Rabbit-derived polyclonal IgG targeting human T-cell antigens; depletes T cells (and some B/NK cells) via complement-dependent cytotoxicity, ADCC, and apoptosis.
Rabbit-derived polyclonal IgG that binds multiple human T‑cell antigens and depletes T cells (with some B/NK cell effects) via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and induction of apoptosis, producing profound lymphodepletion.
NO
INDIRECT
rATG is a polyclonal anti–T-cell IgG that binds multiple T-cell antigens (e.g., CD2/CD3/CD4/CD8) and depletes T cells via complement-dependent cytotoxicity, ADCC, and apoptosis; it is not directed against CD44, so CD44+ cells are not directly killed.
Chimeric anti-CD20 monoclonal antibody that depletes CD20+ B cells (including memory B cells) via CDC, ADCC, and apoptosis; spares plasma cells.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on pre-B and mature B cells and depletes them via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and apoptosis; spares CD20-negative plasma cells.
YES
DIRECT
Anti-CD20 mAb binds CD20 on B cells and triggers complement-dependent cytotoxicity and Fc-mediated ADCC by NK/macrophages, and can directly induce apoptosis.
Anti-CD47 monoclonal antibody that blocks the CD47–SIRPα 'don't-eat-me' signal to enhance macrophage phagocytosis and antigen presentation.
Anti-CD47 monoclonal antibody that blocks the CD47–SIRPα interaction, removing the tumor cell 'don't-eat-me' signal to promote macrophage phagocytosis and enhance antigen presentation, supporting innate and adaptive antitumor immunity.
YES
INDIRECT
Blocks CD47–SIRPα “don’t‑eat‑me” signaling, enabling macrophage Fc-receptor–mediated phagocytosis (ADCP) of CD47+ cells and subsequent immune-mediated killing; may also enhance downstream T‑cell responses via antigen presentation.
Adoptive cellular therapy using engineered T cells (commonly CD19‑targeted) to mediate cytotoxicity against B‑cell malignancies.
Engineered autologous T cells expressing a chimeric antigen receptor (commonly targeting CD19) recognize B‑cell antigens independent of MHC, triggering T‑cell activation and cytotoxic killing of malignant B cells via perforin/granzyme release and cytokine production.
YES
DIRECT
CAR T cells recognize CD19 on target cells via the CAR and kill them through perforin/granzyme-mediated cytolysis (and death receptor signaling), inducing apoptosis.
Autologous gene-modified chimeric antigen receptor T-cell therapy; patient T cells engineered ex vivo to express a CAR targeting Nectin-4 (PVRL4) on tumor cells, enabling MHC-independent recognition, T-cell activation, cytokine release, and cytotoxic killing.
Autologous T cells are genetically engineered ex vivo to express a chimeric antigen receptor that recognizes Nectin-4 (PVRL4) on tumor cells. CAR engagement triggers CD3ζ/co-stimulatory signaling, leading to MHC-independent T-cell activation, cytokine release, expansion, and direct cytotoxic killing of Nectin-4–positive cancer cells.
YES
DIRECT
CAR-T cells bind Nectin-4 on target cells and, via CD3ζ/co-stimulatory signaling, activate cytotoxic effector functions (perforin/granzyme release and death-receptor pathways) to lyse Nectin-4–positive cells.