Potent LIMK1/2 inhibitor (IC50 values are 0.3 and 1 nM at LIMK 1 and 2, respectively). Disrupts microtubule organization, inhibits cofilin phosphorylation and increases α-tubulin acetylation in vitro.
|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.
|Solvent||Max Conc. mg/mL||Max Conc. mM|
Preparing Stock Solutions
The following data is based on the product molecular weight 393.89. 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|
|1 mM||2.54 mL||12.69 mL||25.39 mL|
|5 mM||0.51 mL||2.54 mL||5.08 mL|
|10 mM||0.25 mL||1.27 mL||2.54 mL|
|50 mM||0.05 mL||0.25 mL||0.51 mL|
References are publications that support the biological activity of the product.
Charles et al (2015) Discovery, development, and SAR of aminothiazoles as LIMK inhibitors with cellular anti-invasive properties. J.Med.Chem. 58 8309 PMID: 26356364
Mardilovich et al (2015) LIM kinase inhibitors disrupt mitotic microtubule organization and impair tumor cell proliferation. Oncotarget. 6 38469 PMID: 26540348
If you know of a relevant reference for CRT 0105950, please let us know.
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Keywords: CRT 0105950, CRT 0105950 supplier, CRT0105950, LIMK2, LIMK1, inhibitors, inhibits, lim, kinases, antitumour, antitumor, cofilin, microtubules, LIMK, Microtubules, 6273, 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.