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Merck
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文件

SML1416

Sigma-Aldrich

KU-60019

≥97% (HPLC)

别名:

(2R,6S)-rel-2,6-Dimethyl-N-[5-[6-(4-morpholinyl)-4-oxo-4H-pyran-2-yl]-9H-thioxanthen-2-yl]-4-morpholineacetamide

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About This Item

经验公式（希尔记法）:
C30H33N3O5S
CAS号:
925701-49-1
分子量:
547.67
MDL號碼:
MFCD19690944
分類程式碼代碼:
12352200
PubChem物質ID:
329825862
NACRES:
NA.77

品質等級

100

化驗

≥97% (HPLC)

形狀

powder

顏色

white to beige

溶解度

DMSO: 20 mg/mL, clear

儲存溫度

−20°C

SMILES 字串

O=C(CN1C[C@H](C)O[C@H](C)C1)NC(C=C2)=CC3=C2SC4=C(C5=CC(C=C(N6CCOCC6)O5)=O)C=CC=C4C3

InChI

1S/C30H33N3O5S/c1-19-16-32(17-20(2)37-19)18-28(35)31-23-6-7-27-22(13-23)12-21-4-3-5-25(30(21)39-27)26-14-24(34)15-29(38-26)33-8-10-36-11-9-33/h3-7,13-15,19-20H,8-12,16-18H2,1-2H3,(H,31,35)/t19-,20+

InChI 密鑰

SCELLOWTHJGVIC-BGYRXZFFSA-N

應用

KU-60019 has been used to block ataxia telangiectasia mutated (ATM), to study its association of with the regulation of H2AX (H2A histone family, member X) and apoptosis inducing factor (AIF)-mediated cell death.

生化／生理作用

KU-60019 is a potent inhitor of ATM (ataxia telangiectasia mutated) kinase, a member of phosphatidylinositol-3-kinase-related kinase family that is critical in regulating cell cycle checkpoints and DNA repair. KU-60019 has an IC50 value of 6.3 nM. KU-60019 radiosensitizes U1242 human glioma cells, and also blocks U1242 cell migration and invasion through matrigel.

其他說明

KU-60019 has been expertly reviewed and recommended by the Chemical Probes Portal. For more information, please visit the KU-60019 probe summary on the Chemical Probes Portal website.

儲存類別代碼

11 - Combustible Solids

水污染物質分類（WGK）

WGK 3

閃點（°F）

Not applicable

閃點（°C）

Not applicable

分析证书(COA)

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Pancreatic beta cell death is a hallmark of type 1 and 2 diabetes (T1D/T2D), but the underlying molecular mechanisms are incompletely understood. Key proteins of the DNA damage response (DDR), including tumor protein P53 (P53, also known as TP53 or
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The DNA-methylating drug temozolomide, which induces cell death through apoptosis, is used for the treatment of malignant glioma. Here, we investigate the mechanisms underlying the ability of temozolomide to induce senescence in glioblastoma cells. Temozolomide-induced senescence was triggered by the

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