Methods of improving Anti-fcrn therapies

Abstract

The present disclosure relates to methods of improving anti-FcRn therapies (eg., anti- FcRn antibody dosing regimens) for treating autoimmune diseases (e.g., Graves' disease (GD), thyroid eye disease (TED), Rheumatoid Arthritis (RA), Myasthenia Gravis (MG), Chronic Inflammatory Demyelinating Polyradiculoneuropathy (CIDP), etc.)

Description

METHODS OF IMPROVING ANTI-FCRN THERAPIESRELATED APPLICATIONS

[0001] This application claims priority under 35 U.S. C. § 119(e) to U.S. Provisional Application, U.S.S.N. 63 / 594,708, filed October 31, 2023, U.S. Provisional Application, U.S.S.N.63 / 603,009, filed November 27, 2023, the entire contents of each of which are herein incorporated by reference.REFERENCE TO AN ELECTRONIC SEQUENCE LISTING

[0002] The contents of the electronic sequence listing (I062870008WO00-SEQ-LJG.xml; Size: 22,486 bytes; and Date of Creation: October 29, 2024) are herein incorporated by reference in its entirety.FIELD

[0003] The present disclosure relates to methods of improving anti-FcRn therapies.BACKGROUND

[0004] The neonatal Fc receptor (FcRn) is a non-covalent heterodimer that typically resides in the endosomes of endothelial and epithelial cells. FcRn is a membrane bound receptor having three heavy chain alpha domains (al, a2, and a3) and a single soluble light chain 02- microglobulin (02m) domain. Structurally, it belongs to a family of major histocompatibility complex class 1 molecules that have 02m as a common light chain. The FcRn chain has a molecular weight of about 46 kDa and is composed of an ectodomain containing the al, a2, and a3 heavy chain domains and a 02m light chain domain and having a single sugar chain, a singlepass transmembrane, and a relatively short cytoplasmic tail.

[0005] Antibodies and other therapies targeting FcRn are being developed for the treatment of autoimmune diseases.SUMMARY

[0006] The neonatal Fc receptor (FcRn) regulates the half-life of IgG antibodies, via binding the Fc region, and albumin in the body. FcRn extends the half-life of IgG by shielding it fromlysosomal degradation upon Fc binding and immunoglobulin internalization. FcRn-Fc interactions are beneficial for facilitating long-term protection against pathogens or in response to vaccination, but in the context of antibody-mediated diseases, such as autoimmune diseases, FcRn function can exacerbate the disease state by extending the half-life of autoantibodies. Anti- FcRn therapy can therefore treat or ameliorate antibody-driven autoimmune diseases, such as Graves’ disease, thyroid eye disease (TED), rheumatoid arthritis (RA), myasthenia gravis (MG), immune thrombocytopenia, pemphigus vulgaris, chronic inflammatory demyelinating polyneuropathy (CIDP), systemic lupus erythematosus (SLE), and others. However, due to the chronic and cyclical (e.g., having periods of remission and periods of flare-up) nature of many autoimmune conditions, as well as the pharmacokinetics of different anti-FcRn therapies, determining the appropriate amount, frequency, and length of dosing for adequate treatment is challenging.

[0007] In one aspect, provided herein is a method of treating an autoimmune disease in a subject in need thereof, the method comprising administering to the subject a loading dose, and induction dose and a maintenance dose of an anti-FcRn therapy. In some embodiments, the method comprises administering the induction dose for 12 weeks. In some embodiments, the method comprises administering the maintenance dose for 12 weeks. In some embodiments, the method comprises administering the maintenance dose for 12 months. In some embodiments, the method comprises administering the loading dose on day 4 of the first week of the induction dose. In some embodiments, the method comprises administering the loading dose on day 4 and day 11 during the first two weeks of administration of the induction dose.

[0008] In some embodiments, the induction dose comprises 680 mg of batoclimab administered subcutaneously once per week. In some embodiments, the maintenance dose comprises 340 mg of batoclimab administered subcutaneously once per week. In some embodiments, the maintenance dose comprises 340 mg of batoclimab administered subcutaneously once every other week. In some embodiments, the loading dose comprises a dose of 680 mg of batoclimab administered subcutaneously.

[0009] In some embodiments, the autoimmune disease is rheumatoid arthritis. In other embodiments, the autoimmune disease is Graves’ disease.

[0010] In some embodiments, the induction dose comprises 600 mg of IMVT-1402 administered subcutaneously once per week. In some embodiments, the maintenance dose comprises 300 mgof IMVT-1402 administered subcutaneously once per week. In some embodiments, the maintenance dose comprises 300 mg of IMVT-1402 administered subcutaneously once every other week. In some embodiments, the loading dose comprises a dose of 600 mg of IMVT-1402 administered subcutaneously.

[0011] In some embodiments, the autoimmune disease is a progressive autoimmune disease. In some embodiments, the autoimmune disease is CIDP. In some embodiments, the autoimmune disease is Myasthenia Gravis.

[0012] In some aspects, provided herein is a method of treating an autoimmune disease in a subject in need thereof, the method comprising administering to the subject (a) 680 mg of batoclimab on day 1; (b) 680 mg of batoclimab on day 4; (c) 680 mg of batoclimab on day 8; (d) 680 mg of batoclimab on day 11; and (e) 680 mg of batoclimab once weekly beginning on day 15, for a total treatment duration of 12 weeks.

[0013] In some embodiments, the method further comprises step (f): administering to the subject 340 mg of batoclimab once weekly beginning on day 85, for a total treatment duration of 24 weeks. In some embodiments, the method comprises step (g): administering the subject 680 mg of batoclimab once weekly beginning on day 168 for a total treatment duration of 36 weeks. In some embodiments, the method comprises administering the batoclimab subcutaneously.

[0014] In some embodiments, the method results in a reduction in the level of at least one autoantibody in the subject of at least 50% by 7 days post-initial dose compared to baseline. In some embodiments, the method results in a reduction in the level of at least one autoantibody in the subject of at least 75% by 7 days post- initial dose compared to baseline. In some embodiments, the methods result in a reduction in the level of at least one autoantibody in the subject of at least 85% by 7 days post-initial dose compared to baseline. In some embodiments, the autoantibody is an antibody against AChR, MuSK, LRP4, agrin, Kvl.4 potassium channel, rapsyn, cortactin, acetylcholinesterase, collagen Q, or collagen XIII.

[0015] In some embodiments, the method results in a reduction in the level of total IgG in the subject of at least 50% by 7 days post-initial dose compared to baseline. In some embodiments, the method results in a reduction in the level of total IgG in the subject of at least 75% by 7 days post-initial dose compared to baseline. In some embodiments, the method results in a reduction in the level of total IgG in the subject of at least 85% by 7 days post-initial dose compared to baseline. In some embodiments, the autoimmune disease is a progressive autoimmune disease. Insome embodiments, the autoimmune disease is CIDP. In some embodiments, the autoimmune disease is Myasthenia Gravis.

[0016] In some aspects, provided herein is a method of treating an autoimmune disease in a subject in need thereof, the method comprising administering to the subject: (a) 600 mg of IMVT-1402 on day 1; (b) 600 mg of IMVT-1402 on day 4; (c) 600 mg of IMVT-1402 on day 8; (d) 600 mg of IMVT-1402 on day 11; and 600 mg of IMVT-1402 once weekly beginning on day 15, for a total treatment duration of 12 weeks.

[0017] In some embodiments, the method further comprises step (f): administering to the subject 300 mg of IMVT-1402 once weekly beginning on day 85, for a total treatment duration of 24 weeks. In some embodiments, the method further comprises step (g): administering the subject 600 mg of IMVT-1402 once weekly beginning on day 169 for a total treatment duration of 36 weeks. In some embodiments, the method comprises administering the IMVT-1402 subcutaneously.

[0018] In some embodiments, the method results in a reduction in the level of at least one autoantibody in the subject of at least 50% by 7 days post-initial dose compared to baseline. In some embodiments, the method results in a reduction in the level of at least one autoantibody in the subject of at least 75% by 7 days post- initial dose compared to baseline. In some embodiments, the method results in a reduction in the level of at least one autoantibody in the subject of at least 85% by 7 days post-initial dose compared to baseline. In some embodiments, the autoantibody is an antibody against AChR, MuSK, LRP4, agrin, Kvl.4 potassium channel, rapsyn, cortactin, acetylcholinesterase, collagen Q, or collagen XIII.

[0019] In some embodiments, the method results in a reduction in the level of total IgG in the subject of at least 50% by 7 days post-initial dose compared to baseline. In some embodiments, the method results in a reduction in the level of total IgG in the subject of at least 75% by 7 days post-initial dose compared to baseline. In some embodiments, the method results in a reduction in the level of total IgG in the subject of at least 85% by 7 days post-initial dose compared to baseline.

[0020] In some embodiments, the autoimmune disease is a progressive autoimmune disease. In some embodiments, the autoimmune disease is CIDP. In some embodiments, the autoimmune disease is Myasthenia Gravis.

[0021] In another aspect, provided herein is a method of controlling a flare-up of an autoimmune disease in a subject being treated with an anti-FcRn therapy, the method comprising administering to the subject at least four doses of an anti-FcRn antibody.

[0022] In some embodiments, the method comprises administering the anti-FcRn antibody on days 1, 8, 15, and 22. In some embodiments, the method comprises administering the anti-FcRn antibody on days 1, 4, 8, 15, and 22. In some embodiments, the anti-FcRn antibody is batoclimab. In some embodiments, the batoclimab is administered subcutaneously. In some embodiments, the method comprises administering 680 mg of batoclimab. In some embodiments, the anti-FcRn antibody is IMVT-1402. In some embodiments, the IMVT-1402 is administered subcutaneously. In some embodiments, the method comprises administering 600 mg of IMVT-1402. In some embodiments, the autoimmune disease is a progressive autoimmune disease. In some embodiments, a subject has been administered intravenous immunoglobulin (IVIg). In some embodiments, a subject is further administered IVIg. In some embodiments, the autoimmune disease is being treated with PLEX. In some embodiments, the autoimmune disease is CIDP. In some embodiments, the autoimmune disease is Myasthenia Gravis.

[0023] In some aspects, the present disclosure provides a method for treating Graves’ Disease (GD) in a subject, the method comprising administering the subject an anti-FcRn antibody at 550-700 mg once weekly. In some embodiments, the present disclosure provides a method for treating Graves’ Disease (GD) in a subject, the method comprising administering the subject an anti-FcRn antibody at 200-300 mg (e.g., 300 mg IMVT-1402) once weekly. In some embodiments, the present disclosure provides a method for treating Graves’ Disease (GD) in a subject, the method comprising administering the subject an anti-FcRn antibody at 550-700 mg once weekly for 20-60 weeks.

[0024] In some aspects, the present disclosure provides a method for treating or preventing thyroid eye disease (TED) in a subject having Graves’ Disease (GD), the method comprising administering the subject an anti-FcRn antibody at 550-700 mg (e.g., 600 mg of IMVT-1402) once weekly.

[0025] In some aspects, the present disclosure provides a method for treating or preventing thyroid eye disease (TED) in a subject having Graves’ Disease (GD), the method comprising administering the subject an anti-FcRn antibody at 200-400 mg (e.g., 300 mg of IMVT-1402) once weekly. In some aspects, the present disclosure provides a method for treating or preventingthyroid eye disease (TED) in a subject having Graves’ Disease (GD), the method comprising administering the subject an anti-FcRn antibody at 200-400 mg or 550-700 mg once weekly In some aspects, the present disclosure provides a method for treating or preventing thyroid eye disease (TED) in a subject having Graves’ Disease (GD), the method comprising administering the subject an anti-FcRn antibody at 200-400 mg or 550-700 mg once weekly for 20-60 weeks or for 20-30 weeks. In some embodiments, the administration decreases TED symptoms in the subject relative to prior to the administration. In some embodiments, the administration decreases proptosis in the subject relative to prior to the administration. In some embodiments, the administration decreases lid aperture in the subject relative to prior to the administration. In some embodiments, the administration decreases thyroid volume in the subject relative to prior to the administration.

[0026] In some aspects, the present disclosure provides a method for inducing remission in a subject having Graves’ Disease (GD), the method comprising administering the subject an anti- FcRn antibody at 550-700 mg once weekly.

[0027] In some embodiments, the antibody is administered to the subject for a period of 20-60 weeks. In some embodiments, the antibody is administered to the subject for 52 weeks. In some embodiments, the antibody is administered to the subject for 26 weeks. In some embodiments, the subject is administered the antibody at a reduced dose after 26 weeks. In some embodiments, the subject is administered the reduced dose of the antibody at 300 mg once weekly. In some embodiments, the subject is administered the reduced dose of the antibody at 300 mg once weekly for 26 weeks.

[0028] In some embodiments, the subject is administered 600 mg of the anti-FcRn antibody once weekly for 20-60 weeks. In some embodiments, the subject is administered 600 mg of the anti- FcRn antibody once weekly for 52 weeks. In some embodiments, the subject is administered 600 mg of the anti-FcRn antibody once weekly for 26 weeks.

[0029] In some embodiments, the anti-FcRn antibody is IMVT-1402. In some embodiments, the antibody comprises a heavy chain variable region (VH) comprising a heavy chain complementarity determining region (HCDR) 1 comprising the amino acid sequence of SEQ ID NO: 7, a HCDR2 comprising the amino acid sequence of SEQ ID NO: 8, and a HCDR3 comprising the amino acid sequence of SEQ ID NO: 9, and a light chain variable region comprising a light chain complementarity determining region (LCDR) 1 comprising the aminoacid sequence of SEQ ID NO: 10, a LCDR2 comprising the amino acid sequence of SEQ ID NO: 11, and a LCDR3 comprising the amino acid sequence of SEQ ID NO: 12. In some embodiments, the antibody comprises a VH comprising the amino acid sequence of SEQ ID NO: 15, and a VL comprising the amino acid sequence of SEQ ID NO: 16. In some embodiments, the antibody comprises a heavy chain comprising the amino acid sequence of SEQ ID NO: 19, and a light chain comprising the amino acid sequence of SEQ ID NO: 20. In some embodiments, the antibody comprises a heavy chain comprising the amino acid sequence of SEQ ID NO: 21, and a light chain comprising the amino acid sequence of SEQ ID NO: 22.

[0030] In some embodiments, the subject has overt hyperthyroidism prior to the administration. In some embodiments, the subject has a baseline triiodothyronine (T3) level higher than upper limit of normal (ULN). In some embodiments, the subject has a baseline free thyroxine (FT4) level higher than ULN. In some embodiments, the subject has a baseline TSH level no more than the lower limit of normal (LLN).

[0031] In some embodiments, the subject has subclinical hyperthyroidism prior to the administration. In some embodiments, the subject has a T3 level within a clinically normal T3 level. In some embodiments, the subject has a FT4 level within a clinically normal FT4. In some embodiments, the subject has a thyroid-stimulating hormone (TSH) level less than 0.1 mU / L.

[0032] In some embodiments, the subject is receiving antithyroid drug (ATD) at the time of the administration. In some embodiments, the subject has previously received antithyroid drug (ATD) for at least 3 months prior to the administration. In some embodiments, the ATD is methimazole, carbimazole, propylthiouracil. In some embodiments, the subject is receiving an ATD dose of at least 20 mg / day methimazole prior to the administration. In some embodiments, the subject is receiving an ATD dose of at least 30 mg / day carbimazole prior to the administration. In some embodiments, the subject is receiving an ATD dose of at least 200 mg / day propylthiouracil prior to the administration.

[0033] In some embodiments, the subject is receiving the ATD for the four- weeks immediately preceding a baseline assessment. In some embodiments, the subject has been receiving antithyroid drug (ATD) for at least six months prior to a baseline assessment. In some embodiments, the ATD is methimazole, carbimazole, propylthiouracil. In some embodiments, the subject is receiving an ATD dose of at least 15 mg / day methimazole prior to the administration. In some embodiments, the subject is receiving an ATD dose of at least 20mg / day carbimazole prior to the administration. In some embodiments, the subject is receiving an ATD dose of at least 150 mg / day propylthiouracil prior to the administration.

[0034] In some embodiments, the subject is concurrently receiving an ATD. In some embodiments, the subject is on ATD at a dose of at least 10 mg / day methimazole. In some embodiments, the subject is on ATD at a dose of at least 15 mg / day carbimazole. In some embodiments, the subject is on ATD at a dose of at least 100 mg / day propylthiouracil.

[0035] In some embodiments, the subject does not have or previously had hyperthyroidism not caused by GD.

[0036] In some embodiments, the subject does not have toxic adenoma or toxic multinodular goiter.

[0037] In some embodiments, the subject does not have a history of thyroid storm within six months of the administration of the anti-FcRn antibody (e.g., IMVT-1402 or batoclimab).

[0038] In some embodiments, the subject does not have active autoimmune disease.

[0039] In some embodiments, the subject does not have TED. In some embodiments, the subject does not have moderate to severe active TED that require immediate surgical intervention, corrective surgery, irradiation and / or medical therapy.

[0040] In some embodiments, the subject does not have a history of noncompliance with ATD therapy.

[0041] In some embodiments, the anti-FcRn antibody is administered subcutaneously.

[0042] In some embodiments, the administration induces a state of euthyroidism in the subject at or before week 25 of administration.

[0043] In some embodiments, the administration of an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) reduces the level of T3 in the subject to be within normal range.

[0044] In some embodiments, administration of an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) reduces the level of FT4 in the subject to be within normal range. In some embodiments, the administration of an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) increases the level of TSH in the subject to be within normal range. In some embodiments, the subject stops receiving ATD at or before week 26 of administration of an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab).

[0045] In some embodiments, the administration induces euthyroidism in the subject at or before week 52 of administration. In some embodiments, the administration reduces the level of T3 inthe subject to be within normal range. In some embodiments, the administration reduces the level of FT4 in the subject to be within normal range. In some embodiments, the administration increases the level of TSH in the subject to be within normal range. In some embodiments, the subject stops receiving ATD at or before week 52 of administration.

[0046] In some embodiments, the administration prevents the development or improves one or more following eye symptoms in the subject: bulging eyes; gritty feeling in the eyes; pressure or pain in the eyes; retracted eyelids; red or inflamed eyes; light sensitivity; blurred or double vision, or vision loss.

[0047] In some embodiments, the administration induces remission in the subject (i.e., being in a state of euthyroid for at least 6 months or more following discontinuation of anti-FcRn and / or ATD therapies).

[0048] In some aspects, the present disclosure provides a method for treating Rheumatoid Arthritis (RA) in a subject, the method comprising administering the subject an anti-FcRn antibody at 550-700 mg once weekly.

[0049] In some embodiments, a subject having RA is administered 600 mg of the anti-FcRn antibody once weekly. In some embodiments, the subject is administered 300 mg of the anti- FcRn antibody once weekly. In some embodiments, a subject having RA is administered 600 mg of the anti-FcRn antibody once weekly for at least 16 weeks, and is subsequently administered (i) 600 mg of the anti-FcRn antibody once weekly; or (ii) 300 mg of the anti-FcRn antibody once weekly.

[0050] In some embodiments, the anti-FcRn antibody is administered subcutaneously to a subject having RA.

[0051] In some embodiments, the subject has active RA.

[0052] In some embodiments, the subject has refractory RA. In some embodiments, the subject has moderate disease activity. In some embodiments, the subject has a DAS28-ESR score of more than 3.2. In some embodiments, the subject has a CD Al score of more than 10. In some embodiments, the subject has one or more symptoms suggestive of active RA. In some embodiments, the subject cannot taper glucocorticoid treatment to be less than 7.5 mg / day. In some embodiments, the subject shows rapid radiographic progression of RA as indicated by change in van der Heijde-modified Sharp score 5= 5 points at 1 year.

[0053] In some embodiments, a subject having RA is positive for rheumatoid factor (RF). In some embodiments, a subject having RA is positive for IgG or IgA RF in RA synovial fluid. In some embodiments, a subject having RA has a RF level higher than 25 U / ml. In some embodiments, a subject having RA has a RF level higher than 100 U / ml.

[0054] In some embodiments, a subject having RA is positive for anti-citrullinated protein autoantibodies (ACPA).

[0055] In some embodiments, a subject having RA has at least 6 / 68 tender and / or painful joints (TJC) at baseline. In some embodiments, a subject having RA has at least 6 / 66 swollen joints (SJC) at baseline.

[0056] In some embodiments, a subject having RA has a baseline level of circulating C-reactive protein (CRP) of at least 1.5x ULN.

[0057] In some embodiments, a subject having RA has a baseline Disease Activity score 28 using C-reactive protein (DAS28-CRP) of more than 4.1.

[0058] In some embodiments, a subject having RA does not respond to 2-3 class of biologic (b) or targeted synthetic (ts) disease-modifying antirheumatic drug (b / tsDMARDs).

[0059] In some embodiments, a subject having RA has been treated with a biologic TNF-oc inhibitor (e.g., infliximab, certolizumab, golimumab, etanercept, adalimumab).

[0060] In some embodiments, a subject having RA a subject having RA has been treated with a JAK inhibitor.

[0061] In some embodiments, a subject having RA has been treated with a bDMARD other than a TNF-a inhibitor.

[0062] In some embodiments, a subject having RA responds to rituximab.

[0063]

[0064] In some embodiments, a subject having RA is not on glucocorticoids at doses > 10 mg per day.

[0065] In some embodiments, a subject having RA did not have 3 or more joints injections within 6 weeks of baseline assessment.

[0066] In some embodiments, a subject having RA did not receive systemic glucocorticoid administered by intramuscular or intravenous (IV) injection within six weeks of baseline assessment.

[0067] In some embodiments, the administration decreases the level of RF in the subject.

[0068] In some embodiments, the administration decreases ACAP in the subject.

[0069] In some embodiments, a subject having RA achieves ACR20 response at week 14, 16, or 32 of administration of the anti-FcRn antibody.

[0070] In some embodiments, a subject having RA has at least 20% improvement from baseline in TJC68. In some embodiments, a subject having RA has at least 20% improvement from baseline in SJC66.

[0071] In some embodiments, a subject having RA has at least 20% improvement from baseline in at least 3 of the following parameters: (i) Physician's Global Assessment of Disease Activity (PhGA); (ii) Patient's Global Assessment of Disease Activity (PtGA); (iii) Patient’s Assessment of Pain (100 mm VAS); (iv) Health Assessment Questionnaire - Disability Index (HAQ-DI); and (v) High-sensitivity C-reactive protein (hsCRP)

[0072] In some embodiments, a subject having RA achieves ACR20 response at week 14 or 16 of administration of the anti-FcRn antibody, and has change in CD Al score from week 16 to 32 of administration.

[0073] In some embodiments, a subject having RA achieves ACR20 response at week 14 or 16 of administration of the anti-FcRn antibody, and has a change in SDAI score from week 16 to 32 of administration.

[0074] In some embodiments, the anti-FcRn antibody is IMVT-1402. In some embodiments, the anti-FcRn antibody comprises a heavy chain variable region (VH) comprising a heavy chain complementarity determining region (HCDR) 1 comprising the amino acid sequence of SEQ ID NO: 7, a HCDR2 comprising the amino acid sequence of SEQ ID NO: 8, and a HCDR3 comprising the amino acid sequence of SEQ ID NO: 9, and a light chain variable region comprising a light chain complementarity determining region (LCDR) 1 comprising the amino acid sequence of SEQ ID NO: 10, a LCDR2 comprising the amino acid sequence of SEQ ID NO: 11, and a LCDR3 comprising the amino acid sequence of SEQ ID NO: 12. In some embodiments, the antibody comprises a VH comprising the amino acid sequence of SEQ ID NO: 15, and a VL comprising the amino acid sequence of SEQ ID NO: 16. In some embodiments, the antibody comprises a heavy chain comprising the amino acid sequence of SEQ ID NO: 19, and a light chain comprising the amino acid sequence of SEQ ID NO: 20.

[0075] In some embodiments, the anti-FcRn antibody comprises a heavy chain comprising the amino acid sequence of SEQ ID NO: 21, and a light chain comprising the amino acid sequence of SEQ ID NO: 22.

[0076] In some aspects, the present disclosure provides a method of treating Graves’ Disease (GD) in a subject that is receiving antithyroid drug (ATD) at a dose, the method comprising: (i) administering an anti-FcRn antibody at a dose in the range of 580-700 mg to the subject; (ii) measuring T3 and T4 levels in the subject; (iii) decreasing the dosage of the ATD or stopping the ATD if T3 and / or T4 levels are below ULN; (iii) decreasing the dosage of the anti-FcRn antibody to a dose in the range of 280-400 mg / dose; and (iv) increasing the dosage of the ATD or restarting ATD in the subject to maintain T3 and T4 levels below ULN.

[0077] In some aspects, the present disclosure provides a method of treating Graves’ Disease (GD) in a subject that is receiving antithyroid drug (ATD) at a dose, the method comprising: (i) administering an anti-FcRn antibody to the subject; (ii) measuring T3 and T4 levels in the subject; (iii) decreasing the dosage of the ATD or stopping the ATD if T3 and / or T4 levels are below ULN; (iii) decreasing the dosage of the anti-FcRn antibody to a dose in the range of 280- 400 mg / dose; and (iv) increasing the dosage of the ATD or restarting ATD in the subject to maintain T3 and T4 levels below ULN.

[0078] In some aspects, the present disclosure provides a method of treating Graves’ Disease (GD) in a subject that is receiving antithyroid drug (ATD) at a dose, the method comprising: (i) administering an anti-FcRn antibody at a dose in the range of 580-700 mg to the subject; (ii) measuring T3 and T4 level in the subject; (iii) decreasing the dosage of the ATD or stopping the ATD if T3 and / or T4 levels are below ULN; and (iii) maintaining the dosage of the anti-FcRn antibody while administering the subject with low dose ATD or no ATD to maintain T3 and T4 levels below ULN.

[0079] In some aspects, the present disclosure provides a method of treating Graves’ Disease (GD) in a subject that is receiving antithyroid drug (ATD) at a dose, the method comprising: (i) administering an anti-FcRn antibody to the subject; (ii) measuring T3 and T4 level in the subject; (iii) decreasing the dosage of the ATD or stopping the ATD if T3 and / or T4 levels are below ULN; and (iii) maintaining the dosage of the anti-FcRn antibody while administering the subject with low dose ATD or no ATD to maintain T3 and T4 levels below ULN.

[0080] In some aspects, the present disclosure provides a method for treating Myasthenia Gravis (MG) in a subject, the method comprising administering the subject an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) at 550-700 mg once weekly.

[0081] In some aspects, the present disclosure provides a method for inducing remission in a subject having Myasthenia Gravis (MG), the method comprising administering the subject an anti-FcRn antibody at 550-700 mg once weekly.

[0082] In some embodiments, the subject having MG is administered 600 mg of the anti-FcRn antibody once weekly.

[0083] In some embodiments, the antibody is administered to the subject having MG for a period of 20-60 weeks. In some embodiments, the antibody is administered to the subject having MG for 52 weeks. In some embodiments, the antibody is administered to the subject having MG for 26 weeks.

[0084] In some embodiments, the subject having MG is administered the antibody at a reduced dose after 26 weeks. In some embodiments, the subject having MG is administered the reduced dose of the antibody at 300 mg once weekly. In some embodiments, the subject having MG is administered the reduced dose of the antibody at 300 mg once weekly for 26 weeks. In some embodiments, the subject having MG is administered the reduced dose of the antibody at 300 mg once weekly indefinitely.

[0085] In some embodiments, the subject having MG is positive for anti-acetylcholine receptor (AChR) autoantibodies (anti-AChR+). In some embodiments, the subject having MG is positive for anti-muscles-specific kinase (MuSK) autoantibodies (anti-MuSK+). In some embodiments, the subject having MG is positive for anti-lipoprotein receptor-related protein 4 (LRP4) autoantibodies (anti-LRP4+).

[0086] In some embodiments, the administration of an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) decreases anti- AChR autoantibody levels in the serum of the subject relative to anti- AChR autoantibody levels in the serum prior to the administration.

[0087] In some embodiments, the administration of an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) decreases anti-MuSK autoantibody levels in the serum of the subject having MG relative to anti-MuSK autoantibody levels in the serum prior to the administration.In some embodiments, the administration of an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) decreases anti-LRP4 autoantibody levels in the serum of the subject having MGrelative to anti-LRP4 autoantibody levels in the serum prior to the administration. In some embodiments, the administration of an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) prevents the development or improves one or more following symptoms in the subject having MG: weakness in some or all muscles of the body, double vision, slurred speech, arm weakness, falling, unsteady walking, difficulty swallowing, chronic fatigue, and / or trouble breathing.

[0088] In some aspects, the present disclosure provides a method for treating chronic inflammatory demyelinating polyneuropathy (CIDP) in a subject, the method comprising administering the subject an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) at 200-400 mg once weekly.

[0089] In some aspects, the present disclosure provides a method for treating chronic inflammatory demyelinating polyneuropathy (CIDP) in a subject, the method comprising administering the subject an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) at 550-700 mg once weekly.

[0090] In some embodiments, the subject having CIDP is administered the anti-FcRn antibody for 20-60 weeks. In some embodiments, the subject having CIDP is administered the anti-FcRn antibody for 24 weeks.

[0091] In some embodiments, the method further comprises administering to the subject having CIDP a loading dose of the anti-FcRn antibody on days 3-5 in the first week of administration.

[0092] In some embodiments, the subject having CIDP is administered the anti-FcRn antibody loading dose on day 4 in the first week of administration. In some embodiments, the loading dose of the anti-FcRn antibody is the same as the weekly dose of the anti-FcRn antibody. In some embodiments, the loading dose of the anti-FcRn antibody is 600 mg.

[0093] In some embodiments, the subject having CIDP is administered the anti-FcRn antibody for additional 52 weeks. In some embodiments, the subject having CIDP is administered the anti- FcRn antibody at 600 mg once weekly. In some embodiments, the subject having CIDP is administered the anti-FcRn antibody at 300 mg once weekly.

[0094] In some embodiments, the method further comprises administering to the subject having CIDP a loading dose of the anti-FcRn antibody on days 3-5 in the first week of the additional 52 weeks. In some embodiments, the subject is administered the anti-FcRn antibody loading dose on day 4 in the first week of the additional 52 weeks. In some embodiments, the loading dose ofthe anti-FcRn antibody is the same as the weekly dose of the anti-FcRn antibody. In some embodiments, the loading dose of the anti-FcRn antibody is 600 mg.

[0095] In some embodiments, the subject has typical CIDP. In some embodiments, the subject has a CIDP variant. In some embodiments, the CIDP variant is multifocal CIDP. In some embodiments, the CIDP variant is motor CIDP. In some embodiments, the subject does not have sensory CIDP. In some embodiments, the subject does not have distal CIDP.

[0096] In some embodiments, the subject having CIDP is on or has been on first-line therapy for CIDP. In some embodiments, the first-line therapy for CIDP is corticosteroid. In some embodiments, the subject having CIDP is receiving corticosteroid orally every day or every other day. In some embodiments, the subject having CIDP is receiving corticosteroid via pulse regimen. In some embodiments, the subject having CIDP is tapered off corticosteroid while receiving the anti-FcRn antibody. In some embodiments, the subject having CIDP discontinues corticosteroid prior to receiving the anti-FcRn antibody.

[0097] In some embodiments, the first-line therapy for CIDP is Immunoglobulin (Ig) therapy. In some embodiments, the Ig therapy is intravenous Ig infusion (IVIg). In some embodiments, the Ig therapy is subcutaneous Ig infusion (SCIg). In some embodiments, the subject having CIDP discontinues Ig therapy prior to receiving the anti-FcRn antibody.

[0098] In some embodiments, the first-line therapy for CIDP is plasma exchange (PLEX).

[0099] In some embodiments, the subject having CIDP relapses during the 24- week period of administration of an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) as measured by adjusted Inflammatory Neuropathy Cause and Treatment (aINCAT) score. In some embodiments, the subject having CIDP does not relapse during the 24- week period of administration of an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) as measured by aINCAT score.

[0100] In some embodiments, the administration of an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) increases mean grip strength relative to prior to the administration.

[0101] In some embodiments, the administration of an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) increases Inflammatory Rasch-built Overall Disability Scale (I-RODS) score relative to prior to the administration.

[0102] In some embodiments, the administration of an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) increases MCR-SS score relative to prior to the administration.

[0103] In some embodiments, the administration of an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) decreases Timed Up and Go (TUG) Test score relative to prior to the administration.

[0104] In some embodiments, the administration of an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) decreases total IgG relative to prior to the administration.

[0105] In some embodiments, the administration of an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) decreases IgG subclasses relative to prior to the administration.

[0106] In some embodiments, the administration of an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) decreases autoantibodies targeting myelin glycoproteins relative to prior to the administration.

[0107] In some embodiments, the administration of an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) decreases immune complexes (ICs) relative to prior to the administration.

[0108] In some embodiments, the administration of an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) decreases neurofilament light chain (NfL) relative to prior to the administration.BRIEF DESCRIPTION OF DRAWINGS

[0109] FIG. 1 shows a representative clinical study protocol for healthy subjects. IV = intravenous; MAD = multiple ascending dose; PK = pharmacokinetics; QW = once weekly; SAD = single ascending dose; SC = subcutaneous.

[0110] FIG. 2 shows the mean (SD) albumin concentrations versus nominal time for SAD (linear scale) (safety analysis set). SAD = single ascending dose; SC = subcutaneous; SD = standard deviation. Note: Baseline is defined as the last non-missing value before first treatment. Results including ‘<’ or ‘>’ are imputed as numeric part.

[0111] FIG. 3 shows the mean (SD) albumin concentrations versus nominal time for MAD (linear scale) (safety analysis set). MAD = multiple ascending dose; QW = once weekly; SC = subcutaneous; SD = standard deviation. Note: Baseline is defined as the last non-missing value before first treatment. Results including ‘<’ or ‘>’ are imputed as numeric part.

[0112] FIG. 4 shows the mean (SD) albumin concentrations versus nominal time for alternative dose regimen (linear scale) (safety analysis set). SC = subcutaneous; SD = standard deviation.

[0113] FIG. 5 shows the mean (SD) total cholesterol concentrations versus nominal time for SAD (linear scale) (safety analysis set). IV = intravenous; N = number of participants; SAD = single ascending dose; SC = subcutaneous; SD = standard deviation. Notes: Baseline is definedas the last non-missing value before first treatment. Results including ‘<’ or ‘>’ are imputed as numeric part.

[0114] FIG. 6 shows the mean (SD) LDL cholesterol concentrations versus nominal time for SAD (linear scale) (safety analysis set). IV = intravenous; LDL = low-density lipoprotein; N = number of participants; SAD = single ascending dose; SC = subcutaneous; SD = standard deviation. Notes: Baseline is defined as the last non-missing value before first treatment. Results including ‘<’ or ‘>’ are imputed as numeric part.

[0115] FIG. 7 shows the mean (SD) total cholesterol concentrations versus nominal time for MAD (linear scale) (safety analysis set). MAD = multiple ascending dose; N = number of participants; SC = subcutaneous; SD = standard deviation; QW = once weekly. Notes: Baseline is defined as the last non-missing value before first treatment. Results including '<' or '>' are imputed as numeric part.

[0116] FIG. 8 shows the mean (SD) LDL cholesterol concentrations versus nominal time for MAD (linear scale) (safety analysis set). LDL = low-density lipoprotein; MAD = multiple ascending dose; N = number of participants; QW = once weekly; SC = subcutaneous; SD = standard deviation. Notes: Baseline is defined as the last non-missing value before first treatment. Results including '<' or '>' are imputed as numeric part.

[0117] FIG. 9 shows the mean (SD) total cholesterol concentrations versus nominal time for alternative dose regimen (linear scale) (safety analysis set). N = number of participants; SC = subcutaneous; SD = standard deviation; QW = once weekly. Notes: Baseline is defined as the last non-missing value before first treatment. Results including '<' or '>' are imputed as numeric part.

[0118] FIG. 10 shows the mean (SD) LDL cholesterol concentrations versus nominal time for alternative dose regimen (linear scale) (safety analysis set). LDL = low-density lipoprotein; MAD = multiple ascending dose; N = number of participants; QW = once weekly; SC = subcutaneous; SD = standard deviation. Notes: Baseline is defined as the last non-missing value before first treatment. Results including '<' or '>' are imputed as numeric part.

[0119] FIG. 11 shows the mean (SD) serum concentration of IMVT-1402 in serum versus time following SAD IV administration in healthy participants (semi-logarithmic scale) (pharmacokinetic analysis set). BLQ = below the limit of quantification; IV = intravenous;LLOQ = lower limit of quantification; N = number of participants in the cohort; SAD = singleascending dose; SD = standard deviation. LLOQ value for IMVT-1402 is 0.01 mg / L (dashed line). Notes: All BLQ values are presented as 1 / 2 of LLOQ. Mean ± SD bars with negative values are not presented at the timepoint where SD value is greater than mean.

[0120] FIG. 12 shows the mean (SD) concentration of IMVT-1402 in serum versus time following SAD SC administration in healthy participants (semi-logarithmic scale) (pharmacokinetic analysis set). BLQ = below the limit of quantification; LLOQ = lower limit of quantification; single ascending dose = SAD; SC = subcutaneous. Notes: LLOQ value for IMVT-1402 is 0.01 mg / L (dashed line). All BLQ values are presented as 1 / 2 of LLOQ. Mean ± SD bars with negative values are not presented at the timepoint where SD value is greater than mean.

[0121] FIG. 13 shows the mean (SD) concentration of IMVT-1402 in serum versus time profiles following MAD SC administration - day 1 and day 22 in healthy participants (semi-logarithmic scale) (pharmacokinetic analysis set). BLQ = below the limit of quantification; LLOQ = lower limit of quantification; MAD = multiple ascending dose; SC = subcutaneous; SD = standard deviation. LLOQ value for IMVT-1402 is 0.01 mg / L (dashed line). All BLQ values are presented as 1 / 2 of LLOQ. Mean ± SD bars with negative values are not presented at the timepoint where SD value is greater than mean. Note: In 300 mg MAD cohort, one participant was terminated early after Day 15 visit.

[0122] FIG. 14 shows the mean (SD) concentration of IMVT-1402 in serum versus time profiles following SC administration in healthy participants - alternative dose regimen (semi-logarithmic scale) (pharmacokinetic analysis set). BLQ = below the limit of quantification; LLOQ = lower limit of quantification; SC = subcutaneous; SD = standard deviation. LLOQ value for IMVT- 1402 is 0.01 mg / L (dashed line). All BLQ values are presented as 1 / 2 of LLOQ. Mean ± SD bars with negative values are not presented at the timepoint where SD value is greater than mean.

[0123] FIG. 15 shows the mean (SD) percent change from baseline in total immunoglobulin G (IgG) subclasses concentrations versus nominal time for SAD IV cohorts (linear scale) (pharmacodynamic analysis set). Abbreviations: IgG = immunoglobulin G; IV = intravenous; N = number of participants; SAD = single ascending dose; SD = standard deviation. Note: Baseline is defined as the last non-missing value prior to the first dose of study treatment.

[0124] FIG. 16 shows the mean (SD) percent change from baseline in total immunoglobulin G (IgG) subclasses concentrations versus nominal time for SAD SC cohorts (linear scale)(pharmacodynamic analysis set). Abbreviations: IgG = immunoglobulin G; IV = intravenous; N = number of participants; SAD = single ascending dose; SC = subcutaneous; SD = standard deviation. Note: Baseline is defined as the last non-missing value prior to the first dose of study treatment.

[0125] FIG. 17 shows the mean (SD) percent change from baseline in total immunoglobulin G (IgG) concentrations versus nominal time for MAD cohorts (linear scale) pharmacodynamic analysis set. IgG = immunoglobulin G; MAD = multiple ascending dose; SC = subcutaneous; SD = standard deviation. Note: Baseline is defined as the last non-missing value prior to the first dose of study treatment.

