High affinity and selective PLK4 inhibitor (Ki = 0.16 nM). Exhibits >1000-fold selectivity for PLK4 over Aurora A and Aurora B. Depletes centriole and centrosome levels in vitro. Induces cell cycle arrest in normal human cell lines in a p53-dependent manner.
Sold with the permission of the Ludwig Institute for Cancer Research Ltd
|Storage||Store at -20°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 633.65. 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||1.58 mL||7.89 mL||15.78 mL|
|5 mM||0.32 mL||1.58 mL||3.16 mL|
|10 mM||0.16 mL||0.79 mL||1.58 mL|
|50 mM||0.03 mL||0.16 mL||0.32 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.
Wong et al (2015) Reversible centriole depletion with an inhibitor of Polo-like kinase 4. Science 348 1155 PMID: 25931445
If you know of a relevant reference for Centrinone, please let us know.
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Keywords: Centrinone, supplier, High, affinity, selective, PLK4, inhibitors, inhibits, centriole, centrosome, Polo-like, Kinase, Tocris Bioscience
Citations for Centrinone
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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.