TALVEY® is a bispecific GPRC5D-directed CD3 T-cell engager indicated for the treatment of adult patients with relapsed or refractory multiple myeloma who have received at least four prior lines of therapy, including a proteasome inhibitor, an immunomodulatory agent and an anti-CD38 monoclonal antibody.
This indication is approved under accelerated approval based on response rate and durability of response. Continued approval for this indication may be contingent upon verification and description of clinical benefit in a confirmatory trial(s).
WARNING: CYTOKINE RELEASE SYNDROME and NEUROLOGIC TOXICITY, including IMMUNE EFFECTOR CELL-ASSOCIATED NEUROTOXICITY SYNDROME
See full prescribing information for complete boxed warning
Cytokine release syndrome (CRS), including life-threatening or fatal reactions, can occur in patients receiving TALVEY®. Initiate TALVEY® treatment with step-up dosing to reduce the risk of CRS. Withhold TALVEY® until CRS resolves or permanently discontinue based on severity.
Neurologic toxicity, including immune effector cell-associated neurotoxicity syndrome (ICANS), and serious and life-threatening or fatal reactions, can occur with TALVEY®. Monitor patients for signs and symptoms of neurologic toxicity including ICANS during treatment and treat promptly. Withhold or permanently discontinue TALVEY® based on severity.
Because of the risk of CRS and neurologic toxicity, including ICANS, TALVEY® is available only through a restricted program called the TECVAYLI® and TALVEY® Risk Evaluation and Mitigation Strategy (REMS).
Contraindications2:
- None
Warnings and precautions2:
Cytokine release syndrome
TALVEY® can cause cytokine release syndrome, including life-threatening or fatal reactions. In the clinical trial, CRS occurred in 76% of patients who received TALVEY® at the recommended dosages, with Grade 1 CRS occurring in 57% of patients, Grade 2 in 17%, and Grade 3 in 1.5%. Recurrent CRS occurred in 30% of patients. Most events occurred following step-up dose 1 (29%) or step-up dose 2 (44%) at the recommended dosages. CRS occurred in 33% of patients with step-up dose 3 in the biweekly dosing schedule (N=153). CRS occurred in 30% of patients with the first 0.4 mg/kg treatment dose and in 12% of patients treated with the first 0.8 mg/kg treatment dose. The CRS rate for both dosing schedules combined was less than 3% for each of the remaining doses in Cycle 1 and less than 3% cumulatively from Cycle 2 onward. The median time to onset of CRS was 27 (range: 0.1 to 167) hours from the last dose, and the median duration was 17 (range: 0 to 622) hours. Clinical signs and symptoms of CRS include but are not limited to pyrexia, hypotension, chills, hypoxia, headache, and tachycardia. Potentially life-threatening complications of CRS may include cardiac dysfunction, acute respiratory distress syndrome, neurologic toxicity, renal and/or hepatic failure, and disseminated intravascular coagulation (DIC).
Initiate therapy with step-up dosing and administer pre-treatment medications (corticosteroids, antihistamine, and antipyretics) prior to each dose of TALVEY® in the step-up dosing schedule to reduce the risk of CRS. Monitor patients following administration accordingly. In patients who experience CRS, pre-treatment medications should be administered prior to the next TALVEY® dose.
Counsel patients to seek medical attention should signs or symptoms of CRS occur. At the first sign of CRS, immediately evaluate patient for hospitalization and institute treatment with supportive care based on severity, and consider further management per current practice guidelines. Withhold TALVEY® until CRS resolves or permanently discontinue based on severity.
Neurologic toxicity including ICANS
TALVEY® can cause serious, life-threatening neurologic toxicity or fatal neurologic toxicity, including immune effector cell-associated neurotoxicity syndrome (ICANS).
In the clinical trial, neurologic toxicity, including ICANS, occurred in 55% of patients who received the recommended dosages, with Grade 3 or 4 neurologic toxicity occurring in 6% of patients. The most frequent neurologic toxicities were headache (20%), encephalopathy (15%), sensory neuropathy (14%), and motor dysfunction, including ataxia/cerebellar ataxia (10%). ICANS was reported in 9% of 265 patients where ICANS was collected and who received the recommended dosages. Recurrent ICANS occurred in 3% of patients. Most patients experienced ICANS following step-up dose 1 (3%), step-up dose 2 (3%), step-up dose 3 of the biweekly dosing schedule (1.8%), or the initial treatment dose of the weekly dosing schedule (2.6%) (N=156) or the biweekly dosing schedule (3.7%) (N=109). The median time to onset of ICANS was 2.5 (range: 1 to 16) days after the most recent dose with a median duration of 2 (range: 1 to 22) days. The onset of ICANS can be concurrent with CRS, following resolution of CRS, or in the absence of CRS. Clinical signs and symptoms of ICANS may include but are not limited to confusional state, depressed level of consciousness, disorientation, somnolence, lethargy, and bradyphrenia.
Monitor patients for signs and symptoms of neurologic toxicity during treatment and treat promptly. At the first sign of neurologic toxicity, including ICANS, immediately evaluate the patient and provide supportive care based on severity. Withhold or permanently discontinue TALVEY® based on severity and consider further management per current practice guidelines [see Dosage and Administration (2.5)].
Due to the potential for neurologic toxicity, patients receiving TALVEY® are at risk of depressed level of consciousness. Advise patients to refrain from driving or operating heavy or potentially dangerous machinery during the step-up dosing schedule and for 48 hours after completion of the step-up dosing schedule, and in the event of new onset of any neurological symptoms, until symptoms resolve.
TECVAYLI® and TALVEY® REMS
TALVEY® is available only through a restricted program under a REMS, called the TECVAYLI® and TALVEY® REMS because of the risks of CRS and neurologic toxicity, including ICANS.
Further information about the TECVAYLI® and TALVEY® REMS program is available at www.TEC-TALREMS.com or by telephone at 1-855-810-8064.
Oral toxicity and weight loss
TALVEY® can cause oral toxicities, including dysgeusia, dry mouth, dysphagia, and stomatitis.
In the clinical trial, 80% of patients had oral toxicity, with Grade 3 occurring in 2.1% of patients who received the recommended dosages. The most frequent oral toxicities were dysgeusia (49%), dry mouth (34%), dysphagia (23%), and ageusia (18%). The median time to onset of oral toxicity was 15 (range: 1 to 634) days, and the median time to resolution to baseline was 43 (1 to 530) days. Oral toxicity did not resolve to baseline in 65% of patients.
