The plasma cell dyscrasia oral abstract session at the 2026 ASCO Annual Meeting featured several pivotal trials that advanced the field, including those highlighted here. Coverage of new treatments for amyloidosis will appear in a separate article.

Mezigdomide-Based Regimen Improves Progression-Free Survival in Highly Refractory Myeloma

Mezigdomide given in combination with carfilzomib and dexamethasone (MeziKd) significantly reduced the risk of disease progression or death in patients with relapsed or refractory multiple myeloma in the phase III SUCCESSOR-2 trial,¹ reported Paul G. Richardson, MD, Clinical Program Leader and the Director of Clinical Research at the Jerome Lipper Multiple Myeloma Center, Dana-Farber Cancer Institute, and the R.J. Corman Professor of Medicine at Harvard Medical School. The findings have also been published in The Lancet.²

Paul G. Richardson, MD

At a median follow-up of 10.6 months, median progression-free survival was 18.0 months with MeziKd vs 8.3 months with carfilzomib and dexamethasone (Kd) (hazard ratio [HR] = 0.48; P < .0001). The benefit was consistent across all prespecified subgroups, regardless of prior therapy, age, refractory status, cytogenetic risk, or the presence of extramedullary disease. MeziKd also deepened responses, doubling the rate of very good partial responses or better (≥ VGPR) and tripling the complete response rate among patients previously exposed or refractory to an anti-CD38 antibody and/or lenalidomide.

“We can reasonably conclude that oral mezigdomide combined with weekly intravenous carfilzomib is a potential new standard of care in relapsed/refractory disease and, most importantly, can be easily used across diverse care settings, including community practice,” Dr. Richardson said.

Mezigdomide is a potent oral and distinct cereblon E3 ligase modulator (CELMoD) that has demonstrated greater myeloma cell killing and immune stimulation than currently approved immunomodulatory drugs. It has also shown clinical activity in patients refractory to three classes of therapy and in those exposed or refractory to anti–B-cell maturation antigen (BCMA) agents, thereby addressing an important unmet need, he noted.

“SUCCESSOR-2 identified a patient population that was both anti-CD38–exposed and/or –refractory as well as lenalidomide-exposed and/or -refractory, with traditionally poor outcomes. This is one of the few studies to prospectively target this population in a very specific way. We were trying to identify a convenient, highly effective regimen that could benefit these patients not only in specialized centers but also in the community,” Dr. Richardson said.

The randomized, multicenter, open-label SUCCESSOR-2 trial enrolled patients who had received at least one prior line of therapy that included both lenalidomide and an anti-CD38 antibody. About one-third of patients had received at least two prior lines of therapy, two-thirds had been exposed to both lenalidomide and an anti-CD38 antibody in combination, 76% were refractory to lenalidomide, with 32% refractory to pomalidomide, 86% were refractory to anti-CD38s autobody therapy, 93% were refractory to their most recent treatment, and one-third to one-half (depending on criteria) had high-risk cytogenetics.

Following dose optimization, patients in the efficacy and safety phase received oral mezigdomide at 1 mg once daily for 21 days with one week off. The primary endpoint was progression-free survival as assessed by independent review.

Additional Key Findings with MeziKd

Median progression-free survival 2 was 23.6 months with MeziKd vs 13.0 months with Kd (HR = 0.53; 95% confidence interval [CI] = 0.39–0.72). The MeziKd arm also achieved higher objective response (80.2% vs 53.4%), ≥ VGPR (60.1% vs 30.9%), and complete response rates (26.7% vs 8.9%), as well as a longer duration of response. Although overall survival data remain immature, a trend favoring MeziKd was observed (HR = 0.79; 95% CI = 0.54–1.15), with no overlap seen.

