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.
YES
DIRECT
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.
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.
YES
DIRECT
Amivantamab binds MET on target cells and its IgG1 Fc engages FcγR-expressing effector cells (e.g., NK cells/macrophages) to mediate ADCC/ADCP, killing MET-expressing cells; it also downregulates MET/EGFR signaling.
Third-generation, mutant-selective, irreversible EGFR tyrosine kinase inhibitor used as background anticancer therapy.
Third-generation, mutant-selective, irreversible EGFR tyrosine kinase inhibitor that covalently binds mutant EGFR (e.g., T790M, exon 19 deletions, L858R), suppressing downstream signaling (e.g., MAPK/PI3K) and inducing death of EGFR-mutant tumor cells. Shows minimal activity against wild-type EGFR and penetrates the blood–brain barrier. Has also been reported to reduce PD-L1 expression and inflammatory cytokines in some EGFR-mutant contexts.
YES
DIRECT
Mutant-selective, irreversible inhibition of EGFR L858R kinase activity (covalent binding) blocks MAPK/PI3K-AKT signaling, triggering apoptosis of EGFR-mutant tumor cells.
Third-generation, mutant-selective, irreversible EGFR tyrosine kinase inhibitor used as background anticancer therapy.
Third-generation, mutant-selective, irreversible EGFR tyrosine kinase inhibitor that covalently binds mutant EGFR (e.g., T790M, exon 19 deletions, L858R), suppressing downstream signaling (e.g., MAPK/PI3K) and inducing death of EGFR-mutant tumor cells. Shows minimal activity against wild-type EGFR and penetrates the blood–brain barrier. Has also been reported to reduce PD-L1 expression and inflammatory cytokines in some EGFR-mutant contexts.
YES
DIRECT
Mutant-selective, irreversible inhibition of EGFR exon 19–deleted kinase suppresses MAPK/PI3K-AKT signaling, causing growth arrest and apoptosis of the EGFR-mutant tumor cells.
Third-generation, mutant-selective, irreversible EGFR tyrosine kinase inhibitor used as background anticancer therapy.
Third-generation, mutant-selective, irreversible EGFR tyrosine kinase inhibitor that covalently binds mutant EGFR (e.g., T790M, exon 19 deletions, L858R), suppressing downstream signaling (e.g., MAPK/PI3K) and inducing death of EGFR-mutant tumor cells. Shows minimal activity against wild-type EGFR and penetrates the blood–brain barrier. Has also been reported to reduce PD-L1 expression and inflammatory cytokines in some EGFR-mutant contexts.
YES
DIRECT
Mutant-selective, irreversible inhibition of EGFR T790M blocks downstream MAPK/PI3K signaling, causing growth arrest and apoptosis of EGFR T790M–positive tumor cells.