突变体
化学
表皮生长因子受体
表皮生长因子受体抑制剂
体内
野生型
酪氨酸激酶
肺癌
癌症研究
突变
药理学
受体
生物化学
生物
肿瘤科
医学
基因
遗传学
作者
Benjamin C. Milgram,Deanna R. Borrelli,Natasja Brooijmans,Jack A. Henderson,Brendan Hilbert,Michael R. Huff,Takahiro Ito,Erica L. Jackson,Philip Jonsson,Brendon Ladd,Erin O’Hearn,Raymond Pagliarini,Simon Roberts,Sébastien Ronseaux,Darrin D. Stuart,Weixue Wang,Angel Guzman-Perez
标识
DOI:10.1021/acs.jmedchem.4c02377
摘要
After L858R and ex19del epidermal growth factor receptor (EGFR) mutations, ex20ins mutations are the third most common class of driver-mutations in non-small cell lung cancer (NSCLC). Unfortunately, first-, second-, and third-generation EGFR tyrosine kinase inhibitors (TKIs) are generally ineffective for ex20ins patients due to insufficient mutant activity and selectivity over wild-type EGFR, leading to dose-limiting toxicities. While significant advances in recent years have been made toward identifying potent EGFR ex20ins mutant inhibitors, mutant vs wild-type EGFR selectivity remains a significant challenge. STX-721 (53) is a potent, irreversible inhibitor of the majority of EGFR/HER2 ex20ins mutants and demonstrates excellent mutant vs wild-type selectivity both in vitro and in vivo. STX-721 is currently in phase 1/2 clinical trials for EGFR/HER2 ex20ins-driven NSCLC.
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