Treatment-emergent adverse events were more common with MeziKd, particularly grade 3 or 4 hematologic toxicities. Neutropenia was the most common grade 3 or 4 adverse event, occurring in 61.1% of patients with MeziKd and 9.1% receiving Kd; one patient discontinued treatment because of neutropenia, which was effectively managed with dose interruptions or modifications and growth factor support. Most infections (69% with MeziKd and 98% with Kd) were not associated with neutropenia; fatal infections occurred in 2.4% and 1.1% of patients, respectively, with opportunistic infections occurring in less than 2% of patients overall.

MajesTEC-9: Teclistamab Monotherapy Improves Progression-Free and Overall Survival

In the phase III MajesTEC-9 trial, treatment with the bispecific T-cell engager teclistamab-cqyv (BCMA, CD3) as a single agent, reduced the risk of disease progression or death by 71% and improved overall survival compared with investigator’s choice of pomalidomide, bortezomib, and dexamethasone (PVd) or carfilzomib and dexamethasone (Kd) in patients with myeloma previously treated with an anti-CD38 antibody and lenalidomide.³ The results were simultaneously published in The New England Journal of Medicine.⁴

“MajesTEC-9 is the second positive phase III study of teclistamab-based therapy to demonstrate significant progression-free and overall survival benefits in second-line relapsed/refractory myeloma,” said Roberto Mina, MD, of Winship Cancer Institute of Emory University and the AOU Città della Salute e della Scienza di Torino, Università di Torino, Italy. “The data support teclistamab-based therapy as a new standard of care for patients with at least one prior line of therapy across practice settings.”

Roberto Mina, MD

The earlier MajesTEC-3 trial established teclistamab plus daratumumab as a new second-line standard by demonstrating significant improvements in progression-free and overall survival with BCMA-directed immunotherapy.⁵ MajesTEC-9 extended those findings by evaluating teclistamab monotherapy in patients who had received one to three prior lines of therapy, including prior exposure to both an anti-CD38 antibody and lenalidomide.

The phase III MajesTEC-9 trial enrolled 593 patients who had received one to three prior lines of therapy, including at least two consecutive cycles each of an anti-CD38 monoclonal antibody and lenalidomide, but no prior BCMA-directed therapy. Approximately three-fourths of patients were refractory to both drug classes; one-third were also refractory to a proteasome inhibitor (ie, triple-class refractory), and high-risk disease was fairly common.

Patients were randomly assigned to receive subcutaneous teclistamab or investigator’s choice of PVd or Kd. Subcutaneous teclistamab was initiated at 1.5 mg/kg and increased to 3 mg/kg beginning on Cycle 3.Beginning with Cycle 7 (earlier for patients with ≥ VGPR), teclistamab was dosed monthly. Premedication with steroids was no longer required after Cycle 1, Day 5.

Improvements Across Multiple Outcomes

At a median follow-up of 17.3 months, median progression-free survival was not reached with teclistamab vs 8.2 months with PVd or Kd (HR = 0.29; P < .0001). The 18-month progression-free survival rates were 69.8% and 26.9%, respectively. The progression-free survival benefit favoring teclistamab was observed across all clinically relevant subgroups, including patients refractory to lenalidomide and daratumumab as well as patients with high-risk disease.

Overall survival also favored teclistamab (HR = 0.60; P = .0020), with an estimated 18-month overall survival rate of 79.2% with teclistamab and 68.6% with PVd or Kd. The survival benefit was observed despite more than two-thirds of patients in the control arm receiving a bispecific antibody or chimeric antigen receptor (CAR) T-cell therapy as subsequent treatment.

Response rates were also higher with teclistamab than with PVd or Kd (84.5% vs 54.2%; P < .0001), as were complete response rates (65.9% vs 16.8%; P < .0001), representing an almost fourfold increase (odds ratio [OR] = 10.42), Dr. Mina reported. “Teclistamab also drove deeper responses, with an 86% MRD-negative complete response or better rate among MRD-evaluable patients,” he said. The corresponding rate in the control arm was 45.5% (OR = 6.60; 95% CI = 3.05–15.16). Patient-reported outcomes also favored teclistamab, with the single agent significantly delaying time to symptom worsening (HR = 0.50; P < .0001).

