Chimeric IgG1 anti-EGFR monoclonal antibody that inhibits EGFR signaling and mediates antibody-dependent cellular cytotoxicity (ADCC).
Cetuximab is a chimeric IgG1 anti-EGFR monoclonal antibody that binds the EGFR extracellular domain, blocking ligand binding and receptor dimerization/activation. This inhibits downstream RAS/RAF/MEK/ERK and PI3K/AKT signaling to reduce proliferation and survival, and its Fc region can trigger antibody-dependent cellular cytotoxicity (ADCC) against EGFR-expressing tumor cells.
Cetuximab binds EGFR on target cells and its IgG1 Fc engages Fcγ receptor–bearing effector cells (e.g., NK cells) to mediate antibody-dependent cellular cytotoxicity, killing EGFR-positive cells.
A small-molecule, third-generation, irreversible EGFR tyrosine kinase inhibitor selective for mutant EGFR (including T790M), inhibiting EGFR signaling and downstream MAPK/ERK and PI3K/AKT pathways.
Third-generation, irreversible, mutant-selective EGFR tyrosine kinase inhibitor that covalently binds EGFR (including T790M at Cys797), shutting down EGFR signaling and downstream MAPK/ERK and PI3K/AKT pathways to inhibit proliferation and induce tumor cell death.
Osimertinib covalently inhibits mutant EGFR (including L858R), blocking MAPK/ERK and PI3K/AKT signaling and inducing tumor cell apoptosis.
A small-molecule, third-generation, irreversible EGFR tyrosine kinase inhibitor selective for mutant EGFR (including T790M), inhibiting EGFR signaling and downstream MAPK/ERK and PI3K/AKT pathways.
Third-generation, irreversible, mutant-selective EGFR tyrosine kinase inhibitor that covalently binds EGFR (including T790M at Cys797), shutting down EGFR signaling and downstream MAPK/ERK and PI3K/AKT pathways to inhibit proliferation and induce tumor cell death.
Osimertinib covalently inhibits mutant EGFR (Ex19del) kinase activity, blocking MAPK/ERK and PI3K/AKT survival signaling and inducing tumor cell apoptosis.
A small-molecule, third-generation, irreversible EGFR tyrosine kinase inhibitor selective for mutant EGFR (including T790M), inhibiting EGFR signaling and downstream MAPK/ERK and PI3K/AKT pathways.
Third-generation, irreversible, mutant-selective EGFR tyrosine kinase inhibitor that covalently binds EGFR (including T790M at Cys797), shutting down EGFR signaling and downstream MAPK/ERK and PI3K/AKT pathways to inhibit proliferation and induce tumor cell death.
Covalent, irreversible inhibition of mutant EGFR (including T790M) blocks downstream MAPK/ERK and PI3K/AKT survival signaling, leading to apoptosis of EGFR-mutant tumor cells.
A bispecific IgG1 monoclonal antibody targeting EGFR and MET that blocks ligand binding, promotes receptor internalization and degradation, and mediates Fc-dependent ADCC/ADCP against EGFR/MET-expressing tumor cells.
Amivantamab is a human bispecific IgG1 monoclonal antibody targeting EGFR and MET. It blocks ligand binding and receptor phosphorylation, induces receptor internalization and degradation, and engages Fc-dependent effector functions (ADCC/ADCP) to eliminate EGFR/MET-expressing tumor cells and inhibit downstream signaling.
Amivantamab binds EGFR on target cells and its IgG1 Fc recruits Fc receptor–bearing immune cells to mediate ADCC and ADCP, killing EGFR-expressing cells; it also promotes receptor internalization/degradation.