Dosage regimen for reducing cytokine release syndrome (CRS) with Anti-fcrh5 / Anti-CD3 bispecific antibodies in multiple myeloma therapy

Abstract

The disclosure provides methods of dosing for the treatment of cancers, such as multiple myelomas, with anti-fragment crystallizable receptor-like 5 (FcRH5) / anti-cluster of differentiation 3 (CD3) bispecific antibodies (e.g., cevostamab).

Description

DOSAGE REGIMEN FOR REDUCING CYTOKINE RELEASE SYNDROME (CRS) WITH ANTI-FCRH5 / ANTI-CD3 BISPECIFIC ANTIBODIES IN MULTIPLE MYELOMA THERAPYCROSS-REFERENCE TO RELATED APPLICATIONSThis application claims the benefit of U.S. Patent Application Serial No. 63 / 677,374, filed on July 30, 2024, and U.S. Patent Application Serial No. 63 / 727,146, filed on December 2, 2024, the disclosures of which are incorporated herein by reference in their entirety.SEQUENCE LISTINGThe instant application contains a Sequence Listing which has been submitted electronically in XML format and is hereby incorporated by reference in its entirety. Said XML copy, created on July 30, 2025, is named “50474-360W03_Sequence_Listing_7_30_25” and is 41 ,595 bytes in size.TECHNICAL FIELDThe present disclosure relates to the treatment of cancers, such as B cell proliferative disorders. More specifically, the disclosure concerns the specific treatment of human patients having multiple myeloma (MM) using anti-fragment crystallizable receptor-like 5 (FcRH5) / anti-cluster of differentiation 3 (CD3) bispecific antibodies (e.g., cevostamab).BACKGROUNDCancer remains one of the most deadly threats to human health. In the U.S., cancer affects more than 1 .7 million new patients each year and is the second leading cause of death after heart disease, accounting for approximately one in four deaths.Hematologic cancers, in particular, are the second leading cause of cancer-related deaths. Hematologic cancers include multiple myeloma (MM), a neoplasm characterized by the proliferation and accumulation of malignant plasma cells. Worldwide, approximately 1 10,000 people are diagnosed with MM annually. MM remains incurable despite advances in treatment, with an estimated median survival of 8-10 years for standard-risk myeloma and 2-3 years for high-risk disease, despite receipt of an autologous stem-cell transplant. Despite the significant improvement in patient’s survival over the past 20 years, only 10-15% of patients achieve or exceed expected survival compared with the matched general population. Increased survival has been achieved with the introduction of proteasome inhibitors, immunomodulatory drugs (IMiDs), and monoclonal antibodies. Nevertheless, most patients (if not all) eventually relapse, and the outcome of patients with MM after they become refractory, or ineligible to receive a current treatment (e.g., a proteasome inhibitor or an I Mi D) , is quite poor, with survival less than 1 year. Therefore, relapsed or refractory (R / R) MM, in particular, continues to constitute a significant unmet medical need, and novel therapeutic agents are needed. For such patients, alternative or secondary treatment modalities, such as bispecific antibody-based immunotherapies, may be particularly efficacious. However, the administration of such bispecific-based immunotherapies may cause unwanted side effects, such as cytokine release syndrome (CRS) and other adverse events (AEs). There is an unmet need in the field not only for the development of efficacious therapeutic bispecific antibodies (e.g.,anti-FcRH5 / anti-CD3 bispecific antibodies), but also safe and tolerable methods of dosing in order to achieve a more favorable benefit-risk profile.SUMMARYIn one aspect, the disclosure provides a method of reducing the likelihood of cytokine release syndrome (CRS) in a subject (e.g., a human subject) having multiple myeloma (MM) (e.g., relapsed or refractory (R / R) MM), wherein the method comprises administering to the subject cevostamab in a dosing regimen comprising at least a first dosing cycle (C1 ), wherein the C1 comprises a first dose (C1 D1 ), a second dose (C1 D2), and a third dose (C1 D3) of cevostamab, wherein the C1 D2 is greater than the C1 D1 , and the C1 D3 is greater than the C1 D2, and wherein each dose less than the therapeutically effective amount of cevostamab.In another aspect, the disclosure provides a method of reducing the CRS in a subject (e.g., a human subject) having MM (e.g., R / R MM) and being administered an effective amount of cevostamab, wherein, prior to a first administration to the subject of the effective amount of cevostamab, the method comprises administering to the subject cevostamab in a dosing regimen comprising at least a first dosing cycle (C1 ), wherein the C1 comprises a first dose (C1 D1 ), a second dose (C1 D2), and a third dose (C1 D3) of cevostamab, wherein the C1 D1 is about 0.3 mg, the C1 D2 is between about 1 .2 mg to about 3.3 mg (e.g., 1 .2 mg or 3.3 mg), and the C1 D3 is between about 3.6 mg to about 7.2 mg (e.g., 3.6 mg or 7.2 mg).In another aspect, the disclosure provides a method of reducing the likelihood of CRS in a subject (e.g., a human subject) having MM (e.g., R / R MM) and being administered an effective amount of cevostamab, wherein, prior to a fist administration to the subject of the effective amount of cevostamab, the method comprises administering to the subject cevostamab in a dosing regimen comprising at least a first dosing cycle (C1 ), wherein the C1 comprises a first dose (C1 D1 ), a second dose (C1 D2), and a third dose (C1 D3) of cevostamab, wherein the C1 D1 is about 0.3 mg; the C1 D2 is about 1 .2 mg; and the C1 D3 is about 3.6 mg.In another aspect, the disclosure features a method of reducing the likelihood of CRS in a subject (e.g., a human subject) having MM (e.g., R / R MM) and being administered an effective amount of cevostamab, wherein, prior to a first administration to the subject of the effective amount of cevostamab, the method comprises administering to the subject cevostamab in a dosing regimen comprising at least a first dosing cycle (C1 ), wherein the C1 comprises a first dose (C1 D1 ), a second dose (C1 D2), and a third dose (C1 D3) of cevostamab, wherein the C1 D1 is about 0.3 mg; the C1 D2 is about 3.3 mg; and the C1 D3 is about 7.2 mg.In yet another aspect, the disclosure provides a method of limiting median peak IL-6 levels in a population of human subjects having MM (e.g., R / R MM) to be administered a therapeutically effective amount of cevostamab, .wherein the method comprises administering to each subject (e.g., a human subject) in the population prior to administration of the therapeutically effective amount of cevostamab a dosing regimen comprising a first dose (C1 D1 ), a second dose (C1 D2), and a third dose (C1 D3) of cevostamab, wherein the C1 D2 is greater than the C1 D1 , and the C1 D3 is greater than the C1 D2, and wherein each dose less than the therapeutically effective amount of cevostamab.In yet another aspect, the disclosure provides a method of achieving a median peak IL-6 level of less than about 30 pg / mL in a population of subjects having MM (e.g., R / R MM) and being administered an effective amount of cevostamab, the method comprising administering to a subject (e.g., a human subject) in the population, prior to being administered the effective amount of cevostamab, a dosing regimen comprising at least a first dosing cycle (C1 ), wherein the C1 comprises a first dose (C1 D1 ), a second dose (C1 D2), and a third dose (C1 D3) of cevostamab, wherein the C1 D1 is about 0.3 mg, the C1 D2 is between about 1 .2 mg to about 3.3 mg, and the C1 D3 is between about 3.6 mg to about 7.2 mg.In yet another aspect, the disclosure provides a method of limiting peak IL-6 level to less than about 30 pg / mL in a human subject having MM and being administered an effective amount of cevostamab, the method comprising administering to the subject cevostamab in a dosing regimen comprising at least a first dosing cycle (C1 ), wherein the C1 comprises a first dose (C1 D1 ), a second dose (C1 D2), and a third dose (C1 D3) of cevostamab, wherein the C1 D1 is about 0.3, the C1 D2 is between about 1 mg to about 2.9 mg, and the C1 D3 is between about 3 mg to about 5.9 mg.In some embodiments of the foregoing aspect, the C1 D1 is about 0.3 mg; the C1 D2 is about 1 .2 mg; and the C1 D3 is about 3.6 mg.In some embodiments, the median peak IL-6 level is about 18 pg / mL following administration of the effective amount of cevostamab.In yet another aspect, the disclosure provides a method of achieving a peak IL-6 level of less than about 30 pg / mL in a subject (e.g. a human subject) having MM (e.g., R / R MM) and being administered an effective amount of cevostamab, the method comprising administering to the subject, prior to being administered the effective amount of cevostamab, a dosing regimen comprising at least a first dosing cycle (C1 ), wherein the C1 comprises a first dose (C1 D1 ), a second dose (C1 D2), and a third dose (C1 D3) of cevostamab, wherein the C1 D1 is about 0.3, the C1 D2 is between about 1 .2 mg to about 3.3 mg, and the C1 D3 is between about 3.6 mg to about 7.2 mg.In some embodiments, the C1 D1 is about 0.3 mg; the C1 D2 is about 1 .2 mg; and the C1 D3 is about 3.6 mg.In some embodiments, the peak IL-6 level is about 18 pg / mL following administration of cevostamab.In yet another aspect, the disclosure provides a method of reducing the likelihood of the occurrence of CRS events in a subject (e.g., a human subject) being treated for MM (e.g., R / R MM) with a target dose of cevostamab, the method comprising administering to the subject, prior to a first administration of the target dose to the subject, a dosing regimen comprising a first dose (C1 D1 ), a second dose (C1 D2), and a third dose (C1 D3) of cevostamab, wherein the C1 D2 is greater than the C1 D1 , and the C1 D3 is greater than the C1 D2, and wherein each dose less than the therapeutically effective amount of cevostamab.In yet another aspect, the disclosure provides a method of reducing the occurrence of CRS events in a subject (e.g., a human subject) being treated for MM (e.g., R / R MM) with a target dose of cevostamab, the method comprising administering to the subject, prior to a first administration of the target dose to the subject, a dosing regimen comprising a first dose (C1 D1 ), a second dose (C1 D2), anda third dose (C1 D3) of cevostamab, wherein the C1 D2 is greater than the C1 D1 , and the C1 D3 is greater than the C1 D2, and wherein each dose less than the therapeutically effective amount of cevostamab.In yet another aspect, the disclosure provides a method of reducing the occurrence of CRS events in a subject (e.g., a human subject) being treated for MM (e.g., R / R MM) with a target dose of cevostamab, the method comprising administering to the subject, prior to a first administration of the target dose to the subject in a dosing regimen comprising a first dosing cycle (C1 ), (i) a first dose (C1 D1 ), (ii) a second dose (C1 D2), and (iii) a third dose (C1 D3) of cevostamab, wherein the C1 D1 is about 0.03 mg, the C1 D2 is between about 1 .2 mg to about 3.3 mg, and the C1 D3 is between about 3.6 mg to about 7.2 mg (e.g., 3.6 mg or 7.2 mg).In another aspect, the disclosure provides a method of reducing the occurrence of CRS events in a subject (e.g., a human subject) being treated for MM (e.g., R / R MM) with a target dose of cevostamab, the method comprising administering to the subject, prior to a first administration of the target dose to the subject in a dosing regimen comprising a first dosing cycle (C1 ), (i) a first dose (C1 D1 ) of about 0.3 mg, (ii) a second dose (C1 D2) of about 1 .2 mg, and (iii) a third dose (C1 D3) of about 3.6 mg of cevostamab.In another aspect, the disclosure provides a method of reducing the occurrence of CRS events in a subject (e.g., a human subject) being treated for MM (e.g., R / R MM) with a target dose of cevostamab, the method comprising administering to the subject, prior to a first administration of the target dose to the subject in a dosing regimen comprising a first dosing cycle (C1 ), (i) a first dose (C1 D1 ) of about 0.3 mg, (ii) a second dose (C1 D2) of about 3.3 mg, and (ii) a third dose (C1 D3) of about 7.2 mg of cevostamab.In some embodiments of the foregoing aspect, the method reduces the occurrence of CRS events in a subject as compared to a subject who, prior to a first administration of a target dose, received two or fewer step-up / priming doses (e.g., received no step-up doses, only a C1 D1 , or only a C1 D1 and C1 D2).In some embodiments, the C1 is 21 days in length, and: (i) the C1 D1 is administered on Day 1 of the C1 ; (ii) the C1 D2 is administered on Day 2, Day 3, or Day 4 of the C1 ; and (iii) the C1 D3 is administered on Day 8 of the C1 .In some embodiments, the target dose is greater than the C1 D3. In some embodiments the target dose is between about 20 mg to about 252 mg (e.g., about 160 mg).In some embodiments of the foregoing aspects, the method further comprises administering to the subject an additional dose of cevostamab, wherein the additional dose of cevostamab is greater than the C1 D3. In some embodiments, the additional dose of cevostamab is administered during the C1 as a fourth dose (C1 D4) of cevostamab, wherein the C1 D4 is an effective amount of cevostamab. In some embodiments, the C1 D4 is between about 20 mg to about 252 mg (e.g., about 160 mg). In some embodiments, the C1 D4 is an effective amount of cevostamab and is administered after the C1 D3.In another aspect, the disclosure provides a method of treating MM (e.g., R / R MM) in a subject (e.g., a human subject), wherein the method comprises administering to the subject cevostamab in a dosing regimen comprising at least a first dosing cycle (C1 ), wherein the C1 comprises a first dose (C1 D1 ), a second dose (C1 D2), a third dose (C1 D3) and a target dose of cevostamab.In another aspect, the disclosure provides a method of treating MM (e.g., R / R MM) in a subject (e.g., a human subject), wherein the method comprises administering to the subject cevostamab in adosing regimen comprising at least a first dosing cycle (C1 ), wherein the C1 comprises a first dose (C1 D1 ), a second dose (C1 D2), a third dose (C1 D3) and a target dose of cevostamab, wherein the target dose of cevostamab is a therapeutically effective amount of cevostamab and C1 D1 , C1 D2, and C1 D3 are less than therapeutically effective amount of cevostamab.In another aspect, the disclosure provides a method of treating MM (e.g., R / R MM) in a subject (e.g., a human subject), wherein the method comprises administering to the subject cevostamab in a dosing regimen comprising at least a first dosing cycle (C1 ), wherein the C1 comprises a first dose (C1 D1 ), a second dose (C1 D2), a third dose (C1 D3) and a target dose of cevostamab, wherein the target dose of cevostamab is an effective amount of cevostamab, the C1 D1 , C1 D2, and C1 D3 are less than the effective amount of cevostamab, the C1 D1 is less than C1 D2, and C1 D2 is less than C1 D3.In another aspect, the disclosure provides a method of treating a subject (e.g., a human subject) having MM (e.g., R / R MM), wherein the method comprises administering to the subject cevostamab in a dosing regimen comprising at least a first dosing cycle (C1 ), wherein the C1 comprises a first dose (C1 D1 ), a second dose (C1 D2), a third dose (C1 D3), and a fourth dose (C1 D4) of cevostamab, wherein C1 D4 is a therapeutically effective amount of cevostamab, and wherein C1 D1 is less than C1 D2, which is less than C1 D3, which is less than C1 D4.In another aspect, the disclosure provides a method of treating a subject (e.g., a human subject) having a MM (e.g., a R / R MM), wherein the method comprises administering to the subject cevostamab in a dosing regimen comprising at least a first dosing cycle (C1 ), wherein the C1 comprises a first dose (C1 D1 ), a second dose (C1 D2), a third dose (C1 D3), and a fourth dose (C1 D4) of cevostamab, wherein the C1 D1 is about 0.3 mg, the C1 D2 is about 1 .2 mg to about 3.3 mg (e.g., 1 .2 mg or 3.3 mg) , the C1 D3 is about 3.6 mg to about 7.2 mg (e.g., 3.6 mg or 7.2 mg), and the C1 D4 is between about 20 mg to about 252 mg (e.g., about 160 mg).In some embodiments, the C1 D4 is an effective amount of cevostamab. In some embodiments, the C1 D4 is about 160 mg.In some embodiments, the C1 D1 is about 0.3 mg; the C1 D2 is about 1 .2 mg; and the C1 D3 is about 3.6 mg. In some embodiments, the C1 D1 is about 0.3 mg; the C1 D2 is about 3.3 mg; and the C1 D3 is about 7.2 mg.In another aspect, the disclosure provides a method of treating a subject (e.g., a human subject) having MM (e.g., R / R MM), wherein the method comprises administering to the subject cevostamab in a dosing regimen comprising at least a first dosing cycle (C1 ), wherein the C1 comprises a first dose (C1 D1 ), a second dose (C1 D2), a third dose (C1 D3), and a fourth dose (C1 D4) of cevostamab, wherein the C1 D1 is about 0.3 mg; the C1 D2 is about 1 .2 mg; the C1 D3 is about 3.6 mg; and the C1 D4 is about 160 mg.In another aspect, the disclosure provides a method of treating a subject (e.g., a human subject) having MM (e.g., R / R MM), wherein the method comprises administering to the subject cevostamab in a dosing regimen comprising at least a first dosing cycle (C1 ), wherein the C1 comprises a first dose (C1 D1 ), a second dose (C1 D2), a third dose (C1 D3), and a fourth dose (C1 D4) of cevostamab, the C1 D1 is about 0.3 mg; the C1 D2 is about 3.3 mg; the C1 D3 is about 7.2 mg; and the C1 D4 is about 160 mg.In some embodiments of any one of the foregoing aspects, the length of the C1 is 21 days. In some embodiments, the method comprises administering to the subject: (a) the C1 D1 on or about Day 1 of the C1 ; (b) the C1 D2 on or about Day 2, Day 3, or Day 4 of the C1 ; and (c) the C1 D3 on or about Day 8 of the C1 .In some embodiments of the foregoing aspects, the method comprises administering to the subject the C1 D4 on or about Day 9, Day 10, or Day 1 1 of the C1 .In some embodiments, the method comprises administering to the subject the C1 D4 about 1 day, 2 days, or 3 days after the C1 D3 of the C1 (e.g., after the resolution of a CRS event, if any, that may have occurred after administration of the C1 D3).In some embodiments of any one of the foregoing aspects, the dosing regimen further comprises a second dosing cycle (C2) comprising a single dose (C2D1 ) of cevostamab, wherein the C2D1 is an effective amount of cevostamab that is equal to or greater than the last administered dose of cevostamab and is between about 20 mg to about 252 mg (e.g., about 160 mg). In some embodiments, the C2D1 is about 160 mg. In some embodiments, the length of the C2 is 21 days. In some embodiments, the method comprises administering to the subject the C2D1 on Day 1 of the C2.In some embodiments, the dosing regimen further comprises one or more additional dosing cycles. In some embodiments, the dosing regimen comprises one to 15 additional dosing cycles. In some embodiments, the length of each of the one or more additional dosing cycles is 21 days. In some embodiments, each of the one or more additional dosing cycles comprises a single effective dose of cevostamab. In some embodiments, the method comprises administering to the subject the single dose of cevostamab on Day 1 of the one or more additional dosing cycles. In some embodiments, the single dose is between about 20 mg to about 252 mg (e.g., about 160 mg). In some embodiments, the single dose is about 160 mg.In some embodiments, a median peak IL-6 level in a population of subjects treated according to the method does not exceed 80 pg / mL (e.g., does not exceed 80 pg / mL, 79 pg / mL, 78 pg / mL, 77 pg / mL, 76 pg / mL, 75 pg / mL, 74 pg / mL, 73 pg / mL, 72 pg / mL, 71 pg / mL, 70 pg / mL, 69 pg / mL, 68 pg / mL, 67 pg / mL, 66 pg / mL, 65 pg / mL, 64 pg / mL, 63 pg / mL, 62 pg / mL, 61 pg / mL, 60 pg / mL, 59 pg / mL, 58 pg / mL,57 pg / mL, 56 pg / mL, 55 pg / mL, 54 pg / mL, 53 pg / mL, 52 pg / mL, 51 pg / mL, 50 pg / mL, 49 pg / mL, 48 pg / mL, 47 pg / mL, 46 pg / mL, 45 pg / mL, 44 pg / mL, 43 pg / mL, 42 pg / mL, 41 pg / mL, or 40 pg / mL, 39 pg / mL,38 pg / mL, 37 pg / mL, 36 pg / mL, 35 pg / mL, 34 pg / mL, 33 pg / mL, 32 pg / mL, 31 pg / mL, or 30 pg / mL) between the C1 D1 and the C1 D2. In some embodiments, the median peak IL-6 level in a population of subjects treated according to the method does not exceed 30 pg / mL (e.g., does not exceed 30 pg / mL, 29 pg / mL, 28 pg / mL, 27 pg / mL, 26 pg / mL, 25 pg / mL, 24 pg / mL, 23 pg / mL, 22 pg / mL, 21 pg / mL, 20 pg / mL, 19 pg / mL, 18 pg / mL, 17 pg / mL, 16 pg / mL, 15 pg / mL, 14 pg / mL, 13 pg / mL, 12 pg / mL, 1 1 pg / mL, 10 pg / mL, 9 pg / mL, 8 pg / mL, 7 pg / mL, 6 pg / mL, 5 pg / mL, 4 pg / mL, 3 pg / mL, 2 pg / mL, or 1 pg / mL) between the C1 D1 and the C1 D2.In some embodiments, a median peak IL-6 level in a population of subjects treated according to the method does not exceed 80 pg / mL (e.g., does not exceed 80 pg / mL, 79 pg / mL, 78 pg / mL, 77 pg / mL, 76 pg / mL, 75 pg / mL, 74 pg / mL, 73 pg / mL, 72 pg / mL, 71 pg / mL, 70 pg / mL, 69 pg / mL, 68 pg / mL, 67 pg / mL, 66 pg / mL, 65 pg / mL, 64 pg / mL, 63 pg / mL, 62 pg / mL, 61 pg / mL, 60 pg / mL, 59 pg / mL, 58 pg / mL,57 pg / mL, 56 pg / mL, 55 pg / mL, 54 pg / mL, 53 pg / mL, 52 pg / mL, 51 pg / mL, 50 pg / mL, 49 pg / mL, 48 pg / mL, 47 pg / mL, 46 pg / mL, 45 pg / mL, 44 pg / mL, 43 pg / mL, 42 pg / mL, 41 pg / mL, or 40 pg / mL, 39 pg / mL, 38 pg / mL, 37 pg / mL, 36 pg / mL, 35 pg / mL, 34 pg / mL, 33 pg / mL, 32 pg / mL, 31 pg / mL, or 30 pg / mL) between the C1 D2 and the C1 D3. In some embodiments, the median peak IL-6 level in a population of subjects treated according to the method does not exceed 30 pg / mL (e.g., does not exceed 30 pg / mL, 29 pg / mL, 28 pg / mL, 27 pg / mL, 26 pg / mL, 25 pg / mL, 24 pg / mL, 23 pg / mL, 22 pg / mL, 21 pg / mL, 20 pg / mL, 19 pg / mL, 18 pg / mL, 17 pg / mL, 16 pg / mL, 15 pg / mL, 14 pg / mL, 13 pg / mL, 12 pg / mL, 11 pg / mL, 10 pg / mL, 9 pg / mL, 8 pg / mL, 7 pg / mL, 6 pg / mL, 5 pg / mL, 4 pg / mL, 3 pg / mL, 2 pg / mL, or 1 pg / mL) between the C1 D2 and the C1 D3.In some embodiments, the method further comprises administering to the subject a fourth dose (C1 D4) of cevostamab during the C1 , wherein the C1 D4 is between about 20 mg to about 252 mg (e.g., 160 mg), and wherein the median peak IL-6 level in a population of subjects treated according to the method does not exceed 30 pg / mL (e.g., does not exceed 30 pg / mL, 29 pg / mL, 28 pg / mL, 27 pg / mL, 26 pg / mL, 25 pg / mL, 24 pg / mL, 23 pg / mL, 22 pg / mL, 21 pg / mL, 20 pg / mL, 19 pg / mL, 18 pg / mL, 17 pg / mL, 16 pg / mL, 15 pg / mL, 14 pg / mL, 13 pg / mL, 12 pg / mL, 11 pg / mL, 10 pg / mL, 9 pg / mL, 8 pg / mL, 7 pg / mL, 6 pg / mL, 5 pg / mL, 4 pg / mL, 3 pg / mL, 2 pg / mL, or 1 pg / mL) between the C1 D3 and the C1 D4.In some embodiments, a median peak IL-6 level in a population of subjects treated according to the method does not exceed 30 pg / mL (e.g., does not exceed 30 pg / mL, 29 pg / mL, 28 pg / mL, 27 pg / mL, 26 pg / mL, 25 pg / mL, 24 pg / mL, 23 pg / mL, 22 pg / mL, 21 pg / mL, 20 pg / mL, 19 pg / mL, 18 pg / mL, 17 pg / mL, 16 pg / mL, 15 pg / mL, 14 pg / mL, 13 pg / mL, 12 pg / mL, 11 pg / mL, 10 pg / mL, 9 pg / mL, 8 pg / mL, 7 pg / mL, 6 pg / mL, 5 pg / mL, 4 pg / mL, 3 pg / mL, 2 pg / mL, or 1 pg / mL) between the C1 D3 and the C1 D4.In some embodiments, a peak IL-6 level in the subject does not exceed 80 pg / mL (e.g., does not exceed 80 pg / mL, 79 pg / mL, 78 pg / mL, 77 pg / mL, 76 pg / mL, 75 pg / mL, 74 pg / mL, 73 pg / mL, 72 pg / mL, 71 pg / mL, 70 pg / mL, 69 pg / mL, 68 pg / mL, 67 pg / mL, 66 pg / mL, 65 pg / mL, 64 pg / mL, 63 pg / mL, 62 pg / mL, 61 pg / mL, 60 pg / mL, 59 pg / mL, 58 pg / mL, 57 pg / mL, 56 pg / mL, 55 pg / mL, 54 pg / mL, 53 pg / mL, 52 pg / mL, 51 pg / mL, 50 pg / mL, 49 pg / mL, 48 pg / mL, 47 pg / mL, 46 pg / mL, 45 pg / mL, 44 pg / mL, 43 pg / mL, 42 pg / mL, 41 pg / mL, or 40 pg / mL, 39 pg / mL, 38 pg / mL, 37 pg / mL, 36 pg / mL, 35 pg / mL, 34 pg / mL, 33 pg / mL, 32 pg / mL, 31 pg / mL, or 30 pg / mL) between the C1 D1 and the C1 D2. In some embodiments, the peak IL-6 level in the subject does not exceed 30 pg / mL (e.g., does not exceed 30 pg / mL, 29 pg / mL, 28 pg / mL, 27 pg / mL, 26 pg / mL, 25 pg / mL, 24 pg / mL, 23 pg / mL, 22 pg / mL, 21 pg / mL, 20 pg / mL, 19 pg / mL, 18 pg / mL, 17 pg / mL, 16 pg / mL, 15 pg / mL, 14 pg / mL, 13 pg / mL, 12 pg / mL, 11 pg / mL, 10 pg / mL, 9 pg / mL, 8 pg / mL, 7 pg / mL, 6 pg / mL, 5 pg / mL, 4 pg / mL, 3 pg / mL, 2 pg / mL, or 1 pg / mL) between the C1 D1 and the C1 D2.In some embodiments, a peak IL-6 level in the subject does not exceed 80 pg / mL (e.g., does not exceed 80 pg / mL, 79 pg / mL, 78 pg / mL, 77 pg / mL, 76 pg / mL, 75 pg / mL, 74 pg / mL, 73 pg / mL, 72 pg / mL, 71 pg / mL, 70 pg / mL, 69 pg / mL, 68 pg / mL, 67 pg / mL, 66 pg / mL, 65 pg / mL, 64 pg / mL, 63 pg / mL, 62 pg / mL, 61 pg / mL, 60 pg / mL, 59 pg / mL, 58 pg / mL, 57 pg / mL, 56 pg / mL, 55 pg / mL, 54 pg / mL, 53 pg / mL, 52 pg / mL, 51 pg / mL, 50 pg / mL, 49 pg / mL, 48 pg / mL, 47 pg / mL, 46 pg / mL, 45 pg / mL, 44 pg / mL, 43 pg / mL, 42 pg / mL, 41 pg / mL, or 40 pg / mL, 39 pg / mL, 38 pg / mL, 37 pg / mL, 36 pg / mL, 35 pg / mL, 34 pg / mL, 33 pg / mL, 32 pg / mL, 31 pg / mL, or 30 pg / mL) between the C1 D2 and the C1 D3. In some embodiments,the peak IL-6 level in the subject does not exceed 30 pg / mL (e.g., does not exceed 30 pg / mL, 29 pg / mL, 28 pg / mL, 27 pg / mL, 26 pg / mL, 25 pg / mL, 24 pg / mL, 23 pg / mL, 22 pg / mL, 21 pg / mL, 20 pg / mL, 19 pg / mL, 18 pg / mL, 17 pg / mL, 16 pg / mL, 15 pg / mL, 14 pg / mL, 13 pg / mL, 12 pg / mL, 11 pg / mL, 10 pg / mL, 9 pg / mL, 8 pg / mL, 7 pg / mL, 6 pg / mL, 5 pg / mL, 4 pg / mL, 3 pg / mL, 2 pg / mL, or 1 pg / mL) between the C1 D2 and the C1 D3.In some embodiments, a peak IL-6 level in the subject does not exceed 30 pg / mL (e.g., does not exceed 30 pg / mL, 29 pg / mL, 28 pg / mL, 27 pg / mL, 26 pg / mL, 25 pg / mL, 24 pg / mL, 23 pg / mL, 22 pg / mL, 21 pg / mL, 20 pg / mL, 19 pg / mL, 18 pg / mL, 17 pg / mL, 16 pg / mL, 15 pg / mL, 14 pg / mL, 13 pg / mL, 12 pg / mL, 11 pg / mL, 10 pg / mL, 9 pg / mL, 8 pg / mL, 7 pg / mL, 6 pg / mL, 5 pg / mL, 4 pg / mL, 3 pg / mL, 2 pg / mL, or 1 pg / mL) between the C1 D3 and the C1 D4.In some embodiments, the method further comprises administering to the subject a fourth dose (C1 D4) of cevostamab during the C1 , wherein the C1 D4 is between about 20 mg to about 252 mg, and wherein the peak IL-6 level in the subject does not exceed 30 pg / mL (e.g., does not exceed 30 pg / mL, 29 pg / mL, 28 pg / mL, 27 pg / mL, 26 pg / mL, 25 pg / mL, 24 pg / mL, 23 pg / mL, 22 pg / mL, 21 pg / mL, 20 pg / mL, 19 pg / mL, 18 pg / mL, 17 pg / mL, 16 pg / mL, 15 pg / mL, 14 pg / mL, 13 pg / mL, 12 pg / mL, 11 pg / mL, 10 pg / mL, 9 pg / mL, 8 pg / mL, 7 pg / mL, 6 pg / mL, 5 pg / mL, 4 pg / mL, 3 pg / mL, 2 pg / mL, or 1 pg / mL) between the C1 D3 and the C1 D4.In some embodiments of the foregoing aspects, the method further comprises administering to the subject a fourth dose (C1 D4) of cevostamab during the C1 , wherein the C1 D4 is between about 20 mg to about 252 mg, and wherein the peak IL-6 level in the subject does not exceed 30 pg / mL (e.g., does not exceed 30 pg / mL, 29 pg / mL, 28 pg / mL, 27 pg / mL, 26 pg / mL, 25 pg / mL, 24 pg / mL, 23 pg / mL, 22 pg / mL, 21 pg / mL, 20 pg / mL, 19 pg / mL, 18 pg / mL, 17 pg / mL, 16 pg / mL, 15 pg / mL, 14 pg / mL, 13 pg / mL, 12 pg / mL, 11 pg / mL, 10 pg / mL, 9 pg / mL, 8 pg / mL, 7 pg / mL, 6 pg / mL, 5 pg / mL, 4 pg / mL, 3 pg / mL, 2 pg / mL, or 1 pg / mL) between the C1 D3 and the C1 D4.In some embodiments of any one of the foregoing aspects, a peak level of CD8+ T cell activation in the subject in the C1 occurs between administration of the C1 D1 and the C1 D2.In some embodiments of any one of the foregoing aspects, a peak level of CD8+ T cell activation in the subject in the C1 occurs between administration of the C1 D2 and the C1 D3.In some embodiments, a peak level of CD8+ T cell activation in the subject in the C1 occurs between administration of the C1 D3 and the C1 D4.ln some embodiments, the peak level of CD8+ T cell activation in the subject in the C1 within 24 hours after administration of cevostamab.In some embodiments of any one of the foregoing aspects, the method further comprises evaluating CRS after administration of at least one of the C1 D1 , the C1 D2, and / or the C1 D3. In some embodiments, the method further comprises evaluating CRS after each of the C1 D1 , the C1 D2, and the C1 D3. In some embodiments, after administration of at least one of the C1 D1 , the C1 D2, and / or the C1 D3 (i) no CRS event has occurred, or (ii) CRS signs and symptoms from the previous dose have resolved, and the subject is administered the next dose of cevostamab. In some embodiments, the subject is not administered the next dose of cevostamab unless (i) no CRS event has occurred from administration of at least one of the C1 D1 , the C1 D2, and / or the C1 D3, or (ii) CRS signs and symptoms have resolved after administration of at least one of the C1 D1 , the C1 D2, and / or the C1 D3. In someembodiments, the subject is administered the next dose of cevostamab no earlier than 20 hours from administration of the previous dose.In some embodiments of any one of the foregoing aspects, the method further comprises measuring CRS after the C1 D1 , the C1 D2, and / or the C1 D3. In some embodiments, the method further comprises measuring CRS after the C1 D1 , the C1 D2, and the C1 D3. In some embodiments, (i) there is no CRS or (ii) CRS signs and symptoms from the previous dose have resolved, and the subject is administered the next dose of cevostamab. In some embodiments, the subject is administered the next dose of cevostamab no earlier than 20 hours from administration of the previous dose.In some embodiments, the method reduces the likelihood of the subject experiencing a CRS event. In some embodiments, the method reduces the likelihood of the subject experiencing Grade >1 CRS. In some embodiments, the method reduces the likelihood of the subject experiencing Grade >2 CRS. In some embodiments, the method reduces the likelihood of the subject experiencing Grade >3 CRS.In some embodiments, the likelihood of the subject experiencing Grade 1 CRS after the C1 D1 is less than 10% (e.g., less than 10%, less than 9%, less than 8%, less than 7%, less than 6%, less than 5%, less than 4%, less than 3%, less than 2%, or less than 1 %, e.g. 0%). In some embodiments, the likelihood of the subject experiencing Grade 1 CRS after the C1 D2 is less than 25% (e.g., less than 25%, less than 24%, less than 23%, less than 22%, less than 21 %, less than 20%, less than 19%, less than 18%, less than 17%, less than 16%, less than 15%, less than 14%, less than 13%, less than 12%, less than 1 1 %, less than 10%, less than 9%, less than 8%, less than 7%, less than 6%, less than 5%, less than 4%, less than 3%, less than 2%, or less than 1 %, e.g. 0%). In some embodiments, the likelihood of the subject experiencing Grade 1 CRS after the C1 D3 is less than 15% (e.g., less than 15%, less than 14%, less than 13%, less than 12%, less than 1 1 %, less than 10%, less than 9%, less than 8%, less than 7%, less than 6%, less than 5%, less than 4%, less than 3%, less than 2%, or less than 1 %, e.g. 0%).In some embodiments, the likelihood of the subject experiencing Grade 2 CRS after the C1 D1 is less than 10% (e.g., less than 10%, less than 9%, less than 8%, less than 7%, less than 6%, less than 5%, less than 4%, less than 3%, less than 2%, or less than 1 %, e.g. 0%). In some embodiments, the likelihood of the subject experiencing Grade 2 CRS after the C1 D2 is less than 25% (e.g., less than 25%, less than 24%, less than 23%, less than 22%, less than 21 %, less than 20%, less than 19%, less than 18%, less than 17%, less than 16%, less than 15%, less than 14%, less than 13%, less than 12%, less than 1 1 %, less than 10%, less than 9%, less than 8%, less than 7%, less than 6%, less than 5%, less than 4%, less than 3%, less than 2%, or less than 1 %, e.g. 0%). In some embodiments, the likelihood of the subject experiencing Grade 2 CRS after the C1 D3 is less than 15% (e.g., less than 15%, less than 14%, less than 13%, less than 12%, less than 1 1 %, less than 10%, less than 9%, less than 8%, less than 7%, less than 6%, less than 5%, less than 4%, less than 3%, less than 2%, or less than 1 %, e.g. 0%).In some embodiments, the likelihood of the subject experiencing at least one Grade 1 or Grade 2 CRS event after the first administration of the C1 D4 is less than 65% (e.g., less than 65%, less than 64%, less than 63%, less than 62%, less than 61 %, less than 60%, less than 59%, or less than 58%).In some embodiments of any one of the foregoing aspects, the dosing regimen results in a CRS event in less than about 90% (e.g., less than about 90%, less than about 85%, less than about 80%, lessthan about 75%, less than about 70%, less than about 65%, or less than about 60%) of a population of subjects having MM (e.g., R / R MM). In some embodiments, the dosing regimen results in the CRS event in about 58% to about 90% (e.g., about 58%, about 59%, about 60%, about 61%, about 62%, about 63%, about 64%, about 65%, about 66%, about 67%, about 68%, about 69%, about 70%, about 71%, about 72%, about 73%, about 74%, about 75%, about 76%, about 77%, about 78%, about 79%, about 80%, about 81 %, about 82%, about 83%, about 84%, about 85%, about 86%, about 87%, about 88%, about 89%, or about 90%) of the population of subjects having MM (e.g., R / R MM). In some embodiments, the dosing regimen results in the CRS event in about 58% to about 68% (e.g., about 58%, about 59%, about 60%, about 61%, about 62%, about 63%, about 64%, about 65%, about 66%, about 67%, or about 68%) of the population of subjects having MM (e.g., R / R MM). In some embodiments, the dosing regimen results in the CRS event in about 63% of the population of subjects having MM (e.g., R / R MM).In some embodiments of any one of the foregoing aspects, the dosing regimen results in a grade >2 CRS event in less than about 50% of a population of subjects having MM (e.g., R / R MM). In some embodiments, the dosing regimen results in the grade >2 CRS event in about 10% to about 25% (e.g., about 10%, about 11%, about 12%, about 13%, about 14%, about 15%, about 16%, about 17%, about 18%, about 19%, about 20%, about 21%, about 22%, about 23%, about 24%, or about 25%) of the population of subjects having MM (e.g., R / R MM). In some embodiments, the dosing regimen results in the grade >2 CRS event in about 17% (e.g., 16%, 17%, or 18%) of the population of subjects having MM (e.g., R / R MM).In some embodiments of any one of the foregoing aspects, the dosing regimen results in a grade >3 CRS event in less than about 10% of a population of subjects having MM (e.g., R / R MM). In some embodiments, the dosing regimen results in the grade >3 CRS event in about 0% to about 5% (e.g., about 0%, about 1%, about 2%, about 3%, about 4%, or about 5%) of the population of subjects having MM (e.g., R / R MM). In some embodiments, the dosing regimen does not result in any grade >3 CRS event in the population of subjects having MM (e.g., R / R MM).In some embodiments of any one of the foregoing aspects, cevostamab is administered to the subject as a monotherapy. In some embodiments of any one of the foregoing aspects, cevostamab is administered to the subject as a combination therapy. In some embodiments, cevostamab is administered to the subject concurrently with one or more additional therapeutic agents. In some embodiments, cevostamab is administered to the subject before one or more additional therapeutic agents.In some embodiments, cevostamab is administered to the subject prior to the administration of one or more additional therapeutic agents. In some embodiments, cevostamab is administered to the subject subsequent to the administration of one or more additional therapeutic agents. In some embodiments, the one or more additional therapeutic agents comprise an effective amount of tocilizumab. In some embodiments, tocilizumab is administered to the subject by intravenous infusion.In some embodiments: (a) the subject weighs > 100 kg, and tocilizumab is administered to the subject at a dose of 800 mg; (b) the subject weighs > 30 kg and < 100 kg, and tocilizumab is administered to the subject at a dose of 8 mg / kg; or (c) the subject weighs < 30 kg, and tocilizumab is administered to the subject at a dose of 12 mg / kg.In some embodiments, 1 to 2 doses of tocilizumab are administered to the subject if the subject experiences no CRS event. In some embodiments, 4 to 5 doses of tocilizumab are administered to the subject if the subject experiences a Grade 1 CRS event. In some embodiments, 4 doses of tocilizumab are administered to the subject if the subject experiences a Grade 2 CRS event.In some embodiments, tocilizumab is administered to the subject about 2 hours before administration of cevostamab.In some embodiments of any one of the foregoing aspects and embodiments, cevostamab is administered to the subject by intravenous infusion. In some embodiments, cevostamab is administered to the subject subcutaneously. In some embodiments, the subject has a CRS event, and treatment with cevostamab is suspended as a result of the CRS event. In some embodiments, the subject has a CRS event, and the method further comprises treating the symptoms of the CRS event while suspending treatment with cevostamab. In some embodiments, the method further comprises administering to the subject an effective amount of tocilizumab to treat the CRS event. In some embodiments, the effective amount is 800 mg if the subject weighs > 100 kg, 8 mg / kg if the subject weighs > 30 kg and < 100 kg, and 12 mg / kg if the subject weighs < 30 kg.In some embodiments of any one of the foregoing aspects, the subject has received prior treatment for MM. the prior treatment for MM is selected from one or more of a proteasome inhibitor, an IMiD, an anti-CD38 therapeutic agent, an anti-SLAMF7 therapeutic agent, a nuclear export inhibitor, a histone deacetylase (HDAC) inhibitor, an autologous stem cell transplant (ASCT), a bispecific antibody, an antibody-drug conjugate (ADC), a CAR-T cell therapy, and a BCMA-directed therapyIn some embodiments the subject has received a standard of care treatment for MM prior to being administered the C1 D1 . In some embodiments the subject has received prior treatment for MM selected from one or more of a proteasome inhibitor, an immunomodulatory drug (IMiD), and an anti- CD38 therapeutic agent. In some embodiments, the subject has relapsed or become refractory to the standard of care treatment for MM.In some embodiments of any one of the foregoing aspects, the subject has received at least three prior lines of treatment for the MM. In some embodiments, the subject has received at least four prior lines of treatment for the MM. In some embodiments, the subject has received at least five prior lines of treatment for the MM. In some embodiments, the subject has received at least six prior lines of treatment for the MM. In some embodiments, the subject has received at least seven prior lines of treatment for the MM. In some embodiments, the subject has received at least eight prior lines of treatment for the MM. In some embodiments, the subject has received at least nine prior lines of treatment for the MM. In some embodiments, the subject has received at least ten prior lines of treatment for the MM.In some embodiments of any one of the foregoing aspects and embodiments, the MM is relapsed or refractory (R / R) MM. drug (IMiD), and an anti-cluster of differentiation 38 (CD38) monoclonal antibody (mAb).In another aspect, the disclosure provides a method of treating a subject (e.g., a human subject) having R / R MM, wherein the method comprises administering to the subject cevostamab in a dosing regimen comprising at least a first dosing cycle (C1 ), wherein the length of the C1 is 21 days, wherein the C1 comprises a first dose (C1 D1 ), a second dose (C1 D2), a third dose (C1 D3), and a fourth dose (C1 D4)of cevostamab, wherein the C1 D1 is about 0.3 mg and is administered on Day 1 of C1 ; the C1 D2 is about1 .2 mg and is administered on Day 2, Day 3, or Day 4 of C1 ; the C1 D3 is about 3.6 mg and is administered on Day 8 of C1 ; and the C1 D4 is an effective amount of cevostamab and is administered on Day 9, Day 10, or Day 11 of C1 .In another aspect, the disclosure provides a method of treating a subject (e.g., a human subject) having R / R MM, wherein the method comprises administering to the subject an effective amount of cevostamab in a dosing regimen comprising at least a first dosing cycle (C1 ), wherein the length of the C1 is 21 days, wherein the C1 comprises a first dose (C1 D1 ), a second dose (C1 D2), a third dose (C1 D3), and a fourth dose (C1 D4) of cevostamab, wherein the C1 D1 is about 0.3 mg and is administered on Day 1 ; the C1 D2 is about 1 .2 mg and is administered on Day 2, Day 3, or Day 4; the C1 D3 is about 3.6 mg and is administered on Day 8; and the C1 D4 is about 160 mg and is administered on Day 9, Day 10, or Day 11 .In another aspect, the disclosure provides a method of treating a subject (e.g., a human subject) having R / R MM, wherein the method comprises administering to the subject an effective amount of cevostamab in a dosing regimen comprising at least a first dosing cycle (C1 ), wherein the length of the C1 is 21 days, wherein the C1 comprises a first dose (C1 D1 ), a second dose (C1 D2), a third dose (C1 D3), and a fourth dose (C1 D4) of cevostamab, wherein the C1 D1 is about 0.3 mg and is administered on Day 1 ; the C1 D2 is about 3.3 mg and is administered on Day 2, Day 3, or Day 4; the C1 D3 is about7.2 mg and is administered on Day 8; and the C1 D4 is about 160 mg and is administered on Day 9, Day 10, or Day 11 .In another aspect, the disclosure provides a method of reducing the likelihood of CRS in a subject (e.g., a human subject) being treated for R / R MM with a target dose of cevostamab in at least a first dosing cycle (C1 ) of 21 days, wherein prior to administration of the target dose of cevostamab, the C1 further comprises a first dose (C1 D1 ), a second dose (C1 D2), and a third dose (C1 D3) of cevostamab, wherein the C1 D1 is about 0.3 mg and is administered on Day 1 ; the C1 D2 is about 1 .2 mg and is administered on Day 2, Day 3, or Day 4; and the C1 D3 is about 3.6 mg and is administered on Day 8.In another aspect, the disclosure provides a method of reducing the likelihood of CRS in a subject (e.g., a human