The c-MET signalling pathway consists of the mesenchymal epithelial transition factor (c-MET) transmembrane tyrosine kinase receptor and its ligand hepatocyte growth factor (HGF) or scatter factor (SF). Binding of HGF/SF to c-MET activates downstream signalling pathways such as Rho, focal adhesion kinase (FAK) and PI3K. These pathways regulate cancer cell growth, survival angiogenesis, invasion and metastasis. Thus, prevention of c-MET dependent neoplastic processes may provide a means for managing invasive tumors of high metastatic potential. In fact, c-MET/HGF has evolved as an attractive target for the pharmaceutical industry.

At present, at least 16 different molecules including four antibodies are in clinical development and quite a number of projects are in preclinical development. The majority of approaches are directed at inhibiting the c-MET receptor tyrosine kinsase (RTK) by small molecules. The first generation of c-MET RTK inhibitors are dual- or multi-targeting c-MET inhibitors. These multi-target c-MET inhibitors are most advanced in clinical development with two projects in phase III. The next wave of c-MET inhibitors typically are ATP-competitive potent and highly selective c-MET inhibitors with lead compounds in phase II.

Related report:
Competitor Analysis: c-MET/HGF Inhibitors
 

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