Skip to Content
Merck

SML1109

KU-55933

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

Synonym(s):

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

Sign In to View Organizational & Contract Pricing.

Select a Size

All Photos(1)

About This Item

Empirical Formula (Hill Notation):
C21H17NO3S2
CAS Number:
587871-26-9
Molecular Weight:
395.49
UNSPSC Code:
12352200
PubChem Substance ID:
329825484
NACRES:
NA.77
MDL number:
MFCD08276985

Product Name

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

100

Looking for similar products? Visit Product Comparison Guide

Related Categories

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.

Storage Class

11 - Combustible Solids

wgk

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable

Choose from one of the most recent versions:

Certificates of Analysis (COA)

Lot/Batch Number
0000515124
0000515113
0000515113
0000515124
0000502948

Don't see the Right Version?

If you require a particular version, you can look up a specific certificate by the Lot or Batch number.

Search for a COA

Already Own This Product?

Find documentation for the products that you have recently purchased in the Document Library.

Visit the Document Library

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.
A surveillance mechanism ensures repair of DNA lesions during zygotic reprogramming.
Ladstatter S and Kikue T K
Cell, 167(7), 1774-1787 (2016)
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
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
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
View All Related Papers

Our team of scientists has experience in all areas of research including Life Science, Material Science, Chemical Synthesis, Chromatography, Analytical and many others.

Contact Technical Service