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.
YES
DIRECT
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.
YES
DIRECT
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 T-cell engager (BiTE) that links CD3 on T cells to CD19 on B cells, activating T-cell–mediated cytotoxicity.
A bispecific single-chain antibody (BiTE) that binds CD19 on B cells and CD3 on T cells, physically bringing T cells into contact with CD19+ cells to trigger TCR/CD3-mediated activation, cytolytic synapse formation, cytokine release, and perforin/granzyme-dependent killing of malignant B cells.
NO
INDIRECT
Blinatumomab binds CD3 on T cells to activate and redirect them to CD19+ cells; T cells kill CD19+ targets via perforin/granzyme, not the CD3+ cells.
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.
YES
DIRECT
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).
YES
DIRECT
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.