Fcrn antibodies and methods of use thereof

Abstract

Composition and methods for treating an autoimmune disease in a subject in need thereof, the method comprising subcutaneously administering nipocalimab to the subject.

Description

FCRN ANTIBODIES AND METHODS OF USE THEREOFCROSS REFERENCE TO RELATED APPLICATIONS

[0001] This application claims priority to U.S. Provisional Application No. 63 / 770,795, filed on March 12, 2025, and U.S. Provisional Application No. 63 / 987,168, filed on February 20, 2026, the disclosure of each of which is hereby incorporated by reference in its entirety.SEQUENCE LISTING

[0002] The instant application contains a sequence listing which is being submitted herewith electronically in xml format and is hereby incorporated by reference in its entirety. Said xml copy, created on March 6, 2026, is named 103693004420_SequenceListing_ST26.xml and is 10,585 bytes in size.BACKGROUND

[0003] Therapeutic proteins, e.g., therapeutic antibodies, have rapidly become a clinically important drug class for patients with immunological diseases. Numerous autoimmune and alloimmune diseases are mediated by pathogenic antibodies. There exists a need for novel methods of treating immunological diseases.SUMMARY

[0004] The present disclosure provides a method of treating an autoimmune disease in a subject in need thereof, the method comprising subcutaneously administering nipocalimab to the subject at a dose from about 1000 mg to about 2000 mg every two weeks, or a dose from about 400 mg to about 600 mg every week.

[0005] The present disclosure provides a method of reducing serum IgG in a subject in need thereof, the method comprising administering nipocalimab to the subject at a dose from about 1000 mg to about 2000 mg every two weeks, or a dose from about 400 mg to about 600 mg every week, wherein the administration of nipocalimab reduce serum IgG in the subject by at least 60% from baseline serum IgG, at least 65% from baseline serum IgG, at least 70% from baseline serum IgG, at least 75% from baseline serum IgG, or at least 80% from baseline serum IgG.103693.004420\4914-0795-9446.2DOCKET NO.: 103693.004420 (MPI6028WOPCT1)

[0006] The present disclosure provides a method of treating generalized myasthenia gravis (gMG) in a subject in need thereof, the method comprising subcutaneously administering nipocalimab to the subject at a dose from about 1000 mg to about 2000 mg every two weeks, or a dose from about 400 mg to about 600 mg every week.

[0007] The present disclosure provides a method of treating warm autoimmune hemolytic anemia (wAIHA) in a subject in need thereof, the method comprising subcutaneously administering nipocalimab to the subject at a dose from about 1000 mg to about 2000 mg every two weeks, or a dose from about 400 mg to about 600 mg every week.

[0008] The present disclosure provides a method of treating chronic inflammatory demyelinating polyneuropathy (CIDP) in a subject in need thereof, the method comprising subcutaneously administering nipocalimab to the subject at a dose from about 1000 mg to about 2000 mg every two weeks, or a dose from about 400 mg to about 600 mg every week.

[0009] The present disclosure provides a method of treating idiopathic inflammatory myopathies (IIM) in a subject in need thereof, the method comprising subcutaneously administering nipocalimab to the subject at a dose from about 1000 mg to about 2000 mg every two weeks, or a dose from about 400 mg to about 600 mg every week.

[0010] The present disclosure provides a pharmaceutical product, comprising a therapeutic agent, comprising: a bi-weekly dose from about 1000 mg to about 2000 mg of nipocalimab; or a weekly dose from about 400 mg to about 600 mg of nipocalimab; and a subcutaneous injection device, comprising: a container configured to contain the therapeutic agent; a discharge nozzle sized to deliver the therapeutic agent to a subject subcutaneously; and a driver configured to drive the therapeutic agent from the container and out of the discharge nozzle.DESCRIPTION OF THE DRAWINGS

[0011] The following description of the illustrative examples may be better understood when read in conjunction with the appended drawings. It is understood that potential examples of the disclosed systems and methods are not limited to those depicted.

[0012] FIG. 1 is a schematic overview of the CIDP study.-2- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)

[0013] FIG. 2 is the gMG trial profile. The primary efficacy analysis dataset included all randomly assigned patients who received at least one dose (partial or complete) of study drug in the double-blind phase and were antibody-positive for a generalized myasthenia gravis-related pathogenic antibody (antibodies to acetylcholine receptor, anti-muscle-specific tyrosine kinase, or anti-lipoprotein-related protein receptor 4), confirmed before randomization. The safety analysis dataset included all randomly assigned patients who received at least one dose (partial or complete) of either study drug in the double-blind phase (including both antibody-positive and antibodynegative patients). *49 patients did not meet one or more of the study inclusion or exclusion criteria.

[0014] FIG. 3A and FIG.3B are graphs of MG-ADL and QMG least-squares mean change from baseline (SE) over 24 weeks. Symbols represent least squares mean at each timepoint and error bars represent the SE. A significantly greater average reduction from baseline in MG-ADL total score was observed over weeks 22, 23, and 24 for the nipocalimab group (least squares mean change -4-70 [SE 0-329]) than for the placebo group (-3-25 [0-335]), with least-squares mean difference from placebo of-1 -45 (95% CI -2-38 to -0-52, p=0 0024). A significantly greater average reduction from baseline in QMG total score was observed over weeks 22 and 24 for the nipocalimab group (least-squares mean change -4-86 [SE 0-504]) than for the placebo group (-2 05 [0-499]) with least-squares mean difference from placebo of -2-81 (95% CI -4-22 to -1-41; p=0-00012). MG-ADL total score ranges from 0 to 24; a higher score indicates greater symptom severity. QMG total score ranges from 0 to 39; a higher score indicates greater symptom severity. Negative change in score indicates improvement. MG-ADL=Myasthenia Gravis-Activities of Daily Living. QMG=Quantitative Myasthenia Gravis. SE=standard error. SOC=standard of care.

[0015] FIG. 4 is a graph of MG-ADL responder endpoints. Improvements of at least 2 points (response) and at least 50% are based on average improvement over weeks 22, 23, and 24. Early response is at least a 2-point improvement at week 1, week 2, or week 1 and 2. Response from weeks 4 to 24 is at least a 2-point improvement from week 4 to week 24 with up to two non-consecutive excursions from week 6 to week 23. p values from the Cochran-Mantel-Haenszel test controlling for baseline MG-ADL total score (<9 or >9), antibody status, and region. The p values were not reported for response (from weeks 4-24) or at least 50% improvement (weeks 22-24) because the preceding comparison in the hierarchy (ie, early response [week 1, week 2, or week 1 and 2] was not statistically significant at a two-sided a of 0-05). MG-ADL=Myasthenia Gravis-Activities of Daily Living. SOC=standard of care.-3- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)

[0016] FIG. 5 is a graph of Median (IQR) percent change from baseline IgG in the doubleblind phase. Symbols represent the median and error bars the IQR. SOC=standard of care.

[0017] FIG. 6A is a graph of Cumulative Distribution of Improvement in MG-ADL Total Score at Week 24 in an exemplary embodiment.

[0018] FIG. 6B is a graph of Cumulative Distribution of Improvement in QMG Total Score at Week 24 in an exemplary embodiment.

[0019] FIG. 7 is a schematic overview of the IIM study of an exemplary embodiment.

[0020] FIG. 8 is a schematic overview of the wAIHA study of an exemplary embodiment.

[0021] FIG. 9 is a graph of the mean (±SD) serum nipocalimab concentration versus time by Cohort and Day / Week.

[0022] FIG. 10 is a graph of the mean (±SD) serum nipocalimab concentration versus time by Cohort and Day / Week.

[0023] FIG. 11 is a graph of the mean (±SD) serum nipocalimab concentration versus time by Cohort and Day / Week.

[0024] FIG. 12 is a graph of the mean (±SD) serum nipocalimab concentration versus time by Cohort and Day / Week.

[0025] FIG. 13 is a graph of the median (IQR) percent change from baseline of total serum IgG over time through Day 50 (IQR= Interquartile Range).

[0026] FIG. 14A-14C is a panel of graphs showing the predicted free drug concentration, total serum IgG % change from baseline, and MG-ADL placebo-corrected change from baseline for the population following intravenous (IV) 15mg / kg Q2W (with 30mg / kg loading dose) and subcutaneous (SC) 1500mg Q2W (without loading dose).

[0027] FIG. 15A-15C is a panel of graphs showing the predicted free drug concentration, total serum IgG % change from baseline, and MG-ADL placebo-corrected change from baseline for the population following IV 15mg / kg Q2W (with 30mg / kg loading dose) and SC 1500mg Q2W (with 3000mg loading dose).-4- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)

[0028] FIG. 16A-16C is a panel of graphs showing the predicted free drug concentration, total serum IgG % change from baseline (CFB), and MG-ADL placebo-corrected change from baseline for the population following IV 15mg / kg Q2W (with 30mg / kg loading dose) and SC 518mg QW (without loading dose).

[0029] FIG. 17 shows a drug product according to one example that comprises a syringe containing a therapeutic agent of this disclosure.

[0030] FIG. 18 shows a drug product according to one example that comprises a syringe supported in a housing, the syringe containing a therapeutic agent of this disclosure.

[0031] FIG. 19 shows a drug product according to one example that comprises an autoinjector having a cartridge containing a therapeutic agent of this disclosure.

[0032] FIG. 20 shows a drug product according to one example that comprises an autoinjector having a syringe containing a therapeutic agent of this disclosure.

[0033] FIG. 21 shows a perspective view drug product according to one example that comprises an on-body delivery system having a container that contains a therapeutic agent of this disclosure.

[0034] FIG. 22 shows a perspective view of the drug product of FIG. 21 with the container removed.

[0035] FIG. 23 shows a side view of the drug product of FIG. 21.

[0036] FIG. 24 shows a simplified schematic of the drug product of FIG. 21 according to one example.

[0037] FIG. 25 shows a simplified schematic of the drug product of FIG. 21 according to another example.

[0038] FIG. 26 is a schematic overview of the Phase 2 / 3 wAIHA study described in Example 7.

[0039] FIG. 27 is a bar chart showing the proportion of participants each of the three groups (placebo, 15 mg / kg q2w, and 30 mg / kg q4w) that achieved durable response.-5- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)

[0040] FIG. 28 is a graph showing the time to durable Hemoglobin (Hgb) response during the double-blind (DB) period in each of the three groups (placebo, 15 mg / kg q2w, and 30 mg / kg q4w).

[0041] FIG. 29 is a graph showing the mean change from baseline in Hgb values by visit through Week 24.

[0042] FIG. 30 is a plot showing the percentage of participants who achieved sustained Hgb response in each of the three groups (placebo, 15 mg / kg q2w, and 30 mg / kg q4w).

[0043] FIG. 31 is a graph showing change from baseline in FACIT-Fatigue total score at the time of durable Hgb response.

[0044] FIG. 32 is a plot showing mean change from baseline in FACIT-Fatigue total scores by visit through Week 24.

[0045] FIG. 33 is a plot showing the mean (+ / - SE) values for albumin laboratory values over time in DB period.

[0046] FIG. 34A is a plot showing the mean (+ / - SE) percent change from baseline values for fasting total cholesterol laboratory values over time in DB period.

[0047] FIG. 34B is a plot showing the mean (+ / - SE) percent change from baseline values for HDL laboratory values over time in DB period.

[0048] FIG. 34C is a plot showing the mean (+ / - SE) percent change from baseline values for LDL laboratory values over time in DB period.

[0049] FIG. 35A is a plot showing the mean (+ / - SE) percent change from baseline values for fasting total cholesterol laboratory values over time in DB and open label extension (OLE) periods combined.

[0050] FIG. 35B is a plot showing the mean (+ / - SE) percent change from baseline values for HDL laboratory values over time in DB and OLE periods combined.

[0051] FIG. 35C is a plot showing the mean (+ / - SE) percent change from baseline values for LDL laboratory values over time in DB and OLE periods combined.-6- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)

[0052] FIG. 36 is a plot showing median (+ / - IQR) percent change from baseline values for total Immunoglobulin G (IgG) in DB Period.

[0053] FIG. 37 is a plot showing median (+ / - IQR) percent change from baseline values for pathogenic autoantibodies in DB Period.

[0054] FIG. 38 is a plot showing mean change from baseline in Hgb level (g / dL) among responders within 15 mg / kg q2w group (15 mg / kg q2w-R), non-responders within 15 mg / kg q2w group (15 mg / kg q2w - NR); responders within 30 mg / kg q4w group (30 mg / kg q4w - R); and non-responders within 30 mg / kg q4w group (30 mg / kg q4w - NR).

[0055] FIG. 39A is a plot comparing mean indirect bilirubin and mean Hgb between responders and non-responders within 15 mg / kg q2w group.

[0056] FIG. 39B is a plot comparing mean indirect bilirubin and mean Hgb between responders and non-responders within 30 mg / kg q4w group.

[0057] FIG. 40 is a chart showing mean improvement in FACIT-Fatigue total score between responders and non-responders.

[0058] FIG. 41 is a schematic overview of phase 3 study including the SC Substudy described in Example 8.

[0059] FIG. 42 is a graph showing the visit schedule of the SC Substudy in Example 8.

[0060] FIG. 43 is a plot showing mean change of IMACS FIS from baseline through Week 52 among patients in nipocalimab group and placebo group.

[0061] FIG. 44 is a plot showing mean change of PROMIS -PF-20 from baseline through Week 52 among patients in nipocalimab group and placebo group.

[0062] FIG. 45 is a plot showing mean change of MMT-8 from baseline through Week 52 among patients in nipocalimab group and placebo group.

[0063] FIG. 46 is a plot showing mean change of PhGA from baseline through Week 52 among patients in nipocalimab group and placebo group.-7- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)

[0064] FIG. 47 is a plot showing mean change of PtGA from baseline through Week 52 among patients in nipocalimab group and placebo group.

[0065] FIG. 48 is a plot showing mean change of MDAAT from baseline through Week 52 among patients in nipocalimab group and placebo group.

[0066] FIG. 49 is a plot showing mean change of HAQ-DI from baseline through Week 52 among patients in nipocalimab group and placebo group.

[0067] FIG. 50 is a plot showing mean change of muscle enzyme CK from baseline through Week 52 among patients in nipocalimab group and placebo group.

[0068] FIG. 51 is a plot showing mean change of muscle enzyme ALT from baseline through Week 52 among patients in nipocalimab group and placebo group.

[0069] FIG. 52 is a plot showing mean change of muscle enzyme AST from baseline through Week 52 among patients in nipocalimab group and placebo group.

[0070] FIG. 53 is a plot showing mean change of muscle enzyme LDH from baseline through Week 52 among patients in nipocalimab group and placebo group.

[0071] FIG. 54 is a plot showing mean change of muscle enzyme aldolase from baseline through Week 52 among patients in nipocalimab group and placebo group.

[0072] FIG. 55 is a plot showing mean change of total IgG from baseline through Week 52 among patients in nipocalimab group and placebo group.

[0073] FIG. 56 is a plot showing mean change of myositis specific autoantibodies (MSA) from baseline through Week 52 among patients in nipocalimab group and placebo group.

[0074] FIG. 57 is a graph showing IgG % change from baseline for 2*518 mg SC LD, 518 mg QW from week 1 and 30 mg / kg Q4W IV. The medians from 1000 simulated patients are presented.

[0075] FIG. 58 is a graph showing Hgb (g / dL) increase from baseline for 2*518 mg SC LD, 518 mg QW from week 1 and 30 mg / kg Q4W IV. The medians from 1000 simulated patients are presented.-8- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)

[0076] FIG. 59 is a graph showing IgG % change from baseline for 2*518 mg SC LD, 518 mg QW from week 1, 30 mg / kg Q4W IV, and 518 mg QW from week 0. The medians from 1000 simulated patients are presented.

[0077] FIG. 60 is a graph showing Hgb (g / dL) increase from baseline for 2*518 mg SC LD, 518 mg QW from week 1, 30 mg / kg Q4W IV, and 518 mg QW from week 0. The medians from 1000 simulated patients are presented.

[0078] FIG. 61 is a panel of graphs showing nipocalimab concentration (pg / mL) (FIG. 61 A), unoccupied receptor (%) (FIG. 6 IB), and IgG percent change from baseline (%) (FIG. 61C) over the weeks since the first dose for 460 mg QW, 518 mg QW, and 15 mg / kg Q2W dosing regimens.

[0079] FIG. 62 is a graph showing lipid ratio to baseline changes over the weeks since the first dose for 460 mg QW, 518 mg QW, and 15 mg / kg Q2W dosing regimens.

[0080] FIG. 63 is a graph showing IgG percent change from baseline (%) over the weeks since the first dose for 2*460 mg SC LD, 460 mg QW from week 1 and 2*518 mg SC LD, 518 mg QW from week 1 dosing regimens.

[0081] FIG. 64 is a graph showing IMACS FIS score over the weeks since the first dose for 2*460 mg SC LD, 460 mg QW from week 1, 460 mg QW from week 0, 2*518 mg SC LD, 518 mg QW from week 1, 518 mg QW from week 0 dosing regimens.DETAILED DESCRIPTIONCertain Terminology

[0082] As used herein and in the appended claims, the singular forms “a”, “an” and “the” include plural reference unless the context clearly dictates otherwise.

[0083] As used herein, the term “about” means that the numerical value is approximate and small variations would not significantly affect the practice of the disclosed embodiments. Where a numerical limitation is used, unless indicated otherwise by the context, “about” means the numerical value can vary by ±10% and remain within the scope of the disclosed embodiments.-9- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)

[0084] As used herein, the terms “comprising” (and any form of comprising, such as “comprise”, “comprises”, and “comprised”), “having” (and any form of having, such as “have” and “has”), “including” (and any form of including, such as “includes” and “include”), or “containing” (and any form of containing, such as “contains” and “contain”), are inclusive or open-ended and do not exclude additional, unrecited elements or method steps. Any composition or method that recites the term “comprising” should also be understood to also describe such compositions as consisting, consisting of, or consisting essentially of the recited components or elements.

[0085] As used herein, the term “individual,” “subject,” or “patient,” can be used interchangeably, means any animal, including mammals, such as mice, rats, other rodents, rabbits, dogs, cats, swine, cattle, sheep, horses, or primates, such as humans. As used herein, the term “mammal” means a rodent (i.e., a mouse, a rat, or a guinea pig), a monkey, a cat, a dog, a cow, a horse, a pig, or a human. In some embodiments, the mammal is a human.

[0086] As used herein, the phrase “in need thereof’ means that the subject has been identified as having a need for the particular method or treatment. In some embodiments, the identification can be by any means of diagnosis. In any of the methods and treatments described herein, the subject can be in need thereof. In some embodiments, the subject is in an environment or will be traveling to an environment in which a particular disease, disorder, or condition is prevalent.

[0087] As used herein, the term “therapeutically effective amount” refers to an amount, e.g., pharmaceutical dose, effective in inducing a desired biological effect in a subject or patient or in treating a patient having a condition or disorder described herein. It is also to be understood herein that a “therapeutically effective amount” may be interpreted as an amount giving a desired therapeutic effect, either taken in one dose or in any dosage or route, taken alone or in combination with other therapeutic agents.

[0088] As used herein, the term “no more than” refers to an amount that is less than equal to. This may be an amount in integers. For example, no more than two substitutions can refer to 0, 1, or 2 substitutions.

[0089] As used herein, the terms “treatment” or “treating” refer to reducing, decreasing, decreasing the risk of, or decreasing the side effects of a particular disease or condition. Reducing,-10- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)decreasing, decreasing the risk of, or decreasing the side effects of are relative to a subject who did not receive treatment, e.g., a control, a baseline, or a known control level or measurement.

[0090] As used herein, the term “bi-weekly” refers to one dose administered every two weeks. As used herein, the term “weekly” refers to one dose administered every one week.

[0091] As used herein, the term “baseline” in reference to amount, concentration or level of a molecule refers to the amount, concentration, or level of the molecule prior to the administration of a therapeutic (e.g., antibody) provided for herein. For example, baseline may refer to the time prior to the initial anti-FcRn antibody administration. As another example, baseline may refer to serum IgG prior to the initial anti-FcRn antibody administration. As another example, baseline may refer to serum albumin prior to the initial anti-FcRn antibody administration. As another example, baseline may refer to an International Myositis Assessment and Clinical Studies Total Improvement Score (IMACS TIS) prior to the initial anti-FcRn antibody administration.

[0092] As used herein, the term “initial anti-FcRn antibody administration” refers to the administration of the very first dose of the anti-FcRn antibody. For example, in cases where a loading dose of the anti-FcRn antibody is administered, the term refers to the administration of the loading dose of the anti-FcRn antibody. As another example, in cases where no loading dose is administered, the term refers to the administration of the first dose of the anti-FcRn antibody.

[0093] As used herein, the term “change” in reference to a baseline refers to a subject having an improvement as compared to that subject’s conditions, scores, symptoms, and the like prior to being treated with the anti-FcRn antibodies as provided for herein.

[0094] As used herein, the term “sustained” refers to a clinical benefit that is maintained at or above the specified level continuously over the specified period. When it is stated that a clinical benefit is sustained for a period of time (i.e., 28 days), it is meant that the clinical benefit is maintained for such period of time (i.e., 28 days) starting from the time the clinical benefit is first achieved.

[0095] As used herein, the term “pharmaceutical composition” refers to a medicinal or pharmaceutical formulation that contains an active ingredient as well as one or more excipients and diluents to enable the active ingredient suitable for the method of administration. The pharmaceutical composition of the present disclosure includes pharmaceutically acceptable -11- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)components that are compatible with the anti-FcRn antibody. The pharmaceutical composition may be in aqueous form for intravenous or subcutaneous administration or in tablet or capsule form for oral administration. In some embodiments, the composition is suitable for intravenous administration. In some embodiments, the composition is suitable for subcutaneous administration.

[0096] As used herein, the term “pharmaceutically acceptable carrier” refers to an excipient or diluent in a pharmaceutical composition. The pharmaceutically acceptable carrier must be compatible with the other ingredients of the formulation and not deleterious to the recipient. In the present disclosure, the pharmaceutically acceptable carrier must provide adequate pharmaceutical stability to the Fc construct. The nature of the carrier differs with the mode of administration. For example, for intravenous administration, an aqueous solution carrier is generally used; for oral administration, a solid carrier is preferred.Anti-FcRn antibodies

[0097] The term “antibody” herein is used in the broadest sense and encompasses various antibody structures, including but not limited to monoclonal antibodies, polyclonal antibodies, multispecific antibodies (e.g., bispecific antibodies), scFVs, nanobodies, VHH, and antibody fragments so long as they exhibit FcRn antigen-binding activity.

[0098] Additionally, antibody or antibody molecule, as that term is used herein, refers to a polypeptide, e.g., an immunoglobulin chain or fragment thereof, comprising at least one functional immunoglobulin variable domain sequence. An antibody molecule encompasses antibodies (e.g., full-length antibodies) and antibody fragments.

[0099] Immunoglobulin chains exhibit the same general structure of relatively conserved framework regions (FR) joined by three hypervariable regions, also called complementarity determining regions or CDRs. The CDRs from the two chains of each pair are aligned by the framework regions, enabling binding to a specific epitope. From N-terminus to C-terminus, both light and heavy chains comprise the domains FR1, CDR1, FR2, CDR2, FR3, CDR3 and FR4. The assignment of amino acids to each domain is in accordance with the definitions of Kabat Sequences of Proteins of Immunological Interest (National Institutes of Health, Bethesda, Md. (1987 and 1991)), or Chothia & Lesk J. Mol. Biol. 196:901-917 (1987); Chothia et al. Nature 342:878-883 (1989). In some embodiments, the antibodies provided herein comprise the same FRs and different-12- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)CDRs. In some embodiments, the antibodies provided herein comprise the same CDRs and different FRs. In some embodiments, mutations in the FR are in the heavy chain. In some embodiments, mutations in the FR are in the FR1 of the heavy chain. In some embodiments, mutations in the FR are in the FR2 of the heavy chain. In some embodiments, mutations in the FR are in the FR3 of the heavy chain. In some embodiments, mutations in the FR are in the FR4 of the heavy chain. In some embodiments, mutations in the FR are in the light chain. In some embodiments, mutations in the FR are in the FR1 of the light chain. In some embodiments, mutations in the FR are in the FR2 of the light chain. In some embodiments, mutations in the FR are in the FR3 of the light chain. In some embodiments, mutations in the FR are in the FR4 of the light chain. In some embodiments, mutations in the FR are in the heavy and light chains. In some embodiments, mutations in the FR are in any one or more of the FRs of the heavy and light chains.

[0100] As used herein, the terms “variable region” and “variable domain” refer to the portions of the light and heavy chains of an antibody that include amino acid sequences of complementary determining regions (CDRs, e g., CDRL1, CDRL2, CDRL3, CDRH1, CDRH2, and CDRH3) and framework regions (FRs). According to the methods used in this disclosure, the amino acid positions assigned to CDRs and FRs are defined according to Kabat (Sequences of Proteins of Immunological Interest, 5th Ed. Public Health Service, National Institutes of Health, Bethesda, MD. (1991)). Using this numbering system, the actual linear amino acid sequence may contain fewer or additional amino acids corresponding to a shortening of, or insertion into, a CDR (defined further herein) or FR (defined further herein) of the variable region. For example, a heavy chain variable region may include a single inserted residue (i.e., residue 52a according to Kabat) after residue 52 of CDRH2 and inserted residues (i.e., residues 82a, 82b, 82c, etc. according to Kabat) after residue 82 of heavy chain FR. The Kabat numbering of residues may be determined for a given antibody by alignment at regions of homology of the sequence of the antibody with a “standard” Kabat numbered sequence.

[0101] As used herein, the terms “complementary determining regions” and “CDRs” refer to the regions of an antibody variable domain or variable region which are hypervariable in sequence and / or form structurally defined loops. A CDR is also known as a hypervariable region. The light chain and heavy chain variable regions each have three CDRs. The light chain variable region contains CDR LI, CDR L2, and CDR L3. The heavy chain variable region contains CDR Hl, CDR H2, and CDR H3. Each CDR may include amino acid residues from a complementarity determining -13- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)region as defined by Kabat (i.e., about residues 24-34 (CDRL1), 50-56 (CDRL2) and 89-97 (CDR L3) in the light chain variable region and about residues 31-35 (CDR Hl), 50-65 (CDR H2) and 95-102 (CDR H3) in the heavy chain variable region.

[0102] As used herein, the term “FcRn” refers a neonatal Fc receptor that binds to the Fc region of an IgG antibody, e.g., an IgGl antibody. An exemplary FcRn is human FcRn having UniProt ID No. P55899, which is hereby incorporated by reference in its entirety. Without being bound to any particular theory, human FcRn is believed to be responsible for maintaining the half-life of IgG by binding and trafficking constitutively internalized IgG back to the cell surface for the recycling of IgG.

[0103] In some embodiments, the anti-FcRn antibody comprises a heavy chain or light chain. In some embodiments, the anti-FcRn antibody comprises a heavy chain and a light chain in a scFv format. In some embodiments, the heavy and light chain are linked with a peptide linker, such a glycine / serine or glycine / alanine linker.

[0104] In some embodiments, the anti-FcRn antibody is nipocalimab, which can also be referred to as M281. Nipocalimab is an antibody that binds to human neonatal Fc receptor (FcRn). Nipocalimab is described in US Patent No. 10,676,526, PCT Publication No. W02020 / 023310, PCT Publication No. W02020 / 018910, each of which are hereby incorporated by reference in their entirety.

[0105] FcRn is a type I transmembrane protein that functions as an IgG- and serum albuminbinding, intracellular vesicular trafficking protein. FcRn is expressed in endothelial cells, luminal epithelial cells, hepatocytes, podocytes, granulocytes, monocytes, macrophages, dendritic cells, and NK cells, but not on B or T cells. FcRn maintains the half-life of IgG by binding and trafficking constitutively internalized IgG back to the cell surface. Binding of both Fc and serum albumin by FcRn occurs in the early endosome at pH 6.0, followed by sorting of the FcRn into vesicles, which traffic the FcRn-bound IgG or albumin back to the cell surface where FcRn rapidly releases the IgG or albumin at pH 7.4. This trafficking cycle maintains the half-life of IgG and albumin by recycling both into the circulation and preventing trafficking to the lysosomes for degradation. FcRn also captures internalized IgGFc in epithelial cells and transports them bidirectionally to the opposing apical or basolateral membranes. This function allows IgG to traffic to the lumen of organs such as-14- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)the gastrointestinal tract or the transport of IgG or IgG-antigen complexes from the lumen to the vasculature or lymphoid tissues in the stromal layers.

[0106] The present disclosure provides isolated anti-FcRn antibodies that bind to human FcRn with high affinity. The anti-FcRn antibodies compete with and effectively inhibit the binding of other anti-FcRn antibodies (e.g., IgG, IgG autoantibodies) to FcRn, thereby increasing the catabolism and decreasing the half-life of other anti-FcRn antibodies (e.g., IgG, IgG autoantibodies). The anti-FcRn antibodies may be used in a method of treating or reducing immune complex-based activation of an immune response in a subject, such as an immune response caused by autoantibodies in an autoimmune disease.

[0107] In some embodiments, the anti-FcRn antibody used herein comprises or consists of: a light chain comprising or consisting of the sequence:QSALTQPASVSGSPGQSITISCTGTGSDVGSYNLVSWYQQHPG KAPKLMIYGDSERPSGVSNRFSGSKSGNTASLTISGLQAEDEA DYYCSSYAGSGIYVFGTGTKVTVLGQPKAAPSVTLFPPSSEEL QANKATLVCLISDFYPGAVTVAWKADSSPVKAGVETTTPSKQ SNNKYAASSYLSLTPEQWKSHKSYSCQVTHEGSTVEKTVAPT ECS (SEQ ID NO: 1);

[0108] and a heavy chain comprises or consists of the sequence:EVQLLESGGGLVQPGGSLRLSCAASGFTFSTYAMGWVRQAPG KGLEWVSSIGASGSQTRYADSVKGRFTISRDNSKNTLYLQMN SLRAEDTAVYYCARLAIGDSYWGQGTMVTVSSASTKGPSVFP LAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTF P A VLQ S S GLYSLS S WTVPS S SLGTQT YICNVNHKPSNTKVDK KVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTP EVTCVVVDVSHEDPEVI<FNWYVDGVEVHNAI<TI<PREEQYAS TYRVVSVLTVLHQDWLNGI<EYI<CI<VSNI<ALPAPIEI<TISI<AI< GQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWES NGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSC SVMHEALHNHYTQKSLSLSPG (SEQ ID NO: 2).

[0109] In some embodiments, the anti-FcRn antibody used herein comprises (a) a light chain comprising complementary determining region (CDR) LI, CDRL2, and CDRL3 and (b) a heavy chain comprising CDR Hl, CDR H2, and CDR H3, wherein the CDR LI comprises the sequence TGTGSDVGSYNLVS (SEQ ID NO: 3), the CDRL2 comprises the sequence GDSERPS (SEQ ID NO: 4), the CDR L3 comprises the sequence SSYAGSGIYV (SEQ ID NO: 5), the CDR Hl-15- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)comprises the sequence TYAMG (SEQ ID NO: 6), the CDR H2 comprises the sequence SIGASGSQTRYADS (SEQ ID NO: 7), and the CDRH3 comprises the sequence LAIGDSY (SEQ ID NO: 8). In some embodiments, the anti-FcRn antibody used herein comprises: (a) a light chain sequence that is at least 95%, 96%, 97% 98%, or 99% identical to SEQ ID NO: 1 and comprises the CDR LI (SEQ ID NO: 3), the CDR L2 (SEQ ID NO: 4), the CDR L3 (SEQ ID NO: 5); and (b) a heavy chain sequence that is at least 95%, 96%, 97% 98%, or 99% identical to SEQ ID NO: 2 and comprises the CDR Hl (SEQ ID NO: 6), the CDR H2 (SEQ ID NO: 7), and the CDR H3 SEQ ID NO: 8).

[0110] In some embodiments, the heavy chain of the anti-FcRn antibody used herein comprises an amino acid sequence at least 95%, 96%, 97% 98%, or 99% identical to SEQ ID NO: 2 with one or more of the following amino acid substitutions: A23V, S30R, L80V, A84T, E85D, A93V, relative to the sequence of SEQ ID NO: 2. In some embodiments, the light chain of the anti-FcRn antibody comprises an amino acid sequence at least 95%, 96%, 97% 98%, or 99% identical the amino acid sequence of SEQ ID NO: 1 with one or more of the following amino acid substitutions: Q38H, V58I, and G99D, relative to the sequence of SEQ ID NO: 1.

[0111] In some embodiments, the anti-FcRn antibody used herein comprises a light chain variable region comprising an amino acid sequence that is at least 95%, 97%, 99%, or 100% identical to:QSALTQPASVSGSPGQSITISCTGTGSDVGSYNLVSWYQQHPGKAPKLMIYGDSERPSGVSN RFSGSKSGNTASLTISGLQAEDEADYYCSSYAGSGIYVFGTGTKVTVL (SEQ ID NO: 9). In some embodiments, the light chain variable region comprises the CDR LI (SEQ ID NO: 3), the CDR L2 (SEQ ID NO: 4), the CDR L3 (SEQ ID NO: 5). In some embodiments, the anti-FcRn antibody used herein comprises a heavy chain variable region comprising an amino acid sequence that is at least 95%, 97%, 99%, or 100% identical to:EVQLLESGGGLVQPGGSLRLSCAASGFTFSTYAMGWVRQAPGKGLEWVSSIGASGSQTRY ADSVKGRFHSRDNSKNTLYLQMNSLRAEDTAVYYCARLAIGDSYWGQGTMVTVSS (SEQ ID NO: 10). In some embodiments, the heavy chain variable region contains the CDR Hl (SEQ ID NO: 6), the CDR H2 (SEQ ID NO: 7), and the CDR H3 (SEQ ID NO: 8).

[0112] In some embodiments, the light chain of the anti-FcRn antibody used herein comprises a sequence having at least 90% identity to the sequence of SEQ ID NO: 1.-16- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)

[0113] In some embodiments, the heavy chain of the anti-FcRn antibody used herein comprises a sequence having at least 90% identity to the sequence of SEQ ID NO: 2.

[0114] In some embodiments, the anti-FcRn antibody used herein has a light chain and a heavy chain, wherein the light chain comprises a sequence having at least 90%, 95%, 98% or 99% identity to the sequence of SEQ ID NO: 1, and the heavy chain comprises a sequence having at least 90%, 95%, 98% or 99% identity to the sequence of SEQ ID NO: 2.

[0115] As used herein, the term “percent (%) identity” refers to the percentage of amino acid (or nucleic acid) residues of a candidate sequence, e.g., an anti-FcRn antibody of the disclosure, that are identical to the amino acid (or nucleic acid) residues of a reference sequence, e.g., a wild-type anti-FcRn antibody, after aligning the sequences and introducing gaps, if necessary, to achieve the maximum percent identity (i.e., gaps can be introduced in one or both of the candidate and reference sequences for optimal alignment and non-homologous sequences can be disregarded for comparison purposes). Alignment for purposes of determining percent identity can be achieved in various ways that are within the skill in the art, for instance, using publicly available computer software such as BLAST, ALIGN, or Megalign (DNASTAR) software. Those skilled in the art can determine appropriate parameters for measuring alignment, including any algorithms needed to achieve maximal alignment over the full length of the sequences being compared. In some embodiments, the percent amino acid (or nucleic acid) sequence identity of a given candidate sequence to, with, or against a given reference sequence (which can alternatively be phrased as a given candidate sequence that has or includes a certain percent amino acid (or nucleic acid) sequence identity to, with, or against a given reference sequence) is calculated as follows:100 x (fraction of A / B)where A is the number of amino acid (or nucleic acid) residues scored as identical in the alignment of the candidate sequence and the reference sequence, and where B is the total number of amino acid (or nucleic acid) residues in the reference sequence. In some embodiments where the length of the candidate sequence does not equal to the length of the reference sequence, the percent amino acid (or nucleic acid) sequence identity of the candidate sequence to the reference sequence would not equal to the percent amino acid (or nucleic acid) sequence identity of the reference sequence to the candidate sequence.-17- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)

[0116] In some embodiments, a reference sequence aligned for comparison with a candidate sequence may show that the candidate sequence exhibits from 50% to 100% identity across the full length of the candidate sequence or a selected portion of contiguous amino acid (or nucleic acid) residues of the candidate sequence. The length of the candidate sequence aligned for comparison purpose is at least 30%, e.g., at least 40%, e.g., at least 50%, 60%, 70%, 80%, 90%, or 100% of the length of the reference sequence. When a position in the candidate sequence is occupied by the same amino acid (or nucleic acid) residue as the corresponding position in the reference sequence, then the molecules are identical at that position. A position may be altered by a substitution, deletion, or insertion. A substitution, deletion, or insertion may comprise a certain number of amino acids, (e.g., 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, or more). When describing a substitution, deletion, or insertion of no more than n amino acids, this is meant that the substitution, deletion, or insertion comprises, e.g., 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, or n amino acids. The number or substitutions, deletions, or insertions can comprise a percent of the total sequence (e.g., 1%, 5%, 10%, 15%, 20%, or more) where the number of substitutions, deletions, or insertions alters 5%, 10%, 15%, 20% or more, of the amino acids in the total sequence.

[0117] In some embodiments of all the methods described herein, the Fc domain of the antibody is not fucosylated. In some embodiments of all the methods described herein, the Fc domain of the antibody is not glycosylated. In some embodiments of all the methods described herein, the antibody lacks effector function. In some embodiments of all the methods described herein, the antibody is an IgGl antibody.Pharmaceutical Compositions and Methods of Administration

[0118] In some embodiments, the methods described herein comprise administering the anti-FcRn antibody to the subject or patient. The terms “subject and “patient” can be used interchangeably. In some embodiments, the antibody is administered as part of a pharmaceutical composition comprising 5-60 mg / ml of the antibody.

