Anti-CD20 monoclonal antibody that depletes CD20+ B cells via ADCC/CDC, modulating the tumor microenvironment.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B lymphocytes and depletes CD20+ cells via Fc-mediated ADCC, complement-dependent cytotoxicity, and antibody-dependent phagocytosis, thereby modulating the tumor microenvironment.
Rituximab binds CD20 on B cells and triggers Fc-mediated effector functions—ADCC by NK cells/macrophages, complement-dependent lysis, and antibody-dependent phagocytosis—depleting CD20+ cells.
Anti-HER2 monoclonal antibody that inhibits HER2 dimerization (especially with HER3) and mediates ADCC.
Humanized anti-HER2 monoclonal antibody that binds the HER2 extracellular dimerization domain to prevent HER2 heterodimerization (especially with HER3), thereby blocking downstream PI3K/AKT/MAPK signaling, inhibiting tumor cell proliferation and promoting apoptosis; also mediates antibody-dependent cellular cytotoxicity (ADCC).
Pertuzumab binds the HER2 subdomain II, recruits FcγR-expressing immune effectors (e.g., NK cells) to mediate ADCC, killing HER2+ cells; it also blocks HER2 heterodimerization, suppressing survival signaling and promoting apoptosis.
Chimeric IgG1 anti-EGFR monoclonal antibody that blocks ligand binding to EGFR, suppressing downstream RAS-RAF-MEK-ERK and PI3K-AKT signaling; can also trigger antibody-dependent cellular cytotoxicity (ADCC).
Chimeric IgG1 monoclonal antibody against EGFR that binds the extracellular domain to block ligand binding and receptor activation/dimerization, inhibiting downstream RAS-RAF-MEK-ERK and PI3K-AKT signaling; Fc-mediated ADCC may also contribute to antitumor activity.
Cetuximab binds EGFR on target cells and its IgG1 Fc engages Fcγ receptors on NK cells/macrophages to trigger ADCC (and some CDC), resulting in lysis of EGFR-expressing cells; EGFR signaling blockade is mainly antiproliferative.
Bispecific IgG1 monoclonal antibody targeting EGFR and MET that blocks signaling, promotes receptor downregulation, and triggers Fc-mediated ADCC; background anticancer therapy.
Bispecific IgG1 monoclonal antibody targeting EGFR and MET that blocks receptor phosphorylation and downstream signaling, promotes receptor internalization/degradation, and induces Fc-mediated ADCC to inhibit tumor cell proliferation.
Amivantamab binds EGFR on target cells and engages Fcγ receptor–bearing effector cells (e.g., NK cells, macrophages) to induce ADCC/ADCP, leading to killing of EGFR+ cells; it also blocks signaling and promotes receptor internalization/degradation.