Methods, therapies and uses for treating cancer

Abstract

The present disclosure describes therapies and uses including an anti-BCMA / anti-CD3 bispecific antibody for the treatment of cancer and / or cancer-associated diseases.

Description

[0001]PC073018A - 1 - METHODS, THERAPIES FOR TREATING CANCER REFERENCE TO SEQUENCE LISTING 5 The instant application contains a Sequence Listing which has been submitted electronically and is hereby incorporated by reference in its entirety. Said Sequence Listing, created on August 10, 2023, is named PC073018_sequence_listing_ST26.xml and is 25 KB in size. 10 Background B-cell maturation antigen (BCMA, CD269, or TNFRSF17) is a member of the tumor necrosis factor receptor (TNFR) superfamily. BCMA was identified in a malignant human T cell lymphoma containing a t(4; 16) translocation. The gene is selectively expressed in the B-cell lineage with the highest expression in plasma blasts and plasma 15 cells, antibody secreting cells. BCMA binds two ligands, B-cell activation factor (BAFF) (also called B-lymphocyte stimulator (BLyS) and APOL-related leukocyte expressed ligand (TALL-1)) and a proliferation-inducing ligand (APRIL) with affinity of 1 µM and 16nM, respectively. Binding of APRIL or BAFF to BCMA promotes a signaling cascade involving NF-kappa B, Elk-1, c-Jun N-terminal kinase and the p38 mitogen-activated 20 protein kinase, which produce signals for cell survival and proliferation. BCMA is also expressed on malignant B cells and several cancers that involve B lymphocytes including multiple myeloma, plasmacytoma, Hodgkin's Lymphoma, and chronic lymphocytic leukemia. In autoimmune diseases where plasmablasts are involved such as systemic lupus erythematosus (SLE) and rheumatoid arthritis, BCMA expressing antibody- 25 producing cells secrete autoantibodies that attack self. BCMA also found in a soluble form (i.e., soluble BCMA or sBCMA) in peripheral blood of multiple myeloma patients and can result in a sink for BCMA-specific therapies. Several BCMA-specific therapies are currently in development. Exemplary anti-BCMA / anti-CD3 bispecific antibodies include AMG420 (Amgen), AMG701 (Amgen), CC-93269 (Bristol Myers Squibb), elranatamab 30 (Pfizer), REGN5458 (Regeneron), REGN5459 (Regeneron), teclistamab (Janssen), and TNB-383B (TeneoBio). MM is a hematological B-cell malignancy characterized by dysregulated proliferation of bone marrow (BM) plasma cells. Globally, there are approximately 176,000 new cases and 117,000 deaths per year attributed to MM (Sung H, et al., CA Cancer J Clin.2021; 71(3): 209-49). Cancer Society estimates that for the US in 2021, approximately 34,920 new MM cases will be diagnosed and approximately 12,410 MM related deaths will occur. Despite recent advances in treatment, MM remains an incurable disease and almost all patients, even those who initially respond to treatment, are expected to relapse. Even for patients who receive autologous stem cell transplant (ASCT), the median time to relapse is only 17.2 months (Jimenez-Zepeda et al., Bone Marrow Transplant.2015; 50(2): 204-8). Similarly, for patients who are treated with novel proteasome inhibitor (PI)-based or immunomodulatory drug (IMiD)-based combination regimens as frontline treatment, the median time to relapse is 16.4 months (Lopez A et al, Leuk Res Rep.2015; 4(2): 64-9). MM patients typically receive many lines of treatment as their disease progresses and becomes refractory to various therapeutic approaches. Trials that have treated patients with BCMA-directed therapy in the relapsed / refractory multiple myeloma (RRMM) population have included heavily pretreated patients. Outcomes in the RRMM population are quite poor; for example, patients with RRMM who respond poorly to PI-based or IMiD-based regimens showed a median overall survival (OS) of 13 months (95% CI: 11, 15) (Kumar SK et al. Leukemia.2017; 31(11): 2443-48). Newer and more effective therapies have substantially increased patient benefit; however, in this real-world setting (N=3449), the most recent 4-year survival is only 75% (Nandakumar B et al. Journal of Clinical Oncology.2019; 37 (15_suppl): 8039). The lack of effective and durable therapeutic options highlights the unmet medical need in the RRMM patient population. There remains a need for improved therapies for the treatment of cancers and / or cancer-associated diseases, such as multiple myeloma. Furthermore, there is a need for therapies having greater efficacy than existing therapies. Summary Provided herein are therapies for the treatment of cancer and / or cancer- associated diseases. Provided herein are methods of treating a cancer and / or a cancer- associated disease in a subject. The methods of treatment include the use of an anti- BCMA / anti-CD3 bispecific antibody. In some embodiments, the anti-BCMA / anti-CD3 bispecific antibody is Elranatamab. In some embodiments, provided is a method of treating a cancer in a subject, the method comprising administering an anti-BCMA / anti-CD3 bispecific antibody to the subject according to a primary dosing schedule and a re-starting dosing schedule, wherein the primary dosing schedule includes a first priming dose, a second priming dose followed by a treatment dose; and wherein if the subject experiences a dose delay: (i) after the first priming dose but before the second priming dose the antibody is administered to the subject according to a re-starting dosing schedule according to the following: a) if two weeks or less since the first priming dose, the subject is administered the antibody at the second priming dose, optionally wherein if the second priming dose is tolerated, the dose in increased to the treatment dose after four days; or b) if greater than two weeks since the first priming dose, the subject is administered the antibody at the first priming dose. (ii) after the second priming dose but before the treatment dose the antibody is administered to the subject according to a re-starting dosing schedule according to the following: a) if two weeks or less since the second priming dose, the subject is administered the antibody at the treatment dose; b) if greater than two weeks and less than or equal to four weeks since the second priming dose, the subject is administered the antibody at the second priming dose optionally wherein if the second priming dose is tolerated, the dose in increased to the treatment dose after four days; or c) if greater than four weeks since the second priming dose, the subject is administered the antibody at the first priming dose. (iii) after a treatment dose but before the next treatment dose the antibody is administered to the subject according to a re-starting dosing schedule according to the following: a) if six weeks or less since the last treatment dose, the subject is administered the antibody at the treatment dose; b) if greater than six weeks and less than or equal to twelve weeks since the last treatment dose, the subject is administered the antibody at the second priming dose, optionally wherein if priming dose is tolerated, the dose in increased to the treatment dose after four days; or c) if greater than twelve weeks since the last treatment dose, the subject is administered the antibody at the first priming dose. In some embodiments, a dose delay occurs when a subject experiences toxicity and / or other adverse event related to the administration of the anti-BCMA / anti-CD3 antibody as part of the primary dosing schedule. In some embodiments, if the subject experiences a dose delay after the first priming dose but before the second priming dose the antibody is administered to the subject according to a re-starting dosing schedule in which the antibody is administered at the second priming dose, optionally wherein if the second priming dose is tolerated, the dose is increased to the treatment dose after four days. In some embodiments, if the subject experiences a dose delay after the second priming dose but before the treatment dose the antibody is administered to the subject according to a re-starting dosing schedule if more than two weeks since the second priming dose in which the antibody is administered at the second priming dose, optionally wherein if the second priming dose is tolerated, the dose is increased to the treatment dose after one week. In some embodiments, if the subject experiences a dose delay after a treatment dose the antibody is administered to the subject according to a re-starting dosing schedule if more than four weeks since the last treatment dose in which the antibody is administered at the second priming dose, optionally wherein if the second priming dose is tolerated, the dose is increased to the treatment dose after one week. In some embodiments, after the antibody is administered according to the re- starting dosing schedule, the dosing is continued according to the primary dosing schedule. In some embodiments the anti-BCMA / anti-CD3 bispecific antibody is Elranatamab. In some embodiments, the cancer is multiple myeloma. In some embodiments, the cancer is advanced multiple myeloma. In some embodiments, the cancer is relapsed or refractory multiple myeloma. In some embodiments, the cancer is triple class refractory multiple myeloma. In some embodiments, the multiple myeloma of the subject is refractory to all three types of the following multiple myeloma therapies (1) a prior multiple myeloma therapy that comprises a proteasome inhibitor, (2) a multiple myeloma therapy that comprises an immunomodulatory agent and (3) a prior multiple myeloma therapy that comprises an anti-CD38 antibody. In some embodiments, the cancer is double class refractory multiple myeloma. In some embodiments, the multiple myeloma of the subject is refractory to at least two of the following three types of multiple myeloma therapies (1) a prior multiple myeloma therapy that comprises a proteasome inhibitor, (2) a prior multiple myeloma therapy that comprises an immunomodulatory agent and (3) a prior multiple myeloma therapy that comprises an anti-CD38 antibody. In some embodiments, the cancer is newly diagnosed multiple myeloma. In some embodiments, the cancer is multiple myeloma, and the subject has received stem cell transplant. In some embodiments, the subject has received autologous stem cell transplant. In some embodiments, the subject has received autologous stem cell transplant or allogeneic stem cell transplant. In some embodiments, the subject is minimum residual disease positive post stem cell transplant. In some embodiments, the cancer is multiple myeloma, wherein in some embodiments the subject has progressed or is intolerant of an established multiple myeloma therapy. In some embodiments, the established multiple myeloma therapy comprises at least one drug selected from the group consisting of a proteasome inhibitor, an IMid drug and an anti-CD38 antibody. In some embodiments, the cancer is multiple myeloma wherein the subject has received at least four prior therapies and the subject’s multiple myeloma is refractory or relapsed to (1) a prior multiple myeloma therapy that comprises an proteasome inhibitor, (2) a prior multiple myeloma therapy that comprises an immunomodulatory agent and (3) a prior multiple myeloma therapy that comprises an anti-CD38 monoclonal antibody, and wherein the subject has demonstrated disease progression on the last therapy. In one aspect of these embodiments, the subject has received a prior therapy of a BCMA targeted ADC or a BCMA targeted CAR-T. In another aspect of these embodiments, the subject has not received any prior therapy of a BCMA targeted ADC or a BCMA targeted CAR-T. In some embodiments, the cancer is multiple myeloma, the subject has received at least one, at least two, at least three or at least four prior multiple myeloma therapies, and the subject’s multiple myeloma is refractory or relapsed to (1) a prior multiple myeloma therapy that comprises a inhibitor, (2) a prior multiple myeloma therapy that comprises an immunomodulatory agent and (3) a prior multiple myeloma therapy that comprises an anti-CD38 antibody, and the subject has demonstrated disease progression on the last multiple myeloma therapy. In one aspect of this embodiment, the subject has received at least three prior multiple myeloma therapies. In another aspect of this embodiment, the subject has received at least four prior multiple myeloma therapies. In some embodiments, the previous multiple myeloma therapies the subject received comprise a BCMA directed ADC therapy or a BCMA directed CAR-T cell therapy. In some embodiments, the previous multiple myeloma therapies the subject received comprise a BCMA directed therapy. In some embodiments, the previous multiple myeloma therapies the subject received do not comprise a BCMA directed ADC therapy or a BCMA directed CAR-T cell therapy. In some embodiments, the previous multiple myeloma therapies the subject received do not comprise a BCMA directed therapy. In some embodiments, the cancer is multiple myeloma, and the subject has received at least one or at least two prior multiple myeloma therapies, the subject’s multiple myeloma is refractory or relapsed to (1) a prior multiple myeloma therapy that comprises a proteasome inhibitor and (2) a prior multiple myeloma therapy that comprises an immunomodulatory agent. In some embodiments, the subject has demonstrated disease progression on the last multiple myeloma therapy. In some embodiments, the cancer is multiple myeloma, and the subject has not received any prior multiple myeloma therapies. In some embodiments, the subject has not received any prior multiple myeloma therapies after the diagnosis of multiple myeloma. In some embodiments, the subject is stem cell transplant ineligible. In some embodiments, the cancer is multiple myeloma and the subject is stem cell transplant ineligible. In some embodiments, the subject is autologous stem cell transplant ineligible. In some embodiments, the subject is allogeneic stem cell transplant ineligible. In some embodiments, the subject is ineligible for autologous stem cell transplant and is also ineligible for allogeneic stem cell transplant. Brief Description of the Figures / Drawings FIG. 1 depicts the restarting for Elranatamab following a dose interruption. FIG. 2 depicts infections of any grade (A) and grade ≥3 (B) in patients with or without Ig replacement therapy. FIG. 3 depicts infections of any grade (A) and grade ≥3 (B) in patients with or without hypogammaglobulinemia. DETAILED DESCRIPTION The present invention may be understood more readily by reference to the following detailed description of the embodiments of the invention and the Examples included herein. It is to be understood that this invention is not limited to specific methods of making that may of course vary. It is to be also understood that the terminology used herein is for the purpose of describing specific embodiments only and is not intended to be limiting. Exemplary embodiments (E) of the invention provided herein include: E1. A method of treating cancer, comprising administering an anti-BCMA / anti-CD3 bispecific antibody to a subject according to a primary dosing schedule and a re-starting dosing schedule, and wherein the dosing schedule is described by a week number, a dose amount and a dose frequency corresponding to each week number, wherein the primary dosing schedule is selected from: (a) Week Number Dose Amount (mg) Dose Frequency 1 44; 32; 12 plus 32; or A Weekly plus B; 2 – 24; 32; 44; 76; 116; or 152 Weekly 32; 44; 76; 116; or 152 Weekly; every two weeks; 25 onwards; every three weeks; or every four weeks , (b) Week Number Dose Amount (mg) Dose Frequency 1 44; 32; 12 or A Weekly plus B; 2 – 25; 32; 44; 76; 116; or 152 Weekly 32; 44; 76; 116; or 152 Weekly; every two weeks; 26 onwards; every three weeks; or every four weeks , (c) Week Number Dose Amount (mg) Dose Frequency 1 44; 32; 12 plus 32; or A Weekly plus B; 2 – 26; 44; or 76 Weekly 44; or 76 Weekly; every two weeks; 27 onwards; every three weeks; or every four weeks ,(d) Week Number Dose Amount (mg) Dose Frequency 1 44; 32; 12 plus 32; or A Weekly plus B; 2 – 24 32; 44; 76; 116; or 152 Every two weeks 25 onwards 32; 44; 76; 116; or 152 Every two weeks; every three weeks; or every four weeks , (e) Week Number Dose Amount (mg) Dose Frequency 1 44; 32; 12 plus 32; or A Weekly plus B; 2 – 25 32; 44; 76; 116; or 152 Every two