Cyclin-dependent kinase 2 (cdk2) inhibitor; induces cell-cycle arrest at the G2-M phase. 10- to 36-fold more selective for cdk2-cyclin A over other cdks (IC50 = 0.41 μM for cdk2-cyclin A). Potentiates the apoptotic effect of taxol (Cat. No. 1097) in HeLa cells; down-regulates the antiapoptotic protein survivin.
|Storage||Desiccate 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 422.52. 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||2.37 mL||11.83 mL||23.67 mL|
|5 mM||0.47 mL||2.37 mL||4.73 mL|
|10 mM||0.24 mL||1.18 mL||2.37 mL|
|50 mM||0.05 mL||0.24 mL||0.47 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.
Pennati et al (2005) Potentiation of paclitaxel-induced apoptosis by the novel cyclin-dependent kinase inhibitor NU6140: a possible role for survivin down-regulation. Mol.Cancer.Ther. 4 1328 PMID: 16170024
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Keywords: NU6140 cdk2 inhibitor cyclin-dependent kinase inhibitors inhibits anti-apoptotic arrests cell cycle Cyclin-dependent Kinase
Citations for NU 6140
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Literature in this Area
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.