subject) having R / R MM and being administered an effective amount of cevostamab, wherein, prior to a first administration to the subject of the effective amount of cevostamab, the method comprises administering to the subject cevostamab in a dosing regimen comprising at least a first dosing cycle (C1 ), wherein the length of the C1 is 21 days, wherein the C1 comprises a first dose (C1 D1 ), a second dose (C1 D2), and a third dose (C1 D3) of cevostamab, wherein the C1 D1 is about 0.3 mg and is administered on Day 1 ; the C1 D2 is about 1 .2 mg and is administered on Day 2, Day 3, or Day 4; and the C1 D3 is about 3.6 mg and is administered on Day 8.In another aspect, the disclosure provides a method of reducing the likelihood of CRS in a subject (e.g., a human subject) having R / R MM and being administered an effective amount of cevostamab, wherein, prior to a first administration to the subject of the effective amount of cevostamab, the method comprises administering to the subject cevostamab in a dosing regimen comprising at least a first dosing cycle (C1 ), wherein the length of the C1 is 21 days, wherein the C1 comprises a first dose (C1 D1 ), a second dose (C1 D2), and a third dose (C1 D3) of cevostamab, wherein the C1 D1 is about 0.3 mg and isadministered on Day 1 ; the C1 D2 is about 3.3 mg and is administered on Day 2, Day 3, or Day 4; and the C1 D3 is about 7.2 mg and is administered on Day 8.In another aspect, the disclosure provides a method of achieving a median peak IL-6 level of less than about 30 pg / mL (e.g., less than about 30 pg / mL, 29 pg / mL, 28 pg / mL, 27 pg / mL, 26 pg / mL, 25 pg / mL, 24 pg / mL, 23 pg / mL, 22 pg / mL, 21 pg / mL, 20 pg / mL, 19 pg / mL, 18 pg / mL, 17 pg / mL, 16 pg / mL, 15 pg / mL, 14 pg / mL, 13 pg / mL, 12 pg / mL, 11 pg / mL, 10 pg / mL, 9 pg / mL, 8 pg / mL, 7 pg / mL, 6 pg / mL, 5 pg / mL, 4 pg / mL, 3 pg / mL, 2 pg / mL, or 1 pg / mL) in a population of subjects (e.g., human subjects) having R / R MM and being administered an effective amount of cevostamab, the method comprising administering to a subject (e.g., a human subject) in the population, prior to being administered the effective amount of cevostamab, a dosing regimen comprising at least a first dosing cycle (C1 ), wherein the length of the C1 is 21 days, wherein the C1 comprises a first dose (C1 D1 ), a second dose (C1 D2), and a third dose (C1 D3) of cevostamab, wherein the C1 D1 is about 0.3 mg and is administered on Day 1 ; the C1 D2 is about 1 .2 mg and is administered on Day 2, Day 3, or Day 4; and the C1 D3 is about 3.6 mg and is administered on Day 8.In yet another aspect, the disclosure provides a method of treating a subject (e.g., a human subject) having R / R MM, wherein the method comprises administering to the subject cevostamab in a dosing regimen comprising at least a first dosing cycle (C1 ), wherein the length of the C1 is 21 days, wherein the C1 comprises a first dose (C1 D1 ), a second dose (C1 D2), and a third dose (C1 D3) of cevostamab, wherein the C1 D1 is about 0.3 mg and is administered on Day 1 ; the C1 D2 is about 3.3 mg and is administered on Day 2, Day 3, or Day 4; the C1 D3 is about 160 mg and is administered on Day 8, and wherein tocilizumab is administered to the subject about 2 hours prior to administering the first dose of cevostamab.In another aspect, the disclosure provides a method of treating a subject (e.g., a human subject) having R / R MM, wherein the method comprises administering to the subject cevostamab in a dosing regimen comprising at least a first dosing cycle (C1 ), wherein the length of the C1 is 21 days, wherein the C1 comprises a first dose (C1 D1 ), a second dose (C1 D2), and a third dose (C1 D3), wherein the C1 D1 is about 0.3 mg and is administered on Day 1 ; the C1 D2 is about 3.3 mg and is administered on Day 4; and the C1 D3 is about 160 mg and is administered on Day 8.In some embodiments of any one of the preceding aspects, the dosing regimen further comprises a second dosing cycle (C2) comprising a single dose (C2D1 ) of cevostamab, wherein the length of the C2 is 21 days, and wherein the C2D1 is about 160 mg and is administered to the subject on Day 1 of the second dosing cycle. In some embodiments, the dosing regimen comprises one or more additional dosing cycles, wherein the length of each of the one or more additional dosing cycles is 21 days, wherein each of the one or more additional dosing cycles comprises a single 160 mg dose of cevostamab, and wherein the single 160 mg dose of cevostamab is administered to the subject on Day 1 of each of the one or more additional dosing cycles.In another aspect, the disclosure provides a method of reducing the occurrence of CRS events in a subject (e.g., a human subject) being treated for R / R MM with a target dose of cevostamab, the method comprising administering to the subject, prior to a first administration of the target dose to the subject in a dosing regimen comprising a first dosing cycle (C1 ), (i) a first dose (C1 D1 ), (ii) a second dose (C1 D2),and (iii) a third dose (C1 D3) of cevostamab, wherein the C1 D1 is about 0.3 mg and is administered on Day 1 ; the C1 D2 is about 1 .2 mg and is administered on Day 2, Day 3, or Day 4; and the C1 D3 is about 3.6 mg and is administered on Day 8, wherein the length of the C1 is 21 days.In another aspect, the disclosure provides a method of reducing the occurrence of CRS events in a subject (e.g., a human subject) being treated for R / R MM with a target dose of cevostamab, the method comprising administering to the subject, prior to a first administration of the target dose to the subject in a dosing regimen comprising a first dosing cycle (C1 ), (i) a first dose (C1 D1 ), (ii) a second dose (C1 D2), and (iii) a third dose (C1 D3) of cevostamab, wherein the C1 D1 is about 0.3 mg and is administered on Day 1 ; the C1 D2 is about 3.3 mg and is administered on Day 2, Day 3, or Day 4; and the C1 D3 is about 7.2 mg and is administered on Day 8, wherein the length of the C1 is 21 daysIn another aspect, the disclosure provides a method of reducing the occurrence of CRS events in a subject (e.g., a human subject) being treated for R / R MM with a target dose of cevostamab, wherein, prior to a first administration of the target dose to the subject in a dosing regimen comprising a first dosing cycle (C1 ), the method comprises administering to the subject (i) a first dose (TS-C1 D1 ), (ii) a second dose (TS-C1 D2), and (iii) a third dose (TS-C1 D3) of cevostamab, wherein administering such target dose to a first plurality of such subjects results in a reduction in the number of subjects experiencing a CRS event after first administration of the target dose, as compared to a second plurality of such subjects administered such target dose after administration of a first dose (DS-C1 D1 ) and a second dose (DS- C1 D2), with no third dose (DS-C1 D3), and wherein the TS-D1 D2 is greater than the TS-C1 D1 , the TS- C1 D3 is greater than the TS-C1 D2, and the DS-C1 D2 is greater than the DS-C1 D1 .In some embodiments of the foregoing aspect, administering such target dose to the first plurality of such subjects results in at least a 10% reduction (e.g., at least a 10% reduction, at least an 1 1 % reduction, at least a 12% reduction, at least a 13% reduction, at least a 14% reduction, or at least a 15% reduction) in the number of subjects experiencing a CRS event after first administration of the target dose. In some embodiments, administering such target dose to the first plurality of such subjects results in a 15% reduction in the number of subjects experiencing a CRS event after first administration of the target dose.In yet another aspect, the disclosure provides a method of reducing the occurrence of CRS events in a subject (e.g., a human subject) being treated for R / R MM with a target dose of cevostamab, wherein, prior to a first administration of the target dose to the subject in a dosing regimen comprising a first dosing cycle (C1 ), the method comprises administering to the subject (i) a first dose (TS-C1 D1 ), (ii) a second dose (TS-C1 D2), and (iii) a third dose (TS-C1 D3) of cevostamab, wherein administering such target dose to a first plurality of such subjects results in at least a 10% reduction (e.g., at least a 10% reduction, at least an 1 1 % reduction, at least a 12% reduction, at least a 13% reduction, or at least a 14% reduction) in the number of subjects experiencing a CRS event during the C1 , as compared to a second plurality of such subjects administered such target dose after administration of a first dose (DS-C1 D1 ) and a second dose (DS-C1 D2), with no third dose (DS-C1 D3), and wherein the TS-D1 D2 is greater than the TS-C1 D1 , the TS-C1 D3 is greater than the TS-C1 D2, and the DS-C1 D2 is greater than the DS-C1 D1 . In some embodiments, wherein administering such target dose to the first plurality of such subjects results in a 14% reduction in the number of subjects experiencing a CRS event during the C1 .In another aspect, the disclosure provides a method of reducing the occurrence of CRS events in a subject (e.g., a human subject) being treated for R / R MM with a target dose of cevostamab, wherein, prior to a first administration of the target dose to the subject in a dosing regimen comprising a first dosing cycle (C1 ), the method comprises administering to the subject (i) a first dose (TS-C1 D1 ); (ii) a second dose (TS-C1 D2); and (iii) a third dose (TS-C1 D3) of cevostamab, wherein administering cevostamab in the C1 to a first plurality of such human subjects results in at least a 30% reduction in the number of CRS events experienced by each subject during the C1 , as compared to a second plurality of human patients administered the target dose of cevostamab after a first dose (DS-C1 D1 ) and a second dose (DS-C1 D2), but not a third dose (DS-C1 D3) of cevostamab, and wherein the TS-D1 D2 is greater than the TS-C1 D1 , the TS-C1 D3 is greater than the TS-C1 D2, and the DS-C1 D2 is greater than the DS-C1 D1 .In some embodiments of the foregoing aspect, administering such target dose to the first plurality of such subjects results in at least a 10% reduction (e.g., at least a 10% reduction, at least an 11% reduction, at least a 12% reduction, or at least a 13% reduction) in the number of subjects experiencing a CRS event during the C1 . In some embodiments, administering such target dose to the first plurality of such subjects results in a 14% reduction in the number of subjects experiencing a CRS event during the C1.In yet another aspect, the disclosure provides a method of reducing the occurrence of CRS events in a subject being treated for MM (e.g., R / R MM) at a target dose of cevostamab, wherein, prior to a first administration of the target dose to the subject in a dosing regimen comprising a first dosing cycle (C1 ), the method comprises administering to the subject (i) a first dose (TS-C1 D1 ); (ii) a second dose (TS-C1 D2); and (iii) a third dose (TS-C1 D3) of cevostamab, wherein administering cevostamab in the C1 to a first plurality of such subjects results in a reduction in the number of CRS events experienced by each subject during the C1 , as compared to a second plurality of subjects administered the target dose of cevostamab after a first dose (DS-C1 D1 ) and a second dose (DS-C1 D2), but not a third dose (DS-C1 D3) of cevostamab, and wherein the TS-D1 D2 is greater than the TS-C1 D1 , the TS-C1 D3 is greater than the TS-C1 D2, and the DS-C1 D2 is greater than the DS-C1 D1 . In some embodiments, administering cevostamab in the C1 to the first plurality of such subjects results in at least a 30% reduction in the number of CRS events experienced by each subject during the C1 .In yet another aspect, the disclosure provides a method of reducing the occurrence of CRS events in a subject (e.g., a human subject) being treated for MM (e.g., R / R MM) at a target dose of cevostamab, wherein, prior to first administration of the target dose to the subject in a first treatment cycle (C1 ), the subject is administered cevostamab at (i) a first dose (TS-C1 D1 ); (ii) a second dose (TS-C1 D2); and (iii) a third dose (TS-C1 D3), wherein administering cevostamab in the first treatment cycle to a first plurality of such human subjects results in a reduction in the number of subjects requiring tocilizumab treatment for CRS during first treatment cycle, as compared to a second plurality of human subjects administered a target dose of cevostamab after a first dose (DS-C1 D1 ) and a second dose (DS-C1 D2), but not a third dose (DS-C1 D3) of cevostamab, and wherein the TS-D1 D2 is greater than the TS-C1 D1 , the TS-C1 D3 is greater than the TS-C1 D2, and the DS-C1 D2 is greater than the DS-C1 D1 .In some embodiments of the foregoing aspect, administering cevostamab in the C1 to the first plurality of such subjects results in at least a 10% reduction in the number of subjects requiring tocilizumab treatment for CRS during the C1 .In yet another aspect, the disclosure provides a method of pre-treating a subject (e.g., a human subject) for receiving a target dose of cevostamab, wherein the method comprises administering to the subject (i) a first dose (C1 D1 ), (ii) a second dose (C1 D2), and (iii) a third dose (C1 D3) of cevostamab, wherein the C1 D2 is greater than the C1 D1 , and the C1 D3 is greater than the C1 D2, wherein the risk of CRS events in the subject, after administration of the C1 D1 , C1 D2, and C1 D3 to the subject, is at a level that is safe for the subject to receive the target dose of cevostamab.In some embodiments of the foregoing aspect, following administration of the C1 D1 , C1 D2, and C1 D3 to the subject, the subject achieves a peak IL-6 level of less than about 80 pg / mL (e.g., less than 80 pg / mL, 79 pg / mL, 78 pg / mL, 77 pg / mL, 76 pg / mL, 75 pg / mL, 74 pg / mL, 73 pg / mL, 72 pg / mL, 71 pg / mL, 70 pg / mL, 69 pg / mL, 68 pg / mL, 67 pg / mL, 66 pg / mL, 65 pg / mL, 64 pg / mL, 63 pg / mL, 62 pg / mL,61 pg / mL, 60 pg / mL, 59 pg / mL, 58 pg / mL, 57 pg / mL, 56 pg / mL, 55 pg / mL, 54 pg / mL, 53 pg / mL, 52 pg / mL, 51 pg / mL, 50 pg / mL, 49 pg / mL, 48 pg / mL, 47 pg / mL, 46 pg / mL, 45 pg / mL, 44 pg / mL, 43 pg / mL,42 pg / mL, 41 pg / mL, or 40 pg / mL, 39 pg / mL, 38 pg / mL, 37 pg / mL, 36 pg / mL, 35 pg / mL, 34 pg / mL, 33 pg / mL, 32 pg / mL, 31 pg / mL, or 30 pg / mL), thereby indicating that the risk of CRS events in the subject is at a level that is safe for the subject to receive the target dose of cevostamab. In some embodiments, the subject achieves a peak IL-6 level of less than about 30 pg / mL (e.g., less than about 30 pg / mL, 29 pg / mL, 28 pg / mL, 27 pg / mL, 26 pg / mL, 25 pg / mL, 24 pg / mL, 23 pg / mL, 22 pg / mL, 21 pg / mL, 20 pg / mL, 19 pg / mL, 18 pg / mL, 17 pg / mL, 16 pg / mL, 15 pg / mL, 14 pg / mL, 13 pg / mL, 12 pg / mL, 11 pg / mL, 10 pg / mL, 9 pg / mL, 8 pg / mL, 7 pg / mL, 6 pg / mL, 5 pg / mL, 4 pg / mL, 3 pg / mL, 2 pg / mL, or 1 pg / mL) prior to the administration of the target dose of cevostamab. In some embodiments, the method further comprises administering to the pre-treated subject a target dose of cevostamab.In yet another aspect, the disclosure provides a method of reducing the occurrence of CRS events in a subject being treated for R / R MM at a target dose of cevostamab, wherein, prior to a first administration of the target dose to the subject in a dosing regimen comprising a first dosing cycle (C1 ), the method comprises administering to the subject (i) a first dose (TS-C1 D1 ); (ii) a second dose (TS- C1 D2); and (iii) a third dose (TS-C1 D3) of cevostamab, wherein administering cevostamab in the C1 to a first plurality of such human subjects results in a reduction in the number of CRS events experienced by each subject during the C1 , as compared to a second plurality of subjects administered the target dose of cevostamab after a first dose (DS-C1 D1 ) and a second dose (DS-C1 D2), but not a third dose (DS-C1 D3) of cevostamab, and wherein the TS-D1 D2 is greater than the TS-C1 D1 , the TS-C1 D3 is greater than the TS-C1 D2, and the DS-C1 D2 is greater than the DS-C1 D1 .In some embodiments of the foregoing aspect, administering cevostamab in the C1 to the first plurality of such subjects results in at least a 25% reduction in the number of CRS events experienced by each subject during the C1 .In yet another aspect, the disclosure provides a method of reducing the occurrence of CRS events in a subject being treated for R / R MM at a target dose of cevostamab, wherein, prior to a first administration of the target dose to the subject in a dosing regimen comprising a first dosing cycle (C1 ), the method comprises administering to the subject (i) a first dose (TS-C1 D1 ); (ii) a second dose (TS-C1 D2); and (iii) a third dose (TS-C1 D3) of cevostamab, wherein administering cevostamab in the C1 to a first plurality of such subjects results in an increase in the number of subjects experiencing no CRS event during the C1 , as compared to a second plurality of subjects administered the target dose of cevostamab after a first dose (DS-C1 D1 ) and a second dose (DS-C1 D2), but not a third dose (DS-C1 D3) of cevostamab, and wherein the TS-D1 D2 is greater than the TS-C1 D1 , the TS-C1 D3 is greater than the TS-C1 D2, and the DS-C1 D2 is greater than the DS-C1 D1 .In some embodiments of the foregoing aspect, administering cevostamab in the C1 to the first plurality of such subjects results in at least a 50% increase in the number of subjects experiencing no CRS event during the C1 .In yet another aspect, the disclosure provides a method of reducing the occurrence of CRS events in a subject being treated for R / R MM at a target dose of cevostamab, wherein, prior to a first administration of the target dose to the subject in a dosing regimen comprising a first dosing cycle (C1 ), the method comprises administering to the subject (i) a first dose (TS-C1 D1 ); (ii) a second dose (TS- C1 D2); and (iii) a third dose (TS-C1 D3) of cevostamab, wherein administering cevostamab in the C1 to a first plurality of such subjects results in a reduction in the number of subjects experiencing at least two CRS events during the C1 , as compared to a second plurality of subjects administered the target dose of cevostamab after a first dose (DS-C1 D1 ) and a second dose (DS-C1 D2), but not a third dose (DS-C1 D3) of cevostamab, and wherein the TS-D1 D2 is greater than the TS-C1 D1 , the TS-C1 D3 is greater than the TS-C1 D2, and the DS-C1 D2 is greater than the DS-C1 D1 .In some embodiments of the foregoing aspect, administering cevostamab in the C1 to the first plurality of such subjects results in at least a 50% reduction in the number of subjects experiencing at least two CRS events during the C1 .In some embodiments of any one of the foregoing aspects, the subject is a human subject.In yet another aspect, the disclosure features a method of reducing the likelihood of cytokine release syndrome (CRS) in a subject (e.g., a human subject) having multiple myeloma (MM), wherein the method comprises administering to the subject a bispecific antibody that binds to Fc receptor-like 5 (FcRH5) and cluster of differentiation 3 (CD3) (e.g., cevostamab) in a dosing regimen comprising at least a first dosing cycle (C1 ), wherein the first dosing cycle (C1 ) comprises a first dose (C1 D1 ), a second dose (C1 D2), and a third dose (C1 D3) of the bispecific antibody, wherein the C1 D1 is between about 0.01 mg to about 0.9 mg (e.g., about 0.01 mg to about 0.1 mg, about 0.1 mg to about 0.5 mg, about 0.25 mg to about 0.75 mg, about 0.5 mg to about 0.9 mg, or about 0.2 mg to about 0.4 mg, e.g., about 0.01 mg, about 0.05 mg, about 0.1 mg, about 0.15 mg, about 0.2 mg, about 0.25 mg, about 0.3 mg, about 0.35 mg, about 0.4 mg, about 0.45 mg, about 0.5 mg, about 0.55 mg, about 0.6 mg, about 0.65 mg, about 0.7 mg, about 0.75 mg, about 0.8 mg, about 0.85 mg, or about 0.9 mg), the C1 D2 is between about 1 mg to about 5.9 mg (e.g., about 1 mg to about 1 .5 mg, about 1 mg to about 2 mg, about 1 mg to about 2.9 mg, about 1 mg to about 3.4 mg, about 1 .1 mg to about 1 .3 mg, about 1 .2 mg to about 3.3 mg, about 1 .5 mg to about 4 mg, about 2 mg to about 3 mg, about 2 mg to about 4.5 mg, about 2.5 mg to about 5 mg, about 3 mg to about 4 mg, about 3 mg to about 5 mg, about 3.5 mg to about 5.9 mg, about 3.2 mg to about 3.4 mg, or about 3.5 mg to about 3.7 mg, e.g., about 1 mg, about 1 .1 mg, about 1 .2 mg, about 1 .3 mg, about 1 .4 mg, about 1 .5 mg, about 1 .6 mg, about 1 .7 mg, about 1 .8 mg, about 1 .9 mg, about 2 mg, about 2.1 mg, about2.2 mg, about 2.3 mg, about 2.4 mg, about 2.5 mg, about 2.6 mg, about 2.7 mg, about 2.8 mg, about 2.9 mg, about 3 mg, about 3.1 mg, about 3.2 mg, about 3.3 mg, about 3.4 mg, about 3.5 mg, about 3.6 mg, about 3.7 mg, about 3.8 mg, about 3.9 mg, about 4 mg, about 4.1 mg, about 4.2 mg, about 4.3 mg, about4.4 mg, about 4.5 mg, about 4.6 mg, about 4.7 mg, about 4.8 mg, about 4.9 mg, about 5 mg, about 5.1 mg, about 5.2 mg, about 5.3 mg, about 5.4 mg, about 5.5 mg, about 5.6 mg, about 5.7 mg, about 5.8 mg, or about 5.9 mg), and the C1 D3 is between about 3 mg to about 19.9 mg (e.g., about 3 mg to about 10 mg, about 3 mg to about 7.5 mg, about 3 mg to about 5 mg, about 3 mg to about 4 mg, about 3.5 mg to about 3.7 mg, about 3.5 mg to about 7 mg, about 3.6 mg to about 7.2 mg, about 5 mg to about 7 mg, about 5 mg to about 10 mg, about 5 mg to about 15 mg, about 6 mg to about 19.9 mg, about 6.5 mg to about 10 mg, about 7 mg to about 15 mg, about 7.1 mg to about 7.3 mg, about 10 mg to about 15 mg, about 12 mg to about 17 mg, or about 15 mg to about 19.9 mg, e.g., about 3.5 mg, about 3.6 mg, about 3.7 mg, about 3.8 mg, about 3.9 mg, about 4 mg, about 4.1 mg, about 4.2 mg, about 4.3 mg, about 4.4 mg, about 4.5 mg, about 4.6 mg, about 4.7 mg, about 4.8 mg, about 4.9 mg, about 5 mg, about 5.1 mg, about 5.2 mg, about 5.3 mg, about 5.4 mg, about 5.5 mg, about 5.6 mg, about 5.7 mg, about 5.8 mg, about 5.9 mg, about 6 mg, about 6.1 mg, about 6.2 mg, about 6.3 mg, about 6.4 mg, about 6.5 mg, about 6.6 mg, about 6.7 mg, about 6.8 mg, about 6.9 mg, about 7 mg, about 7.1 mg, about 7.2 mg, about 7.3 mg, about 7.4 mg, about 7.5 mg, about 7.6 mg, about 7.7 mg, about 7.8 mg, about 7.9 mg, about 8 mg, about 8.1 mg, about 8.2 mg, about 8.3 mg, about 8.4 mg, about 8.5 mg, about 8.6 mg, about 8.7 mg, about 8.8 mg, about 8.9 mg, about 9 mg, about 9.1 mg, about 9.2 mg, about 9.3 mg, about 9.4 mg, about9.5 mg, about 9.6 mg, about 9.7 mg, about 9.8 mg, about 9.9 mg, about 10 mg, about 10.1 mg, about10.2 mg, about 10.3 mg, about 10.4 mg, about 10.5 mg, about 10.6 mg, about 10.7 mg, about 10.8 mg, about 10.9 mg, about 11 mg, about 11.1 mg, about 11 .2 mg, about 11 .3 mg, about 11 .4 mg, about 11 .5 mg, about 11 .6 mg, about 11 .7 mg, about 11 .8 mg, about 11 .9 mg, about 12 mg, about 12.1 mg, about12.2 mg, about 12.3 mg, about 12.4 mg, about 12.5 mg, about 12.6 mg, about 12.7 mg, about 12.8 mg, about 12.9 mg, about 13 mg, about 13.1 mg, about 13.2 mg, about 13.3 mg, about 13.4 mg, about 13.5 mg, about 13.6 mg, about 13.7 mg, about 13.8 mg, about 13.9 mg, about 14 mg, about 14.1 mg, about14.2 mg, about 14.3 mg, about 14.4 mg, about 14.5 mg, about 14.6 mg, about 14.7 mg, about 14.8 mg, about 14.9 mg, about 15 mg, about 15.1 mg, about 15.2 mg, about 15.3 mg, about 15.4 mg, about 15.5 mg, about 15.6 mg, about 15.7 mg, about 15.8 mg, about 15.9 mg, about 16 mg, about 16.1 mg, about16.2 mg, about 16.3 mg, about 16.4 mg, about 16.5 mg, about 16.6 mg, about 16.7 mg, about 16.8 mg, about 16.9 mg, about 17 mg, about 17.1 mg, about 17.2 mg, about 17.3 mg, about 17.4 mg, about 17.5 mg, about 17.6 mg, about 17.7 mg, about 17.8 mg, about 17.9 mg, about 18 mg, about 18.1 mg, about18.2 mg, about 18.3 mg, about 18.4 mg, about 18.5 mg, about 18.6 mg, about 18.7 mg, about 18.8 mg, about 18.9 mg, about 19 mg, about 19.1 mg, about 19.2 mg, about 19.3 mg, about 19.4 mg, about 19.5 mg, about 19.6 mg, about 19.7 mg, about 19.8 mg, or about 19.9 mg) and is greater than the C1 D2.In another aspect, the disclosure features a method of achieving a median peak IL-6 level of less than about 30 pg / mL (e.g., about 10 pg / mL, about 11 pg / mL, about 12 pg / mL, about 13 pg / mL, about 14 pg / mL, about 15 pg / mL, about 16 pg / mL, about 17 pg / mL, about 18 pg / mL, about 19 pg / mL, about 20 pg / mL, about 21 pg / mL, about 22 pg / mL, about 23 pg / mL, about 24 pg / mL, about 25 pg / mL, about 26 pg / mL, about 27 pg / mL, about 28 pg / mL, about 29 pg / mL, or about 30 pg / mL) in a population of subjects(e.g., human subjects) having MM following administration of a bispecific antibody that binds to FcRH5 and CD3 (e.g., cevostamab), wherein the method comprises administering to a subject in the population the bispecific antibody in a dosing regimen comprising at least a first dosing cycle (C1 ), wherein the first dosing cycle (C1 ) comprises a first dose (C1 D1 ), a second dose (C1 D2), and a third dose (C1 D3) of the bispecific antibody, wherein the C1 D1 is between about 0.01 mg to about 0.9 mg (e.g., about 0.01 mg to about 0.1 mg, about 0.1 mg to about 0.5 mg, about 0.25 mg to about 0.75 mg, about 0.5 mg to about 0.9 mg, or about 0.2 mg to about 0.4 mg, e.g., about 0.01 mg, about 0.05 mg, about 0.1 mg, about 0.15 mg, about 0.2 mg, about 0.25 mg, about 0.3 mg, about 0.35 mg, about 0.4 mg, about 0.45 mg, about 0.5 mg, about 0.55 mg, about 0.6 mg, about 0.65 mg, about 0.7 mg, about 0.75 mg, about 0.8 mg, about 0.85 mg, or about 0.9 mg), the C1 D2 is between about 1 mg to about 5.9 mg (e.g., about 1 mg to about 1 .5 mg, about 1 mg to about 2 mg, about 1 mg to about 2.9 mg, about 1 mg to about 3.4 mg, about 1 .1 mg to about 1 .3 mg, about 1 .2 mg to about 3.3 mg, about 1 .5 mg to about 4 mg, about 2 mg to about 3 mg, about 2 mg to about 4.5 mg, about 2.5 mg to about 5 mg, about 3 mg to about 4 mg, about 3 mg to about 5 mg, about 3.5 mg to about 5.9 mg, about 3.2 mg to about 3.4 mg, or about 3.5 mg to about 3.7 mg, e.g., about 1 mg, about 1 .1 mg, about 1 .2 mg, about 1 .3 mg, about 1 .4 mg, about 1 .5 mg, about 1 .6 mg, aboutI .7 mg, about 1 .8 mg, about 1 .9 mg, about 2 mg, about 2.1 mg, about 2.2 mg, about 2.3 mg, about 2.4 mg, about 2.5 mg, about 2.6 mg, about 2.7 mg, about 2.8 mg, about 2.9 mg, about 3 mg, about 3.1 mg, about 3.2 mg, about 3.3 mg, about 3.4 mg, about 3.5 mg, about 3.6 mg, about 3.7 mg, about 3.8 mg, about 3.9 mg, about 4 mg, about 4.1 mg, about 4.2 mg, about 4.3 mg, about 4.4 mg, about 4.5 mg, about 4.6 mg, about 4.7 mg, about 4.8 mg, about 4.9 mg, about 5 mg, about 5.1 mg, about 5.2 mg, about 5.3 mg, about 5.4 mg, about 5.5 mg, about 5.6 mg, about 5.7 mg, about 5.8 mg, or about 5.9 mg), and the C1 D3 is between about 3 mg to about 19.9 mg (e.g., about 3 mg to about 10 mg, about 3 mg to about 7.5 mg, about 3 mg to about 5 mg, about 3 mg to about 4 mg, about 3.5 mg to about 3.7 mg, about 3.5 mg to about 7 mg, about 3.6 mg to about 7.2 mg, about 5 mg to about 7 mg, about 5 mg to about 10 mg, about 5 mg to about 15 mg, about 6 mg to about 19.9 mg, about 6.5 mg to about 10 mg, about 7 mg to about 15 mg, about 7.1 mg to about 7.3 mg, about 10 mg to about 15 mg, about 12 mg to about 17 mg, or about 15 mg to about 19.9 mg, e.g., about 3.5 mg, about 3.6 mg, about 3.7 mg, about 3.8 mg, about 3.9 mg, about 4 mg, about 4.1 mg, about 4.2 mg, about 4.3 mg, about 4.4 mg, about 4.5 mg, about 4.6 mg, about 4.7 mg, about 4.8 mg, about 4.9 mg, about 5 mg, about 5.1 mg, about 5.2 mg, about 5.3 mg, about 5.4 mg, about 5.5 mg, about 5.6 mg, about 5.7 mg, about 5.8 mg, about 5.9 mg, about 6 mg, about 6.1 mg, about 6.2 mg, about 6.3 mg, about 6.4 mg, about 6.5 mg, about 6.6 mg, about 6.7 mg, about 6.8 mg, about 6.9 mg, about 7 mg, about 7.1 mg, about 7.2 mg, about 7.3 mg, about 7.4 mg, about 7.5 mg, about 7.6 mg, about 7.7 mg, about 7.8 mg, about 7.9 mg, about 8 mg, about 8.1 mg, about 8.2 mg, about 8.3 mg, about 8.4 mg, about 8.5 mg, about 8.6 mg, about 8.7 mg, about 8.8 mg, about 8.9 mg, about 9 mg, about 9.1 mg, about 9.2 mg, about 9.3 mg, about 9.4 mg, about 9.5 mg, about 9.6 mg, about 9.7 mg, about 9.8 mg, about 9.9 mg, about 10 mg, about 10.1 mg, about 10.2 mg, about 10.3 mg, about 10.4 mg, about 10.5 mg, about 10.6 mg, about 10.7 mg, about 10.8 mg, about 10.9 mg, about 1 1 mg, about 1 1 .1 mg, aboutI I .2 mg, about 1 1 .3 mg, about 1 1 .4 mg, about 1 1 .5 mg, about 1 1 .6 mg, about 1 1 .7 mg, about 1 1 .8 mg, about 1 1 .9 mg, about 12 mg, about 12.1 mg, about 12.2 mg, about 12.3 mg, about 12.4 mg, about 12.5 mg, about 12.6 mg, about 12.7 mg, about 12.8 mg, about 12.9 mg, about 13 mg, about 13.1 mg, about13.2 mg, about 13.3 mg, about 13.4 mg, about 13.5 mg, about 13.6 mg, about 13.7 mg, about 13.8 mg, about 13.9 mg, about 14 mg, about 14.1 mg, about 14.2 mg, about 14.3 mg, about 14.4 mg, about 14.5 mg, about 14.6 mg, about 14.7 mg, about 14.8 mg, about 14.9 mg, about 15 mg, about 15.1 mg, about15.2 mg, about 15.3 mg, about 15.4 mg, about 15.5 mg, about 15.6 mg, about 15.7 mg, about 15.8 mg, about 15.9 mg, about 16 mg, about 16.1 mg, about 16.2 mg, about 16.3 mg, about 16.4 mg, about 16.5 mg, about 16.6 mg, about 16.7 mg, about 16.8 mg, about 16.9 mg, about 17 mg, about 17.1 mg, about17.2 mg, about 17.3 mg, about 17.4 mg, about 17.5 mg, about 17.6 mg, about 17.7 mg, about 17.8 mg, about 17.9 mg, about 18 mg, about 18.1 mg, about 18.2 mg, about 18.3 mg, about 18.4 mg, about 18.5 mg, about 18.6 mg, about 18.7 mg, about 18.8 mg, about 18.9 mg, about 19 mg, about 19.1 mg, about19.2 mg, about 19.3 mg, about 19.4 mg, about 19.5 mg, about 19.6 mg, about 19.7 mg, about 19.8 mg, or about 19.9 mg).In some embodiments, the median peak IL-6 level is about 10 pg / mL to about 80 pg / mL (e.g., about 10 pg / mL, about 1 1 pg / mL, about 12 pg / mL, about 13 pg / mL, about 14 pg / mL, about 15 pg / mL, about 16 pg / mL, about 17 pg / mL, about 18 pg / mL, about 19 pg / mL, about 20 pg / mL, about 21 pg / mL, about 22 pg / mL, about 23 pg / mL, about 24 pg / mL, about 25 pg / mL, about 26 pg / mL, about 27 pg / mL, about 28 pg / mL, about 29 pg / mL, about 30 pg / mL, about 31 pg / mL, about 32 pg / mL, about 33 pg / mL, about 34 pg / mL, about 35 pg / mL, about 36 pg / mL, about 37 pg / mL, about 38 pg / mL, about 39 pg / mL, about 40 pg / mL, about 41 pg / mL, about 42 pg / mL, about 43 pg / mL, about 44 pg / mL, about 45 pg / mL, about 46 pg / mL, about 47 pg / mL, about 48 pg / mL, about 49 pg / mL, about 50 pg / mL, about 51 pg / mL, about 52 pg / mL, about 53 pg / mL, about 54 pg / mL, about 55 pg / mL, about 56 pg / mL, about 57 pg / mL, about 58 pg / mL, about 59 pg / mL, about 60 pg / mL, about 61 pg / mL, about 62 pg / mL, about 63 pg / mL, about 64 pg / mL, about 65 pg / mL, about 66 pg / mL, about 67 pg / mL, about 68 pg / mL, about 69 pg / mL, about 70 pg / mL, about 71 pg / mL, about 72 pg / mL, about 73 pg / mL, about 74 pg / mL, about 75 pg / mL, about 76 pg / mL, about 77 pg / mL, about 78 pg / mL, about 79 pg / mL, or about 80 pg / mL) following administration of the bispecific antibody. In some embodiments, the median peak IL-6 level is about 80 pg / mL following administration of the bispecific antibody. In some embodiments, the median peak IL-6 level is about 30 pg / mL following administration of the bispecific antibody. In some embodiments, the median peak IL-6 level is about 18 pg / mL following administration of the bispecific antibody.In some embodiments, the median peak IL-6 level is measured in blood samples obtained from the population of subjects (e.g., human subjects). In some embodiments, the blood samples are peripheral blood samples.In some embodiments, the method further comprises administering to the subject (e.g., human subjects) an additional dose of the bispecific antibody, wherein the additional dose of the bispecific antibody is greater than the C1 D3. In some embodiments, the additional dose of the bispecific antibody that is greater than the C1 D3 is a target dose of the bispecific antibody. In some embodiments, the additional dose of the bispecific antibody is administered during the first dosing cycle (C1 ) as a fourth dose (C1 D4) of the bispecific antibody and is between about 20 mg to about 252 mg (e.g., about 30 mg to about 252 mg, about 40 mg to about 252 mg, about 60 mg to about 252 mg, about 80 mg to about 252 mg, about 100 mg to about 200 mg, about 140 mg to about 180 mg, about 150 mg to about 170 mg, about 132 mg to about 160 mg, about 70 mg to about 105 mg, or about 100 mg to about 180 mg, e.g.,about 20 mg, about 25 mg, about 30 mg, about 35 mg, about 40 mg, about 45 mg, about 50 mg, about 55 mg, about 60 mg, about 65 mg, about 70 mg, about 75 mg, about 80 mg, about 85 mg, about 90 mg, about 95 mg, about 100 mg, about 105 mg, about 110 mg, about 115 mg, about 120 mg, about 125 mg, about 130 mg, about 131 mg, about 132 mg, about 133 mg, about 134 mg, about 135 mg, about 140 mg, about 145 mg, about 150 mg, about 155 mg, about 160 mg, about 165 mg, about 170 mg, about 175 mg, about 180 mg, about 185 mg, about 190 mg, about 195 mg, about 200 mg, about 205 mg, about 210 mg, about 215 mg, about 220 mg, about 225 mg, about 230 mg, about 235 mg, about 240 mg, about 245 mg, about 250 mg, or about 252 mg). In some embodiments, the C1 D4 of the bispecific antibody is a target dose of the bispecific antibody.In another aspect, the disclosure features a method of treating a subject (e.g., a human subject) having MM, wherein the method comprises administering to the subject an effective amount of a bispecific antibody that binds to FcRH5 and CD3 (e.g., cevostamab) in a dosing regimen comprising at least a first dosing cycle (C1 ), wherein the first dosing cycle (C1 ) comprises a first dose (C1 D1 ), a second dose (C1 D2), a third dose (C1 D3), and a fourth dose (C1 D4) of the bispecific antibody, wherein the C1 D1 is between about 0.01 mg to about 0.9 mg (e.g., about 0.01 mg to about 0.1 mg, about 0.1 mg to about 0.5 mg, about 0.25 mg to about 0.75 mg, about 0.5 mg to about 0.9 mg, or about 0.2 mg to about 0.4 mg, e.g., about 0.01 mg, about 0.05 mg, about 0.1 mg, about 0.15 mg, about 0.2 mg, about 0.25 mg, about 0.3 mg, about 0.35 mg, about 0.4 mg, about 0.45 mg, about 0.5 mg, about 0.55 mg, about 0.6 mg, about 0.65 mg, about 0.7 mg, about 0.75 mg, about 0.8 mg, about 0.85 mg, or about 0.9 mg), the C1 D2 is between about 1 mg to about 5.9 mg (e.g., about 1 mg to about 1 .5 mg, about 1 mg to about 2 mg, about 1 mg to about 2.9 mg, about 1 mg to about 3.4 mg, about 1 .1 mg to about 1 .3 mg, about 1 .2 mg to about3.3 mg, about 1 .5 mg to about 4 mg, about 2 mg to about 3 mg, about 2 mg to about 4.5 mg, about 2.5 mg to about 5 mg, about 3 mg to about 4 mg, about 3 mg to about 5 mg, about 3.5 mg to about 5.9 mg, about 3.2 mg to about 3.4 mg, or about 3.5 mg to about 3.7 mg, e.g., about 1 mg, about 1 .1 mg, about 1 .2 mg, about 1 .3 mg, about 1 .4 mg, about 1 .5 mg, about 1 .6 mg, about 1 .7 mg, about 1 .8 mg, about 1 .9 mg, about 2 mg, about 2.1 mg, about 2.2 mg, about 2.3 mg, about 2.4 mg, about 2.5 mg, about 2.6 mg, about2.7 mg, about 2.8 mg, about 2.9 mg, about 3 mg, about 3.1 mg, about 3.2 mg, about 3.3 mg, about 3.4 mg, about 3.5 mg, about 3.6 mg, about 3.7 mg, about 3.8 mg, about 3.9 mg, about 4 mg, about 4.1 mg, about 4.2 mg, about 4.3 mg, about 4.4 mg, about 4.5 mg, about 4.6 mg, about 4.7 mg, about 4.8 mg, about 4.9 mg, about 5 mg, about 5.1 mg, about 5.2 mg, about 5.3 mg, about 5.4 mg, about 5.5 mg, about5.6 mg, about 5.7 mg, about 5.8 mg, or about 5.9 mg), the C1 D3 is between about 3 mg to about 19.9 mg(e.g., about 3 mg to about 10 mg, about 3 mg to about 7.5 mg, about 3 mg to about 5 mg, about 3 mg to about 4 mg, about 3.5 mg to about 3.7 mg, about 3.5 mg to about 7 mg, about 3.6 mg to about 7.2 mg, about 5 mg to about 7 mg, about 5 mg to about 10 mg, about 5 mg to about 15 mg, about 6 mg to about19.9 mg, about 6.5 mg to about 10 mg, about 7 mg to about 15 mg, about 7.1 mg to about 7.3 mg, about 10 mg to about 15 mg, about 12 mg to about 17 mg, or about 15 mg to about 19.9 mg, e.g., about 3.5 mg, about 3.6 mg, about 3.7 mg, about 3.8 mg, about 3.9 mg, about 4 mg, about 4.1 mg, about 4.2 mg, about4.3 mg, about 4.4 mg, about 4.5 mg, about 4.6 mg, about 4.7 mg, about 4.8 mg, about 4.9 mg, about 5 mg, about 5.1 mg, about 5.2 mg, about 5.3 mg, about 5.4 mg, about 5.5 mg, about 5.6 mg, about 5.7 mg, about 5.8 mg, about 5.9 mg, about 6 mg, about 6.1 mg, about 6.2 mg, about 6.3 mg, about 6.4 mg, about6.5 mg, about 6.6 mg, about 6.7 mg, about 6.8 mg, about 6.9 mg, about 7 mg, about 7.1 mg, about 7.2 mg, about 7.3 mg, about 7.4 mg, about 7.5 mg, about 7.6 mg, about 7.7 mg, about 7.8 mg, about 7.9 mg, about 8 mg, about 8.1 mg, about 8.2 mg, about 8.3 mg, about 8.4 mg, about 8.5 mg, about 8.6 mg, about 8.7 mg, about 8.8 mg, about 8.9 mg, about 9 mg, about 9.1 mg, about 9.2 mg, about 9.3 mg, about 9.4 mg, about 9.5 mg, about 9.6 mg, about 9.7 mg, about 9.8 mg, about 9.9 mg, about 10 mg, about 10.1 mg, about 10.2 mg, about 10.3 mg, about 10.4 mg, about 10.5 mg, about 10.6 mg, about 10.7 mg, about 10.8 mg, about 10.9 mg, about 11 mg, about 11 .1 mg, about 11 .2 mg, about 11 .3 mg, about 11 .4 mg, about11 .5 mg, about 11 .6 mg, about 11 .7 mg, about 11 .8 mg, about 11 .9 mg, about 12 mg, about 12.1 mg, about 12.2 mg, about 12.3 mg, about 12.4 mg, about 12.5 mg, about 12.6 mg, about 12.7 mg, about 12.8 mg, about 12.9 mg, about 13 mg, about 13.1 mg, about 13.2 mg, about 13.3 mg, about 13.4 mg, about13.5 mg, about 13.6 mg, about 13.7 mg, about 13.8 mg, about 13.9 mg, about 14 mg, about 14.1 mg, about 14.2 mg, about 14.3 mg, about 14.4 mg, about 14.5 mg, about 14.6 mg, about 14.7 mg, about 14.8 mg, about 14.9 mg, about 15 mg, about 15.1 mg, about 15.2 mg, about 15.3 mg, about 15.4 mg, about15.5 mg, about 15.6 mg, about 15.7 mg, about 15.8 mg, about 15.9 mg, about 16 mg, about 16.1 mg, about 16.2 mg, about 16.3 mg, about 16.4 mg, about 16.5 mg, about 16.6 mg, about 16.7 mg, about 16.8 mg, about 16.9 mg, about 17 mg, about 17.1 mg, about 17.2 mg, about 17.3 mg, about 17.4 mg, about17.5 mg, about 17.6 mg, about 17.7 mg, about 17.8 mg, about 17.9 mg, about 18 mg, about 18.1 mg, about 18.2 mg, about 18.3 mg, about 18.4 mg, about 18.5 mg, about 18.6 mg, about 18.7 mg, about 18.8 mg, about 18.9 mg, about 19 mg, about 19.1 mg, about 19.2 mg, about 19.3 mg, about 19.4 mg, about19.5 mg, about 19.6 mg, about 19.7 mg, about 19.8 mg, or about 19.9 mg) and is greater than the C1 D2, and the C1 D4 is between about 20 mg to about 252 mg (e.g., about 30 mg to about 252 mg, about 40 mg to about 252 mg, about 60 mg to about 252 mg, about 80 mg to about 252 mg, about 100 mg to about 200 mg, about 140 mg to about 180 mg, about 150 mg to about 170 mg, about 132 mg to about 160 mg, about 70 mg to about 105 mg, or about 100 mg to about 180 mg, e.g., about 20 mg, about 25 mg, about 30 mg, about 35 mg, about 40 mg, about 45 mg, about 50 mg, about 55 mg, about 60 mg, about 65 mg, about 70 mg, about 75 mg, about 80 mg, about 85 mg, about 90 mg, about 95 mg, about 100 mg, about105 mg, about 110 mg, about 115 mg, about 120 mg, about 125 mg, about 130 mg, about 131 mg, about132 mg, about 133 mg, about 134 mg, about 135 mg, about 140 mg, about 145 mg, about 150 mg, about155 mg, about 160 mg, about 165 mg, about 170 mg, about 175 mg, about 180 mg, about 185 mg, about190 mg, about 195 mg, about 200 mg, about 205 mg, about 210 mg, about 215 mg, about 220 mg, about225 mg, about 230 mg, about 235 mg, about 240 mg, about 245 mg, about 250 mg, or about 252 mg). In some embodiments, the C1 D4 of the bispecific antibody is a target dose of the bispecific antibody.In some embodiments, the C1 D4 is between about 132 mg to about 160 mg. In some embodiments, the C1 D4 is about 160 mg. In some embodiments, the C1 D4 of the bispecific antibody is a target dose of the bispecific antibody.In some embodiments, the C1 D1 is between about 0.1 mg to about 0.6 mg (e.g., about 0.1 mg, about 0.2 mg, about 0.3 mg, about 0.4 mg, about 0.5 mg, or about 0.6 mg); the C1 D2 is between about 1 mg to about 5 mg (e.g., about 1 mg, about 2 mg, about 3 mg, about 4 mg, or about 5 mg); and the C1 D3 is between about 3 mg to about 10 mg (e.g., about 3 mg, about 4 mg, about 5 mg, about 6 mg, about 7 mg, about 8 mg, about 9 mg, or about 10 mg) and is greater than the C1 D2. In some embodiments, theC1 D1 is about 0.3 mg; the C1 D2 is between about 1 mg to about 2.9 mg (e.g., about 1 mg, about 1 .1 mg, about 1 .2 mg, about 1 .3 mg, about 1 .4 mg, about 1 .5 mg, about 1 .6 mg, about 1 .7 mg, about 1 .8 mg, about 1 .9 mg, about 2 mg, about 2.1 mg, about 2.2 mg, about 2.3 mg, about 2.4 mg, about 2.5 mg, about2.6 mg, about 2.7 mg, about 2.8 mg, or about 2.9 mg); and the C1 D3 is between about 3 mg to about 5.9 mg.In some embodiments, the C1 D1 is about 0.3 mg; the C1 D2 is about 1 .2 mg; and the C1 D3 is about 3.6 mg. In some embodiments, the C1 D1 is about 0.3 mg; the C1 D2 is between about 3 mg to about 5 mg (e.g., about 3 mg, about 3.1 mg, about 3.2 mg, about 3.3 mg, about 3.4 mg, about 3.5 mg, about 3.6 mg, about 3.7 mg, about 3.8 mg, about 3.9 mg, about 4 mg, about 4.1 mg, about 4.2 mg, about4.3 mg, about 4.4 mg, about 4.5 mg, about 4.6 mg, about 4.7 mg, about 4.8 mg, about 4.9 mg, or about 5 mg); and the C1 D3 is between about 6 mg to about 10 mg (e.g., about 6 mg, about 6.1 mg, about 6.2 mg, about 6.3 mg, about 6.4 mg, about 6.5 mg, about 6.6 mg, about 6.7 mg, about 6.8 mg, about 6.9 mg, about 7 mg, about 7.1 mg, about 7.2 mg, about 7.3 mg, about 7.4 mg, about 7.5 mg, about 7.6 mg, about7.7 mg, about 7.8 mg, about 7.9 mg, about 8 mg, about 8.1 mg, about 8.2 mg, about 8.3 mg, about 8.4 mg, about 8.5 mg, about 8.6 mg, about 8.7 mg, about 8.8 mg, about 8.9 mg, about 9 mg, about 9.1 mg, about 9.2 mg, about 9.3 mg, about 9.4 mg, about 9.5 mg, about 9.6 mg, about 9.7 mg, about 9.8 mg, about 9.9 mg, or about 10 mg). In some embodiments, the C1 D1 is about 0.3 mg; the C1 D2 is about 3.3 mg; and the C1 D3 is about 7.2 mg.In another aspect, the disclosure features a method of treating a subject (e.g., a human subject) having MM, wherein the method comprises administering to the subject a bispecific antibody that binds to FcRH5 and CD3 (e.g., cevostamab) in a dosing regimen comprising at least a first dosing cycle (C1 ), wherein the first dosing cycle (C1 ) comprises a first dose (C1 D1 ), a second dose (C1 D2), a third dose (C1 D3), and a fourth dose (C1 D4) of the bispecific antibody, wherein the C1 D1 is about 0.3 mg; the C1 D2 is about 1 .2 mg; the C1 D3 is about 3.6 mg; and the C1 D4 is about 160 mg. In some embodiments, the C1 D4 of the bispecific antibody is a target dose of the bispecific antibody.In another aspect, the disclosure features method of treating a subject (e.g., a human subject) having MM, wherein the method comprises administering to the subject a bispecific antibody that binds to