Methods for treating multiple myeloma

Abstract

Embodiments of the present invention relate to methods of reducing oral toxicities, such as taste impairment, in subjects that undergo treatment with a GPRC5D- targeted therapeutic.

Description

[0001] Attorney Docket No.258199.061702 JBI6826WOPCT1 METHODS FOR TREATING MULTIPLE MYELOMA CROSS-REFERENCE TO RELATED APPLICATIONS This application claims priority to United States Provisional Application Serial Number 63 / 514,744, filed July 20, 2023, the entire contents of which are incorporated herein by reference in their entirety. REFERENCE TO SEQUENCE LISTING SUBMITTED ELECTRONICALLY This application contains a sequence listing, which is submitted electronically in XML format and is hereby incorporated by reference in its entirety. Said XML copy, created on June 21, 2024, is named “258199061702 (JBI6826WOPCT1) Sequence Listing.xml” and is 25,460 bytes in size. FIELD OF THE INVENTION Methods of treating multiple myeloma are disclosed. BACKGROUND OF THE INVENTION Multiple myeloma (MM) is a cancer of the plasma cells. Mechanistically, multiple myeloma is characterized by production of monoclonal proteins (M-proteins) comprised of pathological immunoglobulins or fragments of such, which have lost their function. The proliferation of multiple myeloma cells leads to subsequent displacement from the normal bone marrow niche, while overproduction of M-proteins causes characteristic osteolytic lesions, increased susceptibility to infections, hypercalcemia, renal insufficiency or failure, and neurological complications. Treatment options for multiple myeloma have improved over time and vary depending on the aggressiveness of the disease, underlying prognostic factors, physical condition of the patient, and existing comorbidities. Therapeutic options include proteasome inhibitors (PIs), immunomodulatory drugs (IMiDs), alkylating agents, monoclonal antibodies (mAbs), antibody drug conjugate, histone deacetylase inhibitor, nuclear protein export inhibitor, chimeric antigen receptor (CAR) T cell therapy and stem cell transplantation. Attorney Docket No.258199.061702 JBI6826WOPCT1 Despite these therapeutic achievements, the disease recurs and is associated with additional risk factors (e.g., comorbidities or increasing age), thus warranting the need for novel therapeutic approaches, such as new dosage and treatment regimens. In particular in the elderly population, for which stem cell transplantation is often not a viable option, and in patients with refractory disease who exhausted several therapies, multiple myeloma remains an incurable malignancy and an unmet medical need with significant morbidity and mortality. In particular, there remains a need for therapeutic regimens that achieve rapid, deep and durable clinical responses, while providing manageable safety profiles. There also remains a need for therapeutic regimens that provide improved side effect profiles and quality of life for patients. SUMMARY OF THE INVENTION An embodiment of the present invention provides a method of decreasing oral toxicity in a subject under treatment with a GPRC5D-targeted therapeutic, the method comprising administering to the subject a prophylactic intervention for oral toxicity prior to administering a therapeutically effective amount of the GPRC5D-targeted therapeutic throughout a treatment phase, wherein the prophylactic intervention is selected from the group consisting of dexamethasone, pregabalin, clonazepam, and a combination thereof. In certain embodiments, the GPRC5D-targeted therapeutic is a GPRC5DxCD3 bispecific antibody, such as talquetamab. In certain embodiments, the GPRC5DxCD3 bispecific antibody comprises a GPRC5D binding domain comprising the HCDR1 of SEQ ID NO: 4, the HCDR2 of SEQ ID NO: 5, the HCDR3 of SEQ ID NO: 6, the LCDR1 of SEQ ID NO: 7, the LCDR2 of SEQ ID NO: 8 and the LCDR3 of SEQ ID NO: 9, and a CD3 binding domain comprising the HCDR1 of SEQ ID NO: 14, the HCDR2 of SEQ ID NO: 15, the HCDR3 of SEQ ID NO: 16, the LCDR1 of SEQ ID NO: 17, the LCDR2 of SEQ ID NO: 18 and the LCDR3 of SEQ ID NO: 19. In certain embodiments, the GPRC5D binding domain comprises a heavy chain variable region (VH) having the amino acid sequence of SEQ ID NO: 10 and a light chain variable region (VL) having the amino acid sequence of SEQ ID NO: 11, and the CD3 binding domain comprises a heavy chain variable region (VH) having the amino Attorney Docket No.258199.061702 JBI6826WOPCT1 acid sequence of SEQ ID NO: 20 and a light chain variable region (VL) having the amino acid sequence of SEQ ID NO: 21. In certain embodiments, the GPRC5DxCD3 bispecific antibody is an IgG1, an IgG2, an IgG3 or an IgG4 isotype. In certain embodiments, the GPRC5DxCD3 bispecific antibody is an IgG4 isotype. In certain embodiments, the GPRC5DxCD3 bispecific antibody comprises one or more substitutions in its Fc region. In certain embodiments, the GPRC5DxCD3 bispecific antibody is an IgG4 isotype and comprises S228P, F234A and L235A substitutions in its Fc region. In certain embodiments, the GPRC5DxCD3 bispecific antibody is an IgG4 isotype and comprises S228P, F234A, L235A F405L and R409K substitutions in its Fc region. In certain embodiments, the Fc region of the GPRC5D -specific IgG4 antibody from which the GPRC5D-binding arm is derived comprises S228P, L234A and L235A substitutions in its Fc region. In certain embodiments, the Fc region of the CD3-specific IgG4 antibody from which the CD3-binding arm is derived comprises S228P, L234A, L235A, F405L, and R409K substitutions in its Fc region.In certain embodiments, the GPRC5DxCD3 bispecific antibody comprises a first heavy chain (HC1) having the amino acid sequence of SEQ ID NO: 12, a first light chain (LC1) having the amino acid sequence of SEQ ID NO: 13, a second heavy chain (HC2) having the amino acid sequence of SEQ ID NO: 22 and a second light chain (LC2) having the amino acid sequence of SEQ ID NO: 23. In certain embodiments, the GPRC5DxCD3 bispecific antibody comprises a first heavy chain (HC1) having at least 90% identity to the amino acid sequence of SEQ ID NO: 12, a first light chain (LC1) having at least 90% identity to the amino acid sequence of SEQ ID NO: 13, a second heavy chain (HC2) having at least 90% identity to the amino acid sequence of SEQ ID NO: 22 and a second light chain (LC2) having at least 90% identity to the amino acid sequence of SEQ ID NO: 23. In certain embodiments, the GPRC5DxCD3 bispecific antibody comprises a first heavy chain (HC1) having at least 95% identity to the amino acid sequence of SEQ ID NO: 12, a first light chain (LC1) having at least 95% identity to the amino acid sequence Attorney Docket No.258199.061702 JBI6826WOPCT1 of SEQ ID NO: 13, a second heavy chain (HC2) having at least 95% identity to the amino acid sequence of SEQ ID NO: 22 and a second light chain (LC2) having at least 95% identity to the amino acid sequence of SEQ ID NO: 23. In certain embodiments, the GPRC5DxCD3 bispecific antibody comprises a first heavy chain (HC1) having at least 98% identity to the amino acid sequence of SEQ ID NO: 12, a first light chain (LC1) having at least 98% identity to the amino acid sequence of SEQ ID NO: 13, a second heavy chain (HC2) having at least 98% identity to the amino acid sequence of SEQ ID NO: 22 and a second light chain (LC2) having at least 98% identity to the amino acid sequence of SEQ ID NO: 23. In certain embodiments, the GPRC5DxCD3 bispecific antibody is talquetamab. In certain embodiments, the subject has been diagnosed with multiple myeloma. In certain embodiments, the subject has relapsed or refractory multiple myeloma (RRMM). In certain embodiments, the subject has received at least three prior lines of therapy. In certain embodiments, the subject has received at least four prior lines of therapy. In certain embodiments, the subject has received at least five prior lines of therapy (penta-drug exposed). In certain embodiments, the subject has received at least three prior lines of therapy, including a proteasome inhibitor, an immunomodulatory agent and an anti- CD38 monoclonal antibody. In certain embodiments, the subject has received at least four prior lines of therapy, including a proteasome inhibitor, an immunomodulatory agent and an anti- CD38 monoclonal antibody. In certain embodiments, the prophylactic intervention is dexamethasone. In certain embodiments, the prophylactic intervention is a dexamethasone mouthwash (an oral solution comprising dexamethasone), e.g., 0.5 mg dexamethasone, twice daily. In certain embodiments, the prophylactic intervention is 0.1 mg / mL dexamethasone mouthwash (e.g., 0.5 mg dexamethasone, twice daily). Attorney Docket No.258199.061702 JBI6826WOPCT1 In certain embodiments, the method comprises administering the dexamethasone mouthwash in an amount of 5 mL (e.g., 0.5 mg / 5 mL), twice daily (e.g., wherein the subject washes his or her mouth with the mouthwash for about 5 minutes without swallowing the mouthwash, and preferably does not consume food or drinks for about 30 minutes afterwards). In certain embodiments, the method comprises administering the dexamethasone mouthwash in an amount of 5 mL twice daily, and administering 50 mg fluconazole once daily (e.g., to prevent thrush). In certain embodiments, the method comprises increasing the dose of the dexamethasone mouthwash to a maximum of 4 times daily after an event of decreased taste score (≥6) has occurred. In certain embodiments, the prophylactic intervention is pregabalin (e.g., in the form of a capsule or tablet, preferably a 50 mg capsule). In certain embodiments, the method comprises administering the pregabalin at a dose of 50 mg, twice daily. In certain embodiments, the method comprises increasing the dose of pregabalin after an event of decreased taste score (≥6) has occurred. In certain embodiments, the method comprises increasing the dose of pregabalin after an event of decreased taste score (≥6) has occurred, first to 150 mg / day, and after a week to a maximum of 300 mg / day. In certain embodiments, the prophylactic intervention is clonazepam. In certain embodiments, the prophylactic intervention is clonazepam mouthwash (e.g., 0.5 mg clonazepam, twice daily). In certain embodiments, the prophylactic intervention is clonazepam orally dissolving tablet (ODT) (e.g., 0.5 mg clonazepam orally dissolving tablet (ODT), twice daily). In certain embodiments, the prophylactic intervention is 0.1 mg / mL clonazepam mouthwash. In certain embodiments, the method comprises administering 0.1 mg / mL clonazepam mouthwash at a dose of 5 mL (e.g., 0.5 mg / 5 mL), twice daily (e.g., wherein the subject washes his or her mouth with the mouthwash for about 5 minutes without Attorney Docket No.258199.061702 JBI6826WOPCT1 swallowing the mouthwash, and preferably does not consume food or drinks for about 30 minutes afterwards). In certain embodiments, the method comprises continuing clonazepam mouthwash at the same dose if a decrease of 6 points or more in the taste score (measured by taste strips) has developed. In certain embodiments, the method comprises administering the first dose of the prophylactic intervention 5-9 days prior to administering a first dose (e.g. a first step-up dose) of the GPRC5D-targeted therapeutic. In certain embodiments, the method comprises administering the first dose of the prophylactic intervention 6-8 days prior to administering a first dose (e.g. a first step-up dose) of the GPRC5D-targeted therapeutic, and continuing daily administration of the prophylactic intervention throughout the treatment phase. In certain embodiments, the method comprises administering the first dose of the prophylactic intervention 7 days prior to administering a first dose (e.g. a first step-up dose) of the GPRC5D-targeted therapeutic, and continuing daily administration of the prophylactic intervention throughout the treatment phase. In certain embodiments, the method comprises administering the prophylactic intervention daily for 5-9 days prior to administering a first dose (e.g. a first step-up dose) of the GPRC5D-targeted therapeutic, and continuing daily administration of the prophylactic intervention throughout the treatment phase. In certain embodiments, the method comprises administering the prophylactic intervention daily for 6-8 days prior to administering a first dose (e.g. a first step-up dose) of the GPRC5D-targeted therapeutic. In certain embodiments, the method comprises administering the prophylactic intervention daily for 7 days prior to administering a first dose (e.g. a first step-up dose) of the GPRC5D-targeted therapeutic. In certain embodiments, the method comprises subcutaneously administering to the subject one or more step-up doses of the GPRC5DxCD3 bispecific antibody prior to administering a treatment dose of the GPRC5DxCD3 bispecific antibody. In certain embodiments, the method comprises subcutaneously administering to the subject a treatment dose of the GPRC5DxCD3 bispecific antibody weekly (QW). Attorney Docket No.258199.061702 JBI6826WOPCT1 In certain embodiments, the method comprises subcutaneously administering to the subject a treatment dose of the GPRC5DxCD3 bispecific antibody every two weeks (Q2W). In certain embodiments, the method comprises subcutaneously administering the GPRC5DxCD3 bispecific antibody weekly (QW) at a treatment dose of about 400 μg / kg. In certain embodiments, the method comprises subcutaneously administering the GPRC5DxCD3 bispecific antibody every two weeks (Q2W) at a treatment dose of about 800 μg / kg. In certain embodiments, the method comprises subcutaneously administering 2 or 3 step-up doses of the GPRC5DxCD3 bispecific antibody prior to subcutaneously administering a treatment dose. In certain embodiments, the method comprises subcutaneously administering step-up doses of 10 μg / kg and 60 μg / kg of the GPRC5DxCD3 bispecific antibody prior to subcutaneously administering a treatment dose. In certain embodiments, the method comprises subcutaneously administering step-up doses of 10 μg / kg and 60 μg / kg and 400 μg / kg of the GPRC5DxCD3 bispecific antibody prior to subcutaneously administering a treatment dose. In certain embodiments, the method comprises subcutaneously administering step-up doses of the GPRC5DxCD3 bispecific antibody 2-4 days apart from each other. In certain embodiments, the method comprises subcutaneously administering the GPRC5DxCD3 bispecific antibody according to the following dosing schedule for a first 28-day treatment cycle: step-up dose 1 (Day 1) at 0.01 mg / kg, followed by step-up dose 2 (Day 4) at 0.06 mg / kg, followed by step-up dose 3 (Day 8) at 0.4 mg / kg, followed by a first treatment dose (Day 15) at 0.8 mg / kg. In certain embodiments, the step-up doses are administered ≥2 days apart and the first treatment dose is administered ≥2 days after the step-up dose 3, between Day 7 and Day 15. In certain embodiments, for subsequent 28-day treatment cycles after the first 28- day treatment cycle (Cycles 2+), the GPRC5DxCD3 bispecific antibody is administered 14±3 days after prior treatment dose, at 0.8 mg / kg Q2W (e.g., on Days 1 and 15 of each treatment cycle). Attorney Docket No.258199.061702 JBI6826WOPCT1 In certain embodiments, the subject has decreased oral toxicity (e.g., decreased taste impairment) compared to a subject that has not received the same prophylactic intervention, e.g., as determined by taste assessment using taste strips. In certain embodiments, the subject has decreased occurrence of oral toxicity (e.g., decreased occurrence of taste impairment) compared to a subject that has not received the same prophylactic intervention, e.g., as determined by taste assessment using taste strips. In certain embodiments, the subject has decreased severity of oral toxicity (e.g., decreased severity of taste impairment) compared to a subject that has not received the same prophylactic intervention, e.g., as determined by taste assessment using taste strips. In certain embodiments, the subject does not have an occurrence of oral toxicity (e.g., does not have an occurrence of taste impairment) as a result of the prophylactic intervention (oral toxicity, such as taste impairment, is prevented), e.g., as determined by taste assessment using taste strips. In certain embodiments, the method decreases the proportion of subjects in a population that have at least 1 occurrence of 6 points or more of deterioration from a baseline taste score during the treatment phase, as measured by taste strips, e.g., by standard taste assessment. In certain embodiments, the subject exhibits one or more of the following clinical results (e.g., as determined by a total WETT testing score): 1. lower rate of occurrence of taste dysfunction (hypogeusia) compared to a subject that has not received the same prophylactic intervention, and / or 2. lower rate of occurrence of severe hypogeusia / ageusia compared to a subject that has not received the same prophylactic intervention, and / or 3. longer time to first onset of severe hypogeusia / ageusia compared to a subject that has not received the same prophylactic intervention, and / or 4. higher rate of resolution / improvement of hypogeusia / ageusia at 3 and 6 months, compared to a subject that has not received the same prophylactic intervention. All methods described herein, however expressed, may be described as corresponding uses, in particular medical uses. BRIEF DESCRIPTION OF THE FIGURES Attorney Docket No.258199.061702 JBI6826WOPCT1 The following figures form part of the present specification and are included to further demonstrate certain aspects of the present invention. The invention may be better understood by reference to one or more of these figures in combination with the description of specific embodiments presented herein. Fig.1 provides a Study Design of the Phase 2, Open-label, Randomized Study to Evaluate Prophylactic Interventions on Talquetamab-related Oral Toxicity (TALISMAN study). Fig.2 provides the Normative WETT-SA53 Percentile Table. DETAILED DESCRIPTION OF THE INVENTION The disclosed methods can be understood more readily by reference to the following detailed description. It is to be understood that the disclosed methods are not limited to the specific methods described and / or shown herein, and that the terminology used herein is for the purpose of describing particular embodiments by way of example only and is not intended to be limiting of the claimed methods. All patents, published patent applications and publications cited herein are incorporated by reference as if set fourth fully herein. As used herein, the singular forms “a,” “an,” and “the” include the plural. Various terms relating to aspects of the description are used throughout the specification and claims. Such terms are to be given their ordinary meaning in the art unless otherwise indicated. Other specifically defined terms are to be construed in a manner consistent with the definitions provided herein. “About” when used in reference to numerical ranges, cutoffs, or specific values means within an acceptable error range for the particular value as determined by one of ordinary skill in the art, which will depend in part on how the value is measured or determined, i.e., the limitations of the measurement system. Unless explicitly stated otherwise within the Examples or elsewhere in the Specification in the context of an assay, result or embodiment, “about” means within one standard deviation per the practice in the art, or a range of up to 5%, whichever is larger. “Antibodies” is meant in a broad sense and includes immunoglobulin molecules including monoclonal antibodies including murine, human, humanized and chimeric monoclonal antibodies, antigen binding fragments, multispecific antibodies, such as Attorney Docket No.258199.061702 JBI6826WOPCT1 bispecific, trispecific, tetraspecific etc., dimeric, tetrameric or multimeric antibodies, single chain antibodies, domain antibodies and any other modified configuration of the immunoglobulin molecule that comprises an antigen binding site of the required specificity. “Full length antibodies” are comprised of two heavy chains (HC) and two light chains (LC) inter-connected by disulfide bonds as well as multimers thereof (e.g. IgM). Each heavy chain is comprised of a heavy chain variable region (VH) and a heavy chain constant region (comprised of domains CH1, hinge, CH2 and CH3). Each light chain is comprised of a light chain variable region (VL) and a light chain constant region (CL). The VH and the VL regions can be further subdivided into regions of