The safety profile was consistent with the established profile of teclistamab monotherapy. Cytokine-release syndrome was predominantly low grade, and all cases resolved without treatment discontinuation. Discontinuations because of toxicity occurred in 10.7% of the teclistamab arm and 13.1% of the PVd/Kd arm. Treatment-related deaths were reported in 6.5% and 3.5% of patients, respectively.

“Infections certainly were common, especially in the first 6 months of treatment, when disease burden was highest,” Dr. Mina acknowledged. Grade 5 infections occurred in 16 patients (5.5%) on the teclistamab arm and 8 (2.8%) on the PVd/Kd arm, almost all within the first 6 months. The incidence of grade 3 or higher infections declined substantially after 6 months. These findings reinforce the importance of established immunoglobulin replacement therapy and antimicrobial prophylaxis.

FORTE: Five Years of Sustained MRD Negativity Associated With Long-Term Outcomes

Newly diagnosed patients with multiple myeloma who achieved sustained MRD negativity for more than 3 years—and ideally for 5 years—experienced significantly improved progression-free and overall survival, according to an analysis of the phase II FORTE trial.⁶ The benefit was so pronounced that it appeared to overcome the adverse prognostic impact of high-risk baseline features. “Newly diagnosed patients with at least 5 years of sustained MRD negativity had a 7-year progression-free survival rate of 91%,” said Mattia D’Agostino, MD, of AOU Città della Salute e della Scienza di Torino, Università di Torino, Italy.

“We know that achieving MRD negativity is the single most powerful prognostic factor in multiple myeloma. With novel combinations, we can achieve MRD negativity in 80% of patients receiving quadruplets and in basically 100% of those with novel immunotherapies. We also know that one year of sustained MRD negativity at a sensitivity of 10^-5 outperforms single-timepoint MRD assessment in predicting progression-free survival. However, the optimal duration of sustained MRD negativity for predicting outcomes remains unclear,” Dr. D’Agostino said.

To address this question, the investigators analyzed the impact of different durations of sustained MRD negativity in the phase II FORTE trial. In newly diagnosed transplant-eligible patients, FORTE found that induction with carfilzomib, lenalidomide, and dexamethasone (KRd) yielded higher ≥ VGPR rates than carfilzomib, cyclophosphamide, and dexamethasone (KCd), and that 2 years of maintenance with carfilzomib plus dexamethasone was superior to lenalidomide alone.⁷ Among patients achieving ≥ VGPR before maintenance, bone marrow MRD was measured every 6 months at a sensitivity of 10^-5. Sustained MRD negativity was defined as consecutive MRD negativity for at least 1, 2, 3, 4, or 5 years without an intervening MRD-positive result.

At the start of maintenance therapy, 65% of patients were MRD-negative. The MRD negativity rate increased to 76% during the first year of maintenance and reached 80% at 5 years. Sustained MRD negativity for at least 3 years was achieved by 36% of patients, declining to 20% at 5 years, Dr. D’Agostino reported.

“MRD dynamics during the first 5 years of maintenance were key predictors of progression-free and overall survival,” he said.After 7 years of follow-up, the best outcomes were observed among patients who remained MRD-negative throughout maintenance and those who converted from MRD-positive to MRD-negative during maintenance. At 7 years, progression-free survival rates were 93% and 71%, respectively, and overall survival rates were 94% and 92%.

Patients who remained MRD-positive or experienced MRD resurgence after initially achieving MRD negativity during maintenance had 7-year progression-free survival rates below 30%.

The association between sustained MRD negativity and 7-year progression-free survival was striking. Rates increased progressively with longer durations of sustained MRD negativity, from 26% in patients with less than 1 year of sustained MRD negativity (HR = 0.72; P = .12 vs MRD-positive) to 34% after 1 year (HR = 0.40; P = .003 vs MRD-positive), 44% after 2 years (HR = 0.36; P < .001 vs MRD-positive), 70% after 3 years (HR = 0.17; P < .001 vs MRD-positive), 81% after 4 years (HR = 0.15; P < .001 vs MRD-positive), and 91% after at least 5 years (HR = 0.06; P < .001 vs MRD-positive). The investigators estimated that a median duration of sustained MRD negativity of >3 years corresponded to an approximately 80% reduction in the risk of progression.

