Autologous T cells genetically engineered to express a chimeric antigen receptor targeting B-cell maturation antigen (BCMA) on plasma cells; used for multiple myeloma. CAR engagement triggers T-cell activation and cytotoxicity.
Autologous T cells are engineered to express a chimeric antigen receptor that binds BCMA on malignant plasma cells; CAR engagement triggers CD3ζ and costimulatory signaling, leading to T-cell activation, expansion, cytokine release, and perforin/granzyme-mediated cytotoxic killing of BCMA-expressing myeloma cells.
CAR recognition of BCMA activates engineered T cells, which kill BCMA-expressing cells via perforin/granzyme-mediated cytotoxicity (and Fas–FasL pathways).
A bispecific T‑cell engager (BiTE) antibody construct linking CD3 on T cells to CD19 on B‑cell ALL blasts to drive T‑cell–mediated cytotoxicity and MRD clearance.
A bispecific T‑cell engager that binds CD19 on B‑cell blasts and CD3 on T cells, forming an immunologic synapse that activates and redirects T cells to kill CD19+ cells via perforin/granzyme‑mediated cytotoxicity, leading to clearance of minimal residual disease.
Blinatumomab links CD3 on T cells to CD19 on target cells, forming an immunologic synapse that triggers perforin/granzyme-mediated killing of CD19+ 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.
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.
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.
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.