hypervariability, termed complementarity determining regions (CDR), interspersed with framework regions (FR). Each VH and VL is composed of three CDRs and four FR segments, arranged from amino-to-carboxy-terminus in the following order: FR1, CDR1, FR2, CDR2, FR3, CDR3 and FR4. Immunoglobulins can be assigned to five major classes, IgA, IgD, IgE, IgG and IgM, depending on the heavy chain constant domain amino acid sequence. IgA and IgG are further sub-classified as the isotypes IgA1, IgA2, IgG1, IgG2, IgG3 and IgG4. Antibody light chains of any vertebrate species can be assigned to one of two clearly distinct types, namely kappa (κ) and lambda (λ), based on the amino acid sequences of their constant domains. “Antigen binding fragment” or “antigen binding domain” refers to a portion of an immunoglobulin molecule that binds an antigen. Antigen binding fragments can be synthetic, enzymatically obtainable or genetically engineered polypeptides and include the VH, the VL, the VH and the VL, Fab, F(ab’)2, Fd and Fv fragments, domain antibodies (dAb) consisting of one VH domain or one VL domain, shark variable IgNAR domains, camelized VH domains, minimal recognition units consisting of the amino acid residues that mimic the CDRs of an antibody, such as FR3-CDR3-FR4 portions, the HCDR1, the HCDR2 and / or the HCDR3 and the LCDR1, the LCDR2 and / or the LCDR3. VH and VL domains can be linked together via a synthetic linker to form various types of single chain antibody designs where the VH / VL domains can pair intramolecularly, or intermolecularly in those cases when the VH and VL domains are expressed by separate single chain antibody constructs, to form a monovalent antigen binding site, such as single chain Fv (scFv) or diabody; described for example in Int. Attorney Docket No.258199.061702 JBI6826WOPCT1 Patent Publ. Nos. WO1998 / 44001, WO1988 / 01649, WO1994 / 13804 and WO1992 / 01047. “Bispecific” refers to an antibody that specifically binds two distinct antigens or two distinct epitopes within the same antigen. The bispecific antibody can have cross- reactivity to other related antigens, for example to the same antigen from other species (homologs), such as human or monkey, for example Macaca cynomolgus (cynomolgus, cyno) or Pan troglodytes, or can bind an epitope that is shared between two or more distinct antigens. “Cancer” refers to a broad group of various diseases characterized by the uncontrolled growth of abnormal cells in the body. Unregulated cell division and growth results in the formation of malignant tumors that invade neighboring tissues and can also metastasize to distant parts of the body through the lymphatic system or bloodstream. A “cancer” or “cancer tissue” can include a tumor. “CD3” refers to a human antigen which is expressed on T cells as part of the multimolecular T cell receptor (TCR) complex and which consists of a homodimer or heterodimer formed from the association of two or four receptor chains: CD3 epsilon, CD3 delta, CD3 zeta and CD3 gamma. Human CD3 epsilon comprises the amino acid sequence of SEQ ID NO: 2. SEQ ID NO: 3 shows the extracellular domain of CD3 epsilon. SEQ ID NO: 2 MQSGTHWRVLGLCLLSVGVWGQDGNEEMGGITQTPYKVSISGTTVILTC PQYPGSEILWQHNDKNIGGDEDDKNIGSDEDHLSLKEFSELEQSGYYVCY PRGSKPEDANFYLYLRARVCENCMEMDVMSVATIVIVDICITGGLLLLVY YWSKNRKAKAKPVTRGAGAGGRQRGQNKERPPPVPNPDYEPIRKGQRD LYSGLNQRRI SEQ ID NO: 3 DGNEEMGGITQTPYKVSISGTTVILTCPQYPGSEILWQHNDKNIGGDEDD KNIGSDEDHLSLKEFSELEQSGYYVCYPRGSKPEDANFYLYLRARVCENC MEMD “CH3 region” or “CH3 domain” refers to the CH3 region of an immunoglobulin. The CH3 region of human IgG1 antibody corresponds to amino acid Attorney Docket No.258199.061702 JBI6826WOPCT1 residues 341-446. However, the CH3 region can also be any of the other antibody isotypes as described herein. “Combination” means that two or more therapeutics are administered to a subject together in a mixture, concurrently as single agents or sequentially as single agents in any order. “Complementarity determining regions” (CDR) are antibody regions that bind an antigen. CDRs can be defined using various delineations such as Kabat (Wu et al. J Exp Med 132: 211-50, 1970) (Kabat et al., Sequences of Proteins of Immunological Interest, 5thEd. Public Health Service, National Institutes of Health, Bethesda, Md., 1991), Chothia (Chothia et al. J Mol Biol 196: 901-17, 1987), IMGT (Lefranc et al. Dev Comp Immunol 27: 55-77, 2003) and AbM (Martin and Thornton J Bmol Biol 263: 800- 15, 1996). The correspondence between the various delineations and variable region numbering are described (see e.g. Lefranc et al. Dev Comp Immunol 27: 55-77, 2003; Honegger and Pluckthun, J Mol Biol 309:657-70, 2001; International ImMunoGeneTics (IMGT) database; Web resources, http: / / www_imgt_org). Available programs such as abYsis by UCL Business PLC can be used to delineate CDRs. The term “CDR”, “HCDR1”, “HCDR2”, “HCDR3”, “LCDR1”, “LCDR2” and “LCDR3” as used herein includes CDRs defined by any of the methods described supra, Kabat, Chothia, IMGT or AbM, unless otherwise explicitly stated in the specification. Preferably, the term “CDR”, “HCDR1”, “HCDR2”, “HCDR3”, “LCDR1”, “LCDR2” and “LCDR3” as used herein includes CDRs defined by the method of Kabat. “Comprising” is intended to include examples encompassed by the terms “consisting essentially of” and “consisting of”; similarly, the term “consisting essentially of” is intended to include examples encompassed by the term “consisting of.” Unless the context clearly requires otherwise, throughout the description and the claims, the words “comprise”, “comprising”, and the like are to be construed in an inclusive sense as opposed to an exclusive or exhaustive sense; that is to say, in the sense of “including, but not limited to”. “Decreasing oral toxicity” refers to decreasing the severity of oral toxicity in a subject, and / or decreasing the occurrence of oral toxicity in a subject, and / or preventing the occurrence of oral toxicity in a subject. Attorney Docket No.258199.061702 JBI6826WOPCT1 “Fc gamma receptor” (Fc ^R) refers to well-known Fc ^RI, Fc ^RIIa, Fc ^RIIb or Fc ^RIII. Activating Fc ^R includes Fc ^RI, Fc ^RIIa and Fc ^RIII. “GPRC5D-targeted therapeutic” refers to a therapeutic, such as an antibody, that binds to GPRC5D on multiple myeloma cells. “GPRC5DxCD3 bispecific antibody” refers to a bispecific antibody that specifically binds GPRC5D and CD3. “Human antibody” refers to an antibody that is optimized to have minimal immune response when administered to a human subject. Variable regions of human antibody are derived from human immunoglobulin sequences. If human antibody contains a constant region or a portion of the constant region, the constant region is also derived from human immunoglobulin sequences. Human antibody comprises heavy and light chain variable regions that are “derived from” sequences of human origin if the variable regions of the human antibody are obtained from a system that uses human germline immunoglobulin or rearranged immunoglobulin genes. Such exemplary systems are human immunoglobulin gene libraries displayed on phage, and transgenic non-human animals such as mice or rats carrying human immunoglobulin loci. “Human antibody” typically contains amino acid differences when compared to the immunoglobulins expressed in humans due to differences between the systems used to obtain the human antibody and human immunoglobulin loci, introduction of somatic mutations or intentional introduction of substitutions into the frameworks or CDRs, or both. Typically, “human antibody” is at least about 80%, 81%, 82%, 83%, 84%, 85%, 86%, 87%, 88%, 89%, 90%, 91%, 92%, 93%, 94%, 95%, 96%, 97%, 98% or 99% identical in amino acid sequence to an amino acid sequence encoded by human germline immunoglobulin or rearranged immunoglobulin genes. In some cases, “human antibody” can contain consensus framework sequences derived from human framework sequence analyses, for example as described in Knappik et al., (2000) J Mol Biol 296:57-86, or synthetic HCDR3 incorporated into human immunoglobulin gene libraries displayed on phage, for example as described in Shi et al., (2010) J Mol Biol 397:385-96, and in Int. Patent Publ. No. WO2009 / 085462. Antibodies in which at least one CDR is derived from a non-human species are not included in the definition of “human antibody”. “Humanized antibody” refers to an antibody in which at least one CDR is derived from non-human species and at least one framework is derived from human Attorney Docket No.258199.061702 JBI6826WOPCT1 immunoglobulin sequences. Humanized antibody can include substitutions in the frameworks so that the frameworks can not be exact copies of expressed human immunoglobulin or human immunoglobulin germline gene sequences. “Identity” refers to a relationship between the sequences of two or more polypeptide molecules or two or more nucleic acid molecules, as determined by aligning and comparing the sequences. “Percent (%) 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, Inc.) software. Those skilled in the art can determine appropriate parameters for aligning sequences, including any algorithms needed to achieve maximal alignment over the full length of the sequences being compared. “Isolated” refers to a homogenous population of molecules (such as synthetic polynucleotides or a protein such as an antibody) which have been substantially separated and / or purified away from other components of the system the molecules are produced in, such as a recombinant cell, as well as a protein that has been subjected to at least one purification or isolation step. “Isolated antibody” refers to an antibody that is substantially free of other cellular material and / or chemicals and encompasses antibodies that are isolated to a higher purity, such as to 80%, 81%, 82%, 83%, 84%, 85%, 86%, 87%, 88%, 89%, 90%, 91%, 92%, 93%, 94%, 95%, 96%, 97%, 98%, 99% or 100% purity. “Monoclonal antibody” refers to an antibody obtained from a substantially homogenous population of antibody molecules, i.e., the individual antibodies comprising the population are identical except for possible well-known alterations such as removal of C-terminal lysine from the antibody heavy chain or post-translational modifications such as amino acid isomerization or deamidation, methionine oxidation or asparagine or glutamine deamidation. Monoclonal antibodies typically bind one antigenic epitope. A Attorney Docket No.258199.061702 JBI6826WOPCT1 bispecific monoclonal antibody binds two distinct antigenic epitopes. Monoclonal antibodies can have heterogeneous glycosylation within the antibody population. Monoclonal antibody can be monospecific or multispecific such as bispecific, monovalent, bivalent or multivalent. “Mutation” refers to an engineered or naturally occurring alteration in a polypeptide or polynucleotide sequence when compared to a reference sequence. The alteration can be a substitution, insertion or deletion of one or more amino acids or polynucleotides. “Negative minimal residual disease status” or “negative MRD status” or “MRD negative” refers to the PerMillionCount (i.e., a point estimate of malignant myeloma cells per million nucleated cells) in a patients on-study bone marrow sample relative to their reference bone marrow sample (i.e., talquetamab treatment naïve bone marrow sample). Based on this PerMillionCount, each sample is determined to be positive or negative. Samples are positive if the PerMillionCount is greater than or equal to the limit of sensitivity, otherwise they are negative. Negative minimal residual disease status can be determined at a sensitivity of 0.01% (10-4), 0.001% (10-5) or 0.0001% (10-6). Negative minimal residual disease status was determined using next generation sequencing (NGS). “Pharmaceutical composition” refers to composition that comprises an active ingredient and a pharmaceutically acceptable carrier. “Pharmaceutically acceptable carrier” or “excipient” refers to an ingredient in a pharmaceutical composition, other than the active ingredient, which is nontoxic to a subject. “Prophylactic intervention for oral toxicity” as used herein, means that treatment with the prophylactic intervention begins before a treatment phase with the GPRC5D-targeted therapeutic is initiated (i.e., before the subject’s first dose of the GPRC5D-targeted therapeutic); preferably, treatment with the prophylactic intervention then continues after the subject begins treatment with the GPRC5D-targeted therapeutic (i.e., the subject is treated with the prophylactic intervention before, and preferably during, the treatment phase with the GPRC5D-targeted therapeutic). Attorney Docket No.258199.061702 JBI6826WOPCT1 “Recombinant” refers to DNA, antibodies and other proteins that are prepared, expressed, created or isolated by recombinant means when segments from different sources are joined to produce recombinant DNA, antibodies or proteins. “Refractory” refers to a cancer that is not amendable to surgical intervention and is initially unresponsive to therapy. “Relapsed” refers to a cancer that responded to treatment but then returns. “Step-up dose” refers to a dose of an active agent that is administered to a subject prior to a treatment dose. A step-up dose is lower than the treatment dose. To prevent or lessen certain toxicities, such as cytokine release syndrome (CRS), a “priming” dose strategy may include one or more lower step-up dose(s) followed by higher treatment doses. “Subject” includes any human or nonhuman animal. “Nonhuman animal” includes all vertebrates, e.g., mammals and non-mammals, such as nonhuman primates, sheep, dogs, cats, horses, cows, chickens, amphibians, reptiles, etc. Except when noted, the terms “patient” or “subject” are used interchangeably. “T cell redirecting therapeutic” refers to a molecule containing two or more binding regions, wherein one of the binding regions specifically binds a cell surface antigen on a target cell or tissue and wherein a second binding region of the molecule specifically binds a T cell antigen. Examples of cell surface antigen include a tumor associated antigen, such as GPRC5D. Examples of T cell antigen include, e.g., CD3. This dual / multi-target binding ability recruits T cells to the target cell or tissue leading to the eradication of the target cell or tissue. “Therapeutically effective amount” refers to an amount effective, at doses and for periods of time necessary, to achieve a desired therapeutic result. A therapeutically effective amount can vary depending on factors such as the disease state, age, sex, and weight of the individual, and the ability of a therapeutic or a combination of therapeutics to elicit a desired response in the individual. Exemplary indicators of an effective therapeutic or combination of therapeutics that include, for example, improved well- being of the patient. “Treat” or “treatment” refers to both therapeutic treatment and prophylactic or preventative measures, wherein the object is to prevent or slow down (lessen) an undesired physiological change or disorder. Beneficial or desired clinical results include Attorney Docket No.258199.061702 JBI6826WOPCT1 alleviation of symptoms, diminishment of extent of disease, stabilized (i.e., not worsening) state of disease, delay or slowing of disease progression, amelioration or palliation of the disease state, and remission (whether partial or total), whether detectable or undetectable. “Treatment” can also mean prolonging survival as compared to expected survival if a subject was not receiving treatment. Those in need of treatment include those already with the condition or disorder as well as those prone to have the condition or disorder or those in which the condition or disorder is to be prevented. “Treatment dose” refers to a dose of the active agent that is administered to a subject to treat a disease. A treatment dose may be administered at a regular dosing interval on a repetitive basis (e.g. weekly, biweekly). A treatment dose may be preceded by one or more step-up doses. “Treatment phase” as used herein refers to a time period throughout which a subject is administered a GPRC5D-targeted therapeutic on a dosing schedule, including any step-doses and treatment doses, starting from the subject’s first dose of the GPRC5D-targeted therapeutic (e.g., the first step-up dose) until the subject discontinues treatment with the GPRC5D-targeted therapeutic. For example, a treatment phrase may begin when a subject receives a first step-up dose and continue for several weeks or months as the subject receives subsequent step-up doses and treatment doses. A patient that is “triple-class exposed” refers to a patient diagnosed with multiple myeloma (MM) that has previously been treated with (at a minimum) a proteasome inhibitor (PI), an immunomodulatory agent and an anti-CD38 monoclonal antibody. “Tumor cell” or a “cancer cell” refers to a cancerous, pre-cancerous or transformed cell, either in vivo, ex vivo, or in tissue culture, that has spontaneous or induced phenotypic changes. These changes do not necessarily involve the uptake of new genetic material. Although transformation can arise from infection with a transforming virus and incorporation of new genomic nucleic acid, uptake of exogenous nucleic acid or it can also arise spontaneously or following exposure to a carcinogen, thereby mutating an endogenous gene. Transformation / cancer is exemplified by morphological changes, immortalization of cells, aberrant growth control, foci formation, proliferation, malignancy, modulation of tumor specific marker levels, invasiveness, tumor growth in suitable animal hosts such as nude mice, and the like, in vitro, in vivo, and ex vivo. Attorney Docket No.258199.061702 JBI6826WOPCT1 The numbering of amino acid residues in the antibody constant region throughout the specification is according to the EU index as described in Kabat et al., Sequences of Proteins of Immunological Interest, 5thEd. Public Health Service, National Institutes of Health, Bethesda, MD. (1991), unless otherwise explicitly stated. Antibody constant chain numbering can be found for example at ImMunoGeneTics website, at IMGT Web resources at IMGT Scientific charts. Conventional one and three-letter amino acid codes are used herein as shown in Table 1. Table 1. Amino acid Three-letter code One-letter code Alanine Ala A Arginine Arg R Asparagine Asn N Aspartate Asp D Cysteine Cys C Glutamate Gln E Glutamine Glu Q Glycine Gly G Histidine His H Isoleucine Ile I Leucine Leu L Lysine Lys K Methionine Met M Phenylalanine Phe F Proline Pro P Serine Ser S Threonine Thr T Tryptophan Trp W Tyrosine Tyr Y Valine Val V GPRC5DxCD3 bispecific antibodies and uses thereof In patients with relapsed or refractory disease who have exhausted several therapies, multiple myeloma (MM) remains an incurable malignancy and an unmet medical need with significant morbidity and mortality. Despite therapeutic achievements including agents such as proteasome inhibitors (Pis), immunomodulatory drugs (ImiDs), and monoclonal antibodies (mAbs), the disease most often recurs. In the first prospective Attorney Docket No.258199.061702 JBI6826WOPCT1 study of real-life standard of care in triple-class exposed patients with relapsed or refractory multiple myeloma (RRMM), regimens utilized showed no clear standard of care and resulted in poor outcomes in heavily pretreated, triple-class exposed patients. T- cell redirecting agents targeting CD3 and epitopes such as BCMA, FcRH5 and GPRC5D, and anti-BCMA CAR-T cells have broadened the therapeutic armamentarium. These new therapeutic options directed at alternative mechanisms of action can better control the disease, provide deeper, more sustained responses, and better long-term outcomes including maintenance of health-related quality of life. However, specific toxicity of these new agents should be better studied and managed. Despite major developments, MM remains an incurable malignancy and an unmet medical need with significant morbidity and mortality. GPRC5D is a 7-transmembrane receptor protein for which is shown that expression is limited to normal plasma cells and hard keratinized tissues such as hair follicles. The relatively restricted expression of GPRC5D makes it a relatively low risk target for on-target / off-tumor toxicity and designates it as a suitable target for T lymphocyte (T cell) mediated therapy to treat plasma cell disorders like multiple myeloma. Talquetamab is a novel, humanized IgG4 bispecific antibody designed to target the CD3 receptor complex on T cells and GPRC5D-expressing multiple myeloma cells, resulting