ATP-competitive inhibitor of Aurora B kinase (IC50 = 250 nM). Prevents chromosome alignment and segregation; also induces polyploidy and prevents histone H3-Ser10 phosphorylation. Overrides the spindle assembly checkpoint and induces mitotic exit in monastrol- and taxol-treated HeLa cells.
|Storage||Desiccate at RT|
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 553.12. 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||1.81 mL||9.04 mL||18.08 mL|
|5 mM||0.36 mL||1.81 mL||3.62 mL|
|10 mM||0.18 mL||0.9 mL||1.81 mL|
|50 mM||0.04 mL||0.18 mL||0.36 mL|
References are publications that support the biological activity of the product.
Hauf et al (2003) The small molecule Hesperadin reveals a role for Aurora B in correcting kinetochore-microtubule attachment and in maintaining the spindle assembly checkpoint. J.Cell.Biol. 161 281 PMID: 12707311
Jetton et al (2009) The cell cycle as a therapeutic target against Trypanosoma brucei: Hesperadin inhibits Aurora kinase-1 and blocks mitotic progression in bloodstream forms. Mol.Microbiol. 72 442 PMID: 19320832
Sessa et al (2005) Mechanism of Aurora B activation by INCENP and inhibition by Hesperadin. Mol.Cell. 18 379 PMID: 15866179
If you know of a relevant reference for Hesperadin hydrochloride, please let us know.
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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.