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.
YES
DIRECT
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.
YES
DIRECT
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 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.
NO
INDIRECT
Forimtamig crosslinks CD3 on T cells to GPRC5D on myeloma cells, activating T-cell cytotoxicity (perforin/granzyme) against GPRC5D-positive cells; CD3+ T cells are effectors, not targets.
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.
YES
DIRECT
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.
Chimeric anti-CD20 monoclonal antibody that mediates B-cell depletion via antibody-dependent cellular cytotoxicity, complement activation, and apoptosis.
Rituximab is a chimeric monoclonal antibody against CD20 that depletes CD20-positive B cells via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and induction of apoptosis.
YES
DIRECT
Anti-CD20 antibody binds CD20+ cells and triggers killing via Fc-mediated ADCC (e.g., NK cells/macrophages), complement-dependent cytotoxicity, and can induce apoptosis upon crosslinking.