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Biological Activity for TC-S 7010
TC-S 7010 is a potent and selective inhibitor of Aurora kinase A (IC50 = 3.4 nM); exhibits 1000-fold selectivity for Aurora kinase A over Aurora kinase B. Displays antiproliferative activity in HCT116 and HT29 cells (IC50 values are 0.19 and 2.9 μM respectively).
Compound Libraries for TC-S 7010
Technical Data for TC-S 7010
|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.
Solubility Data for TC-S 7010
|Solvent||Max Conc. mg/mL||Max Conc. mM|
Preparing Stock Solutions for TC-S 7010
The following data is based on the product molecular weight 588.07. 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||1.7 mL||8.5 mL||17 mL|
|5 mM||0.34 mL||1.7 mL||3.4 mL|
|10 mM||0.17 mL||0.85 mL||1.7 mL|
|50 mM||0.03 mL||0.17 mL||0.34 mL|
References for TC-S 7010
References are publications that support the biological activity of the product.
Aliagas-Martin et al (2009) A class of 2,4-bisanilinopyrimidine Aurora A inhibitors with unusually high selectivity against Aurora B. J.Med.Chem. 52 3300 PMID: 19402633
Yuan et al (2012) Overcoming CML acquired resistance by specific inhibition of Aurora A kinse in the KCL-22 cell model. Carcinogenesis 33 285 PMID: 22116466
If you know of a relevant reference for TC-S 7010, please let us know.
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Citations for TC-S 7010
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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.