C-Met inhibitor

rdf:langString C-Met inhibitor

rdf:langString SND: structure not disclosed; RON: Recepteur d'origine nantais ALK: Anaplastic lymphoma kinase; VEGFR2: Vascular-Endothelial Growth Factor Receptor 2; MiT: microphthalmia transcription factor tumors; PDAC: pancreatic ductal adenocarcinoma; NSCLC: non-small cell lung carcinoma; HCC: hepatocellular carcinoma; MTC: medullary thyroid carcinoma; GBM: glioblastoma; RCC: renal cell carcinoma; HNSCC: head and neck squamous cell cainoma; IND: Investigational New Drug.

rdf:langString Current status in c-met inhibitors 2010.tif

rdf:langString c-Met inhibitors are a class of small molecules that inhibit the enzymatic activity of the c-Met tyrosine kinase, the receptor of hepatocyte growth factor/scatter factor (HGF/SF). These inhibitors may have therapeutic application in the treatment of various types of cancers. Many c-Met inhibitors are currently in clinical trials. Crizotinib and cabozantinib were the first to be approved by the U.S. FDA. Crizotinib received accelerated approval in 2011 for the treatment of patients with locally advanced or metastatic non-small cell lung cancer, while cabozantinib was approved in 2012 for the treatment of medullary thyroid cancer and it has also started clinical trials for the treatment of several other types of cancer. c-Met stimulates cell scattering, invasion, protection from apoptosis and angiogenesis. c-Met is a receptor tyrosine kinase, which can cause a wide variety of different cancers, such as renal, gastric and small cell lung carcinomas, central nervous system tumours, as well as several sarcomas when its activity is dysregulated. Targeting the ATP binding site of c-Met by small molecules inhibitors is one strategy for inhibition of the tyrosine kinase.