[0126] FIG. 18 shows the mean (SD) percent change from baseline in total immunoglobulin G (IgG) and IgG subclasses concentrations versus nominal time for alternative dose regimen (linear scale) (pharmacodynamic analysis set). IgG = immunoglobulin G; SC = subcutaneous; SD = standard deviation; Note: Baseline is last non-missing value before first treatment.

[0127] FIG. 19 shows the individual percent change from baseline in total immunoglobulin G (IgG) concentrations versus actual time by ADA status for SAD (pharmacodynamic analysis set). ADA = anti-drug antibody; IgG = immunoglobulin G; IV = intravenous; N = number of participants; SAD = single ascending dose; SC = Subcutaneous. Note: Baseline is defined as the last non-missing value before first treatment. Results including '<' or '>' are imputed as numeric part.

[0128] FIG. 20 shows the individual percent change from baseline in total immunoglobulin G (IgG) concentrations versus actual time by ADA status for MAD (pharmacodynamic analysis set). ADA = anti-drug antibody; IgG = immunoglobulin G; MAD = multiple ascending dose; N = number of participants; QW = once weekly; SC = Subcutaneous. Note: Baseline is defined as the last non-missing value before first treatment. Results including '<' or '>' are imputed as numeric part.

[0129] FIG. 21 shows the individual percent change from baseline in total immunoglobulin G (IgG) concentrations versus actual time by ADA status for alternative dose regimen (linear scale) (pharmacodynamic analysis set). ADA = anti-drug antibody; IgG = immunoglobulin G; MAD = multiple ascending dose; N = number of participants; SC = Subcutaneous. Note: Baseline is defined as the last non-missing value before first treatment. Results including '<' or '>' are imputed as numeric part.

[0130] FIG. 22 shows the mean (SD) percent change from baseline in circulating immune complex concentrations versus nominal time for MAD (linear scale) (safety analysis set). MAD = multiple ascending dose; pchg = percent change; SC = subcutaneous; SD = standard deviation; QW = Once Weekly. Notes: Baseline is defined as the last non-missing value before first treatment. Results including '<' or '>' are imputed as numeric part. The calculation of pchg is based on the imputed value.

[0131] FIG. 23 shows the mean (SD) percent change from baseline in circulating immune complex concentrations versus nominal time for alternative dose regimen (linear scale) (safety analysis set), pchg = percent change; SC = subcutaneous; SD = standard deviation. Notes: Baseline is defined as the last non-missing value before first treatment. Results including '<' or '>' are imputed as numeric part. The calculation of pchg is based on the imputed value.

[0132] FIG. 24 shows a Rheumatoid Arthritis (RA) influence diagram: interactions between cells, cytokines, and therapies and their effects on inflammation used in an RA Quantitative Systems Pharmacology (QSP) Model.

[0133] FIG. 25 shows a representative Graves’ disease clinical study diagram. ATD = antithyroid drugs; D = Day; EOS = end of study; ET = early termination; EuThy = euthyroid; N = no; QW = once weekly; R = randomization; SC = subcutaneous; SFU = safety follow-up; TRAb = TSHR antibody; W = Week; Y = yes. *Confirmed by 2 consecutive assessments.

[0134] FIG. 26 shows a representative clinical study diagram. *Meets ACR20 criteria at week 14 and week 16. NR=Did not meet ACR20 criteria at week 14 and week 16.

[0135] FIG. 27 shows the ATD dose change versus nominal time following weekly SC doses of batoclimab in safety analysis set of Graves’ disease subjects who discontinued earlier or reached week 12 (N = 21). ATD = antithyroid drug; QI = first quartile; Q3 = third quartile; SC = subcutaneous. Notes: Hyperthyroid participants received batoclimab 680 mg SC QW for 12 weeks.

[0136] FIG. 28 shows the ATD dose change versus nominal time following weekly SC doses of batoclimab in safety analysis set of Graves’ disease subjects who discontinued earlier or reached week 24 (N = 14). ATD = antithyroid drug; QI = first quartile; Q3 = third quartile; SC = subcutaneous. Notes: Hyperthyroid participants received batoclimab 680 mg SC QW for 12 weeks, followed by batoclimab 340 mg SC QW starting from Day 85 for an additional 12 weeks.

[0137] FIG. 29 is a schematic outline of the Phase 2 Graves’ disease trial design for batoclimab.

[0138] FIG. 30 shows percent change from baseline in total IgG at week 6, week 12, or week 24 of Graves’ disease subjects receiving batoclimab treatment.

[0139] FIG. 31 shows free serum T3 levels over time in Graves’ disease subjects receiving batoclimab treatment.

[0140] FIG. 32 shows free serum T4 levels over time in Graves’ disease subjects receiving batoclimab treatment.

[0141] FIG. 33 shows free serum T3 / free serum T4 levels (top panel), and TRAb / TSH levels (bottom panel) over time in Graves’ disease subjects receiving batoclimab treatment while decreasing CMZ dose to stop CMS treatment.

[0142] FIG. 34 shows proptosis level / lid aperture and thyroid volume (bottom panel) over time with batoclimab treatment while decreasing CMZ dose to stop CMS treatment.

[0143] FIG. 35 shows proportion of Graves’ disease patients with FT3 and FT4 at or below ULN with batoclimab treatment.

[0144] FIG. 36 shows proportion of Graves’ disease patients with FT3 and FT4 at or below ULN with batoclimab treatment while being on reduced ATD dose and off ATD.

[0145] FIG. 37 shows proportion of Graves’ disease patients with FT3 and FT4 at or below ULN with batoclimab treatment while being on reduced ATD dose or off ATD.

[0146] FIG. 38 shows that high dose batoclimab drives rapid normalization of T3 and T4 and ATD tapering in Graves’ disease patients.

[0147] FIG. 39 shows that deep IgG reduction at 24 weeks was associated with a meaningfully higher ATD-free responder rate.

[0148] FIG. 40 is an exemplary study schematic related to myasthenia gravis (MG).

[0149] FIG. 41 is an exemplary study schematic related to chronic inflammatory demyelinating polyradiculoneuropathy (CIDP).DETAILED DESCRIPTION

[0150] Provided herein are methods for improving anti-FcRn therapies as well as methods of treating autoimmune diseases (e.g., Graves’ Disease (GD), thyroid eye disease (TED), Rheumatoid Arthritis (RA), Myasthenia Gravis (MG), Chronic Inflammatory Demyelinating Polyradiculoneuropathy (CIDP), etc.), and treating flare-ups of an autoimmune disease. In some embodiments, the present disclosure provides treatment regimens for various autoimmune diseases (e.g., GD, RA, MG, CIDP, etc.) that confers therapeutic effects, such as reduction inautoantibodies, amelioration / prevention of thyroid eye disease (TED) symptoms, and return to euthyroid state. In some embodiments, the methods comprise administering one or more doses (e.g., a loading dose) of an anti-FcRn antibody (e.g., batoclimab or IMVT-1402).Anti-FcRn Antibodies

[0151] In various embodiments of the therapeutic methods disclosed herein, an anti-FcRn antibody or antigen-binding fragment can non-competitively inhibit the binding of at least one autoantibody and / or pathogenic antibody (e.g., at least one IgG) to FcRn at physiological pH (i.e., pH 7.0-7.4). Without wishing to be bound by theory, it is believed that FcRn binds to its ligand (i.e., IgG) and does not substantially show affinity for IgG at physiological pH rather than acidic pH. Thus, in various embodiments, at physiological pH, the anti-FcRn antibody or antigen-binding fragment may act as a non-competitive inhibitor of the binding of IgG to FcRn, and the binding of the anti-FcRn antibody or antigen-binding fragment to FcRn is not influenced by the presence of IgG. Thus, in various embodiments, the anti-FcRn antibody or antigenbinding fragment that binds specifically to FcRn non-competitively with IgG in a pH- independent manner has an advantage over conventional competitive inhibitors (i.e., antibodies that bind to FcRn competitively with IgG) in that it can provide therapeutic or prophylactic effects even at significantly low concentrations by the FcRn-mediated signaling of IgG.

[0152] In addition, in various embodiments, in the procedure of intracellular migration in a state bound to FcRn, the anti-FcRn antibody or antigen-binding fragment can maintain its binding to FcRn with an affinity higher than IgG in blood. Thus, in various embodiments, the anti-FcRn antibody or antigen-binding fragment can inhibit the binding of IgG to FcRn even in endosomes that are acidic pH environments in which IgG can bind to FcRn, thereby promoting the clearance of IgG.

[0153] In some embodiments, the anti-FcRn antibody or antigen-binding fragment is batoclimab (also referred to herein as HL161BKN and RVT-1401). RVT- 1401 / batoclimab is also described in, e.g., international patent application publication WO2015 / 167293 (where it is referred to as HL161BKN), which is incorporated by reference herein in its entirety.

[0154] In some embodiments, the anti-FcRn antibody or antigen-binding fragment thereof is IMVT-1402. IMVT-1402 is also described in international patent application No. PCT / US2023 / 067539 (where it is also referred to as HL161ANS), which is incorporated by reference herein in its entirety. 1

[0155] The CDR sequences of batoclimab and IMVT-1402 are set forth in Table 1Table 1: CDR sequences of heavy chain and light chain variable domains of selected human FcRn antibodies

[0156] In some embodiments, the antibody or antigen-binding fragment comprises three heavy chain CDR ammo acid sequences of SEQ ID No: 1 (HCDR1), SEQ ID No: 2 (HCDR2), SEQ ID No: 3 (HCDR3); and three light chain CDR amino acid sequences of SEQ ID No: 4 (LCDR1), SEQ ID No: 5 (LCDR2), SEQ ID No: 6 (LCDR3). In some embodiments, the antibody or antigen-binding fragment comprises three heavy chain CDR amino acid sequences of SEQ ID No: 7 (HCDR1), SEQ ID No: 8 (HCDR2), SEQ ID No: 9 (HCDR3); and three light chain CDR ammo acid sequences of SEQ ID No: 10 (LCDR1), SEQ ID No: 11 (LCDR2), SEQ ID No: 12 (LCDR3).

[0157] Illustrative heavy and light chain variable regions of anti-FcRn antibodies are set forth in Table 2.Table 2: Amino acid sequences of heavy chain and light chain variable domains of selected human FcRn antibodies

[0158] In some embodiments, the antibody or antigen-binding fragment comprises a heavy chain variable region comprising an amino acid sequence that is at least 90%, at least 95%, at least 98%, or least 99 identical to the sequence set forth in SEQ ID No: 13; and a light chain variable region comprising an amino acid sequence that is at least 90%, at least 95%, at least 98%, or least 99 identical to the sequence set forth in SEQ ID No: 14. In some embodiments, the antibody or antigen-binding fragment comprises a heavy chain amino acid comprising an amino acid sequence that is at least 90%, at least 95%, at least 98%, or least 99 identical to the sequence set forth in SEQ ID No: 15; and a light chain amino acid comprising an amino acid sequence that is at least 90%, at least 95%, at least 98%, or least 99 identical to the sequence set forth in SEQ ID No: 16.

[0159] In some embodiments, the antibody or antigen-binding fragment comprises a heavy chain variable region amino acid sequence of SEQ ID No: 13; and a light chain variable region amino acid sequence of SEQ ID No: 14. In some embodiments, the antibody or antigen-binding fragment comprises a heavy chain amino acid sequence of SEQ ID No: 15; and a light chain amino acid sequence of SEQ ID No: 16.

[0160] Illustrative heavy chains and light chains of the anti-FcRn antibodies are set forth in Table 3.Table 3: Amino acid sequences of full-length heavy chain and light chain of selected human FcRn antibodies

[0161] In some embodiments, the antibody or antigen-binding fragment comprises a heavy chain comprising an amino acid sequence that is at least 90%, at least 95%, at least 98%, or least 99 identical to the sequence set forth in SEQ ID No: 17, 19 or 21; and a light chain comprising an amino acid sequence that is at least 90%, at least 95%, at least 98%, or least 99 identical to the sequence set forth in SEQ ID No: 18, 20 or 22. In some embodiments, the antibody or antigenbinding fragment comprises a heavy chain comprising the sequence set forth in SEQ ID No: 17, 19 or 21; and a light chain comprising the sequence set forth in SEQ ID No: 18, 20 or 22.

[0162] Binding “affinity” refers to the strength of interaction between antibody and antigen at single antigenic sites. Within each antigenic site, the variable region of the antibody "arm" interacts through weak non-covalent forces with the antigen at numerous sites. In general, the more interactions, the higher the affinity.

[0163] As used herein, the term "specific," "specifically binds," and "binds specifically" refers to a binding reaction between an antibody or an antigen-binding fragment thereof (e.g., an anti- FcRn antibody or an antigen-binding fragment thereof) and a target antigen (e.g., FcRn) in a heterogeneous population of proteins and other biologies. Antibodies can be tested for specificity of binding by comparing binding to an appropriate antigen with binding to an alternate antigen or antigen mixture under a given set of conditions. If the antibody binds to the appropriate antigen with at least 2 times, at least 5 times, or at least 10 times (or more) higher affinity than to the alternate antigen or antigen mixture, then it is considered to be specific.

[0164] A “specific antibody” or a “target-specific antibody” is one that only binds the target antigen (e.g., FcRn), but does not bind (or exhibits minimal binding) to other antigens. In some embodiments, an antibody or an antigen-binding fragment thereof that specifically binds the target antigen (e.g., FcRn) has a KD of less than IxlO'6M, less than IxlO'7M, less than IxlO'8M, less than IxlO'9M, less than IxlO'10M, less than IxlO'11M, less than IxlO'12M, or less than IxlO'13M at pH 6.0 or pH 7.4. In some embodiments, the KD is about 0.01 nM to about 2 nM at pH 6.0 or pH 7.4. In some embodiments, the KD is about 300 pM or less to about 2 nM or less at pH 7.4. In some embodiments, the KD is about 2 nM or less to 900 pM or less at pH 6.0.

[0165] As used herein, the term “KD” refers to the equilibrium dissociation constant for antibody -antigen binding, which is obtained from the ratio of kd to ka(i.e., kd / ka) and is generally expressed as a molar concentration (M). The term "kassoc" or "ka" refers to the association rate of a particular antibody-antigen interaction, whereas the term "kdis" or "kd" refers to the dissociation rate of a particular antibody-antigen interaction. The measurement of kd and / or kacan be performed at 25 °C or 37°C. KD values for antibodies and antigen-binding fragments can be determined using methods well established in the art (see, e.g., Pollard, Mol. Biol. Cell 21(23):4061-7, 2010). In some embodiments, the KD is measured by direct binding and / or competition binding assays (e.g., surface plasmon resonance and / or competition ELISA). In some embodiments, the KD is measured by surface plasmon resonance (e.g., human FcRn- immobilized surface plasmon resonance). In some embodiments, the KD of an anti-FcRn antibody or antigen-binding fragment disclosed herein is measured by human FcRn-immobilized surface plasmon resonance.

[0166] In some embodiments of the therapeutic methods, uses, and compositions disclosed herein, the anti-FcRn antibody or antigen-binding fragment has a KD (dissociation constant) of about 0.01 nM to 2 nM at pH 6.0 and pH 7.4, as determined by, e.g., surface plasmon resonance. In some embodiments, the anti-FcRn antibody or antigen-binding fragment has a KD from about 300 pM or less to about 2 nM or less at pH 7.4 and / or has a KD from about 2 nM or less to about 900 pM or less at pH 6.0, as determined by, e.g., surface plasmon resonance. In some embodiments, the anti-FcRn antibody or antigen-binding fragment binds to the outside of cells and when bound maintains its binding to endosomes. In some embodiments, the anti-FcRn antibody or antigen-binding fragment effectively blocks the binding of one or moreautoantibodies to FcRn (e.g., human FcRn), as determined by, e.g., a blocking assay performed using human FcRn-expressing cells and FACS.

[0167] As used herein, the term “anti-FcRn antibody” or “antibody that binds specifically to FcRn” refers to any form of an antibody or an antigen-binding fragment thereof that binds specifically to FcRn, e.g., those binding with a KD of less than 2 nM at pH 6.0 or pH 7.4, as determined by, e.g., surface plasmon resonance (e.g., human FcRn-immobilized surface plasmon resonance). The term encompasses monoclonal antibodies (including full-length monoclonal antibodies), polyclonal antibodies, and biologically functional fragments so long as they bind specifically to FcRn.

[0168] In some embodiments of the therapeutic methods, uses, and compositions disclosed herein, the anti-FcRn antibody or antigen-binding fragment comprises:• a CDR1 comprising an amino acid sequence that is at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, or at least 99% identical to the amino acid sequence set forth in SEQ ID No. 1, 4, 7 or 10;• a CDR2 comprising an amino acid sequence that is at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, or at least 99% identical to the amino acid sequence set forth in SEQ ID 2, 5, 8 or 11 ; and• a CDR3 comprising an amino acid sequence that is at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, or at least 99% identical to the amino acid sequence set forth in SEQ ID No. 3, 6, 9 or 12.

[0169] In some embodiments of the therapeutic methods, uses, and compositions disclosed herein, the anti-FcRn antibody or antigen-binding fragment may comprise one or more amino acid deletions, additions, or substitutions in the amino acid sequences described herein.

[0170] In some embodiments of the therapeutic methods, uses, and compositions disclosed herein, the anti-FcRn antibody or antigen-binding fragment may comprise amino acid sequences identical to or having homology with the amino acid sequences described herein. The term “identity” or “homology” refers to a relationship between the sequences of two or more polypeptides, as determined by comparing the sequences. The term "identity" also means thedegree of sequence relatedness between the polypeptides, as determined by the number of matches between strings of two or more amino acid residues. The percent “identity” between the two sequences is a function of the number of identical positions shared by the sequences (i.e., percent identity equals number of identical positions / total number of positions x 100), taking into account the number of gaps, and the length of each gap, which need to be introduced for optimal alignment of the two sequences. The comparison of sequences and determination of percent identity between two sequences can be accomplished using a mathematical algorithm. For sequence comparison, typically one sequence acts as a reference sequence, to which test sequences are compared. When using a sequence comparison algorithm, test and reference sequences are entered into a computer, subsequence coordinates are designated, if necessary, and sequence algorithm program parameters are designated. Default program parameters can be used, or alternative parameters can be designated. The sequence comparison algorithm then calculates the percent sequence identities for the test sequences relative to the reference sequence, based on the program parameters. Additionally, or alternatively, the amino acid sequences disclosed herein can further be used as a “query sequence” to perform a search against public databases to, for example, identify related sequences. For example, such searches can be performed using the BLAST program of Altschul et al. (J. Mol. Biol. 215:403-10, 1990).

[0171] Two sequences are “substantially identical” if two sequences have a specified percentage of amino acid residues that are the same (i.e., 60% identity, optionally 65%, 70%, 75%, 80%, 85%, 90%, 95%, or 99% identity over a specified region, or, when not specified, over the entire sequence), when compared and aligned for maximum correspondence over a comparison window, or designated region as measured using one of the following sequence comparison algorithms or by manual alignment and visual inspection. Optionally, the identity exists over a region that is at least about 10 amino acids in length, or over a region that is about 20, 50, 200 or more amino acids in length. In some embodiments, the anti-FcRn antibodies and antigen-binding fragments described herein comprise at least one amino acid sequence that is at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, or at least 99% identical to the sequence set forth in any one of SEQ ID NOs: 1-22.

[0172] In some embodiments, the antibody or antigen-binding fragment comprises a heavy chain variable region comprising:• a CDR1 comprising an amino acid sequence of SEQ ID No: 1, CDR2 comprising an amino acid sequence of SEQ ID No: 2, and CDR3 comprising an amino acid sequence of SEQ ID No: 3; or• a CDR1 comprising an amino acid sequence of SEQ ID No: 7, CDR2 comprising an amino acid sequence of SEQ ID No: 8, and CDR3 comprising an amino acid sequence of SEQ ID No: 9.

[0173] In some embodiments, the antibody or antigen-binding fragment comprises a light chain variable region comprising:• a CDR1 comprising an amino acid sequence of SEQ ID No: 4, CDR2 comprising an amino acid sequence of SEQ ID No: 5, and CDR3 comprising an amino acid sequence of SEQ ID No: 6; or• a CDR1 comprising an amino acid sequence of SEQ ID No: 10, CDR2 comprising an amino acid sequence of SEQ ID No: 11, and CDR3 comprising an amino acid sequence of SEQ ID No: 12.

[0174] In some embodiments, the antibody or antigen-binding fragment comprises one or more heavy chain variable regions and one or more light chain variable regions selected from the group consisting of:• a heavy chain variable region comprising CDR1 comprising an amino acid sequence of SEQ ID No: 1 (HCDR1), CDR2 comprising an amino acid sequence of SEQ ID No: 2 (HCDR2), and CDR3 comprising an amino acid sequence of SEQ ID No: 3 (HCDR3); and a light chain variable region comprising CDR1 comprising an amino acid sequence of SEQ ID No: 4 (LCDR1), CDR2 comprising an amino acid sequence of SEQ ID No:5 (LCDR2), and CDR3 comprising an amino acid sequence of SEQ ID No: 6 (LCDR3); or• a heavy chain variable region comprising CDR1 comprising an amino acid sequence of SEQ ID No: 7 (HCDR1), CDR2 comprising an amino acid sequence of SEQ ID No: 8 (HCDR2), and CDR3 comprising an amino acid sequence of SEQ ID No: 9 (HCDR3); and a light chain variable region comprising CDR1 comprising an amino acid sequence of SEQ ID No: 10 (LCDR1), CDR2 comprising an amino acid sequence of SEQ ID No: 11 (LCDR2), and CDR3 comprising an amino acid sequence of SEQ ID NO: 12 (LCDR3).

[0175] In some embodiments, the antibody or antigen-binding fragment comprises one or more heavy chain variable regions and / or one or more light chain variable regions comprising one or more amino acid sequences selected from the group consisting of amino acid sequences of SEQ ID Nos: 13-16.

[0176] In some embodiments, the antibody or antigen-binding fragment comprises heavy chain variable region comprising an amino acid sequence of SEQ ID Nos: 13 or 15 and / or light chain variable region comprising an amino acid sequence of SEQ ID Nos: 14 or 16.

[0177] In some embodiments, the antibody or antigen-binding fragment comprises one or more heavy chain variable regions and one or more light chain variable regions selected from the group consisting of:• a heavy chain variable region comprising an amino acid sequence of SEQ ID No: 13 and a light chain variable region comprising an amino acid sequence of SEQ ID No: 14; and• a heavy chain variable region comprising an amino acid sequence of SEQ ID No: 15 and a light chain variable region comprising an amino acid sequence of SEQ ID No: 16.

[0178] The terms “fragment,” “antibody fragment,” and “antigen-binding fragment,” as used herein in reference to an antibody, all refer to one or more fragments of a full-length antibody that retain the ability to specifically bind to the target antigen (e.g., FcRn) and / or provide a function of the full-length antibody (e.g., non-competitive interference with the binding of IgGto FcRn). Antigen-binding fragments can also be present in larger macromolecules, e.g., bispecific, trispecific, and multispecific antibodies, such as diabodies, triabodies and tetrabodies. Examples of antigen-binding fragments include, but are not limited to, single-chain antibodies, Fab fragments, F(ab')2 fragments, Fd, scFv, domain antibodies, dual-specific antibodies, minibodies, scap (sterol regulatory binding protein cleavage activating protein), chelating recombinant antibodies, tribodies or bibodies, intrabodies, nanobodies, and small modular immunopharmaceuticals (SMIP).

[0179] In some embodiments, the antibody or antigen-binding fragment is a binding-domain immunoglobulin fusion protein, camelized antibody, VHH containing antibody, IgD antibody, IgE antibody, IgM antibody, IgGl antibody, IgG2 antibody, IgG3 antibody, or IgG4 antibody. In some embodiments, the antibody or antigen-binding fragment comprises derivatives in theantibody constant regions. In some embodiments, the antibody or antigen-binding fragment is a synthetic antibody based on protein scaffolds that have the ability to bind to FcRn.

[0180] In some embodiments, an antigen-binding fragment shows the same or similar properties as those of the full-length antibody. Without limitation, an antigen-binding fragment can be produced by any suitable method known in the art. For instance, the various antigen-binding fragments described herein may be produced by enzymatic or chemical modification of full- length antibodies, synthesized de novo using recombinant DNA methodologies (e.g., scFv), or identified using phage display libraries (see, e.g., Pini and Bracci, Curr. Protein Pept. Sci.1(2): 155-69, 2000). Antigen-binding fragments may be screened for utility (e.g., specificity, binding affinity, activity) in the same manner as are full-length antibodies.

[0181] In addition, antibodies or antigen-binding fragments having a mutation in the variable and / or constant region may be used in the therapeutic methods, uses, and compositions described herein. Examples of such antibodies or antigen-binding fragments include antibodies having a conservative substitution of an amino acid residue in the variable region and / or constant region. As used herein, the term “conservative substitution” refers to a substitution with another amino acid residue having properties similar to those of the original amino acid residue. For example, lysine, arginine and histidine have similar properties in that they have a basic side-chain, and aspartic acid and glutamic acid have similar properties in that they have an acidic side chain. In addition, glycine, asparagine, glutamine, serine, threonine, tyrosine, cysteine and tryptophan have similar properties in that they have an uncharged polar side-chain, and alanine, valine, leucine, threonine, isoleucine, proline, phenylalanine and methionine have similar properties in that they have a non-polar side-chain. Also, tyrosine, phenylalanine, tryptophan and histidine have similar properties in that they have an aromatic side-chain. Thus, it will be obvious to those skilled in the art that, even when substitution of amino acid residues in groups showing similar properties as described above occurs, it will likely show no significant change in the properties of the antibody or antigen-binding fragment.

[0182] In addition, in some embodiments, the antibody or antigen-binding fragment may be conjugated to another substance (e.g., a therapeutic agent or a detectable label). Substances that may be conjugated to, or administered in combination with, an antibody or antigen-binding fragment described herein include but are not limited to therapeutic agents that are generally used for the treatment of autoimmune diseases (e.g., a standard-of-care agent, e.g., any one ormore of the standard-of-care agents described and / or incorporated by reference herein); substances that are capable of inhibiting the activity of FcRn; and moieties that may be physically associated with the antibody or antigen-binding fragment, e.g., to improve its stabilization and / or retention in circulation, e.g., in blood, serum, lymph, or other tissues. For example, the antibody or antigen-binding fragment can be associated with a polymer, e.g., a non- antigenic polymer such as polyalkylene oxide or polyethylene oxide. Suitable polymers will vary substantially by weight. Polymers having molecular number average weights ranging from about 200 to about 35,000 (or about 1,000 to about 15,000, and 2,000 to about 12,500) can be used. For example, the antibody or antigen-binding fragment can be conjugated to water soluble polymers, e.g., hydrophilic polyvinyl polymers, e.g., polyvinylalcohol and polyvinylpyrrolidone. Nonlimiting examples of such polymers include, but are not limited to, polyalkylene oxide homopolymers such as polyethylene glycol (PEG) or polypropylene glycols, polyoxyethylenated polyols, copolymers thereof and block copolymers thereof, provided that the water solubility of the block copolymers is maintained.

[0183] In various embodiments, the antibody or antigen-binding fragment binds to FcRn with a KD (dissociation constant) of 0.01 nM to 2 nM at pH 6.0 or pH 7.4, as measured by, e.g., surface plasmon resonance.Pharmaceutical Compositions

[0184] Also provided herein are pharmaceutical compositions comprising the anti-FcRn antibody or an antigen-binding fragment thereof formulated together with at least one pharmaceutically acceptable carrier. The compositions may also contain one or more additional therapeutic agents that are suitable for treating autoimmune diseases. Methods of formulating pharmaceutical compositions and suitable formulations are known in the art (see, e.g., "Remington's Pharmaceutical Sciences," Mack Publishing Co., Easton, PA). Appropriate formulation may depend on the route of administration.

[0185] As used herein, a "pharmaceutical composition" refers to a preparation of an anti-FcRn antibody or an antigen-binding fragment thereof in addition to other components suitable for administration to a patient, such as a pharmaceutically acceptable carrier and / or excipient. The pharmaceutical compositions provided herein may be suitable for administration in vitro and / or in vivo. In some embodiments, the pharmaceutical compositions provided herein are in such form as to permit administration and subsequently provide the intended biological activity of theactive ingredient(s) and / or to achieve a therapeutic effect. The pharmaceutical compositions provided herein preferably contain no additional components which are unacceptably toxic to a subject to which the formulation would be administered.

[0186] As used herein, the terms "pharmaceutically acceptable carrier" and "physiologically acceptable carrier," which may be used interchangeably, refer to a carrier, diluent, or excipient that does not cause significant irritation to a subject and does not abrogate the biological activity and properties of the administered antibody or antigen-binding fragment. Thus, pharmaceutically acceptable carriers should be compatible with the active ingredient such as the antibody or an antigen-binding fragment thereof, and may include physiological saline, sterile water, Ringer’s solution, buffered saline, dextrose solution, maltodextrin solution, glycerol, ethanol, or a mixture of two or more thereof. Pharmaceutically acceptable carriers may also enhance or stabilize the composition or can be used to facilitate preparation of the composition. Pharmaceutically acceptable carriers can include other conventional additives, such as antioxidants, buffers, solvents, bacteriostatic agents, dispersion media, coatings, antibacterial and antifungal agents, isotonic and absorption delaying agents, and the like that are physiologically compatible. The carrier may be selected to minimize adverse side effects in the subject, and / or to minimize degradation of the active ingredient(s).

[0187] As used herein, the term "excipient" refers to an inert substance added to a pharmaceutical composition to further facilitate administration of an active ingredient. Formulations for parenteral administration can, for example, contain excipients such as sterile water or saline, polyalkylene glycols such as polyethylene glycol, vegetable oils, or hydrogenated napthalenes. Other excipients include, but are not limited to, calcium bicarbonate, calcium phosphate, various sugars and types of starch, cellulose derivatives, gelatin, ethylenevinyl acetate co-polymer particles, and surfactants, including, for example, polysorbate 20.

[0188] In various embodiments of the therapeutic methods, uses, and compositions disclosed herein, the anti-FcRn antibody, antigen-binding fragment, or pharmaceutical composition can be administered by a variety of methods known in the art. The route and / or mode of administration may vary depending upon the desired results. In some embodiments, the antibody, antigenbinding fragment, or pharmaceutical composition is administered by oral, intravenous, intramuscular, intra-arterial, intramedullary, intradural, intracardial, transdermal, subcutaneous, intraperitoneal, gastrointestinal, sublingual, or local routes. In some embodiments, the antibody,antigen-binding fragment, or pharmaceutical composition is administered orally or parenterally. In some embodiments, the antibody, antigen-binding fragment, or pharmaceutical composition is administered parenterally, e.g., intravenously or subcutaneously (e.g., by injection or infusion). In some embodiments, the antibody, antigen-binding fragment, or pharmaceutical composition is administered subcutaneously (e.g., by injection or infusion). In some embodiments, the antibody, antigen-binding fragment, or pharmaceutical composition is administered as one or more subcutaneous injections. In some embodiments, the antibody, antigen-binding fragment, or pharmaceutical composition is administered as a single (i.e., one) subcutaneous injection. In some embodiments, the antibody, antigen-binding fragment, or pharmaceutical composition is administered as two or more (e.g., two) consecutive subcutaneous injections. In some embodiments, the antibody, antigen-binding fragment, or pharmaceutical composition is administered without intravenous administration (e.g., intravenous induction) prior to the one or more subcutaneous injections. In some embodiments, the antibody, antigen-binding fragment, or pharmaceutical composition is delivered via a syringe, a catheter, a pump delivery system, or a stent. In some embodiments, the antibody, antigen-binding fragment, or pharmaceutical composition is delivered via a syringe (e.g., a pre-filled syringe). Depending on the route of administration, the active compound(s), i.e., the anti-FcRn antibody or antigen-binding fragment, may be coated in a material to protect the compound(s) from the action of acids and other natural conditions that may inactivate the compound(s).

[0189] An antibody, antigen-binding fragment, or pharmaceutical composition may be formulated as various forms such as a powder, tablet, capsule, liquid, injection, ointment, or syrup, and / or comprised in a single-dosage or multi-dosage container such as a sealed ampoule, vial, or syringe. In some embodiments, the antibody, antigen-binding fragment, or pharmaceutical composition is formulated as an injectable form. In some embodiments, the antibody, antigen-binding fragment, or pharmaceutical composition is formulated as an aqueous solution, suspension, or emulsion, with one or more excipients, diluents, dispersants, surfactants, binders, and / or lubricants. In some embodiments, the antibody, antigen-binding fragment, or pharmaceutical composition is comprised in a syringe (e.g., a pre-filled syringe). In some embodiments, the antibody, antigen-binding fragment, or pharmaceutical composition is comprised in a syringe having and / or compatible with a small gauge needle (e.g., a needlegreater than about 25 gauge, greater than about 26 gauge, greater than about 27 gauge, greater than about 28 gauge, greater than about 29 gauge, and / or greater than about 30 gauge).

[0190] In some embodiments, the antibody, antigen-binding fragment, or pharmaceutical composition is formulated to achieve stability and / or to prevent or minimize physical and / or chemical degradation prior to administration. Physical instability may involve processes such as denaturation and aggregation, while common chemical degradation pathways include but are not limited to cross-linking, deamidation, isomerization, oxidation, and fragmentation (see, e.g., Wang et al., J. Pharm. Sci. 91(1): 1-26, 2007). As used herein, the term “stable” or “stability” when used to describe an antibody or an antigen-binding fragment thereof means that the antibody or antigen-binding fragment remains intact in a manner to retain activity (e.g., binding to FcRn) and / or achieve a therapeutic effect. In some embodiments, the antibody, antigenbinding fragment, or pharmaceutical composition is formulated with one or more pharmaceutically acceptable carriers (e.g., one or more excipients) such that it is stable under standard storage conditions. In some embodiments, the antibody, antigen-binding fragment, or pharmaceutical composition is formulated with one or more pharmaceutically acceptable carriers (e.g., one or more excipients) such that it is stable at high concentrations. In some embodiments, the antibody or antigen-binding fragment can be stably concentrated at formulations up to about 150 mg / mL or above. In some embodiments, the antibody or antigen-binding fragment can be stably concentrated at formulations up to about 170 mg / mL or above. In some embodiments, the antibody or antigen-binding fragment can be stably concentrated at formulations above about 170 mg / mL (e.g., at about 180 mg / mL, at about 200 mg / mL, at about 220 mg / mL, or above). In some embodiments, the stably concentrated formulation (e.g., a formulation comprising up to about 170 mg / mL or above of the antibody or antigen-binding fragment) retains acceptable viscosity for administration via a small gauge needle. In some embodiments, the small gauge needle is greater than about 25 gauge, greater than about 26 gauge, greater than about 27 gauge, greater than about 28 gauge, greater than about 29 gauge, or greater than about 30 gauge.

[0191] The anti-FcRn antibody or antigen-binding fragment may be formulated into pharmaceutically acceptable dosage forms by conventional methods known to those of skill in the art. Parenteral compositions, for example, may be formulated in dosage unit form for ease of administration and uniformity of dosage. As used herein, “dosage unit form” refers to physically discrete units suited as unitary dosages for the subjects to be treated; each unit contains apredetermined quantity of active compound calculated to produce the desired therapeutic effect in association with a pharmaceutically acceptable carrier. In some embodiments, the antibody, antigen-binding fragment, or pharmaceutical composition is formulated in dosage unit form. In some embodiments, the antibody, antigen-binding fragment, or pharmaceutical composition is formulated in dosage unit form for subcutaneous administration. In some embodiments, the antibody, antigen-binding fragment, or pharmaceutical composition is formulated in dosage unit form for administration as one or more subcutaneous injections (e.g., one subcutaneous injection or two or more (e.g., two) consecutive subcutaneous injections). In some embodiments, the antibody, antigen-binding fragment, or pharmaceutical composition is formulated in dosage unit form (e.g., as one or more subcutaneous injections) for self-administration by the patient and / or for administration by a treating clinician.Methods of Use

[0192] Provided herein are methods of improving anti-FcRn therapy comprising administering the antibodies or antigen-binding fragments thereof provided herein. In some embodiments, provided herein are methods of treating an autoimmune disease (e.g., GD, RA, TED, MG, CIDP, etc.) in a subject via dosing regiments of administering an anti-FcRn therapy (e.g., batoclimab or IMVT-1402). Autoimmune diseases that can be treated with an anti-FcRn therapy described herein include, but are not limited to, Graves’ disease (GD), thyroid eye disease (TED), rheumatoid arthritis (RA), myasthenia gravis (MG), immune thrombocytopenia, pemphigus vulgaris, chronic inflammatory demyelinating polyneuropathy (CIDP), and systemic lupus erythematosus (SLE). In some embodiments, the autoimmune disease is a progressive autoimmune disease. An autoimmune disease is characterized as progressive when symptoms worsen or are exacerbated over time, with or without treatment.Dosing Regimen for Graves’ Disease (GD)

[0193] In some aspects, the present disclosure provides compositions and methods for treating Graves’ disease. In some embodiments, the method comprises a dosing regimen (e.g., dose, dosing frequency, etc.) for GD that improves the efficacy of the treatment (e.g., relative to using a different dosing regimen).

[0194] Graves’ Disease (GD) is an autoimmune condition in which autoantibodies bind to thyroid cells, mimicking thyroid-stimulating hormone (TSH). Autoantibody binding to thyroidcells (e.g., Thyroid Stimulating Hormone receptor (THSR; also known as thyrotrophin) autoantibodies (TRAb)), in some embodiments, induces excessive thyroid hormone production, resulting in inflammation and an enlarged thyroid, and can cause symptoms in systems throughout the body, including irregular heart rate, pretibial myxedema, weight loss, muscle weakness, temperature sensitivity, and others. In some embodiments, TRAbs comprise Thyroid Stimulating Immunoglobulin (TSI), and can be measured using suitable TSI assays. GD is chronic and can negatively impact life expectancy if not treated appropriately. Assays to determine the onset and severity of GD are known in the art (see, e.g., Ehlers et al. Graves, disease in clinical perspective. Front Biosci, 2019. 24(1): 33-45).

[0195] A subject is typically first suspected of having hyperthyroidism upon presenting in the clinic with low basal serum levels of TSH. The normal range of TSH is 0.5 to 5.0 mU / L.Diagnostic accuracy is improved upon assessment of thyroxine (T4) and triiodothyronine (T3) in the blood, as elevation of one or both can further confirm hyperthyroidism diagnosis. In some embodiments, the normal range of total T4 in adults is 5.0-12.0 pg / dL. In some embodiments, a normal level of free T4 (FT4) is 0.7-1.9 ng / dL. In some embodiments, a normal total T3 level in adults is 79-165 ng / dL. Accordingly, the upper limit of normal (ULN) of free T4 (FT4) is considered to be about 1.9 ng / dL, and the ULN of total T3 is considered to be about 165 ng / dL. TSH, T3, and T4 levels are typically determined by electrochemiluminescent immunoassays or enzyme-linked immunosorbent assays (ELISAs) but can be measured via any suitable assay.

[0196] In some embodiments, the present disclosure provides compositions (e.g., anti-FcRn antibody, IMVT-1402 or batoclimab) and methods (e.g., dosing regimens) for treating GD in a subject. In some embodiments, a subject is administered an anti-FcRn antibody (e.g., IMVT- 1402 or batoclimab) at a range of 550-700 mg once weekly. In some embodiments, a subject is administered an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) at a range of 550-700 mg once weekly. In some embodiments, a subject is administered an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) at a range of 550-700 mg once weekly for 20-60 weeks.

