Hepatocyte growth factor receptor (c-Met), Proto-oncogene tyrosine-protein kinase Src (c-Src), Epidermal growth factor receptor (EGFR), and Receptor tyrosine-protein kinase erbB-2 (HER2) (c-Met, c-Src, EGFR, HER2)

This target profile comprises four distinct tyrosine kinases: the Hepatocyte Growth Factor Receptor (c-Met), the Proto-oncogene tyrosine-protein kinase Src (c-Src), the Epidermal Growth Factor Receptor (EGFR), and the Receptor tyrosine-protein kinase erbB-2 (HER2) [UniProt P08581, P12931, P00533, P04626]. These proteins are integral to intracellular signaling networks that govern essential cellular processes such as proliferation, differentiation, and survival [PubMed: 21460848]. EGFR and HER2 belong to the ErbB family of receptor tyrosine kinases (RTKs), while c-Met is an RTK activated by hepatocyte growth factor. c-Src is a non-receptor tyrosine kinase that frequently interacts with these RTKs to amplify downstream signaling and facilitate cross-talk between pathways [PubMed: 20889916]. In many cancers, such as non-small cell lung cancer (NSCLC) and breast cancer, these kinases are often overexpressed or mutated, driving oncogenesis. They are also frequently implicated in the development of resistance to targeted therapies, where one kinase may compensate for the inhibition of another through bypass signaling mechanisms [Nature Reviews Cancer, 2010]. Consequently, they are major focal points for therapeutic intervention using small-molecule kinase inhibitors and monoclonal antibodies, which aim to disrupt their enzymatic activity or ligand binding to halt tumor progression.

Other names

METHGFRSRCErbB1ErbB2NeuCD340HER-2/neuProto-oncogene c-Srcp60-Src

Tyrosine kinase inhibition (ATP-competitive inhibition)