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Potent and selective ATP-competitive CDK9 inhibitor (IC50 = 0.5 nM). Exhibits selectivity for CDK9 over a panel of 468 kinases, but inhibits DYRK1B (IC50 = 350 nM), displays <90% binding to CDK7 (IC50 >10 μM) and CDK13. Inhibits proliferation of MOLT4 cells in vitro. Induces apoptosis.
|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 513.07. 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||1.95 mL||9.75 mL||19.49 mL|
|5 mM||0.39 mL||1.95 mL||3.9 mL|
|10 mM||0.19 mL||0.97 mL||1.95 mL|
|50 mM||0.04 mL||0.19 mL||0.39 mL|
References are publications that support the biological activity of the product.
Olson et al (2018) Pharmacological perturbation of CDK9 using selective CDK9 inhibition or degradation. Nat.Chem.Biol. 14 163 PMID: 29251720
Winter et al (2017) BET bromodomain proteins function as master transcription elongation factors independent of CDK9 recruitment. Mol.Cell 67 5 PMID: 28673542
If you know of a relevant reference for NVP 2, please let us know.
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Keywords: NVP 2, NVP 2 supplier, NVP2, Cyclin-dependent, protein, kinases, inhibitors, inhibits, Cdk9, potent, selective, Kinase, 6535, 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.