FcRH5 and CD3 (e.g., cevostamab) in a dosing regimen comprising at least a first dosing cycle (C1 ), wherein the first dosing cycle (C1 ) comprises a first dose (C1 D1 ), a second dose (C1 D2), a third dose (C1 D3), and a fourth dose (C1 D4) of the bispecific antibody, the C1 D1 is about 0.3 mg; the C1 D2 is about3.3 mg; the C1 D3 is about 7.2 mg; and the C1 D4 is about 160 mg. In some embodiments, the C1 D4 of the bispecific antibody is a target dose of the bispecific antibody.In one aspect, the disclosure features a method of reducing the likelihood of CRS in a subject (e.g., a human subject) having MM, wherein the method comprises administering to the subject a bispecific antibody that binds to FcRH5 and CD3 (e.g., cevostamab) in a dosing regimen comprising at least a first dosing cycle (C1 ), wherein the first dosing cycle (C1 ) comprises a first dose (C1 D1 ), a second dose (C1 D2), and a third dose (C1 D3) of the bispecific antibody, wherein the C1 D1 is about 0.3 mg; the C1 D2 is about 1 .2 mg; and the C1 D3 is about 3.6 mg.In another aspect, the disclosure features a method of reducing the likelihood of CRS in a subject (e.g., a human subject) having MM, wherein the method comprises administering to the subject abispecific antibody that binds to FcRH5 and CD3 (e.g., cevostamab) in a dosing regimen comprising at least a first dosing cycle (C1 ), wherein the first dosing cycle (C1 ) comprises a first dose (C1 D1 ), a second dose (C1 D2), and a third dose (C1 D3) of the bispecific antibody, wherein the C1 D1 is about 0.3 mg; the C1 D2 is about 3.3 mg; and the C1 D3 is about 7.2 mg.In one aspect, the disclosure features a method of achieving a median peak IL-6 level of about 30 pg / mL in a population of subjects (e.g., human subjects) having MM following administration of a bispecific antibody that binds to FcRH5 and CD3 (e.g., cevostamab), wherein the method comprises administering to a subject in the population the bispecific antibody in a dosing regimen comprising at least a first dosing cycle (C1 ), wherein the first dosing cycle (C1 ) comprises a first dose (C1 D1 ), a second dose (C1 D2), and a third dose (C1 D3) of the bispecific antibody, wherein the C1 D1 is about 0.3 mg; the C1 D2 is about 1 .2 mg; and the C1 D3 is about 3.6 mg.In some embodiments, the length of the first dosing cycle (C1 ) is 21 days. In some embodiments, the method comprises administering to the subject: (a) the C1 D1 on or about Day 1 of the first dosing cycle (C1 ); (b) the C1 D2 on or about Day 2, Day 3, or Day 4 of the first dosing cycle; and (c) the C1 D3 on or about Day 8 of the first dosing cycle.In some embodiments, the length of the first dosing cycle (C1 ) is 21 days, and the method comprises administering to the subject the C1 D4 on or about Day 9, Day 10, or Day 11 of the first dosing cycle (C1 ).In some embodiments, the length of the first dosing cycle (C1 ) is 21 days, and the method comprises administering to the subject the C1 D4 about 1 day, 2 days, or 3 days after the C1 D3 of the first dosing cycle (C1 ).In some embodiments, the C1 D4 of the bispecific antibody is a target dose of the bispecific antibody.In one aspect, the disclosure features a method of treating a subject (e.g., a human subject) having MM, wherein the method comprises administering to the subject a bispecific antibody that binds to FcRH5 and CD3 (e.g., cevostamab) in a dosing regimen comprising at least a first dosing cycle (C1 ), wherein the length of the first dosing cycle (C1 ) is 21 days, wherein the first dosing cycle (C1 ) comprises a first dose (C1 D1 ), a second dose (C1 D2), and a third dose (C1 D3) of the bispecific antibody, and wherein: (a) the C1 D1 is between about 0.01 mg to about 0.9 mg (e.g., about 0.01 mg to about 0.1 mg, about 0.1 mg to about 0.5 mg, about 0.25 mg to about 0.75 mg, about 0.5 mg to about 0.9 mg, or about 0.2 mg to about 0.4 mg, e.g., about 0.01 mg, about 0.05 mg, about 0.1 mg, about 0.15 mg, about 0.2 mg, about 0.25 mg, about 0.3 mg, about 0.35 mg, about 0.4 mg, about 0.45 mg, about 0.5 mg, about 0.55 mg, about 0.6 mg, about 0.65 mg, about 0.7 mg, about 0.75 mg, about 0.8 mg, about 0.85 mg, or about 0.9 mg) and is administered to the subject on or about Day 1 of the first dosing cycle (C1 ); (b) the C1 D2 is between about 1 mg to about 5.9 mg (e.g., about 1 mg to about 1 .5 mg, about 1 mg to about 2 mg, about 1 mg to about 2.9 mg, about 1 mg to about 3.4 mg, about 1 .1 mg to about 1 .3 mg, about 1 .2 mg to about 3.3 mg, about 1 .5 mg to about 4 mg, about 2 mg to about 3 mg, about 2 mg to about 4.5 mg, about 2.5 mg to about 5 mg, about 3 mg to about 4 mg, about 3 mg to about 5 mg, about 3.5 mg to about 5.9 mg, about 3.2 mg to about 3.4 mg, or about 3.5 mg to about 3.7 mg, e.g., about 1 mg, about 1 .1 mg, about 1 .2 mg, about 1 .3 mg, about 1 .4 mg, about 1 .5 mg, about 1 .6 mg, about 1 .7 mg, about 1 .8 mg, about 1 .9 mg,about 2 mg, about 2.1 mg, about 2.2 mg, about 2.3 mg, about 2.4 mg, about 2.5 mg, about 2.6 mg, about 2.7 mg, about 2.8 mg, about 2.9 mg, about 3 mg, about 3.1 mg, about 3.2 mg, about 3.3 mg, about 3.4 mg, about 3.5 mg, about 3.6 mg, about 3.7 mg, about 3.8 mg, about 3.9 mg, about 4 mg, about 4.1 mg, about 4.2 mg, about 4.3 mg, about 4.4 mg, about 4.5 mg, about 4.6 mg, about 4.7 mg, about 4.8 mg, about 4.9 mg, about 5 mg, about 5.1 mg, about 5.2 mg, about 5.3 mg, about 5.4 mg, about 5.5 mg, about 5.6 mg, about 5.7 mg, about 5.8 mg, or about 5.9 mg) and is administered to the subject on or about Day 2, Day 3, or Day 4 of the first dosing cycle (C1 ); and (c) the C1 D3 is between about 100 mg to about 180 mg and is administered to the subject on or about Day 8 of the first dosing cycle (C1 ).In some embodiments, the C1 D1 is between about 0.1 mg to about 0.6 mg; the C1 D2 is between about 1 mg to about 5 mg; and the C1 D3 is between about 132 mg to about 160 mg.In another aspect, the disclosure features a method of treating a subject (e.g., a human subject) having MM, wherein the method comprises administering to the subject an effective amount of a bispecific antibody that binds to FcRH5 and CD3 (e.g., cevostamab) in a dosing regimen comprising at least a first dosing cycle (C1 ), wherein the length of the first dosing cycle is 21 days, wherein the first dosing cycle (C1 ) comprises a first dose (C1 D1 ), a second dose (C1 D2), and a third dose (C1 D3) of the bispecific antibody, and wherein: (a) the C1 D1 is about 0.3 mg and is administered to the subject on or about Day 1 of the first dosing cycle (C1 ); (b) the C1 D2 is about 3.3 mg and is administered to the subject on or about Day 2, Day 3, or Day 4 of the first dosing cycle (C1 ); and (c) the C1 D3 is about 160 mg and is administered to the subject on or about Day 8 of the first dosing cycle (C1 ).In some embodiments, the method further comprises administering to the subject (e.g., a human subject) an effective amount of tocilizumab about 2 hours prior to administering the first dose of the bispecific antibody. In some embodiments, the subject weighs > 100 kg, and tocilizumab is administered to the subject at a dose of 800 mg. In some embodiments, the subject weighs > 30 kg and < 100 kg, and tocilizumab is administered to the subject at a dose of 8 mg / kg. In some embodiments, the subject weighs < 30 kg, and tocilizumab is administered to the subject at a dose of 12 mg / kg.In some embodiments, the dosing regimen further comprises a second dosing cycle comprising a single dose (C2D1 ) of the bispecific antibody, wherein the C2D1 is equal to or greater than the last administered dose of the bispecific antibody and is between about 100 mg to about 180 mg. In some embodiments, the C2D1 is between about 132 mg to about 160 mg. In some embodiments, the C2D1 is about 160 mg.In some embodiments, the length of the second dosing cycle is 21 days. In some embodiments, the method comprises administering to the subject (e.g., a human subject) the C2D1 on Day 1 of the second dosing cycle. In some embodiments, the dosing regimen comprises one or more additional dosing cycles. In some embodiments, the dosing regimen comprises one to 15 additional dosing cycles. In some embodiments, the length of each of the one or more additional dosing cycles is 21 days. In some embodiments, each of the one or more additional dosing cycles comprises a single dose of the bispecific antibody. In some embodiments, the method comprises administering to the subject the single dose of the bispecific antibody on Day 1 of the one or more additional dosing cycles. In some embodiments, the single dose is between about 100 mg to about 180 mg. In some embodiments, the single dose is between about 132 mg to about 160 mg. In some embodiments, the single dose is about 160 mg.In some embodiments, a median peak IL-6 level in a population of subjects (e.g., human subjects) treated according to the method does not exceed 80 pg / mL between the C1 D1 and the C1 D2. In some embodiments, the median peak IL-6 level in a population of subjects treated according to the method does not exceed 30 pg / mL between the C1 D1 and the C1 D2.In some embodiments, a median peak IL-6 level in a population of subjects (e.g., human subjects) treated according to the method does not exceed 80 pg / mL between the C1 D2 and the C1 D3. In some embodiments, the median peak IL-6 level in a population of subjects treated according to the method does not exceed 30 pg / mL between the C1 D2 and the C1 D3.In some embodiments, a median peak IL-6 level in a population of subjects treated according to the method does not exceed 30 pg / mL between the C1 D3 and the C1 D4. In some embodiments, the C1 D4 of the bispecific antibody is a target dose of the bispecific antibody.In some embodiments, the IL-6 level is measured in a blood sample. In some embodiments, the blood sample is a peripheral blood sample.In some embodiments, a peak level of CD8+ T cell activation in the subject (e.g., a human subject) in the first dosing cycle occurs between administration of the C1 D1 and the C1 D2. In some embodiments, a peak level of CD8+ T cell activation in the subject in the first dosing cycle occurs between administration of the C1 D2 and the C1 D3. In some embodiments, a peak level of CD8+ T cell activation in the subject in the first dosing cycle occurs between administration of the C1 D3 and the C1 D4. In some embodiments, the peak level of CD8+ T cell activation in the subject in the first dosing cycle occurs within 24 hours after administration of the bispecific antibody.In some embodiments, the bispecific antibody (e.g., cevostamab) comprises an anti-FcRH5 arm comprising a first binding domain comprising the following six hypervariable regions (HVRs): (a) an HVR- H1 comprising the amino acid sequence of RFGVH (SEQ ID NO: 1 ); (b) an HVR-H2 comprising the amino acid sequence of VIWRGGSTDYNAAFVS (SEQ ID NO: 2); (c) an HVR-H3 comprising the amino acid sequence of HYYGSSDYALDN (SEQ ID NO:3); (d) an HVR-L1 comprising the amino acid sequence of KASQDVRNLVV (SEQ ID NO: 4); (e) an HVR-L2 comprising the amino acid sequence of SGSYRYS (SEQ ID NO: 5); and (f) an HVR-L3 comprising the amino acid sequence of QQHYSPPYT (SEQ ID NO: 6); and an anti-CD3 arm comprising a second binding domain comprising the following six HVRs: (a) an HVR-H1 comprising the amino acid sequence of SYYIH (SEQ ID NO: 9); (b) an HVR-H2 comprising the amino acid sequence of WIYPENDNTKYNEKFKD (SEQ ID NO: 10); (c) an HVR-H3 comprising the amino acid sequence of DGYSRYYFDY (SEQ ID NO: 11 ); (d) an HVR-L1 comprising the amino acid sequence of KSSQSLLNSRTRKNYLA (SEQ ID NO: 12); (e) an HVR-L2 comprising the amino acid sequence of WTSTRKS (SEQ ID NO: 13); and (f) an HVR-L3 comprising the amino acid sequence of KQSFILRT (SEQ ID NO: 14).In some embodiments, the bispecific antibody comprises an anti-FcRH5 arm comprising a first binding domain comprising a heavy chain variable (VH) domain comprising an amino acid sequence having at least 95% (e.g., 95%, 96%, 97%, 98%, 99%, or 100%) sequence identity to the amino acid sequence of SEQ ID NO: 7. In some embodiments, the bispecific antibody comprises an anti-FcRH5 arm comprising a first binding domain comprising a light chain variable (VL) domain comprising an amino acid sequence having at least 95% (e.g., 95%, 96%, 97%, 98%, 99%, or 100%) sequence identity to theamino acid sequence of SEQ ID NO: 8. In some embodiments the binding domain comprises a VH domain comprising an amino acid sequence having at least 95% (e.g., 95%, 96%, 97%, 98%, 99%, or 100%) sequence identity to the amino acid sequence of SEQ ID NO: 7 and a VL domain comprising an amino acid sequence having at least 95% sequence identity to the amino acid sequence of SEQ ID NO: 8. In some embodiments, the first binding domain comprises a VH domain comprising an amino acid sequence of SEQ ID NO: 7 and a VL domain comprising an amino acid sequence of SEQ ID NO: 8.In some embodiments, the bispecific antibody comprises an anti-CD3 arm comprising a second binding domain comprising a VH domain comprising an amino acid sequence having at least 95% (e.g., 95%, 96%, 97%, 98%, 99%, or 100%) sequence identity to the amino acid sequence of SEQ ID NO: 15. In some embodiments the bispecific antibody comprises an anti-CD3 arm comprising a second binding domain comprising a VL domain comprising an amino acid sequence having at least 95% (e.g., 95%, 96%, 97%, 98%, 99%, or 100%) sequence identity to the amino acid sequence of SEQ ID NO: 16. In some embodiments, the second binding arm comprises a VH domain comprising an amino acid sequence having at least 95% (e.g., 95%, 96%, 97%, 98%, 99%, or 100%) sequence identity to the amino acid sequence of SEQ ID NO: 15 and a VL domain comprising an amino acid sequence having at least 95% (e.g., 95%, 96%, 97%, 98%, 99%, or 100%) sequence identity to the amino acid sequence of SEQ ID NO: 16. In some embodiments, the second binding domain comprises a VH domain comprising an amino acid sequence of SEQ ID NO: 15 and a VL domain comprising an amino acid sequence of SEQ ID NO: 16.In some embodiments, the bispecific antibody comprises an aglycosylation site mutation. In some embodiments, the aglycosylation site mutation reduces effector function of the bispecific antibody. In some embodiments, the aglycosylation site mutation is a substitution mutation. In some embodiments, the bispecific antibody comprises a substitution mutation in the Fc region that reduces effector function.In some embodiments, the bispecific antibody is a monoclonal antibody. In some embodiments, the bispecific antibody is a humanized antibody. In some embodiments, the bispecific antibody is a chimeric antibody. In some embodiments, the bispecific antibody is a full-length antibody. In some embodiments, the bispecific antibody is an IgG antibody. In some embodiments, wherein the IgG antibody is an IgG 1 antibody.In some embodiments, the bispecific antibody comprises one or more heavy chain constant domains, wherein the one or more heavy chain constant domains are selected from a first CH1 (CH1?) domain, a first CH2 (CH2j) domain, a first CH3 (CH3y) domain, a second CH1 (CH12) domain, second CH2 (CH22) domain, and a second CH3 (CH32) domain. In some embodiments, at least one of the one or more heavy chain constant domains is paired with another heavy chain constant domain. In some embodiments, the CH3y and CH32domains each comprise a protuberance or cavity, and wherein the protuberance or cavity in the CH3y domain is positionable in the cavity or protuberance, respectively, in the CH32domain. In some embodiments, the CH3j and CH32domains meet at an interface between the protuberance and cavity. In some embodiments, the CH2j and CH22domains each comprise a protuberance or cavity, and wherein the protuberance or cavity in the CH2j domain is positionable in the cavity or protuberance, respectively, in the CH22domain. In some embodiments, the CH2j and CH22domains meet at an interface between said protuberance and cavity. In some embodiments, the anti-FcRH5 arm comprises the protuberance and the anti-CD3 arm comprises the cavity. In some embodiments, a CH3 domain of the anti-FcRH5 arm comprises a protuberance comprising a T366W amino acid substitution mutation (EU numbering) and a CH3 domain of the anti-CD3 arm comprises a cavity comprising T366S, L368A, and Y407V amino acid substitution mutations (EU numbering).In some embodiments, the bispecific antibody comprises an anti-FcRH5 arm comprising a heavy chain polypeptide (H1 ) and a light chain polypeptide (L1 ) and an anti-CD3 arm comprising a heavy chain polypeptide (H2) and a light chain polypeptide (L2), and wherein: (a) H1 comprises the amino acid sequence of SEQ ID NO: 35; (b) L1 comprises the amino acid sequence of SEQ ID NO: 36; (c) H2 comprises the amino acid sequence of SEQ ID NO: 37; and (d) L2 comprises the amino acid sequence of SEQ ID NO: 38.In some embodiments, the bispecific antibody is cevostamab.In some embodiments, the bispecific antibody is an antibody fragment that binds FcRH5 and CD3. In some embodiments, the antibody fragment is selected from the group consisting of Fab, Fab’-SH, Fv, scFv, and (Fab’)2 fragments.In some embodiments, the dosing regimen results in a CRS event in less than about 90% of a population of subjects (e.g., human subjects) having MM. In some embodiments, the dosing regimen results in a CRS event in less than about 68% of a population of subjects having MM. In some embodiments, the dosing regimen results in the CRS event in about 58% to about 90% (e.g., about 58%, about 59%, about 60%, about 61%, about 62%, about 63%, about 64%, about 65%, about 66%, about 67%, about 68%, about 69%, about 70%, about 71%, about 72%, about 73%, about 74%, about 75%, about 76%, about 77%, about 78%, about 79%, about 80%, about 81%, about 82%, about 83%, about 84%, about 85%, about 86%, about 87%, about 88%, about 89%, or about 90%) of the population of subjects having MM.In some embodiments, the dosing regimen results in the CRS event in about 58% to about 68% (e.g., about 58%, about 59%, about 60%, about 61%, about 62%, about 63%, about 64%, about 65%, about 66%, about 67%, or about 68%) of the population of subjects (e.g., human subjects) having MM.In some embodiments, the dosing regimen results in the CRS event in about 63% of the population of subjects (e.g., human subjects) having MM.In some embodiments, the dosing regimen results in a grade >2 CRS event in less than about 50% of a population of subjects (e.g., human subjects) having MM. In some embodiments, the dosing regimen results in a grade >2 CRS event in less than about 25% (e.g., about 1%, about 2%, about 3%, about 4%, about 5%, about 6%, about 7%, about 8%, about 9%, about 10%, about 11%, about 12%, about 13%, about 14%, about 15%, about 16%, about 17%, about 18%, about 19%, about 20%, about 21%, about 22%, about 23%, or about 24%) of a population of subjects having a MM. In some embodiments, the dosing regimen results in the grade >2 CRS event in about 10% to about 50% (e.g., about 10%, about 11%, about 12%, about 13%, about 14%, about 15%, about 16%, about 17%, about 18%, about 19%, about 20%, about 21%, about 22%, about 23%, about 24%, about 25%, about 26%, about 27%, about 28%, about 29%, about 30%, about 31%, about 32%, about 33%, about 34%, about 35%, about 36%, about 37%, about 38%, about 39%, about 40%, about 41%, about 42%, about 43%,about 44%, about 45%, about 46%, about 47%, about 48%, about 49%, or about 50%) of the population of subjects having MM.In some embodiments, the dosing regimen results in the grade >2 CRS event in about 17% of the population of subjects (e.g., human subjects) having MM.In some embodiments, the dosing regimen results in a grade >3 CRS event in less than about 10% (e.g., about 1%, about 2%, about 3%, about 4%, about 5%, about6%, about 7%, about 8%, about 9%, or about 10%) of a population of subjects (e.g., human subjects) having MM. In some embodiments, the dosing regimen results in the grade >3 CRS event in about 0% to about 5% (e.g., about 0%, about 1%, about 2%, about 3%, about 4%, or about 5%) of the population of subjects having MM.In some embodiments, the dosing regimen does not result in any grade >3 CRS event in the population of subjects having MM.In some embodiments, the bispecific antibody is administered to the subject as a monotherapy.In some embodiments, the bispecific antibody is administered to the subject as a combination therapy. In some embodiments, the bispecific antibody is administered to the subject concurrently with one or more additional therapeutic agents. In some embodiments, the bispecific antibody is administered to the subject prior to the administration of one or more additional therapeutic agents. In some embodiments, the bispecific antibody is administered to the subject subsequent to the administration of one or more additional therapeutic agents. In some embodiments, the one or more additional therapeutic agents comprise an effective amount of tocilizumab. In some embodiments, tocilizumab is administered to the subject by intravenous infusion. In some embodiments, the subject weighs > 100 kg, and tocilizumab is administered to the subject at a dose of 800 mg. In some embodiments, the subject weighs > 30 kg and < 100 kg, and tocilizumab is administered to the subject at a dose of 8 mg / kg. In other embodiments, the subject weighs < 30 kg, and tocilizumab is administered to the subject at a dose of 12 mg / kg. In some embodiments, tocilizumab is administered to the subject 2 hours before administration of the bispecific antibody. In some embodiments, the one or more additional therapeutic agents comprise an effective amount of pomalidomide, daratumumab, and / or a B-cell maturation antigen (BCMA)-directed therapy.In some embodiments, the bispecific antibody is administered to the subject by intravenous infusion.In some embodiments, the bispecific antibody is administered to the subject subcutaneously.In some embodiments, the subject has a CRS event, and the method further comprises treating the symptoms of the CRS event while suspending treatment with the bispecific antibody. In some embodiments, the method further comprises administering to the subject an effective amount of tocilizumab to treat the CRS event. In some embodiments, tocilizumab is administered intravenously to the subject as a single dose of about 8 mg / kg. In some embodiments, the CRS event does not resolve or worsens within 24 hours of treating the symptoms of the CRS event, and the method further comprises administering to the subject one or more additional doses of tocilizumab to manage the CRS event. In some embodiments, the one or more additional doses of tocilizumab are administered intravenously to the subject at a dose of about 8 mg / kg.In some embodiments, the one or more additional therapeutic agents comprises an effective amount of a corticosteroid. In some embodiments, the corticosteroid is administered intravenously to the subject. In some embodiments, the corticosteroid is methylprednisolone. In some embodiments, methylprednisolone is administered at a dose of about 80 mg. In some embodiments, the corticosteroid is dexamethasone. In some embodiments, dexamethasone is administered at a dose of about 20 mg.In some embodiments, the one or more additional therapeutic agents comprise an effective amount of acetaminophen or paracetamol. In some embodiments, acetaminophen or paracetamol is administered at a dose of between about 500 mg to about 1000 mg (e.g., about 500 mg, about 600 mg, about 700 mg, about 800 mg, about 900 mg, or about 1000 mg). In some embodiments, acetaminophen or paracetamol is administered orally to the subject.In some embodiments, the one or more additional therapeutic agents comprise an effective amount of diphenhydramine. In some embodiments, diphenhydramine is administered at a dose of between about 25 mg to about 50 mg (e.g., about 25 mg, about 26 mg, about 27 mg, about 28 mg, about 29 mg, about 30 mg, about 31 mg, about 32 mg, about 33 mg, about 34 mg, about 35 mg, about 36 mg, about 37 mg, about 38 mg, about 39 mg, about 40 mg, about 41 mg, about 42 mg, about 43 mg, about 44 mg, about 45 mg, about 46 mg, about 47 mg, about 48 mg, about 49 mg, or about 50 mg). In some embodiments, diphenhydramine is administered orally to the subject.In some embodiments, the MM is relapsed or refractory (R / R) MM. In some embodiments, the individual has received at least three prior lines of treatment for the MM. In some embodiments, the individual has received at least four prior lines of treatment for the MM. In some embodiments, the individual has been exposed to a prior treatment comprising a proteasome inhibitor, an IMiD, and / or an anti-CD38 therapeutic agent. In some embodiments, the proteasome inhibitor is bortezomib, carfilzomib, or ixazomib. In some embodiments, the IMiD is thalidomide, lenalidomide, or pomalidomide. In some embodiments, the anti-CD38 therapeutic agent is an anti-CD38 antibody. In some embodiments, the anti- CD38 antibody is daratumumab, MOR202, or isatuximab. In some embodiments, the anti-CD38 antibody is daratumumab.In some embodiments, the individual has been exposed to a prior treatment comprising an anti- SLAMF7 therapeutic agent, a nuclear export inhibitor, a histone deacetylase (HDAC) inhibitor, an autologous stem cell transplant (ASCT), a bispecific antibody, an antibody-drug conjugate (ADC), a CAR- T cell therapy, or a BCMA-directed therapy. In some embodiments, the anti-SLAMF7 therapeutic agent is an anti-SLAMF7 antibody. In some embodiments, the anti-SLAMF7 antibody is elotuzumab. In some embodiments, the nuclear export inhibitor is selinexor. In some embodiments, the HDAC inhibitor is panobinostat. In some embodiments, the BCMA-directed therapy is an antibody-drug conjugate targeting BCMA.In another aspect, the disclosure features a method of treating a subject having R / R MM, wherein the method comprises administering to the subject an effective amount of cevostamab in a dosing regimen comprising at least a first dosing cycle (C1 ), wherein the length of the first dosing cycle (C1 ) is 21 days, wherein the first dosing cycle (C1 ) comprises a first dose (C1 D1 ), a second dose (C1 D2), a third dose (C1 D3), and a fourth dose (C1 D4) of the bispecific antibody, wherein the C1 D1 is about 0.3 mg and is administered on Day 1 of C1 ; the C1 D2 is about 1 .2 mg and is administered on Day 2, Day 3, or Day 4of C1 ; the C1 D3 is about 3.6 mg and is administered on Day 8; and the C1 D4 is the effective amount of cevostamab and is administered on Day 9, Day 10, or Day 1 1 of C1 . In some embodiments, the C1 D4 is about 160 mg.In another aspect, the disclosure features a method of treating a subject having R / R MM, wherein the method comprises administering to the subject an effective amount of cevostamab in a dosing regimen comprising at least a first dosing cycle (C1 ), wherein the length of the first dosing cycle (C1 ) is 21 days, wherein the first dosing cycle (C1 ) comprises a first dose (C1 D1 ), a second dose (C1 D2), a third dose (C1 D3), and a fourth dose (C1 D4) of the bispecific antibody, wherein the C1 D1 is about 0.3 mg and is administered on Day 1 of C1 ; the C1 D2 is about 3.3 mg and is administered on Day 2, Day 3, or Day 4 of C1 ; the C1 D3 is about 7.2 mg and is administered on Day 8 of C1 ; and the C1 D4 is the effective amount of cevostamab and is administered on Day 9, Day 10, or Day 1 1 . In some embodiments, the C1 D4 is about 160 mg.In another aspect, the disclosure features a method of reducing the likelihood of CRS in a subject having R / R MM, wherein the method comprises administering to the subject cevostamab in a dosing regimen comprising at least a first dosing cycle (C1 ), wherein the length of the first dosing cycle (C1 ) is 21 days, wherein the first dosing cycle (C1 ) comprises a first dose (C1 D1 ), a second dose (C1 D2), and a third dose (C1 D3) of the bispecific antibody, wherein the C1 D1 is about 0.3 mg and is administered on Day 1 of C1 ; the C1 D2 is about 1 .2 mg and is administered on Day 2, Day 3, or Day 4 of C1 ; and the C1 D3 is about 3.6 mg and is administered on Day 8 of C1 .In another aspect, the disclosure features a method of reducing the likelihood of CRS in a subject having R / R MM, wherein the method comprises administering to the subject cevostamab in a dosing regimen comprising at least a first dosing cycle (C1 ), wherein the length of the first dosing cycle (C1 ) is 21 days, wherein the first dosing cycle (C1 ) comprises a first dose (C1 D1 ), a second dose (C1 D2), and a third dose (C1 D3) of the bispecific antibody, wherein the C1 D1 is about 0.3 mg and is administered on Day 1 ; the C1 D2 is about 3.3 mg and is administered on Day 2, Day 3, or Day 4; and the C1 D3 is about7.2 mg and is administered on Day 8.In another aspect, the disclosure features a method of achieving a median peak IL-6 level of less than about 30 pg / mL (e.g., about 10pg / mL, about 1 1 pg / mL, about 12pg / mL, about 13pg / mL, about 14pg / mL, about 15pg / mL, about 16pg / mL, about 17pg / mL, about 18pg / mL, about 19pg / mL, about 20pg / mL, about 21 pg / mL, about 22pg / mL, about 23pg / mL, about 24pg / mL, about 25pg / mL, about 26pg / mL, about 27pg / mL, about 28pg / mL, about 25pg / mL, about 26pg / mL, about 27pg / mL, about 28pg / mL, or about 29pg / mL) in a population of subjects having R / R MM, wherein the method comprises administering to a subject in the population cevostamab in a dosing regimen comprising at least a first dosing cycle (C1 ), wherein the length of the first dosing cycle (C1 ) is 21 days, wherein the first dosing cycle (C1 ) comprises a first dose (C1 D1 ), a second dose (C1 D2), and a third dose (C1 D3) of the bispecific antibody, wherein the C1 D1 is about 0.3 mg and is administered on Day 1 ; the C1 D2 is about1 .2 mg and is administered on Day 2, Day 3, or Day 4; and the C1 D3 is about 3.6 mg and is administered on Day 8.In another aspect, the disclosure features a method of treating a subject having R / R MM, wherein the method comprises administering to each subject an effective amount of cevostamab in a dosingregimen comprising at least a first dosing cycle (C1 ), wherein the length of the first dosing cycle (C1 ) is 21 days, wherein the first dosing cycle (C1 ) comprises a first dose (C1 D1 ), a second dose (C1 D2), and a third dose (C1 D3) of the bispecific antibody, wherein the C1 D1 is about 0.3 mg and is administered on Day 1 ; the C1 D2 is about 3.3 mg and is administered on Day 2, Day 3, or Day 4; the C1 D3 is about 160 mg and is administered on Day 8, and wherein an effective amount of tocilizumab is administered to the subject about 2 hours prior to administering the first dose of cevostamab.In another aspect, the disclosure features a method of treating a subject having R / R MM, wherein the method comprises administering to the subject an effective amount of cevostamab in a dosing regimen comprising at least a first dosing cycle (C1 ), wherein the length of the first dosing cycle (C1 ) is 21 days, wherein the first dosing cycle (C1 ) comprises a first dose (C1 D1 ), a second dose (C1 D2), and a third dose (C1 D3), wherein the C1 D1 is about 0.3 mg and is administered on Day 1 ; the C1 D2 is about 3.3 mg and is administered on Day 4; and the C1 D3 is about 160 mg and is administered on Day 8.In some embodiments of any of the foregoing aspects, the dosing regimen further comprises a second dosing cycle (C2) comprising a single dose (C2D1 ) of cevostamab, wherein the length of the C2 is 21 days, and wherein the C2D1 is an effective amount of cevostamab and is administered to the subject on Day 1 of the second dosing cycle. In some embodiments, the dosing regimen further comprises one or more additional dosing cycles, wherein the length of each of the one or more additional dosing cycles is 21 days, wherein each of the one or more additional dosing cycles comprises a single dose of the effective amount of cevostamab administered to the subject on Day 1 of each of the one or more additional dosing cycles.In another aspect, the disclosure features a method of reducing the occurrence of CRS events in a subject being treated for R / R MM with a target dose of cevostamab, the method comprising administering to the subject, prior to a first administration of the target dose to the subject in a dosing regimen comprising a first dosing cycle (C1 ), (i) a first dose (C1 D1 ), (ii) a second dose (C1 D2), and (iii) a third dose (C1 D3) of cevostamab, wherein the C1 D1 is about 0.3 mg and is administered on Day 1 ; the C1 D2 is about 1 .2 mg and is administered on Day 2, Day 3, or Day 4; and the C1 D3 is about 3.6 mg and is administered on Day 8, wherein the length of the C1 is 21 days.In another aspect, the disclosure features a method of reducing the occurrence of CRS events in a subject being treated for R / R MM with a target dose of cevostamab, the method comprising administering to the subject, prior to a first administration of the target dose to the subject in a dosing regimen comprising a first dosing cycle (C1 ), (i) a first dose (C1 D1 ), (ii) a second dose (C1 D2), and (iii) a third dose (C1 D3) of cevostamab, wherein the C1 D1 is about 0.3 mg and is administered on Day 1 ; the C1 D2 is about 3.3 mg and is administered on Day 2, Day 3, or Day 4; and the C1 D3 is about 7.2 mg and is administered on Day 8, wherein the length of the C1 is 21 days.In another aspect, the disclosure features a method of reducing the occurrence of CRS events in a subject being treated for R / R MM with a target dose of cevostamab, wherein, prior to a first administration of the target dose to the subject in a dosing regimen comprising a first dosing cycle (C1 ), the method comprises administering to the subject (i) a first dose (TS-C1 D1 ), (ii) a second dose (TS- C1 D2), and (iii) a third dose (TS-C1 D3) of cevostamab, wherein administering such target dose to a first plurality of such subjects results in a reduction in the number of subjects experiencing a CRS event afterfirst administration of the target dose, as compared to a second plurality of such subjects (e.g., human subjects) being treated for R / R MM with a target dose of cevostamab and administered such target dose after administration of a first dose (DS-C1 D1 ) and a second dose (DS-C1 D2), with no third dose (DS- C1 D3)of cevostamab, and wherein the TS-D1 D2 is greater than the TS-C1 D1 , the TS-C1 D3 is greater than the TS-C1 D2, and the DS-C1 D2 is greater than the DS-C1 D1 . In some embodiments, administering such target dose to the first plurality of such subjects results in at least a 10% reduction in the number of subjects experiencing a CRS event after first administration of the target dose. In some embodiments, administering such target dose to the first plurality of such subjects results in a 15% reduction in the number of subjects experiencing a CRS event after first administration of the target dose.In another aspect, the disclosure features a method of reducing the occurrence of CRS events in a subject being treated for R / R MM with a target dose of cevostamab, wherein, prior to a first administration of the target dose to the subject in a dosing regimen comprising a first dosing cycle (C1 ), the method comprises administering to the subject (i) a first dose (TS-C1 D1 ), (ii) a second dose (TS- C1 D2), and (iii) a third dose (TS-C1 D3) of cevostamab, wherein administering such target dose to a first plurality of such subjects results in a reduction in the number of subjects experiencing a CRS event during the C1 , as compared to a second plurality of subjects (e.g., human subjects) being treated for R / R MM with a target dose of cevostamab and administered such target dose after administration of a first dose (DS-C1 D1 ) and a second dose (DS-C1 D2), with no third dose of cevostamab, and wherein the TS- D1 D2 is greater than the TS-C1 D1 , the TS-C1 D3 is greater than the TS-C1 D2, and the DS-C1 D2 is greater than the DS-C1 D1 . In some embodiments, administering such target dose to the first plurality of such subjects results in at least a 10% reduction in the number of subjects experiencing a CRS event during the C1 . In some embodiments, administering such target dose to the first plurality of such subjects results in a 14% reduction in the number of subjects experiencing a CRS event during the C1 .In another aspect, the disclosure features a method of reducing the occurrence of CRS events in a subject being treated for R / R MM at an target dose of cevostamab, wherein, prior to a first administration of the target dose to the subject in a dosing regimen comprising a first dosing cycle (C1 ), the method comprises administering to the subject (i) a first dose (TS-C1 D1 ); (ii) a second dose (TS- C1 D2); and (iii) a third dose (TS-C1 D3) of cevostamab, wherein administering cevostamab in the C1 to a first plurality of such subjects results in a reduction in the number of CRS events experienced by each subject during the C1 , as compared to a second plurality of subjects administered the target dose of cevostamab after a first dose (DS-C1 D1 ) and a second dose (DS-C1 D2), but not a third dose (DS-C1 D3) of cevostamab, and wherein the TS-D1 D2 is greater than the TS-C1 D1 , the TS-C1 D3 is greater than the TS-C1 D2, and the DS-C1 D2 is greater than the DS-C1 D1 . In some embodiments, administering cevostamab in the C1 to the first plurality of such subjects results in at least a 30% reduction in the number of CRS events experienced by each subject during the C1 .In another aspect, the disclosure features a method of reducing the occurrence of CRS events in a subject being treated for R / R MM at a target dose of cevostamab, wherein, prior to first administration of the target dose to the subject in a first treatment cycle (C1 ), the subject is administered cevostamab at (i) a first dose (TS-C1 D1 ); (ii) a second dose (TS-C1 D2); and (iii) a third dose (TS-C1 D3), wherein administering cevostamab in the C1 to a first plurality of such subjects results in a reduction in thenumber of subjects requiring tocilizumab treatment for CRS during the C1 , as compared to a second plurality of subjects being treated for MM and administered a target dose of cevostamab after a first dose (DS-C1 D1 ) and a second dose (DS-C1 D2), but not a third dose (DS-C1 D3) of cevostamab, and wherein the TS-D1 D2 is greater than the TS-C1 D1 , and the TS-C1 D3 is greater than the TS-C1 D2, and the DS- C1 D2 is greater than the DS-C1 D1 . In some embodiments, administering cevostamab in the C1 to the first plurality of such subjects results in at least a 10% reduction in the number of subjects requiring tocilizumab treatment for CRS during the C1 .In another aspect, the disclosure features a method of pre-treating a subject for receiving a target dose of cevostamab, wherein the method comprises administering to the subject (i) a first dose (C1 D1 ), (ii) a second dose (C1 D2), and (iii) a third dose (C1 D3) of cevostamab, wherein the C1 D2 is greater than the C1 D1 , and the C1 D3 is greater than the C1 D2, wherein the risk of CRS events in the subject, after administration of the C1 D1 , C1 D2, and C1 D3 to the subject, is at a level that is safe for the subject to receive the target dose of cevostamab. In some embodiments following administration of the C1 D1 , C1 D2, and C1 D3 to the subject, the subject achieves a peak IL-6 level of less than about 80 pg / mL, thereby indicating that the risk of CRS events in the subject is at a level that is safe for the subject to receive the target dose of cevostamab. In some embodiments, the subject achieves a peak IL-6 level of less than about 30 pg / mL prior to the administration of the target dose of cevostamab. In some embodiments, the method further comprises administering to the pre-treated subject a target dose of cevostamab.In another aspect, the disclosure features a method of reducing the occurrence of CRS events in a subject being treated for R / R MM at a target dose of cevostamab, wherein, prior to a first administration of the target dose to the subject in a dosing regimen comprising a first dosing cycle (C1 ), the method comprises administering to the subject (i) a first dose (TS-C1 D1 ); (ii) a second dose (TS-C1 D2); and (iii) a third dose (TS-C1 D3) of cevostamab, wherein administering cevostamab in the C1 to a first plurality of such human subjects results in a reduction in the number of CRS events experienced by each subject during the C1 , as compared to a second plurality of subjects being treated for R / R MM and administered the target dose of cevostamab after a first dose (DS-C1 D1 ) and a second dose (DS-C1 D2), but not a third dose (DS-C1 D3) of cevostamab, and wherein the TS-D1 D2 is greater than the TS-C1 D1 , the TS-C1 D3 is greater than the TS-C1 D2, and the DS-C1 D2 is greater than the DS-C1 D1 . In some embodiments, administering cevostamab in the C1 to the first plurality of such subjects results in at least a 25% reduction in the number of CRS events experienced by each subject during the C1 .In another aspect, the disclosure features a method of reducing the occurrence of CRS events in a subject being treated for R / R MM at a target dose of cevostamab, wherein, prior to a first administration of the target dose to the subject in a dosing regimen comprising a first dosing cycle (C1 ), the method comprises administering to the subject (i) a first dose (TS-C1 D1 ); (ii) a second dose (TS-C1 D2); and (iii) a third dose (TS-C1 D3) of cevostamab, wherein administering cevostamab in the C1 to a first plurality of such subjects results in an increase in the number of subjects experiencing no CRS event during the C1 , as compared to a second plurality of subjects being treated for R / R MM and administered the target dose of cevostamab after a first dose (DS-C1 D1 ) and a second dose (DS-C1 D2), but not a third dose (DS- C1 D3) of cevostamab, and wherein the TS-D1 D2 is greater than the TS-C1 D1 , the TS-C1 D3 is greaterthan the TS-C1 D2, and the DS-C1 D2 is greater than the DS-C1 D1 . In some embodiments, administering cevostamab in the C1 to the first plurality of such subjects results in at least a 50% increase in the number of subjects experiencing no CRS event during the C1 .In another aspect, the disclosure features a method of reducing the occurrence of CRS events in a subject being treated for R / R MM at a target dose of cevostamab, wherein, prior to a first administration of the target dose to the subject in a dosing regimen comprising a first dosing cycle (C1 ), the method comprises administering to the subject (i) a first dose (TS-C1 D1 ); (ii) a second dose (TS-C1 D2); and (iii) a third dose (TS-C1 D3) of cevostamab, wherein administering cevostamab in the C1 to a first plurality of such subjects results in a reduction in the number of subjects experiencing Grade >2 CRS events during