TALVEY® can cause weight loss. In the clinical trial, 62% of patients experienced weight loss, regardless of having an oral toxicity, including 29% of patients with Grade 2 (10% or greater) weight loss and 2.7% of patients with Grade 3 (20% or greater) weight loss. The median time to onset of Grade 2 or higher weight loss was 67 (range: 6 to 407) days, and the median time to resolution was 50 (range: 1 to 403) days. Weight loss did not resolve in 57% of patients who reported weight loss.
Monitor patients for signs and symptoms of oral toxicity. Counsel patients to seek medical attention should signs or symptoms of oral toxicity occur and provide supportive care as per current clinical practice, including consultation with a nutritionist. Monitor weight regularly during therapy. Evaluate clinically significant weight loss further. Withhold TALVEY® or permanently discontinue based on severity.
Infections
TALVEY® can cause infections, including life-threatening or fatal infections.
Serious infections occurred in 16% of patients, with fatal infections in 1.5% of patients. Grade 3 or 4 infections occurred in 17% of patients. The most common serious infections reported were bacterial infection (8%), which included sepsis, and COVID-19 (2.7%).
Monitor patients for signs and symptoms of infection prior to and during treatment with TALVEY® and treat appropriately. Administer prophylactic antimicrobials according to local guidelines. Withhold or consider permanent discontinuation of TALVEY® as recommended based on severity.
Cytopenias
TALVEY® can cause cytopenias, including neutropenia and thrombocytopenia.
In the clinical trial, Grade 3 or 4 decreased neutrophils occurred in 35% of patients, and Grade 3 or 4 decreased platelets occurred in 22% of patients who received TALVEY®. The median time to onset for Grade 3 or 4 neutropenia was 22 (range: 1 to 312) days, and the median time to resolution to Grade 2 or lower was 8 (range: 1 to 79) days. The median time to onset for Grade 3 or 4 thrombocytopenia was 12 (range: 2 to 183) days, and the median time to resolution to Grade 2 or lower was 10 (range: 1 to 64) days. Monitor complete blood counts during treatment and withhold TALVEY® as recommended based on severity.
Skin toxicity
TALVEY® can cause serious skin reactions, including rash, maculo-papular rash, erythema, and erythematous rash.
In the clinical trial, skin reactions occurred in 62% of patients, with Grade 3 skin reactions in 0.3%. The median time to onset was 25 (range: 1 to 630) days. The median time to improvement to Grade 1 or less was 33 days.
Monitor for skin toxicity, including rash progression. Consider early intervention and treatment to manage skin toxicity. Withhold TALVEY® as recommended based on severity.
Hepatotoxicity
TALVEY® can cause hepatotoxicity. Elevated ALT occurred in 33% of patients, with Grade 3 or 4 ALT elevation occurring in 2.7%; elevated AST occurred in 31% of patients, with Grade 3 or 4 AST elevation occurring in 3.3%. Grade 3 or 4 elevations of total bilirubin occurred in 0.3% of patients. Liver enzyme elevation can occur with or without concurrent CRS.
Monitor liver enzymes and bilirubin at baseline and during treatment as clinically indicated. Withhold TALVEY® or consider permanent discontinuation of TALVEY® based on severity [see Dosage and Administration (2.5)].
Embryo-fetal toxicity
Based on its mechanism of action, TALVEY® may cause fetal harm when administered to a pregnant woman. Advise pregnant women of the potential risk to the fetus. Advise females of reproductive potential to use effective contraception during treatment with TALVEY® and for 3 months after the last dose.
Adverse reactions
The most common adverse reactions (≥20%) are pyrexia, CRS, dysgeusia, nail disorder, musculoskeletal pain, skin disorder, rash, fatigue, weight decreased, dry mouth, xerosis, dysphagia, upper respiratory tract infection, diarrhea, hypotension, and headache.
The most common Grade 3 or 4 laboratory abnormalities (≥30%) are lymphocyte count decreased, neutrophil count decreased, white blood cell decreased, and hemoglobin decreased.
cp-394174v6
DARZALEX FASPRO® is a combination of daratumumab, a CD38-targeted antibody, and hyaluronidase, an endoglycosidase, indicated for the treatment of adult patients with:
- multiple myeloma in combination with bortezomib, lenalidomide, and dexamethasone for induction and consolidation in newly diagnosed patients who are eligible for autologous stem cell transplant
- multiple myeloma in combination with bortezomib, lenalidomide, and dexamethasone in newly diagnosed patients who are ineligible for autologous stem cell transplant
- multiple myeloma in combination with bortezomib, melphalan and prednisone in newly diagnosed patients who are ineligible for autologous stem cell transplant
- multiple myeloma in combination with lenalidomide and dexamethasone in newly diagnosed patients who are ineligible for autologous stem cell transplant and in patients with relapsed or refractory multiple myeloma who have received at least one prior therapy
- multiple myeloma in combination with bortezomib, thalidomide, and dexamethasone in newly diagnosed patients who are eligible for autologous stem cell transplant
- multiple myeloma in combination with bortezomib and dexamethasone in patients who have received at least one prior therapy
- multiple myeloma in combination with pomalidomide and dexamethasone in patients who have received at least one prior line of therapy including lenalidomide and a proteasome inhibitor
- multiple myeloma in combination with carfilzomib and dexamethasone in patients with relapsed or refractory multiple myeloma who have received one to three prior lines of therapy
- multiple myeloma as monotherapy, in patients who have received at least three prior lines of therapy including a proteasome inhibitor (PI) and an immunomodulatory agent or who are double-refractory to a PI and an immunomodulatory agent
- high-risk smoldering multiple myeloma as monotherapy
- light chain (AL) amyloidosis in combination with bortezomib, cyclophosphamide and dexamethasone in newly diagnosed patients
Limitations of use:
- DARZALEX FASPRO® is not indicated and is not recommended for the treatment of patients with light chain (AL) amyloidosis who have NYHA Class IIIB or Class IV cardiac disease or Mayo Stage IIIB outside of controlled clinical trials
Contraindications3:
- DARZALEX FASPRO® is contraindicated in patients with a history of severe hypersensitivity to daratumumab, hyaluronidase, or any of the components of the formulation.
Warnings and precautions3:
Hypersensitivity and other administration reactions
Both systemic administration-related reactions, including severe or life-threatening reactions, and local injection-site reactions can occur with DARZALEX FASPRO®. Fatal reactions have been reported with daratumumab-containing products, including DARZALEX FASPRO®.
Systemic reactions
In a pooled safety population of 1446 patients with multiple myeloma (N=1253) or light chain (AL) amyloidosis (N=193) who received DARZALEX FASPRO® as monotherapy or as part of a combination therapy, 7% of patients experienced a systemic administration-related reaction (Grade 2: 3%, Grade 3: 0.8%, Grade 4: 0.1%). In patients with high-risk smoldering multiple myeloma (N=193), systemic administration-related reactions occurred in 17% of patients in AQUILA (Grade 2: 7%, Grade 3: 1%).
