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Biological Activity for Salirasib
Salirasib is an inhibitor of active Ras proteins. Displaces active Ras from the plasma membrane; impairs downstream signaling and inhibits proliferation of endometrial carcinoma cells. Also facilitates Ras degradation. Shown to induce autophagy in several human cancer cell lines.
Technical Data for Salirasib
|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 Data for Salirasib
|Solvent||Max Conc. mg/mL||Max Conc. mM|
Preparing Stock Solutions for Salirasib
The following data is based on the product molecular weight 358.54. Batch specific molecular weights may vary from batch to batch due to the degree of hydration, which will affect the solvent volumes required to prepare stock solutions.
|Concentration / Solvent Volume / Mass||1 mg||5 mg||10 mg|
|1 mM||2.79 mL||13.95 mL||27.89 mL|
|5 mM||0.56 mL||2.79 mL||5.58 mL|
|10 mM||0.28 mL||1.39 mL||2.79 mL|
|50 mM||0.06 mL||0.28 mL||0.56 mL|
References for Salirasib
References are publications that support the biological activity of the product.
Schmukler et al (2013) Ras inhibition enhances autophagy, which partially protects cells from death. Oncotarget 4 142 PMID: 23370967
Faigenbaum et al (2013) Growth of poorly differentiated endometrial carcinoma is inhibited by combined action of medroxyprogesterone acetate and the Ras inhibitor Salirasib. Oncotarget 4 316 PMID: 23530112
Haklai et al (1998) Dislodgement and accelerated degradation of Ras. Biochemistry 37 1306 PMID: 9477957
If you know of a relevant reference for Salirasib, please let us know.
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Keywords: Salirasib, Salirasib supplier, Ras, inhibitors, inhibits, induces, autophagy, Autophagy, GTPases, 4989, Tocris Bioscience
2 Citations for Salirasib
Citations are publications that use Tocris products. Selected citations for Salirasib include:
Lee et al (2015) A systems-biological study on the identification of safe and effective molecular targets for the reduction of ultraviolet B-induced skin pigmentation. J Virol 5 10305 PMID: 25980672
Li et al (2018) Is Ras a potential target in treatment against cutaneous squamous cell carcinoma?. J Cancer 9 3373 PMID: 30271499
Do you know of a great paper that uses Salirasib from Tocris? Please let us know.
Reviews for Salirasib
Average Rating: 5 (Based on 1 Review.)
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Human osteosarcoma cells were incubated with 20 μM Salirasib for 30 min prior to treatment with 10 μM LPA to estimate COX-2 expression using Western blot analysis. Salirasib abolished LPA-induced COX-2 expression.
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.