the C1 , as compared to a second plurality of subjects being treated for R / R MM and administered the target dose of cevostamab after a first dose (DS-C1 D1 ) and a second dose (DS-C1 D2), but not a third dose (DS-C1 D3) of cevostamab, and wherein the TS-D1 D2 is greater than the TS-C1 D1 , the TS-C1 D3 is greater than the TS-C1 D2, and the DS-C1 D2 is greater than the DS-C1 D1 . In some embodiments, administering cevostamab in the C1 to the first plurality of such subjects results in at least a 35% reduction in the number of subjects experiencing Grade >2 CRS events during the C1 .In another aspect, the disclosure features a method of reducing the occurrence of CRS events in a subject being treated for R / R MM at a target dose of cevostamab, wherein, prior to a first administration of the target dose to the subject in a dosing regimen comprising a first dosing cycle (C1 ), the method comprises administering to the subject (i) a first dose (TS-C1 D1 ); (ii) a second dose (TS-C1 D2); and (iii) a third dose (TS-C1 D3) of cevostamab, wherein administering cevostamab in the C1 to a first plurality of such subjects results in a reduction in the number of subjects experiencing at least two CRS events during the C1 , as compared to a second plurality of subjects being treated for R / R MM and administered the target dose of cevostamab after a first dose (DS-C1 D1 ) and a second dose (DS-C1 D2), but not a third dose (DS-C1 D3) of cevostamab, and wherein the TS-D1 D2 is greater than the TS-C1 D1 , the TS-C1 D3 is greater than the TS-C1 D2, and the DS-C1 D2 is greater than the DS-C1 D1 . In some embodiments, administering cevostamab in the C1 to the first plurality of such subjects results in at least a 50% reduction in the number of subjects experiencing at least two CRS events during the C1 .In some embodiments of any of the foregoing aspects, the subject is a human subject.In another aspect, the disclosure provides cevostamab for use in a method of reducing the likelihood of CRS in a subject (e.g., a human subject) having MM (e.g., R / R MM) and being administered an effective amount of cevostamab, wherein, prior to a first administration to the subject of an effective amount of cevostamab, cevostamab is to be administered to the subject in a dosing regimen comprising at least a first dosing cycle (C1 ), wherein the C1 comprises a first dose (C1 D1 ), a second dose (C1 D2), and a third dose (C1 D3) of cevostamab, wherein the C1 D1 is about 0.3 mg, the C1 D2 is between about 1 .2 mg to about 3.3 mg, and the C1 D3 is between about 3.6 mg to about 7.2 mg.In another aspect, the disclosure provides cevostamab for use in a method of reducing the likelihood of CRS in a subject (e.g., a human subject) having MM (e.g., R / R MM) and being administered an effective amount of cevostamab, wherein, prior to a first administration to the subject of the effective amount of cevostamab, cevostamab is to be administered to the subject in a dosing regimen comprising at least a first dosing cycle (C1 ), wherein the C1 comprises a first dose (C1 D1 ), a second dose (C1 D2),and a third dose (C1 D3) of cevostamab, wherein the C1 D1 is about 0.3 mg; the C1 D2 is about 1 .2 mg; and the C1 D3 is about 3.6 mg.In another aspect, the disclosure provides cevostamab for use in a method of reducing the likelihood of CRS in a subject (e.g., a human subject) having MM (e.g., R / R MM) and being administered an effective amount of cevostamab, wherein, prior to a first administration to the subject of the effective amount of cevostamab, cevostamab is to be administered to the subject in a dosing regimen comprising at least a first dosing cycle (C1 ), wherein the C1 comprises a first dose (C1 D1 ), a second dose (C1 D2), and a third dose (C1 D3) of cevostamab, wherein the C1 D1 is about 0.3 mg; the C1 D2 is about 3.3 mg; and the C1 D3 is about 7.2 mg.In yet another aspect, the disclosure provides cevostamab for use in a method of achieving a median peak IL-6 level of less than about 30 pg / mL in a population of subjects having a MM (e.g., a R / R MM) and being administered an effective amount of cevostamab, wherein, prior to the subject being administered the effective amount of cevostamab, cevostamab is to be administered to a subject in the population a dosing regimen comprising at least a first dosing cycle (C1 ), wherein the C1 comprises a first dose (C1 D1 ), a second dose (C1 D2), and a third dose (C1 D3) of cevostamab, wherein the C1 D1 is about 0.3 mg, the C1 D2 is between about 1 .2 mg to about 3.3 mg, and the C1 D3 is between about 3.6 mg to about 7.2 mg.In yet another aspect, the disclosure provides cevostamab for use in a method of achieving a peak IL-6 level of less than about 30 pg / mL in a subject (e.g., a human subject) having a MM (e.g., a R / R MM) and being administered an effective amount of cevostamab, wherein prior to the subject being administered the effective amount of cevostamab, cevostamab is to be administered to the subject in a dosing regimen comprising at least a first dosing cycle (C1 ), wherein the C1 comprises a first dose (C1 D1 ), a second dose (C1 D2), and a third dose (C1 D3) of cevostamab, wherein the C1 D1 is about 0.3, the C1 D2 is between about 1 .2 mg to about 3.3 mg, and the C1 D3 is between about 3.6 mg to about 7.2 mg.In yet another aspect, the disclosure provides cevostamab for use in a method of treating a subject (e.g., a human subject) having MM (e.g., R / R MM), wherein an effective amount of cevostamab is to be administered to the subject in a dosing regimen comprising at least a first dosing cycle (C1 ), wherein the C1 comprises a first dose (C1 D1 ), a second dose (C1 D2), a third dose (C1 D3), and a fourth dose (C1 D4) of cevostamab, wherein the C1 D1 is about 0.3 mg, the C1 D2 is about 1 .2 mg to about 3.3 mg (e.g., about 1 .2 mg or about 3.3 mg), the C1 D3 is about 3.6 mg to about 7.2 mg (e.g., about 3.6 mg or about 7.2 mg), and the C1 D4 is between about 20 mg to about 252 mg (e.g., about 160 mg).In another aspect, the disclosure provides cevostamab for use in a method of treating a subject (e.g., a human subject) having MM (e.g., R / R MM), wherein an effective amount of cevostamab is to be administered to the subject in a dosing regimen comprising at least a first dosing cycle (C1 ), wherein the C1 comprises a first dose (C1 D1 ), a second dose (C1 D2), a third dose (C1 D3), and a fourth dose (C1 D4) of cevostamab, wherein the C1 D1 is about 0.3 mg; the C1 D2 is about 1 .2 mg; the C1 D3 is about 3.6 mg; and the C1 D4 is about 160 mg.In another aspect, the disclosure provides cevostamab for use in a method of treating a subject (e.g., a human subject) having MM (e.g., R / R MM), wherein an effective amount of cevostamab is to beadministered to the subject in a dosing regimen comprising at least a first dosing cycle (C1 ), wherein the C1 comprises a first dose (C1 D1 ), a second dose (C1 D2), a third dose (C1 D3), and a fourth dose (C1 D4) of cevostamab, the C1 D1 is about 0.3 mg; the C1 D2 is about 3.3 mg; the C1 D3 is about 7.2 mg; and the C1 D4 is about 160 mg.In yet another aspect, the disclosure provides cevostamab for use in a method of treating a subject (e.g., a human subject) having an R / R MM, an effective amount of cevostamab is to be administered to the subject in a dosing regimen comprising at least a first dosing cycle (C1 ), wherein the length of the C1 is 21 days, wherein the C1 comprises a first dose (C1 D1 ), a second dose (C1 D2), a third dose (C1 D3), and a fourth dose (C1 D4) of cevostamab, wherein the C1 D1 is about 0.3 mg and is to be administered on Day 1 of C1 ; the C1 D2 is about 1 .2 mg and is to be administered on Day 2, Day 3, or Day 4 of C1 ; the C1 D3 is about 3.6 mg and is to be administered on Day 8 of C1 ; and the C1 D4 is the effective amount of cevostamab and is to be administered on Day 9, Day 10, or Day 11 of C1 .In another aspect, the disclosure provides cevostamab for use in a method of treating a subject (e.g., a human subject) having an R / R MM, wherein an effective amount of cevostamab is to be administered to the subject in a dosing regimen comprising at least a first dosing cycle (C1 ), wherein the length of the C1 is 21 days, wherein the C1 comprises a first dose (C1 D1 ), a second dose (C1 D2), a third dose (C1 D3), and a fourth dose (C1 D4) of cevostamab, wherein the C1 D1 is about 0.3 mg and is to be administered on Day 1 ; the C1 D2 is about 3.3 mg and is to be administered on Day 2, Day 3, or Day 4; the C1 D3 is about 7.2 mg and is to be administered on Day 8; and the C1 D4 is the effective amount of cevostamab and is to be administered on Day 9, Day 10, or Day 11 .In another aspect, the disclosure provides cevostamab for use in a method reducing the likelihood of CRS in a subject having an R / R MM and being administered an effective amount of cevostamab, wherein, prior to a first administration to the subject of the effective amount of cevostamab, cevostamab is to be administered to the subject in a dosing regimen comprising at least a first dosing cycle (C1 ), wherein the length of the C1 is 21 days, wherein the C1 comprises a first dose (C1 D1 ), a second dose (C1 D2), and a third dose (C1 D3) of cevostamab, wherein the C1 D1 is about 0.3 mg and is to be administered on Day 1 ; the C1 D2 is about 1 .2 mg and is to be administered on Day 2, Day 3, or Day 4; and the C1 D3 is about 3.6 mg and is to be administered on Day 8.In another aspect, the disclosure provides cevostamab for use in a method of achieving a median peak IL-6 level of less than about 30 pg / mL in a population of subjects having an R / R MM and being administered an effective amount of cevostamab, wherein prior to being administered the effective amount of cevostamab, each subject in the population is to be administered a dosing regimen comprising at least a first dosing cycle (C1 ), wherein the length of the C1 is 21 days, wherein the C1 comprises a first dose (C1 D1 ), a second dose (C1 D2), and a third dose (C1 D3) of cevostamab, wherein the C1 D1 is about 0.3 mg and is to be administered on Day 1 ; the C1 D2 is about 1 .2 mg and is to be administered on Day 2, Day 3, or Day 4; and the C1 D3 is about 3.6 mg and is to be administered on Day 8.In another aspect, the disclosure provides cevostamab for use in a method of treating a subject having an R / R MM, wherein an effective amount of cevostamab is to be administered to the subject in a dosing regimen comprising at least a first dosing cycle (C1 ), wherein the length of the C1 is 21 days, wherein the C1 comprises a first dose (C1 D1 ), a second dose (C1 D2), and a third dose (C1 D3) ofcevostamab, wherein the C1 D1 is about 0.3 mg and is to be administered on Day 1 ; the C1 D2 is about 1 .2 mg and is to be administered on Day 2, Day 3, or Day 4; the C1 D3 is about 3.6 mg and is to be administered on Day 8, and wherein an effective amount of tocilizumab is to be administered to the subject about 2 hours prior to administration of the first dose of cevostamab.In another aspect, the disclosure provides cevostamab for use in a method of treating a subject having an R / R MM, wherein an effective amount of cevostamab is to be administered to the subject in a dosing regimen comprising at least a first dosing cycle (C1 ), wherein the length of the C1 is 21 days, wherein the C1 comprises a first dose (C1 D1 ), a second dose (C1 D2), and a third dose (C1 D3), wherein the C1 D1 is about 0.3 mg and is to be administered on Day 1 ; the C1 D2 is about 3.3 mg and is to be administered on Day 4; and the C1 D3 is about 160 mg and is to be administered on Day 8.In another aspect, the disclosure provides cevostamab for use in a method of reducing the occurrence of CRS events in a subject being treated for an R / R MM with a target dose of cevostamab, wherein prior to a first administration of the target dose to the subject, cevostamab is to be administered to the subject in a dosing regimen comprising a first dosing cycle (C1 ) comprising (i) a first dose (C1 D1 ), (ii) a second dose (C1 D2), and (iii) a third dose (C1 D3) of cevostamab, wherein the C1 D1 is about 0.3 mg and is to be administered on Day 1 ; the C1 D2 is about 1 .2 mg and is to be administered on Day 2, Day 3, or Day 4; and the C1 D3 is about 3.6 mg and is to be administered on Day 8, wherein the length of the C1 is 21 days.In another aspect, the disclosure provides cevostamab for use in a method of reducing the occurrence of CRS events in a subject being treated for a R / R MM with a target dose of cevostamab, wherein prior to a first administration of the target dose to the subject, cevostamab is to be administered to the subject in a dosing regimen comprising a first dosing cycle (C1 ) comprising (i) a first dose (C1 D1 ), (ii) a second dose (C1 D2), and (iii) a third dose (C1 D3) of cevostamab, wherein the C1 D1 is about 0.3 mg and is to be administered on Day 1 ; the C1 D2 is about 3.3 mg and is to be administered on Day 2, Day 3, or Day 4; and the C1 D3 is about 7.2 mg and is to be administered on Day 8, wherein the length of the C1 is 21 days.In another aspect, the disclosure provides cevostamab for use in a method of reducing the occurrence of CRS events in a subject being treated for R / R MM with a target dose of cevostamab, wherein, prior to a first administration of the target dose to the subject, cevostamab is to be administered to the subject in a dosing regimen comprising a first dosing cycle (C1 ) comprising (i) a first dose (TS- C1 D1 ), (ii) a second dose (TS-C1 D2), and (iii) a third dose (TS-C1 D3) of cevostamab, wherein administering such target dose to a first plurality of such subjects results in a reduction in the number of subjects experiencing a CRS event after first administration of the target dose, as compared to a second plurality of subjects (e.g., human subjects) being treated for R / R MM with a target dose of cevostamab and administered such target dose after administration of a first dose (DS-C1 D1 ) and a second dose (DS- C1 D2), with no third dose of cevostamab, and wherein the TS-D1 D2 is greater than the TS-C1 D1 , the TS-C1 D3 is greater than the TS-C1 D2, and the DS-C1 D2 is greater than the DS-C1 D1 .In another aspect, the disclosure provides cevostamab for use in a method of reducing the occurrence of CRS events in a subject being treated for MM at an target dose of cevostamab, wherein, prior to a first administration of the target dose to the subject, cevostamab is to be administered to thesubject in a dosing regimen comprising a first dosing cycle (C1 ) comprising (i) a first dose (TS-C1 D1 ); (ii) a second dose (TS-C1 D2); and (iii) a third dose (TS-C1 D3) of cevostamab, wherein administration of cevostamab in the C1 to a first plurality of such subjects results in a reduction in the number of CRS events experienced by each subject during the C1 , as compared to a second plurality of subjects administered the target dose of cevostamab after a first dose (DS-C1 D1 ) and a second dose (DS-C1 D2), but not a third dose of cevostamab, and wherein the TS-D1 D2 is greater than the TS-C1 D1 , the TS-C1 D3 is greater than the TS-C1 D2, and the DS-C1 D2 is greater than the DS-C1 D1 .In another aspect, the disclosure provides cevostamab for use in a method of reducing the occurrence of CRS events in a subject being treated for R / R MM at a target dose of cevostamab, wherein, prior to first administration of the target dose to the subject, cevostamab is to be administered to the subject in a first treatment cycle (C1 ) comprising (i) a first dose (TS-C1 D1 ); (ii) a second dose (TS- C1 D2); and (iii) a third dose (TS-C1 D3), wherein administration of cevostamab in the C1 to a first plurality of such subjects results in a reduction in the number of subjects requiring tocilizumab treatment for CRS during the C1 , as compared to a second plurality of subjects being treated for MM and administered a target dose of cevostamab after a first dose (DS-C1 D1 ) and a second dose (DS-C1 D2), but not a third dose of cevostamab, and wherein the TS-D1 D2 is greater than the TS-C1 D1 , and the TS-C1 D3 is greater than the TS-C1 D2, and the DS-C1 D2 is greater than the DS-C1 D1 .In another aspect, the disclosure features cevostamab for use in a method of pre-treating a subject for receiving a target dose of cevostamab, wherein cevostamab is to be administered to the subject as (i) a first dose (C1 D1 ), (ii) a second dose (C1 D2), and (iii) a third dose (C1 D3) of cevostamab, wherein the C1 D2 is greater than the C1 D1 , and the C1 D3 is greater than the C1 D2, wherein the risk of CRS events in the subject, after administration of the C1 D1 , C1 D2, and C1 D3 to the subject, is at a level that is safe for the subject to receive the target dose of cevostamab.In another aspect, the disclosure features cevostamab for use in a method of reducing the occurrence of CRS events in a subject being treated for R / R MM at a target dose of cevostamab, wherein, prior to a first administration of the target dose to the subject in a dosing regimen comprising a first dosing cycle (C1 ), cevostamab is to be administered to the subject as (i) a first dose (TS-C1 D1 ); (ii) a second dose (TS-C1 D2); and (iii) a third dose (TS-C1 D3), wherein administration of cevostamab in the C1 to a first plurality of such human subjects results in a reduction in the number of CRS events experienced by each subject during the C1 , as compared to a second plurality of subjects being treated for R / R MM and administered the target dose of cevostamab after a first dose (DS-C1 D1 ) and a second dose (DS-C1 D2), but not a third dose (DS-C1 D3) of cevostamab, and wherein the TS-D1 D2 is greater than the TS-C1 D1 , the TS-C1 D3 is greater than the TS-C1 D2, and the DS-C1 D2 is greater than the DS- C1 D1 .In yet another aspect, the disclosure provides cevostamab for use in a method of reducing the occurrence of CRS events in a subject being treated for R / R MM at a target dose of cevostamab, wherein, prior to a first administration of the target dose to the subject in a dosing regimen comprising a first dosing cycle (C1 ), cevostamab is to be administered to the subject as (i) a first dose (TS-C1 D1 ); (ii) a second dose (TS-C1 D2); and (iii) a third dose (TS-C1 D3) of cevostamab, wherein administration cevostamab in the C1 to a first plurality of such subjects results in a reduction in the number of subjectsexperiencing Grade >2 CRS events during the C1 , as compared to a second plurality of subjects being treated for R / R MM and administered the target dose of cevostamab after a first dose (DS-C1 D1 ) and a second dose (DS-C1 D2), but not a third dose of cevostamab, and wherein the TS-D1 D2 is greater than the TS-C1 D1 , the TS-C1 D3 is greater than the TS-C1 D2, and the DS-C1 D2 is greater than the DS-C1 D1 .In another aspect, the disclosure provides cevostamab for use in a method of reducing the occurrence of CRS events in a subject being treated for R / R MM at a target dose of cevostamab, wherein, prior to a first administration of the target dose to the subject in a dosing regimen comprising a first dosing cycle (C1 ), cevostamab is to be administered to the subject as (i) a first dose (TS-C1 D1 ); (ii) a second dose (TS-C1 D2); and (iii) a third dose (TS-C1 D3) of cevostamab, wherein administration of cevostamab in the C1 to a first plurality of such subjects results in a reduction in the number of subjects experiencing at least two CRS events during the C1 , as compared to a second plurality of subjects being treated for R / R MM and administered the target dose of cevostamab after a first dose (DS-C1 D1 ) and a second dose (DS-C1 D2), but not a third dose of cevostamab, and wherein the TS-D1 D2 is greater than the TS-C1 D1 , the TS-C1 D3 is greater than the TS-C1 D2, and the DS-C1 D2 is greater than the DS-C1 D1 .In another aspect, the disclosure provides a use of cevostamab in a manufacture of a medicament for reducing the likelihood of CRS in a subject (e.g., a human subject) having MM (e.g., R / R MM), wherein the medicament is formulated for administration in a dosing regimen prior to a first administration of an effective amount of cevostamab to the subject, wherein the dosing regimen comprises at least a first dosing cycle (C1 ), wherein the C1 comprises a first dose (C1 D1 ), a second dose (C1 D2), and a third dose (C1 D3) of cevostamab, wherein the C1 D1 is about 0.3 mg, the C1 D2 is between about 1 .2 mg to about 3.3 mg, and the C1 D3 is between about 3.6 mg to about 7.2 mg.In another aspect, the disclosure provides a use of cevostamab in a manufacture of a medicament for reducing the likelihood of CRS in a subject (e.g., a human subject) having MM (e.g., R / R MM) and being administered an effective amount of cevostamab, wherein the medicament is formulated for administration in a dosing regimen prior to a first administration of an effective amount of cevostamab to the subject, wherein the dosing regimen comprises at least a first dosing cycle (C1 ), wherein the C1 comprises a first dose (C1 D1 ), a second dose (C1 D2), and a third dose (C1 D3) of cevostamab, wherein the C1 D1 is about 0.3 mg; the C1 D2 is about 1 .2 mg; and the C1 D3 is about 3.6 mg.In another aspect, the disclosure provides a use of cevostamab in a manufacture of a medicament for reducing the likelihood of CRS in a subject (e.g., a human subject) having MM (e.g., R / R MM) and being administered an effective amount of cevostamab, wherein the medicament is formulated for administration in a dosing regimen prior to a first administration of an effective amount of cevostamab to the subject, wherein the dosing regimen comprises at least a first dosing cycle (C1 ), wherein the C1 comprises a first dose (C1 D1 ), a second dose (C1 D2), and a third dose (C1 D3) of cevostamab, wherein the C1 D1 is about 0.3 mg; the C1 D2 is about 3.3 mg; and the C1 D3 is about 7.2 mg.In yet another aspect, the disclosure provides a use of cevostamab in a manufacture of a medicament for achieving a median peak IL-6 level of less than about 30 pg / mL in a population of subjects having a MM (e.g., a R / R MM) and being administered an effective amount of cevostamab, wherein the medicament is formulated for administration to a subject in the population in a dosing regimen prior to the subject being administered the effective amount of cevostamab, wherein the dosingregimen comprises at least a first dosing cycle (C1 ), wherein the C1 comprises a first dose (C1 D1 ), a second dose (C1 D2), and a third dose (C1 D3) of cevostamab, wherein the C1 D1 is about 0.3 mg, the C1 D2 is between about 1 .2 mg to about 3.3 mg, and the C1 D3 is between about 3.6 mg to about 7.2 mg.In yet another aspect, the disclosure provides a use of cevostamab in a manufacture of a medicament for achieving a peak IL-6 level of less than about 30 pg / mL in a subject (e.g., a human subject) having a MM (e.g., a R / R MM) and being administered an effective amount of cevostamab, wherein the medicament is formulated for administration to a subject in a dosing regimen prior to the subject being administered the effective amount of cevostamab, wherein the dosing regimen comprises at least a first dosing cycle (C1 ), wherein the C1 comprises a first dose (C1 D1 ), a second dose (C1 D2), and a third dose (C1 D3) of cevostamab, wherein the C1 D1 is about 0.3, the C1 D2 is between about 1 .2 mg to about 3.3 mg, and the C1 D3 is between about 3.6 mg to about 7.2 mg.In yet another aspect, the disclosure provides a use of cevostamab in the manufacture of a medicament for treating a subject (e.g., a human subject) having MM (e.g., R / R MM), wherein the medicament is formulated for administration to the subject in an effective amount in a dosing regimen comprising at least a first dosing cycle (C1 ), wherein the C1 comprises a first dose (C1 D1 ), a second dose (C1 D2), a third dose (C1 D3), and a fourth dose (C1 D4) of cevostamab, wherein the C1 D1 is about 0.3 mg, the C1 D2 is about 1 .2 mg to about 3.3 mg (e.g., about 1 .2 mg or about 3.3 mg), the C1 D3 is about 3.6 mg to about 7.2 mg (e.g., about 3.6 mg or about 7.2 mg), and the C1 D4 is between about 20 mg to about 252 mg (e.g., about 160 mg).In another aspect, the disclosure provides a use of cevostamab in a manufacture of a medicament for treating a subject (e.g., a human subject) having MM (e.g., R / R MM), wherein the medicament is formulated for administration to the subject in an effective amount in a dosing regimen comprising at least a first dosing cycle (C1 ), wherein the C1 comprises a first dose (C1 D1 ), a second dose (C1 D2), a third dose (C1 D3), and a fourth dose (C1 D4) of cevostamab, wherein the C1 D1 is about 0.3 mg; the C1 D2 is about 1 .2 mg; the C1 D3 is about 3.6 mg; and the C1 D4 is about 160 mg.In another aspect, the disclosure provides a use of cevostamab in a manufacture of a medicament for treating a subject (e.g., a human subject) having MM (e.g., R / R MM), wherein the medicament is formulated for administration to the subject in an effective amount in a dosing regimen comprising at least a first dosing cycle (C1 ), wherein the C1 comprises a first dose (C1 D1 ), a second dose (C1 D2), a third dose (C1 D3), and a fourth dose (C1 D4) of cevostamab, the C1 D1 is about 0.3 mg; the C1 D2 is about 3.3 mg; the C1 D3 is about 7.2 mg; and the C1 D4 is about 160 mg.In yet another aspect, the disclosure provides a use of cevostamab in a manufacture of a medicament for treating a subject (e.g., a human subject) having an R / R MM, wherein the medicament is formulated for administration to the subject in an effective amount in a dosing regimen comprising at least a first dosing cycle (C1 ), wherein the length of the C1 is 21 days, wherein the C1 comprises a first dose (C1 D1 ), a second dose (C1 D2), a third dose (C1 D3), and a fourth dose (C1 D4) of cevostamab, wherein the C1 D1 is about 0.3 mg and is to be administered on Day 1 of C1 ; the C1 D2 is about 1 .2 mg and is to be administered on Day 2, Day 3, or Day 4 of C1 ; the C1 D3 is about 3.6 mg and is to be administered on Day 8 of C1 ; and the C1 D4 is the effective amount of cevostamab and is to be administered on Day 9, Day 10, or Day 11 of C1 .In another aspect, the disclosure provides use of cevostamab in a manufacture of a medicament for treating a subject (e.g., a human subject) having an R / R MM, wherein the medicament is formulated for administration to the subject in an effective amount in a dosing regimen comprising at least a first dosing cycle (C1 ), wherein the length of the C1 is 21 days, wherein the C1 comprises a first dose (C1 D1 ), a second dose (C1 D2), a third dose (C1 D3), and a fourth dose (C1 D4) of cevostamab, wherein the C1 D1 is about 0.3 mg and is to be administered on Day 1 ; the C1 D2 is about 3.3 mg and is to be administered on Day 2, Day 3, or Day 4; the C1 D3 is about 7.2 mg and is to be administered on Day 8; and the C1 D4 is the effective amount of cevostamab and is to be administered on Day 9, Day 10, or Day 11 .In another aspect, the disclosure provides a use of cevostamab in a manufacture of a medicament for reducing the likelihood of CRS in a subject having an R / R MM and being administered an effective amount of cevostamab, wherein the medicament is formulated for administration in a dosing regimen prior to a first administration to the subject of the effective amount of cevostamab, wherein the dosing regimen comprises at least a first dosing cycle (C1 ), wherein the length of the C1 is 21 days, wherein the C1 comprises a first dose (C1 D1 ), a second dose (C1 D2), and a third dose (C1 D3) of cevostamab, wherein the C1 D1 is about 0.3 mg and is to be administered on Day 1 ; the C1 D2 is about1 .2 mg and is to be administered on Day 2, Day 3, or Day 4; and the C1 D3 is about 3.6 mg and is to be administered on Day 8.In another aspect, the disclosure provides a use of cevostamab in a manufacture of a medicament for reducing the likelihood of CRS in a subject having an R / R MM and being administered an effective amount of cevostamab, wherein the medicament is formulated for administration in a dosing regimen prior to a first administration to the subject of the effective amount of cevostamab, wherein the dosing regimen comprises at least a first dosing cycle (C1 ), wherein the length of the C1 is 21 days, wherein the C1 comprises a first dose (C1 D1 ), a second dose (C1 D2), and a third dose (C1 D3) of cevostamab, wherein the C1 D1 is about 0.3 mg and is to be administered on Day 1 ; the C1 D2 is about3.3 mg and is to be administered on Day 2, Day 3, or Day 4; and the C1 D3 is about 7.2 mg and is to be administered on Day 8.In another aspect, the disclosure provides a use of cevostamab in a manufacture of a medicament for achieving a median peak IL-6 level of less than about 30 pg / mL in a population of subjects having an R / R MM and being administered an effective amount of cevostamab, wherein the medicament is formulated for administration in a dosing regimen prior to administration of the effective amount of cevostamab to each subject in the population, wherein the dosing regimen comprises at least a first dosing cycle (C1 ), wherein the length of the C1 is 21 days, wherein the C1 comprises a first dose (C1 D1 ), a second dose (C1 D2), and a third dose (C1 D3) of cevostamab, wherein the C1 D1 is about 0.3 mg and is to be administered on Day 1 ; the C1 D2 is about 1 .2 mg and is to be administered on Day 2, Day 3, or Day 4; and the C1 D3 is about 3.6 mg and is to be administered on Day 8.In another aspect, the disclosure provides a use of cevostamab in a manufacture of a medicament for treating a subject having an R / R MM, wherein the medicament is formulated for administration in a dosing regimen comprising at least a first dosing cycle (C1 ), wherein the length of the C1 is 21 days, wherein the C1 comprises a first dose (C1 D1 ), a second dose (C1 D2), and a third dose (C1 D3) of cevostamab, wherein the C1 D1 is about 0.3 mg and is to be administered on Day 1 ; the C1 D2is about 3.3 mg and is to be administered on Day 2, Day 3, or Day 4; the C1 D3 is about 7.2 mg and is to be administered on Day 8, and wherein an effective amount of tocilizumab is to be administered to the subject about 2 hours prior to administering the first dose of cevostamab.In another aspect, the disclosure provides a use of cevostamab in a manufacture of a medicament for treating a subject having an R / R MM, wherein the medicament is formulated for administration to the subject in a dosing regimen comprising at least a first dosing cycle (C1 ), wherein the length of the C1 is 21 days, wherein the C1 comprises a first dose (C1 D1 ), a second dose (C1 D2), and a third dose (C1 D3), wherein the C1 D1 is about 0.3 mg and is to be administered on Day 1 ; the C1 D2 is about 1 .2 mg and is to be administered on Day 2, Day 3, or Day 4; the C1 D3 is about 3.6 mg and is to be administered on Day 8, and wherein an effective amount of tocilizumab is to be administered to the subject about 2 hours prior to administration of the first dose of cevostamab.In another aspect, the disclosure provides a use of cevostamab in a manufacture of a medicament for reducing the occurrence of CRS events in a subject being treated for an R / R MM with a target dose of cevostamab, wherein the medicament is formulated for administration in a dosing regimen prior to a first administration of the target dose to the subject, wherein the dosing regimen comprises a first dosing cycle (C1 ) comprising (i) a first dose (C1 D1 ), (ii) a second dose (C1 D2), and (iii) a third dose (C1 D3) of cevostamab, wherein the C1 D1 is about 0.3 mg and is to be administered on Day 1 ; the C1 D2 is about 1 .2 mg and is to be administered on Day 2, Day 3, or Day 4; and the C1 D3 is about 3.6 mg and is to be administered on Day 8, wherein the length of the C1 is 21 days.In another aspect, the disclosure provides a use of cevostamab in a manufacture of a medicament for reducing the occurrence of CRS events in a subject being treated for a R / R MM with a target dose of cevostamab, wherein the medicament is formulated for administration in a dosing regimen prior to a first administration of the target dose to the subject, wherein the dosing regimen comprises a first dosing cycle (C1 ) comprising (i) a first dose (C1 D1 ), (ii) a second dose (C1 D2), and (iii) a third dose (C1 D3) of cevostamab, wherein the C1 D1 is about 0.3 mg and is to be administered on Day 1 ; the C1 D2 is about 3.3 mg and is to be administered on Day 2, Day 3, or Day 4; and the C1 D3 is about 7.2 mg and is to be administered on Day 8, wherein the length of the C1 is 21 days.In another aspect, the disclosure provides a use of cevostamab in a manufacture of a medicament for reducing the occurrence of CRS events in a subject being treated for R / R MM with a target dose of cevostamab, wherein the medicament is formulated for administration to the subject prior to a first administration of the target dose in a first dosing cycle (C1 ) comprising (i) a first dose (TS-C1 D1 ), (ii) a second dose (TS-C1 D2), and (iii) a third dose (TS-C1 D3) of cevostamab, wherein administration of such target dose to a first plurality of such subjects results in a reduction in the number of subjects experiencing a CRS event after first administration of the target dose, as compared to a second plurality of subjects (e.g., human subjects) being treated for R / R MM with a target dose of cevostamab and administered such target dose after administration of a first dose (DS-C1 D1 ) and a second dose (DS- C1 D2), with no third dose of cevostamab, and wherein the TS-D1 D2 is greater than the TS-C1 D1 , the TS-C1 D3 is greater than the TS-C1 D2, and the DS-C1 D2 is greater than the DS-C1 D1 .In another aspect, the disclosure provides a use of cevostamab in a manufacture of a medicament for reducing the occurrence of CRS events in a subject being treated for MM at a target doseof cevostamab, wherein the medicament is formulated for administration prior to a first administration of the target dose to the subject, and is formulated for administration to the subject in a first dosing cycle (C1 ) comprising (i) a first dose (TS-C1 D1 ); (ii) a second dose (TS-C1 D2); and (iii) a third dose (TS-C1 D3) of cevostamab, wherein the administration of cevostamab in the C1 to a first plurality of such subjects results in a reduction in the number of CRS events experienced by each subject during the C1 , as compared to a second plurality of subjects administered the target dose of cevostamab after a first dose (DS-C1 D1 ) and a second dose (DS-C1 D2), but not a third dose of cevostamab, and wherein the TS- D1 D2 is greater than the TS-C1 D1 , the TS-C1 D3 is greater than the TS-C1 D2, and the DS-C1 D2 is greater than the DS-C1 D1 .In another aspect, the disclosure provides a use of cevostamab in a manufacture of a medicament for reducing the occurrence of CRS events in a subject being treated for MM at a target dose of cevostamab, wherein the medicament is formulated for administration in a first treatment cycle (C1 ) prior to first administration of the target dose to the subject, wherein C1 comprises (i) a first dose (TS- C1 D1 ); (ii) a second dose (TS-C1 D2); and (iii) a third dose (TS-C1 D3), wherein administration of cevostamab in the C1 to a first plurality of such subjects results in a reduction in the number of subjects requiring tocilizumab treatment for CRS during the C1 , as compared to a second plurality of subjects administered a target dose of cevostamab after a first dose (DS-C1 D1 ) and a second dose (DS-C1 D2), but not a third dose of cevostamab, and wherein the TS-D1 D2 is greater than the TS-C1 D1 , and the TS- C1 D3 is greater than the TS-C1 D2, and the DS-C1 D2 is greater than the DS-C1 D1 .In another aspect, the disclosure provides a use of cevostamab in a manufacture of a medicament for reducing the occurrence of CRS events in a subject being treated for R / R MM at a target dose of cevostamab, wherein the medicament is formulated for administration in a first treatment cycle (C1 ) prior to first administration of the target dose to the subject, wherein C1 comprises (i) a first dose (TS-C1 D1 ); (ii) a second dose (TS-C1 D2); and (iii) a third dose (TS-C1 D3), wherein administration of cevostamab in the C1 to a first plurality of such subjects results in a reduction in the number of subjects requiring tocilizumab treatment for CRS during the C1 , as compared to a plurality of subjects being treated for MM and administered a target dose of cevostamab after a first dose (DS-C1 D1 ) and a second dose (DS-C1 D2), but not a third dose of cevostamab, and wherein the TS-D1 D2 is greater than the TS- C1 D1 , and the TS-C1 D3 is greater than the TS-C1 D2, and the DS-C1 D2 is greater than the DS-C1 D1 .In another aspect, the disclosure features a use of cevostamab in a manufacture of a medicament for pre-treating a subject for receiving a target dose of cevostamab, whreein the medicament is formulated for administration to the subject as (i) a first dose (C1 D1 ), (ii) a second dose (C1 D2), and (iii) a third dose (C1 D3) of cevostamab, wherein the C1 D2 is greater than the C1 D1 , and the C1 D3 is greater than the C1 D2, wherein the risk of CRS events in the subject, after administration of the C1 D1 , C1 D2, and C1 D3 to the subject, is at a level that is safe for the subject to receive the target dose of cevostamab.In another aspect, the disclosure features a use of cevostamab in the manufacture of a medicament for reducing the occurrence of CRS events in a subject being treated for R / R MM at a target dose of cevostamab, wherein, the medicament is formulated for administration to the subject prior to a first administration of the target dose to the subject in a dosing regimen comprising a first dosing cycle(C1 ), and wherein the medicament is formulated for administration to the subject as (i) a first dose (TS- C1 D1 ); (ii) a second dose (TS-C1 D2); and (iii) a third dose (TS-C1 D3), wherein administration of cevostamab in the C1 to a first plurality of such human subjects results in a reduction in the number of CRS events experienced by each subject during the C1 , as compared to a second plurality of subjects being treated for R / R MM and administered the target dose of cevostamab after a first dose (DS-C1 D1 ) and a second dose (DS-C1 D2), but not a third dose (DS-C1 D3) of cevostamab, and wherein the TS- D1 D2 is greater than the TS-C1 D1 , the TS-C1 D3 is greater than the TS-C1 D2, and the DS-C1 D2 is greater than the DS-C1 D1 .In another aspect, the disclosure provides a use of cevostamab in a manufacture of a medicament for reducing the occurrence of CRS events in a subject being treated for R / R MM at a target dose of cevostamab, wherein the medicament is formulated for administration prior to a first administration of the target dose to the subject in a dosing regimen comprising a first dosing cycle (C1 ), and wherein the medicament is formulated for administration to the subject as (i) a first dose (TS-C1 D1 ); (ii) a second dose (TS-C1 D2); and (iii) a third dose (TS-C1 D3) of cevostamab, wherein administration of cevostamab in the C1 to a first plurality of such subjects results in an increase in the number of subjects experiencing no CRS event during the C1 , as compared to a second plurality of subjects being treated for R / R MM and administered the target dose of cevostamab after a first dose (DS-C1 D1 ) and a second dose (DS-C1 D2), but not a third dose of cevostamab, and wherein the TS-D1 D2 is greater than the TS-C1 D1 , the TS-C1 D3 is greater than the TS-C1 D2, and the DS-C1 D2 is greater than the DS-C1 D1 .In yet another aspect, the disclosure provides a use of cevostamab in a manufacture of a medicament for reducing the occurrence of CRS events in a subject being treated for R / R MM at a target dose of cevostamab, wherein the medicament is formulated for administration prior to a first administration of the target dose to the subject in a dosing regimen comprising a first dosing cycle (C1 ), and wherein the medicament is formulated for administration to the subject as (i) a first dose (TS-C1 D1 ); (ii) a second dose (TS-C1 D2); and (iii) a third dose (TS-C1 D3) of cevostamab, wherein administration cevostamab in the C1 to a first plurality of such subjects results in a reduction in the number of subjects experiencing Grade >2 CRS events during the C1 , as compared to a second plurality of subjects being treated for R / R MM and administered the target dose of cevostamab after a first dose (DS-C1 D1 ) and a second dose (DS-C1 D2), but not a third dose of cevostamab, and wherein the TS-D1 D2 is greater than the TS-C1 D1 , the TS-C1 D3 is greater than the TS-C1 D2, and the DS-C1 D2 is greater than the DS-C1 D1 .In another aspect, the disclosure provides a use of cevostamab in a manufacture of a medicament for reducing the occurrence of CRS events in a subject being treated for R / R MM at a target dose of cevostamab, wherein the medicament is formulated for administration prior to a first administration of the target dose to the subject in a dosing regimen comprising a first dosing cycle (C1 ), and wherein the medicament is formulated for administration to the subject as (i) a first dose (TS-C1 D1 ); (ii) a second dose (TS-C1 D2); and (iii) a third dose (TS-C1 D3) of cevostamab, wherein administration of cevostamab in the C1 to a first plurality of such subjects results in a reduction in the number of subjects experiencing at least two CRS events during the C1 , as compared to a second plurality of subjects being treated for R / R MM and administered the target dose of cevostamab after a first dose (DS-C1 D1 ) and asecond dose (DS-C1 D2), but not a third dose of cevostamab, and wherein the TS-D1 D2 is greater than the TS-C1 D1 , the TS-C1 D3 is greater than the TS-C1 D2, and the DS-C1 D2 is greater than the DS-C1 D1 .BRIEF DESCRIPTION OF THE DRAWINGSThe accompanying drawings are included to illustrate embodiments of the disclosure and further an understanding of its implementations.FIG. 1 is a schematic diagram showing dose escalation schedules for triple step-up dose escalation Arm H1 and Arm H2 of Study GO39775, as described in Example 1 . C: cycle; D: day; Q21 : every 3 weeks (or 21 -days).FIGS. 2A-2C are schematic diagrams showing the dose escalation schedules and suitable doses for the single step-up (FIG. 2A), double step-up (FIG. 2B), and triple step-up (FIG. 2C) dosing regimens described herein. Doses are depicted in milligrams.FIG. 3 is a schematic diagram showing an exemplary triple step-up dose-escalation scenario for Arm H1 and Arm H2 across three different cohorts of Study GO39775, as described further in Example 1 . Doses are depicted in milligrams (mg). Asterisks (*) indicate hypothetical scenarios for dose exploration.FIGS. 4A-4B are Sankey plots showing the proportion of patients that experienced no cytokine release syndrome (CRS), Grade 1 CRS, Grade 2 CRS, or Grade 3 CRS in Arms H1 and Arm 11 (FIG. 4A) or Arm H2 and Arm I2 (FIG. 4B) of the triple step-up regimen in Study GO39775, as described further in Example 1 . The CRS grade (e.g., Grade 1 , Grade 2, or no CRS), tocilizumab (toci) administration (e.g., yes or no), and no administered dose of cevostamab (“No Dose”) is also shown for each patient.T= five patients with Grade 1 CRS and treated with tocilizumab were not accounted for by the clinical cutoff date.FIG. 5 is a table showing the number (n) and proportion of patients that experienced one or more CRS events and the grade of the highest CRS event in all cycles of the indicated dose-escalation regimen in Study GO39775, as described further in Example 1 . SS = single step-up dosing; DS = double step-up dosing; TS = triple step-up dosing; SU = step-up.FIG. 6 is a table showing rates of CRS events in patients across all cycles of the indicated doseescalation regimen at the clinical cutoff date of October 9, 2023. CRS grade (Gr), number of CRS events, average number of events per patient, and proportion of CRS events with tocilizumab (TCZ) treatment is also shown.T= five patients with Grade 1 CRS and treated with tocilizumab were not accounted for by the clinical cutoff date. *** = one Grade 3 CRS, 1 Gr4 CRS.FIG. 7 is a box-and-whiskers plot showing peak interleukin-6 (IL-6) levels following the 3.3 mg or 3.6 mg step-up dose across different dose-escalation treatment regimens in Study GO39775, as described further in Example 1 . Peak IL-6 levels are depicted as nanograms per liter (ng / L). Sample size (n), median peak IL-6 levels, and the range of peak IL-6 levels are depicted below the plot. SS = single step-up; DS = double step-up; TS = triple step-up.FIG. 8 are tables presenting the efficacy of the indicated Arms in Study GO39775. sCR = stringent complete response; SD = stable disease; VGPR = very good partial response; MR = minimal response; SD = stable disease; PD = progressive disease; ORR = objective response rate. ORR is defined as the proportion of patients who achieved sCR, CR, VGPR, or PR as determined by investigatorassessment according to the International Myeloma Working Group (IMWG) response criteria. Nonresponse includes MR, SD, and PD. * = Cohort B and G utilize same dose / schedule but enrollment occurred ~ 14 months apart. # = High proportion of PD as best overall response (BOR) noted for H1 / I1 .FIGS. 9A-9B is a set of exposure-response (E-R) plots showing the exposure-efficacy relationship of cevostamab for the probability of occurrence of partial response (PR) or better and the average concentrations at cycle 3 (Cavg, cycle 3; FIG. 9A) or the minimum concentrations at cycle 3 (Cmin, cycle 3; FIG. 9B) across the pooled single step-up, double step-up, and triple step-up dosing regimens. The E-R plot is divided into four intervals denoted by dashed vertical lines, which indicate the quartiles of the exposure metric. Filled circles shown at 0% and 100% probabilities represent the observed data across the cohorts using pooled data from the step-up dosing regimens. Black error bars represent the standard error for quartiles of exposure, plotted at the median value within each quartile. The shaded area of the curve represents the 90% confidence intervals (Cis), and the dashed lines bordering the shaded area median of fitted logistic regression model from 1 ,000 bootstrap samples. Horizontal bars in the graph below represent the population pharmacokinetic model-predicted exposures represented by geometric mean and 90% Cis at the planned dose cohorts of 500 simulations at each cohort. AIC = Akaike information criterion; EC50 = half-maximal effective concentration; EC90 = 90% maximal effective concentrationFIGS. 