In all patients (N=1639), systemic administration-related reactions occurred in 7% of patients with the first injection, 0.5% with the second injection, and cumulatively 1% with subsequent injections. The median time to onset was 3.2 hours (range: 4 minutes to 3.5 days). Of the 283 systemic administration related reactions that occurred in 135 patients, 240 (85%) occurred on the day of DARZALEX FASPRO® administration. Delayed systemic administration-related reactions have occurred in 1% of the patients.
Severe reactions include hypoxia, dyspnea, hypertension, and tachycardia, and ocular adverse reactions, including choroidal effusion, acute myopia, and acute angle closure glaucoma. Other signs and symptoms of systemic administration-related reactions may include respiratory symptoms, such as bronchospasm, nasal congestion, cough, throat irritation, allergic rhinitis, and wheezing, as well as anaphylactic reaction, pyrexia, chest pain, pruritus, chills, vomiting, nausea, hypotension, and blurred vision.
Pre-medicate patients with histamine-1 receptor antagonist, acetaminophen and corticosteroids. Monitor patients for systemic administration-related reactions, especially following the first and second injections. For anaphylactic reaction or life-threatening (Grade 4) administration-related reactions, immediately and permanently discontinue DARZALEX FASPRO®. Consider administering corticosteroids and other medications after the administration of DARZALEX FASPRO® depending on dosing regimen and medical history to minimize the risk of delayed (defined as occurring the day after administration) systemic administration-related reactions.
Ocular adverse reactions, including acute myopia and narrowing of the anterior chamber angle due to ciliochoroidal effusions with potential for increased intraocular pressure or glaucoma, have occurred with daratumumab-containing products. If ocular symptoms occur, interrupt DARZALEX FASPRO® and seek immediate ophthalmologic evaluation prior to restarting DARZALEX FASPRO®.
Local reactions
In this pooled safety population of 1446 patients with multiple myeloma (N=1253) or light chain (AL) amyloidosis (N=193), injection-site reactions occurred in 8% of patients, including Grade 2 reactions in 1.1%. The most frequent (>1%) injection-site reactions were injection site erythema and injection site rash. In patients with high-risk smoldering multiple myeloma (N=193), injection-site reactions occurred in 28% of patients, including Grade 2 reactions in 3%. These local reactions occurred a median of 6 minutes (range: 0 minutes to 6.5 days) after starting administration of DARZALEX FASPRO®. Monitor for local reactions and consider symptomatic management.
Cardiac toxicity in patients with light chain (AL) amyloidosis
Serious or fatal cardiac adverse reactions occurred in patients with light chain (AL) amyloidosis who received DARZALEX FASPRO® in combination with bortezomib, cyclophosphamide and dexamethasone. Serious cardiac disorders occurred in 16% and fatal cardiac disorders occurred in 10% of patients. Patients with NYHA Class IIIA or Mayo Stage IIIA disease may be at greater risk. Patients with NYHA Class IIIB or IV disease were not studied.
Monitor patients with cardiac involvement of light chain (AL) amyloidosis more frequently for cardiac adverse reactions and administer supportive care as appropriate.
Infections
DARZALEX FASPRO® can cause serious, life-threatening, or fatal infections. In patients who received DARZALEX FASPRO® in a pooled safety population including patients with smoldering multiple myeloma and light chain (AL) amyloidosis (N=1639), serious infections, including opportunistic infections, occurred in 24% of patients, Grade 3 or 4 infections occurred in 22%, and fatal infections occurred in 2.5%. The most common type of serious infection reported was pneumonia (8.5%).
Monitor patients for signs and symptoms of infection prior to and during treatment with DARZALEX FASPRO® and treat appropriately. Administer prophylactic antimicrobials according to guidelines.
Neutropenia
Daratumumab may increase neutropenia induced by background therapy. Monitor complete blood cell counts periodically during treatment according to manufacturer’s prescribing information for background therapies. Monitor patients with neutropenia for signs of infection. Consider withholding DARZALEX FASPRO® until recovery of neutrophils. In lower body weight patients receiving DARZALEX FASPRO®, higher rates of Grade 3-4 neutropenia were observed.
Thrombocytopenia
Daratumumab may increase thrombocytopenia induced by background therapy. Monitor complete blood cell counts periodically during treatment according to manufacturer’s prescribing information for background therapies. Consider withholding DARZALEX FASPRO® until recovery of platelets.
Embryo-fetal toxicity
Based on the mechanism of action, DARZALEX FASPRO® can cause fetal harm when administered to a pregnant woman. DARZALEX FASPRO® may cause depletion of fetal immune cells and decreased bone density. Advise pregnant women of the potential risk to a fetus. Advise females with reproductive potential to use effective contraception during treatment with DARZALEX FASPRO® and for 3 months after the last dose.
The combination of DARZALEX FASPRO® with lenalidomide, thalidomide, or pomalidomide is contraindicated in pregnant women because lenalidomide, thalidomide, and pomalidomide may cause birth defects and death of the unborn child. Refer to the lenalidomide, thalidomide, or pomalidomide prescribing information on use during pregnancy.
Interference with serological testing
Daratumumab binds to CD38 on RBCs and results in a positive Indirect Antiglobulin Test (Indirect Coombs test). Daratumumab-mediated positive indirect antiglobulin test may persist for up to 6 months after the last daratumumab administration. Daratumumab bound to RBCs masks detection of antibodies to minor antigens in the patient’s serum. The determination of a patient’s ABO and Rh blood type are not impacted.
Notify blood transfusion centers of this interference with serological testing and inform blood banks that a patient has received DARZALEX FASPRO®. Type and screen patients prior to starting DARZALEX FASPRO®.
Interference with determination of complete response
Daratumumab is a human IgG kappa monoclonal antibody that can be detected on both the serum protein electrophoresis and immunofixation assays used for the clinical monitoring of endogenous M‑protein. This interference can impact the determination of complete response and of disease progression in some DARZALEX FASPRO®-treated patients with IgG kappa myeloma protein.
Adverse reactions
In multiple myeloma, the most common adverse reaction (≥20%) with DARZALEX FASPRO® monotherapy is upper respiratory tract infection. The most common adverse reactions with combination therapy (≥20% for any combination) include fatigue, nausea, diarrhea, dyspnea, sleep disorder, headache, rash, renal impairment, motor dysfunction, pyrexia, cough, muscle spasms, back pain, vomiting, hypertension, upper respiratory tract infection, peripheral neuropathy, peripheral sensory neuropathy, constipation, pneumonia, edema, dizziness, bruising, and COVID-19.
