Description

SAH-SOS1A TFA is a peptide-based SOS1/KRAS protein interaction inhibitor. SAH-SOS1A TFA binds to wild-type and mutant KRAS (G12D, G12V, G12C, G12S, and Q61H) with nanomolar affinity (EC50=106-175 nM). SAH-SOS1A TFA directly and independently blocks nucleotide association. SAH-SOS1A TFA impairs KRAS-driven cancer cell viability and exerts its effects by on-mechanism blockade of the ERK-MAPK phosphosignaling cascade downstream of KRAS[1].–80°C, 2 years; -20°C, 1 year (Powder, sealed storage, away from moisture and light, under nitrogen)–Cancer-Kinase/protease–C102H160N27F3O30—-[1]Leshchiner ES, et al. Direct inhibition of oncogenic KRAS by hydrocarbon-stapled SOS1 helices. Proc Natl Acad Sci U S A. 2015;112(6):1761-1766.–2896737-31-6–2301.55–99.16–C[C@]1(C(N[C@H](C(N[C@@](C(N[C@H](C(N[C@@](C)(CCC/C=C/CCC1)C(N[C@@H](CC(C)C)C(N[C@@H](CCCCN)C(N[C@@H]([C@H](O)C)C(N[C@@H](CCC(O)=O)C(N[C@@H](CCC(O)=O)C(NCC(N[C@H](C(O)=O)CC(N)=O)=O)=O)=O)=O)=O)=O)=O)=O)CC(N)=O)=O)([H])[C@H](O)C)=O)CC(C)C)=O)NC([C@H]([C@@H](C)CC)NC(CNC([C@H](CC2=CC=CC=C2)NC([C@@H](NC([C@H](CCCNC(N)=N)NC([C@@H](NC(C)=O)CCCNC(N)=N)=O)=O)CC3=CC=CC=C3)=O)=O)=O)=O.OC(C(F)(F)F)=O–Cancer–H2O : 33.33 mg/mL (ultrasonic)–Ras–K-Ras–GPCR/G Protein;MAPK/ERK Pathway–Peptides