[0197] In some embodiments, a subject is administered an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) at a range of 550-700 mg, 550-690 mg, 550-680 mg, 550-670 mg, 550-660 mg, 550-650 mg, 550-640 mg, 550-630 mg, 550-620 mg, 550-610 mg, 550-600 mg, 550-590 mg,550-580 mg, 550-570 mg, 550-560 mg, 580-700 mg, 580-690 mg, 580-680 mg, 580-670 mg,580-660 mg, 580-650 mg, 580-640 mg, 580-630 mg, 580-620 mg, 580-610 mg, 580-600 mg,580-590 mg, 600-700 mg, 600-690 mg, 600-680 mg, 600-670 mg, 600-660 mg, 600-650 mg, 600-640 mg, 600-630 mg, 600-620 mg, 600-610 mg, 620-700 mg, 620-690 mg, 620-680 mg, 620-670 mg, 620-660 mg, 620-650 mg, 620-640 mg, 620-630 mg, 650-700 mg, 650-690 mg, 650-680 mg, 650-670 mg, 650-660 mg, 680-700 mg, or 680-690 mg once weekly. In some embodiments, a subject having or suspected of having GD is administered IMVT-1402 at a range of 550-700 mg, 550-690 mg, 550-680 mg, 550-670 mg, 550-660 mg, 550-650 mg, 550-640 mg, 550-630 mg, 550-620 mg, 550-610 mg, 550-600 mg, 550-590 mg, 550-580 mg, 550-570 mg, 550-560 mg, 580-700 mg, 580-690 mg, 580-680 mg, 580-670 mg, 580-660 mg, 580-650 mg, 580-640 mg, 580-630 mg, 580-620 mg, 580-610 mg, 580-600 mg, 580-590 mg, 600-700 mg, 600-690 mg, 600-680 mg, 600-670 mg, 600-660 mg, 600-650 mg, 600-640 mg, 600-630 mg, 600-620 mg, 600-610 mg, 620-700 mg, 620-690 mg, 620-680 mg, 620-670 mg, 620-660 mg, 620-650 mg, 620-640 mg, 620-630 mg, 650-700 mg, 650-690 mg, 650-680 mg, 650-670 mg, 650-660 mg, 680-700 mg, or 680-690 mg once weekly. In some embodiments, a subject is administered IMVT-1402 at a dose of 600 mg once weekly. In some embodiments, a subject having or suspected of having GD is administered batoclimab at a range of 550-700 mg, 550-690 mg, 550-680 mg, 550-670 mg, 550-660 mg, 550-650 mg, 550-640 mg, 550-630 mg, 550-620 mg, 550-610 mg, 550-600 mg, 550-590 mg, 550-580 mg, 550-570 mg, 550-560 mg, 580-700 mg, 580-690 mg, 580-680 mg, 580-670 mg, 580-660 mg, 580-650 mg, 580-640 mg, 580-630 mg, 580-620 mg, 580-610 mg, 580-600 mg, 580-590 mg, 600-700 mg, 600-690 mg, 600-680 mg, 600-670 mg, 600-660 mg, 600-650 mg, 600-640 mg, 600-630 mg, 600-620 mg, 600-610 mg, 620-700 mg, 620-690 mg, 620-680 mg, 620-670 mg, 620-660 mg, 620-650 mg, 620-640 mg, 620-630 mg, 650-700 mg, 650-690 mg, 650-680 mg, 650-670 mg, 650-660 mg, 680-700 mg, or 680-690 mg once weekly. In some embodiments, a subject having or suspected of having GD is administered batoclimab at a dose of 680 mg once weekly.

[0198] In some embodiments, a subject having or suspected of having GD is administered an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) at a range of 550-700 mg (e.g., any of the doses described herein) once weekly for 20-60 weeks, 20-58 weeks, 20-55 weeks, 20-52 weeks, 20-50 weeks, 20-45 weeks, 20-42 weeks, 20-40 weeks, 20-35 weeks, 20-30 weeks, 20-25 weeks,25-60 weeks, 25-58 weeks, 25-55 weeks, 25-52 weeks, 25-50 weeks, 25-45 weeks, 25-42 weeks,25-40 weeks, 25-35 weeks, 25-30 weeks, 30-60 weeks, 30-58 weeks, 30-55 weeks, 30-52 weeks,30-50 weeks, 30-45 weeks, 30-42 weeks, 30-40 weeks, 30-35 weeks, 35-60 weeks, 35-58 weeks,35-55 weeks, 35-52 weeks, 35-50 weeks, 35-45 weeks, 35-42 weeks, 35-40 weeks, 40-60 weeks,40-58 weeks, 40-55 weeks, 40-52 weeks, 40-50 weeks, 40-45 weeks, 40-42 weeks, 45-60 weeks,45-58 weeks, 45-55 weeks, 45-52 weeks, 45-50 weeks, 50-60 weeks, 50-58 weeks, 50-55 weeks,50-52 weeks, 55-60 weeks, or 55-58 weeks.

[0199] In some embodiments, a subject is administered IMVT-1402. In some embodiments, the subject is administered IMVT-1402 at 600 mg once weekly for 26 weeks. In some embodiments, the subject is administered IMVT-1402 at 600 mg once weekly for 52 weeks.

[0200] In some embodiments, a subject is administered batoclimab. In some embodiments, the subject is administered batoclimab at 680 mg once weekly for 26 weeks. In some embodiments, the subject is administered batoclimab at 680 mg once weekly for 26 weeks, and 340 mg once weekly for another 26 weeks. In some embodiments, the subject is administered batoclimab at 680 mg once weekly for 52 weeks.

[0201] In some embodiments, a subject with GD is administered an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) at 300 mg once weekly indefinitely. In some embodiments, a subject with GD is administered an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) at 600 mg or 680 mg once weekly indefinitely. In some embodiments, a subject with GD is administered IMVT-1402 at 300 mg once weekly indefinitely. In some embodiments, a subject with GD is administered IMVT-1402 at 600 mg once weekly indefinitely. In some embodiments, a subject with GD is administered batoclimab at 340 mg once weekly indefinitely. In some embodiments, a subject with GD is administered batoclimab at 680 mg once weekly indefinitely.

[0202] In some embodiments, prior to administration, the subject has hyperthyroidism. Hyperthyroidism is further subdivided into two types: (i) overt hyperthyroidism, in which total T3 and / or free T4 is greater than the ULN and TSH levels are below the LLN; and (ii) subclinical hyperthyroidism, in which T3 and free T4 are within normal limits (WNL) and TSH levels are below the LLN (see Ross et al. 2016 American Thyroid Association Guidelines for Diagnosis and Management of Hyperthyroidism and Other Causes of Thyrotoxicosis. Thyroid. 26(1)).

[0203] In some embodiments, prior to administration, the subject has overt hyperthyroidism. In some embodiments, prior to administration, a GD subject with overt hyperthyroidism has a baseline T3 level higher than T3 ULN (e.g., more than lx ULN, more than 2x ULN, more than 3x ULN, more than 4x ULN, more than 5x ULN, more than 6x ULN, more than 7x ULN, morethan 8x ULN, more than 9x ULN, more than 1 Ox ULN, more than 15x ULN, more than 20x ULN, more than 50x ULN, more than lOOx ULN, or more). In some embodiments, prior to administration, a GD subject with overt hyperthyroidism has a baseline T3 level higher than T3 ULN (e.g., baseline T3 in the range of Llx-lOOOx ULN, l.lx-900x ULN, l.lx-800x ULN, l.lx- 700xULN, l.lx-600x ULN, Llx-500xULN, Llx-400xULN, Llx-300xULN, Llx-200xULN, Llx-lOOxULN, Llx-lOOxULN, Llx-25xULN, l.lx-lOxULN, Llx-5xULN, l.lx-3xULN, Llx-2xULN, L5x-1000xULN, L5x-900xULN, L5x-800xULN, L5x-700xULN, L5x-600x ULN, L5x-500xULN, L5x-400xULN, L5x-300xULN, L5x-200xULN, L5x-100xULN, L5x-100xULN, L5x-25xULN, L5x-10xULN, L5x-5xULN, L5x-3xULN, L5x-2xULN, 1.5x-1000x ULN, L5x-900xULN, L5x-800xULN, L5x-700xULN, L5x-600xULN, 1.5x- 500xULN, L5x-400xULN, L5x-300xULN, L5x-200xULN, L5x-100xULN, L5x-100xULN, L5x-25xULN, L5x-10xULN, L5x-5xULN, L5x-3xULN, L5x-2xULN, 2x-1000xULN, 2x- 900x ULN, 2x-800x ULN, 2x-700x ULN, 2x-600x ULN, 2x-500x ULN, 2x-400x ULN, 2x-300x ULN, 2x-200x ULN, 2x-100x ULN, 2x-100x ULN, 2x-25x ULN, 2x-10x ULN, 2x-5x ULN, 2x- 3xULN, 5x-1000xULN, 5x-900xULN, 5x-800xULN, 5x-700xULN, 5x-600xULN, 5x-500x ULN, 5x-400xULN, 5x-300xULN, 5x-200xULN, 5x-100xULN, 5x-100xULN, 5x-25xULN, 5x-10xULN, lOx-lOOOx ULN, 10x-900xULN, 10x-800xULN, 10x-700xULN, 10x-600x ULN, 10x-500xULN, 10x-400xULN, 10x-300xULN, 10x-200xULN, IOX-IOOXULN, lOx- lOOxULN, 10x-20xULN, lOOx-lOOOx ULN, 100x-900x ULN, 100x-800x ULN, 100x-700x ULN, 100x-600x ULN, 100x-500x ULN, 100x-400x ULN, 100x-300x ULN, 100x-200x ULN, IOOX-IOOOXULN, 100x-900x ULN, 100x-800x ULN, 100x-700x ULN, 100x-600x ULN, lOOx- 500xULN, 100x-400x ULN, 100x-300x ULN, 100x-200x ULN, 250x-1000x ULN, 250x-900x ULN, 250x-800x ULN, 250x-700x ULN, 250x-600x ULN, 250x-500x ULN, 250x-400x ULN, 500x-1000x ULN, 500x-900x ULN, 500x-800x ULN, 500x-700x ULN, 500x-600x ULN, 750x- lOOOx ULN, 750x-900x ULN, 750x-800x ULN). In some embodiments, prior to administration, a GD subject with overtly hyperthyroidism has a baseline FT4 level higher than FT4 ULN (e.g., more than lx ULN, more than 2x ULN, more than 3x ULN, more than 4x ULN, more than 5x ULN, more than 6x ULN, more than 7x ULN, more than 8x ULN, more than 9x ULN, more than 1 Ox ULN, more than 15x ULN, more than 20x ULN, more than 5 Ox ULN, more than lOOx ULN, or more). In some embodiments, prior to administration, a GD subject with overt hyperthyroidism has a baseline FT4 level higher than FT4 ULN (e.g., in the range of l.lx-lOOOx ULN, l.lx-900xULN, Llx-800xULN, l.lx-700x ULN, l.lx-600x ULN, l.lx-500x ULN, l.lx-400x ULN, Llx-300xULN, Llx-200xULN, l.lx-lOOx ULN, l.lx-lOOx ULN, Llx-25xULN, Llx-lOx ULN, Llx-5xULN, Llx-3xULN, Llx-2xULN, L5x-1000x ULN, L5x-900xULN, L5x-800x ULN, L5x-700xULN, L5x-600xULN, L5x-5OOxULN, L5x-400xULN, L5x-300xULN, L5x-200xULN, L5x-100xULN, L5x-100xULN, L5x-25xULN, L5x-10xULN, L5x-5x ULN, 1.5x-3xULN, L5x-2xULN, L5x-1000x ULN, L5x-900xULN, L5x-800xULN, 1.5x- 700xULN, L5x-600xULN, L5x-5OOxULN, L5x-400xULN, L5x-300xULN, L5x-200xULN, L5x-100xULN, L5x-100xULN, L5x-25xULN, L5x-10xULN, L5x-5xULN, L5x-3xULN, L5x-2x ULN, 2x-1000x ULN, 2x-900x ULN, 2x-800x ULN, 2x-700x ULN, 2x-600x ULN, 2x- 5OOx ULN, 2x-400x ULN, 2x-300x ULN, 2x-200x ULN, 2x-100x ULN, 2x-100x ULN, 2x-25x ULN, 2x-10x ULN, 2x-5x ULN, 2x-3x ULN, 5x-1000x ULN, 5x-900x ULN, 5x-800x ULN, 5x- 700xULN, 5x-600xULN, 5x-500xULN, 5x-400xULN, 5x-300xULN, 5x-200xULN, 5x-100x ULN, 5x-100xULN, 5x-25xULN, 5x-10xULN, lOx-lOOOx ULN, 10x-900xULN, 10x-800x ULN, 10x-700xULN, 10x-600xULN, 10x-500xULN, 10x-400xULN, 10x-300xULN, lOx- 200xULN, lOx-lOOxULN, lOx-lOOxULN, 10x-20xULN, lOOx-lOOOx ULN, 100x-900x ULN, 100x-800x ULN, 100x-700x ULN, 100x-600x ULN, 100x-500x ULN, 100x-400x ULN, lOOx- 300xULN, 100x-200x ULN, lOOx-lOOOx ULN, 100x-900x ULN, 100x-800x ULN, 100x-700x ULN, 100x-600x ULN, 100x-500x ULN, 100x-400x ULN, 100x-300x ULN, 100x-200x ULN, 250x-1000x ULN, 250x-900x ULN, 250x-800x ULN, 250x-700x ULN, 250x-600x ULN, 250x- 500xULN, 250x-400x ULN, 500x-1000x ULN, 500x-900x ULN, 500x-800x ULN, 500x-700x ULN, 500x-600x ULN, 750x-1000x ULN, 750x-900x ULN, 750x-800x ULN). In some embodiments, prior to administration, a GD subject with overt hyperthyroidism has a baseline TSH level lower than TSH LLN (e.g., less than lx LLN, less than 0.9x LLN, less than 0.8x LLN, less than 0.7x LLN, less than 0.6x LLN, less than 0.5x LLN, less than 0.4x LLN, less than 0.3x LLN, less than 0.2x LLN, less than O.lx LLN, less than 0.075x LLN, less than 0.05x LLN, less than 0.025x LLN, less than O.Olx LLN, or less). In some embodiments, prior to administration, a GD subject with overt hyperthyroidism has a baseline TSH level lower than TSH LLN (e.g., in the range of 0.001x-0.99x LLN, 0.005x-0.99x LLN, 0.0008x-0.99x LLN, 0.01x-0.99x LLN, 0.05x-0.99x LLN, 0.08x-0.99x LLN, 0.1x-0.99x LLN, 0.2x-0.99x LLN, 0.3x-0.99x LLN, 0.4x- 0.99xLLN, 0.5x-0.99x LLN, 0.6x-0.99x LLN, 0.7x-0.99x LLN, 0.8x-0.99x LLN, 0.9x-0.99x LLN, 0.001x-0.8x LLN, 0.005x-0.8x LLN, 0.0008x-0.8x LLN, 0.01x-0.8x LLN, 0.05x-0.8xLLN, 0.08x-0.8x LLN, 0.1x-0.8x LLN, 0.2x-0.8x LLN, 0.3x-0.8x LLN, 0.4x-0.8x LLN, 0.5x- 0.8x LLN, 0.6x-0.8x LLN, 0.7x-0.8x LLN, 0.001x-0.5x LLN, 0.005x-0.5x LLN, 0.0008x-0.5x LLN, 0.01x-0.5x LLN, 0.05x-0.5x LLN, 0.08x-0.5x LLN, O.lx-O.5x LLN, 0.2x-0.5x LLN, 0.3x- 0.5x LLN, 0.4x-0.5x LLN, 0.001x-0.3x LLN, 0.005x-0.3x LLN, 0.0008x-0.3x LLN, 0.01x-0.3x LLN, 0.05x-0.3x LLN, 0.08x-0.3x LLN, O.lx-O.3x LLN, 0.2x-0.3x LLN, O.OOlx-O.lx LLN, 0.005x-0.1x LLN, 0.0008x-0.1x LLN, O.Olx-O.lx LLN, 0.05x-0.1x LLN, 0.08x-0.1x LLN, 0.001x-0.075x LLN, 0.005x-0.075x LLN, 0.0008x-0.075x LLN, 0.01x-0.075x LLN, 0.05x- 0.075x LLN, 0.08x-0.075x LLN, 0.001x-0.05x LLN, 0.005x-0.05x LLN, 0.0008x-0.05x LLN, 0.01x-0.05x LLN, 0.001x-0.02x LLN, 0.005x-0.02x LLN, 0.0008x-0.02x LLN, or 0.01x-0.02x LLN.

[0204] In some embodiments, prior to administration, the subject has subclinical hyperthyroidism. In some embodiments, prior to administration, a GD subject with subclinical hyperthyroidism has a T3 and FT4 within normal range. In some embodiments, prior to administration, a GD subject with subclinical hyperthyroidism has a TSH level less than 0.1 mU / L (e.g., a TSH level less than 0.1 mU / L, less than 0.09 mU / L, less than 0.08 mU / L, less than 0.07 mU / L, less than 0.06 mU / L, less than 0.05 mU / L, less than 0.04 mU / L, less than 0.03 mU / L, less than 0.02 mU / L, less than 0.01 mU / L, less than 0.0075 mU / L, less than 0.005 mU / L, less than 0.002 mU / L, less than 0.001 mU / L, or less). In some embodiments, prior to administration, a GD subject with subclinical hyperthyroidism has a TSH level less than 0.1 mU / L (e.g., in the range of 0.001-0.1 mU / L, 0.001-0.1 mU / L, 0.001-0.1 mU / L, 0.001-0.1 mU / L, 0.001-0.1 mU / L, 0.001-0.1 mU / L, 0.001-0.1 mU / L, 0.001-0.09 mU / L, 0.001-0.08 mU / L, 0.001- 0.07 mU / L, 0.001-0.06 mU / L, 0.001-0.05 mU / L, 0.001-0.04 mU / L, 0.001-0.03 mU / L, 0.001- 0.02 mU / L, 0.001-0.01 mU / L, 0.001-0.009 mU / L, 0.001-0.008 mU / L, 0.001-0.007 mU / L, 0.001- 0.006 mU / L, 0.001-0.005 mU / L, 0.001-0.004 mU / L, 0.001-0.003 mU / L, 0.001-0.002 mU / L, 0.005-0.1 mU / L, 0.005-0.1 mU / L, 0.005-0.1 mU / L, 0.005-0.1 mU / L, 0.005-0.1 mU / L, 0.005-0.1 mU / L, 0.005-0.1 mU / L, 0.005-0.09 mU / L, 0.005-0.08 mU / L, 0.005-0.07 mU / L, 0.005-0.06 mU / L, 0.005-0.05 mU / L, 0.005-0.04 mU / L, 0.005-0.03 mU / L, 0.005-0.02 mU / L, 0.005-0.01 mU / L, 0.005-0.009 mU / L, 0.005-0.008 mU / L, 0.005-0.007 mU / L, 0.005-0.006 mU / L, 0.008-0.1 mU / L, 0.008-0.1 mU / L, 0.008-0.1 mU / L, 0.008-0.1 mU / L, 0.008-0.1 mU / L, 0.008-0.1 mU / L, 0.008-0.1 mU / L, 0.008-0.09 mU / L, 0.008-0.08 mU / L, 0.008-0.07 mU / L, 0.008-0.06 mU / L, 0.008-0.05 mU / L, 0.008-0.04 mU / L, 0.008-0.03 mU / L, 0.008-0.02 mU / L, 0.008-0.01 mU / L,0.008-0.009 mU / L, 0.01-0.1 mU / L, 0.01-0.1 mU / L, 0.01-0.1 mU / L, 0.01-0.1 mU / L, 0.01-0.1 mU / L, 0.01-0.1 mU / L, 0.01-0.1 mU / L, 0.01-0.09 mU / L, 0.01-0.08 mU / L, 0.01-0.07 mU / L, 0.01- 0.06 mU / L, 0.01-0.05 mU / L, 0.01-0.04 mU / L, 0.01-0.03 mU / L, 0.01-0.02 mU / L, 0.05-0.1 mU / L, 0.05-0.1 mU / L, 0.05-0.1 mU / L, 0.05-0.1 mU / L, 0.05-0.1 mU / L, 0.05-0.1 mU / L, 0.05-0.1 mU / L, 0.05-0.09 mU / L, 0.05-0.08 mU / L, 0.05-0.07 mU / L, 0.05-0.06 mU / L, 0.08-0.1 mU / L, or 0.08-0.1 mU / L.

[0205] The presence of autoantibodies against thyroid stimulating hormone receptor (TSHR) (TRAbs) is highly specific for GD. In some embodiments, prior to administration, a subject with GD has elevated TRAb levels. In some embodiments, a normal range of TRAb is 0-0.9 IU / L.

[0206] Approximately 20-25% of subjects with GD develop thyroid eye disease (TED), also known as Graves’ ophthalmopathy, and 80% of GD patients who develop TED do so within 18 months of the onset of GD. TED affects the eye muscles and fatty tissues behind the eye. In some embodiments, a subject with GD has one or more TED symptoms include blurred or double vision, changes in the appearance of the eye (e.g., bulging), difficulty moving the eyes, low tolerance of bright lights, pain and / or redness of the eye, and swelling or fullness of the eyelids. The development of TED symptoms is usually progressive for the first year after their onset, and severe TED can require steroids and / or orbital radiotherapy for treatment. In some embodiments, a subject has GD may have one or more eye symptoms but is not diagnosed as having TED. In some embodiments, a subject has GD but does not have any eye symptoms. In some embodiments, a subject has GD but is not diagnosed as having TED. In some embodiments, a subject has GD but does not have any eye symptoms and is not diagnosed as having TED. In some embodiments, an anti-FcRn therapy (e.g., batoclimab or IMVT-1402) described herein prevents or delays onset or development of TED relative to a subject not receiving the anti-FcRn therapy. In some embodiments, amelioration of TED symptoms is indicative of a positive response to an anti-FcRn therapy (e.g., batoclimab or IMVT-1402) described herein. In some embodiments, administration of the anti-FcRn antibody (e.g., IMVT- 1402 or batoclimab) prevents the onset of TED in a subject having GD. In some embodiments, administration of the anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) delays the onset of TED in a subject having GD by one month, two months, three months, four months, five months, six months, seven months, eight months, nine months, ten months, eleven months, twelve months, fifteen months, eighteen months, two years, three years, four years, five years, or more.In some embodiments, administration of the anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) reduces or eliminates one or more eye symptoms in a subject having GD. In some embodiments, the administration of an anti-FcRn antibody as described herein decreases proptosis in the subject relative to prior to the administration. In some embodiments, the administration of an anti-FcRn antibody decreases lid aperture in the subject relative to prior to the administration. In some embodiments, the administration of an anti-FcRn antibody decreases thyroid volume in the subject relative to prior to the administration.

[0207] In some embodiments, an anti-FcRn therapy (e.g., batoclimab or IMVT-1402) induces remission of GD in a subject receiving the therapy. A subject is typically considered to be in remission of GD when a patient is euthyroid for at least 6 months or more following discontinuation of ATD therapy; for subjects receiving anti-FcRn therapy and ATD therapy a subject would be considered to be in remission when a subject is euthyroid for at least 6 months or more following discontinuation of both therapies. In some embodiments, administration of the anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) using the dosing regimen described herein induces remission in the subject and the subject maintains the remission by at least six months, at least one year, at least two years, at least three years, at least four years, at least five years, or longer.

[0208] In some embodiments, a subject with GD receiving the anti-FcRn antibody dosing regimen described herein has been previously treated with one or more antithyroid drugs (ATD). In some embodiments, a subject with GD has been on an ATD for longer than 3 months immediately preceding the administration of an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab). In some embodiments, a subject with GD is on an ATD while receiving the anti- FcRn antibody dosing regimen described herein. Non-limiting examples of ATD include methimazole, carbimazole, or propylthiouracil. In some embodiments, a subject with GD has been on a dose of at least 20 mg / day of methimazole (e.g., for at least four weeks prior to the baseline assessment). In some embodiments, a subject with GD has been on a dose of at least 30 mg / day of carbimazole (e.g., for at least four weeks prior to the baseline assessment). In some embodiments, a subject with GD has been on a dose of at least 200 mg / day of propylthiouracil (e.g., for at least four weeks prior to the baseline assessment). In some embodiments, a subject with GD has been on ATD for at least six months prior to the baseline assessment and prior to initiating treatment with an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab). In someembodiments, a subject with GD has been on a dose of at least 15 mg / day of methimazole (e.g., at any point of treatment history) prior to the baseline assessment and prior to initiating treatment with an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab). In some embodiments, a subject with GD has been on a dose of at least 20 mg / day of carbimazole (e.g., at any point of treatment history) prior to the baseline assessment and prior to initiating treatment with an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab). In some embodiments, a subject with GD has been on a dose of at least 150 mg / day of propylthiouracil (e.g., at any point of treatment history) prior to the baseline assessment and prior to initiating treatment with an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab). In some embodiments, a subject with GD is on a dose of at least 10 mg / day of methimazole (e.g., at the time of the baseline assessment) prior to initiating treatment with an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab). In some embodiments, a subject with GD is on a dose of at least 15 mg / day of carbimazole (e.g., at the time of the baseline assessment) prior to initiating treatment with an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab). In some embodiments, a subject with GD is on a dose of at least 100 mg / day of propylthiouracil (e.g., at the time of the baseline assessment) prior to initiating treatment with an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab).

[0209] In some embodiments, an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) dosing regimens described herein are more suitable for subjects with GD but not having certain conditions or comorbidities. For example, in some embodiments, the subject with GD has not previously been treated with radioactive iodine (RAI) therapy. In some embodiments, a subject with GD has not undergone total thyroidectomy. In some embodiments, a subject with GD does not have T3 and / or FT4 lower than the LLN prior to initiating the administration of an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab). In some embodiments, a subject with GD has not received levothyroxine, desiccated thyroid extract, or T3 at any dose within 6 weeks of baseline assessment prior to initiating treatment with an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab). In some embodiments, a subject with GD has not received a block block-and- replace treatment. In some embodiments, a subject with GD does not have a history of hyperthyroidism not caused by GD (e.g., toxic adenoma or toxic multinodular goiter) and / or history of thyroid storm within 6 months of baseline assessment prior to initiating treatment with an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab). In some embodiments, a subject with GD does not have a known active autoimmune disease requiring treatment that may put thesubject at an undue risk. In some embodiments, a subject with GD does not have moderate- to- severe active thyroid eye disease (TED) and are expected to require immediate surgical intervention and / or are planning corrective surgery / irradiation or medical therapy for TED during treatment. In some embodiments, a subject with GD does not have a documented history of noncompliance with ATD therapy.

[0210] Subjects with GD may suffer from a rare but deadly disease flare-up known as a thyroid storm. A sudden and sharp rise in thyroid hormones can induce fever, sweating, delirium, severe weakness, tremors, irregular heartbeat, and severe low blood pressure and coma. In some embodiments, an anti-FcRn therapy (e.g., batoclimab or IMVT-1402) described herein prevents or ameliorates a GD flare-up and / or thyroid storm.

[0211] In some embodiments, prior to the initiation of administration of an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab), baseline levels of the subject’s thyroid function (e.g., T3, T4, TSH, and / or TRAb) can be assessed and recorded. The levels of these parameters can be measured throughout treatment to assess treatment efficacy. T3, T4, TSH, and / or TRAb can be measured using any suitable methods.

[0212] In some embodiments, administration of an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) dosing regimen described herein decreases TSI level in the subject (e.g., relative to baseline TSI level prior to the administration) by at least at least 1%, at least 5%, at least 10%, at least 15%, at least 20%, at least 25%, at least 30%, at least 35%, at least 40%, at least 45%, at least 50%, at least 55%, at least 60%, at least 65%, at least 70%, at least 75%, at least 80%, at least 85%, at least 90%, at least 95%, at least 96%, at least 97%, at least 98%, at least 99%, or 100%. In some embodiments, the administration of an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) dosing regimen described herein decreases TSI level in the subject (e.g., relative to baseline TSI level prior to the administration) by between 1% and 100%, between 5% and 100%, between 5% and 90%, between 5% and 80%, between 5% and 70%, between 5% and 60%, between 5% and 50%, between 5% and 40%, between 5% and 30%, between 5% and 20%, between 5% and 15%, between 10% and 100%, between 10% and 90%, between 10% and 80%, between 10% and 70%, between 10% and 60%, between 10% and 50%, between 10% and 40%, between 10% and 30%, between 10% and 20%, between 10% and 15%, between 20% and 100%, between 20% and 90%, between 20% and 80%, between 20% and 70%, between 20% and 60%, between 20% and 50%, between 20% and 40%, between 20% and 30%, between 30%and 100%, between 30% and 90%, between 30% and 80%, between 30% and 70%, between 30% and 60%, between 30% and 50%, between 30% and 40%, between 40% and 100%, between 40% and 90%, between 40% and 80%, between 40% and 70%, between 40% and 60%, between 40% and 50%, between 50% and 100%, between 50% and 90%, between 50% and 80%, between 50% and 70%, between 50% and 60%, between 60% and 100%, between 60% and 90%, between 60% and 80%, between 60% and 70%, between 70% and 100%, between 70% and 90%, between 70% and 80%, between 80% and 100%, between 80% and 90%, or between 90% and 100%.

[0213] In some embodiments, administration of an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) dosing regimen described herein decreases total IgG level in the subject (e.g., relative to baseline total IgG level prior to the administration) by at least at least 1%, at least 5%, at least 10%, at least 15%, at least 20%, at least 25%, at least 30%, at least 35%, at least 40%, at least 45%, at least 50%, at least 55%, at least 60%, at least 65%, at least 70%, at least 75%, at least 80%, at least 85%, at least 90%, at least 95%, at least 96%, at least 97%, at least 98%, at least 99%, or 100%. In some embodiments, the administration of an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) dosing regimen described herein decreases total IgG level in the subject (e.g., relative to baseline total IgG level prior to the administration) by between 1% and 100%, between 5% and 100%, between 5% and 90%, between 5% and 80%, between 5% and 70%, between 5% and 60%, between 5% and 50%, between 5% and 40%, between 5% and 30%, between 5% and 20%, between 5% and 15%, between 10% and 100%, between 10% and 90%, between 10% and 80%, between 10% and 70%, between 10% and 60%, between 10% and 50%, between 10% and 40%, between 10% and 30%, between 10% and 20%, between 10% and 15%, between 20% and 100%, between 20% and 90%, between 20% and 80%, between 20% and 70%, between 20% and 60%, between 20% and 50%, between 20% and 40%, between 20% and 30%, between 30% and 100%, between 30% and 90%, between 30% and 80%, between 30% and 70%, between 30% and 60%, between 30% and 50%, between 30% and 40%, between 40% and 100%, between 40% and 90%, between 40% and 80%, between 40% and 70%, between 40% and 60%, between 40% and 50%, between 50% and 100%, between 50% and 90%, between 50% and 80%, between 50% and 70%, between 50% and 60%, between 60% and 100%, between 60% and 90%, between 60% and 80%, between 60% and 70%, between 70%and 100%, between 70% and 90%, between 70% and 80%, between 80% and 100%, between 80% and 90%, or between 90% and 100%.

[0214] In some embodiments, a subject administered an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) dosing regimen described herein achieves a euthyroid state (e.g., becomes euthyroid) within 25 weeks of administration (e.g., within 25 weeks, within 24 weeks, within 23 weeks, within 22 weeks, within 21 weeks, within 20 weeks, within 19 weeks, within 18 weeks, within 17 weeks, within 16 weeks, within 15 weeks, within 14 weeks, within 13 weeks, within 12 weeks, within 11 weeks, within 10 weeks, within 9 weeks, within 8 weeks, within 7 weeks, within 6 weeks, within 5 weeks, within 4 weeks, within 3 weeks, within 2 weeks, or within 1 week). Euthyroid, as used herein, refers to the state of having normal thyroid gland function. In some embodiments, a subject that is euthyroid has T3 (total T3 or FT3), FT4, and TSH within normal ranges, respectively. In some embodiments, continuing administration of anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) dosing regimen described herein maintains the euthyroid state in the subject relative to subjects that stop the treatment at 26 weeks.

[0215] In some embodiments, the administration of an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) dosing regimen described herein decreases T3 level in the subject (e.g., relative to baseline T3 level prior to the administration) by at least at least 1%, at least 5%, at least 10%, at least 15%, at least 20%, at least 25%, at least 30%, at least 35%, at least 40%, at least 45%, at least 50%, at least 55%, at least 60%, at least 65%, at least 70%, at least 75%, at least 80%, at least 85%, at least 90%, at least 95%, at least 96%, at least 97%, at least 98%, at least 99%, or100%. In some embodiments, the administration of an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) dosing regimen described herein decreases T3 level in the subject (e.g., relative to baseline T3 level prior to the administration) by between 1% and 100%, between 5% and 100%, between 5% and 90%, between 5% and 80%, between 5% and 70%, between 5% and 60%, between 5% and 50%, between 5% and 40%, between 5% and 30%, between 5% and 20%, between 5% and 15%, between 10% and 100%, between 10% and 90%, between 10% and 80%, between 10% and 70%, between 10% and 60%, between 10% and 50%, between 10% and 40%, between 10% and 30%, between 10% and 20%, between 10% and 15%, between 20% and 100%, between 20% and 90%, between 20% and 80%, between 20% and 70%, between 20% and 60%, between 20% and 50%, between 20% and 40%, between 20% and 30%, between 30% and 100%, between 30% and 90%, between 30% and 80%, between 30% and 70%, between30% and 60%, between 30% and 50%, between 30% and 40%, between 40% and 100%, between 40% and 90%, between 40% and 80%, between 40% and 70%, between 40% and 60%, between 40% and 50%, between 50% and 100%, between 50% and 90%, between 50% and 80%, between 50% and 70%, between 50% and 60%, between 60% and 100%, between 60% and 90%, between 60% and 80%, between 60% and 70%, between 70% and 100%, between 70% and 90%, between 70% and 80%, between 80% and 100%, between 80% and 90%, or between 90% and 100%. In some embodiments, the administration of an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) dosing regimen described herein decreases T3 level in the subject to be within the normal range of T3 (e.g., 79-165 ng / dL).

[0216] In some embodiments, the administration of an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) dosing regimen described herein decreases FT4 level in the subject (e.g., relative to baseline FT4 level prior to the administration) by at least at least 1%, at least 5%, at least 10%, at least 15%, at least 20%, at least 25%, at least 30%, at least 35%, at least 40%, at least 45%, at least 50%, at least 55%, at least 60%, at least 65%, at least 70%, at least 75%, at least 80%, at least 85%, at least 90%, at least 95%, at least 96%, at least 97%, at least 98%, at least 99%, or100%. In some embodiments, the administration of an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) dosing regimen described herein decreases FT4 level in the subject (e.g., relative to baseline FT4 level prior to the administration) by between 1% and 100%, between 5% and 100%, between 5% and 90%, between 5% and 80%, between 5% and 70%, between 5% and 60%, between 5% and 50%, between 5% and 40%, between 5% and 30%, between 5% and 20%, between 5% and 15%, between 10% and 100%, between 10% and 90%, between 10% and 80%, between 10% and 70%, between 10% and 60%, between 10% and 50%, between 10% and 40%, between 10% and 30%, between 10% and 20%, between 10% and 15%, between 20% and 100%, between 20% and 90%, between 20% and 80%, between 20% and 70%, between 20% and 60%, between 20% and 50%, between 20% and 40%, between 20% and 30%, between 30% and 100%, between 30% and 90%, between 30% and 80%, between 30% and 70%, between 30% and 60%, between 30% and 50%, between 30% and 40%, between 40% and 100%, between 40% and 90%, between 40% and 80%, between 40% and 70%, between 40% and 60%, between 40% and 50%, between 50% and 100%, between 50% and 90%, between 50% and 80%, between 50% and 70%, between 50% and 60%, between 60% and 100%, between 60% and 90%, between 60% and 80%, between 60% and 70%, between 70% and 100%, between70% and 90%, between 70% and 80%, between 80% and 100%, between 80% and 90%, or between 90% and 100%. In some embodiments, the administration of an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) dosing regimen described herein decreases FT4 level in the subject to be within the normal range of FT4 (e.g., 0.7-1.9 ng / dL).In some embodiments, the administration of an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) dosing regimen described herein increases TSH level in the subject (e.g., relative to baseline TSH level prior to the administration) by at least at least at least 5%, at least 10%, at least 15%, at least 20%, at least 25%, at least 30%, at least 35%, at least 40%, at least 45%, at least 50%, at least 55%, at least 60%, at least 65%, at least 70%, at least 75%, at least 80%, at least 85%, at least 90%, at least 95%, at least 100%, at least 1.5 times, at least 2 times, at least 3 times, at least 4 times, at least 5 times, at least 10 times, at least 20 times, at least 50 times, at least 100 times or more. In some embodiments, administration of an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) dosing regimen described herein increases TSH level in the subject (e.g., relative to baseline TSH level prior to the administration) by between 1% and 100%, between 5% and 100%, between 5% and 90%, between 5% and 80%, between 5% and 70%, between 5% and 60%, between 5% and 50%, between 5% and 40%, between 5% and 30%, between 5% and 20%, between 5% and 15%, between 10% and 100%, between 10% and 90%, between 10% and 80%, between 10% and 70%, between 10% and 60%, between 10% and 50%, between 10% and 40%, between 10% and 30%, between 10% and 20%, between 10% and 15%, between 20% and 100%, between 20% and 90%, between 20% and 80%, between 20% and 70%, between 20% and 60%, between 20% and 50%, between 20% and 40%, between 20% and 30%, between 30% and 100%, between 30% and 90%, between 30% and 80%, between 30% and 70%, between 30% and 60%, between 30% and 50%, between 30% and 40%, between 40% and 100%, between 40% and 90%, between 40% and 80%, between 40% and 70%, between 40% and 60%, between 40% and 50%, between 50% and 100%, between 50% and 90%, between 50% and 80%, between 50% and 70%, between 50% and 60%, between 60% and 100%, between 60% and 90%, between 60% and 80%, between 60% and 70%, between 70% and 100%, between 70% and 90%, between 70% and 80%, between 80% and 100%, between 80% and 90%, between 90% and 100%, between 1 and 100 times, between 1 and 90 times, between 1 and 80 times, between 1 and 70 times, between 1 and 60 times, between 1 and 50 times, between 1 and 40 times, between 1 and 30 times, between 1 and 20 times, between 1 and10 times, between 1 and 8 times, between 1 and 5 times, between 1 and 3 times, between 5 and 100 times, between 5 and 90 times, between 5 and 80 times, between 5 and 70 times, between 5 and 60 times, between 5 and 50 times, between 5 and 40 times, between 5 and 30 times, between 5 and 20 times, between 5 and 10 times, between 5 and 8 times, between 10 and 100 times, between 10 and 90 times, between 10 and 80 times, between 10 and 70 times, between 10 and 60 times, between 10 and 50 times, between 10 and 40 times, between 10 and 30 times, between 10 and 20 times, between 25 and 100 times, between 25 and 90 times, between 25 and 80 times, between 25 and 70 times, between 25 and 60 times, between 25 and 50 times, between 25 and 40 times, between 25 and 30 times, between 50 and 100 times, between 50 and 90 times, between 50 and 80 times, between 50 and 70 times, between 50 and 60 times, between 75 and 100 times, between 75 and 90 times, and between 75 and 80 times. In some embodiments, administration of an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) dosing regimen described herein increases TSH level in the subject to be within the normal range (e.g., 0.5 to 5.0 mll / L).

