A HER2-directed antibody–drug conjugate in which an anti-HER2 monoclonal antibody binds ERBB2 on tumor cells, is internalized, and releases an intracellular cytotoxic payload, leading to tumor cell death; also attenuates HER2-driven signaling and may exert a bystander effect on neighboring HER2-low cells.
HER2-directed antibody–drug conjugate: an anti-HER2 monoclonal antibody binds ERBB2 on tumor cells, is internalized, and a cleavable linker releases a camptothecin-derived topoisomerase I inhibitor payload that induces DNA damage and apoptosis; additionally attenuates HER2 signaling and may exert a bystander effect on neighboring HER2-low cells.
NO
INDIRECT
SHR-A1811 binds HER2 on tumor cells, is internalized, and releases a camptothecin-derived topoisomerase I inhibitor that causes DNA damage and apoptosis. DNA topoisomerase I is the intracellular enzymatic target of the payload, not the recognition antigen; cells expressing topo I alone are not specifically targeted.
Rabbit polyclonal anti-thymocyte globulin that depletes T cells to prevent rejection and GVHD.
Rabbit polyclonal anti-thymocyte IgG that binds multiple T-cell surface antigens and depletes T cells via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and apoptosis, producing immunosuppression to prevent rejection and GVHD.
YES
DIRECT
Polyclonal rabbit IgG in Thymoglobulin binds CD25 on T cells, triggering complement-dependent cytotoxicity and Fc-mediated ADCC, and can induce apoptosis, depleting CD25+ cells.
Anti-CD47 monoclonal antibody (IgG4) that blocks the CD47–SIRPα 'don't‑eat‑me' signal to promote macrophage phagocytosis (ADCP) of tumor cells.
Humanized IgG4 anti-CD47 monoclonal antibody that blocks the CD47-SIRPalpha checkpoint, removing the 'don't-eat-me' signal to enable macrophage antibody-dependent cellular phagocytosis (ADCP) of tumor cells and stimulate downstream antitumor immune responses.
YES
DIRECT
Anti-CD47 antibody blocks the CD47–SIRPα checkpoint and opsonizes CD47+ cells, enabling macrophage Fcγ receptor-mediated antibody-dependent cellular phagocytosis; secondary T-cell responses may also contribute.
Anti‑EGFR monoclonal antibody (IgG1) that inhibits EGFR signaling and mediates NK‑cell antibody‑dependent cellular cytotoxicity (ADCC).
Chimeric IgG1 monoclonal antibody targeting EGFR; binds the extracellular domain to block ligand binding and receptor dimerization, inhibiting downstream signaling (RAS/RAF/MEK/ERK and PI3K/AKT) and tumor proliferation. The IgG1 Fc also engages Fc gamma receptors on NK cells to mediate ADCC.
YES
DIRECT
Cetuximab binds EGFR on target cells and its IgG1 Fc engages Fcγ receptors on effector cells (e.g., NK cells), inducing antibody-dependent cellular cytotoxicity (perforin/granzyme lysis; may also contribute via ADCP/CDC).
Anti‑EGFR monoclonal antibody (IgG1) that inhibits EGFR signaling and mediates NK‑cell antibody‑dependent cellular cytotoxicity (ADCC).
Chimeric IgG1 monoclonal antibody targeting EGFR; binds the extracellular domain to block ligand binding and receptor dimerization, inhibiting downstream signaling (RAS/RAF/MEK/ERK and PI3K/AKT) and tumor proliferation. The IgG1 Fc also engages Fc gamma receptors on NK cells to mediate ADCC.
NO
INDIRECT
Cetuximab binds EGFR on tumor cells; its Fc engages CD16a on NK cells to trigger ADCC that kills EGFR+ targets. CD16a+ cells are effectors and are not killed by the drug.