Epidermal growth factor receptor (EGFR) and Hepatocyte growth factor receptor (c-MET) (EGFR/c-MET)

The target refers to the dual inhibition of the Epidermal growth factor receptor (EGFR) and the Hepatocyte growth factor receptor (c-MET), both of which are receptor tyrosine kinases (RTKs) essential for cell signaling (Source: UniProt, P00533; P08581). These receptors are frequently co-expressed or mutated in various solid tumors, including non-small cell lung cancer (NSCLC) and head and neck squamous cell carcinoma (HNSCC), where they drive oncogenic processes such as cell proliferation, survival, and metastasis (Source: PubMed, PMID: 33163435). MCLA-129 (petosemtamab) is a bispecific antibody that targets both EGFR and c-MET to provide a more robust blockade of tumor growth and to overcome resistance to standard EGFR inhibitors, which often occurs through the activation of the MET pathway (Source: Merus, Petosemtamab (MCLA-129)). The therapeutic mechanism involves the simultaneous inhibition of ligand binding, receptor degradation, and the recruitment of immune cells via antibody-dependent cellular cytotoxicity (ADCC) to enhance anti-tumor activity (Source: ClinicalTrials.gov, NCT04394624). This dual-targeting strategy is particularly relevant for patients who have progressed on prior tyrosine kinase inhibitors or who exhibit MET-driven resistance (Source: PubMed, PMID: 34534445).

Other names

EGFR/METErbB-1/HGFRHER1/METErbB-1/MET

Simultaneous binding and inhibition of EGFR and c-MET signaling, induction of receptor degradation, and activation of antibody-dependent cellular cytotoxicity (ADCC).