[0119] As provided for herein, in some embodiments, pharmaceutical compositions comprising an anti-FcRn antibody are provided. In some embodiments, pharmaceutical compositions comprising an anti-FcRn antibody for administration to a patient suffering from autoimmune disease wherein the anti-FcRn antibody is administered to the patient in a therapeutically effective amount from about 1000 mg to about 2000 mg every 2 weeks are provided. In some embodiments,-18- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)pharmaceutical compositions comprising an anti-FcRn antibody for administration to a patient suffering from autoimmune disease wherein the anti-FcRn antibody is administered to the patient in a therapeutically effective amount from about 400 mg to about 600 mg every week are provided. In some embodiments, pharmaceutical compositions comprising an anti-FcRn antibody for administration to a patient suffering from autoimmune disease who previously received at least one therapy, wherein the anti-FcRn antibody is administered to the patient in a therapeutically effective amount from about 1000 mg to about 2000 mg every 2 weeks are provided. In some embodiments, pharmaceutical compositions comprising an anti-FcRn antibody for administration to a patient suffering from autoimmune disease who previously received at least one therapy, wherein the anti-FcRn antibody is administered to the patient in a therapeutically effective amount from about 400 mg to about 600 mg every week are provided. In some embodiments, the anti-FcRn antibody is nipocalimab.

[0120] In some embodiments, the pharmaceutical compositions of the invention that contain an anti-FcRn antibody as the therapeutic proteins may be formulated for subcutaneous administration. For injectable formulations, various effective pharmaceutical carriers are known in the art. In some embodiments, the formulation is administered with an infusion pump, a patch pump, or a wearable injector. In some embodiments, the formulation is administered with an on-body device. In some embodiments, the formulation is administered using a subcutaneous injection device. In some embodiments, the subcutaneous injection device comprises a container configured to contain the therapeutic agent, a discharge nozzle sized to deliver the therapeutic agent to a subject subcutaneously, and a driver configured to drive the therapeutic agent from the container and out of the discharge nozzle.

[0121] In some embodiments, the composition is administered subcutaneously. In some embodiments, the composition is administered using an infusion pump. In some embodiments, the composition is administered using an auto injector. In some embodiments, the composition is administered using a patch pump injector. In some embodiments, the composition is administered using a wearable injector. In some embodiments, the composition is administered using an on-body device. In some embodiments, the composition is administered using a subcutaneous injection device, comprising a container configured to contain the therapeutic agent, a discharge nozzle sized to deliver the therapeutic agent to a subject subcutaneously, and a driver configured to drive the therapeutic agent from the container and out of the discharge nozzle.-19- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)

[0122] In some embodiments, the pharmaceutical composition comprises a therapeutically effective amount of the anti-FcRn antibody. In some embodiments, the pharmaceutical composition comprises a therapeutically effective amount of the anti-FcRn antibody. In some embodiments, the therapeutically effective amount is from about 400 mg to about 2000 mg, about 400 mg to about 1000 mg, about 600 mg to about 1000 mg, about 600 mg to about 2000 mg, about 400 mg to about 1500 mg, about 1000 mg to about 2000 mg, about 400 mg to about 600 mg of the anti-FcRn antibody. In some embodiments, the therapeutically effective amount is about 400 mg, about 600 mg, about 1000 mg, or about 2000 mg. In some embodiments, the therapeutically effective amount is about 518 mg. In some embodiments, the therapeutically effective amount is about 460 mg.

[0123] In some embodiments, the pharmaceutical composition is administered every week, every two weeks, or monthly. In some embodiments, the pharmaceutical composition is administered every week. In some embodiments, the pharmaceutical composition is administered every two weeks. In some embodiments, the pharmaceutical composition is administered monthly. In some embodiments, the initial dose is different from the every week or once every two weeks dose. In some embodiments, the dose is the same every time it is administered.

[0124] In some embodiments, the antibody or pharmaceutical composition is administered every week. In some embodiments, the antibody or pharmaceutical composition is administered subcutaneously every week via autoinjector (Al). In some embodiments, the antibody or pharmaceutical composition is administered once every two weeks. In some embodiments, the antibody or pharmaceutical composition is administered subcutaneously once every two weeks via on-body device (OBDS).

[0125] In some embodiments, the pharmaceutical composition comprises from about 1000 mg to about 2000 mg the pharmaceutical composition is administered every two weeks. In some embodiments, the pharmaceutical composition comprises from about 400 mg to about 600 mg the pharmaceutical composition is administered every week.

[0126] In some embodiments, the administration of the antibody or pharmaceutical composition takes place over about 30-90 minutes. In some embodiments, the administration takes place over about 15-60 minutes. In some embodiments, the administration takes place in about 15 to about 30 minutes. In some embodiments, the administration takes place in about 15 to about 45 minutes. In some embodiments, the administration takes place in about 15 to about 90 minutes. In -20- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)some embodiments, the administration takes place in about 15 to about 120 minutes. In some embodiments, the administration takes place in about 15 minutes, about 30 minutes, about 45 minutes, about 60 minutes, about 90 minutes, or about 120 minutes.

[0127] In some embodiments, the pharmaceutical composition comprises one or more of sodium phosphate, sodium chloride, trehalose, or polysorbate.Methods of Treatment and Uses

[0128] The present disclosure provides for embodiments for methods of treating autoimmune disorders including, but not limited to, generalized myasthenia gravis (gMG), warm autoimmune hemolytic anemia (wAIHA), chronic inflammatory demyelinating polyneuropathy (CIDP), and idiopathic inflammatory myopathies (IIM), and related symptoms or pathologies associated with the same. In some embodiments, a subject with an autoimmune disorder is treated with an anti-FcRn antibody. In some embodiments, the anti-FcRn antibody is nipocalimab.

[0129] The present disclosure provides a method of treating an autoimmune disease in a subject in need thereof, the method comprising subcutaneously administering nipocalimab to the subject at a dose from about 1000 mg to about 2000 mg every two weeks, or a dose from about 400 mg to about 600 mg every week. In some embodiments, the subject receives a second subcutaneous administration of nipocalimab at a dose from about 400 mg to about 600 mg in the first week. Also provided herein is nipocalimab for use in a method of treating an autoimmune disease in a subject in need thereof, the method comprising subcutaneously administering nipocalimab to the subject at a dose from about 1000 mg to about 2000 mg every two weeks, or a dose from about 400 mg to about 600 mg every week. In some embodiments, the subject receives a second subcutaneous administration of nipocalimab at a dose from about 400 mg to about 600 mg in the first week. Also provided herein is a use of nipocalimab for the manufacture of a medicament for treating an autoimmune disease in a subject in need thereof, the method comprising subcutaneously administering nipocalimab to the subject at a dose from about 1000 mg to about 2000 mg every two weeks, or a dose from about 400 mg to about 600 mg every week. In some embodiments, the subject receives a second subcutaneous administration of nipocalimab at a dose from about 400 mg to about 600 mg in the first week.-21- 103693.004420\4914-0795-9446.2DOCKET NO.: 103693.004420 (MPI6028WOPCT1)

[0130] In some embodiments, nipocalimab is administered every two weeks subcutaneously at a dose from about 1200 mg to about 1800 mg via an on-body device. In some embodiments, nipocalimab is administered every two weeks subcutaneously at a dose from about 1400 mg to about 1600 mg via an on-body device. In some embodiments, nipocalimab is administered every two weeks subcutaneously at a dose about 1500 mg via an on-body device.

[0131] In some embodiments, nipocalimab is administered every week subcutaneously at a dose from about 400 mg to about 600 mg via an auto injector. In some embodiments, the subject receives a second subcutaneous administration of nipocalimab at a dose from about 400 mg to about 600 mg in the first week via an autoinjector. In some embodiments, nipocalimab is administered every week subcutaneously at a dose from about 450 mg to about 550 mg via an autoinjector. In some embodiments, the subject receives a second subcutaneous administration of nipocalimab at a dose from about 450 mg to about 550 mg in the first week via an autoinjector. In some embodiments, nipocalimab is administered every week subcutaneously at a dose of about 518 mg via an autoinjector. In some embodiments, the subject receives a second subcutaneous administration of nipocalimab at a dose of about 518 mg in the first week via an autoinjector. In some embodiments, the subject receives a second subcutaneous administration of nipocalimab at a dose of about 518 mg in the first day via an autoinjector. In some embodiments, nipocalimab is administered every week subcutaneously at a dose of about 460 mg via an autoinjector. In some embodiments, the subject receives a second subcutaneous administration of nipocalimab at a dose of about 460 mg via an autoinjector in the first week. In some embodiments, the subject receives a second subcutaneous administration of nipocalimab at a dose of about 460 mg in the first day via an auto injector.

[0132] In some embodiments, the subject being treated for autoimmune disease has or shows a reduction in one or more immunoglobulin isotypes or total IgG. In some embodiments, the administration of nipocalimab reduce serum IgG in the subject by at least 60% from baseline serum IgG, at least 65% from baseline serum IgG, at least 70% from baseline serum IgG, at least 75% from baseline serum IgG, or at least 80% from baseline serum IgG. In some embodiments, the isotype of immunoglobulins reduced is IgGl, IgG2, IgG3, IgG4, IgA, IgM or IgE, or any combination thereof.

[0133] In some embodiments, the administration of the pharmaceutical composition to the patient does not significantly increase levels of total cholesterol, high-density lipoprotein (HDL), -22- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)calculated low-density lipoprotein (LDL), and triglycerides after administration of the pharmaceutical composition comprising the antibody. In some embodiments, the antibody is nipocalimab. In some embodiments, the administration of the pharmaceutical composition to the patient does not significantly increase levels of total cholesterol after administration of the pharmaceutical composition comprising the antibody. In some embodiments, the administration of the pharmaceutical composition to the patient does not significantly increase levels of high-density lipoprotein (HDL) after administration of the pharmaceutical composition comprising the antibody. In some embodiments, the administration of the pharmaceutical composition to the patient does not significantly increase levels of calculated low-density lipoprotein (LDL) after administration of the pharmaceutical composition comprising the antibody. In some embodiments, the administration of the pharmaceutical composition to the patient does not significantly increase levels of triglycerides after administration of the pharmaceutical composition comprising the antibody. In some embodiments, the administration of the pharmaceutical composition to the patient does not significantly increase levels of total cholesterol after administration of the pharmaceutical composition comprising nipocalimab. In some embodiments, the administration of the pharmaceutical composition to the patient does not significantly increase levels of high-density lipoprotein (HDL) after administration of the pharmaceutical composition comprising nipocalimab. In some embodiments, the administration of the pharmaceutical composition to the patient does not significantly increase levels of calculated low-density lipoprotein (LDL) after administration of the pharmaceutical composition comprising nipocalimab. In some embodiments, the administration of the pharmaceutical composition to the patient does not significantly increase levels of triglycerides after administration of the pharmaceutical composition comprising nipocalimab.

[0134] As used herein, the phrase “does not significantly increase” when used in reference to levels (measurements) of total cholesterol, high-density lipoprotein (HDL), calculated low-density lipoprotein (LDL), or triglycerides” means that any increase is less than 30% as compared to the level(s) prior (baseline) to the administration of the antibody or compositions provided for herein. In some embodiments, the increase is less than 25%, 20%, 15%, 10%, or 5%. In some embodiments, the increase is no greater than about 1 to about 30%, about 5% to about 25%, about 1% to about 20%, about 1% to about 15%, about 1% to about 10%, about 5% to about 15%, about 5% to about 20%, about 10% to about 20%, about 1%, about 5%, about 10%, about 15%, about 20%, about 25%, or about 30%..-23- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)

[0135] In some embodiments, the administration of nipocalimab treats or ameliorates tingling of the arms, tingling of the legs, weakening of arms, weakening of legs, loss of reflexes, loss of balance, loss of ability to walk, impaired coordination, abnormal walk, trouble walking, trouble bending over, trouble reaching, trouble squatting, loss of feeling in arms, loss of feeling in legs, fatigue, burning, pain, clumsiness, difficulty swallowing, double vision, muscle atrophy, dysphagia. In some embodiments, the improvement in symptoms or conditions are referred to as occurring over time, 12 weeks, or 48 weeks after initiation of treatment. Although reference is made to determining whether those improvements are measurable over time, at 12 weeks, or at 48 weeks after initiation of treatment, in some embodiments, the improvements or changes described herein will occur within 2, 4, 6, 8, 10, 12, 14, 16, 18, 20, 22, 24, 26, 28, 30, 32, 34, 36, 38, 40, 42, 44, 46, and 48 weeks. In some embodiments, the changes or improvements will last at least 2, 4, 6, 8, 10, 12, 14, 16, 18, 20, 22, 24, 26, 28, 30, 32, 34, 36, 38, 40, 42, 44, 46, and 48 weeks.Reducing Serum IgG

[0136] Provided herein are methods of reducing serum IgG in a subject in need thereof, the method comprising administering nipocalimab to the subject at a dose from about 1000 mg to about 2000 mg every two weeks, or a dose from about 400 mg to about 600 mg every week, wherein the administration of nipocalimab reduce serum IgG in the subject by at least 60% from baseline serum IgG, at least 65% from baseline serum IgG, at least 70% from baseline serum IgG, at least 75% from baseline serum IgG, or at least 80% from baseline serum IgG. In some embodiments, the subject receives a second subcutaneous administration of nipocalimab at a dose from about 400 mg to about 600 mg in the first week. Also provided herein is nipocalimab for use in a method of reducing serum IgG in a subject in need thereof, the method comprising administering nipocalimab to the subject at a dose from about 1000 mg to about 2000 mg every two weeks, or a dose from about 400 mg to about 600 mg every week, wherein the administration of nipocalimab reduce serum IgG in the subject by at least 60% from baseline serum IgG, at least 65% from baseline serum IgG, at least 70% from baseline serum IgG, at least 75% from baseline serum IgG, or at least 80% from baseline serum IgG. In some embodiments, the subject receives a second subcutaneous administration of nipocalimab at a dose from about 400 mg to about 600 mg in the first week. Also provided herein is a use of nipocalimab for the manufacture of a medicament for reducing serum IgG in a subject in need thereof, the method comprising administering nipocalimab to the subject at a dose from about 1000 mg to about 2000 mg every two weeks, or a dose from about 400 mg to -24- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)about 600 mg every week, wherein the administration of nipocalimab reduce serum IgG in the subject by at least 60% from baseline serum IgG, at least 65% from baseline serum IgG, at least 70% from baseline serum IgG, at least 75% from baseline serum IgG, or at least 80% from baseline serum IgG. In some embodiments, the subject receives a second subcutaneous administration of nipocalimab at a dose from about 400 mg to about 600 mg in the first week.

[0137] In some embodiments, nipocalimab is administered every two weeks subcutaneously at a dose from about 1200 mg to about 1800 mg via an on-body device. In some embodiments, nipocalimab is administered every two weeks subcutaneously at a dose from about 1400 mg to about 1600 mg via an on-body device. In some embodiments, nipocalimab is administered every two weeks subcutaneously at a dose about 1500 mg via an on-body device.

[0138] In some embodiments, nipocalimab is administered every week subcutaneously at a dose from about 400 mg to about 600 mg via an auto injector. In some embodiments, the subject receives a second subcutaneous administration of nipocalimab at a dose from about 400 mg to about 600 mg in the first week via an autoinjector. In some embodiments, nipocalimab is administered every week subcutaneously at a dose from about 450 mg to about 550 mg via an autoinjector. In some embodiments, the subject receives a second subcutaneous administration of nipocalimab at a dose from about 450 mg to about 550 mg in the first week via an autoinjector.

[0139] In some embodiments, nipocalimab is administered every week subcutaneously at a dose about 518 mg via an autoinjector. In some embodiments, the subject receives a second subcutaneous administration of nipocalimab at a dose of about 518 mg in the first week via an autoinjector. In some embodiments, the subject receives a second subcutaneous administration of nipocalimab at a dose of about 518 mg in the first day via an autoinjector.

[0140] In some embodiments, nipocalimab is administered every week subcutaneously at a dose of about 460 mg via an autoinjector. In some embodiments, the subject receives a second subcutaneous administration of nipocalimab at a dose of about 460 mg via an autoinjector in the first week. In some embodiments, the subject receives a second subcutaneous administration of nipocalimab at a dose of about 460 mg in the first day via an autoinjector.-25- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)

[0141] In some embodiments, the subject has warm autoimmune hemolytic anemia (wAIHA), generalized myasthenia gravis (gMG), chronic inflammatory demyelinating polyneuropathy (CIDP), or idiopathic inflammatory myopathies (IIM).

[0142] In some embodiments, the administration of nipocalimab increases total cholesterol in the subject by at most 18 mg / dL, at most 17 mg / dL, at most 16 mg / dL, at most 15 mg / dL, at most 14 mg / dL, at most 13 mg / dL, or at most 12 mg / dL from baseline total cholesterol.

[0143] In some embodiments, the administration of nipocalimab increases HDL in the subject at most 8 mg / dL, at most 7 mg / dL, at most 6 mg / dL, at most 5 mg / dL, at most 4 mg / dL, at most 3 mg / dL, or at most 2 mg / dL from baseline HDL.

[0144] In some embodiments, the administration of nipocalimab increases LDL in the subject at most 12 mg / dL, at most 11 mg / dL, at most 10 mg / dL, at most 9 mg / dL, at most 8 mg / dL, at most 7 mg / dL, at most 6 mg / dL, or at most 5 mg / dL from baseline LDL.

[0145] In some embodiments, the administration of nipocalimab reduces serum albumin in the subject by at most 18%, at most 16%, at most 14%, at most 12%, at most 10%, at most 8%, at most 6%, at most 4%, or at most 2% from baseline serum albumin.

[0146] In some embodiments, the administering of the anti-LcRn agent (e.g. nipocalimab) to a subject does not increase (or even lowers) the chances of serious infection in the subject.Myasthenia Gravis

[0147] The present disclosure also provides methods of treating generalized myasthenia gravis (gMG) in a subject. Generalized myasthenia gravis is a chronic autoimmune disease associated with functional impairment, which is characterized by fluctuating, fatigable muscle weakness.Approximately 95% of patients with generalized myasthenia gravis are antibody-positive (85% antiacetylcholine receptor [AChR] -positive, about 8% anti-muscle-specific tyrosine kinase [MuSK]-positive, and about 1-2% anti-low-density lipoprotein receptor-related protein 4 [LRP4] -positive) (Meriggioli, M, et al. Expert Rev Clin Immunol, 8 (2012), pp. 427-438). These IgG antibodies mediate disruption of cholinergic transmission at the neuromuscular junction. The burden of illness in generalized myasthenia gravis, including medications, outpatient visits, hospital admissions, and intensive care treatment, is substantial.-26- 103693.004420\4914-0795-9446.2DOCKET NO.: 103693.004420 (MPI6028WOPCT1)

[0148] Provided herein is a method of treating generalized myasthenia gravis (gMG) in a subject in need thereof, the method comprising subcutaneously administering nipocalimab to the subject at a dose from about 1000 mg to about 2000 mg every two weeks; or from about 400 mg to about 600 mg every week. In some embodiments, the subject receives a second subcutaneous administration of nipocalimab at a dose from about 400 mg to about 600 mg in the first week. Also provided herein is nipocalimab for use in a method of treating generalized myasthenia gravis (gMG) in a subject in need thereof, the method comprising subcutaneously administering nipocalimab to the subject at a dose from about 1000 mg to about 2000 mg every two weeks; or from about 400 mg to about 600 mg every week. In some embodiments, the subject receives a second subcutaneous administration of nipocalimab at a dose from about 400 mg to about 600 mg in the first week. Also provided herein is a use of nipocalimab for the manufacture of a medicament for treating generalized myasthenia gravis (gMG) in a subject in need thereof, the method comprising subcutaneously administering nipocalimab to the subject at a dose from about 1000 mg to about 2000 mg every two weeks; or from about 400 mg to about 600 mg every week. In some embodiments, the subject receives a second subcutaneous administration of nipocalimab at a dose from about 400 mg to about 600 mg in the first week.

[0149] In some embodiments, nipocalimab is administered every two weeks subcutaneously at a dose from about 1200 mg to about 1800 mg via an on-body device. In some embodiments, nipocalimab is administered every two weeks subcutaneously at a dose from about 1400 mg to about 1600 mg via an on-body device. In some embodiments, nipocalimab is administered every two weeks subcutaneously at a dose about 1500 mg via an on-body device.

[0150] In some embodiments, nipocalimab is administered every week subcutaneously at a dose from about 400 mg to about 600 mg via an auto injector. In some embodiments, the subject receives a second subcutaneous administration of nipocalimab at a dose from about 400 mg to about 600 mg in the first week via an autoinjector. In some embodiments, nipocalimab is administered every week subcutaneously at a dose from about 450 mg to about 550 mg via an autoinjector. In some embodiments, the subject receives a second subcutaneous administration of nipocalimab at a dose from about 450 mg to about 550 mg in the first week via an autoinjector. In some embodiments, nipocalimab is administered every week subcutaneously at a dose about 518 mg via an autoinjector. In some embodiments, the subject receives a second subcutaneous administration of nipocalimab at a dose of about 518 mg in the first week via an auto injector. In some embodiments,-27- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)the subject receives a second subcutaneous administration of nipocalimab at a dose of about 518 mg in the first day via an autoinjector. In some embodiments, nipocalimab is administered every week subcutaneously at a dose of about 460 mg via an auto injector. In some embodiments, the subject receives a second subcutaneous administration of nipocalimab at a dose of about 460 mg via an autoinjector in the first week. In some embodiments, the subject receives a second subcutaneous administration of nipocalimab at a dose of about 460 mg in the first day via an auto injector.

[0151] In some embodiments, the method provides a clinical benefit as measured by a decrease in MG-ADL score in the subject by more than 4.0, 4.1, 4.2, 4.3, 4.4, 4.5, 4.6, 4.7, 4.8, 4.9, 5.0, 5.1, 5.2, 5.3, 5.4, 5.6, 5.7, 5.8, 5.9 or 6.0 from baseline within 12, 14, 16, 18, 20, 22, 24, 26, 28, 30, 36, 42, 48 or 52 weeks of initiation of said administering.

[0152] In some embodiments, the method provides a clinical benefit as measured by a decrease in QMG score in the subject by more than 4.0, 4.1, 4.2, 4.3, 4.4, 4.5, 4.6, 4.7, 4.8, 4.9, or 5.0 from baseline within 12, 14, 16, 18, 20, 22, 24, 26, 28, 30, 36, 42, 48 or 52 weeks of initiation of said administering.

[0153] In some embodiments, the subject is positive for one or more of anti-AChR antibody, anti-MuSK antibody, and anti-LRP4 antibody.

[0154] In some embodiments, the administration of nipocalimab increase total cholesterol in the subject by at most 18 mg / dL, at most 17 mg / dL, at most 16 mg / dL, at most 15 mg / dL, at most 14 mg / dL, at most 13 mg / dL, or at most 12 mg / dL from baseline total cholesterol.

[0155] In some embodiments, the administration of nipocalimab increase HDL in the subject at most 8 mg / dL, at most 7 mg / dL, at most 6 mg / dL, at most 5 mg / dL, at most 4 mg / dL, at most 3 mg / dL, or at most 2 mg / dL from baseline HDL.

[0156] In some embodiments, the administration of nipocalimab increase LDL in the subject at most 12 mg / dL, at most 11 mg / dL, at most 10 mg / dL, at most 9 mg / dL, at most 8 mg / dL, at most 7 mg / dL, at most 6 mg / dL, or at most 5 mg / dL from baseline LDL.

[0157] In some embodiments, the administration of nipocalimab reduces serum albumin in the subject by at most 18%, at most 16%, at most 14%, at most 12%, at most 10%, at most 8%, at most 6%, at most 4%, or at most 2% from baseline serum albumin.-28- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)Warm Autoimmune Hemolytic Anemia

[0158] The present disclosure also provides methods of treating warm autoimmune hemolytic anemia (wAIHA) in a subject. Autoimmune hemolytic anemia (AIHA) is a rare, life-threatening autoimmune disorder caused by autoantibodies that attach to and prematurely destroy self-red blood cells (RBCs). AIHA is generally classified into warm (wAIHA), cold, and mixed forms according to the thermal range of the autoantibodies involved. Warm AIHA is the most common form of AIHA, and hemolysis is mediated by autoantibodies that bind to RBCs at body temperature (ie, 37°C / 98.6°F), leading primarily to extravascular hemolysis in the spleen and, to a lesser extent, the liver.

[0159] Provided herein is a method of treating warm autoimmune hemolytic anemia (wAIHA) in a subject in need thereof, the method comprising subcutaneously administering nipocalimab to the subject at a dose from about 1000 mg to about 2000 mg every two weeks, or a dose from about 400 mg to about 600 mg every week. Also provided herein is nipocalimab for use in a method of treating warm autoimmune hemolytic anemia (wAIHA) in a subject in need thereof, the method comprising subcutaneously administering nipocalimab to the subject at a dose from about 1000 mg to about 2000 mg every two weeks, or a dose from about 400 mg to about 600 mg every week. Also provided herein is a use of nipocalimab for the manufacture of a medicament for treating warm autoimmune hemolytic anemia (wAIHA) in a subject in need thereof, the method comprising subcutaneously administering nipocalimab to the subject at a dose from about 1000 mg to about 2000 mg every two weeks, or a dose from about 400 mg to about 600 mg every week.

[0160] In some embodiments, nipocalimab is administered every two weeks subcutaneously at a dose from about 1200 mg to about 1800 mg via an on-body device. In some embodiments, nipocalimab is administered every two weeks subcutaneously at a dose from about 1400 mg to about 1600 mg via an on-body device. In some embodiments, nipocalimab is administered every two weeks subcutaneously at a dose about 1500 mg via an on-body device.

[0161] In some embodiments, nipocalimab is administered every week subcutaneously at a dose from about 400 mg to about 600 mg via an auto injector. In some embodiments, the subject receives a second subcutaneous administration of nipocalimab at a dose from about 400 mg to about 600 mg via an autoinjector in the first week. In some embodiments, nipocalimab is administered every week subcutaneously at a dose from about 450 mg to about 550 mg via an autoinjector. In -29- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)some embodiments, the subject receives a second subcutaneous administration of nipocalimab at a dose from about 450 mg to about 550 mg via an autoinjector in the first week. In some embodiments, nipocalimab is administered every week subcutaneously at a dose about 518 mg via an autoinjector. In some embodiments, the subject receives a second subcutaneous administration of nipocalimab at a dose about 518 mg via an autoinjector in the first week. In some embodiments, the subject receives a second subcutaneous administration of nipocalimab at a dose of about 518 mg in the first day via an autoinjector.

[0162] In some embodiments, nipocalimab is administered every week subcutaneously at a dose of about 460 mg via an autoinjector. In some embodiments, the subject receives a second subcutaneous administration of nipocalimab at a dose of about 460 mg via an autoinjector in the first week. In some embodiments, the subject receives a second subcutaneous administration of nipocalimab at a dose of about 460 mg in the first day via an autoinjector.

[0163] In some embodiments, the method provides a clinical benefit as measured by an increase in a hemoglobin (Hgb) level in the subject of more than 0.5, 1, 1.5, 2, 2.5, 3, 3.5, 4, 4.5, 5, 5.5, 6, 6.5, 7, 7.5, 8, 8.5, 9, 9.5, or 10 g / dL within 1, 2, 4, 6, 8, 10, 12, 14, 16, 18, 20, 22, 24, 30, 36, 42, 48 or 52 weeks of initiation of said administering relative to a baseline Hgb level in the subject prior to initiation of said administering.

[0164] In some embodiments, the administering of the anti-FcRn agent (e.g. nipocalimab) to a subject provides a clinical benefit as measured by an increase in the hemoglobin (Hgb) level in the subject of 1 g / dL or more relative to the baseline within 1 week of initiation of said administering. In some embodiments, the administering of the anti-FcRn agent (e.g. nipocalimab) to a subject provides a clinical benefit as measured by an increase in the hemoglobin (Hgb) level in the subject of 1 g / dL or more relative to the baseline within 2 weeks of initiation of said administering. In some embodiments, the administering of the anti-FcRn agent (e.g. nipocalimab) to a subject provides a clinical benefit as measured by an increase in the hemoglobin (Hgb) level in the subject of 1 g / dL or more relative to the baseline within 3 weeks of initiation of said administering. In some embodiments, the administering of the anti-FcRn agent (e.g. nipocalimab) to a subject provides a clinical benefit as measured by an increase in the hemoglobin (Hgb) level in the subject of 1 g / dL or more relative to the baseline within 4 weeks of initiation of said administering.-30- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)

[0165] In some embodiments, the administering of the anti-FcRn agent (e.g. nipocalimab) to a subject provides a clinical benefit as measured by an increase in the hemoglobin (Hgb) level in the subject of 1.5 g / dL or more relative to the baseline within 1, 2, 3 or 4 weeks of initiation of said administering.

[0166] In some embodiments, the administering of the anti-FcRn agent (e.g. nipocalimab) to a subject provides a clinical benefit as measured by an increase in the hemoglobin (Hgb) level in the subject of 2 g / dL or more relative to the baseline within 1, 2, 3 or 4 weeks of initiation of said administering. In some embodiments, the administering of the anti-FcRn agent (e.g. nipocalimab) to a subject provides a clinical benefit as measured by achievement of a hemoglobin (Hgb) level in the subject of 10 g / dL or more within 1, 2, 3 or 4 weeks of initiation of said administering.

[0167] In some embodiments, the method provides a clinical benefit as measured by an increase in the hemoglobin (Hgb) level in the subject of 1.5 g / dL or more relative to the baseline within 4 weeks of initiation of said administering. In some embodiments, the method provides a clinical benefit as measured by an increase in the hemoglobin (Hgb) level in the subject of 2 g / dL or more relative to the baseline within 4 weeks of initiation of said administering.

[0168] In some embodiments, the method provides a clinical benefit within 16 weeks of initiation of said administering as measured by:• achievement of a hemoglobin (Hgb) level in the subject of 10 g / dL or more; and• an increase in a hemoglobin (Hgb) level in the subject of 2 g / dL or more relative to a baseline level of Hgb in the subject prior to initiation of said administering.

[0169] In some embodiments, the clinical benefit is sustained for at least 28 days. In some embodiments, the clinical benefit is sustained for at least 6, 8, or 12 weeks. In some embodiments, the clinical benefit is sustained for at least 16 weeks. In some embodiments, the clinical benefit is sustained for at least 24 weeks. In some embodiments, the clinical benefit is sustained for at least 52 weeks.

[0170] In some embodiments, the method provides a clinical benefit as measured by:• achievement of a hemoglobin (Hgb) level in the subject of 10 g / dL or more; and• an increase in a hemoglobin (Hgb) level in the subject by 2 g / dL or more relative to a baseline level of Hgb in the subject prior to initiation of said administering, wherein the -31- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)clinical benefit is sustained for at least 28 days, wherein the clinical benefit is achieved within 16 weeks of initiation of said administering, and wherein the subject did not receive a rescue therapy.

[0171] In some embodiments, the rescue therapy comprises increased corticosteroids, blood transfusion, or intravenous immunoglobulin (IVIg) administration.

[0172] In some embodiments, the method provides a clinical benefit as measured by an increase in a Functional Assessment of Chronic Illness Therapy -Fatigue (FACIT-Fatigue) score in the subject by more than 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31, or 32 relative to a baseline FACIT-Fatigue score in the subject prior to initiation of said administering within 2, 4, 6, 8, 10, 12, 14, 16, 18, 20, 22, 24, 30, 36, 42, 48 or 52 weeks of initiation of said administering.

[0173] In some embodiments, the administering of the anti-FcRn agent (e.g. nipocalimab) to a subject suffering from wAIHA provides a clinical benefit within 16 weeks of initiation of said administering as measured by:achievement of a hemoglobin (Hgb) level in the subject of 10 g / dL or more; and an increase in a hemoglobin (Hgb) level in the subject of 1.5 g / dL or more relative to a baseline level of Hgb in the subject prior to initiation of said administering.

[0174] In some embodiments, the method provides a clinical benefit as measured by an increase in a Functional Assessment of Chronic Illness Therapy -Fatigue (FACIT-Fatigue) score in the subject by 2.95 or more relative to a baseline FACIT-Fatigue score in the subject prior to initiation of said administering within 24 weeks of initiation of said administering.

[0175] In some embodiments, the method provides a clinical benefit as measured by an increase in a Functional Assessment of Chronic Illness Therapy -Fatigue (FACIT-Fatigue) score in the subject by 3.4 or more relative to a baseline FACIT-Fatigue score in the subject prior to initiation of said administering within 24 weeks of initiation of said administering.

[0176] In some embodiments, the subject receives corticosteroid at a first dose before initiation of said administering, and the method provides a clinical benefit as indicated by the subject receives corticosteroid at a second dose that is at least 10%, 15%, 20%, 25%, 30%, 35%,-32- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)40%, 45%, 50%, 55%, 60%, 65%, or 70% lower than the first dose within 24, 30, 36, 42, 48 or 52 weeks or more weeks of initiation of said administering.

[0177] In some embodiments, the subject receives corticosteroid at a first dose before initiation of said administering, and the method provides a clinical benefit as indicated by the subject receives corticosteroid at a second dose that is at least 20% lower than the first dose within 24 weeks or more weeks of initiation of said administering.

[0178] In some embodiments, the subject receives corticosteroid at a first dose before initiation of said administering, and the method provides a clinical benefit as indicated by the subject receives corticosteroid at a second dose that is at least 60% lower than the first dose within 48 weeks or more weeks of initiation of said administering. In some embodiments, the corticosteroid is prednisone.

[0179] In some embodiments, the method provides a clinical benefit as measured by:• achievement of a hemoglobin (Hgb) level in the subject of 10 g / dL or more;• an increase in a hemoglobin (Hgb) level in the subject by 2 g / dL or more relative to a baseline level of Hgb in the subject prior to initiation of said administering,wherein the clinical benefit is sustained for at least 28 days, wherein the clinical benefit is achieved within 16 weeks of initiation of said administering, and wherein the subject did not receive a rescue therapy; and wherein the method provides a further clinical benefit as measured by:• an increase in a Functional Assessment of Chronic Illness Therapy -Fatigue (FACIT-Fatigue) score in the subject by more than 3 within 24 weeks of initiation of said administering relative to a baseline FACIT-Fatigue score in the subject prior to initiation of said administering; and• the subject receives corticosteroid at a second dose that is at least 20% lower than the first dose within 24 weeks or more weeks of initiation of said administering, wherein the subject receives corticosteroid at a first dose before initiation of said administering.

[0180] In some embodiments, the rescue therapy comprises corticosteroids, blood transfusion, or intravenous immunoglobulin (IVIg).

[0181] In some embodiments, the method provides a clinical benefit as measured by a reduction in total IgG in the subject by more than 20%, 30%, 40%, 50%, 60%, 70%, 80%, or 90%-33- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)relative to a baseline level of total IgG in the subject prior to initiation of said administering within 8, 10, 12, 14, 16, 18, 20, 22, 24, 30, 36, 42, 48 or 52 weeks of initiation of said administering.

[0182] In some embodiments, the administration of nipocalimab increases total cholesterol in the subject by at most 18 mg / dL, at most 17 mg / dL, at most 16 mg / dL, at most 15 mg / dL, at most 14 mg / dL, at most 13 mg / dL, or at most 12 mg / dL from baseline total cholesterol.

[0183] In some embodiments, the administration of nipocalimab increases total cholesterol in the subject by at most about 5%, about 10%, about 12%, about 14%, about 16%, about 18%, or about 20%, relative to a baseline level of total cholesterol in the subject prior to initiation of said administering.

[0184] In some embodiments, the administration of nipocalimab increases total cholesterol in the subject by at most about 14%, relative to a baseline level of total cholesterol in the subject prior to initiation of said administering. In some embodiments, the administration of nipocalimab increases total cholesterol in the subject by at most about 13.5%, relative to a baseline level of total cholesterol in the subject prior to initiation of said administering.

[0185] In some embodiments, the administration of nipocalimab increase HDL in the subject at most 8 mg / dL, at most 7 mg / dL, at most 6 mg / dL, at most 5 mg / dL, at most 4 mg / dL, at most 3 mg / dL, or at most 2 mg / dL from baseline HDL.

[0186] In some embodiments, the administration of nipocalimab increases LDL in the subject at most 12 mg / dL, at most 11 mg / dL, at most 10 mg / dL, at most 9 mg / dL, at most 8 mg / dL, at most 7 mg / dL, at most 6 mg / dL, or at most 5 mg / dL from baseline LDL.

[0187] In some embodiments, the administration of nipocalimab increases LDL in the subject by at most about 1%, about 3%, about 4%, about 5%, about 6%, about 8%, or about 10% relative to a baseline level of LDL in the subject prior to initiation of said administering.

[0188] In some embodiments, the administration of nipocalimab increases LDL in the subject by at most about 5% relative to a baseline level of LDL in the subject prior to initiation of said administering. In some embodiments, the administration of nipocalimab increases LDL in the subject by at most about 4.5% relative to a baseline level of LDL in the subject prior to initiation of said administering.-34- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)

[0189] In some embodiments, the administration of nipocalimab reduces serum albumin in the subject by at most 18%, at most 16%, at most 14%, at most 12%, at most 10%, at most 8%, at most 6%, at most 4%, or at most 2% from baseline serum albumin.

[0190] In some embodiments, the administration of nipocalimab reduces serum albumin in the subject by at most about 2 g / L, about 4 g / L, about 6 g / L, about 8 g / L, about 10 g / L, about 12 g / L, about 14 g / L, about 16 g / L, about 18 g / L, or about 20 g / L relative to a baseline serum albumin in the subject prior to initiation of said administering.

[0191] In some embodiments, the administration of nipocalimab reduces serum albumin in the subject by at most about 10 g / L relative to a baseline serum albumin in the subject prior to initiation of said administering.

[0192] In some embodiments, the subject is 12 years or older. In some embodiments, the subject is 18 years or older. In some embodiments, the subject is from 12 to 18 years old.

[0193] In some embodiments, the method provides a clinical benefit as measured by a reduction in wAIHA-related pathogenic autoantibodies in the subject by more than 15%, 20%, 30%, or 40% relative to a baseline level of wAIHA-related pathogenic autoantibodies in the subject prior to initiation of said administering and within 1, 2, 4, 6, 8, 10, 12, 14, 16, 18, 20, 22, 24, 30, 36, 42, 48, or 52 weeks of initiation of said administering.

