Low-fucose, fully human IgG1 bispecific monoclonal antibody targeting EGFR and MET; inhibits EGFR/MET signaling and active against EGFR activating/resistance mutations (e.g., T790M/C797S) and MET pathway activation.
Low-fucose, fully human IgG1 bispecific antibody that targets EGFR and MET (wild-type and mutant), blocks ligand binding and receptor phosphorylation, promotes receptor internalization/degradation, and mediates Fc-dependent ADCC; collectively shuts down EGFR/MET downstream signaling (e.g., MAPK, PI3K-AKT) and inhibits tumor cell proliferation, including in EGFR-activating/resistance and MET-driven settings.
YES
DIRECT
Amivantamab binds EGFR on target cells and engages Fcγ receptors on immune effectors to trigger ADCC (and ADCP), killing EGFR-positive cells; it also induces receptor internalization/degradation and signaling blockade (mainly cytostatic).
Low-fucose, fully human IgG1 bispecific monoclonal antibody targeting EGFR and MET; inhibits EGFR/MET signaling and active against EGFR activating/resistance mutations (e.g., T790M/C797S) and MET pathway activation.
Low-fucose, fully human IgG1 bispecific antibody that targets EGFR and MET (wild-type and mutant), blocks ligand binding and receptor phosphorylation, promotes receptor internalization/degradation, and mediates Fc-dependent ADCC; collectively shuts down EGFR/MET downstream signaling (e.g., MAPK, PI3K-AKT) and inhibits tumor cell proliferation, including in EGFR-activating/resistance and MET-driven settings.
YES
DIRECT
Amivantamab binds MET on target cells and engages Fcγ receptor–bearing effector cells to mediate Fc-dependent ADCC (and phagocytosis), leading to target-cell killing; it also induces receptor internalization/degradation and signaling blockade.