| Literature DB >> 31085175 |
Bryan D Smith1, Michael D Kaufman1, Wei-Ping Lu1, Anu Gupta1, Cynthia B Leary1, Scott C Wise1, Thomas J Rutkoski1, Yu Mi Ahn1, Gada Al-Ani1, Stacie L Bulfer1, Timothy M Caldwell1, Lawrence Chun2, Carol L Ensinger1, Molly M Hood1, Arin McKinley3, William C Patt1, Rodrigo Ruiz-Soto1, Ying Su1, Hanumaiah Telikepalli1, Ajia Town3, Benjamin A Turner1, Lakshminarayana Vogeti1, Subha Vogeti1, Karen Yates1, Filip Janku4, Albiruni Ryan Abdul Razak5, Oliver Rosen1, Michael C Heinrich3, Daniel L Flynn6.
Abstract
Ripretinib (DCC-2618) was designed to inhibit the full spectrum of mutant KIT and PDGFRA kinases found in cancers and myeloproliferative neoplasms, particularly in gastrointestinal stromal tumors (GISTs), in which the heterogeneity of drug-resistant KIT mutations is a major challenge. Ripretinib is a "switch-control" kinase inhibitor that forces the activation loop (or activation "switch") into an inactive conformation. Ripretinib inhibits all tested KIT and PDGFRA mutants, and notably is a type II kinase inhibitor demonstrated to broadly inhibit activation loop mutations in KIT and PDGFRA, previously thought only achievable with type I inhibitors. Ripretinib shows efficacy in preclinical cancer models, and preliminary clinical data provide proof-of-concept that ripretinib inhibits a wide range of KIT mutants in patients with drug-resistant GISTs.Entities:
Keywords: GIST; KIT; PDGFRA; conformational switch control; imatinib; mastocytosis; regorafenib; resistance; ripretinib; sunitinib
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Year: 2019 PMID: 31085175 DOI: 10.1016/j.ccell.2019.04.006
Source DB: PubMed Journal: Cancer Cell ISSN: 1535-6108 Impact factor: 31.743