in T cell activation and subsequent lysis of GPRC5D-expressing cells. Oral toxicities are among the most frequently reported adverse events (AEs) with talquetamab treatment. Oral toxicity, characterized by dry mouth, dysgeusia, and / or dysphagia, is of special interest since it can decrease the patient’s quality of life and potentially result in weight reduction and could lead to discontinuation of the talquetamab treatment. In the MonumenTAL-1 clinical study, the discontinuation rate was about 5%. The etiology of oral toxicity after talquetamab treatment remains to be elucidated. On target, off tumor effect of the GPRC5D-directed T-cell could be a factor; however, GPRC5D expression can only be demonstrated in the filiform papillae. Filiform papillae are the most numerous papillae and are found all over the dorsum of the anterior two-thirds of the tongue, which are not associated with taste receptors. Drugs that can treat or reverse oral toxicity associated with GPRC5D-targeted therapeutics remain to be identified, and pathogenesis of this oral toxicity side effect needs further investigation. Attorney Docket No.258199.061702 JBI6826WOPCT1 The present inventors have developed novel treatment regimens to decrease or prevent the occurrence and / or severity of oral toxicity in subjects that receive a GPRC5D-targeted therapeutic, such as a GPRC5DxCD3 bispecific antibody. In preferred embodiments, prophylactic use of one or more of these treatment regimens mitigates the oral side effects of GPRC5D-targeted treatment (e.g., taste impairment) compared to no prophylaxis, thereby improving quality of life and maintaining the subject’s adherence to the GPRC5D-targeted dosing regimen. As used herein, oral toxicity includes dry mouth and / or taste impairment (altered taste and / or loss of taste) and / or difficulty swallowing. A taste impairment may include dysgeusia and / or hypogeusia and / or ageusia. Antibodies of the present invention Any suitable GPRC5D-targeted therapeutic known to those skilled in the art in view of the present disclosure can be used in the invention. In preferred embodiments, the GPRC5D-targeted therapeutic is a GPRC5DxCD3 bispecific antibody. Various bispecific antibody formats include formats described herein and recombinant IgG-like dual targeting molecules, wherein the two sides of the molecule each contain the Fab fragment or part of the Fab fragment of at least two different antibodies; IgG fusion molecules, wherein full length IgG antibodies are fused to an extra Fab fragment or parts of Fab fragment; Fc fusion molecules, wherein single chain Fv molecules or stabilized diabodies are fused to heavy-chain constant-domains, Fc-regions or parts thereof; Fab fusion molecules, wherein different Fab-fragments are fused together; ScFv- and diabody-based and heavy chain antibodies (e.g., domain antibodies, nanobodies) wherein different single chain Fv molecules or different diabodies or different heavy-chain antibodies (e.g. domain antibodies, nanobodies) are fused to each other or to another protein or carrier molecule, or bispecific antibodies generated by arm exchange. Exemplary bispecific formats include dual targeting molecules include Dual Targeting (DT)-Ig (GSK / Domantis), Two-in-one Antibody (Genentech) and mAb2 (F-Star), Dual Variable Domain (DVD)-Ig (Abbott), DuoBody (Genmab), Ts2Ab (MedImmune / AZ) and BsAb (Zymogenetics), HERCULES (Biogen Idec) and TvAb (Roche), ScFv / Fc Fusions (Academic Institution), SCORPION (Emergent BioSolutions / Trubion, Zymogenetics / BMS) and Dual Affinity Retargeting Technology (Fc-DART) (MacroGenics), F(ab)2 Attorney Docket No.258199.061702 JBI6826WOPCT1 (Medarex / AMGEN), Dual-Action or Bis-Fab (Genentech), Dock-and-Lock (DNL) (ImmunoMedics), Bivalent Bispecific (Biotecnol) and Fab-Fv (UCB-Celltech), Bispecific T Cell Engager (BITE) (Micromet), Tandem Diabody (Tandab) (Affimed), Dual Affinity Retargeting Technology (DART) (MacroGenics), Single-chain Diabody (Academic), TCR- like Antibodies (AIT, ReceptorLogics), Human Serum Albumin ScFv Fusion (Merrimack) and COMBODY (Epigen Biotech), dual targeting nanobodies (Ablynx), dual targeting heavy chain only domain antibodies. Various formats of bispecific antibodies have been described, for example in Chames and Baty (2009) Curr Opin Drug Disc Dev 12: 276 and in Nunez-Prado et al., (2015) Drug Discovery Today 20(5):588-594. In some embodiments, the GPRC5DxCD3 bispecific antibody comprises any one of the GPRC5D binding domains described in U.S. Patent No.10,562,968, the content of which is incorporated herein by reference in its entirety. In some embodiments, the GPRC5DxCD3 bispecific antibody comprises any one of the CD3 binding domains described in U.S. Patent No.10,562,968. In some embodiments, the GPRC5DxCD3 bispecific antibody comprises any one of the GPRC5DxCD3 bispecific antibodies described in U.S. Patent No.10,562,968. In some embodiments, the GPRC5DxCD3 bispecific antibody is chimeric, humanized or human. In some embodiments, the bispecific antibody is an IgG1, an IgG2, an IgG3 or an IgG4 isotype. In preferred embodiments, the bispecific antibody is an IgG4 isotype. An exemplary wild-type IgG4 comprises an amino acid sequence of SEQ ID NO: 34. SEQ ID NO: 34: ASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGV HTFPAVLQSSGLYSLSSVVTVPSSSLGTKTYTCNVDHKPSNTKVDKRVES KYGPPCPSCPAPEFLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDP EVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKE YKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCL VKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRW QEGNVFSCSVMHEALHNHYTQKSLSLSLGK Attorney Docket No.258199.061702 JBI6826WOPCT1 The bispecific antibody can be of any allotype. It is expected that allotype has no influence on properties of the bispecific antibodies, such as binding or Fc-mediated effector functions. Immunogenicity of therapeutic antibodies is associated with increased risk of infusion reactions and decreased duration of therapeutic response (Baert et al., (2003) N Engl J Med 348:602-08). The extent to which therapeutic antibodies induce an immune response in the host can be determined in part by the allotype of the antibody (Stickler et al., (2011) Genes and Immunity 12:213-21). Antibody allotype is related to amino acid sequence variations at specific locations in the constant region sequences of the antibody. Table 2 shows select IgG1, IgG2 and IgG4 allotypes. Table 2. AllotypeAmino acid residue at position of diversity(residue numbering: EU Index) IgG2 IgG4 IgG1 189 282 309 422 214 356 358 431 G2m(n) T M G2m(n-) P V G2m(n) / (n- T V nG4m(a) L R G1m(17) K E M A G1m(17,1) K D L A In some embodiments, the bispecific antibody comprises one or more Fc substitutions that reduces binding of the bispecific antibody to a Fc ^ receptor (Fc ^R) and / or reduces Fc effector functions such as C1q binding, complement dependent cytotoxicity (CDC), antibody-dependent cell-mediated cytotoxicity (ADCC) or phagocytosis (ADCP). The specific substitutions can be made in comparison to the wild- type IgG4 of SEQ ID NO: 34. Fc positions that can be substituted to reduce binding of the Fc to the activating Fc ^R and subsequently to reduce effector function are substitutions L234A / L235A on IgG1, V234A / G237A / P238S / H268A / V309L / A330S / P331S on IgG2, F234A / L235A on IgG4, S228P / F234A / L235A on IgG4, N297A on all Ig isotypes, V234A / G237A on IgG2, K214T / E233P / L234V / L235A / G236-deleted / A327G / P331A / D365E / L358M on IgG1, H268Q / V309L / A330S / P331S on IgG2, S267E / L328F on IgG1, L234F / L235E / D265A on IgG1, L234A / L235A / G237A / P238S / H268A / A330S / P331S on Attorney Docket No.258199.061702 JBI6826WOPCT1 IgG1, S228P / F234A / L235A / G237A / P238S on IgG4, and S228P / F234A / L235A / G236- deleted / G237A / P238S on IgG4, wherein residue numbering is according to the EU index. Fc substitutions that can be used to reduce CDC are a K322A substitution. Well-known S228P substitution can further be made in IgG4 antibodies to enhance IgG4 stability. In some embodiments, the bispecific antibody comprises one or more asymmetric substitutions in a first CH3 domain or in a second CH3 domain, or in both the first CH3 domain and the second CH3 domain. In some embodiments, the one or more asymmetric substitutions is selected from the group consisting of F405L / K409R, wild-type / F405L_R409K, T366Y / F405A, T366W / F405W, F405W / Y407A, T394W / Y407T, T394S / Y407A, T366W / T394S, F405W / T394S and T366W / T366S_L368A_Y407V, L351Y_F405A_Y407V / T394W, T366I_K392M_T394W / F405A_Y407V, T366L_K392M_T394W / F405A_Y407V, L351Y_Y407A / T366A_K409F, L351Y_Y407A / T366V_K409F, Y407A / T366A_K409F and T350V_L351Y_F405A_Y407V / T350V_T366L_K392L_T394W. In some embodiments, the GPRC5DxCD3 bispecific antibody is an IgG4 isotype and comprises phenylalanine at position 405 and arginine at position 409 in a first heavy chain (HC1) and leucine at position 405 and lysine at position 409 in a second heavy chain (HC2), wherein residue numbering is according to the EU Index. In some embodiments, the GPRC5DxCD3 bispecific antibody further comprises proline at position 228, alanine at position 234 and alanine at position 235 in both the HC1 and the HC2. Tables 3 and 4 provide sequences of an exemplary embodiment of a GPRC5DxCD3 bispecific antibody, according to the Kabat numbering system. Table 3. Sequences of GPRC5D binding arm Region Sequence SEQ ID NO:HCDR1 GYTMN 4 HCDR2 LINPYNSDTNYAQKLQG 5 HCDR3 VALRVALDY 6 LCDR1 KASQNVATHVG 7 LCDR2 SASYRYS 8 LCDR3 QQYNRYPYT 9 Attorney Docket No.258199.061702 JBI6826WOPCT1 VH QVQLVQSGAEVKKPGASVKVSCKASGYSF 10 TGYTMNWVRQAPGQGLEWMGLINPYNSD TNYAQKLQGRVTMTTDTSTSTAYMELRSL RSDDTAVYYCARVALRVALDYWGQGTLV TVSS VL DIQMTQSPSSLSASVGDRVTITCKASQNVA 11 THVGWYQQKPGKAPKRLIYSASYRYSGVP SRFSGSGSGTEFTLTISNLQPEDFATYYCQQ YNRYPYTFGQGTKLEIK HC QVQLVQSGAEVKKPGASVKVSCKASGYSF 12 TGYTMNWVRQAPGQGLEWMGLINPYNSD TNYAQKLQGRVTMTTDTSTSTAYMELRSL RSDDTAVYYCARVALRVALDYWGQGTLV TVSSASTKGPSVFPLAPCSRSTSESTAALGC LVKDYFPEPVTVSWNSGALTSGVHTFPAV LQSSGLYSLSSVVTVPSSSLGTKTYTCNVD HKPSNTKVDKRVESKYGPPCPPCPAPEAAG GPSVFLFPPKPKDTLMISRTPEVTCVVVDV SQEDPEVQFNWYVDGVEVHNAKTKPREE QFNSTYRVVSVLTVLHQDWLNGKEYKCK VSNKGLPSSIEKTISKAKGQPREPQVYTLPP SQEEMTKNQVSLTCLVKGFYPSDIAVEWE SNGQPENNYKTTPPVLDSDGSFFLYSRLTV DKSRWQEGNVFSCSVMHEALHNHYTQKS LSLSLGK LC DIQMTQSPSSLSASVGDRVTITCKASQNVA 13 THVGWYQQKPGKAPKRLIYSASYRYSGVP SRFSGSGSGTEFTLTISNLQPEDFATYYCQQ YNRYPYTFGQGTKLEIKRTVAAPSVFIFPPS DEQLKSGTASVVCLLNNFYPREAKVQWK VDNALQSGNSQESVTEQDSKDSTYSLSSTL TLSKADYEKHKVYACEVTHQGLSSPVTKS FNRGEC Table 4. Sequences of CD3 binding arm Region Sequence SEQ ID NO: HCDR1 TYAMN 14 HCDR2 RIRSKYNNYATYYAASVKG 15 HCDR3 HGNFGNSYVSWFAY 16 LCDR1 RSSTGAVTTSNYAN 17 LCDR2 GTNKRAP 18 Attorney Docket No.258199.061702 JBI6826WOPCT1 LCDR3 ALWYSNLWV 19 VH EVQLVESGGGLVQPGGSLRLSCAASGFTFNT 20 YAMNWVRQAPGKGLEWVARIRSKYNNYAT YYAASVKGRFTISRDDSKNSLYLQMNSLKTE DTAVYYCARHGNFGNSYVSWFAYWGQGTL VTVSS VL QTVVTQEPSLTVSPGGTVTLTCRSSTGAVTT 21 SNYANWVQQKPGQAPRGLIGGTNKRAPGTP ARFSGSLLGGKAALTLSGVQPEDEAEYYCAL WYSNLWVFGGGTKLTVLGQP HC EVQLVESGGGLVQPGGSLRLSCAASGFTFNT 22 YAMNWVRQAPGKGLEWVARIRSKYNNYAT YYAASVKGRFTISRDDSKNSLYLQMNSLKTE DTAVYYCARHGNFGNSYVSWFAYWGQGTL VTVSSASTKGPSVFPLAPCSRSTSESTAALGC LVKDYFPEPVTVSWNSGALTSGVHTFPAVL QSSGLYSLSSVVTVPSSSLGTKTYTCNVDHK PSNTKVDKRVESKYGPPCPPCPAPEAAGGPS VFLFPPKPKDTLMISRTPEVTCVVVDVSQED PEVQFNWYVDGVEVHNAKTKPREEQFNSTY RVVSVLTVLHQDWLNGKEYKCKVSNKGLPS SIEKTISKAKGQPREPQVYTLPPSQEEMTKNQ VSLTCLVKGFYPSDIAVEWESNGQPENNYKT TPPVLDSDGSFLLYSKLTVDKSRWQEGNVFS CSVMHEALHNHYTQKSLSLSLGK LC QTVVTQEPSLTVSPGGTVTLTCRSSTGAVTT 23 SNYANWVQQKPGQAPRGLIGGTNKRAPGTP ARFSGSLLGGKAALTLSGVQPEDEAEYYCAL WYSNLWVFGGGTKLTVLGQPKAAPSVTLFP PSSEELQANKATLVCLISDFYPGAVTVAWKA Attorney Docket No.258199.061702 JBI6826WOPCT1 DSSPVKAGVETTTPSKQSNNKYAASSYLSLT PEQWKSHRSYSCQVTHEGSTVEKTVAPTECS In some embodiments, the GPRC5DxCD3 bispecific antibody is JNJ-64407564 or Talquetamab (also referred to herein as Tal), which has the sequences described in Tables 3 and 4. Talquetamab is a GPRC5D-directed bispecific antibody in development for treatment of patients with relapsed or refractory multiple myeloma. See, e.g., Chari A, et al. Blood 2022; 140 (suppl 1): 384-387, which is incorporated by reference herein. Talquetamab is a bispecific GPRC5D-directed CD3 T cell engager in development as a monotherapy for the treatment of adult patients with relapsed or refractory multiple myeloma who have received at least three or four prior therapies, including a proteasome inhibitor, an immunomodulatory agent and an anti-CD38 monoclonal antibody. Talquetamab and its methods of use are described, for example, in WO 2018 / 017786 and WO 2022 / 058445, which are incorporated by reference herein. According to particular embodiments, the GPRC5DxCD3 bispecific antibody has an amino acid sequence with at least 80%, at least 85%, at least 90%, at least 95%, at least 98%, or at least 99% sequence identity to the amino acid sequence of talquetamab. Additional embodiments of GPRC5DxCD3 bispecific antibodies that may be used in accordance with the present invention are described below. In certain embodiments, the GPRC5DxCD3 bispecific antibody comprises a GPRC5D binding domain comprising the HCDR1 of SEQ ID NO: 4, the HCDR2 of SEQ ID NO: 5, the HCDR3 of SEQ ID NO: 6, the LCDR1 of SEQ ID NO: 7, the LCDR2 of SEQ ID NO: 8 and the LCDR3 of SEQ ID NO: 9, and a CD3 binding domain comprising the HCDR1 of SEQ ID NO: 14, the HCDR2 of SEQ ID NO: 15, the HCDR3 of SEQ ID NO: 16, the LCDR1 of SEQ ID NO: 17, the LCDR2 of SEQ ID NO: 18 and the LCDR3 of SEQ ID NO: 19. In certain embodiments, the GPRC5D binding domain comprises a heavy chain variable region (VH) having the amino acid sequence of SEQ ID NO: 10 and a light chain variable region (VL) having the amino acid sequence of SEQ ID NO: 11, and the CD3 binding domain comprises a heavy chain variable region (VH) having the amino Attorney Docket No.258199.061702 JBI6826WOPCT1 acid sequence of SEQ ID NO: 20 and a light chain variable region (VL) having the amino acid sequence of SEQ ID NO: 21. In certain embodiments, the GPRC5DxCD3 bispecific antibody is an IgG1, an IgG2, an IgG3 or an IgG4 isotype. In certain embodiments, the GPRC5DxCD3 bispecific antibody is an IgG4 isotype. In certain embodiments, the GPRC5DxCD3 bispecific antibody comprises one or more substitutions in its Fc region. In certain embodiments, the GPRC5DxCD3 bispecific antibody is an IgG4 isotype and comprises S228P, F234A and L235A substitutions in its Fc region. In certain embodiments, the GPRC5DxCD3 bispecific antibody is an IgG4 isotype and comprises S228P, F234A, L235A F405L and R409K substitutions in its Fc region. In certain embodiments, the Fc region of the GPRC5D-specific IgG4 antibody from which the GPRC5D-binding arm is derived comprises S228P, L234A and L235A substitutions in its Fc region. In certain embodiments, the Fc region of the CD3-specific IgG4 antibody from which the CD3-binding arm is derived comprises S228P, L234A, L235A, F405L, and R409K substitutions in its Fc region.In certain embodiments, the GPRC5DxCD3 bispecific antibody comprises a first heavy chain (HC1) having the amino acid sequence of SEQ ID NO: 12, a first light chain (LC1) having the amino acid sequence of SEQ ID NO: 13, a second heavy chain (HC2) having the amino acid sequence of SEQ ID NO: 22 and a second light chain (LC2) having the amino acid sequence of SEQ ID NO: 23. In certain embodiments, the GPRC5DxCD3 bispecific antibody comprises a first heavy chain (HC1) having at least 90% identity to the amino acid sequence of SEQ ID NO: 12, a first light chain (LC1) having at least 90% identity to the amino acid sequence of SEQ ID NO: 13, a second heavy chain (HC2) having at least 90% identity to the amino acid sequence of SEQ ID NO: 22 and a second light chain (LC2) having at least 90% identity to the amino acid sequence of SEQ ID NO: 23. In certain embodiments, the GPRC5DxCD3 bispecific antibody comprises a first heavy chain (HC1) having at least 95% identity to the amino acid sequence of SEQ ID NO: 12, a first light chain (LC1) having at least 95% identity to the amino acid sequence Attorney Docket No.258199.061702 JBI6826WOPCT1 of SEQ ID NO: 13, a second heavy chain (HC2) having at least 95% identity to the amino acid sequence of SEQ ID NO: 22 and a second light chain (LC2) having at least 95% identity to the amino acid sequence of SEQ ID NO: 23. In certain embodiments, the GPRC5DxCD3 bispecific antibody comprises a first heavy chain (HC1) having at least 98% identity to the amino acid sequence of SEQ ID NO: 12, a first light chain (LC1) having at least 98% identity to the amino acid sequence of SEQ ID NO: 13, a second heavy chain (HC2) having at least 98% identity to the amino acid sequence of SEQ ID NO: 22 and a second light chain (LC2) having at least 98% identity to the amino acid sequence of SEQ ID NO: 23. In certain embodiments, the GPRC5DxCD3 bispecific antibody is talquetamab. Patient populations with multiple myeloma In certain embodiments, GPRC5DxCD3 bispecific antibodies disclosed herein are for use in treating multiple myeloma in a subject, for example a human subject, wherein the subject is relapsed or refractory to treatment with one or more prior anti- cancer treatments. Relapsed disease means a cancer has come back. Refractory disease means a cancer has not improved with treatment or has stopped responding to treatment. In some embodiments, the subject is relapsed or refractory to treatment with a therapeutic used to treat multiple myeloma or other hematological malignancies. In certain embodiments, the subject has had been treated with from 1 to 11 prior lines of therapy, or from 1 to 10 prior lines of therapy. In certain embodiments, the subject has previously received an autologous stem cell transplant (ASCT). In certain embodiments, the subject has received at least three prior lines of therapy. In certain embodiments, the subject has received at least four prior lines of therapy. In certain embodiments, the subject has received at least five prior lines of therapy (penta-drug exposed). In certain embodiments, the subject has received at least three prior lines of therapy, including a proteasome inhibitor, an immunomodulatory agent and an anti- CD38 monoclonal antibody. Attorney Docket No.258199.061702 JBI6826WOPCT1 In certain embodiments, the subject has received at least four prior lines of therapy, including a proteasome inhibitor, an immunomodulatory agent and an anti- CD38 monoclonal antibody. In particular embodiments, the patients are relapsed or refractory or intolerant to the last line of therapy (LOT); were exposed to a proteasome inhibitor, immunomodulatory drug, and anti-CD38 therapy; and had measurable disease. In some embodiments, the subject has received three anti-cancer therapies prior to administration of the GPRC5DxCD3 bispecific antibody. In one embodiment, the three prior anti-cancer therapies are a proteasome inhibitor (PI), an immunomodulatory drug (iMiD), and an anti-CD38 antibody. In certain such embodiments, the proteasome inhibitor is bortezomib, carfilzomib or ixazomib, the immunomodulatory drug (iMiD) is lenalidomide, pomalidomide or thalidomide and the anti-CD38 antibody is daratumumab or isatuximab. In one embodiment, the proteasome inhibitor is bortezomib, the immunomodulatory drug (iMiD) is lenalidomide and the anti-CD38 antibody is daratumumab. In one embodiment, the proteasome inhibitor is bortezomib, the immunomodulatory drug (iMiD) is lenalidomide and the anti-CD38 antibody is isatuximab. In one embodiment, the proteasome inhibitor is bortezomib, the immunomodulatory drug (iMiD) is pomalidomide and the anti-CD38 antibody is daratumumab. In one embodiment, the proteasome inhibitor is bortezomib, the immunomodulatory drug (iMiD) is pomalidomide and the anti-CD38 antibody is isatuximab. In one embodiment, the proteasome inhibitor is bortezomib, the immunomodulatory drug (iMiD) is thalidomide and the anti-CD38 antibody is daratumumab. In one embodiment, the proteasome inhibitor is bortezomib, the immunomodulatory drug (iMiD) is thalidomide and the anti-CD38 antibody is isatuximab. In one embodiment, the proteasome inhibitor is carfilzomib, the immunomodulatory drug (iMiD) is lenalidomide and the anti-CD38 antibody is daratumumab. In one embodiment, the proteasome inhibitor is carfilzomib, the immunomodulatory drug (iMiD) is lenalidomide and the anti-CD38 antibody is isatuximab. In one embodiment, the proteasome inhibitor is carfilzomib, the immunomodulatory drug (iMiD) is pomalidomide and the anti-CD38 antibody is Attorney Docket No.258199.061702 JBI6826WOPCT1 daratumumab. In