[0194] In some embodiments, the subject receives a plurality of 30 mg / kg intravenous doses of nipocalimab based on the weight of the subject, wherein the first dose is administered to the subject over at least 30 minutes, and wherein the subsequent doses are administered over at least 15 minutes.Chronic Inflammatory Demyelinating Polyneuropathy

[0195] The present disclosure also provides methods of treating chronic inflammatory demyelinating polyneuropathy (CIDP) in a subject. In some embodiments, the CIDP is probable CIDP. In some embodiments, the CIDP is definite active CIDP. In some embodiments, the CIDP is classified as probable or definite active CIDP according to the European Federation of Neurological Societies / Peripheral Nerve Society (EFNS / PNS 2010) criteria. In some embodiments, the method-35- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)comprises administering a pharmaceutical composition comprising administering an anti-FcRn antibody to the subject. In some embodiments, the anti-FcRn antibody is nipocalimab.

[0196] Provided herein are methods of treating chronic inflammatory demyelinating polyneuropathy (CIDP) in a subject in need thereof, the method comprising subcutaneously administering nipocalimab to the subject at a dose from about 1000 mg to about 2000 mg every two weeks, or a dose from about 400 mg to about 600 mg every week. In some embodiments, the subject receives a second subcutaneous administration of nipocalimab at a dose from about 400 mg to about 600 mg in the first week. Also provided herein is nipocalimab for use in a method of treating chronic inflammatory demyelinating polyneuropathy (CIDP) in a subject in need thereof, the method comprising subcutaneously administering nipocalimab to the subject at a dose from about 1000 mg to about 2000 mg every two weeks, or a dose from about 400 mg to about 600 mg every week. In some embodiments, the subject receives a second subcutaneous administration of nipocalimab at a dose from about 400 mg to about 600 mg in the first week. Also provided herein is a use of nipocalimab for the manufacture of a medicament for treating chronic inflammatory demyelinating polyneuropathy (CIDP) in a subject in need thereof, the method comprising subcutaneously administering nipocalimab to the subject at a dose from about 1000 mg to about 2000 mg every two weeks, or a dose from about 400 mg to about 600 mg every week. In some embodiments, the subject receives a second subcutaneous administration of nipocalimab at a dose from about 400 mg to about 600 mg in the first week.

[0197] In some embodiments, nipocalimab is administered every two weeks subcutaneously at a dose from about 1200 mg to about 1800 mg via an on-body device. In some embodiments, nipocalimab is administered every two weeks subcutaneously at a dose from about 1400 mg to about 1600 mg via an on-body device. In some embodiments, nipocalimab is administered every two weeks subcutaneously at a dose about 1500 mg via an on-body device.

[0198] In some embodiments, nipocalimab is administered every week subcutaneously at a dose from about 400 mg to about 600 mg via an auto injector. In some embodiments, the subject receives a second subcutaneous administration of nipocalimab at a dose from about 400 mg to about 600 mg in the first week via an auto injector.

[0199] In some embodiments, nipocalimab is administered every week subcutaneously at a dose from about 450 mg to about 550 mg via an autoinjector. In some embodiments, the subject -36- 103693.004420\4914-0795-9446.2DOCKET NO.: 103693.004420 (MPI6028WOPCT1)receives a second subcutaneous administration of nipocalimab at a dose from about 450 mg to about 550 mg in the first week via an autoinjector.

[0200] In some embodiments, nipocalimab is administered every week subcutaneously at a dose of about 518 mg via an autoinjector. In some embodiments, the subject receives a second subcutaneous administration of nipocalimab at a dose of about 518 mg in the first week via an autoinjector. In some embodiments, the subject receives a second subcutaneous administration of nipocalimab at a dose of about 518 mg in the first day via an autoinjector. In some embodiments, nipocalimab is administered every week subcutaneously at a dose of about 460 mg via an autoinjector. In some embodiments, the subject receives a second subcutaneous administration of nipocalimab at a dose of about 460 mg via an auto injector in the first week. In some embodiments, the subject receives a second subcutaneous administration of nipocalimab at a dose of about 460 mg in the first day via an autoinjector.

[0201] In some embodiments, the method provides a clinical benefit as measured by a reduction of at least 1 in adjusted Inflammatory Neuropathy Cause and Treatment (INCAT) score in the subject within 10 weeks of initiation of said administering, compared to an initial INCAT score determined at baseline.

[0202] In some embodiments, the subject maintains or has a further reduction in the adjusted INCAT score from week 10 to week 12, week 16, week 20, week 24, week 28, week 32, week 36, week 40, week 42, week 44, week 48, or week 52 from initiation of said administering.

[0203] In some embodiments, the method provides a clinical benefit as measured by an increase of at least 8kPa, lOkPa, 12kPa, or 14kPa in grip strength for the dominant hand of the subject by week 10 from initiation of said administering, compared to an initial grip strength determined at baseline.

[0204] In some embodiments, the subject maintains or has a further increase in the grip strength for the dominant hand of the subject from week 10 to week 12, week 16, week 20, week 24, week 28, week 32, week 36, week 40, week 42, week 44, week 48, or week 52 from initiation of said administering.

[0205] In some embodiments, the method provides a clinical benefit as measured by an increase of at least 8kPa, lOkPa, 12kPa, or 14kPa in grip strength for the non-dominant hand of the -37- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)subject by week 10 from initiation of said administering, compared to an initial grip strength determined at baseline.

[0206] In some embodiments, the subject maintains or has a further increase in the grip strength for the non-dominant hand of the subject from week 10 to week 12, week 16, week 20, week 24, week 28, week 32, week 36, week 40, week 42, week 44, week 48, or week 52 from initiation of said administering.

[0207] In some embodiments, the method provides a clinical benefit as measured by an increase in Inflammatory Rasch-built Overall Disability Scale (I-RODS) centile score in the subject by at least 4, 5, 6, 7, or 8 points by week 12, 16, 20, 24, 28, 32, 36, 40, 42, 44, 48, or 52 from initiation of said administering, compared to an initial I-RODS score determined at baseline.

[0208] In some embodiments, the method provides a clinical benefit as measured by an increase in MRC Muscle Grading Sale Sum score in the subject by at least 4, 5, 6, 7, or 8 by week 12, 16, 20, 24, 28, 32, 36, 40, 42, 44, 48, or 52 from initiation of said administering, compared to an initial MRC Muscle Grading Sale Sum score determined at baseline.

[0209] In some embodiments, the administration of nipocalimab increase total cholesterol in the subject by at most 18 mg / dL, at most 17 mg / dL, at most 16 mg / dL, at most 15 mg / dL, at most 14 mg / dL, at most 13 mg / dL, or at most 12 mg / dL from baseline total cholesterol.

[0210] In some embodiments, the administration of nipocalimab increase HDL in the subject at most 8 mg / dL, at most 7 mg / dL, at most 6 mg / dL, at most 5 mg / dL, at most 4 mg / dL, at most 3 mg / dL, or at most 2 mg / dL from baseline HDL.

[0211] In some embodiments, the administration of nipocalimab increase LDL in the subject at most 12 mg / dL, at most 11 mg / dL, at most 10 mg / dL, at most 9 mg / dL, at most 8 mg / dL, at most 7 mg / dL, at most 6 mg / dL, or at most 5 mg / dL from baseline LDL.

[0212] In some embodiments, the administration of nipocalimab reduces serum albumin in the subject by at most 18%, at most 16%, at most 14%, at most 12%, at most 10%, at most 8%, at most 6%, at most 4%, or at most 2% from baseline serum albumin.Idiopathic Inflammatory Myopathies-38- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)

[0213] The present disclosure also provides methods of treating idiopathic inflammatory myopathies (IIM) in a subject. IIM is characterized by common features of insidious painless, proximal skeletal muscle weakness, low endurance, and elevated serum muscle enzyme levels. Most IIM have an inflammatory pattern on muscle biopsy. IIM are a heterogeneous group of rare diseases which includes dermatomyositis (DM), immune-mediated necrotizing myopathy (IMNM), anti-synthetase syndrome (ASyS), inclusion body myositis (IBM), overlap myositis (OM), and polymyositis (PM).

[0214] Provided herein is a method of the method treating idiopathic inflammatory myopathies (IIM) in a subject in need thereof, the method comprising subcutaneously administering nipocalimab to the subject at a dose from about 1000 mg to about 2000 mg every two weeks, or a dose from about 400 mg to about 600 mg every week. In some embodiments, the subject receives a second subcutaneous administration of nipocalimab at a dose from about 400 mg to about 600 mg in the first week. Also provided herein is nipocalimab for use in a method of treating idiopathic inflammatory myopathies (IIM) in a subject in need thereof, the method comprising subcutaneously administering nipocalimab to the subject at a dose from about 1000 mg to about 2000 mg every two weeks, or a dose from about 400 mg to about 600 mg every week. In some embodiments, the subject receives a second subcutaneous administration of nipocalimab at a dose from about 400 mg to about 600 mg in the first week. Also provided herein is a use of nipocalimab for the manufacture of a medicament for treating idiopathic inflammatory myopathies (IIM) in a subject in need thereof, the method comprising subcutaneously administering nipocalimab to the subject at a dose from about 1000 mg to about 2000 mg every two weeks, or a dose from about 400 mg to about 600 mg every week. In some embodiments, the subject receives a second subcutaneous administration of nipocalimab at a dose from about 400 mg to about 600 mg in the first week.

[0215] In some embodiments, nipocalimab is administered every two weeks subcutaneously at a dose from about 1200 mg to about 1800 mg via an on-body device. In some embodiments, nipocalimab is administered every two weeks subcutaneously at a dose from about 1400 mg to about 1600 mg via an on-body device. In some embodiments, nipocalimab is administered every two weeks subcutaneously at a dose about 1500 mg via an on-body device.

[0216] In some embodiments, nipocalimab is administered every week subcutaneously at a dose from about 400 mg to about 600 mg via an auto injector. In some embodiments, the subject receives a second subcutaneous administration of nipocalimab at a dose from about 400 mg to about -39- 103693.004420\4914-0795-9446.2DOCKET NO.: 103693.004420 (MPI6028WOPCT1)600 mg in the first week via an autoinjector. In some embodiments, nipocalimab is administered every week subcutaneously at a dose from about 450 mg to about 550 mg via an autoinjector. In some embodiments, the subject receives a second subcutaneous administration of nipocalimab at a dose from about 450 mg to about 550 mg in the first week via an autoinjector. In some embodiments, nipocalimab is administered every week subcutaneously at a dose from about 518 mg via an autoinjector. In some embodiments, the subject receives a second subcutaneous administration of nipocalimab at a dose of about 518 mg in the first week via an autoinjector. In some embodiments, the subject receives a second subcutaneous administration of nipocalimab at a dose of about 518 mg in the first day via an autoinjector. In some embodiments, nipocalimab is administered every week subcutaneously at a dose of about 460 mg via an autoinjector. In some embodiments, the subject receives a second subcutaneous administration of nipocalimab at a dose of about 460 mg via an autoinjector in the first week. In some embodiments, the subject receives a second subcutaneous administration of nipocalimab at a dose of about 460 mg in the first day via an auto injector.

[0217] In some embodiments, the method provides a clinical benefit as measured by an increase in International Myositis Assessment and Clinical Studies Total Improvement Score (IMACS TIS) in the subject by at least 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31, 32, 33, 34, 35, 36, 37, 38, 39, 40, 41, 42, 43, 44, 45, 46, 47, 48, 49, 50, 51, 52, 53, 54, 55, 56, 57, 58, 59, 60, 61, 62, 63, 64, 65, 66, 67, 68, 69, 70, 71, 72, 73, 74, 75, 76, 77, 78, 79, 80, 81, 82, 83, 84, 85, 86, 87, 88, 89, 90, 91, 92, 93, 94, or 95 from baseline within 12, 16, 20, 24, 30, 36, 42, 48 or 52 weeks of initiation of said administering.

[0218] In some embodiments, the method provides a clinical benefit as measured by an increase in International Myositis Assessment and Clinical Studies Total Improvement Score (IMACS TIS) in the subject by 20 or more from baseline within 4 weeks of initiation of said administering. In some embodiments, the method provides a clinical benefit as measured by an increase in International Myositis Assessment and Clinical Studies Total Improvement Score (IMACS TIS) in the subject by 40 or more from baseline within 12 weeks of initiation of said administering.

[0219] In some embodiments, the increase in IMACS TIS is sustained for at least 20 weeks. In some embodiments, the increase in IMACS US is sustained for at least 20, 24, 36, 40, 44, or 48 weeks. In some embodiments, the increase in IMACS TIS is sustained for at least 48 weeks.-40- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)

[0220] In some embodiments, the method provides a clinical benefit as measured by an increase in International Myositis Assessment and Clinical Studies Total Improvement Score (IMACS TIS) in the subject by 40 or more from baseline within 12 weeks of initiation of said administering.

[0221] In some embodiments, the increase in IMACS TIS is sustained for at least 20 weeks. In some embodiments, the increase in IMACS TIS is sustained for at least 32, 36, or 40 weeks. In some embodiments, the increase in IMACS TIS is sustained for at least 40 weeks.

[0222] In some embodiments, the method provides a clinical benefit as measured by an increase in International Myositis Assessment and Clinical Studies Total Improvement Score (IMACS TIS) in the subject by 20 or more from baseline within 8 weeks of initiation of said administering. In some embodiments, the method provides a clinical benefit as measured by an increase in IMACS TIS in the subject by 40 or more from baseline within 16 weeks of initiation of said administering. In some embodiments, the method provides a clinical benefit as measured by an increase in IMACS TIS in the subject by 60 or more from baseline within 24 weeks of initiation of said administering

[0223] In any of the foregoing embodiments, the subject receives 5 mg / day, 7.5 mg / day, 10 mg / day, 12.5 mg / day, 15 mg / day, 17.5 mg / day, or 20 mg / day or less of glucocorticoid. In certain embodiments, the subject receives 5 mg / day or less of glucocorticoid. In some embodiments, the glucocorticoid is prednisone. In some embodiments, the glucocorticoid is prednisone or prednisone equivalent.

[0224] As used herein, the term "prednisone equivalent dose" refers to a dose of prednisone or an equivalent dose of a systemic corticosteroid other than prednisone. Systemic corticosteroids are well-known and include compounds of various potencies. Systemic corticosteroids may be formulated as injectables or pills. For examples, commercially available systemic corticosteroids include, but are not limited to, betamethasone, cortisone, dexamethasone, hydrocortisone, methylprednisolone, prednisone, prednisolone, and triamcinolone.

[0225] In some embodiments, the subject receives 5 mg / day or less of glucocorticoid from weeks 44 to week 52 of initiation of said administering.-41- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)

[0226] In some embodiments, the method provides a clinical benefit as measured by an increase in Manual Muscle Testing (MMT-8) score in the subject by more than 5, 10, 15, 20, 25, 30, 35, 40, 45, 50, 55, 60, 65, 70, 75, 80, 85, 90, 95, 100, 105, 110, 115, 120, 125, 130, 135, 140, or 145 from baseline within 12, 16, 20, 24, 30, 36, 42, 48 or 52 weeks of initiation of said administering. In some embodiments, the method provides a clinical benefit as measured by an increase in MMT-8 score in the subject by more than 10 from baseline within 12 weeks of initiation of said administering

[0227] In some embodiments, the increase in MMT-8 is sustained for at least 8, 12, 16, 20, 24, 30, 36, or 40 weeks. In some embodiments, the increase in MMT-8 is sustained for at least 40 weeks.

[0228] In some embodiments, the method provides a clinical benefit as measured by a decrease in Extramuscular Global Assessment (MDAAT) score in the subject by more than 1, 1.5, 2, 3, or 4 from baseline within 10, 12, 16, 20, 24, 30, 36, 42, 48 or 52 weeks of initiation of said administering. In some embodiments, the method provides a clinical benefit as measured by a decrease in MDAAT score in the subject by more than 1.5 from baseline within 12 weeks of initiation of said administering

[0229] In some embodiments, the decrease in MDAAT score is sustained for at least 12, 16, 20, 24, 30, 36, or 40 weeks. In some embodiments, the decrease in MDAAT score is sustained for at least 12 weeks. In some embodiments, the decrease in MDAAT score is sustained for at least 16 weeks. In some embodiments, the decrease in MDAAT score is sustained for at least 20 weeks. In some embodiments, the decrease in MDAAT score is sustained for at least 24 weeks. In some embodiments, the decrease in MDAAT score is sustained for at least 30 weeks. In some embodiments, the decrease in MDAAT score is sustained for at least 36 weeks. In some embodiments, the decrease in MDAAT score is sustained for at least 40 weeks.

[0230] In some embodiments, the method provides a clinical benefit as measured by a decrease in Physician Global Assessment (PhGA) score in the subject by more than 1, 2, 3, 4, 5, 6, 7, 8, 9 or 10 from baseline within 6, 8, 12, 16, 20, 24, 30, 36, 42, 48 or 52 weeks of initiation of said administering. In some embodiments, the method provides a clinical benefit as measured by a decrease in PhGA score in the subject by more than 2 from baseline within 8 weeks of initiation of said administering-42- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)

[0231] In some embodiments, the decrease in PhGA score is sustained for at least 12, 16, 20, 24, 30, 36, 40, or 44 weeks. In some embodiments, the decrease in PhGA score is sustained for at least 44 weeks.

[0232] In some embodiments, the method provides a clinical benefit as measured by a decrease in Cutaneous Dermatomyositis Activity-Investigator Global Assessment (CDA-IGA) score in the subject by more than 1, 2, 3, or 4 from baseline within 12, 16, 20, 24, 30, 36, 42, 48 or 52 weeks of initiation of said administering.

[0233] In some embodiments, the method provides a clinical benefit as measured by a decrease in Health Assessment Questionnaire Disability Index (HAQ-DI) score in the subject by more than 0.3 from baseline within 12 weeks of initiation of said administering. In some embodiments, the decrease in HAQ-DI score is sustained for at least 12, 16, 20, 24, 30, 36, or 40 weeks. In some embodiments, the decrease in HAQ-DI score is sustained for at least 40 weeks.

[0234] In some embodiments, the subject receives glucocorticoid at a first dose before initiation of said administering, and the method provides a clinical benefit as indicated by the subject receiving glucocorticoid at a second dose that is lower than the first dose within 8, 10, 12, 14, 16, 18, 20, 22, 24, 26, 28, 30, 32, 34, 36, 38, 40, 42, 44, 46, 48, 50 or 52 weeks or more weeks of initiation of said administering. In some embodiments, the method provides a clinical benefit as indicated by the subject receiving glucocorticoid at a second dose that is lower than the first dose within 8, 12, 16, 24, 40, or 44 weeks of initiation of said administering

[0235] In some embodiments, the first dose of glucocorticoid is higher than 7.5 mg, higher than 10 mg, higher than 12.5 mg, higher than 15 mg, or higher than 17.5 mg per day. In some embodiments, the first dose is higher than 7.5 mg per day. In some embodiments, the first dose is higher than 5 mg per day.

[0236] In some embodiments, the second dose of glucocorticoid is 5 mg per day or lower. In some embodiments, the second dose of glucocorticoid is 0.5 mg per day, 1 mg per day, 1.5 mg per day, 2 mg per day, or 2.5 mg per day lower than the first dose of glucocorticoid. In some embodiments, the second dose of glucocorticoid is 2.5 mg per day lower than the first dose of glucocorticoid-43- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)

[0237] As used herein, the term "glucocorticoid" refers to a compound that belongs to the family of compounds called corticosteroids (steroids). Prednisone is an example of a glucocorticoid.

[0238] In some embodiments, the method provides a clinical benefit as measured by an increase of 20 or more in International Myositis Assessment and Clinical Studies Total Improvement Score (IMACS TIS) in the subject from baseline; and the subject receives glucocorticoid at a first dose before initiation of said administering, and the method provides a clinical benefit as indicated by the subject receiving glucocorticoid at a second dose that is lower than the first dose, wherein the second dose is 5 mg per day or lower within 44, 48, 50, or 52 weeks of initiation of said administering.

[0239] In some embodiments, the administration of nipocalimab increases total cholesterol in the subject by at most 18 mg / dL, at most 17 mg / dL, at most 16 mg / dL, at most 15 mg / dL, at most 14 mg / dL, at most 13 mg / dL, or at most 12 mg / dL from baseline total cholesterol.

[0240] In some embodiments, the administration of nipocalimab increases HDL in the subject at most 8 mg / dL, at most 7 mg / dL, at most 6 mg / dL, at most 5 mg / dL, at most 4 mg / dL, at most 3 mg / dL, or at most 2 mg / dL from baseline HDL.

[0241] In some embodiments, the administration of nipocalimab increases LDL in the subject at most 12 mg / dL, at most 11 mg / dL, at most 10 mg / dL, at most 9 mg / dL, at most 8 mg / dL, at most 7 mg / dL, at most 6 mg / dL, or at most 5 mg / dL from baseline LDL.

[0242] In some embodiments, the administration of nipocalimab reduces serum albumin in the subject by at most 18%, at most 16%, at most 14%, at most 12%, at most 10%, at most 8%, at most 6%, at most 4%, or at most 2% from baseline serum albumin.

[0243] In some embodiments, the method provides a clinical benefit as measured by a reduction in creatine kinase (CK) in the subject by 500 IU / L relative to a baseline CK level in the subject prior to initiation of said administering within 4 weeks of initiation of said administering. In some embodiments, the reduction in CK is sustained for at least 48 weeks.

[0244] In some embodiments, the method provides a clinical benefit as measured by a reduction in creatine kinase (CK) in the subject by 1000 IU / L relative to a baseline CK level in the-44- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)subject prior to initiation of said administering within 12 weeks of initiation of said administering. In some embodiments, the reduction in CK is sustained for at least 40 weeks.

[0245] In some embodiments, the method provides a clinical benefit as measured by a reduction in Alanine aminotransferase (ALT) in the subject by 25 IU / L relative to a baseline ALT level in the subject prior to initiation of said administering within 12 weeks of initiation of said administering. In some embodiments, the reduction in ALT is sustained for at least 40 weeks.

[0246] In some embodiments, the method provides a clinical benefit as measured by a reduction in Aspartate aminotransferase (AST) in the subject by 20 IU / L relative to a baseline AST level in the subject prior to initiation of said administering within 12 weeks of initiation of said administering. In some embodiments, the reduction in AST is sustained for at least 40 weeks

[0247] In some embodiments, the method provides a clinical benefit as measured by a reduction in lactate dehydrogenase (LDH) in the subject by 50 IU / L relative to a baseline LDH level in the subject prior to initiation of said administering within 12 weeks of initiation of said administering. In some embodiments, the reduction in LDH is sustained for at least 40 weeks.

[0248] In some embodiments, the method provides a clinical benefit as measured by a reduction in aldolase in the subject by 10 IU / L relative to a baseline aldolase level in the subject prior to initiation of said administering within 12 weeks of initiation of said administering. In some embodiments, the reduction in aldolase is sustained for at least 40 weeks

[0249] In some embodiments, the subject is positive for at least one autoantibody selected from the group consisting of anti-Jo-1, anti-PL7, anti-PL12, anti-0 J, and anti-EJ antibodies. In some embodiments, the subject is positive for at least one autoantibody selected from the group consisting of anti-SRP and anti-HMGCR antibodies. In some embodiments, the subject is positive for at least one autoantibody selected from the group consisting of anti-Mi-2, anti-TTFl, anti-NXP-2, anti-SAE, and anti-MDA-5 antibodies.

[0250] In some embodiments, the idiopathic inflammatory myopathy (IIM) is anti-synthetase Syndrome (ASyS). In some embodiments, the idiopathic inflammatory myopathy (IIM) is dermatomyositis (DM). In some embodiments, the idiopathic inflammatory myopathy (IIM) is immune-mediated necrotizing myopathy (IMNM). In some embodiments, the idiopathic inflammatory myopathy (IIM) is inclusion body myositis (IBM).-45- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)

[0251] It will be appreciated by those skilled in the art that changes could be made to the embodiments described above without departing from the broad inventive concept thereof. It is understood, therefore, that this invention is not limited to the particular embodiments disclosed, but it is intended to cover modifications within the spirit and scope of the present invention as defined by the present description.

[0252] The following list of embodiments is intended to complement, rather than displace or supersede, the previous descriptions:

[0253] Embodiment Section

[0254] Embodiment 1. A method of treating an autoimmune disease in a subject in need thereof, the method comprising subcutaneously administering nipocalimab to the subject at a dose (a) from about 1000 mg to about 2000 mg every two weeks; or (b) from about 400 mg to about 600 mg every week.

[0255] Embodiment 2. The method of embodiment 1, wherein nipocalimab is administered every two weeks subcutaneously at a dose from about 1200 mg to about 1800 mg via an on-body device.

[0256] Embodiment 3. The method of embodiment 1 or embodiment 2, wherein nipocalimab is administered every two weeks subcutaneously at a dose from about 1400 mg to about 1600 mg via an on-body device.

[0257] Embodiment 4. The method of any one of embodiments 1-3, wherein nipocalimab is administered every two weeks subcutaneously at a dose of about 1500 mg via an on-body device.

[0258] Embodiment 5. The method of embodiment 1, wherein nipocalimab is administered every week subcutaneously at a dose from about 400 mg to about 600 mg via an autoinjector.

[0259] Embodiment 6. The method of embodiment 5, wherein the subject receives a second subcutaneous administration of nipocalimab at a dose from about 400 mg to about 600 mg via an auto injector in the first week.-46- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)

[0260] Embodiment 7. The method of embodiment 1 or embodiment 5, wherein nipocalimab is administered every week subcutaneously at a dose from about 450 mg to about 550 mg via an auto injector.

[0261] Embodiment 8. The method of embodiment 7, wherein the subject receives a second subcutaneous administration of nipocalimab at a dose from about 450 mg to about 550 mg via an auto injector in the first week.

[0262] Embodiment 9. The method of any one of embodiments 1, 5-8, wherein nipocalimab is administered every week subcutaneously at a dose of about 518 mg via an autoinjector.

[0263] Embodiment 10. The method of embodiment 9, wherein the subject receives a second subcutaneous administration of nipocalimab at a dose of about 518 mg via an autoinjector in the first week.

[0264] Embodiment 11. The method of embodiment 9, wherein the subject receives a second subcutaneous administration of nipocalimab at a dose of about 518 mg via an autoinjector in the first day.

[0265] Embodiment 12. The method of any one of embodiments 1, 5-8, wherein nipocalimab is administered every week subcutaneously at a dose of about 460 mg via an autoinjector.

[0266] Embodiment 13. The method of embodiment 12, wherein the subject receives a second subcutaneous administration of nipocalimab at a dose of about 460 mg via an autoinjector in the first week.

[0267] Embodiment 14. The method of embodiment 12, wherein the subject receives a second subcutaneous administration of nipocalimab at a dose of about 460 mg via an autoinjector in the first day.

[0268] Embodiment 15. The method of any one of embodiments 1-14, wherein the autoimmune disease is warm autoimmune hemolytic anemia (wAIHA), generalized myasthenia gravis (gMG), chronic inflammatory demyelinating polyneuropathy (CIDP), or idiopathic inflammatory myopathies (IIM).-47- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)

[0269] Embodiment 16. The method of any one of embodiments 1-15, wherein the administration of nipocalimab reduces serum IgG in the subject by at least 60% from baseline serum IgG, at least 65% from baseline serum IgG, at least 70% from baseline serum IgG, at least 75% from baseline serum IgG, or at least 80% from baseline serum IgG.

[0270] Embodiment 17. The method of any one of embodiments 1-16, wherein the administration of nipocalimab increases total cholesterol in the subject by at most 18 mg / dL, at most 17 mg / dL, at most 16 mg / dL, at most 15 mg / dL, at most 14 mg / dL, at most 13 mg / dL, or at most 12 mg / dL from baseline total cholesterol.

[0271] Embodiment 18. The method of any one of embodiments 1-17, wherein the administration of nipocalimab increases HDL in the subject at most 8 mg / dL, at most 7 mg / dL, at most 6 mg / dL, at most 5 mg / dL, at most 4 mg / dL, at most 3 mg / dL, or at most 2 mg / dL from baseline HDL.

[0272] Embodiment 19. The method of any one of embodiments 1-18, wherein the administration of nipocalimab increases LDL in the subject at most 12 mg / dL, at most 11 mg / dL, at most 10 mg / dL, at most 9 mg / dL, at most 8 mg / dL, at most 7 mg / dL, at most 6 mg / dL, or at most 5 mg / dL from baseline LDL.

[0273] Embodiment 20. The method of any one of embodiments 1-19, wherein the administration of nipocalimab reduces serum albumin in the subject by at most 18%, at most 16%, at most 14%, at most 12%, at most 10%, at most 8%, at most 6%, at most 4%, or at most 2% from baseline serum albumin.

[0274] Embodiment 21. A method of reducing serum IgG in a subject in need thereof, the method comprising administering nipocalimab to the subject at a dose (a) from about 1000 mg to about 2000 mg every two weeks; or (b) from about 400 mg to about 600 mg every week; wherein the administration of nipocalimab reduces serum IgG in the subject by at least 60% from baseline serum IgG, at least 65% from baseline serum IgG, at least 70% from baseline serum IgG, at least 75% from baseline serum IgG, or at least 80% from baseline serum IgG.

[0275] Embodiment 22. The method of embodiment 21, wherein nipocalimab is administered every two weeks subcutaneously at a dose from about 1200 mg to about 1800 mg via an on-body device.-48- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)

[0276] Embodiment 23. The method of embodiment 21 or embodiment 22, wherein nipocalimab is administered every two weeks subcutaneously at a dose from about 1400 mg to about 1600 mg via an on-body device.

[0277] Embodiment 24. The method of any one of embodiments 21-23, wherein nipocalimab is administered every two weeks subcutaneously at a dose of about 1500 mg via an on-body device.

[0278] Embodiment 25. The method of embodiment 21, wherein nipocalimab is administered every week subcutaneously at a dose from about 400 mg to about 600 mg via an autoinjector.

[0279] Embodiment 26. The method of embodiment 25, wherein the subject receives a second subcutaneous administration of nipocalimab at a dose from about 400 mg to about 600 mg via an auto injector in the first week.

[0280] Embodiment 27. The method of embodiment 21 or embodiment 25, wherein nipocalimab is administered every week subcutaneously at a dose from about 450 mg to about 550 mg via an autoinjector.

[0281] Embodiment 28. The method of embodiment 27, wherein the subject receives a second subcutaneous administration of nipocalimab at a dose from about 450 mg to about 550 mg via an auto injector in the first week.

[0282] Embodiment 29. The method of any one of embodiments 21, 25, or 27, wherein nipocalimab is administered every week subcutaneously at a dose of about 518 mg via an auto injector.

[0283] Embodiment 30. The method of embodiment 29, wherein the subject receives a second subcutaneous administration of nipocalimab at a dose of about 518 mg via an autoinjector in the first week.

[0284] Embodiment 31. The method of embodiment 29, wherein the subject receives a second subcutaneous administration of nipocalimab at a dose of about 518 mg via an autoinjector in the first day.-49- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)

[0285] Embodiment 32. The method of any one of embodiments 21, 25, or 27, wherein nipocalimab is administered every week subcutaneously at a dose of about 460 mg via an auto injector.

[0286] Embodiment 33. The method of embodiment 32, wherein the subject receives a second subcutaneous administration of nipocalimab at a dose of about 460 mg via an autoinjector in the first week.

[0287] Embodiment 34. The method of embodiment 32, wherein the subject receives a second subcutaneous administration of nipocalimab at a dose of about 460 mg via an autoinjector in the first day.

[0288] Embodiment 35. The method of any one of embodiments 21-34, wherein the subject has warm autoimmune hemolytic anemia (wAIHA), generalized myasthenia gravis (gMG), chronic inflammatory demyelinating polyneuropathy (CIDP), or idiopathic inflammatory myopathies (IIM).

[0289] Embodiment 36. The method of any one of embodiments 21-35, wherein the administration of nipocalimab increases total cholesterol in the subject by at most 18 mg / dL, at most 17 mg / dL, at most 16 mg / dL, at most 15 mg / dL, at most 14 mg / dL, at most 13 mg / dL, or at most 12 mg / dL from baseline total cholesterol.

[0290] Embodiment 37. The method of any one of embodiments 21-36, wherein the administration of nipocalimab increases HDL in the subject at most 8 mg / dL, at most 7 mg / dL, at most 6 mg / dL, at most 5 mg / dL, at most 4 mg / dL, at most 3 mg / dL, or at most 2 mg / dL from baseline total HDL.

[0291] Embodiment 38. The method of any one of embodiments 21-37, wherein the administration of nipocalimab increases LDL in the subject at most 12 mg / dL, at most 11 mg / dL, at most 10 mg / dL, at most 9 mg / dL, at most 8 mg / dL, at most 7 mg / dL, at most 6 mg / dL, or at most 5 mg / dL from baseline LDL.

[0292] Embodiment 39. The method of any one of embodiments 21-38, wherein the administration of nipocalimab reduces serum albumin in the subject by at most 18%, at most 16%, at most 14%, at most 12%, at most 10%, at most 8%, at most 6%, at most 4%, or at most 2% from baseline serum albumin.-50- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)

[0293] Embodiment 40. A method of treating generalized myasthenia gravis (gMG) in a subject in need thereof, the method comprising subcutaneously administering nipocalimab to the subject at a dose (a) from about 1000 mg to about 2000 mg every two weeks; or (b) from about 400 mg to about 600 mg every week.

[0294] Embodiment 41. The method of embodiment 40, wherein nipocalimab is administered every two weeks subcutaneously at a dose from about 1200 mg to about 1800 mg via an on-body device.

[0295] Embodiment 42. The method of embodiment 40 or embodiment 41, wherein nipocalimab is administered every two weeks subcutaneously at a dose from about 1400 mg to about 1600 mg via an on-body device.

[0296] Embodiment 43. The method of any one of embodiments 40-42, wherein nipocalimab is administered every two weeks subcutaneously at a dose of about 1500 mg via an on-body device.

[0297] Embodiment 44. The method of embodiment 43, wherein nipocalimab is administered every week subcutaneously at a dose from about 400 mg to about 600 mg via an autoinjector.

[0298] Embodiment 45. The method of embodiment 44, wherein the subject receives a second subcutaneous administration of nipocalimab at a dose from about 400 mg to about 600 mg via an auto injector in the first week.

[0299] Embodiment 46. The method of embodiment 40 or embodiment 44, wherein nipocalimab is administered every week subcutaneously at a dose from about 450 mg to about 550 mg via an autoinjector.

[0300] Embodiment 47. The method of embodiment 46, wherein the subject receives a second subcutaneous administration of nipocalimab at a dose from about 450 mg to about 550 mg via an auto injector in the first week.

[0301] Embodiment 48. The method of any one of embodiments 40, 44, or 46, wherein nipocalimab is administered every week subcutaneously at a dose of about 518 mg via an auto injector.-51- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)

[0302] Embodiment 49. The method of embodiment 48, wherein the subject receives a second subcutaneous administration of nipocalimab at a dose of about 518 mg via an autoinjector in the first week.

[0303] Embodiment 50. The method of embodiment 48, wherein the subject receives a second subcutaneous administration of nipocalimab at a dose of about 518 mg via an autoinjector in the first day.

[0304] Embodiment 51. The method of any one of embodiments 40, 44, or 46, wherein nipocalimab is administered every week subcutaneously at a dose of about 460 mg via an auto injector.

[0305] Embodiment 52. The method of embodiment 51, wherein the subject receives a second subcutaneous administration of nipocalimab at a dose of about 460 mg via an autoinjector in the first week.

[0306] Embodiment 53. The method of embodiment 51, wherein the subject receives a second subcutaneous administration of nipocalimab at a dose of about 460 mg via an autoinjector in the first day.

[0307] Embodiment 54. The method of any one of embodiments 40-53, wherein the method provides a clinical benefit as measured by a decrease in MG-ADL score in the subject by more than 4.0, 4.1, 4.2, 4.3, 4.4, 4.5, 4.6, 4.7, 4.8, 4.9, 5.0, 5.1, 5.2, 5.3, 5.4, 5.6, 5.7, 5.8, 5.9 or 6.0 from baseline within 12, 14, 16, 18, 20, 22, 24, 26, 28, 30, 36, 42, 48 or 52 weeks of initiation of said administering.

[0308] Embodiment 55. The method of any one of embodiments 40-54, wherein the method provides a clinical benefit as measured by a decrease in QMG score in the subject by more than 4.0, 4.1, 4.2, 4.3, 4.4, 4.5, 4.6, 4.7, 4.8, 4.9, or 5.0 from baseline within 12, 14, 16, 18, 20, 22, 24, 26, 28, 30, 36, 42, 48 or 52 weeks of initiation of said administering.

[0309] Embodiment 56. The method of any one of embodiments 40-55, wherein the subject is positive for one or more of anti-AChR antibody, anti-MuSK antibody, and anti-LRP4 antibody.

[0310] Embodiment 57. The method of any one of embodiments 40-56, wherein the administration of nipocalimab increases total cholesterol in the subject by at most 18 mg / dL, at -52- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)most 17 mg / dL, at most 16 mg / dL, at most 15 mg / dL, at most 14 mg / dL, at most 13 mg / dL, or at most 12 mg / dL from baseline total cholesterol.

[0311] Embodiment 58. The method of any one of embodiments 40-57, wherein the administration of nipocalimab increases HDL in the subject at most 8 mg / dL, at most 7 mg / dL, at most 6 mg / dL, at most 5 mg / dL, at most 4 mg / dL, at most 3 mg / dL, or at most 2 mg / dL from baseline HDL.

[0312] Embodiment 59. The method of any one of embodiments 40-58, wherein the administration of nipocalimab increases LDL in the subject at most 12 mg / dL, at most 11 mg / dL, at most 10 mg / dL, at most 9 mg / dL, at most 8 mg / dL, at most 7 mg / dL, at most 6 mg / dL, or at most 5 mg / dL from baseline LDL.

