癌症研究
化学
癌基因
信号转导
基因
医学
生物化学
细胞周期
作者
Erin Sheffels,Robert L. Kortum
标识
DOI:10.1021/acs.jmedchem.1c00698
摘要
In RTK/RAS-mutated cancers, therapeutic resistance is driven by rebound activation of multiple RTKs; broad inhibition of RTK signaling can potentially delay therapeutic resistance for a majority of patients. A new SOS1 inhibitor, BI-3406, broadly inhibits proximal RTK signaling will greatly expand the efficacy of therapies used to treat RTK/RAS-mutated cancers.
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