The most common adverse reactions (≥20%) in patients with high-risk smoldering multiple myeloma who received DARZALEX FASPRO® monotherapy are upper respiratory tract infection, musculoskeletal pain, fatigue, diarrhea, rash, sleep disorder, sensory neuropathy, and injection site reactions.
The most common adverse reactions (≥20%) in patients with AL amyloidosis are upper respiratory tract infection, diarrhea, peripheral edema, constipation, fatigue, peripheral sensory neuropathy, nausea, insomnia, dyspnea, and cough.
The most common hematology laboratory abnormalities (≥40%) with DARZALEX FASPRO® are decreased leukocytes, decreased lymphocytes, decreased neutrophils, decreased platelets, and decreased hemoglobin.
- MonumenTAL-3 is a phase 3, multicenter, open-label, study that randomized 864 patients between November 4, 2022, and March 13, 2025, at 182 sites across 18 countries/regions.
- Patients were randomly assigned 1:1:1 to receive Tal-DP, Tal-D, or DPd. Randomization was stratified by ISS stage (I, II, or III) at screening, prior Dara exposure, and number of prior LOTs (1, 2 or 3, >3).
- Tal and Dara were administered in 28-day cycles in the Tal-DP and Tal-D arms.
- Patients randomized to the DPd arm received treatment according to established schedules.
- Patients received study treatment until confirmed progressive disease, death, intolerable toxicity, consent withdrawal, or study end, whichever occurred first.
Tal-DP dosing schedule
| 28-day cycles | Cycle 1 | Cycle 2 | Cycle 3 | Cycle 4 | Cycle 5 | Cycle 6 | Cycle 7+ |
|---|---|---|---|---|---|---|---|
| Tal SC | Step-up doses* | 0.8 mg/kg Q2W d1 and 15 |
0.8 mg/kg Q2W d1 and 15 |
0.8 mg/kg Q2W d1 and 15 |
0.8 mg/kg Q2W† d1 and 15 |
0.8 mg/kg Q2W† d1 and 15 |
0.8 mg/kg Q4W‡ d1 |
| Dara SC§ | 1800 mg QW d1, 8, 15 and 22 |
1800 mg QW d1, 8, 15 and 22 |
1800 mg Q2W d1 and 15 |
1800 mg Q2W d1 and 15 |
1800 mg Q2W d1 and 15 |
1800 mg Q2W d1 and 15 |
1800 mg Q4W d1 |
| Pom PO | - | 2 mg QD d1-21 |
2 mg QD d1-21¶ |
2 mg QD d1-21¶ |
2 mg QD d1-21¶ |
2 mg QD d1-21¶ |
2 mg QD d1-21¶ |
| Dex PO/IV# | - | 40 mg QW d1, 8, 15 and 22 |
40 mg QW d1, 8, 15 and 22 |
40 mg QW d1, 8, 15 and 22 |
- | - | - |
Tal-D dosing schedule
| 28-day cycles | Cycle 1 | Cycle 2 | Cycle 3 | Cycle 4 | Cycle 5 | Cycle 6 | Cycle 7+ |
|---|---|---|---|---|---|---|---|
| Tal SC | Step-up doses* | 0.8 mg/kg Q2W d1 and 15 |
0.8 mg/kg Q2W d1 and 15 |
0.8 mg/kg Q2W d1 and 15 |
0.8 mg/kg Q2W† d1 and 15 |
0.8 mg/kg Q2W† d1 and 15 |
0.8 mg/kg Q4W‡ d1 |
| Dara SC§ | 1800 mg QW d1, 8, 15 and 22 |
1800 mg QW d1, 8, 15 and 22 |
1800 mg Q2W d1 and 15 |
1800 mg Q2W d1 and 15 |
1800 mg Q2W d1 and 15 |
1800 mg Q2W d1 and 15 |
1800 mg Q4W d1 |
| Dex PO/IV# | - | 40 mg QW d1, 8, 15 and 22 |
40 mg QW d1, 8, 15 and 22 |
40 mg QW d1, 8, 15 and 22 |
- | - | - |
DPd dosing (approved schedule)||
| 28-day cycles | Cycles 1-2 | Cycles 3-6 | Cycle 7+ |
|---|---|---|---|
| Dara SC§ | 1800 mg QW d1, 8, 15 and 22 |
1800 mg Q2W d1 and 15 |
1800 mg Q4W d1 |
| Pom PO** | 4 mg QD d1-21 |
4 mg QD d1-21 |
4 mg QD d1-21 |
| Dex PO/IV# | 40 mg QW | 40 mg QW | 40 mg QW |
*Step-up Tal doses in cycle 1: day 2, 0.01 mg/kg; day 4, 0.06 mg/kg; day 8, 0.4 mg/kg; day 15, 0.8 mg/kg. †Patients with confirmed ≥VGPR could switch to Q4W Tal dosing starting at Cycle 5. ‡Q4W Tal dosing if confirmed ≥PR, otherwise Tal continued at Q2W until confirmed PR or better. §There must have been ≥4 days between each dose of Dara SC. ¶Pom dose could be escalated to 4 mg starting Cycle 3, Day 1 at investigator discretion. #Dex also served as pretreatment medication administered ~1-3 hr prior to Dara in Cycles 2-4; dose could be adjusted to 20 mg for pts ≥75 years or with BMI <18.5 kg/m2. ||Required pretreatment medications included acetaminophen and diphenhydramine. **There must have been ≥7 days between the courses of Pom for each cycle.
Key eligibility criteria1
Inclusion criteria:
- Patients were aged ≥18 years
- Patients had measurable RRMM, defined by serum M-protein levels ≥0.5 g/dL, urine M-protein level ≥200 mg/24 hours or light chain myeloma without measurable M-protein in the serum or the urine
- Patients had received ≥1 prior LOT, including lenalidomide and a proteasome inhibitor
- Patients who had received only 1 prior line of therapy were required to be lenalidomide-refractory
- ECOG PS score of 0-2
Exclusion criteria:
- Refractoriness to anti-CD38 mAbs
- Prior GPRC5D-directed therapy
- Prior exposure to Pom, or T-cell-redirecting therapy within 3 months before randomization
Primary endpoint1,*
- PFS defined as time from randomization to first documentation of disease progression or death from any cause, whichever was reported first, as assessed by an IRC.
Key secondary endpoints1,*
- Overall response (PR or better)
- CR or better (CR or sCR)
- MRD-negative CR (10-5 threshold)
- OS
Additional secondary endpoints:
- Safety
- Pharmacokinetics
- Immunogenicity
*Response and disease progression were assessed by an IRC according to the criteria of the IMWG 2016 guidelines.
