Genetically modified autologous T cells engineered to express an HLA-A2–restricted T-cell receptor specific for NY-ESO-1, enabling recognition and cytotoxic killing of NY-ESO-1–expressing tumor cells.
Autologous T lymphocytes genetically modified to express an HLA-A2-restricted T-cell receptor specific for NY-ESO-1. These TCR-T cells recognize NY-ESO-1 peptide presented by HLA-A2 on tumor cells and, upon TCR engagement, activate cytotoxic effector functions (perforin/granzyme and cytokine release) to kill NY-ESO-1-positive cancer cells.
NO
INDIRECT
TCR-engineered T cells kill only cells presenting the NY-ESO-1 peptide in HLA-A2 via perforin/granzyme after TCR engagement; HLA-A2 expression alone is insufficient for killing.
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.
YES
DIRECT
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.
YES
DIRECT
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.
YES
DIRECT
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.
YES
DIRECT
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.