SAH-SOS1A TFA |
| رقم الكتالوجGC62034 |
SAH-SOS1A TFA هو مثبط تفاعل البروتين SOS1 / KRAS القائم على الببتيديرتبط SAH-SOS1A TFA بـ KRAS من النوع البري والمتحور (G12D و G12V و G12C و G12S و Q61H) مع تقارب نانومولار (EC50 = 106-175 نانومتر)يقوم SAH-SOS1A TFA بحظر ارتباط النوكليوتيدات بشكل مباشر ومستقليضعف SAH-SOS1A TFA قابلية بقاء الخلايا السرطانية التي يقودها KRAS ويمارس آثاره من خلال الحصار المفروض على آلية سلسلة إشارات الفسفوز ERK-MAPK في اتجاه مجرى KRAS
Products are for research use only. Not for human use. We do not sell to patients.
Sample solution is provided at 25 µL, 10mM.
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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), directly and independently blocks nucleotide association, impairs KRAS-driven cancer cell viability, and exerts its effects by on-mechanism blockade of the ERK-MAPK phosphosignaling cascade downstream of KRAS[1].
SAH-SOS1A (0.625-40 μM; 24 hours) dose-responsively impairs the viability of cancer cells bearing G12D, G12C, G12V, G12S, G13D, and Q61H mutations with IC50 values in the 5- to 15-μM range. Cancer cells expressing wild-type KRAS, such as HeLa and Colo320-HSR cells, are similarly affected[1].SAH-SOS1A (5-40 μM; 4 hours) dose-responsively inhibits MEK1/2, ERK1/2, and AKT phosphorylation[1].
SAH-SOS1A (0.2 μL of 10 mM solution; injection; 48 hours; abdomens of D. melanogaster Ras85DV12/ActinGS) treatment notably decreases the phosphorylation state of ERK1/2[1].
[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.
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