Potent, selective inhibitor of cyclin-dependent kinases (cdk). Inhibits cdc2/cyclin B (IC50 = 650 nM), cdk2/cyclin A (IC50 = 700 nM), cdk2/cyclin E (IC50 = 700 nM), cdk5 / p35 (IC50 = 160 nM) and is selective over cdk4/cyclin D1 and cdk6/cyclin D3 (IC50 > 100 μM). Also selective over a wide range of related kinases including ERK1 and ERK2. Arrests L1210 cells in G1 phase. Inhibits phosphorylation of vimentin in vivo. Antimitotic.
|Storage||Store at -20°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 354.45. 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||2.82 mL||14.11 mL||28.21 mL|
|5 mM||0.56 mL||2.82 mL||5.64 mL|
|10 mM||0.28 mL||1.41 mL||2.82 mL|
|50 mM||0.06 mL||0.28 mL||0.56 mL|
References are publications that support the products' biological activity.
De Azevedo et al (1997) Inhibition of cyclin-dependent kinases by purine analogues. Eur.J.Biochem. 243 518 PMID: 9030780
Meijer (1996) Chemical inhibitors of cyclin-dependent kinases. Trends Cell.Biol. 6 393 PMID: 15157522
Meijer et al (1997) Biochemical and cellular effects of roscovitine, a potent and selective inhibitor of the cyclin-dependent kinases cdc2, cdk2 and cdk5. Eur.J.Biochem. 243 527 PMID: 9030781
If you know of a relevant reference for Roscovitine, please let us know.
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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.