CGP 74514 dihydrochloride
Potent cdk1 inhibitor (IC50 = 25 nM). Reduces Akt phosphorylation and increases mitochondrial damage in leukemia cells in vitro in combination with LY 294002.
|Storage||Desiccate at RT|
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
All Tocris products are intended for laboratory research use only.
|Solvent||Max Conc. mg/mL||Max Conc. mM|
Preparing Stock Solutions
The following data is based on the product molecular weight 458.82. 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||2.18 mL||10.9 mL||21.8 mL|
|5 mM||0.44 mL||2.18 mL||4.36 mL|
|10 mM||0.22 mL||1.09 mL||2.18 mL|
|50 mM||0.04 mL||0.22 mL||0.44 mL|
The reconstitution calculator allows you to quickly calculate the volume of a reagent to reconstitute your vial. Simply enter the mass of reagent and the target concentration and the calculator will determine the rest.
References are publications that support the products' biological activity.
Yu et al (2013) The lethal effects of pharmacological cyclin-dependent kinase inhibitors in human leukemia cells proceed through a phosphatidylinositol 3-kinase/Akt-dependent process. Cancer Res. 63 1822 PMID: 12702569
Furet et al (2000) Structure-based design of potent CDK1 inhibitors derived from olomoucine. J.Comput.Aided Mol.Des. 14 403 PMID: 10896313
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Keywords: CGP74514 dihydrochloride cyclin dependent kinase inhibitors inhibits CDK1 Cyclin-dependent Kinase
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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.