weeks 26 onwards 32; 44; 76; 116; or 152 Every two weeks; every three weeks; or every four weeks , or (f) Week Number Dose Amount (mg) Dose Frequency 1 44; 32; 12 plus 32; or A Weekly plus B; 2 – 26 32; 44; 76; 152 Every two weeks 27 onwards 32; 44; 76; 116; or 152 Every two weeks; every three weeks; or every four weeks wherein when the dose amount is 12 mg plus 32 mg during week 1, the dose amount of 12 mg is administered on one day, subsequently, the dose amount of 32 mg is administered on another day, wherein A plus B is 4 (A) plus 20 (B), 8 (A) plus 16 (B), 12 (A) plus 12 (B), or 8 (A) plus 24 (B), and wherein when the dose amount is A mg plus B mg during week 1, the dose amount of A mg is administered on one day, subsequently, the dose amount of B mg is administered on another day; wherein the dose amount and the dose frequency during week 1 are together referred to as a priming dosing, and if the subject is administered only one dose of antibody in the priming dosing, such one dose is referred to as a single priming dose, if the subject is sequentially administered two doses of antibody during week 1, the two doses are referred to as a first priming dose and a second priming dose respectively; the dose amount and dose frequency during weeks 2 - 24, weeks 2 – 25 and weeks 2 – 26 in the respective dosing schedules (a) and (d), (b) and (e) and (c) and (f), respectively, are in each dosing schedule together referred to as a first treatment dosing, the dose amount and the dose frequency during week 25 and onwards, week 26 onwards, and week 27 onwards in the respective dosing schedules (a) and (d), (b) and (e) and (c) and (f), are in each dosing schedule together referred to as a second treatment dosing; and wherein if the subject experiences a dose delay: (i) after the first priming dose but before the second priming dose the antibody is administered to the subject according to a re-starting dosing schedule according to the following: a) if two weeks or less since the first priming dose, the subject is administered the antibody at the second priming dose, optionally wherein if the second priming dose is tolerated, the dose in increased to the treatment dose after four days; or b) if greater than two weeks since the first priming dose, the subject is administered the antibody at the first priming dose. (ii) after the second priming before the treatment dose the antibody is administered to the subject according to a re-starting dosing schedule according to the following: a) if two weeks or less since the second priming dose, the subject is administered the antibody at the treatment dose; b) if greater than two weeks and less than or equal to four weeks since the second priming dose, the subject is administered the antibody at the second priming dose optionally wherein if the second priming dose is tolerated, the dose in increased to the treatment dose after four days, optionally after one week; or c) if greater than four weeks since the second priming dose, the subject is administered the antibody at the first priming dose. (iii) after a treatment dose but before the next treatment dose the antibody is administered to the subject according to a re-starting dosing schedule according to the following: a) if six weeks or less since the last treatment dose, the subject is administered the antibody at the treatment dose; b) if greater than six weeks and less than or equal to twelve weeks since the last treatment dose, the subject is administered the antibody at the second priming dose, optionally wherein if the second priming dose is tolerated, the dose in increased to the treatment dose after four days, optionally after one week; or c) if greater than twelve weeks since the last treatment dose, the subject is administered the antibody at the first priming dose. E2. The method of E1, wherein after the antibody is administered according to the re- starting dosing schedule, the dosing is continued according to the primary dosing schedule. E3. The method of E1 or E2, wherein the anti-BCMA / anti-CD3 antibody is Elranatamab. E4. The method of any one of E1 to E3, wherein the subject is administered the antibody according to the primary dosing schedule as shown below, (a) Week Number Dose Amount (mg) Dose Frequency 1 44 Weekly 2 – 24 76 Weekly 25 onwards 76 Weekly; every two weeks; every three weeks; or every four weeks , (b) Week Number Dose Amount (mg) Dose Frequency 1 44 Weekly 2 – 25 76 Weekly 26 onwards 76 Weekly; every two weeks; every three weeks; or every four weeks , (c) Week Number Dose Amount (mg) Dose Frequency 1 44 Weekly 2 – 26 76 Weekly 27 onwards 76 Weekly; every two weeks; every three weeks; or every four weeks , (d) Week Number Dose Amount (mg) Dose Frequency 1 44 Weekly 2 – 24 76 Every two weeks 25 onwards 76 Every two weeks; every three weeks; or every four weeks , (e) Week Number Dose Amount (mg) Dose Frequency 1 44 Weekly 2 – 25 76 Every two weeks 26 onwards 76 Every two weeks; every three weeks; or every four weeks , or (f) Week Number Dose Amount Dose Frequency 1 44 Weekly 2 – 26 76 Every two weeks 27 onwards 76 Every two weeks; every three weeks; or every four weeks . E5. The method of E4, wherein the subject is administered the antibody according to the dosing schedule (a), (b) or (c), and the dose frequency for week 25 onwards, week 26 onwards, and week 27 onwards in the dosing schedule (a), (b), and (c), respectively, is (i) weekly, (ii) every two weeks, or (iii) weekly or every two weeks. E6. The method of any one of E1 to E3, wherein the subject is administered the antibody according to the primary dosing schedule as shown below, (a) Week Number Dose Amount (mg) Dose Frequency 1 12 plus 32 Weekly 2 – 24 76 Weekly 25 onwards 76 Weekly; every two weeks; every three weeks; or every four weeks , (b) Week Number Dose Amount (mg) Dose Frequency 1 12 plus 32 Weekly 2 – 25 76 Weekly 26 onwards 76 Weekly; every two weeks; every three weeks; or every four weeks , (c) Week Number Dose Amount (mg) Dose Frequency 1 12 plus 32 Weekly 2 – 26 76 Weekly 27 onwards 76 Weekly; every two weeks; every three weeks; or every four weeks , (d) Week Number Dose Amount (mg) Dose Frequency 1 12 plus 32 Weekly 2 – 24 76 Every two weeks 25 onwards 76 Every two weeks; every three weeks; or every four weeks , (e) Week Number Dose Amount (mg) Dose Frequency 1 12 plus 32 Weekly 2 – 25 76 Every two weeks 26 onwards 76 Every two weeks; every three weeks; or every four weeks , or (f) Week Number Dose Amount (mg) Dose Frequency 1 12 plus 32 Weekly 2 – 26 76 Every two weeks 27 onwards 76 Every two weeks; every three weeks; or every four weeks . E7. The method of E6, wherein the subject is administered the antibody according to the dosing schedule (a), (b) or (c), and the dose frequency for week 25 onwards, week 26 onwards, and week 27 onwards in the dosing schedule (a), (b), and (c), respectively, is (i) weekly, (ii) every two weeks, or (iii) weekly or every two weeks. E8. The method of any one of E1 to E3, wherein the subject is administered the antibody according to the primary dosing schedule as shown below, (a) Week Number Dose Amount (mg) Dose Frequency 1 32; or 12 plus Weekly 2 – 24 44 Weekly 25 onwards 44 Weekly; every two weeks; every three weeks; or every four weeks , (b) Week Number Dose Amount (mg) Dose Frequency 1 32; or 12 plus 32 Weekly 2 – 25 44 Weekly 26 onwards 44 Weekly; every two weeks; every three weeks; or every four weeks , (c) Week Number Dose Amount (mg) Dose Frequency 1 32; or 12 plus 32 Weekly 2 – 26 44 Weekly 27 onwards 44 Weekly; every two weeks; every three weeks; or every four weeks , (d) Week Number Dose Amount (mg) Dose Frequency 1 32; or 12 plus 32 Weekly 2 – 24 44 Every two weeks 25 onwards 44 Every two weeks; every three weeks; or every four weeks , (e) Week Number Dose Amount (mg) Dose Frequency 1 32; or 12 plus 32 Weekly 2 – 25 44 Every two weeks 26 onwards 44 Every two weeks; every three weeks; or every four weeks , or (f) Week Number Dose Amount Dose Frequency 1 32; or 12 plus 32 Weekly 2 – 26 44 Every two weeks 27 onwards 44 Every two weeks; every three weeks; or every four weeks . E9. The method of E8, wherein the subject is administered the antibody according to the dosing schedule (a), (b) or (c), and the dose frequency for week 25 onwards, week 26 onwards, and week 27 onwards in the dosing schedule (a), (b), and (c), respectively, is (i) weekly, (ii) every two weeks, or (iii) weekly or every two weeks. E10. The method of any one of E1 to E9, wherein the subject is administered the antibody of the second treatment dosing for 6 to 18 cycles, thereafter, the subject is administered a third treatment dosing of the antibody subcutaneously, wherein the third treatment dosing is 32 mg Q2W, 32 mg Q4W, 44 mg Q2W, 44 mg Q4W, 76 mg Q2W, 76 mg Q4W, 116 mg Q2W, 116 mg Q4W, 152 mg Q2W, or 152 mg Q4W, wherein a cycle is 21 days or 28 days, and cycle 1 starts on day 1 week 1, day 1 week 2, or day 1 week 3. E11. The method of E10, wherein (i) the first treatment dosing is 32 mg Q1W, the second treatment dosing is 32 mg Q1W or 32 mg Q2W and the third treatment dosing is 32 mg Q2W or 32 mg Q4W, (ii) first treatment dosing is 32 mg Q1W, the second treatment dosing is 32 mg Q2W and the third treatment dosing is 32 mg Q4W, (iii) the first treatment dosing is 44 mg Q1W, the second treatment dosing is 44 mg Q1W or 44 mg Q2W and the third treatment dosing is 44 mg Q2W or 44 mg Q4W; (iv) the first treatment dosing is 44 mg Q1W, the second treatment dosing is 44 mg Q2W and the third treatment dosing is 44 mg Q4W; (v) first treatment dosing is 76 mg Q1W, the second treatment dosing is 76 mg Q1W or 76 mg Q2W and the third treatment dosing is 76 mg Q2W or 76 mg Q4W, (vi) the first treatment dosing is 76 mg Q1W, the second treatment dosing is 76 mg Q2W and the third treatment dosing is 76 mg Q4W, (vii) the first treatment dosing is 116 mg Q1W, the second treatment dosing is 116 mg Q1W or 116 mg Q2W and the third treatment dosing is 116 mg Q2W or 116 mg Q4W; (viii) the first treatment dosing is 116 mg Q1W, the second treatment dosing is 116 mg Q2W and the third treatment dosing is 116 mg Q4W, (ix) the first treatment 152 mg Q1W, the second treatment dosing is 152 mg Q1W or 152 mg Q2W and the third treatment dosing is 152 mg Q2W or 152 mg Q4W, or (x) the first treatment dosing is 152 mg Q1W, the second treatment dosing is 152 Q2W and the third treatment dosing is 152 mg Q4W. E12. The method of E3, wherein the subject is administered Elranatamab according to the following primary dosing schedule: first priming dose of 12 mg on Day 1; second priming dose of 32 mg on Day 4; first treatment dose of 76 mg on Day 8. E13. The method of E12, wherein subsequent treatment doses are administered one week after the first treatment dose and weekly thereafter through week 24. E14. The method of E13, wherein further treatment doses are administered every two weeks (Q2W) from week 25. E15. The method of any one of E1 to E14, wherein if a subject has received treatment for at least six months and disease response shows at least a partial response (PR) or better with responses persisting for at least two months, the dose interval may be changed from QW to Q2W at the same dose level / dosage. E16. The method of any one of E1 to E15, wherein the method further comprising administering to the subject at least one dose of a premedication prior to each of the single priming dose, the first priming dose, the second priming dose and / or the first treatment dose of the anti-BCMA / anti-CD3 bispecific antibody is administered to the subject. E17. The method of E16, wherein the premedication is administered prior to the first and second priming doses as part of the re-starting dosing schedule. E18. The method of E16 or E17, wherein the premedication is administered prior to the treatment dose as part of the re-starting dosing schedule. E19. The method of any one of E18, wherein the premedication may be acetaminophen (or equivalent such as paracetamol), diphenhydramine (or equivalent) and / or dexamethasone (or equivalent). E20. The method of any one of E16 to E19, wherein dexamethasone is administered at a dexamethasone dosing of about 10 mg to about 40 mg daily oral or intravenous, such as 20 mg. E21. The method of any one of E16 to E20, wherein acetaminophen is administered at a dose of 650 mg or paracetamol is administered at a dose of 500 mg. E22. The method of any of E16 to E21, wherein diphenhydramine is administered at a dose of 25 mg, oral or intravenous. E23. The method of any one of E16 to E22, wherein the premedication dosing can be the same or different while the subject is on the priming dosing, the first treatment and subsequent dosing of the bispecific antibody. E24. The method of any one of E1 to E23, wherein the antibody is administered subcutaneously. E25. The method of any one of E1 to E24, wherein a dose delay results from the subject experiencing cytokine release syndrome (CRS) or neurologic toxicity including immune effector cell-associated neurotoxicity syndrome (ICANS). E26. The method of any one of E1 to E25, wherein a dose delay results from the subject experiencing infections; neutropenia; hepatotoxicity. E27. The method of any one of E1 to E26 wherein the cancer is multiple myeloma. E28. The method of E27, wherein the cancer is relapsed or refractory (R / R) multiple myeloma (MM). E29. The method of E27 or E28, subject has previously been treated with at least four prior lines of therapy, including a proteasome inhibitor, an immunomodulatory agent, and an anti-CD38 monoclonal antibody. E30. The method of E27 or E28, wherein the subject has previously been treated with at least three prior lines of therapy, which may include a proteasome inhibitor, an immunomodulatory agent, and an anti-CD38 monoclonal antibody. E31. The method of E27 or E28, wherein the subject has previously been treated with at least two prior lines of therapy, which may include two of the following: a proteasome inhibitor, an immunomodulatory agent, and an anti-CD38 monoclonal antibody. E32. The method of E27 or E28, wherein the cancer is newly diagnosed multiple myeloma. E33. The method of E32, wherein the subject has received stem cell transplant, optionally autologous stem cell transplant or allogeneic stem cell transplant. E34. The method of E27 or E28, wherein the subject has not received any prior multiple myeloma therapies. E35. The method of any one of E1 to E34, further comprising administering to the subject a second therapeutic agent. E36. The method of any one of E1 to E35, further comprising administering to the subject radiotherapy. E37. The method of E35, wherein the second therapeutic agent is selected from one or more of lenalidomide, daratumumab, dexamethasone. E38. The method of E37, wherein the second therapeutic agent is lenalidomide. E39. The method of E37, wherein the second therapeutic agent is daratumumab. E40. The method of E37 or E38, wherein lenalidomide is administered at a dose of 5-25 mg. E41. The method of E40, wherein lenalidomide is administered at a dose of 5, 10, 15, 20 or 25 mg, optionally by PO administration. E42. The method of E37 or E39, wherein daratumumab is administered at a dose of 1800 mg, optionally by subcutaneous administration. E43. The method of E42, wherein daratumumab is administered QW, Q2W or Q4W. E44. The method of E42 or E43, wherein the method further comprising administering to the subject at least one dose of a premedication prior to each daratumumab dose. E45. The method of E44, wherein the premedication is acetaminophen (or equivalent such as paracetamol), diphenhydramine (or equivalent) and / or dexamethasone (or equivalent). E46. The method of any one of E1-E45, wherein the method further comprises administered immunoglobulin replacement therapy. E47. The method of E46, wherein immunoglobulin replacement therapy is administered if IgG level < 400 mg / dL. E48. The method of E46 or E47, wherein the immunoglobulin replacement therapy is administered if immunoparesis / hypogammaglobulinemia is determined. E49. The method of E47 or E48, wherein the immunoglobulin replacement therapy is administered every 4 weeks. E50. The method of E49, wherein the immunoglobulin replacement therapy is administered during the first six 28 day treatment cycles. E51. The method of E47 or E48, wherein the immunoglobulin replacement therapy is administered to patients