SAH-SOS1A

发表于由

SAH-SOS1A;

SAH-SOS1A 是一种基于肽的 SOS1/KRAS 蛋白相互作用抑制剂。SAH-SOS1A 以纳摩尔亲和力 (EC50=106-175 nM) 与野生型和突变型 KRAS (G12D, G12V, G12C, G12S, and 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。

SAH-SOS1Aamp;;

SAH-SOS1A Chemical Structure

CAS No. : 1652561-87-9

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SAH-SOS1A 的其他形式现货产品:

SAH-SOS1A TFA

生物活性

SAH-SOS1A is a peptide-based SOS1/KRAS protein interaction inhibitor. SAH-SOS1A 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].

IC50 Target[1]

KRAS-SOS1

;

KRas G12C

140 nM (EC50)

KRas G12D

109 nM (EC50)

KRas G12V

154 nM (EC50)

KRas G12S

155 nM (EC50)

KRas Q61H

175 nM (EC50)

K-Ras WT

106 nM (EC50)

体外研究
(In Vitro)

SAH-SOS1A (0.625-40 μM) 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].

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

Cell Viability Assay[1]

Cell Line: Panc 10.05 cells bearing the KRAS G12D mutation
Concentration: 0.625-40 μM
Incubation Time: 24 hours
Result: Dose-responsively impaired the viability of cancer cells bearing KRAS G12D.

Western Blot Analysis[1]

Cell Line: Panc 10.05 cells
Concentration: 5-40 μM
Incubation Time: Indicated doses for 4 h, followed by 15-min stimulation with EGF
Result: Dose-responsively inhibited MEK1/2, ERK1/2, and AKT phosphorylation.

体内研究
(In Vivo)

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].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.
分子量

2187.53

Formula

C100H159N27O28
CAS 号

1652561-87-9
Sequence Shortening

RRFFGI{Aaa}LTN{Aaa}LKTEEGN (Covalent bridge:Aaa7-Aaa11)
运输条件

Room temperature in continental US; may vary elsewhere.
储存方式

Please store the product under the recommended conditions in the Certificate of Analysis.
参考文献

  • [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.