You can now submit reviews for your favorite Tocris products. Your review will help other researchers decide on the best products for their research. Why not submit a review today?!Submit Review
Cyclin-dependent kinase (cdk) inhibitor (reported IC50 values are 6 nM for cdk1 and cdk5, and 6 - 9 nM for cdk2, depending on binding partner). Selective over a range of other protein kinases (IC50 >10,000 nM). Shown to have antiproliferative properties, mediated by ERK1 and ERK2.
Sold under license from the Regents of the University of California
|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|
|1eq. NaOH||43.29||100 with gentle warming|
Preparing Stock Solutions
The following data is based on the product molecular weight 432.91. 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||2.31 mL||11.55 mL||23.1 mL|
|5 mM||0.46 mL||2.31 mL||4.62 mL|
|10 mM||0.23 mL||1.15 mL||2.31 mL|
|50 mM||0.05 mL||0.23 mL||0.46 mL|
References are publications that support the biological activity of the product.
Gray et al (1998) Exploiting chemical libraries, structure, and genomics in the search for kinase inhibitors. Science 281 533 PMID: 9677190
Gray et al (1999) ATP-site directed inhibitors of cyclin-dependent kinases. Curr.Med.Chem. 6 859 PMID: 10495356
Knockaert et al (2002) p42/p44 MAPKs are intracellular targets of the CDK inhibitor purvalanol. Oncogene 21 6413 PMID: 12226745
Jorda et al (2018) How selective are pharmacological inhibitors of cell-cycle-regulating cyclin-dependent kinases? J.Med.Chem. 61 9105 PMID: 30234987
If you know of a relevant reference for Purvalanol B, please let us know.
View Related Products by Product Action
Keywords: Purvalanol B, Purvalanol B supplier, Cyclin-dependent, protein, kinases, inhibitors, inhibits, Cdk, PurvalanolB, NG95, potent, cdk1, cdk2, cdk5, selective, NG, 95, Kinase, 1581, Tocris Bioscience
3 Citations for Purvalanol B
Citations are publications that use Tocris products. Selected citations for Purvalanol B include:
Wissing et al (2007) Proteomics analysis of protein kinases by target class-selective prefractionation and tandem mass spectrometry. J Pharmacol Exp Ther 6 537 PMID: 17192257
Ma et al (2019) Characterization of the Src-regulated kinome identifies SGK1 as a key mediator of Src-induced transformation. Nat Commun 10 296 PMID: 30655532
Schreiber et al (2010) An integrated phosphoproteomics work flow reveals extensive network regulation in early lysophosphatidic acid signaling. Mol Cell Proteomics 9 1047 PMID: 20071362
Do you know of a great paper that uses Purvalanol B from Tocris? Please let us know.
Reviews for Purvalanol B
There are currently no reviews for this product. Be the first to review Purvalanol B and earn rewards!
Have you used Purvalanol B?
Submit a review and receive an Amazon gift card.
$50/€35/£30/$50CAN/¥300 Yuan/¥5000 Yen for first to review with an image
$25/€18/£15/$25CAN/¥75 Yuan/¥1250 Yen for a review with an image
$10/€7/£6/$10 CAD/¥70 Yuan/¥1110 Yen for a review without an image
Literature in this Area
Tocris offers the following scientific literature in this area to showcase our products. We invite you to request* or download your copy today!
*Please note that Tocris will only send literature to established scientific business / institute addresses.
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.