[0217] In some embodiments, during the treatment course, the dose of ATD the subject is on can be adjusted based on T3, T4, and / or TSH level and / or the subject’s clinical response. For example, in some embodiments, the administration of an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) dosing regimen described herein decreases T3 and / or T4 levels in the subject to be below ULN, whereupon the subject receives a reduced dose of ATD. In some embodiments, a subject administered an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) dosing regimen described herein can decrease the dose of ATD within 60 weeks, within 55 weeks, within 50 weeks, within 45 weeks, within 40 weeks, within 35 weeks, within 30 weeks, within 25 weeks, within 20 weeks, within 15 weeks, within 10 weeks, or within 5 weeks of administration. In some embodiments, administration of an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) dosing regimen described herein induces a euthyroid state in the subject, and the subject can stop taking ATDs. In some embodiments, a subject administered an anti-FcRn antibody (e.g., IMVT- 1402 or batoclimab) dosing regimen described herein stops taking ATD within 60 weeks, within 55 weeks, within 50 weeks, within 45 weeks, within 40 weeks, within 35 weeks, within 30 weeks, within 25 weeks, within 20 weeks, within 15 weeks, within 10 weeks, or within 5 weeks of administration.

[0218] In some aspects, the subject can taper down the dose of ATD while on high dose of an anti-FcRn antibody (e.g., batoclimab at 680 mg or IMVT-1402 at 600 mg) to eventually stoptaking ATD. In some embodiments, the subject then switches on a lower dose of an anti-FcRn antibody (e.g., batoclimab at 340 mg or IMVT-1402 at 300 mg) but requires increased dose or reintroduction of ATD to maintain a normal T3 and / or T4 levels. In other embodiments, the subject stays on high dose of an anti-FcRn antibody (e.g., batoclimab at 680 mg or IMVT-1402 at 600 mg) while staying on low dose of ATD or staying off of ATD and maintains a normal level of T3 and / or T4. Accordingly, in some embodiments, the present disclosure provides a method of treating Graves’ disease (GD) in a subject that is receiving antithyroid drug (ATD) at a dose, the method comprising: (i) administering a subject with an anti-FcRn antibody at a dose in the range of 580-700 mg (e.g., batoclimab at 680 mg or IMVT-1402 at 600 mg); (ii) measuring T3 and T4 levels in the subject; (iii) decreasing the dosage of the ATD or stop the ATD if T3 and / or T4 levels are below ULN; (iii) decreasing the dosage of the anti-FcRn antibody to a dose in the rage of 280-400 mg / dose (e.g., batoclimab at 340 mg or IMVT-1402 at 300 mg); and (iv) increasing the dosage of the ATD or restarting ATD in the subject to maintain T3 and T4 levels below ULN. In some embodiments, the present disclosure provides a method of treating Graves’ disease (GD) in a subject that is receiving antithyroid drug (ATD) at a dose, the method comprising: (i) administering a subject with an anti-FcRn antibody at a dose in the range of 580-700 mg (e.g., batoclimab at 680 mg or IMVT-1402 at 600 mg); (ii) measuring T3 and T4 level in the subject; (iii) decreasing the dosage of the ATD or stop the ATD if T3 and / or T4 levels are below ULN; and (iii) maintaining the dosage of the anti-FcRn antibody (e.g., batoclimab at 680 mg or IMVT- 1402 at 600 mg) while administering the subject with low dose ATD or no ATD to maintain T3 and T4 levels below ULN.

[0219] In some embodiments, administering an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) to a subject with GD improves the subject’s quality of life (QOL) score. QOL scoring includes self-assessment questionnaires that measure multiple aspects relating to quality of life, such as anxiety, cognitive problems, composite QOL, cosmetic complaints, depression (depressivity), emotional susceptibility, eye symptoms, goiter symptoms, hyperthyroid symptoms, hypothyroid symptoms, impaired daily life, overall QOL, social impairment, tiredness. Item responses in assessing QQL are scored as: 0 = “Not at all”; 1 = “A little”; 2 = “Some”; 3 = “Quite a bit”; and 4 = “Very much / Completely”. An exemplary questionnaire to assess QOL in a subject having GD is the ThyPRO (thyroid- related patient-reported outcome) 39Scale (see, e.g., Watt el al. Development of a short version of the Thyroid-Related Patient- Reported Outcome Thy PRO. Thyroid, 2015. 25(10): 1069-1079.)

[0220] In some embodiments, administering an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) to a subject with GD improves the subject’s anxiety score within 12 weeks and / or 24 weeks compared to the subject’s anxiety score prior to administering the anti-FcRn antibody. In some embodiments, administering an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) to a subject with GD improves the subject’s cognitive problems score within 12 weeks and / or 24 weeks compared to the subject’s cognitive problems score prior to administering the anti-FcRn antibody. In some embodiments, administering an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) to a subject with GD improves the subject’s composite QOL score within 12 weeks and / or 24 weeks compared to the subject’s composite QOL score prior to administering the anti- FcRn antibody. In some embodiments, administering an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) to a subject with GD improves the subject’s cosmetic complaints score within 12 weeks and / or 24 weeks compared to the subject’s cosmetics complaints score prior to administering the anti-FcRn antibody. In some embodiments, administering an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) to a subject with GD improves the subject’s depressivity score within 12 weeks and / or 24 weeks compared to the subject’s depressivity score prior to administering the anti-FcRn antibody. In some embodiments, administering an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) to a subject with GD improves the subject’s emotional susceptibility score within 12 weeks and / or 24 weeks compared to the subject’s emotional susceptibility score prior to administering the anti-FcRn antibody. In some embodiments, administering an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) to a subject with GD improves the subject’s eye symptoms score within 12 weeks and / or 24 weeks compared to the subject’s eye symptoms score prior to administering the anti-FcRn antibody. In some embodiments, administering an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) to a subject with GD improves the subject’s goiter symptoms score within 12 weeks and / or 24 weeks compared to the subject’s goiter symptoms score prior to administering the anti-FcRn antibody.

[0221] In some embodiments, administering an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) to a subject with GD improves the subject’s hyperthyroid symptoms score within 12 weeks and / or 24 weeks compared to the subject’s hyperthyroid symptoms score prior to administering the anti-FcRn antibody. In some embodiments, administering an anti-FcRnantibody (e.g., IMVT-1402 or batoclimab) to a subject with GD improves the subject’s hypothyroid score within 12 weeks and / or 24 weeks compared to the subject’s hypothyroid score prior to administering the anti-FcRn antibody. In some embodiments, administering an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) to a subject with GD improves the subject’s anxiety score within 12 weeks and / or 24 weeks compared to the subject’s anxiety score prior to administering the anti-FcRn antibody. In some embodiments, administering an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) to a subject with GD improves the subject’s impaired daily life score within 12 weeks and / or 24 weeks compared to the subject’s impaired daily life score prior to administering the anti-FcRn antibody. In some embodiments, administering an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) to a subject with GD improves the subject’s overall QOL score within 12 weeks and / or 24 weeks compared to the subject’s overall QOL score prior to administering the anti-FcRn antibody. In some embodiments, administering an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) to a subject with GD improves the subject’s social impairment score within 12 weeks and / or 24 weeks compared to the subject’s social impairment score prior to administering the anti-FcRn antibody. In some embodiments, administering an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) to a subject with GD improves the subject’s tiredness score within 12 weeks and / or 24 weeks compared to the subject’s tiredness score prior to administering the anti-FcRn antibody.

[0222] In some embodiments, administering an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) to a subject with GD improves the subject’s anxiety score, cognitive problems score, composite QOL score, cosmetic complains score, depressivity score, emotional susceptibility score, eye symptoms score, goiter symptoms score, hyperthyroid symptoms score, hypothyroid symptoms score, impaired daily life score, overall QOL score, social impairment sore, and / or tiredness score compared to the corresponding score prior to administering the anti-FcRn antibody within 12 weeks and / or 24 weeks.

[0223] In some embodiments, a subject that showed improved QQL score described herein is euthyroid and no longer receiving ATD following or during administration of an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab). In some embodiments, a subject that showed improved QQL score described herein is euthyroid and still receiving ATD following or during administration of an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab).Dosing Regimen for Rheumatoid Arthritis (RA)

[0224] Rheumatoid arthritis (RA) is a chronic autoimmune disease that causes inflammation in the joints. In some instances, RA can cause inflammation in the lungs, eyes, mouth, and skin. RA has an estimated worldwide prevalence of 0.5% to 1.0% of the population. Symptoms of RA include joint pain, stiffness, and swelling of the large and small joints. The pathophysiology of RA involves chronic inflammation of the synovial membrane, which can destroy articular cartilage and juxta-articular bone. If RA is left untreated or inadequately treated, RA can cause joint destruction with severe disability, poor quality of life, and premature mortality.

[0225] Autoantibodies are detected in approximately 70% to 80% of RA patients and include rheumatoid factor (RF) and anti-citrullinated protein autoantibodies (ACPA). RF is defined as autoantibodies against the Fc portion of IgG and, despite their name, are not exclusive to RA and can be found in other disease conditions. RF is found in multiple Ig isotypes (IgM, IgG, and IgA), and all 3 isotypes are presents in over half of subjects with RA but less than 5% of healthy individuals.

[0226] Seropositive RA is associated with severe disease and poor outcomes, including increased mortality. Seropositivity for both RF and ACPA has an amplifying effect on disease and results in an aggressive phenotype including severe extra-articular manifestations.Additionally, seropositivity for both RF and ACPA, as well as high disease activity at baseline and pulmonary involvement, is associated with difficult-to-treat (D2T) RA. High affinity and high titer of IgG RF in RA synovial fluid are believed to potentiate inflammation and antigen trapping in joints by forming IgG-IC complexes, activating complement, and causing leukocyte (immune cell) infiltration. Accordingly, treatment of subjects suffering from RA, and especially seropositive RA, with an anti-FcRn therapy ( .g., batoclimab or IMVT-1402) described herein, can ameliorate or prevent progression of symptoms, by decreasing the half-life of destructive autoantibodies in the subject’s system.

[0227] Criteria for determining whether a subject has RA have been laid out according to the American College of Rheumatology (ACR) / European League Against Rheumatism Collaborative Initiative (EULAR) (Aletaha et al., Rheumatoid arthritis classification criteria: an American College of Rheumatology / European League Against Rheumatism collaborative initiative. Arthritis Rheum, 2010. 62(9): 2569-2581). The criteria for definite RA is based on: synovitis in at least 1 joint, absence of an alternative diagnosis that explains the synovitis, andachievement of a total score of > 6 from individual scores in 4 domains including number and site of involved joints (0-5), serological abnormality (0-3), elevated acute-phase response (0-1), and symptom duration (2 levels, score range 0-1).

[0228] In some embodiments, an anti-FcRn therapy (e.g., batoclimab or IMVT-1402) is administered to a subject having RA to treat or ameliorate symptoms thereof. In some embodiments, the present disclosure provides compositions (e.g., IMVT-1402 or batoclimab) and methods (e.g., dosing regimens) for treating RA in a subject.

[0229] In some embodiments, a subject having RA is administered with an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) at a range of 550-700 mg once weekly.

[0230] In some embodiments, a subject having RA is administered an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) at a range of 550-700 mg, 550-690 mg, 550-680 mg, 550-670 mg, 550-660 mg, 550-650 mg, 550-640 mg, 550-630 mg, 550-620 mg, 550-610 mg, 550-600 mg, 550-590 mg, 550-580 mg, 550-570 mg, 550-560 mg, 580-700 mg, 580-690 mg, 580-680 mg, 580-670 mg, 580-660 mg, 580-650 mg, 580-640 mg, 580-630 mg, 580-620 mg, 580-610 mg, 580-600 mg, 580-590 mg, 600-700 mg, 600-690 mg, 600-680 mg, 600-670 mg, 600-660 mg, 600-650 mg, 600-640 mg, 600-630 mg, 600-620 mg, 600-610 mg, 620-700 mg, 620-690 mg, 620-680 mg, 620-670 mg, 620-660 mg, 620-650 mg, 620-640 mg, 620-630 mg, 650-700 mg, 650-690 mg, 650-680 mg, 650-670 mg, 650-660 mg, 680-700 mg, or 680-690 mg once weekly.

[0231] In some embodiments, a subject is administered an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) at a range of 550-700 mg once weekly for at least 16 weeks (e.g., at least 16 weeks, at least 17 weeks, at least 18 weeks, at least 19 weeks, at least 20 weeks, at least 21 weeks, at least 22 weeks, at least 23 weeks, at least 24 weeks, at least 25 weeks, at least 25 weeks, at least 27 weeks, at least 28 weeks, at least 29 weeks, at least 30 weeks, at least 31 weeks, at least 32 weeks, at least 33 weeks, at least 34 weeks, at least 35 weeks, at least 36 weeks, at least 37 weeks, at least 38 weeks, at least 39 weeks, at least 40 weeks, or more). In some embodiments, a subject with RA is administered an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) at a range of 550-700 mg once weekly indefinitely. In some embodiments, a subject with RA is administered an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) at 300 mg or 340 mg once weekly indefinitely. In some embodiments, a subject with RA is administered an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab at 600 mg or 680 mg once weekly indefinitely. In some embodiments, a subject with RA is administered IMVT-1402 at 300mg once weekly indefinitely. In some embodiments, a subject with RA is administered IMVT- 1402 at 600 mg once weekly indefinitely. In some embodiments, a subject with RA is administered batoclimab at 340 mg once weekly indefinitely. In some embodiments, a subject with RA is administered batoclimab at 680 mg once weekly indefinitely.

[0232] In some embodiments, a subject with RA is administered IMVT-1402. In some embodiments, the subject with RA is administered IMVT-1402 at 600 mg once weekly for 16 weeks. In some embodiments, after the initial 16-week administration, the subject continues to receive IMVT-1402 at 600 mg once weekly. In some embodiments, after the initial 16-week administration, the subject is subsequently administered 300 mg IMVT-1402 once weekly.

[0233] In some embodiments, a subject with RA has active RA. In some embodiments, a subject with RA has refractory RA. A subject having refractory RA is a subject that, despite the availability of advanced therapies and having been exposed to multiple disease-modifying antirheumatic drugs (DMARDs), does not benefit from such treatment. Such subjects are variously designated as having “difficult-to-treat (D2T) RA”, “treatment-resistant RA”, or “refractory RA”. In some embodiments, refractory RA is defined by the following criteria: (i) 1 Treatment according to EULAR recommendations and failure of >2 b / tsDMARDs (with different mechanisms of action) after failing csDMARD therapy (unless contraindicated); (ii). Signs suggestive of active / progressive disease, defined as at least one of: a. At least moderate disease activity (according to validated composite measures including joint counts, for example, DAS28-ESR >3.2 or CD Al >10); b. Signs (including acute phase reactants and imaging) and / or symptoms suggestive of active disease (joint related or other); c. Inability to taper glucocorticoid treatment (below 7.5 mg / day prednisone or equivalent); d. Rapid radiographic progression (with or without signs of active disease) as indicated by change in van der Heijde-modified Sharp score >5 points at 1 year; e. Well-controlled disease according to above standards, but still having RA symptoms that are causing a reduction in quality of life; (iii). The management of signs and / or symptoms is perceived as problematic by the rheumatologist and / or the subject.

[0234] In some embodiments, the subject with RA is positive for RF. In some embodiments, the subject is positive for IgG or IgA RF in RA synovial fluid. In some embodiments, the subject has a baseline RF level higher than 25U / ml, higher than 30U / ml, higher than 35U / ml, higher than 40U / ml, higher than 45U / ml, higher than 50U / ml, higher than 55U / ml, higher than 60U / ml, higher than 65U / ml, higher than 70U / ml, higher than 75U / ml, higher than 80U / ml, higher than85U / ml, higher than 90U / ml, higher than 95U / ml, higher than lOOU / ml, higher than 120U / ml, higher than 150U / ml, higher than 180U / ml, higher than 200U / ml, higher than 250U / ml, higher than 300U / ml, higher than 350U / ml, higher than 400U / ml, higher than 450U / ml, higher than 500U / ml, or higher. In some embodiments, the subject has a baseline RF level in the range of 25- 500 U / ml, 25-450 U / ml, 25-400 U / ml, 25-350 U / ml, 25-300 U / ml, 25-250 U / ml, 25-200 U / ml, 25-150 U / ml, 25-100 U / ml, 25-75 U / ml, 25-50 U / ml, 50-500 U / ml, 50-450 U / ml, 50-400 U / ml, 50-350 U / ml, 50-300 U / ml, 50-250 U / ml, 50-200 U / ml, 50-150 U / ml, 50-100 U / ml, 50-75 U / ml, 100-500 U / ml, 100-450 U / ml, 100-400 U / ml, 100-350 U / ml, 100-300 U / ml, 100-250 U / ml, 100- 200 U / ml, 100-150 U / ml, 150-500 U / ml, 150-450 U / ml, 150-400 U / ml, 150-350 U / ml, 150-300 U / ml, 150-250 U / ml, 150-200 U / ml, 200-500 U / ml, 200-450 U / ml, 200-400 U / ml, 200-350 U / ml, 200-300 U / ml, 200-250 U / ml, 250-500 U / ml, 250-450 U / ml, 250-400 U / ml, 250-350 U / ml, 250-300 U / ml, 300-500 U / ml, 300-450 U / ml, 300-400 U / ml, 300-350 U / ml, 400-500 U / ml, 400-450 U / ml, or 450-500 U / ml.

[0235] In some embodiments, a subject with RA has at least 6 / 68 (e.g., at least 7 / 68, at least 10 / 68, at least 15 / 68, at least 20 / 68, at least 25 / 68, at least 30 / 68, at least 35 / 68, at least 40 / 68, at least 45 / 68, at least 50 / 68, at least 55 / 68, at least 60 / 68, at least 65 / 68, or 68 / 68) tender / painful joints (TJC) at a baseline.

[0236] In some embodiments, a subject with RA has at least 6 / 66 (e.g., at least 6 / 66, at least 7 / 66, at least 10 / 66, at least 15 / 66, at least 20 / 66, at least 25 / 66, at least 30 / 66, at least 35 / 66, at least 40 / 66, at least 45 / 66, at least 50 / 66, at least 55 / 66, at least 60 / 66, at least 65 / 66, or 66 / 66) swollen joints (SJC) at a baseline.

[0237] In some embodiments, a subject with RA has a baseline Disease Activity Score of 28 using C-reactive protein (DAS28-CRP > 4.1).

[0238] In some embodiments, a subject with RA has an inadequate response to 2-3 classes of biologic and targeted synthetic DMARDs (b / tsDMARDs). In some embodiments, a subject with RA has been treated with a biologic TNFa inhibitor (e.g., infliximab, certolizumab, golimumab, etanercept, or adalimumab) and were intolerant to or experienced insufficient efficacy (including loss of efficacy) at a dose and duration. In some embodiments, a subject has been treated with a JAK inhibitor or at least 1 additional bDMARD other than a TNFa inhibitor and experienced insufficient efficacy (including loss of efficacy) at a dose and duration. In some embodiments, the subject has not had an inadequate response to rituximab. In some embodiments, a subjectwith RA has regular use of at least 1 cDMARD (e.g., MTX, hydroxychloroquine, and / or sulfasalazine) for > 12 weeks at baseline. In some embodiments, a subject initiating an anti-FcRn therapy (e.g., batoclimab or IMVT-1402) described herein is on MTX at a stable, unchanging oral dose of 15 to 25 mg / week (e.g., for at least the 8 weeks prior to the administration).

[0239] In some embodiments, a subject with RA has not been on more than three DMARDs prior to administration. In some embodiments, a subject with RA is not receiving glucocorticoids at doses > 10 mg / day. In some embodiments, a subject with RA has not had 3 or more joints injected with intraarticular glucocorticoids. In some embodiments, a subject with RA has not received any parenteral glucocorticoid administered by intramuscular (IM) or intravenous (IV) injection. In some embodiments, a subject with RA is not anticipated to require parenteral injection of glucocorticoids while receiving an anti-FcRn therapy (e.g., batoclimab or IMVT- 1402) described herein. In some embodiments, a subject with RA has not received rituximab and experienced insufficient efficacy (including loss of efficacy). In some embodiments, a subject with RA has not had an inadequate response to more than 3 b / tsDMARDs of differing mechanisms of action as treatment for RA. In some embodiments, a subject with RA has not started treatment with NSAIDS, for which the NSAID use is intended for treatment of signs and symptoms of RA) within 2 weeks of initiating an anti-FcRn therapy (e.g., batoclimab or IMVT- 1402) described herein or within 6 weeks of a baseline assessment. In some embodiments, a subject with RA does not have Felty’s syndrome.

[0240] In some embodiments, administration of an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) dosing regimen described herein decreases the RF level in the subject (e.g., relative to baseline RF level prior to the administration) by at least at least 1%, at least 5%, at least 10%, at least 15%, at least 20%, at least 25%, at least 30%, at least 35%, at least 40%, at least 45%, at least 50%, at least 55%, at least 60%, at least 65%, at least 70%, at least 75%, at least 80%, at least 85%, at least 90%, at least 95%, at least 96%, at least 97%, at least 98%, at least 99%, or 100%. administration of an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) dosing regimen described herein decreases the RF level in the subject (e.g., relative to baseline RF level prior to the administration) by between 1% and 100%, between 5% and 100%, between 5% and 90%, between 5% and 80%, between 5% and 70%, between 5% and 60%, between 5% and 50%, between 5% and 40%, between 5% and 30%, between 5% and 20%, between 5% and 15%, between 10% and 100%, between 10% and 90%, between 10% and 80%, between 10% and70%, between 10% and 60%, between 10% and 50%, between 10% and 40%, between 10% and 30%, between 10% and 20%, between 10% and 15%, between 20% and 100%, between 20% and 90%, between 20% and 80%, between 20% and 70%, between 20% and 60%, between 20% and 50%, between 20% and 40%, between 20% and 30%, between 30% and 100%, between 30% and 90%, between 30% and 80%, between 30% and 70%, between 30% and 60%, between 30% and 50%, between 30% and 40%, between 40% and 100%, between 40% and 90%, between 40% and 80%, between 40% and 70%, between 40% and 60%, between 40% and 50%, between 50% and 100%, between 50% and 90%, between 50% and 80%, between 50% and 70%, between 50% and 60%, between 60% and 100%, between 60% and 90%, between 60% and 80%, between 60% and 70%, between 70% and 100%, between 70% and 90%, between 70% and 80%, between 80% and 100%, between 80% and 90%, or between 90% and 100%.

[0241] In some embodiments, administration of an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) dosing regimen described herein decreases the ACAP level in the subject (e.g., relative to baseline ACAP level prior to the administration) by at least at least 1%, at least 5%, at least 10%, at least 15%, at least 20%, at least 25%, at least 30%, at least 35%, at least 40%, at least 45%, at least 50%, at least 55%, at least 60%, at least 65%, at least 70%, at least 75%, at least 80%, at least 85%, at least 90%, at least 95%, at least 96%, at least 97%, at least 98%, at least 99%, or 100%. administration of an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) dosing regimen described herein decreases the ACAP level in the subject (e.g., relative to baseline ACAP level prior to the administration) by between 1% and 100%, between 5% and 100%, between 5% and 90%, between 5% and 80%, between 5% and 70%, between 5% and 60%, between 5% and 50%, between 5% and 40%, between 5% and 30%, between 5% and 20%, between 5% and 15%, between 10% and 100%, between 10% and 90%, between 10% and 80%, between 10% and 70%, between 10% and 60%, between 10% and 50%, between 10% and 40%, between 10% and 30%, between 10% and 20%, between 10% and 15%, between 20% and 100%, between 20% and 90%, between 20% and 80%, between 20% and 70%, between 20% and 60%, between 20% and 50%, between 20% and 40%, between 20% and 30%, between 30% and 100%, between 30% and 90%, between 30% and 80%, between 30% and 70%, between 30% and 60%, between 30% and 50%, between 30% and 40%, between 40% and 100%, between 40% and 90%, between 40% and 80%, between 40% and 70%, between 40% and 60%, between 40% and 50%, between 50% and 100%, between 50% and 90%, between 50% and80%, between 50% and 70%, between 50% and 60%, between 60% and 100%, between 60% and 90%, between 60% and 80%, between 60% and 70%, between 70% and 100%, between 70% and 90%, between 70% and 80%, between 80% and 100%, between 80% and 90%, or between 90% and 100%.

[0242] In some embodiments, a subject administered an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) dosing regimen described herein achieves ACR20 response at week 14, 16, or 32 of administration. In some embodiments, administration of an anti-FcRn antibody (e.g., IMVT- 1402 or batoclimab) dosing regimen described herein improves TJC68 by at least 20%, at least 25%, at least 30%, at least 35%, at least 40%, at least 45%, at least 50%, at least 55%, at least 60%, at least 65%, at least 70%, at least 75%, at least 80%, at least 85%, at least 90%, at least 95%, at least 96%, at least 97%, at least 98%, at least 99%, or 100% relative to baseline TJC68. In some embodiments, administration of an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) dosing regimen described herein improves SJC66 by at least 20%, at least 25%, at least 30%, at least 35%, at least 40%, at least 45%, at least 50%, at least 55%, at least 60%, at least 65%, at least 70%, at least 75%, at least 80%, at least 85%, at least 90%, at least 95%, at least 96%, at least 97%, at least 98%, at least 99%, or 100% relative to baseline SJC66.

[0243] In some embodiments, administration of an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) dosing regimen described herein improves at least 3 of the following parameters by at least 20% (e.g., at least 20%, at least 25%, at least 30%, at least 35%, at least 40%, at least 45%, at least 50%, at least 55%, at least 60%, at least 65%, at least 70%, at least 75%, at least 80%, at least 85%, at least 90%, at least 95%, at least 96%, at least 97%, at least 98%, at least 99%, or 100%) relative to their respective baseline level: (i) Physician's Global Assessment of Disease Activity (PhGA); (ii) Patient's Global Assessment of Disease Activity (PtGA); (iii) Patient’s Assessment of Pain (100 mm VAS); (iv) Health Assessment Questionnaire - Disability Index (HAQ-DI); and (v) High-sensitivity C-reactive protein (hsCRP).

[0244] In some embodiments, a subject with RA administered an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) dosing regimen described herein has change in achieves ACR20 response at week 14-16, and CD Al score from week 16 to 32 of administration. In some embodiments, a subject with RA administered an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) dosing regimen described herein has achieves ACR20 response at week 14-16, and change in SDAI score from week 16 to 32 of administration.

[0245] Subjects suffering from RA may occasionally suffer RA flare-ups, in which symptoms worsen or new symptoms appear. An RA flare can involve the exacerbation of any symptom but most commonly involves intense pain and stiffness in the joints. Aside from worsening of joint- related symptoms, RA flare-ups may cause fatigue, weight loss, fever, total-body pain, inflammatory nodules under the skin, rashes, dry eyes, and / or flu-like symptoms. Less common symptoms of RA flare-ups can include hearing problems such as tinnitus, difficulty breathing, numbness and tingling, disrupted sleep, and gastrointestinal problems. RA flares typically last about 3 days, but may last longer or resolve sooner. In some embodiments, an anti-FcRn therapy (e.g., batoclimab or IMVT-1402) described herein prevents or ameliorates an RA flare-up.Dosing Regimen for Myasthenia Gravis (MG)

[0246] In some aspects, the present disclosure provides compositions and methods for treating myasthenia graves (MG). In some embodiments, the method comprises a dosing regiment (e.g., dose, dosing frequency, etc.) for MG that improves the efficacy of the treatment (e.g., relative to using a different dosing regimen) for MG.

[0247] Myasthenia gravis (MG) is a rare, potentially fatal chronic autoimmune neuromuscular disease caused by autoantibodies directed against the postsynaptic muscle membrane at the neuromuscular junction, which leads to muscle weakness and fatigability. There are 2 peaks of incidence: early-onset MG in the third decade (mostly females) and late-onset MG in the elderly (mostly males). Depending on the geographic region, the prevalence of MG ranges between 2.19 to 36.71 cases / 100,000 population.

[0248] Most patients with MG present with unilateral or bilateral involvement of the muscles that control eye and eyelid movement, as they are particularly susceptible to weakness (i.e., ocular myasthenia gravis, oMG). Typical symptoms of oMG include intermittent drooping of the upper eyelid (ptosis) and double vision (diplopia). In approximately 80% of patients, oMG precedes the more severe generalized myasthenia gravis (gMG), in which involvement of bulbar, axial, limb, and / or respiratory muscles controlling chewing, talking, and swallowing are frequently affected. If patients have restricted ocular disease for 2 years without developing gMG, they are not likely to develop it later.

[0249] The diagnosis of MG is confirmed by the combination of relevant signs and symptoms and a positive test for specific autoantibodies. Autoantibody specificity and clinical manifestations characterize different subgroups of MG. Approximately 80% of patients with MGhave detectable immunoglobulin G1 (IgGl) and immunoglobulin G3 (IgG3) subclass antibodies against the acetylcholine receptor (AChR) expressed on the muscle membrane (“anti-AChR+”). Autoantibody binding to AChR can have multiple effects, including activation of the complement cascade, which leads to formation of the membrane attack complex and damage of the postsynaptic membrane.

[0250] Muscle-specific kinase (MuSK), in conjunction with lipoprotein receptor-related protein 4 (LRP4), is responsible for AChR clustering and maintenance of the neuromuscular junction. Autoantibodies to MuSK are detected in approximately 1% to 10% of patients and are immunoglobulin G4 (IgG4) subclass autoantibodies (“anti-MuSK+”). Therefore, they cannot activate the complement cascade but instead exert their pathogenicity through blocking the interaction between MuSK and LRP4 that is required for the clustering of AChR. In patients with anti-MuSK+ MG, concentrations of anti-MuSK tend to correlate with disease severity, and changes in antibody concentration over time can reflect disease activity.

[0251] Antibodies to LRP4 are detected in 1% to 5% of patients with MG of any type and in 7% to 33% of patients without AChR and MuSK antibodies (“anti-LRP4+”). Autoantibodies to LRP4 are IgGl subclass, and their predominant pathogenic mechanism of action is through the activation of the complement cascade. Patients without detectable antibodies against any of these 3 antigens are referred to as seronegative (10% to 15% of patients with MG). Diagnosis of MG in seronegative patients is based on a thorough clinical examination and neurophysiological testing.

[0252] The primary objective of treatment is to improve functional ability and quality of life by minimizing the severity of MG symptoms to the point of minimal manifestations, while also avoiding considerable drug-induced adverse effects. Treatment should be tailored to the individual patient depending on their MG subgroup. Cholinesterase inhibitors, such as pyridostigmine, prevent the degradation of acetylcholine and thus increase its availability at the neuromuscular junction, which improves neuromuscular transmission and symptoms, particularly for anti-AChR+ patients. For patients who do not adequately respond to symptomatic therapy, immunosuppressive therapy can lead to improvement. Glucocorticoids are the first-line immunosuppressant; however, nonsteroidal immunosuppressive agents can be used (e.g., azathioprine, cyclosporine, mycophenolate mofetil, methotrexate, rituximab, and tacrolimus). Plasma exchange (PLEX) and intravenous immunoglobulin (IVIg) are fast-actingtreatments and are typically used in patients with acute, severe MG when a rapid response is crucial. As their effect is short-lived (4 to 12 weeks), additional immunotherapy is usually needed.

[0253] The treatment paradigm for managing MG is evolving with the introduction of new therapies. For anti-AChR+ patients, complement inhibitors (e.g., eculizumab, ravulizumab, zilucoplan) that prevent the formation of the membrane attack complex have demonstrated clinical efficacy and have been approved by the United States (US) Food and Drug Administration (FDA). Reducing the levels of pathogenic immunoglobulin G (IgG) autoantibodies in gMG is associated with a clinical benefit based on data from IVIg, rituximab, and neonatal fragment crystallizable receptor (FcRn) blockers. For efgartigimod and rozanolixizumab, which are FcRn blockers, reductions in pathogenic autoantibodies ranged from 40% to 70%, depending on the study and treatment duration, and both have been approved by the US FDA for the treatment of gMG. Additional FcRn blockers are in clinical development; for example, nipocalimab and batoclimab. The emergence of new therapies has the potential to revolutionize the treatment of MG.

[0254] The current immunomodulating therapies have improved the prognosis for patients with MG. However, high doses of corticosteroids are typically necessary to achieve improvement or remission, and long-term treatment with corticosteroids and other immunosuppressive therapies is often necessary. Complement inhibitors have a significant risk of meningococcal meningitis and require vaccination prior to initiation of therapy and careful monitoring. Additionally, patients who are not included in the approved indication populations (anti-AChR+ or anti- MuSK+), such as the 10% to 15% of seronegative patients with MG cannot access such treatments.

[0255] There are widespread and significant negative effects on quality of life, including daily activities such as eating, walking, and speaking, for patients with gMG. Overall, the persistent muscle weakness associated with gMG often negatively interferes with patients’ ability to engage in daily activities, including demands of work, family, social functions, and physical activities.

[0256] Despite chronic immunosuppressive therapies, patients with gMG can have acute exacerbations of disease. Within the first 2 years after diagnosis of MG, approximately 15% to 20% of patients with MG develop a potentially life-threatening myasthenic crisis that requiresmechanical ventilation and extended intensive care management. Hospitalization rates average an annualized rate of 4.4% for acute exacerbation of disease and 6.8% for myasthenic crisis. The average length of a hospital stay ranges from 11.3 to 13.1 days for acute exacerbation, but it may be considerably longer for crisis admissions. A myasthenic crisis is associated with an in-hospital mortality rate of 5% to 12%, even with established critical care protocols. The most common causes of death are multiorgan failure due to sepsis and respiratory failure. Therefore, there remains an unmet need for a more efficacious treatment that can be safely administered on a chronic basis and can achieve benefit more quickly to protect against risk of precipitous physical decline.

[0257] Accordingly, treatment of subjects suffering from MG, and especially seropositive MG, with an anti-FcRn therapy (e.g., batoclimab or IMVT-1402) described herein, can ameliorate or prevent progression of symptoms, by decreasing the half-life of destructive autoantibodies in the subject’s system.

[0258] Criteria for determining whether a subject has MG and the severity of the MG, divided into classes I-V, have been laid out according to the Myasthenia Gravis Foundation of America (MGFA) (Jaretzki et al., Myasthenia gravis: recommendations for clinical research standards. Nurology, 2000. 55(1): 16-23). The classes and respective criteria for MG are:

[0259] Class I: Any ocular muscle weakness; may have weakness of eye closure. All other muscle strength is normal.

[0260] Class II: Mild weakness affecting muscles other than ocular muscles; may also have ocular muscle weakness of any severity.

[0261] Ila. Predominantly affecting limb, axial muscles, or both. May also have lesser

[0262] involvement of oropharyngeal muscles.

[0263] lib. Predominantly affecting oropharyngeal, respiratory muscles, or both. May also have lesser or equal involvement of limb, axial muscles, or both.

[0264] Class III: Moderate weakness affecting muscles other than ocular muscles; may also have ocular muscle weakness of any severity.

[0265] Illa. Predominantly affecting limb, axial muscles, or both. May also have lesser

[0266] involvement of oropharyngeal muscles.

[0267] Illb. Predominantly affecting oropharyngeal, respiratory muscles, or both. May also have lesser or equal involvement of limb, axial muscles, or both.

[0268] Class IV: Severe weakness affecting muscles other than ocular muscles; may also have ocular muscle weakness of any severity.

[0269] IVa. Predominantly affecting limb, axial muscles, or both. May also have lesser

[0270] involvement of oropharyngeal muscles.

[0271] IVb. Predominantly affecting oropharyngeal, respiratory muscles, or both. May also have lesser or equal involvement of limb, axial muscles, or both.

[0272] Class V: Defined as intubation, with or without mechanical ventilation, except when employed during routine postoperative management. The use of a feeding tube without intubation places the patient in class IVb.

[0273] In some embodiments, an anti-FcRn therapy (e.g., batoclimab or IMVT-1402) is administered to a subject having MG to treat or ameliorate symptoms thereof. In some embodiments, the present disclosure provides compositions (e.g., IMVT-1402 or batoclimab) and methods (e.g., dosing regimens) for treating MG in a subject.

[0274] In some embodiments, a subject having MG is administered an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) at a range of 550-700 mg once weekly.

[0275] In some embodiments, a subject having MG is administered an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) at a range of 550-700 mg, 550-690 mg, 550-680 mg, 550-670 mg, 550-660 mg, 550-650 mg, 550-640 mg, 550-630 mg, 550-620 mg, 550-610 mg, 550-600 mg,550-590 mg, 550-580 mg, 550-570 mg, 550-560 mg, 580-700 mg, 580-690 mg, 580-680 mg,580-670 mg, 580-660 mg, 580-650 mg, 580-640 mg, 580-630 mg, 580-620 mg, 580-610 mg,580-600 mg, 580-590 mg, 600-700 mg, 600-690 mg, 600-680 mg, 600-670 mg, 600-660 mg,600-650 mg, 600-640 mg, 600-630 mg, 600-620 mg, 600-610 mg, 620-700 mg, 620-690 mg,620-680 mg, 620-670 mg, 620-660 mg, 620-650 mg, 620-640 mg, 620-630 mg, 650-700 mg,650-690 mg, 650-680 mg, 650-670 mg, 650-660 mg, 680-700 mg, or 680-690 mg once weekly.

[0276] In some embodiments, a subject is administered an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) at a range of 550-700 mg once weekly for at least 12 weeks (e.g., at least 12 weeks, at least 13 weeks, at least 14 weeks, at least 16 weeks, at least 17 weeks, at least 18 weeks, at least 19 weeks, at least 20 weeks, at least 21 weeks, at least 22 weeks, at least 23 weeks, at least 24 weeks, at least 25 weeks, at least 25 weeks, at least 27 weeks, at least 28 weeks, at least 29 weeks, at least 30 weeks, at least 31 weeks, at least 32 weeks, at least 33 weeks, at least 34 weeks, at least 35 weeks, at least 36 weeks, at least 37 weeks, at least 38weeks, at least 39 weeks, at least 40 weeks, or more). In some embodiments, a subject with MG is administered an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) at a range of 550-700 mg once weekly indefinitely. In some embodiments, a subject is administered an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) at 600 mg or 680 mg once weekly for 12 weeks. In some embodiments, a subject with MG is administered an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) at 300 mg or 340 mg once weekly indefinitely. In some embodiments, a subject with MG is administered an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) at 600 mg once weekly indefinitely. In some embodiments, a subject with MG is administered IMVT-1402 at 300 mg once weekly indefinitely. In some embodiments, a subject with MG is administered IMVT-1402 at 600 mg once weekly indefinitely. In some embodiments, a subject with MG is administered batoclimab at 340 mg once weekly indefinitely. In some embodiments, a subject with MG is administered batoclimab at 680 mg once weekly indefinitely.

[0277] In some embodiments, a subject with MG is administered IMVT-1402. In some embodiments, the subject with MG is administered IMVT-1402 at 600 mg once weekly for 12 weeks. In some embodiments, after the initial 12-week administration, the subject continues to receive IMVT-1402 at 600 mg once weekly. In some embodiments, after the initial 12-week administration, the subject is subsequently administered 300 mg IMVT-1402 once weekly.

