Selective LIM kinase 2 (LIMK2) inhibitor; inhibits cofilin phosphorylation in cells that overexpress LIMK2 but not LIMK1. Attenuates the growth of several cancer cell lines. Reduces phospho-cofilin levels and Panc-1 tumor size in a mouse xenograft model.
|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|
Preparing Stock Solutions
The following data is based on the product molecular weight 389.33. Batch specific molecular weights may vary from batch to batch due to solvent of hydration, which will affect the solvent volumes required to prepare stock solutions.
|Concentration / Solvent Volume / Mass||1 mg||5 mg||10 mg|
|0.5 mM||5.14 mL||25.69 mL||51.37 mL|
|2.5 mM||1.03 mL||5.14 mL||10.27 mL|
|5 mM||0.51 mL||2.57 mL||5.14 mL|
|25 mM||0.1 mL||0.51 mL||1.03 mL|
References are publications that support the biological activity of the product.
Rak et al (2014) Novel LIMK2 inhibitor blocks Panc-1 tumor growth in a mouse xenograft model. Oncoscience 1 39 PMID: 25593987
Mashiach-Farkash et al (2012) Computer-based identification of a novel LIMK1/2 inhibitor that synergizes with salirasib to destabilize the actin cytoskeleton. Oncotarget 3 629 PMID: 22776759
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Keywords: T 5601640, T 5601640 supplier, T5601640, Selective, LIMK2, inhibitors, inhibits, lim, kinases, antitumour, antitumor, cofilin, T56-LIMKi, LIMK, 5269, Tocris Bioscience
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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.