[0313] Embodiment 60. The method of any one of embodiments 40-59, wherein the administration of nipocalimab reduces serum albumin in the subject by at most 18%, at most 16%, at most 14%, at most 12%, at most 10%, at most 8%, at most 6%, at most 4%, or at most 2% from baseline serum albumin.

[0314] Embodiment 61. A method of treating warm autoimmune hemolytic anemia (wAIHA) in a subject in need thereof, the method comprising subcutaneously administering nipocalimab to the subject at a dose (a) from about 1000 mg to about 2000 mg every two weeks; or (b) from about 400 mg to about 600 mg every week.

[0315] Embodiment 62. The method of embodiment 61, wherein nipocalimab is administered every two weeks subcutaneously at a dose from about 1200 mg to about 1800 mg via an on-body device.

[0316] Embodiment 63. The method of embodiment 61 or embodiment 62, wherein nipocalimab is administered every two weeks subcutaneously at a dose from about 1400 mg to about 1600 mg via an on-body device.

[0317] Embodiment 64. The method of any one of embodiments 61-63, wherein nipocalimab is administered every two weeks subcutaneously at a dose of about 1500 mg via an on-body device.

[0318] Embodiment 65. The method of embodiment 61, wherein nipocalimab is administered every week subcutaneously at a dose from about 400 mg to about 600 mg via an autoinjector.-53- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)

[0319] Embodiment 66. The method of embodiment 65, wherein the subject receives a second subcutaneous administration of nipocalimab at a dose from about 400 mg to about 600 mg via an auto injector in the first week.

[0320] Embodiment 67. The method of any one of embodiments 61 or 65, wherein nipocalimab is administered every week subcutaneously at a dose from about 450 mg to about 550 mg via an autoinjector.

[0321] Embodiment 68. The method of embodiment 67, wherein the subject receives a second subcutaneous administration of nipocalimab at a dose from about 450 mg to about 550 mg via an auto injector in the first week.

[0322] Embodiment 69. The method of any one of embodiments 61, 65, or 67, wherein nipocalimab is administered every week subcutaneously at a dose of about 518 mg via an auto injector.

[0323] Embodiment 70. The method of embodiment 69, wherein the subject receives a second subcutaneous administration of nipocalimab at a dose of about 518 mg via an autoinjector in the first week.

[0324] Embodiment 71. The method of embodiment 69, wherein the subject receives a second subcutaneous administration of nipocalimab at a dose of about 518 mg via an autoinjector in the first day.

[0325] Embodiment 72. The method of any one of embodiments 61-71, wherein the method provides a clinical benefit as measured by an increase in a hemoglobin (Hgb) level in the subject of more than 0.5, 1, 1.5, 2, 2.5, 3, 3.5, 4, 4.5, 5, 5.5, 6, 6.5, 7, 7.5, 8, 8.5, 9, 9.5, or 10 g / dL within 1, 2, 4, 6, 8, 10, 12, 14, 16, 18, 20, 22, 24, 30, 36, 42, 48 or 52 weeks of initiation of said administering relative to a baseline Hgb level in the subject prior to initiation of said administering.

[0326] Embodiment 73. The method of embodiment 4, wherein the method provides a clinical benefit as measured by an increase in the hemoglobin (Hgb) level in the subject of 1.5 g / dL or more relative to the baseline within 4 weeks of initiation of said administering.-54- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)

[0327] Embodiment 74. The method of embodiment 4, wherein the method provides a clinical benefit as measured by an increase in the hemoglobin (Hgb) level in the subject of 2 g / dL or more relative to the baseline within 4 weeks of initiation of said administering.

[0328] Embodiment 75. The method of any one of embodiments 1-6, wherein the method provides a clinical benefit as measured by achievement of a hemoglobin (Hgb) level in the subject of 10 g / dL or more within 1, 2, 3, or 4 weeks of initiation of said administering.

[0329] Embodiment 76. The method of any one of embodiments 1-7, wherein the method provides a clinical benefit within 16 weeks of initiation of said administering as measured by: achievement of a hemoglobin (Hgb) level in the subject of 10 g / dL or more; and an increase in a hemoglobin (Hgb) level in the subject of 1.5 g / dL or more relative to a baseline level of Hgb in the subject prior to initiation of said administering.

[0330] Embodiment 77. The method of any one of embodiments 1-7, wherein the method provides a clinical benefit within 16 weeks of initiation of said administering as measured by: achievement of a hemoglobin (Hgb) level in the subject of 10 g / dL or more; and an increase in a hemoglobin (Hgb) level in the subject of 2 g / dL or more relative to a baseline level of Hgb in the subject prior to initiation of said administering.

[0331] Embodiment 78. The method of any one of embodiments 72-77, wherein the clinical benefit is sustained for at least 28 days.

[0332] Embodiment 79. The method of any one of embodiments 72-77, wherein the clinical benefit is sustained for at least 6, 8, or 12 weeks.

[0333] Embodiment 80. The method of any one of embodiments 72-77, wherein the clinical benefit is sustained for at least 16 weeks.

[0334] Embodiment 81. The method of any one of embodiments 72-77, wherein the clinical benefit is sustained for at least 24 weeks.

[0335] Embodiment 82. The method of any one of embodiments 72-77, wherein the clinical benefit is sustained for at least 52 weeks.-55- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)

[0336] Embodiment 83. The method of any one of embodiments 72-77, wherein the method provides a clinical benefit as measured by:achievement of a hemoglobin (Hgb) level in the subject of 10 g / dL or more; andan increase in a hemoglobin (Hgb) level in the subject by 2 g / dL or more relative to a baseline level of Hgb in the subject prior to initiation of said administering,wherein the clinical benefit is sustained for at least 28 days, wherein the clinical benefit is achieved within 16 weeks of initiation of said administering, and wherein the subject did not receive a rescue therapy.

[0337] Embodiment 84. The method of embodiment 83, wherein the rescue therapy comprises increased corticosteroids, blood transfusion, or intravenous immunoglobulin (IVIg) administration.

[0338] Embodiment 85. The method of any one of embodiments 61-84, wherein the method provides a clinical benefit as measured by an increase in a Functional Assessment of Chronic Illness Therapy-Fatigue (FACIT-Fatigue) score in the subject by more than 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31, or 32 relative to a baseline FACIT-Fatigue score in the subject prior to initiation of said administering within 2, 4, 6, 8, 10, 12, 14, 16, 18, 20, 22, 24, 30, 36, 42, 48 or 52 weeks of initiation of said administering.

[0339] Embodiment 86. The method of any one of embodiments 61-85, wherein the method provides a clinical benefit as measured by an increase in a Functional Assessment of Chronic Illness Therapy -Fatigue (FACIT-Fatigue) score in the subject by 2.95 or more relative to a baseline FACIT-Fatigue score in the subject prior to initiation of said administering within 24 weeks of initiation of said administering.

[0340] Embodiment 87. The method of any one of embodiments 61-86, wherein the method provides a clinical benefit as measured by an increase in a Functional Assessment of Chronic Illness Therapy-Fatigue (FACIT-Fatigue) score in the subject by 3.4 or more relative to a baseline FACIT-Fatigue score in the subject prior to initiation of said administering within 24 weeks of initiation of said administering.

[0341] Embodiment 88. The method of any one of embodiments 61-87, wherein the subject receives corticosteroid at a first dose before initiation of said administering, and the method provides a clinical benefit as indicated by the subject receives corticosteroid at a second dose that is-56- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)at least 10%, 15%, 20%, 25%, 30%, 35%, 40%, 45%, 50%, 55%, 60%, 65%, or 70% lower than the first dose within 24, 30, 36, 42, 48 or 52 weeks or more weeks of initiation of said administering.

[0342] Embodiment 89. The method of any one of embodiments 61-88, wherein the subject receives corticosteroid at a first dose before initiation of said administering, and the method provides a clinical benefit as indicated by the subject receives corticosteroid at a second dose that is at least 20% lower than the first dose within 24 weeks or more weeks of initiation of said administering.

[0343] Embodiment 90. The method of any one of embodiments 61-89, wherein the subject receives corticosteroid at a first dose before initiation of said administering, and the method provides a clinical benefit as indicated by the subject receives corticosteroid at a second dose that is at least 60% lower than the first dose within 48 weeks or more weeks of initiation of said administering.

[0344] Embodiment 91. The method of embodiment 90, wherein the corticosteroid is prednisone.

[0345] Embodiment 92. The method of any one of embodiments 61-91, wherein the method provides a clinical benefit as measured by:achievement of a hemoglobin (Hgb) level in the subject of 10 g / dL or more;an increase in a hemoglobin (Hgb) level in the subject by 2 g / dL or more relative to a baseline level of Hgb in the subject prior to initiation of said administering,wherein the clinical benefit is sustained for at least 28 days, wherein the clinical benefit is achieved within 16 weeks of initiation of said administering, and wherein the subject did not receive a rescue therapy;and wherein the method provides a further clinical benefit as measured by:an increase in a Functional Assessment of Chronic Illness Therapy -Fatigue (FACIT-Fatigue) score in the subject by more than 3 within 24 weeks of initiation of said administering relative to a baseline FACIT-Fatigue score in the subject prior to initiation of said administering; and-57- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)the subject receives corticosteroid at a second dose that is at least 20% lower than the first dose within 24 weeks or more weeks of initiation of said administering, wherein the subject receives corticosteroid at a first dose before initiation of said administering.

[0346] Embodiment 93. The method of embodiment 92, wherein the rescue therapy comprises corticosteroids, blood transfusion, or intravenous immunoglobulin (IVIg).

[0347] Embodiment 94. The method of any one of embodiments 61-93, wherein the method provides a clinical benefit as measured by a reduction in total IgG in the subject by more than 20%, 30%, 40%, 50%, 60%, 70%, 80%, or 90% relative to a baseline level of total IgG in the subject prior to initiation of said administering within 8, 10, 12, 14, 16, 18, 20, 22, 24, 30, 36, 42, 48 or 52 weeks of initiation of said administering.

[0348] Embodiment 95. The method of any one of embodiments 61-94, wherein the administration of nipocalimab increases total cholesterol in the subject by at most 14%, relative to a baseline level of total cholesterol in the subject prior to initiation of said administering.

[0349] Embodiment 96. The method of any one of embodiments 61-95, wherein the administration of nipocalimab increases LDL in the subject at most 5% relative to a baseline level of LDL in the subject prior to initiation of said administering.

[0350] Embodiment 97. The method of any one of embodiments 61-96, wherein the administration of nipocalimab reduces serum albumin in the subject by at most 10 g / L relative to a baseline serum albumin in the subject prior to initiation of said administering.

[0351] Embodiment 98. The method of any one of embodiments 61-97, wherein the subject is 12 years or older.

[0352] Embodiment 99. The method of any one of embodiments 61-98, wherein the subject is 18 years or older.

[0353] Embodiment 100. The method of any one of embodiments 61-99, wherein the subject is from 12 to 18 years old.

[0354] Embodiment 101. The method of any one of embodiments 61-100, wherein the method provides a clinical benefit as measured by a reduction in wAIHA-related pathogenic autoantibodies -58- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)in the subject by more than 15%, 20%, 30%, or 40% relative to a baseline level of wAIHA-related pathogenic autoantibodies in the subject prior to initiation of said administering and within 1, 2, 4, 6, 8, 10, 12, 14, 16, 18, 20, 22, 24, 30, 36, 42, 48, or 52 weeks of initiation of said administering.

[0355] Embodiment 102. The method of any one of embodiments 61-101, wherein the subject receives a plurality of 30 mg / kg intravenous doses of nipocalimab based on the weight of the subject, wherein the first dose is administered to the subject over at least 30 minutes, and wherein the subsequent doses are administered over at least 15 minutes.

[0356] Embodiment 103. A method of treating chronic inflammatory demyelinating polyneuropathy (CIDP) in a subject in need thereof, the method comprising subcutaneously administering nipocalimab to the subject at a dose(a) from about 1000 mg to about 2000 mg every two weeks; or(b) from about 400 mg to about 600 mg every week.

[0357] Embodiment 104. The method of embodiment 103, wherein nipocalimab is administered every two weeks subcutaneously at a dose from about 1200 mg to about 1800 mg via an on-body device.

[0358] Embodiment 105. The method of embodiment 103 or embodiment 104, wherein nipocalimab is administered every two weeks subcutaneously at a dose from about 1400 mg to about 1600 mg via an on-body device.

[0359] Embodiment 106. The method of any one of embodiments 103-105, wherein nipocalimab is administered every two weeks subcutaneously at a dose of about 1500 mg via an on-body device.

[0360] Embodiment 107. The method of embodiment 103, wherein nipocalimab is administered every week subcutaneously at a dose from about 400 mg to about 600 mg via an auto injector.

[0361] Embodiment 108. The method of embodiment 107, wherein the subject receives a second subcutaneous administration of nipocalimab at a dose from about 400 mg to about 600 mg via an autoinjector in the first week.-59- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)

[0362] Embodiment 109. The method of embodiment 103 or embodiment 107, wherein nipocalimab is administered every week subcutaneously at a dose from about 450 mg to about 550 mg via an autoinjector.

[0363] Embodiment 110. The method of embodiment 109, wherein the subject receives a second subcutaneous administration of nipocalimab at a dose from about 450 mg to about 550 mg via an autoinjector in the first week.

[0364] Embodiment 111. The method of any one of embodiments 103, 107, or 109, wherein nipocalimab is administered every week subcutaneously at a dose of about 518 mg via an auto injector.

[0365] Embodiment 112. The method of embodiment 111, wherein the subject receives a second subcutaneous administration of nipocalimab at a dose of about 518 mg via an autoinjector in the first week.

[0366] Embodiment 113. The method of embodiment 111, wherein the subject receives a second subcutaneous administration of nipocalimab at a dose of about 518 mg via an autoinjector in the first day.

[0367] Embodiment 114. The method of any one of embodiments 103-113, wherein the method provides a clinical benefit as measured by a reduction of at least 1 in adjusted Inflammatory Neuropathy Cause and Treatment (INCAT) score in the subject within 10 weeks of initiation of said administering, compared to an initial INCAT score determined at baseline.

[0368] Embodiment 115. The method of embodiment 114, wherein the subject maintains or has a further reduction in the adjusted INCAT score from week 10 to week 12, week 16, week 20, week 24, week 28, week 32, week 36, week 40, week 42, week 44, week 48, or week 52 from initiation of said administering.

[0369] Embodiment 116. The method of any one of embodiments 103-115, wherein the method provides a clinical benefit as measured by an increase of at least 8kPa, lOkPa, 12kPa, or 14kPa in grip strength for the dominant hand of the subject by week 10 from initiation of said administering, compared to an initial grip strength determined at baseline.-60- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)

[0370] Embodiment 117. The method of embodiment 116, wherein the subject maintains or has a further increase in the grip strength for the dominant hand of the subject from week 10 to week 12, week 16, week 20, week 24, week 28, week 32, week 36, week 40, week 42, week 44, week 48, or week 52 from initiation of said administering.

[0371] Embodiment 118. The method of any one of embodiments 103-117, wherein the method provides a clinical benefit as measured by an increase of at least 8kPa, lOkPa, 12kPa, or 14kPa in grip strength for the non-dominant hand of the subject by week 10 from initiation of said administering, compared to an initial grip strength determined at baseline.

[0372] Embodiment 119. The method of embodiment 118, wherein the subject maintains or has a further increase in the grip strength for the non-dominant hand of the subject from week 10 to week 12, week 16, week 20, week 24, week 28, week 32, week 36, week 40, week 42, week 44, week 48, or week 52 from initiation of said administering.

[0373] Embodiment 120. The method of any one of embodiments 103-119, wherein the method provides a clinical benefit as measured by an increase in Inflammatory Rasch-built Overall Disability Scale (I-RODS) centile score in the subject by at least 4, 5, 6, 7, or 8 points by week 12, 16, 20, 24, 28, 32, 36, 40, 42, 44, 48, or 52 from initiation of said administering, compared to an initial I-RODS score determined at baseline.

[0374] Embodiment 121. The method of any one of embodiments 103-120, wherein the method provides a clinical benefit as measured by an increase in MRC Muscle Grading Sale Sum score in the subject by at least 4, 5, 6, 7, or 8 by week 12, 16, 20, 24, 28, 32, 36, 40, 42, 44, 48, or 52 from initiation of said administering, compared to an initial MRC Muscle Grading Sale Sum score determined at baseline.

[0375] Embodiment 122. The method of any one of embodiments 103-121, wherein the administration of nipocalimab increases total cholesterol in the subject by at most 18 mg / dL, at most 17 mg / dL, at most 16 mg / dL, at most 15 mg / dL, at most 14 mg / dL, at most 13 mg / dL, or at most 12 mg / dL from baseline total cholesterol.

[0376] Embodiment 123. The method of any one of embodiments 103-122, wherein the administration of nipocalimab increases HDL in the subject at most 8 mg / dL, at most 7 mg / dL, at-61- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)most 6 mg / dL, at most 5 mg / dL, at most 4 mg / dL, at most 3 mg / dL, or at most 2 mg / dL from baseline HDL.

[0377] Embodiment 124. The method of any one of embodiments 103-123, wherein the administration of nipocalimab increases LDL in the subject at most 12 mg / dL, at most 11 mg / dL, at most 10 mg / dL, at most 9 mg / dL, at most 8 mg / dL, at most 7 mg / dL, at most 6 mg / dL, or at most 5 mg / dL from baseline LDL.

[0378] Embodiment 125. The method of any one of embodiments 103-124, wherein the administration of nipocalimab reduces serum albumin in the subject by at most 18%, at most 16%, at most 14%, at most 12%, at most 10%, at most 8%, at most 6%, at most 4%, or at most 2% from baseline serum albumin.

[0379] Embodiment 126. A method of treating idiopathic inflammatory myopathies (IIM) in a subject in need thereof, the method comprising subcutaneously administering nipocalimab to the subject at a dose(a) from about 1000 mg to about 2000 mg every two weeks; or(b) from about 400 mg to about 600 mg every week.

[0380] Embodiment 127. The method of embodiment 126, wherein nipocalimab is administered every two weeks subcutaneously at a dose from about 1200 mg to about 1800 mg via an on-body device.

[0381] Embodiment 128. The method of embodiment 126 or embodiment 127, wherein nipocalimab is administered every two weeks subcutaneously at a dose from about 1400 mg to about 1600 mg via an on-body device.

[0382] Embodiment 129. The method of any one of embodiments 126-128, wherein nipocalimab is administered every two weeks subcutaneously at a dose of about 1500 mg via an on-body device.

[0383] Embodiment 130. The method of embodiment 126, wherein nipocalimab is administered every week subcutaneously at a dose from about 400 mg to about 600 mg via an auto injector.-62- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)

[0384] Embodiment 131. The method of embodiment 130, wherein the subject receives a second subcutaneous administration of nipocalimab at a dose from about 400 mg to about 600 mg via an autoinjector in the first week.

[0385] Embodiment 132. The method of embodiment 126 or embodiment 130, wherein nipocalimab is administered every week subcutaneously at a dose from about 450 mg to about 550 mg via an autoinjector.

[0386] Embodiment 133. The method of embodiment 132, wherein the subject receives a second subcutaneous administration of nipocalimab at a dose from about 450 mg to about 550 mg via an autoinjector in the first week.

[0387] Embodiment 134. The method of any one of embodiments 126, 130, or 132, wherein nipocalimab is administered every week subcutaneously at a dose from about 518 mg via an auto injector.

[0388] Embodiment 135. The method of embodiment 134, wherein the subject receives a second subcutaneous administration of nipocalimab at a dose of about 518 mg via an autoinjector in the first week.

[0389] Embodiment 136. The method of embodiment 134, wherein the subject receives a second subcutaneous administration of nipocalimab at a dose of about 518 mg via an autoinjector in the first day.

[0390] Embodiment 137. The method of any one of embodiments 126, 130, or 132, wherein nipocalimab is administered every week subcutaneously at a dose of about 460 mg via an auto injector.

[0391] Embodiment 138. The method of embodiment 137, wherein the subject receives a second subcutaneous administration of nipocalimab at a dose of about 460 mg via an autoinjector in the first week.

[0392] Embodiment 139. The method of embodiment 137, wherein the subject receives a second subcutaneous administration of nipocalimab at a dose of about 460 mg via an autoinjector in the first day.-63- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)

[0393] Embodiment 140. The method of any one of embodiments 126-139, wherein the method provides a clinical benefit as measured by an increase in International Myositis Assessment and Clinical Studies Total Improvement Score (IMACS TIS) in the subject by at least 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31, 32, 33, 34, 35, 36, 37, 38, 39, 40, 41, 42, 43, 44, 45, 46, 47, 48, 49, 50, 51, 52, 53, 54, 55, 56, 57, 58, 59, 60, 61, 62, 63, 64, 65, 66, 67, 68, 69, 70, 71, 72, 73, 74, 75, 76, 77, 78, 79, 80, 81, 82, 83, 84, 85, 86, 87, 88, 89, 90, 91, 92, 93, 94, or 95 from baseline within 12, 16, 20, 24, 30, 36, 42, 48 or 52 weeks of initiation of said administering.

[0394] Embodiment 141. The method of any one of embodiments 126-140, wherein the method provides a clinical benefit as measured by an increase in Manual Muscle Testing (MMT-8) score in the subject by more than 5, 10, 15, 20, 25, 30, 35, 40, 45, 50, 55, 60, 65, 70, 75, 80, 85, 90, 95, 100, 105, 110, 115, 120, 125, 130, 135, 140, or 145 from baseline within 12, 16, 20, 24, 30, 36, 42, 48 or 52 weeks of initiation of said administering.

[0395] Embodiment 142. The method of any one of embodiments 126-141, wherein the method provides a clinical benefit as measured by a decrease in Extramuscular Global Assessment (MDAAT) score in the subject by more than 1, 1.5, 2, 3, or 4 from baseline within 10, 12, 16, 20, 24, 30, 36, 42, 48 or 52 weeks of initiation of said administering.

[0396] Embodiment 143. The method of any one of embodiments 126-142, wherein the method provides a clinical benefit as measured by a decrease in Physician Global Assessment (PhGA) score in the subject by more than 1, 2, 3, 4, 5, 6, 7, 8, 9 or 10 from baseline within 6, 8, 12, 16, 20, 24, 30, 36, 42, 48 or 52 weeks of initiation of said administering.

[0397] Embodiment 144. The method of any one of embodiments 126-143, wherein the method provides a clinical benefit as measured by a decrease in Cutaneous Dermatomyositis Activity -Investigator Global Assessment (CDA-IGA) score in the subject by more than 1, 2, 3, or 4 from baseline within 12, 16, 20, 24, 30, 36, 42, 48 or 52 weeks of initiation of said administering.

[0398] Embodiment 145. The method of any one of embodiments 126-144, wherein the subject receives glucocorticoid at a first dose before initiation of said administering, and the method provides a clinical benefit as indicated by the subject receiving glucocorticoid at a second dose that is lower than the first dose within 8, 10, 12, 14, 16, 18, 20, 22, 24, 26, 28, 30, 32, 34, 36, 38, 40, 42, 44, 46, 48, 50 or 52 weeks or more weeks of initiation of said administering.-64- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)

[0399] Embodiment 146. The method of embodiment 145, wherein the first dose is higher than 7.5 mg, 10 mg, 12.5 mg, 15 mg, or 17.5 mg per day.

[0400] Embodiment 147. The method of embodiment 145, wherein the first dose is higher than 5 mg per day.

[0401] Embodiment 148. The method of any one of embodiments 126-147, wherein the administration of nipocalimab increases total cholesterol in the subject by at most 18 mg / dL, at most 17 mg / dL, at most 16 mg / dL, at most 15 mg / dL, at most 14 mg / dL, at most 13 mg / dL, or at most 12 mg / dL from baseline total cholesterol.

[0402] Embodiment 149. The method of any one of embodiments 126-148, wherein the administration of nipocalimab increases HDL in the subject at most 8 mg / dL, at most 7 mg / dL, at most 6 mg / dL, at most 5 mg / dL, at most 4 mg / dL, at most 3 mg / dL, or at most 2 mg / dL from baseline HDL.

[0403] Embodiment 150. The method of any one of embodiments 126-149, wherein the administration of nipocalimab increases LDL in the subject at most 12 mg / dL, at most 11 mg / dL, at most 10 mg / dL, at most 9 mg / dL, at most 8 mg / dL, at most 7 mg / dL, at most 6 mg / dL, or at most 5 mg / dL from baseline LDL.

[0404] Embodiment 151. The method of any one of embodiments 126-150, wherein the administration of nipocalimab reduces serum albumin in the subject by at most 18%, at most 16%, at most 14%, at most 12%, at most 10%, at most 8%, at most 6%, at most 4%, or at most 2% from baseline serum albumin.

[0405] Embodiment 152. A pharmaceutical product, comprising:a therapeutic agent, comprising:a bi-weekly dose from about 1000 mg to about 2000 mg of nipocalimab; or a weekly dose from about 400 mg to about 600 mg of nipocalimab; and a subcutaneous injection device, comprising:a container configured to contain the therapeutic agent;a discharge nozzle sized to deliver the therapeutic agent to a subject subcutaneously; and-65- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)a driver configured to drive the therapeutic agent from the container and out of the discharge nozzle.

[0406] Embodiment 153. The pharmaceutical product of embodiment 152, wherein the therapeutic agent comprises the bi-weekly dose and the therapeutic agent has a volume from 13mL to 17mL.

[0407] Embodiment 154. The pharmaceutical product of embodiment 153, wherein the injection device is configured to deliver about 15mL + 0.5mL of the therapeutic agent to the subject.

[0408] Embodiment 155. The pharmaceutical product of any one of embodiments 152 and 153, wherein the subcutaneous injection device is an on-body delivery device.

[0409] Embodiment 156. The pharmaceutical product of embodiment 155, wherein the driver has a drive force that drives the therapeutic agent out of the discharge nozzle and into the subject at a rate from 0.5mL / minute to 2.0mL / minute.

[0410] Embodiment 157. The pharmaceutical product of any one of embodiments 152-156, wherein the bi-weekly dose is from about 1200 mg to about 1800 mg.

[0411] Embodiment 158. The pharmaceutical product of any one of embodiments 152-156, wherein the bi-weekly dose is from about 1400 mg to about 1600 mg.

[0412] Embodiment 159. The pharmaceutical product of any one of embodiments 152-156, wherein the bi-weekly dose is about 1500 mg.

[0413] Embodiment 160. The pharmaceutical product of embodiment 152, wherein the therapeutic agent comprises the weekly dose and the therapeutic agent has a volume from about 2mL to 4mL.

[0414] Embodiment 161. The pharmaceutical product of embodiment 160, wherein the injection device is configured to deliver 2.8mL + 0.5mL of the therapeutic agent to the subject.

[0415] Embodiment 162. The pharmaceutical product of any one of embodiments 160 and 161, wherein the subcutaneous injection device is an auto injector.-66- 103693.004420\4914-0795-9446.2DOCKET NO.: 103693.004420 (MPI6028WOPCT1)

[0416] Embodiment 163. The pharmaceutical product of embodiment 162, wherein the driver has a drive force that drives the therapeutic agent out of the discharge nozzle and into air at a rate from 0.08mL / second to 0.4mL / second.

[0417] Embodiment 164. The pharmaceutical product of any one of embodiments 160-163, wherein the weekly dose is from about 450 mg to about 550 mg.

[0418] Embodiment 165. The pharmaceutical product of any one of embodiments 160-163, wherein the weekly dose is about 518 mg via an autoinjector.

[0419] Embodiment 166. The pharmaceutical product of any one of embodiments 160-163, wherein the weekly dose is about 460 mg via an autoinjector.

[0420] Embodiment 167. The pharmaceutical product of any one of embodiments 152-166, wherein the subcutaneous injection device comprises a skin-contacting surface that contacts skin of the subject during an injection, and the discharge nozzle is a needle that (i) extends beyond the skincontacting by about 6.5mm + 1mm when the drug is delivered to the subject, and / or (ii) has a needle gage from 23Gto 27G, or both (i) and (ii).

[0421] Embodiment 168. The pharmaceutical product of any one of embodiments 152-167, wherein:the container is a cartridge having a septum;the subcutaneous injection device pierces the septum to fluidly couple the cartridge to the discharge nozzle; andthe subcutaneous injection device delivers the therapeutic agent out of the discharge nozzle such that no particulate matter generated during piercing of the septum is discharged from the discharge nozzle that has a particle diameter >150 pm.

[0422] Embodiment 169. The pharmaceutical product of any one of embodiments 152-161, wherein the therapeutic agent, when delivered to the subject, reduces serum IgG in the subject by at least 60% from baseline serum IgG, at least 65% from baseline serum IgG, at least 70% from baseline serum IgG, at least 75% from baseline serum IgG, or at least 80% from baseline serum IgG.-67- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)

[0423] Embodiment 170. The pharmaceutical product of any one of embodiments 152-169, wherein the therapeutic agent, when delivered to the subject, increases total cholesterol in the subject by at most 18 mg / dL, at most 17 mg / dL, at most 16 mg / dL, at most 15 mg / dL, at most 14 mg / dL, at most 13 mg / dL, or at most 12 mg / dL from baseline total cholesterol.

[0424] Embodiment 171. The pharmaceutical product of any one of embodiments 152-170, wherein the therapeutic agent, when delivered to the subject, increases HDL in the subject at most 8 mg / dL, at most 7 mg / dL, at most 6 mg / dL, at most 5 mg / dL, at most 4 mg / dL, at most 3 mg / dL, or at most 2 mg / dL from baseline HDL.

[0425] Embodiment 172. The pharmaceutical product of any one of embodiments 152-171, wherein the therapeutic agent, when delivered to the subject, increases LDL in the subject at most 12 mg / dL, at most 11 mg / dL, at most 10 mg / dL, at most 9 mg / dL, at most 8 mg / dL, at most 7 mg / dL, at most 6 mg / dL, or at most 5 mg / dL from baseline LDL.

[0426] Embodiment 173. The pharmaceutical product of any one of embodiments 152-172, wherein the therapeutic agent, when delivered to the subject, reduces serum albumin in the subject by at most 18%, at most 16%, at most 14%, at most 12%, at most 10%, at most 8%, at most 6%, at most 4%, or at most 2% from baseline serum albumin.

[0427] Embodiment 174. The pharmaceutical product of embodiment 152, wherein the pharmaceutical product is disposed in the container.

[0428] Embodiment 175. The pharmaceutical product of embodiment 152, wherein the pharmaceutical product is a kit comprising a separate container that is separate from the subcutaneous injection device, and the separate container contains the therapeutic agent.

[0429] Embodiment 176. The pharmaceutical product of embodiment 152, wherein the pharmaceutical product is a kit comprising at least one other subcutaneous injection device, and the subcutaneous injection device and the at least one other subcutaneous injection device (i) are each sized to contain only a portion of the dose and (i) together contain an entirety of the dose.Pharmaceutical Product-68- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)

[0430] Throughout this description, like reference labels depict like features. For succinctness, descriptions of like features might not be repeated. It will be understood that any description of a feature in relation to a figure applies equally to like features in other figures.

[0431] In various examples of this disclosure, a pharmaceutical product comprises a therapeutic agent and a subcutaneous injection device. The therapeutic agent comprises a weekly or a bi-weekly dose as discussed above. The injection device comprises a container configured to contain the therapeutic agent. The container can be a syringe barrel, a vial, a cartridge, a bladder, or any other suitable container. The injection device comprises a discharge nozzle sized to deliver the therapeutic agent to a subject subcutaneously. The discharge nozzle can be a needle, catheter, other suitable discharge nozzle for delivering the therapeutic agent to a subject subcutaneously.

[0432] In some embodiments, the present disclosure provides a pharmaceutical product, comprising: a therapeutic agent, comprising: a bi-weekly dose from about 1000 mg to about 2000 mg of nipocalimab; or a weekly dose from about 400 mg to about 600 mg of nipocalimab; and a subcutaneous injection device, comprising: a container configured to contain the therapeutic agent; a discharge nozzle sized to deliver the therapeutic agent to a subject subcutaneously; and a driver configured to drive the therapeutic agent from the container and out of the discharge nozzle.

[0433] In some embodiments, the therapeutic agent comprises the bi-weekly dose and the therapeutic agent has a volume from 13mL to 17mL.

[0434] In some embodiments, the injection device is configured to deliver about 15mL ± 0.5mL of the therapeutic agent to the subject.

[0435] In some embodiments, the subcutaneous injection device is an on-body delivery device.

[0436] In some embodiments, the driver has a drive force that drives the therapeutic agent out of the discharge nozzle and into the subject at a rate from 0.5mL / minute to 2.0mL / minute.

[0437] In some embodiments, the bi-weekly dose is from about 1200 mg to about 1800 mg. In some embodiments, the bi-weekly dose is from about 1400 mg to about 1600 mg. In some embodiments, the bi-weekly dose is about 1500 mg.

[0438] In some embodiments, the therapeutic agent comprises the weekly dose and the therapeutic agent has a volume from about 2mL to 4mL.-69- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)

[0439] In some embodiments, the injection device is configured to deliver 2.8mL ± 0.5mL of the therapeutic agent to the subject.

[0440] In some embodiments, the subcutaneous injection device is an autoinjector.

[0441] In some embodiments, the driver has a drive force that drives the therapeutic agent out of the discharge nozzle and into air at a rate from 0.08mL / second to 0.4mL / second.

[0442] In some embodiments, the weekly dose is from about 450 mg to about 550 mg. In some embodiments, the weekly dose is about 518 mg via an autoinjector. In some embodiments, the weekly dose is about 460 mg via an autoinjector.

[0443] In some embodiments, the subcutaneous injection device comprises a skin-contacting surface that contacts skin of the subject during an injection, and the discharge nozzle is a needle that (i) extends beyond the skin- contacting by about 6.5mm ± 1mm when the drug is delivered to the subject, and / or (ii) has a needle gage from 23G to 27G, or both (i) and (ii).

[0444] In some embodiments, the container is a cartridge having a septum; the subcutaneous injection device pierces the septum to fluidly couple the cartridge to the discharge nozzle; and the subcutaneous injection device delivers the therapeutic agent out of the discharge nozzle such that no particulate matter generated during piercing of the septum is discharged from the discharge nozzle that has a particle diameter >150 pm.

[0445] In some embodiments, the therapeutic agent, when delivered to the subject, reduces serum IgG in the subject by at least 60% from baseline serum IgG, at least 65% from baseline serum IgG, at least 70% from baseline serum IgG, at least 75% from baseline serum IgG, or at least 80% from baseline serum IgG.

[0446] In some embodiments, the therapeutic agent, when delivered to the subject, increases total cholesterol in the subject by at most 18 mg / dL, at most 17 mg / dL, at most 16 mg / dL, at most 15 mg / dL, at most 14 mg / dL, at most 13 mg / dL, or at most 12 mg / dL from baseline total cholesterol.

[0447] In some embodiments, the therapeutic agent, when delivered to the subject, increases HDL in the subject at most 8 mg / dL, at most 7 mg / dL, at most 6 mg / dL, at most 5 mg / dL, at most 4 mg / dL, at most 3 mg / dL, or at most 2 mg / dL from baseline HDL.-70- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)

[0448] In some embodiments, the therapeutic agent, when delivered to the subject, increases LDL in the subject at most 12 mg / dL, at most 11 mg / dL, at most 10 mg / dL, at most 9 mg / dL, at most 8 mg / dL, at most 7 mg / dL, at most 6 mg / dL, or at most 5 mg / dL from baseline LDL.

[0449] In some embodiments, the therapeutic agent, when delivered to the subject, reduces serum albumin in the subject by at most 18%, at most 16%, at most 14%, at most 12%, at most 10%, at most 8%, at most 6%, at most 4%, or at most 2% from baseline serum albumin.

[0450] In some embodiments, the pharmaceutical product is disposed in the container.

[0451] The present disclosure provides a pharmaceutical product, comprising: a therapeutic agent, comprising from about 400 mg to about 600 mg of nipocalimab; and a subcutaneous injection device, comprising: (a) a container configured to contain the therapeutic agent; (b) a discharge nozzle sized to deliver the therapeutic agent to a subject subcutaneously; and (c) a driver configured to drive the therapeutic agent from the container and out of the discharge nozzle.

[0452] In some embodiments, the therapeutic agent has a volume from about 1.4 mL to 2.5 mL. In some embodiments, the therapeutic agent has a volume of about 2.09 mL ± 0.25 mL.

[0453] In some embodiments, the subcutaneous injection device is an autoinjector.

[0454] In some embodiments, the driver has a drive force that drives the therapeutic agent out of the discharge nozzle and into air at a rate from 0.09 mL / second to 0.3 mL / second.

[0455] In some embodiments, the subcutaneous injection device comprises a skin-contacting surface that contacts skin of the subject during an injection, and the discharge nozzle is a needle that (i) extends beyond the skin- contacting by about 6.5 mm + 1 mm when the drug is delivered to the subject, and / or (ii) has a needle gage from 23 G to 27 G, or both (i) and (ii).

[0456] In some embodiments, the pharmaceutical product is disposed in the container.

[0457] In some embodiments, the therapeutic agent comprises 200 mg / mL to 250 mg / mL nipocalimab. In some embodiments, the therapeutic agent comprises from about 400 mg to about 500 mg of nipocalimab. In some embodiments, the therapeutic agent comprises about 460 mg of nipocalimab.-71- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)

[0458] In some embodiments, the pharmaceutical product is a kit comprising a separate container that is separate from the subcutaneous injection device, and the separate container contains the therapeutic agent.

[0459] In some embodiments, the pharmaceutical product is a kit comprising at least one other subcutaneous injection device, and the subcutaneous injection device and the at least one other subcutaneous injection device (i) are each sized to contain only a portion of the dose and (i) together contain an entirety of the dose.