at high risk of infection if IgG level < 400 mg / dL. E52. The method of E51, wherein the immunoglobulin replacement therapy is administered during a seventh to twelfth 28 day treatment cycles. E53. The method of E51 or E52, wherein the patients are at high risk of developing Grade 3-4 infection during the method of treatment. E54. The method of any of E46 to E53, wherein the immunoglobulin replacement therapy is administered intravenously or subcutaneously. E55. The method of any of E46 to E54, wherein the immunoglobulin replacement therapy results in decreased infection rates. E56. The method of any of E46 to E55, wherein the immunoglobulin replacement therapy is administered until IgG level > 400 mg / dL and / or resolution of immunoparesis / hypogammaglobulinemia. E57. A method of treating cancer, comprising administering Elranatamab to a subject according to a primary dosing schedule and a re-starting dosing schedule, wherein the primary dosing schedule comprises a first priming dose of 12 mg on Day 1; a second priming dose of 32 mg on Day 4; and a first treatment dose of 76 mg on Day 8; wherein subsequent treatment doses are administered one week after the first treatment dose and weekly thereafter through week 24; wherein further treatment doses are administered every two weeks (Q2W) from week 25 if a subject has received treatment for at least six months and disease response shows at least a partial response (PR) or better with responses persisting for at least two months; and wherein if the subject experiences a dose delay: (i) after the first priming dose but before the second priming dose the antibody is administered to the subject according to a re-starting dosing schedule according to the following: a) if two weeks or less since the dose, the subject is administered the antibody at the second priming dose, optionally wherein if the second priming dose is tolerated, the dose in increased to the treatment dose after four days; or b) if greater than two weeks since the first priming dose, the subject is administered the antibody at the first priming dose. (ii) after the second priming dose but before the treatment dose the antibody is administered to the subject according to a re-starting dosing schedule according to the following: a) if two weeks or less since the second priming dose, the subject is administered the antibody at the treatment dose; b) if greater than two weeks and less than or equal to four weeks since the second priming dose, the subject is administered the antibody at the second priming dose optionally wherein if the second priming dose is tolerated, the dose in increased to the treatment dose after four days, optionally after one week; or c) if greater than four weeks since the second priming dose, the subject is administered the antibody at the first priming dose. (iii) after a treatment dose but before the next treatment dose the antibody is administered to the subject according to a re-starting dosing schedule according to the following: a) if six weeks or less since the last treatment dose, the subject is administered the antibody at the treatment dose; b) if greater than six weeks and less than or equal to twelve weeks since the last treatment dose, the subject is administered the antibody at the second priming dose, optionally wherein if the second priming dose is tolerated, the dose in increased to the treatment dose after four days, optionally after one week; or c) if greater than twelve weeks since the last treatment dose, the subject is administered the antibody at the first priming dose; and wherein after re-starting dosing, the dosing is continued according to the primary dosing schedule. E58. The method of E57, wherein if the subject experiences a dose delay after the first priming dose but before the second priming dose the antibody is administered to the subject according to a re-starting in which the antibody is administered at the second priming dose, optionally wherein if the second priming dose is tolerated, the dose is increased to the treatment dose after four days. E59. The method of E57 or E58, wherein if the subject experiences a dose delay after the second priming dose but before the treatment dose the antibody is administered to the subject according to a re-starting dosing schedule if more than two weeks since the second priming dose in which the antibody is administered at the second priming dose, optionally wherein if the second priming dose is tolerated, the dose is increased to the treatment dose after one week. E60. The method of any one of E57-E59, wherein if the subject experiences a dose delay after a treatment dose the antibody is administered to the subject according to a re- starting dosing schedule if more than four weeks since the last treatment dose in which the antibody is administered at the second priming dose, optionally wherein if the second priming dose is tolerated, the dose is increased to the treatment dose after one week. E61. The method of any one of E1 to E60, wherein if the subject experiences CRS, the subject is administered supportive therapy for CRS. E62. The method of E61, wherein the subject is administered an effective amount of tocilizumab. The section headings used herein are for organizational purposes only and are not to be construed as limiting the subject matter described. All references cited herein, including patent applications, patent publications, UniProtKB accession numbers are herein incorporated by reference, as if each individual reference were specifically and individually indicated to be incorporated by reference in its entirety. The techniques and procedures described or referenced herein are generally well understood and commonly employed using conventional methodology by those skilled in the art, such as, for example, the widely utilized methodologies described in Sambrook et al, Molecular Cloning: A Laboratory Manual 3rd. edition (2001) Cold Spring Harbor Laboratory Press, Cold Harbor, N.Y. CURRENT PROTOCOLS IN MOLECULAR BIOLOGY (F. M. Ausubel, et al. eds., (2003)); the series METHODS IN ENZYMOLOGY (Academic Press, Inc.): PCR 2: A PRACTICAL APPROACH (M. J. MacPherson, B. D. Hames and G. R. Taylor eds. (1995)), Harlow and Lane, eds. (1988) ANTIBODIES, A LABORATORY MANUAL, and ANIMAL CELL CULTURE (R. I. Freshney, ed. (1987)); Oligonucleotide Synthesis (M. J. Gait, ed., 1984); Methods in Molecular Biology, Humana Press; Cell Biology: A Laboratory Notebook (J. E. Cellis, ed., 1998) Academic Press; Animal Cell Culture (R. I. Freshney), ed., 1987); Introduction to Cell and Tissue Culture (J. P. Mather and P. E. Roberts, 1998) Plenum Press; Cell and Tissue Culture Laboratory Procedures (A. Doyle, J. B. Griffiths, and D. G. Newell, eds., 1993-8) J. Wiley and Sons; Handbook of Experimental Immunology (D. M. Weir and C. C. Blackwell, eds); Gene Transfer Vectors for Mammalian Cells (J. M. Miller and M. P. Calos, eds., 1987); PCR: The Polymerase Chain Reaction, (Mullis et al, eds., 1994); Current Protocols in Immunology (J. E. Coligan et al, eds., 1991); Short Protocols in Molecular Biology (Wiley and Sons, 1999); Immunobiology (C. A. Janeway and P. Travers, 1997); Antibodies (P. Finch, 1997); Antibodies: A Practical Approach (D. Catty., ed., IRL Press, 1988-1989); Monoclonal Antibodies: A Practical Approach (P. Shepherd and C. Dean, eds., Oxford University Press, 2000); Using Antibodies: A Laboratory Manual (E. Harlow and D. Lane (Cold Spring Harbor Laboratory Press, 1999)); The Antibodies (M. Zanetti and J. D. Capra, eds., Harwood Academic Publishers, 1995); and updated versions thereof. Definitions Unless otherwise defined herein, scientific and technical terms used in connection with the present invention have the meanings that are commonly understood by those of ordinary skill in the art. As used herein, the singular form "a", "an", and "the" include plural references unless indicated otherwise. For example, "an" antibody includes one or more antibodies. Where aspects or embodiments of the invention are described in terms of a Markush group or other grouping of alternatives, the present invention encompasses not only the entire group listed as a whole, but each member of the group individually and all possible subgroups of the main group, but also the main group absent one or more of the group members. The present envisages the explicit exclusion of one or more of any of the group members in the claimed invention. Any example(s) following the term “e.g.” or “for example” is not meant to be exhaustive or limiting. As used herein, the term “about” when used to modify a numerically defined parameter means that the parameter may vary by as much as 10% below or above the stated numerical value for that parameter. For example, a dose of about 5 mg means 5% ± 10%, i.e., it may vary between 4.5 mg and 5.5 mg. The term “identity” or “identical to” refers to the overall relatedness between polymeric molecules, e.g., between nucleic acid molecules (e.g., DNA molecules or RNA molecules) or between polypeptide molecules. “Identity” measures the percent of identical matches between two or more sequences with gap alignments addressed by a particular mathematical model of computer programs (e.g., algorithms), which are well known in the art. The terms "treating", "treat" or "treatment" refer to any type of treatment, e.g., such as to relieve, alleviate, or slow the progression of the patient’s disease, disorder or condition or any tissue damage associated with the disease. In some embodiments, the disease, disorder or condition is cancer. The term “therapeutically effective amount” refers to the amount of active ingredient that elicits the biological or medicinal response in a tissue, system, animal, individual or human that is being sought by a researcher, veterinarian, medical doctor or other clinician, which may include one or more of the following: (1) preventing the disease; for example, preventing a disease, condition or disorder in an individual that may be predisposed to the disease, condition or disorder but does not yet experience or display the pathology or symptomatology of the disease; (2) inhibiting the disease; for example, inhibiting a disease, condition or disorder in an individual that is experiencing or displaying the pathology or symptomatology of the disease, condition or disorder (i.e., arresting or slowing further development of the pathology or symptomatology); and (3) ameliorating the disease; for example, ameliorating a disease, condition or disorder in an individual that is experiencing or displaying the pathology or symptomatology of the disease, condition or disorder (i.e., reversing the pathology or symptomatology). An “antibody” refers to an molecule capable of specific binding to a target, such as a polypeptide, carbohydrate, polynucleotide, lipid, etc., through at least one antigen binding site, located in the variable region of the immunoglobulin molecule. As used herein, the term “antibody” can encompass any type of antibody (e.g., monospecific, bispecific), and includes portions of intact antibodies that retain the ability to bind to a given antigen (e.g., an “antigen-binding fragment”), and any other modified configuration of an immunoglobulin molecule that comprises an antigen binding site. An exemplary antibody comprises i) a variable region of the light chain, heavy chain or both and ii) a constant region of the heavy chain comprising three sequential immunoglobulin domains (CH1, CH2, and CH3) and of the light chain comprising a single immunoglobulin domain (CL). A “bispecific antibody” refers to a molecule that has binding specificity for at least two different epitopes. In some embodiments, bispecific antibodies can bind simultaneously two different antigens. In other embodiments, the two different epitopes may reside on the same antigen. In certain embodiments, the bispecific antibody is capable of simultaneously binding two antigens expressed on two distinct cells. A “variable region” of an antibody refers to the variable region of the antibody light chain or the variable region of the antibody heavy chain, either alone or in combination. As known in the art, the variable regions of the heavy and light chains each consist of four framework regions (FRs) connected by three complementarity determining regions (CDRs) also known as hypervariable regions and contribute to the formation of the antigen binding site of antibodies. If variants of a subject variable region are desired, particularly with substitution in amino acid residues outside of a CDR region (i.e., in the framework region), appropriate amino acid substitution, preferably, conservative amino acid substitution, can be identified by comparing the subject variable region to the variable regions of other antibodies which contain CDR1 and CDR2 sequences in the same canonincal class as the subject variable region (Chothia and Lesk, J Mol Biol 196(4): 901-917, 1987). Antibodies produced by host cells may undergo post-translational cleavage of one or more, particularly one or two, amino acids from the C-terminus of the heavy chain. Therefore, an antibody produced by a host cell by expression of a specific nucleic acid molecule encoding a full-length heavy chain may include the full-length heavy chain, or it may include a cleaved variant of the full-length heavy chain. This particularly may be the case where the final two C-terminal of the heavy chain are glycine (G446) and lysine (K447, numbering according to Kabat EU index). Therefore, the C-terminal lysine, or the C-terminal glycine and lysine, of an anti-BCMA / anti-CD3 bispecific antibody provided herein may or may not be present. Dosing regimens and methods provided herein include an anti-BCMA / anti-CD3 bispecific antibody. As used herein, an anti-BCMA / anti-CD3 bispecific antibody can be any molecule that can simultaneously bind to both BCMA (e.g., on B cells) and CD3 (e.g., on T cells). Anti-BCMA / anti-CD3 bispecific antibodies are also referred to herein as “BCMA x CD3” or “BCMA” bispecific antibodies. B-cell maturation antigen (BCMA, also known as TNFRSF17 and CD269) is a candidate for bispecific antibody based immunotherapy. BCMA expression is upregulated during B-cell maturation into plasma blasts and plasma cells, but it is not expressed on naïve B cells, hematopoietic stem cells or normal tissues such as the heart, lung, kidney, or tonsil. In multiple myeloma, BCMA expression was identified at each disease stage, and on patients with differing cytogenetic risks. Furthermore, BCMA expression was not influenced by treatment with autologous stem cell transplant (ASCT) or chemotherapy. In vivo, bispecific antibodies against BCMA have been shown to induce T-cell activation, reduce tumor burden and prolong survival. Examples of anti-BCMA / anti-CD3 bispecific antibodies that may be useful in the therapies of the present invention include, but are not limited to, AMG 420 (BCMAxCD3 bispecific T-cell engager, BiTE®, Amgen), AMG 701 (BCMAxCD3 BiTE®, Amgen), CC- 93269 (BCMAxCD3 bispecific antibody, Celgene), teclistamab (JNJ-64007957 - Jansen), elranatamab (BCMAxCD3 bispecific antibody, Pfizer Inc.), TNB-383B (TeneoBio / AbbVie), linvoseltamab (REGN5458 - BCMAxCD3 bispecific antibody, Regeneron), alnuctamab (CC-93269 – BMS), AFM26 (BCMAxCD16 tetravalent bispecific antibody, Affimed GmbH), HPN217 (BCMAxALBxCD3 trispecific, Harpoon Therapeutics). In some aspects, the anti-BCMA / anti-CD3 bispecific antibody comprises a first antigen binding site and a second antigen binding site, wherein the first antigen binding site specifically binds to CD3, and wherein the second antigen binding site specifically binding to a BCMA. In some aspects, an anti-BCMA / anti-CD3 bispecific antibody may have any of the features or characteristics of any of the BCMA bispecific antibodies provided in WO2016 / 166629, which is hereby by reference for all purposes. Elranatamab is an anti-BCMA / anti-CD3 bispecific antibody. Elranatamab is described, for example in US Patent No.9,969,809, incorporated by reference in its entirety. The selected sequences of Elranatamab are shown in Table 1 herein. Elranatamab is also known as PF-06863135 and these terms are used interchangeably herein. In some aspects, the first antigen binding site specifically binds to CD3. Information about CD3 is provided, for example, via UniProtKB #P07766. In some aspects, the first