one embodiment, the proteasome inhibitor is carfilzomib, the immunomodulatory drug (iMiD) is pomalidomide and the anti-CD38 antibody is isatuximab. In one embodiment, the proteasome inhibitor is carfilzomib, the immunomodulatory drug (iMiD) is thalidomide and the anti-CD38 antibody is daratumumab. In one embodiment, the proteasome inhibitor is carfilzomib, the immunomodulatory drug (iMiD) is thalidomide and the anti-CD38 antibody is isatuximab. In one embodiment, the proteasome inhibitor is ixazomib, the immunomodulatory drug (iMiD) is lenalidomide and the anti-CD38 antibody is daratumumab. In one embodiment, the proteasome inhibitor is ixazomib, the immunomodulatory drug (iMiD) is lenalidomide and the anti-CD38 antibody is isatuximab. In one embodiment, the proteasome inhibitor is ixazomib, the immunomodulatory drug (iMiD) is pomalidomide and the anti-CD38 antibody is daratumumab. In one embodiment, the proteasome inhibitor is ixazomib, the immunomodulatory drug (iMiD) is pomalidomide and the anti-CD38 antibody is isatuximab. In one embodiment, the proteasome inhibitor is ixazomib, the immunomodulatory drug (iMiD) is thalidomide and the anti-CD38 antibody is daratumumab. In one embodiment, the proteasome inhibitor is ixazomib, the immunomodulatory drug (iMiD) is thalidomide and the anti-CD38 antibody is isatuximab. In some embodiments, the subject is refractory or relapsed to treatment with one or more treatments or therapies, such as THALOMID®(thalidomide), REVLIMID®(lenalidomide), POMALYST®(pomalidomide), VELCADE®(bortezomib), NINLARO (ixazomib), KYPROLIS®(carfilzomib), FARADYK®30elinexor30att), AREDIA®(pamidronate), ZOMETA®(zoledronic acid), DARZALEX®(daratumumab), elotozumab or melphalan, Xpovio ® (Selinexor), Venclexta ® (Venetoclax), GSK 916, CAR-T therapies, or other BCMA-directed therapies. Various qualitative and / or quantitative methods can be used to determine relapse or refractory nature of the disease. Symptoms that can be associated are for example a decline or plateau of the well-being of the patient or re-establishment or worsening of various symptoms associated with solid tumors, and / or the spread of cancerous cells in the body from one location to other organs, tissues or cells. Attorney Docket No.258199.061702 JBI6826WOPCT1 In some embodiments, the multiple myeloma is relapsed or refractory to treatment with an anti-CD38 antibody,31elinexorr, venetoclax, lenalinomide, bortezomib, pomalidomide, carfilzomib, elotozumab, ixazomib, melphalan or thalidomide, or any combination thereof. In one embodiment, the anti-CD38 antibody is daratumumab. In another embodiment, the anti-CD38 antibody is isatuximab In some embodiments, the multiple myeloma is a high-risk multiple myeloma. Subjects with high-risk multiple myeloma are known to relapse early and have poor prognosis and outcome. Subjects can be classified as having high-risk multiple myeloma is they have one or more of the following cytogenetic abnormalities: t(4;14)(p16;q32), t(14;16)(q32;q23), del17p, 1qAmp, t(4;14)(p16;q32) and t(14;16)(q32;q23), t(4;14)(p16;q32) and del17p, t(14;16)(q32;q23) and del17p, or t(4;14)(p16;q32), t(14;16)(q32;q23) and del17p. In some embodiments, the subject having the high-risk multiple myeloma has one or more chromosomal abnormalities comprising: t(4;14)(p16;q32), t(14;16)(q32;q23), del17p, 1qAmp, t(4;14)(p16;q32) and t(14;16)(q32;q23), t(4;14)(p16;q32) and del17p, t(14;16)(q32;q23) and del17p; or t(4;14)(p16;q32), t(14;16)(q32;q23) and del17p, or any combination thereof. The cytogenetic abnormalities can be detected for example by fluorescent in situ hybridization (FISH). In chromosomal translocations, an oncogene is translocated to the IgH region on chromosome 14q32, resulting in dysregulation of these genes. t(4;14)(p16;q32) involves translocation of fibroblast growth factor receptor 3 (FGFR3) and multiple myeloma SET domain containing protein (MMSET) (also called WHSC1 / NSD2), and t(14;16)(q32;q23) involves translocation of the MAF transcription factor C-MAF. Deletion of 17p (del17p) involves loss of the p53 gene locus. Chromosomal rearrangements can be identified using well known methods, for example fluorescent in situ hybridization, karyotyping, pulsed field gel electrophoresis, or sequencing. Prophylactic interventions for GPRC5D-related oral toxicity The inventors have developed novel treatment regimens to decrease or prevent the occurrence and / or severity of oral toxicity, such as taste impairment, in subjects that Attorney Docket No.258199.061702 JBI6826WOPCT1 receive a GPRC5D-targeted therapeutic, such as a GPRC5DxCD3 bispecific antibody (e.g., talquetamab). As used herein, “weight-based” refers to administration of a dose amount that is based on the subject’s specific body weight; for example, 3 mg / kg refers to a dose of 3 milligrams of antibody per kilogram of the subject’s body weight. Unless otherwise specified herein, when a dose is described in a unit of “mg / kg” or “µg / kg,” weight-based dosing is being employed. Unless otherwise specified herein, a GPRC5DxCD3 bispecific antibody, such as talquetamab, is administered on a dosing schedule based on sequential 28-day cycles, for example, Cycle 1 starts on Day 1 of Cycle 1 and ends on Day 28 of Cycle 1, and then Day 1 of Cycle 2 starts the day after Day 28 of Cycle 1 and ends on Day 28 of Cycle 2, and then Day 1 of Cycle 3 starts the day after Day 28 of Cycle 2 and ends on Day 28 of Cycle 3, and so on. In certain embodiments, one or more step-up doses are administered prior to the first treatment cycle, i.e., prior to Cycle 1 Day 1. Thus, a treatment cycle, as used herein, refers to a 28-day treatment cycle. As used herein “Q2W” (also referred to as “bi-weekly” or “biweekly”) means once every two weeks, and “QW” (also referred to as “weekly”) means once weekly. Administration of a treatment dose once weekly (QW) is also referred to herein as a weekly dosing schedule. Administration of a treatment dose once every two weeks (Q2W) is also referred to herein as a bi-weekly dosing schedule. As used herein “Q4W” means once every four weeks. Q4W is sometimes referred to herein as “monthly” but technically refers to once every 4 weeks or once every 28 days (e.g., in 28-day cycles, a first treatment dose occurs on Day 1 of Cycle 1, a second treatment dose occurs on Day 1 of Cycle 2, etc.). According to embodiments of the present invention, methods of treating multiple myeloma are effective in eliciting a clinical response in a subject as determined by International Myeloma Working Group (IMWG) 2016 response criteria. According to particular embodiments, the methods of treatment are effective in eliciting a partial response, a very good partial response, a complete response or a stringent complete response, as determined by IMWG response criteria. As used herein, overall response rate (ORR) refers to the percentage of patients in a population that achieve a partial response (PR) or better, i.e., a partial response, very good partial response, complete Attorney Docket No.258199.061702 JBI6826WOPCT1 response or stringent complete response. IMWG 2016 criteria for response to Multiple Myeloma treatment are provided in Table 7 below. Table 7 Response Response Criteria sCR=stringent complete ^ CR as defined below, plus response ^ Normal FLC ratio, and ^ Absence of clonal PCs by immunohistochemistry, immunofluorescenceaor 2- to 4-color flow cytometry CR=complete response ^ Negative immunofixation on the serum and urine, and ^ Disappearance of any soft tissue plasmacytomas, and ^ <5% PCs in bone marrow VGPR=very good partial response ^ Serum and urine M-component detectable by immunofixation but not on electrophoresis, or ^ ≥90% reduction in serum M-protein plus urine M- protein <100 mg / 24 hours PR=partial response ^ ≥50% reduction of serum M-protein and reduction in 24-hour urinary M-protein by ≥90% or to <200 mg / 24 hours ^ If the serum and urine M-protein are not measurable, a decrease of ≥50% in the difference between involved and uninvolved FLC levels is required in place of the M-protein criteria ^ If serum and urine M-protein are not measurable, and serum free light assay is also not measurable, ≥50% reduction in bone marrow PCs is required in place of M-protein, provided baseline bone marrow plasma cell percentage was ≥30% ^ In addition to the above criteria, if present at baseline, a ≥50% reduction in the size of soft tissue plasmacytomas is also required. CR=complete response; FLC=free light chain; IMWG=International Myeloma Working Group; M-protein=monoclonal paraprotein; MR=minimal response; PC=plasma cell; PD=progressive disease; PR=partial response; sCR=stringent complete response; SD=stable disease; VGPR=very good partial responseaPresence / absence of clonal cells is based upon the kappa / lambda ratio. An abnormal kappa / lambda ratio by immunohistochemistry or immunofluorescence requires a minimum of 100 plasma cells for analysis. An abnormal ratio reflecting presence of an abnormal clone is kappa / lambda of >4:1 or <1:2. Attorney Docket No.258199.061702 JBI6826WOPCT1 * Clarifications to IMWG criteria for coding CR and VGPR in subjects in whom the only measurable disease is by serum FLC levels: CR in such subjects indicates a normal FLC ratio of 0.26 to 1.65 in addition to CR criteria listed above. VGPR in such subjects requires a >90% decrease in the difference between involved and uninvolved FLC levels. IMWG criteria for response to Multiple Myeloma treatment are also described, for example, in Durie et al., Kumar et al. and Rajkumar et al., which are incorporated by reference herein: Durie BG, Harousseau JL, Miguel JS, et al. International uniform response criteria for multiple myeloma. Leukemia.2006;20(9):1467-1473; Kumar S, Paiva B, Anderson KC, et al. International Myeloma Working Group consensus criteria for response and minimal residual disease assessment in multiple myeloma. Lancet Oncol.2016;17(8):e328-346; Rajkumar SV, Harousseau JL, Durie B, et al. Consensus recommendations for the uniform reporting of clinical Trials: report of the International Myeloma Workshop Consensus Panel 1. Blood.2011;117(18):4691-4695. In certain embodiments, a subject’s response to the prophylactic interventions described herein may be tested by one or more of the following procedures: - Taste assessment using WETT, as described herein; - Taste assessment using taste strips (e.g., according to the standard taste assessment described herein); - Grade of dysgeusia by NCI-CTCAE, Version 5.0; - PROs: EORTC-QLQ-C30 / OH-15, STTA, xerostomia inventory, and PRO- CTCAE oral toxicity items; - Measurement of stimulated and unstimulated salivary flow; - Tongue and / or salivary gland biopsies (optional); According to an embodiment, a subject’s taste is assessed with taste strips according to the procedure below, referred to herein as the “standard taste assessment”: Standard taste assessment: - The taste strip, with a length of 8 cm and an area of 2 cm2, is impregnated with a taste stimulant. The lowest concentrations of each taste quality should be identified by half of healthy individuals only; the highest concentration should be identified by approximately 100% of the participants. Attorney Docket No.258199.061702 JBI6826WOPCT1 - Four concentrations (4=lowest concentration, 1=highest concentration) are used for each taste quality: sweet, sour, salty, bitter, and umami. - The taste strips (plus 2 blank strips without taste) are presented in increasing concentrations (Table 11). Each of the 2 sequences of the 22 taste strips (4 concentrations of each taste quality plus 2 blanks) are applied in a pseudorandomized order. - Before the procedure, subjects are instructed to refrain from eating, drinking, or using tobacco products (including e-cigarettes or the equivalent of e-cigarettes, except for nicotine patches) 30 minutes to 1 hour before the procedure. Procedure: 1. Choose 1 of the sequences of A / C, A / D, B / C or B / D for the assessment as described in Table 11. Change the order for every assessment. 2. Place the taste strip at the middle of the tongue, at approximately 1.5 cm from the tip of the tongue. 3. Ask the subject to close the mouth and choose 1 of 6 possible answers (sweet, sour, salty, bitter, umami, or no taste) on a form. 4. Ask the subject to rinse the mouth with water before assessment with the next taste strip. 5. After the assessment completion, calculate the total score, based on the highest score per taste. The test will result in a maximum score of 4 for each taste quality and a maximum (i.e., the best) total score of 20. Table 11: Sequences of Taste Strips treatment with a GPRC5D-targeted therapeutic; for example, the subject’s baseline taste Attorney Docket No.258199.061702 JBI6826WOPCT1 score may be taken within 7 days prior to the subject’s first dose of the GPRC5D- targeted therapeutic. In a preferred embodiment, a baseline taste score is determined by averaging the 2 scores from taste assessments: (a) 1-7 days prior to Day 1 of GPRC5D treatment (i.e., Day -7 to -1) and (b) Day 1 of GPRC5D treatment (wherein “Day 1 of GPRC5D treatment” refers to the day that a first dose of the GPRC5D-targeted therapeutic is administered to the subject). According to an alternative embodiment, a subject’s taste is assessed according to the procedure below, referred to herein as the Waterless Empirical Taste Test (WETT), which is commercially available. Taste Assessment Using Taste Strips (WETT): Performance of this taste assessment uses 1 x 6 cm plastic strips with proprietary pads of monomer cellulose that are embedded with either sucrose (sweet), citric acid (sour), sodium chloride (salty), caffeine (bitter), monosodium glutamate (umami), or blank tastants. Four concentrations (4=lowest concentration, 1=highest concentration) are used for each taste quality: sweet, sour, salty, bitter, and umami. No liquid rinsing is required. The taste strips (plus 7 blank strips without taste) is presented in a predetermined pseudo- randomized order. The test is divided into 2 phases. In the first half, taste stimulants are presented in increasing concentrations using 27 taste strips (4 concentrations of each taste quality plus 7 blanks). In the second half, taste stimulants are presenting in decreasing concentrations using 26 taste strips (4 concentrations of each taste quality plus 6 blanks). Preparation Before the Procedure: Instruct the participants to refrain from eating, drinking, or using tobacco products (including e-cigarettes or the equivalent of e-cigarettes, except for nicotine patches) 3 hours before the procedure. Procedure: 1. The taste test is self-administered by the participant. 2. Each taste strip is numbered sequentially and provided in 4 packs. 3. Participant will place each strip, one at a time, beginning with strip number 1 on and around the tongue, especially the sides, for 10 to 15 seconds. Attorney Docket No.258199.061702 JBI6826WOPCT1 4. Using the provided response sheet, fill in the appropriate circle under the taste identified on the strip as sweet, sour, salty, bitter, brothy (soupy, savory taste), or no taste at all. 5. Upon completion, participants will submit the response sheet to the clinical staff. 6. Test administration time varies, depending upon the taste ability of the participant. For most normal subjects, the administration test time is 5 to 10 minutes. Scoring: 1. Use the scoring key provided with the kit to evaluate the test result. 2. To score the test, place the WETT™ Scoring Key 1 of 2, and 2 of 2 on top of the WETT RESPONSE SHEET / WETT-SA-53) so that the red arrow on the WETT Scoring Key aligns to the red dot on the WETT™ RESPONSE SHEET. The correct responses (as indicated by the filled in circles showing up in the score card) should be added and indicated at the bottom of the response sheet for each column. These values represent the number of correct responses for each test quality, as well as the number of correct responses for the blanks. The total score is obtained by adding the column numbers and putting their sum in the box on the right side of the second page of the response card (WETT-SA-53). The total score added on the WETT-SA-53 card will be used against the Normative WETT-SA53 Percentile Table for healthy men and women. As shown in FIG.2Error! Reference source not found.: a. Scores at or below 19-21 (10thpercentile) suggest dysfunction. b. Scores at or below 14 (5thpercentile) strongly suggest severe hypogeusia or ageusia. Dosing Schedules In certain embodiments, a treatment phase comprises subcutaneous administration of talquetamab according to one or both of the following weight-based dosing schedules (QW and / or Q2W) shown in Tables 9 and 10, wherein mg / kg refers to mg of talquetamab per kg of the patient’s body weight: Table 9: Weekly Dosing Schedule Dosing schedule Day DoseaDay 1 Step-up dose 1 0.01 mg / kg Step-up dosing schedule Day 4bStep-up dose 2 0.06 mg / kg Day 7bFirst treatment dose 0.4 mg / kg Attorney Docket No.258199.061702 JBI6826WOPCT1 Dosing schedule Day DoseaWeekly dosing One week after first treatmen Subsequent 0.4 mg / kg once schedule t dose and weekly thereafterctreatment doses weekly Based on actual body weight.bDose may be administered between 2 to 4 days after the previous dose and may be given up to 7 days after the previous dose to allow for resolution of adverse reactions.cMaintain a minimum of 6 days between weekly doses. Table 10: Bi-Weekly Dosing Schedule Dosing schedule Day DoseaDay 1 Step-up dose 1 0.01 mg / kg Step-up dosing schedule Day 4bStep-up dose 2 0.06 mg / kg Day 7bStep-up dose 3 0.4 mg / kg Day 10cFirst treatment dose 0.8 mg / kg Biweekly (every 2 Two weeks after first weeks) dosing treatment dose and Subsequent 0.8 mg / kg every 2 schedule every 2 weeks treatment doses weeks thereafterdaBased on actual body weight.bDose may be administered between 2 to 4 days after the previous dose and may be given up to 7 days after the previous dose to allow for resolution of adverse reactions.cDose may be administered between 2 to 7 days after step-up dose 3.dMaintain a minimum of 12 days between biweekly (every 2 weeks) doses. Additional embodiments of the present invention are described below. An embodiment of the present invention provides a method of decreasing oral toxicity (e.g., taste impairment) in a subject under treatment with a GPRC5D-targeted therapeutic, the method comprising administering to the subject a prophylactic intervention for oral toxicity prior to administering a therapeutically effective amount of the GPRC5D-targeted therapeutic (e.g., to treat multiple myeloma) throughout a treatment phase, wherein the prophylactic intervention is selected from the group consisting of dexamethasone, pregabalin, clonazepam, and a combination thereof. In certain embodiments, the prophylactic intervention is dexamethasone. Attorney Docket No.258199.061702 JBI6826WOPCT1 In certain embodiments, the prophylactic intervention is a dexamethasone mouthwash (an oral solution comprising dexamethasone), e.g., 0.5 mg dexamethasone, twice daily. In certain embodiments, the prophylactic intervention is 0.1 mg / mL dexamethasone mouthwash (e.g., 0.5 mg dexamethasone, twice daily). In certain embodiments, the method comprises administering the dexamethasone mouthwash in an amount of 5 mL (e.g., 0.5 mg / 5 mL), twice daily (e.g., wherein the subject washes his or her mouth with the mouthwash for about 5 minutes without swallowing the mouthwash, and preferably does not consume food or drinks for about 30 minutes afterwards). In certain embodiments, the method comprises administering the dexamethasone mouthwash in an amount of 5 mL twice daily, and administering 50 mg fluconazole once daily (e.g., to prevent thrush). In certain embodiments, the method comprises increasing the dose of the dexamethasone mouthwash to a maximum of 4 times daily after an event of decreased taste score (≥6) has occurred. In certain embodiments, the prophylactic intervention is pregabalin (e.g., in the form of a capsule or tablet). In an embodiment, pregabalin is administered as a 50 mg capsule. In certain embodiments, the method comprises administering the pregabalin at a dose of 50 mg, twice daily. In certain embodiments, the method comprises increasing the dose of pregabalin after an event of decreased taste score (≥6) has occurred. In certain embodiments, the method comprises increasing the dose of pregabalin after an event of decreased taste score (≥6) has occurred, first to 150 mg / day, and after a week to a maximum of 300 mg / day. In certain embodiments, the prophylactic intervention