[0278] In some embodiments, a subject with MG has mild to severe MG of Class I, II, III, or IV at an initial screening visit. In some embodiments, for a subject with MG of Class I, duration of disease is no more than 2 years (e.g., the subject has not had MG of Class I for greater than 2 years). In some embodiments, a subject with MG has diagnostic autoantibody confirmation of MG at an initial screening visit, wherein the autoantibodies include anti-AChR autoantibodies, anti-MuSK autoantibodies, and / or anti-LRP4 autoantibodies. In some embodiments, a subject with MG who is seronegative to known antibodies has a history of abnormal neuromuscular transmission test demonstrated by single-fiber electromyography or repetitive nerve stimulation and one of: (i) a history of positive edrophonium chloride test; and / or (ii) demonstrate improvement in MG signs on oral cholinesterase inhibitors, IVIg, or PLEX as assessed by a physician. In some embodiments, a subject with MG has a MG-ADL score of > 5 at an initial screening visit and a baseline visit (e.g., day 1 of treatment with an anti-FcRn antibody). In some embodiments, a subject with MG has a quantitative myasthenia gravis (QMG) score of > 11 at an initial screening visit and a baseline visit (e.g., day 1 of treatment with an anti-FcRn antibody). Insome embodiments, a subject with MG of Class I does not have a QMG score of > 11 at an initial screening visit and a baseline visit (e.g., day 1 of treatment with an anti-FcRn antibody). In some embodiments, a subject with MG has been treated or is being treated with one or more of:

[0279] (a) corticosteroids and / or cholinesterase inhibitors, providing the following circumstances are met:

[0280] (i) corticosteroids: stable dose of < 30 mg of prednisone weekly (QD) or equivalent for > 6 weeks before an initial screening visit, within which changes to the dosage regimen are permitted as follows:

[0281] (1) for participants receiving < 15 mg of prednisone QD or equivalent, excursions in the daily dose of < 2.5 mg or equivalent are permitted once; and

[0282] (2) for participants receiving > 15 mg to < 30 mg of prednisone QD or equivalent, excursions in the daily dose of < 5 mg or equivalent are permitted once;

[0283] (ii) cholinesterase inhibitors: stable dose (no change) for > 4 weeks before an initial screening visit; and / or

[0284] (b) nonsteroidal immunosuppressants: use of up to one of the following medications that meet the below criteria:

[0285] (i) methotrexate, azathioprine, or my cophenolate mofetil use < 6 months or > 18 months prior to an initial screening visit with no dose adjustments for > 3 months; and

[0286] (ii) cyclosporine, cyclophosphamide, or tacrolimus use for > 5 months prior to an initial screening visit with no dose adjustments for > 3 months.

[0287] In some embodiments, administration of an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) dosing regimen described herein decreases anti-AChR autoantibody levels in the subject (e.g., relative to baseline anti-AChR autoantibody levels prior to the administration) by at least at least 1%, at least 5%, at least 10%, at least 15%, at least 20%, at least 25%, at least 30%, at least 35%, at least 40%, at least 45%, at least 50%, at least 55%, at least 60%, at least 65%, at least 70%, at least 75%, at least 80%, at least 85%, at least 90%, at least 95%, at least 96%, at least 97%, at least 98%, at least 99%, or 100%. administration of an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) dosing regimen described herein decreases anti-AChR autoantibody levels in the subject (e.g., relative to baseline anti-AChR autoantibody levels prior to the administration) by between 1% and 100%, between 5% and 100%, between 5% and 90%, between 5% and 80%, between 5% and 70%, between 5% and 60%, between 5% and 50%,between 5% and 40%, between 5% and 30%, between 5% and 20%, between 5% and 15%, between 10% and 100%, between 10% and 90%, between 10% and 80%, between 10% and 70%, between 10% and 60%, between 10% and 50%, between 10% and 40%, between 10% and 30%, between 10% and 20%, between 10% and 15%, between 20% and 100%, between 20% and 90%, between 20% and 80%, between 20% and 70%, between 20% and 60%, between 20% and 50%, between 20% and 40%, between 20% and 30%, between 30% and 100%, between 30% and 90%, between 30% and 80%, between 30% and 70%, between 30% and 60%, between 30% and 50%, between 30% and 40%, between 40% and 100%, between 40% and 90%, between 40% and 80%, between 40% and 70%, between 40% and 60%, between 40% and 50%, between 50% and 100%, between 50% and 90%, between 50% and 80%, between 50% and 70%, between 50% and 60%, between 60% and 100%, between 60% and 90%, between 60% and 80%, between 60% and 70%, between 70% and 100%, between 70% and 90%, between 70% and 80%, between 80% and 100%, between 80% and 90%, or between 90% and 100%.

[0288] In some embodiments, administration of an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) dosing regimen described herein decreases anti-MuSK autoantibody levels in the subject (e.g., relative to baseline anti-MuSK autoantibody levels prior to the administration) by at least at least 1%, at least 5%, at least 10%, at least 15%, at least 20%, at least 25%, at least 30%, at least 35%, at least 40%, at least 45%, at least 50%, at least 55%, at least 60%, at least 65%, at least 70%, at least 75%, at least 80%, at least 85%, at least 90%, at least 95%, at least 96%, at least 97%, at least 98%, at least 99%, or 100%. administration of an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) dosing regimen described herein decreases anti-MuSK autoantibody levels in the subject (e.g., relative to baseline anti-MuSK autoantibody levels prior to the administration) by between 1% and 100%, between 5% and 100%, between 5% and 90%, between 5% and 80%, between 5% and 70%, between 5% and 60%, between 5% and 50%, between 5% and 40%, between 5% and 30%, between 5% and 20%, between 5% and 15%, between 10% and 100%, between 10% and 90%, between 10% and 80%, between 10% and 70%, between 10% and 60%, between 10% and 50%, between 10% and 40%, between 10% and 30%, between 10% and 20%, between 10% and 15%, between 20% and 100%, between 20% and 90%, between 20% and 80%, between 20% and 70%, between 20% and 60%, between 20% and 50%, between 20% and 40%, between 20% and 30%, between 30% and 100%, between 30% and 90%, between 30% and 80%, between 30% and 70%, between 30% and 60%, between30% and 50%, between 30% and 40%, between 40% and 100%, between 40% and 90%, between 40% and 80%, between 40% and 70%, between 40% and 60%, between 40% and 50%, between 50% and 100%, between 50% and 90%, between 50% and 80%, between 50% and 70%, between 50% and 60%, between 60% and 100%, between 60% and 90%, between 60% and 80%, between 60% and 70%, between 70% and 100%, between 70% and 90%, between 70% and 80%, between 80% and 100%, between 80% and 90%, or between 90% and 100%.

[0289] In some embodiments, administration of an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) dosing regimen described herein decreases anti-LRP4 autoantibody levels in the subject (e.g., relative to baseline anti-LRP4 autoantibody levels prior to the administration) by at least at least 1%, at least 5%, at least 10%, at least 15%, at least 20%, at least 25%, at least 30%, at least 35%, at least 40%, at least 45%, at least 50%, at least 55%, at least 60%, at least 65%, at least 70%, at least 75%, at least 80%, at least 85%, at least 90%, at least 95%, at least 96%, at least 97%, at least 98%, at least 99%, or 100%. administration of an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) dosing regimen described herein decreases anti-LRP4 autoantibody levels in the subject (e.g., relative to baseline anti-LRP4 autoantibody levels prior to the administration) by between 1% and 100%, between 5% and 100%, between 5% and 90%, between 5% and 80%, between 5% and 70%, between 5% and 60%, between 5% and 50%, between 5% and 40%, between 5% and 30%, between 5% and 20%, between 5% and 15%, between 10% and 100%, between 10% and 90%, between 10% and 80%, between 10% and 70%, between 10% and 60%, between 10% and 50%, between 10% and 40%, between 10% and 30%, between 10% and 20%, between 10% and 15%, between 20% and 100%, between 20% and 90%, between 20% and 80%, between 20% and 70%, between 20% and 60%, between 20% and 50%, between 20% and 40%, between 20% and 30%, between 30% and 100%, between 30% and 90%, between 30% and 80%, between 30% and 70%, between 30% and 60%, between 30% and 50%, between 30% and 40%, between 40% and 100%, between 40% and 90%, between 40% and 80%, between 40% and 70%, between 40% and 60%, between 40% and 50%, between 50% and 100%, between 50% and 90%, between 50% and 80%, between 50% and 70%, between 50% and 60%, between 60% and 100%, between 60% and 90%, between 60% and 80%, between 60% and 70%, between 70% and 100%, between 70% and 90%, between 70% and 80%, between 80% and 100%, between 80% and 90%, or between 90% and 100%.

[0290] In some embodiments, administration of an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) dosing regimen described herein decreases anti-AChR autoantibody levels, anti- MuSK autoantibody levels, and / or anti-LRP4 autoantibody levels in the subject (e.g., relative to baseline anti-AChR autoantibody levels, anti-MuSK autoantibody levels, and / or anti-LRP4 autoantibody levels prior to the administration) by at least at least 1%, at least 5%, at least 10%, at least 15%, at least 20%, at least 25%, at least 30%, at least 35%, at least 40%, at least 45%, at least 50%, at least 55%, at least 60%, at least 65%, at least 70%, at least 75%, at least 80%, at least 85%, at least 90%, at least 95%, at least 96%, at least 97%, at least 98%, at least 99%, or 100%. administration of an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) dosing regimen described herein decreases anti-AChR autoantibody levels, anti-MuSK autoantibody levels, and / or anti-LRP4 autoantibody levels in the subject (e.g., relative to baseline anti-AChR autoantibody levels, anti-MuSK autoantibody levels, and / or anti-LRP4 autoantibody levels prior to the administration) by between 1% and 100%, between 5% and 100%, between 5% and 90%, between 5% and 80%, between 5% and 70%, between 5% and 60%, between 5% and 50%, between 5% and 40%, between 5% and 30%, between 5% and 20%, between 5% and 15%, between 10% and 100%, between 10% and 90%, between 10% and 80%, between 10% and 70%, between 10% and 60%, between 10% and 50%, between 10% and 40%, between 10% and 30%, between 10% and 20%, between 10% and 15%, between 20% and 100%, between 20% and 90%, between 20% and 80%, between 20% and 70%, between 20% and 60%, between 20% and 50%, between 20% and 40%, between 20% and 30%, between 30% and 100%, between 30% and 90%, between 30% and 80%, between 30% and 70%, between 30% and 60%, between 30% and 50%, between 30% and 40%, between 40% and 100%, between 40% and 90%, between 40% and 80%, between 40% and 70%, between 40% and 60%, between 40% and 50%, between 50% and 100%, between 50% and 90%, between 50% and 80%, between 50% and 70%, between 50% and 60%, between 60% and 100%, between 60% and 90%, between 60% and 80%, between 60% and 70%, between 70% and 100%, between 70% and 90%, between 70% and 80%, between 80% and 100%, between 80% and 90%, or between 90% and 100%.

[0291] In some embodiments, a subject administered an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) dosing regimen described herein exhibits a change in QMG score at week 10, 12, and / or 24 of administration compared to QMG score at a baseline visit.

[0292] In some embodiments, a subject administered an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) dosing regimen described herein exhibits a change in MG-ADL (MG activities of daily living) score at week 10, 12, and / or 24 of administration compared to MG-ADL score at a baseline visit. The MG-ADL score includes scoring assessments related to talking, chewing, swallowing, breathing, brushing teeth or hair, arising from sitting, double vision, and eyelid droop. In some embodiments, a subject administered an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) dosing regimen described herein exhibits a > 2-point change in MG-ADL score at week 10, 12, and / or 24 of administration compared to MG-ADL score at a baseline visit. In some embodiments, a subject administered an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) dosing regimen described herein exhibits a MG-ADL score of 0 or 1 by week 10 or 12 of administration. In some embodiments, a subject administered an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) dosing regimen described herein exhibits a change in QOL15r score at week 10, 12, and / or 24 of administration compared to QOL15r score at a baseline visit. The myasthenia gravis QOL15r scale is a 15-item quality of life scale designed to assess aspects of a subject’s experience with MG. The QOL15r scale includes assessing the subject’s: frustration; trouble with eyes (e.g., double vision); difficult eating; limited social activity; enjoyment of hobbies or fun activities; trouble meeting the needs of family members; planning; limitations in performing work (including work at home); difficulty speaking; personal independence (e.g., driving, shopping, running errands, etc.); depression; trouble walking; getting around public places; overwhelm; and trouble performing personal grooming needs as it relates to the subject’s MG.

[0293] In some embodiments, a subject administered an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) dosing regimen described herein exhibits a change in Myasthenia Gravis Impairment Index (MGII) generalized domain score at week 10, 12, and / or 24 of administration compared to MGII generalized domain score at a baseline visit. In some embodiments, a subject administered an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) dosing regimen described herein exhibits a change in serum total IgG and IgG subclasses 1-4 at week 10, 12, and / or 24 of administration compared to serum total IgG and IgG subclasses 1-4 at a baseline visit.

[0294] Subjects suffering from MG may occasionally suffer MG flare-ups, in which symptoms worsen or new symptoms appear. An MG flare can involve the exacerbation of any symptom but most commonly involves weakness or intensified weakness in some or all muscles of the body.1MG flare-ups may also result in double vision or worsened double vision, slurred speech, increased arm weakness, falling, unsteady walking, difficulty swallowing, chronic fatigue, or trouble breathing. MG flareups last a day, with symptoms fluctuating from one day to the next, but can also last weeks or even months. In some embodiments, an anti-FcRn therapy (e.g., batoclimab or IMVT-1402) described herein prevents or ameliorates an MG flare-up.Dosing Regimen for chronic inflammatory demyelinating polyneuropathy (CIDP)

[0295] In some aspects, the present disclosure provides compositions and methods for treating chronic inflammatory demyelinating polyneuropathy (CIDP). In some embodiments, the method comprises a dosing regimen (e.g., dose, dosing frequency, etc.) for CIDP that improves the efficacy of the treatment (e.g., relative to using a different dosing regimen) for CIDP.

[0296] Chronic inflammatory demyelinating polyneuropathy (CIDP) is an acquired, immune- mediated neuropathy affecting the peripheral nerves and nerve roots. CIDP presents with symmetric involvement of both proximal and distal extremity muscle weakness. In some embodiments, CIDP is initiated by an inciting process such as molecular mimicry causes activation of autoreactive T cells. Activated T cells cross the blood-nerve barrier (BNB) via adhesion molecules and diapedesis, where they secrete metalloproteinases and pro-inflammatory cytokines that increase the permeability of the BNB and stimulate autoantibody production by plasma cells. The damaged BNB permits passage of soluble factors such as antibodies and complement as well as activated macrophages, which also release pro-inflammatory cytokines and reactive oxygen species, thus propagating the inflammatory cycle. In some conditions, upon accessing the nerve, autoantibodies can bind to neuronal proteins including myelin glycoproteins resulting in complement activation and macrophage mediated axonal degeneration and demyelination. Autoantibody induced degeneration and demyelination causes characteristic electrophysiologic alterations of the peripheral nerves (e.g., distal latency prolongation and reduced motor conduction velocity). In some embodiments, degeneration and demyelination is clinically manifested by the sensorimotor deficits in CIDP.

[0297] The diagnosis of CIDP is based on the fulfillment of both clinical criteria and electrodiagnostic criteria. Clinical criteria for typical CIDP in a subject include: (a) progressive or relapsing, symmetric, proximal, and distal muscle weakness of the upper and lower limbs as well as sensory involvement of at least two limbs; and (b) clinical course developing over at least8 weeks; with, (c) absent or reduced tendon reflexes in all limbs. In some embodiments, a subject has a CIDP variant, which presents with the clinical criteria for typical CIDP, except that tendon reflexes may be normal in unaffected limbs, and one or more of other symptoms based on the particular variant. In some embodiments, a CIDP variant is distal CIDP, which presents as distal sensory loss and muscle weakness predominantly in the lower limbs. In some embodiments, a CIDP variant is Multifocal CIDP, which presents as sensory loss and muscle weakness in a multifocal pattern, usually asymmetric, upper limb predominant. In some embodiments, a CIDP variant is focal CIDP, which presents as sensory loss and muscle weakness in only 1 limb. In some embodiments, a CIDP variant is motor CIDP, which presents as motor signs and symptoms without sensory involvement. In some embodiments, a CIDP variant is a sensory CIDP, which presents as sensory signs and symptoms without motor involvement. In addition to the clinical criteria, electrodiagnostic testing (e.g., nerve conduction studies of both sensory and motor nerves) is required to make the diagnosis, and criteria have been established that support either the diagnosis of CIDP or possible CIDP. In the event that only the “possible” level of diagnosis is achieved, then additional diagnostic testing may provide supportive evidence to confirm the diagnosis - provided at least 2 of the following criteria are met: o Study of empiric therapy: objective response on impairment and disability scales such as:• Inflammatory neuropathy cause and treatment (INCAT);• Inflammatory Rasch built Overall Disability Scale (I-RODS); or• Medical Research Council Sum Score (MRC-SS) to treatment with intravenous immunoglobulin (IVIg), Corticosteroids or plasm exchange (PLEX);

[0298] Diagnostic imaging: to identify enlargement in the cross-sectional area of at least 2 sites in the proximal median nerve and / or brachial plexus by ultrasound; or, to identify enlargement in the size of spinal nerve root(s) by Magnetic resonance imaging (MRI);

[0299] Cerebrospinal fluid (CSF): demonstrating albuminocytologic dissociation (i.e., elevated CSF protein level with normal CSF white blood cell [WBC] level);

[0300] Nerve biopsy: demonstrating features such as edema, demyelination, and / or onion bulb formation; biopsy is typically taken from the sural nerve and is generally only undertaken when less invasive diagnostic methods have failed to confirm the diagnosis.

[0301] Given the heterogeneity in the clinical presentation of CIDP, its differential diagnosis includes an extensive list of potential alternative diagnoses (e.g., hereditary neuropathies) thatmerit consideration and may prompt additional laboratory testing (e.g., for diabetic neuropathy, multiple myeloma, inflammatory myopathy, vitamin Bl 2 deficiency). Additionally, in some cases, the presence of certain antibodies (anti-neurofascin-155 (i.e., anti-NF155 autoantibody), anti-contactin- 1 (i.e., anti-CNTNl autoantibody), anti-contact in associated protein 1 (i.e., anti- CASPR1 autoantibody), anti-NF140 / NF186 (i.e., anti-NF140 / NF186 autoantibody)) may signal the diagnosis of an autoimmune “nodopathy.” These conditions respond poorly to typical CIDP therapies and are considered separate entities outside the framework of the European Academy of Neurology / Peripheral Nerve Society (EAN / PNS) diagnostic criteria for CIDP, as currently revised.

[0302] First line treatment for CIDP include one or more of IVIg, subcutaneous immunoglobulin (SCIg), corticosteroids, and PLEX. In some embodiments, a subject having CIDP is treated with one of the three first line treatment. In some embodiments, for patients who fail to achieve objective improvement (e.g., of impairment and disability) after 3 months of treatment, the other first-line agents may be tried. In some embodiments, alternative treatment options include rituximab, cyclophosphamide, or cyclosporine. In some embodiments, once objective improvement is achieved, the patient may be switched to maintenance therapy to reduce the dose or frequency of treatment to the minimum effective level. For maintenance therapy, patients may be switched from IVIg to SCIg and immunomodulatory agents such as azathioprine, cyclosporine, or mycophenolate may be used for IVIg dose-reducing, corticosteroid-sparing, or PLEX frequency-reducing effect. In some cases, increasing the dose or frequency of treatment or combining first line treatments is a consideration for patients who continue to experience active disease. For long-term management of clinically stable patients, therapy should be periodically reduced or stopped to assess if treatment is still required.

[0303] Despite the availability of the therapies described above, there remains significant unmet medical need for patients with CIDP. For example, although immunoglobulin therapy (IVIg, SCIg) is effective, it may be associated with significant side effects and complications such as severe headache, thromboembolism, and hemolysis. Additionally, IVIg therapy imposes a burden on patients’ time and requires visits at an infusion center, because access to home health agency support for at-home administration remains limited. The availability of IVIg has also been constrained at times due to supply conditions. Currently available SCIg therapy often requires frequent administration across multiple infusion sites using an external pump to deliverthe requisite volume of therapy. Corticosteroid therapy, though also effective, is associated with a number of well-known adverse events (e.g., weight gain, hypertension, diabetes, and osteoporosis), especially with chronic use. PLEX is a specialized procedure requiring central venous access and is not universally available. The immunomodulatory therapies that may be used in CIDP are all associated with significant potential risks including the possibility of malignancy and / or infection. Others include azathioprine - cytopenias; cyclosporine hypertension, nephrotoxicity; my cophenolate - blood dyscrasias including neutropenia and red blood cell (RBC) aplasia; rituximab - renal toxicity; and cyclophosphamide - cardiac, pulmonary, and renal toxicity as well as bone marrow suppression and infertility.

[0304] In some aspects, the present disclosure, provides a method for treating CIDP, the method comprises a dosing regimen (e.g., dose, dosing frequency, etc.) for CIDP that improves the efficacy of the treatment (e.g., relative to using a different dosing regimen) for CIDP. In some embodiments, the method comprises administering a subject having CIDP an effective amount of an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) at a dosing frequency for improved efficacy of the treatment.

[0305] Various FcRn blocker have been tested clinically (e.g., nipocalimab) and some have been approved by FDA for treating CIDP (e.g., efgartigimod). By competitively binding with the IgG binding site on FcRn, an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) blocks FcRn- mediated recycling of IgG, resulting in increased lysosomal degradation and decreased serum levels of IgG. Accordingly, in autoimmune disorders mediated by pathogenic IgG autoantibodies, FcRn blockade can decrease the concentration of these antibodies. Importantly, FcRn blockade does not decrease the concentration of immunoglobulin M (IgM) or immunoglobulin A (IgA), thus leaving this part of the humoral immune system intact.

[0306] In some embodiments, the present disclosure provides compositions (e.g., anti-FcRn antibody IMVT-1402 or batoclimab) and methods (e.g., dosing regimens) for treating CIDP in a subject. In some embodiments, a subject has typical CIDP and associated clinical manifestations. In some embodiments, a subject has a CIDP variant described herein and associated clinical manifestations.

[0307] In some embodiments, the present disclosure provides methods (e.g., dosing regimens) for treating CIDP in a subject, the method comprising administering the subject with an anti-FcRn antibody at a dose effective for inhibiting FcRn-mediated recycling of IgG autoantibodies, thereby reducing IgG autoantibodies (e.g., pathogenic IgG autoantibody levels).

[0308] In some embodiments, a subject having CIDP is administered an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) at a range of 200-400 mg. In some embodiments, a subject having CIDP is administered an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) at a range of 200-400 mg once weekly. In some embodiments, a subject having CIDP is administered an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) at a range of 200-400 mg once weekly for 20-60 weeks.

[0309] In some embodiments, a subject having CIDP is administered an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) in the range of 200-400 mg, 220-400 mg, 250-400 mg, 280-400 mg, 300-400 mg, 320-400 mg, 350-400 mg, 380-400 mg, 200-380 mg, 220-380 mg, 250-380 mg, 280-380 mg, 300-380 mg, 320-380 mg, 350-380 mg, 200-350 mg, 220-350 mg, 250-350 mg, 280-350 mg, 300-350 mg, 320-350 mg, 200-320 mg, 220-320 mg, 250-320 mg, 280-320 mg, 300-320 mg, 200-300 mg, 220-300 mg, 250-300 mg, 280-300 mg, 200-280 mg, 220-280 mg, 250-280 mg, 200-250mg, 220-250 mg, 200-220 mg once weekly. In some embodiments, a subject having CIDP is administered IMVT-1402 at a dose of 300 mg once weekly. In some embodiments, a subject having CIDP is administered batoclimab at a dose of 340 mg once weekly. In some embodiments, a subject having CIDP is administered an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) at 300 mg or 340 mg indefinitely. In some embodiments, whether a subject having CIDP can stop an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) treatment can be evaluated by improvement of one or more symptom and / or whether the subject is tapering off first line treatment (e.g., IVIg, etc.). Evaluation of symptoms of a subject having CIDP can be done by a physician using any suitable methods.

[0310] In some embodiments, a subject having CIDP is administered an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) at a range of 550-700 mg. In some embodiments, a subject having CIDP is administered an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) at a range of 550-700 mg once weekly. In some embodiments, a subject having CIDP is administered an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) at a range of 550-700 mg once weekly for 20-60 weeks.

[0311] In some embodiments, a subject having CIDP is administered an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) at a range of 550-700 mg, 550-690 mg, 550-680 mg, 550-670mg, 550-660 mg, 550-650 mg, 550-640 mg, 550-630 mg, 550-620 mg, 550-610 mg, 550-600 mg, 550-590 mg, 550-580 mg, 550-570 mg, 550-560 mg, 580-700 mg, 580-690 mg, 580-680 mg, 580-670 mg, 580-660 mg, 580-650 mg, 580-640 mg, 580-630 mg, 580-620 mg, 580-610 mg, 580-600 mg, 580-590 mg, 600-700 mg, 600-690 mg, 600-680 mg, 600-670 mg, 600-660 mg, 600-650 mg, 600-640 mg, 600-630 mg, 600-620 mg, 600-610 mg, 620-700 mg, 620-690 mg, 620-680 mg, 620-670 mg, 620-660 mg, 620-650 mg, 620-640 mg, 620-630 mg, 650-700 mg, 650-690 mg, 650-680 mg, 650-670 mg, 650-660 mg, 680-700 mg, or 680-690 mg once weekly. In some embodiments, a subject having CIDP is administered IMVT-1402 at a range of 550-700 mg, 550-690 mg, 550-680 mg, 550-670 mg, 550-660 mg, 550-650 mg, 550-640 mg, 550-630 mg, 550-620 mg, 550-610 mg, 550-600 mg, 550-590 mg, 550-580 mg, 550-570 mg, 550-560 mg, 580-700 mg, 580-690 mg, 580-680 mg, 580-670 mg, 580-660 mg, 580-650 mg, 580-640 mg, 580-630 mg, 580-620 mg, 580-610 mg, 580-600 mg, 580-590 mg, 600-700 mg, 600-690 mg, 600-680 mg, 600-670 mg, 600-660 mg, 600-650 mg, 600-640 mg, 600-630 mg, 600-620 mg, 600-610 mg, 620-700 mg, 620-690 mg, 620-680 mg, 620-670 mg, 620-660 mg, 620-650 mg, 620-640 mg, 620-630 mg, 650-700 mg, 650-690 mg, 650-680 mg, 650-670 mg, 650-660 mg, 680-700 mg, or 680-690 mg once weekly. In some embodiments, a subject having CIDP is administered IMVT-1402 at a dose of 600 mg once weekly. In some embodiments, a subject having CIDP is administered batoclimab at a range of 550-700 mg, 550-690 mg, 550-680 mg, 550-670 mg, 550-660 mg, 550-650 mg, 550-640 mg, 550-630 mg, 550-620 mg, 550-610 mg, 550-600 mg, 550-590 mg, 550-580 mg, 550-570 mg, 550-560 mg, 580-700 mg, 580-690 mg, 580-680 mg, 580-670 mg, 580-660 mg, 580-650 mg, 580-640 mg, 580-630 mg, 580-620 mg, 580-610 mg, 580-600 mg, 580-590 mg, 600-700 mg, 600-690 mg, 600-680 mg, 600-670 mg, 600-660 mg, 600-650 mg, 600-640 mg, 600-630 mg, 600-620 mg, 600-610 mg, 620-700 mg, 620-690 mg, 620-680 mg, 620-670 mg, 620-660 mg, 620-650 mg, 620-640 mg, 620-630 mg, 650-700 mg, 650-690 mg, 650-680 mg, 650-670 mg, 650-660 mg, 680-700 mg, or 680-690 mg once weekly. In some embodiments, a subject having CIDP is administered batoclimab at a dose of 680 mg once weekly.

[0312] In some embodiments, a subject having CIDP is administered an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) at a range of 550-700 mg (e.g., any of the doses described herein) once weekly for 20-60 weeks, 20-58 weeks, 20-55 weeks, 20-52 weeks, 20-50 weeks, 20-45 weeks, 20-42 weeks, 20-40 weeks, 20-35 weeks, 20-30 weeks, 20-25 weeks, 25-60 weeks,25-58 weeks, 25-55 weeks, 25-52 weeks, 25-50 weeks, 25-45 weeks, 25-42 weeks, 25-40 weeks,25-35 weeks, 25-30 weeks, 30-60 weeks, 30-58 weeks, 30-55 weeks, 30-52 weeks, 30-50 weeks,30-45 weeks, 30-42 weeks, 30-40 weeks, 30-35 weeks, 35-60 weeks, 35-58 weeks, 35-55 weeks,35-52 weeks, 35-50 weeks, 35-45 weeks, 35-42 weeks, 35-40 weeks, 40-60 weeks, 40-58 weeks,40-55 weeks, 40-52 weeks, 40-50 weeks, 40-45 weeks, 40-42 weeks, 45-60 weeks, 45-58 weeks,45-55 weeks, 45-52 weeks, 45-50 weeks, 50-60 weeks, 50-58 weeks, 50-55 weeks, 50-52 weeks,55-60 weeks, or 55-58 weeks. In some embodiments, a subject having CIDP is administered an IMVT-1402 at 600 mg for 24 weeks. In some embodiments, a subject having CIDP is administered an IMVT-1402 at 600 mg for 52 weeks. In some embodiments, a subject having CIDP is administered batoclimab at 680 mg for 24 weeks. In some embodiments, a subject having CIDP is administered batoclimab at 680 mg for 52 weeks.

[0313] In some embodiments, after the first dose of an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) on day 1, a subject having CIDP is administered a loading dose of the anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) between days 3-5 in the first week of treatment. In some embodiments, a loading dose is administered to the subjecting having CIDP on day 4 in the first week of treatment. In some embodiments, a loading dose is between 550-700 mg (e.g., 550- 700 mg, 550-690 mg, 550-680 mg, 550-670 mg, 550-660 mg, 550-650 mg, 550-640 mg, 550- 630 mg, 550-620 mg, 550-610 mg, 550-600 mg, 550-590 mg, 550-580 mg, 550-570 mg, 550- 560 mg, 580-700 mg, 580-690 mg, 580-680 mg, 580-670 mg, 580-660 mg, 580-650 mg, 580- 640 mg, 580-630 mg, 580-620 mg, 580-610 mg, 580-600 mg, 580-590 mg, 600-700 mg, 600- 690 mg, 600-680 mg, 600-670 mg, 600-660 mg, 600-650 mg, 600-640 mg, 600-630 mg, 600- 620 mg, 600-610 mg, 620-700 mg, 620-690 mg, 620-680 mg, 620-670 mg, 620-660 mg, 620- 650 mg, 620-640 mg, 620-630 mg, 650-700 mg, 650-690 mg, 650-680 mg, 650-670 mg, 650- 660 mg, 680-700 mg, or 680-690 mg) of the anti-FcRn antibody. In some embodiments, a loading dose is 600 mg of IMVT-1402. In some embodiments, a loading dose is 680 mg of batoclimab. In some embodiments, a loading does of an anti-FcRn antibody is to administer the subject having CIDP with the same anti-FcRn antibody at the same dose as the weekly treatment.

[0314] In some embodiments, a subject is administered with an anti-FcRn antibody (e.g., IMVT- 1402) at 600 mg once weekly for 24 weeks with a loading dose of the anti-FcRn antibody at 600 mg on day 4 of treatment. In some embodiments, the subject having CIDP enters further anti- FcRn antibody treatment after week 24. In some embodiments, a subject receives anotherloading dose on days 3-5 of week 25. In some embodiments, the subject having CIDP receives the anti-FcRn antibody up to additional 52 weeks.

[0315] In some embodiments, a subject being diagnosed as having CIDP is suitable for the treatment described herein. In some embodiments, a subject has typical CIDP according to the European Academy of Neurology / Peripheral Nerve Society (EAN / PNS) Guideline on Diagnosis and Treatment of CIDP. In some embodiments, a subject having CIDP meet all of the following criteria: (i) Progressive or relapsing, symmetric, proximal, and distal muscle weakness of upper and lower limbs and sensory involvement of at least 2 limbs (at any point in the disease course); (ii). Developing over at least 8 weeks; (iii). Absent or reduced tendon reflexes in all limbs. In some embodiments, a subject has a CIDP variant according to the EAN / PNS Guideline on Diagnosis and Treatment of CIDP. In some embodiments, a subject having a CIDP variant meets the same clinical as typical CIDP only that tendon reflexes may be normal in unaffected limbs. In some embodiments, a subject has multifocal CIDP. In some embodiments, a subject having multifocal CIDP meets all the clinical criteria of typical CIDP, and also has documented sensory loss and muscle weakness in a multifocal pattern, usually asymmetric, upper limb predominant. In some embodiments, a subject has motor CIDP. In some embodiments, a subject having motor CIDP meets all the clinical criteria of typical CIDP, and also has motor symptoms and signs without sensory involvement.

[0316] In addition to the clinical criteria of CIDP, a subject having CIDP also has electrodiagnostic test results supporting the diagnosis of CIDP per the EAN / PNS guideline on diagnosis and treatment of CIDP. In some embodiments, a subject having CIDP meets either or both of criterion (a) or (b): (a) Motor nerve conduction criteria strongly supportive of demyelination.; b. Motor nerve conduction criteria weakly supportive of demyelination and 2 or more of the following additional diagnostic criteria (e.g., based on historical data: (i) Objective improvement to an empiric trial of therapy with immunoglobulin treatment, plasma exchange (PLEX) or corticosteroids; (ii). Diagnostic imaging by ultrasound or magnetic resonance imaging (MRI) supporting the diagnosis of CIDP by demonstrating nerve enlargement; (iii). Cerebrospinal fluid (CSF) demonstrating albuminocytologic dissociation (i.e., elevated CSF protein level [defined as > 70 mg / dL or > 10 mg / dL greater than years of age for those who are > 60 years old] with normal CSF white blood cell level); (iv). Nerve biopsy demonstratingfeatures supporting the diagnosis of CIDP, such as edema, demyelination, and / or onion bulb formation.

[0317] In some embodiments, a subject having CIDP suitable for an anti-FcRn antibody treatment is currently on, or have been receiving corticosteroids (e.g., systemic corticosteroids on a chronic stable dose). In some embodiments, a subject having CIDP is receiving systemic corticosteroids daily. In some embodiments, a subject having CIDP is receiving systemic corticosteroids every other day. In some embodiments, a subject having CIDP is receiving systemic corticosteroids daily or every other day orally. In some embodiments, a subject having CIDP is receiving systemic corticosteroids daily or every other day via pulse regimen. In some embodiments, a subject taking systemic corticosteroids as their main CIDP therapy are suitable for the anti-FcRn antibody treatment provided that they are taking chronic oral corticosteroids with a maximum dose equivalent to prednisolone / prednisone 20 mg / day (including every other day or similar regimen) and are willing to follow the dose taper requirements after randomization (described elsewhere herein). In oral dosing, stable dose is considered to be daily excursions < 2.5 mg prednisone or prednisone equivalent for > 3 months prior to administration. In some embodiments, a subject taking systemic corticosteroids as their main CIDP therapy are suitable for the anti-FcRn antibody treatment provided that they are taking chronic pulsed corticosteroid regimens defined as doses of > 100 mg / day prednisolone / prednisone equivalent (i.e., IV / intramuscularly [IM] or orally [PO]) with a minimum interval between pulse treatments of > 3 weeks and are willing to discontinue pulse treatments upon randomization. In pulse regimen, stable dose is considered to be repetitive cycles without the need for dose adjustment to maintain disease control for > 3 months prior to administration.

[0318] In some embodiments, a subject having CIDP suitable for an anti-FcRn antibody treatment shows an underlying active disease process even if symptoms are controlled (e.g., show improvement on starting a first-line therapy, or deterioration after reduction of a first-line therapy). In some embodiments, a subject having CIDP with underlying active disease process meet either one of the following criteria (a) or (b):

[0319] (a) Within 36 months of screening, a clinically meaningful improvement following initiation of standard of care therapy is documented in the medical records, and there is clinical evidence to support ongoing disease activity. In some embodiments, clinically meaningful improvement may be defined as 1 of the following:o > 1 -point decrease in adjusted inflammatory neuropathy cause and treatment (aINCAT ) score; o Increase in Inflammatory Rasch-Built Overall Disability Scale (I-RODS) total score > 4 points; o Increase in Research Council Sum Score (MRC-SS) > 3; o Grip strength improvement of > 8 kilopascals; or o An equivalent improvement that is documented in the medical record and is considered to be meaningful in the Investigator’s judgement.

[0320] In some embodiments, evidence to support ongoing disease activity may be any of the following (within 12 months of Screening): o Clinical worsening at the end of recent IVIG cycle; or o Improvement after recent IVIG infusions, or o An equivalent change in clinical status that is documented in the medical record.

[0321] (b). Within 36 months of Screening, a clinically meaningful deterioration following reduction of standard of care therapy (planned dose reduction or increased dosing interval to test for continued disease activity) or after a missed dose is documented in the medical records. In some embodiments, clinically meaningful deterioration may be defined as one of the following: o > 1 -point increase in aINCAT score; o Decrease in I-RODS total score > 4 points; o Decrease in MRC-SS > 3; o Grip strength worsening of > 8 kilopascals; or o An equivalent deterioration of an objective measure that is documented in the medical record and is considered to be meaningful in the Investigator’s judgement.

[0322] In some embodiments, changes in more subjective measures, for example, pain perception, would not meet the above criteria.

[0323] In some embodiments, a subject suitable for the anti-FcRn antibody treatment described herein does not have certain conditions. In some embodiments, a subject does not have current or prior history of immunoglobulin M (IgM) paraproteinemia with or without anti-myelin associated-glycoprotein antibodies. In some embodiments, a subject does not have distal CIDP. In some embodiments, a subject does not have sensory CIDP.

[0324] In some embodiments, a subject does not have focal CIDP. In some embodiments, a subject does not have distal CIDP. In some embodiments, a subject does not have autoimmune nodopathy per the EAN / PNS guideline on diagnosis and treatment of CIDP. In some embodiments, a subject does not have polyneuropathy with etiology other than CIDP including but not limited to multifocal motor neuropathy; hereditary demyelinating neuropathy; polyneuropathy, organomegaly, endocrinopathy, monoclonal protein and skin change syndromes; lumbosacral radiculoplexus neuropathy; systemic illnesses (e.g., vitamin deficiency syndromes and paraneoplastic neuropathies), or drug- or toxin-induced.

[0325] In some embodiments, a subject does not have diabetes mellitus (DM). In some embodiments, a subject shows evidence of poorly controlled DM (e.g., two or more hemoglobin Ale (HbAlc) levels above 9%) immediately preceding a diagnosis of CIDP. In some embodiments, a subject does not have poorly controlled DM at screening (e.g., 2 or more HbAlc levels above 8% within the past year).

[0326] In some embodiments, a subject does not have myelopathy. In some embodiments, a subject does not have central demyelination.

[0327] In some embodiments, a subject is on oral corticosteroids as main therapy for CIDP and begins to taper off oral corticosteroids at the beginning of the anti-FcRn antibody (e.g., IMVT- 1402 or batoclimab) treatment. In some embodiments, a subject is on low dose oral corticosteroids (e.g., equivalent to 5-10 mg / day prednisolone / prednisone) along with IVIg as main therapy for CIDP begins to taper off oral corticosteroids and / or IVIg at the beginning of the anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) treatment.

[0328] In some embodiments, a subject is on pulsed corticosteroids as the main therapy for CIDP must be discontinued prior to for the duration of the anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) treatment. In some embodiments, a subject is on pulsed corticosteroids as the main therapy for CIDP receives the last pulsed corticosteroids 5-9 days (e.g., 7 days) prior to the first administration of the anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) treatment.

[0329] In some embodiments, a subject is receiving Immunoglobulin (Ig) therapy (e.g., IVIg or SCIg) as the main therapy for CIDP must be discontinued prior to for the duration of the anti- FcRn antibody (e.g., IMVT-1402 or batoclimab) treatment. In some embodiments, a subject is on pulsed corticosteroids as the main therapy for CIDP receives the last Ig therapy 5-9 days (e.g., 7days) prior to the first administration of the anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) treatment.