[0460] The injection device comprises a driver configured to drive the therapeutic agent from the container and out of the discharge nozzle. The driver comprises one or more plungers, one or more springs, one or more motors, one or more compressed gas canisters, one or more hydraulic actuator, one or more pneumatic actuators, one or more other suitable drivers for driving the therapeutic agent from the container, or any combination thereof. In examples in which the driver comprises one or more springs, each spring can be a helical spring, a compression spring, an extension spring, a torsion spring, a constant force spring, a leaf spring, a gas spring, any other suitable spring, or any combination thereof. In some examples, the pharmaceutical product can be a kit comprising the subcutaneous injection device and the therapeutic agent disposed in a container that is separate from the subcutaneous injection device. In some examples, the pharmaceutical product can be a kit comprising the therapeutic agent, the subcutaneous injection device, and at least one other subcutaneous injection device, where a dose of the therapeutic agent is divided between the subcutaneous injection device and the at least one other subcutaneous injection device.

[0461] Referring to FIG. 17, a pharmaceutical product 100 is shown according to one example in which the subcutaneous pharmaceutical injection device 102 is a syringe. The pharmaceutical injection device 102 comprises a container 110 in the form of a syringe barrel. The container 110 has a proximal end 110a and a distal end 110b. The proximal end 110a can define an opening to receive a driver 114 therein. The distal end 110b can be offset from the proximal end 110a along a central axis along a distal direction. The container 110 contains the therapeutic agent 116 therein.

[0462] The injection device 102 comprises a discharge nozzle 112 which can be in the form of a subcutaneous injection needle or catheter. The injection needle can be a 25 gage, 26 gage, or 27 gage needle. For instance, the injection device 102 can comprise an abutment surface that is configured to abut a subject’s skin while the therapeutic agent is delivered to the subject, and the -72- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)discharge nozzle 112 can extend from the abutment surface by a distance in a range from 4.5mm to 8.5mm, such as in a range from 5mm to 8mm, such as in a range from 5.5mm to 7.5mm, such as in a range from 6mm to 7mm, such as by a distance of 6.5mm. In one example, the abutment surface can be at the distal end 110b of the container 110. In other examples, the injection device can comprise a housing that houses the container 110, and the abutment surface can be defined by the housing. For instance, the injection device can comprise the Becton Dickinson® UltraSafe®, the West Pharmaceutical® SelfDose®, or the grip accessory of FIG. 18, and the housing can be a housing of such devices.

[0463] Referring briefly to FIG. 18, an alternative injection device 100' comprises a housing 130 that houses the container 110. The housing 130 has a proximal end 130a and a distal end 130b. The proximal end 130a can define an opening that receives the container 110 into the housing 130 to support the container 110 therein, although the opening could alternatively extend into a different surface of the housing 130 such as into a side of the housing 130. The distal end 130b defines an abutment surface that is configured to abut a subject’s skin while the therapeutic agent 116 is delivered to the subject. The housing 130 supports the container 110 such that the discharge nozzle 112 extends from the abutment surface by a distance in a range from 4.5mm to 8.5mm, such as in a range from 5mm to 8mm, such as in a range from 5.5mm to 7.5mm, such as in a range from 6mm to 7mm, such as by a distance of 6.5mm.

[0464] Referring back to FIG. 17, the injection device 102 comprises a driver 114 in the form of a plunger. The driver 114 comprises a plunger rod 114a that extends into the proximal end 110a of the container 110. The driver 114 comprises a gasket 114b disposed in the syringe barrel 110 at a distal end of the plunger rod 114a. The gasket 114b forms a seal with an interior surface of the container 110 that prevents the therapeutic agent 116 from escaping past the gasket 114b along a proximal direction, opposite the distal direction. The driver 114 can be operated by a user applying a manual force to a proximal end of the driver 114 to move the driver 114 in the distal direction to drive the therapeutic agent 116 from the container 110 and out of the discharge nozzle 112.

[0465] Optionally, the injection device 102 can comprise a cap 118. Fluid flow between the discharge nozzle 112 and the container 110 can be enabled by removing a cap 118 from the discharge nozzle 112. In operation, a user such as the subject or a healthcare provider can remove the cap 118 from the discharge nozzle 112, insert the discharge nozzle 112 into a subcutaneous-73- 103693.004420\4914-0795-9446.2DOCKET NO.: 103693.004420 (MPI6028WOPCT1)layer of the subject, and actuate the diver 114 to drive the contents of the injection device 110 from the container 110 and out of the discharge nozzle 112.

[0466] In the example shown in FIG. 17, the injection device 102 is a pre-filled syringe that is preloaded with the therapeutic agent 116 prior to delivery of the pharmaceutical product 100 to a subject or healthcare provider. In other examples, the pharmaceutical product 100 can be in the form of a kit that comprises the injection device 102, and a separate container (not shown) that is separate from the injection device 102, wherein the separate container contains the therapeutic agent 116 disposed therein. The separate container can be any suitable container such as (without limitation) a vial, cartridge, syringe, or bag. In such examples, a health care provider or the subject can introduce a volume of the therapeutic agent 116 into the container 110 by inserting the discharge nozzle 112 into the separate container containing the therapeutic agent 116, and withdrawing the driver 114 along the proximal direction to draw the therapeutic agent 116 from container, through the discharge nozzle 112, and into the container 110. In yet still other examples, the pharmaceutical product 100 can be in the form of a kit that comprises the therapeutic agent 116, the injection device 102, and at least one other injection device 102, where a dose of the therapeutic agent 116 is divided between the injection device 102 and the at least one other injection device 102 prior to delivery to the subject or healthcare provider, or is divided by the subject or healthcare provider.

[0467] In some examples, the therapeutic agent 116 can comprise a bi-weekly dose from about 1000 mg to about 2000 mg of nipocalimab, such as from about 1200 mg to about 1800 mg, such as from about 1400 mg to about 1600 mg, such as 1500mg. The bi-weekly dose of the therapeutic agent 116 has a volume from 13mL to 17mL, such as a volume of about 15.4mL ± ImL. The container 110 can define a volume of at least 13mL, such as at least 14mL, such as at least 15mL, such as at least 16 mL, such as at least 17mL, such as at least 18mL, such as at least 19mL, or such as at least 20 mL that contains the bi-weekly dose of the therapeutic agent 116. The injection device 102 is configured to deliver at least 14.25mL of the therapeutic agent 116 to the subject. In some examples, the injection device 102 is configured to deliver 15mL ± ImL to the subject.

[0468] In other examples, the therapeutic agent 116 can comprise a weekly dose from about 400 mg to about 600 mg of nipocalimab, such as from about 450 mg to about 550 mg, such as about 518 mg. In such examples, the weekly dose of the therapeutic agent 116 has a volume from 2mL to 4mL, such as a volume of about 2.8mL ± 0.5mL. The injection device 102 is configured to deliver -74- 103693.004420\4914-0795-9446.2DOCKET NO.: 103693.004420 (MPI6028WOPCT1)about 2.8mL ± 0.5mL to the subject. The container 110 can define a volume of at least 2.5mL, such as at least 3.0mL, or such as at least 3.5mL that contains the weekly dose of the therapeutic agent 116.

[0469] Referring to FIG. 19, a pharmaceutical product 200 is shown according to one example in which the subcutaneous pharmaceutical injection device 202 is an autoinjector. The pharmaceutical product 200 comprises the injection device 202 and a therapeutic agent 116. The pharmaceutical injection device 202 comprises a container 210 in the form of a cartridge that contains the therapeutic agent 116. In alternative examples, the pharmaceutical product 200 can comprise a container 210 in the form of a syringe barrel 110 as shown in FIG. 20 in which corresponding features are labeled using the same reference labels. The container 110 has a proximal end 210a and a distal end 210b. The proximal end 210a defines an opening to receive a driver 214 therein. The distal end 210b can be offset from the proximal end 210a along a central axis along a distal direction. The container 210 contains the therapeutic agent 116 therein. The distal end 210b of the container 210 comprises a head 211 with a septum disposed therein that prevents the therapeutic agent 116 from escaping in the distal direction until the septum is pierced by a piercing nozzle. The container 210 can comprise a gasket 222 disposed in the cartridge 210. The gasket 222 forms a seal with an interior surface of the container 210 that prevents the therapeutic agent 116 from escaping past the gasket 222 along a proximal direction, opposite the distal direction.

[0470] The injection device 202 comprises a discharge nozzle 112 which can be in the form of a subcutaneous injection needle or catheter. The injection needle can be a 25 gage, 26 gage, or 27 gage needle. For instance, the injection device 202 can comprise an abutment surface that is configured to abut a subject’s skin while the therapeutic agent is delivered to the subject, and the discharge nozzle 112 can extend from the abutment surface by a distance in a range from 4.5mm to 8.5mm, such as in a range from 5mm to 8mm, such as in a range from 5.5mm to 7.5mm, such as in a range from 6mm to 7mm, such as by a distance of 6.5mm, when the abutment surface is pressed against the skin. In one example, the abutment surface can be at the distal end 230 of a housing 230 of the injection device 202.

[0471] The injection device 202 comprises a septum-piercing nozzle 212 that is configured to move so as to pierce the septum of the cartridge 210, thereby placing the discharge nozzle 112 in fluid communication with the therapeutic agent 116. For example, pressing a sleeve 234 of the -75- 103693.004420\4914-0795-9446.2DOCKET NO.: 103693.004420 (MPI6028WOPCT1)injection device 202 against a subject’s skin can cause the septum-piercing nozzle 212 to move proximally to pierce the septum. The septum-piercing nozzle 212 can be a needle. In some examples, the septum-piercing nozzle 212 and the discharge nozzle 112 can be opposing ends of a double-sided needle. In other examples, as shown in FIG. 20, the injection device 202' can be devoid of a septum-piercing nozzle, and instead, the discharge nozzle 112 can extend from the container 110.

[0472] The injection device 202 comprises a driver 213. The driver 213 comprises a plunger 214 that extends into the proximal end 210a of the container 210. The driver 213 comprises a motive force device 227 that is configured to apply a motive force to the plunger 214 to move the plunger 214 in the distal direction to drive the therapeutic agent 216 from the container 210 and out of the discharge nozzle 112. The motive force device 227 comprises a spring, although the motive force device could alternatively comprise a motor, a compressed gas canister, a hydraulic actuator, a pneumatic actuator, any other suitable motive force device, or any combination thereof.

[0473] The injection device 202 comprises a latch 251 that is configured to transition between a latched position in which the driver 213 is prevented causing the plunger 214 to move, and an unlatched position in which the plunger 214 is permitted to move. The injection device 202 can comprise an actuator that is configured to transition the latch 251 between the latched position and the unlatched position. The actuator can be any suitable actuator. In one example, the actuator can be a button that is depressed by a user. In another example, the actuator can be a sleeve 241 of the housing 230.

[0474] The housing 230 houses the container 116 and the driver 213 therein. The housing 230 comprises a main body 232 and the sleeve 234 that is retractable relative to the main body 232. In particular, pressing the sleeve 234 against the skin of the subject can cause the sleeve 234 to retract relative to the main body 232. As discussed above, in some examples, the sleeve 234 can be an actuator that causes the latch 251 to transition between the latched position and the unlatched position when the sleeve 234 is retracted. In some examples, the sleeve 234 can be a needle guard that is configured to transition between an initial position in which a distal end of the discharge nozzle 112 is contained within the sleeve 234, and a retracted position in which the distal end of the discharge nozzle 112 extends from sleeve 234. The sleeve 234 can be transitioned between the initial and retracted positions by pressing the sleeve 234 against the subject’s skin. As the sleeve 234 transitions to the retracted position, the discharge nozzle 112 is inserted into the subject’s skin.-76- 103693.004420\4914-0795-9446.2DOCKET NO.: 103693.004420 (MPI6028WOPCT1)

[0475] A distal end of the housing 230 can define the abutment surface. For instance, a distal end of the sleeve 234 can define the abutment surface such that, when the sleeve 234 is in the retracted position, the discharge nozzle 112 extends from the abutment surface by a distance in the range discussed above. The sleeve 234 can be configured to transition from the retracted potion to an extended position in which the distal end of the discharge nozzle 112 is contained within the sleeve 234 after the injection device 202 is removed from the subject’s skin. For example, the injection device 202 can comprise a return spring 242 that is configured to bias the sleeve 234 towards the extended position. The injection device 202 can comprise a latch that is configured lock the sleeve 234 in the extended position so as to guard against inadvertent needle sticks.

[0476] In alternative examples, the sleeve 234 does not serve as a needle guard, and instead, the container 210 can be configured to move within the housing 230 relative to the main body 232 between an initial position in which a distal end of the discharge nozzle 112 is contained within the housing 230, and a retracted position in which the distal end of the discharge nozzle 112 extends from the housing 230. In such examples, the sleeve 234 can retract a sufficient amount to transition the latch 251 between the latched position and the unlatched position, without exposing the full length of the discharge nozzle 112.

[0477] In some examples, the therapeutic agent 116 can comprise a weekly dose from about 400 mg to about 600 mg of nipocalimab, such as from about 450 mg to about 550 mg, such as about 518 mg. The weekly dose of the therapeutic agent 116 has a volume from 2mL to 4mL, such as a volume of about 2.8mL ± 0.5mL. The injection device 202 is configured to deliver about 2.8mL ± 0.5mL to the subject. The container 110 can define a volume of at least 2.5mL, such as at least 3.0mL, or such as at least 3.5mL that contains the weekly dose of the therapeutic agent 116. To deliver the weekly dose, the driver has a drive force that drives the therapeutic agent out of the discharge nozzle and into air at a rate from 0.08mL / second to 0.4mL / second.

[0478] In other examples, the pharmaceutical product 200 can be in the form of a kit that comprises the injection device 202 and at least one other injection device 202, wherein the weekly dose of the therapeutic agent 116 is divided between the injection device 202 and the at least one other injection device 202. For instance, the therapeutic agent 116 can comprise about one halfweek dose from about 200 mg to about 300 mg of nipocalimab, such as from about 225 mg to about 275 mg, such as about 259 mg. The one half-week dose of the therapeutic agent 116 has a volume from 1 ,25mL to 1 ,6mL, such as a volume of about 1 ,4mL ± 0.25mL. The container 110 can define a -77- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)volume of at least 1.25mL, such as at least 1.3mL, such as at least 1.35mL, or such as at least 1.4mL that contains the one half- week dose of the therapeutic agent 116. It will be understood that the therapeutic agent 116 need not be divided equally between the injection device 202 and the at least one other injection device 202.

[0479] The injection device 200 can be configured to deliver the therapeutic agent 116 out of the discharge nozzle 112 such that no particulate matter generated during piercing of the septum is discharged from the discharge nozzle 112 that has a particle diameter >150 pm. For instance, in some examples, the injection device 202 can comprise a filter in a flow path that extends from the container 210 (or 110) to a distal end of the discharge nozzle 112.

[0480] While the foregoing description relates to one example of an autoinjector, the present invention is not limited to such an autoinjector. The skilled person would understand that various other modifications to the described autoinjector may be used with the present invention. For example, the autoinjector may be gas powered, electrically powered, or powered by a torsion spring.

[0481] Turning to FIGs. 21 to 23, a pharmaceutical product 300 is shown according to one example in which the subcutaneous pharmaceutical injection device 302 is a patch pump or on-body delivery system (OBDS). The pharmaceutical product 300 comprises the injection device 302, a container 210, and a therapeutic agent 116. The injection device 302 has a housing 303 that can support, such as house, a container 210 that contains the therapeutic agent 116. The container 210 can be a cartridge as shown. Alternatively, the container 210 can be a syringe, a vial, an expandable bladder, or any other suitable container for containing the therapeutic agent 116. The housing 303 can support, such as house, other components of the injection device 302, such as a driver, a discharge nozzle 112, a septum piercing mechanism, control circuitry, a nozzle insertion mechanism, or any combination thereof. The driver is configured to drive the therapeutic agent 116 from the container 210 and out of the discharge nozzle 112. The driver can comprise one or more plungers, one or more springs, one or more motors, one or more compressed gas canisters, one or more hydraulic drivers, one or more pneumatic actuators, one or more other suitable drivers for driving the therapeutic agent from the container, or any combination thereof.

[0482] The housing 303 can be configured to support, such as house, at least a portion up to an entirety of the container 210 therein. The housing 303 can be configured to receive, and in some -78- 103693.004420\4914-0795-9446.2DOCKET NO.: 103693.004420 (MPI6028WOPCT1)cases removably receive, the drug container 210. Thus, the container 210 can be insertable into and / or removable from the housing 303. The housing 303 can define an opening 306 therein that is configured to receive the container 210 at least partially or fully into the housing 303. In some examples, the housing 303 can comprise a closure 308, such as a cap or a door, that is configured to close at least a portion of the opening 306 to maintain the container 210 in the opening 306. The opening 306 can be configured such that the drug container 210 is received into the opening 306 along an insertion direction I. The insertion direction I can be transverse to a longitudinal axis of the drug container 210 as shown or can be aligned with the longitudinal axis of the drug container 210. In other examples, the housing 303 can be devoid of the opening 306 and closure 308, and the container 210 can be sealed within the housing 303.

[0483] The drug delivery device housing 303 can have a bottom 303a and an opposing top 303b that are opposite from one another along a first direction Di. The injection device 302 is configured such that the bottom 303a faces the skin of the subject when the injection device 302 is attached to the subject. The housing 303 can have a first side 303c and a second side 303d opposite from one another along a second direction D2. The first and second sides 303c and 303d can extend between the bottom 303a and the top 303b. The housing 303 can have a first end 303e and a second end 303f that are opposite one another along a third direction D3. The first and second ends 303e and 303f can extend between the first and second sides 303c and 303d and between the bottom 303a and bottom 303b. The opening 306 can extend into the top 303b. In alternative examples, the opening can extend into another suitable surface or surfaces, such as one or more of the bottom 303a, the first side 303c, the second side 303d, the first end 303e, and the second end 303f.

[0484] The injection device 202 comprises a discharge nozzle 112 which can be in the form of a subcutaneous injection needle or catheter. The injection needle can be a 25 gage, 26 gage, or 27 gage needle. For instance, the discharge nozzle 112 can extend from the bottom 303a of the housing 303 by a distance in a range from 4.5mm to 8.5mm, such as in a range from 5mm to 8mm, such as in a range from 5.5mm to 7.5mm, such as in a range from 6mm to 7mm, such as by a distance of 6.5mm, when the abutment surface is pressed against the skin.

[0485] The injection device 302 comprises a fastener 304 configured to attach the housing 303 to a subject’s body. The fastener 304 can be any suitable fastener for attaching to a subject’s body, such as (without limitation) an adhesive, including a tape with adhesive, a strap, or other suitable fastener. The fastener 304 can be supported by the bottom 303a of the housing 303.-79- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)

[0486] Turning now to FIG. 24, a simplified schematic of the drug product 300 of FIGs. 19 to 21 is shown according to one example. The delivery device 302 comprises a driver 313 configured to drive the therapeutic agent 116 from the container 210 out of the discharge nozzle 112. The driver 313 can be any suitable driver for expelling the therapeutic agent 116 from the drug container 200. The driver 313 can comprise a plunger 314 that is configured to move the gasket 222 of the container 210 to drive the therapeutic agent 116 from the container 210. The driver 313 can comprise a motive force device 315 that is configured to cause the plunger 314 to move the gasket 222. The motive force device 315 can be any suitable device for moving the plunger 314. For example, the motive force device 315 can be (without limitation) a motor, a spring, a hydraulic actuator, a pneumatic actuator, a compressed gas canister, any other suitable motive force device, or any combination thereof. In the example of FIG. 24, the motive force device 315 is a motor that is controlled by control circuitry 328.

[0487] The injection device 302 can comprise a septum piercing needle 312 that is configured to pierce the septum of the container 210. At least one of the septum piercing needle 312 and the container 210 can be configured to move towards the other to cause the piercing needle 312 to pierce the septum. The injection device 302 can comprise a septum piercing mechanism 318 that is configured to cause the least one of the septum piercing needle 312 and the container 210 to move towards the other to cause the piercing needle 312 to pierce the septum. The septum piercing mechanism 318 can comprise any suitable driver for piercing the septum such as (without limitation) a motor, a spring, a hydraulic actuator, a pneumatic actuator, a compressed gas canister, any other suitable driver, or any combination thereof. Piercing the septum places the septum piercing needle 312 in fluid communication with the therapeutic agent 116 contained within the container 210. The injection device 302 can be configured to deliver the therapeutic agent 116 out of the discharge nozzle 112 such that no particulate matter generated during piercing of the septum is discharged from the discharge nozzle 112 that has a particle diameter >150 pm. For instance, in some examples, the injection device 302 can comprise a filter in a flow path that extends from the container 210 to a distal end of the discharge nozzle 112, such as between the septum piercing needle 312 and the distal end of the discharge nozzle 112.

[0488] The injection device 302 can comprise a conduit 320, such as tubing, that fluidly connects the septum piercing needle 312 to the discharge nozzle 112. Thus, piercing the septum can-80- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)place the discharge nozzle 112 in fluid communication with the therapeutic agent 116 contained within the container 210 via the septum piercing needle 312 and the conduit 320.

[0489] The injection device 302 can comprise a nozzle insertion mechanism 322 that is configured to cause the discharge nozzle 112 to be inserted into a subject, such as into a subject’s skin. The nozzle insertion mechanism 322 can be configured to cause the discharge nozzle 112 to extend out of the housing 303 (labeled in FIGs. 21 to 23) of the injection device 302 and into the subject. In some examples, the nozzle insertion mechanism 322 can be configured to cause the discharge nozzle 112 to retract back into the housing after injection. The nozzle insertion mechanism 322 can comprise any suitable driver for inserting the discharge nozzle 112 into the subject’s skin, such as (without limitation) a motor, a spring, a hydraulic actuator, a pneumatic actuator, a compressed gas canister, any other suitable motive force device, or any combination thereof. Additionally, or alternatively, the injection device 302 can comprise a needle guard (not shown) that extends over the discharge nozzle 112 after injection. Retracting and / or covering the discharge nozzle 112 after injection can prevent inadvertent needle sticks and / or limit human contact with biological materials remaining on the discharge nozzle 112.

[0490] The injection device 302 can comprise control circuitry 328 that is configured to control various features of the injection device 302. For example, the control circuitry 328 can be configured to control operation of the driver 313. The control circuitry 328 can be configured to cause the driver 313 to begin driving the therapeutic agent 116 from the container 210. The control circuitry 328 can be configured to control the flow rate in which the therapeutic agent 116 is driven from the container 210. The control circuitry 328 can be configured to cause the driver 313 to stop driving the therapeutic agent 116 when an injection is complete and / or when an error is detected during the injection. The control circuitry 328 can also be configured to control operation of the nozzle insertion mechanism 322 to cause the discharge nozzle 112 to be inserted into the subject before injection and / or removed from the subject after injection.

[0491] The injection device 302 can comprise a user interface 324 that is configured to be engaged by a user such as a health care provider or subject to operate the injection device 302. The user interface 324 can comprise an input device that is configured to receive commands and / or instructions from the user. For example, the input device can be a button, a touchscreen, or other input device that is engaged by the user to begin an injection. As another example, the input device can be an audio input device.-81- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)

[0492] The user interface 324 can be configured to provide information to a user of the injection device 302. The user can be, for example, a subject, or a subject’s care giver or health care professional assisting the subject in using the injection device 302. The user interface 324 can have a variety of configurations, and the injection device 302 can include a single type of user interface or can include more than one type of user interface. For example, the user interface 324 can include one or more lights, e.g., a light emitting diode (LED) or other type of light, configured to illuminate to provide various information. Examples of the information indicated by the user interface 324 include power (on / off) status, error state (e.g., low power supply, improper nozzle advancement into the subject, incompatible type of container 210 loaded into the injection device 302, etc.), drug delivery status (e.g., indication that drug delivery is currently occurring), drug delivery progress information, an orientation of the injection device 302 relative to gravity, an indication of a dose of the therapeutic agent 116 to be provided in each delivery of the therapeutic agent 116 to the subject, and any other suitable type of information.

[0493] As another example, the user interface 324 can include a display configured to show information thereon, such as by using text and / or graphics. The display can include a display screen having any of a variety of configurations, such as a cathode ray tube (CRT), a liquid crystal display (LCD), a touchscreen, etc. As yet another example, the user interface 324 can include a vibration mechanism configured to vibrate with the vibration being configured to be felt by the subject wearing the injection device 302. As still another example, the user interface 324 can include a speaker configured to provide an audio signal. As another example, the user interface 324 can include a mechanical level configured to indicate an orientation of the injection device 302 relative to gravity.

[0494] In some examples, the therapeutic agent 116 can comprise a bi-weekly dose from about 1000 mg to about 2000 mg of nipocalimab, such as from about 1200 mg to about 1800 mg, such as from about 1400 mg to about 1600 mg, such as 1500mg. The bi-weekly dose of the therapeutic agent 116 has a volume from 13mL to 17mL, such as a volume of about 15.4mL ± ImL. The container 210 can define a volume of at least 13mL, such as at least 14mL, such as at least 15mL, such as at least 16 mL, such as at least 17mL, such as at least 18mL, such as at least 19mL, or such as at least 20 mL that contains the bi-weekly dose of the therapeutic agent 116. The injection device 302 is configured to deliver at least 14.25mL of the therapeutic agent 116 to the subject. In some examples, the injection device 302 is configured to deliver 15mL ± ImL to the subject. To deliver -82- 103693.004420\4914-0795-9446.2DOCKET NO.: 103693.004420 (MPI6028WOPCT1)the bi-weekly dose, the driver 313 can have a drive force that drives the therapeutic agent 116 out of the discharge nozzle 112 and into the subject at a rate from 0.5mL / minute to 2.0mL / minute.

[0495] Referring now to FIG. 25, a simplified schematic of the drug product 300 of FIGs. 21 to 23 is shown according to another example. In this example, the container 210 is shown as a cartridge, although in alternative examples, the container could be another suitable container such as a vial. Unlike the example drug injection device 302 of FIG. 24 in which the driver 313 acts on the gasket 222 of the container 210, the example drug injection device 302 of FIG. 25 has a pump 450 that is configured to drive the therapeutic agent 116 from the container 210. The injection device 300 can comprise a conduit 430, such as tubing, that fluidly couples the pump 450 to the container 210, e.g., via the septum piercing needle 312. The pump 450 can be configured to apply a suction to the container 210 to draw the therapeutic agent 116 from the container 210 into a pump chamber 434 of the pump 450, and then drive the therapeutic agent 116 from the pump chamber 434 to the discharge nozzle 112.

[0496] The pump 450 can be any suitable pump. In this specific example, the pump 450 is shown as a piston pump. The pump 450 comprises the pump chamber 434, a driver 413, an inlet valve 432, and an outlet valve 436. The driver 413 comprises a plunger 414 and a motive force device 415. The motive force device 415 can be (without limitation) a motor, a spring, a hydraulic actuator, a pneumatic actuator, a compressed gas canister, any other suitable motive force device, or any combination thereof. In the example of FIG. 25, the motive force device 415 is a motor that is controlled by control circuitry 328.

[0497] The pump 450 is configured such that the motive force device 415 moves the plunger 414 in a reciprocating manner. In a first pumping phase, the control circuitry 328 is configured to drive the plunger 414 (e.g., slidably move the plunger 414 within the pump chamber 434) to draw the therapeutic agent 116 from the container 210 into the conduit 430, then through an inlet valve 432 and into the pump chamber 434. The inlet valve 432 is configured to be opened and closed such that when the inlet valve 324 is open there is fluid communication between the container 210 and the pump chamber 434, and when the inlet valve 432 is closed there is no fluid communication between the container 210 and the pump chamber 434. During the first pumping phase, the control circuitry 328 is configured to cause the inlet valve 432 to open, cause an outlet valve 436 to close, and drive the plunger 434 to draw the therapeutic agent 116 from the container 210 into the pump chamber 434. For instance, the control circuitry 328 is configured to set the inlet valve 432 and the -83- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)outlet valve 436 such that the therapeutic agent 116 can flow only between the container 210 and the pump chamber 434. Thus, as the plunger 414 is drawn back, the therapeutic agent 116 is drawn into pump chamber 434. The control circuitry 328 causing the inlet valve 432 to open and the outlet valve 436 to close can be active control or can be passive control in which the valves 432, 436 are mechanical valves that automatically open / close due to the driving of the plunger 414.

[0498] In some instances, the control circuitry 328 is configured to drive the plunger 414 to draw the therapeutic agent 116 into the pump chamber 434 in a single motion of the plunger 414. For example, the plunger 414 is pulled back in a single motion to draw a volume of the therapeutic agent 116 into the pump chamber 434 during the first pumping phase. In other instances, the control circuitry 328 is configured to drive the plunger 414 to draw the therapeutic agent 116 into the pump chamber 434 in a plurality of discrete motions of the plunger 414. For example, the plunger 414 is incrementally pulled back into the pump chamber 434 in a plurality of discrete motions thereby drawing the therapeutic agent 116 into the pump chamber 434 in a plurality of discrete dosages. For instance, the plunger 414 can be pulled halfway into the pump chamber 434 in one motion and then the rest of the way into the pump chamber 434 in a second, separate motion.

[0499] In a second pumping phase, the control circuitry 328 is configured to drive the plunger 414 to deliver the therapeutic agent 116 from the pump chamber 434 through the outlet valve 436 to an outlet fluid path 438 and then to the discharge nozzle 112 for delivery into the subject. The outlet valve 436 is configured to be opened and closed such that when the outlet valve 436 is open, there is fluid communication between the pump chamber 434 and the discharge nozzle 112, and when the outlet valve 436 is closed, there is no fluid communication between the pump chamber 434 and the discharge nozzle 112. During the second pumping phase, the control circuitry 328 is configured to cause the inlet valve 432 to close, cause the outlet valve 436 to open, and drive the plunger 414 to deliver the therapeutic agent 116 from the pump chamber 434 to the discharge nozzle 112. For instance, the control circuitry 326 can be configured to set the inlet valve 432 and the outlet valve 436 such that the therapeutic agent 116 can flow only between the pump chamber 434 and the discharge nozzle 112. Thus, as the plunger 414 is pushed into the pump chamber 434, the therapeutic agent 116 is pushed out of the pump chamber 434. Similar to that discussed above, the control circuitry 328 causing the inlet valve 432 to close and the outlet valve 436 to open can be active control or can be passive control in which the valves 432, 436 are mechanical valves that automatically open / close due to the driving of the plunger 414.-84- 103693.004420\4914-0795-9446.2DOCKET NO.: 103693.004420 (MPI6028WOPCT1)

[0500] In some examples, the control circuitry 328 is configured to drive the plunger 414 to drive the therapeutic agent 116 from the pump chamber 434 in a single motion. For instance, the plunger 414 is pushed into the pump chamber 434 in a single motion to drive a volume of the therapeutic agent 116 from the pump chamber 434 to the discharge nozzle 112. Alternatively, the control circuitry 36 can be configured to drive the plunger 34 to drive the therapeutic agent 116 from the pump chamber 28 in one or more discrete expansion motions of the plunger 414. For instance, the plunger 414 can be pushed halfway into of the pump chamber 434 in one motion and then the rest of the way into the pump chamber 434 in a second, separate motion.

[0501] The injection device 302 can be configured to deliver the therapeutic agent 116 out of the discharge nozzle 112 such that no particulate matter generated during piercing of the septum is discharged from the discharge nozzle 112 that has a particle diameter >150 pm. For instance, in some examples, the injection device 302 can comprise a filter in a flow path that extends from the container 210 to a distal end of the discharge nozzle 112, such as between the septum piercing needle 312 and the pump 450 or between the pump 450 and the discharge nozzle 112.

[0502] In some examples, the therapeutic agent 116 can comprise a bi-weekly dose from about 1000 mg to about 2000 mg of nipocalimab, such as from about 1200 mg to about 1800 mg, such as from about 1400 mg to about 1600 mg, such as 1500mg. The bi-weekly dose of the therapeutic agent 116 has a volume from 13mL to 17mL, such as a volume of about 15.4mL ± ImL. The container 210 can define a volume of at least 13mL, such as at least 14mL, such as at least 15mL, such as at least 16 mL, such as at least 17mL, such as at least 18mL, such as at least 19mL, or such as at least 20 mL that contains the bi-weekly dose of the therapeutic agent 116. The injection device 302 is configured to deliver at least 14.25mL of the therapeutic agent 116 to the subject. In some examples, the injection device 302 is configured to deliver 15.4mL ± ImL to the subject. To deliver the bi-weekly dose, the driver 313 can have a drive force that drives the therapeutic agent 116 out of the discharge nozzle 112 and into the subject at a rate from 0.5mL / minute to 2.0mL / minute.

[0503] It should be noted that the illustrations and descriptions of the examples and embodiments shown in the figures are for exemplary purposes only and should not be construed limiting the disclosure. One skilled in the art will appreciate that the present disclosure contemplates various embodiments. Additionally, it should be understood that the concepts described above with the above-described examples and embodiments may be employed alone or in combination with any of the other examples and embodiments described above. It should further be -85- 103693.004420\4914-0795-9446.2DOCKET NO.: 103693.004420 (MPI6028WOPCT1)appreciated that the various alternative examples and embodiments described above with respect to one illustrated embodiment can apply to all examples and embodiments as described herein, unless otherwise indicated.

[0504] Conditional language used herein, such as, among others, “can,” “could,” “might,” “may,” “e.g.,” and the like, unless specifically stated otherwise, or otherwise understood within the context as used, is generally intended to convey that certain embodiments include, while other embodiments do not include, certain features, elements, and / or steps. Thus, such conditional language is not generally intended to imply that features, elements, and / or steps are in any way required for one or more embodiments or that one or more embodiments necessarily include logic for deciding, with or without author input or prompting, whether these features, elements and / or steps are included or are to be performed in any particular embodiment. The terms “comprising,” “including,” “having,” and the like are synonymous and are used inclusively, in an open-ended fashion, and do not exclude additional elements, features, acts, operations, and so forth. Also, the term “or” is used in its inclusive sense (and not in its exclusive sense) so that when used, for example, to connect a list of elements, the term “or” means one, some, or all of the elements in the list.

[0505] While certain example embodiments have been described, these embodiments have been presented by way of example only and are not intended to limit the scope of the inventions disclosed herein. Thus, nothing in the foregoing description is intended to imply that any particular feature, characteristic, step, module, or block is necessary or indispensable. Indeed, the novel methods and systems described herein may be embodied in a variety of other forms; furthermore, various omissions, substitutions, and changes in the form of the methods and systems described herein may be made without departing from the spirit of the inventions disclosed herein. The accompanying claims and their equivalents are intended to cover such forms or modifications as would fall within the scope and spirit of certain of the inventions disclosed herein.

[0506] It will be understood that reference herein to “a” or “one” to describe a feature such as a component or step does not foreclose additional features or multiples of the feature. For instance, reference to a device having or defining “one” of a feature does not preclude the device from having or defining more than one of the feature, as long as the device has or defines at least one of the feature. Similarly, reference herein to “one of’ a plurality of features does not foreclose the invention from including two or more, up to all, of the features. For instance, reference to a device -86- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)having or defining “one of a protrusion and a recess” does not foreclose the device from having both the protrusion and the recess.

[0507] The following examples are illustrative, but not limiting, of the compounds, compositions and methods described herein. Other suitable modifications and adaptations known to those skilled in the art are within the scope of the following embodiments.EXAMPLESEXAMPLE 1. Treatment with nipocalimab in participants diagnosed with active CIDP

[0508] Study Design. This is a multicenter, randomized, double-blind, placebo-controlled withdrawal, Phase 2 / 3 study to evaluate treatment with nipocalimab in participants diagnosed with active CIDP according to the European Academy of Neurology / Peripheral Nerve Society (EAN / PNS) 2021 criteria. The study consists of the following periods: (1) identification of participants with active CIDP (including screening and Run-in), (2) open-label treatment with nipocalimab (Stage A), (3) double-blind, placebo controlled, randomized withdrawal (Stage B) and (4) an open-label extension (OLE). See Schema in FIG.1. Efficacy, safety, pharmacokinetics (PK), immunogenicity, and biomarker evaluations will be assessed according to the Schedule of Activities (SoA). Participants who discontinue or withdraw at any point during the treatment periods (Stage A, Stage B, or the OLE) are requested to enter an 8-week follow-up after the last dose of study intervention; this includes participants who are considered a non-responder in Stage A. Participants who discontinue from Stage B due to protocol defined relapse and plan to enter the OLE will not need 8-week follow-up after the last dose of study intervention.

[0509] Screening Period-The duration of this period will be up to 4 weeks. Participants is required to have a diagnosis of CIDP according to criteria of the EAN / PNS 2021 guidelines and active disease as determined by the CIDP Disease Activity Status score (CD AS >3). Confirmation of CIDP diagnosis during this period will be verified by an external and independent CIDP adjudication committee. Participants must be either treated or untreated with SoC medications (intravenous immunoglobulin [IVIg] or subcutaneous immunoglobulin [SCIg] and / or corticosteroids [CS]) at the time of study enrollment. The participants who are treated with these SoC medications at the study entry must be willing to discontinue (IVIg, SCIg, or pulsed CS) or taper (oral CS) treatment during the first Run-in Visit. Untreated CIDP participants who-87- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)demonstrate active disease status, including those newly diagnosed / treatment naive or untreated with SoC in the prior 3 months, will complete Screening and bypass the Run-in Period, and thus, will directly enter Stage A.

[0510] Run-in Period-The duration of this period will be up to 12 weeks. This period is designed to identify participants with active CIDP who are not in remission. The EAN / PNS 2021 diagnosis and treatment guidelines define active disease by the following: progression, relapse or demonstration of persistent treatment dependence, without deficits that cannot improve related to severe chronic axonal degeneration. Participants will be discontinued from IVIg, SCIg or pulsed CS, or tapered down from oral CS therapy (to a dose or regimen equivalent to prednisolone / prednisone <20 mg / day) and monitored for worsening of disease within the 12-week period. Evidence of clinical deterioration (ECD) is defined by one of the following: >1 -point increase in adjusted INCAT disability score or >8 kPa decrease in grip strength, which are considered clinically meaningful changes. This period will ensure that only participants with active CIDP who meet the deterioration criteria may proceed to the open-label treatment (Stage A). The transition to Stage A will occur at the first timepoint of ECD. Participants who do not demonstrate ECD by week 12 will be considered to be in remission and will be discontinued from the study.