Sustained MRD negativity for 3 years also appeared to overcome adverse baseline prognostic features. Comparable benefits were observed in patients with high-risk and standard-risk disease, as well as in those with and without circulating tumor cells. In each subgroup, approximately 84% of patients remained progression-free at 7 years, Dr. D’Agostino noted.

ERASMM (EMN34): Elranatamab Shows Activity in High-Risk Smoldering Myeloma

The first results from the phase II ERASMM trial demonstrated a “strong efficacy signal” for the BCMAxCD3 bispecific antibody elranatamab-bcmm as early intervention in patients with high-risk smoldering myeloma, according to researchers.⁸ At a median follow-up of 14 months, the overall response rate was 92%, including a complete response rate of 72%. Among the 29 patients available for assessment, MRD was undetectable in 90%. “These results support further evaluation of elranatamab in high-risk smoldering multiple myeloma,” said Cyrille Touzeau, MD, PhD, of University Hospital of Nantes, France.

Cyrille Touzeau, MD, PhD

The study enrolled 50 patients with high-risk smoldering myeloma, defined by the presence of at least two high-risk features according to the 2/20/20 criteria (see IMWG inset). Patients received fixed-duration treatment with single-agent subcutaneous elranatamab for 2 years. At the data cutoff, 86% remained on treatment, 96% were progression-free, and no patient had progressed to active myeloma. Seven patients (14%) had discontinued treatment, five because of adverse events and two because of biochemical progression.

Grade 3 nonhematologic adverse events were uncommon and consisted primarily of infections (14%). The most common hematologic toxicity was grade 3 or 4 neutropenia, which occurred in 40% of patients. Cytokine-release syndrome was common but was predominantly grade 1 (46%) or grade 2 (20%); grade 3 events occurred in two patients and resolved. No cases of immune effector cell–associated neurotoxicity syndrome (ICANS) were reported. The five treatment discontinuations reported because of adverse events included one case each of Guillain-Barré syndrome (recovered), hypertransaminasemia (recovered), and peripheral neuropathy, as well as two infections; all of these treatment discontinuations occurred in patients who had achieved at least a partial response. 

DISCLOSURE: Dr. Richardson has served in a consulting or advisory role for Celgene/Bristol-Myers Squibb, GlaxoSmithKline, Oncopeptides, and Sanofi. Dr. Mina had personal financial disclosures for AbbVie, Amgen, GlaxoSmithKline, Johnson & Johnson, Menarini Group, Pfizer, Regeneron, Roche, and Sanofi. Dr. D’Agostino had personal disclosures for GlaxoSmithKline, Janssen, Sanofi, Adaptive Biotechnologies, Bristol-Myers Squibb/Celgene, GlaxoSmithKline, and Sanofi. Dr. Touzeau had personal disclosures for AbbVie, Bristol-Myers Squibb, GlaxoSmithKline, Johnson & Johnson, Menarini Group, Pfizer, and Sanofi.

REFERENCES

1. Richardson P, Schjesvold F, Chengcheng F, et al: Mezigdomide, carfilzomib, and dexamethasone vs carfilzomib and dexamethasone in relapsed/refractory multiple myeloma: Results from the phase 3 SUCCESSOR-2 trial. 2026 ASCO Annual Meeting. Abstract LBA 7506. Presented May 29, 2026.

2. Dimopoulos M, Schjesvold F, Fu C, et al: Mezigdomide, carfilzomib, and dexamethasone versus carfilzomib and dexamethasone in patients with relapsed or refractory multiple myeloma (SUCCESSOR-2): A phase 3, open-label, randomized controlled trial. The Lancet. Published June 14, 2026.

