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Potent inhibitor of Aurora kinases (IC50 values are 0.015, 0.019 and 0.025 μM at Aurora A, Aurora C and Aurora B respectively). Displays antiproliferative activity in a range of human tumor cell lines. Orally bioavailable.
|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.
|Solvent||Max Conc. mg/mL||Max Conc. mM|
Preparing Stock Solutions
The following data is based on the product molecular weight 551.48. 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||1.81 mL||9.07 mL||18.13 mL|
|5 mM||0.36 mL||1.81 mL||3.63 mL|
|10 mM||0.18 mL||0.91 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.
Bavetsias et al (2010) Imidazo[4,5-b]pyridine derivatives as inhibitors of Aurora kinases: lead optimization studies toward the identification of an orally bioavailable preclinical development candidate. J.Med.Chem. 53 5213 PMID: 20565112
Faisal et al (2011) The Aurora kinase inhibitor CCT137690 downregulates MYCN and sensitizes MYCN-amplified neuroblastoma in vivo. Mol.Cancer Ther. 10 2115 PMID: 21885865
If you know of a relevant reference for CCT 137690, please let us know.
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Keywords: CCT 137690, CCT 137690 supplier, CCT137690, aurora, kinases, pan-aurora, inhibitors, inhibits, antiproliferative, Aurora, Kinases, 4291, Tocris Bioscience
Citations for CCT 137690
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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.