c-RET
The c-RET proto-oncogene, which was originally identified as a transforming gene by transfection of T-cell lymphoma DNA into NIH3T3 cells, is a member of the receptor tyrosine kinase (RTK) gene superfamily that encodes a receptor tyrosine kinase involved in the regulation of glial cell line-derived neurotrophic factor (GDNF) signaling. Signaling proteins, such as Grb7/Grb10, PLCγ, Shc/Enigma and Grb2, are recruited by activated c-RET protein through binding to the phosphorylated tyrosine residues in c-RET protein’s COOH-terminal sequence, Y905, Y1015, Y1062 and Y1096 respectively. Moreover, results of in vivo studies suggest mutations of c-RET have been implicated in tumorigenesis, in which c-RET mRNA and/or protein have been found in tumors of neuroectodermal origin as well as in human neuroblastoma cell lines.
- A8236 Regorafenib4 CitationTarget: Raf|VEGFR|PDGFR|c-Kit|RETSummary: Inhibitor of VEGFR/PDGFR/FGFR/mutant kit/RET/Raf-1
- C3080 AD57 (hydrochloride)Summary: polypharmacological cancer therapeutic that inhibits RET.
- C4239 RPI-1Summary: ATP-dependent RET kinase inhibitor
- A4145 TG101209Summary: JAK2/3 inhibitor
- A4116 Danusertib (PHA-739358)2 CitationTarget: Aurora KinasesSummary: Pan-aurora kinase inhibitor
- A4237 Amuvatinib (MP-470, HPK 56)Summary: Tyrosine kinase inhibitor
- A3750 Regorafenib hydrochlorideTarget: Raf|VEGFR|PDGFR|c-Kit|c-RETSummary: Tyrosine kinase inhibitor
- A3751 Regorafenib monohydrateSummary: Tyrosine kinase inhibitor
- A3847 SU5416Target: VEGFRSummary: VEGF receptor inhibitor and AHR agonist