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Merck

SML1109

KU-55933

≥98% (HPLC), Ataxia telangiectasia (A-T) mutated (ATM) kinase inhibitor, powder

동의어(들):

2-(4-Morpholinyl)-6-(1-thianthrenyl)-4H-Pyran-4-one, 2-(Morpholin-4-yl)-6-(thianthren-1-yl)-4H-pyran-4-one

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크기 선택


제품정보 (DICE 배송 시 비용 별도)

실험식(Hill 표기법):
C21H17NO3S2
CAS 번호:
Molecular Weight:
395.49
UNSPSC Code:
12352200
PubChem Substance ID:
NACRES:
NA.77
MDL number:
Assay:
≥98% (HPLC)
Form:
powder
Quality level:
Storage condition:
desiccated
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제품 이름

KU-55933, ≥98% (HPLC)

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

assay

≥98% (HPLC)

form

powder

storage condition

desiccated

color

white to beige

solubility

DMSO: 10 mg/mL, clear

storage temp.

−20°C

Quality Level

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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.
KU-55933 is a very potent, specific inhibitor of Ataxia telangiectasia (A-T) mutated (ATM) kinase.

저장 등급

11 - Combustible Solids

wgk

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable


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시험 성적서(COA)

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문서 라이브러리 방문

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A surveillance mechanism ensures repair of DNA lesions during zygotic reprogramming.
Ladstatter S and Kikue T K
Cell, 167(7), 1774-1787 (2016)
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Zhongkai Zhang et al.
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
Mengtan Xing et al.
FEBS open bio, 9(7), 1315-1326 (2019-05-30)
DNA double-strand breaks (DSBs) are highly cytotoxic lesions, and unrepaired or misrepaired DSBs can lead to various human diseases, including immunodeficiency, neurological abnormalities, growth retardation, and cancer. Nonhomologous end joining (NHEJ) is the major DSB repair pathway in mammals. Ku70

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