10A-10B is a set of E-R plots showing the exposure-efficacy relationship of cevostamab for the probability of very good partial response or better (>VGPR) rates and Cavg, cycle 3 (FIG. 10A) or Cmin, cycle 3 (FIG. 10B) the across the pooled single step-up, double step-up, and triple step-up dosing regimens.FIGS. 11A-11B is a set of E-R plots showing the exposure-efficacy relationship of cevostamab for the probability of occurrence of PR or better (FIG. 11 A) or >VGPR rates (FIG. 11 B) and Cavg, cycle 3. Arrow 2 is pointing to a datapoint that represents the observed probability of the occurrence of PR or better or >VGPR rates plotted at the estimated geometric mean of Cavg, cycle 3 at 160 mg administered every three weeks in Study CO43476 (n=23); error bars represent the Wald’s 90% Cis for said observed probability. Arrow 1 is pointing to a datapoint that represents the observed probability of the occurrence of PR or better or >VGPR rates plotted at the estimated geometric mean of Cavg, cycle 3 at the 160 mg target dose administered every three weeks in Study GO39775 (N=152); error bars represent the Wald’s 90% Cis for said observed probability. The E-R plot is divided into five intervals denoted by dashed vertical lines, which indicate the quintiles of the exposure metric.FIGS. 12A-12B is a set of E-R plots showing the exposure-safety relationship of cevostamab for the probability of occurrence of all-grade CRS events and the maximum concentration following the step- up dose administration on cycle 1 day 1 (Cmax at C1 D1 ; FIG. 12A) or the maximum concentration following the first target dose administration (Cmax, cycle 1 target dose; FIG. 12B) across the pooled single step-up, double step-up, and triple step-up dosing regimens, in which the target dose was administered on Day 8 for the single step-up regimen, Day 9-11 for the double step-up regimen, and Day 15 for the triple step-up regimen. Gr+1 = Grade 1 or higher event.FIGS. 13A-13B is a set of E-R plots showing the exposure-safety relationship of cevostamab for the probability of occurrence of Grade >2 CRS events and Cmax at C1 D1 (FIG. 13A) or Cmax, cyle 1target dose (FIG. 13B) across the pooled single step-up, double step-up, and triple step-up dosing regimens described in Study GO39775. Gr2+ = Grade 2 or higher event.FIGS. 14A-14B is a set of E-R plots showing the exposure-safety relationship of cevostamab for the probability of occurrence of Grade >3 neutropenia and the maximum concentration following the step- up dose administration on C1 D1 (Cmax, step-up dose; FIG. 14A) or the maximum concentration following the target dose administration at cycle 3 (Cmax at C3; FIG. 14B) across the pooled single step-up, double step-up, and triple step-up dosing regimens described in Study GO39775. Gr3+ = Grade 3 or higher event.FIGS. 15A-15B is a set of E-R plots showing the exposure-safety relationship of cevostamab for the probability of occurrence of Grade >3 anemia and Cmax, step-up dose (FIG. 15A) or Cmax at C3 (FIG. 15B) across the pooled single step-up, double step-up, and triple step-up dosing regimens described in Study GO39775.FIGS. 16A-16B is a set of E-R plots showing the exposure-safety relationship of cevostamab for the probability of occurrence of Grade >3 thrombocytopenia (TCP) and Cmax, step-up dose (FIG. 16A) or Cmax at C3 (FIG. 16B) across the pooled single step-up, double step-up, and triple step-up dosing regimens described in Study GO39775.FIGS. 17A-17B is a set of E-R plots showing the exposure-safety relationship of cevostamab for the probability of occurrence of Grade >3 lymphopenia and Cmax, step-up dose (FIG. 17A) or Cmax at C3 (FIG. 17B) across the pooled single step-up, double step-up, and triple step-up dosing regimens described in Study GO39775.FIGS. 18A-18B is a set of E-R plots showing the exposure-safety relationship of cevostamab for the probability of occurrence of Grade >3 infections and Cmax, step-up dose (FIG. 18A) or Cmax at C3 (FIG. 18B) across the pooled single step-up, double step-up, and triple step-up dosing regimens described in Study GO39775.FIGS. 19A-19B is a set of E-R plots showing the exposure-safety relationship of cevostamab for the probability of occurrence of a severe adverse event (SAE) and Cmax, step-up dose (FIG. 19A) or Cmax at C3 (FIG. 19B) across the pooled single step-up, double step-up, and triple step-up dosing regimens described in Study GO39775.FIGS. 20A-20B is a set of E-R plots showing the exposure-safety relationship of cevostamab for the probability of occurrence of a Grade >3 adverse event (AE) and Cmax, step-up dose (FIG. 20A) or Cmax at C3 (FIG. 20B) across the pooled single step-up, double step-up, and triple step-up dosing regimens described in Study GO39775.FIGS. 21A-21B is a set of E-R plots showing the exposure-safety relationship of cevostamab for the probability of occurrence of an AE that leads to a dose modification and Cmax, step-up dose (FIG. 21 A) or Cmax at C3 (FIG. 21 B) across the pooled single step-up, double step-up, and triple step-up dosing regimens described in Study GO39775. A dose modification included a dose interruption, reduction, or discontinuation.FIG. 22 is an E-R plot showing the exposure-safety relationship of cevostamab for the probability of occurrence of Grade >3 infections and the average concentrations at cycle 3 (Cavg at C3). Arrow 2 is pointing to a datapoint that represents the observed probability of the occurrence of Grade >3 infectionsplotted at the estimated geometric mean of Cavg at C3 at 160 mg administered every three weeks in Study CO43476 (n=25); error bars represent the Wald’s 90% Cis for said observed probability. Arrow 1 is pointing to a datapoint that represents the observed probability of the occurrence of Grade >3 infections plotted at the estimated geometric mean of Cavg at C3 at the 160 mg target dose administered every three weeks in Study GO39775 (1X1=159); error bars represent the Wald’s 90% Cis for said observed probability.FIG. 23 is an E-R plot showing the exposure-safety relationship of cevostamab for the probability of occurrence of an SAE at Cavg at C3. Arrow 2 is pointing to a datapoint that represents the observed probability of the occurrence of SAEs plotted at the estimated geometric mean of Cavg at C3 at 160 mg administered every three weeks in Study CO43476 (n=25); error bars represent the Wald’s 90% Cis for said observed probability. Arrow 1 is pointing to a datapoint that represents the observed probability of the occurrence of SAEs plotted at the estimated geometric mean of Cavg at C3 at the 160 mg target dose administered every three weeks in Study GO39775 (N=159); error bars represent the Wald’s 90% Cis for said observed probability.FIG. 24 is a set of heatmaps that shows the maximum IL-6 peak ratio of the indicated triple step- up dosing regimen (e.g., 0.3 mg / 1 .2 mg / 3.6 mg followed by 160 mg of cevostamab) compared to a single step-up dosing regimen. A schematic diagram of the indicated doses and schedule is shown on the left of each heatmap. D1 = Day 1 ; D2 = Day 2; D3 = Day 3; D4 = Day 4; D8 = Day 8; D9 = Day 9; D10 = Day 10; D11 = Day 11.FIG. 25 is a set of heatmaps that shows the maximum IL-6 peak ratio of the indicated double step-up dosing regimen (e.g., 0.3 mg / 3.6 mg followed by 160 mg of cevostamab (left); or 0.3 mg / 3.3 mg followed by 160 mg of cevostamab (right)) compared to a single step-up dosing regimen. A schematic diagram of the indicated doses and schedule are shown to the left of each heatmap. D1 = Day 1 ; D2 = Day 2; D3 = Day 3; D4 = Day 4; D8 = Day 8; D15 = Day 15.FIG. 26 is a schematic diagram illustrating the overview of the QSP model calibration and validation workflow. Cyno = cynomolgus monkey; DScomp = compressed double step-up dosing regimen (e.g., Arm K); SS = single step-up; DS = double step-up; r / r = relaped or refractory; TDB = T-cell dependent bispecific antibody; Ph = PhaseFIG. 27 is a series of plots showing the model simulation results for IL-6 peak levels of digital twins and patients in each indicated dosing regimen cevostamab treatment cohort. Black line indicates median IL-6 peak concentrations, and the shaded region indicates the 5,h-95,hpercentile of simulation of digital twins. LLOQ: lower-limit of quantification of observed IL-6 concentrations; NPTNM: number of patients in the cohort; Ndigitai twin : number of digital twins corresponding to the patients in the cohort, in which there were 100 digital twins per patient.FIG. 28 is a graph showing the peak IL-6 levels following administration of cevostamab at the indicated C1 D1 step-up doses. The horizontal line indicates the median predicted IL-6 peak levels in the virtual population (8,400 digital twins) of the QSP model, and the shaded bar represents the 90% prediction interval. Filled circles represent observed data used for calibration of the model, and hollow circles represent observed data for validation of the QSP model. Filled diamonds represent the geometricmean of the observed data for the calibration data, and the hollow diamonds represent the geometric mean of the observed data for the validation data.FIG. 29 is a graph showing peak IL-6 levels following administration of the 3.6 mg step-up dose of cevostamab in the single step-up dosing regimen.FIG. 30 is a graph showing peak IL-6 levels following administration of the 3.3 mg or 3.6 mg dose of cevostamab in the indicated step-up dosing regimens.FIG. 31 is a graph showing peak IL-6 levels following administration of the target dose of cevostamab in the indicated step-up dosing regimensFIG. 32 is a series of graphs showing peak IL-6 levels at various days of the indicated dosing regimens. The solid lines indicate median IL-6 levels in the virtual population (8,400 digital twins) of the QSP model, and the shaded region in the graphs represents the 90% prediction interval.FIGS. 33A-33C are a series of forest plots showing the predicted impact of baseline characteristics on steady-state cevostamab exposure based on a 160 mg target dose, in which FIG. 33A shows the steady-state area under the curve (AUC) of cevostamab, FIG. 33B shows the steady-state maximum serum concentrations (Cmax) of cevostamab, and FIG. 33C shows the steady-state minimum serum concentrations (Cmin) of cevostamab.FIGS. 34A-34B are a set of box-and-whisker plots showing the relationship between anti-drug antibody (ADA) titer and dose-normalized Cmin of cevostamab (FIG. 34A) or dose-normalized Cmax of cevostamab (FIG. 34B) across the indicated doses in ADA-negative (ADA-) patients, patients with an ADA titer <4 (low titer), and patients with an ADA titer >4 (high titer).FIGS. 35A-35B are a set of graphs showing the relationship between the observed M-protein blood levels (FIG. 35A) and the observed free-light chain blood levels (FIG. 35B) over time in response to the indicated target dose levels of cevostamab. Dashed lines indicate the median protein levels, and the shaded region represents the 90% Cis. Individual data points and corresponding dashed lines represent individual patient paraprotein dynamics.FIGS. 36A-36B are a set of forest plots showing the predicted impact of baseline characteristics on the M-protein growth rate (FIG. 36A) or M-protein decay half-life as measured in days (FIG. 36B).FIGS. 37A-37B are a set of forest plots showing the predicted impact of baseline characteristics on free-light chain growth rate (FIG. 37A) and free-light chain decay half-life as measured in days (FIG. 37B).FIG. 38 is a graph showing the predicted paraprotein levels over time. FLC: free-light chain; MCPROT: M-protein.FIGS. 39A-39B are a set of graphs showing the posterior predictive check (PPC) of the tumor growth inhibition model based on the overall response rate (FIG. 39A), in which there was at least a 50% decrease of paraprotein reduction at nadir, and VGPR response rate (FIG. 39B), in which VGPR is classified as at least a 90% decrease of paraprotein reduction at nadir, at the indicated target dose levels. Data points without numbers represent the median prediction, and error bars represent the 90% prediction interval. Data points with numbers (n, number of patients) represents observed patient responses in Study GO39775.FIGS. 40A-40B are a set of graphs showing the PPC of the tumor growth inhibition model based on the overall response rate (FIG. 40A) and VGPR response rate (FIG. 40B) at the indicated dose priming sequence of doses in Study GO39775. Data points without numbers represent the median prediction, and error bars represent the 90% prediction interval. Data points with numbers (n, number of patients) represents observed patient responses in Study GO39775.FIGS. 41A-41B are a set of graphs showing the PPC of the tumor growth inhibition model based on the overall response rate (FIG. 41 A) and VGPR response rate (FIG. 41 B) at the indicated single step- up dose priming sequence of doses in Study GO39775.FIGS. 42A-42B are a set of graphs showing the PPC of the tumor growth inhibition model based on the overall response rate (FIG. 42A) and VGPR response rate (FIG. 42B) at the indicated dose priming sequence of doses in Study GO39775.FIGS. 43A-43C are schematic diagrams showing the possible single-step (SS), double-step (DS), and triple-step (TS) dosing regimens from the GO39775 Phase I dose-escalation study. Dose levels are in milligrams. A total of 324 patients were enrolled in the cevostamab monotherapy study (FIG. 43A), 167 patients were enrolled in the 160 mg target dose (TD) study (FIG. 43B), and 30 patients were enrolled in the cycle 1 (C1 ) 0.3mg / 1 .2 mg / 3.6 mg triple step-up plus 160mg TD study (FIG. 43C).FIG. 44 is a table outlining the baseline characteristics of patients enrolled in the GO39775 Phase I dose-escalation study. Most patients enrolled had heavily pretreated and highly refractory disease, while more than 50% of patients had received a prior BCMA-targeted therapy. * = includes t(4;14), t(14;16) and del(17p); t = >1 IMiD, >1 PI and >1 anti-CD38 antibody; t = &2 IMiDs, >2 Pls and >1 anti-CD38 antibody; data cut-off: Aug 22, 2024; HR, high risk.FIG. 45 is a flow chart outlining the treatment disposition of the 167 patients that were enrolled in the 160 mg target dose (TD) study.FIG. 46 is a table (left) and graph (right) characterizing adverse effects that were observed in the GO39775 Phase I dose-escalation study. * = includes time after completion and / or discontinuation of treatment when AE reporting was limited to 90 days after the last dose of study drug or until initiation of another anti-cancer therapy, whichever occurred first, and to treatment-related SAEs thereafter; f = excludes 16 patients with Gr 5 AE of PD; $ = HLH (n=2) and pseudomonal sepsis in the context of DIC (n=1); §group term: neutropenia, neutrophil count decreased and febrile neutropenia; fl = group term: thrombocytopenia and platelet count decreased; data cut-off: Aug 22, 2024; ALT, alanine transaminase; DIC, disseminated intravascular coagulation; Gr, Grade; HLH, hemophagocytic lymphohistiocytosis; PT, Preferred Term; SAE, serious AE.FIG. 47 is a set of tables summarizing adverse events (AE) of infection at the 160 mg target dose (TD) in the 167 patients that were enrolled in the 160 mg target dose (TD) study. * = System Organ Class level term; data cut-off: Aug 22, 2024; URI, upper respiratory tract infection; UTI, urinary tract infection.FIG. 48 is a table (left) and bar graph (right) summarizing cytokine release syndrome (CRS) events that occurred in the 30 patients were enrolled in the cycle 1 (C1 ) 0.3mg / 1 .2 mg / 3.6 mg triple step- up plus 160mg TD study. Gr, Grade. * = Gr 2 CRS in 1 patient in C2 only; t = D3 or D4 depending on the emergence of CRS with the previous administration; $ = D10 or D11 ; data cut-off: Aug 22, 2024.FIG. 49 is a bar graph summarizing the overall response rate (ORR) of patients at the 160 mg target dose (TD) level. * = <10-5 level by NGS; f = all patients were in VGPR or better (VGPR+); $ = subgroups are not mutually exclusive; § = unvalidated analysis; data cut-off: Aug 22, 2024; CR, complete response; MRD, minimal residual disease; NGS, next generation sequencing; ORR, overall response rate; PR, partial response; sCR, stringent CR; VGPR, very good PR; BsAb, bispecific antibody.FIG. 50 is a graph showing the durability of response of patients at the 160 mg target dose (TD) level. * = unvalidated analysis; data cut-off: Aug 22, 2024; DoR, duration of response; mDoR, median DoR.FIG. 51 is a graph showing the durability of response after completion of cevostamab treatment in patients administered the 160mg target dose (TD) of cevostamab.FIGS. 52A-52B are plots showing the best ORR in all patients and in those with or without prior BCMA-targeted therapies who received cevostamab at the 160 mg TD level (FIG. 52A) and duration of response among patients in PR, PR or better (PR+) or VGPR+ who received cevostamab at the 160 mg target-dose level (FIG. 52B).FIG. 53 is a flow chart outlining the treatment disposition of the 324 patients that were enrolled in the 160 mg TD study described in Example 7.FIG. 54 is a plot showing the PK profile of cevostamab within the indicated cohorts.FIG. 55 shows a series of box and whisker plots demonstrating the relationship between patient response and FcRH5 expression levels on myeloma cells that were collected at baseline in patients who received cevostamab treatment at the 160 mg TD. Myeloma cells were collected by bone marrow aspiration. Bone marrow aspirates that were considered hemodiluted by the study pathologists were not included in the analysis. FcRH5 expression was assessed by flow cytometry (FC).FIG. 56 is a line graph of progression-free survival (PFS) among patients who received cevostamab at the 160 mg TD, as described in Example 7.FIGS. 57A-57D are Sankey plots showing the proportion of patients that experienced no CRS, Grade 1 CRS, Grade 2 CRS, or Grade 3 CRS in Arm A, Arm C, and Arm F of the single step-up regimen (FIG. 57A), in Arm B and Arm D of the double step-up regimen (FIG. 57B), in Arm B and Arm G of the double step-up regimen (FIG. 57C), and in Arm K of the double step-up regimen (FIG. 57D) in Study GO39775. The CRS grade (e.g., Grade 1 , Grade 2, or no CRS), tocilizumab (toci) administration (e.g., yes or no), and no administered dose of cevostamab (“No Dose”) is also shown for each patient.DETAILED DESCRIPTIONI. DEFINITIONSThe term “about” as used herein refers to the usual error range for the respective value readily known to the skilled person in this technical field. Reference to “about” a value or parameter herein includes (and describes) aspects that are directed to that value or parameter per se.It is understood that aspects of the disclosure described herein include “comprising,” “consisting,” and “consisting essentially of” aspects.The term “FcRH5” or “fragment crystallizable receptor-like 5,” as used herein, refers to any native FcRH5 from any vertebrate source, including mammals such as primates (e.g. humans) and rodents(e.g., mice and rats), unless otherwise indicated, and encompasses “full-length,” unprocessed FcRH5, as well as any form of FcRH5 that results from processing in the cell. The term also encompasses naturally occurring variants of FcRH5, including, for example, splice variants or allelic variants. FcRH5 includes, for example, human FcRH5 protein (UniProtKB / Swiss-Prot ID: Q96RD9.3), which is 977 amino acids in length.The terms “anti-FcRH5 antibody” and “an antibody that binds to FcRH5” refer to an antibody that is capable of binding FcRH5 with sufficient affinity such that the antibody is useful as a diagnostic and / or therapeutic agent in targeting FcRH5. In one embodiment, the extent of binding of an anti-FcRH5 antibody to an unrelated, non-FcRH5 protein is less than about 10% of the binding of the antibody to FcRH5 as measured, e.g., by a radioimmunoassay (RIA). In certain embodiments, an antibody that binds to FcRH5 has a dissociation constant (KD) of < 1 pM, < 250 nM, < 100 nM, < 15 nM, < 10 nM, < 6 nM, < 4 nM, < 2 nM, < 1 nM, < 0.1 nM, < 0.01 nM, or < 0.001 nM (e.g. 10-8M or less, e.g. from 10-8M to 10-13M, e.g., from 10-9M to 10-13M). In certain embodiments, an anti-FcRH5 antibody binds to an epitope of FcRH5 that is conserved among FcRH5 from different species.The term “cluster of differentiation 3” or “CD3,” as used herein, refers to any native CD3 from any vertebrate source, including mammals such as primates (e.g. humans) and rodents (e.g., mice and rats), unless otherwise indicated, including, for example, CD3e, CD3y, CD3a, and CD3p chains. The term encompasses “full-length,” unprocessed CD3 (e.g., unprocessed or unmodified CD3e or CD3y), as well as any form of CD3 that results from processing in the cell. The term also encompasses naturally occurring variants of CD3, including, for example, splice variants or allelic variants. CD3 includes, for example, human CD3e protein (NCBI RefSeq No. NP_000724), which is 207 amino acids in length, and human CD3y protein (NCBI RefSeq No. NP_000064), which is 182 amino acids in length.The terms “anti-CD3 antibody” and “an antibody that binds to CD3” refer to an antibody that is capable of binding CD3 with sufficient affinity such that the antibody is useful as a diagnostic and / or therapeutic agent in targeting CD3. In one embodiment, the extent of binding of an anti-CD3 antibody to an unrelated, non-CD3 protein is less than about 10% of the binding of the antibody to CD3 as measured, e.g., by a radioimmunoassay (RIA). In certain embodiments, an antibody that binds to CD3 has a dissociation constant (KD) of < 1 pM, < 250 nM, < 100 nM, < 15 nM, < 10 nM, < 5 nM, < 1 nM, < 0.1 nM, < 0.01 nM, or < 0.001 nM (e.g. 10-8M or less, e.g. from 10-8M to 10-13M, e.g., from 10-9M to 10-13M). In certain embodiments, an anti-CD3 antibody binds to an epitope of CD3 that is conserved among CD3 from different species.For the purposes herein, “cevostamab,” also referred to as BFCR4350A or RO7187797, is an Fc- engineered, humanized, full-length non-glycosylated lgG1 kappa T-cell-dependent bispecific antibody (TDB) that binds FcRH5 and CD3 and comprises an anti-FcRH5 arm comprising the heavy chain polypeptide sequence of SEQ ID NO: 35 and the light chain polypeptide sequence of SEQ ID NO: 36 and an anti-CD3 arm comprising the heavy chain polypeptide sequence of SEQ ID NO: 37 and the light chain polypeptide sequence of SEQ ID NO: 38. Cevostamab comprises a threonine to tryptophan amino acid substitution at position 366 on the heavy chain of the anti-FcRH5 arm (T366W) using EU numbering of Fc region amino acid residues and three amino acid substitutions (tyrosine to valine at position 407, threonine to serine at position 366, and leucine to alanine at position 368) on the heavy chain of the anti-CD3 arm (Y407V, T366S, and L368A) using EU numbering of Fc region amino acid residues to drive heterodimerization of the two arms (half-antibodies). Cevostamab also comprises an amino acid substitution (asparagine to glycine) at position 297 on each heavy chain (N297G) using EU numbering of Fc region amino acid residues, which results in a non-glycosylated antibody that has minimal binding to Fc (Fey) receptors and, consequently, prevents Fc-effector function. Cevostamab is also described in WHO Drug Information (International Nonproprietary Names for Pharmaceutical Substances), Recommended INN: List 84, Vol. 34, No. 3, published 2020 (see page 701 ). Cevostamab is also listed as CAS Registry No.: 2249888-53-5.The term “antibody” herein is used in the broadest sense and encompasses various antibody structures, including but not limited to monoclonal antibodies, polyclonal antibodies, multispecific antibodies (e.g., bispecific antibodies), and antibody fragments (e.g., bis-Fabs) so long as they exhibit the desired antigen-binding activity.“Affinity” refers to the strength of the sum total of noncovalent interactions between a single binding site of a molecule (e.g., an antibody) and its binding partner (e.g., an antigen). Unless indicated otherwise, as used herein, “binding affinity” refers to intrinsic binding affinity which reflects a 1 :1 interaction between members of a binding pair (e.g., antibody and antigen). The affinity of a molecule X for its partner Y can generally be represented by the dissociation constant (KD). Affinity can be measured by common methods known in the art, including those described herein. Specific illustrative and exemplary aspects for measuring binding affinity are described in the following.An “affinity matured” antibody refers to an antibody with one or more alterations in one or more hypervariable regions (HVRs), compared to a parent antibody which does not possess such alterations, such alterations resulting in an improvement in the affinity of the antibody for antigen.The terms “full-length antibody,” “intact antibody,” and “whole antibody” are used herein interchangeably to refer to an antibody having a structure substantially similar to a native antibody structure or having heavy chains that contain an Fc region as defined herein.An “antibody fragment” refers to a molecule other than an intact antibody that comprises a portion of an intact antibody that binds the antigen to which the intact antibody binds. Examples of antibody fragments include but are not limited to bis-Fabs; Fv; Fab; Fab, Fab’-SH; F(ab’)2; diabodies; linear antibodies; single-chain antibody molecules (e.g., scFv, ScFab); and multispecific antibodies formed from antibody fragments.A “single-domain antibody” refers to an antibody fragment comprising all or a portion of the heavy chain variable domain or all or a portion of the light chain variable domain of an antibody. In certain aspects, a single-domain antibody is a human single-domain antibody (see, e.g., U.S. Patent No. 6,248,516 B1 ). Examples of single-domain antibodies include but are not limited to a VHH.A “Fab” fragment is an antigen-binding fragment generated by papain digestion of antibodies and consists of an entire L chain along with the variable region domain of the H chain (VH), and the first constant domain of one heavy chain (CH1 ). Papain digestion of antibodies produces two identical Fab fragments. Pepsin treatment of an antibody yields a single large F(ab’)2 fragment which roughly corresponds to two disulfide linked Fab fragments having divalent antigen-binding activity and is still capable of cross-linking antigen. Fab’ fragments differ from Fab fragments by having an additional fewresidues at the carboxy terminus of the CH1 domain including one or more cysteines from the antibody hinge region. Fab’-SH is the designation herein for Fab’ in which the cysteine residue(s) of the constant domains bear a free thiol group. F(ab’)2 antibody fragments originally were produced as pairs of Fab’ fragments which have hinge cysteines between them. Other chemical couplings of antibody fragments are also known.“Fv” consists of a dimer of one heavy- and one light-chain variable region domain in tight, non- covalent association. From the folding of these two domains emanate six hypervariable loops (3 loops each from the H and L chain) that contribute the amino acid residues for antigen binding and confer antigen binding specificity to the antibody. However, even a single variable domain (or half of an Fv comprising only three CDRs specific for an antigen) has the ability to recognize and bind antigen, although often at a lower affinity than the entire binding site.The term “Fc region” herein is used to define a C-terminal region of an immunoglobulin heavy chain, including native sequence Fc regions and variant Fc regions. Although the boundaries of the Fc region of an immunoglobulin heavy chain might vary, the human IgG heavy chain Fc region is usually defined to stretch from an amino acid residue at position Cys226, or from Pro230, to the carboxylterminus thereof. The C-terminal lysine (residue 447 according to the EU numbering system) of the Fc region may be removed, for example, during production or purification of the antibody, or by recombinantly engineering the nucleic acid encoding a heavy chain of the antibody. Accordingly, a composition of intact antibodies may comprise antibody populations with all Lys447 residues removed, antibody populations with no Lys447 residues removed, and antibody populations having a mixture of antibodies with and without the Lys447 residue.A “functional Fc region” possesses an “effector function” of a native sequence Fc region. Exemplary “effector functions” include C1q binding; CDC; Fc receptor binding; ADCC; phagocytosis; down regulation of cell surface receptors {e.g., B cell receptor; BCR), etc. Such effector functions generally require the Fc region to be combined with a binding domain {e.g., an antibody variable domain) and can be assessed using various assays as disclosed, for example, in definitions herein.A “native sequence Fc region” comprises an amino acid sequence identical to the amino acid sequence of an Fc region found in nature. Native sequence human Fc regions include a native sequence human IgG I Fc region (non-A and A allotypes); native sequence human lgG2 Fc region; native sequence human lgG3 Fc region; and native sequence human lgG4 Fc region as well as naturally occurring variants thereof.A “variant Fc region” comprises an amino acid sequence which differs from that of a native sequence Fc region by virtue of at least one amino acid modification, preferably one or more amino acid substitution(s). Preferably, the variant Fc region has at least one amino acid substitution compared to a native sequence Fc region or to the Fc region of a parent polypeptide, e.g., from about one to about ten amino acid substitutions, and preferably from about one to about five amino acid substitutions in a native sequence Fc region or in the Fc region of the parent polypeptide. The variant Fc region herein will preferably possess at least about 80% homology with a native sequence Fc region and / or with an Fc region of a parent polypeptide, preferably at least about 90% homology therewith, or preferably at least about 95% homology therewith.“Fc complex” as used herein refers to CH3 domains of two Fc regions interacting together to form a dimer or, as in certain aspects, two Fc regions interact to form a dimer, wherein the cysteine residues in the hinge regions and / or the CH3 domains interact through bonds and / or forces (e.g., Van der Waals, hydrophobic forces, hydrogen bonds, electrostatic forces, or disulfide bonds).“Fc component” as used herein refers to a hinge region, a CH2 domain or a CH3 domain of an Fc region.“Hinge region” is generally defined as stretching from about residue 216 to 230 of an IgG (EU numbering), from about residue 226 to 243 of an IgG (Kabat numbering), or from about residue 1 to 15 of an IgG (IMGT unique numbering).The “lower hinge region” of an Fc region is normally defined as the stretch of residues immediately C-terminal to the hinge region, i.e., residues 233 to 239 of the Fc region (EU numbering).A “variant Fc region” comprises an amino acid sequence which differs from that of a native sequence Fc region by virtue of at least one amino acid modification, preferably one or more amino acid substitution(s). Preferably, the variant Fc region has at least one amino acid substitution compared to a native sequence Fc region or to the Fc region of a parent polypeptide, e.g., from about one to about ten amino acid substitutions, and preferably from about one to about five amino acid substitutions in a native sequence Fc region or in the Fc region of the parent polypeptide. The variant Fc region herein will preferably possess at least about 80% homology with a native sequence Fc region and / or with an Fc region of a parent polypeptide, and preferably at least about 90% homology therewith, more preferably at least about 95% homology therewith.“Fc receptor” or “FcR” describes a receptor that binds to the Fc region of an antibody. A preferred FcR is a native sequence human FcR. Moreover, a preferred FcR is one that binds an IgG antibody (a gamma receptor) and includes receptors of the FcyRI, FcyRII, and FcyRIII subclasses, including allelic variants and alternatively spliced forms of these receptors. FcyRII receptors include FcyRIIA (an “activating receptor”) and FcyRIIB (an “inhibiting receptor”), which have similar amino acid sequences that differ primarily in the cytoplasmic domains thereof. Activating receptor FcyRIIA contains an immunoreceptor tyrosine-based activation motif (ITAM) in its cytoplasmic domain. Inhibiting receptor FcyRIIB contains an immunoreceptor tyrosine-based inhibition motif (ITIM) in its cytoplasmic domain (see review M. in Daeron, Annu. Rev. Immunol. 15:203-234 (1997)). FcRs are reviewed in Ravetch and Kinet, Annu. Rev. Immunol. 9:457-492 (1991 ); Capel et al., Immunomethods 4:25-34 (1994); and de Haas et al., J. Lab. Clin. Med. 126:330-41 (1995). Other FcRs, including those to be identified in the future, are encompassed by the term “FcR” herein. The term also includes the neonatal receptor, FcRn, which is responsible for the transfer of maternal IgGs to the fetus (Guyer et al., J. Immunol. 117:587 (1976) and Kim et al., J. Immunol. 24:249 (1994)).The term “knob-into-hole” or “KnH” technology as mentioned herein refers to the technology directing the pairing of two polypeptides together in vitro or in vivo by introducing a protuberance (knob) into one polypeptide and a cavity (hole) into the other polypeptide at an interface in which they interact. For example, KnHs have been introduced in the Fc:Fc interaction interfaces, CL:CH1 interfaces or VH / VL interfaces of antibodies (e.g., US2007 / 0178552, WO 96 / 027011 , WO 98 / 050431 and Zhu et al. (1997) Protein Science 6:781 -788). This is especially useful in driving the pairing of two different heavy chainstogether during the manufacture of multispecific antibodies. For example, multispecific antibodies having KnH in their Fc regions can further comprise single variable domains linked to each Fc region, or further comprise different heavy chain variable domains that pair with identical, similar, or different light chain variable domains. KnH technology can also be used to pair two different receptor extracellular domains together or any other polypeptide sequences that comprise different target recognition sequences.“Framework” or “FR” refers to variable domain residues other than hypervariable region (HVR) residues. The FR of a variable domain generally consists of four FR domains: FR1 , FR2, FR3, and FR4. Accordingly, the HVR and FR sequences generally appear in the following sequence in VH (or VL): FR1 - H1 (L1 )-FR2-H2(L2)-FR3-H3(L3)-FR4.The “CH1 region” or “CH1 domain” comprises the stretch of residues from about residue 118 to residue 215 of an IgG (EU numbering), from about residue 114 to 223 of an IgG (Kabat numbering), or from about residue 1 .4 to residue 121 of an IgG (IMGT unique numbering) (Lefranc M-P, Giudicelli V, Duroux P, Jabado-Michaloud J, Folch G, Aouinti S, Carillon E, Duvergey H, Houles A, Paysan-Lafosse T, Hadi-Saljoqi S, Sasorith S, Lefranc G, Kossida S. IMGT®, the international ImMunoGeneTics information system® 25 years on. Nucleic Acids Res. 2015 Jan;43(Database issue):D413-22).The “CH2 domain” of a human IgG Fc region usually extends from about residues 244 to about 360 of an IgG (Kabat numbering), from about residues 231 to about 340 of an IgG (EU numbering), or from about residues 1 .6 to about 125 of an IgG (IGMT unique numbering). The CH2 domain is unique in that it is not closely paired with another domain. Rather, two N-linked branched carbohydrate chains are interposed between the two CH2 domains of an intact native IgG molecule. It has been speculated that the carbohydrate may provide a substitute for the domain-domain pairing and help stabilize the CH2 domain. Burton, Molec. Immunol.22: 161 -206 (1985).The “CH3 domain” comprises the stretch of residues C-terminal to a CH2 domain in an Fc region (i.e., from about amino acid residue 361 to about amino acid residue 478 of an IgG (Kabat numbering), from about amino acid residue 341 to about amino acid residue 447 of an IgG (EU numbering), or from about amino acid residue 1 .4 to about amino acid residue 130 of an IgG (IGMT unique numbering)).The “CL domain” or “constant light domain” comprises the stretch of residues C-terminal to a light-chain variable domain (VL). The light chain of an antibody may be a kappa (K) (“CK”) or lambda (A) (“CA”) light chain region. The CK region generally extends from about residue 108 to residue 214 of an IgG (Kabat or EU numbering) or from about residue 1 .4 to residue 126 of an IgG (IMGT unique numbering). The CA residue generally extends from about residue 107a to residue 215 (Kabat numbering) or from about residue 1 .5 to residue 127 (IMGT unique numbering) (Lefranc M-P, Giudicelli V, Duroux P, Jabado-Michaloud J, Folch G, Aouinti S, Carillon E, Duvergey H, Houles A, Paysan-Lafosse T, Hadi-Saljoqi S, Sasorith S, Lefranc G, Kossida S. IMGT®, the international ImMunoGeneTics information system® 25 years on. Nucleic Acids Res. 2015 Jan;43(Database issue):D413-22).The light chain (LC) from any vertebrate species can be assigned to one of two clearly distinct types, called kappa and lambda, based on the amino acid sequences of their constant domains. Depending on the amino acid sequence of the constant domain of their heavy chains (CH), immunoglobulins can be assigned to different classes or isotypes. There are five classes of immunoglobulins: IgA, IgD, IgE, IgG, and IgM, having heavy chains designated a, 5, y, e, and p,respectively. The y and a classes are further divided into subclasses on the basis of relatively minor differences in CH sequence and function, e.g., humans express the following subclasses: IgG 1 , lgG2, lgG3, lgG4, lgA1 , and lgA2.The term “chimeric” antibody refers to an antibody in which a portion of the heavy and / or light chain is derived from a particular source or species, while the remainder of the heavy and / or light chain is derived from a different source or species.The “class” of an antibody refers to the type of constant domain or constant region possessed by its heavy chain. There are five major classes of antibodies: IgA, IgD, IgE, IgG, and IgM, and several of these may be further divided into subclasses (isotypes), e.g., IgGi, lgG2, IgGs, lgG4, IgAi, and lgA2. The heavy chain constant domains that correspond to the different classes of immunoglobulins are called a, 5, E, y, and p., respectively.A “human antibody” is one which possesses an amino acid sequence which corresponds to that of an antibody produced by a human or a human cell or derived from a non-human source that utilizes human antibody repertoires or other human antibody-encoding sequences. This definition of a human antibody specifically excludes a humanized antibody comprising non-human antigen-binding residues. Human antibodies can be produced using various techniques known in the art, including phage-display libraries. Hoogenboom and Winter. J. Mol. Biol. 227:381 ,1991 ; Marks et al. J. Mol. Biol. 222:581 , 1991 . Also available for the preparation of human monoclonal antibodies are methods described in Cole et al. Monoclonal Antibodies and Cancer Therapy, Alan R. Liss, p. 77 (1985); Boerner et al. J. Immunol., 147(1 ):86-95, 1991 . See also van Dijk and van de Winkel. Curr. Opin. Pharmacol. 