Oral small-molecule tyrosine kinase inhibitor of ABL, PDGFR, and KIT; intended to suppress parallel/bypass RTK and tumor–stroma signaling.
ATP-competitive tyrosine kinase inhibitor of ABL (including BCR-ABL), PDGFR, and KIT; prevents kinase autophosphorylation and downstream MAPK and PI3K/AKT signaling, inhibiting proliferation and inducing apoptosis in oncogene-driven cells and suppressing PDGF-mediated tumor–stroma signaling.
Imatinib directly inhibits PDGFRβ kinase activity by binding the ATP site, blocking autophosphorylation and downstream MAPK and PI3K/AKT signaling, leading to growth arrest and apoptosis in PDGFR-driven cells.
Oral small-molecule tyrosine kinase inhibitor of ABL, PDGFR, and KIT; intended to suppress parallel/bypass RTK and tumor–stroma signaling.
ATP-competitive tyrosine kinase inhibitor of ABL (including BCR-ABL), PDGFR, and KIT; prevents kinase autophosphorylation and downstream MAPK and PI3K/AKT signaling, inhibiting proliferation and inducing apoptosis in oncogene-driven cells and suppressing PDGF-mediated tumor–stroma signaling.
ATP-competitive inhibition of KIT blocks autophosphorylation and downstream MAPK/PI3K–AKT survival signaling in KIT-dependent cells, causing growth arrest and apoptosis.
Bispecific IgG1 monoclonal antibody targeting EGFR and MET; blocks ligand binding and signaling, promotes receptor internalization and degradation, and mediates Fc-dependent ADCC.
Bispecific IgG1 monoclonal antibody against EGFR and MET that blocks ligand binding and receptor phosphorylation, promotes receptor internalization and degradation, suppresses EGFR/MET downstream signaling, and induces Fc-dependent ADCC, resulting in inhibition of tumor cell proliferation.
Amivantamab binds EGFR on target cells and its IgG1 Fc engages Fcγ receptor–bearing effector cells (e.g., NK cells) to induce antibody-dependent cellular cytotoxicity (ADCC), leading to target-cell lysis; it also blocks signaling but killing is via ADCC.
Bispecific IgG1 monoclonal antibody targeting EGFR and MET; blocks ligand binding and signaling, promotes receptor internalization and degradation, and mediates Fc-dependent ADCC.
Bispecific IgG1 monoclonal antibody against EGFR and MET that blocks ligand binding and receptor phosphorylation, promotes receptor internalization and degradation, suppresses EGFR/MET downstream signaling, and induces Fc-dependent ADCC, resulting in inhibition of tumor cell proliferation.
Amivantamab binds MET on target cells and engages Fcγ receptor–bearing effector cells (e.g., NK cells, macrophages) to induce ADCC/ADCP, killing MET-expressing cells; it also blocks signaling and promotes receptor internalization.
Chimeric IgG1 monoclonal antibody against EGFR; inhibits EGFR signaling and mediates antibody-dependent cellular cytotoxicity (ADCC).
Chimeric IgG1 monoclonal antibody against EGFR that binds the extracellular domain, blocking ligand binding and receptor dimerization/activation, thereby inhibiting downstream RAS–RAF–MEK–ERK and PI3K–AKT signaling to suppress tumor cell proliferation; Fc region mediates antibody-dependent cellular cytotoxicity (ADCC).
Cetuximab binds EGFR on target cells and its Fc engages Fc-gamma receptor–bearing effector cells (e.g., NK cells) to induce antibody-dependent cellular cytotoxicity (± complement-mediated lysis), killing EGFR+ cells.