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. Author manuscript; available in PMC: 2021 Sep 27.
Published in final edited form as: Structure. 2017 Aug 3;25(9):1442–1448.e3. doi: 10.1016/j.str.2017.07.003

Figure 2. KRAS G12C-1 and KRAS G12C-ARS-632 Both Show Enhanced Thermal Stability and Similar in Potency for Inhibition of KRAS G12C-Depenent MAPK Signaling in H358 Cells.

Figure 2.

(A) Raw DSF measurements for KRAS G12C fully labeled with either ARS-632 or 1.

(B) First derivative of (A) shows the shifts in Tm (dashed vertical lines) associated with protein labeling.

(C) Impact of compound exposure on MAPK signaling. Levels of pERK were evaluated in the KRAS-G12C-containing cancer cell line H358 as a surrogate for RAS signaling through the MAPK pathway. Cells were treated with compound 1 or ARS-632 as indicated for 6 hr. Phosphorylation of ERK1/2 was determined by immunoblotting.