5:368-74, 2001 . Human antibodies can be prepared by administering the antigen to a transgenic animal that has been modified to produce such antibodies in response to antigenic challenge, but whose endogenous loci have been disabled, e.g., immunized xenomice (see, e.g., U.S. Pat. Nos. 6,075,181 and 6,150,584 regarding XENOMOUSE™ technology). See also, for example, Li et al. Proc. Natl. Acad. Sci. USA. 103:3557-3562, 2006 regarding human antibodies generated via a human B-cell hybridoma technology.A “human consensus framework” is a framework which represents the most commonly occurring amino acid residues in a selection of human immunoglobulin VL or VH framework sequences. Generally, the selection of human immunoglobulin VL or VH sequences is from a subgroup of variable domain sequences. Generally, the subgroup of sequences is a subgroup as in Kabat et al. Sequences of Proteins of Immunological Interest, Fifth Edition, NIH Publication 91 -3242, Bethesda MD (1991 ), vols. 1 -3. In one aspect, for the VL, the subgroup is subgroup kappa I as in Kabat et al. supra. In one aspect, for the VH, the subgroup is subgroup III as in Kabat et al. supra.A “humanized” antibody refers to a chimeric antibody comprising amino acid residues from non- human HVRs and amino acid residues from human FRs. In certain aspects, a humanized antibody will comprise substantially all of at least one, and typically two, variable domains, in which all or substantially all of the HVRs (e.g., CDRs) correspond to those of a non-human antibody, and all or substantially all of the FRs correspond to those of a human antibody. In certain aspects in which all or substantially all of the FRs of a humanized antibody correspond to those of a human antibody, any of the FRs of the humanized antibody may contain one or more amino acid residues (e.g., one or more Vernier position residues of FRs) from non-human FR(s). A humanized antibody optionally may comprise at least a portion of anantibody constant region derived from a human antibody. A “humanized form” of an antibody, e.g., a nonhuman antibody, refers to an antibody that has undergone humanization.The term “variable region” or “variable domain” refers to the domain of an antibody heavy or light chain that is involved in binding the antibody to antigen. The variable domains of the heavy chain and light chain (VH and VL, respectively) of a native antibody generally have similar structures, with each domain comprising four conserved framework regions (FRs) and three hypervariable regions (HVRs). (See, e.g., Kindt et al. Kuby Immunology, 6thed. W.H. Freeman and Co., page 91 (2007).) A single VH or VL domain may be sufficient to confer antigen-binding specificity. Furthermore, antibodies that bind a particular antigen may be isolated using a VH or VL domain from an antibody that binds the antigen to screen a library of complementary VL or VH domains, respectively. See, e.g., Portolano et al. J. Immunol. 150:880-887, 1993; Clarkson et al. Nature 352:624-628, 1991.The term “hypervariable region” or “HVR” as used herein refers to each of the regions of an antibody variable domain which are hypervariable in sequence (“complementarity determining regions” or “CDRs”). Generally, antibodies comprise six CDRs: three in the VH (CDR-H1 , CDR-H2, CDR-H3), and three in the VL (CDR-L1 , CDR-L2, CDR-L3). Exemplary CDRs herein include:(a) CDRs occurring at amino acid residues 26-32 (L1 ), 50-52 (L2), 91 -96 (L3), 26-32 (H1 ), 53-55 (H2), and 96-101 (H3) (Chothia and Lesk, J. Mol. Biol. 196:901 -917, 1987);(b) CDRs occurring at amino acid residues 24-34 (L1 ), 50-56 (L2), 89-97 (L3), 31 -35b (H1 ), SO- 65 (H2), and 95-102 (H3) (Kabat et al. Sequences of Proteins of Immunological Interest, 5th Ed. Public Health Service, National Institutes of Health, Bethesda, MD (1991 )); and(c) antigen contacts occurring at amino acid residues 27c-36 (L1 ), 46-55 (L2), 89-96 (L3), 30-35b (H1 ), 47-58 (H2), and 93-101 (H3) (MacCallum et al. J. Mol. Biol. 262: 732-745, 1996).Unless otherwise indicated, HVR residues and other residues in the variable domain (e.g., FR residues) are numbered herein according to Kabat et al. supra.“Single-chain Fv” also abbreviated as “sFv” or “scFv” are antibody fragments that comprise the VH and VL antibody domains connected into a single polypeptide chain. Preferably, the scFv polypeptide further comprises a polypeptide linker between the VH and VL domains, which enables the scFv to form the desired structure for antigen binding. For a review of scFv, see Pluckthun, The Pharmacology of Monoclonal Antibodies, vol. 113, Rosenburg and Moore eds., Springer- Verlag, New York, pp. 269-315 (1994); Malmborg et al., J. Immunol. Methods 183:7-13, 1995.By “targeting domain” is meant a part of a compound or a molecule that specifically binds to a target epitope, antigen, ligand, or receptor. Targeting domains include but are not limited to antibodies (e.g., monoclonal, polyclonal, recombinant, humanized, and chimeric antibodies), antibody fragments or portions thereof (e.g., bis-Fab fragments, Fab fragments, F(ab’)2, scFab, scFv antibodies, SMIP, singledomain antibodies, diabodies, minibodies, scFv-Fc, affibodies, nanobodies, and VH and / or VL domains of antibodies), receptors, ligands, aptamers, peptide targeting domains (e.g., cysteine knot proteins (CKP)), and other molecules having an identified binding partner. A targeting domain may target, block, agonize, or antagonize the antigen to which it binds.The term “monoclonal antibody” as used herein refers to an antibody obtained from a population of substantially homogeneous antibodies, i.e., the individual antibodies comprising the population areidentical and / or bind the same epitope, except for possible variant antibodies, e.g., containing naturally occurring mutations or arising during production of a monoclonal antibody preparation, such variants generally being present in minor amounts. In contrast to polyclonal antibody preparations, which typically include different antibodies directed against different determinants (epitopes), each monoclonal antibody of a monoclonal antibody preparation is directed against a single determinant on an antigen. Thus, the modifier “monoclonal” indicates the character of the antibody as being obtained from a substantially homogeneous population of antibodies, and is not to be construed as requiring production of the antibody by any particular method. For example, the monoclonal antibodies to be used in accordance with the present disclosure may be made by a variety of techniques, including but not limited to the hybridoma method, recombinant DNA methods, phage-display methods, and methods utilizing transgenic animals containing all or part of the human immunoglobulin loci, such methods and other exemplary methods for making monoclonal antibodies being described herein.The term “multispecific antibody” is used in the broadest sense and specifically covers an antibody that has polyepitopic specificity. In one aspect, the multispecific antibody binds to two different targets (e.g., bispecific antibody). Such multispecific antibodies include, but are not limited to, an antibody comprising a heavy chain variable domain (VH) and a light chain variable domain (VL), where the VH / VL unit has polyepitopic specificity, antibodies having two or more VL and VH domains with each VH / VL unit binding to a different epitope, antibodies having two or more single variable domains with each single variable domain binding to a different epitope, full-length antibodies, antibody fragments such as Fab, Fv, dsFv, scFv, diabodies, bispecific diabodies and triabodies, antibody fragments that have been linked covalently or non-covalently. “Polyepitopic specificity” refers to the ability to specifically bind to two or more different epitopes on the same or different target(s). “Monospecific” refers to the ability to bind only one antigen. In one aspect, the monospecific biepitopic antibody binds two different epitopes on the same target / antigen. In one aspect, the monospecific polyepitopic antibody binds to multiple different epitopes of the same target / antigen. According to one aspect, the multispecific antibody is an IgG antibody that binds to each epitope with an affinity of 5 pM to 0.001 pM, 3 pM to 0.001 pM, 1 pM to 0.001 pM, 0.5 pM to 0.001 pM, or 0.1 pM to 0.001 pM.A “naked antibody” refers to an antibody that is not conjugated to a heterologous moiety (e.g., a cytotoxic moiety) or radiolabel. The naked antibody may be present in a pharmaceutical formulation.“Native antibodies” refer to naturally occurring immunoglobulin molecules with varying structures. For example, native IgG antibodies are heterotetrameric glycoproteins of about 150,000 daltons, composed of two identical light chains and two identical heavy chains that are disulfide-bonded. From N- to C-terminus, each heavy chain has a variable region (VH), also called a variable heavy domain or a heavy chain variable domain, followed by three constant domains (CH1 , CH2, and CH3). Similarly, from N- to C-terminus, each light chain has a variable region (VL), also called a variable light domain or a light chain variable domain, followed by a constant light (CL) domain. The light chain of an antibody may be assigned to one of two types, called kappa (K) and lambda (A), based on the amino acid sequence of its constant domain.As used herein, the term “immunoadhesin” designates molecules which combine the binding specificity of a heterologous protein (an “adhesin”) with the effector functions of immunoglobulin constantdomains. Structurally, the immunoadhesins comprise a fusion of an amino acid sequence with a desired binding specificity, which amino acid sequence is other than the antigen recognition and binding site of an antibody {i.e., is “heterologous” compared to a constant region of an antibody), and an immunoglobulin constant domain sequence {e.g., CH2 and / or CH3 sequence of an IgG). The adhesin and immunoglobulin constant domains may optionally be separated by an amino acid spacer. Exemplary adhesin sequences include contiguous amino acid sequences that comprise a portion of a receptor or a ligand that binds to a protein of interest. Adhesin sequences can also be sequences that bind a protein of interest, but are not receptor or ligand sequences {e.g., adhesin sequences in peptibodies). Such polypeptide sequences can be selected or identified by various methods, include phage display techniques and high throughput sorting methods. The immunoglobulin constant domain sequence in the immunoadhesin can be obtained from any immunoglobulin, such as IgG 1 , lgG2, lgG3, or lgG4 subtypes, IgA (including lgA1 and lgA2), IgE, IgD, or IgM.“Chemotherapeutic agent” includes chemical compounds useful in the treatment of cancer. Examples of chemotherapeutic agents include erlotinib (TARCEVA®, Genentech / OSI Pharm.), bortezomib (VELCADE®, Millennium Pharm.), disulfiram, epigallocatechin gallate , salinosporamide A, carfilzomib, 17-AAG (geldanamycin), radicicol, lactate dehydrogenase A (LDH-A), fulvestrant (FASLODEX®, AstraZeneca), sunitib (SUTENT®, Pfizer / Sugen), letrozole (FEMARA®, Novartis), imatinib mesylate (GLEEVEC®, Novartis), finasunate (VATALANIB®, Novartis), oxaliplatin (ELOXATIN®, Sanofi), 5-FU (5-fluorouracil), leucovorin, Rapamycin (Sirolimus, RAPAMUNE®, Wyeth), Lapatinib (TYKERB®, GSK572016, Glaxo Smith Kline), Lonafamib (SCH 66336), sorafenib (NEXAVAR®, Bayer Labs), gefitinib (IRESSA®, AstraZeneca), AG1478, alkylating agents such as thiotepa and CYTOXAN® cyclosphosphamide; alkyl sulfonates such as busulfan, improsulfan and piposulfan; aziridines such as benzodopa, carboquone, meturedopa, and uredopa; ethylenimines and methylamelamines including altretamine, triethylenemelamine, triethylenephosphoramide, triethylenethiophosphoramide and trimethylomelamine; acetogenins (especially bullatacin and bullatacinone); a camptothecin (including topotecan and irinotecan); bryostatin; callystatin; CC-1065 (including its adozelesin, carzelesin and bizelesin synthetic analogs); cryptophycins (particularly cryptophycin 1 and cryptophycin 8); adrenocorticosteroids (including prednisone and prednisolone); cyproterone acetate; 5a-reductases including finasteride and dutasteride); vorinostat, romidepsin, panobinostat, valproic acid, mocetinostat dolastatin; aldesleukin, talc duocarmycin (including the synthetic analogs, KW-2189 and CB1 -TM1 ); eleutherobin; pancratistatin; a sarcodictyin; spongistatin; nitrogen mustards such as chlorambucil, chlomaphazine, chlorophosphamide, estramustine, ifosfamide, mechlorethamine, mechlorethamine oxide hydrochloride, melphalan, novembichin, phenesterine, prednimustine, trofosfamide, uracil mustard; nitrosoureas such as carmustine, chlorozotocin, fotemustine, lomustine, nimustine, and ranimnustine; antibiotics such as the enediyne antibiotics (e.g., calicheamicin, especially calicheamicin y11 and calicheamicin w11 (Angew Chem. Inti. Ed. Engl. 199433:183-186); dynemicin, including dynemicin A; bisphosphonates, such as clodronate; an esperamicin; as well as neocarzi nostatin chromophore and related chromoprotein enediyne antibiotic chromophores), aclacinomysins, actinomycin, authramycin, azaserine, bleomycins, cactinomycin, carabicin, caminomycin, carzinophilin, chromomycinis, dactinomycin, daunorubicin, detorubicin, 6-diazo-5-oxo-L-norleucine, ADRIAMYCIN® (doxorubicin),morpholino-doxorubicin, cyanomorpholino-doxorubicin, 2-pyrrolino-doxorubicin and deoxydoxorubicin), epirubicin, esorubicin, idarubicin, marcellomycin, mitomycins such as mitomycin C, mycophenolic acid, nogalamycin, olivomycins, peplomycin, porfiromycin, puromycin, quelamycin, rodorubicin, streptonigrin, streptozocin, tubercidin, ubenimex, zinostatin, zorubicin; anti-metabolites such as methotrexate and 5- fluorouracil (5-FU); folic acid analogs such as denopterin, methotrexate, pteropterin, trimetrexate; purine analogs such as fludarabine, 6-mercaptopurine, thiamiprine, thioguanine; pyrimidine analogs such as ancitabine, azacitidine, 6-azauridine, carmofur, cytarabine, dideoxyuridine, doxifluridine, enocitabine, floxuridine; androgens such as calusterone, dromostanolone propionate, epitiostanol, mepitiostane, testolactone; anti-adrenals such as aminoglutethimide, mitotane, trilostane; folic acid replenisher such as frolinic acid; aceglatone; aldophosphamide glycoside; aminolevulinic acid; eniluracil; amsacrine; bestrabucil; bisantrene; edatraxate; defofamine; demecolcine; diaziquone; elfomithine; elliptinium acetate; an epothilone; etoglucid; gallium nitrate; hydroxyurea; lentinan; lonidainine; maytansinoids such as maytansine and ansamitocins; mitoguazone; mitoxantrone; mopidamnol; nitraerine; pentostatin; phenamet; pirarubicin; losoxantrone; podophyllinic acid; 2-ethylhydrazide; procarbazine; PSK® polysaccharide complex (JHS Natural Products, Eugene, Oreg.); razoxane; rhizoxin; sizofuran; spirogermanium; tenuazonic acid; triaziquone; 2,2’,2”-trichlorotriethylamine; trichothecenes (especially T- 2 toxin, verracurin A, roridin A and anguidine); urethan; vindesine; dacarbazine; mannomustine; mitobronitol; mitolactol; pipobroman; gacytosine; arabinoside (“Ara-C”); cyclophosphamide; thiotepa; taxoids, e.g., TAXOL (paclitaxel; Bristol-Myers Squibb Oncology, Princeton, N.J.), ABRAXANE® (Cremophor-free), albumin-engineered nanoparticle formulations of paclitaxel (American Pharmaceutical Partners, Schaumberg, III.), and TAXOTERE® (docetaxel, doxetaxel; Sanofi-Aventis); chloranmbucil; GEMZAR® (gemcitabine); 6-thioguanine; mercaptopurine; methotrexate; platinum analogs such as cisplatin and carboplatin; vinblastine; etoposide (VP-16); ifosfamide; mitoxantrone; vincristine;NAVELBINE® (vinorelbine); novantrone; teniposide; edatrexate; daunomycin; aminopterin; capecitabine (XELODA®); ibandronate; CPT-11 ; topoisomerase inhibitor RFS 2000; difluoromethylornithine (DMFO); retinoids such as retinoic acid; and pharmaceutically acceptable salts, acids and derivatives of any of the above.Chemotherapeutic agent also includes (i) anti-hormonal agents that act to regulate or inhibit hormone action on tumors such as anti-estrogens and selective estrogen receptor modulators (SERMs), including, for example, tamoxifen (including NOLVADEX®; tamoxifen citrate), raloxifene, droloxifene, iodoxyfene , 4-hydroxytamoxifen, trioxifene, keoxifene, LY117018, onapristone, and FARESTON® (toremifine citrate); (ii) aromatase inhibitors that inhibit the enzyme aromatase, which regulates estrogen production in the adrenal glands, such as, for example, 4(5)-imidazoles, aminoglutethimide, MEGASE® (megestrol acetate), AROMASIN® (exemestane; Pfizer), formestanie, fadrozole, RIVISOR® (vorozole), FEMARA® (letrozole; Novartis), and ARIMIDEX® (anastrozole; AstraZeneca); (iii) anti-androgens such as flutamide, nilutamide, bicalutamide, leuprolide and goserelin; buserelin, tripterelin, medroxyprogesterone acetate, diethylstilbestrol, premarin, fluoxymesterone, all transretionic acid, fenretinide, as well as troxacitabine (a 1 ,3-dioxolane nucleoside cytosine analog); (iv) protein kinase inhibitors; (v) lipid kinase inhibitors; (vi) antisense oligonucleotides, particularly those which inhibit expression of genes in signaling pathways implicated in aberrant cell proliferation, such as, for example,PKC-alpha, Ralf and H-Ras; (vii) ribozymes such as VEGF expression inhibitors (e.g., ANGIOZYME®) and HER2 expression inhibitors; (viii) vaccines such as gene therapy vaccines, for example, ALLOVECTIN®, LEUVECTIN®, and VAXID®; PROLEUKIN®, rlL-2; a topoisomerase 1 inhibitor such as LURTOTECAN®; ABARELIX® rmRH; and (ix) pharmaceutically acceptable salts, acids and derivatives of any of the above.Chemotherapeutic agent also includes antibodies such as alemtuzumab (Campath), bevacizumab (AVASTIN®, Genentech); cetuximab (ERBITUX®, Imclone); panitumumab (VECTIBIX®, Amgen), rituximab (RITUXAN®, Genentech / Biogen Idee), pertuzumab (OMNITARG®, 2C4, Genentech), trastuzumab (HERCEPTIN®, Genentech), tositumomab (Bexxar, Corixia), and the antibody drug conjugate, gemtuzumab ozogamicin (MYLOTARG®, Wyeth). Additional humanized monoclonal antibodies with therapeutic potential as agents in combination with the compounds of the disclosure include: apolizumab, aselizumab, atlizumab, bapineuzumab, bivatuzumab mertansine, cantuzumab mertansine, cedelizumab, certolizumab pegol, cidfusituzumab, cidtuzumab, daclizumab, eculizumab, efalizumab, epratuzumab, erlizumab, felvizumab, fontolizumab, gemtuzumab ozogamicin, inotuzumab ozogamicin, ipilimumab, labetuzumab, lintuzumab, matuzumab, mepolizumab, motavizumab, motovizumab, natalizumab, nimotuzumab, nolovizumab, numavizumab, ocrelizumab, omalizumab, palivizumab, pascolizumab, peefusituzumab, pectuzumab, pexelizumab, ralivizumab, ranibizumab, reslivizumab, reslizumab, resyvizumab, rovelizumab, ruplizumab, sibrotuzumab, siplizumab, sontuzumab, tacatuzumab tetraxetan, tadocizumab, talizumab, tefibazumab, tocilizumab, toralizumab, tucotuzumab celmoleukin, tucusituzumab, umavizumab, urtoxazumab, ustekinumab, visilizumab, and the antiinterleukin-12 (ABT-874 / J695, Wyeth Research and Abbott Laboratories) which is a recombinant exclusively human-sequence, full-length lgG1 A antibody genetically modified to recognize interleukin-12 p40 protein.Chemotherapeutic agent also includes “EGFR inhibitors,” which refers to compounds that bind to or otherwise interact directly with EGFR and prevent or reduce its signaling activity, and is alternatively referred to as an “EGFR antagonist.” Examples of such agents include antibodies and small molecules that bind to EGFR. Examples of antibodies which bind to EGFR include MAb 579 (ATCC CRL HB 8506), MAb 455 (ATCC CRL HB8507), MAb 225 (ATCC CRL 8508), MAb 528 (ATCC CRL 8509) (see, US Patent No. 4,943, 533, Mendelsohn et al.) and variants thereof, such as chimerized 225 (C225 or Cetuximab; ERBUTIX®) and reshaped human 225 (H225) (see, WO 96 / 40210, Imclone Systems Inc.); IMC-11 F8, a fully human, EGFR-targeted antibody (Imclone); antibodies that bind type II mutant EGFR (US Patent No. 5,212,290); humanized and chimeric antibodies that bind EGFR as described in US Patent No. 5,891 ,996; and human antibodies that bind EGFR, such as ABX-EGF or Panitumumab (see WO98 / 50433, Abgenix / Amgen); EMD 55900 (Stragliotto et al. Eur. J. Cancer 32A:636-640 (1996)); EMD7200 (matuzumab) a humanized EGFR antibody directed against EGFR that competes with both EGF and TGF-alpha for EGFR binding (EMD / Merck); human EGFR antibody, HuMax-EGFR (GenMab); fully human antibodies known as E1 .1 , E2.4, E2.5, E6.2, E6.4, E2.11 , E6. 3 and E7.6. 3 and described in US 6,235,883; MDX-447 (Medarex Inc); and mAb 806 or humanized mAb 806 (Johns et al., J. Biol. Chem. 279(29) :30375-30384 (2004)). The anti-EGFR antibody may be conjugated with a cytotoxic agent, thus generating an immunoconjugate (see, e.g., EP659,439A2, Merck Patent GmbH). EGFR antagonistsinclude small molecules such as compounds described in US Patent Nos: 5,616,582, 5,457,105, 5,475,001 , 5,654,307, 5,679,683, 6,084,095, 6,265,410, 6,455,534, 6,521 ,620, 6,596,726, 6,713,484, 5,770,599, 6,140,332, 5,866,572, 6,399,602, 6,344,459, 6,602,863, 6,391 ,874, 6,344,455, 5,760,041 , 6,002,008, and 5,747,498, as well as the following PCT publications: WO98 / 14451 , W098 / 50038, W099 / 09016, and WO99 / 24037. Particular small molecule EGFR antagonists include OSI-774 (CP- 358774, erlotinib, TARCEVA® Genentech / OSI Pharmaceuticals); PD 183805 (Cl 1033, 2-propenamide, N-[4-[(3-chloro-4-fluorophenyl)amino]-7-[3-(4-morpholinyl)propoxy]-6-quinazolinyl]-, dihydrochloride, Pfizer Inc.); ZD1839, gefitinib (IRESSA®) 4-(3’-Chloro-4’-fluoroanilino)-7-methoxy-6-(3- morpholinopropoxy)quinazoline, AstraZeneca); ZM 105180 ((6-amino-4-(3-methylphenyl-amino)- quinazoline, Zeneca); BIBX-1382 (N8-(3-chloro-4-fluoro-phenyl)-N2-(1 -methyl-piperidin-4-yl)- pyrimido[5,4-d]pyrimidine-2,8-diamine, Boehringer Ingelheim); PKI-166 ((R)-4-[4-[(1 -phenylethyl)amino]- 1 H-pyrrolo[2,3-d]pyrimidin-6-yl]-phenol); (R)-6-(4-hydroxyphenyl)-4-[(1 -phenylethyl)amino]-7H-pyrrolo[2,3- d]pyrimidine); CL-387785 (N-[4-[(3-bromophenyl)amino]-6-quinazolinyl]-2-butynamide); EKB-569 (N-[4- [(3-chloro-4-fluorophenyl)amino]-3-cyano-7-ethoxy-6-quinolinyl]-4-(dimethylamino)-2-butenamide) (Wyeth); AG1478 (Pfizer); AG1571 (SU 5271 ; Pfizer); dual EGFR / HER2 tyrosine kinase inhibitors such as lapatinib (TYKERB®, GSK572016 or N-[3-chloro-4-[(3 fluorophenyl)methoxy]phenyl]- 6[5[[[2methylsulfonyl)ethyl]amino]methyl]-2-furanyl]-4-quinazolinamine).Chemotherapeutic agents also include “tyrosine kinase inhibitors” including the EGFR-targeted drugs noted in the preceding paragraph; small molecule HER2 tyrosine kinase inhibitor such as TAK165 available from Takeda; CP-724,714, an oral selective inhibitor of the ErbB2 receptor tyrosine kinase (Pfizer and OSI); dual-HER inhibitors such as EKB-569 (available from Wyeth) which preferentially binds EGFR but inhibits both HER2 and EGFR-overexpressing cells; lapatinib (GSK572016; available from Glaxo-SmithKline), an oral HER2 and EGFR tyrosine kinase inhibitor; PKI-166 (available from Novartis); pan-HER inhibitors such as canertinib (CI-1033; Pharmacia); Raf-1 inhibitors such as antisense agent ISIS-5132 available from ISIS Pharmaceuticals which inhibit Raf-1 signaling; non-HER targeted TK inhibitors such as imatinib mesylate (GLEEVEC®, available from Glaxo SmithKline); multi-targeted tyrosine kinase inhibitors such as sunitinib (SUTENT®, available from Pfizer); VEGF receptor tyrosine kinase inhibitors such as vatalanib (PTK787 / ZK222584, available from Novartis / Schering AG); MAPK extracellular regulated kinase I inhibitor CI-1040 (available from Pharmacia); quinazolines, such as PD 153035, 4-(3-chloroanilino) quinazoline; pyridopyrimidines; pyrimidopyrimidines; pyrrolopyrimidines, such as CGP 59326, CGP 60261 and CGP 62706; pyrazolopyrimidines, 4-(phenylamino)-7H-pyrrolo[2,3-d] pyrimidines; curcumin (diferuloyl methane, 4,5-bis (4-fluoroanilino)phthalimide); tyrphostines containing nitrothiophene moieties; PD-0183805 (Warner-Lamber); antisense molecules (e.g. those that bind to HER-encoding nucleic acid); quinoxalines (US Patent No. 5,804,396); tryphostins (US Patent No. 5,804,396); ZD6474 (Astra Zeneca); PTK-787 (Novartis / Schering AG); pan-HER inhibitors such as CI- 1033 (Pfizer); Affinitac (ISIS 3521 ; Isis / Lilly); imatinib mesylate (GLEEVEC®); PKI 166 (Novartis); GW2016 (Glaxo SmithKline); CI-1033 (Pfizer); EKB-569 (Wyeth); Semaxinib (Pfizer); ZD6474 (AstraZeneca); PTK-787 (Novartis / Schering AG); INC-1 C1 1 (Imclone), rapamycin (sirolimus, RAPAMUNE®); or as described in any of the following patent publications: US Patent No. 5,804,396; WO 1999 / 09016 (American Cyanamid); WO 1998 / 43960 (American Cyanamid); WO 1997 / 38983 (WarnerLambert); WO 1999 / 06378 (Warner Lambert); WO 1999 / 06396 (Warner Lambert); WO 1996 / 30347 (Pfizer, Inc); WO 1996 / 33978 (Zeneca); WO 1996 / 3397 (Zeneca) and WO 1996 / 33980 (Zeneca).Chemotherapeutic agents also include dexamethasone, interferons, colchicine, metoprine, cyclosporine, amphotericin, metronidazole, alemtuzumab, alitretinoin, allopurinol, amifostine, arsenic trioxide, asparaginase, BCG live, bevacuzimab, bexarotene, cladribine, clofarabine, darbepoetin alfa, denileukin, dexrazoxane, epoetin alfa, elotinib, filgrastim, histrelin acetate, ibritumomab, interferon alfa- 2a, interferon alfa-2b, lenalidomide, levamisole, mesna, methoxsalen, nandrolone, nelarabine, nofetumomab, oprelvekin, palifermin, pamidronate, pegademase, pegaspargase, pegfilgrastim, pemetrexed disodium, plicamycin, porfimer sodium, quinacrine, rasburicase, sargramostim, temozolomide, VM-26, 6-TG, toremifene, tretinoin, ATRA, valrubicin, zoledronate, and zoledronic acid, and pharmaceutically acceptable salts thereof.Chemotherapeutic agents also include hydrocortisone, hydrocortisone acetate, cortisone acetate, tixocortol pivalate, triamcinolone acetonide, triamcinolone alcohol, mometasone, amcinonide, budesonide, desonide, fluocinonide, fluocinolone acetonide, betamethasone, betamethasone sodium phosphate, dexamethasone, dexamethasone sodium phosphate, fluocortolone, hydrocortisone-17- butyrate, hydrocortisone-17-valerate, aclometasone dipropionate, betamethasone valerate, betamethasone dipropionate, prednicarbate, clobetasone-17-butyrate, clobetasol-17-propionate, fluocortolone caproate, fluocortolone pivalate and fluprednidene acetate; immune selective antiinflammatory peptides (ImSAIDs) such as phenylalanine-glutamine-glycine (FEG) and its D-isomeric form (feG) (IMULAN BioTherapeutics, LLC); anti-rheumatic drugs such as azathioprine, ciclosporin (cyclosporine A), D-penicillamine, gold salts, hydroxychloroquine, leflunomideminocycline, sulfasalazine, tumor necrosis factor alpha (TNFa) blockers such as etanercept (Enbrel), infliximab (Remicade), adalimumab (Humira), certolizumab pegol (Cimzia), golimumab (Simponi), interleukin 1 (IL-1 ) blockers such as anakinra (Kineret), T cell costimulation blockers such as abatacept (Orencia), interleukin 6 (IL-6) blockers such as tocilizumab (ACTEMRA®); interleukin 13 (IL-13) blockers such as lebrikizumab; interferon alpha (IFN) blockers such as Rontalizumab; beta 7 integrin blockers such as rhuMAb Beta7; IgE pathway blockers such as Anti-M1 prime; Secreted homotrimeric LTa3 and membrane bound heterotrimer LTa1 / p2 blockers such as anti-lymphotoxin alpha (LTa); radioactive isotopes (e.g., At211, I131, I125, Y90, Re186, Re188, Sm153, Bi212, P32, Pb212, and radioactive isotopes of Lu); miscellaneous investigational agents such as thioplatin, PS-341 , phenylbutyrate, ET-18- OCH3, or farnesyl transferase inhibitors (L-739749, L-744832); polyphenols such as quercetin, resveratrol, piceatannol, epigallocatechine gallate, theaflavins, flavanols, procyanidins, betulinic acid and derivatives thereof; autophagy inhibitors such as chloroquine; delta-9-tetrahydrocannabinol (dronabinol, MARINOL®); beta- lapachone; lapachol; colchicines; betulinic acid; acetylcamptothecin, scopolectin, and 9- aminocamptothecin); podophyllotoxin; tegafur (UFTORAL®); bexarotene (TARGRETIN®); bisphosphonates such as clodronate (for example, BONEFOS® or OSTAC®), etidronate (DIDROCAL®), NE-58095, zoledronic acid / zoledronate (ZOMETA®), alendronate (FOSAMAX®), pamidronate (AREDIA®), tiludronate (SKELID®), or risedronate (ACTONEL®); and epidermal growth factor receptor (EGF-R); vaccines such as THERATOPE® vaccine; perifosine, COX-2 inhibitor (e.g. celecoxib or etoricoxib), proteosome inhibitor (e.g. PS341 ); CCI-779; tipifarnib (R1 1577); orafenib, ABT510; Bcl-2inhibitor such as oblimersen sodium (GENASENSE®); pixantrone; farnesyltransferase inhibitors such as lonafarnib (SCH 6636, SARASARTM); and pharmaceutically acceptable salts, acids or derivatives of any of the above; as well as combinations of two or more of the above such as CHOP, an abbreviation for a combined therapy of cyclophosphamide, doxorubicin, vincristine, and prednisolone; and FOLFOX, an abbreviation for a treatment regimen with oxaliplatin (ELOXATIN™) combined with 5-FU and leucovorin.Chemotherapeutic agents also include non-steroidal anti-inflammatory drugs with analgesic, antipyretic and anti-inflammatory effects. NSAIDs include non-selective inhibitors of the enzyme cyclooxygenase. Specific examples of NSAIDs include aspirin, propionic acid derivatives such as ibuprofen, fenoprofen, ketoprofen, flurbiprofen, oxaprozin and naproxen, acetic acid derivatives such as indomethacin, sulindac, etodolac, diclofenac, enolic acid derivatives such as piroxicam, meloxicam, tenoxicam, droxicam, lornoxicam and isoxicam, fenamic acid derivatives such as mefenamic acid, meclofenamic acid, flufenamic acid, tolfenamic acid, and COX-2 inhibitors such as celecoxib, etoricoxib, lumiracoxib, parecoxib, rofecoxib, and valdecoxib. NSAIDs can be indicated for the symptomatic relief of conditions such as rheumatoid arthritis, osteoarthritis, inflammatory arthropathies, ankylosing spondylitis, psoriatic arthritis, Reiter’s syndrome, acute gout, dysmenorrhoea, metastatic bone pain, headache and migraine, postoperative pain, mild-to-moderate pain due to inflammation and tissue injury, pyrexia, ileus, and renal colic.The term “cytotoxic agent” as used herein refers to a substance that inhibits or prevents a cellular function and / or causes cell death or destruction. Cytotoxic agents include, but are not limited to, radioactive isotopes (e.g., At211, I131, 1125, Y90, Re186, Re188, Sm153, Bi212, P32, Pb212, and radioactive isotopes of Lu); chemotherapeutic agents or drugs (e.g., methotrexate, adriamicin, vinca alkaloids (vincristine, vinblastine, etoposide), doxorubicin, melphalan, mitomycin C, chlorambucil, daunorubicin or other intercalating agents); growth inhibitory agents; enzymes and fragments thereof such as nucleolytic enzymes; antibiotics; toxins such as small molecule toxins or enzymatically active toxins of bacterial, fungal, plant or animal origin, including fragments and / or variants thereof; and the various antitumor or anticancer agents disclosed below.A “disorder” is any condition that would benefit from treatment including, but not limited to, chronic and acute disorders or diseases including those pathological conditions which predispose a mammal to the disorder in question. In one aspect, the disorder is a cancer, e.g., a multiple myeloma (MM).The terms “cell proliferative disorder” and “proliferative disorder” refer to disorders that are associated with some degree of abnormal cell proliferation. In one aspect, the cell proliferative disorder is cancer. In one aspect, the cell proliferative disorder is a tumor.“Tumor,” as used herein, refers to all neoplastic cell growth and proliferation, whether malignant or benign, and all pre-cancerous and cancerous cells and tissues. The terms “cancer,” “cancerous,” “cell proliferative disorder,” “proliferative disorder,” and “tumor” are not mutually exclusive as referred to herein.The terms “cancer” and “cancerous” refer to or describe the physiological condition in mammals that is typically characterized by unregulated cell growth / proliferation. Aspects of cancer include solid tumor cancers and non-solid tumor cancers. Examples of cancer include, but are not limited to, B cell proliferative disorders, such as multiple myeloma (MM), which may be relapsed or refractory MM. TheMM may be, e.g., typical MM (e.g., immunoglobulin G (IgG) MM, IgA MM, IgD MM, IgE MM, or IgM MM), light chain MM (LCMM) (e.g., lambda light chain MM or kappa light chain MM), or non-secretory MM. The MM may have one or more cytogenetic features (e.g., high-risk cytogenic features), e.g., t(4;14), t(11 ;14), t(14;16), and / or del ( 17p), as described in Table 1 and in the International Myeloma Working Group (IMWG) criteria provided in Sonneveld et al., Blood, 127(24): 2955-2962, 2016, and / or 1 q21 , as described in Chang et al., Bone Marrow Transplantation, 45: 117-121 , 2010. Cytogenic features may be detected, e.g., using fluorescent in situ hybridization (FISH).Table 1. Cytogenic features of MMThe term “B cell proliferative disorder” or “B cell malignancy” refers to a disorder that is associated with some degree of abnormal B cell proliferation and includes, for example, lymphoma, leukemia, myeloma, and myelodysplastic syndrome. In one embodiment, the B cell proliferative disorder is a lymphoma, such as non-Hodgkin’s lymphoma (NHL), including, for example, diffuse large B cell lymphoma (DLBCL) (e.g., relapsed or refractory DLBCL). In another embodiment, the B cell proliferative disorder is a leukemia, such as chronic lymphocytic leukemia (CLL). Other specific examples of cancer also include germinal-center B cell-like (GCB) diffuse large B cell lymphoma (DLBCL), activated B celllike (ABC) DLBCL, follicular lymphoma (FL), mantle cell lymphoma (MCL), acute myeloid leukemia (AML), chronic lymphoid leukemia (CLL), marginal zone lymphoma (MZL), small lymphocytic leukemia (SLL), lymphoplasmacytic lymphoma (LL), Waldenstrom macroglobulinemia (WM), central nervous system lymphoma (CNSL), Burkitt’s lymphoma (BL), B cell prolymphocytic leukemia, splenic marginal zone lymphoma, hairy cell leukemia, splenic lymphoma / leukemia, unclassifiable, splenic diffuse red pulp small B cell lymphoma, hairy cell leukemia variant, heavy chain diseases, a heavy chain disease, y heavy chain disease, p heavy chain disease, plasma cell myeloma, solitary plasmacytoma of bone, extraosseous plasmacytoma, extranodal marginal zone lymphoma of mucosa-associated lymphoid tissue (MALT lymphoma), nodal marginal zone lymphoma, pediatric nodal marginal zone lymphoma, pediatric follicular lymphoma, primary cutaneous follicle center lymphoma, T cell / histiocyte rich large B celllymphoma, primary DLBCL of the CNS, primary cutaneous DLBCL, leg type, EBV-positive DLBCL of the elderly, DLBCL associated with chronic inflammation, lymphomatoid granulomatosis, primary mediastinal (thymic) large B cell lymphoma, intravascular large B cell lymphoma, ALK-positive large B cell lymphoma, plasmablastic lymphoma, large B cell lymphoma arising in HHV8-associated multicentric Castleman disease, primary effusion lymphoma: B cell lymphoma, unclassifiable, with features intermediate between DLBCL and Burkitt lymphoma, and B cell lymphoma, unclassifiable, with features intermediate between DLBCL and classical Hodgkin’s lymphoma. Further examples of cancer include, but are not limited to, carcinoma, lymphoma, blastoma, sarcoma, and leukemia or lymphoid malignancies, including B cell lymphomas. More particular examples of such cancers include, but are not limited to, low grade / follicu lar NHL; small lymphocytic (SL) NHL; intermediate grade / follicular NHL; intermediate grade diffuse NHL; high grade immunoblastic NHL; high grade lymphoblastic NHL; high grade small non-cleaved cell NHL; bulky disease NHL; AIDS-related lymphoma; and acute lymphoblastic leukemia (ALL); chronic myeloblastic leukemia; and post-transplant lymphoproliferative disorder (PTLD). Examples of solid tumors include squamous cell cancer (e.g., epithelial squamous cell cancer), lung cancer including smallcell lung cancer, non-small cell lung cancer, adenocarcinoma of the lung and squamous carcinoma of the lung, cancer of the peritoneum, hepatocellular cancer, gastric or stomach cancer including gastrointestinal cancer and gastrointestinal stromal cancer, pancreatic cancer, glioblastoma, cervical cancer, ovarian cancer, liver cancer, bladder cancer, cancer of the urinary tract, hepatoma, breast cancer, colon cancer, rectal cancer, colorectal cancer, endometrial or uterine carcinoma, salivary gland carcinoma, kidney or renal cancer, prostate cancer, vulval cancer, thyroid cancer, hepatic carcinoma, anal carcinoma, penile carcinoma, melanoma, superficial spreading melanoma, lentigo maligna melanoma, acral lentiginous melanomas, nodular melanomas, as well as abnormal vascular proliferation associated with phakomatoses, edema (such as that associated with brain tumors), Meigs' syndrome, brain, as well as head and neck cancer, and associated metastases. In certain embodiments, cancers that are amenable to treatment by the antibodies of the disclosure include breast cancer, colorectal cancer, rectal cancer, non-small cell lung cancer, glioblastoma, non-Hodgkins lymphoma (NHL), renal cell cancer, prostate cancer, liver cancer, pancreatic cancer, soft-tissue sarcoma, Kaposi's sarcoma, carcinoid carcinoma, head and neck cancer, ovarian cancer, and mesothelioma.“Effector functions” refer to those biological activities attributable to the Fc region of an antibody, which vary with the antibody isotype. Examples of antibody effector functions include: C1q binding and complement dependent cytotoxicity (CDC); Fc receptor binding; antibody-dependent cell-mediated cytotoxicity (ADCC); phagocytosis; down regulation of cell surface receptors (e.g., B cell receptor); and B cell activation.“Complement dependent cytotoxicity” or “CDC” refers to the lysis of a target cell in the presence of complement. Activation of the classical complement pathway is initiated by the binding of the first component of the complement system (C1q) to antibodies (of the appropriate subclass) that are bound to their cognate antigen. To assess complement activation, a CDC assay, e.g., as described in Gazzano- Santoro et al., J. Immunol. Methods 202:163 (1996), can be performed.“Antibody-dependent cell-mediated cytotoxicity” or “ADCC” refers to a form of cytotoxicity in which secreted Ig bound onto Fc receptors (FcRs) present on certain cytotoxic cells {e.g., Natural Killer (NK)cells, neutrophils, and macrophages) enable these cytotoxic effector cells to bind specifically to an antigen-bearing target cell and subsequently kill the target cell with cytotoxic agents. The antibodies “arm” the cytotoxic cells and are absolutely required for such killing. The primary cells for mediating ADCC, NK cells, express FcyRIII only, whereas monocytes express FcyRI, FcyRII, and FcyRIII. FcR expression on hematopoietic cells is summarized in Table 3 on page 464 of Ravetch and Kinet. Annu. Rev. Immunol. 9:457-92, 1991 . To assess ADCC activity of a molecule of interest, an in vitro ADCC assay, such as that described in U.S. Patent No. 5,500,362 or 5,821 ,337 can be performed. Useful effector cells for such assays include peripheral blood mononuclear cells (PBMC) and Natural Killer (NK) cells. Alternatively, or additionally, ADCC activity of the molecule of interest can be assessed in vivo, e.g., in an animal model such as that disclosed in Clynes et al. Proc. Natl. Acad. Sci. USA. 95:652-656, 1998.