Cyclin-dependent kinase (cdk) inhibitor (reported IC50 values are 0.4, 0.6, 4.4 - 5.6 μM for cdk5, cdk1 and cdk2, respectively). Also inhibits GSK-3 (IC50 = 1 uM).
|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|
Preparing Stock Solutions
The following data is based on the product molecular weight 185.19. 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||5.4 mL||27 mL||54 mL|
|5 mM||1.08 mL||5.4 mL||10.8 mL|
|10 mM||0.54 mL||2.7 mL||5.4 mL|
|50 mM||0.11 mL||0.54 mL||1.08 mL|
References are publications that support the biological activity of the product.
Ortega et al (2002) Pyrazolo[3,4-b]quinoxalines. A new class of cyclin-dependent kinases inhibitors. Bioorg.Med.Chem.Lett. 10 2177 PMID: 11983514
Monge et al (1995) 3-Amino-2-quinoxalinecarbonitrile. New fused quinoxalines with potential cytotoxic activity. J.Heterocycl.Chem. 31 1135
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 NSC 693868, please let us know.
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Keywords: NSC 693868, NSC 693868 supplier, GSK-3, inhibitors, inhibits, cdks, GSK, Glycogen, Synthase, Kinases, 3, Cyclin-Dependent, Protein, Carbohydrate, Metabolism, NSC693868, Cyclin-dependent, Kinase, 1937, Tocris Bioscience
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Literature in this Area
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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.