- A total of 864 patients underwent randomization, and 833 patients received the assigned treatment (276, Tal-DP; 274, Tal-D; 283, DPd)
*“Other” ethnic groups includes native Hawaiian or other Pacific Islander, multiple ethnicities, not reported, or unknown. †Assessed with the use of bone marrow biopsies or aspirates in patients with available data (N=855). ‡A patient may have both true extramedullary and paraskeletal plasmacytomas. Percentages calculated with the number of patients with ≥1 soft-tissue plasmacytoma in each treatment arm as the denominator. §Assessed by central FISH testing, or local FISH and karyotype testing if central FISH was unavailable. High risk was defined as positive for one or more of the following chromosome abnormalities: del(17p), t(4;14), or t(14;16). ¶Derived based on serum β2-macroglobulin and albumin at baseline. **Scores regarding ECOG PS range from 0 to 5, with higher scores indicating greater disability. ††Two participants were not previously exposed to a proteasome inhibitor. One of these patients was reported as a major protocol deviation and the second patient was randomized but not treated due to not meeting laboratory criteria 72 hours prior to the planned dosing.
- As of November 3, 2025 (clinical cutoff), median follow-up was 24.6 months (range, 0.03-35.4)
- Pom dose reductions occurred in 42.2% (Tal-DP) and 60.4% (DPd) of patients
- In Tal-DP, 10.1% of patients escalated to Pom 4 mg from 2 mg
|
Tal-DP (N=276) |
Tal-D (N=274) |
DPd (N=283) |
|
|---|---|---|---|
| Median treatment duration (months) | 21.9 | 21.5 | 18.9 |
| Treatment discontinuation | 29.7% | 30.3% | 52.7% |
| Treatment discontinuation due to progressive disease | 13.4% | 15.7% | 40.3% |
| Treatment discontinuation due to AEs | 12.7% | 8.4% | 7.1% |
- Treatment with Tal-DP and Tal-D resulted in a significantly lower risk of disease progression or death compared with treatment with DPd1
- Estimated 24-month PFS rates (95% CIs): Tal-DP, 81.3% (75.8-85.7); Tal-D, 77.6% (71.7-82.5); DPd, 51.2% (44.8-57.1)1
- The O’Brien-Fleming stopping boundary for superiority was crossed for Tal-DP and Tal-D at the prespecified interim analysis (P<0.0001 both arms; Tal-DP boundary, P=0.0069; Tal-D boundary, P=0.0145)1
- The HR (95% CI) for progression or death versus DPd was 0.28 (0.20-0.40) for Tal-DP and 0.33 (0.24-0.46) for Tal-D1
PFS (ITT population)
- PFS across prespecified subgroups in the ITT population4
From The New England Journal of Medicine, Mina R, et al, Talquetamab Plus Daratumumab ± Pomalidomide in Relapsed/Refractory Myeloma. doi: 10.1056/NEJMoa2604657. Copyright © 2026 Massachusetts Medical Society. Reprinted with permission from Massachusetts Medical Society.
HR and 95% CI from a Cox proportional hazards model with treatment as the sole explanatory variable. An HR <1.0 indicates an advantage for the Tal-containing regimen as compared with DPd. The subgroup analysis for each parameter includes patients with available data for that parameter. Median PFS in months is displayed for each subgroup. CI widths have not been adjusted for multiplicity and may not be used in place of hypothesis testing.
*Includes patients only in the United States. †Baseline renal function was categorized according to an estimated glomerular filtration rate of 60 mL/min/1.73 m2. ‡The ISS consists of three stages (with a higher stage indicating more advanced disease) and is based on levels of serum β2-microglobulin and albumin. §Scores regarding ECOG PS range from 0 to 5, with higher scores indicating greater disability. ¶Assessed by central FISH testing, or local FISH and karyotype testing if central FISH was unavailable. High risk was defined as positive for one or more of the following chromosome abnormalities: del(17p), t(4;14), or t(14;16).
- Response rates were significantly higher in the Tal-DP (88.2%) and Tal-D (88.5%) arms when compared with DPd (77.6%), with RRs (95% CI) of 1.14 (1.06-1.23) for both Tal-DP and Tal-D relative to DPd1
- A significantly greater proportion of patients in the Tal-DP (71.1%) and Tal-D (69.0%) groups achieved a CR compared with DPd (34.5%), with RRs (95% CI) of 2.07 (1.72-2.46) for Tal-DP and 2.01 (1.68-2.39) for Tal-D versus DPd1
- Median time to CR or better: Tal-DP, 7.0 months; Tal-D, 7.7 months; DPd, 6.6 months1
- Duration of response rate (95% CI) at 24 months: Tal-DP, 86.0% (80.6-89.9); Tal-D, 79.8% (73.4-84.8); DPd, 59.6% (52.1-66.3)1
ORR
- Among the ITT population, MRD-negative CR rates at the 10-5 threshold were significantly higher with Tal-DP (52.3%) and Tal-D (46.3%) than with DPd (15.9%), with RRs (95% CI) of 3.31 (2.48-4.40) and 2.92 (2.19-3.91) for Tal-DP and Tal-D versus DPd, respectively1
- The estimated 24-month OS rates (95% CI) for Tal-DP, Tal-D, and DPd were 89.2% (84.9-92.4), 87.9% (83.0-91.5), and 79.1 (73.7-83.6)1
- The HRs (95% CI) for death from any cause versus DPd were 0.47 (0.30-0.73) for Tal-DP and 0.51 (0.33-0.78) for Tal-D. The corresponding P-values, P=0.0006 (Tal-DP) and P=0.0015 (Tal-D), did not cross the prespecified stopping boundaries for superiority given the nominal alpha allocated (0.0001) for each comparison at the interim analysis1
- Among all randomized patients, 18.1% (Tal-DP), 18.5% (Tal-D), and 40.0% (DPd) received ≥1 subsequent therapy1
- Overall, 6.6% (Tal-DP), 7.3% (Tal-D), and 19.0% (DPd) of patients received subsequent T-cell-redirecting therapies, and 5.9%, 7.3%, and 14.5% received subsequent BCMA-targeted therapy1
- Deaths were reported in 109 patients who received any study treatment: 24 (8.7%) in Tal-DP, 28 (10.2%) in Tal-D, and 57 (20.1%) in DPd, and were mainly due to AEs and disease progression1
- The number of deaths from AEs during study treatment was 5 (1.8%), 11 (4.0%), and 13 (4.6%), for Tal-DP, Tal-D and DPd, respectively1
CRS & ICANS1,4
- CRS was reported in 67.8% of patients in Tal-DP (55.8% grade 1, 11.2% grade 2) and 58.4% in Tal-D (48.9% grade 1, 8.8% grade 2)
- Events were transient with a median duration of 2 days (range, 1-57), and occurred mostly during the SUD schedule; 4 grade 2 events occurred after cycle 1 (all Tal-DP)
- All events resolved except one in Tal-D
- CRS led to Tal discontinuation in 4 patients (one Tal-DP and three Tal-D) and discontinuation of all study treatment in 2 patients (both Tal-D)
- ICANS was reported in 2.9% of patients in Tal-DP and 1.8% in Tal-D; 3 patients in Tal-DP had grade 3 events, and all events resolved
Infections1,4
- Infections of any grade were reported in 87.3% (Tal-DP), 84.3% (Tal-D), and 83.0% (DPd) of patients; the most common (occurring in ≥20% of patients) any-grade infections were URTIs (46.4% [Tal-DP], 44.5% [Tal-D], and 36.4% [DPd])
- Grade 3 or 4 infections were reported in 37.7% (Tal-DP), 29.2% (Tal-D), and 42.4% (DPd), and were most commonly pneumonia (13.8% [Tal-DP], 9.5% [Tal-D], and 19.1% [DPd])
- Fatal infections occurred in 2 (0.7%) patients in Tal-DP, 4 (1.5%) in Tal-D, and 5 (1.8%) in DPd.
