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118502

Sigma-Aldrich

ATM Kinase Inhibitor

InSolution, ≥95%

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Synonym(s):
InSolution ATM Kinase Inhibitor
Empirical Formula (Hill Notation):
C21H17NO3S2
Molecular Weight:
395.49

Quality Level

Assay

≥95% (HPLC)

form

liquid

manufacturer/tradename

Calbiochem®

storage condition

OK to freeze
desiccated (hygroscopic)
protect from light

shipped in

wet ice

storage temp.

−20°C

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This Item
506148118510528101
ATM Kinase Inhibitor InSolution, ≥95%

Sigma-Aldrich

118502

ATM Kinase Inhibitor

PI-103 InSolution, ≥97%, potent ATP-competitive inhibitor of DNA-PK, PI3-K, and mTOR

Sigma-Aldrich

528101

PI-103

form

liquid

form

liquid

form

powder

form

liquid

manufacturer/tradename

Calbiochem®

manufacturer/tradename

Calbiochem®

manufacturer/tradename

Calbiochem®

manufacturer/tradename

Calbiochem®

storage condition

OK to freeze, desiccated (hygroscopic), protect from light

storage condition

OK to freeze, desiccated (hygroscopic), protect from light

storage condition

OK to freeze, protect from light

storage condition

OK to freeze, desiccated (hygroscopic), protect from light

shipped in

wet ice

shipped in

wet ice

shipped in

wet ice

shipped in

wet ice

storage temp.

−20°C

storage temp.

2-8°C

storage temp.

2-8°C

storage temp.

−20°C

General description

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.

Packaging

Packaged under inert gas

Warning

Toxicity: Irritant (B)

Physical form

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

Reconstitution

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

Other Notes

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.

Legal Information

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

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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
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
Consuelo Pitolli et al.
Journal of experimental & clinical cancer research : CR, 42(1), 214-214 (2023-08-21)
Medulloblastoma (MB) is the most common cerebellar malignancy during childhood. Among MB, MYC-amplified Group 3 tumors display the worst prognosis. MYC is an oncogenic transcription factor currently thought to be undruggable. Nevertheless, targeting MYC-dependent processes (i.e. transcription and RNA processing
Estelle Vincendeau et al.
Nature communications, 13(1), 3707-3707 (2022-06-29)
SHLD1 is part of the Shieldin (SHLD) complex, which acts downstream of 53BP1 to counteract DNA double-strand break (DSB) end resection and promote DNA repair via non-homologous end-joining (NHEJ). While 53BP1 is essential for immunoglobulin heavy chain class switch recombination

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