| c-Met (MET or mesenchymal-epithelial transition factor) is a prototype member of a subfamily of heterodimeric receptor tyrosine kinases (RTKs) and is the receptor for hepatocyte growth factor (HGF). MET can be activated through ligand-dependent or ligand-independent mechanisms. Binding of HGF to the MET extracellular domain results in receptor multimerization, phosphorylation, and activation of MET-dependent signal transduction inside the cell. Activation of the MET receptor leads to the activation of downstream signals, including the mitogen-activated protein kinase (ERK/ MAPK) and phosphatidylinositol 3-kinase (PI3K/AKT) pathways, STAT3, and RAS. Dysregulated HGF/c-Met signaling is a driving factor for several malignancies and promotes tumor growth, invasion, dissemination and angiogenesis. Dysregulated HGF/c-Met signaling has also been associated with poor clinical outcomes and resistance acquisition to some approved targeted therapies. Thus, c-Met kinase has emerged as a promising target for cancer drug development. Different therapeutic approaches targeting the HGF/c-Met signaling pathway are under development for targeted cancer therapy, among which small molecule inhibitors of c-Met kinase constitute the largest effort within the pharmaceutical industry. BioVision is proud to offer several structurally diverse small molecule c-Met kinase inhibitors for research. |
