Autologous, second-generation, bispecific CD20/BCMA-directed chimeric antigen receptor T-cell (CAR-T) therapy. Patient T cells are gene-engineered to express a CAR recognizing CD20 and BCMA; engagement triggers T-cell activation, cytotoxic killing, and cytokine release, depleting CD20+ B cells and BCMA+ plasmablasts/long-lived plasma cells to reduce autoantibody-mediated pathology. Administered as a single IV infusion.
Autologous second-generation bispecific CD20/BCMA-directed CAR T cells. Patient T cells are engineered to express a CAR that recognizes CD20 on B cells and BCMA on plasmablasts/plasma cells; antigen binding triggers T-cell activation, cytotoxic killing, and cytokine release, leading to depletion of pathogenic B-lineage cells and reduction of autoantibody production.
YES
DIRECT
CAR-T cells recognize CD20 on B cells; antigen engagement activates T cells to kill the bound cell via perforin/granzyme-mediated cytolysis and apoptosis (and Fas–FasL), leading to lysis of CD20+ cells.
Autologous, second-generation, bispecific CD20/BCMA-directed chimeric antigen receptor T-cell (CAR-T) therapy. Patient T cells are gene-engineered to express a CAR recognizing CD20 and BCMA; engagement triggers T-cell activation, cytotoxic killing, and cytokine release, depleting CD20+ B cells and BCMA+ plasmablasts/long-lived plasma cells to reduce autoantibody-mediated pathology. Administered as a single IV infusion.
Autologous second-generation bispecific CD20/BCMA-directed CAR T cells. Patient T cells are engineered to express a CAR that recognizes CD20 on B cells and BCMA on plasmablasts/plasma cells; antigen binding triggers T-cell activation, cytotoxic killing, and cytokine release, leading to depletion of pathogenic B-lineage cells and reduction of autoantibody production.
YES
DIRECT
Anti-BCMA CAR T cells bind BCMA on target cells, become activated, and kill via T-cell cytotoxic mechanisms (perforin/granzyme release and death-receptor signaling).
An antibody-drug conjugate (also known as izalontamab brengitecan, BMS-986507, iza-bren) targeting TROP2 that delivers the camptothecin-derived topoisomerase I inhibitor payload brengitecan to induce DNA damage and apoptosis.
TROP2-targeting antibody-drug conjugate that binds TROP2 on tumor cells, is internalized, and releases the camptothecin-derived topoisomerase I inhibitor brengitecan to induce DNA damage and apoptosis.
YES
DIRECT
An EGFR/HER3-targeting antibody–drug conjugate binds EGFR on tumor cells, is internalized, and releases a cytotoxic topoisomerase I inhibitor payload that causes DNA damage and apoptosis.
An antibody-drug conjugate (also known as izalontamab brengitecan, BMS-986507, iza-bren) targeting TROP2 that delivers the camptothecin-derived topoisomerase I inhibitor payload brengitecan to induce DNA damage and apoptosis.
TROP2-targeting antibody-drug conjugate that binds TROP2 on tumor cells, is internalized, and releases the camptothecin-derived topoisomerase I inhibitor brengitecan to induce DNA damage and apoptosis.
YES
DIRECT
The ADC binds HER3 on tumor cells, is internalized, and releases a cytotoxic payload that induces DNA damage and apoptosis, directly killing HER3-expressing cells.
Gene-modified natural killer (NK) cells engineered to express an NKG2D-based chimeric antigen receptor (CAR) that recognizes NKG2D ligands (MICA, MICB, ULBP family) on tumor cells, activating NK cytotoxicity for treatment of relapsed/refractory multiple myeloma.
Gene‑modified NK cells expressing an NKG2D‑based CAR recognize stress‑induced NKG2D ligands (MICA, MICB, ULBP family) on tumor cells. CAR signaling activates NK cytotoxic functions, inducing degranulation (perforin/granzyme), cytokine‑mediated killing, and apoptosis of malignant cells, targeting relapsed/refractory multiple myeloma.
YES
DIRECT
NKG2D-CAR NK cells bind ULBP4 on target cells, triggering CAR signaling and NK effector functions (degranulation with perforin/granzyme and death receptor pathways), leading to apoptotic lysis of the target cells.