[0330] In some embodiments, a subject that tapers off or discontinues first-line CIDP therapy during and / or prior to the anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) treatment described herein does not relapse (e.g., does not relapse in first 24 weeks of 600 mg IMVT-1402 treatment). Relapse, as used herein, refers to a worsening (increase) of > 1 point (e.g., at least 1 point, at least 2 points, at least 3 points, at least 4 points, at least 5 points, at least 6 points, at least 7 points, at least 8 points, at least 9 points, or at least 10 points) on the aINCAT score at any time point relative to baseline. Baseline aINCAT score can be taken prior to the first administration. In some embodiments, a subject has relapsed if the initial increase is more than 1 point on the aINCAT score. In some embodiments, a subject can be assessed further during treatment if the initial increase is 1 point on the aINCAT score, and if the initial increase of 1 point is maintained or increases, the subject has relapsed. The INCAT disability scale is a widely used and validated efficacy assessment of neurologic dysfunction in CIDP. Upper and lower limb dysfunction are each separately assessed on a scale of 0-5, and the results are summed together for a total composite score of 0-10. Higher scores represent greater disability. The minimum clinically important difference for the INCAT disability scale is 1 point. In some embodiments, a subject has not relapsed if the subject has reduced aINCAT score relative to baseline after anti-FcRn antibody treatment (e.g., 600 mg IMVT-1402 for 24 weeks). In some embodiments, a subject has not relapsed if the subject has increased aINCAT score of 1 point above baseline at initial assessment but aINCAT score reduced in subsequence assessment after anti-FcRn antibody treatment (e.g., 600 mg IMVT-1402 for 24 weeks). In some embodiments, a subject that relapsed does not continue the anti-FcRn treatment but resumes first-line therapy for CIDP (e.g., corticosteroids and / or Ig therapy). In some embodiments, a subject that relapsed continue to receive the anti-FcRn antibody treatment.

[0331] In some embodiments, administration of an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) described herein reduces Adjusted Inflammatory Neuropathy Cause and Treatment (aINCAT) score in a subject having CIDP.

[0332] In some embodiments, administration of the anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) to a subject having CIDP increases mean grip strength by at least 1%, at least 5%, at least 10%, at least 15%, at least 20%, at least 25%, at least 30%, at least 35%, at least 40%, atleast 45%, at least 50%, at least 55%, at least 60%, at least 65%, at least 70%, at least 75%, at least 80%, at least 85%, at least 90%, at least 95%, at least 96%, at least 97%, at least 98%, at least 99%, at least 100%, at least 2-fold, at least 3-fold, at least 4-fold, at least 5-fold, at least 6- fold, at least 7-fold, at least 8-fold, at least 9-fold, at least lOfold, or more relative to baseline mean grip strength. Mean Grip Strength provides an objective, quantitative, and immediate assessment of strength impairment. The Jamar dynamometer and the Martin vigorimeter are both commonly used to assess Mean Grip Strength.

[0333] In some embodiments, administration of the anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) to a subject having CIDP increases Medical Research Council Sum Score (MRC- SS) score by at least 1%, at least 5%, at least 10%, at least 15%, at least 20%, at least 25%, at least 30%, at least 35%, at least 40%, at least 45%, at least 50%, at least 55%, at least 60%, at least 65%, at least 70%, at least 75%, at least 80%, at least 85%, at least 90%, at least 95%, at least 96%, at least 97%, at least 98%, at least 99%, at least 100%, at least 2-fold, at least 3 -fold, at least 4-fold, at least 5 -fold, at least 6-fold, at least 7-fold, at least 8-fold, at least 9-fold, at least 10-fold, or more relative to baseline MCR-SS score. The MRC-SS is a standardized methodology for objectively assessing and reporting muscle unction. Six muscle groups are assessed bilaterally, and each are scored on a scale of 0 (no visible contraction) to 5 (normal) yielding a sum ranging from 0 (paralysis) to 60 (normal strength).

[0334] In some embodiments, administration of the anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) to a subject having CIDP increases Inflammatory Rasch-built Overall Disability Scale (I-RODS) by at least 1%, at least 5%, at least 10%, at least 15%, at least 20%, at least 25%, at least 30%, at least 35%, at least 40%, at least 45%, at least 50%, at least 55%, at least 60%, at least 65%, at least 70%, at least 75%, at least 80%, at least 85%, at least 90%, at least 95%, at least 96%, at least 97%, at least 98%, at least 99%, at least 100%, at least 2-fold, at least 3 -fold, at least 4-fold, at least 5 -fold, at least 6-fold, at least 7-fold, at least 8-fold, at least 9-fold, at least 10-fold, or more relative to baseline I-RODS score. The I-RODS for immune-mediated peripheral neuropathies is a linearly weighted scale that captures activity and social participation limitations in participants with CIDP. It is completed by the participant in the presence of or with the oversight of the blinded assessor. The assessment consists of a 24-question instrument that addresses upper and lower limb tasks that range in difficulty from reading a book and eating tostanding and running. Answers are scored on a scale of 0 to 2 (complete disability to no disability) and the raw scores are then transformed into a final score ranging from 0-100.

[0335] In some embodiments, administration of the anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) to a subject having CIDP decreases “Timed Up and Go” (TUG) Test score by at least 1%, at least 5%, at least 10%, at least 15%, at least 20%, at least 25%, at least 30%, at least35%, at least 40%, at least 45%, at least 50%, at least 55%, at least 60%, at least 65%, at least70%, at least 75%, at least 80%, at least 85%, at least 90%, at least 95%, at least 96%, at least97%, at least 98%, at least 99%, or at least 100%. The TUG test is an overall method to measure lower extremity function, mobility, and fall risk. It entails timing a patient while they: 1. Stand up from a chair, 2. Walk a distance of 3 meters (about 10 feet), 3. Turn, 4. Walk back to the chair, and 5. sit down. The TUG has been able to demonstrate clinical improvement following an intervention. The average time to complete the test varies with age and ability, or the need for assisting devices. Participants with a TUG score > 3.5 seconds are likely to have an increased risk of fall.

[0336] In some embodiments, administration of an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) dosing regimen described herein decreases total IgG level in the subject having CIDP (e.g., relative to baseline total IgG level prior to the administration) by at least at least 1%, at least 5%, at least 10%, at least 15%, at least 20%, at least 25%, at least 30%, at least 35%, at least 40%, at least 45%, at least 50%, at least 55%, at least 60%, at least 65%, at least 70%, at least 75%, at least 80%, at least 85%, at least 90%, at least 95%, at least 96%, at least 97%, at least 98%, at least 99%, or 100%. In some embodiments, the administration of an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) dosing regimen described herein decreases total IgG level in the subject (e.g., relative to baseline total IgG level prior to the administration) by between 1% and 100%, between 5% and 100%, between 5% and 90%, between 5% and 80%, between 5% and 70%, between 5% and 60%, between 5% and 50%, between 5% and 40%, between 5% and 30%, between 5% and 20%, between 5% and 15%, between 10% and 100%, between 10% and 90%, between 10% and 80%, between 10% and 70%, between 10% and 60%, between 10% and 50%, between 10% and 40%, between 10% and 30%, between 10% and 20%, between 10% and 15%, between 20% and 100%, between 20% and 90%, between 20% and 80%, between 20% and 70%, between 20% and 60%, between 20% and 50%, between 20% and 40%, between 20% and 30%, between 30% and 100%, between 30% and 90%, between 30%and 80%, between 30% and 70%, between 30% and 60%, between 30% and 50%, between 30% and 40%, between 40% and 100%, between 40% and 90%, between 40% and 80%, between 40% and 70%, between 40% and 60%, between 40% and 50%, between 50% and 100%, between 50% and 90%, between 50% and 80%, between 50% and 70%, between 50% and 60%, between 60% and 100%, between 60% and 90%, between 60% and 80%, between 60% and 70%, between 70% and 100%, between 70% and 90%, between 70% and 80%, between 80% and 100%, between 80% and 90%, or between 90% and 100%.

[0337] In some embodiments, administration of an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) dosing regimen described herein decreases IgG subclasses (e.g., IgG2, IgG2, IgG3 and / or IgG4) level in the subject having CIDP (e.g., relative to baseline total IgG level prior to the administration) by at least at least 1%, at least 5%, at least 10%, at least 15%, at least 20%, at least 25%, at least 30%, at least 35%, at least 40%, at least 45%, at least 50%, at least 55%, at least 60%, at least 65%, at least 70%, at least 75%, at least 80%, at least 85%, at least 90%, at least 95%, at least 96%, at least 97%, at least 98%, at least 99%, or 100%. In some embodiments, the administration of an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) dosing regimen described herein decreases IgG subclass (e.g., IgGl, IgG2, IgG3, or IgG4) level in the subject having CIDP (e.g., relative to baseline total IgG level prior to the administration) by between 1% and 100%, between 5% and 100%, between 5% and 90%, between 5% and 80%, between 5% and 70%, between 5% and 60%, between 5% and 50%, between 5% and 40%, between 5% and 30%, between 5% and 20%, between 5% and 15%, between 10% and 100%, between 10% and 90%, between 10% and 80%, between 10% and 70%, between 10% and 60%, between 10% and 50%, between 10% and 40%, between 10% and 30%, between 10% and 20%, between 10% and 15%, between 20% and 100%, between 20% and 90%, between 20% and 80%, between 20% and 70%, between 20% and 60%, between 20% and 50%, between 20% and 40%, between 20% and 30%, between 30% and 100%, between 30% and 90%, between 30% and 80%, between 30% and 70%, between 30% and 60%, between 30% and 50%, between 30% and 40%, between 40% and 100%, between 40% and 90%, between 40% and 80%, between 40% and 70%, between 40% and 60%, between 40% and 50%, between 50% and 100%, between 50% and 90%, between 50% and 80%, between 50% and 70%, between 50% and 60%, between 60% and 100%, between 60% and 90%, between 60% and 80%, between 60% and 70%, between 70%and 100%, between 70% and 90%, between 70% and 80%, between 80% and 100%, between 80% and 90%, or between 90% and 100%.

[0338] In some embodiments, administration of an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) dosing regimen described herein decreases levels of autoantibodies targeting myelin glycoproteins in the subject having CIDP (e.g., relative to baseline total autoantibodies targeting myelin glycoproteins level prior to the administration) by at least at least 1%, at least 5%, at least10%, at least 15%, at least 20%, at least 25%, at least 30%, at least 35%, at least 40%, at least45%, at least 50%, at least 55%, at least 60%, at least 65%, at least 70%, at least 75%, at least80%, at least 85%, at least 90%, at least 95%, at least 96%, at least 97%, at least 98%, at least99%, or 100%. In some embodiments, the administration of an anti-FcRn antibody (e.g., IMVT- 1402 or batoclimab) dosing regimen described herein decreases levels of autoantibodies targeting myelin glycoproteins in the subject having CIDP (e.g., relative to baseline total autoantibodies targeting myelin glycoproteins level prior to the administration) by between 1% and 100%, between 5% and 100%, between 5% and 90%, between 5% and 80%, between 5% and 70%, between 5% and 60%, between 5% and 50%, between 5% and 40%, between 5% and 30%, between 5% and 20%, between 5% and 15%, between 10% and 100%, between 10% and 90%, between 10% and 80%, between 10% and 70%, between 10% and 60%, between 10% and 50%, between 10% and 40%, between 10% and 30%, between 10% and 20%, between 10% and 15%, between 20% and 100%, between 20% and 90%, between 20% and 80%, between 20% and 70%, between 20% and 60%, between 20% and 50%, between 20% and 40%, between 20% and 30%, between 30% and 100%, between 30% and 90%, between 30% and 80%, between 30% and 70%, between 30% and 60%, between 30% and 50%, between 30% and 40%, between 40% and 100%, between 40% and 90%, between 40% and 80%, between 40% and 70%, between 40% and 60%, between 40% and 50%, between 50% and 100%, between 50% and 90%, between 50% and 80%, between 50% and 70%, between 50% and 60%, between 60% and 100%, between 60% and 90%, between 60% and 80%, between 60% and 70%, between 70% and 100%, between 70% and 90%, between 70% and 80%, between 80% and 100%, between 80% and 90%, or between 90% and 100%.

[0339] In some embodiments, administration of an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) dosing regimen described herein decreases immune complexes (ICs) in the subject having CIDP (e.g., relative to baseline total ICs level prior to the administration) by at least atleast 1%, at least 5%, at least 10%, at least 15%, at least 20%, at least 25%, at least 30%, at least 35%, at least 40%, at least 45%, at least 50%, at least 55%, at least 60%, at least 65%, at least 70%, at least 75%, at least 80%, at least 85%, at least 90%, at least 95%, at least 96%, at least 97%, at least 98%, at least 99%, or 100%. In some embodiments, the administration of an anti- FcRn antibody (e.g., IMVT-1402 or batoclimab) dosing regimen described herein decreases immune complexes (ICs) in the subject having CIDP (e.g., relative to baseline total ICs level prior to the administration) by between 1% and 100%, between 5% and 100%, between 5% and 90%, between 5% and 80%, between 5% and 70%, between 5% and 60%, between 5% and 50%, between 5% and 40%, between 5% and 30%, between 5% and 20%, between 5% and 15%, between 10% and 100%, between 10% and 90%, between 10% and 80%, between 10% and 70%, between 10% and 60%, between 10% and 50%, between 10% and 40%, between 10% and 30%, between 10% and 20%, between 10% and 15%, between 20% and 100%, between 20% and 90%, between 20% and 80%, between 20% and 70%, between 20% and 60%, between 20% and 50%, between 20% and 40%, between 20% and 30%, between 30% and 100%, between 30% and 90%, between 30% and 80%, between 30% and 70%, between 30% and 60%, between 30% and 50%, between 30% and 40%, between 40% and 100%, between 40% and 90%, between 40% and 80%, between 40% and 70%, between 40% and 60%, between 40% and 50%, between 50% and 100%, between 50% and 90%, between 50% and 80%, between 50% and 70%, between 50% and 60%, between 60% and 100%, between 60% and 90%, between 60% and 80%, between 60% and 70%, between 70% and 100%, between 70% and 90%, between 70% and 80%, between 80% and 100%, between 80% and 90%, or between 90% and 100%.

[0340] In some embodiments, administration of an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) dosing regimen described herein decreases neurofilament light chain (NfL) in the subject having CIDP (e.g., relative to baseline total NfL level prior to the administration) by at least at least 1%, at least 5%, at least 10%, at least 15%, at least 20%, at least 25%, at least 30%, at least 35%, at least 40%, at least 45%, at least 50%, at least 55%, at least 60%, at least 65%, at least 70%, at least 75%, at least 80%, at least 85%, at least 90%, at least 95%, at least 96%, at least 97%, at least 98%, at least 99%, or 100%. In some embodiments, the administration of an anti-FcRn antibody (e.g., IMVT-1402 or batoclimab) dosing regimen described herein decreases neurofilament light chain (NfL) in the subject having CIDP (e.g., relative to baseline total NfL level prior to the administration) by between 1% and 100%, between 5% and 100%, between 5%and 90%, between 5% and 80%, between 5% and 70%, between 5% and 60%, between 5% and 50%, between 5% and 40%, between 5% and 30%, between 5% and 20%, between 5% and 15%, between 10% and 100%, between 10% and 90%, between 10% and 80%, between 10% and 70%, between 10% and 60%, between 10% and 50%, between 10% and 40%, between 10% and 30%, between 10% and 20%, between 10% and 15%, between 20% and 100%, between 20% and 90%, between 20% and 80%, between 20% and 70%, between 20% and 60%, between 20% and 50%, between 20% and 40%, between 20% and 30%, between 30% and 100%, between 30% and 90%, between 30% and 80%, between 30% and 70%, between 30% and 60%, between 30% and 50%, between 30% and 40%, between 40% and 100%, between 40% and 90%, between 40% and 80%, between 40% and 70%, between 40% and 60%, between 40% and 50%, between 50% and 100%, between 50% and 90%, between 50% and 80%, between 50% and 70%, between 50% and 60%, between 60% and 100%, between 60% and 90%, between 60% and 80%, between 60% and 70%, between 70% and 100%, between 70% and 90%, between 70% and 80%, between 80% and 100%, between 80% and 90%, or between 90% and 100%.Additional Dosing Schedules

[0341] Dosage regimens for the anti-FcRn antibody or antigen-binding fragment, either alone or in combination with one or more additional therapeutic agents or therapy, may be adjusted to provide the optimum desired response (e.g., a therapeutic response). For example, a single bolus of the anti-FcRn antibody or antigen-binding fragment may be administered at one time, several divided doses may be administered over a predetermined period of time, or the dose of the anti- FcRn antibody or antigen-binding fragment may be proportionally reduced or increased as indicated by the exigencies of the therapeutic situation. For any particular subject, specific dosage regimens may be adjusted over time according to the individual’s need, and the professional judgment of the treating clinician. For instance, in some embodiments, the dose of the anti-FcRn antibody or antigen-binding fragment can be suitably determined by taking into consideration the patient’s severity, condition, age, case history, and the like.

[0342] Dosage values for the anti-FcRn antibody or antigen-binding fragment, compositions comprising the anti-FcRn antibody or antigen-binding fragment, and / or any additional therapeutic agent(s), may be selected based on the unique characteristics of the active compound(s) and the particular therapeutic effect to be achieved. A physician can start doses ofthe antibodies or antigen-binding fragments at levels lower than those required to achieve the desired therapeutic effect and gradually increase the dosage until the desired effect is achieved. A physician can also start doses of the antibodies or antigen-binding fragments at levels higher than those required to achieve the desired therapeutic effect and gradually decrease the dosage until the desired effect is achieved. In general, effective doses of the antibodies or antigenbinding fragments for the treatment of an autoimmune disease may vary depending upon many different factors, for example, on the stage of the disease, the severity of symptoms, and the subject’s prognosis. The selected dosage level may also depend upon a variety of pharmacokinetic factors including the activity of the particular compositions employed, or the ester, salt or amide thereof, the route of administration, the time of administration, the rate of excretion of the particular compound being employed, the duration of the treatment, other drugs, compounds and / or materials used in combination with the particular compositions employed, the age, sex, weight, condition, general health and prior medical history of the patient being treated, and like factors. In some embodiments, the treatment may be administered once or several times. Intermittent and / or chronic (continuous) dosing strategies may be applied in view of the condition of the particular patient.

[0343] In some embodiments, a therapeutically effective amount of the anti-FcRn antibody or antigen-binding fragment is employed in the methods, uses, and pharmaceutical compositions of the present disclosure.

[0344] As used herein, the terms “therapeutically effective amount” and “therapeutically effective dose” are used interchangeably herein to refer to an amount sufficient to decrease at least one symptom or measurable parameter associated with a disease, disorder, or condition; to normalize body functions in a disease, disorder, or condition that results in the impairment of specific bodily functions; and / or to provide improvement in, or slow the progression of, one or more clinically measured parameters of a disease, disorder, or condition. A therapeutically effective amount may, for example, be sufficient to treat, reduce the severity, delay the onset, and / or reduce the risk of occurrence of one or more symptoms of an autoimmune disease. A therapeutically effective amount, as well as a therapeutically effective frequency of administration, can be determined by methods known in the art and discussed herein. In some embodiments of the methods, uses, and compositions described herein, the anti-FcRn antibody or antigen-binding fragment is administered in an amount that is therapeutically effective whenadministered as a single agent. In some embodiments, the anti-FcRn antibody or antigen-binding fragment and at least one additional therapeutic agent are each administered in an amount that is therapeutically effective when the agents are used in combination. In some embodiments, a therapeutically effective amount of the anti-FcRn antibody or antigen-binding fragment is the amount required to reduce the level of total serum IgG and / or the level of at least one autoantibody (e.g., at least one IgG) in a patient having or suspected of having an autoimmune disease.

[0345] Provided herein are methods of improving anti-FcRn therapies in a subject in need thereof comprising administering to the subject an anti-FcRn antibody. In some embodiments, the antibody or antigen-binding fragment is administered to the patient at one or more doses (e.g., two or more different doses). For example, in some embodiments, the antibody or antigenbinding fragment is administered to the patient at two different doses, e.g., at least one higher dose, followed by at least one lower dose.

[0346] In some aspects of the present disclosure, provided herein is a method of treating an autoimmune disease in a subject in need thereof, the method comprising administering to the subject a loading dose, and induction dose and a maintenance dose of an anti-FcRn therapy.

[0347] In some embodiments of the methods of treating an autoimmune disease, the autoimmune disease is a progressive disease. In some embodiments of the methods of treating an autoimmune disease, the autoimmune disease is a demyelinating disease. In some embodiments of the methods of treating an autoimmune disease, the autoimmune disease is chronic inflammatory demyelinating polyneuropathy (CIDP). In some embodiments of the methods of treating an autoimmune disease, the autoimmune disease is Myasthenia Gravis. In some embodiments of the methods of treating an autoimmune disease, the autoimmune disease is Graves’ Disease. In some embodiments of the methods of treating an autoimmune disease, the autoimmune disease is rheumatoid arthritis (e.g., refractory rheumatoid arthritis). In some embodiments of the methods of treating an autoimmune disease, the autoimmune disease is systemic lupus erythematosus. In some embodiments of the methods of treating an autoimmune disease, the autoimmune disease is cutaneous lupus erythematosus. In some embodiments of the methods of treating an autoimmune disease, the autoimmune disease is thyroid eye disease. In some embodiments of the methods of treating an autoimmune disease, the autoimmune disease is warm autoimmune hemolytic anemia.

[0348] In some embodiments of the methods of treating an autoimmune disease, the subject being treated is already receiving one or more anti-FcRn therapies. The anti-FcRn therapy may be, for example, an anti-FcRn antibody. Examples of anti-FcRn antibodies include efgartigimod (ARGX-113), rozanolixizumab (UCB7665), nipocalimab (M281), orilanolimab (SYNT001), as well as batoclimab and IMVT-1402. In some embodiments, the anti-FcRn therapy comprises Abdegs, Seldegs, SYN1436 and / or SYN1327.

[0349] In some embodiments of the methods of treating an autoimmune disease, the subject being treated is receiving intravenous immunoglobulin (IVIg). In some embodiments of the methods of treating an autoimmune disease, the subject being treated is receiving plasma exchange or plasmapheresis (PLEX).Induction Dose

[0350] The induction dose may be a dose of an anti-FcRn antibody that is administered for an initial period to achieve control of disease symptoms.

[0351] In some embodiments, the induction dose is a dose of about 100 mg to about 200 mg of an anti-FcRn antibody (e.g., batoclimab or IMVT-1402). In some embodiments, the induction dose is a dose of about 100 mg, about 110 mg, about 120 mg, about 130 mg, about 140 mg, about 150 mg, about 160 mg, about 170 mg, about 180 mg, about 190 mg, or about 200 mg of an anti-FcRn antibody (e.g., batoclimab or IMVT-1402).

[0352] In some embodiments, the induction dose is a dose of about 200 mg to about 300 mg of an anti-FcRn antibody (e.g., batoclimab or IMVT-1402). In some embodiments, the induction dose is a dose of about 200 mg, about 210 mg, about 220 mg, about 230 mg, about 240 mg, about 250 mg, about 260 mg, about 270 mg, about 280 mg, about 290 mg, or about 300 mg of an anti-FcRn antibody (e.g., batoclimab or IMVT-1402).

[0353] In some embodiments, the induction dose is a dose of about 300 mg to about 500 mg of an anti-FcRn antibody (e.g., batoclimab or IMVT-1402). In some embodiments, the induction dose is a dose of about 300 mg, about 310 mg, about 320 mg, about 330 mg, about 340 mg, about 350 mg, about 360 mg, about 370 mg, about 380 mg, about 390 mg, about 400 mg, about 410 mg, about 420 mg, about 430 mg, about 440 mg, about 450 mg, about 460 mg, about 470 mg, about 480 mg, about 490 mg, or about 500 mg of an anti-FcRn antibody (e.g., batoclimab or IMVT-1402).

[0354] In some embodiments, the induction dose is a dose of about 500 mg to about 700 mg of an anti-FcRn antibody (e.g., batoclimab or IMVT-1402). In some embodiments, the induction dose is a dose of about 500 mg, about 510 mg, about 520 mg, about 530 mg, about 540 mg, about 550 mg, about 560 mg, about 570 mg, about 580 mg, about 590 mg, about 600 mg, about 610 mg, about 620 mg, about 630 mg, about 640 mg, about 650 mg, about 660 mg, about 670 mg, about 680 mg, about 690 mg, or about 700 mg of an anti-FcRn antibody (e.g., batoclimab or IMVT-1402).

[0355] In some embodiments, the induction dose is a dose of about 700 mg to about 1000 mg an anti-FcRn antibody (e.g., batoclimab or IMVT-1402). In some embodiments, the induction dose is a dose of about 700 mg, about 710 mg, about 720 mg, about 730 mg, about 740 mg, about 750 mg, about 760 mg, about 765 mg, about 770 mg, about 780 mg, about 790 mg, about 800 mg, about 810 mg, about 820 mg, about 830 mg, about 840 mg, about 850 mg, about 860 mg, about 870 mg, about 880 mg, about 890 mg, about 900 mg, about 910 mg, about 920 mg, about 930 mg, about 940 mg, about 950 mg, about 960 mg, about 970 mg, about 980 mg, about 990 mg, or about 1000 mg an anti-FcRn antibody (e.g., batoclimab or IMVT-1402).

[0356] In some embodiments, the induction dose is a dose of about 1000 mg to about 1500 mg of an anti-FcRn antibody (e.g., batoclimab or IMVT-1402). In some embodiments, the induction dose is a dose of about 1000 mg, about 1010 mg, about 1020 mg, about 1030 mg, about 1040 mg, about 1050 mg, about 1060 mg, about 1070 mg, about 1080 mg, about 1090 mg, about 1100 mg, about 1110 mg, about 1120 mg, about 1130 mg, about 1140 mg, about 1150 mg, about 1160 mg, about 1170 mg, about 1180 mg, about 1190 mg, about 1200 mg, about 1210 mg, about 1220 mg, about 1230 mg, about 1240 mg, about 1250 mg, about 1260 mg, about 1270 mg, about 1280 mg, about 1290 mg, about 1300 mg, about 1310 mg, about 1320 mg, about 1330 mg, about 1340 mg, about 1350 mg, about 1360 mg, about 1370 mg, about 1380 mg, about 1390 mg, about 1400 mg, about 1410 mg, about 14 mg, about 1430 mg, about 1440 mg, about 1450 mg, about 1460 mg, about 1470 mg, about 1480 mg, about 1490 mg, or about 1500 mg of an anti-FcRn antibody (e.g., batoclimab or IMVT-1402).

[0357] In some embodiments, the induction dose of an anti-FcRn antibody (e.g., batoclimab or IMVT-1402) is administered to the patient once or more than once over a period of about 1 day, 2 days, 3 days, 4 days, 5 days, 6 days, 7 days, 8 days, 9 days, 10 days, 11 days, 12 days, 13 days, 14 days, 1 week, 2 weeks, 3 weeks, 4 weeks, 1 month, 2 months, 3 months, 4 months, 5 months,6 months, 7 months, 8 months, 9 months, 10 months, 11 months, 12 months, 18 months, 24 months, 30 months, 36 months, 48 months, 52 months, 60 months, or longer.

[0358] In some embodiments, the induction dose of an anti-FcRn antibody (e.g., batoclimab or IMVT-1402) is administered to the patient once weekly. In some embodiments, the induction dose of an anti-FcRn antibody (e.g., batoclimab or IMVT-1402) is administered to the patient once weekly for at least 1 week, at least 2 weeks, at least 3 weeks, at least 4 weeks, at least 5 weeks, at least 6 weeks, at least 7 weeks, at least 8 weeks, at least 9 weeks, at least 10 weeks, at least 12 weeks, at least 20 weeks, at least 24 weeks, at least 30 weeks, at least 40 weeks, at least 50 weeks, at least 60 weeks, at least 70 weeks, at least 76 weeks, at least 80 weeks, or longer. In some embodiments, the induction dose of an anti-FcRn antibody (e.g., batoclimab or IMVT- 1402) is administered to the patient once weekly for at least 12 weeks. In some embodiments, the induction dose of an anti-FcRn antibody (e.g., batoclimab or IMVT-1402) once weekly for at least 24 weeks.

[0359] In some embodiments, the induction dose of an anti-FcRn antibody (e.g., batoclimab or IMVT-1402) is administered to the patient once weekly as a single (i.e., one) subcutaneous injection. In some embodiments, the induction dose of an anti-FcRn antibody (e.g., batoclimab or IMVT-1402) is administered to the patient once weekly as two or more consecutive subcutaneous injections (e.g., two consecutive subcutaneous injections). The term “consecutive,” as used herein in the context of subcutaneous injections (or other routes of administration), refers to two or more subcutaneous injections administered one after another, but sufficiently close in time so as to provide the desired therapeutic or prophylactic effect. In some embodiments, consecutive subcutaneous injections are administered within about 30 seconds, within about 1 minute, within about 2 minutes, within about 5 minutes, within about 10 minutes, within about 30 minutes, within about 1 hour, within about 2 hours, or within about 5 hours of one another.

[0360] In some embodiments, the induction dose of an anti-FcRn antibody (e.g., batoclimab or IMVT-1402) is administered to the patient once every 2 weeks (bi-weekly). In some embodiments, the induction dose of an anti-FcRn antibody (e.g., batoclimab or IMVT-1402) is administered to the patient once every 2 weeks for at least 2 weeks, at least 4 weeks, at least 6 weeks, at least 8 weeks, at least 10 weeks, at least 12 weeks, at least 20 weeks, at least 24 weeks, at least 30 weeks, at least 40 weeks, at least 50 weeks, at least 60 weeks, at least 70 weeks, at least 76 weeks, at least 80 weeks, or longer. In some embodiments, the induction dose of an anti-FcRn antibody (e.g., batoclimab or IMVT-1402) is administered to the patient once every 2 weeks for at least 12 weeks. In some embodiments, the induction dose of an anti-FcRn antibody (e.g., batoclimab or IMVT-1402) is administered to the patient weekly for at least 24 weeks.

[0361] In some embodiments, the induction dose of an anti-FcRn antibody (e.g., batoclimab or IMVT-1402) is administered to the patient once monthly. In some embodiments, the induction dose of an anti-FcRn antibody (e.g., batoclimab or IMVT-1402) is administered to the patient once monthly for at least 1 month, at least 2 months, at least 3 months, at least 4 months, at least 5 months, at least 6 months, at least 7 months, at least 8 months, at least 9 months, at least 10 months, at least 11 months, at least 12 months, at least 18 months, at least 24 months, at least 30 months, at least 36 months, or longer. In some embodiments, the induction dose of an anti-FcRn antibody (e.g., batoclimab or IMVT-1402) is administered to the patient once monthly as a single subcutaneous injection. In some embodiments, the induction dose of an anti-FcRn antibody (e.g., batoclimab or IMVT-1402) is administered to the patient once monthly as two or more consecutive subcutaneous injections.

[0362] In some embodiments, the induction dose is a dose of 680 mg of batoclimab. In some embodiments, the induction dose is a dose of 680 mg of batoclimab, administered subcutaneously once per week. In some embodiments, the induction dose is a dose of 680 mg of batoclimab, administered subcutaneously every other week. In some embodiments, the induction dose is a dose of 680 mg of batoclimab, administered subcutaneously once per week for 12 weeks.

[0363] In some embodiments, the induction dose is 600 mg of IMVT-1402. In some embodiments, the induction dose is 600 mg of IMVT-1402 administered subcutaneously once per week. In some embodiments, the induction dose is 600 mg of IMVT-1402 administered subcutaneously every other week. In some embodiments, the induction dose is 600 mg of IMVT- 1402 administered subcutaneously once per week for 12 weeks.Graves ’ Disease (GD)

[0364] In some embodiments, an induction dose for treatment of Graves’ disease (GD) comprises a dose of about 100 mg to about 200 mg of IMVT-1402. In some embodiments, an induction dose for treatment of GD comprises a dose of about 100 mg, about 110 mg, about 120 mg, about 130 mg, about 140 mg, about 150 mg, about 160 mg, about 170 mg, about 180 mg, about 190 mg, or about 200 mg of IMVT-1402. In some embodiments, an induction dose fortreatment of GD comprises a dose of about 200 mg to about 300 mg of IMVT-1402. In some embodiments, an induction dose comprises a dose of about 200 mg, about 210 mg, about 220 mg, about 230 mg, about 240 mg, about 250 mg, about 260 mg, about 270 mg, about 280 mg, about 290 mg, or about 300 mg of IMVT-1402. In some embodiments, an induction dose for treatment of GD comprises a dose of about 300 mg to about 500 mg of IMVT-1402. In some embodiments, an induction dose for treatment of GD comprises a dose of about 300 mg, about 310 mg, about 320 mg, about 330 mg, about 340 mg, about 350 mg, about 360 mg, about 370 mg, about 380 mg, about 390 mg, about 400 mg, about 410 mg, about 420 mg, about 430 mg, about 440 mg, about 450 mg, about 460 mg, about 470 mg, about 480 mg, about 490 mg, or about 500 mg of IMVT-1402. In some embodiments, an induction dose for treatment of GD comprises a dose of about 500 mg to about 700 mg of IMVT-1402. In some embodiments, an induction dose for treatment of GD comprises a dose of about 500 mg, about 510 mg, about 520 mg, about 530 mg, about 540 mg, about 550 mg, about 560 mg, about 570 mg, about 580 mg, about 590 mg, about 600 mg, about 610 mg, about 620 mg, about 630 mg, about 640 mg, about 650 mg, about 660 mg, about 670 mg, about 680 mg, about 690 mg, or about 700 mg of IMVT- 1402. In some embodiments, an induction dose for treatment of GD comprises a dose of about 700 mg to about 1000 mg IMVT-1402. In some embodiments, an induction dose for treatment of GD comprises a dose of about 700 mg, about 710 mg, about 720 mg, about 730 mg, about 740 mg, about 750 mg, about 760 mg, about 765 mg, about 770 mg, about 780 mg, about 790 mg, about 800 mg, about 810 mg, about 820 mg, about 830 mg, about 840 mg, about 850 mg, about 860 mg, about 870 mg, about 880 mg, about 890 mg, about 900 mg, about 910 mg, about 920 mg, about 930 mg, about 940 mg, about 950 mg, about 960 mg, about 970 mg, about 980 mg, about 990 mg, or about 1000 mg of IMVT-1402. In some embodiments, an induction dose for treatment of GD comprises a dose of about 1000 mg to about 1500 mg of IMVT-1402. In some embodiments, an induction dose for treatment of GD comprises a dose of about 1000 mg, about 1010 mg, about 1020 mg, about 1030 mg, about 1040 mg, about 1050 mg, about 1060 mg, about1070 mg, about 1080 mg, about 1090 mg, about 1100 mg, about 1110 mg, about 1120 mg, about1130 mg, about 1140 mg, about 1150 mg, about 1160 mg, about 1170 mg, about 1180 mg, about1190 mg, about 1200 mg, about 1210 mg, about 1220 mg, about 1230 mg, about 1240 mg, about1250 mg, about 1260 mg, about 1270 mg, about 1280 mg, about 1290 mg, about 1300 mg, about1310 mg, about 1320 mg, about 1330 mg, about 1340 mg, about 1350 mg, about 1360 mg, about1370 mg, about 1380 mg, about 1390 mg, about 1400 mg, about 1410 mg, about 1420 mg, about 1430 mg, about 1440 mg, about 1450 mg, about 1460 mg, about 1470 mg, about 1480 mg, about 1490 mg, or about 1500 mg of IMVT-1402.

[0365] In some embodiments, an induction dose of IMVT-1402 for treating GD is administered to the patient once or more than once over a period of about 1 day, 2 days, 3 days, 4 days, 5 days, 6 days, 7 days, 8 days, 9 days, 10 days, 11 days, 12 days, 13 days, 14 days, 1 week, 2 weeks, 3 weeks, 4 weeks, 1 month, 2 months, 3 months, 4 months, 5 months, 6 months, 7 months, 8 months, 9 months, 10 months, 11 months, 12 months, 18 months, 24 months, 30 months, 36 months, 48 months, 52 months, 60 months, or longer.

[0366] In some embodiments, an induction dose of IMVT-1402 for treating GD is administered to the patient once weekly. In some embodiments, an induction dose of IMVT-1402 for treating GD is administered to the patient once weekly for at least 1 week, at least 2 weeks, at least 3 weeks, at least 4 weeks, at least 5 weeks, at least 6 weeks, at least 7 weeks, at least 8 weeks, at least 9 weeks, at least 10 weeks, at least 12 weeks, at least 20 weeks, at least 24 weeks, at least 30 weeks, at least 40 weeks, at least 50 weeks, at least 60 weeks, at least 70 weeks, at least 76 weeks, at least 80 weeks, or longer. In some embodiments, an induction dose of IMVT-1402 for treating GD is administered to the patient once weekly for at least 12 weeks. In some embodiments, an induction dose of IMVT-1402 for treating GD once weekly for at least 24 weeks.

[0367] In some embodiments, an induction dose of IMVT-1402 for treating GD is administered to the patient once weekly as a single (i.e., one) subcutaneous injection. In some embodiments, an induction dose of IMVT-1402 for treating GD is administered to the patient once weekly as two or more consecutive subcutaneous injections (e.g., two consecutive subcutaneous injections). The term “consecutive,” as used herein in the context of subcutaneous injections (or other routes of administration), refers to two or more subcutaneous injections administered one after another, but sufficiently close in time so as to provide the desired therapeutic or prophylactic effect. In some embodiments, consecutive subcutaneous injections are administered within about 30 seconds, within about 1 minute, within about 2 minutes, within about 5 minutes, within about 10 minutes, within about 30 minutes, within about 1 hour, within about 2 hours, or within about 5 hours of one another.

[0368] In some embodiments, an induction dose of IMVT-1402 for treating GD is administered to the patient once every 2 weeks (bi-weekly). In some embodiments, an induction dose of IMVT-1402 for treating GD is administered to the patient once every 2 weeks for at least 2 weeks, at least 4 weeks, at least 6 weeks, at least 8 weeks, at least 10 weeks, at least 12 weeks, at least 20 weeks, at least 24 weeks, at least 30 weeks, at least 40 weeks, at least 50 weeks, at least 60 weeks, at least 70 weeks, at least 76 weeks, at least 80 weeks, or longer. In some embodiments, an induction dose of IMVT-1402 for treating GD is administered to the patient once every 2 weeks for at least 12 weeks. In some embodiments, an induction dose of IMVT- 1402 for treating GD is administered to the patient weekly for at least 24 weeks.

[0369] In some embodiments, an induction dose of IMVT-1402 for treating GD is administered to the patient once monthly. In some embodiments, an induction dose of IMVT-1402 for treating GD is administered to the patient once monthly for at least 1 month, at least 2 months, at least 3 months, at least 4 months, at least 5 months, at least 6 months, at least 7 months, at least 8 months, at least 9 months, at least 10 months, at least 11 months, at least 12 months, at least 18 months, at least 24 months, at least 30 months, at least 36 months, or longer. In some embodiments, an induction dose of IMVT-1402 for treating GD is administered to the patient once monthly as a single subcutaneous injection. In some embodiments, an induction dose of IMVT-1402 for treating GD is administered to the patient once monthly as two or more consecutive subcutaneous injections.