3. Mina R, Touzeau C, Hungria V, et al: MajesTEC-9: a phase 3 randomized study of teclistamab monotherapy vs investigator’s choice of pomalidomide, bortezomib, and dexamethasone or carfilzomib and dexamethasone (PVd/Kd) in patients (pts) with relapsed refractory multiple. 2026 ASCO Annual Meeting. Abstract 7507. Presented May 29, 2026.

4. Touzeau C, Mina R, Quach H, et al: Teclistamab in multiple myeloma with one to three previous lines of therapy. N Engl J Med. Published May 29, 2026.

5. Costa LJ, Bahlis NJ, Perrot A, et al: Teclistamab plus daratumumab in relapsed or refractory multiple myeloma. N Engl J Med 394(8):739-752, 2026.

6. D’Agostino M, Bertuglia G, Rota-Scalabrini D, et al: Impact of sustained MRD negativity for up to 5 years on long-term outcome of transplant-eligible newly diagnosed multiple myeloma patients enrolled in the randomized phase 2 FORTE trial. 2026 ASCO Annual Meeting. Abstract 7504. Presented May 29, 2026.

7. Gay F, Musto P, Rota-Scalabrini D, et al: Carfilzomib with cyclophosphamide and dexamethasone or lenalidomide and dexamethasone plus autologous transplantation or carfilzomib plus lenalidomide and dexamethasone, followed by maintenance with carfilzomib plus lenalidomide or lenalidomide alone for patients with newly diagnosed multiple myeloma (FORTE): A randomised, open-label, phase 2 trial. Lancet Oncol (12):1705-1720, 2021.

8. Touzeau C, Schjesvold F, Cerchione C, et al: Safety and efficacy of elranatamab as early intervention in patients with high-risk smoldering myeloma: First results from the phase 2 ERASMM (EMN34) study. 2026 ASCO Annual Meeting. Abstract 7500. Presented May 29, 2026.

EXPERT POINT OF VIEW

Providing expert perspective on these pivotal studies were Ajai Chari, MD, professor of clinical medicine at the University of California San Francisco School of Medicine, and Amrita Krishnan, MD, director of the Judy and Bernard Briskin Center for Multiple Myeloma Research at City of Hope, Duarte, California.

Dr. Chari emphasized the growing importance and clinical challenge of treatment refractoriness, noting that patients are becoming resistant to both anti-CD38 agents and lenalidomide earlier in their disease course, yet this population has historically been underrepresented in randomized clinical trials. Based on the results of MajesTEC-9¹ and SUCCESSOR-2,² the field can now envision new off-the-shelf standards of care for these patients.

Ajai Chari, MD

Amrita Krishnan, MD

Six phase III trials evaluating anti-BCMA therapies have now demonstrated superiority over standard-of-care regimens.Reviewing the pivotal trials of pomalidomide, carfilzomib, and BCMA-targeting therapies—including CAR T-cell therapies and belantamab mafodotin-blmf—Dr. Chari highlighted the marked heterogeneity of the study populations, with rates of lenalidomide-refractory disease ranging from 30% to 100% and anti-CD38-refractory disease from 0% to 95%. Such differences greatly limit direct comparisons of progression-free survival, which is the primary endpoint of most relapsed and refractory multiple myeloma studies, across trials, he said, “but we can at least look at the hazard ratios in conjunction with the absolute progression-free survival numbers. Despite better control arms in modern studies (eg triplets vs doublets).” Those hazard ratios have steadily improved, ranging from 0.60 in the earliest trials to 0.17 in MajesTEC-3 with teclistamab-cqyv.³ “That’s the best hazard ratio we have seen in a phase III clinical trial,” Dr. Chari noted.

He added that although improvements in progression-free survival were historically not always expected to translate into an overall survival benefit, multiple studies have now shown significant gains in overall survival as well.