antigen binding site comprises three CDRs of a heavy chain variable region (VH) comprising the amino acid sequence shown in SEQ ID NO: 15, and / or three CDRs of a light chain variable region (VL) comprising the amino acid sequence shown in SEQ ID NO: 16. In some aspects, the VH comprises a VH CDR1 comprising the sequence shown in one or more of SEQ ID NO: 9, 24, and 25, a VH CDR2 comprising the sequence shown in one or more of SEQ ID NO: 10 and 26, a VH CDR3 comprising the sequence shown in SEQ ID NO: 11, and / or the VL comprises a VL CDR1 comprising the sequence shown in SEQ ID NO: 12, a VL CDR2 comprising the sequence shown in SEQ ID NO: 13, a VL CDR3 comprising the sequence shown in SEQ ID NO: 14. In some aspects, the VH comprises the sequence shown in SEQ ID NO: 15, and / or the VL comprises the sequence shown in SEQ ID NO: 16. In some aspects, the bispecific antibody comprises a first heavy chain and a first light chain comprising the first antigen binding site, wherein the first heavy chain comprises the amino acid sequence shown in SEQ ID NO: 19, and / or the first light chain comprises the amino acid sequence shown in SEQ ID NO: 20. In some aspects, the second antigen binding site specifically binds to BCMA. Information about BCMA is provided, for example, via UniProtKB ID # Q02223. In some aspects, the antigen binding site comprises three CDRs of a heavy chain variable region (VH) comprising the amino acid sequence shown in SEQ ID NO: 7, and / or three CDRs of a light chain variable region (VL) comprising the amino acid sequence shown in SEQ ID NO: 8. In some aspects, the VH comprises a VH CDR1 comprising the sequence shown in one or more of SEQ ID NO: 1, 21, and 22, a VH CDR2 comprising the sequence shown in one or more of SEQ ID NO: 2 and 23 , a VH CDR3 comprising the sequence shown in SEQ ID NO: 3, and / or the VL comprises a VL CDR1 comprising the sequence shown in SEQ ID NO: 4, a VL CDR2 comprising the sequence shown in SEQ ID NO: 5, a VL CDR3 comprising the sequence shown in SEQ ID NO: 6. In some aspects, the VH comprises the sequence shown in SEQ 7, and / or the VL comprises the sequence shown in SEQ ID NO: 8. In some aspects, the bispecific antibody comprises a second heavy chain and a second light chain comprising the second antigen binding site, wherein the second heavy chain comprises the amino acid sequence shown in SEQ ID NO: 17, and / or the second light chain comprises the amino acid sequence shown in SEQ ID NO: 18. In some embodiments, the first antigen binding site VH comprises a sequence that is at least about 95%, 96%, 97%, 98%, 99%, or 100% identical to the amino acid sequence of SEQ ID NO: 15, the first antigen binding site VL comprises a sequence that is at least about 95%, 96%, 97%, 98%, 99%, or 100% identical to the amino acid sequence of SEQ ID NO: 16, the second antigen binding site VH comprises a sequence that is at least about 95%, 96%, 97%, 98%, 99%, or 100% identical to the amino acid sequence of SEQ ID NO: 7, and the second antigen binding site VL comprises a sequence that is at least about 95%, 96%, 97%, 98%, 99%, or 100% identical to the amino acid sequence of SEQ ID NO: 8. In some embodiments, the heavy chain polypeptide sequence for the anti-BCMA arm (second heavy chain) of elranatamab may lack the C-terminal lysine residue that is present in SEQ ID NO: 17. In some examples, the heavy chain polypeptide sequence for the anti-CD3 arm (first heavy chain) of elranatamab may lack the C-terminal lysine residue that is present in SEQ ID NO: 19. In some examples, the heavy chain polypeptide sequence for the anti-BCMA arm (second heavy chain) of elranatamab may lack the C- terminal lysine residue that is present in SEQ ID NO: 17 and the heavy chain polypeptide sequence for the anti-CD3 arm (first heavy chain) of elranatamab may lack the C-terminal lysine residue that is present in SEQ ID NO: 19. In some aspects, the BCMA bispecific antibody is elranatamab. Elranatamab is a heterodimeric full-length bispecific antibody comprised of one B-cell maturation antigen (BCMA) binding arm and one cluster of differentiation (CD3) binding arm paired through hinge mutation technology. It utilizes a modified human IgG2Δa fragment crystallizable (Fc) region. Elranatamab is described, for example in US Patent No.9,969,809, which is hereby incorporated for all purposes. The sequences of elranatamab are shown in Table 1. Elranatamab is also known as PF-06863135 and these terms are used interchangeably herein. Elranatamab is further described, e.g., in Chemical Abstract Services (CAS) Registry Number 2408850-14-4, United States Adopted Names (USAN) File Number (HI-199), and the WHO Information ((International Nonproprietary Names for Pharmaceutical Substances), Recommended INN: List 87, Vol. 36, No. 1, published 2022, pages 100-103. In some embodiments the dosage of elranatamab may be selected from one of the following: 4 mg, 8 mg, 12 mg, 16 mg, 20 mg, 24 mg, 32 mg, 44 mg, 76 mg, 116 mg and 152 mg. In some embodiments, a dosing method or regimen provided herein involving an anti-BCMA / anti-CD3 bispecific antibody may include one, two, or more priming doses. Priming doses can be utilised to initially sensitize the immune system at lower doses therefore reducing the rate, duration and grade of cytokine release syndrome (CRS) and Immune Effector Cell-Associated Neurotoxicity Syndrome (ICANS). In some embodiments, a first priming dose may be 4 mg to 32 mg and a second priming dose may be from 12 mg to 44 mg. Exemplary priming doses for elranatamab are a first dose of 12 mg and a second dose of 32 mg. An exemplary priming dose schedule is to administer the first priming dose (e.g., 12 mg) on day 1, the second priming dose (e.g., 32 mg) on day 4, followed by a treatment dose. In some embodiments the treatment dose (e.g., 44 mg or 76 mg) is on day 8 (i.e., 1 week after the first priming dose). In some embodiments, the treatment dose is 32 mg to 76 mg. The treatment dose may be selected from 44 mg or 76 mg. In some embodiments, the first priming dose is 12 mg, the second priming dose is 32 mg, and the treatment dose is 44 mg or 76 mg. In some embodiments, an anti-BCMA / anti-CD3 bispecific antibody may be administered in methods and regimens provided herein once a week (Q1W or QW), once every two weeks (Q2W), once every three weeks (Q3W), or once every four weeks (Q4W). In some embodiments, the antibody is administered QW or Q2W. In some embodiments, if a subject has received treatment for at least six months and disease response shows at least a partial response (PR) or better with responses persisting for at least two months, the dose interval may be changed from QW to Q2W at the same dose level / dosage (for example, 76 mg QW to 76 mg Q2W or 44 mg QW to 44 mg Q2W). These dosing frequencies may be part of dosing cycles, such as 14-day, 21-day, or 28- day cycles. In some embodiments, the method further comprising administering to the subject at least one dose of a premedication prior to each of the single priming dose, the first priming dose, the second priming dose and / or the first treatment dose of the anti-BCMA / anti-CD3 bispecific antibody is to the subject. In some embodiments, the premedication is administered prior to the first and second priming doses and the first treatment dose. The premeditation may be acetaminophen (or equivalent such as paracetamol), diphenhydramine (or equivalent) and / or dexamethasone (or equivalent. In some embodiments, dexamethasone is administered at a dexamethasone dosing of about 10 mg to about 40 mg daily oral or intravenous, such as 20 mg. In some embodiments, acetaminophen is administered at a dose of 650 mg or paracetamol is administered at a dose of 500 mg. In some embodiments, diphenhydramine is administered at a dose of 25 mg, oral or intravenous. In some embodiments, the premedication dosing can be the same or different while the subject is on the priming dosing, the first therapeutic and subsequent dosing of the bispecific antibody. In some embodiments, a cancer treated with a dosing regimen or method provided herein is relapsed and / or refractory (R / R). In some embodiments, a subject treated with a dosing regimen or method provided herein has been previously treated with 1-4 lines of therapy for the cancer. In some embodiments, the cancer is multiple myeloma. In some embodiments, the cancer is advanced multiple myeloma. In some embodiments, the cancer is relapsed or refractory multiple myeloma. In some embodiments, the cancer is triple class refractory multiple myeloma. In some embodiments, the multiple myeloma of the subject is refractory to all three types of the following multiple myeloma therapies (1) a prior multiple myeloma therapy that comprises a proteasome inhibitor, (2) a prior multiple myeloma therapy that comprises an immunomodulatory agent and (3) a prior multiple myeloma therapy that comprises an anti-CD38 antibody. In some embodiments, the cancer is double class refractory multiple myeloma. In some embodiments, the multiple myeloma of the subject is refractory to at least two of the following three types of multiple myeloma therapies (1) a prior multiple myeloma therapy that comprises a proteasome inhibitor, (2) a prior multiple myeloma therapy that comprises an immunomodulatory agent and (3) a prior multiple myeloma therapy that comprises an anti-CD38 antibody. In some embodiments, the cancer is newly diagnosed multiple myeloma. In some embodiments, the cancer is multiple myeloma, and the subject has received stem cell transplant. In some embodiments, the subject has received autologous stem cell transplant. In some embodiments, has received autologous stem cell transplant or allogeneic stem cell transplant. In some embodiments, the subject is minimum residual disease positive post stem cell transplant. In some embodiments, the cancer is multiple myeloma, wherein in some embodiments the subject has progressed or is intolerant of an established multiple myeloma therapy. In some embodiments, the established multiple myeloma therapy comprises at least one drug selected from the group consisting of a proteasome inhibitor, an IMid drug and an anti-CD38 antibody. In some embodiments, the cancer is multiple myeloma wherein the subject has received at least four prior therapies and the subject’s multiple myeloma is refractory or relapsed to (1) a prior multiple myeloma therapy that comprises an proteasome inhibitor, (2) a prior multiple myeloma therapy that comprises an immunomodulatory agent and (3) a prior multiple myeloma therapy that comprises an anti-CD38 monoclonal antibody, and wherein the subject has demonstrated disease progression on the last therapy. In one aspect of these embodiments, the subject has received a prior therapy of a BCMA targeted ADC or a BCMA targeted CAR-T. In another aspect of these embodiments, the subject has not received any prior therapy of a BCMA targeted ADC or a BCMA targeted CAR-T. In some embodiments, the cancer is multiple myeloma, the subject has received at least one, at least two, at least three or at least four prior multiple myeloma therapies, and the subject’s multiple myeloma is refractory or relapsed to (1) a prior multiple myeloma therapy that comprises a proteasome inhibitor, (2) a prior multiple myeloma therapy that comprises an immunomodulatory agent and (3) a prior multiple myeloma therapy that comprises an anti-CD38 antibody. In one aspect of this embodiment, the subject has demonstrated disease progression on the last multiple myeloma therapy. In one aspect of this embodiment, the subject has received at least three prior multiple myeloma therapies. In another aspect of this embodiment, the subject has received at least four prior multiple myeloma therapies. In some embodiments, the previous multiple myeloma therapies the subject received comprise a BCMA directed ADC therapy or a BCMA directed CAR-T cell therapy. In some embodiments, the previous multiple myeloma therapies the subject received comprise a BCMA directed therapy. In some embodiments, the multiple myeloma therapies the subject received do not comprise a BCMA directed ADC therapy or a BCMA directed CAR-T cell therapy. In some embodiments, the previous multiple myeloma therapies the subject received do not comprise a BCMA directed therapy. In some embodiments, the cancer is multiple myeloma, and the subject has received at least one or at least two prior multiple myeloma therapies, the subject’s multiple myeloma is refractory or relapsed to (1) a prior multiple myeloma therapy that comprises a proteasome inhibitor and (2) a prior multiple myeloma therapy that comprises an immunomodulatory agent. In some embodiments, the subject has demonstrated disease progression on the last multiple myeloma therapy. In some embodiments, the cancer is multiple myeloma, and the subject has not received any prior multiple myeloma therapies. In some embodiments, the subject has not received any prior multiple myeloma therapies after the diagnosis of multiple myeloma. In some embodiments, the subject is stem cell transplant ineligible. In some embodiments, the cancer is multiple myeloma and the subject is stem cell transplant ineligible. In some embodiments, the subject is autologous stem cell transplant ineligible. In some embodiments, the subject is allogeneic stem cell transplant ineligible. In some embodiments, the subject is ineligible for autologous stem cell transplant and is also ineligible for allogeneic stem cell transplant. An anti-BCMA / anti-CD3 bispecific antibody provided herein can be administered to the subject through any of the routes established for protein delivery, in particular, intravenous, intradermal and subcutaneous injection or infusion, or by oral or nasal administration. In some embodiments, the anti-BCMA / anti-CD3 bispecific antibody (e.g., elranatamab) is administered subcutaneously. In some embodiments, the method further comprises administered a second therapeutic agent. In some embodiments, the second therapeutic agent is selected from immunomodulating agents, including thalidomide, lenalidomide, pomalidomide, iberdomide and apremilast, which may stimulate an immune response in a subject. Further immunomodulating agents include, pattern recognition receptor (PRR) agonists, immunostimulatory cytokines, immune cell therapy and cancer vaccines. In some embodiments, the second therapeutic agent is selected from an agent directed or targeted to 5T4; A33; alpha-folate receptor 1 (e.g. mirvetuximab soravtansine); Alk-1; BCMA (e.g. see WO2016166629 and others disclosed herein); BTN1A1 (e.g. see CA19-9; CA-125 (e.g. abagovomab); Carboanhydrase IX; CCR2; CCR4 (e.g. mogamulizumab); CCR5 (e.g. leronlimab); CCR8; CD3 [e.g. blinatumomab (CD3 / CD19 bispecific), PF-06671008 (CD3 / P-cadherin bispecific), PF-06863135 (CD3 / BCMA bispecific)]; CD19 (e.g. blinatumomab, MOR208); CD20 (e.g. ibritumomab tiuxetan, obinutuzumab, ofatumumab, rituximab, ublituximab); CD22 (inotuzumab ozogamicin, moxetumomab pasudotox); CD25; CD28; CD30 (e.g. brentuximab vedotin); CD33 (e.g. gemtuzumab ozogamicin); CD38 (e.g. daratumumab, daratumumab and hyaluronidase, and isatuximab), CD40; CD-40L; CD44v6; CD47 (e.g. Hu5F9-G4, CC-90002, SRF231, B6H12); CD52 (e.g. alemtuzumab); CD56; CD63; CD79 (e.g. polatuzumab vedotin); CD80; CD86; CD123; CD276 / B7-H3 (e.g. omburtamab); CDH17; CEA; ClhCG; CTLA-4 (e.g. ipilimumab, tremelimumab), CXCR4; desmoglein 4; DLL3 (e.g. rovalpituzumab tesirine); DLL4; E-cadherin; EDA; EDB; EFNA4; EGFR (e.g. cetuximab, depatuxizumab mafodotin, necitumumab, panitumumab); EGFRvIII; Endosialin; EpCAM (e.g. oportuzumab monatox); FAP; Fetal Acetylcholine Receptor; FLT3 (e.g. see WO2018 / 220584); 4-1BB (CD137) [e.g. utomilumab / PF-05082566 (see WO2012 / 032433) or urelumab / BMS-663513], GD2 (e.g. dinutuximab, 3F8); GD3; GITR (e.g. TRX518); GloboH; GM1; GM2; HER2 / neu [e.g. margetuximab, pertuzumab, trastuzumab; ado-trastuzumab emtansine, trastuzumab duocarmazine, PF-06804103 (see US8828401)]; HER3; HER4; ICOS; IL-10; ITG-AvB6; LAG-3 (e.g. relatlimab, IMP701); Lewis-Y; LG; Ly-6; M-CSF [e.g. PD-0360324 (see US7326414)]; (membrane- bound) IgE; MCSP; mesothelin; MIS Receptor type II; MUC1; MUC2; MUC3; MUC4; MUC5AC; MUC5B; MUC7; MUC16; Notch1; Notch3; Nectin-4 (e.g. enfortumab vedotin); OX40 [e.g. PF-04518600 (see US7960515)]; P-Cadherin [e.g. PF-06671008 (see WO2016 / 001810)]; PCDHB2; PD-1 [e.g. BCD-100, camrelizumab, cemiplimab, genolimzumab (CBT-501), MEDI0680, nivolumab, pembrolizumab, sasanlimab (PF- 06801591, see WO2016 / 092419), sintilimab, spartalizumab, STI-A1110, tislelizumab, TSR-042, and others disclosed herein]; PD-L1 (e.g. atezolizumab, durvalumab, BMS- 936559 (MDX-1105), LY3300054, and others disclosed herein); PDGFRA (e.g. olaratumab); Plasma Cell Antigen; PolySA; PSCA; PSMA; PTK7 [e.g. PF-06647020 (see US9409995)]; Ror1; SAS; SLAMF7 (e.g. elotuzumab); SHH; SIRPa (e.g. ED9, Effi-DEM); STEAP; sTn; TGF-beta; TIGIT; TIM-3; TMPRSS3; TNF-alpha precursor; TROP-2 (e.g., sacituzumab govitecan); TSPAN8; VEGF (e.g. bevacizumab, brolucizumab); VEGFR1 (e.g. ranibizumab); VEGFR2 (e.g. ramucirumab, ranibizumab); and Wue-1. In some embodiments, the comprising administering lenalidomide to the subject. In some embodiments, both elranatamab and lenalidomide are administered in a treatment cycle of four weeks, for at least a first treatment cycle, and wherein if a priming dosing of elranatamab is administered, the first treatment cycle starts on the seventh day after the single priming dose or the last dose of the priming dosing is administered, and wherein lenalidomide is administered at a dose of 25 mg daily orally on day 1 to day 21 of each treatment cycle. In some embodiments, lenalidomide is administered at a dose of 25 mg daily orally on day 1 to day 21 of each treatment cycle without dexamethasone. In some embodiments, the first dose of elranatamab in a treatment cycle is administered on day 1 of the treatment cycle. In some embodiments, a priming dosing of elranatamab is administered, a cycle is 28 days, lenalidomide is administered at a daily oral dose of about 5 mg, about 10 mg, about 15 mg, about 20 mg or about 25 mg on day 8-28 or day 15 - 28 of the first cycle, and on day 1-28 of the second and third cycle, afterwards, starting on the fourth cycle, lenalidomide is administered at a daily oral dose of about 5 to 10 mg higher than that is administered during the third cycle, or continued to be administered at the same daily oral dose as that of the third cycle on day 1-28 of each cycle. In some embodiments, a priming dosing of elranatamab is administered, lenalidomide is administered at a daily oral dose of about 10 mg, or about 15 mg starting on day 8 of cycle 1 for at least 10 consecutive days in each cycle. In some embodiments, the method further comprising administering daratumumab to the subject. In some embodiments, daratumumab is administered subcutaneously at a daratumumab dosing of about 1800 mg weekly, every two weeks, every three weeks, or every four weeks. In some embodiments, daratumumab dosing starts as about 1800 weekly in cycle 1 for about 8 doses, followed by about 1800 mg every two weeks for about 8 to about 10 doses, followed by about 1800 mg every four weeks thereafter. In some embodiments, the method further comprises administering lenalidomide and daratumumab to the subject. A "heterodimer," "heterodimeric protein," “heterodimeric complex,” or "heteromultimeric polypeptide" is a molecule comprising a first polypeptide and a second polypeptide, wherein the differs in amino acid sequence from the first polypeptide by at least one amino acid residue. A “human antibody” refers to an antibody which possesses an amino acid sequence which corresponds to that of an antibody produced by a human or has been made using any technique for making fully human antibodies. For example, fully human antibodies may be obtained by using commercially available mice that have been engineered to express specific human immunoglobulin proteins, or by library (e.g., phage, yeast, or ribosome) display techniques for preparing fully human antibodies. This definition of a human antibody specifically excludes a humanized antibody comprising non-human antigen binding residues. A "humanized" antibody refers to a non-human (e.g., murine) antibody that is a chimeric antibody that contains minimal sequence derived from non-human immunoglobulin. Preferably, humanized antibodies are human immunoglobulins (recipient antibody) in which residues from a CDR of the recipient are replaced by residues from a CDR of a non-human species (donor antibody) such as mouse, rat, or rabbit having the desired specificity, affinity, and capacity. The humanized antibody may comprise residues that are found neither in the recipient antibody nor in the imported CDR or framework sequences, but are included to further refine and optimize antibody performance. An “IMiD drug”, “imid drug”, or an “immunomodulatory agent”, as used herein, interchangeably, refers to a drug that is understood by a practicing physician treating multiple myeloma as an IMiD drug or immunomodulatory agent in the context of the treatment of multiple myeloma. Examples of an IMid drug or an immunomodulating agent, includes, without limitation, thalidomide, lenalidomide and pomalidomide. Daratumumab (Darzalex, Darzalex Faspro) is an IgG1 kappa human monoclonal antibody that binds to the CD38 antigen and is available in formulations for intravenous and subcutaneous administration. Daratumumab is indicated in combination with lenalidomide and dexamethasone, for the treatment of adult patients with newly diagnosed multiple myeloma who are ineligible for autologous stem cell transplant. Immunoglobulin replacement therapy (also referred to as IVIG) refers to administration of a composition of IgG immunoglobulins to a subject. The composition can be administered intravenously or subcutaneously. “BCMA directed ADC to a multiple myeloma therapy that comprises an antibody drug conjugate, wherein the antibody binds to B-cell maturation antigen (BCMA). Examples of a BCMA directed ADC includes, without limitation, belantamab mafodotin -blmf, which was approved by USFDA and marketed under the brand name BLENREP. “BCMA directed CAR-T cell therapy”, or “anti-BCMA CAR-T cell” as used herein, interchangeably, refers to a multiple myeloma therapy that comprises a chimeric antigen receptor T cell wherein the chimeric antigen receptor recognizes B-cell maturation antigen (BCMA). Examples of a “BCMA targeted CAR-T therapy”, or “anti-BCMA CAR T cell therapy” includes, without limitation, idecabtgene vicleucel (ide-cel; or bb2121) and JNJ-4528, also known as LCAR-B38M. “BCMA directed therapy”, refers to a multiple myeloma therapy which active ingredient comprises a component that binds to the B-Cell maturation antigen. BCMA directed therapy includes BCMA directed ADC Therapy, BCMA directed CAR-T therapy, and multiple myeloma therapies that comprises BCMA bispecific antibodies. “Newly diagnosed multiple myeloma” refers to multiple myeloma wherein the patient (subject) has not yet received any treatment for the diagnosis of multiple myeloma. "Homology" refers to sequence similarity between two polypeptide sequences when they are optimally aligned. When a position in both of the two compared sequences is occupied by the same amino acid monomer subunit, e.g., if a position in a light chain CDR of two different Abs is occupied by alanine, then the two Abs are homologous at that position. The percent of homology is the number of homologous positions shared by the two sequences divided by the total number of positions compared ×100. For example, if 8 of 10 of the positions in two sequences are matched or homologous when the sequences are optimally aligned then the two sequences are 80% homologous. Generally, the comparison is made when two sequences are aligned to give maximum percent homology. For example, the comparison can be performed by a BLAST algorithm wherein the parameters of the algorithm are selected to give the largest match between the respective sequences over the entire length of the respective reference sequences. The following references relate to BLAST algorithms often used for sequence analysis: BLAST ALGORITHMS: Altschul, S.F., et al., (1990) J. Mol. Biol.215:403-410; Gish, W., et al., (1993) Nature Genet. 3:266-272; Madden, T.L., et al., (1996) Meth. Enzymol. 266:131-141; Altschul, S.F., (1997) Nucleic Acids Res. 25:3389-3402; Zhang, J., et al., (1997) Genome Res.7:649-656; Wootton, J.C., et al., (1993) Comput. Chem. 17:149-163; Hancock, J.M. et al., (1994) Comput. Appl. Biosci. 10:67-70; ALIGNMENT SCORING SYSTEMS: Dayhoff, M.O., et al., "A model of evolutionary change in proteins." in Atlas of Protein Sequence and Structure, (1978) vol.5, suppl.3. M.O. Dayhoff (ed.), pp.345-352, Natl. Biomed. Res. Found., Washington, DC; Schwartz, R.M., et al., "Matrices for detecting distant relationships." in Atlas of Protein Sequence and Structure, (1978) vol. 5, suppl. 3." M.O. Dayhoff (ed.), pp. 353-358, Natl. Biomed. Res. Found., Washington, DC; Altschul, S.F., (1991) J. Mol. Biol.219:555-565; States, D.J., et al., (1991) Methods 3:66-70; Henikoff, S., et al., (1992) Proc. Natl. Acad. Sci. USA 89:10915-10919; Altschul, S.F., et al., (1993) J. Mol. Evol. 36:290-300; ALIGNMENT STATISTICS: Karlin, S., et al., (1990) Proc. Natl. Acad. Sci. USA 87:2264- 2268; Karlin, S., et al., (1993) Proc. Natl. Acad. Sci. USA 90:5873-5877; Dembo, A., et al., (1994) Ann. Prob. 22:2022-2039; and Altschul, S.F. "Evaluating the statistical significance of multiple distinct local alignments." in Theoretical and Computational Methods in Genome Research (S. Suhai, ed.), (1997) pp.1-14, Plenum, New York. "Patient", "subject" or “individual” refers to any living organism suffering from or prone to a condition that can be prevented or treated by administration of a therapeutic agent or composition, or combination as provided herein, such as a cancer and / or a cancer-associated disease and includes both humans and animals. The terms “patients”, “subjects” and “individuals” include, but are not limited to, mammals (e.g., murines, simians, equines, bovines, porcines, canines, felines, and the like), and preferably are human. “Sustained response” means a sustained therapeutic effect after cessation of treatment with a therapeutic agent, or a combination therapy described herein. In some aspects, the sustained response has a duration that is at least the same as the treatment duration, or at least 1.5, 2.0, 2.5 or 3 times longer than the treatment duration. As used in herein, “administering" refers to the delivery of a therapeutic agent to a subject, using any of the various methods and delivery systems known to those skilled in the art. Exemplary routes of administration include intravenous, intramuscular, subcutaneous, intraperitoneal, spinal, or other parenteral routes of administration, for example by injection or infusion. The phrase "parenteral administration" as used herein means modes of administration other than enteral and topical administration, usually by injection, and includes, without intravenous, intramuscular, intraarterial, intrathecal, intralymphatic, intralesional, intracapsular, intraorbital, intracardiac, intradermal, intraperitoneal, transtracheal, subcutaneous, subcuticular, intraarticular, subcapsular, subarachnoid, intraspinal, epidural and intrasternal injection and infusion, as well as in vivo electroporation. A therapeutic agent can be administered via a non- parenteral route, or orally. Other non-parenteral routes include a topical, epidermal or mucosal route of administration, for example, intranasally, vaginally, rectally, sublingually or topically. Administering can also be performed, for example, once, a plurality of times, and / or over one or more extended periods. "Treat" or "treating" a cancer and / or a cancer-associated disease as used herein means to administer a therapy according to the present invention to a subject, patient or individual having a cancer, or diagnosed with a cancer, to achieve at least one positive therapeutic effect, such as, for example, reduced number of cancer cells, reduced tumor size, reduced rate of cancer cell infiltration into peripheral organs, or reduced rate of tumor metastasis or tumor growth, reversing, alleviating, inhibiting the progress of, or preventing the disorder or condition to which such term applies, or one or more symptoms of such disorder or condition. The term "treatment", as used herein, unless otherwise indicated, refers to the act of treating as "treating" is defined immediately above. The term “treating” also includes adjuvant and neo-adjuvant treatment of a subject. For the purposes of this invention, beneficial or desired clinical results include, but are not limited to, one or more of the following: reducing the proliferation of (or destroying) neoplastic or cancerous cell; inhibiting metastasis or neoplastic cells; shrinking or decreasing the size of tumor; remission of the cancer; decreasing symptoms resulting from the cancer; increasing the quality of life of those suffering from the cancer; decreasing the dose of other medications required to treat the cancer; delaying the progression the cancer; curing the cancer; overcoming one or more resistance mechanisms of the cancer; and / or prolonging survival of patients the cancer. Positive therapeutic effects in cancer can be measured in a number of ways (see, for example, W. A. Weber, J. Nucl. Med.50:1S- 10S (2009)). In some aspects, the treatment achieved by the invention is any of the partial response (PR), complete response (CR), overall response (OR), objective response rate (ORR), progression free survival (PFS), radiographic PFS, disease free survival (DFS) and overall survival (OS). PFS, also referred to as “Time to Tumor Progression” indicates the length of time during and after treatment that the cancer does not grow and includes the amount of time patients have a CR or PR, as well as the amount of time patients have experienced stable disease (SD). DFS refers to the length of time during and after treatment that the patient remains free of disease. OS refers to a prolongation in life expectancy as compared to naïve or untreated subjects or patients. In some aspects, response to the invention is any of PR, CR, PFS, DFS, ORR, OR or OS that is assessed using Response Evaluation Criteria in Solid Tumors (RECIST 1.1) response criteria (Eisenhauer et al., E.A. et al., Eur. J Cancer 45:228-247 (2009)). In some aspects, anti-myeloma activity may be evaluated by Overall response rate (ORR), time to response (TTR), complete response rate (CRR), duration of response (DOR), duration of complete response (DoCR), duration of stable disease (DOSD), progression-free survival (PFS), overall survival (OS), using International Myeloma Working Group (IMWG) criteria. The treatment regimen for a therapy as provided herein that is effective to treat a cancer patient may vary according to factors such as the disease state, age, and weight of the patient, and the ability of the therapy to elicit an anti-cancer response in the subject. While an aspect of any of the aspects of the invention may not be effective in achieving a positive therapeutic effect in every subject, it should do so in a statistically significant number of subjects as determined by any statistical test known in the art such as , but not limited to, the Cox log-rank test, the Cochran-Mantel-Haenszel log-rank test, the Student’s t-test, the chi2-test, the U-test according to Mann and Whitney, the Kruskal- Wallis test (H-test), Jonckheere-Terpstrat-test and the Wilcon on-test. The term “treatment” also encompasses in vitro and ex vivo treatment, e.g., of a cell, by a reagent, diagnostic, binding compound, or by another cell. As used herein, “pharmaceutical product” refers to a drug product that comprises an actively pharmaceutical ingredient and is regulated by the US FDA, EMA or other counterpart regulatory agencies in the other markets. A pharmaceutical product can be an investigational drug or a drug product that has already been approved by a regulatory agency. The terms “treatment regimen”, “dosing protocol” and “dosing regimen” are used interchangeably to refer to the dose and timing of administration of the antibody. As used herein “dosing” refers to both the “dose amount”, for example 1 mg, 20 mg, and the “dose frequency”, for example, once a day (QD), once a week (Q1W or QW), every two weeks (Q2W), every three weeks (Q3W) and every four weeks (Q4W). Dosing may also include the administration route of a drug, such as for example, subcutaneously (SC), intravenously (IV), oral (PO), if Similarly, a “priming dosing”, a “first treatment dosing”, a “second treatment