Fig. 1: Active-state KRASG12C inhibitors inhibit ERK pathway output more potently and durably than inactive-state KRASG12C inhibitors.
From: Combined inhibition of KRASG12C and mTORC1 kinase is synergistic in non-small cell lung cancer
Cell viability data of KRASG12C mutant cell lines following treatment with (a) inactive-state KRASG12C inhibitors or (b) active-state KRASG12C inhibitors for 72 h. Data are the mean ± SD of n = 8 experimental replicates. c LU65 and H23 cell lines were treated with 100 nM Adagrasib or 100 nM RM-018 for the indicated times and lysates were analyzed by immunoblot. In parallel, the amount of active GTP-bound KRAS was determined by a RAS-GTP pulldown assay. d The mRNA expression of the indicated target genes was determined by quantitative PCR in LU65 and H23 cell lines following 100 nM Adagrasib or 100 nM RM-018 treatment for the indicated times. The data shown represent the means ± SD of n = 3 experimental replicates. P values are shown and were calculated by two-sided t test.