[0511] Open-label Nipocalimab Treatment Period. Stage A is designed to identify nipocalimab treatment responders and restabilizing participants who deteriorated in Run-in.Treatment response is assessed by evidence of clinical improvement (ECI) in the setting of openlabel treatment with nipocalimab. In this 12-week study period, participants received 30 mg / kg nipocalimab IV loading dose followed by 15 mg / kg nipocalimab administered intravenous (IV) every 2 weeks (q2w). Participants are eligible to enter Stage B if the following responder criteria are met. Participants must: (1) demonstrate ECI from Stage A baseline, defined as improvement in either adjusted INCAT disability score (>1 -point decrease) or grip strength (>8kPa increase).Participants who entered Stage A from the Run-in period should improve on the same assessment that declined in the Run-in period. (2) maintain the same or improved scores on these assessments (INCAT disability score or grip strength) for at least the last 2 consecutive visits of Stage A (eg, weeks 10 and 12); and (3) demonstrate no deterioration on the adjusted INCAT disability score from either Run-in baseline (for participants on IVIg / SCIg / corticosteroids [CS] at screening) or Stage A baseline (for untreated or treatment naive participants). Participants showing no evidence of improvement on nipocalimab by week 6, demonstrating ECD, or who are nipocalimab non- -88- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)responders by week 12 will be discontinued from the study and treated with IVIg or other standard of care rescue therapy at the investigator's discretion and requested to return for a safety follow-up visit, see details below for Rescue Medications. No improvement is defined as no improvement in either adjusted INCAT disability score or grip strength by week 6.

[0512] Randomized Withdrawal, Placebo-controlled Period (Documentation of Efficacy and Safety of nipocalimab vs placebo). Stage B is a double-blind, placebo-controlled, randomized withdrawal period which will evaluate the efficacy and safety of nipocalimab versus placebo in nipocalimab treatment responders for up to 52 weeks. Participants will be randomly assigned in a 1 : 1 ratio to receive either placebo or nipocalimab (15 mg / kg IV q2w) starting on Day 1 in Stage B. The participants will receive study intervention (placebo or nipocalimab) and undergo safety, efficacy, PK, pharmacodynamics (PD), and immunogenicity assessments, as outlined in the SoA. Participants who meet protocol-defined criteria for relapse during this period will be discontinued from study intervention. Relapse is defined as one of the following: (1)1 -point or greater increase in adjusted INCAT disability score relative to Stage B baseline or (2) switch to IVIg or other SoC as a result of investigator-assessed lack of efficacy. In case both relapse criteria are met, the earlier date will be defined as the date of relapse for this participant. In the case of the second criteria listed above, evaluation based on clinically relevant deterioration demonstrated by minimal clinical important difference (MCID) changes in clinical outcome assessments, medical history, physical / neurologic examination, and additional outpatient or inpatient management for CIDP should be used to guide investigator decision of a switch to IVIg or other SoC based on lack of efficacy.

[0513] Open-label Extension (variable duration). After completion of Stage B participants have the option to enter the OLE to evaluate long-term safety and efficacy of nipocalimab and may continue until 2 years after marketing authorization in a participant’s local country / territory or until nipocalimab becomes available commercially or via other continued access program, whichever comes first. The OLE will be of variable duration per participating country / territory depending on the timing of market authorization and commercial availability of nipocalimab. Participants who discontinue from Stage B for a reason other than relapse, including those who are switched to IVIg or other SoC as a result of investigator-assessed lack of efficacy without confirmation of relapse by the RAC, will not be eligible for OLE entry. Participants will receive nipocalimab 15 mg / kg q2w by IV infusion starting on OLE Day 1. Participants who relapse as defined by INCAT disability score -89- 103693.004420\4914-0795-9446.2DOCKET NO.: 103693.004420 (MPI6028WOPCT1)in the OLE will stop treatment with nipocalimab, should return for an OLE EOP visit, and be requested to return for a Follow-up Safety Visit 8 weeks after last nipocalimab infusion.

[0514] Efficacy Evaluations. Efficacy is assessed prior to dosing during the treatment periods (Stage A, Stage B and OLE). Investigator-rated assessments include the INCAT disability scale, grip strength, Medical Research Council (MRC) Muscle Grading Scale, and Timed Up and Go (TUG). Patient reported outcomes (PROs) are recommended to be collected in the following sequence: Inflammatory Rasch-Built Overall Disability Score (I-RODS), Patient Global Impression of Severity (PGI-S), Short Form Health Survey version 2 (SF-36v2), EuroQol 5-dimension 5-level quality of life questionnaire (EQ-5D-5L), Rasch Transformed-Fatigue Severity Scale (RT-FSS), Work Productivity and Activity Impairment Questionnaire: Specific Health Problem (WPAI-SHP), Treatment Satisfaction Questionnaire for Medication (TSQM vll), and Neuropathic Pain Intensity-Numeric Rating Scale (PI-NRS).

[0515] The INCAT disability scale is a clinician-rated assessment that measures activity limitation and degree of functional disability. The INCAT scale is an ordinal scale scored from 0 to 10, with higher scores indicating more disability (Table 2). The adjusted INCAT disability score excludes changes in upper limb function from 0 [normal] to 1 [minor symptoms in the fingers which do not impair any functional activities]. The adjusted INCAT has been used in multiple CIDP clinical trials as the primary endpoint defining relapse. A 1 -point change in the adjusted INCAT disability score is considered to be a MCID.

[0516] Grip Strength is a quantifiable, objective performance outcome measure of hand strength, which can be measured using various devices (Table 2). In CIDP clinical trials, grip strength is used to capture important changes in hand strength that occur throughout the study using supplied devices. The final grip strength measurement is the average of the 3 recordings. The right and left hand are reported separately. Grip strength will be captured at home by the patient prior the scheduled phone or clinic visit. Only the assessment recorded at a clinic visit (scheduled or unscheduled) will be used for analysis. Medical Research Council (MRC) Muscle Grading Scale is a clinician-rated outcome (Table 2) that provides a strength rating (on a scale from 0 [no visible contraction] to 5 [normal]) in 6 muscles collected bilaterally: deltoid, biceps, wrist extensors, iliopsoas, quadriceps, tibialis anterior. Lower scores indicate greater impairment. Inflammatory Rasch-Built Overall Disability Scale (I-RODS) is a widely used, reliable and well validated patient-reported, linearly weighted scale intended to specifically assess activity and social participation -90- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)limitations in patients with CIDP. The I-RODS is comprised of 24 items representing common daily activities that address upper and lower limb disability and range in difficulty from very easy to very difficult (Table 2). Lower scores indicate greater activity and social participation limitations. The patient assigns a score, 0 which represents “impossible to perform,” 1 “performed with difficulty” or 2 representing “easily performed.” Both the ability of the patient and the perceived difficulty of a task are tallied for a raw I-RODS score that ranges between 0 and 48. The resulting raw I-RODS score is then transformed to a final I-RODS score ranging from 0 (most severe activity and social participation limitations) to 100 (no activity and social participation limitations).

[0517] Timed Up and Go (TUG) is a performance outcome measure that evaluates mobility, balance, walking ability, and gait impairment in CIDP. The TUG measures the time taken to stand up from a chair, walk 3 meters, turn, walk back to the chair, and sit down again. The SF-36 version 2 is a self-administered, 36-item questionnaire measuring health-related quality of life (HRQoL). The recall period for all items is the past week. The SF-36 version 2 Acute includes 8 domains that measure Physical Functioning (10), Role-Physical (4), Bodily Pain (2), General Health (5), Vitality (4), Social Functioning (2), Role-Emotional (3) and Mental Health (5). The 8 domains can be aggregated into 2 summary scales that reflect physical and mental health: Physical Component Summary (PCS) and Mental Component Summary (MCS). Responses to all items are rated on a 3-, 5- or 6-point Likert scale. The EQ-5D-5L Descriptive System is a self-administered, standardized measure of health status in a wide range of health conditions and treatments. It provides a descriptive profile and a single index value for health status that can be used in the clinical and economic evaluation of health care. The recall period for all items is ‘Today.’ The EQ-5D-5L consists of the EQ-5D descriptive system and the EQ visual analog scale (EQ-VAS). The EQ-5D descriptive system is comprised of 5 items across the following 5 dimensions: mobility, self-care, usual activities, pain / discomfort and anxiety / depression. The EQ-5D-5L uses a 5-point Likert response scale ranging from “No problems” to “Extreme problems.” Treatment Satisfaction Questionnaire for Medication (TSQM vll)

[0518] The TSQM vll is a generic 11 -item patient reported outcome instrument that is used to assess patient satisfaction with treatment. The recall period for this instrument is 2 to 3 weeks, or since the last medication use. Response options are 5 or 7-point Likert or Likert-type scales. Four domain scores can be calculated Effectiveness (2), Side Effects (4), Convenience (3) and Global Satisfaction Scale (2) on a 0 to 100 scale, with higher scores indicating a higher level of satisfaction -91- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)with treatment. Patient Global Impression of Severity (PGI-S) is a single item, patient-reported outcome measure that will enable an anchor-based methodology that will allow calculation of meaningful within patient change for a desired concept. These will support the analysis of the I-RODS as a secondary endpoint. As supportive evidence, percentage of participants with meaningful I-RODS score change will be compared among treatment groups in Stage B. Rasch Transformed-Fatigue Severity Scale (RT-FSS) is a 7-item patient-reported outcome, linearly weighted Raschbased scale that measures fatigue severity and impact on activities and lifestyle. The recall period is ‘over the past 1 week.’ Responses are scored on a 4-point scale from 0 (disagree) to 3 (agree), a total score a can be calculated with a range from 0 (no signs of fatigue) to 21 (most disabling fatigue). Higher scores indicate higher level of fatigue severity and impact. Work Productivity and Activity Impairment-Specific Health Problem (WPAI-SHP) is a 6-item patient-reported outcome questionnaire that measures the effect of CIDP on work productivity and impairment. The WPAI-SHP yields 4 scores: absenteeism (work time missed); presenteeism (impairment at work / reduced one the job effectiveness); work productivity loss (overall work impairment / absenteeism plus presenteeism); and activity impairment. Each score is expressed as a percentage (0-100%) with higher numbers indicating greater impairment and less productivity. The recall period is past 7 days. Neuropathic Pain Intensity-Numeric Rating Scale (PI-NRS) is used to rate patient-reported pain in the past 24 hours on a scale of 0 to 10, where 0 represents “no pain” and 10 represents “the worst possible pain”, using whole numbers. The single-item scale is a standard method for assessment of pain in clinical settings and patients find it intuitively easy to use. Completion of the scale requires less than 1 minute. The clinically meaningful change of 2 points is identified when using the scale to assess neuropathic pain.Table 1. Objectives And Endpoints-92- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)-93- 103693.004420\4914-0795-9446.2DOCKET NO.: 103693.004420 (MPI6028WOPCT1)>-94- 103693.004420\4914-0795-9446.2DOCKET NO.: 103693.004420 (MPI6028WOPCT1)Table 2. Functional and Disability Assessments Used in CIDP

[0519] Nipocalimab is effective in treating CIDP. Nipocalimab is proved to be superior to placebo in delaying relapse in participants with CIDP, who are responders to nipocalimab.Nipocalimab treatment achieves at least a 50%, 55%, 60%, 65%, 70%, or 75% reduction in the risk of relapse in the participants compared to placebo. Relapse is defined as a deterioration of symptoms as measured by an increase in adjusted INCAT disability score (>1 point increase) or the switch to IVIg or other standard of care (SoC) as a result of investigator-assessed lack of efficacy. A subject is evaluated, prior to treatment with nipocalimab, utilizing EFNS / PNS 2010 and other metrics as provided in this example. A subject with CIDP is evaluated utilizing INCAT, grip strength, and I-RODS prior to treatment with nipocalimab to generate a INCAT, grip strength, and I-RODS score. The subject is administered nipocalimab at an initial loading dose of 30 mg / kg, and subsequent maintenance dose of 15 mg / kg every 2 weeks for 12 weeks. After 12 weeks and over time, the subject is evaluated for INCAT, grip strength, and I-RODS scores. The subject is found to have achieved an ECI if the following conditions are satisfied: improvement in INCAT total score (>=1); improvement in grip strength (>=8kpa); or improvement in I-RODS (>=4 points); and-95- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)wherein the improvement is to at least the scores recorded at screening visit, and wherein the subject maintained stable scores for at least 2 consecutive visits.

[0520] Nipocalimab is effective in treating CIDP based on change from baseline in INTAC, grip strength, MRC, I-RODS, and TUG scores. A subject is evaluated, prior to treatment with nipocalimab, utilizing the metrics as provided in this example. A subject with CDIP is evaluated with INTAC, grip strength, MRC, I-RODS, and TUG scales prior to treatment with nipocalimab to generate a baseline INTAC, grip strength, MRC, I-RODS, and TUG scores. The subject is administered nipocalimab at an initial loading dose of 30 mg / kg, and subsequent maintenance dose of 15 mg / kg every 2 weeks for 12 weeks. Over time and after 12 weeks, the subject is evaluated with INTAC, grip strength, MRC, I-RODS, and TUG scales. The subject is found to have an improvement on the adjusted INTAC scale over time following administration of the first dose. The subject is found to have an improvement on the adjusted INTAC scale at week 12 following administration of the first dose. The subject is found to have an improvement on the grip strength scale over time following administration of the first dose. The subject is found to have an improvement on the grip strength scale at week 12 following administration of the first dose. The subject is found to have an improvement on the MRC sum scale over time following administration of the first dose. The subject is found to have an improvement on the MRC sum scale at week 12 following administration of the first dose. The subject is found to have an improvement on the I-RODS disability scale over time following administration of the first dose. The subject is found to have an improvement on the I-RODS disability scale at week 12 following administration of the first dose. The subject is found to have an improvement on the TUG scale over time following administration of the first dose. The subject is found to have an improvement on the TUG scale at week 12 following administration of the first dose.

[0521] Nipocalimab is effective in treating CIDP based on change from baseline in INTAC, grip strength, MRC, I-RODS, and TUG scores following treatment with nipocalimab.A subject is evaluated, prior to treatment with nipocalimab, utilizing the metrics as provided in this example. A subject with CDIP is evaluated with INTAC, grip strength, MRC, I-RODS, and TUG scales after 12 weeks of treatment with nipocalimab to generate a baseline INTAC, grip strength, MRC, I-RODS, and TUG scores. The subject is administered nipocalimab at a dose of 15 mg / kg every 2 weeks for 48 weeks. Over time and after 48 weeks, the subject is evaluated with INTAC, grip strength, MRC, I-RODS, and TUG scales. The subject is found to have a delayed adjusted -96- 103693.004420\4914-0795-9446.2DOCKET NO.: 103693.004420 (MPI6028WOPCT1)INTAC deterioration on the adjusted INTAC scale over time following administration of the first dose. The subject is found to have a delayed adjusted INTAC deterioration on the adjusted INTAC scale at 48 weeks following administration of the first dose. The subject is found to have an improvement on the adjusted INTAC scale over time following administration of the first dose. The subject is found to have an improvement on the adjusted INTAC scale at week 48 following administration of the first dose. The subject is found to have an improvement on the grip strength scale over time following administration of the first dose. The subject is found to have an improvement on the grip strength scale at week 48 following administration of the first dose. The subject is found to have an improvement on the MRC sum scale over time following administration of the first dose. The subject is found to have an improvement on the MRC sum scale at week 48 following administration of the first dose. The subject is found to have an improvement on the I-RODS disability scale over time following administration of the first dose. The subject is found to have an improvement on the I-RODS disability scale at week 48 following administration of the first dose. The subject is found to have an improvement on the I-RODS disability scale that is a change greater than or equal to 4 points on the I-RODS scale over time following administration of the first dose. The subject is found to have an improvement on the I-RODS disability scale that is a change greater than or equal to 4 points on the I-RODS scale at week 48 following administration of the first dose. The subject is found to have an improvement on the TUG scale over time following administration of the first dose. The subject is found to have an improvement on the TUG scale at week 48 following administration of the first dose.

[0522] Treatment of CIDP with an anti-FcRn antibody leads to an improvement in HRQoL, Modified Rasch-based FSS, TSQM-9, EQ-5D-5L, PGI-S, and WPALSHP scores. A subject with CIDP is evaluated utilizing HRQoL, Modified Rasch-based FSS, TSQM-9, EQ-5D-5L, PGI-S, and WPAESHP scales prior to treatment with nipocalimab to generate a baseline HRQoL, Modified Rasch-based FSS, TSQM-9, EQ-5D-5L, PGI-S, and WPAESHP scores. The subject is administered nipocalimab at dose of 15 mg / kg every 2 weeks, or at an initial loading dose of 30 mg / kg, followed by subsequent maintenance dose of 15 mg / kg every 2 weeks for 12 weeks, followed by administration of a single dose of 15 mg / kg every 2 weeks for 48 weeks. Over time and after 12 and 48 weeks following first dose, the subject is evaluated utilizing HRQoL, Modified Rasch-based FSS, TSQM-9, EQ-5D-5L, PGI-S, and WPAESHP scales. The subject is found to have an improvement on the HRQoL scale over time following administration of the first dose. The subject is found to have an improvement on the HRQoL scale at week 12 following administration -97- 103693.004420\4914-0795-9446.2DOCKET NO.: 103693.004420 (MPI6028WOPCT1)of the first dose. The subject is found to have an improvement on the HRQoL scale at week 48 following administration of the first dose. The subject is found to have an improvement on the Modified Rasch-based FSS scale over time following administration of the first dose. The subject is found to have an improvement on the Modified Rasch-based FSS scale at week 12 following administration of the first dose. The subject is found to have an improvement on the Modified Rasch- based FSS scale at week 48 following administration of the first dose. The subject is found to have an improvement on the TSQM-9 scale over time following administration of the first dose. The subject is found to have an improvement on the TSQM-9 scale at week 12 following administration of the first dose. The subject is found to have an improvement on the TSQM-9 scale at week 48 following administration of the first dose. The subject is found to have an improvement on the EQ-5D-5L scale over time following administration of the first dose. The subject is found to have an improvement on the EQ-5D-5L scale at week 12 following administration of the first dose. The subject is found to have an improvement on the EQ-5D-5L scale at week 48 following administration of the first dose. The subject is found to have an improvement on the PGI-S scale over time following administration of the first dose. The subject is found to have an improvement on the PGI-S scale at week 12 following administration of the first dose. The subject is found to have an improvement on the PGI-S scale at week 48 following administration of the first dose. The subject is found to have an improvement on the WPAESHP scale over time following administration of the first dose. The subject is found to have an improvement on the WPAESHP scale at week 12 following administration of the first dose. The subject is found to have an improvement on the WPAESHP scale at week 48 following administration of the first dose.

[0523] Treatment of CIDP with nipocalimab does not elevate cholesterol. Elevations in total cholesterol and low-density lipoprotein (LDL) were reported recently with another experimental anti-FcRn antibody that is not nipocalimab in the same pharmacological class of FcRn antagonists. This finding triggered a review of lipid data in Sponsor-completed and ongoing nipocalimab studies. In the Phase 1 healthy volunteer MOM-M281-001 and Phase 2 generalized myasthenia gravis MOM-M281-004 studies, asymptomatic, dose dependent, reversible elevations in non-fasting mean total cholesterol were observed up to 25% from baseline. In study MOM-M281-004, at the highest dose of 60 mg / kg every 2 weeks (Q2W), the mean percent change in total cholesterol increased to a stable maximum of 21% to 23% above baseline within 1 month of initiation of dosing and declined to near baseline level 1-2 months after the last dose. As a result of these findings, the following assessments are conducted: 1) assessment for lipids (total cholesterol,-98- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)HDL, calculated LDL, and triglycerides) in fasting and non-fasting conditions at multiple time points on and off treatment, 2) exclusion criterion for patients with a recent significant cardiovascular event, 3) recommendation for lipid abnormalities management according to local health guidelines.

[0524] The example provided herein demonstrates that an anti-FcRn antibody, such as, but not limited to, nipocalimab is effective to treat CIDP as measured one or more of the indices and outcomes as provided for herein.EXAMPLE 2. Safety and efficacy of nipocalimab in adults with generalized myasthenia gravis.

[0525] Results. 199 patients were enrolled and randomly assigned, of whom 196 (98 in each treatment group) received at least one dose of study drug and were included in the safety analysis dataset (FIG. 2). A major protocol deviation was noted for 20 patients in the nipocalimab group and 28 patients in the placebo group; the majority were either addressed by prespecified statistical methods described in the statistical analysis plan or were missed safety assessments that did not affect the overall safety of the participants. The primary efficacy analysis dataset comprised 153 randomly assigned and treated patients who were antibody-positive (77 in the nipocalimab group and 76 in the placebo group). Among the patients who were antibody-positive, 134 (88%) were antibody-positive for AChR, 16 (11%) for MuSK, and three (2%) for LRP4. Most patients completed 24 weeks of double-blind treatment (FIG. 2).

[0526] A significantly greater reduction from baseline in MG-ADL total score was observed over weeks 22, 23, and 24 (primary efficacy endpoint) for the nipocalimab group (least-squares mean change -4-70 [SE 0-329]) than for the placebo group (-3-25 [0-335]), with a difference between groups of-1 -45 (95% CI -2-38 to -0-52; p=0-0024; FIG. 3A and 3B). The estimated treatment difference for nipocalimab versus placebo in male patients was -2-39 (95% CI -3 -87 to -0-91) and in female patients was -0-86 [-2-06 to 0-34). A statistically significantly greater reduction from baseline in QMG total score was also observed over weeks 22 and 24 (first key secondary endpoint) for the nipocalimab group (least squares mean change -4-86 [SE 0-504]) compared with the placebo group (least squares mean change -2 -05 [0-499]), with a difference between groups of -2 -81 (95% CI -4-22 to -1 - 41; p=0- 00012; FIG 3 A and 3B).-99- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)

[0527] A statistically significant treatment effect, favoring nipocalimab, was observed for the key secondary responder endpoint of percentage of patients with at least a 2 point improvement in average MG-ADL total score over weeks 22, 23, and 24 (between-group difference 16-2% [95% CI 0-9 to 31-5]; p=0 021; FIG. 4). The between-group difference for the third key secondary endpoint of early response, defined as response at week 1, week 2, or week 1 and week 2, was not statistically significant (between-group difference 8-4% [95% CI -7 2 to 24 0]; p=0-23; FIG. 4). Given that the between-group difference for the third key secondary endpoint was not statistically significant, the two subsequent key secondary endpoints could not be formally tested according to the predefined testing sequence. Estimates for these endpoints showed a higher percentage of patients had a response from weeks 4 to 24 in the nipocalimab group than in the placebo group, and a higher percentage of patients showed at least 50% symptom improvement in the nipocalimab group compared with the placebo group (FIG. 4). Approximately a third of patients (24 [31%] of 77) treated with nipocalimab reached the predefined other secondary endpoint of minimal symptom expression at any time during the double-blind phase, compared with ten (13%) of 76 patients treated with placebo. Further, eight (10%) of 77 patients treated with nipocalimab reached minimal symptom expression at least 75% of all timepoints during the double-blind phase, compared with one (1%) of 76 patients treated with placebo. Patients treated with nipocalimab reached numerically higher levels of improvement (up to >8 points in MG-ADL and up to >9 points in QMG) at predefined visit weeks, compared with patients treated with placebo.

[0528] Nipocalimab demonstrated rapid and sustained lowering of IgG (FIG. 5). The median predose (minimal) total IgG reduction from baseline after the loading dose was -74-6% (IQR -79-4 to -68-7) at week 2 and -68-8% (-75-3 to -62-2) at week 24. A significant reduction in each IgG subclass was observed; AChR antibody and MuSK antibody concentrations also showed reductions over the 6-month double-blind phase. No changes in total IgM, IgA, or IgE were observed.

[0529] Increases in fasting total cholesterol, high-density lipoprotein (HDL), and low-density lipoprotein (LDL) were observed in the nipocalimab group. At week 24, mean percent change from baseline was 7-8% (SD 16-86) for total cholesterol, 7 0% (20 -87) for HDL, and 8 -3% (23 12) for LDL in the nipocalimab group, and was -4 - 1% (12-30) for total cholesterol, -1 -6% (13 • 84) for HDL, and -3 0% (18-56) for LDL in the placebo group. Given the concomitant increase in total cholesterol and HDL, the mean total cholesterol: HDL ratio in the nipocalimab group remained-100- 103693.004420\4914-0795-9446.2DOCKET NO.: 103693.004420 (MPI6028WOPCT1)lower than 4 throughout the 24-week double-blind phase and similar to placebo at 24 weeks (nipocalimab 3-6

[0136] , placebo 3-5 [1-21]).

[0530] No clinically meaningful changes were reported in vital signs, electrocardiogram recordings, or other clinical laboratory evaluations (including leukocytes), and no liver abnormalities met Hy's law criteria. There was a mild decrease of albumin in the nipocalimab group (mean percent change from baseline in albumin was -7-2% [SD 5-37] with nipocalimab and -2 1%

[0708] with placebo at week 24); however, all albumin values stayed within the normal laboratory reference range.

[0531] Discussion. In this study, nipocalimab showed clinically meaningful and sustained efficacy over 6 months in a broad cohort of patients with antibody-positive (anti-AChR-positive, anti-MuSK-positive, or anti-LRP4-positive) generalized myasthenia gravis, in both the primary, clinician-assessed and patient-reported outcome (MG-ADL) and the key secondary, clinician-assessed outcome (QMG). Statistically significant effects in both patient-reported and clinician-reported outcomes support the clinically meaningful benefits of nipocalimab in generalized myasthenia gravis. More patients in the nipocalimab group than in the placebo group also achieved MG-ADL responder status at both weeks 1 and 2. A secondary endpoint assessed the sustainability of therapeutic effect; approximately two times more patients in the nipocalimab group than in the placebo group reached MG-ADL responder status by week 4, with response sustained through the end of the 6-month double-blind phase.This study demonstrates the uninterrupted sustained treatment efficacy in a broader group of patients who are antibody-positive. The antibody-positive study cohort (88% positive for AChR antibodies, 10% for MuSK antibodies, and 2% for LRP4 antibodies) is representative of the general myasthenia gravis patient population. In addition, these results show nipocalimab was well tolerated among patients. IgG lowering was rapid and substantial (-75% at week 2) and sustained over 6 months (minimum steady-state predose reduction of around 70%), with no evidence of diminishing pharmacodynamic effect. Consistent with these findings, patients treated with nipocalimab showed numerically greater treatment differences for MG-ADL and QMG compared with placebo as early as week 1, and the magnitude of separation from placebo achieved at week 2 was generally maintained and similar to the separation seen at week 24 (EIG. 3). Nipocalimab also reduced IgG subclass concentrations; anti-AChR and anti-MuSK antibodies followed a similar pattern in patients who were antibody-positive. The magnitude of lowering for both IgG was generally associated with -101- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)greater improvement in symptoms, suggesting a correlation between the reduction of IgG and clinical improvement in generalized myasthenia gravis.

[0532] FIGs. 3A and 3B show the time course of response for the primary efficacy measure (MG-ADL) and the key secondary efficacy measure (QMG). FIGs. 6A and 6B show the distribution of response on the MG-ADL and QMG following 24 weeks of treatment with nipocalimab.

[0533] Adolescents with gMG. The pharmacodynamics, pharmacokinetics, and efficacy of nipocalimab for the treatment of generalized myasthenia gravis (gMG) in adolescents (12 to less than 18 years of age), who are antibody-positive (anti- AChR and anti-MuSK), were evaluated over 24 weeks in an open-label study. The study enrolled patients who met the following criteria at screening: MGFA clinical classification class II to IV; Positive for antibodies to AChR or MuSK; On stable dose of SOC therapy prior to screening, including AChE inhibitors, steroids or NSISTs, either in combination or alone.

[0534] Seven adolescent patients received nipocalimab at the recommended dosage regimen described above over 24 weeks. Patients had a median age of 14 years at screening (range 12 to 16 years) and a median time since diagnosis of three years. Six patients were female; four were Asian, one was black, and two were of unknown race. Median MG-ADL total score at baseline was 3.5, and median QMG total score was 14. All patients were AChR antibody-positive. At baseline, three patients were on AChE inhibitors, five were on steroids, and six were on NSISTs at stable doses.

[0535] The primary endpoint was the effect of nipocalimab on total serum IgG. At Week 24, the median pre-dose percent reduction in total IgG from baseline (N = 5) was 70%, consistent with the IgG reduction seen in adults. For the secondary endpoints, the mean (SD) change at Week 24 in MG-ADL was -2.40 (0.418) and in QMG was -3.80 (2.683) the pattern of improvement was consistent with those seen in adults.EXAMPLE 3. Efficacy and Safety of Nipocalimab in Participants with Active Idiopathic Inflammatory Myopathies.Provided herein is a phase 2, multicenter, randomized, double-blind, placebo-controlled, parallel-group study to evaluate the efficacy and safety of nipocalimab in participants with active idiopathic inflammatory myopathies.-102- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)

[0536] Objectives and Endpoints. Active IIM for this study includes active DM, IMNM, and ASyS subtypes.Table 3. Objectives and Endpoints> <>>>>-103- 103693.004420\4914-0795-9446.2DOCKET NO.: 103693.004420 (MPI6028WOPCT1)>> <<> >> << >> < >-104- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)> >> > >> > >> > >> > >-105- 103693.004420\4914-0795-9446.2DOCKET NO.: 103693.004420 (MPI6028WOPCT1)-106- 103693.004420\4914-0795-9446.2DOCKET NO.: 103693.004420 (MPI6028WOPCT1)Note: Both the nipocalimab and placebo arms are in addition to protocol-permitted, oral standard-of-care treatments but are referred to as “nipocalimab” and “placebo” throughout.

[0537] Study Design. This is a Phase 2, single-dose, randomized, double-blind, placebo-controlled, parallel, multicenter, interventional study in participants >18 years of age with active IIM (including DM, IMNM, and ASyS subtypes) despite being on standard-of-care treatments, to evaluate the efficacy, safety, tolerability, PK, PD, and immunogenicity of 15 mg / kg IV q2w nipocalimab. This Phase 2 study is designed to be an adequate and well-controlled clinical investigation. Participants must be serologically positive and have clinically active disease while-107- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)receiving at least 1 standard-of-care treatment within at least 6 weeks prior to the first administration of the study intervention. The number of participants to be enrolled in this study in each of the 3 subtypes is expected to be reflective of the relative prevalence of these IIM subtypes.

[0538] The total duration of the study is up to 112 weeks, consisting of 4 study periods: a <6-week screening period (rescreening is permitted once per participant), a 52-week double-blind period, a 48-week LTE, and a safety follow-up 8 weeks post last administration of study intervention. A 20-week mandatory protocol- defined oral GC taper will be applied to both study groups from Week 24 to Week 44, for those participants on oral GC (>5 mg / day of prednisone or equivalent) at baseline. At Week 52, participants will be assessed by the investigator for eligibility to continue into a 48-week LTE. If a participant is not enrolled in the LTE, or ends participation in study prior to Week 52, they will be followed for 8 weeks after the last administration of study intervention. If a participant is enrolled in the LTE, the safety follow-up visit will occur 8 weeks post last administration of study intervention of the LTE (FIG. 7).

[0539] Nipocalimab group: Body weight based IV administration of nipocalimab (15 mg / kg) at Week 0 then q2w thereafter.

[0540] Placebo group: IV administration of placebo at Week 0 then q2w thereafter

[0541] Randomization will utilize the following 2 stratification factors:

[0542] 1. Groups of specific MSA profile at screening: a. DM: anti-Mi-2, anti-TTFl-y, anti- NXP-2, anti-SAE, anti-MDA-5 antibodies, b. IMNM: anti-SRP and anti-HMGCR antibodies, c. ASyS: anti-Jo-1, anti-PL7, anti-PL12, anti-OJ, and anti-EJ antibodies

[0543] 2. Disease severity at Week 0: a. Moderate disease, b. Severe disease

[0544] Endpoints. The proportion of participants who achieve at least minimal improvement (>20) in IMACS FIS at Week 52 and on <5 mg / day of oral prednisone (or equivalent) from Week 44 through Week 52 is selected as the primary endpoint. Secondary endpoints will be analyzed at Week 24 and Week 52.

[0545] Efficacy, safety, PK, PD, immunogenicity, and biomarkers (where local regulations permit) will be assessed according to the SoA. An optional pharmacogenomic blood sample will be-108- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)collected from participants who consent to this component of the study (where local regulations permit).

[0546] Key safety assessments include AEs, SAEs, AESIs, laboratory parameters (hematology and chemistry, including lipid panel), vital signs, and physical examination.

[0547] Based on benefit-risk analysis, the LTE may be delayed or stopped at the sponsor’s discretion. Participants will be randomly assigned into 1 of 2 treatment groups (nipocalimab or placebo) and will be stratified by MSA profile and disease severity. Approximately 35 participants will be enrolled. All enrolled participants will complete the study per protocol.

[0548] Participants on GC at baseline should remain on a stable dose of oral GC (<20 mg / day prednisone or equivalent) from 4 weeks prior to the first administration of study intervention to Week 0. No changes in GC doses are allowed between Week 0 and Week 24. From Week 24 to Week 44, GC doses should be tapered based on a mandatory protocol-defined GC tapering schedule. No changes to GC doses are allowed from Week 44 to Week 52. Participants who are on GC other than prednisone during screening should preferably be switched to prednisone to follow the GC taper. If the participant continues on GC other than prednisone, the investigator should contact the sponsor designee / medical monitor to ensure that the taper is appropriately adjusted for the GC equivalency compared with prednisone. If participants have GC-induced side effects or develop them during the study (such as osteoporosis and hyperglycemia), appropriate treatment must be given in the judgment of the investigator.

[0549] Efficacy, safety, PK, PD, immunogenicity, and biomarkers (where local regulations permit) will be assessed according to the SoA. An optional pharmacogenomic blood sample will be collected from participants who consent to this component of the study (where local regulations permit). Key safety assessments include AEs, SAEs, AESIs, laboratory parameters (hematology and chemistry, including lipid panel), vital signs, and physical examination.

[0550] Long-Term Extension. All participants entering the LTE will receive nipocalimab 15 mg / kg IV q2w through Week 98. The first dose in the LTE will be at Week 52 and the last dose will be at Week 98. Participants and Investigators will remain blinded to initial treatment assignment until after the DBL at end of study.-109- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)

[0551] The objective of the LTE is to evaluate the long-term efficacy and safety of nipocalimab treatment beyond 1 year. Participants who meet the eligibility criteria will be considered for the LTE. The study intervention in the LTE begins after the assessments per the SoA have been completed at Week 52 and will continue for up to an additional 48 weeks of treatment or until the sponsor decides not to pursue an indication in IIM, whichever occurs first. Participants on placebo in the initial double-blind period will be crossed over to nipocalimab at the point of entering the LTE. Participants and investigators will remain blinded to the initial treatment assignments.

[0552] Study Population. Screening for eligible participants will be performed within 6 weeks before administration of the study intervention. Only 1 retest and 1 rescreening are allowed. If there is a question about the inclusion and exclusion criteria, the investigator must consult with the appropriate sponsor representative and resolve any issues before enrolling a participant in the study. Waivers are not allowed.Inclusion Criteria

[0553] Main Study Inclusion Criteria. Each potential participant must satisfy all of the following criteria to be enrolled in the study:

[0554] Type of Participant and Disease Characteristic 1. >18 years of age.

[0555] Disease Characteristics.2. Disease classification criteria: Participant meets the diagnostic criteria of probable or definite IIM based on 2017 EULAR / ACR classification criteria for adult IIM at least 6 weeks prior to first administration of the study intervention. All historical or current clinical features are included for determination of classification criteria.

[0556] Active disease criteria: Participant has active IIM confirmed by a physician (such as a rheumatologist, neurologist, or dermatologist experienced in treatment of inflammatory myopathies), and meeting at least 1 of the following at screening:a. Active myositis-associated rash (Gottron's papules / sign or heliotrope rash or CDASI total activity score >6).b. A recent available (within 12 weeks prior to screening) muscle biopsy, muscle MRI, or EMG report confirming active disease:-110- 103693.004420\4914-0795-9446.2DOCKET NO.: 103693.004420 (MPI6028WOPCT1)- Muscle biopsy findings: eg, endomysial mononuclear inflammation, or perimysial and / or perivascular mononuclear inflammation, or randomly distributed necrotic muscle fibers without significant mononuclear inflammation.- MRI findings: eg, muscle and / or fascia edema in proximal upper or lower extremity indicative of myositis and absence of severe atrophy or fibro fatty replacement of proximal muscles.- EMG findings: eg, irritable proximal myopathy with positive sharp wave, or fibrillation potential, or increased insertional activity in proximal upper or lower extremity.c. Any 1 muscle enzyme elevation (from screening laboratory values) by >4xULN (muscle enzymes include CK, LDH, aldolase, AST, ALT) secondary to myositis (guided by the GGT <3xULN, total bilirubin <E5xULN, and the ratio of AST or ALTxULN / CKxULN is <1.5)(Chandra 2020).

[0557] Disease severity criteria and minimal core set measure abnormality criteria: Participants should have MMT-8 score of 136 or less and at least 2 of the 5 other core set measures abnormalities at screening and confirmed at Week 0 (except muscle enzymes which use the screening values): PhGA >2; PtGA >2; Extra-muscular global assessment MDAAT >2; HAQ-DI >0.25; Any muscle enzyme (CK, LDH, aldolase, AST, ALT) >2xULN.Table 4. IIM Disease Severity> < <>>>>>-111- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)

[0558] Antibody positivity criteria: Any 1 of the MS As positive: DM: anti-Mi-2, anti-TIFl-y, anti-NXP-2, anti-SAE; anti-MDA-5 antibodies. IMNM: anti-SRP and anti-HMGCR antibodies. ASyS: anti-Jo-1, anti-PL7, anti-PL12, anti-OJ, and anti-EJ antibodies.

[0559] If all MSAs are negative or more than 1 MSA is positive within different subtypes (defined by the central laboratory) at screening, the tests should be repeated during the screening period. If the same results are observed at retesting, the participant should not be enrolled in the study.