Teclistamab Monotherapy Impresses

Turning to the MajesTEC-9 study, Dr. Chari highlighted the “dismal” progression-free survival of 8.2 months with the control regimens PVd and Kd. By comparison, progression-free survival of anti-CD38-KD approached 17 months in the less heavily refractory populations enrolled in the CANDOR⁴ and IKEMA⁵ trials, he noted. In MajesTEC-9, single-agent teclistamab significantly improved progression-free survival across multiple subgroups, as well as overall response, MRD negativity, and time to symptom worsening, compared with standard of care.

“One thing that caught my attention is that the CD38-naive patients had a hazard ratio of 0.16, which is nearly identical to the hazard ratio we saw with teclistamab and daratumumab in MajesTEC-3.³ In other words, the question becomes: doublet vs monotherapy in the CD38-naive patient. To answer that question, we need longer term follow-up and mature progression-free survival and overall survival data,” he said.

Also noteworthy was the overall survival benefit, despite two-thirds of the patients in the control arm receiving subsequent T-cell–redirecting therapy. “I think that trying to save your best therapies for later may not be the best strategy because even when you do that, you still see superiority with earlier use of teclistamab perhaps due to attrition and/or better T Cell health in earlier lines of therapy,” he said.

Dr. Chari also expressed some concern about the 17% rate of grade 2 cytokine-release syndrome. “This could present a challenge for community sites that may never have given T-cell engagers,” he said. Although infections, including some fatal events, were more common with teclistamab, most occurred within the first 6 months, underscoring the importance of initiating immunoglobulin replacement early, he added.

Bispecific Antibody or CAR T-Cell Therapy?

The findings naturally raise the question of which approach is best suited for a given patient: a bispecific antibody or CAR T-cell therapy? Dr. Chari suggested that CAR T-cell therapy may be preferred for patients who are fit, have more indolent disease, or would be inconvenienced by frequent visits to the treatment center. Bispecific antibodies, by contrast, may be better suited for patients who are frail/have comorbidities, have “explosive disease” requiring prompt intervention, or live close to the treatment center.

He added that treatment selection should take into account the prolonged risks of infection associated with bispecific antibodies, the need for ongoing immunoglobulin replacement therapy,and access to teclistamab, balanced against the upfront risks and access considerations associated with CAR T-cell therapy.

Finding a Place for Mezigdomide

Moving to SUCCESSOR-2—the first phase III study of a CELMoD, in this case mezigdomide—Dr. Chari noted that the progression-free survival of just 8.3 months with the control regimen, Kd, underscored the “dismal” outcomes observed in patients with dual-refractory disease, even early in the disease course. Mezigdomide plus Kd significantly improved progression-free survival (HR = 0.48) across multiple subgroups, as well as response rates and progression-free survival 2 (HR = 0.53). The progression-free survival 2 findings are noteworthy, he said, because the benefit was observed despite the relatively short follow-up and the availability of novel therapies in the control arm, with more than 30% of patients receiving CAR T-cell therapy or a bispecific antibody. “Overall survival is also trending favorably (HR = 0.79), which is encouraging to see with short follow-up,” he added.

“What’s important about SUCCESSOR-2 is that this is an off-the-shelf therapy, and it’s probably reasonable to use MeziKd in the ‘holding therapy’ period, ie, that period prior to BCMA CAR T apheresis, where we don’t want use bispecifics or antibody drug conjugates. I think it’s going to be an important option,” Dr. Chari said.

Regarding safety, he noted that dose reductions were often required, although treatment-related discontinuation rates were comparable between the two arms. He suggested that the higher frequency of adverse events with the triplet regimen was not unexpected, given the substantially longer duration of treatment (18 months vs 8 months with Kd alone). Fatal infections were uncommon in both arms, and rates of nonhematologic toxicities were reassuring, he said.

Dr. Chari concluded by noting that mezigdomide dose intensity was 83% and 42% required dose reductions. This raises several questions about the optimal use of mezigdomide, including the best starting dose particularly in patients of different races and ethnicities, the impact of prior infections and extensive bone marrow involvement, and the best use of growth factor support.

