Cyclin-dependent kinase (CDK) inhibitor that causes cell cycle arrest at G1 and G2 phase. Potently inhibits the growth of breast and lung cancer cell lines (IC50 = 25 - 160 nM) in vitro.
|Storage||Store 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 438.3. 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||2.28 mL||11.41 mL||22.82 mL|
|5 mM||0.46 mL||2.28 mL||4.56 mL|
|10 mM||0.23 mL||1.14 mL||2.28 mL|
|50 mM||0.05 mL||0.23 mL||0.46 mL|
References are publications that support the products' biological activity.
Kaur et al (1992) Growth inhibition with reversible cell cycle arrest of carcinoma cells by Flavone L86-8275. J.Natl.Cancer.Inst. 84 1736 PMID: 1279187
Ambrosini et al (2008) The cyclin-dependent kinase inhibitor flavopiridol potentiates the effects of topoisomerase I poisons by suppressing Rad51 expression in a p53-dependent manner. Cancer Res. 68 2312 PMID: 18381438
If you know of a relevant reference for Flavopiridol hydrochloride, please let us know.
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Keywords: Flavopiridol hydrochloride, supplier, L86-8275, HMR1275, cyclin, dependent, kinases, inhibitors, inhibits, CDKs, cell, cycle, arrest, antitumor, antiproliferative, anticancer, L, 86-8275, Cyclin-dependent, Kinase, Cyclin-dependent, Kinase, Tocris Bioscience
Citations for Flavopiridol hydrochloride
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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.