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Real World Efficacy of BCMA Directed Therapies in Patients with Multiple Myeloma after Receiving Belantamab Mafodotin
Abstract   Peer reviewed

Real World Efficacy of BCMA Directed Therapies in Patients with Multiple Myeloma after Receiving Belantamab Mafodotin

Rachel DiLeo, Prerna Mewawalla, Kalaivani Babu, Yue Yin, Christopher Sun Strouse, Ethan Chen, Hira Shaikh, James Davis, Kimberly Green, Omar Alkharabsheh, …
Transplantation and cellular therapy, Vol.31(2), pp.S414-S415
02/2025
DOI: 10.1016/j.jtct.2025.01.635

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Abstract

Multiple myeloma is an inherently incurable plasma cell malignancy characterized by periods of remissions and inevitable relapses. Belantamab mafodotin, an anti-BCMA ADC was previously approved for patients that have failed ≥4 prior therapies.While BCMA directed therapies with different mechanisms of action are increasingly utilized for RRMM, outcomes after sequential therapies with BCMA directed treatments remains an area of active investigation. This study aims to assess the real-world outcomes of patients treated with BCMA-directed therapies following progression on belantamab mafodotin. This retrospective analysis was conducted on adult patients with RRMM who had received belantamab mafodotin and were subsequently treated with BCMA directed therapies from October 10, 2019 to September 28, 2023. This multicenter study was a collaborative effort of five large academic centers in the US Myeloma Innovations Research Collaborative (USMIRC). Key outcomes included response rates, progression free survival (PFS) and overall survival (OS). Subgroup analyses were performed to compare patients who received bispecific antibodies (BsAb) or CAR T-cell therapy, as well as those who had a ≥6-month interval versus those with a <6 month interval between belantamab mafodotin and subsequent BCMA therapy. The PFS and OS were estimated using the Kaplan-Meier curves. A total of 23 patients (12 males, 11 females) were included in the analysis. The median age was 68 (range 37-82) years with 10 patients (43%) with high-risk cytogenetics, 20 patients (87%) who had received at least ≥4 prior lines of treatment, and 8 patients (35%) with extra medullary disease (EMD) at the time of treatment. Of these 23 patients, 14 received CAR-T and 9 received BsAb. The overall response rate (ORR) for the entire population was 65% (15/23), 44% (4/9) in the BsAb subgroup and 79% (11/14) in the CAR-T subgroup. With a median follow up of 24 months for the entire population, median PFS and OS were 5 (range 2-10) months and 28 (16-NR) months, respectively. There was no statistically significant difference in median PFS between patients who received a BsAb (5 mos, range 2-10) versus CAR-T (7 mos range 2-9) (p= 0.8); Figure 1. When comparing the timing of subsequent BCMA directed therapy, no statistically significant difference was seen between BCMA therapy within 6 months (5 mos, range 3-9) and BCMA therapy ≥ 6-month post belantamab (7 mos, range 2-10) (p= 0.8) Figure 2. In patients with RRMM receiving BCMA directed BsAb or CAR T-cell therapy after failure of belantamab mafodotin, outcomes in general remain inferior compared to those without prior BCMA exposure (historical cohort). Choice of subsequent BCMA directed therapy as well as treatment free interval from BCMA exposure are not predictive of outcomes. Our findings need to be confirmed with larger studies and longer follow-up.

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