AT7519 hydrochloride

CHF 72.00
In stock
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Product Details
Synonyms AT-7519
Product Type Chemical
Properties
Formula C16H17Cl2N5O2 . HCl
MW 382.2 . 36.5
CAS 902135-91-5
Purity Chemicals ≥95%
Appearance Solid.
Solubility Soluble in DMSO or ethanol.
Declaration Manufactured by SynKinase.
Other Product Data Target: CDK2 - CDK7 - CDK5 - CDK4 | Kinase Group: CMGC | Substrate: Serine-Threonine

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Our product description may differ slightly from the original manufacturers product datasheet.
InChi Key PAOFPNGYBWGKCO-UHFFFAOYSA-N
Shipping and Handling
Shipping AMBIENT
Short Term Storage +4°C
Long Term Storage -20°C
Use/Stability Stable for at least 2 years after receipt when stored at -20°C.
Documents
MSDS Download PDF
Product Specification Sheet
Datasheet Download PDF
AT7519 is a potent inhibitor of several CDK family members. AT7519 showed potent antiproliferative activity (40-940nM) in a panel of human tumor cell lines, and the mechanism of action was shown here to be consistent with the inhibition of CDK1 and CDK2 in solid tumor cell lines. AT7519 caused cell cycle arrest followed by apoptosis in human tumor cells and inhibited tumor growth in human tumor xenograft models. Tumor regression was observed following twice daily dosing of AT7519 in the HCT116 and HT29 colon cancer xenograft models. Also it has been shown that the biological effects are linked to inhibition of CDKs in vivo and that AT7519 induces tumor cell apoptosis in these xenograft models. Moreover, AT7519 has an attractive biological profile and is well tolerated and effective making it a more plausible candidate for clinical development than previously available CDK inhibitors. In in vitro kinase assays AT7519 showed nanomolar levels of activity from <10 to 2400 for cyclins; only one other non-cyclin related kinase was inhibited at levels below 10µM (GSK3β, 89nM), all others tested had IC(50)'s of greater than 10,000nM.
Product References
  1. Biological characterization of AT7519, a small-molecule inhibitor of cyclin-dependent kinases, in human tumor cell lines: M.S. Squires, et al.; Mol. Cancer Ther. 8, 324 (2009)
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