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Merck
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Documentos clave

118502

Sigma-Aldrich

ATM Kinase Inhibitor

InSolution, ≥95%

Sinónimos:

InSolution ATM Kinase Inhibitor

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About This Item

Fórmula empírica (notación de Hill):
C21H17NO3S2
Peso molecular:
395.49
Código UNSPSC:
12352200
NACRES:
NA.77

Nivel de calidad

Análisis

≥95% (HPLC)

formulario

liquid

fabricante / nombre comercial

Calbiochem®

condiciones de almacenamiento

OK to freeze
desiccated (hygroscopic)
protect from light

Condiciones de envío

wet ice

temp. de almacenamiento

−20°C

Descripción general

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.

Envase

Packaged under inert gas

Advertencia

Toxicity: Irritant (B)

Forma física

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

Reconstitución

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

Otras notas

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.

Información legal

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

Código de clase de almacenamiento

10 - Combustible liquids

Clase de riesgo para el agua (WGK)

WGK 2

Punto de inflamabilidad (°F)

188.6 °F - closed cup - (Dimethylsulfoxide)

Punto de inflamabilidad (°C)

87 °C - closed cup - (Dimethylsulfoxide)


Certificados de análisis (COA)

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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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