[0370] In some embodiments, an induction dose for treating GD is 600 mg of IMVT-1402. In some embodiments, an induction dose for treating GD is 600 mg of IMVT-1402 administered subcutaneously once per week. In some embodiments, an induction dose for treating GD is 600 mg of IMVT-1402 administered subcutaneously every other week. In some embodiments, an induction dose for treating GD is 600 mg of IMVT-1402 administered subcutaneously once per week for 26 weeks. In some embodiments, an induction dose for treating GD is 600 mg of IMVT-1402 administered subcutaneously once per week for 26 weeks. In some embodiments, an induction dose for treating GD is 600 mg of IMVT-1402 administered subcutaneously once per week for 52 weeks. In some embodiments, an induction dose of IMVT-1402 for treating GD is combined with a flare dose (e.g., a concurrent or additional dose of IMVT-1402 to control a flare-up of GD) for treating GD.Rheumatoid Arthritis (RA)

[0371] In some embodiments, an induction dose for treatment of Rheumatoid Arthritis (RA) comprises a dose of about 100 mg to about 200 mg of IMVT-1402. In some embodiments, an induction dose for treatment of RA comprises a dose of about 100 mg, about 110 mg, about 120 mg, about 130 mg, about 140 mg, about 150 mg, about 160 mg, about 170 mg, about 180 mg, about 190 mg, or about 200 mg of IMVT-1402. In some embodiments, an induction dose for treatment of RA comprises a dose of about 200 mg to about 300 mg of IMVT-1402. In some embodiments, an induction dose comprises a dose of about 200 mg, about 210 mg, about 220 mg, about 230 mg, about 240 mg, about 250 mg, about 260 mg, about 270 mg, about 280 mg, about 290 mg, or about 300 mg of IMVT-1402. In some embodiments, an induction dose for treatment of RA comprises a dose of about 300 mg to about 500 mg of IMVT-1402. In some embodiments, an induction dose for treatment of RA comprises a dose of about 300 mg, about 310 mg, about 320 mg, about 330 mg, about 340 mg, about 350 mg, about 360 mg, about 370 mg, about 380 mg, about 390 mg, about 400 mg, about 410 mg, about 420 mg, about 430 mg, about 440 mg, about 450 mg, about 460 mg, about 470 mg, about 480 mg, about 490 mg, or about 500 mg of IMVT-1402. In some embodiments, an induction dose for treatment of RA comprises a dose of about 500 mg to about 700 mg of IMVT-1402. In some embodiments, an induction dose for treatment of RA comprises a dose of about 500 mg, about 510 mg, about 520 mg, about 530 mg, about 540 mg, about 550 mg, about 560 mg, about 570 mg, about 580 mg, about 590 mg, about 600 mg, about 610 mg, about 620 mg, about 630 mg, about 640 mg, about 650 mg, about 660 mg, about 670 mg, about 680 mg, about 690 mg, or about 700 mg of IMVT- 1402. In some embodiments, an induction dose for treatment of RA comprises a dose of about 700 mg to about 1000 mg IMVT-1402. In some embodiments, an induction dose for treatment of RA comprises a dose of about 700 mg, about 710 mg, about 720 mg, about 730 mg, about 740 mg, about 750 mg, about 760 mg, about 765 mg, about 770 mg, about 780 mg, about 790 mg, about 800 mg, about 810 mg, about 820 mg, about 830 mg, about 840 mg, about 850 mg, about 860 mg, about 870 mg, about 880 mg, about 890 mg, about 900 mg, about 910 mg, about 920 mg, about 930 mg, about 940 mg, about 950 mg, about 960 mg, about 970 mg, about 980 mg, about 990 mg, or about 1000 mg of IMVT-1402. In some embodiments, an induction dose for treatment of RA comprises a dose of about 1000 mg to about 1500 mg of IMVT-1402. In some embodiments, an induction dose for treatment of RA comprises a dose of about 1000 mg, about1010 mg, about 1020 mg, about 1030 mg, about 1040 mg, about 1050 mg, about 1060 mg, about1070 mg, about 1080 mg, about 1090 mg, about 1100 mg, about 1110 mg, about 1120 mg, about1130 mg, about 1140 mg, about 1150 mg, about 1160 mg, about 1170 mg, about 1180 mg, about1190 mg, about 1200 mg, about 1210 mg, about 1220 mg, about 1230 mg, about 1240 mg, about1250 mg, about 1260 mg, about 1270 mg, about 1280 mg, about 1290 mg, about 1300 mg, about1310 mg, about 1320 mg, about 1330 mg, about 1340 mg, about 1350 mg, about 1360 mg, about1370 mg, about 1380 mg, about 1390 mg, about 1400 mg, about 1410 mg, about 1420 mg, about1430 mg, about 1440 mg, about 1450 mg, about 1460 mg, about 1470 mg, about 1480 mg, about1490 mg, or about 1500 mg of IMVT-1402.

[0372] In some embodiments, an induction dose of IMVT-1402 for treating RA is administered to the patient once or more than once over a period of about 1 day, 2 days, 3 days, 4 days, 5 days, 6 days, 7 days, 8 days, 9 days, 10 days, 11 days, 12 days, 13 days, 14 days, 1 week, 2 weeks, 3 weeks, 4 weeks, 1 month, 2 months, 3 months, 4 months, 5 months, 6 months, 7 months, 8 months, 9 months, 10 months, 11 months, 12 months, 18 months, 24 months, 30 months, 36 months, 48 months, 52 months, 60 months, or longer.

[0373] In some embodiments, an induction dose of IMVT-1402 for treating RA is administered to the patient once weekly. In some embodiments, an induction dose of IMVT-1402 for treating RA is administered to the patient once weekly for at least 1 week, at least 2 weeks, at least 3 weeks, at least 4 weeks, at least 5 weeks, at least 6 weeks, at least 7 weeks, at least 8 weeks, at least 9 weeks, at least 10 weeks, at least 12 weeks, at least 20 weeks, at least 24 weeks, at least 30 weeks, at least 40 weeks, at least 50 weeks, at least 60 weeks, at least 70 weeks, at least 76 weeks, at least 80 weeks, or longer. In some embodiments, an induction dose of IMVT-1402 for treating RA is administered to the patient once weekly for at least 12 weeks. In some embodiments, an induction dose of IMVT-1402 for treating RA once weekly for at least 24 weeks.

[0374] In some embodiments, an induction dose of IMVT-1402 for treating RA is administered to the patient once weekly as a single (i.e., one) subcutaneous injection. In some embodiments, an induction dose of IMVT-1402 for treating RA is administered to the patient once weekly as two or more consecutive subcutaneous injections (e.g., two consecutive subcutaneous injections). The term “consecutive,” as used herein in the context of subcutaneous injections (or other routes of administration), refers to two or more subcutaneous injections administered one after another,but sufficiently close in time so as to provide the desired therapeutic or prophylactic effect. In some embodiments, consecutive subcutaneous injections are administered within about 30 seconds, within about 1 minute, within about 2 minutes, within about 5 minutes, within about 10 minutes, within about 30 minutes, within about 1 hour, within about 2 hours, or within about 5 hours of one another.

[0375] In some embodiments, an induction dose of IMVT-1402 for treating RA is administered to the patient once every 2 weeks (bi-weekly). In some embodiments, an induction dose of IMVT-1402 for treating RA is administered to the patient once every 2 weeks for at least 2 weeks, at least 4 weeks, at least 6 weeks, at least 8 weeks, at least 10 weeks, at least 12 weeks, at least 20 weeks, at least 24 weeks, at least 30 weeks, at least 40 weeks, at least 50 weeks, at least 60 weeks, at least 70 weeks, at least 76 weeks, at least 80 weeks, or longer. In some embodiments, an induction dose of IMVT-1402 for treating RA is administered to the patient once every 2 weeks for at least 12 weeks. In some embodiments, an induction dose of IMVT- 1402 for treating RA is administered to the patient weekly for at least 24 weeks.

[0376] In some embodiments, an induction dose of IMVT-1402 for treating RA is administered to the patient once monthly. In some embodiments, an induction dose of IMVT-1402 for treating RA is administered to the patient once monthly for at least 1 month, at least 2 months, at least 3 months, at least 4 months, at least 5 months, at least 6 months, at least 7 months, at least 8 months, at least 9 months, at least 10 months, at least 11 months, at least 12 months, at least 18 months, at least 24 months, at least 30 months, at least 36 months, or longer. In some embodiments, an induction dose of IMVT-1402 for treating RA is administered to the patient once monthly as a single subcutaneous injection. In some embodiments, an induction dose of IMVT-1402 for treating RA is administered to the patient once monthly as two or more consecutive subcutaneous injections.

[0377] In some embodiments, an induction dose for treating RA is 600 mg of IMVT-1402. In some embodiments, an induction dose for treating RA is 600 mg of IMVT-1402 administered subcutaneously once per week. In some embodiments, an induction dose for treating RA is 600 mg of IMVT-1402 administered subcutaneously every other week. In some embodiments, an induction dose for treating RA is 600 mg of IMVT-1402 administered subcutaneously once per week for 16 weeks. In some embodiments, an induction dose for treating RA is 600 mg of IMVT-1402 administered subcutaneously once per week for 16 weeks. In some embodiments, aninduction dose for treating RA is 600 mg of IMVT-1402 administered subcutaneously once per week for 32 weeks. In some embodiments, an induction dose for treating RA is 600 mg of IMVT-1402 administered subcutaneously once per week for 16 weeks, after which the induction dose is stopped and a maintenance dose is administered. In some embodiments, an induction dose of IMVT-1402 for treating RA is combined with a flare dose (e.g., a concurrent or additional dose of IMVT-1402 to control a flare-up of RA) for treating RA.Maintenance Dose

[0378] The maintenance dose may be a lower dose (compared to the induction dose) of an anti- FcRn antibody that is administered to maintain control of disease symptoms after the initial administration of the induction dose. However, in some circumstances the induction dose and the maintenance dose may be the same or similar.

[0379] In some embodiments, the maintenance dose is a dose of about 100 mg to about 200 mg of an anti-FcRn antibody (e.g., batoclimab or IMVT-1402). In some embodiments, the maintenance dose is a dose of about 100 mg, about 110 mg, about 120 mg, about 130 mg, about 140 mg, about 150 mg, about 160 mg, about 170 mg, about 180 mg, about 190 mg, or about 200 mg of an anti-FcRn antibody (e.g., batoclimab or IMVT-1402).

[0380] In some embodiments, the maintenance dose is a dose of about 200 mg to about 300 mg of an anti-FcRn antibody (e.g., batoclimab or IMVT-1402). In some embodiments, the maintenance dose is a dose of about 200 mg, about 210 mg, about 220 mg, about 230 mg, about 240 mg, about 250 mg, about 260 mg, about 270 mg, about 280 mg, about 290 mg, or about 300 mg of an anti-FcRn antibody (e.g., batoclimab or IMVT-1402).

[0381] In some embodiments, the maintenance dose is a dose of about 300 mg to about 500 mg of an anti-FcRn antibody (e.g., batoclimab or IMVT-1402). In some embodiments, the maintenance dose is a dose of about 300 mg, about 310 mg, about 320 mg, about 330 mg, about 340 mg, about 350 mg, about 360 mg, about 370 mg, about 380 mg, about 390 mg, about 400 mg, about 410 mg, about 420 mg, about 430 mg, about 440 mg, about 450 mg, about 460 mg, about 470 mg, about 480 mg, about 490 mg, or about 500 mg of an anti-FcRn antibody (e.g., batoclimab or IMVT-1402).

[0382] In some embodiments, the maintenance dose is a dose of about 500 mg to about 700 mg of an anti-FcRn antibody (e.g., batoclimab or IMVT-1402). In some embodiments, the maintenance dose is a dose of about 500 mg, about 510 mg, about 520 mg, about 530 mg, about540 mg, about 550 mg, about 560 mg, about 570 mg, about 580 mg, about 590 mg, about 600 mg, about 610 mg, about 620 mg, about 630 mg, about 640 mg, about 650 mg, about 660 mg, about 670 mg, about 680 mg, about 690 mg, or about 700 mg of an anti-FcRn antibody (e.g., batoclimab or IMVT-1402).

[0383] In some embodiments, the maintenance dose is a dose of about 700 mg to about 1000 mg an anti-FcRn antibody (e.g., batoclimab or IMVT-1402). In some embodiments, the maintenance dose is a dose of about 700 mg, about 710 mg, about 720 mg, about 730 mg, about 740 mg, about 750 mg, about 760 mg, about 765 mg, about 770 mg, about 780 mg, about 790 mg, about 800 mg, about 810 mg, about 820 mg, about 830 mg, about 840 mg, about 850 mg, about 860 mg, about 870 mg, about 880 mg, about 890 mg, about 900 mg, about 910 mg, about 920 mg, about 930 mg, about 940 mg, about 950 mg, about 960 mg, about 970 mg, about 980 mg, about 990 mg, or about 1000 mg an anti-FcRn antibody (e.g., batoclimab or IMVT-1402).

[0384] In some embodiments, the maintenance dose is a dose of about 1000 mg to about 1500 mg of an anti-FcRn antibody (e.g., batoclimab or IMVT-1402). In some embodiments, the maintenance dose is a dose of about 1000 mg, about 1010 mg, about 1020 mg, about 1030 mg, about 1040 mg, about 1050 mg, about 1060 mg, about 1070 mg, about 1080 mg, about 1090 mg, about 1100 mg, about 1110 mg, about 1120 mg, about 1130 mg, about 1140 mg, about 1150 mg, about 1160 mg, about 1170 mg, about 1180 mg, about 1190 mg, about 1200 mg, about 1210 mg, about 1220 mg, about 1230 mg, about 1240 mg, about 1250 mg, about 1260 mg, about 1270 mg, about 1280 mg, about 1290 mg, about 1300 mg, about 1310 mg, about 1320 mg, about 1330 mg, about 1340 mg, about 1350 mg, about 1360 mg, about 1370 mg, about 1380 mg, about 1390 mg, about 1400 mg, about 1410 mg, about 1420 mg, about 1430 mg, about 1440 mg, about 1450 mg, about 1460 mg, about 1470 mg, about 1480 mg, about 1490 mg, or about 1500 mg of an anti- FcRn antibody (e.g., batoclimab or IMVT-1402).

[0385] In some embodiments, the maintenance dose of an anti-FcRn antibody (e.g., batoclimab or IMVT-1402) is administered to the patient once or more than once over a period of about 1 day, 2 days, 3 days, 4 days, 5 days, 6 days, 7 days, 8 days, 9 days, 10 days, 11 days, 12 days, 13 days, 14 days, 1 week, 2 weeks, 3 weeks, 4 weeks, 1 month, 2 months, 3 months, 4 months, 5 months, 6 months, 7 months, 8 months, 9 months, 10 months, 11 months, 12 months, 18 months, 24 months, 30 months, 36 months, 48 months, 52 months, 60 months, or longer. In some embodiments, the maintenance dose is administered for the rest of a patient’s life.

[0386] In some embodiments, the maintenance dose of an anti-FcRn antibody (e.g., batoclimab or IMVT-1402) is administered to the patient once weekly. In some embodiments, the maintenance dose of an anti-FcRn antibody (e.g., batoclimab or IMVT-1402) is administered to the patient once weekly for at least 1 week, at least 2 weeks, at least 3 weeks, at least 4 weeks, at least 5 weeks, at least 6 weeks, at least 7 weeks, at least 8 weeks, at least 9 weeks, at least 10 weeks, at least 12 weeks, at least 20 weeks, at least 24 weeks, at least 30 weeks, at least 40 weeks, at least 50 weeks, at least 60 weeks, at least 70 weeks, at least 76 weeks, at least 80 weeks, or longer. In some embodiments, the maintenance dose of an anti-FcRn antibody (e.g., batoclimab or IMVT-1402) is administered to the patient once weekly for at least 12 weeks. In some embodiments, the maintenance dose of an anti-FcRn antibody (e.g., batoclimab or IMVT- 1402) once weekly for at least 24 weeks.

[0387] In some embodiments, the maintenance dose of an anti-FcRn antibody (e.g., batoclimab or IMVT-1402) is administered to the patient once weekly as a single (i.e., one) subcutaneous injection. In some embodiments, the maintenance dose of an anti-FcRn antibody (e.g., batoclimab or IMVT-1402) is administered to the patient once weekly as two or more consecutive subcutaneous injections (e.g., two consecutive subcutaneous injections).

[0388] In some embodiments, the maintenance dose of an anti-FcRn antibody (e.g., batoclimab or IMVT-1402) is administered to the patient once every 2 weeks (bi-weekly). In some embodiments, the maintenance dose of an anti-FcRn antibody (e.g., batoclimab or IMVT-1402) is administered to the patient once every 2 weeks for at least 2 weeks, at least 4 weeks, at least 6 weeks, at least 8 weeks, at least 10 weeks, at least 12 weeks, at least 20 weeks, at least 24 weeks, at least 30 weeks, at least 40 weeks, at least 50 weeks, at least 60 weeks, at least 70 weeks, at least 76 weeks, at least 80 weeks, or longer. In some embodiments, the maintenance dose of an anti-FcRn antibody (e.g., batoclimab or IMVT-1402) is administered to the patient once every 2 weeks for at least 12 weeks. In some embodiments, the maintenance dose of an anti-FcRn antibody (e.g., batoclimab or IMVT-1402) is administered to the patient weekly for at least 24 weeks.

[0389] In some embodiments, the maintenance dose of an anti-FcRn antibody (e.g., batoclimab or IMVT-1402) is administered to the patient once monthly. In some embodiments, the maintenance dose of an anti-FcRn antibody (e.g., batoclimab or IMVT-1402) is administered to the patient once monthly for at least 1 month, at least 2 months, at least 3 months, at least 4months, at least 5 months, at least 6 months, at least 7 months, at least 8 months, at least 9 months, at least 10 months, at least 11 months, at least 12 months, at least 18 months, at least 24 months, at least 30 months, at least 36 months, or longer. In some embodiments, the maintenance dose of an anti-FcRn antibody (e.g., batoclimab or IMVT-1402) is administered to the patient once monthly as a single subcutaneous injection. In some embodiments, the maintenance dose of an anti-FcRn antibody (e.g., batoclimab or IMVT-1402) is administered to the patient once monthly as two or more consecutive subcutaneous injections.

[0390] In some embodiments, the maintenance dose is 340 mg of batoclimab. In some embodiments, the maintenance dose is 340 mg of batoclimab administered subcutaneously once per week. In some embodiments, the maintenance dose is 340 mg of batoclimab administered subcutaneously every other week. In some embodiments, the maintenance dose is 340 mg of batoclimab administered subcutaneously once per week for 12 months or longer. In some embodiments, the maintenance dose is 340 mg of batoclimab administered subcutaneously every other week for 12 months or longer.

[0391] In some embodiments, the maintenance dose is 680 mg of batoclimab. In some embodiments, the maintenance dose is 680 mg of batoclimab administered subcutaneously once per week. In some embodiments, the maintenance dose is 680 mg of batoclimab administered subcutaneously every other week. In some embodiments, the maintenance dose is 680 mg of batoclimab administered subcutaneously once per week for 12 months or longer. In some embodiments, the maintenance dose is 680 mg of batoclimab administered subcutaneously every other week for 12 months or longer.

[0392] In some embodiments, the maintenance dose is 300 mg of IMVT-1402. In some embodiments, the maintenance dose is 300 mg of IMVT-1402 administered subcutaneously once per week. In some embodiments, the maintenance dose is 300 mg of IMVT-1402 administered subcutaneously every other week. In some embodiments, the maintenance dose is 300 mg of IMVT-1402 administered subcutaneously once per week for 12 months or longer. In some embodiments, the maintenance dose is 300 mg of IMVT-1402 administered subcutaneously every other week for 12 months or longer.

[0393] In some embodiments, the maintenance dose is 600 mg of IMVT-1402. In some embodiments, the maintenance dose is 600 mg of IMVT-1402 administered subcutaneously once per week. In some embodiments, the maintenance dose is 600 mg of IMVT-1402 administeredsubcutaneously every other week. In some embodiments, the maintenance dose is 600 mg of IMVT-1402 administered subcutaneously once per week for 12 months or longer. In some embodiments, the maintenance dose is 600 mg of IMVT-1402 administered subcutaneously every other week for 12 months or longer.

[0394] In some embodiments, the induction dose and the maintenance dose are alternated, e.g., the patient may receive the induction dose for a first period of time followed by the maintenance dose for a first period of time, followed by the induction dose for a second period of time, optionally followed by the maintenance dose for a second period of time. In some embodiments, the cycle of induction and maintenance dose (administration of the induction dose for a period of time followed by administration of the maintenance dose for a period of time being one cycle) is repeated one twice, three times, four times, five times, six times seven times, or ten times. In some embodiments, the cycle of induction and maintenance dose is repeated for about 3 months, about 6 months, about 12 months, about 15 months, about 18 months, about 24 months, or longer.

[0395] In another aspect, a method described here comprises (i) administering to a subject 680 mg of an anti-FcRn antibody subcutaneously once weekly for 12 weeks, followed by (ii) administering to the subject 340 mg of the anti-FcRn antibody subcutaneously once weekly for 12 weeks. In another aspect, a method described here comprises (i) administering to a subject 600 mg of an anti-FcRn antibody subcutaneously once weekly for 12 weeks, followed by (ii) administering to the subject 300 mg of the anti-FcRn antibody subcutaneously once weekly for 12 weeks. These steps (i) and (ii) may be repeated as needed, for example, repeated twice (for a total treatment time of 48 weeks) three times (for a total treatment time of 72 weeks), four times (for a total treatment time of 96 weeks), or five times (for a total treatment time of 120 weeks).Graves ’ Disease (GD)

[0396] A maintenance dose for treatment of Graves’ disease (GD) may be a lower dose (compared to the induction dose) of IMVT-1402 that is administered to maintain control of disease symptoms after the initial administration of the induction dose. In some embodiments, a maintenance dose for treatment of GD comprises the same dose as an induction dose for treatment of GD.

[0397] In some embodiments, a maintenance dose for treatment of GD is a dose of about 100 mg to about 200 mg of IMVT-1402. In some embodiments, a maintenance dose for treatment of GDis a dose of about 100 mg, about 110 mg, about 120 mg, about 130 mg, about 140 mg, about 150 mg, about 160 mg, about 170 mg, about 180 mg, about 190 mg, or about 200 mg of IMVT-1402. In some embodiments, a maintenance dose for treatment of GD is a dose of about 200 mg to about 300 mg of IMVT-1402. In some embodiments, a maintenance dose for treatment of GD is a dose of about 200 mg, about 210 mg, about 220 mg, about 230 mg, about 240 mg, about 250 mg, about 260 mg, about 270 mg, about 280 mg, about 290 mg, or about 300 mg of IMVT-1402. In some embodiments, a maintenance dose for treatment of GD is a dose of about 300 mg to about 500 mg of IMVT-1402. In some embodiments, a maintenance dose for treatment of GD is a dose of about 300 mg, about 310 mg, about 320 mg, about 330 mg, about 340 mg, about 350 mg, about 360 mg, about 370 mg, about 380 mg, about 390 mg, about 400 mg, about 410 mg, about 420 mg, about 430 mg, about 440 mg, about 450 mg, about 460 mg, about 470 mg, about 480 mg, about 490 mg, or about 500 mg of IMVT-1402. In some embodiments, a maintenance dose for treatment of GD is a dose of about 500 mg to about 700 mg of IMVT-1402. In some embodiments, a maintenance dose for treatment of GD is a dose of about 500 mg, about 510 mg, about 520 mg, about 530 mg, about 540 mg, about 550 mg, about 560 mg, about 570 mg, about 580 mg, about 590 mg, about 600 mg, about 610 mg, about 620 mg, about 630 mg, about 640 mg, about 650 mg, about 660 mg, about 670 mg, about 680 mg, about 690 mg, or about 700 mg of IMVT-1402. In some embodiments, a maintenance dose for treatment of GD is a dose of about 700 mg to about 1000 mg IMVT-1402. In some embodiments, a maintenance dose for treatment of GD is a dose of about 700 mg, about 710 mg, about 720 mg, about 730 mg, about 740 mg, about 750 mg, about 760 mg, about 765 mg, about 770 mg, about 780 mg, about 790 mg, about 800 mg, about 810 mg, about 820 mg, about 830 mg, about 840 mg, about 850 mg, about 860 mg, about 870 mg, about 880 mg, about 890 mg, about 900 mg, about 910 mg, about 920 mg, about 930 mg, about 940 mg, about 950 mg, about 960 mg, about 970 mg, about 980 mg, about 990 mg, or about 1000 mg IMVT-1402. In some embodiments, a maintenance dose for treatment of GD is a dose of about 1000 mg to about 1500 mg of IMVT-1402. In some embodiments, a maintenance dose for treatment of GD is a dose of about 1000 mg, about 1010 mg, about 1020 mg, about 1030 mg, about 1040 mg, about 1050 mg, about 1060 mg, about 1070 mg, about 1080 mg, about 1090 mg, about 1100 mg, about 1110 mg, about 1120 mg, about 1130 mg, about 1140 mg, about 1150 mg, about 1160 mg, about 1170 mg, about 1180 mg, about 1190 mg, about 1200 mg, about 1210 mg, about 1220 mg, about 1230 mg, about 1240 mg, about1250 mg, about 1260 mg, about 1270 mg, about 1280 mg, about 1290 mg, about 1300 mg, about 1310 mg, about 1320 mg, about 1330 mg, about 1340 mg, about 1350 mg, about 1360 mg, about 1370 mg, about 1380 mg, about 1390 mg, about 1400 mg, about 1410 mg, about 1420 mg, about 1430 mg, about 1440 mg, about 1450 mg, about 1460 mg, about 1470 mg, about 1480 mg, about 1490 mg, or about 1500 mg of IMVT-1402.

[0398] In some embodiments, a maintenance dose for treatment of GD of IMVT-1402 is administered to the patient once or more than once over a period of about 1 day, 2 days, 3 days, 4 days, 5 days, 6 days, 7 days, 8 days, 9 days, 10 days, 11 days, 12 days, 13 days, 14 days, 1 week, 2 weeks, 3 weeks, 4 weeks, 1 month, 2 months, 3 months, 4 months, 5 months, 6 months, 7 months, 8 months, 9 months, 10 months, 11 months, 12 months, 18 months, 24 months, 30 months, 36 months, 48 months, 52 months, 60 months, or longer. In some embodiments, a maintenance dose for treatment of GD is administered for the rest of a patient’s life.

[0399] In some embodiments, a maintenance dose for treatment of GD of IMVT-1402 is administered to the patient once weekly. In some embodiments, a maintenance dose for treatment of GD of IMVT-1402 is administered to the patient once weekly for at least 1 week, at least 2 weeks, at least 3 weeks, at least 4 weeks, at least 5 weeks, at least 6 weeks, at least 7 weeks, at least 8 weeks, at least 9 weeks, at least 10 weeks, at least 12 weeks, at least 20 weeks, at least 24 weeks, at least 30 weeks, at least 40 weeks, at least 50 weeks, at least 60 weeks, at least 70 weeks, at least 76 weeks, at least 80 weeks, or longer. In some embodiments, a maintenance dose for treatment of GD of IMVT-1402 is administered to the patient once weekly for at least 12 weeks. In some embodiments, a maintenance dose for treatment of GD of IMVT- 1402 once weekly for at least 24 weeks.

[0400] In some embodiments, a maintenance dose for treatment of GD of IMVT-1402 is administered to the patient once weekly as a single (i.e., one) subcutaneous injection. In some embodiments, a maintenance dose for treatment of GD of IMVT-1402 is administered to the patient once weekly as two or more consecutive subcutaneous injections (e.g., two consecutive subcutaneous injections).

[0401] In some embodiments, a maintenance dose for treatment of GD of IMVT-1402 is administered to the patient once every 2 weeks (bi-weekly). In some embodiments, a maintenance dose for treatment of GD of IMVT-1402 is administered to the patient once every 2weeks for at least 2 weeks, at least 4 weeks, at least 6 weeks, at least 8 weeks, at least 10 weeks, at least 12 weeks, at least 20 weeks, at least 24 weeks, at least 30 weeks, at least 40 weeks, at least 50 weeks, at least 60 weeks, at least 70 weeks, at least 76 weeks, at least 80 weeks, or longer. In some embodiments, a maintenance dose for treatment of GD of IMVT-1402 is administered to the patient once every 2 weeks for at least 12 weeks. In some embodiments, a maintenance dose for treatment of GD of IMVT-1402 is administered to the patient weekly for at least 24 weeks.

[0402] In some embodiments, a maintenance dose for treatment of GD of IMVT-1402 is administered to the patient once monthly. In some embodiments, a maintenance dose for treatment of GD of IMVT-1402 is administered to the patient once monthly for at least 1 month, at least 2 months, at least 3 months, at least 4 months, at least 5 months, at least 6 months, at least 7 months, at least 8 months, at least 9 months, at least 10 months, at least 11 months, at least 12 months, at least 18 months, at least 24 months, at least 30 months, at least 36 months, or longer. In some embodiments, a maintenance dose for treatment of GD of IMVT-1402 is administered to the patient once monthly as a single subcutaneous injection. In some embodiments, a maintenance dose for treatment of GD of IMVT-1402 is administered to the patient once monthly as two or more consecutive subcutaneous injections.

[0403] In some embodiments, a maintenance dose for treatment of GD comprises a dose of 300 mg of IMVT-1402. In some embodiments, a maintenance dose for treatment of GD comprises a dose of 300 mg of IMVT-1402 administered subcutaneously once per week. In some embodiments, a maintenance dose for treatment of GD comprises a dose of 300 mg of IMVT- 1402 administered subcutaneously every other week. In some embodiments, a maintenance dose for treatment of GD comprises a dose of 300 mg of IMVT-1402 administered subcutaneously once per week for 12 months or longer. In some embodiments, a maintenance dose for treatment of GD comprises a dose of 300 mg of IMVT-1402 administered subcutaneously every other week for 12 months or longer.

[0404] In some embodiments, a maintenance dose for treatment of GD comprises a dose of 600 mg of IMVT-1402. In some embodiments, a maintenance dose for treatment of GD comprises a dose of 600 mg of IMVT-1402 administered subcutaneously once per week. In some embodiments, a maintenance dose for treatment of GD comprises a dose of 600 mg of IMVT- 1402 administered subcutaneously every other week. In some embodiments, a maintenance doseI l lfor treatment of GD comprises a dose of 600 mg of IMVT-1402 administered subcutaneously once per week for 12 months or longer. In some embodiments, a maintenance dose for treatment of GD comprises a dose of 600 mg of IMVT-1402 administered subcutaneously every other week for 12 months or longer.

[0405] In some embodiments, the induction dose and a maintenance dose for treatment of GD are alternated, e.g., the patient may receive the induction dose for a first period of time followed by a maintenance dose for treatment of GD for a first period of time, followed by the induction dose for a second period of time, optionally followed by a maintenance dose for treatment of GD for a second period of time. In some embodiments, the cycle of induction and maintenance dose (administration of the induction dose for a period of time followed by administration of a maintenance dose for treatment of GD for a period of time being one cycle) is repeated one twice, three times, four times, five times, six times seven times, or ten times. In some embodiments, the cycle of induction and maintenance dose is repeated for about 3 months, about 6 months, about 12 months, about 15 months, about 18 months, about 24 months, or longer.

[0406] In another aspect, a method described here comprises (i) administering to a subject 600 mg of IMVT-1402 subcutaneously once weekly for 26 weeks, followed by (ii) administering to the subject 300 mg of IMVT-1402 subcutaneously once weekly for 26 weeks. In another aspect, a method described here comprises (i) administering to a subject 600 mg of IMVT-1402 subcutaneously once weekly for 26 weeks, followed by (ii) administering to the subject 600 mg of IMVT-1402 subcutaneously once weekly for 26 weeks. These steps (i) and (ii) may be repeated as needed, for example, repeated twice (for a total treatment time of 52 weeks) three times (for a total treatment time of 78 weeks), four times (for a total treatment time of 104 weeks), or five times (for a total treatment time of 130 weeks).

[0407] In some embodiments, a maintenance dose for treatment of GD comprises a dose of 600 mg of IMVT-1402 administered subcutaneously once weekly for 26 weeks. In some embodiments, a maintenance dose for treatment of GD comprises a dose of 600 mg of IMVT- 1402 administered subcutaneously once weekly for 52 weeks. In some embodiments, a maintenance dose for treatment of GD comprises a dose of 600 mg of IMVT-1402 administered subcutaneously once weekly for at least 52 weeks. In some embodiments, a maintenance dose of IMVT-1402 for treating GD is combined with a flare dose (e.g., a concurrent or additional dose of IMVT-1402 to control a flare-up of GD) for treating GD.Rheumatoid Arthritis (RA)

[0408] A maintenance dose for treatment of Rheumatoid Arthritis (RA) may be a lower dose (compared to the induction dose) of IMVT-1402 that is administered to maintain control of disease symptoms after the initial administration of the induction dose. In some embodiments, a maintenance dose for treatment of RA comprises the same dose as an induction dose for treatment of RA.

[0409] In some embodiments, a maintenance dose for treatment of RA is a dose of about 100 mg to about 200 mg of IMVT-1402. In some embodiments, a maintenance dose for treatment of RA is a dose of about 100 mg, about 110 mg, about 120 mg, about 130 mg, about 140 mg, about 150 mg, about 160 mg, about 170 mg, about 180 mg, about 190 mg, or about 200 mg of IMVT-1402. In some embodiments, a maintenance dose for treatment of RA is a dose of about 200 mg to about 300 mg of IMVT-1402. In some embodiments, a maintenance dose for treatment of RA is a dose of about 200 mg, about 210 mg, about 220 mg, about 230 mg, about 240 mg, about 250 mg, about 260 mg, about 270 mg, about 280 mg, about 290 mg, or about 300 mg of IMVT-1402. In some embodiments, a maintenance dose for treatment of RA is a dose of about 300 mg to about 500 mg of IMVT-1402. In some embodiments, a maintenance dose for treatment of RA is a dose of about 300 mg, about 310 mg, about 320 mg, about 330 mg, about 340 mg, about 350 mg, about 360 mg, about 370 mg, about 380 mg, about 390 mg, about 400 mg, about 410 mg, about 420 mg, about 430 mg, about 440 mg, about 450 mg, about 460 mg, about 470 mg, about 480 mg, about 490 mg, or about 500 mg of IMVT-1402. In some embodiments, a maintenance dose for treatment of RA is a dose of about 500 mg to about 700 mg of IMVT-1402. In some embodiments, a maintenance dose for treatment of RA is a dose of about 500 mg, about 510 mg, about 520 mg, about 530 mg, about 540 mg, about 550 mg, about 560 mg, about 570 mg, about 580 mg, about 590 mg, about 600 mg, about 610 mg, about 620 mg, about 630 mg, about 640 mg, about 650 mg, about 660 mg, about 670 mg, about 680 mg, about 690 mg, or about 700 mg of IMVT-1402. In some embodiments, a maintenance dose for treatment of RA is a dose of about 700 mg to about 1000 mg IMVT-1402. In some embodiments, a maintenance dose for treatment of RA is a dose of about 700 mg, about 710 mg, about 720 mg, about 730 mg, about 740 mg, about 750 mg, about 760 mg, about 765 mg, about 770 mg, about 780 mg, about 790 mg, about 800 mg, about 810 mg, about 820 mg, about 830 mg, about 840 mg, about 850 mg, about 860 mg, about 870 mg, about 880 mg, about 890 mg, about 900 mg, about 910 mg, about920 mg, about 930 mg, about 940 mg, about 950 mg, about 960 mg, about 970 mg, about 980 mg, about 990 mg, or about 1000 mg IMVT-1402. In some embodiments, a maintenance dose for treatment of RA is a dose of about 1000 mg to about 1500 mg of IMVT-1402. In some embodiments, a maintenance dose for treatment of RA is a dose of about 1000 mg, about 1010 mg, about 1020 mg, about 1030 mg, about 1040 mg, about 1050 mg, about 1060 mg, about 1070 mg, about 1080 mg, about 1090 mg, about 1100 mg, about 1110 mg, about 1120 mg, about 1130 mg, about 1140 mg, about 1150 mg, about 1160 mg, about 1170 mg, about 1180 mg, about 1190 mg, about 1200 mg, about 1210 mg, about 1220 mg, about 1230 mg, about 1240 mg, about 1250 mg, about 1260 mg, about 1270 mg, about 1280 mg, about 1290 mg, about 1300 mg, about 1310 mg, about 1320 mg, about 1330 mg, about 1340 mg, about 1350 mg, about 1360 mg, about 1370 mg, about 1380 mg, about 1390 mg, about 1400 mg, about 1410 mg, about 1420 mg, about 1430 mg, about 1440 mg, about 1450 mg, about 1460 mg, about 1470 mg, about 1480 mg, about 1490 mg, or about 1500 mg of IMVT-1402.

[0410] In some embodiments, a maintenance dose for treatment of RA of IMVT-1402 is administered to the patient once or more than once over a period of about 1 day, 2 days, 3 days, 4 days, 5 days, 6 days, 7 days, 8 days, 9 days, 10 days, 11 days, 12 days, 13 days, 14 days, 1 week, 2 weeks, 3 weeks, 4 weeks, 1 month, 2 months, 3 months, 4 months, 5 months, 6 months, 7 months, 8 months, 9 months, 10 months, 11 months, 12 months, 18 months, 24 months, 30 months, 36 months, 48 months, 52 months, 60 months, or longer. In some embodiments, a maintenance dose for treatment of RA is administered for the rest of a patient’s life.

[0411] In some embodiments, a maintenance dose for treatment of RA of IMVT-1402 is administered to the patient once weekly. In some embodiments, a maintenance dose for treatment of RA of IMVT-1402 is administered to the patient once weekly for at least 1 week, at least 2 weeks, at least 3 weeks, at least 4 weeks, at least 5 weeks, at least 6 weeks, at least 7 weeks, at least 8 weeks, at least 9 weeks, at least 10 weeks, at least 12 weeks, at least 20 weeks, at least 24 weeks, at least 30 weeks, at least 40 weeks, at least 50 weeks, at least 60 weeks, at least 70 weeks, at least 76 weeks, at least 80 weeks, or longer. In some embodiments, a maintenance dose for treatment of RA of IMVT-1402 is administered to the patient once weekly for at least 12 weeks. In some embodiments, a maintenance dose for treatment of RA of IMVT-1402 once weekly for at least 24 weeks. In some embodiments, a maintenance dose for treatment of GD of IMVT-1402 once weekly for at least 52 weeks.

[0412] In some embodiments, a maintenance dose for treatment of RA of IMVT-1402 is administered to the patient once weekly as a single (i.e., one) subcutaneous injection. In some embodiments, a maintenance dose for treatment of RA of IMVT-1402 is administered to the patient once weekly as two or more consecutive subcutaneous injections (e.g., two consecutive subcutaneous injections).

[0413] In some embodiments, a maintenance dose for treatment of RA of IMVT-1402 is administered to the patient once every 2 weeks (bi-weekly). In some embodiments, a maintenance dose for treatment of RA of IMVT-1402 is administered to the patient once every 2 weeks for at least 2 weeks, at least 4 weeks, at least 6 weeks, at least 8 weeks, at least 10 weeks, at least 12 weeks, at least 20 weeks, at least 24 weeks, at least 30 weeks, at least 40 weeks, at least 50 weeks, at least 60 weeks, at least 70 weeks, at least 76 weeks, at least 80 weeks, or longer. In some embodiments, a maintenance dose for treatment of RA of IMVT-1402 is administered to the patient once every 2 weeks for at least 12 weeks. In some embodiments, a maintenance dose for treatment of RA of IMVT-1402 is administered to the patient weekly for at least 24 weeks.

[0414] In some embodiments, a maintenance dose for treatment of RA of IMVT-1402 is administered to the patient once monthly. In some embodiments, a maintenance dose for treatment of RA of IMVT-1402 is administered to the patient once monthly for at least 1 month, at least 2 months, at least 3 months, at least 4 months, at least 5 months, at least 6 months, at least 7 months, at least 8 months, at least 9 months, at least 10 months, at least 11 months, at least 12 months, at least 18 months, at least 24 months, at least 30 months, at least 36 months, or longer. In some embodiments, a maintenance dose for treatment of RA of IMVT-1402 is administered to the patient once monthly as a single subcutaneous injection. In some embodiments, a maintenance dose for treatment of RA of IMVT-1402 is administered to the patient once monthly as two or more consecutive subcutaneous injections.

[0415] In some embodiments, a maintenance dose for treatment of RA comprises a dose of 300 mg of IMVT-1402. In some embodiments, a maintenance dose for treatment of RA comprises a dose of 300 mg of IMVT-1402 administered subcutaneously once per week. In some embodiments, a maintenance dose for treatment of RA comprises a dose of 300 mg of EMVT-1402 administered subcutaneously every other week. In some embodiments, a maintenance dose for treatment of RA comprises a dose of 300 mg of IMVT-1402 administered subcutaneously once per week for 12 months or longer. In some embodiments, a maintenance dose for treatment ofRA comprises a dose of 300 mg of IMVT-1402 administered subcutaneously every other week for 12 months or longer.