- Deaths due to infections occurred between study days 208-388 in Tal-DP, days 52-626 in Tal-D, and days 18-224 in DPd
- Grade ≥3 infections were most common in the first 6 months of treatment, then declined
- Hypogammaglobulinemia, as assessed by AEs or IgG <400 mg/dL, occurred in 81.5%, 70.1%, and 62.5% of patients in Tal-DP, Tal-D and DPd, respectively. Overall, 63.8% (Tal-DP), 56.2% (Tal-D), and 36.7% of patients received ≥1 dose of IgG replacement therapy, irrespective of hypogammaglobulinemia
- Opportunistic infections were reported in 16.3%, 17.9% and 12.0% in Tal-DP, Tal-D and DPd, respectively
*Most common treatment-emergent infection of any grade defined as occurring in ≥20% of patients in any treatment group; shown with percent occurrence of respective grade 3/4 infection. †The safety population was defined as all randomized participants who received at least one dose of study treatment. ‡Hypogammaglobulinemia AEs are based on investigator-reported events. Laboratory-defined hypogammaglobulinemia includes patients with ≥1 post-baseline IgG value <400 mg/dL.
GPRC5D-related AEs1,4
- In Tal-DP and Tal-D, 14.5% (grade 3: 2.9%) and 12.4% (grade 3: 2.2%) of patients experienced ataxia/balance disorder events (including ataxia, dysarthria, balance disorder, nystagmus, cerebellar ataxia, cerebellar, syndrome, dysmetria and gait disturbance) respectively
- The median (range) time to onset of ataxia/balance disorders from the first dose of study treatment was 292 (3-1034) and 326 (24-873) days for Tal-DP and Tal-D
- Event onset was infrequent in cycle 1 (0.4% in all arms), increased during cycles 2–6 (4.7% [Tal-DP], 2.6% [Tal-D]), and was most common from cycle 7 onward (10.9% [Tal-DP], 10.2% [Tal-D])
- Ataxia/balance events led to Tal discontinuation in 4.7% (Tal-DP) and 2.2% (Tal-D) of patients
- Taste changes were reported in 72.8%, 74.8%, and 3.9% of patients in Tal-DP, Tal-D, and DPd
- Taste changes led to Tal discontinuation in 4.0% and 2.2% of patients in Tal-DP and Tal-D
- Non-rash skin, nail-related, and rash events were also common with Tal-containing regimens, occurring more frequently than with DPd
- AEs of decreased weight were reported in 45.7% (Tal-DP), 38.3% (Tal-D), and 7.4% (DPd) of patients
- Of these events, most were grade 1 (5 to <10% from baseline; 21%) or grade 2 (10 to <20% from baseline; 65.1%)
- The majority of events improved or resolved over time (68.5% in Tal-DP and 79.0% in Tal-D)
- Weight loss led to Tal discontinuation in 2.2% (Tal-DP) and 1.8% (Tal-D) of patients
- Decreases in mean body mass index in Tal-DP and Tal-D were observed primarily in the first 6 months and then stabilized
GPRC5D-associated AEs
*Including ageusia, dysgeusia (maximum grade 2 severity per CTCAE v5.0), hypogeusia, and taste disorder. †Including skin exfoliation, dry skin, pruritus, and palmar-plantar erythrodysesthesia syndrome. ‡Including nail discoloration, nail disorder, onycholysis, onychomadesis, onychoclasis, nail dystrophy, nail toxicity, and nail ridging. §Including rash, maculopapular rash, erythematous rash, and erythema. ¶Including ataxia, dysarthria, balance disorder, nystagmus, cerebellar ataxia, cerebellar syndrome, dysmetria, and gait disturbance.
- The most common TEAEs are shown below. The most common grade 3 or 4 AE was neutropenia (76.4% [Tal-DP], 29.2% [Tal-D], and 86.2% [DPd])1
- Serious AEs occurred in 63.0% (Tal-DP), 52.6% (Tal-D), and 53.7 (DPd) of patients, most commonly pneumonia (11.2%, 9.1%, and 19.4%)1
- AEs leading to discontinuation of all study treatment occurred in 10.5% (Tal-DP), 8.0% (Tal-D), and 6.7% (DPd) of patients1
*The safety population included all randomized patients who received ≥1 study treatment. Safety analyses are conducted according to the treatment received. †Defined as those occurring in ≥20% of patients in any trial group. AEs were graded per CTCAE v5.0. ‡Taste changes included dysgeusia, ageusia, hypogeusia, and taste disorder. Per CTCAE, the maximum severity for taste changes is grade 2. §Non-rash skin AEs included skin exfoliation, dry skin, pruritus, and palmar-plantar erythrodysesthesia syndrome. ||Nail-related AEs included nail discoloration, nail disorder, onycholysis, onychomadesis, onychoclasis, and nail ridging.
- Second primary malignancy was observed in 7.6% (Tal-DP), 3.6% (Tal-D), and 4.2% (DPd) of patients1
Primary publication
Conflict of interest:
- The MonumenTAL-3 study is sponsored by Janssen Research & Development, LLC.
