Article
Abrogation of Oncogenic RAS Signaling by a RAS(ON) Inhibitor Doublet Primes Immune-Refractory KRASG12C-Mutant NSCLC for Immune Checkpoint Blockade.
Cancer discovery - 1 Jun 2026
Wei Xing, Blaj Cristina, Ali Al-Radhawi M, Lai Lick Pui, Maldonato Benjamin J, Yang Yu Chi, Seu Lillian, Gundlapalli Harika, Jiang Lingyan, Moreno Ayala Mariela A, Spradlin Jessica N, Garrick Brett, Cai Shurui, Salmon Avery, Pham Anna, Bredeson Sean, Liang Rich, Helland Ciara, Evans James W, Labrecque Mark P, Yu Xinxing, Song Avian Hyun Joo, Dinglasan Nuntana, Tran Linh, Kumamoto Alice, Grigoryan Lilit, Malliri Angeliki, Brown Katherine D, Carter Mathew, Simpson Kathryn L, Crosbie Philip A, Galvin Melanie, Chang Stephanie, Huang Yue, Tovbis Shifrin Nataliya, Pechuan-Jorge Ximo, Raghulan Rashi, Zhuang Yongxian, Coles Darryl I, Dive Caroline, Aronchik Ida, Holderfield Matthew, Lindsay Colin R, Wang Zhengping, Wang Zhican, Singh Mallika, Smith Jacqueline A M, Jiang Jingjing, Quintana Elsa
Abstract excerpt
To address RAS pathway hyperactivation and targeted therapy resistance in KRASG12C-mutant non-small cell lung cancer (NSCLC), we evaluated the potential of the RAS(ON) G12C-selective covalent inhibitor elironrasib and the RAS(ON) multi-selective inhibitor daraxonrasib combination to maximize RAS pathway suppression and forestall pathway reactivation in a series of preclinical models. We demonstrate that the...
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