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CDK8/19i is a potent and selective CDK8 and CDK19 inhibitor (IC50 values are 2.9 and 14.1 nM, respectively). CDK8/19i maintains pluripotency of mouse PSCs in culture. It induces the formation of dome-shaped colonies and upregulates Nanog-GFP reporter and endogenous Nanog expression in mouse ESCs in vitro.
|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 253.3. 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||3.95 mL||19.74 mL||39.48 mL|
|5 mM||0.79 mL||3.95 mL||7.9 mL|
|10 mM||0.39 mL||1.97 mL||3.95 mL|
|50 mM||0.08 mL||0.39 mL||0.79 mL|
References are publications that support the biological activity of the product.
Lynch et al (2020) Global hyperactivation of enhancers stabilizes human and mouse naive pluripotency through inhibition of CDK8/19 Mediator kinases. Nat.Cell.Bio. 22 1223 PMID: 32989249
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Keywords: CDK8/19i, CDK8/19i supplier, cyclin, dependent, kinases, inhibitors, inhibits, CDK8, CDK19, stem, cells, pluripotency, pluripotent, maintenance, self-renewal, potent, selective, Cyclin-dependent, Kinase, Stem, Cell, Proliferation, 7372, 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.