“Complex” or “complexed” as used herein refers to the association of two or more molecules that interact with each other through bonds and / or forces {e.g., Van der Waals, hydrophobic, hydrophilic forces) that are not peptide bonds. In one aspect, the complex is heteromultimeric. It should be understood that the term “protein complex” or “polypeptide complex” as used herein includes complexes that have a non-protein entity conjugated to a protein in the protein complex {e.g., including, but not limited to, chemical molecules such as a toxin or a detection agent).As used herein, “delaying progression” of a disorder or disease means to defer, hinder, slow, retard, stabilize, and / or postpone development of the disease or disorder (e.g., a cell proliferative disorder, e.g., cancer). This delay can be of varying lengths of time, depending on the history of the disease and / or individual being treated. As is evident to one skilled in the art, a sufficient or significant delay can, in effect, encompass prevention, in that the individual does not develop the disease. For example, a late-stage cancer, such as development of metastasis, may be delayed.As used herein, an “effective amount” or “therapeutically effective amount” of a compound, for example, an anti-FcRH5 / anti-CD3 T-cell-dependent bispecific antibody (TDB) of the disclosure (e.g., cevostamab) or a composition (e.g., pharmaceutical composition) thereof, is at least the minimum amount required to achieve the desired therapeutic or prophylactic result, such as a measurable improvement or prevention of a particular disorder (e.g., a cell proliferative disorder, e.g., cancer). An effective amount herein may vary according to factors such as the disease state, age, sex, and weight of the patient, and the ability of the antibody to elicit a desired response in the individual. An effective amount is also one in which any toxic or detrimental effects of the treatment are outweighed by the therapeutically beneficial effects. For prophylactic use, beneficial or desired results include results such as eliminating or reducing the risk, lessening the severity, or delaying the onset of the disease, including biochemical, histological and / or behavioral symptoms of the disease, its complications, and intermediate pathological phenotypes presenting during development of the disease. For therapeutic use, beneficial or desired results include clinical results such as decreasing one or more symptoms resulting from the disease, increasing the quality of life of those suffering from the disease, decreasing the dose of other medications required to treat the disease, enhancing effect of another medication such as via targeting, delaying the progression of the disease, and / or prolonging survival. In the case of cancer or tumor, an effective amount of the drug may have the effect in reducing the number of cancer cells; reducing the tumor size; inhibiting {i.e., slow to some extent or desirably stop) cancer cell infiltration into peripheral organs; inhibit {i.e., slow to someextent and desirably stop) tumor metastasis; inhibiting to some extent tumor growth; and / or relieving to some extent one or more of the symptoms associated with the disorder. An effective amount can be administered in one or more administrations. For purposes of this disclosure, an effective amount of drug, compound, or pharmaceutical composition is an amount sufficient to accomplish prophylactic or therapeutic treatment either directly or indirectly. As is understood in the clinical context, an effective amount of a drug, compound, or pharmaceutical composition may or may not be achieved in conjunction with another drug, compound, or pharmaceutical composition. Thus, an “effective amount” may be considered in the context of administering one or more therapeutic agents, and a single agent may be considered to be given in an effective amount if, in conjunction with one or more other agents, a desirable result may be or is achieved.As used herein, “overall survival” or “OS” refers to the percentage of individuals in a group who are likely to be alive after a particular duration of time.As used herein, “objective response rate” (ORR) refers to the sum of stringent complete response (sCR), complete response (CR), very good partial response (VGPR), and partial response (PR) rates as determined using the International Myeloma Working Group response criteria (Table 7).The term “epitope” refers to the particular site on an antigen molecule to which an antibody binds. In some aspects, the particular site on an antigen molecule to which an antibody binds is determined by hydroxyl radical footprinting. In some aspects, the particular site on an antigen molecule to which an antibody binds is determined by crystallography.A “growth inhibitory agent” when used herein refers to a compound or composition which inhibits growth of a cell either in vitro or in vivo. In one aspect, growth inhibitory agent is growth inhibitory antibody that prevents or reduces proliferation of a cell expressing an antigen to which the antibody binds. In another aspect, the growth inhibitory agent may be one which significantly reduces the percentage of cells in S phase. Aspects of growth inhibitory agents include agents that block cell cycle progression (at a place other than S phase), such as agents that induce G1 arrest and M-phase arrest. Classical M-phase blockers include the vincas (vincristine and vinblastine), taxanes, and topoisomerase II inhibitors such as doxorubicin, epirubicin, daunorubicin, etoposide, and bleomycin. Those agents that arrest G1 also spill over into S-phase arrest, for example, DNA alkylating agents such as tamoxifen, prednisone, dacarbazine, mechlorethamine, cisplatin, methotrexate, 5-fluorouracil, and ara-C. Further information can be found in Mendelsohn and Israel, eds., The Molecular Basis of Cancer, Chapter 1 , entitled “Cell cycle regulation, oncogenes, and antineoplastic drugs” by Murakami et al. (W.B. Saunders, Philadelphia, 1995), e.g., p. 13. The taxanes (paclitaxel and docetaxel) are anticancer drugs both derived from the yew tree. Docetaxel (TAXOTERE®, Rhone-Poulenc Rorer), derived from the European yew, is a semisynthetic analogue of paclitaxel (TAXOL®, Bristol-Myers Squibb). Paclitaxel and docetaxel promote the assembly of microtubules from tubulin dimers and stabilize microtubules by preventing depolymerization, which results in the inhibition of mitosis in cells.An “immunoconjugate” is an antibody conjugated to one or more heterologous molecule(s), including but not limited to a cytotoxic agent.The term “immunomodulatory agent” refers to a class of molecules that modifies the immune system response or the functioning of the immune system. Immunomodulatory agents include, but are notlimited to, PD-L1 axis binding antagonists, thalidomide (a-N-phthalimido-glutarimide) and its analogues, OTEZLA® (apremilast), REVLIMID® (lenalidomide) and POMALYST® (pomalidomide), and pharmaceutically acceptable salts or acids thereof.A “subject” or an “individual” is a mammal. Mammals include, but are not limited to, domesticated animals (e.g., cows, sheep, cats, dogs, and horses), primates (e.g., humans and non-human primates such as monkeys), rabbits, and rodents (e.g., mice and rats). In certain aspects, the subject or individual is a human.An “isolated” protein or peptide is one which has been separated from a component of its natural environment. In some aspects, a protein or peptide is purified to greater than 95% or 99% purity as determined by, for example, electrophoresis (e.g., SDS-PAGE, isoelectric focusing (IEF), capillary electrophoresis) or chromatography (e.g., ion exchange or reverse phase HPLC).An “isolated” nucleic acid refers to a nucleic acid molecule that has been separated from a component of its natural environment. An isolated nucleic acid includes a nucleic acid molecule contained in cells that ordinarily contain the nucleic acid molecule, but the nucleic acid molecule is present extrachromosomally or at a chromosomal location that is different from its natural chromosomal location.The term “PD-L1 axis binding antagonist” refers to a molecule that inhibits the interaction of a PD- L1 axis binding partner with either one or more of its binding partners, so as to remove T cell dysfunction resulting from signaling on the PD-L1 signaling axis - with a result being to restore or enhance T cell function (e.g., proliferation, cytokine production, target cell killing). As used herein, a PD-L1 axis binding antagonist includes a PD-1 binding antagonist, a PD-L1 binding antagonist and a PD-L2 binding antagonist. The term “PD-1 binding antagonist” refers to a molecule that decreases, blocks, inhibits, abrogates or interferes with signal transduction resulting from the interaction of PD-1 with one or more of its binding partners, such as PD-L1 , PD-L2. In some aspects, the PD-1 binding antagonist is a molecule that inhibits the binding of PD-1 to one or more of its binding partners. In a specific aspect, the PD-1 binding antagonist inhibits the binding of PD-1 to PD-L1 and / or PD-L2. For example, PD-1 binding antagonists include anti-PD-1 antibodies, antigen binding fragments thereof, immunoadhesins, fusion proteins, oligopeptides and other molecules that decrease, block, inhibit, abrogate or interfere with signal transduction resulting from the interaction of PD-1 with PD-L1 and / or PD-L2. In one aspect, a PD-1 binding antagonist reduces the negative co-stimulatory signal mediated by or through cell surface proteins expressed on T lymphocytes mediated signaling through PD-1 so as render a dysfunctional T cell less dysfunctional (e.g., enhancing effector responses to antigen recognition). In some aspects, the PD-1 binding antagonist is an anti-PD-1 antibody. In a specific aspect, a PD-1 binding antagonist is MDX- 1 106 (nivolumab). In another specific aspect, a PD-1 binding antagonist is MK-3475 (pembrolizumab). In another specific aspect, a PD-1 binding antagonist is AMP-224. In another specific aspect, a PD-1 binding antagonist is MED1 -0680. In another specific aspect, a PD-1 binding antagonist is PDR001 . In another specific aspect, a PD-1 binding antagonist is REGN2810. In another specific aspect, a PD-1 binding antagonist is BGB-108.The term “PD-L1 binding antagonist” refers to a molecule that decreases, blocks, inhibits, abrogates or interferes with signal transduction resulting from the interaction of PD-L1 with either one or more of its binding partners, such as PD-1 , B7-1 . In some aspects, a PD-L1 binding antagonist is amolecule that inhibits the binding of PD-L1 to its binding partners. In a specific aspect, the PD-L1 binding antagonist inhibits binding of PD-L1 to PD-1 and / or B7-1 . In some aspects, the PD-L1 binding antagonists include anti-PD-L1 antibodies, antigen binding fragments thereof, immunoadhesins, fusion proteins, oligopeptides and other molecules that decrease, block, inhibit, abrogate or interfere with signal transduction resulting from the interaction of PD-L1 with one or more of its binding partners, such as PD- 1 , B7-1 . In one aspect, a PD-L1 binding antagonist reduces the negative co-stimulatory signal mediated by or through cell surface proteins expressed on T lymphocytes mediated signaling through PD-L1 so as to render a dysfunctional T cell less dysfunctional (e.g., enhancing effector responses to antigen recognition). In some aspects, a PD-L1 binding antagonist is an anti-PD-L1 antibody. In still another specific aspect, an anti-PD-L1 antibody is MPDL3280A (atezolizumab, marketed as TECENTRIQ™ with a WHO Drug Information (International Nonproprietary Names for Pharmaceutical Substances), Recommended INN: List 74, Vol. 29, No. 3, 2015 (see page 387)). In a specific aspect, an anti-PD-L1 antibody is YW243.55.S70. In another specific aspect, an anti-PD-L1 antibody is MDX-1105. In another specific aspect, an anti PD-L1 antibody is MSB0015718C. In still another specific aspect, an anti-PD-L1 antibody is MEDI4736.The term “PD-L2 binding antagonist” refers to a molecule that decreases, blocks, inhibits, abrogates or interferes with signal transduction resulting from the interaction of PD-L2 with either one or more of its binding partners, such as PD-1 . In some aspects, a PD-L2 binding antagonist is a molecule that inhibits the binding of PD-L2 to one or more of its binding partners. In a specific aspect, the PD-L2 binding antagonist inhibits binding of PD-L2 to PD-1 . In some aspects, the PD-L2 antagonists include anti-PD-L2 antibodies, antigen binding fragments thereof, immunoadhesins, fusion proteins, oligopeptides and other molecules that decrease, block, inhibit, abrogate or interfere with signal transduction resulting from the interaction of PD-L2 with either one or more of its binding partners, such as PD-1 . In one aspect, a PD-L2 binding antagonist reduces the negative co-stimulatory signal mediated by or through cell surface proteins expressed on T lymphocytes mediated signaling through PD-L2 so as render a dysfunctional T cell less dysfunctional (e.g., enhancing effector responses to antigen recognition). In some aspects, a PD-L2 binding antagonist is an immunoadhesin.The term “protein,” as used herein, refers to any native protein from any vertebrate source, including mammals such as primates (e.g., human subjects) and rodents (e.g., mice and rats), unless otherwise indicated. The term encompasses “full-length,” unprocessed protein as well as any form of the protein that results from processing in the cell. The term also encompasses naturally occurring variants of the protein, e.g., splice variants or allelic variants.“Percent (%) amino acid sequence identity” with respect to a reference polypeptide sequence is defined as the percentage of amino acid residues in a candidate sequence that are identical with the amino acid residues in the reference polypeptide sequence, after aligning the sequences and introducing gaps, if necessary, to achieve the maximum percent sequence identity, and not considering any conservative substitutions as part of the sequence identity. Alignment for purposes of determining percent amino acid sequence identity can be achieved in various ways that are within the skill in the art, for instance, using publicly available computer software such as BLAST, BLAST-2, ALIGN or Megalign (DNASTAR) software. Those skilled in the art can determine appropriate parameters for aligningsequences, including any algorithms needed to achieve maximal alignment over the full-length of the sequences being compared. For purposes herein, however, % amino acid sequence identity values are generated using the sequence comparison computer program ALIGN-2. The ALIGN-2 sequence comparison computer program was authored by Genentech, Inc., and the source code has been filed with user documentation in the U.S. Copyright Office, Washington D.C., 20559, where it is registered under U.S. Copyright Registration No. TXU510087. The ALIGN-2 program is publicly available from Genentech, Inc., South San Francisco, California, or may be compiled from the source code. The ALIGN-2 program should be compiled for use on a UNIX operating system, including digital UNIX V4.0D. All sequence comparison parameters are set by the ALIGN-2 program and do not vary.In situations where ALIGN-2 is employed for amino acid sequence comparisons, the % amino acid sequence identity of a given amino acid sequence A to, with, or against a given amino acid sequence B (which can alternatively be phrased as a given amino acid sequence A that has or comprises a certain % amino acid sequence identity to, with, or against a given amino acid sequence B) is calculated as follows:100 times the fraction X / Y where X is the number of amino acid residues scored as identical matches by the sequence alignment program ALIGN-2 in that program’s alignment of A and B, and where Y is the total number of amino acid residues in B. It will be appreciated that where the length of amino acid sequence A is not equal to the length of amino acid sequence B, the % amino acid sequence identity of A to B will not equal the % amino acid sequence identity of B to A. Unless specifically stated otherwise, all % amino acid sequence identity values used herein are obtained as described in the immediately preceding paragraph using the ALIGN-2 computer program.The term “pharmaceutical formulation” refers to a preparation which is in such form as to permit the biological activity of an active ingredient contained therein to be effective, and which contains no additional components which are unacceptably toxic to a subject to which the formulation would be administered.A “pharmaceutically acceptable carrier” refers to an ingredient in a pharmaceutical formulation, other than an active ingredient, which is nontoxic to a subject. A pharmaceutically acceptable carrier includes, but is not limited to, a buffer, excipient, stabilizer, or preservative.By “radiation therapy” is meant the use of directed gamma rays or beta rays to induce sufficient damage to a cell so as to limit its ability to function normally or to destroy the cell altogether. It will be appreciated that there will be many ways known in the art to determine the dosage and duration of treatment. Typical treatments are given as a one-time administration and typical dosages range from 10 to 200 units (Grays) per day.As used herein, “treatment” (and grammatical variations thereof such as “treat” or “treating”) refers to clinical intervention in an attempt to alter the natural course of the individual being treated, and can be performed either for prophylaxis or during the course of clinical pathology. Desirable effects of treatment include, but are not limited to, preventing occurrence or recurrence of disease, alleviation of symptoms, diminishment of any direct or indirect pathological consequences of the disease, preventing metastasis, decreasing the rate of disease progression, amelioration or palliation of the disease state,and remission or improved prognosis. In some aspects, antibodies of the disclosure (e.g., anti- FcRH5 / anti-CD3 TDBs of the disclosure) are used to delay development of a disease or to slow the progression of a disease.By “reduce” or “inhibit” is meant the ability to cause an overall decrease, for example, of 20% or greater, of 50% or greater, or of 75%, 85%, 90%, 95%, or greater. In certain aspects, reduce or inhibit can refer to the incidence or recurrence of cytokine release syndrome or events thereof. In certain aspects, reduce or inhibit can refer to the effector function of an antibody that is mediated by the antibody Fc region, such effector functions specifically including complement-dependent cytotoxicity (CDC), antibody-dependent cellular cytotoxicity (ADCC), and antibody-dependent cellular phagocytosis (ADCP).According to the disclosure, the term "vaccine" relates to a pharmaceutical preparation (pharmaceutical composition) or product that upon administration induces an immune response, in particular a cellular immune response, which recognizes and attacks a pathogen or a diseased cell such as a cancer cell. A vaccine may be used for the prevention or treatment of a disease. A vaccine may be a cancer vaccine. A “cancer vaccine” as used herein is a composition that stimulates an immune response in a subject against a cancer. Cancer vaccines typically consist of a source of cancer-associated material or cells (antigen) that may be autologous (from self) or allogenic (from others) to the subject, along with other components {e.g., adjuvants) to further stimulate and boost the immune response against the antigen. Cancer vaccines can result in stimulating the immune system of the subject to produce antibodies to one or several specific antigens, and / or to produce killer T cells to attack cancer cells that have those antigens.As used herein, “administering” is meant a method of giving a dosage of a compound (e.g., an anti-FcRH5 / anti-CD3 TDB) to a subject. In some aspects, the compositions utilized in the methods herein are administered intravenously. The compositions utilized in the methods described herein can be administered, for example, intramuscularly, intravenously, intradermally, percutaneously, intraarterially, intraperitoneally, intralesionally, intracranially, intraarticularly, intraprostatically, intrapleurally, intratracheally, intranasally, intravitreally, intravaginally, intrarectally, topically, intratumorally, peritoneally, subcutaneously, subconjunctivally, intravesicularlly, mucosally, intrapericardially, intraumbilically, intraocularly, orally, topically, locally, by inhalation, by injection, by infusion, by continuous infusion, by localized perfusion bathing target cells directly, by catheter, by lavage, in cremes, or in lipid compositions. The method of administration can vary depending on various factors (e.g., the compound or composition being administered and the severity of the condition, disease, or disorder being treated).“CD38” as used herein refers to a CD38 glycoprotein found on the surface of many immune cells, including CD4+, CD8+, B lymphocytes, and natural killer (NK) cells, and includes any native CD38 from any vertebrate source, including mammals such as primates (e.g., human subjects) and rodents (e.g., mice and rats), unless otherwise indicated. CD38 is expressed at a higher level and more uniformly on myeloma cells as compared to normal lymphoid and myeloid cells. The term encompasses “full-length,” unprocessed CD38, as well as any form of CD38 that results from processing in the cell. The term also encompasses naturally occurring variants of CD38, e.g., splice variants or allelic variants. CD38 is also referred to in the art as cluster of differentiation 38, ADP-ribosyl cyclase 1 , cADPr hydrolase 1 , and cyclic ADP-ribose hydrolase 1 . CD38 is encoded by the CD38 gene. The nucleic acid sequence of anexemplary human CD38 is shown under NCBI Reference Sequence: NM_001775.4 or in SEQ ID NO: 33. The amino acid sequence of an exemplary human CD38 protein encoded by CD38 is shown under UniProt Accession No. P28907 or in SEQ ID NO: 34.The term “anti-CD38 antibody” encompasses all antibodies that bind CD38 with sufficient affinity such that the antibody is useful as a therapeutic agent in targeting a cell expressing the antigen, and does not significantly cross-react with other proteins such as a negative control protein in the assays described below. For example, an anti-CD38 antibody may bind to CD38 on the surface of a MM cell and mediate cell lysis through the activation of complement-dependent cytotoxicity, ADCC, antibody-dependent cellular phagocytosis (ADCP), and apoptosis mediated by Fc cross-linking, leading to the depletion of malignant cells and reduction of the overall cancer burden. An anti-CD38 antibody may also modulate CD38 enzyme activity through inhibition of ribosyl cyclase enzyme activity and stimulation of the cyclic adenosine diphosphate ribose (cADPR) hydrolase activity of CD38. In certain aspects, an anti-CD38 antibody that binds to CD38 has a dissociation constant (KD) of < 1 pM, < 100 nM, < 10 nM, < 1 nM, < 0.1 nM, < 0.01 nM, or < 0.001 nM (e.g., 10-8M or less, e.g., from 10-8M to 10-13M, e.g., from 10-9M to 10-13M). In certain aspects, the anti-CD38 antibody may bind to both human CD38 and chimpanzee CD38. Anti-CD38 antibodies also include anti-CD38 antagonist antibodies. Bispecific antibodies wherein one arm of the antibody binds CD38 are also contemplated. Also encompassed by this definition of anti-CD38 antibody are functional fragments of the preceding antibodies. Examples of antibodies which bind CD38 include: daratumumab (DARZALEX®) (U.S. Patent No: 7,829,673 and U.S. Pub. No: 20160067205 A1 ); “MOR202” (U.S. Patent No: 8,263,746); and isatuximab (SAR-650984).As used herein, the term “target dose” refers to an effective amount of an anti-fragment crystallizable receptor-like 5 (FcRH5) / anti-cluster of differentiation 3 (CD3) bispecific antibody (e.g., cevostamab) that achieves a desired therapeutic effect, such as a desired clinical efficacy (e.g., an improved ORR, VGPR, CR, or PR rate) and, optionally, a desired safety profile (e.g., a reduced likelihood of an infection, serious adverse event (SAE), and / or adverse event (AE)). Target doses for a bispecific antibody that binds to FcRH5 and CD3 (e.g., an anti-FcRH5 / anti-CD3 antibody, e.g., cevostamab) may, for example, be about 20 mg to about 252 mg (e.g., about 160 mg). In some aspects, the dosage of a target dose may increase or decrease during a given dosing regimen, depending upon the frequency of its administration. As non-limiting examples, a target dose of about 20 mg to about 160 mg may be administered once every week (QW), a target dose of about 60 mg to about 180 mg (e.g., 90 mg) may be administered about once every two weeks (Q2W), a target dose of about 90 mg to about 240 mg (e.g., 160 mg) may be administered about once every three weeks (Q3W), and a target dose of about 60 mg to about 252 mg may be administered about once every four weeks (Q4W).As used herein, the phrase “relapsed or refractory” or “R / R” refers to a status of a disease (e.g., a cancer, e.g., a MM) in patient in which the disease has either returned after a period of improvement (relapsed) or has failed to respond to treatment (refractory). Relapsed disease occurs when a patient initially achieves remission but later experiences disease progression, while refractory disease does not respond to therapy or it progresses shortly after treatment.As used herein, the phrase “heavily pre-treated” refers to a cancer patient (e.g., subjects with an R / R MM) who has received at least three prior lines of treatment for their cancer (e.g., 3, 4, 5, 6, 7, 8, 9,10, 11 , 12, 13, or 14 prior lines of treatment, or more, for their cancer (e.g., R / R MM)). Exemplary prior lines of treatment include proteasome inhibitors (e.g., bortezomib, carfilzomib, and ixazomib), immunomodulatory drugs (e.g., thalidomide, lenalidomide, and pomalidomide), and anti-CD38 antibodies (e.g., daratumumab, MOR202, and isatuximab).As used herein, a level that is “safe” for the subject to receive a target dose of a bispecific antibody that binds to FcRH5 and CD3 (e.g., cevostamab) is a level at which the subject is unlikely to develop further CRS events or further signs or symptoms of CRS upon administration of a target dose (e.g., a C1 D4 or C2D1 dose) of a bispecific antibody that binds to FcRH5 and CD3 (e.g., cevostamab), which can be determined, for example, by assessment of a biomarker (e.g., IL-6). In some instances, a peak IL-6 level of less than about 80 pg / mL (e.g., less than about 30 pg / mL) indicates that risk of CRS events in the subject is at a level that is safe for the subject to receive a target dose of the bispecific antibody that binds to FcRH5 and CD3 (e.g., cevostamab).11. THERAPEUTIC METHODSThe disclosure is based, in part, on methods of treating a subject having cancer (e.g., multiple myeloma (MM), e.g., relapsed or refractory (R / R) MM) using dose-escalation dosing regimens with antifragment crystallizable receptor-like 5 (FcRH5) / anti-cluster of differentiation 3 (CD3) bispecific antibodies (e.g., cevostamab). The methods are expected to reduce the likelihood of, minimize, or inhibit unwanted treatment effects, which include cytokine-driven toxicities (e.g., cytokine release syndrome (CRS)), infusion-related reactions (IRRs), macrophage activation syndrome (MAS), neurologic toxicities, severe tumor lysis syndrome (TLS), neutropenia, thrombocytopenia, and / or elevated liver enzymes. Therefore, the methods are useful for treating the subject while achieving a favorable benefit-risk profile.A. Double Step-Up Dosing RegimensThe disclosure provides methods for treating a subject having a cancer (e.g., MM, e.g., R / R MM). The method includes a step of administering to the subject a bispecific antibody that binds to FcRH5 and CD3 (e.g., an anti-FcRH5 / anti-CD3 antibody, e.g., cevostamab) in a double step-up dose-escalation dosing regimen described herein.For example, the bispecific antibody may be administered to the subject in a double step-up dosing regimen comprising at least a first dosing cycle, wherein the first dosing cycle comprises a first dose (C1 D1 ; cycle 1 , dose 1 ), a second dose (C1 D2; cycle 1 , dose 2), and a third dose (C1 D3; cycle 1 , dose 3) of the bispecific antibody. The first dosing cycle may be three weeks or 21 days long. In such instances, the C1 D1 of the bispecific antibody may be administered to the subject on Day 1 of the first dosing cycle; the C1 D2 of the bispecific antibody may be administered to the subject on Day 2, Day 3, or Day 4 (“D2-4”) of the first dosing cycle; and the C1 D3 of the bispecific antibody may be administered to the subject on Day 8 of the first dosing cycle.In some embodiments, the method further includes the administration of one or more additional therapeutic agents described herein (e.g., tocilizumab). In such instances, the one or more additional therapeutic agents (e.g., tocilizumab) may be administered prior to (e.g., about 2 hours), subsequent to (e.g., about 2 hours), or concurrently with the administration of the bispecific antibody.In some embodiments, administration of the bispecific antibody that binds to FcRH5 and CD3 (e.g., an anti-FcRH5 / anti-CD3 antibody, e.g., cevostamab) occurs in a dosing regimen described herein for at least two months, at least three months, at least four months, at least five months, at least six months, at least seven months, at least eight months, at least nine months, at least ten months, at least eleven months, or at least one year. In some embodiments, administration of the bispecific antibody that binds to FcRH5 and CD3 (e.g., an anti-FcRH5 / anti-CD3 antibody, e.g., cevostamab) occurs in a dosing regimen described herein for about two months, about three months, about four months, about five months, about six months, about seven months, about eight months, about nine months, about ten months, about eleven months, or about twelve months (e.g., up to one year, e.g., up to 52 weeks).The double step-up dosing regimens outlined above are described in further detail below, including exemplary dosages and days of administering the bispecific antibody.DosagesThe C1 D1 of the bispecific antibody (e.g., an anti-FcRH5 / anti-CD3 antibody, e.g., cevostamab) may be administered to the subject at a dosage that is between about 0.01 milligram (mg) to about 0.9 mg. For example, the C1 D1 may be about 0.01 mg to about 0.1 mg, about 0.1 mg to about 0.5 mg, about 0.25 mg to about 0.75 mg, about 0.5 mg to about 0.9 mg, or about 0.2 mg to about 0.4 mg. In another example, the C1 D1 may be about 0.01 mg, about 0.05 mg, about 0.1 mg, about 0.15 mg, about 0.2 mg, about 0.25 mg, about 0.3 mg, about 0.35 mg, about 0.4 mg, about 0.45 mg, about 0.5 mg, about 0.55 mg, about 0.6 mg, about 0.65 mg, about 0.7 mg, about 0.75 mg, about 0.8 mg, about 0.85 mg, or about 0.9 mg. In some aspects, the C1 D1 is about 0.3 mg.The C1 D2 of the bispecific antibody (e.g., an anti-FcRH5 / anti-CD3 antibody, e.g., cevostamab) may be administered to the subject at a dosage that is greater than the C1 D1 (e.g., greater than 0.9 mg), preferably wherein the dosage is between about 1 mg to about 5.9 mg. For example, the C1 D2 may be about 1 mg to about 1 .5 mg, about 1 mg to about 2 mg, about 1 mg to about 2.9 mg, about 1 mg to about3.4 mg, about 1 .1 mg to about 1 .3 mg, about 1 .2 mg to about 3.3 mg, about 1 .5 mg to about 4 mg, about 2 mg to about 3 mg, about 2 mg to about 4.5 mg, about 2.5 mg to about 5 mg, about 3 mg to about 4 mg, about 3 mg to about 5 mg, about 3.5 mg to about 5.9 mg, about 3.2 mg to about 3.4 mg, or about 3.5 mg to about 3.7 mg. In another example, the C1 D2 may be about 1 mg, about 1 .1 mg, about 1 .2 mg, about1 .3 mg, about 1 .4 mg, about 1 .5 mg, about 1 .6 mg, about 1 .7 mg, about 1 .8 mg, about 1 .9 mg, about 2 mg, about 2.1 mg, about 2.2 mg, about 2.3 mg, about 2.4 mg, about 2.5 mg, about 2.6 mg, about 2.7 mg, about 2.8 mg, about 2.9 mg, about 3 mg, about 3.1 mg, about 3.2 mg, about 3.3 mg, about 3.4 mg, about3.5 mg, about 3.6 mg, about 3.7 mg, about 3.8 mg, about 3.9 mg, about 4 mg, about 4.1 mg, about 4.2 mg, about 4.3 mg, about 4.4 mg, about 4.5 mg, about 4.6 mg, about 4.7 mg, about 4.8 mg, about 4.9 mg, about 5 mg, about 5.1 mg, about 5.2 mg, about 5.3 mg, about 5.4 mg, about 5.5 mg, about 5.6 mg, about 5.7 mg, about 5.8 mg, or about 5.9 mg. In some aspects, the C1 D2 is about 3.3 mg.The C1 D3 of the bispecific antibody (e.g., an anti-FcRH5 / anti-CD3 antibody, e.g., cevostamab) may be administered to the subject at a dosage that is greater than the C1 D2 (e.g., greater than 5.9 mg), preferably wherein the dosage is between about 20 mg to about 600 mg. For example, the C1 D3 may be about 30 mg to about 500 mg, about 40 mg to about 400 mg, about 60 mg to about 350 mg, about 80 mgto about 300 mg, about 100 mg to about 200 mg, about 140 mg to about 180 mg, about 150 mg to about 170 mg, about 132 mg to about 160 mg, about 20 to about 252 mg, or about 100 mg to about 180 mg. In another example, the C1 D3 may be about 20 mg, about 25 mg, about 30 mg, about 35 mg, about 40 mg, about 45 mg, about 50 mg, about 55 mg, about 60 mg, about 65 mg, about 70 mg, about 75 mg, about 80 mg, about 85 mg, about 90 mg, about 95 mg, about 100 mg, about 105 mg, about 110 mg, about 115 mg, about 120 mg, about 125 mg, about 130 mg, about 131 mg, about 132 mg, about 133 mg, about 134 mg, about 135 mg, about 140 mg, about 145 mg, about 150 mg, about 155 mg, about 160 mg, about 165 mg, about 170 mg, about 175 mg, about 180 mg, about 185 mg, about 190 mg, about 195 mg, about 200 mg, about 205 mg, about 210 mg, about 215 mg, about 220 mg, about 225 mg, about 230 mg, about 235 mg, about 240 mg, about 245 mg, about 250 mg, about 252 mg, about 255 mg, about 260 mg, about 265 mg, about 270 mg, about 275 mg, about 280 mg, about 285 mg, about 290 mg, about 295 mg, about 300 mg, about 305 mg, about 310 mg, about 315 mg, about 320 mg, about 325 mg, about 330 mg, about 335 mg, about 340 mg, about 345 mg, about 350 mg, about 355 mg, about 360 mg, about 365 mg, about 370 mg, about 375 mg, about 380 mg, about 385 mg, about 390 mg, about 395 mg, about 400 mg, about 405 mg, about 410 mg, about 415 mg, about 420 mg, about 425 mg, about 430 mg, about 435 mg, about 440 mg, about 445 mg, about 450 mg, about 455 mg, about 460 mg, about 465 mg, about 470 mg, about 475 mg, about 480 mg, about 485 mg, about 490 mg, about 495 mg, about 500 mg, about 505 mg, about 510 mg, about 515 mg, about 520 mg, about 525 mg, about 530 mg, about 535 mg, about 540 mg, about 545 mg, about 550 mg, about 555 mg, about 560 mg, about 565 mg, about 570 mg, about 575 mg, about 580 mg, about 585 mg, about 590 mg, about 595 mg, or about 600 mg. In some aspects, the C1 D3 is about 160 mg.Exemplary combinations of double step-up dosagesWhile any combination of dosages (e.g., C1 D1 , C1 D2, and / or C1 D3, or later) described above can be used in a dosing regimen described herein, the following represent non-limiting examples of particular dosing combinations that can be used in a dosing regimen described herein.As an example, the disclosure provides a method of treating a subject (e.g., a human subject) having a cancer (e.g., a MM, e.g., R / R MM), the method comprising administering to the subject a bispecific antibody that binds to FcRH5 and CD3 (e.g., cevostamab) in a dosing regimen comprising at least a first dosing cycle (e.g., a first 21 -day dosing cycle), wherein the first dosing cycle comprises a C1 D1 , a C1 D2, and a C1 D3 of the bispecific antibody, and wherein the C1 D1 is between about 0.2 mg to about 0.4 mg (e.g., about 0.3 mg), the C1 D2 is greater than the C1 D1 (e.g., the C1 D2 is about 1 mg to about 5.9 mg, e.g., about 3.3 mg), and the C1 D3 is greater than the C1 D2 (e.g., the C1 D3 is about 20 mg to about 252 mg, about 100 mg to about 180 mg, or about 132 mg to about 160 mg, e.g., about 160 mg). The C1 D1 , C1 D2, and C1 D3 may be administered at any dosage described above so long as the C1 D2 is greater than the C1 D1 , and the C1 D3 is greater than the C1 D2. In some aspects, the method further includes the administration of tocilizumab about one to three hours (e.g., about 1 hour, about 1 .5 hours, about 2 hours, about 2.5 hours, or about 3 hours) prior to administering the first dose of the bispecific antibody.As another example, the disclosure provides a method of treating a subject (e.g., a human subject) having a cancer (e.g., a MM, e.g., a R / R MM), the method comprising administering to the subject a bispecific antibody that binds to FcRH5 and CD3 (e.g., cevostamab) in a dosing regimen comprising at least a first dosing cycle (e.g., a first 21 -day dosing cycle), wherein the first dosing cycle comprises a C1 D1 , a C1 D2, and a C1 D3 of the bispecific antibody, and wherein the C1 D1 is between about 0.01 mg to about 0.9 mg (e.g., between about 0.1 mg to about 0.6 mg, e.g., about 0.3 mg), the C1 D2 is between about 1 mg to about 5.9 mg (e.g., between about 3 mg to about 5 mg, e.g., 3.3 mg), and the C1 D3 is between about 20 mg to about 252 mg (e.g., between about 100 to about 180 mg or about 132 mg to about 160 mg, e.g., about 160 mg). In some aspects, the method further includes the administration of tocilizumab about one to three hours (e.g., about 1 hour, about 1 .5 hours, about 2 hours, about 2.5 hours, or about 3 hours) prior to administering the first dose of the bispecific antibody.Days of administrationThe bispecific antibody (e.g., an anti-FcRH5 / anti-CD3 antibody, e.g., cevostamab) may be administered to the subject in a double step-up dosing regimen described herein (e.g., a dosing regimen comprising a C1 D1 , a C1 D2, and a C1 D3, as described above) comprising at least a first dosing cycle, wherein the first dosing cycle is three weeks or 21 days long.In some aspects, the C1 D1 of the bispecific antibody is administered to the subject on Day 1 of the first dosing cycle; the C1 D2 of the bispecific antibody is administered to the subject on Day 2, Day 3, or Day 4 of the first dosing cycle; and the C1 D3 of the bispecific antibody is administered to the subject on Day 8 of the first dosing cycle.In some aspects, the C1 D1 of the bispecific antibody is administered to the subject on Day 1 of the first dosing cycle; the C1 D2 of the bispecific antibody is administered to the subject on Day 2 of the first dosing cycle; and the C1 D3 of the bispecific antibody is administered to the subject on Day 8 of the first dosing cycle. In some aspects, the C1 D1 of the bispecific antibody is administered to the subject on Day 1 of the first dosing cycle; the C1 D2 of the bispecific antibody is administered to the subject on Day 3 of the first dosing cycle; and the C1 D3 of the bispecific antibody is administered to the subject on Day 8 of the first dosing cycle. In some aspects, the C1 D1 of the bispecific antibody is administered to the subject on Day 1 of the first dosing cycle; the C1 D2 of the bispecific antibody is administered to the subject on Day 4 of the first dosing cycle; and the C1 D3 of the bispecific antibody is administered to the subject on Day 8 of the first dosing cycle.As an example, the disclosure provides a method of treating a subject (e.g., a human subject) having a cancer (e.g., a MM, e.g., R / R MM), the method comprising administering to the subject a bispecific antibody that binds to FcRH5 and CD3 (e.g., cevostamab) in a dosing regimen comprising at least a first dosing cycle, wherein the length of the first dosing cycle is 21 days, wherein the first dosing cycle comprises a C1 D1 , a C1 D2, and a C1 D3 of the bispecific antibody being administered on Day 1 , Day 2-4 (i.e., Day 2, Day 3, or Day 4), and Day 8, respectively, and wherein the C1 D1 is between about 0.2 mg to about 0.4 mg (e.g., about 0.3 mg), the C1 D2 is greater than the C1 D1 (e.g., the C1 D2 is about 1 mg to about 5.9 mg, e.g., about 3.3 mg), and the C1 D3 is greater than the C1 D2 (e.g., the C1 D3 is about 20 mg to about 252 mg, about 100 mg to about 180 mg, or about 132 mg to about 160 mg, e.g.,about 160 mg). The C1 D1 , C1 D2, and C1 D3 may be administered at any dosage described above so long as the C1 D2 is greater than the C1 D1 , and the C1 D3 is greater than the C1 D2. In some aspects, the C1 D1 , C1 D2, and C1 D3 are administered on Day 1 , Day 2, and Day 8, respectively, of the first dosing cycle. In some aspects, the C1 D1 , C1 D2, and C1 D3 are administered on Day 1 , Day 3, and Day 8, respectively, of the first dosing cycle. In some aspects, the C1 D1 , C1 D2, and C1 D3 are administered on Day 1 , Day 4, and Day 8, respectively, of the first dosing cycle. In some aspects, the method further includes administering tocilizumab about one to three hours (e.g., about 1 hour, about 1 .5 hours, about 2 hours, about 2.5 hours, or about 3 hours) prior to administering the bispecific antibody.As another example, the disclosure provides a method of treating a subject (e.g., a human subject) having a cancer (e.g., a MM, e.g., a R / R MM), the method comprising administering to the subject a bispecific antibody that binds to FcRH5 and CD3 (e.g., cevostamab) in a dosing regimen comprising at least a first dosing cycle, wherein the length of the first dosing cycle is 21 days, wherein the first dosing cycle comprises a C1 D1 , a C1 D2, and a C1 D3 of the bispecific antibody being administered on Day 1 , Day 2-4 (i.e., Day 2, Day 3, or Day 4), and Day 8, respectively, and wherein the C1 D1 is between about 0.01 mg to about 0.9 mg (e.g., between about 0.1 mg to about 0.6 mg, e.g., about 0.3 mg), the C1 D2 is between about 1 mg to about 5.9 mg (e.g., between about 3 mg to about 5 mg, e.g., 3.3 mg), and the C1 D3 is between about 20 mg to about 252 mg (e.g., between about 100 mg to about 180 mg, e.g., between about 132 mg to about 160 mg, e.g., about 160 mg). In some aspects, the C1 D1 , C1 D2, and C1 D3 are administered on Day 1 , Day 2, and Day 8, respectively, of the first dosing cycle. In some aspects, the C1 D1 , C1 D2, and C1 D3 are administered on Day 1 , Day 3, and Day 8, respectively, of the first dosing cycle. In some aspects, the C1 D1 , C1 D2, and C1 D3 are administered on Day 1 , Day 4, and Day 8, respectively, of the first dosing cycle. In some aspects, the method further includes administering tocilizumab about one to three hours (e.g., about 1 hour, about 1 .5 hours, about 2 hours, about 2.5 hours, or about 3 hours) prior to administering the bispecific antibody.As yet another example, the disclosure provides a method of treating a subject having a MM, wherein the method comprises administering to the subject a bispecific antibody that binds to FcRH5 and CD3 in a dosing regimen comprising at least a first dosing cycle, wherein the length of the first dosing cycle is 21 days, wherein the first dosing cycle comprises a first dose (C1 D1 ), a second dose (C1 D2), and a third dose (C1 D3) of the bispecific antibody, and wherein: (a) the C1 D1 is about 0.3 mg and is administered to the subject on or about Day 1 of the first dosing cycle; (b) the C1 D2 is about 3.3 mg and is administered to the subject on or about Day 2, day 3, or Day 4 of the first dosing cycle; and (c) the C1 D3 is about 160 mg and is administered to the subject on or about Day 8 of the first dosing cycle. In some aspects, the method further comprises administering to the subject tocilizumab about 2 hours prior to administering the first dose (e.g., C1 D1 ) of the bispecific antibody.Dosing cyclesThe bispecific antibody (e.g., an anti-FcRH5 / anti-CD3 antibody, e.g., cevostamab) may be administered to the subject in a dosing regimen described above (e.g., a dosing regimen comprising a C1 D1 , a C1 D2, and a C1 D3) with only a single dosing cycle (e.g., one dosing cycle comprising a C1 D1 , a C1 D2, and a C1 D3). However, in some aspects, the dosing regimen further comprises a second dosingcycle, wherein the second dosing cycle includes at least a single dose (C2D1 ; cycle 2, dose 1 ) of the bispecific antibody. The second dosing cycle may be three weeks or 21 days long and may include administering to the subject the C2D1 on or about Day 1 of the second dosing cycle.In some aspects, the C2D1 is equal to or greater than the C1 D3. For example, the C2D1 may be about 20 mg to about 600 mg, about 30 mg to about 500 mg, about 40 mg to about 400 mg, about 60 mg to about 350 mg, about 80 mg to about 300 mg, about 100 mg to about 200 mg, about 140 mg to about 180 mg, about 150 mg to about 170 mg, about 132 mg to about 160 mg, about 20 mg to about 252 mg, or about 100 mg to about 180 mg. In another example, the C2D1 may be about 20 mg, about 25 mg, about 30 mg, about 35 mg, about 40 mg, about 45 mg, about 50 mg, about 55 mg, about 60 mg, about 65 mg, about 70 mg, about 75 mg, about 80 mg, about 85 mg, about 90 mg, about 95 mg, about 100 mg, about 105 mg, about 110 mg, about 115 mg, about 120 mg, about 125 mg, about 130 mg, about 131 mg, about 132 mg, about 133 mg, about 134 mg, about 135 mg, about 140 mg, about 145 mg, about 150 mg, about155 mg, about 160 mg, about 165 mg, about 170 mg, about 175 mg, about 180 mg, about 185 mg, about190 mg, about 195 mg, about 200 mg, about 205 mg, about 210 mg, about 215 mg, about 220 mg, about225 mg, about 230 mg, about 235 mg, about 240 mg, about 245 mg, about 250 mg, about 252 mg, about255 mg, about 260 mg, about 265 mg, about 270 mg, about 275 mg, about 280 mg, about 285 mg, about290 mg, about 295 mg, about 300 mg, about 305 mg, about 310 mg, about 315 mg, about 320 mg, about325 mg, about 330 mg, about 335 mg, about 340 mg, about 345 mg, about 350 mg, about 355 mg, about360 mg, about 365 mg, about 370 mg, about 375 mg, about 380 mg, about 385 mg, about 390 mg, about395 mg, about 400 mg, about 405 mg, about 410 mg, about 415 mg, about 420 mg, about 4...

