Inhibition of ULK1/2 and KRAS controls tumor growth in preclinical models of lung cancer.

Mutational activation of occurs commonly in lung carcinogenesis and, with the recent U.S. Food and Drug Administration approval of covalent inhibitors of KRAS such as sotorasib or adagrasib, KRAS oncoproteins are important pharmacological targets in non-small cell lung cancer (NSCLC).

Inhibition of ULK1/2 and KRAS controls tumor growth in preclinical models of lung cancer.

Mutational activation of occurs commonly in lung carcinogenesis and, with the recent FDA approval of covalent inhibitors of KRAS such as sotorasib or adagrasib, KRAS oncoproteins are important pharmacological targets in non-small cell lung cancer (NSCLC). However, not all KRAS -driven NSCLCs respond to these inhibitors, and the emergence of drug resistance in those patients that do respond can be rapid and pleiotropic. Hence, based on a backbone of covalent inhibition of KRAS , efforts are underway to develop effective combination therapies.