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Submit ReviewTC-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).
M. Wt | 588.07 |
Formula | C31H31ClFN7O2 |
Storage | Store at +4°C |
Purity | ≥99% (HPLC) |
CAS Number | 1158838-45-9 |
PubChem ID | 44139710 |
InChI Key | AKSIZPIFQAYJGF-UHFFFAOYSA-N |
Smiles | O=C(NC3=CC=CC=C3Cl)C(C=C2)=CC=C2NC1=C(F)C=NC(NC4=CC=C(CC(N5CCN(CC)CC5)=O)C=C4)=N1 |
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.
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
Keywords: TC-S 7010, TC-S 7010 supplier, TC-S7010, Aurora, kinase, A, potent, selective, inhibitors, inhibits, antiproliferative, Kinases, 5286, Tocris Bioscience
Citations are publications that use Tocris products. Selected citations for TC-S 7010 include:
Alexandre et al (2020) KIF14 controls ciliogenesis via regulation of Aurora A and is important for Hedgehog signaling. J Cell Biol 219 PMID: 32348467
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This product guide provides a review of the cell cycle and DNA damage research area and lists over 150 products, including research tools for:
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. 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.