Claims

1. WHAT IS CLAIMED IS:1 . A method of reducing the likelihood of cytokine release syndrome (CRS) in a subject having multiple myeloma (MM) and being administered an effective amount of cevostamab, wherein, prior to a first administration to the subject of the effective amount of cevostamab, the method comprises administering to the subject cevostamab in a dosing regimen comprising at least a first dosing cycle (C1 ), wherein the C1 comprises a first dose (C1 D1 ), a second dose (C1 D2), and a third dose (C1 D3) of cevostamab, wherein the C1 D1 is about 0.3 mg, the C1 D2 is between about 1 .2 mg to about 3.3 mg, and the C1 D3 is between about 3.6 mg to about 7.2 mg.

2. A method of reducing the likelihood of CRS in a subject having MM and being administered an effective amount of cevostamab, wherein, prior to a first administration to the subject of the effective amount of cevostamab, the method comprises administering to the subject cevostamab in a dosing regimen comprising at least a first dosing cycle (C1 ), wherein the C1 comprises a first dose (C1 D1 ), a second dose (C1 D2), and a third dose (C1 D3) of cevostamab, wherein the C1 D1 is about 0.3 mg; the C1 D2 is about 1 .2 mg; and the C1 D3 is about 3.6 mg.

3. A method of reducing the likelihood of CRS in a subject having MM and being administered an effective amount of cevostamab, wherein, prior to a first administration to the subject of the effective amount of cevostamab, the method comprises administering to the subject cevostamab in a dosing regimen comprising at least a first dosing cycle (C1 ), wherein the C1 comprises a first dose (C1 D1 ), a second dose (C1 D2), and a third dose (C1 D3) of cevostamab, wherein the C1 D1 is about 0.3 mg; the C1 D2 is about 3.3 mg; and the C1 D3 is about 7.2 mg.

4. A method of achieving a median peak IL-6 level of less than about 30 pg / mL in a population of subjects having MM and being administered an effective amount of cevostamab, the method comprising administering to a subject in the population, prior to being administered the effective amount of cevostamab, a dosing regimen comprising at least a first dosing cycle (C1 ), wherein the C1 comprises a first dose (C1 D1 ), a second dose (C1 D2), and a third dose (C1 D3) of cevostamab, wherein the C1 D1 is about 0.3 mg, the C1 D2 is between about 1 .2 mg to about 3.3 mg, and the C1 D3 is between about 3.6 mg to about 7.2 mg.

5. The method of claim 4, wherein the C1 D1 is about 0.3 mg; the C1 D2 is about 1 .2 mg; and the C1 D3 is about 3.6 mg.

6. The method of claim 4 or 5, wherein the median peak IL-6 level is about 18 pg / mL following administration of the effective amount of cevostamab.

7. A method of achieving a peak IL-6 level of less than about 30 pg / mL in a subject having MM and being administered an effective amount of cevostamab, the method comprising administering to the subject, prior to being administered the effective amount of cevostamab, a dosing regimen comprising at least afirst dosing cycle (C1 ), wherein the C1 comprises a first dose (C1 D1 ), a second dose (C1 D2), and a third dose (C1 D3) of cevostamab, wherein the C1 D1 is about 0.3, the C1 D2 is between about 1 .2 mg to about 3.3 mg, and the C1 D3 is between about 3.6 mg to about 7.2 mg.

8. The method of claim 7, wherein the C1 D1 is about 0.3 mg; the C1 D2 is about 1 .2 mg; and the C1 D3 is about 3.6 mg.

9. The method of claim 7 or 8, wherein the peak IL-6 level is about 18 pg / mL following administration of cevostamab.

10. A method of reducing the occurrence of CRS events in a subject being treated for MM with a target dose of cevostamab, the method comprising administering to the subject, prior to a first administration of the target dose to the subject in a dosing regimen comprising a first dosing cycle (C1 ), (i) a first dose (C1 D1 ), (ii) a second dose (C1 D2), and (iii) a third dose (C1 D3) of cevostamab, wherein the C1 D1 is about 0.03 mg, the C1 D2 is between about 1 .2 mg to about 3.3 mg, and the C1 D3 is between about 3.6 mg to about 7.2 mg.11 . A method of reducing the occurrence of CRS events in a subject being treated for MM with a target dose of cevostamab, the method comprising administering to the subject, prior to a first administration of the target dose to the subject in a dosing regimen comprising a first dosing cycle (C1 ), (i) a first dose(C1 D1 ) of about 0.3 mg, (ii) a second dose (C1 D2) of about 1 .2 mg, and (iii) a third dose (C1 D3) of about 3.6 mg of cevostamab.

12. A method of reducing the occurrence of CRS events in a subject being treated for MM with a target dose of cevostamab, the method comprising administering to the subject, prior to a first administration of the target dose to the subject in a dosing regimen comprising a first dosing cycle (C1 ), (i) a first dose (C1 D1 ) of about 0.3 mg, (ii) a second dose (C1 D2) of about 3.3 mg, and (ii) a third dose (C1 D3) of about 7.2 mg of cevostamab.

13. The method of any one of claims 10-12, wherein the C1 is 21 days in length, and wherein:(i) the C1 D1 is administered on Day 1 of the C1 ;(ii) the C1 D2 is administered on Day 2, Day 3, or Day 4 of the C1 ; and(iii) the C1 D3 is administered on Day 8 of the C1 .

14. The method of any one of claims 10-13, wherein the target dose is greater than the C1 D3.

15. The method of claim 14, wherein the target dose is between about 20 mg to about 252 mg.

16. The method of any one of claims 1 -15, wherein the method further comprises administering to the subject an additional dose of cevostamab, wherein the additional dose of cevostamab is greater than the C1 D3.

17. The method of claim 16, wherein the additional dose of cevostamab is administered during the C1 after the C1 D3 as a fourth dose (C1 D4) of cevostamab, wherein the C1 D4 is an effective amount of cevostamab.

18. A method of treating a subject having MM, wherein the method comprises administering to the subject an effective amount of cevostamab in a dosing regimen comprising at least a first dosing cycle (C1 ), wherein the C1 comprises a first dose (C1 D1 ), a second dose (C1 D2), a third dose (C1 D3), and a fourth dose (C1 D4) of cevostamab, wherein the C1 D1 is about 0.3 mg, the C1 D2 is about 1 .2 mg to about 3.3 mg, the C1 D3 is about 3.6 mg to about 7.2 mg, and the C1 D4 is between about 20 mg to about 252 mg.

19. The method of claim 18, wherein the C1 D4 is an effective amount of cevostamab.

20. The method of claim 18 or 19, wherein the C1 D1 is about 0.3 mg; the C1 D2 is about 1 .2 mg; and the C1 D3 is about 3.6 mg.21 . The method of claim 18 or 19, wherein the C1 D1 is about 0.3 mg; the C1 D2 is about 3.3 mg; and the C1 D3 is about 7.2 mg.

22. A method of treating a subject having MM, wherein the method comprises administering to the subject an effective amount of cevostamab in a dosing regimen comprising at least a first dosing cycle (C1 ), wherein the C1 comprises a first dose (C1 D1 ), a second dose (C1 D2), a third dose (C1 D3), and a fourth dose (C1 D4) of cevostamab, wherein the C1 D1 is about 0.3 mg; the C1 D2 is about 1 .2 mg; the C1 D3 is about 3.6 mg; and the C1 D4 is about 160 mg.

23. A method of treating a subject having MM, wherein the method comprises administering to the subject an effective amount of cevostamab in a dosing regimen comprising at least a first dosing cycle (C1 ), wherein the C1 comprises a first dose (C1 D1 ), a second dose (C1 D2), a third dose (C1 D3), and a fourth dose (C1 D4) of cevostamab, the C1 D1 is about 0.3 mg; the C1 D2 is about 3.3 mg; the C1 D3 is about 7.2 mg; and the C1 D4 is about 160 mg.

24. The method of any one of claims 1 -23, wherein the length of the C1 is 21 days.

25. The method of claim 24, wherein the method comprises administering to the subject:(a) the C1 D1 on or about Day 1 of the C1 ;(b) the C1 D2 on or about Day 2, Day 3, or Day 4 of the C1 ; and(c) the C1 D3 on or about Day 8 of the C1 .

26. The method of any one of claims 17-25, wherein the method comprises administering to the subject the C1 D4 on or about Day 9, Day 10, or Day 11 of the C1 .

27. The method of any one of claims 17-26, wherein the method comprises administering to the subject the C1 D4 about 1 day, 2 days, or 3 days after the C1 D3 of the C1 .

28. The method of any one of claims 1 -27, wherein the dosing regimen further comprises a second dosing cycle (C2) comprising a single dose (C2D1 ) of cevostamab, wherein the C2D1 is an effective amount of cevostamab that is equal to or greater than the last administered dose of cevostamab and is between about 20 mg to about 252 mg.

29. The method of claim 28, wherein the C2D1 is about 160 mg.

30. The method of claim 28 or 29, wherein the length of the C2 is 21 days.31 . The method of claim 30, wherein the method comprises administering to the subject the C2D1 on Day 1 of the C2.

32. The method of any one of claims 28-31 , wherein the dosing regimen further comprises one or more additional dosing cycles.

33. The method of claim 32, wherein the dosing regimen comprises one to 15 additional dosing cycles.

34. The method of claim 32 or 33, wherein the length of each of the one or more additional dosing cycles is 21 days.

35. The method of any one of claims 32-34, wherein each of the one or more additional dosing cycles comprises a single effective dose of cevostamab.

36. The method of claim 35, wherein the method comprises administering to the subject the single effective dose of cevostamab on Day 1 of the one or more additional dosing cycles.

37. The method of claim 36, wherein the single dose is between about 20 mg to about 252 mg.

38. The method of claim 37, wherein the single dose is about 160 mg.

39. The method of any one of claims 18-23, wherein a median peak IL-6 level in a population of subjects treated according to the method does not exceed 80 pg / mL between the C1 D1 and the C1 D2.

40. The method of any one of claims 4-6 and 39, wherein the median peak IL-6 level in the population of subjects treated according to the method does not exceed 30 pg / mL between the C1 D1 and the C1 D2.41 . The method of any one of claims 18-23, 39, and 40, wherein a median peak IL-6 level in a population of subjects treated according to the method does not exceed 80 pg / mL between the C1 D2 and the C1 D3.

42. The method of any one of claims 4-6, 40, and 41 , wherein the median peak IL-6 level in the population of subjects treated according to the method does not exceed 30 pg / mL between the C1 D2 and the C1 D3.

43. The method of any one of claims 4-6, wherein the method further comprises administering to the subject a fourth dose (C1 D4) of cevostamab during the C1 , wherein the C1 D4 is between about 20 mg to about 252 mg, and wherein the median peak IL-6 level in a population of subjects treated according to the method does not exceed 30 pg / mL between the C1 D3 and the C1 D4.

44. The method of any one of claims 18-23 and 39-42, wherein a median peak IL-6 level in a population of subjects treated according to the method does not exceed 30 pg / mL between the C1 D3 and the C1 D4.

45. The method of any one of claims 18-23, wherein a peak IL-6 level in the subject does not exceed 80 pg / mL between the C1 D1 and the C1 D2.

46. The method of any one of claims 7-9 and 45, wherein the peak IL-6 level in the subject does not exceed 30 pg / mL between the C1 D1 and the C1 D2.

47. The method of any one of claims 18-23, 45, and 46, wherein a peak IL-6 level in the subject does not exceed 80 pg / mL between the C1 D2 and the C1 D3.

48. The method of any one of claims 7-9, 46, and 47, wherein the peak IL-6 level in the subject does not exceed 30 pg / mL between the C1 D2 and the C1 D3.

49. The method of any one of claims 7-9, wherein the method further comprises administering to the subject a fourth dose (C1 D4) of cevostamab during the C1 , wherein the C1 D4 is between about 20 mg to about 252 mg, and wherein the peak IL-6 level in the subject does not exceed 30 pg / mL between the C1 D3 and the C1 D4.

50. The method of any one of claims 18-23 and 45-48, wherein a peak IL-6 level in the subject does not exceed 30 pg / mL between the C1 D3 and the C1 D4.51 . The method of any one of claims 1 -50, wherein a peak level of CD8+ T cell activation in the subject in the C1 occurs between administration of the C1 D1 and the C1 D2.

52. The method of any one of claims 1 -50, wherein a peak level of CD8+ T cell activation in the subject in the C1 occurs between administration of the C1 D2 and the C1 D3.

53. The method of any one of claims 1 -50, wherein a peak level of CD8+ T cell activation in the subject in the C1 occurs between administration of the C1 D3 and the C1 D4.

54. The method of any one of claims 51 -53, wherein the peak level of CD8+ T cell activation in the subject in the C1 occurs within 24 hours after administration of cevostamab.

55. The method of any one of claims 1 -54, wherein the method further comprises evaluating CRS after at least one of the C1 D1 , the C1 D2, and / or the C1 D3.

56. The method of claim 55, wherein the method further comprises measuring CRS after each of the C1 D1 , the C1 D2, and the C1 D3.

57. The method of claim 55 or 56, wherein, after administration of at least one of the C1 D1 , the C1 D2, and / or the C1 D3 (i) no CRS event has occurred, or (ii) CRS signs and symptoms from the previous dose have resolved, and the subject is administered the next dose of cevostamab.

58. The method of any one of claims 55-57, wherein the subject is not administered the next dose of cevostamab unless (i) no CRS event has occurred from administration of at least one of the C1 D1 , the C1 D2, and / or the C1 D3, or (ii) CRS signs and symptoms have resolved after administration of at least one of the C1 D1 , the C1 D2, and / or the C1 D3.

59. The method of claim 57, wherein the subject is administered the next dose of cevostamab no earlier than 20 hours from administration of the previous dose.

60. The method of any one of claims 55-59, wherein the method reduces the likelihood of the subject experiencing a CRS event.61 . The method of any one of claims 55-60, wherein the method reduces the likelihood of the subject experiencing Grade >1 CRS.

62. The method of any one of claims 55-61 , wherein the method reduces the likelihood of the subject experiencing Grade >2 CRS.

63. The method of any one of claim 55-62, wherein the method reduces the likelihood of the subject experiencing Grade >3 CRS.

64. The method of claim 60, wherein the likelihood of the subject experiencing Grade 1 CRS after the C1 D1 is less than 10%.

65. The method of claim 60, wherein the likelihood of the subject experiencing Grade 1 CRS after the C1 D2 is less than 25%.

66. The method of claim 60, wherein the likelihood of the subject experiencing Grade 1 CRS after the C1 D3 is less than 15%.

67. The method of claim 62, wherein the likelihood of the subject experiencing Grade 2 CRS after the C1 D1 is less than 10%.

68. The method of claim 62, wherein the likelihood of the subject experiencing Grade 2 CRS after the C1 D2 is less than 25%.

69. The method of claim 62, wherein the likelihood of the subject experiencing Grade 2 CRS after the C1 D3 is less than 15%.

70. The method of any one of claims 55-69, wherein the likelihood of the subject experiencing at least one Grade 1 or Grade 2 CRS event after the first administration of the C1 D4 is less than 65%.71 . The method of any one of claims 1 -70, wherein the dosing regimen results in a CRS event in less than about 90% of a population of subjects having MM.

72. The method of claim 71 , wherein the dosing regimen results in the CRS event in about 58% to about 90% of the population of subjects having MM.

73. The method of claim 72, wherein the dosing regimen results in the CRS event in about 58% to about 68% of the population of subjects having MM.

74. The method of claim 73, wherein the dosing regimen results in the CRS event in about 63% of the population of subjects having MM.

75. The method of any one of claims 1 -74, wherein the dosing regimen results in a grade >2 CRS event in less than about 50% of a population of subjects having MM.

76. The method of claim 75, wherein the dosing regimen results in the grade >2 CRS event in about 10% to about 25% of the population of subjects having MM.

77. The method of claim 75 or 76, wherein the dosing regimen results in the grade >2 CRS event in about 17% of the population of subjects having MM.

78. The method of any one of claims 1 -77, wherein the dosing regimen results in a grade >3 CRS event in less than about 10% of a population of subjects having MM.

79. The method of claim 78, wherein the dosing regimen results in the grade >3 CRS event in about 0% to about 5% of the population of subjects having MM.

80. The method of claim 78 or 79, wherein the dosing regimen does not result in any grade >3 CRS event in the population of subjects having MM.81 . The method of any one of claims 1 -80, wherein cevostamab is administered to the subject as a monotherapy.

82. The method of any one of claims 1 -80, wherein cevostamab is administered to the subject as a combination therapy.

83. The method of claim 82, wherein cevostamab is administered to the subject concurrently with one or more additional therapeutic agents.

84. The method of claim 83, wherein cevostamab is administered to the subject prior to the administration of one or more additional therapeutic agents.

85. The method of claim 83, wherein cevostamab is administered to the subject subsequent to the administration of one or more additional therapeutic agents.

86. The method of any one of claims 83-85, wherein the one or more additional therapeutic agents comprise an effective amount of tocilizumab.

87. The method of claim 86, wherein tocilizumab is administered to the subject by intravenous infusion.

88. The method of claim 86 or 87, wherein:(a) the subject weighs > 100 kg, and tocilizumab is administered to the subject at a dose of 800 mg;(b) the subject weighs > 30 kg and < 100 kg, and tocilizumab is administered to the subject at a dose of 8 mg / kg; or(c) the subject weighs < 30 kg, and tocilizumab is administered to the subject at a dose of 12 mg / kg.

89. The method of any one of claims 86-88, wherein tocilizumab is administered to the subject 2 hours before administration of cevostamab.

90. The method of any one of claims 1 -89, wherein cevostamab is administered to the subject by intravenous infusion.91 . The method of any one of claims 1 -89, wherein cevostamab is administered to the subject subcutaneously.

92. The method of any one of claims 1 -91 , wherein the subject experiences a CRS event, and treatment with cevostamab is suspended as a result of the CRS event to enable treatment of the CRS event.

93. The method of claim 92, wherein the method further comprises administering to the subject an effective amount of tocilizumab to treat the CRS event.

94. The method of any one of claims 1 -93, wherein the subject has received prior treatment for MM.

95. The method of claim 94, wherein the prior treatment for MM is selected from one or more of a proteasome inhibitor, an I MiD, an anti-CD38 therapeutic agent, an anti-SLAMF7 therapeutic agent, a nuclear export inhibitor, a histone deacetylase (HDAC) inhibitor, an autologous stem cell transplant (ASCT), a bispecific antibody, an antibody-drug conjugate (ADC), a CAR-T cell therapy, and a BCMA- directed therapy.

96. The method of claim 94 or 95, wherein the subject has received a standard of care treatment for MM prior to being administered the C1 D1 .

97. The method of claim 96, wherein the standard of care treatment comprises a proteasome inhibitor (PI), an immunomodulatory drug (IMiD), and an anti-cluster of differentiation 38 (CD38) monoclonal antibody (mAb).

98. The method of any one of claims 94-97, wherein the subject has received at least three prior lines of treatment for the MM.

99. The method of claim 98, wherein the subject has received at least four prior lines of treatment for the MM.

100. The method of any one of claims 96-99, wherein the subject has relapsed or become refractory to the standard of care treatment for MM.101 . The method of any one of claims 1 -100, wherein the MM is relapsed or refractory (R / R) MM.

102. A method of treating a subject having R / R MM, wherein the method comprises administering to the subject an effective amount of cevostamab in a dosing regimen comprising at least a first dosing cycle (C1 ), wherein the length of the C1 is 21 days, wherein the C1 comprises a first dose (C1 D1 ), a second dose (C1 D2), a third dose (C1 D3), and a fourth dose (C1 D4) of cevostamab, wherein the C1 D1 is about 0.3 mg and is administered on Day 1 of C1 ; the C1 D2 is about 1 .2 mg and is administered on Day 2, Day 3, or Day 4 of C1 ; the C1 D3 is about 3.6 mg and is administered on Day 8 of C1 ; and the C1 D4 is the effective amount of cevostamab and is administered on Day 9, Day 10, or Day 11 of C1 .

103. A method of treating a subject having R / R MM, wherein the method comprises administering to the subject an effective amount of cevostamab in a dosing regimen comprising at least a first dosing cycle (C1 ), wherein the length of the C1 is 21 days, wherein the C1 comprises a first dose (C1 D1 ), a second dose (C1 D2), a third dose (C1 D3), and a fourth dose (C1 D4) of cevostamab, wherein the C1 D1 is about 0.3 mg and is administered on Day 1 of C1 ; the C1 D2 is about 3.3 mg and is administered on Day 2, Day 3, or Day 4 of C1 ; the C1 D3 is about 7.2 mg and is administered on Day 8; and the C1 D4 is the effective amount of cevostamab and is administered on Day 9, Day 10, or Day 11 of C1 .

104. A method of reducing the likelihood of CRS in a subject having R / R MM and being administered an effective amount of cevostamab, wherein, prior to a first administration to the subject of the effective amount of cevostamab, the method comprises administering to the subject cevostamab in a dosing regimen comprising at least a first dosing cycle (C1 ), wherein the length of the C1 is 21 days, wherein the C1 comprises a first dose (C1 D1 ), a second dose (C1 D2), and a third dose (C1 D3) of cevostamab, wherein the C1 D1 is about 0.3 mg and is administered on Day 1 of C1 ; the C1 D2 is about 1 .2 mg and is administered on Day 2, Day 3, or Day 4 of C1 ; and the C1 D3 is about 3.6 mg and is administered on Day 8 of C1.

105. A method of reducing the likelihood of CRS in a subject having R / R MM and being administered an effective amount of cevostamab, wherein, prior to a first administration to the subject of the effective amount of cevostamab, the method comprises administering to the subject cevostamab in a dosing regimen comprising at least a first dosing cycle (C1 ), wherein the length of the C1 is 21 days, wherein the C1 comprises a first dose (C1 D1 ), a second dose (C1 D2), and a third dose (C1 D3) of cevostamab, wherein the C1 D1 is about 0.3 mg and is administered on Day 1 of C1 ; the C1 D2 is about 3.3 mg and is administered on Day 2, Day 3, or Day 4 C1 ; and the C1 D3 is about 7.2 mg and is administered on Day 8 C1.

106. A method of achieving a median peak IL-6 level of less than about 30 pg / mL in a population of subjects having R / R MM and being administered an effective amount of cevostamab, the method comprising administering to each subject in the population, prior to being administered the effective amount of cevostamab, a dosing regimen comprising at least a first dosing cycle (C1 ), wherein the length of the C1 is 21 days, wherein the C1 comprises a first dose (C1 D1 ), a second dose (C1 D2), and a thirddose (C1 D3) of cevostamab, wherein the C1 D1 is about 0.3 mg and is administered on Day 1 of C1 ; the C1 D2 is about 1 .2 mg and is administered on Day 2, Day 3, or Day 4 of C1 ; and the C1 D3 is about 3.6 mg and is administered on Day 8 of C1 .

107. A method of treating a subject having R / R MM, wherein the method comprises administering to the subject an effective amount of cevostamab in a dosing regimen comprising at least a first dosing cycle (C1 ), wherein the length of the C1 is 21 days, wherein the C1 comprises a first dose (C1 D1 ), a second dose (C1 D2), and a third dose (C1 D3) of cevostamab, wherein the C1 D1 is about 0.3 mg and is administered on Day 1 ; the C1 D2 is about 3.3 mg and is administered on Day 2, Day 3, or Day 4; the C1 D3 is about 160 mg and is administered on Day 8, and wherein an effective amount of tocilizumab is administered to the subject about 2 hours prior to administering the first dose of cevostamab.

108. A method of treating a subject having R / R MM, wherein the method comprises administering to the subject an effective amount of cevostamab in a dosing regimen comprising at least a first dosing cycle (C1 ), wherein the length of the C1 is 21 days, wherein the C1 comprises a first dose (C1 D1 ), a second dose (C1 D2), and a third dose (C1 D3), wherein the C1 D1 is about 0.3 mg and is administered on Day 1 ; the C1 D2 is about 3.3 mg and is administered on Day 4; and the C1 D3 is about 160 mg and is administered on Day 8.

109. The method of any one of claims 102-108, wherein the dosing regimen further comprises a second dosing cycle (C2) comprising a single dose (C2D1 ) of cevostamab, wherein the length of the C2 is 21 days, and wherein the C2D1 is an effective amount of cevostamab and is administered to the subject on Day 1 of the second dosing cycle.

110. The method of claim 109, wherein the dosing regimen comprises one or more additional dosing cycles, wherein the length of each of the one or more additional dosing cycles is 21 days, wherein each of the one or more additional dosing cycles comprises a single dose of the effective amount of cevostamab administered to the subject on Day 1 of each of the one or more additional dosing cycles.111 . A method of reducing the occurrence of CRS events in a subject being treated for R / R MM with a target dose of cevostamab, the method comprising administering to the subject, prior to a first administration of the target dose to the subject in a dosing regimen comprising a first dosing cycle (C1 ), (i) a first dose (C1 D1 ), (ii) a second dose (C1 D2), and (iii) a third dose (C1 D3) of cevostamab, wherein the C1 D1 is about 0.3 mg and is administered on Day 1 ; the C1 D2 is about 1 .2 mg and is administered on Day 2, Day 3, or Day 4; and the C1 D3 is about 3.6 mg and is administered on Day 8, wherein the length of the C1 is 21 days.

112. A method of reducing the occurrence of CRS events in a subject being treated for R / R MM with a target dose of cevostamab, the method comprising administering to the subject, prior to a first administration of the target dose to the subject in a dosing regimen comprising a first dosing cycle (C1 ),(i) a first dose (C1 D1 ), (ii) a second dose (C1 D2), and (iii) a third dose (C1 D3) of cevostamab, wherein the C1 D1 is about 0.3 mg and is administered on Day 1 ; the C1 D2 is about 3.3 mg and is administered on Day 2, Day 3, or Day 4; and the C1 D3 is about 7.2 mg and is administered on Day 8, wherein the length of the C1 is 21 days.

113. A method of reducing the occurrence of CRS events in a subject being treated for R / R MM with a target dose of cevostamab, wherein, prior to a first administration of the target dose to the subject in a dosing regimen comprising a first dosing cycle (C1 ), the method comprises administering to the subject (i) a first dose (TS-C1 D1 ), (ii) a second dose (TS-C1 D2), and (iii) a third dose (TS-C1 D3) of cevostamab, wherein administering such target dose to a first plurality of such subjects results in a reduction in the number of subjects experiencing a CRS event after first administration of the target dose, as compared to a second plurality of subjects (e.g., human subjects) being treated for R / R MM with a target dose of cevostamab and administered such target dose after administration of a first dose (DS-C1 D1 ) and a second dose (DS-C1 D2), with no third dose of cevostamab, and wherein the TS-D1 D2 is greater than the TS-C1 D1 , the TS-C1 D3 is greater than the TS-C1 D2, and the DS-C1 D2 is greater than the DS-C1 D1 .

114. The method of claim 113, wherein administering such target dose to the first plurality of such subjects results in at least a 10% reduction in the number of subjects experiencing a CRS event after first administration of the target dose.

115. The method of claim 113 or 114, wherein administering such target dose to the first plurality of such subjects results in a 15% reduction in the number of subjects experiencing a CRS event after first administration of the target dose.

116. A method of reducing the occurrence of CRS events in a subject being treated for R / R MM with a target dose of cevostamab, wherein, prior to a first administration of the target dose to the subject in a dosing regimen comprising a first dosing cycle (C1 ), the method comprises administering to the subject (i) a first dose (TS-C1 D1 ), (ii) a second dose (TS-C1 D2), and (iii) a third dose (TS-C1 D3) of cevostamab, wherein administering such target dose to a first plurality of such subjects results in a reduction in the number of subjects experiencing a CRS event during the C1 , as compared to a second plurality of subjects (e.g., human subjects) being treated for R / R MM with a target dose of cevostamab and administered such target dose after administration of a first dose (DS-C1 D1 ) and a second dose (DS-C1 D2), with no third dose of cevostamab, and wherein the TS-D1 D2 is greater than the TS-C1 D1 , the TS-C1 D3 is greater than the TS-C1 D2, and the DS-C1 D2 is greater than the DS-C1 D1 .

117. The method of claim 116, wherein administering such target dose to the first plurality of such subjects results in at least a 10% reduction in the number of subjects experiencing a CRS event during the C1 .

118. The method of claim 116 or 117, wherein administering such target dose to the first plurality of such subjects results in a 14% reduction in the number of subjects experiencing a CRS event during the C1.

119. A method of reducing the occurrence of CRS events in a subject being treated for R / R MM at an target dose of cevostamab, wherein, prior to a first administration of the target dose to the subject in a dosing regimen comprising a first dosing cycle (C1 ), the method comprises administering to the subject (i) a first dose (TS-C1 D1 ); (ii) a second dose (TS-C1 D2); and (iii) a third dose (TS-C1 D3) of cevostamab, wherein administering cevostamab in the C1 to a first plurality of such subjects results in a reduction in the number of CRS events experienced by each subject during the C1 , as compared to a second plurality of subjects administered the target dose of cevostamab after a first dose (DS-C1 D1 ) and a second dose (DS-C1 D2), but not a third dose of cevostamab, and wherein the TS-D1 D2 is greater than the TS-C1 D1 , the TS-C1 D3 is greater than the TS-C1 D2, and the DS-C1 D2 is greater than the DS-C1 D1 .

120. The method of claim 119, wherein administering cevostamab in the C1 to the first plurality of such subjects results in at least a 30% reduction in the number of CRS events experienced by each subject during the C1 .121 . A method of reducing the occurrence of CRS events in a subject being treated for R / R MM at a target dose of cevostamab, wherein, prior to first administration of the target dose to the subject in a first treatment cycle (C1 ), the subject is administered cevostamab at (i) a first dose (TS-C1 D1 ); (ii) a second dose (TS-C1 D2); and (iii) a third dose (TS-C1 D3), wherein administering cevostamab in the C1 to a first plurality of such subjects results in a reduction in the number of subjects requiring tocilizumab treatment for CRS during the C1 , as compared to a second plurality of subjects being treated for MM and administered a target dose of cevostamab after a first dose (DS-C1 D1 ) and a second dose (DS-C1 D2), but not a third dose of cevostamab, and wherein the TS-D1 D2 is greater than the TS-C1 D1 , and the TS- C1 D3 is greater than the TS-C1 D2, and the DS-C1 D2 is greater than the DS-C1 D1 .

122. The method of claim 121 , wherein administering cevostamab in the C1 to the first plurality of such subjects results in at least a 10% reduction in the number of subjects requiring tocilizumab treatment for CRS during the C1 .

123. A method of pre-treating a subject for receiving a target dose of cevostamab, wherein the method comprises administering to the subject (i) a first dose (C1 D1 ), (ii) a second dose (C1 D2), and (iii) a third dose (C1 D3) of cevostamab, wherein the C1 D2 is greater than the C1 D1 , and the C1 D3 is greater than the C1 D2, wherein the risk of CRS events in the subject, after administration of the C1 D1 , C1 D2, andC1 D3 to the subject, is at a level that is safe for the subject to receive the target dose of cevostamab.

124. The method of claim 123, wherein, following administration of the C1 D1 , C1 D2, and C1 D3 to the subject, the subject achieves a peak IL-6 level of less than about 80 pg / mL, thereby indicating that therisk of CRS events in the subject is at a level that is safe for the subject to receive the target dose of cevostamab.

125. The method of claim 124, wherein the subject achieves a peak IL-6 level of less than about 30 pg / mL prior to the administration of the target dose of cevostamab.

126. The method of claim 124 or 125, wherein the method further comprises administering to the pretreated subject a target dose of cevostamab.

127. A method of reducing the occurrence of CRS events in a subject being treated for R / R MM at a target dose of cevostamab, wherein, prior to a first administration of the target dose to the subject in a dosing regimen comprising a first dosing cycle (C1 ), the method comprises administering to the subject (i) a first dose (TS-C1 D1 ); (ii) a second dose (TS-C1 D2); and (iii) a third dose (TS-C1 D3) of cevostamab, wherein administering cevostamab in the C1 to a first plurality of such human subjects results in a reduction in the number of CRS events experienced by each subject during the C1 , as compared to a second plurality of subjects being treated for R / R MM and administered the target dose of cevostamab after a first dose (DS-C1 D1 ) and a second dose (DS-C1 D2), but not a third dose (DS-C1 D3) of cevostamab, and wherein the TS-D1 D2 is greater than the TS-C1 D1 , the TS-C1 D3 is greater than the TS-C1 D2, and the DS-C1 D2 is greater than the DS-C1 D1 .

128. The method of claim 127, wherein administering cevostamab in the C1 to the first plurality of such subjects results in at least a 25% reduction in the number of CRS events experienced by each subject during the C1 .

129. A method of reducing the occurrence of CRS events in a subject being treated for R / R MM at a target dose of cevostamab, wherein, prior to a first administration of the target dose to the subject in a dosing regimen comprising a first dosing cycle (C1 ), the method comprises administering to the subject (i) a first dose (TS-C1 D1 ); (ii) a second dose (TS-C1 D2); and (iii) a third dose (TS-C1 D3) of cevostamab, wherein administering cevostamab in the C1 to a first plurality of such subjects results in an increase in the number of subjects experiencing no CRS event during the C1 , as compared to a second plurality of subjects being treated for R / R MM and administered the target dose of cevostamab after a first dose (DS- C1 D1 ) and a second dose (DS-C1 D2), but not a third dose of cevostamab, and wherein the TS-D1 D2 is greater than the TS-C1 D1 , the TS-C1 D3 is greater than the TS-C1 D2, and the DS-C1 D2 is greater than the DS-C1 D1.

130. The method of claim 129, wherein administering cevostamab in the C1 to the first plurality of such subjects results in at least a 50% increase in the number of subjects experiencing no CRS event during the C1 .131 . A method of reducing the occurrence of CRS events in a subject being treated for R / R MM at a target dose of cevostamab, wherein, prior to a first administration of the target dose to the subject in a dosing regimen comprising a first dosing cycle (C1 ), the method comprises administering to the subject (i) a first dose (TS-C1 D1 ); (ii) a second dose (TS-C1 D2); and (iii) a third dose (TS-C1 D3) of cevostamab, wherein administering cevostamab in the C1 to a first plurality of such subjects results in a reduction in the number of subjects experiencing Grade >2 CRS events during the C1 , as compared to a second plurality of subjects being treated for R / R MM and administered the target dose of cevostamab after a first dose (DS-C1 D1 ) and a second dose (DS-C1 D2), but not a third dose of cevostamab, and wherein the TS-D1 D2 is greater than the TS-C1 D1 , the TS-C1 D3 is greater than the TS-C1 D2, and the DS-C1 D2 is greater than the DS-C1 D1 .

132. The method of claim 131 , wherein administering cevostamab in the C1 to the first plurality of such subjects results in at least a 35% reduction in the number of subjects experiencing Grade >2 CRS events during the C1 .

133. A method of reducing the occurrence of CRS events in a subject being treated for R / R MM at a target dose of cevostamab, wherein, prior to a first administration of the target dose to the subject in a dosing regimen comprising a first dosing cycle (C1 ), the method comprises administering to the subject (i) a first dose (TS-C1 D1 ); (ii) a second dose (TS-C1 D2); and (iii) a third dose (TS-C1 D3) of cevostamab, wherein administering cevostamab in the C1 to a first plurality of such subjects results in a reduction in the number of subjects experiencing at least two CRS events during the C1 , as compared to a second plurality of subjects being treated for R / R MM and administered the target dose of cevostamab after a first dose (DS-C1 D1 ) and a second dose (DS-C1 D2), but not a third dose of cevostamab, and wherein the TS-D1 D2 is greater than the TS-C1 D1 , the TS-C1 D3 is greater than the TS-C1 D2, and the DS-C1 D2 is greater than the DS-C1 D1 .

134. The method of claim 133, wherein administering cevostamab in the C1 to the first plurality of such subjects results in at least a 50% reduction in the number of subjects experiencing at least two CRS events during the C1 .

135. The method of any one of claims 1 -134, wherein the subject is a human subject.