is clonazepam. In certain embodiments, the prophylactic intervention is clonazepam mouthwash (e.g., 0.5 mg clonazepam, twice daily). In certain embodiments, the prophylactic intervention is clonazepam orally dissolving tablet (ODT) (e.g., 0.5 mg clonazepam orally dissolving tablet (ODT), twice daily). Attorney Docket No.258199.061702 JBI6826WOPCT1 In certain embodiments, the prophylactic intervention is 0.1 mg / mL clonazepam mouthwash. In certain embodiments, the method comprises administering 0.1 mg / mL clonazepam mouthwash in an amount of 5 mL (e.g., 0.5 mg / 5 mL), twice daily (e.g., wherein the subject washes his or her mouth with the mouthwash for about 5 minutes without swallowing the mouthwash, and preferably does not consume food or drinks for about 30 minutes afterwards). In certain embodiments, the method comprises continuing clonazepam mouthwash at the same dose if a decrease of 6 points or more in the taste score (measured by taste strips) has developed. In certain embodiments, the method comprises administering the first dose of the prophylactic intervention at least 1 day, or at least 2 days, or at least 3 days, or at least 4 days, or at least 5 days, or at least 6 days, or at least 7 days prior to administering a first dose (e.g. a first step-up dose) of the GPRC5D-targeted therapeutic In certain embodiments, the method comprises administering the first dose of the prophylactic intervention 5-9 days prior to administering a first dose (e.g. a first step-up dose) of the GPRC5D-targeted therapeutic, and preferably continuing administration (e.g., daily administration) of the prophylactic intervention throughout the treatment phase. In certain embodiments, the method comprises administering the first dose of the prophylactic intervention 6-8 days prior to administering a first dose (e.g. a first step-up dose) of the GPRC5D-targeted therapeutic, and preferably continuing administration (e.g., daily administration) of the prophylactic intervention throughout the treatment phase. In certain embodiments, the method comprises administering the first dose of the prophylactic intervention 7 days prior to administering a first dose (e.g. a first step-up dose) of the GPRC5D-targeted therapeutic, and preferably continuing administration (e.g., daily administration) of the prophylactic intervention throughout the treatment phase. In certain embodiments, the method comprises administering the prophylactic intervention daily for 5-9 days prior to administering a first dose (e.g. a first step-up Attorney Docket No.258199.061702 JBI6826WOPCT1 dose) of the GPRC5D-targeted therapeutic, and continuing administration (e.g., daily administration) of the prophylactic intervention throughout the treatment phase. In certain embodiments, the method comprises administering the prophylactic intervention daily for 6-8 days prior to administering a first dose (e.g. a first step-up dose) of the GPRC5D-targeted therapeutic. In certain embodiments, the method comprises administering the prophylactic intervention daily for 7 days prior to administering a first dose (e.g. a first step-up dose) of the GPRC5D-targeted therapeutic. In certain embodiments, the treatment phase comprises subcutaneously administering to the subject one or more step-up doses of the GPRC5DxCD3 bispecific antibody prior to administering a treatment dose of the GPRC5DxCD3 bispecific antibody. In certain embodiments, the treatment phase comprises subcutaneously administering to the subject a treatment dose of the GPRC5DxCD3 bispecific antibody weekly (QW). In certain embodiments, the treatment phase comprises subcutaneously administering to the subject a treatment dose of the GPRC5DxCD3 bispecific antibody every two weeks (Q2W). In certain embodiments, the treatment phase comprises subcutaneously administering to the subject a treatment dose of the GPRC5DxCD3 bispecific antibody every four weeks (Q4W). In certain embodiments, the treatment phase comprises subcutaneously administering to the subject a treatment dose of the GPRC5DxCD3 bispecific antibody every two weeks (Q2W) and then every four weeks (Q4W). In certain embodiments, the treatment phase subcutaneously administering the GPRC5DxCD3 bispecific antibody weekly (QW) at a treatment dose of about 400 μg / kg. In certain embodiments, the treatment phase comprises subcutaneously administering the GPRC5DxCD3 bispecific antibody every two weeks (Q2W) at a treatment dose of about 800 μg / kg. In certain embodiments, the treatment phase comprises subcutaneously administering the GPRC5DxCD3 bispecific antibody every two weeks (Q2W) at a Attorney Docket No.258199.061702 JBI6826WOPCT1 treatment dose of about 800 μg / kg, and then administering the GPRC5DxCD3 bispecific antibody every 4 weeks (Q4W) at a treatment dose of about 800 μg / kg. In certain embodiments, the treatment phase comprises subcutaneously administering the GPRC5DxCD3 bispecific antibody every two weeks (Q2W) at a treatment dose of about 800 μg / kg, and then administering the GPRC5DxCD3 bispecific antibody every 4 weeks (Q4W) at a treatment dose of about 800 μg / kg starting at C5D1 if the subject has response of VGPR or better, or starting at C7D1 if the participant has a response of PR or better, according to IMWG 2016 criteria. In certain embodiments, the treatment phase comprises subcutaneously administering 2 or 3 step-up doses of the GPRC5DxCD3 bispecific antibody prior to subcutaneously administering a treatment dose. In certain embodiments, the treatment phase comprises subcutaneously administering step-up doses of 10 μg / kg and 60 μg / kg of the GPRC5DxCD3 bispecific antibody prior to subcutaneously administering a treatment dose. In certain embodiments, the treatment phase comprises subcutaneously administering step-up doses of 10 μg / kg and 60 μg / kg and 400 μg / kg of the GPRC5DxCD3 bispecific antibody prior to subcutaneously administering a treatment dose. In certain embodiments, the treatment phase comprises subcutaneously administering step-up doses of the GPRC5DxCD3 bispecific antibody 2-4 days apart from each other. In certain embodiments, the treatment phase comprises subcutaneously administering the GPRC5DxCD3 bispecific antibody according to the following dosing schedule for a first 28-day treatment cycle: step-up dose 1 (Day 1) at 0.01 mg / kg, followed by step-up dose 2 (Day 4) at 0.06 mg / kg, followed by step-up dose 3 (Day 8) at 0.4 mg / kg, followed by a first treatment dose (Day 15) at 0.8 mg / kg. In certain embodiments, the step-up doses are administered ≥2 days apart and the first treatment dose is administered ≥2 days after the step-up dose 3, between Day 7 and Day 15. In certain embodiments, for subsequent 28-day treatment cycles after the first 28- day treatment cycle (Cycles 2+), the GPRC5DxCD3 bispecific antibody is administered Attorney Docket No.258199.061702 JBI6826WOPCT1 14±3 days after prior treatment dose, at 0.8 mg / kg Q2W (e.g., on Days 1 and 15 of each treatment cycle). In certain embodiments, the method comprises administering talquetamab in 28- day cycles as follows: during Cycle 1, administering the following step-up doses and first treatment dose of the talquetamab: ^ Step-up dose 1 (e.g., Day 1): 0.01 mg / kg, ^ Step-up dose 2 (e.g, Day 4): 0.06 mg / kg, ^ Step-up dose 3 (e.g., Day 8): 0.4 mg / kg, ^ First Treatment dose (e.g., Day 15): 0.8 mg / kg, wherein the step-up doses are administered at least 2 days apart, and the first treatment dose is administered at least 2 days after step-up dose 3 (e.g., between Days 8 and 15); and during Cycle 2 and all subsequent cycles, talquetamab is administered 14±3 days after prior treatment dose, at 0.8 mg / kg Q2W (e.g., on Days 1 and 15 of each cycle), wherein frequency of dosing is optionally decreased to Q4W starting at Cycle 5 Day 1 (C5D1) if the subject has a response of VGPR or better, or starting at Cycle 7 Day 1 (C7D1) if the subject has a response of PR or better, according to IMWG 2016 criteria. In certain embodiments, the subject has decreased oral toxicity (e.g., decreased taste impairment) compared to a subject that has not received the same prophylactic intervention, e.g., as determined by taste assessment using taste strips. In certain embodiments, the subject has decreased occurrence of oral toxicity (e.g., decreased occurrence of taste impairment) compared to a subject that has not received the same prophylactic intervention, e.g., as determined by taste assessment using taste strips. In certain embodiments, the subject has decreased severity of oral toxicity (e.g., decreased severity of taste impairment) compared to a subject that has not received the same prophylactic intervention, e.g., as determined by taste assessment using taste strips. In certain embodiments, the subject does not have an occurrence of oral toxicity (e.g., does not have an occurrence of taste impairment) as a result of the prophylactic intervention (oral toxicity, such as taste impairment, is prevented), e.g., as determined by taste assessment using taste strips. Attorney Docket No.258199.061702 JBI6826WOPCT1 In certain embodiments, the method decreases oral toxicity (e.g., decreases taste impairment) in a population of subjects compared to a population of subjects that have not received the same prophylactic intervention, e.g., as determined by taste assessment using taste strips. In certain embodiments, the method decreases occurrence of oral toxicity (e.g., decreases occurrence of taste impairment) in a population of subjects compared to a population of subjects that have not received the same prophylactic intervention, e.g., as determined by taste assessment using taste strips. In certain embodiments, the method decreases severity of oral toxicity (e.g., decreases severity of taste impairment) in a population of subjects compared to a population of subjects that have not received the same prophylactic intervention, e.g., as determined by taste assessment using taste strips. In certain embodiments, the method prevents oral toxicity (e.g., prevents taste impairment) in a population of subjects as a result of the prophylactic intervention (oral toxicity, such as taste impairment, is prevented), e.g., as determined by taste assessment using taste strips. In certain embodiments, the method decreases the proportion of subjects in a population that have at least 1 occurrence of 6 points or more of deterioration from a baseline taste score during the treatment phase, as measured by taste strips, e.g., by standard taste assessment. In certain embodiments, the subject exhibits one or more of the following clinical results, e.g., as determined by a Waterless Empirical Taste Test (WETT) score: 1. lower rate of occurrence of taste dysfunction (hypogeusia) compared to a subject that has not received the same prophylactic intervention, and / or 2. lower rate of occurrence of severe hypogeusia / ageusia compared to a subject that has not received the same prophylactic intervention, and / or 3. longer time to first onset of severe hypogeusia / ageusia compared to a subject that has not received the same prophylactic intervention, and / or 4. higher rate of resolution / improvement of hypogeusia / ageusia at 3 and 6 months, compared to a subject that has not received the same prophylactic intervention. EXEMPLARY EMBODIMENTS Attorney Docket No.258199.061702 JBI6826WOPCT1 Provided below are enumerated embodiments of the present invention. These embodiments are illustrative only and do not limit the scope of the present disclosure or of the claims attached hereto. 1. A method of decreasing oral toxicity (e.g., taste impairment) in a subject under treatment with a GPRC5D-targeted therapeutic, the method comprising administering to the subject a prophylactic intervention for oral toxicity prior to administering a therapeutically effective amount of the GPRC5D-targeted therapeutic throughout a treatment phase, wherein the prophylactic intervention is selected from the group consisting of dexamethasone, pregabalin, clonazepam, and a combination thereof. 2. The method of embodiment 1, wherein the GPRC5D-targeted therapeutic is a GPRC5DxCD3 bispecific antibody. 3. The method of embodiment 2, wherein the GPRC5DxCD3 bispecific antibody comprises a GPRC5D binding domain comprising the HCDR1 of SEQ ID NO: 4, the HCDR2 of SEQ ID NO: 5, the HCDR3 of SEQ ID NO: 6, the LCDR1 of SEQ ID NO: 7, the LCDR2 of SEQ ID NO: 8 and the LCDR3 of SEQ ID NO: 9, and a CD3 binding domain comprising the HCDR1 of SEQ ID NO: 14, the HCDR2 of SEQ ID NO: 15, the HCDR3 of SEQ ID NO: 16, the LCDR1 of SEQ ID NO: 17, the LCDR2 of SEQ ID NO: 18 and the LCDR3 of SEQ ID NO: 19. 4. The method of embodiment 2 or 3, wherein the GPRC5DxCD3 bispecific antibody comprises a GPRC5D binding domain comprising a heavy chain variable region (VH) having the amino acid sequence of SEQ ID NO: 10 and a light chain variable region (VL) having the amino acid sequence of SEQ ID NO: 11, and the CD3 binding domain comprises a heavy chain variable region (VH) having the amino acid sequence of SEQ ID NO: 20 and a light chain variable region (VL) having the amino acid sequence of SEQ ID NO: 21. 5. The method of any of embodiments 2-4, wherein the GPRC5DxCD3 bispecific antibody is an IgG1, an IgG2, an IgG3 or an IgG4 isotype. 6. The method of any of embodiments 2-5, wherein the GPRC5DxCD3 bispecific antibody is an IgG4 isotype. 7. The method of any of embodiments 2-6, wherein the GPRC5DxCD3 bispecific antibody comprises one or more substitutions in its Fc region. Attorney Docket No.258199.061702 JBI6826WOPCT1 8. The method of any of embodiments 2-7, wherein the GPRC5DxCD3 bispecific antibody is an IgG4 isotype and comprises S228P, F234A and L235A substitutions in its Fc region. 9. The method of any of embodiments 2-8, wherein the GPRC5DxCD3 bispecific antibody is an IgG4 isotype and comprises S228P, F234A, L235A F405L and R409K substitutions in its Fc region. 10. The method of any of embodiments 2-9, wherein the Fc region of the GPRC5D-specific IgG4 antibody from which the GPRC5D-binding arm is derived comprises S228P, L234A and L235A substitutions in its Fc region. 11. The method of any of embodiments 2-10, wherein the Fc region of the CD3- specific IgG4 antibody from which the CD3-binding arm is derived comprises S228P, L234A, L235A, F405L, and R409K substitutions in its Fc region. 12. The method of any of embodiments 2-11, wherein the GPRC5DxCD3 bispecific antibody comprises a first heavy chain (HC1) having the amino acid sequence of SEQ ID NO: 12, a first light chain (LC1) having the amino acid sequence of SEQ ID NO: 13, a second heavy chain (HC2) having the amino acid sequence of SEQ ID NO: 22 and a second light chain (LC2) having the amino acid sequence of SEQ ID NO: 23. 13. The method of any of embodiments 2-11, wherein the GPRC5DxCD3 bispecific antibody comprises a first heavy chain (HC1) having at least 90% identity to the amino acid sequence of SEQ ID NO: 12, a first light chain (LC1) having at least 90% identity to the amino acid sequence of SEQ ID NO: 13, a second heavy chain (HC2) having at least 90% identity to the amino acid sequence of SEQ ID NO: 22 and a second light chain (LC2) having at least 90% identity to the amino acid sequence of SEQ ID NO: 23. 14. The method of any of embodiments 2-11, wherein the GPRC5DxCD3 bispecific antibody comprises a first heavy chain (HC1) having at least 95% identity to the amino acid sequence of SEQ ID NO: 12, a first light chain (LC1) having at least 95% identity to the amino acid sequence of SEQ ID NO: 13, a second heavy chain (HC2) having at least 95% identity to the amino acid sequence of SEQ ID NO: 22 and a second light chain (LC2) having at least 95% identity to the amino acid sequence of SEQ ID NO: 23. Attorney Docket No.258199.061702 JBI6826WOPCT1 15. The method of any of embodiments 2-11, wherein the GPRC5DxCD3 bispecific antibody comprises a first heavy chain (HC1) having at least 98% identity to the amino acid sequence of SEQ ID NO: 12, a first light chain (LC1) having at least 98% identity to the amino acid sequence of SEQ ID NO: 13, a second heavy chain (HC2) having at least 98% identity to the amino acid sequence of SEQ ID NO: 22 and a second light chain (LC2) having at least 98% identity to the amino acid sequence of SEQ ID NO: 23. 16. The method of any of embodiments 2-12, wherein the GPRC5DxCD3 bispecific antibody is talquetamab. 17. The method of any of embodiments 1-16, wherein the subject has been diagnosed with multiple myeloma. 18. The method of any of embodiments 1-17, wherein the subject has received at least three prior lines of therapy. 19. The method of any of embodiments 1-17, wherein the subject has received at least four prior lines of therapy. 20. The method of any of embodiments 1-17, wherein the subject has relapsed or refractory multiple myeloma myeloma (RRMM). 21. The method of any of embodiments 1-17, wherein the subject has received at least three prior lines of therapy, including a proteasome inhibitor, an immunomodulatory agent and an anti-CD38 monoclonal antibody. 22. The method of any of embodiments 1-17, wherein the subject has received at least four prior lines of therapy, including a proteasome inhibitor, an immunomodulatory agent and an anti-CD38 monoclonal antibody. 23. The method of any of embodiments 1-22, wherein the prophylactic intervention is dexamethasone. 24. The method of embodiment 23, wherein the prophylactic intervention is a dexamethasone mouthwash (an oral solution comprising dexamethasone), e.g., 0.5 mg dexamethasone, twice daily. 25. The method of embodiment 23 or 24, wherein the prophylactic intervention is 0.1 mg / mL dexamethasone mouthwash (e.g., 0.5 mg dexamethasone, twice daily). 26. The method of embodiment 24 or 25 comprising administering the dexamethasone mouthwash at a dose of 5 mL (e.g., 0.5 mg / 5 mL)), twice daily (e.g., Attorney Docket No.258199.061702 JBI6826WOPCT1 wherein the subject washes his or her mouth with the mouthwash for about 5 minutes without swallowing the mouthwash, and preferably does not consume food or drinks for about 30 minutes afterwards). 27. The method of embodiment 24 or 25 comprising administering the dexamethasone mouthwash at a dose of of 5 mL twice daily, and administering 50 mg fluconazole once daily (e.g., to prevent thrush). 28. The method of any of embodiments 24-27 comprising increasing the dose of the dexamethasone mouthwash to a maximum of 4 times daily after an event of decreased taste score (≥6) has occurred. 29. The method of any of embodiments 1-22, wherein the prophylactic intervention is pregabalin (e.g., in the form of a capsule or tablet, preferably a 50 mg capsule). 30. The method of embodiment 29 comprising administering the pregabalin at a dose of 50 mg, twice daily. 31. The method of embodiment 29 or 30 comprising increasing the dose of pregabalin after an event of decreased taste score (≥6) has occurred. 32. The method of embodiment 29 or 30 comprising increasing the dose of pregabalin after an event of decreased taste score (≥6) has occurred, first to 150 mg / day, and after a week to a maximum of 300 mg / day. 33. The method of any of embodiments 1-22, wherein the prophylactic intervention is clonazepam. 34. The method of embodiment 33, wherein the prophylactic intervention is (i) clonazepam mouthwash (e.g., 0.5 mg clonazepam, twice daily), or (ii) clonazepam orally dissolving tablet (ODT) (e.g., 0.5 mg clonazepam orally dissolving tablet (ODT), twice daily). 35. The method of embodiment 33, wherein the prophylactic intervention is (i) 0.1 mg / mL clonazepam mouthwash, or (ii) 0.5 mg clonazepam orally dissolving tablet (ODT), twice daily. 36. The method of any of embodiments 33-35 comprising administering 0.1 mg / mL clonazepam mouthwash at a dose of 5 mL (e.g., 0.5 mg / 5 mL), twice daily (e.g., wherein the subject washes his or her mouth with the mouthwash for about 5 minutes Attorney Docket No.258199.061702 JBI6826WOPCT1 without swallowing the mouthwash, and preferably does not consume food or drinks for about 30 minutes afterwards). 37. The method of embodiment 36 comprising continuing clonazepam mouthwash at the same dose if a decrease of 6 points or more in the taste score (measured by taste strips) has developed. 38. The method of any of embodiments 1-37 comprising administering the first dose of the prophylactic intervention 5-9 days prior to administering a first dose (e.g. a first step-up dose) of the GPRC5D-targeted therapeutic. 