EGFR and c-MET (EGFR, c-MET)

EGFR (epidermal growth factor receptor) and c-MET (hepatocyte growth factor receptor) are distinct, non-redundant receptor tyrosine kinases; both are established therapeutic targets, highly relevant for targeted cancer therapies, frequently mutated or overexpressed in tumors, and targeted by both small molecule inhibitors and monoclonal antibodies. Both receptors are implicated in cancer biology and can show functional cross-talk, leading to combinatorial strategies using EGFR and MET inhibitors to overcome resistance or achieve synergistic anti-tumor response, especially in NSCLC and TNBC. Resistance to one can involve compensatory activation of the other, reinforcing the relevance of dual inhibition. Listing 'EGFR, c-MET' together in a single entry is incorrect for structured information purposes, as each has unique biology, biomarkers, drugs, and safety profiles.

Other names

ErbB-1HER1ERBBmENANISBD2p170METc-MET proto-oncogenemesenchymal-epithelial transition factor

Tyrosine kinase inhibition (competitive binding to ATP-binding site for EGFR, blocks ATP binding for c-MET), Antibody-mediated EGFR blockade (prevents ligand binding/activation) and MET inhibition (blocks receptor dimerization/activation). Often targeted concurrently for synergistic anti-tumor effects or to overcome resistance.