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. 2025 Apr 16;2(3):100103.
doi: 10.1016/j.bneo.2025.100103. eCollection 2025 Aug.

Belantamab mafodotin in patients with relapsed/refractory multiple myeloma: a real-world experience

Affiliations

Belantamab mafodotin in patients with relapsed/refractory multiple myeloma: a real-world experience

Malin Hultcrantz et al. Blood Neoplasia. .

Abstract

Belantamab mafodotin is an antibody-drug conjugate targeting B-cell maturation antigen (BCMA) for the treatment of multiple myeloma. To evaluate the efficacy and safety of belantamab mafodotin in a real-world setting in the United States, we assessed all patients treated with commercial belantamab mafodotin at the Memorial Sloan Kettering Cancer Center between 2020 and 2023. Ninety-four patients were identified; 57 had high-risk cytogenetics, 77 were triple-class refractory, the median prior lines of therapy was 6, and 18 patients had received prior BCMA-targeted treatment. The overall response rate (ORR) was 43%, and 21% achieved a very good partial response or better. The median progression-free survival (PFS) was 3.8 months, median overall survival (OS) was 17.2 months, and the median duration of response was 10.5 months. In patients with prior BCMA exposure (median prior lines of therapy = 9), the ORR was 29%, PFS was 2 months, and OS was 20.4 months. Sixty-one patients (65%) had any grade of ocular toxicity and 15 patients had grade 3 or more keratopathy. All keratopathy was reversible and resolved or reduced to grade 1 by the end of the follow-up. Most patients could continue on a reduced dose or with a longer dose interval while maintaining the clinical response. Eighteen patients had 1 or more infections, most of which were grade 1/2. In summary, belantamab mafodotin showed significant ORR, including those of patients with prior BCMA exposure. Ocular toxicity was similar to that in previous reports, and the risk of serious infections was low in this cohort of heavily pretreated patients with multiple myeloma.

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Conflict of interest statement

Conflict-of-interest disclosure: M.H. reports research funding from AbbVie, Bristol Myers Squibb (BMS), Daiichi Sankyo, Cosette Pharmaceuticals, GlaxoSmithKline (GSK), Johnson & Johnson, and The Binding Site; and has received honoraria for consultancy/participation in advisory boards for BMS, Janssen, and GSK. H.H. reports grants from Takeda and Janssen. N.K. reports research funding through Amgen, Janssen, Epizyme, and AbbVie; consults for CCOPharma, OncLive, and Intellisphere Remedy Health; and participated in an advisory board for Janssen and MedImmune. K.M. reports grant support from American Society of Hematology (ASH), Multiple Myeloma Research Foundation, and International Myeloma Foundation. S.M. reports research funding from Janssen Oncology, BMS, Allogene Therapeutics, Fate Therapeutics, Caribou Therapeutics, and Takeda Oncology; received consulting fees from Evicore, Optum, BioAscend, Janssen Oncology, BMS, AbbVie, HMP Education, and Legend Biotech; and honoraria from OncLive, Physician Education Resource, MJH Life Sciences, and Plexus Communications. U.A.S. reports research funding from the Memorial Sloan Kettering Paul Calabresi Career Development Award for Clinical Oncology K12CA184746, Paula and Rodger Riney Foundation, Parker Institute for Cancer Immunotherapy at MSK, HealthTree Foundation, International Myeloma Society, ASH, and Allen Foundation Inc, as well as nonfinancial support from the ASH Clinical Research Training Institute and Transdisciplinary Research on Energetis and Cancer Training Workshop R25CA203650 (PI: Melinda Irwin). U.A.S. also reports other research support from Celgene/BMS and Janssen; personal fees from Association of Cancer Care Centers, MashUpMD, Janssen Biotech, Sanofi, BMS, MJH LifeSciences, Intellisphere, Phillips Gilmore Oncology Communications, i3 Health, and RedMedEd. C.R.T. reports research funding from Janssen and Takeda; personal fees from Physician Educations Resource and MJH Life Sciences; and has participated in advisory boards for Janssen and Sanofi, outside of the submitted work. D.J.C. receives research funding from Genentech. O.B.L. reports serving on the advisory board for MorphoSys, Kite, and Daiichi Sankyo; and has served as a paid consultant for Incyte. H.J.L. has served as a paid consultant for Takeda, Genzyme, Janssen, Karyopharm, Pfizer, Celgene, and Caelum Biosciences; and has received research support from Takeda. M.S. served as a paid consultant for McKinsey & Company, Angiocrine Bioscience, Inc, and Omeros Corporation; received research funding from Angiocrine Bioscience, Inc, Omeros Corporation, and Amgen, Inc; served on ad hoc advisory boards for Kite, a Gilead company; and received honoraria from i3 Health, Medscape, and CancerNetwork for Continuous Medical Education-related activity. G.L.S. reports research funding from Janssen, Amgen, BMS, Beyond Spring; and serves on the data safety monitoring board for ArcellX. S.A.G. reports personal fees and advisory role (scientific advisory board) from Actinium, Celgene, BMS, Sanofi, Amgen, Pfizer, GSK, Jazz Pharmaceuticals, Janssen, Omeros, Takeda, and Kite. T.S. reports honoraria from Roche-Genentech. A.M.L. reports grants from Novartis during the conduct of the study; grants from BMS; personal fees from Trillium Therapeutics; grants, personal fees, and nonfinancial support from Pfizer; and grants and personal fees from Janssen outside the submitted work. A.M.L. also has a patent US20150037346A1 with royalties paid. S.Z.U. reports grants and personal fees from AbbVie, Amgen, BMS, Celgene, GSK, Janssen, Merck, MundiPharma, Oncopeptides, Pharmacyclics, Sanofi, Seattle Genetics, SkylineDX, and Takeda. D.J.C. receives research funding from Genentech. The remaining authors declare no competing financial interests.

Figures

None
Graphical abstract
Figure 1.
Figure 1.
Survival outcomes. (A) PFS. (B) OS.
Figure 2.
Figure 2.
Median duration of response.
Figure 3.
Figure 3.
Swimmer plot of treatment response to belantamab mafodotin. Patients who had previous exposure to BCMA-targeted therapies are marked with an asterisk. LOT, line of therapy; POD, progression of disease.
Figure 4.
Figure 4.
PFS in patients who had 1 or more prior BCMA-targeted therapy vs BCMA therapy–naïve patients.

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