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SML1109

Sigma-Aldrich

KU-55933

≥98% (HPLC)

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Synonym(s):
2-(4-Morpholinyl)-6-(1-thianthrenyl)-4H-Pyran-4-one, 2-(Morpholin-4-yl)-6-(thianthren-1-yl)-4H-pyran-4-one
Empirical Formula (Hill Notation):
C21H17NO3S2
CAS Number:
Molecular Weight:
395.49
MDL number:
PubChem Substance ID:
NACRES:
NA.77

Quality Level

assay

≥98% (HPLC)

form

powder

storage condition

desiccated

color

white to beige

solubility

DMSO: 10 mg/mL, clear

storage temp.

−20°C

SMILES string

O=C1C=C(OC(=C1)c2cccc3Sc4ccccc4Sc23)N5CCOCC5

InChI

1S/C21H17NO3S2/c23-14-12-16(25-20(13-14)22-8-10-24-11-9-22)15-4-3-7-19-21(15)27-18-6-2-1-5-17(18)26-19/h1-7,12-13H,8-11H2

InChI key

XRKYMMUGXMWDAO-UHFFFAOYSA-N

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1 of 4

This Item
SML1416SML1257SML0813
vibrant-m

SML1109

KU-55933

vibrant-m

SML1416

KU-60019

vibrant-m

SML1257

KU-0060648

vibrant-m

SML0813

BRD56491

form

powder

form

powder

form

powder

form

powder

assay

≥98% (HPLC)

assay

≥97% (HPLC)

assay

≥98% (HPLC)

assay

≥98% (HPLC)

solubility

DMSO: 10 mg/mL, clear

solubility

DMSO: 20 mg/mL, clear

solubility

DMSO: 1 mg/mL, clear (warmed)

solubility

DMSO: 2 mg/mL, clear (warmed)

storage temp.

−20°C

storage temp.

−20°C

storage temp.

−20°C

storage temp.

2-8°C

color

white to beige

color

white to beige

color

white to light brown

color

white to beige

Application

KU-55933 has been used as an ataxia-telangiectasia mutated (Atm) inhibitor.

Biochem/physiol Actions

KU-55933 is a very potent, specific inhibitor of Ataxia telangiectasia (A-T) mutated (ATM) kinase (IC50 = 13 nM). KU-22933 treatment sensitizes cancer cells to ionizing radiation and cytotoxic drugs. The compound KU-22933 blocks ATM-mediated phosphorylyation of p53, gH2AX, NBS1, and SMC1.

Storage Class

11 - Combustible Solids

wgk_germany

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable


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Christianne Hoey et al.
Molecular oncology, 12(8), 1324-1341 (2018-05-31)
Recurrence of high-grade prostate cancer after radiotherapy is a significant clinical problem, resulting in increased morbidity and reduced patient survival. The molecular mechanisms of radiation resistance are being elucidated through the study of microRNA (miR) that negatively regulate gene expression.
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Journal of experimental & clinical cancer research : CR, 39(1), 247-247 (2020-11-18)
SIRT6 has diverse roles in cells, and the role of SIRT6 in tumorigenesis is controversial. Considering the role of SIRT6 as an inducer of DNA damage repair, it might be involved in resistance to anti-cancer therapy. We evaluated the prognostic
A surveillance mechanism ensures repair of DNA lesions during zygotic reprogramming.
Ladstatter S and Kikue T K
Cell, 167(7), 1774-1787 (2016)
Bo-Hua Chen et al.
Nature communications, 11(1), 5267-5267 (2020-10-21)
Peroxisomes perform beta-oxidation of branched and very-long chain fatty acids, which leads to the formation of reactive oxygen species (ROS) within the peroxisomal lumen. Peroxisomes are therefore prone to ROS-mediated damages. Here, using light to specifically and acutely induce ROS
Sanket Awate et al.
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The Tousled like kinase 1B (TLK1B) is critical for DNA repair and survival of cells. Upon DNA damage, Chk1 phosphorylates TLK1B at S457 leading to its transient inhibition. Once TLK1B regains its kinase activity it phosphorylates Rad9 at S328. In

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