Autologous, gene-modified T cells engineered to express a bispecific chimeric antigen receptor targeting BCMA (TNFRSF17) and GPRC5D on myeloma cells; CAR engagement triggers CD3ζ/costimulatory signaling to drive T-cell proliferation, cytokine release, and cytotoxic killing, aiming to reduce antigen escape and tumor heterogeneity.
Autologous T cells are engineered to express a bispecific CAR that recognizes BCMA and GPRC5D on myeloma cells. Antigen binding activates CD3ζ and costimulatory signaling, driving T‑cell proliferation, cytokine release, and cytotoxic killing of target cells, with dual targeting intended to limit antigen escape and address tumor heterogeneity.
Bispecific CAR T cells bind BCMA on target cells, triggering CD3ζ/costimulatory signaling and T‑cell activation, leading to perforin/granzyme- and death receptor–mediated killing of BCMA+ cells.
Autologous, gene-modified T cells engineered to express a bispecific chimeric antigen receptor targeting BCMA (TNFRSF17) and GPRC5D on myeloma cells; CAR engagement triggers CD3ζ/costimulatory signaling to drive T-cell proliferation, cytokine release, and cytotoxic killing, aiming to reduce antigen escape and tumor heterogeneity.
Autologous T cells are engineered to express a bispecific CAR that recognizes BCMA and GPRC5D on myeloma cells. Antigen binding activates CD3ζ and costimulatory signaling, driving T‑cell proliferation, cytokine release, and cytotoxic killing of target cells, with dual targeting intended to limit antigen escape and address tumor heterogeneity.
CAR-T cells bind GPRC5D on target cells, activating CD3ζ/costimulatory signaling and degranulation to kill via perforin/granzyme-mediated apoptosis (with additional Fas–FasL/cytokine effects).
Gene-modified, CD19-directed T-cell therapy (engineered cytotoxic T cells; single infusion ~3×10^6 cells/kg) designed to deplete CD19+ B cells to reduce autoantibody production and modulate humoral immunity in refractory autoimmune diseases.
Gene‑modified autologous T cells expressing an anti‑CD19 chimeric receptor recognize and kill CD19+ B cells and plasmablasts, producing B‑cell depletion that lowers autoantibody production and modulates humoral immunity in refractory autoimmune disease.
Anti-CD19 CAR-T cells recognize CD19 on B cells/plasmablasts and kill them via T-cell cytotoxic pathways (perforin/granzyme-mediated lysis and apoptosis, ± Fas/FasL).
Subcutaneous bispecific T‑cell–engaging antibody that binds GPRC5D on myeloma cells and CD3 on T cells, activating T‑cell cytotoxicity against GPRC5D-positive plasma cells.
Bispecific antibody that binds GPRC5D on myeloma cells and CD3 on T cells, cross-linking them to activate T-cell cytotoxicity and kill GPRC5D-positive plasma cells.
Bispecific antibody links CD3 on T cells to GPRC5D on target cells, forming an immune synapse and activating T-cell perforin/granzyme–mediated killing of GPRC5D-positive cells.
Subcutaneous anti‑CD38 IgG1 monoclonal antibody that induces direct apoptosis and mediates CDC, ADCC, and ADCP, while depleting CD38-positive immunosuppressive cells.
Human IgG1 monoclonal antibody targeting CD38 on plasma/tumor cells; binding triggers direct apoptosis and Fc‑mediated effector functions (CDC, ADCC, ADCP) to kill CD38+ cells, while depleting CD38-expressing immunosuppressive cells (Tregs, Bregs, MDSCs) to enhance antitumor immunity.
Daratumumab binds CD38 on target cells, inducing apoptosis and Fc-mediated effector killing—complement-dependent cytotoxicity (CDC), NK cell ADCC, and macrophage ADCP—of CD38+ cells.