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KRAS Inhibitor that Simultaneously Inhibits Nucleotide Exchange Activity and Effector Engagement
Journal article   Open access   Peer reviewed

KRAS Inhibitor that Simultaneously Inhibits Nucleotide Exchange Activity and Effector Engagement

CynthiaV Pagba, Amit K. Gupta, Ali K Naji, Dharini van der Hoeven, Kelly Churion, Xiaowen Liang, Jacob Jakubec, Magnus Hook, Yan Zuo, Marisela Martinez de Kraatz, …
ACS bio & med chem au, Vol.2(6), pp.617-626
12/21/2022
DOI: 10.1021/acsbiomedchemau.2c00045
PMCID: PMC10125367
PMID: 37101428
url
https://doi.org/10.1021/acsbiomedchemau.2c00045View
Published (Version of record) Open Access

Abstract

We describe a small molecule ligand ACA-14 (2-hydroxy-5-{[(2-phenyl-cyclopropyl) carbonyl] amino} benzoic acid) as an initial lead for the development of direct inhibitors of KRAS, a notoriously difficult anticancer drug target. We show that the compound binds to KRAS near the switch regions with affinities in the low micromolar range and exerts different effects on KRAS interactions with binding partners. Specifically, ACA-14 impedes the interaction of KRAS with its effector Raf and reduces both intrinsic and SOS-mediated nucleotide exchange rates. Likely as a result of these effects, ACA-14 inhibits signal transduction through the MAPK pathway in cells expressing mutant KRAS and inhibits the growth of pancreatic and colon cancer cells harboring mutant KRAS. We thus propose compound ACA-14 as a useful initial lead for the development of broad-acting inhibitors that target multiple KRAS mutants and simultaneously deplete the fraction of GTP-loaded KRAS while abrogating the effector-binding ability of the already GTP-loaded fraction.
Biochemistry & Molecular Biology Chemistry, Medicinal Life Sciences & Biomedicine Pharmacology & Pharmacy Science & Technology

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