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Tumor necrosis factor receptor superfamily member 17 (BCMA) is a cell surface receptor primarily expressed on mature B lymphocytes and plasma cells [1, 6]. It plays a critical role in the survival and proliferation of long-lived plasma cells by binding to its ligands, B-cell activating factor (BAFF) and a proliferation-inducing ligand (APRIL) [9, 13]. In multiple myeloma, BCMA is highly and nearly universally overexpressed on malignant plasma cells, making it an ideal therapeutic target with minimal off-target expression in other tissues [12, 14]. Current therapeutic strategies include chimeric antigen receptor (CAR) T-cell therapies, bispecific antibodies, and antibody-drug conjugates, which have shown significant efficacy in relapsed or refractory disease [8, 16]. Approved agents like idecabtagene vicleucel and teclistamab have demonstrated deep and durable responses in patients with heavily pretreated disease [13, 16]. However, treatment is associated with specific safety risks such as cytokine release syndrome, neurotoxicity, and modality-specific issues like ocular toxicity [15, 19]. Additionally, soluble BCMA (sBCMA) serves as a valuable non-invasive biomarker for monitoring disease progression and response to therapy [11, 18].
Antibody-drug conjugate, Bispecific T-cell engager, and Chimeric antigen receptor T-cell therapy
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