dosing” and so on, each refers to both the dose amount and dose frequency of such dosing and optionally also includes the administration route if so specified. In some embodiments, there is one dose amount and one dose frequency in a dosing. In some embodiments, there are more than one dose amounts, and / or more than one dose frequencies in a dosing. As used herein, “dose level”, unless otherwise specified, when used to describe the dose amount of Elranatamab refers to one of the following dose amounts: 4 mg, 8 mg, 12 mg, 16 mg, 20 mg, 24 mg, 32 mg, 44 mg, 76 mg, 116 mg and 152 mg, wherein 8 mg, 12 mg, 16 mg, 20 mg 24 mg, 32 mg, 44 mg, 76 mg, 116 mg and 152 mg are each one dose level higher than 4 mg, 8 mg, 12 mg, 16 mg, 24 mg, 32 mg, 44 mg, 76 mg, and 116 mg, respectively. The terms “dose delay” and “dose interruption” are used interchangeably to refer to therapy being withheld to manage toxicity or other adverse event, or reaction related to the therapy. For example, in some embodiments, a dose delay can result if a subject experiences cytokine release syndrome (CRS), neurologic toxicity including immune effector cell-associated neurotoxicity syndrome (ICANS), infections, neutropenia, hepatoxicity, or other toxicity or adverse event or reaction. After resolution of the toxicity or other adverse event, administration of the anti-BCMA / anti-CD3 bispecific antibody is restarted according to the defined re-starting dosing schedule. As used herein, a “respective regulatory label of the pharmaceutical product” means, an unexpired United States Prescribing Information (USPI) from US Food and Drug Administration (FDA), an unexpired Summary of Product Characteristics (SMPC) from European Medicine Agency (EMA), of the pharmaceutical product or similar labels of the pharmaceutical product from the regulatory agencies in other markets. In some embodiments, a “respective regulatory label of the pharmaceutical product” in a patent or patent application in the United States, refers to an unexpired USPI of the pharmaceutical product, and in a patent or patent application in a European country that adopts EMA marketing authorizations of the pharmaceutical product, an unexpired SMPC of the pharmaceutical product, and similarly in other jurisdictions. As used herein the “subject’s response”, refers to the clinical response of the subject being treated with the pharmaceutical product that comprises elranatamab. The ‘subject’s response” includes one or more aspects with regard to clinical efficacy, such as complete response, partial duration of the response. “Subject’s response” may also include additional aspects such as toxicity and adverse events. As used herein, “IMWG response” refers to a patient’s (subject’s) clinical response to a pharmaceutical product to treat multiple myeloma, wherein the response, such as a complete response, or partial response, is defined according to the most up to date definition from the International Myeloma Working Group. As used herein, “cycle”, and “week” when used in the context of describing a method of treating cancer including uses thereof, a dosing, or a dosing schedule, refer to a duration of time. A cycle is 21 days or 28 days, unless otherwise specified, when a subject is treated with a therapeutic agent, a pharmaceutical product thereof, such as elranatamab, or a pharmaceutical product thereof. Week 1 refers to the first week when the subject is treated under the method, or any of the dosing or dosing schedules therein unless otherwise specified. Week 2 starts immediately after week 1 ends, week 3 starts immediately after week 2 ends, and so on. Cycle 1 starts on the first day of week 1, the first day of week 2, or the first day of week three, unless otherwise specified. Unless stated otherwise, cycle 2 starts immediately after cycle 1 ends, cycle 3 starts immediately after cycle 2 ends, and so on. As used herein, “stem cell transplant ineligible” refers patient diagnosed with multiple myeloma being not eligible for stem cell transplant as a treatment for the multiple myeloma. "Tumor" as it applies to a subject diagnosed with, or suspected of having, a cancer refers to a malignant or potentially malignant neoplasm or tissue mass of any size and includes primary tumors and secondary neoplasms. A solid tumor is an abnormal growth or mass of tissue that usually does not contain cysts or liquid areas. Different types of solid tumors are named for the type of cells that form them. Examples of solid tumors are sarcomas, carcinomas, and lymphomas. Leukemias (cancers of the blood) generally do not form solid tumors (National Cancer Institute, Dictionary of Cancer Terms). Multiple myeloma is a cancer of the plasma cells. "Tumor burden" also referred to as "tumor load", refers to the total amount of tumor material distributed throughout the body. Tumor burden refers to the total number of cancer cells or the total size of tumor(s), throughout the body, including lymph nodes and bone narrow. Tumor burden can be determined by a variety of methods known in the art, such as, e.g., by measuring the dimensions of tumor(s) upon removal from the subject, e.g., using calipers, or while in the body imaging techniques, e.g., ultrasound, bone scan, computed tomography (CT) or magnetic resonance imaging (MRI) scans. The term "tumor size" refers to the total size of the tumor which can be measured as the length and width of a tumor. Tumor size may be determined by a variety of methods known in the art, such as, e.g., by measuring the dimensions of tumor(s) upon removal from the subject, e.g., using calipers, or while in the body using imaging techniques, e.g., bone scan, ultrasound, CT or MRI scans. The term "immunotherapy" refers to the treatment of a subject by a method comprising inducing, enhancing, suppressing, or otherwise modifying an immune response. The term “immune effector cell” or “effector cell” as used herein refers to a cell within the natural repertoire of cells in the human immune system which can be activated to affect the viability of a target cell. The viability of a target cell can include cell survival, proliferation, and / or ability to interact with other cells. "Pharmaceutically acceptable excipient" or "pharmaceutically acceptable carrier" refers to a component that may be included in the compositions described herein and causes no significant adverse toxicological effects to a subject. The terms "protein", "polypeptide" and "peptide" are used interchangeably herein and refer to any peptide-linked chain of amino acids, regardless of length co-translational or post-translational modification. As used in herein, "substantially" or "essentially" means nearly totally or completely, for instance, 95% or greater of a given quantity. The term "substantially homologous" or “substantially identical” means that a particular subject sequence, for example, a mutant sequence, varies from a reference sequence by one or more substitutions, deletions, or additions, the net effect of which does not result in an adverse functional dissimilarity between the reference and subject sequences. For purposes herein, a sequence having greater than 95 percent homology (identity), equivalent biological activity (although not necessarily equivalent strength of biological activity), and equivalent expression characteristics to a given sequence is considered to be substantially homologous (identical). For purposes of determining homology, truncation of the mature sequence should be disregarded. Dosing schedules of Elranatamab, prior to any dose delays, are described, for example in WO2022 / 053990, which is incorporated by reference in its entirety. Another aspect of the invention kits that are suitable for use in performing the methods of treatment described herein. In one embodiment, the kit contains dosage forms in quantities sufficient to carry out the methods of the invention. In another embodiment, the kit comprises quantities sufficient to carry out the methods of the invention and at least a first container for a first dosage and a second container for a second dosage. In aspects and embodiments that refer to a method of treatment as described herein, such aspects and embodiments are also further aspects and embodiments to the anti-BCMA / anti-CD3 bispecific antibody, premedication compound(s) and / or second therapeutic agent(s), for use in that treatment, or alternatively for the manufacture of a medicament for use in that treatment. Sequences Sequences provided herein are summarized in Table 1 below. Table 1: SEQ ID Description Sequence NO: 1 Anti-BCMA GFTFSSYPMS HCDR1 Extended 2 Anti- BCMA AIGGSGGSLPYADIVKG HCDR2 Extended 3 Anti- BCMA YWPMDI HCDR3 4 Anti- BCMA RASQSVSSSYLA LCDR1 Extended 5 Anti- BCMA DASIRAT LCDR2 Extended 6 Anti- BCMA QQYQSWPLT LCDR3 7 Anti- BCMA EVQLLESGGG LVQPGGSLRL SCAASGFTFS VH SYPMSWVRQA PGKGLEWVSA IGGSGGSLPY ADIVKGRFTI SRDNSKNTLY LQMNSLRAED TAVYYCARYW PMDIWGQGTL VTVSS 8 Anti- BCMA EIVLTQSPGT LSLSPGERAT LSCRASQSVS VL SSYLAWYQQK PGQAPRLLMY DASIRATGIP SEQ ID Description Sequence NO: DRFSGSGSGT DFTLTISRLE PEDFAVYYCQ QYQSWPLTFG QGTKVEIK 9 Anti-CD3 GFTFSDYYMT HCDR1 Extended 10 Anti-CD3 FIRNRARGYTSDHNPSVKG HCDR2 Extended 11 Anti-CD3 DRPSYYVLDY HCDR3 12 Anti-CD3 KSSQSLFNVRSRKNYLA LCDR1 Extended 13 Anti-CD3 WASTRES LCDR2 Extended 14 Anti-CD3 KQSYDLFT LCDR3 15 Anti-CD3 VH EVQLVESGGG LVQPGGSLRL SCAASGFTFS DYYMTWVRQA PGKGLEWVAF IRNRARGYTS DHNPSVKGRF TISRDNAKNS LYLQMNSLRA EDTAVYYCAR DRPSYYVLDY WGQGTTVTVSS 16 Anti-CD3 VL DIVMTQSPDS LAVSLGERAT INCKSSQSLF NVRSRKNYLA WYQQKPGQPP KLLISWASTR ESGVPDRFSG SGSGTDFTLT ISSLQAEDVA VYYCKQSYDL FTFGSGTKLE IK 17 Anti- BCMA EVQLLESGGG LVQPGGSLRL SCAASGFTFS heavy chain SYPMSWVRQA PGKGLEWVSA IGGSGGSLPY ADIVKGRFTI SRDNSKNTLY LQMNSLRAED TAVYYCARYW PMDIWGQGTL VTVSSastkg psvfplapcs rstsestaal gclvkdyfpe pvtvswnsga ltsgvhtfpa vlqssglysl ssvvtvpssn fgtqtytcnv dhkpsntkvd ktverkceve cpecpappva gpsvflfppk pkdtlmisrt pevtcvvvav shedpevqfn wyvdgvevhn aktkpreeqf nstfrvvsvl tvvhqdwlng keykckvsnk glpssiekti sktkgqprep qvytlppsre emtknqvslt cevkgfypsd iavewesngq pennykttpp mldsdgsffl yskltvdksr wqqgnvfscs vmhealhnhy tqkslslspg k 18 Anti-BCMA EIVLTQSPGT LSLSPGERAT LSCRASQSVS light chain SSYLAWYQQK PGQAPRLLMY DASIRATGIP DRFSGSGSGT DFTLTISRLE PEDFAVYYCQ QYQSWPLTFG QGTKVEIKrt vaapsvfifp psdeqlksgt asvvcllnnf ypreakvqwk vdnalqsgns SEQ ID Description Sequence NO: qesvteqdsk dstyslsstl tlskadyekh kvyacevthq glsspvtksf nrgec 19 Anti-CD3 EVQLVESGGG LVQPGGSLRL SCAASGFTFS heavy chain DYYMTWVRQA PGKGLEWVAF IRNRARGYTS DHNPSVKGRF TISRDNAKNS LYLQMNSLRA EDTAVYYCAR DRPSYYVLDY WGQGTTVTVS Sastkgpsvf plapcsrsts estaalgclv kdyfpepvtv swnsgaltsg vhtfpavlqs sglyslssvv tvpssnfgtq tytcnvdhkp sntkvdktve rkcrvrcprc pappvagpsv flfppkpkdt lmisrtpevt cvvvavshed pevqfnwyvd gvevhnaktk preeqfnstf rvvsvltvvh qdwlngkeyk ckvsnkglps siektisktk gqprepqvyt lppsreemtk nqvsltclvk gfypsdiave wesngqpenn ykttppmlds dgsfflysrl tvdksrwqqg nvfscsvmhe alhnhytqks lslspgk 20 Anti-CD3 DIVMTQSPDS LAVSLGERAT INCKSSQSLF light chain NVRSRKNYLA WYQQKPGQPP KLLISWASTR ESGVPDRFSG SGSGTDFTLT ISSLQAEDVA VYYCKQSYDL FTFGSGTKLE IKrtvaapsv fifppsdeql ksgtasvvcl lnnfypreak vqwkvdnalq sgnsqesvte qdskdstysl sstltlskad yekhkvyace vthqglsspv tksfnrgec 21 Anti-BCMA GFTFSSY HCDR1 Chothia 22 Anti-BCMA SYPMS HCDR1 Kabat 23 Anti-BCMA GGSGGS HCDR2 Chothia 24 Anti-CD3 HCDR1 GFTFSDY Chothia 25 Anti-CD3 HCDR1 DYYMT Kabat 26 Anti-CD3 RNRARGYT HCDR2 Chothia The following examples of for carrying out the present invention are offered for illustrative purposes only and are not intended to limit the scope of the present invention in any way. The foregoing description and following Examples detail certain specific embodiments of the disclosure and describes the best mode contemplated by the inventors. It will be appreciated, however, that no matter how detailed the foregoing may appear in text, the disclosure may be practiced in many ways and the disclosure should be construed in accordance with the appended claims and any equivalents thereof. Although the disclosed teachings have been described with reference to various applications, methods, kits, and compositions, it will be appreciated that various changes and modifications can be made without departing from the teachings herein and the claimed disclosure below. The following examples are provided to better illustrate the disclosed teachings and are not intended to limit the scope of the teachings presented herein. While the present teachings have been described in terms of these exemplary embodiments, the skilled artisan will readily understand that numerous variations and modifications of these exemplary embodiments are possible without undue experimentation. All such variations and modifications are within the scope of the current teachings. EXAMPLES Example 1 Study of Elranatamab dosing in the event of a dose interruption during therapy In the MagnetisMM-3 (NCT04649359) study, elranatamab (ELRA) administered at a dose of 76 mg once-weekly (QW) with 2 step-up priming doses of 12 mg on day 1 and 32 mg on day 4 had a manageable safety profile, with 56.3% of patients developing cytokine release syndrome (CRS) and 98.8% of events occurring with the first 3 doses. Clinical factors associated with CRS and dosing recommendations for restarting treatment after dose interruptions, due to a CRS event, in patients with relapsed or refractory multiple myeloma (RRMM) undergoing treatment with ELRA. METHODS Eligible patients received ELRA subcutaneously in step-up priming doses of 12 and 32 mg on days 1 and 4 of cycle 1, respectively, followed by 76 mg of ELRA QW. CRS events were graded according to the criteria of the American Society for Transplantation and Cellular Therapy and managed according to published guidelines. A multivariate analysis was performed to identify clinical factors associated with CRS after elranatamab treatment. Blood samples were collected for pharmacokinetic (PK) analyses for MagnetisMM-1: pre-dose (day 1 of 1-week priming cycle, days 1, 8, 15, 22 of cycles 1 and 2, and day 1 of cycle 3+), post-dose (days 1 and 2 of 1-week priming cycle and days 1 and 2 of cycle 1), and end of treatment (EOT); MM-2: pre-dose (day 1 of the priming cycle, days 1, 8 , and 15 of cycles 1 and 2, and day 1 of cycle 3 to cycle 8, thereafter every 4th cycle), post-dose (days 1, 2, and 4 of the priming cycle, days 1, 2, 4, and 8 of cycle 1), and EOT; MM-3: pre-dose (days 1, 4, 8, 15, and 22 of cycle 1, day 1 of cycles 2-4, thereafter every 3rd cycle), post-dose (days 1, 4, and 8 of cycle 1), and EOT; MM-9: pre-dose (days 1, 4, and 8 of cycle 1, day 1 of cycles 2, 4, and 6, thereafter every 6th cycle), post-dose (days 1 and 4 of cycle 1), and EOT. A previously described population PK model using information from the MagnetisMM-1, MM-2, MM-3, and MM-9 studies was used to simulate different interruption scenarios and determine how long it takes for ELRA exposure to drop below the threshold associated with CRS events. RESULTS Of 183 patients who were treated in MagnetisMM-3 with the 2 step-up priming dosing, 106 patients (57.9%) experienced CRS, 43.7% grade 1, 13.7% grade 2, and 0.5% grade 3. Tocilizumab was used to manage CRS. Of the 130 CRS events, 37 (28.5%; 20 grade 1 and 17 grade ≥2) were treated with tocilizumab, and 93 (71.5%; 82 grade 1 and 11 grade ≥2) were not. After receiving doses of 76 mg of ELRA, 16 instances of dose delays lasting >6 to ≤12 weeks were observed. In most of these instances (11 / 16; 68.8%), patients did not repeat the 32-mg step-up dose. In 5 instances, patients restarted treatment with 32 mg of ELRA. No patients experienced CRS after retreatment. For the 4 instances of dose delays lasting >12 weeks after a 76-mg dose, patients repeated the 32-mg step-up dose in 2 instances, and patients received >32 mg ELRA after the interruption in the other 2 instances, with none experiencing retreatment. To minimize the risk of recurrent CRS events after dose interruptions, clinical and pharmacokinetic data and modeling were used to develop recommendations for restarting therapy (see Figure 1). It is recommended that patients receiving 76 mg ELRA who then experience dose delays lasting 6-12 or >12 weeks should restart treatment at doses of 32 or 12 mg, respectively. With dose delays of 6-12 weeks, ELRA exposure decreases below the Cmax after a 32- mg dose but not less than that for the 12-mg dose; therefore, repeating the 32-mg dose is recommended. With