SML1109
KU-55933
≥98% (HPLC), Ataxia telangiectasia (A-T) mutated (ATM) kinase inhibitor, powder
别名:
2-(4-吗啉基)-6-(1-噻蒽基)-4H-吡喃-4-酮, 2-(吗啉-4-基)-6-(噻蒽-1-基)-4H-吡喃-4-酮
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关于此项目
经验公式（希尔记法）:
C21H17NO3S2
CAS Number:
分子量:
395.49
MDL编号:
UNSPSC代码:
12352200
PubChem化学物质编号:
NACRES:
NA.77
Product Name
KU-55933, ≥98% (HPLC)
质量水平
方案
≥98% (HPLC)
表单
powder
储存条件
desiccated
颜色
white to beige
溶解性
DMSO: 10 mg/mL, clear
储存温度
−20°C
SMILES字符串
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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相关类别
应用
KU-55933已被用作共济失调-毛细血管扩张症突变（ATM）抑制剂。
生化/生理作用
KU-55933是一种非常有效的共济失调毛细血管扩张症（A-T）突变（ATM）激酶特异性抑制剂。
KU-55933是一种非常有效的共济失调毛细血管扩张症（A-T）突变（ATM）激酶特异性抑制剂（IC50 = 13 nM）。KU-22933处理可增强癌细胞对电离辐射和细胞毒性药物的敏感性。化合物KU-22933能够阻断ATM介导的p53、gH2AX、NBS1和SMC1的磷酸化。
储存分类代码
11 - Combustible Solids
WGK
WGK 3
闪点(°F)
Not applicable
闪点(°C)
Not applicable
历史批次信息供参考:
分析证书(COA)
Lot/Batch Number
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
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
Sanket Awate et al.
BMC molecular biology, 17, 3-3 (2016-02-11)
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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