- The authors’ conflict of interest disclosures are as follows: Gang An reported no conflicts of interest. Rahul Banerjee reported grants or contracts from AbbVie, Bristol-Myers Squibb, Gilead Sciences Inc, Johnson and Johnson, Karyopharm Therapeutics, Novartis, Pack Health, and Prothena; and consulting relationships with AbbVie, Adaptive Biotechnologies, Arcellx, Bristol Myers Squibb, Caribou Biosciences, Genentech, Gilead Sciences Inc, GlaxoSmithKline, Janssen Biotech, Karyopharm Therapeutics, Legend Biotech, Pfizer, Poseida Therapeutics, Sanofi, and SparkCures. Meral Beksac reported consulting activities for Janssen Global Services and Sanofi Pasteur Biologics through Ankara University, speakers bureau activities for Janssen Global Services through Ankara University, a scientific advisory board role with Pfizer, and other activities with Regeneron Pharmaceuticals. Guldane Cengiz Seval reported consulting activities for Amgen, Pfizer, and Takeda Pharmaceuticals through Ankara University, and speakers bureau or scientific advisory board activities through Ankara University for Amgen, Bristol-Myers Squibb, GlaxoSmithKline, Johnson and Johnson, Menarini International, Novartis, Pfizer, and Sanofi. Wenming Chen reported no conflicts of interest. Yael Cohen reported research grants, honoraria, or consulting for Amgen; consulting for Bristol Myers Squibb, F. Hoffmann-La Roche, Medison Pharma, Pfizer, Sanofi Pharmaceuticals, and Takeda; extensive consulting, advisory board, clinical trial investigator, steering committee, travel grant, research funding, and speakers bureau activities with Janssen Pharmaceuticals; and employment as Head of the Myeloma Unit at Tel Aviv Sourasky Medical Center. Kaitlyn Connors reported employment with Janssen Biotech and stock holdings in Janssen Biotech and Bristol-Myers Squibb. Christelle Courtoux reported no conflicts of interest. Meletios Dimopoulos reported honoraria and advisory board participation for Amgen, AstraZeneca, BeiGene, Bristol-Myers Squibb, GlaxoSmithKline, Janssen Global Services, Menarini Silicon Biosystems, Regeneron Pharmaceuticals, Sanofi, SWIXX Biopharma, and Takeda Oncology, and travel support from Amgen, Bristol-Myers Squibb, Janssen Global Services, and Takeda Oncology. Joao Farias reported consulting for AbbVie and Johnson and Johnson, and clinical research activities with Regeneron Pharmaceuticals. Mariacristina Festa reported no conflicts of interest. Weijun Fu reported no conflicts of interest. Kentaro Fukushima reported honoraria from Janssen Pharmaceuticals and Pfizer, and research funding from Miyarisan Pharmaceutical Co., Ltd. Hartmut Goldschmidt reported numerous speaking engagements, consulting activities, and travel support involving multiple organizations, including Oncopeptides, Amgen, Bristol-Myers Squibb, Janssen, Novartis, Pfizer, and Sanofi. Jue Gong reported employment with Johnson and Johnson and stock holdings in Johnson and Johnson. Sebastian Grosicki reported no conflicts of interest. Christoph Heuck reported employment with Johnson and Johnson and stock and stock options in Johnson and Johnson. Shang Yi Huang reported no conflicts of interest. Vania Hungria reported consulting relationships with AbbVie, Amgen, Bristol-Myers Squibb, Celgene, GlaxoSmithKline, Janssen Biotech, Pfizer, Regeneron, Roche, Sanofi/Genzyme, and Takeda Oncology. Tomas Jelinek reported travel support from GlaxoSmithKline, Janssen Biotech, and Pfizer, and institutional research grant or contract support from Sanofi. Youngil Koh reported consulting for F. Hoffmann-La Roche, Johnson and Johnson, and Novartis, and expert-witness roles for Pfizer and Takeda Pharmaceuticals. Angelique Langlois reported no conflicts of interest. Jian Li reported no conflicts of interest. Xiao Liu reported no conflicts of interest. Jordi Lopez Pardo reported consulting for Johnson and Johnson, Menarini International, Pfizer, and Sanofi. Jiashen Lu reported employment with Johnson and Johnson and stock and stock options in Johnson and Johnson. Hila Magen reported no conflicts of interest. Senem Maral reported no conflicts of interest. Joaquin Martinez-Lopez reported advisory board or consulting roles with Astellas Pharma, Bristol-Myers Squibb, F. Hoffmann-La Roche, Janssen Biotech, Janssen Global Services, Johnson and Johnson, Novartis, Pfizer, and Sanofi Pasteur Biologics; research grants from Bristol-Myers Squibb; service on an end point review committee for Sanofi; and employment with Universidad Complutense de Madrid. Dai Maruyama reported speaking engagements for AbbVie, Bristol-Myers Squibb, Chugai Pharmaceutical, Janssen Pharmaceuticals, Ono Pharmaceuticals, Pfizer, Sanofi, and Takeda Pharmaceuticals. Maria-Victoria Mateos reported lectures, advisory board participation, or consulting for Amgen, Celgene, F. Hoffmann-La Roche, GlaxoSmithKline, Janssen Global Services, Kite Pharma, Pfizer, Oncopeptides, Regeneron, Sanofi, Stemline Therapeutics, and Takeda Oncology, and employment with University Hospital of Salamanca. Changki Min reported no conflicts of interest. Roberto Mina reported speaking, advisory board, consulting, training, and related activities with AbbVie, Amgen, Bristol-Myers Squibb, F. Hoffmann-La Roche, GlaxoSmithKline, Janssen, Pfizer, Regeneron, Sanofi, and Takeda Oncology. Philippe Moreau reported advisory board or consulting activities with AbbVie, Amgen, Celgene, GlaxoSmithKline, Janssen Biotech, Pfizer, and Sanofi US Services. Daniel O'Leary reported participation in an advisory board for Johnson and Johnson. Albert Oriol reported advisory board or consulting activities and sponsored symposia participation with Amgen, Bristol-Myers Squibb, GlaxoSmithKline, Janssen Biotech, Johnson and Johnson, Pfizer Canada, and Sanofi Pasteur, and employment with Institut Catala d'Oncologia. Lisa O'Rourke reported employment with Johnson and Johnson and stock holdings in Johnson and Johnson. Charlotte Pawlyn reported advisory board, consulting, DSMB, trial steering committee, speaking, clinical-trial funding, educational material, collaborative project, and related activities—many paid to her institution—with AbbVie, Adaptive Biotechnologies, AstraZeneca, Bristol