dose delays >12 weeks, ELRA exposure decreases below the Cmaxafter a 12-mg dose; so, repeating the step-dosing schedule starting with the 12-mg dose is recommended. CONCLUSIONS The 2-step-up priming regimen used in the MagnetisMM-3 study mitigated the frequency and severity of CRS, and retreatment at these doses after dose delays helped to reduce additional risk of CRS. The dosing recommendations described here is expected to facilitate the outpatient administration of ELRA for treating RRMM. The dosing after dose interruption is further summarized in the below Table 2. Last Dose Time Since the Last Dose Action for Next Dose Administered Administered Step-up dose 1 (12 mg) 2 weeks or less (≤14 days) Restart Elranatamab at step-up dose 2 (32 mg).aIf tolerated, increase to 76 mg 4 days later. Greater than 2 weeks (>14 Restart Elranatamab days) step-up dosing schedule at step-up dose 1 (12 mg).aStep-up dose 2 (32 mg) 2 weeks or less (≤14 days) Restart Elranatamab at 76 mg.aGreater than 2 weeks to less Restart Elranatamab at than or equal to 4 weeks (15 step-up dose 2 (32 mg).adays to ≤28 days) Last Dose Time Dose Action for Next Dose Administered Administered If tolerated, increase to 76 mg 1 week later. Greater than 4 weeks Restart Elranatamab (>28 days) step-up dosing schedule at step-up dose 1 (12 mg).aAny treatment dose 6 weeks or less (≤42 days) Restart Elranatamab at (76 mg) 76 mg. Greater than 6 weeks to less Restart Elranatamab at or equal to 12 weeks (43 step-up dose 2 (32 mg).adays to ≤84 days)bIf tolerated, increase to 76 mg 1 week later. Greater than 12 weeks (>84 Restart Elranatamab days)bstep-up dosing schedule at step-up dose 1 (12 mg).aa. Administer pre-treatment medications prior to the Elranatamab dose b. Consider benefit-risk of restarting Elranatamab in patients who require a dose delay of more than 42 days due to an adverse reaction. Example 2 Dosage delays may be required to manage toxicities related to Elranatamab, such as cytokine release syndrome (CRS) and ICANS. Management recommendations for CRS are summarized in Table 3 below. If CRS is suspected, Elranatamab is withheld until CRS resolves. Table 3. Recommendations for of CRS GradeaPresenting Symptoms ActionsGrade 1 Temperature ≥100.4 °F (38 °C)b^ Withhold Elranatamab until CRSresolves.c^ Administer pretreatment medications prior to next dose of Elranatamab. Grade 2 Temperature ≥100.4 °F (38 °C) ^ Withhold Elranatamab until CRS with either: resolves.c^ Hypotension responsive to ^ Monitor patients daily for 48 fluid and not requiring hours following the next dose of vasopressors, and / or Elranatamab. Instruct patients to ^ Oxygen requirement of low- remain within proximity of a flow nasal cannulador blow- healthcare facility, and consider by hospitalization. ^ Administer pretreatment medications prior to next dose of Elranatamab. Grade 3 Temperature ≥100.4 °F (38 °C) ^ Withhold Elranatamab until CRS (First with either: resolves.coccurrence) ^ Hypotension requiring one ^ Provide supportive therapy, vasopressor with or without which may include intensive care. vasopressin, and / or ^ Patients should be hospitalized ^ Oxygen requirement of high- for 48 hours following the next flow nasal cannulad, dose of Elranatamab. facemask, non-rebreather ^ Administer pretreatment mask, or Venturi mask medications prior to next dose of Elranatamab. Table 3. Recommendations for of CRS GradeaPresenting Symptoms Actions Grade 3 Temperature ≥100.4 °F (38 °C) ^ Permanently discontinue therapy (Recurrent) with either: with Elranatamab. ^ Hypotension requiring one ^ Provide supportive therapy, vasopressor with or without which may include intensive care. vasopressin, and / or ^ Oxygen requirement of high- flow nasal cannulad, facemask, non-rebreather mask, or Venturi mask Grade 4 Temperature ≥100.4 °F (38 °C) ^ Permanently discontinue therapy with either: with Elranatamab. ^ Hypotension requiring ^ Provide supportive therapy, multiple vasopressors which may include intensive care. (excluding vasopressin), and / or ^ Oxygen requirement of positive pressure (e.g., continuous positive airway pressure [CPAP], bilevel positive airway pressure [BiPAP], intubation, and mechanical ventilation) a. Based on American Society for Transplantation and Cellular Therapy (ASTCT) 2019 grading criteria for CRS. b. Attributed to CRS. Fever may not always be present concurrently with hypotension or hypoxia as it may be masked by interventions such as antipyretics or anti- cytokine therapy. c. See Table 2 in Example 1 for recommendations on restarting Elranatamab after dose delays. d. Low-flow nasal cannula is ≤6 L / min, and high-flow nasal cannula is >6 L / min. Neurologic Toxicity Including ICANS Management recommendations for ICANS and neurologic toxicity are summarized in Table 4 and Table 5. At the first sign of neurologic toxicity, including ICANS, withhold Elranatamab and consider neurology evaluation. Rule out other causes of neurologic symptoms. Provide supportive therapy, which may include intensive care, for severe or life-threatening neurologic toxicities, including ICANS. Manage ICANS according to the recommendations in Table 4 and consider further management per current practice guidelines. Table 4. Recommendations for Management of ICANS Gradea Presenting Symptomsb Actions Grade 1 ICE score 7-9c^ Withhold Elranatamab until ICANS resolves.eOr depressed level of ^ Monitor neurologic symptoms and consciousnessd: awakens consider consultation with a spontaneously. neurologist and other specialists for further evaluation and management. ^ Consider non-sedating, anti-seizure medications (e.g., levetiracetam) for seizure prophylaxis. Grade 2 ICE score 3-6c^ Withhold Elranatamab until ICANS resolves.eOr depressed level of ^ Administer dexamethasonef10 mg consciousnessd: awakens to intravenously every 6 hours. Continue voice. dexamethasone use until resolution to Grade 1 or less, then taper. ^ Monitor neurologic symptoms and consider consultation with a neurologist and other specialists for further evaluation and management. Table 4. Recommendations for of ICANS Gradea Presenting Symptomsb Actions ^ Consider non-sedating, anti-seizure medications (e.g., levetiracetam) for seizure prophylaxis. ^ Monitor patients daily for 48 hours following the next dose of Elranatamab. Instruct patients to remain within proximity of a healthcare facility, and consider hospitalization. Grade 3 ICE score 0-2c^ Withhold Elranatamab until ICANS (First resolves.eoccurrence) or depressed level of ^ Administer dexamethasonef10 mg consciousnessd: awakens intravenously every 6 hours. Continue only to tactile stimulus, dexamethasone use until resolution to Grade 1 or less, then taper. or seizuresd, either: ^ Monitor neurologic symptoms and ^ any clinical seizure, focal consider consultation with a or generalized, that neurologist and other specialists for resolves rapidly, or further evaluation and management. ^ non-convulsive seizures ^ Consider non-sedating, anti-seizure on electroencephalogram medications (e.g., levetiracetam) for (EEG) that resolve with seizure prophylaxis. intervention, ^ Provide supportive therapy, which may include intensive care. or raised intracranial ^ Patients should be hospitalized for 48 pressure: focal / local edema hours following the next dose of on neuroimagingdElranatamab. Grade 3 ICE score 0-2c^ Permanently discontinue (recurrent) Elranatamab. or depressed level of ^ Administer dexamethasonef10 mg consciousnessd: awakens intravenously every 6 hours. Continue only to tactile stimulus, Table 4. Recommendations for of ICANS Gradea Presenting Symptomsb Actions dexamethasone use until resolution to or seizuresd, either: Grade 1 or less, then taper. ^ any clinical seizure, focal ^ Monitor neurologic symptoms and or generalized, that consider consultation with a resolves rapidly, or neurologist and other specialists for ^ non-convulsive seizures further evaluation and management. on electroencephalogram ^ Consider non-sedating, anti-seizure (EEG) that resolve with medications (e.g., levetiracetam) for intervention, seizure prophylaxis. ^ Provide supportive therapy, which or raised intracranial may include intensive care. pressure: focal / local edema on neuroimagingdGrade 4 ICE score 0c^ Permanently discontinue Elranatamab. Or, depressed level of ^ Administer dexamethasonef10 mg consciousnessdeither: intravenously every 6 hours. Continue ^ patient is unarousable or dexamethasone use until resolution to requires vigorous or Grade 1 or less, then taper. repetitive tactile stimuli to ^ Alternatively, consider administration arouse, or of methylprednisolone 1,000 mg per ^ stupor or coma, day intravenously for 3 days. ^ Monitor neurologic symptoms and or seizuresd, either: consider consultation with a ^ life-threatening prolonged neurologist and other specialists for seizure (>5 minutes), or further evaluation and management. ^ repetitive clinical or ^ Consider non-sedating, anti-seizure electrical seizures without medications (e.g., levetiracetam) for return to baseline in seizure prophylaxis. between, ^ Provide supportive therapy, which may include intensive or motor findingsd: care. ^ deep focal motor weakness such as Table 4. Recommendations for of ICANS Gradea Presenting Symptomsb Actions hemiparesis or paraparesis, or raised intracranial pressure / cerebral edemad, with signs / symptoms such as: ^ diffuse cerebral edema on neuroimaging, or ^ decerebrate or decorticate posturing, or ^ cranial nerve VI palsy, or ^ papilledema, or ^ Cushing’s triad a. Based on American Society for Transplantation and Cellular Therapy (ASTCT) 2019 grading criteria for ICANS. b. Management is determined by the most severe event, not attributable to any other cause. c. If patient is arousable and able to perform Immune Effector Cell-Associated Encephalopathy (ICE) Assessment, assess: Orientation (oriented to year, month, city, hospital = 4 points); Naming (name 3 objects, e.g., point to clock, pen, button = 3 points); Following Commands (e.g., “show me 2 fingers” or “close your eyes and stick out your tongue” = 1 point); Writing (ability to write a standard sentence = 1 point); and Attention (count backwards from 100 by ten = 1 point). If patient is unarousable and unable to perform ICE Assessment (Grade 4 ICANS) = 0 points. d. Not attributable to any other cause. e. See Table 2 for recommendations on restarting Elranatamab after dose delays. f. All references to dexamethasone administration are dexamethasone or equivalent medications. Table 5. Recommendations for of Neurologic Toxicity, Excluding ICANS Adverse Severity Actions Reaction NeurologicGrade 1^ Withhold Elranatamab until Toxicity neurologic toxicity symptoms (excluding resolve or stabilize. ICANS) Grade 2 ^ Withhold Elranatamab until Grade 3 (First occurrence) neurologic toxicity symptoms improve to Grade 1 or less. ^ Provide supportive therapy. Grade 3 (Recurrent) ^ Permanently discontinue Grade 4 Elranatamab. ^ Provide supportive therapy, which may include intensive care. Table 6. Recommended Dosage Modifications for Other Adverse Reactions Adverse Severity Actions Reactions Hematologic Absolute neutrophil count ^ Withhold Elranatamab until Adverse less than 0.5 x 109 / L absolute neutrophil count is 0.5 x Reactions 109 / L or higher.b[see WarningsFebrile neutropenia^ Withhold Elranatamab untiland Precautions absolute neutrophil count is 1 x (5.5)] 109 / L or higher and fever resolves.bHemoglobin less than ^ Withhold Elranatamab until 8 g / dL hemoglobin is 8 g / dL or higher.bPlatelet count less than ^ Withhold Elranatamab until 25,000 / mcL platelet count is 25,000 / mcL or higher and no evidence of bleeding.b Table 6. Recommended Dosage for Other Adverse Reactions Adverse Severity Actions Reactions Platelet count between 25,000 / mcL and 50,000 / mcL with bleeding Infections and Grade 3 ^ Withhold Elranatamab until Other adverse reaction improves to Non-hematologic ≤Grade 1 or baseline.bAdverseGrade 4^ Consider permanent Reactionsadiscontinuation of Elranatamab. [see Warnings ^ If Elranatamab is not permanently and Precautions discontinued, withhold subsequent (5.4, 5.6) and treatment doses of Elranatamab Adverse (e.g., doses administered after Reactions (6.1)] Elranatamab step-up dosing schedule) until adverse reaction improves to Grade 1 or less. a. Based on National Cancer Institute Common Terminology Criteria for Adverse Events (NCI-CTCAE), Version 5.0. b. See Table 2 for recommendations on restarting Elranatamab after dose delays. Example 3 – Immunoglobulin replacement therapy Patients with relapsed or refractory multiple myeloma (RRMM) are at increased risk for severe infections due to immunosuppression related to underlying MM as well as anti- myeloma therapies. As a result, management guidelines include recommendations for anti-infective prophylaxis in patients at high risk for infections, including Ig replacement therapy for hypogammaglobulinemia. However, sparse data exist demonstrating the impact of Ig replacement on the incidence of infection in patients treated with BCMA–directed bispecific antibodies. In the phase 2 registrational trial with elranatamab, infections occurred in 71.0% of patients, with grade 3 / 4 infections in 37.2% and fatal infections in 7.7%. The impact of Ig replacement therapy and hypogammaglobulinemia on the rate of infections in patients in the MagnetisMM-3 study who received treatment with Elranatamab was studied. Methods A post-hoc analysis (similar to an analysis described in Lancman et al., Clinical Lymphoma, Myeloma & Leukemia, Vol 21, No.5, e470-6, 2021) was conducted to evaluate the impact of Ig replacement therapy and hypogammaglobulinemia on infections in patients enrolled in MagnetisMM-3. Hypogammaglobulinemia was defined as IgG < 400 mg / dL. The on-treatment time for each patient was divided into the following periods for analysis of the incidence of infections: - On vs off Ig replacement therapy - With vs without hypogammaglobulinemia. The “on Ig” period was defined as the period between the administration of Ig replacement therapy + 30 days. Hypogammaglobulinemia was defined as IgG <400 mg / dL. For patients with non-IgG myeloma, quantitative IgG results were used. For patients with IgG myeloma, functional IgG levels were determined by subtracting the amount of the M-spike paraprotein detected in serum protein electrophoresis from the quantitative IgG result. Any new (i.e., noncontinuous) infection event starting within a period, any increase in grade in a single continuous infection event, and any infection event starting in one period and spanning across the entire next period (if ≥30 days) were counted as distinct infection events. A continuous infection event was defined as any event with a grade change and no gap between start / stop dates. Exposure-adjusted infection rates (EAIRs) were calculated as the number of infection events in each period divided by the total time in months in each period. Results Patients Overall, 187 patients received elranatamab in MagnetisMM-3; the median (range) treatment duration was 4.37 (0.03-25.79) months. In the total patient population (n=187), 77 (41.2%) patients received Ig replacement therapy at some point during the treatment period. The median time “on” vs “off” Ig replacement was 3.02 (range, 0.07-25.03) vs 4.57 (range, 0.16-18.63) months. Among patients with quantitative immunoglobulin data (n=137), the median time without and with hypogammaglobulinemia was 4.12 (range, 0.03-20.47) vs 6.34 (range, 0.03- 17.71) months. Infections Lower monthly EAIRs were observed in patients “on” vs “off” Ig replacement therapy (0.22 [95% CI, 0.18-0.27] vs 0.36 [95% CI, 0.33-0.40]), with similar trends observed regardless of infection type (Figure 2) Lower monthly EAIRs were observed in patients without vs with hypogammaglobulinemia (0.23 [95% CI, 0.19-0.27] vs 0.36 [95% CI, 0.32-0.40]); similar trends were seen across infection types (Figure 3) Conclusion In this phase 2 study of patients with RRMM treated with elranatamab, IgG levels of ≥400 mg / dL or Ig replacement therapy were associated with decreased infection rates, including the rates of grade ≥3 infections. These data support the continued need monitoring of Ig levels during treatment and the benefit of Ig replacement therapy in the management of patients with RRMM treated with B-cell maturation antigen (BCMA)–directed bispecific antibodies.