39. The method of any of embodiments 1-37 comprising administering the first dose of the prophylactic intervention 6-8 days prior to administering a first dose (e.g. a first step-up dose) of the GPRC5D-targeted therapeutic, and continuing daily administration of the prophylactic intervention throughout the treatment phase. 40. The method of any of embodiments 1-37 comprising administering the first dose of the prophylactic intervention 7 days prior to administering a first dose (e.g. a first step-up dose) of the GPRC5D-targeted therapeutic, and continuing daily administration of the prophylactic intervention throughout the treatment phase. 41. The method of any of embodiments 1-30 comprising administering the prophylactic intervention daily for 5-9 days prior to administering a first dose (e.g. a first step-up dose) of the GPRC5D-targeted therapeutic, and continuing daily administration of the prophylactic intervention throughout the treatment phase. 42. The method of any of embodiments 1-37 comprising administering the prophylactic intervention daily for 6-8 days prior to administering a first dose (e.g. a first step-up dose) of the GPRC5D-targeted therapeutic. 43. The method of any of embodiments 1-37 comprising administering the prophylactic intervention daily for 7 days prior to administering a first dose (e.g. a first step-up dose) of the GPRC5D-targeted therapeutic. 44. The method of any of embodiments 2-43 comprising subcutaneously administering to the subject one or more step-up doses of the GPRC5DxCD3 bispecific antibody prior to administering a treatment dose of the GPRC5DxCD3 bispecific antibody. Attorney Docket No.258199.061702 JBI6826WOPCT1 45. The method of any of embodiments 2-44 comprising subcutaneously administering to the subject a treatment dose of the GPRC5DxCD3 bispecific antibody weekly (QW). 46. The method of any of embodiments 2-44 comprising subcutaneously administering to the subject a treatment dose of the GPRC5DxCD3 bispecific antibody every two weeks (Q2W) and then, optionally, administering the GPRC5DxCD3 bispecific antibody every 4 weeks (Q4W) starting at C5D1 if the subject has response of VGPR or better, or starting at C7D1 if the participant has a response of PR or better, according to IMWG 2016 criteria. 47. The method of any of embodiments 2-44 comprising subcutaneously administering the GPRC5DxCD3 bispecific antibody weekly (QW) at a treatment dose of about 400 μg / kg. 48. The method of any of embodiments 2-44 comprising subcutaneously administering the GPRC5DxCD3 bispecific antibody every two weeks (Q2W) at a treatment dose of about 800 μg / kg. 49. The method of any of embodiments 2-48 comprising subcutaneously administering 2 or 3 step-up doses of the GPRC5DxCD3 bispecific antibody prior to subcutaneously administering a treatment dose. 50. The method of any of embodiments 2-48 comprising subcutaneously administering step-up doses of 10 μg / kg and 60 μg / kg of the GPRC5DxCD3 bispecific antibody prior to subcutaneously administering a treatment dose. 51. The method of any of embodiments 2-48 comprising subcutaneously administering step-up doses of 10 μg / kg and 60 μg / kg and 400 μg / kg of the GPRC5DxCD3 bispecific antibody prior to subcutaneously administering a treatment dose. 52. The method of any of embodiments 44-51 comprising subcutaneously administering step-up doses of the GPRC5DxCD3 bispecific antibody 2-4 days apart from each other. 53. The method of any of embodiments 2-44 comprising subcutaneously administering the GPRC5DxCD3 bispecific antibody according to the following dosing schedule for a first 28-day treatment cycle: step-up dose 1 (Day 1) at 0.01 mg / kg, Attorney Docket No.258199.061702 JBI6826WOPCT1 followed by step-up dose 2 (Day 4) at 0.06 mg / kg, followed by step-up dose 3 (Day 8) at 0.4 mg / kg, followed by a first treatment dose (Day 15) at 0.8 mg / kg. 54. The method of embodiment 53, wherein the step-up doses are administered ≥2 days apart and the first treatment dose is administered ≥2 days after the step-up dose 3, between Day 7 and Day 15. 55. The method of embodiment 53 or 54, wherein for subsequent 28-day treatment cycles after the first 28-day treatment cycle (Cycles 2+), the GPRC5DxCD3 bispecific antibody is administered 14±3 days after prior treatment dose, at 0.8 mg / kg Q2W (e.g., on Days 1 and 15 of each treatment cycle). 56. The method of any of embodiments 1-55, wherein the subject has decreased oral toxicity (e.g., decreased taste impairment) compared to a subject that has not received the same prophylactic intervention, e.g., as determined by taste assessment using taste strips. 57. The method of any of embodiments 1-56, wherein the subject has decreased occurrence of oral toxicity (e.g., decreased occurrence of taste impairment) compared to a subject that has not received the same prophylactic intervention, e.g., as determined by taste assessment using taste strips. 58. The method of any of embodiments 1-57, wherein the subject has decreased severity of oral toxicity (e.g., decreased severity of taste impairment) compared to a subject that has not received the same prophylactic intervention, e.g., as determined by taste assessment using taste strips. 59. The method of any of embodiments 1-58, wherein the subject does not have an occurrence of oral toxicity (e.g., does not have an occurrence of taste impairment) as a result of the prophylactic intervention (oral toxicity, such as taste impairment, is prevented), e.g., as determined by taste assessment using taste strips. 60. The method of any of embodiments 1-59, wherein the method decreases the proportion of subjects in a population that have at least 1 occurrence of 6 points or more of deterioration from a baseline taste score during the treatment phase, as measured by taste strips, e.g., by standard taste assessment. 61. The method of any of embodiments 1-60, comprising administering talquetamab in 28-day cycles as follows: Attorney Docket No.258199.061702 JBI6826WOPCT1 during Cycle 1, administering the following step-up doses and first treatment dose of the talquetamab: ^ Step-up dose 1 (e.g., Day 1): 0.01 mg / kg, ^ Step-up dose 2 (e.g, Day 4): 0.06 mg / kg, ^ Step-up dose 3 (e.g., Day 8): 0.4 mg / kg, ^ First Treatment dose (e.g., Day 15): 0.8 mg / kg, wherein the step-up doses are administered at least 2 days apart, and the first treatment dose is administered at least 2 days after step-up dose 3 (e.g., between Days 8 and 15); and during Cycle 2 and all subsequent cycles, talquetamab is administered 14±3 days after prior treatment dose, at 0.8 mg / kg Q2W (e.g., on Days 1 and 15 of each cycle), wherein frequency of dosing is optionally decreased to Q4W starting at Cycle 5 Day 1 (C5D1) if the subject has a response of VGPR or better, or starting at Cycle 7 Day 1 (C7D1) if the subject has a response of PR or better, according to IMWG 2016 criteria. 62. The method of any of embodiments 1-61, wherein the subject exhibits one or more of the following clinical results, as determined by a WETT score: 1. lower rate of occurrence of taste dysfunction (hypogeusia) compared to a subject that has not received the same prophylactic intervention, and / or 2. lower rate of occurrence of severe hypogeusia / ageusia compared to a subject that has not received the same prophylactic intervention, and / or 3. longer time to first onset of severe hypogeusia / ageusia compared to a subject that has not received the same prophylactic intervention, and / or 4. higher rate of resolution / improvement of hypogeusia / ageusia at 3 and 6 months, compared to a subject that has not received the same prophylactic intervention. Those skilled in the art will appreciate that numerous changes and modifications can be made to the preferred embodiments of the invention and that such changes and modifications can be made without departing from the spirit of the invention. It is, therefore, intended that the appended claims cover all such equivalent variations as fall within the true spirit and scope of the invention. The disclosures of each patent, patent application, and publication cited or described in this document are hereby incorporated herein by reference, in its entirety. Attorney Docket No.258199.061702 JBI6826WOPCT1 EXAMPLES The following examples are provided to further describe some of the embodiments disclosed herein. The examples are intended to illustrate, not to limit, the disclosed embodiments. Example 1: A Phase 2, Open-label, Randomized Study to Evaluate Prophylactic Interventions on Talquetamab-related Oral Toxicity (TALISMAN study) The rationale of this study is to further characterize the oral toxicity of talquetamab and study the effects of prophylaxis to decrease or prevent the oral side effects of talquetamab. Bispecific Antibody Anti-GPRC5D / anti-CD3 antibody talquetamab (also called Tal) (e.g., described in U.S. Patent No.10,562,968, the content of which is incorporated herein by reference in its entirety) was made by Janssen Pharmaceuticals. It was produced by cultivation of recombinant Chinese Hamster Ovary cells followed by isolation, chromatographic purification, and formulation. Talquetamab comprises a GPRC5D binding arm GC5B596 and a CD3 binding arm CD3B219, the amino acid sequences of which are shown in Table A and Table B. Table A. Sequences of GPRC5D binding arm Region Sequence SEQ ID NO:HCDR1 GYTMN 4 HCDR2 LINPYNSDTNYAQKLQG 5 HCDR3 VALRVALDY 6 LCDR1 KASQNVATHVG 7 LCDR2 SASYRYS 8 LCDR3 QQYNRYPYT 9 VH QVQLVQSGAEVKKPGASVKVSCKASGYSF 10 TGYTMNWVRQAPGQGLEWMGLINPYNSD TNYAQKLQGRVTMTTDTSTSTAYMELRSL RSDDTAVYYCARVALRVALDYWGQGTLV TVSS VL DIQMTQSPSSLSASVGDRVTITCKASQNVA 11 THVGWYQQKPGKAPKRLIYSASYRYSGVP SRFSGSGSGTEFTLTISNLQPEDFATYYCQQ YNRYPYTFGQGTKLEIK Attorney Docket No.258199.061702 JBI6826WOPCT1 HC QVQLVQSGAEVKKPGASVKVSCKASGYSF 12 TGYTMNWVRQAPGQGLEWMGLINPYNSD TNYAQKLQGRVTMTTDTSTSTAYMELRSL RSDDTAVYYCARVALRVALDYWGQGTLV TVSSASTKGPSVFPLAPCSRSTSESTAALGC LVKDYFPEPVTVSWNSGALTSGVHTFPAV LQSSGLYSLSSVVTVPSSSLGTKTYTCNVD HKPSNTKVDKRVESKYGPPCPPCPAPEAAG GPSVFLFPPKPKDTLMISRTPEVTCVVVDV SQEDPEVQFNWYVDGVEVHNAKTKPREE QFNSTYRVVSVLTVLHQDWLNGKEYKCK VSNKGLPSSIEKTISKAKGQPREPQVYTLPP SQEEMTKNQVSLTCLVKGFYPSDIAVEWE SNGQPENNYKTTPPVLDSDGSFFLYSRLTV DKSRWQEGNVFSCSVMHEALHNHYTQKS LSLSLGK LC DIQMTQSPSSLSASVGDRVTITCKASQNVA 13 THVGWYQQKPGKAPKRLIYSASYRYSGVP SRFSGSGSGTEFTLTISNLQPEDFATYYCQQ YNRYPYTFGQGTKLEIKRTVAAPSVFIFPPS DEQLKSGTASVVCLLNNFYPREAKVQWK VDNALQSGNSQESVTEQDSKDSTYSLSSTL TLSKADYEKHKVYACEVTHQGLSSPVTKS FNRGEC Table B. Sequences of CD3 binding arm Region Sequence SEQ ID NO: HCDR1 TYAMN 14 HCDR2 RIRSKYNNYATYYAASVKG 15 HCDR3 HGNFGNSYVSWFAY 16 LCDR1 RSSTGAVTTSNYAN 17 LCDR2 GTNKRAP 18 LCDR3 ALWYSNLWV 19 VH EVQLVESGGGLVQPGGSLRLSCAASGFTFNT 20 YAMNWVRQAPGKGLEWVARIRSKYNNYAT YYAASVKGRFTISRDDSKNSLYLQMNSLKTE DTAVYYCARHGNFGNSYVSWFAYWGQGTL VTVSS Attorney Docket No.258199.061702 JBI6826WOPCT1 VL QTVVTQEPSLTVSPGGTVTLTCRSSTGAVTT 21 SNYANWVQQKPGQAPRGLIGGTNKRAPGTP ARFSGSLLGGKAALTLSGVQPEDEAEYYCAL WYSNLWVFGGGTKLTVLGQP HC EVQLVESGGGLVQPGGSLRLSCAASGFTFNT 22 YAMNWVRQAPGKGLEWVARIRSKYNNYAT YYAASVKGRFTISRDDSKNSLYLQMNSLKTE DTAVYYCARHGNFGNSYVSWFAYWGQGTL VTVSSASTKGPSVFPLAPCSRSTSESTAALGC LVKDYFPEPVTVSWNSGALTSGVHTFPAVL QSSGLYSLSSVVTVPSSSLGTKTYTCNVDHK PSNTKVDKRVESKYGPPCPPCPAPEAAGGPS VFLFPPKPKDTLMISRTPEVTCVVVDVSQED PEVQFNWYVDGVEVHNAKTKPREEQFNSTY RVVSVLTVLHQDWLNGKEYKCKVSNKGLPS SIEKTISKAKGQPREPQVYTLPPSQEEMTKNQ VSLTCLVKGFYPSDIAVEWESNGQPENNYKT TPPVLDSDGSFLLYSKLTVDKSRWQEGNVFS CSVMHEALHNHYTQKSLSLSLGK LC QTVVTQEPSLTVSPGGTVTLTCRSSTGAVTT 23 SNYANWVQQKPGQAPRGLIGGTNKRAPGTP ARFSGSLLGGKAALTLSGVQPEDEAEYYCAL WYSNLWVFGGGTKLTVLGQPKAAPSVTLFP PSSEELQANKATLVCLISDFYPGAVTVAWKA DSSPVKAGVETTTPSKQSNNKYAASSYLSLT PEQWKSHRSYSCQVTHEGSTVEKTVAPTECS Objectives This is an open-label, randomized study which aims to evaluate the effect of different prophylaxes to mitigate talquetamab-related oral toxicity. Cohort A will be used as control. Presently, no prophylaxis has shown proven efficacy. Attorney Docket No.258199.061702 JBI6826WOPCT1 The primary study objectives are to identify prophylactic interventions that, as measured by the Waterless Empirical Taste Test (WETT®) score, can minimize the incidence, severity, and duration of talquetamab-related hypogeusia, and to better characterize the clinical presentation of talquetamab-related hypogeusia. Key secondary objectives are to determine the effect of prophylaxis on taste dysfunction, body weight, smell, and saliva changes, and to assess health-related quality of life parameters using PROs focused on assessing dysgeusia, oral mucositis, dysphagia, and xerostomia. The hypothesis of this study is that prophylaxis, initiated prior to first dose of talquetamab and continued daily throughout the Treatment Phase, minimizes the incidence, severity, or duration of talquetamab-related hypogeusia when compared to no prophylaxis. This is an open-label, randomized, multicenter study in adult participants with RRMM previously exposed to at least 1 PI, 1 IMiD, and an anti-CD38 mAb and considered for treatment with talquetamab. The study will include a Screening Phase, a Treatment Phase, and a Follow-up Phase. The oral side effects of talquetamab will be closely monitored in 4 cohorts: a standard of care cohort, i.e., a control cohort (Cohort A) and 3 cohorts (Cohorts B, C, and D) in which a prophylaxis is added to prevent the occurrence or decrease the severity of oral side effects, with a special focus on change or loss of taste. The oral side effects of talquetamab will be closely monitored in all 4 cohorts. Decisions to modify the evaluation of prophylactic interventions or the addition of new cohorts or interventions may be considered at a later stage based on study results. Methods Following randomization, participants of Cohorts B, C, and D will start the assigned prophylaxis 1 week before starting talquetamab treatment. The prophylaxis will continue through the Treatment Phase as long as the participant continues to receive talquetamab. After step-up dosing of talquetamab therapy, participants will be treated with a 0.8 mg / kg SC Q2W regimen until progressive disease, death, lost to follow-up, withdrawal of consent, discontinuation, or until 12 months after the start of talquetamab treatment, whichever occurs first. At the investigator’s discretion, a change to 0.8 mg / kg SC Q4W of talquetamab will be allowed starting at Cycle 5 Day 1 (C5D1) if the participant has response of confirmed VGPR or better, and starting at Cycle 7 Day 1 (C7D1) if the participant has response of confirmed PR or better. The participant may Attorney Docket No.258199.061702 JBI6826WOPCT1 receive the doses as outpatient or be admitted for inpatient monitoring of talquetamab SC administration. A total of approximately 120 participants will be randomized (1:1:1:1) to the 4 cohorts. The study design is illustrated in FIG.1. Cohort A will be the control cohort to characterize the oral side effects of talquetamab. Treatment of the oral side effects would be at the discretion of the treating physician. Drugs excluding the prophylactic interventions used in this study could be considered for treatment of oral side effects. Participants in Cohorts B, C, and D will receive the following prophylaxis: Cohort B: 0.1 mg / mL dexamethasone mouthwash, 5 mL twice daily. Cohort C: 50 mg dose pregabalin oral dose, twice daily. Cohort D: 0.5 mg clonazepam orally dissolving tablet (ODT), twice daily. If a taste dysfunction has developed, the investigator may consider dose modifications to any prophylaxis per clinical judgment and by the assessment of severe hypogeusia or ageusia per the WETT score. All participants will be tested with the following key procedures: ^ Taste assessment using taste strips (WETT) ^ Assessment of manifestations of oral toxicity, including dysgeusia, oral mucositis, xerostomia, dysphagia, grading per NCI-CTCAE, Version 5.0 ^ Assessment of smell function, including both odor identification and threshold testing ^ PROs: EORTC-QLQ-C30, EORTC-QLQ-OH-15, Epstein Taste Scale, STTA, short xerostomia inventory, and PRO-CTCAE ^ Tongue and / or salivary gland biopsies (at selected sites only) ^ Tongue swab for microbiome analysis (only participants in Cohort A) ^ Saliva assessment: production and characterization Total estimated accrual time is approximately 18 months. The duration of the treatment period for individual participants will be up to 12 months. Therefore, the duration of individual participation is estimated to be 12 to 30 months. Provision of talquetamab through the study may continue beyond the planned 1- year treatment schedule. Justifications for Dose Attorney Docket No.258199.061702 JBI6826WOPCT1 Rationale for Q2W Dosing of Talquetamab 0.8 mg / kg SC Q2W is effective, well tolerated, and has manageable safety profiles in participants with heavily pretreated RRMM. In addition, a 0.8 mg / kg SC Q2W regimen is more convenient than a more frequent regimen such as 0.4 mg / kg SC QW. The doses and schedule for talquetamab SC (0.01, 0.06, and 0.4 mg / kg step-up doses followed by 0.8 mg / kg SC Q2W treatment dose) was selected based on the PK, pharmacodynamics, safety, and efficacy findings from the Phase 1 parts of the MonumenTAL-1 study (talquetamab monotherapy). The third step-up dose (0.4 mg / kg) in this study is slightly higher than that (0.3 mg / kg) evaluated in Phase 1 and Phase 2 parts of MonumenTAL-1 but this adjustment is supported by the demonstrated safety of the 0.4 mg / kg dose given weekly as the therapeutic dose in the MonumenTAL-1 study. The concentration-time and safety profiles are estimated to be similar between the regimens 0.01, 0.06, and 0.3 mg / kg step-up doses followed by 0.8 mg / kg SC Q2W and 0.01, 0.06, and 0.4 mg / kg step-up doses followed by 0.8 mg / kg SC Q2W treatment dose. Rationale for Q4W Dosing of Talquetamab In the current study, the frequency of dosing may be decreased at the investigator’s discretion to Q4W for talquetamab starting at C5D1 for participants with response of confirmed VGPR or better. For participants with response of confirmed PR or better, talquetamab dosing could be switched to Q4W starting at C7D1. The median concentration-time profile following Q4W dosing at C5D1 or C7D1 is estimated to be above the maximum concentration associated with the EC90value identified in an ex vivo cytotoxicity assay and is estimated to be sufficient to maintain efficacy in low tumor burden setting. Additionally, a dose-response relationship was observed for talquetamab-specific AEs (skin, oral, and nail toxicity) based on a preliminary safety exposure-response analysis. Therefore, patients who switch to a lower dose after becoming responders for a certain period may benefit from a lower (or non-worsening) incidence of AEs. The proposed Q4W dosing schedule of talquetamab would maintain efficacy by balancing maximal reduction of disease burden with biweekly dosing in the initial 6 cycles of treatment with participant convenience and reduced exposure with Q4W dosing from Cycle 7 onward for participants with response of confirmed PR or better (or as early as Cycle 5 for participants who have achieved a confirmed response of VGPR or better). Attorney Docket No.258199.061702 JBI6826WOPCT1 Rationale for Dosing of Dexamethasone Mouthwash Twice daily mouthwash of 0.5 mg / 5 mL is the usual starting dose for mild and active oral cGVHD, and a decrease to a once daily dose after CR can be used to prevent recurrence. To mimic the effect of dexamethasone mouthwash in patients with oral cGVHD, the twice daily dose will be used prophylactically, in conjunction with 50 mg fluconazole once daily, 1 week before the start of talquetamab treatment. Rationale for Dosing of Pregabalin The normal starting dose to treat neuropathic pain is 75 mg twice a day. Since participants will be treated prophylactically, pregabalin will be started at 50 mg twice daily to minimize the occurrence of side effects. Rationale for Dosing of Clonazepam The doses and schedule for clonazepam was selected based on the study of using topical clonazepam in treating burning mouth syndrome where a 1 mg tablet was sucked 3 times / day for 14 days, as discussed in Section Error! Reference source not found.. In this study, a 0.5 mg of clonazepam orally dissolving tablet will be supplied to improve drug distribution in the oral cavity. Participants will start on 0.5 mg clonazepam twice daily, 1 week before the start of talquetamab treatment. Clonazepam orally dissolving tablet (ODT) rapidly disintegrates in the mouth upon contact with saliva; therefore, either no additional water or small amounts of water could be needed during administration. Detailed methods of administration are provided below. Drugs for Prophylaxis Prophylactic interventions are outlined in the following table:

