cetuximab

Cetuximab binds specifically to EGFR on both normal and tumor cells and competitively inhibits the binding of epidermal growth factor (EGF) and other ligands. Animal studies have shown that binding of cetuximab to EGFR blocks phosphorylation and activation of receptor-associated kinases, resulting in inhibition of cell growth, induction of apoptosis, and decreased matrix metalloproteinase and vascular endothelial growth factor production. Signal transduction through EGFR results in activation of wild-type KRAS protein. However, in cells with activating KRAS somatic mutations, the mutant KRAS protein is continuously active and appears independent of EGFR regulation. Cetuximab is indicated* for treatment of head and neck cancer and colorectal cancer.

*Please refer to full prescribing information/package insert for precise indications.

Associated Tumor Types

Associated Biomarkers

Associated Signaling Pathways

Content provided for information purposes only and does not necessarily reflect the markers included in the Caris Molecular Intelligence Service. References on file and available upon request.