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  • SAH-SOS1A TFA
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SAH-SOS1A TFA

SAH-SOS1A TFA 是一种基于肽的 SOS1/KRAS 蛋白相互作用抑制剂。SAH-SOS1A TFA 以纳摩尔亲和力 (EC50=106-175 nM) 与野生型和突变型 KRAS (G12D, G12V, G12C, G12S, Q61H) 结合,直接和独立地阻断核苷酸结合,损害 KRAS 驱动的癌细胞活力,并通过阻断 KRAS 下游 ERK-MAPK 磷酸化信号级联的机制发挥作用。

原价
¥4525-7550
价格
3620-6040
SAH-SOS1A TFA的二维码

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  • 库存: 现货
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  • 货号: ajcx32930
  • CAS: N/A
  • 别名:
  • 分子式: C102H160N27F3O30
  • 分子量: 2301.55
  • 纯度: >98%
  • 溶解度:
  • 储存: Store at -20°C, protect from light, stored under nitrogen
  • 库存: 现货

Background

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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