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Fendiline Hydrochloride is a K-Ras inhibitor. Selectively inhibits K-Ras localization to the plasma membrane (IC50 = 9.64 μM). Blocks proliferation of cancer cell lines expressing oncogenic mutant K-Ras. Also inhibits L-type calcium channels (IC50 = 17 μM).
Fendiline Hydrochloride is also offered as part of the Tocriscreen 2.0 Max. Find out more about compound libraries available from Tocris.
|Storage||Store at +4°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.
|Solvent||Max Conc. mg/mL||Max Conc. mM|
The following data is based on the product molecular weight 351.91. 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||2.84 mL||14.21 mL||28.42 mL|
|5 mM||0.57 mL||2.84 mL||5.68 mL|
|10 mM||0.28 mL||1.42 mL||2.84 mL|
|50 mM||0.06 mL||0.28 mL||0.57 mL|
References are publications that support the biological activity of the product.
Tripathi et al (1993) Fendiline inhibits L-type calcium channels in guinea-pig ventricular myocytes: a whole-cell patch-clamp study. Br.J.Pharmacol. 108 865 PMID: 8485628
van der Hoeven et al (2015) Fendiline inhibits K-Ras plasma membrane localization and blocks K-Ras signal transmission. Mol.Cell.Biol. 33 237 PMID: 23129805
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Keywords: Fendiline Hydrochloride, Fendiline Hydrochloride supplier, K-Ras, membrane, localization, inhibitors, inhibits, L-type, calcium, channel, Ca2+, voltage-gated, Cav, blockers, blocks, Cav1.x, Channels, Ras, GTPases, 6407, Tocris Bioscience
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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.
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.
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.
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.