Half-life–extended bispecific T-cell engager antibody that binds DLL3 on SCLC cells and CD3 on T cells to redirect cytotoxic T-cell killing (immunotherapy).
Half-life–extended bispecific T-cell engager antibody that binds DLL3 on tumor cells and CD3 on T cells, redirecting and activating cytotoxic T lymphocytes to kill DLL3-expressing cancer cells.
Bispecific T‑cell engager links CD3 on T cells to DLL3 on target cells, activating CTLs to kill DLL3-expressing cells via perforin/granzyme-mediated cytotoxicity.
Third-generation, mutant-selective, irreversible EGFR tyrosine kinase inhibitor that covalently binds mutant EGFR (e.g., T790M, L858R, exon 19 deletions), suppressing EGFR signaling to inhibit proliferation and induce apoptosis, with relatively reduced activity on wild-type EGFR.
Mutant‑selective, irreversible EGFR tyrosine kinase inhibition of EGFR T790M suppresses downstream signaling (e.g., MAPK/PI3K‑AKT), leading to growth inhibition and apoptosis of the mutant EGFR–expressing tumor cells.
Cetuximab (C225) is a chimeric IgG1 anti-EGFR monoclonal antibody that blocks ligand binding and EGFR activation/dimerization, promotes receptor internalization, inhibits downstream RAS–RAF–MEK–ERK and PI3K–AKT signaling, and mediates antibody-dependent cellular cytotoxicity (ADCC).
Chimeric IgG1 monoclonal antibody against EGFR that binds the extracellular domain to block ligand binding and receptor activation/dimerization, promotes receptor internalization, inhibits downstream RAS–RAF–MEK–ERK and PI3K–AKT signaling, and mediates Fc-dependent ADCC against EGFR-expressing tumor cells (most effective in RAS wild-type disease).
Cetuximab binds EGFR and its IgG1 Fc engages Fcγ receptors on immune effectors to mediate ADCC (and some CDC), killing EGFR-expressing cells; EGFR blockade can also promote apoptosis.