Myers Squibb, Cellcentric, GlaxoSmithKline, iTeos Therapeutics, Janssen Pharmaceuticals, Menarini Stemline, Opna Bio, Pfizer, and Sanofi. Aurore Perrot reported consulting activities with AbbVie, Adaptive Biotechnologies, Amgen, Bristol-Myers Squibb, GlaxoSmithKline, Janssen Biotech, Pfizer, Sanofi, Stemline Therapeutics, and Takeda Oncology, and service on an end point review committee for Sanofi. Matthew Pianko reported site-principal-investigator, consulting, advisory board, clinical research, and travel-related activities with AbbVie, AstraZeneca, Bristol Myers Squibb, Celgene, E.R. Squibb & Sons, GlaxoSmithKline, Janssen entities, Kite Pharma, Pfizer, Regeneron, and Sanofi Genzyme. Xiang Qin reported employment with Johnson and Johnson. Jakub Radocha reported scientific advisory board activities with Bristol Myers Squibb, GlaxoSmithKline, Johnson and Johnson, Pfizer, and Sanofi; travel support from Johnson and Johnson and Sanofi; and consulting for Takeda Pharmaceutical Company. Leo Rasche reported consulting for Amgen, Johnson and Johnson, and Pfizer; travel support from BeiGene Switzerland and Johnson and Johnson; grants or contracts from Bristol-Myers Squibb, GlaxoSmithKline, and Sanofi; and employment with Julius-Maximilians-Universitat Wurzburg. Paula Rodriguez Otero reported consulting, advisory board, speaker bureau, steering committee, and related activities with AbbVie, AstraZeneca, Bristol Myers Squibb, Caribou Biosciences, F. Hoffmann-La Roche, GlaxoSmithKline, H3 Biomedicine, Janssen Global Services, Johnson and Johnson, Pfizer, Menarini Stemline Espana, Oncopeptides, Regeneron, and Sanofi Pasteur, and employment with Clinica Universidad de Navarra. Samuel Rubinstein reported ad hoc consulting for Bristol-Myers Squibb and Johnson and Johnson. Jayr Schmidt Filho reported honoraria and advisory board roles with AbbVie, AstraZeneca, Johnson and Johnson International, Kite Pharma, and Pfizer Pharmaceuticals. Pawel Steckiewicz reported no conflicts of interest. William Terry reported employment with Johnson and Johnson. Raymond Thertulien reported consulting and advisory board activities with AbbVie and Johnson and Johnson, and speakers bureau activities with GlaxoSmithKline, Johnson and Johnson, and Sanofi. Jaszianne Tolbert reported employment with Johnson and Johnson. Mehmet Turgut reported being an advisor for AbbVie. Agata Tyczynska reported no conflicts of interest. Sandra Vasey reported employment with Johnson and Johnson and stock holdings in Johnson and Johnson. Diego Vieyra reported employment with Johnson & Johnson Health Care Systems. Peter Voorhees reported advisory board or consulting activities with AbbVie, Ascentage Pharma, AstraZeneca, Bristol-Myers Squibb, GlaxoSmithKline, Janssen Biotech, Johnson and Johnson, Legend Biotech, Pfizer, PreDICTA Biosciences, Regeneron, and Sanofi, including steering committee activities for AQUILA and LINKER-3. Jing Ye reported clinical research activities with Bristol-Myers Squibb and Regeneron Pharmaceuticals, and consulting for Janssen Pharmaceuticals, Pfizer, and Sanofi. Elena Zamagni reported consulting or advisory roles with Amgen, AstraZeneca, Bristol-Myers Squibb, GlaxoSmithKline, Janssen Cilag EMEA, Menarini International, Oncopeptides, Pfizer, Sanofi, and Takeda Pharmaceutical Company. Jiangxiu Zhou reported employment with Johnson and Johnson.
Additional information can be found in the publication and supplemental material including:
- Patient disposition
- Dosing schedules for Tal-DP, Tal-D and DPd
- Deaths and causes of death
- Deaths due to TEAEs
- Treatment-emergent CRS and supportive treatments
- Occurrence of CRS by toxicity grade
- ICANS events
- Most common treatment-emergent infections and infestations and hypogammaglobulinemia
- Treatment-emergent grade ≥3 infections over time
- Most common treatment-emergent opportunistic infections
- GPRC5D-associated AEs
- Treatment-emergent ataxia/balance disorders
- Second primary malignancies
- Mina R, et al. N Engl J Med. DOI: 10.1056/NEJMoa2604657.
- TALVEY® [Prescribing Information]. Horsham, PA: Janssen Biotech, Inc.
- DARZALEX FASPRO® [Prescribing Information]. Horsham, PA: Janssen Biotech, Inc.
- Mina R, et al. N Engl J Med. DOI: 10.1056/NEJMoa2604657. Supplemental Appendix.
| AE | Adverse event | MM | Multiple myeloma |
|---|---|---|---|
| BCMA | B-cell maturation antigen | MRD | Minimal residual disease |
| CAR-T | Chimeric antigen receptor T-cell | NYHA | New York Heart Association |
| CD | Cluster of differentiation | NE | Not evaluable |
| CI | Confidence interval | ORR | Overall response rate |
| COVID-19 | Coronavirus disease 2019 | OS | Overall survival |
| CR | Complete response | OR | Odds ratio |
| CRS | Cytokine release syndrome | PFS | Progression-free survival |
| CTCAE | Common Terminology Criteria for Adverse Events | PI | Proteasome inhibitor |
| Dara | Daratumumab | PO | Oral |
| Dex | Dexamethasone | Pom | Pomalidomide |
| DIC | Disseminated intravascular coagulation | PR | Partial response |
| DPd | Daratumumab plus pomalidomide and dexamethasone | QD | Once a day |
| ECOG PS | Eastern Cooperative Oncology Group Performance Status | QW | Weekly |
| FDA | Food and Drug Administration | Q2W | Every other week |
| FISH | Fluorescence in situ hybridization | Q4W | Every 4 weeks |
| GPRC5D | G protein-coupled receptor class C group 5 member D | REMS | Risk Evaluation and Mitigation Strategy |
| HR | Hazard ratio | RR | Risk ratio |
| ICANS | Immune effector cell-associated neurotoxicity syndrome | RRMM | Relapsed/refractory multiple myeloma |
| IRC | Independent Review Committee | SC | Subcutaneous |
| Ig | Immunoglobulin | sCR | Stringent complete response |
| IMWG | International Myeloma Working Group | SUD | Step-up dosing |
| Isa | Isatuximab | Tal | Talquetamab |
| ISS | International Staging System | Tal-D | Talquetamab plus daratumumab |
| ITT | Intent-to-treat | Tal-DP | Talquetamab plus daratumumab and pomalidomide |
| IV | Intravenous | TEAE | Treatment-emergent adverse event |
| LOT | Line of therapy | URTI | Upper respiratory tract infection |
| mAb | Monoclonal antibody | VGPR | Very good partial response |