YF135

YF135 (Multiple concentrations; 72 h) potently and selectively inhibits the proliferation of KRAS^G12C-mutant H358 (IC₅₀ = 153.9 nM) and H23 (IC₅₀ = 243.9 nM) lung cancer cells, but does not inhibit proliferation of KRAS^G12S-mutant A549 lung cancer cells^[1].
YF135 (0.3-30 μM; 12-36 h) induces time- and dose-dependent degradation of endogenous KRAS^G12C and reduction of p-ERK signaling in KRAS^G12C-mutant H358 (DC₅₀ = 3.61 μM for KRAS degradation) and H23 (DC₅₀ = 4.53 μM for KRAS degradation) lung cancer cells, with no activity in KRAS^G12S-mutant A549 lung cancer cells or evidence of a hook effect at high concentrations^[1].
YF135 (3 μM) mediated degradation of KRAS^G12C and reduction of p-ERK signaling in KRAS^G12C-mutant H358 and H23 lung cancer cells is dependent on the proteasome pathway^[1].
YF135 (3 μM; 12-24 h) induces reversible degradation of KRAS^G12C and reduction of p-ERK signaling in KRAS^G12C-mutant H358 and H23 lung cancer cells, as evidenced by recovery of protein levels following compound washout even in the absence of new protein synthesis^[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.