Humanized IgG1 anti-EGFR (HER1) monoclonal antibody that blocks ligand binding, inhibits downstream RAS/RAF/MEK/ERK and PI3K/AKT signaling, enhances radiosensitivity, and can mediate ADCC via Fcγ receptors on NK cells.
Humanized IgG1 monoclonal antibody against EGFR (HER1) that binds the receptor’s extracellular domain to block ligand binding and activation, suppressing downstream RAS/RAF/MEK/ERK and PI3K/AKT signaling to inhibit tumor cell proliferation and survival; also enhances radiosensitivity and can mediate ADCC via Fcγ receptor–bearing effector cells (e.g., NK cells).
IgG1 anti-EGFR antibody opsonizes EGFR+ cells; Fcγ receptor–bearing effector cells (e.g., NK cells) kill via ADCC (and possibly CDC). EGFR signaling blockade mainly inhibits proliferation; cytotoxicity is immune-mediated.
Anti-HER2/ERBB2 IgG1 monoclonal antibody that inhibits HER2 signaling and mediates antibody-dependent cellular cytotoxicity (ADCC).
Humanized IgG1 monoclonal antibody targeting HER2/ERBB2 that blocks receptor signaling (inhibiting dimerization and downstream PI3K/AKT and MAPK pathways), promotes receptor internalization, and elicits antibody-dependent cellular cytotoxicity via Fcγ receptor engagement on immune effector cells against HER2-overexpressing tumor cells.
Trastuzumab binds HER2 on tumor cells and its Fc engages Fcγ receptors on NK cells and other effectors to trigger antibody‑dependent cellular cytotoxicity (ADCC), killing the HER2+ cells; may also contribute via complement activation and apoptosis from HER2 signaling blockade.
Biological monoclonal antibody (VAY736) targeting the BAFF-R receptor; blocks BAFF-R signaling and depletes B cells to reduce anti-platelet autoantibody production.
Fully human monoclonal antibody against BAFF-R (TNFRSF13C) that blocks BAFF/BAFF-R signaling and depletes BAFF-R–expressing B cells (e.g., via Fc-mediated cytotoxicity/apoptosis), reducing B-cell survival and autoantibody production.
Anti–BAFF-R IgG binds BAFF-R on B cells and depletes them via Fc-mediated effector functions (ADCC/ADCP, complement) and BAFF-signal blockade–induced apoptosis.
Allogeneic NK-92–derived CAR-NK cell therapy engineered to recognize PD-L1 and express high-affinity CD16 (FcγRIIIa) for direct tumor killing and enhanced ADCC.
Allogeneic NK-92–derived CAR-NK engineered with a PD-L1–targeting CAR to directly recognize and kill PD-L1–expressing tumor cells, and co-expressing high-affinity CD16 (FcγRIIIa) to mediate robust antibody-dependent cellular cytotoxicity (ADCC) in the presence of IgG1 therapeutic antibodies (e.g., cetuximab).
CAR-NK cells bind PD-L1 via their PD-L1–targeting CAR, triggering NK degranulation and perforin/granzyme-mediated lysis of target cells; high-affinity CD16 also enables ADCC against antibody-coated tumor cells.
Anti-EGFR IgG1 monoclonal antibody that blocks EGFR signaling and opsonizes tumor cells to trigger ADCC.
Chimeric IgG1 monoclonal antibody targeting EGFR; binds the extracellular domain to block ligand binding and receptor dimerization, inhibiting downstream EGFR signaling and tumor proliferation, while Fc-mediated opsonization induces ADCC (and CDC) against EGFR-expressing tumor cells.
Cetuximab opsonizes EGFR-expressing cells and recruits immune effectors via its IgG1 Fc to trigger NK cell–mediated ADCC and complement-dependent cytotoxicity, leading to lysis of EGFR+ cells (while also blocking EGFR signaling).