[0416] In some embodiments, a maintenance dose for treatment of RA comprises a dose of 600 mg of IMVT-1402. In some embodiments, a maintenance dose for treatment of RA comprises a dose of 600 mg of IMVT-1402 administered subcutaneously once per week. In some embodiments, a maintenance dose for treatment of RA comprises a dose of 600 mg of IMVT- 1402 administered subcutaneously every other week. In some embodiments, a maintenance dose for treatment of RA comprises a dose of 600 mg of IMVT-1402 administered subcutaneously once per week for 12 months or longer. In some embodiments, a maintenance dose for treatment of RA comprises a dose of 600 mg of IMVT-1402 administered subcutaneously every other week for 12 months or longer.

[0417] In some embodiments, the induction dose and a maintenance dose for treatment of RA are alternated, e.g., the patient may receive the induction dose for a first period of time followed by a maintenance dose for treatment of RA for a first period of time, followed by the induction dose for a second period of time, optionally followed by a maintenance dose for treatment of RA for a second period of time. In some embodiments, the cycle of induction and maintenance dose (administration of the induction dose for a period of time followed by administration of a maintenance dose for treatment of RA for a period of time being one cycle) is repeated one twice, three times, four times, five times, six times seven times, or ten times. In some embodiments, the cycle of induction and maintenance dose is repeated for about 3 months, about 6 months, about 12 months, about 15 months, about 18 months, about 24 months, or longer.

[0418] In another aspect, a method described here comprises (i) administering to a subject 600 mg of IMVT-1402 subcutaneously once weekly for 16 weeks, followed by (ii) administering to the subject 300 mg of IMVT-1402 subcutaneously once weekly for 16 weeks. In another aspect, a method described here comprises (i) administering to a subject 600 mg of IMVT-1402 subcutaneously once weekly for 16 weeks, followed by (ii) administering to the subject 600 mg of IMVT-1402 subcutaneously once weekly for 16 weeks. These steps (i) and (ii) may be repeated as needed, for example, repeated twice (for a total treatment time of 32 weeks) threetimes (for a total treatment time of 48 weeks), four times (for a total treatment time of 64 weeks), or five times (for a total treatment time of 80 weeks).

[0419] In some embodiments, a maintenance dose for treatment of RA comprises a dose of 600 mg of IMVT-1402 administered subcutaneously once weekly for 16 weeks. In some embodiments, a maintenance dose for treatment of RA comprises a dose of 600 mg of IMVT- 1402 administered subcutaneously once weekly for 16 weeks. In some embodiments, a maintenance dose for treatment of RA comprises a dose of 300 mg of IMVT-1402 administered subcutaneously once weekly for 16 weeks. In some embodiments, a maintenance dose for treatment of RA comprises a dose of 300 mg of IMVT-1402 administered subcutaneously once weekly for at least 16 weeks. In some embodiments, a maintenance dose of IMVT-1402 for treating RA is combined with a flare dose (e.g., a concurrent or additional dose of IMVT-1402 to control a flare-up of RA) for treating RA.Loading Dose

[0420] A loading dose may be added to the administration schedule. Without wishing to be bound by theory, it is believed that the administration of a loading dose of anti-FcRn antibody results in a faster decrease in serum IgG and / or autoantibodies, and, by extension, better control of disease symptoms. This is particularly important in disease with acute symptoms, where additional treatment (e.g., rescue treatment) may be required if the reduction in IgG and / or antibodies is not achieved fast enough. In the context of many autoimmune diseases, reduction in IgG is correlated with clinical efficacy.

[0421] Generally, a loading dose is added to the first 1-2 weeks of the induction dose. Thus, in some embodiments, the loading dose is administered on day 4 of the first week of the induction dose. In some embodiments, the loading dose is administered on day 4 and day 11 during the first two weeks of administration of the induction dose. “Day 4,” “day 11,” etc. refer to the days of treatment, with day 1 being the first day on which the induction dose of the anti-FcRn antibody is administered.

[0422] In some embodiments, the loading dose is a dose of about 100 mg to about 200 mg of an anti-FcRn antibody (e.g., batoclimab or IMVT-1402). In some embodiments, the loading dose is a dose of about 100 mg, about 110 mg, about 120 mg, about 130 mg, about 140 mg, about 150 mg, about 160 mg, about 170 mg, about 180 mg, about 190 mg, or about 200 mg of an anti-FcRn antibody (e.g., batoclimab or IMVT-1402).

[0423] In some embodiments, the loading dose is a dose of about 200 mg to about 300 mg of an anti-FcRn antibody (e.g., batoclimab or IMVT-1402). In some embodiments, the loading dose is a dose of about 200 mg, about 210 mg, about 220 mg, about 230 mg, about 240 mg, about 250 mg, about 260 mg, about 270 mg, about 280 mg, about 290 mg, or about 300 mg of an anti-FcRn antibody (e.g., batoclimab or IMVT-1402).

[0424] In some embodiments, the loading dose is a dose of about 300 mg to about 500 mg of an anti-FcRn antibody (e.g., batoclimab or IMVT-1402). In some embodiments, the loading dose is a dose of about 300 mg, about 310 mg, about 320 mg, about 330 mg, about 340 mg, about 350 mg, about 360 mg, about 370 mg, about 380 mg, about 390 mg, about 400 mg, about 410 mg, about 420 mg, about 430 mg, about 440 mg, about 450 mg, about 460 mg, about 470 mg, about 480 mg, about 490 mg, or about 500 mg of an anti-FcRn antibody (e.g., batoclimab or IMVT- 1402).

[0425] In some embodiments, the loading dose is a dose of about 500 mg to about 700 mg of an anti-FcRn antibody (e.g., batoclimab or IMVT-1402). In some embodiments, the loading dose is a dose of about 500 mg, about 510 mg, about 520 mg, about 530 mg, about 540 mg, about 550 mg, about 560 mg, about 570 mg, about 580 mg, about 590 mg, about 600 mg, about 610 mg, about 620 mg, about 630 mg, about 640 mg, about 650 mg, about 660 mg, about 670 mg, about 680 mg, about 690 mg, or about 700 mg of an anti-FcRn antibody (e.g., batoclimab or IMVT- 1402).

[0426] In some embodiments, the loading dose is a dose of about 700 mg to about 1000 mg an anti-FcRn antibody (e.g., bat...

Claims

CLAIMSWhat is claimed is:

1. A method of treating an autoimmune disease in a subject in need thereof, the method comprising administering to the subject a loading dose, and induction dose and a maintenance dose of an anti-FcRn therapy.

2. The method of claim 1, comprising administering the induction dose for 12 weeks.

3. The method of claim 1, comprising administering the maintenance dose for 12 weeks.

4. The method of claim 1, comprising administering the maintenance dose for 12 months.

5. The method of claim 1, comprising administering the loading dose on day 4 of the first week of the induction dose.

6. The method of claim 1, comprising administering the loading dose on day 4 and day 11 during the first two weeks of administration of the induction dose.

7. The method of claim 1, wherein the induction dose is 680 mg of batoclimab administered subcutaneously once per week.

8. The method of claim 1, wherein the maintenance dose is 340 mg of batoclimab administered subcutaneously once per week.

9. The method of claim 1, wherein the maintenance dose is 340 mg of batoclimab administered subcutaneously once every other week.

10. The method of claim 1, wherein the loading dose is a dose of 680 mg of batoclimab administered subcutaneously.

11. The method of claim 1, wherein the induction dose is 600 mg of IMVT-1402 administered subcutaneously once per week.

12. The method of claim 1, wherein the maintenance dose is 300 mg of IMVT-1402 administered subcutaneously once per week.

13. The method of claim 1, wherein the maintenance dose is 300 mg of IMVT-1402 administered subcutaneously once every other week.

14. The method of claim 1, wherein the loading dose is a dose of 600 mg of IMVT-1402 administered subcutaneously.

15. The method of claim 1 , wherein the autoimmune disease is a progressive autoimmune disease.

16. The method of claim 1 , wherein the autoimmune disease is CIDP.

17. The method of claim 1, wherein the autoimmune disease is Myasthenia Gravis.

18. A method of treating an autoimmune disease in a subject in need thereof, the method comprising administering to the subject:(a) 680 mg of batoclimab on day 1 ;(b) 680 mg of batoclimab on day 4;(c) 680 mg of batoclimab on day 8;(d) 680 mg of batoclimab on day 11 ; and(e) 680 mg of batoclimab once weekly beginning on day 15, for a total treatment duration of 12 weeks.

19. The method of claim 18, further comprising step (f): administering to the subject 340 mg of batoclimab once weekly beginning on day 85, for a total treatment duration of 24 weeks.

20. The method of claim 18, further comprising step (g): administering the subject 680 mg of batoclimab once weekly beginning on day 168 for a total treatment duration of 36 weeks.

21. The method of claim 18, comprising administering the batoclimab subcutaneously.

22. The method of claim 20, wherein the method results in a reduction in the level of at least one autoantibody in the subject of at least 50% by 7 days post-initial dose compared to baseline.

23. The method of claim 18, wherein the method results in a reduction in the level of at least one autoantibody in the subject of at least 75% by 7 days post-initial dose compared to baseline.

24. The method of claim 18, wherein the method results in a reduction in the level of at least one autoantibody in the subject of at least 85% by 7 days post-initial dose compared to baseline.

25. The method of any one of claims 22-24, wherein the autoantibody is an antibody against AChR, MuSK, LRP4, agrin, Kvl.4 potassium channel, rapsyn, cortactin, acetylcholinesterase, collagen Q, or collagen XIII.

26. The method of claim 18, wherein the method results in a reduction in the level of total IgG in the subject of at least 50% by 7 days post-initial dose compared to baseline.

27. The method of claim 18, wherein the method results in a reduction in the level of total IgG in the subject of at least 75% by 7 days post-initial dose compared to baseline.

28. The method of claim 18, wherein the method results in a reduction in the level of total IgG in the subject of at least 85% by 7 days post-initial dose compared to baseline.

29. The method of claim 18, wherein the autoimmune disease is progressive.

30. The method of claim 18, wherein the autoimmune disease is CIDP.

31. The method of claim 18, wherein the autoimmune disease is Myasthenia Gravis.

32. A method of treating an autoimmune disease in a subject in need thereof, the method comprising administering to the subject:(a) 600 mg of IMVT- 1402 on day 1 ;(b) 600 mg of IMVT-1402 on day 4;(c) 600 mg of IMVT- 1402 on day 8 ;(d) 600 mg of IMVT-1402 on day 11; and(e) 600 mg of IMVT-1402 once weekly beginning on day 15, for a total treatment duration of 12 weeks.

33. The method of claim 32, further comprising step (f): administering to the subject 300 mg of IMVT-1402 once weekly beginning on day 85, for a total treatment duration of 24 weeks.

34. The method of claim 32, further comprising step (g): administering the subject 600 mg of IMVT-1402 once weekly beginning on day 168 for a total treatment duration of 36 weeks.

35. The method of claim 32, comprising administering the IMVT-1402 subcutaneously.

36. The method of claim 33, wherein the method results in a reduction in the level of at least one autoantibody in the subject of at least 50% by 7 days post-initial dose compared to baseline.

37. The method of claim 32, wherein the method results in a reduction in the level of at least one autoantibody in the subject of at least 75% by 7 days post-initial dose compared to baseline.

38. The method of claim 32, wherein the method results in a reduction in the level of at least one autoantibody in the subject of at least 85% by 7 days post-initial dose compared to baseline.

39. The method of claim 32, wherein the method results in a reduction in the level of at least one autoantibody in the subject of at least 90% by 7 days post-initial dose compared to baseline.

40. The method of claim 32, wherein the method results in a reduction in the level of total IgG in the subject of at least 50% by 7 days post-initial dose compared to baseline.

41. The method of claim 32, wherein the method results in a reduction in the level of total IgG in the subject of at least 75% by 7 days post-initial dose compared to baseline.

42. The method of claim 32, wherein the method results in a reduction in the level of total IgG in the subject of at least 85% by 7 days post-initial dose compared to baseline.

43. The method of claim 32, wherein the autoimmune disease is a progressive autoimmune disease.

44. The method of claim 32, wherein the autoimmune disease is CIDP.

45. The method of claim 32, wherein the autoimmune disease is Myasthenia Gravis.

46. A method of controlling a flare-up of an autoimmune disease in a subject being treated with an anti-FcRn therapy, the method comprising administering to the subject at least four doses of an anti-FcRn antibody.

47. The method of claim 46, comprising administering the anti-FcRn antibody on days 1, 8, 15, and 22.

48. The method of claim 46, comprising administering the anti-FcRn antibody on days 1, 4, 8, 15, and 22.

49. The method of claim 46, wherein the anti-FcRn antibody is batoclimab.

50. The method of claim 49, wherein the batoclimab is administered subcutaneously.

51. The method of claim 49, comprising administering 680 mg of batoclimab.

52. The method of claim 46, wherein the anti-FcRn antibody is IMVT-1402.

53. The method of claim 52, wherein IMVT-1402 is administered subcutaneously.

54. The method of claim 52, comprising administering 600 mg of IMVT-1402.

55. The method of claim 46, wherein the autoimmune disease is a progressive autoimmune disease.

56. The method of claim 46, wherein the autoimmune disease is treated with TVIg.

57. The method of claim 46, wherein the autoimmune disease is being treated with PLEX.

58. The method of claim 46, wherein the autoimmune disease is CIDP.

59. The method of claim 46, wherein the autoimmune disease is Myasthenia Gravis.

60. A method for treating Graves’ Disease (GD) in a subject, the method comprising administering the subject an anti-FcRn antibody at 550-700 mg once weekly.

61. A method for treating or preventing thyroid eye disease (TED) in a subject having Graves’ disease (GD), the method comprising administering the subject an anti-FcRn antibody at 550-700 mg once weekly.

62. A method for inducing remission in a subject having Graves’ disease (GD), the method comprising administering the subject an anti-FcRn antibody at 550-700 mg once weekly.

63. The method of any one of claims 60-62, wherein the subject is administered 600 mg of the anti-FcRn antibody once weekly.

64. The method of any one of claims 60-63, wherein the antibody is administered to the subject for a period of 20-60 weeks.

65. The method of any one of claims 60-64, wherein the antibody is administered to the subject for 52 weeks.

66. The method of any one of claims 60-64, wherein the antibody is administered to the subject for 26 weeks.

67. The method of claim 66, wherein the subject is administered the antibody at a reduced dose after the initial 26 weeks.

68. The method of claim 67, wherein the subject is administered the reduced dose of the antibody at 300 mg once weekly.

69. The method of claim 68, wherein the subject is administered the reduced dose of the antibody at 300 mg once weekly for 26 weeks.

70. The method of any one of claims 60-69, wherein the anti-FcRn antibody is IMVT-1402.

71. The method of any one of claims 60-70, wherein the antibody comprises a heavy chain variable region (VH) comprising a heavy chain complementarity determining region (HCDR) 1 comprising the amino acid sequence of SEQ ID NO: 7, a HCDR2 comprising the amino acid sequence of SEQ ID NO: 8, and a HCDR3 comprising the amino acid sequence of SEQ ID NO: 9, and a light chain variable region comprising a light chain complementarity determining region (LCDR) 1 comprising the amino acid sequence of SEQ ID NO: 10, a LCDR2 comprising the amino acid sequence of SEQ ID NO: 11, and a LCDR3 comprising the amino acid sequence of SEQ ID NO: 12.

72. The method of any one of claims 60-71, wherein the antibody comprises a VH comprising the amino acid sequence of SEQ ID NO: 15, and a VL comprising the amino acid sequence of SEQ ID NO: 16.

73. The method of any one of claims 60-72, wherein the antibody comprises a heavy chain comprising the amino acid sequence of SEQ ID NO: 19, and a light chain comprising the amino acid sequence of SEQ ID NO: 20.

74. The method of any one of claims 60-72, wherein the antibody comprises a heavy chain comprising the amino acid sequence of SEQ ID NO: 21, and a light chain comprising the amino acid sequence of SEQ ID NO: 22.

75. The method of any one of claims 60-74, wherein the subject has overtly hyperthyroidism prior to the administration.

76. The method of claim 75, wherein the subject has a baseline triiodothyronine (T3) level higher than upper limit of normal (ULN).

77. The method of claims 75 or 76, wherein the subject has a baseline free thyroxine (FT4) level higher than ULN.

78. The method of any one of claims 75-77, wherein the subject a baseline TSH level no more than the lower limit of normal (LLN).

79. The method of any one of claims 60-74, wherein the subject has subclinical hyperthyroidism prior to the administration.

80. The method of claim 79, wherein the subject has a T3 level within a clinically normal T3 level.

81. The method of claim 79 or 80, wherein the subject has a FT4 level within a clinically normal FT4.

82. The method of any one of claims 79-81, wherein the subject has a thyroid-stimulating hormone (TSH) level less than 0.1 mU / L.

83. The method of any one of claims 60-82, wherein the subject is receiving antithyroid drug (ATD) at the time of the administration of the anti-FcRn antibody.

84. The method of claim 83, wherein the subject has previously received antithyroid drug (ATD) for at least 3 months prior to the administration of the anti-FcRn antibody.

85. The method of claim 83 or 84, wherein the ATD is methimazole, carbimazole, propylthiouracil.

86. The method of any one of claims 83-85, wherein the subject is receiving an ATD dose of at least 20 mg / day methimazole prior to the administration of the anti-FcRn antibody.

87. The method of any one of claims 83-86, wherein the subject is receiving an ATD dose of at least 30 mg / day carbimazole prior to the administration of the anti-FcRn antibody.

88. The method of any one of claims 83-87, wherein the subject is receiving an ATD dose of at least 200 mg / day propylthiouracil prior to the administration of the anti-FcRn antibody.

89. The method of any one of claims 83-88, wherein the subject is receiving the ATD for the four- weeks immediately preceding a baseline assessment of the anti-FcRn antibody.

90. The method of any one of claims 83-88, wherein the subject has been receiving antithyroid drug (ATD) for at least six months prior to a baseline assessment.

91. The method of claim 90, wherein the ATD is methimazole, carbimazole, propylthiouracil.

92. The method of any one of claims 83, 90, or 91, wherein the subject is receiving an ATD dose of at least 15 mg / day methimazole prior to the administration of the anti-FcRn antibody.

93. The method of any one of claims 83-85, wherein the subject is receiving an ATD dose of at least 20 mg / day carbimazole prior to the administration of the anti-FcRn antibody.

94. The method of any one of claims 83-85, wherein the subject is receiving an ATD dose of at least 150 mg / day propylthiouracil prior to the administration of the anti-FcRn antibody.

95. The method of claim 94, wherein the subject is concurrently receiving an ATD.

96. The method of claim 95, wherein the subject in on ATD at a dose of at least 10 mg / day methimazole.

97. The method of claim 95, wherein the subject in on ATD at a dose of at least 15 mg / day carbimazole.

98. The method of claim 95, wherein the subject is on ATD at a dose of at least 100 mg / day propylthiouracil.

99. The method of any one of claims 60-98, wherein the subject does not have or previously had hyperthyroidism not caused by GD.

100. The method of claim 99, wherein the subject does not have toxic adenoma or toxic multinodular goiter.

101. The method of claim 99 or 100, wherein the subject does not have a history of thyroid storm within six months of the administration of the anti-FcRn antibody.

102. The method of any one of claims 60-101, wherein the subject does not have TED.

103. The method of any one of claims 60-102, wherein the subject does not have moderate to severe active TED that requires immediate surgical intervention, corrective surgery, irradiation and / or medical therapy.

104. The method of any one of claims 60-103, wherein the subject does not have a history of noncompliance with ATD therapy.

105. The method of any one of claims 60-104, wherein the anti-FcRn antibody is administered subcutaneously.

106. The method of any one of claims 60-105, wherein the administration induces euthyroid in the subject at or before week 25 of administration of the anti-FcRn antibody.

107. The method of claim 106, wherein the administration reduces the level of T3 in the subject to be within normal range.

108. The method of claim 106 or 107, wherein the administration reduces the level of FT4 in the subject to be within normal range.

109. The method of any one of claims 106-108, wherein the administration increases the level of TSH in the subject to be within normal range.

110. The method of any one of claims 60-109, wherein the subject stops receiving ATD at or before week 26 of administration.

111. The method of any one of claims 60-110, wherein the administration of the anti-FcRn antibody induces a state of euthyroidism in the subject at or before week 52 of administration.

112. The method of claim 111, wherein the administration of the anti-FcRn antibody reduces the level of T3 in the subject to be within normal range.

113. The method of claim 111 or 112, wherein the administration of the anti-FcRn antibody reduces the level of FT4 in the subject to be within normal range.

114. The method of any one of claims 111-113, wherein the administration of the anti-FcRn antibody increases the level of TSH in the subject to be within normal range.

115. The method of any one of claims 111-114, wherein the subj ect stops receiving ATD at or before week 52 of administration of the anti-FcRn antibody.

116. The method of any one of claims 60-115, wherein the administration of the anti-FcRn antibody prevents the development or improves one or more following eye symptom in the subject: bulging eyes; gritty feeling in the eyes; pressure or pain in the eyes; retracted eyelids; red or inflamed eyes; light sensitivity; blurred or double vision, or vision loss.

117. The method of any one of claims 60-116, wherein the administration of the anti-FcRn antibody induces remission in the subject (i.e., subject is euthyroid for at least 6 months or more following discontinuation of both therapies).

118. A method for treating Rheumatoid Arthritis (RA) in a subject, the method comprising administering the subject an anti-FcRn antibody at 550-700 mg once weekly.

119. The method of claim 118, wherein the subject is administered 600 mg of the anti-FcRn antibody once weekly.

120. The method of claim 118 or 119, wherein the subject is administered 600 mg of the anti- FcRn antibody once weekly for at least 16 weeks, and is subsequently administered(i) 600 mg of the anti-FcRn antibody once weekly; or(ii) 300 mg of the anti-FcRn antibody once weekly.

121. The method of any one of claims 118-120, wherein the anti-FcRn antibody is administered subcutaneously.

122. The method of any one of claims 118-121, wherein the subject has active RA.

123. The method of any one of claims 118-122, wherein the subject has refractory RA.

124. The method of any one of claims 118-123, wherein the subject has moderate disease activity.

125. The method of any one of claims 118-124, wherein the subject has a DAS28-ESR score of more than 3.2.

126. The method of any one of claims 118-125, wherein the subject has a CD Al score of more than 10.

127. The method of any one of claims 118-126, wherein the subject has one or more symptoms suggestive of active disease.

128. The method of any one of claims 118-127, wherein the subject cannot taper glucocorticoid treatment to be less than 7.5 mg / day.

129. The method of any one of claims 118-128, wherein the subject shows rapid radiographic progression of RA as indicated by change in van der Heijde-modified Sharp score >5 points at 1 year.

130. The method of any one of claims 118-129, wherein the subject is positive for rheumatoid factor (RF).

131. The method of claim 130, wherein the subject is positive for IgG or IgA RF in RA synovial fluid.

132. The method of claim 130 or 131, wherein the subject has a RF level higher than 25 U / ml.

133. The method of any one of claims 130-132, wherein the subject has a RF level higher than 100 U / ml.

134. The method of any one of claims 118-133, wherein the subject is positive for anti- citrullinated protein autoantibodies (ACPA).

135. The method of any one of claims 118-134, wherein the subject has at least 6 / 68 tender and / or painful joints (TJC) at baseline.

136. The method of any one of claims 118-135, wherein the subject has at least 6 / 66 swollen joints (SJC) at baseline.

137. The method of any one of claims 118-136, wherein the subject has a baseline level of circulating C-reactive protein (CRP) of at least 1.5x ULN.

138. The method of any one of claims 118-137, wherein the subject has a baseline Disease Activity score 28 using C-reactive protein (DAS28-CRP) of more than 4.1.

139. The method of any one of claims 118-138, wherein the subject does not respond to 2-3 class of biologic (b) or targeted synthetic (ts) disease-modifying antirheumatic drug (b / tsDMARDs).

140. The method of claim 139, wherein the subject has been treated with a biologic TNF-oc inhibitor (e.g., infliximab, certolizumab, golimumab, etanercept, adalimumab).

141. The method of any one of claim 118-139, wherein the subject has been treated with a JAK inhibitor.

142. The method of any one of claims 119-139, wherein the subject has been treated with a bDMARD other than a TNF-a inhibitor.

143. The method of any one of claims 118-142, wherein the subject responds to rituximab.

144. The method of any one of claims 118-143, wherein the subject is treated with at least 1 conventional (c) DMARD (e.g., MTX, hydroxychloroquine, sulfasalazine).

145. The method of any one of claims 118-144, wherein the subject is not on glucocorticoids at doses > 10 mg per day.

146. The method of any one of claims 118-145, wherein the subject did not have 3 or more joints injections within 6 weeks of baseline assessment.

147. The method of any one of claims 118-146, wherein the subject did not receive systemic glucocorticoid administered by intramuscular or intravenous (IV) injection within six weeks of baseline assessment.

148. The method of any one of claims 118-147, wherein the administration decreases level of RF in the subject.

149. The method of any one of claims 118-148, wherein the administration decreases ACAP in the subject.

150. The method of any one of claims 118-149, wherein the subject achieves ACR20 response at week 14, 16, or 32 of administration.

151. The method of claim 150, wherein the subject has at least 20% improvement from baseline in TJC68.

152. The method of claim 150 or 151 , wherein the subj ect has at least 20% improvement from baseline in SJC66.

153. The method of any one of claims 150-152, wherein the subject has at least 20% improvement from baseline in at least 3 of the following parameters:(i) Physician's Global Assessment of Disease Activity (PhGA);(ii) Patient's Global Assessment of Disease Activity (PtGA);(iii) Patient’s Assessment of Pain (100 mm VAS);(iv) Health Assessment Questionnaire - Disability Index (HAQ-DI); and(v) High-sensitivity C-reactive protein (hsCRP)154. The method of any one of claims 118-153, wherein the subject achieves ACR20 response at week 14 or 16 of administration, and has change in CD Al score from week 16 to 32 of administration.

155. The method of any one of claims 118-154, wherein the subject achieves ACR20 response at week 14 or 16 of administration and has change in SDAI score from week 16 to 32 of administration.

156. The method of any one of claims 118-155, wherein the anti-FcRn antibody is IMVT- 1402.

157. The method of any one of claims 118-156, wherein the antibody comprises a heavy chain variable region (VH) comprising a heavy chain complementarity determining region (HCDR) 1 comprising the amino acid sequence of SEQ ID NO: 7, a HCDR2 comprising the amino acid sequence of SEQ ID NO: 8, and a HCDR3 comprising the amino acid sequence of SEQ ID NO: 9, and a light chain variable region comprising a light chain complementarity determining region (LCDR) 1 comprising the amino acid sequence of SEQ ID NO: 10, a LCDR2 comprising theamino acid sequence of SEQ ID NO: 11, and a LCDR3 comprising the amino acid sequence of SEQ ID NO: 12.

158. The method of any one of claims 118-157, wherein the antibody comprises a VH comprising the amino acid sequence of SEQ ID NO: 15, and a VL comprising the amino acid sequence of SEQ ID NO: 16.

159. The method of any one of claims 118-158, wherein the antibody comprises a heavy chain comprising the amino acid sequence of SEQ ID NO: 19, and a light chain comprising the amino acid sequence of SEQ ID NO: 20.

160. The method of any one of claims 118-159, wherein the antibody comprises a heavy chain comprising the amino acid sequence of SEQ ID NO: 21, and a light chain comprising the amino acid sequence of SEQ ID NO: 22.

161. A method of treating Graves’ Disease (GD) in a subject that is receiving antithyroid drug (AID) at a dose, the method comprising:(i) administering an anti-FcRn antibody at a dose in the range of 580-700 mg to the subject;(ii) measuring T3 and T4 levels in the subject;(iii) decreasing the dosage of the ATD or stop the ATD if T3 and / or T4 levels are below ULN;(iii) decreasing the dosage of the anti-FcRn antibody to a dose in the rage of 280-400 mg / dose; and(iv) increasing the dosage of the ATD or restarting ATD in the subject to maintain T3 and T4 levels below ULN.

162. A method of treating Graves’ Disease (GD) in a subject that is receiving antithyroid drug (ATD) at a dose, the method comprising:(i) administering an anti-FcRn antibody at a dose in the range of 580-700 mg to the subject;(ii) measuring T3 and T4 level in the subject;(iii) decreasing the dosage of the ATD or stop the ATD if T3 and / or T4 levels are below ULN; and(iii) maintaining the dosage of the anti-FcRn antibody while administering the subject with low dose ATD or no ATD to maintain T3 and T4 levels below ULN.

163. A method of treating Graves’ Disease (GD) in a subject that is receiving antithyroid drug (ATD) at a dose, the method comprising:(i) administering an anti-FcRn antibody to the subject;(ii) measuring T3 and T4 levels in the subject;(iii) decreasing the dosage of the ATD or stop the ATD if T3 and / or T4 levels are below ULN;(iii) decreasing the dosage of the anti-FcRn antibody; and(iv) increasing the dosage of the ATD or restarting ATD in the subject to maintain T3 and T4 levels below ULN.

164. A method of treating Graves’ Disease (GD) in a subject that is receiving antithyroid drug (ATD) at a dose, the method comprising:(i) administering an anti-FcRn antibody at a dose to the subject;(ii) measuring T3 and T4 level in the subject;(iii) decreasing the dosage of the ATD or stop the ATD if T3 and / or T4 levels are below ULN; and(iii) maintaining the dosage of the anti-FcRn antibody while administering the subject with low dose ATD or no ATD to maintain T3 and T4 levels below ULN.

165. A method for treating Myasthenia Gravis (MG) in a subject, the method comprising administering the subject an anti-FcRn antibody at 550-700 mg once weekly.

166. A method for inducing remission in a subject having Myasthenia Gravis (MG), the method comprising administering the subject an anti-FcRn antibody at 550-700 mg once weekly.

167. The method of claim 165 or 166, wherein the subject is administered 600 mg of the anti- FcRn antibody once weekly.

168. The method of any one of claims 165-167, wherein the antibody is administered to the subject for a period of 20-60 weeks.

169. The method of any one of claims 165-168, wherein the antibody is administered to the subject for 52 weeks.

170. The method of any one of claims 165-168, wherein the antibody is administered to the subject for 26 weeks.

171. The method of claim 170, wherein the subject is administered the antibody at a reduced dose after 26 weeks.

172. The method of claim 171, wherein the subject is administered the antibody at 300 mg once weekly.

173. The method of claim 171 or 172, wherein the subject is administered the antibody at 300 mg once weekly for 26 weeks.

174. The method of claim 171 or 172, wherein the subject is administered the antibody at 300 mg once weekly indefinitely.

175. The method of any one of claims 165-174, wherein the anti-FcRn antibody is IMVT- 1402.

176. The method of any one of claims 165-175, wherein the antibody comprises a heavy chain variable region (VH) comprising a heavy chain complementarity determining region (HCDR) 1 comprising the amino acid sequence of SEQ ID NO: 7, a HCDR2 comprising the amino acid sequence of SEQ ID NO: 8, and a HCDR3 comprising the amino acid sequence of SEQ ID NO:9, and a light chain variable region comprising a light chain complementarity determining region (LCDR) 1 comprising the amino acid sequence of SEQ ID NO: 10, a LCDR2 comprising the amino acid sequence of SEQ ID NO: 11, and a LCDR3 comprising the amino acid sequence of SEQ ID NO: 12.

177. The method of any one of claims 165-176, wherein the antibody comprises a VH comprising the amino acid sequence of SEQ ID NO: 15, and a VL comprising the amino acid sequence of SEQ ID NO: 16.

178. The method of any one of claims 165-177, wherein the antibody comprises a heavy chain comprising the amino acid sequence of SEQ ID NO: 19, and a light chain comprising the amino acid sequence of SEQ ID NO: 20.

179. The method of any one of claims 165-177, wherein the antibody comprises a heavy chain comprising the amino acid sequence of SEQ ID NO: 21, and a light chain comprising the amino acid sequence of SEQ ID NO: 22.

180. The method of any one of claims 165-179, wherein the subject is positive for antiacetylcholine receptor (AChR) autoantibodies (anti-AChR+).

181. The method of any one of claims 165-180, wherein the subject is positive for anti- muscles-specific kinase (MuSK) autoantibodies (anti-MuSK+).

182. The method of any one of claims 165-181, wherein the subject is positive for antilipoprotein receptor-related protein 4 (LRP4) autoantibodies (anti-LRP4+).

183. The method of any one of claims 165-182, wherein the administration decreases anti- AChR autoantibody levels in the serum of the subject relative to anti- AChR autoantibody levels in the serum prior to the administration.

184. The method of any one of claims 165-183, wherein the administration decreases anti- MuSK autoantibody levels in the serum of the subject relative to anti-MuSK autoantibody levels in the serum prior to the administration.

185. The method of any one of claims 165-184, wherein the administration decreases anti- LRP4 autoantibody levels in the serum of the subject relative to anti-LRP4 autoantibody levels in the serum prior to the administration.

186. The method of any one of claims 165-185, wherein the administration prevents the development or improves one or more following symptoms in the subject: weakness in some or all muscles of the body, double vision, slurred speech, arm weakness, falling, unsteady walking, difficulty swallowing, chronic fatigue, and / or trouble breathing.

187. A method for treating chronic inflammatory demyelinating polyneuropathy (CIDP) in a subject, the method comprising administering the subject an anti-FcRn antibody at 200-400 mg once weekly.

188. A method for treating chronic inflammatory demyelinating polyneuropathy (CIDP) in a subject, the method comprising administering the subject an anti-FcRn antibody at 550-700 mg once weekly.

189. The method of claim 187 or 188, wherein the subject is administered the anti-FcRn antibody for 20-60 weeks.

190. The method of any one of claims claim 187-189, wherein the subject is administered the anti-FcRn antibody for 24 weeks.

191. The method of any one of claims 187-190, wherein the method further comprises administering to the subject a loading dose of the anti-FcRn antibody on days 3-5 in the first week of administration.

192. The method of claim 191, wherein the subject is administered the anti-FcRn antibody loading dose on day 4 in the first week of administration.

193. The method of claim 191 or 192, wherein the loading dose of the anti-FcRn antibody is the same as the weekly dose of the anti-FcRn antibody.

194. The method of any one of claims 191-193, wherein the loading dose of the anti-FcRn antibody is 600 mg.

195. The method of any one of claims 191-194, wherein the subject is administered the anti- FcRn antibody for additional 52 weeks.

196. The method of claim 195, wherein the subject is administered the anti-FcRn antibody at 600 mg once weekly.

197. The method of claim 196, wherein the subject is administered the anti-FcRn antibody at 300 mg once weekly.

198. The method of claim 195-197, wherein the method further comprises administering to the subject a loading dose of the anti-FcRn antibody on days 3-5 in the first week of the additional 52 weeks.

199. The method of claim 198, wherein the subject is administered the anti-FcRn antibody loading dose on day 4 in the first week of the additional 52 weeks.

200. The method of 198 or 199, wherein the loading dose of the anti-FcRn antibody is the same as the weekly dose of the anti-FcRn antibody.

201. The method of any one of claims 190-200, wherein the loading dose of the anti-FcRn antibody is 600 mg.

202. The method of any one of claims 187-201, wherein the subject has typical CIDP.

203. The method of any one of claims 187-202, wherein the subject has a CIDP variant.

204. The method of claim 203, wherein the CIDP variant is multifocal CIDP.

205. The method of claim 203, wherein the CIDP variant is motor CIDP.

206. The method of any one of claims 200-205, wherein the subject does not have sensory CIDP.

207. The method of any one of claims 200-206, wherein the subject does not have distal CIDP.

208. The method of any one of claims 187-207, wherein the subject is on or has been on first- line therapy for CIDP.

209. The method of claim 208, wherein the first-line therapy for CIDP is corticosteroid.

210. The method of claim 209, wherein the subject is receiving corticosteroid orally every day or every other day.

211. The method of claim 211, wherein the subject is receiving corticosteroid via pulse regimen.

212. The method of any one of claims 209-211, wherein the subject is tapered off corticosteroid while receiving the anti-FcRn antibody.

213. The method of any one of claims 209-212, wherein the subject discontinues corticosteroid prior to receiving the anti-FcRn antibody.

214. The method of any one of claims 208, wherein the first-line therapy for CIDP is Immunoglobulin (Ig) therapy.

215. The method of claim 214, wherein the Ig therapy is intravenous Ig infusion (IVIg).

216. The method of claim 215, wherein the Ig therapy is subcutaneous Ig infusion (SCIg).

217. The method of any one of claims 214-216, wherein the subject discontinues Ig therapy prior to receiving the anti-FcRn antibody.

218. The method of claim 208, wherein the first-line therapy for CIDP is plasma exchange (PLEX).

219. The method of claim 218, wherein the subject discontinuous PLEX treatment prior to receiving the anti-FcRn antibody.

220. The method of any one of claims 212, 217 or 219, wherein the subject relapses during the 24- week period of administration as measured by adjusted Inflammatory Neuropathy Cause and Treatment (aINCAT) score.

221. The method of any one of claims 212, 217, or 219, wherein the subject does not relapse during the 24-week period of administration as measured by aINCAT score.

222. The method of any one of claims 187-221, wherein the administration of the anti-FcRn antibody increases mean grip strength relative to prior to the administration.

223. The method of any one of claims 187-222, wherein the administration of the anti-FcRn antibody increases Inflammatory Rasch-built Overall Disability Scale (I-RODS) score relative to prior to the administration.

224. The method of any one of claims 187-223, wherein the administration of the anti-FcRn antibody increases MCR-SS score relative to prior to the administration.

225. The method of any one of claims 187-224, wherein the administration of the anti-FcRn antibody decreases Timed Up and Go (TUG) Test score relative to prior to the administration.

226. The method of any one of claims 187-225, wherein the administration of the anti-FcRn antibody decreases total IgG relative to prior to the administration.

227. The method of any one of claims 187-226, wherein the administration of the anti-FcRn antibody decreases IgG subclasses relative to prior to the administration.

228. The method of any one of claims 187-227, wherein the administration of the anti-FcRn antibody decreases autoantibodies targeting myelin glycoproteins relative to prior to the administration.

229. The method of any one of claims 187-228, wherein the administration of the anti-FcRn antibody decreases immune complexes (ICs) relative to prior to the administration.

230. The method of any one of claims 187-229, wherein the administration of the anti-FcRn antibody decreases neurofilament light chain (NfL) relative to prior to the administration.

231. The method of any one of claims 187-229, wherein the anti-FcRn antibody is IMVT- 1402.

232. The method of any one of claims 187-231, wherein the antibody comprises a heavy chain variable region (VH) comprising a heavy chain complementarity determining region (HCDR) 1 comprising the amino acid sequence of SEQ ID NO: 7, a HCDR2 comprising the amino acid sequence of SEQ ID NO: 8, and a HCDR3 comprising the amino acid sequence of SEQ ID NO: 9, and a light chain variable region comprising a light chain complementarity determining region (LCDR) 1 comprising the amino acid sequence of SEQ ID NO: 10, a LCDR2 comprising theamino acid sequence of SEQ ID NO: 11, and a LCDR3 comprising the amino acid sequence of SEQ ID NO: 12.

233. The method of any one of claims 187-232, wherein the antibody comprises a VH comprising the amino acid sequence of SEQ ID NO: 15, and a VL comprising the amino acid sequence of SEQ ID NO: 16.

234. The method of any one of claims 187-233, wherein the antibody comprises a heavy chain comprising the amino acid sequence of SEQ ID NO: 19, and a light chain comprising the amino acid sequence of SEQ ID NO: 20.

235. The method of any one of claims 187-233, wherein the antibody comprises a heavy chain comprising the amino acid sequence of SEQ ID NO: 21, and a light chain comprising the amino acid sequence of SEQ ID NO: 22.

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