[0560] If more than 1 MSA is positive within the same subtype (defined by the central laboratory) at screening, the participant is eligible, and the retest is not required during the screening period.

[0561] Borderline positivity of any MSA (as reported by central laboratory) will be considered to be negative.

[0562] Participants with positive anti-MDA-5 antibody or positive ASyS at screening should meet the following criteria: a. Participants with positive anti-MDA-5 antibody: Have had a diagnosis of IIM >1 year AND No severe ILD* within 1 year prior to screening, b. Participants with positive ASyS antibody: No severe ILD* within 1 year prior to screening. * Severe ILD is defined as the following: Severe ILD confirmed by chest HRCT OR PFTs of FVC <50% predicted and DLCO (corrected) <40% predicted OR on O2

[0563] For all participants: Age, gender, and risk- appropriate malignancy screening tests should be conducted per local guidelines.

[0564] In addition, for participants with positive anti-TIFl-y antibody at screening or within the prior 3 years, a CT or PET scan of the chest, abdomen and pelvis (within 1 year of screening) is also required. If the malignancy screening is not performed or the result is not available, then the participant should be excluded.

[0565] Concomitant or Previous Medical Therapies Received. Participant must be on 1 or 2 of the following background standard-of-care treatments for active IIM within specified dose range:-112- 103693.004420\4914-0795-9446.2DOCKET NO.: 103693.004420 (MPI6028WOPCT1)

[0566] a. Oral GC alone: Must be receiving oral GC for >6 weeks and at a stable dose with maximum dose of <20 mg / day of prednisone or equivalent for >4 weeks prior to first administration of study intervention OR

[0567] b. Maximum of 2 of the following immunosuppressants: Must be receiving these treatments for >12 weeks and be on a stable dose for >8 weeks prior to first administration of study intervention: MMF <3 g / day; MPA <2160 mg / day; AZA / 6-MP 1 to 2 mg / kg / day; up to 3 mg / kg / day; HCQ <400 mg / day; Oral MTX (or equivalent of subcutaneous [SC] dose) <25 mg / week; LEF <20 mg / day; SSZ <2000 mg / day; Oral TAC with the trough concentration per local guidelines; Oral cyclosporine with the trough concentration per local guidelines, OR

[0568] c. A combination of 1 oral GC and 1 of the immunosuppressant therapies listed b. Investigators can optimize the above background standard-of-care medications prior to randomization and while following the above rules for stable dose duration.Table 5. Permitted Background SOC Medications Washout Periods and Maximally Allowed Stable Doses&> >> >-113- 103693.004420\4914-0795-9446.2DOCKET NO.: 103693.004420 (MPI6028WOPCT1)Table 6. Glucocorticoid Conversion Table (Doses Equivalent to 5 mg Prednisone)

[0569] If a participant is on regular or as needed treatment with low potency topical GC that are allowed in the study or topical TAC to treat skin lesions, the dose and frequency should be stable for >4 weeks prior to first administration of the study intervention as well as maintained at the same dose until Week 52 of the study. Low potency topical GC and topical TAC should not be used within 48 hours prior to each study visit.

[0570] Long-term Extension Inclusion Criteria.

[0571] Each potential participant must satisfy the following criteria to be enrolled in the LTE.

[0572] 1. The participant has completed the Week 52 assessments per Table 2 of the SoA

[0573] 2. The participant would benefit from continuing in the study based on the principal investigator’s clinical judgment.

[0574] Study Results

[0575] A total of 36 MSA (myositis specific antibody) positive patients were screened and randomized into nipocalimab 15 mg / kg q2w group (22) and placebo group (14). The dominant disease drivers for the 36 patients are DM (muscle and skin) (11), ASyS (muscle with frequent, often dominant ILD) (9), and IMNM (severe muscle damage with limited extramuscular disease) (16). 77.3% (17 / 22) of the patients in the nipocalimab group completed double-blind treatment phase while 57.1% (8 / 14) in the placebo group completed double-blind treatment phase. Among the 14 patients in the placebo group, 3 patients discontinued during double-blind treatment phase -114- 103693.004420\4914-0795-9446.2DOCKET NO.: 103693.004420 (MPI6028WOPCT1)due to site issues. Data from these 3 patients were deemed not credible and therefore were not included in efficacy analysis.

[0576] As shown in Table 7, a numerically higher proportion of participants in the nipocalimab group achieved at least minimal improvement (>20) in IMACS TIS at Week 52 and on <5 mg / day of oral prednisone (or equivalent) from Week 44 through Week 52 compared to the placebo group. In addition, patients in nipocalimab group achieved a numerically greater IMACS TIS at Week 52 compared to patients in the placebo group (FIG. 43).Table 7: Primary Endpoint Analysis (Primary Estimand) - Full Analysis Set><

[0577] The Nipocalimab group also showed numerical and proportional improvements across clinician-reported and patient-reported outcomes at Week 52, reflecting global disease improvement:• Nipocalimab group demonstrated numerically greater improvement in physical function (PROMIS-PF20) (FIG. 44);• Nipocalimab group achieved numerically greater and more sustained increase in Muscle strength (MMT-8) (FIG. 45);• Nipocalimab group achieved a greater and more sustained reduction in Physician Global Assessment (PhGA) (FIG. 46);• Nipocalimab group achieved a greater and more sustained reduction in Patient Global Assessment (PtGA) (FIG. 47);• Nipocalimab group demonstrated a greater and more sustained reduction in extramuscular disease (MDAAT) (FIG. 48);• Nipocalimab group demonstrated greater improvement in disability (HAQ-DI) (FIG.49);-115- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)• Nipocalimab group demonstrated a substantial and sustained reduction in muscle enzyme CK (FIG. 50), while 7 / 22 in nipocalimab group and 1 / 11 in placebo group achieved normalized CK level;• Nipocalimab group demonstrated sustained reduction in muscle enzyme ALT through Week 52 (FIG. 51);• Nipocalimab group demonstrated sustained reduction in muscle enzyme AST through Week 52 (FIG 52);• Nipocalimab group demonstrated sustained reduction in muscle enzyme LDH through Week 52 (FIG 53);• Nipocalimab group demonstrated sustained reduction in muscle enzyme aldolase through Week 52 (FIG. 54); and• Nipocalimab reduced accumulative GC exposure through Week 52 (Table 8).Table 8: Cumulative oral GC dose (mg / day) through Week 52

[0578] Moreover, nipocalimab treatment led to rapid and substantial decrease in total IgG (FIG. 55) and myositis specific autoantibodies (MSA) (FIG. 56).

[0579] Finally, nipocalimab was well-tolerated, and the observed safety findings were consistent with nipocalimab’ s established safety profile.-116- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)EXAMPLE 4. Efficacy and Safety of Nipocalimab in Adults with Warm Autoimmune Hemolytic Anemia: A Multicenter, Randomized, Double-blind, Placebo-controlled Study with a Long-term Open-label Extension.

[0580] Study Design. This is a Phase 2 / 3 multicenter, randomized, double-blind, placebo-controlled study in participants with wAIHA to evaluate the efficacy, safety, tolerability, PK, and PD of nipocalimab compared with placebo, followed by an open-label extension (OLE) period. The duration of the double-blind period will be 24 weeks (with end-of-treatment assessments at Week 24 / early termination [ET] for all participants, and post-treatment assessments at Week 30 of the double-blind period only for participants not enrolled in the OLE period). An interim analysis will be done after the first 45 randomized participants have completed their Week 16 visit of the doubleblind period or have been withdrawn prematurely from study therapy.

[0581] At the Week 24 / ET visit of the double-blind period, participants may enroll in the OLE period if they meet the OLE eligibility criteria to continue treatment with nipocalimab for an additional 144 weeks (with end-of-treatment assessments at Week 144 / ET and post-treatment assessments at 8 weeks after the last infusion in the OLE).

[0582] In the double-blind period, approximately 111 eligible participants will be enrolled and randomized 1:1:1 to 1 of 3 treatment groups: Group 1 (n=37): Placebo intravenous (IV) infusion every 2 weeks (Q2W). Group 2 (n=37): 30 mg / kg nipocalimab IV infusion every 4 weeks (Q4W). Group 3 (n=37): 15 mg / kg nipocalimab IV infusion Q2W

[0583] A Screening Period of ~2 weeks will precede the double-blind period. At randomization, participants will be stratified by 3 factors: (1) Concurrent treatment for wAIHA: No treatment or corticosteroids at dose <20mg / day of prednisone or equivalent with no immunosuppressants; Immunosuppressants or corticosteroids at dose >20mg / day of prednisone or equivalent. (2) Primary or secondary wAIHA, and (3) Screening Hgb value (ie, the most recent screening value: <8.5 g / dL or >8.5 g / dL).

[0584] During the double-blind period, study drug infusions begin with Baseline (Day 1, Week 0) and continue every 2 weeks thereafter for 24 weeks for safety, efficacy, PK, and PD assessments. Study drug will be administered during study visits by IV infusion. No infusion will be given at the-117- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)Week 1 visit. To maintain the study blind, all participants will receive an IV infusion of nipocalimab or placebo every 2 weeks, depending on their assigned study group.

[0585] The Week 1, 14, 18, and 22 visits during the double-blind period may be performed at the participant’s home or other offsite location with a visiting nurse and telemedicine (call or videoconference between the site staff and the participant) if all the following conditions are met: 1) the process for providing visiting nurses and telemedicine is in place at the site; 2) approval from Health Authorities and Institutional Review Board (IRB independent Ethics Committee (IEC) has been obtained; and 3) the Investigator agrees that an individual participant can have home visits. If these conditions are met, the

[0586] Week 1, 14, 18, and 22 visits may be performed at the participant’s home or other offsite location. The Week 2, 4, 6, 8, 10, 12, 16, 20, and 24 visits, and the Week 30 Follow-up visit, if applicable, must be performed at the study site. At any time, the Investigator can decide that visits must be performed at the site to ensure participants’ safety.

[0587] Participants who meet predefined failure criteria (ie, failure to demonstrate an increase from baseline in Hgb >1 g / dL and are symptomatic) at or after Week 16 of the double-blind period, or participants who need rescue therapy at or after, Week 4 may, at the Investigator’s discretion, discontinue double blinded treatment and may be assessed for eligibility for the OLE period.

[0588] Participants should continue their baseline stable therapeutic regimen throughout the double-blinded period of the study unless:

[0589] Participant requires rescue therapy OR Participant meets criteria for corticosteroid taper, defined as: At or after Week 8, achieved improvement in Hgb, defined as attainment of the following at 3 consecutive visits (with a minimum duration of 28 days), where at least the first visit is at or before Week 16 of the double-blind period, without the need of rescue therapy: Hgb concentration >10 g / dL AND an increase from baseline in Hgb >2 g / dL. The decision to taper should be confirmed with Medical Monitor OR participant experiences side effects of concomitant medications

[0590] During the double-blind period (post-screening), treatment assignment, laboratory measurements related to expected PD activity and immunogenicity of nipocalimab will be masked to the participant, Investigator, and Sponsor during the study. These laboratory measurements -118- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)include total serum IgG, subclass of IgG (IgGl, IgG2, IgG3, IgG4), IgA, IgM, IgE, albumin, total protein, serum nipocalimab concentration, and anti-nipocalimab antibody results. If an emergency occurs that necessitates knowledge of a participant’s treatment assignment, the Investigator can obtain the information via the web-based interactive response technology (IRT) system.

[0591] At the Week 24 / ET visit of the double-blind period, no blinded study drug will be administered, but study assessments will be conducted. As each participant completes or discontinues from the double-blind period, the Investigator will access the IRT to answer questions regarding participant disposition and participant eligibility for the OLE.

[0592] The post-treatment follow-up after Week 24 / ET through Week 30 after the end of the double-blind treatment does not apply to participants enrolling in the OLE. For participants who are eligible for the OLE, the Week 24 / ET visit of the double-blind period serves as the first visit (Week 0) of the OLE; participants enrolled in the OLE will receive their first open-label infusion of nipocalimab at that visit.

[0593] The OLE treatment assignment for each participant (nipocalimab 15 mg / kg Q2W or 30 mg / kg Q4W), will be determined based on prespecified objective criteria and via the IRT algorithm. During the OLE period, the nipocalimab dosing regimen for a given participant may be increased or decreased once based on prespecified criteria. In addition, corticosteroids, and if necessary other concomitant medications, including immunosuppressants, for wAIHA, may be altered during the OLE period as per the Investigator’s usual clinical practice.

[0594] During the OLE, the Week 1 visit and any visits after 3 visits with study drug administration may be performed at the participant’s home or other offsite location with a visiting nurse and telemedicine (call or videoconference between the site staff and the participant) if all the following conditions are met:

[0595] 1) the process for providing visiting nurses and telemedicine is in place at the site; 2) approval from Health Authorities and IRB / IEC has been obtained; and 3) the Investigator agrees that an individual participant can have home visits. Participants opting for at home visits are required to have an on-site visit at least every 8 weeks. The Week 2, 4, and 144 / ET visits and the Follow-up visit at 8 weeks after the last infusion in the OLE, if applicable, must be performed at the-119- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)study site. At any time, the Investigator can decide that visits must be performed at the site to ensure participants’ safety.

[0596] All participants will be followed for at least 8 weeks after their last dose of study drug, either after their last dose in the double-blind period (for participants not enrolling in the OLE) or after their last dose in the OLE (for participants who enrolled in the OLE). At or following Week 144 of the OLE period, the participant may be eligible to enroll in another nipocalimab protocol if available or have the option to continue nipocalimab through other access programs if available per local regulations. If this occurs, the Follow-up visit at 8 weeks after the last OLE infusion may be waived.

[0597] Study Population. Approximately 111 participants are planned. In the event participants are not able to complete the double-blind period of the study due to restrictions in study site activities or travel restrictions as a direct result of a natural disaster, such as the coronavirus 2019 (COVID-19) pandemic, or other major regional / global circumstance, up to approximately 37 additional participants may be randomized to compensate for the participants lost.

[0598] Test Product, Dose, and Mode of Administration. Nipocalimab for IV infusion at doses of 15 mg / kg Q2W or 30 mg / kg Q4W. Placebo for IV infusion

[0599] Duration of Treatment. Double-blind: 24 weeks. OLE: 144 additional weeks

[0600] Efficacy Assessments: Efficacy assessments will include Hgb, reticulocyte count, and hemolytic parameters (LDH, indirect bilirubin, and haptoglobin), the FACIT-Fatigue Scale, the EQ-5D-5L quality of life questionnaire, the SF-36v2 acute, the PGIS, the PGIC, and the TSQM-9.

[0601] Safety Assessments: Safety assessments will include collection of AEs, SAEs, AESIs, vital signs, physical examinations, clinical laboratory testing (including chemistry, hematology, urinalysis, and lipid panel), and ECG findings. Any new clinically significant clinical laboratory or ECG findings will be reported as an AE. Adverse events of special interest will include events of infection >Grade 3 and hypoalbuminemia >Grade 3 (albumin < 20 g / L) according to the National Cancer Institute (NCI) Common Terminology Criteria for Adverse Events (CTCAE v5.0). Safety oversight for the study will be provided by an independent Data Safety Monitoring Board (DSMB).-120- 103693.004420\4914-0795-9446.2DOCKET NO.: 103693.004420 (MPI6028WOPCT1)

[0602] Pharmacokinetic / Pharmacodynamic Assessments: Blood samples will be drawn for analysis of nipocalimab concentration and total serum IgG, subclass of IgG (IgGl, IgG2, IgG3, IgG4), IgA, IgM, IgE, albumin, ADA, and NAb.Objectives and Outcome MeasuresTable 9. Objectives and Outcome Measures>>-121- 103693.004420\4914-0795-9446.2DOCKET NO.: 103693.004420 (MPI6028WOPCT1)< >-122- 103693.004420\4914-0795-9446.2DOCKET NO.: 103693.004420 (MPI6028WOPCT1)Abbreviations: ADA=anti-drug antibody; AE=adverse event; AESI=adverse event of special interest; DAT=direct antiglobulin test; ECG=electrocardiogram; EQ-5D-5L=EuroQol 5-dimension, 5-level, quality of life questionnaire; FACIT-Fatigue=Functional Assessment of Chronic Illness Therapy -Fatigue; Hgb=hemoglobin; Ig=immunoglobulin; IVIg=intravenous immunoglobulin; LDH=lactate dehydrogenase; NAb= neutralizing antibody; OLE = open-label extension;PD=pharmacodynamic; PGIC=patient global impression of change; PGIS=patient global impression of severity; PK=pharmacokinetic; SAE=serious adverse event; SF-36v2=Medical Outcomes Study Short Form 36-Item health survey version 2; TSQM-9=treatment satisfaction questionnaire for medication; wAIHA=warm autoimmune hemolytic anemia.Eligibility Criteria for the Double-blind Period

[0603] Inclusion Criteria, Double-blind Period. Participants who meet the following criteria will be eligible for enrollment into the double-blind period of the study.

[0604] 1. Participants >18 years of age.

[0605] 2. Diagnosed with active primary or secondary wAIHA, defined as having all of the following: a. Hgb value<10 g / dL (Section 6.2.7) AND b. Signs of hemolysis, defined as: lactate dehydrogenase (LDH) levels above the upper limit of normal (ULN), or haptoglobin below the -123- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)lower limit of normal, or indirect bilirubin above the ULN AND c. Serological evidence of antierythrocyte antibodies associated with a DAT that is either positive for IgG only or is positive for IgG and C3d (fragment of the third component of complement) at screening at the central laboratory. If the DAT is negative, it can be repeated once. If the repeat is negative, the participant is not eligible.

[0606] 3. Have been diagnosed with wAIHA for at least 3 months, and are currently receiving treatment for wAIHA OR have previously received treatment for wAIHA (treatment-naive participants are not eligible)

[0607] 4. If on corticosteroids, participants must have been on treatment for at least 4 weeks with a stable dose during the screening period or for at least 14 days prior to randomization, whichever is longer. Note: Investigators can optimize the above background medications prior to randomization if they are following the above rules for stable dose duration.

[0608] 5. If currently receiving immunosuppressants, the following drugs are allowed: azathioprine, mycophenolate mofetil / mycophenolic acid, methotrexate, cyclosporine, tacrolimus, danazol, and cyclophosphamide. The participant must have been on a stable dose of any of these drugs for >12 weeks prior to screening and during the screening period. If any of these drugs were stopped, it must have been stopped for at least 8 weeks prior to screening. Note: Investigators can optimize the above background medications prior to randomization if they are following the above rules for stable dose duration.

[0609] 6. Have a platelet count >30xl09 / L. Note: Participants with Evans syndrome who do not have primary immunodeficiency will be eligible as long as they meet all other entry criteria, including having a platelet count >30 x 109 / L.

[0610] 7. Participants who have undergone splenectomy must be at least 3 months post resection prior to screening and must be vaccinated as per the United States Center for Disease Control and Prevention (CDC) annual Recommended Immunization Schedule for Adults Aged 19 Years or Older, or must be vaccinated as per country-specific guidelines (Davies 2011).

[0611] 8. Participants with other autoimmune disease (eg, systemic lupus erythematosus or rheumatoid arthritis) or lymphoproliferative disorders may be eligible if they are stable (no changes in concomitant disease-related medications and severity of disease) for at least 3 months prior to -124- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)screening. Participants with lymphoproliferative disease must also have a low grade, be stable and be, in the opinion of the Investigator, unlikely to require chemotherapy or monoclonal antibody therapy during the double-blind period of the study. Participants requiring change of treatment or new treatment for autoimmune or lymphoproliferative diseases (but not rescue therapy for wAIHA) during the double-blind period will be terminated from the study.

[0612] Inclusion Criteria, Open-label Extension. Participants who meet the following criteria will be eligible for continuation in the OLE period of the study.

[0613] 1. Have completed the double-blind period (through Week 24), or have required rescue therapy at or after Week 4 of the double-blind period, or failed to demonstrate an increase from baseline in Hgb of at least 1 g / dL and are symptomatic at or after Week 16 of the double blind period.

[0614] 2. Are able to understand and voluntarily provide written informed consent to participate in the OLE period and comply with all study procedures.EXAMPLE 5. Subcutaneous (SC) administration of nipocalimab in the abdomen using a prefilled syringe autoinjector (PFS-AI) or a syringe

[0615] This was a Phase 1, open-label, two-part, multiple-dose, randomized, parallel-group, safety, tolerability, PD, and PK study in healthy participants. The study evaluated subcutaneous (SC) administration of nipocalimab in the abdomen using a prefilled syringe autoinjector (PFS-AI) (Cohort 1) or a syringe (Cohorts 2, 3, and 4).

[0616] The study consisted of a screening period (within 4 weeks before administration of the first study intervention), an open-label phase (weekly SC administration over a 4-week period), and EOS assessments (done upon completion of end of study (EOS) / early withdrawal assessments on Day 50) or EOS / early withdrawal assessments upon early withdrawal.

[0617] Approximately 60 participants were randomly assigned in a 1 : 1 : 1 : 1 ratio into each of the 4 cohorts (approximately 15 participants / cohort) and received one of the following study interventions:

[0618] Cohort 1 : 460 mg (2 mL) nipocalimab SC every week delivered via PFS-AI for 4 weeks;-125- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)

[0619] Cohort 2: 460 mg (2 mL) nipocalimab SC every week delivered via syringe transfer for 4 weeks;

[0620] Cohort 3: 230 mg (1 mL) nipocalimab SC every week delivered via syringe transfer for 4 weeks;

[0621] Cohort 4: 690 mg (3 mL) nipocalimab SC every week delivered via syringe transfer for 4 weeks;

[0622] A total of 4 doses of nipocalimab per participant in each cohort were planned to be administered. In all cohorts, the participants entered the study site on Day -1 and remained there for the assigned first administration of study intervention and subsequent sampling, until completion of the protocol-related assessments on Day 3, if the investigator considered that the participant was ready for discharge. Participants returned to the study site for subsequent administrations of study intervention (ie, SC administration via PLS-AI or syringe transfer for the second and third dose of nipocalimab) on Days 8 and 15. Participants re-entered the study site on Day 21 or Day 22 for the fourth administration of study intervention administered on Day 22. Participants remained at the study site for subsequent sampling until completion of the protocol-related assessments in-house on Day 24, if the investigator considered the participants ready for discharge.

[0623] Participants were assessed for safety, tolerability, PD, PK, and immunogenicity up to Day 50.

[0624] Two participants from Cohort 4 were excluded from the PK analysis set due to the administration of an incomplete dose. Lor PD analysis, all participants were analyzed.

[0625] Shown in PIGs. 9-12 are the mean (±SD) serum nipocalimab concentration-time profiles for all cohorts, plotted on a linear and semi-logarithmic scale following a single dose and repeated weekly doses. In general, serum nipocalimab concentrations increased steadily during the absorption phase with a dose-dependent decline in concentrations observed in the terminal phase, consistent with target- mediated drug disposition (TMDD). In addition, serum nipocalimab concentrations following a single dose and weekly repeated doses appeared similar with overlapping values between SC delivery via PFS-AI and SC delivery via syringe transfer method (e.g., Cohort 1 and Cohort 2), suggesting similar serum nipocalimab concentration-time profiles when nipocalimab was administered SC using either a PFS-AI or a syringe.-126- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)

[0626] Shown in FIG. 13 is the median (IQR) percent change from baseline of total serum IgG over time through Day 50 (EOS) for Cohorts 1-4. In general, dose-dependent reductions in total serum IgG were observed across all cohorts following nipocalimab administration. Total serum IgG trended downwards following the first dose until the fourth dose. Peak total serum IgG reduction from baseline was observed following the fourth weekly dose (ie, Week 4) across all 4 cohorts. Maximal total serum IgG reduction was observed with the 690-mg dose (ie, Cohort 4), and return to baseline values was the greatest in the 230-mg cohort (ie, Cohort 3).

[0627] In addition, total serum IgG demonstrated similar disposition profiles over time between SC delivery via PFS-AI and SC delivery via syringe transfer method (e.g., Cohorts 1 and 2), suggesting similar IgG lowering when nipocalimab was administered SC using either a PFS-AI or a syringe.EXAMPLE 6. Population PK / PD Model

[0628] A population PK / PD model was built using pharmacokinetic, receptor occupancy, IgG and MG-ADL data from Phi healthy volunteer and Ph2 / Ph3 gMG patient clinical studies of IV nipocalimab. This was combined with a model built from Phi healthy volunteer studies on IV and SC nipocalimab, assuming the same IgG to MG-ADL relationship following SC dosing as identified in IV nipocalimab.

[0629] A virtual population of N=196,000 subjects was simulated, with relevant covariates (body weight, baseline MG-ADL score, age and race) sampled from the participants in the Phase 3 study. Shown in FIGs. 14-16 are model-predicted median and 95% prediction interval in the target population following IV 15mg / kg Q2W (with 30mg / kg loading dose) vs. SC 1500mg Q2W (without loading dose), SC 1500mg Q2W (with 3000mg loading dose), or SC 518mg QW (without loading dose), respectively, for the predicted free drug concentration, total serum IgG % change from baseline (CFB), and MG-ADL placebo-corrected change from baseline.

[0630] The disclosures of each and every patent, patent application, and publication cited herein are hereby incorporated herein by reference in their entirety. While various embodiments have been disclosed with reference to specific aspects, it is apparent that other aspects and variations of these embodiments may be devised by others skilled in the art without departing from-127- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)the true spirit and scope of the embodiments. The appended claims are intended to be construed to include all such aspects and equivalent variations.Example 7. Efficacy and Safety of nipocalimab in Adults with Warm Autoimmune Hemolytic Anemia (wAfflA): A Multicenter, Randomized, Double-blind, Placebo-controlled Study with a Long-term Open-label Extension

[0631] As explained in Example 4, this was a Phase 2 / 3 multicenter, randomized, double-blind (DB), placebo-controlled study in participants with wAIHA to evaluate the efficacy, safety, tolerability, PK, and PD of nipocalimab compared with placebo, followed by an open-label extension (OLE) period.

[0632] A total of 118 participants were enrolled and randomized to study intervention, 38 in the nipocalimab 15 mg / ml q2w group, 38 in the nipocalimab 30 mg / ml q4w group, and 39 in the placebo IV q2w group. Note that 1 participant randomized to the nipocalimab 15 mg / kg IV q2w group did not receive study intervention as the participant was a screening failure and was randomized in error. Note that 3 participants were randomized to nipocalimab 30 mg / kg IV q2w, a dose regimen which was changed to 15 mg / kg IV q2w in an amendment (dated 20 April 2021). All 3 participants completed 24 weeks in the DB period and entered the OLE.Efficacy

[0633] Both evaluated doses of nipocalimab (15 mg / kg IV q2w and 30 mg / kg IV q4w) showed rapid improvement in Hgb response and the improvement was maintained over time when compared with placebo. Both doses also showed overall improvements in Hgb levels that were associated with improvements in hemolytic markers and improvement of patient-reported fatigue.

[0634] A durable Hgb response starting by Week 16 was achieved by a numerically greater proportion of participants in both dose groups compared with placebo (Table 10 and FIG. 27):15 mg / kg IV q2w: 1 -sided p-value=0.04430 mg / kg IV q4w: nominal 1 -sided p-value=0.015Table 10: Proportion of Participants who Achieved Durable Hemoglobin Response (Primary Estimand, Composite Strategy); Full Efficacy Analysis Set-128- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)> >

[0635] Participants who achieved durable hemoglobin response (which is defined as the attainment of Hgb level >10 g / dL and an increase from baseline in Hgb >2 g / dL at 3 consecutive visits (without any missed visits and with a minimum duration of 28 days), where at least the first is at or before DB Week 16) are characterized as responders.

[0636] Additional supportive analyses were planned and performed to assess Hgb improvement using alternative criteria. While the primary endpoint was a composite endpoint, additional analyses of the components were conducted to provide further insight into the consistency, robustness, and clinical relevance of the treatment effect (Table 11).

[0637] All analyses using each of the components or alternative criteria for response demonstrated that a numerically higher proportion of participants in both 15 mg / kg IV q2w and 30 mg / kg IV q4w groups achieved the endpoint compared with the placebo group, with greater responses observed in the 30 mg / kg IV q4w group.-129- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)Table 11: Primary Endpoint Related Analyses (Composite Strategy); Full Efficacy Analysis Set>>> >< >< < > >>> < <-130- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)> >> >> >> >>> >> > >> > >

[0638] Hgb level of >10 g / dL for 3 Consecutive Visits Starting by Week 16

[0639] Most wAIHA patients requiring treatment have Hgb <10 g / dL and successful therapy strives for a stable Hgb level of at least 10 g / dL, resolution of symptoms, and transfusion independence. Sustained Hgb >10 g / dL for 3 consecutive visits and beginning by Week 16, showing a durable hemoglobin improvement above the clinically relevant threshold, was achieved by (Table 9): 36.8% (14 / 38) in the 15 mg / kg IV q2w group (nominal 1-sided p-value=0.498); 55.3% (21 / 38) in the 30 mg / kg IV q4w group (nominal 1-sided p-value=0.046); 35.9% (14 / 39) in the placebo group.-131- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)

[0640] This outcome showed a better durable Hgb response across all treatment groups, with a numerically higher proportion of participants in the 30 mg / kg IV q4w group achieving response compared with placebo.Increase From Baseline Hgb >2 g / dL for 3 Consecutive Visits Starting by Week 16

[0641] An increase of >2 g / dL from baseline in Hgb for 3 consecutive visits and beginning by Week 16 was achieved by (Table 9): 23.7% (9 / 38) in the 15 mg / kg IV q2w group (nominal 1 -sided p-value=0.027); 26.3% (10 / 38) in the 30 mg / kg IV q4w group (nominal 1-sided p-value=0.010); 7.7% (3 / 39) in the placebo group.

[0642] Additional participants in the nipocalimab group met the criteria, whereas no new participants in the placebo group did, highlighting the therapeutic effect of nipocalimab.

[0643] Hgb level of >10 g / dL and Increase From Baseline Hgb >2 g / dL at >1 Visit by Week 24

[0644] Removing the requirement for 3 consecutive visits, the attainment of an Hgb level >10 g / dL and an increase of >2 g / dL from baseline in Hgb at any 1 visit by Week 24 was achieved by (Table 9): 42.1% (16 / 38) in the 15 mg / kg IV q2w group (nominal 1-sided p-value=0.004); 60.5% (23 / 38) in the 30 mg / kg IV q4w group (nominal 1-sided p-value <0.001); 15.4% (6 / 39) in the placebo group.Increase From Baseline Hgb >2 g / dL at >1 Visit by Week 24

[0645] An increase of >2 g / dL from baseline in Hgb at any 1 visit by Week 24 regardless of absolute Hgb level was achieved by (Table 9): 47.4% (18 / 38) in the 15 mg / kg IV q2w group (nominal 1-sided p-value <0.001); 60.5% (23 / 38) in the 30 mg / kg IV q4w group (nominal 1-sided p-value <0.001); 15.4% (6 / 39) in the placebo group.Durable Hgb Response for 3 consecutive Visits by Week 24 of the DB Period

[0646] While the primary endpoint focused on response starting by Week 16, further analysis within the 24-week DB period was performed to assess the benefit of a longer-term treatment effect. Durable hemoglobin response, Hgb level >10 g / dL and an increase from baseline in Hgb >2 g / dL for 3 consecutive visits (with a minimum duration of 28 days), was achieved by (Table 10): 23.7%-132- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)(9 / 38) in the 15 mg / kg IV q2w group (nominal 1-sided p-value=0.020); 28.9% (11 / 38) in the 30 mg / kg IV q4w group (nominal 1-sided p-value=0.006); 7.7% (3 / 39) in the placebo group.

[0647] Extending the time period to 24 weeks resulted in an additional 2 and 1 responders to be observed in the nipocalimab treatment groups of 30 mg / kg IV q4w and 15 mg / kg IV q2w, respectively, after Week 16 while no new responders were observed in the placebo group.Hgb level of >10 g / dL and Increase From Baseline Hgb >1.5 g / dL for 3 Consecutive Visits Starting by Week 16

[0648] An analysis was also conducted to assess durable Hgb response using the criteria of an increase of at least 1.5 g / dL in Hgb from baseline. This threshold, used in the CADENZA study, a randomized, placebo-controlled study evaluating sutimlimab in support of the FDA approval of ENJAYMO® (sutimlimab-jome) for patients with cold agglutinin disease (CAD), was chosen to account for natural variability in Hgb levels during the study period. This threshold was also used in other clinical studies for wAIHA (Zecca 2003; Costa 2025).

[0649] Sustained Hgb level >10 g / dL and an increase from baseline in Hgb >1.5 g / dL for 3 consecutive visits (with a minimum duration of 28 days) and beginning by Week 16 was achieved by 3 additional participants in the 30 mg / kg IV q4w group and 5 additional participants in the 15 mg / kg IV q2w group. In contrast, 1 additional participant in the placebo group met these response criteria: 34.2% (13 / 38) in the 15 mg / kg IV q2w group (nominal 1-sided p-value=0.005); 31.6% (12 / 38) in the 30 mg / kg IV q4w group (nominal 1-sided p-value=0.007); 10.3% (4 / 39) in the placebo group

[0650] With this more clinically relevant threshold, a numerically higher proportion of participants in the 15 mg / kg IV q2w and 30 mg / kg IV q4w groups showed a durable Hgb response compared with placebo. These findings further support the robustness of the observed treatment effect of nipocalimab in this patient population.

[0651] Median (range) time to durable Hgb response was defined as the first time a participant achieved a Hgb level of >10 g / dL and an increase of >2 g / dL from baseline, which was then maintained for at least 3 consecutive visits. Participants treated with nipocalimab showed a faster time to durable Hgb response in both the 15 mg / kg IV q2w and 30 mg / kg IV q4w groups compared-133- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)with the placebo group: 4.21 weeks (2.0; 10.3) in the 15 mg / kg IV q2w group; 4.14 weeks (1.0; 12.3) in the 30 mg / kg IV q4w group; 12.14 weeks (3.7; 16.0) in the placebo group.

[0652] The mean time to durable Hgb response during the DB period was 4.95 weeks in the 15 mg / kg IV q2w group, 4.65 weeks in the 30 mg / kg IV q4w group, and 10.62 weeks in the placebo group. Graphical representation of time to durable Hgb response is shown in (FIG. 28). In addition, patients in the 30 mg / kg IV q4w group achieved a mean 1 g / dL increase in Hgb as early as Week 1 (v.s., -0.1 g / dL for patients in the placebo group).Hgb Over Time

[0653] An increase in Hgb levels from baseline is observed as early as Week 1 for both 15 mg / kg IV q2w and 30 mg / kg IV q4w groups (FIG. 29).

[0654] Participants receiving nipocalimab demonstrated a greater increase in Hgb from baseline compared with those in the placebo group during the DB period. Separation between the nipocalimab groups and placebo was evident from Week 1 and generally maintained through Week 24, with both nipocalimab dose groups showing higher mean Hgb levels across visits. Hgb levels in the placebo group remained near baseline throughout the study. A modest attenuation in mean Hgb levels was observed after approximately Week 16 in the nipocalimab groups. Interpretation after Week 16 is limited by the study design. As per protocol, participants were eligible to enter the OLE after Week 16 of the DB period if their Hgb improvement from baseline was less than 1 g / dL. This pattern is attributable, in part, to the application of the composite strategy, under which data collected after intercurrent events (e.g., change baseline treatment or treatment discontinuation) were set to zero, thereby attenuating mean values at later time points. Despite this attenuation, mean Hgb levels in the nipocalimab groups remained numerically higher than those in the placebo group through Week 24.

[0655] A steady increase in hemoglobin was observed in the 15 mg / kg IV q2w group. Hgb levels in the 30 mg / kg IV q4w group increased rapidly but displayed oscillations that aligned with dosing intervals over time (FIG. 29) and were consistent with the period of nipocalimab pharmacologic activity reflected in the pharmacodynamic profile.

[0656] At Week 24, participants in the 15 mg / kg IV q2w group showed a greater mean change from baseline in Hgb values compared with participants in the placebo group, and participants in -134- 103693.004420\4914-0795-9446.2DOCKET NO.: 103693.004420 (MPI6028WOPCT1)the 30 mg / kg IV q4w group showed modest change from baseline in Hgb values compared with participants in the placebo group, noting that Hgb values in the 30 mg / kg IV q4w group at Week 24 reflect the trough timepoint in the dosing cycle and may not fully characterize post-dose Hgb improvement for this regimen.Duration of Hgb Response: DB Period

[0657] Mean duration from the first timepoint at which the durable Hgb re...

Claims

1. DOCKETNO.: 103693.004420 (MPI6028WOPCT1)CLAIMSWhat is claimed is:

1. A method of treating an autoimmune disease in a subject in need thereof, the method comprising subcutaneously administering nipocalimab to the subject at a dose(a) from about 1000 mg to about 2000 mg every two weeks; or(b) from about 400 mg to about 600 mg every week.

2. The method of claim 1, wherein nipocalimab is administered every two weeks subcutaneously at a dose from about 1200 mg to about 1800 mg via an on-body device.

3. The method of claim 1 or claim 2, wherein nipocalimab is administered every two weeks subcutaneously at a dose from about 1400 mg to about 1600 mg via an on-body device.

4. The method of any one of claims 1-3, wherein nipocalimab is administered every two weeks subcutaneously at a dose of about 1500 mg via an on-body device.

5. The method of claim 1, wherein nipocalimab is administered every week subcutaneously at a dose from about 400 mg to about 600 mg via an autoinjector.

6. The method of claim 5, wherein the subject receives a second subcutaneous administration of nipocalimab at a dose from about 400 mg to about 600 mg via an auto injector in the first week.

7. The method of claim 1 or claim 5, wherein nipocalimab is administered every week subcutaneously at a dose from about 450 mg to about 550 mg via an autoinjector.

8. The method of claim 7, wherein the subject receives a second subcutaneous administration of nipocalimab at a dose from about 450 mg to about 550 mg via an autoinjector in the first week.

9. The method of any one of claims 1, 5-8, wherein nipocalimab is administered every week subcutaneously at a dose of about 518 mg via an autoinjector.-175- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)10. The method of claim 9, wherein the subject receives a second subcutaneous administration of nipocalimab at a dose of about 518 mg via an autoinjector in the first week.

