Patient-derived T cells engineered ex vivo to express a chimeric antigen receptor targeting CD19, then infused intravenously to ablate CD19+ B-lineage cells (naive/memory B cells and plasmablasts), producing B-cell depletion/aplasia and an immune reset.
Autologous T cells engineered to express an anti-CD19 chimeric antigen receptor recognize CD19 on B-lineage cells and, upon engagement, become activated and kill these cells via cytotoxic mechanisms, producing profound depletion/aplasia of CD19+ B cells and reducing autoreactive B cells and autoantibody production (immune reset).
Anti-CD19 CAR-T cells bind CD19 on target B-lineage cells and kill them via contact-dependent cytotoxicity (perforin/granzyme-mediated apoptosis and death-receptor pathways), leading to B-cell depletion.
Polyclonal antibody preparation that depletes T lymphocytes for induction immunosuppression.
Polyclonal anti–T-lymphocyte IgG that binds multiple T-cell surface antigens and depletes T cells via complement-dependent cytotoxicity and Fc-mediated ADCC, with additional T-cell apoptosis and functional inhibition, producing potent immunosuppression.
Polyclonal IgG in ATG binds CD45 on leukocytes and triggers complement-dependent lysis and Fc-mediated ADCC, with additional induction of apoptosis.
Recombinant humanized anti-CD20 monoclonal antibody administered subcutaneously; depletes CD20+ B cells via ADCC, CDC, and apoptosis to reduce autoantibody production. Evaluated in adults with primary membranous nephropathy (Phase I; 350–1000 mg on Days 1 and 15).
Humanized anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes CD20+ B lymphocytes via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and apoptosis, thereby reducing pathogenic autoantibody production.
The anti-CD20 antibody binds CD20 on B cells and induces killing via Fc-mediated ADCC (recruiting NK cells/macrophages), complement-dependent cytotoxicity, and direct apoptosis signaling, depleting CD20+ cells.
An antibody–drug conjugate (Blenrep) targeting BCMA on malignant plasma cells; internalization releases MMAF to disrupt microtubules and induce apoptosis, and can mediate ADCC/ADCP.
Afucosylated anti-BCMA monoclonal antibody conjugated to MMAF; binds BCMA on malignant plasma cells and is internalized, releasing MMAF that inhibits tubulin polymerization leading to G2/M arrest and apoptosis; also engages Fc-mediated effector functions (ADCC/ADCP).
The ADC binds BCMA on target cells, is internalized, and releases MMAF to inhibit tubulin polymerization, causing G2/M arrest and apoptosis; Fc-mediated ADCC/ADCP also kills BCMA+ cells.
Subcutaneous GPRC5D×CD3 bispecific T‑cell–redirecting monoclonal antibody that binds CD3 on T cells and GPRC5D on malignant plasma cells, activating T‑cell cytotoxicity; off‑tumor GPRC5D expression in oral/keratinized tissues is linked to dysgeusia.
Bispecific monoclonal antibody that binds CD3 on T cells and GPRC5D on malignant plasma cells, cross-linking T cells to tumor cells to drive T-cell activation, cytokine release, and cytotoxic lysis of GPRC5D-expressing cells; off-tumor GPRC5D in oral/keratinized tissues is linked to dysgeusia.
Talquetamab links CD3 on T cells to GPRC5D on target cells, triggering T‑cell activation and perforin/granzyme‑mediated lysis of GPRC5D‑expressing cells.