Mechanism

BCMA

Assets acting on this target.

Class
Autologous BCMA-directed CAR-T cell therapy
Pathway
Fully human anti-BCMA scFv (25C2) with CD8α hinge/transmembrane domain, 4-1BB costimulatory domain and CD3ζ signaling domain; NMPA-approved Feb 2024 for relapsed/refractory multiple myeloma (China)

B-cell maturation antigen (BCMA), also known as TNFRSF17, is a cell-surface receptor expressed almost exclusively on mature B lymphocytes and, at high density, on plasma cells—the antibody-producing cells that become malignant in multiple myeloma. BCMA binds two ligands, APRIL and BAFF, and this engagement drives downstream NF-κB signaling that supports plasma cell survival and proliferation. Because malignant plasma cells depend heavily on this survival signal and display BCMA uniformly, the receptor serves as a distinguishing marker that can be exploited therapeutically, largely independent of the survival pathway itself. Chimeric antigen receptor (CAR) T-cell therapy re-engineers a patient's own T lymphocytes to express a synthetic receptor whose extracellular portion recognizes BCMA and whose intracellular portion triggers T-cell activation, bypassing the need for conventional antigen presentation. This allows the engineered T cells to recognize and eliminate BCMA-bearing tumor cells directly. The broader disease relevance of BCMA-directed therapy spans multiple myeloma and, in principle, other plasma-cell and B-cell disorders where this receptor is expressed, making it one of the most actively pursued targets across cellular, antibody-conjugate, and bispecific antibody modalities.

Research

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