Cell-permeable cyclin-dependent kinase inhibitor. IC50 values are 0.033, 0.033, 0.028 and 0.020 μM for cdk1/cyclin B, cdk2/cyclin A, cdk2/cyclin E, and cdk5/p35 respectively. Inhibits ERK1 (IC50 = 12.0 μM) and ERK2 (IC50 = 3.1 μM) and is 3000-fold selective over a range of other protein kinases (IC50 > 100 μM). Arrests cell cycle at G2/M boundary (IC50 = 1.25 μM), and induces apoptosis at concentrations > 10 μM.
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|Storage||Store at +4°C|
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 403.91. 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||2.48 mL||12.38 mL||24.76 mL|
|5 mM||0.5 mL||2.48 mL||4.95 mL|
|10 mM||0.25 mL||1.24 mL||2.48 mL|
|50 mM||0.05 mL||0.25 mL||0.5 mL|
References are publications that support the products' biological activity.
Chang et al (1999) Synthesis and application of functionally diverse 2,6,9-trisubstituted purine libraries as CDK inhibitors. Chem.Biol. 6 361 PMID: 10375538
Knockaert et al (2000) Intracellular targets of cyclin-dependent kinase inhibitors: identification by affinity chromatography using immobilised inhibitors. Chem.Biol. 7 411 PMID: 10873834
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Keywords: Aminopurvalanol A, supplier, Cyclin-dependent, protein, kinases, inhibitors, inhibits, Cdk, AminopurvalanolA, NG97, NG, 97, Cyclin-dependent, Kinase, Cyclin-dependent, Kinase, Tocris Bioscience
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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.