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KRas/son of sevenless 1 (SOS1) interaction inhibitor. Binds within nucleotide binding pocket of KRas (Kd values are 106 - 176 nM for wild type KRas and various KRas mutants). Inhibits nucleotide binding to KRas in a concentration dependent manner. Displays cytotoxicity in KRas-driven cancer cell lines and inhibits downstream ERK-MAPK signaling. Cell permeable.
Sold under license from Dana-Farber Cancer Institute
(Modifications: Arg-1 = N-terminal Ac, X = (S)-2-(4-pentenyl)alanine, X-7 and X-11 stapled together with a double bond)
|Storage||Store at -20°C|
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.
|Solubility||Soluble to 1 mg/ml in water|
References are publications that support the biological activity of the product.
Leshchiner et al (2015) Direct inhibition of oncogenic KRAS by hydrocarbon-stapled SOS1 helices. Proc.Natl.Acad.Sci.USA. 112 1761 PMID: 25624485
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Keywords: SAH-SOS1A, SAH-SOS1A supplier, Dual, SOS1, KRAS, inhibitors, inhibits, cytotoxicity, stabilized, alpha, helices, of, son, sevenless, 1, stapled, peptides, Ras, GTPases, Stapled, Peptides, 6920, Tocris Bioscience
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Literature in this Area
Tocris offers the following scientific literature in this area to showcase our products. We invite you to request* your copy today!
*Please note that Tocris will only send literature to established scientific business / institute addresses.
RAS Oncoproteins Scientific Review
Written by Kirsten L. Bryant, Adrienne D. Cox and Channing J. Der, this review provides a comprehensive overview of RAS protein function and RAS mutations in cancer. Key signaling pathways are highlighted and therapeutic vulnerabilities are explored. This review also includes a detailed section on RAS drug discovery and targeting synthetic lethal interactors of mutant RAS. Compounds available from Tocris are listed.
Cell Cycle & DNA Damage Repair Poster
In normal cells, each stage of the cell cycle is tightly regulated, however in cancer cells many genes and proteins that are involved in the regulation of the cell cycle are mutated or over expressed. Adapted from the 2015 Cancer Product Guide, Edition 3, this poster summarizes the stages of the cell cycle and DNA repair. It also highlights strategies for enhancing replicative stress in cancer cells to force mitotic catastrophe and cell death.
Epigenetics in Cancer Poster
Adapted from the 2015 Cancer Product Guide Edition 3, this poster summarizes the main epigenetic targets in cancer. The dysregulation of epigenetic modifications has been shown to result in oncogenesis and cancer progression. Unlike genetic mutations, epigenetic alterations are considered to be reversible and thus make promising therapeutic targets.