[0002] Attorney Docket No.258199.061702 JBI6826WOPCT1 Cohort NameCohort B Cohort C Cohort DDrug NameDexamethasone Pregabalin ClonazepamDose FormulationMouthwashCapsule 50 mg Orally dissolving (0.1 mg / mL), will betablet (ODT), 0.5 mg provided as 0.5 mg / 5 mL Unit Dose Strength(s)5 mL, twice daily (not50 mg, twice daily 0.5 mg, twice daily to be swallowed)Route of Oral Oral Oral Administration Dosing InstructionsSwish or hold 5 mL inAs indicated The ODT rapidly the mouth fordisintegrates upon 5 minutes, do not contact with saliva. To swallow; no food or be taken without drinks for 30 minutes water or with only afterwards. small amounts of water. Hold the saliva for 3 minutes without swallowing; spit out the saliva after 3 minutes. UseExperimental Experimental ExperimentalInvestigational Yes Yes Yes Medicinal Product (IMP) Non-Investigational No No No Medicinal Product / Auxiliary Medicinal Product (NIMP / AxMP) SourcingSupplied by theSupplied by the Supplied by the sponsorsponsor sponsor Delivery Instructionsa Yes Yes YesaPrescribing information will contain information to meet the applicable regulatory requirements. Talquetamab Treatment Dosing Schedule The duration of each cycle of SC talquetamab will be 28 days. For Cycle 1, talquetamab will be administered according to the following step-up dosing schedule: ^ Step-up dose 1 (Day 1): 0.01 mg / kg ^ Step-up dose 2 (Day 4): 0.06 mg / kg ^ Step-up dose 3 (Day 8): 0.4 mg / kg ^ Treatment dose (Day 15): 0.8 mg / kg Attorney Docket No.258199.061702 JBI6826WOPCT1 Step-up doses are to be administered at least 2 days apart. First treatment dose is to be administered at least 2 days after step-up dose 3, between Days 8 and 15. For Cycles 2+, talquetamab must be administered 14±3 days after prior treatment dose, at 0.8 mg / kg Q2W (ie, on Days 1 and 15 of each cycle). The frequency of dosing may be decreased at the investigator’s discretion to Q4W for talquetamab starting at C5D1 for participants with response of confirmed VGPR or better. For participants with a response of confirmed PR or better, talquetamab dosing could be switched to Q4W starting at C7D1 at the investigator’s discretion. Endpoints Objectives and endpoints are summarized in the following table: Objectives Endpoints Primary ^ To identify prophylaxis or As determined by the total WETT testing score: prophylaxes that can minimize ^ Rate of occurrence of taste dysfunction the incidence, severity, and (hypogeusia) duration of talquetamab-related ^ Rate of occurrence of severe hypogeusia / ageusia hypogeusia, during the study ^ Time to the first onset of severe Treatment Phase hypogeusia / ageusia ^ To better characterize the clinical ^ Rate of resolution / improvement of presentation of talquetamab- hypogeusia / ageusia at 3 and 6 months related hypogeusia Secondary To determine the effect of prophylaxis ^ Change from baseline of WETT testing score on taste dysfunction over time ^ Percentage of time with hypogeusia To assess oral toxicity TEAEs ^ Incidence rate of treatment-emergent dysgeusia, (including dysgeusia, oral mucositis, oral mucositis, dysphagia, and xerostomia dysphagia, and xerostomia) ^ Time to the first onset of treatment-emergent dysgeusia, oral mucositis, dysphagia, and xerostomia ^ Duration of treatment-emergent dysgeusia, oral mucositis, dysphagia, and xerostomia To assess health-related quality of life ^ Change from baseline over time in domains from parameters related to overall health as the EORTC-QLQ-C30, EORTC-QLQ-OH15 well as specific impact of taste ^ Proportion of participants who report oral toxicity changes, xerostomia, dysphagia, oral symptoms overtime using the PRO-CTCAE, mucositis, and other aspects of oral xerostomia inventory, Epstein Taste Scale, and toxicity STTA To assess the effect of prophylaxis on Change from baseline in body weight and BMI over change in body weight time To assess participants’ ability to Frequency of talquetamab dose reductions, adhere to the talquetamab dosing interruptions, and discontinuations schema To assess the effect of prophylaxis on Change from baseline in the results of smell smell function identification and smell detection threshold test Attorney Docket No.258199.061702 JBI6826WOPCT1 Objectives Endpoints To characterize the efficacy of ^ ORR (PR or better), rate of CR or better, rate of talquetamab VGPR or better as defined by the IMWG response criteria ^ Duration of response (DOR) and time to response (TTR) To characterize the safety of Incidence and severity of TEAEs talquetamab and prophylaxes Exploratory To determine talquetamab-related Morphology, tissue architecture, and cellular changes in the tongue and salivary composition of the tongue and / or salivary gland gland biopsies To study the change in composition of Characterization of the microbiome in tongue bacterial flora in the mouth To determine the effect of prophylaxis Change from baseline in stimulated and unstimulated on saliva production salivary flow measurements over time To determine talquetamab-related Characterization of saliva viscosity saliva changes To characterize the efficacy of Progression-free survival (PFS) and overall survival talquetamab (OS) To characterize the PK and assess the ^ Serum concentration of talquetamab immunogenicity of talquetamab ^ Presence of ADAs to talquetamab To evaluate the incidence and severity Incidence and grade of skin and / or nail toxicities of talquetamab-related changes in the according to PRO-CTCAE skin and nails The primary endpoints, assessed by the total WETT testing score during the study Treatment Phase, are as follows: ^ Rate of occurrence of taste dysfunction (hypogeusia), where taste dysfunction is defined as total WETT score ≤19 for males (assigned at birth) and ≤21 for females (assigned at birth) according to the Normative WETT-SA53 Percentile Table (FIG. 2). Of note, validation testing demonstrated a sex-dependent difference in test results that is accounted for in the scoring matrix of WETT. ^ Rate of occurrence of severe hypogeusia / ageusia, where severe hypogeusia / ageusia is defined as a total WETT score ≤14 according to the Normative WETT-SA53 Percentile (see FIG.2). ^ Time to the first onset of severe hypogeusia / ageusia, defined as time from the first dose date of talquetamab to the first onset date of severe hypogeusia / ageusia according to the total WETT score. For participants without severe hypogeusia / ageusia, time to the first onset will be censored. Attorney Docket No.258199.061702 JBI6826WOPCT1 ^ Rate of resolution / improvement of hypogeusia / ageusia at 3 and 6 months, where resolution / improvement is defined as 2 potential scenarios: ^ A taste dysfunction downgraded to taste dysfunction-free, ie, total WETT score ≤19 for males and ≤21 for females at visits prior to Month 3 and Month 6 becomes total WETT score >19 for males and >21 for females at Month 3 and Month 6. ^ Severe hypogeusia / ageusia downgraded to non-severe hypogeusia / ageusia, ie, total WETT score ≤14 prior to Month 3 and Month 6 becomes total WETT score >14 at Month 3 and Month 6. Descriptive statistics will be provided for each primary endpoint. Participation Criteria Inclusion criteria include the following: Be ≥18 years of age (or the legal age of majority in the jurisdiction in which the study is taking place, whichever is greater) at the time of informed consent; and: 1. Both criteria below: a. MM according to IMWG diagnostic criteria. b. Measurable disease at screening, as assessed by local laboratory, defined by any of the following: i. Serum M-protein level ≥0.5 g / dL; or ii. Urine M-protein level ≥200 mg / 24 hours; or iii. Light chain multiple myeloma without measurable M-protein in the serum or the urine: sFLC ≥10 mg / dL and abnormal serum immunoglobulin kappa lambda FLC ratio. iv. For participants without measurable disease in the serum, urine, or involved FLC, presence of plasmacytomas (≥2 cm). 2. Were triple-class exposed (received prior treatment with a PI, an IMiD, and anti-CD38 mAb). NOTE: Relapsed disease is defined as an initial response to prior treatment, followed by confirmed progressive disease by IMWG criteria >60 days after cessation of treatment. Refractory disease is defined as <25% reduction in M- protein or confirmed progressive disease by IMWG criteria during previous treatment or ≤60 days after cessation of treatment. Attorney Docket No.258199.061702 JBI6826WOPCT1 3. Documented evidence of progressive disease based on investigator’s determination of response by IMWG criteria on or after their last regimen. 4. Have an ECOG PS of 0 or 1 at screening (Error! Reference source not found.). Participants with ECOG PS 2 or 3 are eligible for the study if the ECOG PS score is related to stable physical limitations (eg, wheelchair-bound due to prior spinal cord injury) and not related to multiple myeloma or associated therapy. Exclusion criteria include the following: 1. Contraindications or life-threatening known allergies, hypersensitivity, or intolerance to any study drug or its excipients NOTE: Refer to the prescribing information for additional exclusion criteria pertaining to the specific prophylaxes. 2. Stroke, transient ischemic attack, or seizure within 6 months prior to enrollment. 3. Any of the following within 6 months prior to the first dose of study treatment: Severe or unstable angina, myocardial infarction; major thromboembolytic event (eg, pulmonary embolism, cerebrovascular accident), clinically significant ventricular arrythmia or heart failure New York Heart Association functional classification Class III or IV. Uncomplicated deep vein thrombosis is not considered exclusionary. 4. Any of the following: a. Hepatitis B infection (hepatitis B surface antigen or HBV-DNA positive): In the event the infection status is unclear, quantitative viral levels are necessary to determine the infection status. b. Active hepatitis C infection as measured by positive HCV-RNA testing. Participants with a history of HCV antibody positivity must undergo HCV-RNA testing. If a participant with history of chronic hepatitis C infection (defined as both HCV antibody and HCV-RNA positive) completed antiviral therapy and has undetectable HCV-RNA for at least 12 weeks following the completion of therapy, the participant is eligible for the study. Attorney Docket No.258199.061702 JBI6826WOPCT1 5. Major surgery or had significant traumatic injury within 2 weeks prior to the start of administration of study treatment, or will not have fully recovered from surgery, or has major surgery planned during the time the participant is expected to be treated in the study or within 2 weeks after administration of the last dose of study treatment. NOTE: Participants with planned surgical procedures to be conducted under local anesthesia may participate. Kyphoplasty or vertebroplasty are not considered major surgery. If there is a question whether a procedure is considered a major surgery, it is advisable that the investigator consults with the sponsor and resolve any issues before enrolling a participant in the study. 6. A WETT score suggesting severe hypogeusia or ageusia at screening. Also unresolved / severe dysgeusia referred by the participant or a finding in the physical examination / oral cavity inspection. Some examples include leukoplakia, prior mouth cancers, extensive dental caries, severe periodontitis, active oral infections, candidiasis, parotic gland removal, or radiotherapy with resultant xerostomia. 7. Concurrent medical or psychiatric condition or disease that is likely to interfere with study procedures or results, or that in the opinion of the investigator would constitute a hazard for participating in this study, such as: a. Uncontrolled diabetes b. Acute diffuse infiltrative pulmonary disease. c. Evidence of active systemic viral, fungal, or bacterial infection, requiring systemic antimicrobial therapy. d. Active autoimmune disease requiring systemic immunosuppressive therapy within 6 months before start of study treatment. EXCEPTION: Participants with vitiligo, controlled type I diabetes, and prior autoimmune thyroiditis that is currently euthyroid based on clinical symptoms and laboratory testing are eligible regardless of when these conditions were diagnosed. Attorney Docket No.258199.061702 JBI6826WOPCT1 e. Disabling psychiatric conditions (eg, alcohol or drug abuse), severe dementia, or severe impaired mental status that in the investigator’s opinion would compromise compliance with the study procedures. f. Any other issue that would impair the ability of the participant to receive or tolerate the planned treatment at the investigational site, to understand informed consent or any condition for which, in the opinion of the investigator, participation would not be in the best interest of the participant (eg, compromise the well-being) or that could prevent, limit, or confound the protocol-specified assessments. g. History of noncompliance with recommended medical treatments. 8. Known active CNS involvement or exhibits clinical signs of meningeal involvement of MM. If either is suspected, negative whole brain MRI and lumbar cytology are required. 9. Plasma cell leukemia (per IMWG criteria), Waldenström's macroglobulinemia, POEMS syndrome (polyneuropathy, organomegaly, endocrinopathy, M-protein, and skin changes), or primary amyloid light chain amyloidosis at the time of enrolment. 10. Any of the following: a. Any history of malignancy other than multiple myeloma, which is considered at high-risk of recurrence requiring systemic therapy. b. Any ongoing B-cell malignancy (other than multiple myeloma) or myelodysplastic syndrome. c. Any active malignancies (ie, progressing or requiring treatment change in the last 24 months) other than relapsed / refractory multiple myeloma. The only allowed exceptions are malignancies treated within the last 24 months that are considered cured: 1) Non-muscle invasive bladder cancer (solitary Ta-PUNLMP or low grade, <3 cm, no CIS). 2) Non-melanoma skin cancers treated with curative therapy or localized melanoma treated with curative surgical resection alone. 3) Noninvasive cervical cancer. Attorney Docket No.258199.061702 JBI6826WOPCT1 4) Breast cancer: adequately treated lobular carcinoma in situ or ductal carcinoma in situ or history of localized breast cancer (anti-antihormonal therapy is permitted). 5) Localized prostate cancer (M0, N0) with a Gleason Score ≤7a, treated locally only (RP / RT / focal treatment). 6) Other malignancy that is considered cured with minimal risk of recurrence in consultation with the sponsor’s medical monitor. NOTE: In the event of any questions, consult with the sponsor prior to enrolling a participant. 11. Prior or concurrent exposure to any of the following, in the specified time frame prior to randomization: a. Received any prior GPRC5D-directed therapy. b. T-cell redirection therapy (eg, bispecific antibody therapy or bispecific T- cell engager(s)) within 3 weeks. c. Gene-modified adoptive cell therapy (eg, CAR-T cells, natural killer cells) within 3 months. d. Targeted therapy, epigenetic therapy, or treatment with an investigational drug or an invasive investigational medical device within 21 days or ≥5 half-lives, whichever is less. e. Received or plans to receive any live, attenuated vaccine within 4 weeks before the first dose of study drug. Non-live vaccines approved or authorized for emergency use (eg, COVID 19) by local health authorities are allowed. f. Monoclonal antibody therapy within 21 days. g. Cytotoxic therapy within 21 days. h. PI therapy within 14 days. i. IMiD agent therapy within 14 days. j. Radiotherapy within 14 days or focal radiation within 7 days. Any radiotherapy to the oral cavity or anterior neck in the last 3 months. 12. Received either of the following: a. An allogeneic SCT within 6 months before the first dose of study treatment. Participants who received an allogeneic transplant must be off all Attorney Docket No.258199.061702 JBI6826WOPCT1 immunosuppressive medications during the 6 weeks before the start of study treatment administration without signs of graft versus host disease. b. An autologous SCT within 12 weeks before the start of study treatment administration 13. A maximum cumulative dose of corticosteroids of ≥140 mg of prednisone or equivalent within 14-day period before the first dose of study drug (does not include pretreatment medications). 14. Ongoing use of any of the intended prophylactic interventions included in this study Taste Assessment Using Taste Strips (WETT) Performance of this taste assessment uses 1 x 6 cm plastic strips with proprietary pads of monomer cellulose that are embedded with either sucrose (sweet), citric acid (sour), sodium chloride (salty), caffeine (bitter), monosodium glutamate (umami), or blank tastants. Four concentrations (4=lowest concentration, 1=highest concentration) will be used for each taste quality: sweet, sour, salty, bitter, and umami. No liquid rinsing is required. The taste strips (plus 7 blank strips without taste) will be presented in a predetermined pseudo-randomized order. The test is divided into 2 phases. In the first half, taste stimulants are presented in increasing concentrations using 27 taste strips (4 concentrations of each taste quality plus 7 blanks). In the second half, taste stimulants are presenting in decreasing concentrations using 26 taste strips (4 concentrations of each taste quality plus 6 blanks). Preparation Before the Procedure Instruct the participants to refrain from eating, drinking, or using tobacco products (including e-cigarettes or the equivalent of e-cigarettes, except for nicotine patches) 3 hours before the procedure. Procedure 3. The taste test is self-administered by the participant. 4. Each taste strip is numbered sequentially and provided in 4 packs. 5. Participant will place each strip, one at a time, beginning with strip number 1 on and around the tongue, especially the sides, for 10 to 15 seconds. Attorney Docket No.258199.061702 JBI6826WOPCT1 6. Using the provided response sheet, fill in the appropriate circle under the taste identified on the strip as sweet, sour, salty, bitter, brothy (soupy, savory taste), or no taste at all. 7. Upon completion, participants will submit the response sheet to the clinical staff. 8. Test administration time varies, depending upon the taste ability of the participant. For most normal subjects, the administration test time is 5 to 10 minutes. Scoring (to be performed by clinical staff) 9. Use the scoring key provided with the kit to evaluate the test result. 10. To score the test, place the WETT™ Scoring Key 1 of 2, and 2 of 2 on top of the WETT RESPONSE SHEET / WETT-SA-53) so that the red arrow on the WETT Scoring Key aligns to the red dot on the WETT™ RESPONSE SHEET. The correct responses (as indicated by the filled in circles showing up in the score card) should be added and indicated at the bottom of the response sheet for each column. These values represent the number of correct responses for each test quality, as well as the number of correct responses for the blanks. The total score is obtained by adding the column numbers and putting their sum in the box on the right side of the second page of the response card (WETT-SA-53). The total score added on the WETT-SA-53 card will be used against the Normative WETT-SA53 Percentile Table for healthy men and women. As shown in FIG.2Error! Reference source not found.: a. Scores at or below 19-21 (10thpercentile) suggest dysfunction. b. Scores at or below 14 (5thpercentile) strongly suggest severe hypogeusia or ageusia.

