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 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.
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.
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.
Mutant-selective, irreversible inhibition of EGFR T790M blocks downstream MAPK/PI3K signaling, causing growth arrest and apoptosis of EGFR T790M–positive tumor cells.
An autologous anti-CD19 chimeric antigen receptor (CAR) T-cell therapy (second-generation CAR with CD28 costimulation) administered after lymphodepleting chemotherapy to promote CAR-T expansion in relapsed/refractory large B-cell lymphoma.
Autologous T cells engineered to express a CD19-specific chimeric antigen receptor with CD28 costimulation and CD3 zeta signaling selectively bind CD19 on B cells, become activated, expand after lymphodepletion, and mediate cytokine release and cytotoxic killing of CD19-positive malignant cells.
Anti-CD19 CAR T cells bind CD19, become activated, and kill target cells via perforin/granzyme-mediated cytolysis and death-receptor–mediated apoptosis.