Claims

1. A method of treating cancer, comprising administering an anti-BCMA / anti-CD3 bispecific antibody to a subject according to a primary dosing schedule and a re-starting dosing schedule, and wherein the dosing schedule is described by a week number, a dose amount and a dose frequency corresponding to each week number, wherein the primary dosing schedule is selected from: (a) Week Number Dose Amount (mg) Dose Frequency 1 44; 32; 12 plus 32; or A Weekly plus B; 2 – 24; 32; 44; 76; 116; or 152 Weekly 32; 44; 76; 116; or 152 Weekly; every two weeks; 25 onwards; every three weeks; or every four weeks , (b) Week Number Dose Amount (mg) Dose Frequency 1 44; 32; 12 plus 32; or A Weekly plus B; 2 – 25; 32; 44; 76; 116; or 152 Weekly 32; 44; 76; 116; or 152 Weekly; every two weeks; 26 onwards; every three weeks; or every four weeks , (c) Week Number Dose Amount (mg) Dose Frequency 1 44; 32; 12 plus 32; or A Weekly plus B; 2 – 26; 44; or 76 Weekly 44; or 76 Weekly; every two weeks; 27 onwards; every three weeks; or every four weeks , (d) Week Number Dose Amount (mg) Dose Frequency1 44; 32; 12 or A Weekly plus B; 2 – 24 32; 44; 76; 116; or 152 Every two weeks 25 onwards 32; 44; 76; 116; or 152 Every two weeks; every three weeks; or every four weeks , (e) Week Number Dose Amount (mg) Dose Frequency 1 44; 32; 12 plus 32; or A Weekly plus B; 2 – 25 32; 44; 76; 116; or 152 Every two weeks 26 onwards 32; 44; 76; 116; or 152 Every two weeks; every three weeks; or every four weeks , or (f) Week Number Dose Amount (mg) Dose Frequency 1 44; 32; 12 plus 32; or A Weekly plus B; 2 – 26 32; 44; 76; 116; or 152 Every two weeks 27 onwards 32; 44; 76; 116; or 152 Every two weeks; every three weeks; or every four weeks wherein when the dose amount is 12 mg plus 32 mg during week 1, the dose amount of 12 mg is administered on one day, subsequently, the dose amount of 32 mg is administered on another day, wherein A plus B is 4 (A) plus 20 (B), 8 (A) plus 16 (B), 12 (A) plus 12 (B), or 8 (A) plus 24 (B), and wherein when the dose amount is A mg plus B mg during week 1, the dose amount of A mg is administered on one day, subsequently, the dose amount of B mg is administered on another day; wherein the dose amount and the dose frequency during week 1 are together referred to as a priming dosing, and if the subject is administered only one dose of antibody in the priming dosing, such one dose is referred to as a single priming dose, if the subject is sequentially administered two doses of antibody during week 1, the two doses are referred to as a first priming dose and a second priming dose respectively; the dose amount and dose frequency during weeks 2 - 24, weeks 2 – 25 and weeks 2 – 26 in the respective dosing schedules (a) and (d), (b) and (e) and (c) and (f), respectively, are ineach dosing schedule together a first treatment dosing, the dose amount and the dose frequency during week 25 and onwards, week 26 onwards, and week 27 onwards in the respective dosing schedules (a) and (d), (b) and (e) and (c) and (f), are in each dosing schedule together referred to as a second treatment dosing; and wherein if the subject experiences a dose delay: (i) after the first priming dose but before the second priming dose, the antibody is administered to the subject according to a re-starting dosing schedule according to the following: a) if two weeks or less since the first priming dose, the subject is administered the antibody at the second priming dose, optionally wherein if the second priming dose is tolerated, the dose is increased to the treatment dose after four days; or b) if greater than two weeks since the first priming dose, the subject is administered the antibody at the first priming dose. (ii) after the second priming dose but before the treatment dose the antibody is administered to the subject according to a re-starting dosing schedule according to the following: a) if two weeks or less since the second priming dose, the subject is administered the antibody at the treatment dose; b) if greater than two weeks and less than or equal to four weeks since the second priming dose, the subject is administered the antibody at the second priming dose optionally wherein if the second priming dose is tolerated, the dose in increased to the treatment dose after four days; or c) if greater than four weeks since the second priming dose, the subject is administered the antibody at the first priming dose. (iii) after a treatment dose but before the next treatment dose the antibody is administered to the subject according to a re-starting dosing schedule according to the following: a) if six weeks or less since last treatment dose, the subject is administered the antibody at the treatment dose; b) if greater than six weeks and less than or equal to twelve weeks since last treatment dose, the subject is administered the antibody at the second primingdose, optionally wherein if priming dose is tolerated, the dose in increased to the treatment dose after four days; or c) if greater than twelve weeks since last treatment dose, the subject is administered the antibody at the first priming dose.

2. The method of claim 1, wherein after the antibody is administered according to the re- starting dosing schedule, the dosing is continued according to the primary dosing schedule.

3. The method of claim 1 or 2, wherein the anti-BCMA / anti-CD3 antibody is Elranatamab.

4. The method of any one of claims 1 to 3, wherein the subject is administered the antibody according to the primary dosing schedule as shown below, (a) Week Number Dose Amount (mg) Dose Frequency 1 44 Weekly 2 – 24 76 Weekly 25 onwards 76 Weekly; every two weeks; every three weeks; or every four weeks , (b) Week Number Dose Amount (mg) Dose Frequency 1 44 Weekly 2 – 25 76 Weekly 26 onwards 76 Weekly; every two weeks; every three weeks; or every four weeks , (c) Week Number Dose Amount (mg) Dose Frequency 1 44 Weekly 2 – 26 76 Weekly27 onwards 76 Weekly; every two weeks; every three weeks; or every four weeks , (d) Week Number Dose Amount (mg) Dose Frequency 1 44 Weekly 2 – 24 76 Every two weeks 25 onwards 76 Every two weeks; every three weeks; or every four weeks , (e) Week Number Dose Amount (mg) Dose Frequency 1 44 Weekly 2 – 25 76 Every two weeks 26 onwards 76 Every two weeks; every three weeks; or every four weeks , or (f) Week Number Dose Amount (mg) Dose Frequency 1 44 Weekly 2 – 26 76 Every two weeks 27 onwards 76 Every two weeks; every three weeks; or every four weeks .

5. The method of claim 4, wherein the subject is administered the antibody according to the dosing schedule (a), (b) or (c), and the dose frequency for week 25 onwards, week 26 onwards, and week 27 onwards in the dosing schedule (a), (b), and (c), respectively, is (i) weekly, (ii) every two weeks, or (iii) weekly or every two weeks.

6. The method of any one of claims 1 to 3, wherein the subject is administered the antibody according to the primary dosing schedule as shown below, (a) Week Number Dose Amount (mg) Dose Frequency1 12 plus 32 Weekly 2 – 24 76 Weekly 25 onwards 76 Weekly; every two weeks; every three weeks; or every four weeks , (b) Week Number Dose Amount (mg) Dose Frequency 1 12 plus 32 Weekly 2 – 25 76 Weekly 26 onwards 76 Weekly; every two weeks; every three weeks; or every four weeks , (c) Week Number Dose Amount (mg) Dose Frequency 1 12 plus 32 Weekly 2 – 26 76 Weekly 27 onwards 76 Weekly; every two weeks; every three weeks; or every four weeks , (d) Week Number Dose Amount (mg) Dose Frequency 1 12 plus 32 Weekly 2 – 24 76 Every two weeks 25 onwards 76 Every two weeks; every three weeks; or every four weeks , (e) Week Number Dose Amount (mg) Dose Frequency 1 12 plus 32 Weekly 2 – 25 76 Every two weeks 26 onwards 76 Every two weeks; every three weeks; or every four weeks , or (f)Week Number Dose Amount Dose Frequency 1 12 plus 32 Weekly 2 – 26 76 Every two weeks 27 onwards 76 Every two weeks; every three weeks; or every four weeks .

7. The method of claim 6, wherein the subject is administered the antibody according to the dosing schedule (a), (b) or (c), and the dose frequency for week 25 onwards, week 26 onwards, and week 27 onwards in the dosing schedule (a), (b), and (c), respectively, is (i) weekly, (ii) every two weeks, or (iii) weekly or every two weeks 8. The method of any one of claims 1 to 3, wherein the subject is administered the antibody according to the primary dosing schedule as shown below, (a) Week Number Dose Amount (mg) Dose Frequency 1 32; or 12 plus 32 Weekly 2 – 24 44 Weekly 25 onwards 44 Weekly; every two weeks; every three weeks; or every four weeks , (b) Week Number Dose Amount (mg) Dose Frequency 1 32; or 12 plus 32 Weekly 2 – 25 44 Weekly 26 onwards 44 Weekly; every two weeks; every three weeks; or every four weeks , (c) Week Number Dose Amount (mg) Dose Frequency 1 32; or 12 plus 32 Weekly 2 – 26 44 Weekly27 onwards 44 Weekly; every two weeks; every three weeks; or every four weeks , (d) Week Number Dose Amount (mg) Dose Frequency 1 32; or 12 plus 32 Weekly 2 – 24 44 Every two weeks 25 onwards 44 Every two weeks; every three weeks; or every four weeks , (e) Week Number Dose Amount (mg) Dose Frequency 1 32; or 12 plus 32 Weekly 2 – 25 44 Every two weeks 26 onwards 44 Every two weeks; every three weeks; or every four weeks , or (f) Week Number Dose Amount (mg) Dose Frequency 1 32; or 12 plus 32 Weekly 2 – 26 44 Every two weeks 27 onwards 44 Every two weeks; every three weeks; or every four weeks .

9. The method of claim 8, wherein the subject is administered the antibody according to the dosing schedule (a), (b) or (c), and the dose frequency for week 25 onwards, week 26 onwards, and week 27 onwards in the dosing schedule (a), (b), and (c), respectively, is (i) weekly, (ii) every two weeks, or (iii) weekly or every two weeks.

10. The method of any one of claims 1 to 9, wherein the subject is administered the antibody of the second treatment dosing for 6 to 18 cycles, thereafter, the subject is administered a third treatment dosing of the antibody subcutaneously, wherein the third treatment dosing is 32 mg Q2W, 32 mg Q4W, 44 mg Q2W, 44 mg Q4W, 76 mg Q2W, 76 mg Q4W, 116 mg Q2W, 116 mg Q4W, 152 mg Q2W, or 152 mg Q4W, wherein a cycleis 21 days or 28 days, and cycle 1 1 week 1, day 1 week 2, or day 1 week 3.

11. The method of claim 10, wherein (i) the first treatment dosing is 32 mg Q1W, the second treatment dosing is 32 mg Q1W or 32 mg Q2W and the third treatment dosing is 32 mg Q2W or 32 mg Q4W, (ii) first treatment dosing is 32 mg Q1W, the second treatment dosing is 32 mg Q2W and the third treatment dosing is 32 mg Q4W, (iii) the first treatment dosing is 44 mg Q1W, the second treatment dosing is 44 mg Q1W or 44 mg Q2W and the third treatment dosing is 44 mg Q2W or 44 mg Q4W; (iv) the first treatment dosing is 44 mg Q1W, the second treatment dosing is 44 mg Q2W and the third treatment dosing is 44 mg Q4W; (v) first treatment dosing is 76 mg Q1W, the second treatment dosing is 76 mg Q1W or 76 mg Q2W and the third treatment dosing is 76 mg Q2W or 76 mg Q4W, (vi) the first treatment dosing is 76 mg Q1W, the second treatment dosing is 76 mg Q2W and the third treatment dosing is 76 mg Q4W, (vii) the first treatment dosing is 116 mg Q1W, the second treatment dosing is 116 mg Q1W or 116 mg Q2W and the third treatment dosing is 116 mg Q2W or 116 mg Q4W; (viii) the first treatment dosing is 116 mg Q1W, the second treatment dosing is 116 mg Q2W and the third treatment dosing is 116 mg Q4W, (ix) the first treatment dosing is 152 mg Q1W, the second treatment dosing is 152 mg Q1W or 152 mg Q2W and the third treatment dosing is 152 mg Q2W or 152 mg Q4W, or (x) the first treatment dosing is 152 mg Q1W, the second treatment dosing is 152 Q2W and the third treatment dosing is 152152 mg Q4W.

12. The method of claim 3, wherein the subject is administered Elranatamab according to the following primary dosing schedule: first priming dose of 12 mg on Day 1; second priming dose of 32 mg on Day 4; first treatment dose of 76 mg on Day 8.

13. The method of claim 12, wherein subsequent treatment doses are administered one week after the first treatment dose and weekly thereafter through week 24.

14. The method of claim 13, wherein further treatment doses are administered every two weeks (Q2W) from week 25.

15. The method of any one of claims 1 wherein if a subject has received treatment for at least six months and disease response shows at least a partial response (PR) or better with responses persisting for at least two months, the dose interval may be changed from QW to Q2W at the same dose level / dosage.

16. The method of any one of claims 1 to 15, wherein the method further comprising administering to the subject at least one dose of a premedication prior to each of the single priming dose, the first priming dose, the second priming dose and / or the first treatment dose of the anti-BCMA / anti-CD3 bispecific antibody is administered to the subject.

17. The method of claim 16, wherein the premedication is administered prior to the first and second priming doses as part of the re-starting dosing schedule.

18. The method of claim 16 or 17, wherein the premedication is administered prior to the treatment dose as part of the re-starting dosing schedule.

19. The method of any one of claim 16 to 18, wherein the premedication may be acetaminophen (or equivalent such as paracetamol), diphenhydramine (or equivalent) and / or dexamethasone (or equivalent).

20. The method of claim any one of claims 16 to 19, wherein dexamethasone is administered at a dexamethasone dosing of about 10 mg to about 40 mg daily oral or intravenous, such as 20 mg.

21. The method of any one of claims 16 to 20, wherein acetaminophen is administered at a dose of 650 mg or paracetamol is administered at a dose of 500 mg.

22. The method of any of claims 16 to 21, wherein diphenhydramine is administered at a dose of 25 mg, oral or intravenous.

23. The method of any one of claims wherein the premedication dosing can be the same or different while the subject is on the priming dosing, the first treatment and subsequent dosing of the bispecific antibody 24. The method of any one of claims 1 to 23, wherein the antibody is administered subcutaneously.

25. The method of any one of claims 1 to 24, wherein a dose delay results from the subject experiencing cytokine release syndrome (CRS) or neurologic toxicity including immune effector cell-associated neurotoxicity syndrome (ICANS).

26. The method of any one of claims 1 to 25, wherein a dose delay results from the subject experiencing infections; neutropenia; hepatotoxicity.

27. The method of any one of claims 1 to 26, wherein the cancer is multiple myeloma.

28. The method of claim 27, wherein the cancer is relapsed or refractory (R / R) multiple myeloma (MM).

29. The method of claims 27 or 28, wherein the subject has previously been treated with at least four prior lines of therapy, including a proteasome inhibitor, an immunomodulatory agent, and an anti-CD38 monoclonal antibody.

30. The method of claims 27 or 28, wherein the subject has previously been treated with at least three prior lines of therapy, which may include a proteasome inhibitor, an immunomodulatory agent, and an anti-CD38 monoclonal antibody.

31. The method of claims 27 or 28, wherein the subject has previously been treated with at least two prior lines of therapy, which may include two of the following: a proteasome inhibitor, an immunomodulatory agent, and / or an anti-CD38 monoclonal antibody 32. The method of claims 27 or 28, wherein the cancer is newly diagnosed multiple myeloma.

33. The method of claim 32, wherein the subject has received stem cell transplant, optionally autologous stem cell transplant or allogeneic stem cell transplant.

34. The method of claims 27 or 28, wherein the subject has not received any prior multiple myeloma therapies.

35. The method of any one of claims 1 to 34, further comprising administering to the subject a second therapeutic agent.

36. The method of any one of claims 1 to 35, further comprising administering to the subject radiotherapy.

37. The method of claim 35, wherein the second therapeutic agent is selected from one or more of lenalidomide, daratumumab, dexamethasone.

38. The method of any one of claims 1 to 37, wherein the method further comprises administered immunoglobulin replacement therapy.

39. The method of claim 38, wherein immunoglobulin replacement therapy is administered if IgG level < 400 mg / dL and / or if immunoparesis / hypogammaglobulinemia is determined.

40. The method of claim 38 or 39, wherein the immunoglobulin replacement therapy results in decreased infection rates.

41. The method of any of claims 38 to 40, wherein the immunoglobulin replacement therapy is administered until IgG level > 400 mg / dL and / or resolution of immunoparesis / hypogammaglobulinemia.

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