Claims

Attorney Docket No.258199.061702 JBI6826WOPCT1 CLAIMS What is claimed is:

1. A method of decreasing oral toxicity in a subject under treatment with a GPRC5D-targeted therapeutic, the method comprising administering to the subject a prophylactic intervention for oral toxicity prior to administering a therapeutically effective amount of the GPRC5D-targeted therapeutic throughout a treatment phase, wherein the prophylactic intervention is selected from the group consisting of dexamethasone, pregabalin, clonazepam, and a combination thereof.

2. The method of claim 1, wherein the GPRC5D-targeted therapeutic is a GPRC5DxCD3 bispecific antibody.

3. The method of claim 2, wherein the GPRC5DxCD3 bispecific antibody comprises a GPRC5D binding domain comprising the HCDR1 of SEQ ID NO: 4, the HCDR2 of SEQ ID NO: 5, the HCDR3 of SEQ ID NO: 6, the LCDR1 of SEQ ID NO: 7, the LCDR2 of SEQ ID NO: 8 and the LCDR3 of SEQ ID NO: 9, and a CD3 binding domain comprising the HCDR1 of SEQ ID NO: 14, the HCDR2 of SEQ ID NO: 15, the HCDR3 of SEQ ID NO: 16, the LCDR1 of SEQ ID NO: 17, the LCDR2 of SEQ ID NO: 18 and the LCDR3 of SEQ ID NO:

19.

4. The method of claim 2 or 3, wherein the GPRC5DxCD3 bispecific antibody comprises a GPRC5D binding domain comprising a heavy chain variable region (VH) having the amino acid sequence of SEQ ID NO: 10 and a light chain variable region (VL) having the amino acid sequence of SEQ ID NO: 11, and the CD3 binding domain comprises a heavy chain variable region (VH) having the amino acid sequence of SEQ ID NO: 20 and a light chain variable region (VL) having the amino acid sequence of SEQ ID NO:

21.

5. The method of any of claims 2-4, wherein the GPRC5DxCD3 bispecific antibody is an IgG1, an IgG2, an IgG3 or an IgG4 isotype.

6. The method of any of claims 2-5, wherein the GPRC5DxCD3 bispecific antibody is an IgG4 isotype.

7. The method of any of claims 2-6, wherein the GPRC5DxCD3 bispecific antibody comprises one or more substitutions in its Fc region.Attorney Docket No.258199.061702 JBI6826WOPCT1 8. The method of any of claims 2-7, wherein the GPRC5DxCD3 bispecific antibody is an IgG4 isotype and comprises S228P, F234A and L235A substitutions in its Fc region.

9. The method of any of claims 2-8, wherein the GPRC5DxCD3 bispecific antibody is an IgG4 isotype and comprises S228P, F234A, L235A F405L and R409K substitutions in its Fc region.

10. The method of any of claims 2-9, wherein the Fc region of the GPRC5D- specific IgG4 antibody from which the GPRC5D-binding arm is derived comprises S228P, L234A and L235A substitutions in its Fc region.

11. The method of any of claims 2-10, wherein the Fc region of the CD3-specific IgG4 antibody from which the CD3-binding arm is derived comprises S228P, L234A, L235A, F405L, and R409K substitutions in its Fc region.

12. The method of any of claims 2-11, wherein the GPRC5DxCD3 bispecific antibody comprises a first heavy chain (HC1) having the amino acid sequence of SEQ ID NO: 12, a first light chain (LC1) having the amino acid sequence of SEQ ID NO: 13, a second heavy chain (HC2) having the amino acid sequence of SEQ ID NO: 22 and a second light chain (LC2) having the amino acid sequence of SEQ ID NO:

23.

13. The method of any of claims 2-11, wherein the GPRC5DxCD3 bispecific antibody comprises a first heavy chain (HC1) having at least 90% identity to the amino acid sequence of SEQ ID NO: 12, a first light chain (LC1) having at least 90% identity to the amino acid sequence of SEQ ID NO: 13, a second heavy chain (HC2) having at least 90% identity to the amino acid sequence of SEQ ID NO: 22 and a second light chain (LC2) having at least 90% identity to the amino acid sequence of SEQ ID NO:

23.

14. The method of any of claims 2-11, wherein the GPRC5DxCD3 bispecific antibody comprises a first heavy chain (HC1) having at least 95% identity to the amino acid sequence of SEQ ID NO: 12, a first light chain (LC1) having at least 95% identity to the amino acid sequence of SEQ ID NO: 13, a second heavy chain (HC2) having at least 95% identity to the amino acid sequence of SEQ ID NO: 22 and a second light chain (LC2) having at least 95% identity to the amino acid sequence of SEQ ID NO:

23.

15. The method of any of claims 2-11, wherein the GPRC5DxCD3 bispecific antibody comprises a first heavy chain (HC1) having at least 98% identity to the amino acid sequence of SEQ ID NO: 12, a first light chain (LC1) having at least 98% identity toAttorney Docket No.258199.061702 JBI6826WOPCT1 the amino acid sequence of SEQ ID NO: 13, a second heavy chain (HC2) having at least 98% identity to the amino acid sequence of SEQ ID NO: 22 and a second light chain (LC2) having at least 98% identity to the amino acid sequence of SEQ ID NO:

23.

16. The method of any of claims 2-12, wherein the GPRC5DxCD3 bispecific antibody is talquetamab.

17. The method of any of claims 1-16, wherein the subject has been diagnosed with multiple myeloma.

18. The method of any of claims 1-17, wherein the subject has received at least three prior lines of therapy.

19. The method of any of claims 1-17, wherein the subject has received at least four prior lines of therapy.

20. The method of any of claims 1-17, wherein the subject has relapsed or refractory multiple myeloma.

21. The method of any of claims 1-17, wherein the subject has received at least three prior lines of therapy, including a proteasome inhibitor, an immunomodulatory agent and an anti-CD38 monoclonal antibody.

22. The method of any of claims 1-17, wherein the subject has received at least four prior lines of therapy, including a proteasome inhibitor, an immunomodulatory agent and an anti-CD38 monoclonal antibody.

23. The method of any of claims 1-22, wherein the prophylactic intervention is dexamethasone.

24. The method of claim 23, wherein the prophylactic intervention is a dexamethasone mouthwash (an oral solution comprising dexamethasone).

25. The method of claim 23 or 24, wherein the prophylactic intervention is 0.1 mg / mL dexamethasone mouthwash.

26. The method of claim 24 or 25 comprising administering the dexamethasone mouthwash at a dose of 0.5 mg, twice daily.

27. The method of claim 24 or 25 comprising administering the dexamethasone mouthwash at a dose of of 0.5 mg / 5 mL twice daily, and administering 50 mg fluconazole once daily.Attorney Docket No.258199.061702 JBI6826WOPCT1 28. The method of any of claims 24-27 comprising increasing the dose of the dexamethasone mouthwash to a maximum of 4 times daily after an event of decreased taste score (≥6) has occurred.

29. The method of any of claims 1-22, wherein the prophylactic intervention is pregabalin.

30. The method of claim 29 comprising administering the pregabalin at a dose of 50 mg, twice daily.

31. The method of claim 29 or 30 comprising increasing the dose of pregabalin after an event of decreased taste score (≥6) has occurred.

32. The method of claim 29 or 30 comprising increasing the dose of pregabalin after an event of decreased taste score (≥6) has occurred, first to 150 mg / day, and after a week to a maximum of 300 mg / day.

33. The method of any of claims 1-22, wherein the prophylactic intervention is clonazepam.

34. The method of claim 33, wherein the prophylactic intervention is clonazepam mouthwash.

35. The method of claim 33, wherein the prophylactic intervention is 0.1 mg / mL clonazepam mouthwash.

36. The method of any of claims 33-35 comprising administering clonazepam mouthwash at a dose of 0.5 mg, twice daily.

37. The method of claim 36 comprising continuing clonazepam mouthwash at the same dose if a decrease of 6 points or more in a taste score has developed.

38. The method of any of claims 1-37 comprising administering the first dose of the prophylactic intervention 5-9 days prior to administering a first dose of the GPRC5D- targeted therapeutic.

39. The method of any of claims 1-37 comprising administering the first dose of the prophylactic intervention 6-8 days prior to administering a first dose of the GPRC5D- targeted therapeutic, and continuing daily administration of the prophylactic intervention throughout the treatment phase.

40. The method of any of claims 1-37 comprising administering the first dose of the prophylactic intervention 7 days prior to administering a first dose of the GPRC5D-Attorney Docket No.258199.061702 JBI6826WOPCT1 targeted therapeutic, and continuing daily administration of the prophylactic intervention throughout the treatment phase.

41. The method of any of claims 1-30 comprising administering the prophylactic intervention daily for 5-9 days prior to administering a first dose of the GPRC5D- targeted therapeutic, and continuing daily administration of the prophylactic intervention throughout the treatment phase.

42. The method of any of claims 1-37 comprising administering the prophylactic intervention daily for 6-8 days prior to administering a first dose of the GPRC5D- targeted therapeutic.

43. The method of any of claims 1-37 comprising administering the prophylactic intervention daily for 7 days prior to administering a first dose of the GPRC5D-targeted therapeutic.

44. The method of any of claims 2-43 comprising subcutaneously administering to the subject one or more step-up doses of the GPRC5DxCD3 bispecific antibody prior to administering a treatment dose of the GPRC5DxCD3 bispecific antibody.

45. The method of any of claims 2-44 comprising subcutaneously administering to the subject a treatment dose of the GPRC5DxCD3 bispecific antibody weekly (QW).

46. The method of any of claims 2-44 comprising subcutaneously administering to the subject a treatment dose of the GPRC5DxCD3 bispecific antibody every two weeks (Q2W).

47. The method of any of claims 2-44 comprising subcutaneously administering the GPRC5DxCD3 bispecific antibody weekly (QW) at a treatment dose of about 400 μg / kg.

48. The method of any of claims 2-44 comprising subcutaneously administering the GPRC5DxCD3 bispecific antibody every two weeks (Q2W) at a treatment dose of about 800 μg / kg.

49. The method of any of claims 2-48 comprising subcutaneously administering 2 or 3 step-up doses of the GPRC5DxCD3 bispecific antibody prior to subcutaneously administering a treatment dose.

50. The method of any of claims 2-48 comprising subcutaneously administering step-up doses of 10 μg / kg and 60 μg / kg of the GPRC5DxCD3 bispecific antibody prior to subcutaneously administering a treatment dose.Attorney Docket No.258199.061702 JBI6826WOPCT1 51. The method of any of claims 2-48 comprising subcutaneously administering step-up doses of 10 μg / kg and 60 μg / kg and 400 μg / kg of the GPRC5DxCD3 bispecific antibody prior to subcutaneously administering a treatment dose.

52. The method of any of claims 44-51 comprising subcutaneously administering step-up doses of the GPRC5DxCD3 bispecific antibody 2-4 days apart from each other.

53. The method of any of claims 2-44 comprising subcutaneously administering the GPRC5DxCD3 bispecific antibody according to the following dosing schedule for a first 28-day treatment cycle: step-up dose 1 (Day 1) at 0.01 mg / kg, followed by step-up dose 2 (Day 4) at 0.06 mg / kg, followed by step-up dose 3 (Day 8) at 0.4 mg / kg, followed by a first treatment dose (Day 15) at 0.8 mg / kg.

54. The method of claim 53, wherein the step-up doses are administered ≥2 days apart and the first treatment dose is administered ≥2 days after the step-up dose 3, between Day 7 and Day 15.

55. The method of claim 53 or 54, wherein for subsequent 28-day treatment cycles after the first 28-day treatment cycle (Cycles 2+), the GPRC5DxCD3 bispecific antibody is administered 14±3 days after prior treatment dose, at 0.8 mg / kg Q2W.

56. The method of any of claims 1-55, wherein the subject has decreased oral toxicity compared to a subject that has not received the same prophylactic intervention.

57. The method of any of claims 1-56, wherein the subject has decreased occurrence of oral toxicity compared to a subject that has not received the same prophylactic intervention.

58. The method of any of claims 1-57, wherein the subject has decreased severity of oral toxicity compared to a subject that has not received the same prophylactic intervention.

59. The method of any of claims 1-58, wherein the subject does not have an occurrence of oral toxicity as a result of the prophylactic intervention.

60. The method of any of claims 1-59, wherein the method decreases the proportion of subjects in a population that have at least 1 occurrence of 6 points or more of deterioration from a baseline taste score during the treatment phase, as measured by taste strips.

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