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Biological Activity for VX 680
VX 680 is a high affinity and selective Aurora kinase inhibitor (Ki values are 0.6, 5 and 18 nM for Aurora A, Aurora C and Aurora B, respectively). Also exhibits affinity for FLT-3 and Abl. Exhibits selectivity for Aurora kinase over 190 other protein kinases. Inhibits proliferation and induces apoptosis in a number of cancer cell lines in vitro. Reduces tumor size in leukemia and colon cancer cell xenografts in mice.
Technical Data for VX 680
|Storage||Store at -20°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.
References for VX 680
References are publications that support the biological activity of the product.
Bebbington et al (2009) The discovery of the potent aurora inhibitor MK-0457 (VX-680). Bioorg.Med.Chem.Lett. 19 3586 PMID: 19447622
Harrington et al (2004) VX-680, a potent and selective small-molecule inhibitor of the Aurora kinases, suppresses tumor growth in vivo. Nat.Med. 10 262 PMID: 14981513
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Citations for VX 680
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Currently there are no citations for VX 680.
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Literature in this Area
Tocris offers the following scientific literature in this area to showcase our products. We invite you to request* your copy today!
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Cell Cycle and DNA Damage Research Product GuideNew
This product guide provides a review of the cell cycle and DNA damage research area and lists over 170 products, including research tools for:
- Cell Cycle and Mitosis
- DNA Damage Repair
- Targeted Protein Degradation
- Ubiquitin Proteasome Pathway
- Chemotherapy Targets
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.