c-MET / HGFR - SPR Binding Assay

Our service for comprehensive kinetic characterization of your small molecule kinase inhibitors

Theoretical background: c - MET (Mesenchymal epithelial transition factor), also known as hepatocyte growth factor receptor (HGFR) is a receptor tyrosine kinase. The endogenous ligand for c - MET is hepatocyte growth factor/scatter factor (HGF), a disulfide-linked heterodimeric molecule produced predominantly by mesenchymal cells. Ligand-dependent activation of c - MET results in cell proliferation, migration and matrix invasion. These activities facilitate epithelial cell transformation and malignant progression. Thus, abberant activation of the HGF / c - MET pathway leads to a variety of cancers. Amplification of c - MET was also identified as a  mechanism of drug resistance in lung cancer patients initially responsive to the EGFR kinase inhibitors Gefitinib or Erlotinib.


c-MET and inhibitors: SU11274 targets the ATP - binding site of wild type c - MET (IC50 = 20 nM [1]) resulting in an inhibiton of kinase downstream signaling whereas several c - MET mutant forms are resistant to inhibition. AM7, interacting with c - MET in a different binding mode, can bind both the inactive and active form (IC50 = 17 nM [2]) and shows activity against a panel of c - MET mutations found in cancer patients. Crizotinib / PF-2341066 , a multitargeted receptor tyrosine kinase inhibitor, primarily synthesized as ATP - competitive inhibitor for c - MET (IC50 = 11 nM [3]) and ALK is still undergoing clinical trials.

Figure: Real-time kinetic analysis of kinase inhibitor Erlotinib binding to c-MET using surface plasmon resonance.

[1] Sattler M et al.
(2003) Cancer Res. 63(17):5462-9

[2] Bellon SF et al. (2008) J Biol Chem. 283(5):2675-83.

[3] Marion Z et al. (2010) Neoplasia. 12(1): 1–10


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