Direct targeting of KRAS through the Switch-II pocket is an effective therapeutic strategy, but acquired resistance limits clinical benefit. We examine clinically observed resistance mutations (R68S, H95Q, Y96C, Y96D and Q99L) arising during KRAS G12C inhibitor therapy using biochemical, structural, computational and...
M. J. Whitley, M. Dyba, Mayukh Chakrabarti et al.· Nature Communications· 0 citations
We use cookies to run the site and, with your consent, for analytics and to show ads.
See our Cookie Policy.