Sustained MRD Negativity

The FORTE⁶ analysis was a focus of Dr. Krishnan’s discussion. She emphasized that sustained MRD negativity was “extremely important,” identifying 3 years as the minimum duration associated with robust improvements in both progression-free survival (HR = 0.16; P < .001) and overall survival (HR = 0.08; P < .001). “I would argue that 5 or more years, with a 91% progression-free survival rate (HR = 0.06; P < .001), is really quite impressive,” she said.

“But what does this mean for patients?” Dr. Krishnan asked. She noted that in FORTE, sustained MRD negativity was achieved in patients who received lenalidomide until disease progression.“The real question becomes whether, with these other therapies, we can use shorter durations of therapy and still achieve that degree of sustained MRD negativity.”

She noted that ongoing studies—including CARTITUDE-6, MagnetisMM-6, and MajesTEC-7—will help answer that question.

“The other thing is that none of this comes cheaply,” Dr. Krishnan reminded attendees, noting that the current “price of a ticket to remission” can be $500,000 for both CAR T-cell therapy and bispecific antibodies—and bispecifics require ongoing dosing. As a result, global access is severely limited.

Likening advances in myeloma to the exploration of outer space, Dr. Krishnan concluded with a wry observation: “Not everyone can reach the launchpad but we need to make these therapies more accessible to more patients.” 

DISCLOSURE: Dr. Chari reported financial disclosures for AbbVie, Adaptive Biotechnologies, Amgen, Antengene, Bristol-Myers Squibb, Forus, Genentech/Roche, GlaxoSmithKline, Janssen, Karyopharm Therapeutics, Millennium Pharmaceuticals/Takeda, and Sanofi. Dr. Krishnan reported financial disclosures for AbbVie, Arcellx, AstraZeneca, BMS GmbH & Co. KG, Bristol-Myers Squibb, GlaxoSmithKline, Janssen Oncology, Pfizer, Roche, Sanofi/Aventis, and Johnson & Johnson.

REFERENCES

1. Mina R, Touzeau C, Hungria V, et al: MajesTEC-9: a phase 3 randomized study of teclistamab monotherapy vs investigator’s choice of pomalidomide, bortezomib, and dexamethasone or carfilzomib and dexamethasone (PVd/Kd) in patients with relapsed refractory multiple myeloma. 2026 ASCO Annual Meeting. Abstract 7507. Presented May 29, 2026.

2. Richardson P, Schjesvold F, Chengcheng F, et al: Mezigdomide, carfilzomib, and dexamethasone vs carfilzomib and dexamethasone in relapsed/refractory multiple myeloma: results from the phase 3 SUCCESSOR-2 trial. 2026 ASCO Annual Meeting. Abstract LBA 7506. Presented May 29, 2026.

3. Costa LJ, Bahlis NJ, Perrot A, et al: Teclistamab plus daratumumab in relapsed or refractory multiple myeloma. N Engl J Med 394:739-752, 2026.

4. Dimopoulos M, Quach H, Mateos M-V, et al: Carfilzomib, dexamethasone, and daratumumab versus carfilzomib and dexamethasone for patients with relapsed or refractory multiple myeloma (CANDOR): results from a randomised, multicentre, open-label, phase 3 study. Lancet 396:186-197, 2020.

5. Moreau P, Dimopoulos MA, Mikhael J, et al: Isatuximab, carfilzomib, and dexamethasone in relapsed multiple myeloma (IKEMA): a multicentre, open-label, randomised phase 3 trial. Lancet 397:2361-71, 2021.

6. D’Agostino M, Bertuglia G, Rota-Scalabrini D, et al: Impact of sustained MRD negativity for up to 5 years on long-term outcome of transplant-eligible newly diagnosed multiple myeloma patients enrolled in the randomized phase 2 FORTE trial. Abstract 7504. Presented May 29, 2026.