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Merck
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Key Documents

118502

Sigma-Aldrich

ATM Kinase Inhibitor

InSolution, ≥95%

别名:

InSolution ATM Kinase Inhibitor

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About This Item

经验公式(希尔记法):
C21H17NO3S2
分子量:
395.49
分類程式碼代碼:
12352200
NACRES:
NA.77

品質等級

化驗

≥95% (HPLC)

形狀

liquid

製造商/商標名

Calbiochem®

儲存條件

OK to freeze
desiccated (hygroscopic)
protect from light

運輸包裝

wet ice

儲存溫度

−20°C

一般說明

A cell-permeable disubstituted pyranone compound that acts as a potent and ATP-competitive inhibitor of ATM kinase (IC50 = 13 nM; Ki = 2.2 nM). Displays excellent selectivity over other PIKK family kinases (IC50 = 2.5, 9.3, 16.6 µM for DNA-PK, mTOR, PI 3-K, respectively; IC50 >100 µM for PI 4-K and ATR) and exhibits little activity towards a panel of 60 other kinases even at concentrations as high as 10 µM. Inhibits ATM-dependent cellular protein phosphorylation following ionizing radiation (IR) and sensitizes cells with wild-type ATM, but not mutant ATM, to the cytotoxic effects of IR and DNA-damaging agents.

包裝

Packaged under inert gas

警告

Toxicity: Irritant (B)

外觀

A 10 mM (2 mg/506 µl) solution of ATM Kinase Inhibitor (Cat. No. 118500) in DMSO.

重構

Following initial thaw, aliquot and freeze (-20°C).

其他說明

Pereg, Y., et al. 2005. Proc. Natl. Acad. Sci. USA102, 5056.
Lau, A., et al. 2005. Nat. Cell Biol.7, 493.
Hickson, I., et al. 2004. Cancer Res.64, 9152.

法律資訊

CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany

儲存類別代碼

10 - Combustible liquids

水污染物質分類(WGK)

WGK 2

閃點(°F)

188.6 °F - closed cup - (Dimethylsulfoxide)

閃點(°C)

87 °C - closed cup - (Dimethylsulfoxide)


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Alan Lau et al.
Nature cell biology, 7(5), 493-500 (2005-04-19)
Chemotherapy that is used to treat human immunodeficiency virus type-1 (HIV-1) infection focuses primarily on targeting virally encoded proteins. However, the combination of a short retroviral life cycle and high mutation rate leads to the selection of drug-resistant HIV-1 variants.
Yaron Pereg et al.
Proceedings of the National Academy of Sciences of the United States of America, 102(14), 5056-5061 (2005-03-25)
Maintenance of genomic stability depends on the DNA damage response, an extensive signaling network that is activated by DNA lesions such as double-strand breaks (DSBs). The primary activator of the mammalian DSB response is the nuclear protein kinase ataxia-telangiectasia, mutated
Ian Hickson et al.
Cancer research, 64(24), 9152-9159 (2004-12-18)
The serine/threonine protein kinase ATM signals to cell cycle and DNA repair components by phosphorylating downstream targets such as p53, CHK2, NBS1, and BRCA1. Mutation of ATM occurs in the human autosomal recessive disorder ataxia-telangiectasia, which is characterized by hypersensitivity

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