PRINCETON, N.J. — Bristol Myers Squibb (NYSE: BMY) today announced that the U.S. Food and Drug Administration (FDA) has accepted a New Drug Application (NDA) for mezigdomide in combination with carfilzomib and dexamethasone (MeziKd) in patients with relapsed or refractory multiple myeloma (RRMM). Mezigdomide is an oral cereblon E3 ligase modulator, or CELMoD, for the treatment of multiple myeloma. The FDA has granted a Prescription Drug User Fee Act (PDUFA) date of May 13, 2027 for this indication.
“The FDA’s acceptance of our application for mezigdomide highlights the continued momentum of our targeted protein degradation programs, as we now have two distinct agents under review in relapsed or refractory multiple myeloma, which remains a persistent disease,” said Cristian Massacesi, MD, executive vice president, chief medical officer and head of development, Bristol Myers Squibb. “We’re rapidly progressing the development of our CELMoD pipeline and are committed to leveraging this platform to bring the next wave of advances for patients in both hematologic malignancies and solid tumors.”
The filing was based on positive results from the Phase 3 SUCCESSOR-2 trial (NCT05552976) showing MeziKd demonstrated a clinically meaningful and statistically significant improvement in progression-free survival (PFS) (95% CI: 18.0 months vs. 8.3 months [HR:0.48; p<0.0001]), representing a 52% reduction in the risk of disease progression or death compared with Kd in patients with relapsed or refractory multiple myeloma, including those at first relapse after prior treatment with an anti-CD38 monoclonal antibody and lenalidomide. The safety profile of MeziKd was consistent with that observed in prior studies of mezigdomide, as well as with the known safety profiles of the individual agents in the regimen. Results were recently presented at the 2026 American Society of Clinical Oncology (ASCO®) Annual Meeting as a late-breaking oral presentation and published in The Lancet.
Bristol Myers Squibb thanks the patients and investigators involved with the Phase 3 SUCCESSOR-2 study.
About mezigdomide
Mezigdomide is an oral CELMoD specifically optimized to modulate cereblon for maximal and rapid degradation of Ikaros and Aiolos target proteins, leading to higher multiple myeloma cell killing and immune stimulation than traditional immunomodulatory agents. Pre-clinical data suggest mezigdomide enhances T cell function and prevents and reinvigorates an exhausted immune system. Mezigdomide is also being evaluated in the ongoing Phase 3 SUCCESSOR-1 trial vs. standard of care regimen in relapsed or refractory multiple myeloma.
About SUCCESSOR-2
There is a growing number of patients exposed and/or refractory to lenalidomide and anti-CD38 antibodies from first relapse. The SUCCESSOR-2 trial addressed this growing need. SUCCESSOR-2 (NCT05552976) is an inferential, seamless Phase 3, multicenter, randomized, open-label study evaluating the efficacy and safety of mezigdomide in combination with carfilzomib and dexamethasone (MeziKd) versus carfilzomib and dexamethasone (Kd) in patients with relapsed or refractory multiple myeloma (RRMM).
The primary endpoint of the Phase 3 study is progression-free survival. Key secondary endpoints include overall survival, overall response rate, duration of response, time to progression, time to next treatment, minimal residual disease negativity, and health-related quality of life.
Dose optimization for mezigdomide occurred in stage 1. The mezigdomide dose selected for stage 2 of the study was 1.0 mg. In total, 479 patients (288 MeziKd at 1.0 mg of mezigdomide; 191 Kd) were included in the analysis. Across both arms, median age was 68 with 25.1% of patients ≥75 years old; median number of prior therapies was 2; 92.1% of patients were triple-class-exposed, with 85.8% refractory to an anti-CD38 monoclonal antibody and 75.8% to lenalidomide; 37.2% were exposed to pomalidomide and 7.3% to anti-BCMA treatment. At data cutoff, median follow-up was 10.6 months with 52.4% (MeziKd) and 31.4% (Kd) of patients still on treatment.
About Targeted Protein Degradation and CELMoD
Targeted protein degradation (TPD) is a differentiated research platform at Bristol Myers Squibb built on more than two decades of scientific expertise, providing new avenues to degrade therapeutically relevant proteins that were previously considered difficult to address. BMS is the only company that has successfully developed and commercialized protein degrader agents for the treatment of multiple myeloma. These agents, known as immunomodulatory drugs (IMiDs), helped establish the current standard of care in the treatment of this disease, which remains without a cure. BMS is building on this foundation with several investigational protein degraders in clinical trials, leveraging three different modalities including CELMoD, ligand-directed degraders (LDDs), and degrader antibody conjugates (DACs). This three-pronged approach enables matching the right therapeutic modality to a molecular mechanism of action to modulate targets most effectively and ultimately provides more opportunities for potential breakthroughs that may offer meaningful new options for patients across a broad range of diseases, in and beyond hematology and oncology. Learn more about the science behind TPD at Bristol Myers Squibb here.
About Bristol Myers Squibb: Transforming Patients’ Lives Through Science
At Bristol Myers Squibb, our mission is to discover, develop and deliver innovative medicines that help patients prevail over serious diseases. We are pursuing bold science to define what’s possible for the future of medicine and the patients we serve. For more information, visit us at BMS.com and follow us on LinkedIn, X, YouTube, Facebook and Instagram.
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