11. The method of claim 9, wherein the subject receives a second subcutaneous administration of nipocalimab at a dose of about 518 mg via an autoinjector in the first day.

12. The method of any one of claims 1, 5-8, wherein nipocalimab is administered every week subcutaneously at a dose of about 460 mg via an autoinjector.

13. The method of claim 12, wherein the subject receives a second subcutaneous administration of nipocalimab at a dose of about 460 mg via an autoinjector in the first week.

14. The method of claim 12, wherein the subject receives a second subcutaneous administration of nipocalimab at a dose of about 460 mg via an autoinjector in the first day.

15. The method of any one of claims 1-14, wherein the autoimmune disease is warm autoimmune hemolytic anemia (wAIHA), generalized myasthenia gravis (gMG), chronic inflammatory demyelinating polyneuropathy (CIDP), or idiopathic inflammatory myopathies (IIM).

16. The method of any one of claims 1-15, wherein the administration of nipocalimab reduces serum IgG in the subject by at least 60% from baseline serum IgG, at least 65% from baseline serum IgG, at least 70% from baseline serum IgG, at least 75% from baseline serum IgG, or at least 80% from baseline serum IgG.

17. The method of any one of claims 1-16, wherein the administration of nipocalimab increases total cholesterol in the subject by at most 18 mg / dL, at most 17 mg / dL, at most 16 mg / dL, at most 15 mg / dL, at most 14 mg / dL, at most 13 mg / dL, or at most 12 mg / dL from baseline total cholesterol.

18. The method of any one of claims 1-17, wherein the administration of nipocalimab increases HDL in the subject at most 8 mg / dL, at most 7 mg / dL, at most 6 mg / dL, at most 5 mg / dL, at most 4 mg / dL, at most 3 mg / dL, or at most 2 mg / dL from baseline HDL.-176- 103693.004420\4914-0795-9446.2DOCKET NO.: 103693.004420 (MPI6028WOPCT1)19. The method of any one of claims 1-18, wherein the administration of nipocalimab increases LDL in the subject at most 12 mg / dL, at most 11 mg / dL, at most 10 mg / dL, at most 9 mg / dL, at most 8 mg / dL, at most 7 mg / dL, at most 6 mg / dL, or at most 5 mg / dL from baseline LDL.

20. The method of any one of claims 1-19, wherein the administration of nipocalimab reduces serum albumin in the subject by at most 18%, at most 16%, at most 14%, at most 12%, at most 10%, at most 8%, at most 6%, at most 4%, or at most 2% from baseline serum albumin.

21. A method of reducing serum IgG in a subject in need thereof, the method comprising administering nipocalimab to the subject at a dose(a) from about 1000 mg to about 2000 mg every two weeks; or(b) from about 400 mg to about 600 mg every week;wherein the administration of nipocalimab reduces serum IgG in the subject by at least 60% from baseline serum IgG, at least 65% from baseline serum IgG, at least 70% from baseline serum IgG, at least 75% from baseline serum IgG, or at least 80% from baseline serum IgG.

22. The method of claim 21, wherein nipocalimab is administered every two weeks subcutaneously at a dose from about 1200 mg to about 1800 mg via an on-body device.

23. The method of claim 21 or claim 22, wherein nipocalimab is administered every two weeks subcutaneously at a dose from about 1400 mg to about 1600 mg via an on-body device.

24. The method of any one of claims 21-23, wherein nipocalimab is administered every two weeks subcutaneously at a dose of about 1500 mg via an on-body device.

25. The method of claim 21, wherein nipocalimab is administered every week subcutaneously at a dose from about 400 mg to about 600 mg via an autoinjector.

26. The method of claim 25, wherein the subject receives a second subcutaneous administration of nipocalimab at a dose from about 400 mg to about 600 mg via an auto injector in the first week.

27. The method of claim 21 or claim 25, wherein nipocalimab is administered every week subcutaneously at a dose from about 450 mg to about 550 mg via an autoinjector.-177- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)28. The method of claim 27, wherein the subject receives a second subcutaneous administration of nipocalimab at a dose from about 450 mg to about 550 mg via an autoinjector in the first week.

29. The method of any one of claims 21, 25, or 27, wherein nipocalimab is administered every week subcutaneously at a dose of about 518 mg via an autoinjector.

30. The method of claim 29, wherein the subject receives a second subcutaneous administration of nipocalimab at a dose of about 518 mg via an autoinjector in the first week.

31. The method of claim 29, wherein the subject receives a second subcutaneous administration of nipocalimab at a dose of about 518 mg via an autoinjector in the first day.

32. The method of any one of claims 21, 25, or 27, wherein nipocalimab is administered every week subcutaneously at a dose of about 460 mg via an autoinjector.

33. The method of claim 32, wherein the subject receives a second subcutaneous administration of nipocalimab at a dose of about 460 mg via an autoinjector in the first week.

34. The method of claim 32, wherein the subject receives a second subcutaneous administration of nipocalimab at a dose of about 460 mg via an autoinjector in the first day.

35. The method of any one of claims 21-34, wherein the subject has warm autoimmune hemolytic anemia (wAIHA), generalized myasthenia gravis (gMG), chronic inflammatory demyelinating polyneuropathy (CIDP), or idiopathic inflammatory myopathies (IIM).

36. The method of any one of claims 21-35, wherein the administration of nipocalimab increases total cholesterol in the subject by at most 18 mg / dL, at most 17 mg / dL, at most 16 mg / dL, at most 15 mg / dL, at most 14 mg / dL, at most 13 mg / dL, or at most 12 mg / dL from baseline total cholesterol.

37. The method of any one of claims 21-36, wherein the administration of nipocalimab increases HDL in the subject at most 8 mg / dL, at most 7 mg / dL, at most 6 mg / dL, at most 5 mg / dL, at most 4 mg / dL, at most 3 mg / dL, or at most 2 mg / dL from baseline total HDL.-178- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)38. The method of any one of claims 21-37, wherein the administration of nipocalimab increases LDL in the subject at most 12 mg / dL, at most 11 mg / dL, at most 10 mg / dL, at most 9 mg / dL, at most 8 mg / dL, at most 7 mg / dL, at most 6 mg / dL, or at most 5 mg / dL from baseline LDL.

39. The method of any one of claims 21-38, wherein the administration of nipocalimab reduces serum albumin in the subject by at most 18%, at most 16%, at most 14%, at most 12%, at most 10%, at most 8%, at most 6%, at most 4%, or at most 2% from baseline serum albumin.

40. A method of treating generalized myasthenia gravis (gMG) in a subject in need thereof, the method comprising subcutaneously administering nipocalimab to the subject at a dose(a) from about 1000 mg to about 2000 mg every two weeks; or(b) from about 400 mg to about 600 mg every week.

41. The method of claim 40, wherein nipocalimab is administered every two weeks subcutaneously at a dose from about 1200 mg to about 1800 mg via an on-body device.

42. The method of claim 40 or claim 41, wherein nipocalimab is administered every two weeks subcutaneously at a dose from about 1400 mg to about 1600 mg via an on-body device.

43. The method of any one of claims 40-42, wherein nipocalimab is administered every two weeks subcutaneously at a dose of about 1500 mg via an on-body device.

44. The method of claim 43, wherein nipocalimab is administered every week subcutaneously at a dose from about 400 mg to about 600 mg via an autoinjector.

45. The method of claim 44, wherein the subject receives a second subcutaneous administration of nipocalimab at a dose from about 400 mg to about 600 mg via an auto injector in the first week.

46. The method of claim 40 or claim 44, wherein nipocalimab is administered every week subcutaneously at a dose from about 450 mg to about 550 mg via an autoinjector.-179- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)47. The method of claim 46, wherein the subject receives a second subcutaneous administration of nipocalimab at a dose from about 450 mg to about 550 mg via an autoinjector in the first week.

48. The method of any one of claims 40, 44, or 46, wherein nipocalimab is administered every week subcutaneously at a dose of about 518 mg via an autoinjector.

49. The method of claim 48, wherein the subject receives a second subcutaneous administration of nipocalimab at a dose of about 518 mg via an autoinjector in the first week.

50. The method of claim 48, wherein the subject receives a second subcutaneous administration of nipocalimab at a dose of about 518 mg via an autoinjector in the first day.

51. The method of any one of claims 40, 44, or 46, wherein nipocalimab is administered every week subcutaneously at a dose of about 460 mg via an autoinjector.

52. The method of claim 51, wherein the subject receives a second subcutaneous administration of nipocalimab at a dose of about 460 mg via an autoinjector in the first week.

53. The method of claim 51, wherein the subject receives a second subcutaneous administration of nipocalimab at a dose of about 460 mg via an autoinjector in the first day.

54. The method of any one of claims 40-53, wherein the method provides a clinical benefit as measured by a decrease in MG-ADL score in the subject by more than 4.0, 4.1, 4.2, 4.3, 4.4, 4.5, 4.6, 4.7, 4.8, 4.9, 5.0, 5.1, 5.2, 5.3, 5.4, 5.6, 5.7, 5.8, 5.9 or 6.0 from baseline within 12, 14, 16, 18, 20, 22, 24, 26, 28, 30, 36, 42, 48 or 52 weeks of initiation of said administering.

55. The method of any one of claims 40-54, wherein the method provides a clinical benefit as measured by a decrease in QMG score in the subject by more than 4.0, 4.1, 4.2, 4.3, 4.4, 4.5, 4.6, 4.7, 4.8, 4.9, or 5.0 from baseline within 12, 14, 16, 18, 20, 22, 24, 26, 28, 30, 36, 42, 48 or 52 weeks of initiation of said administering.

56. The method of any one of claims 40-55, wherein the subject is positive for one or more of anti- AChR antibody, anti-MuSK antibody, and anti-LRP4 antibody.-180- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)57. The method of any one of claims 40-56, wherein the administration of nipocalimab increases total cholesterol in the subject by at most 18 mg / dL, at most 17 mg / dL, at most 16 mg / dL, at most 15 mg / dL, at most 14 mg / dL, at most 13 mg / dL, or at most 12 mg / dL from baseline total cholesterol.

58. The method of any one of claims 40-57, wherein the administration of nipocalimab increases HDL in the subject at most 8 mg / dL, at most 7 mg / dL, at most 6 mg / dL, at most 5 mg / dL, at most 4 mg / dL, at most 3 mg / dL, or at most 2 mg / dL from baseline HDL.

59. The method of any one of claims 40-58, wherein the administration of nipocalimab increases LDL in the subject at most 12 mg / dL, at most 11 mg / dL, at most 10 mg / dL, at most 9 mg / dL, at most 8 mg / dL, at most 7 mg / dL, at most 6 mg / dL, or at most 5 mg / dL from baseline LDL.

60. The method of any one of claims 40-59, wherein the administration of nipocalimab reduces serum albumin in the subject by at most 18%, at most 16%, at most 14%, at most 12%, at most 10%, at most 8%, at most 6%, at most 4%, or at most 2% from baseline serum albumin.

61. A method of treating warm autoimmune hemolytic anemia (wAIHA) in a subject in need thereof, the method comprising subcutaneously administering nipocalimab to the subject at a dose(a) from about 1000 mg to about 2000 mg every two weeks; or(b) from about 400 mg to about 600 mg every week.

62. The method of claim 61, wherein nipocalimab is administered every two weeks subcutaneously at a dose from about 1200 mg to about 1800 mg via an on-body device.

63. The method of claim 61 or claim 62, wherein nipocalimab is administered every two weeks subcutaneously at a dose from about 1400 mg to about 1600 mg via an on-body device.

64. The method of any one of claims 61-63, wherein nipocalimab is administered every two weeks subcutaneously at a dose of about 1500 mg via an on-body device.-181- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)65. The method of claim 61, wherein nipocalimab is administered every week subcutaneously at a dose from about 400 mg to about 600 mg via an autoinjector.

66. The method of claim 65, wherein the subject receives a second subcutaneous administration of nipocalimab at a dose from about 400 mg to about 600 mg via an auto injector in the first week.

67. The method of any one of claims 61 or 65, wherein nipocalimab is administered every week subcutaneously at a dose from about 450 mg to about 550 mg via an autoinjector.

68. The method of claim 67, wherein the subject receives a second subcutaneous administration of nipocalimab at a dose from about 450 mg to about 550 mg via an autoinjector in the first week.

69. The method of any one of claims 61, 65, or 67, wherein nipocalimab is administered every week subcutaneously at a dose of about 518 mg via an autoinjector.

70. The method of claim 69, wherein the subject receives a second subcutaneous administration of nipocalimab at a dose of about 518 mg via an autoinjector in the first week.

71. The method of claim 69, wherein the subject receives a second subcutaneous administration of nipocalimab at a dose of about 518 mg via an autoinjector in the first day.

72. The method of any one of claims 61-71, wherein the method provides a clinical benefit as measured by an increase in a hemoglobin (Hgb) level in the subject of more than 0.5, 1, 1.5, 2, 2.5, 3, 3.5, 4, 4.5, 5, 5.5, 6, 6.5, 7, 7.5, 8, 8.5, 9, 9.5, or 10 g / dL within 1, 2, 4, 6, 8, 10, 12, 14, 16, 18, 20, 22, 24, 30, 36, 42, 48 or 52 weeks of initiation of said administering relative to a baseline Hgb level in the subject prior to initiation of said administering.

73. The method of claim 72, wherein the method provides a clinical benefit as measured by an increase in the hemoglobin (Hgb) level in the subject of 1.5 g / dL or more relative to the baseline within 4 weeks of initiation of said administering.-182- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)74. The method of claim 72, wherein the method provides a clinical benefit as measured by an increase in the hemoglobin (Hgb) level in the subject of 2 g / dL or more relative to the baseline within 4 weeks of initiation of said administering.

75. The method of any one of claims 61-74, wherein the method provides a clinical benefit as measured by achievement of a hemoglobin (Hgb) level in the subject of 10 g / dL or more within 1, 2, 3, or 4 weeks of initiation of said administering.

76. The method of any one of claims 61-75, wherein the method provides a clinical benefit within 16 weeks of initiation of said administering as measured by:• achievement of a hemoglobin (Hgb) level in the subject of 10 g / dL or more; and• an increase in a hemoglobin (Hgb) level in the subject of 1.5 g / dL or more relative to a baseline level of Hgb in the subject prior to initiation of said administering.

77. The method of any one of claims 61-75, wherein the method provides a clinical benefit within 16 weeks of initiation of said administering as measured by:• achievement of a hemoglobin (Hgb) level in the subject of 10 g / dL or more; and• an increase in a hemoglobin (Hgb) level in the subject of 2 g / dL or more relative to a baseline level of Hgb in the subject prior to initiation of said administering.

78. The method of any one of claims 72-77, wherein the clinical benefit is sustained for at least 28 days.

79. The method of any one of claims 72-77, wherein the clinical benefit is sustained for at least 6, 8, or 12 weeks.

80. The method of any one of claims 72-77, wherein the clinical benefit is sustained for at least 16 weeks.

81. The method of any one of claims 72-77, wherein the clinical benefit is sustained for at least 24 weeks.-183- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)82. The method of any one of claims 72-77, wherein the clinical benefit is sustained for at least 52 weeks.

83. The method of any one of claims 72-77, wherein the method provides a clinical benefit as measured by:• achievement of a hemoglobin (Hgb) level in the subject of 10 g / dL or more; and• an increase in a hemoglobin (Hgb) level in the subject by 2 g / dL or more relative to a baseline level of Hgb in the subject prior to initiation of said administering, wherein the clinical benefit is sustained for at least 28 days, wherein the clinical benefit is achieved within 16 weeks of initiation of said administering, and wherein the subject did not receive a rescue therapy.

84. The method of claim 83, wherein the rescue therapy comprises increased corticosteroids, blood transfusion, or intravenous immunoglobulin (IVIg) administration.

85. The method of any one of claims 61-84, wherein the method provides a clinical benefit as measured by an increase in a Functional Assessment of Chronic Illness Therapy -Fatigue (FACIT-Fatigue) score in the subject by more than 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31, or 32 relative to a baseline FACIT- Fatigue score in the subject prior to initiation of said administering within 2, 4, 6, 8, 10, 12, 14, 16, 18, 20, 22, 24, 30, 36, 42, 48 or 52 weeks of initiation of said administering.

86. The method of any one of claims 61-85, wherein the method provides a clinical benefit as measured by an increase in a Functional Assessment of Chronic Illness Therapy -Fatigue (FACIT-Fatigue) score in the subject by 2.95 or more relative to a baseline FACIT-Fatigue score in the subject prior to initiation of said administering within 24 weeks of initiation of said administering.

87. The method of any one of claims 61-86, wherein the method provides a clinical benefit as measured by an increase in a Functional Assessment of Chronic Illness Therapy -Fatigue (FACIT-Fatigue) score in the subject by 3.4 or more relative to a baseline FACIT-Fatigue score in the subject prior to initiation of said administering within 24 weeks of initiation of said administering.-184- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)88. The method of any one of claims 61-87, wherein the subject receives corticosteroid at a first dose before initiation of said administering, and the method provides a clinical benefit as indicated by the subject receives corticosteroid at a second dose that is at least 10%, 15%, 20%, 25%, 30%, 35%, 40%, 45%, 50%, 55%, 60%, 65%, or 70% lower than the first dose within 24, 30, 36, 42, 48 or 52 weeks or more weeks of initiation of said administering.

89. The method of any one of claims 61-88, wherein the subject receives corticosteroid at a first dose before initiation of said administering, and the method provides a clinical benefit as indicated by the subject receives corticosteroid at a second dose that is at least 20% lower than the first dose within 24 weeks or more weeks of initiation of said administering.

90. The method of any one of claims 61-89, wherein the subject receives corticosteroid at a first dose before initiation of said administering, and the method provides a clinical benefit as indicated by the subject receives corticosteroid at a second dose that is at least 60% lower than the first dose within 48 weeks or more weeks of initiation of said administering.

91. The method of claim 90, wherein the corticosteroid is prednisone.

92. The method of any one of claims 61-91, wherein the method provides a clinical benefit as measured by:• achievement of a hemoglobin (Hgb) level in the subject of 10 g / dL or more;• an increase in a hemoglobin (Hgb) level in the subject by 2 g / dL or more relative to a baseline level of Hgb in the subject prior to initiation of said administering, wherein the clinical benefit is sustained for at least 28 days, wherein the clinical benefit is achieved within 16 weeks of initiation of said administering, and wherein the subject did not receive a rescue therapy;and wherein the method provides a further clinical benefit as measured by:• an increase in a Functional Assessment of Chronic Illness Therapy-Fatigue (FACIT- Fatigue) score in the subject by more than 3 within 24 weeks of initiation of said administering relative to a baseline FACIT-Fatigue score in the subject prior to initiation of said administering; and-185- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)• the subject receives corticosteroid at a second dose that is at least 20% lower than the first dose within 24 weeks or more weeks of initiation of said administering, wherein the subject receives corticosteroid at a first dose before initiation of said administering.

93. The method of claim 92, wherein the rescue therapy comprises corticosteroids, blood transfusion, or intravenous immunoglobulin (IVIg).

94. The method of any one of claims 61-93, wherein the method provides a clinical benefit as measured by a reduction in total IgG in the subject by more than 20%, 30%, 40%, 50%, 60%, 70%, 80%, or 90% relative to a baseline level of total IgG in the subject prior to initiation of said administering within 8, 10, 12, 14, 16, 18, 20, 22, 24, 30, 36, 42, 48 or 52 weeks of initiation of said administering.

95. The method of any one of claims 61-94, wherein the administration of nipocalimab increases total cholesterol in the subject by at most 14%, relative to a baseline level of total cholesterol in the subject prior to initiation of said administering.

96. The method of any one of claims 61-95, wherein the administration of nipocalimab increases LDL in the subject at most 5% relative to a baseline level of LDL in the subject prior to initiation of said administering.

97. The method of any one of claims 61-96, wherein the administration of nipocalimab reduces serum albumin in the subject by at most 10 g / L relative to a baseline serum albumin in the subject prior to initiation of said administering.

98. The method of any one of claims 61-97, wherein the subject is 12 years or older.

99. The method of any one of claims 61-98, wherein the subject is 18 years or older.

100. The method of any one of claims 61-99, wherein the subject is from 12 to 18 years old.-186- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)101. The method of any one of claims 61-100, wherein the method provides a clinical benefit as measured by a reduction in wAIHA-related pathogenic autoantibodies in the subject by more than 15%, 20%, 30%, or 40% relative to a baseline level of wAIHA-related pathogenic autoantibodies in the subject prior to initiation of said administering and within 1, 2, 4, 6, 8, 10, 12, 14, 16, 18, 20, 22, 24, 30, 36, 42, 48, or 52 weeks of initiation of said administering.

102. The method of any one of claims 61-101, wherein the subject receives a plurality of 30 mg / kg intravenous doses of nipocalimab based on the weight of the subject, wherein the first dose is administered to the subject over at least 30 minutes, and wherein the subsequent doses are administered over at least 15 minutes.

103. A method of treating chronic inflammatory demyelinating polyneuropathy (CIDP) in a subject in need thereof, the method comprising subcutaneously administering nipocalimab to the subject at a dose(a) from about 1000 mg to about 2000 mg every two weeks; or(b) from about 400 mg to about 600 mg every week.

104. The method of claim 103, wherein nipocalimab is administered every two weeks subcutaneously at a dose from about 1200 mg to about 1800 mg via an on-body device.

105. The method of claim 103 or claim 104, wherein nipocalimab is administered every two weeks subcutaneously at a dose from about 1400 mg to about 1600 mg via an on-body device.

106. The method of any one of claims 103-105, wherein nipocalimab is administered every two weeks subcutaneously at a dose of about 1500 mg via an on-body device.

107. The method of claim 103, wherein nipocalimab is administered every week subcutaneously at a dose from about 400 mg to about 600 mg via an auto injector.

108. The method of claim 107, wherein the subject receives a second subcutaneous administration of nipocalimab at a dose from about 400 mg to about 600 mg via an auto injector in the first week.-187- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)109. The method of claim 103 or claim 107, wherein nipocalimab is administered every week subcutaneously at a dose from about 450 mg to about 550 mg via an autoinjector.

110. The method of claim 109, wherein the subject receives a second subcutaneous administration of nipocalimab at a dose from about 450 mg to about 550 mg via an autoinjector in the first week.

111. The method of any one of claims 103, 107, or 109, wherein nipocalimab is administered every week subcutaneously at a dose of about 518 mg via an auto injector.

112. The method of claim 111, wherein the subject receives a second subcutaneous administration of nipocalimab at a dose of about 518 mg via an autoinjector in the first week.

113. The method of claim 111, wherein the subject receives a second subcutaneous administration of nipocalimab at a dose of about 518 mg via an autoinjector in the first day.

114. The method of any one of claims 103-113, wherein the method provides a clinical benefit as measured by a reduction of at least 1 in adjusted Inflammatory Neuropathy Cause and Treatment (INCAT) score in the subject within 10 weeks of initiation of said administering, compared to an initial INCAT score determined at baseline.

115. The method of claim 114, wherein the subject maintains or has a further reduction in the adjusted INCAT score from week 10 to week 12, week 16, week 20, week 24, week 28, week 32, week 36, week 40, week 42, week 44, week 48, or week 52 from initiation of said administering.

116. The method of any one of claims 103-115, wherein the method provides a clinical benefit as measured by an increase of at least 8kPa, lOkPa, 12kPa, or 14kPa in grip strength for the dominant hand of the subject by week 10 from initiation of said administering, compared to an initial grip strength determined at baseline.

117. The method of claim 116, wherein the subject maintains or has a further increase in the grip strength for the dominant hand of the subject from week 10 to week 12, week 16, week 20, -188- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)week 24, week 28, week 32, week 36, week 40, week 42, week 44, week 48, or week 52 from initiation of said administering.

118. The method of any one of claims 103-117, wherein the method provides a clinical benefit as measured by an increase of at least 8kPa, lOkPa, 12kPa, or 14kPa in grip strength for the nondominant hand of the subject by week 10 from initiation of said administering, compared to an initial grip strength determined at baseline.

119. The method of claim 118, wherein the subject maintains or has a further increase in the grip strength for the non-dominant hand of the subject from week 10 to week 12, week 16, week 20, week 24, week 28, week 32, week 36, week 40, week 42, week 44, week 48, or week 52 from initiation of said administering.

120. The method of any one of claims 103-119, wherein the method provides a clinical benefit as measured by an increase in Inflammatory Rasch-built Overall Disability Scale (I-RODS) centile score in the subject by at least 4, 5, 6, 7, or 8 points by week 12, 16, 20, 24, 28, 32, 36, 40, 42, 44, 48, or 52 from initiation of said administering, compared to an initial I-RODS score determined at baseline.

121. The method of any one of claims 103-120, wherein the method provides a clinical benefit as measured by an increase in MRC Muscle Grading Sale Sum score in the subject by at least 4, 5, 6, 7, or 8 by week 12, 16, 20, 24, 28, 32, 36, 40, 42, 44, 48, or 52 from initiation of said administering, compared to an initial MRC Muscle Grading Sale Sum score determined at baseline.

122. The method of any one of claims 103-121, wherein the administration of nipocalimab increases total cholesterol in the subject by at most 18 mg / dL, at most 17 mg / dL, at most 16 mg / dL, at most 15 mg / dL, at most 14 mg / dL, at most 13 mg / dL, or at most 12 mg / dL from baseline total cholesterol.-189- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)123. The method of any one of claims 103-122, wherein the administration of nipocalimab increases HDL in the subject at most 8 mg / dL, at most 7 mg / dL, at most 6 mg / dL, at most 5 mg / dL, at most 4 mg / dL, at most 3 mg / dL, or at most 2 mg / dL from baseline HDL.

124. The method of any one of claims 103-123, wherein the administration of nipocalimab increases LDL in the subject at most 12 mg / dL, at most 11 mg / dL, at most 10 mg / dL, at most 9 mg / dL, at most 8 mg / dL, at most 7 mg / dL, at most 6 mg / dL, or at most 5 mg / dL from baseline LDL.

125. The method of any one of claims 103-124, wherein the administration of nipocalimab reduces serum albumin in the subject by at most 18%, at most 16%, at most 14%, at most 12%, at most 10%, at most 8%, at most 6%, at most 4%, or at most 2% from baseline serum albumin.

126. A method of treating idiopathic inflammatory myopathies (IIM) in a subject in need thereof, the method comprising subcutaneously administering nipocalimab to the subject at a dose (a) from about 1000 mg to about 2000 mg every two weeks; or(b) from about 400 mg to about 600 mg every week.

127. The method of claim 126, wherein nipocalimab is administered every two weeks subcutaneously at a dose from about 1200 mg to about 1800 mg via an on-body device.

128. The method of claim 126 or claim 127, wherein nipocalimab is administered every two weeks subcutaneously at a dose from about 1400 mg to about 1600 mg via an on-body device.

129. The method of any one of claims 126-128, wherein nipocalimab is administered every two weeks subcutaneously at a dose of about 1500 mg via an on-body device.

130. The method of claim 126, wherein nipocalimab is administered every week subcutaneously at a dose from about 400 mg to about 600 mg via an auto injector.

131. The method of claim 130, wherein the subject receives a second subcutaneous administration of nipocalimab at a dose from about 400 mg to about 600 mg via an auto injector in the first week.-190- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)132. The method of claim 126 or claim 130, wherein nipocalimab is administered every week subcutaneously at a dose from about 450 mg to about 550 mg via an autoinjector.

133. The method of claim 132, wherein the subject receives a second subcutaneous administration of nipocalimab at a dose from about 450 mg to about 550 mg via an autoinjector in the first week.

134. The method of any one of claims 126, 130, or 132, wherein nipocalimab is administered every week subcutaneously at a dose from about 518 mg via an autoinjector.

135. The method of claim 134, wherein the subject receives a second subcutaneous administration of nipocalimab at a dose of about 518 mg via an autoinjector in the first week.

136. The method of claim 134, wherein the subject receives a second subcutaneous administration of nipocalimab at a dose of about 518 mg via an autoinjector in the first day.

137. The method of any one of claims 126, 130, or 132, wherein nipocalimab is administered every week subcutaneously at a dose of about 460 mg via an auto injector.

138. The method of claim 137, wherein the subject receives a second subcutaneous administration of nipocalimab at a dose of about 460 mg via an autoinjector in the first week.

139. The method of claim 137, wherein the subject receives a second subcutaneous administration of nipocalimab at a dose of about 460 mg via an autoinjector in the first day.

140. The method of any one of claims 126-139, wherein the method provides a clinical benefit as measured by an increase in International Myositis Assessment and Clinical Studies Total Improvement Score (IMACS TIS) in the subject by at least 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31, 32, 33, 34, 35, 36, 37, 38, 39, 40, 41, 42, 43, 44, 45, 46, 47, 48, 49, 50, 51, 52, 53, 54, 55, 56, 57, 58, 59, 60, 61, 62, 63, 64, 65, 66, 67, 68, 69, 70, 71, 72, 73, 74, 75, 76, 77, 78, 79, 80, 81, 82, 83, 84, 85, 86, 87, 88, 89, 90, 91, 92, 93, 94, or 95 from baseline within 12, 16, 20, 24, 30, 36, 42, 48 or 52 weeks of initiation of said administering.-191- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)141. The method of any one of claims 126-140, wherein the method provides a clinical benefit as measured by an increase in Manual Muscle Testing (MMT-8) score in the subject by more than 5, 10, 15, 20, 25, 30, 35, 40, 45, 50, 55, 60, 65, 70, 75, 80, 85, 90, 95, 100, 105, 110, 115, 120, 125, 130, 135, 140, or 145 from baseline within 12, 16, 20, 24, 30, 36, 42, 48 or 52 weeks of initiation of said administering.

142. The method of any one of claims 126-141, wherein the method provides a clinical benefit as measured by a decrease in Extramuscular Global Assessment (MDAAT) score in the subject by more than 1, 1.5, 2, 3, or 4 from baseline within 10, 12, 16, 20, 24, 30, 36, 42, 48 or 52 weeks of initiation of said administering.

143. The method of any one of claims 126-142, wherein the method provides a clinical benefit as measured by a decrease in Physician Global Assessment (PhGA) score in the subject by more than 1, 2, 3, 4, 5, 6, 7, 8, 9 or 10 from baseline within 6, 8, 12, 16, 20, 24, 30, 36, 42, 48 or 52 weeks of initiation of said administering.

144. The method of any one of claims 126-143, wherein the method provides a clinical benefit as measured by a decrease in Cutaneous Dermatomyositis Activity-Investigator Global Assessment (CDA-IGA) score in the subject by more than 1, 2, 3, or 4 from baseline within 12, 16, 20, 24, 30, 36, 42, 48 or 52 weeks of initiation of said administering.

145. The method of any one of claims 126-144, wherein the subject receives glucocorticoid at a first dose before initiation of said administering, and the method provides a clinical benefit as indicated by the subject receiving glucocorticoid at a second dose that is lower than the first dose within 8, 10, 12, 14, 16, 18, 20, 22, 24, 26, 28, 30, 32, 34, 36, 38, 40, 42, 44, 46, 48, 50 or 52 weeks or more weeks of initiation of said administering.

146. The method of claim 145, wherein the first dose is higher than 7.5 mg, 10 mg, 12.5 mg, 15 mg, or 17.5 mg per day.

147. The method of claim 145, wherein the first dose is higher than 5 mg per day.-192- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)148. The method of any one of claims 126-147, wherein the administration of nipocalimab increases total cholesterol in the subject by at most 18 mg / dL, at most 17 mg / dL, at most 16 mg / dL, at most 15 mg / dL, at most 14 mg / dL, at most 13 mg / dL, or at most 12 mg / dL from baseline total cholesterol.

149. The method of any one of claims 126-148, wherein the administration of nipocalimab increases HDL in the subject at most 8 mg / dL, at most 7 mg / dL, at most 6 mg / dL, at most 5 mg / dL, at most 4 mg / dL, at most 3 mg / dL, or at most 2 mg / dL from baseline HDL.

150. The method of any one of claims 126-149, wherein the administration of nipocalimab increases LDL in the subject at most 12 mg / dL, at most 11 mg / dL, at most 10 mg / dL, at most 9 mg / dL, at most 8 mg / dL, at most 7 mg / dL, at most 6 mg / dL, or at most 5 mg / dL from baseline LDL.

151. The method of any one of claims 126-150, wherein the administration of nipocalimab reduces serum albumin in the subject by at most 18%, at most 16%, at most 14%, at most 12%, at most 10%, at most 8%, at most 6%, at most 4%, or at most 2% from baseline serum albumin.

152. A pharmaceutical product, comprising:a therapeutic agent, comprising:a bi-weekly dose from about 1000 mg to about 2000 mg of nipocalimab; ora weekly dose from about 400 mg to about 600 mg of nipocalimab; anda subcutaneous injection device, comprising:a container configured to contain the therapeutic agent;a discharge nozzle sized to deliver the therapeutic agent to a subject subcutaneously; and a driver configured to drive the therapeutic agent from the container and out of the discharge nozzle.

153. The pharmaceutical product of claim 152, wherein the therapeutic agent comprises the biweekly dose and the therapeutic agent has a volume from 13mL to 17mL.-193- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)154. The pharmaceutical product of claim 153, wherein the injection device is configured to deliver about 15mL + 0.5mL of the therapeutic agent to the subject.

155. The pharmaceutical product of any one of claims 152 and 153, wherein the subcutaneous injection device is an on-body delivery device.

156. The pharmaceutical product of claim 155, wherein the driver has a drive force that drives the therapeutic agent out of the discharge nozzle and into the subject at a rate from 0.5mL / minute to 2.0mL / minute.

157. The pharmaceutical product of any one of claims 152-156, wherein the bi-weekly dose is from about 1200 mg to about 1800 mg.

158. The pharmaceutical product of any one of claims 152-156, wherein the bi-weekly dose is from about 1400 mg to about 1600 mg.

159. The pharmaceutical product of any one of claims 152-156, wherein the bi-weekly dose is about 1500 mg.

160. The pharmaceutical product of claim 152, wherein the therapeutic agent comprises the weekly dose and the therapeutic agent has a volume from about 2mL to 4mL.

161. The pharmaceutical product of claim 160, wherein the injection device is configured to deliver 2.8mL + 0.5mL of the therapeutic agent to the subject.

162. The pharmaceutical product of any one of claims 160 and 161, wherein the subcutaneous injection device is an autoinjector.

163. The pharmaceutical product of claim 162, wherein the driver has a drive force that drives the therapeutic agent out of the discharge nozzle and into air at a rate from 0.08mL / second to 0.4mL / second.-194- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)164. The pharmaceutical product of any one of claims 160-163, wherein the weekly dose is from about 450 mg to about 550 mg.

165. The pharmaceutical product of any one of claims 160-163, wherein the weekly dose is about 518 mg via an autoinjector.

166. The pharmaceutical product of any one of claims 160-163, wherein the weekly dose is about 460 mg via an autoinjector.

167. The pharmaceutical product of any one of claims 152-166, wherein the subcutaneous injection device comprises a skin-contacting surface that contacts skin of the subject during an injection, and the discharge nozzle is a needle that (i) extends beyond the skin- contacting by about 6.5mm + 1mm when the drug is delivered to the subject, and / or (ii) has a needle gage from 23Gto 27G, or both (i) and (ii).

168. The pharmaceutical product of any one of claims 152-167, wherein:the container is a cartridge having a septum;the subcutaneous injection device pierces the septum to fluidly couple the cartridge to the discharge nozzle; andthe subcutaneous injection device delivers the therapeutic agent out of the discharge nozzle such that no particulate matter generated during piercing of the septum is discharged from the discharge nozzle that has a particle diameter >150 pm.

169. The pharmaceutical product of any one of claims 152-161, wherein the therapeutic agent, when delivered to the subject, reduces serum IgG in the subject by at least 60% from baseline serum IgG, at least 65% from baseline serum IgG, at least 70% from baseline serum IgG, at least 75% from baseline serum IgG, or at least 80% from baseline serum IgG.

170. The pharmaceutical product of any one of claims 152-169, wherein the therapeutic agent, when delivered to the subject, increases total cholesterol in the subject by at most 18 mg / dL, at most 17 mg / dL, at most 16 mg / dL, at most 15 mg / dL, at most 14 mg / dL, at most 13 mg / dL, or at most 12 mg / dL from baseline total cholesterol.-195- 103693.004420\4914-0795-9446.2DOCKETNO.: 103693.004420 (MPI6028WOPCT1)171. The pharmaceutical product of any one of claims 152-170, wherein the therapeutic agent, when delivered to the subject, increases HDL in the subject at most 8 mg / dL, at most 7 mg / dL, at most 6 mg / dL, at most 5 mg / dL, at most 4 mg / dL, at most 3 mg / dL, or at most 2 mg / dL from baseline HDL.

172. The pharmaceutical product of any one of claims 152-171, wherein the therapeutic agent, when delivered to the subject, increases LDL in the subject at most 12 mg / dL, at most 11 mg / dL, at most 10 mg / dL, at most 9 mg / dL, at most 8 mg / dL, at most 7 mg / dL, at most 6 mg / dL, or at most 5 mg / dL from baseline LDL.

173. The pharmaceutical product of any one of claims 152-172, wherein the therapeutic agent, when delivered to the subject, reduces serum albumin in the subject by at most 18%, at most 16%, at most 14%, at most 12%, at most 10%, at most 8%, at most 6%, at most 4%, or at most 2% from baseline serum albumin.

174. The pharmaceutical product of claim 152, wherein the pharmaceutical product is disposed in the container.

175. The pharmaceutical product of claim 152, wherein the pharmaceutical product is a kit comprising a separate container that is separate from the subcutaneous injection device, and the separate container contains the therapeutic agent.

176. The pharmaceutical product of claim 152, wherein the pharmaceutical product is a kit comprising at least one other subcutaneous injection device, and the subcutaneous injection device and the at least one other subcutaneous injection device (i) are each sized to contain only a portion of the dose and (i) together contain an entirety of the dose.-196- 103693.004420\4914-0795-9446.2

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