CP466722
CP466722 Basic information
- Product Name:
- CP466722
- Synonyms:
-
- CP466722
- 1-(6,7-Dimethoxy-4-quinazolinyl)-3-(2-pyridinyl)-1H-1,2,4-triazol-5-amine
- CP466722;CP 466722;CP-466722
- CS-73
- CP-466722, >98%
- 2-(6,7-dimethoxyquinazolin-4-yl)-5-(pyridin-2-yl)-2H-1,2,4-triazol-3-amine
- 1-(6,7-Dimethoxy-4-quinazolinyl)-3-(2-pyridinyl)-1H-1,2,4-triazol-5-amine CP 466722
- 2-(6,7-dimethoxyquinazolin-4-yl)-5-pyridin-2-yl-1,2,4-triazol-3-amine
- CAS:
- 1080622-86-1
- MF:
- C17H15N7O2
- MW:
- 349.35
- EINECS:
- 808-414-0
- Product Categories:
-
- Inhibitors
- Mol File:
- 1080622-86-1.mol
CP466722 Chemical Properties
- Boiling point:
- 642.3±65.0 °C(Predicted)
- Density
- 1.48
- storage temp.
- Keep in dark place,Sealed in dry,2-8°C
- solubility
- DMSO: soluble0.5mg/mL, clear (warmed)
- pka
- 0.00±0.19(Predicted)
- form
- powder
- color
- white to beige
CP466722 Usage And Synthesis
Description
CP 466,722 is an inhibitor of ataxia-telangiectasia mutated (ATM) kinase that inhibits ionizing radiation-induced ATM autophosphorylation and phosphorylation of the ATM targets SMC1, Chk2, and p53 in HeLa cells when used at a concentration of 10 μM. It is selective for ATM over PI3K and PIKK in HFF(hTERT) and A-T(hTERT) fibroblasts, respectively. CP 466,722 decreases cell survival in response to ionizing radiation in HeLa cells. It is also cytotoxic to MCF-7 and SKBr-3 breast cancer cells (IC50s = 16.92 and 12.78 μM, respectively).
Uses
CP466722 is a competetive, reversible inhbitor of Ataxia telangiectasia (A-T) mutated (ATM) kinase
Definition
ChEBI: 2-(6,7-dimethoxy-4-quinazolinyl)-5-(2-pyridinyl)-1,2,4-triazol-3-amine is a member of quinazolines.
target
ATM
References
[1]. guo, k., et al., development of a cell-based, high-throughput screening assay for atm kinase inhibitors. j biomol screen, 2014. 19(4): p. 538-46.
[2]. nadkarni, a., et al., atm inhibitor ku-55933 increases the tmz responsiveness of only inherently tmz sensitive gbm cells. j neurooncol, 2012. 110(3): p. 349-57.
[3]. rainey, m.d., et al., transient inhibition of atm kinase is sufficient to enhance cellular sensitivity to ionizing radiation. cancer res, 2008. 68(18): p. 7466-74.
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