Humanized anti-EGFR monoclonal antibody that blocks EGFR ligand binding and downstream signaling (RAS/RAF/MEK/ERK; PI3K/AKT) and may induce ADCC.
Humanized anti-EGFR monoclonal antibody that binds EGFR, blocks ligand binding and downstream signaling (RAS/RAF/MEK/ERK and PI3K/AKT), inhibiting tumor cell proliferation and survival; may also induce antibody-dependent cellular cytotoxicity (ADCC).
YES
DIRECT
Anti-EGFR IgG1 binding engages Fcγ receptor–bearing immune cells (e.g., NK cells) to mediate ADCC; EGFR signaling blockade can also promote apoptosis.
Humanized IgG1 monoclonal antibody that binds HER2/ERBB2 domain IV, blocks HER2 signaling and receptor activation/dimerization, and promotes immune-mediated tumor cell killing via antibody‑dependent cellular cytotoxicity (ADCC).
YES
DIRECT
Trastuzumab binds HER2 domain IV on tumor cells and engages FcγR-bearing immune effectors (e.g., NK cells) to induce antibody-dependent cellular cytotoxicity (ADCC), leading to lysis/apoptosis of HER2+ cells; signaling blockade is mainly cytostatic.
Humanized monoclonal antibody that binds HER2 extracellular domain II, blocking HER2–HER3 dimerization and downstream PI3K–AKT/MAPK signaling to inhibit tumor cell growth and promote apoptosis; also mediates ADCC.
YES
DIRECT
Pertuzumab binds HER2 and recruits Fcγ receptor–bearing immune cells to mediate ADCC against HER2+ cells; blockade of HER2–HER3 signaling can also induce apoptosis.
HER2-targeted antibody–drug conjugate of trastuzumab linked to the maytansinoid DM1 microtubule inhibitor; delivers cytotoxic payload to HER2-overexpressing cells while retaining trastuzumab activity.
Ado-trastuzumab emtansine (T-DM1) is a HER2-targeted antibody–drug conjugate in which trastuzumab is linked to the microtubule inhibitor DM1. It binds HER2 on tumor cells, is internalized, and releases DM1 to disrupt microtubules and induce cell death, while trastuzumab concurrently inhibits HER2 signaling and mediates ADCC.
YES
DIRECT
T-DM1 binds HER2, is internalized, and releases the DM1 payload that inhibits microtubules, causing mitotic arrest and apoptosis; the trastuzumab component can also trigger ADCC.
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.
NO
INDIRECT
ATG binds multiple T‑cell surface antigens (e.g., CD2/CD3/CD4/CD8) and depletes T cells via complement-dependent cytotoxicity and Fc-mediated ADCC/apoptosis; HLA-A expression itself is not the target of killing.