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Merck
CN

A7154

Sigma-Aldrich

氧化高碘酸腺苷

≥93%

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别名:
抗氧化剂, 腺苷-2',3'-二醛
经验公式(希尔记法):
C10H11N5O4
CAS号:
分子量:
265.23
MDL编号:
UNSPSC代码:
41106305
PubChem化学物质编号:
NACRES:
NA.51

生物来源

synthetic (organic)

质量水平

检测方案

≥93%

形式

powder

溶解性

0.2 M HCl: 50 mg/mL, clear, colorless to faintly yellow

储存温度

−20°C

SMILES字符串

Nc1ncnc2n(cnc12)C(OC(CO)C=O)C=O

InChI

1S/C10H11N5O4/c11-9-8-10(13-4-12-9)15(5-14-8)7(3-18)19-6(1-16)2-17/h1,3-7,17H,2H2,(H2,11,12,13)

InChI key

ILMNSCQOSGKTNZ-UHFFFAOYSA-N

应用

高碘酸氧化腺苷已用于:
  • 作为人胚胎肾细胞(HEK)-293 T中的精氨酸甲基转移酶抑制剂
  • 作为H4神经胶质瘤的甲基化酶抑制剂
  • 作为小鼠胚胎成纤维细胞NIH3T3的S-腺苷甲硫氨酸(AdoMet)依赖性甲基转移酶的广谱抑制剂

生化/生理作用

腺苷高碘酸氧化物/高碘酸氧化腺苷(Adox)是一种蛋白精氨酸甲基转移酶(PRMT)抑制剂。它还可抑制S-腺苷同型半胱氨酸水解酶并诱导细胞凋亡。可抑制组蛋白甲基转移酶,从而抑制组蛋白甲基化。Adox还可激发内源性细胞毒性。

WGK

WGK 3

闪点(°F)

Not applicable

闪点(°C)

Not applicable

个人防护装备

Eyeshields, Faceshields, Gloves, type N95 (US)


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Yinghong He et al.
Journal of translational medicine, 11, 14-14 (2013-01-16)
Pharmacologic reactivation of fetal hemoglobin expression is a promising strategy for treatment of sickle cell disease and β-thalassemia. The objective of this study was to investigate the effect of the methyl transferase inhibitor adenosine-2',3'-dialdehyde (Adox) on induction of human fetal
Malin Hultberg et al.
Clinical biochemistry, 39(2), 160-163 (2005-12-07)
The metabolism of homocysteine is influenced by several dietary factors, including folate, cobalamin and possibly also the intake of polyhydroxylated phenolic compounds (polyphenols), which were shown to increase plasma homocysteine (tHcy) concentration. In order to reveal the cause of the
Ivon J M van der Linden et al.
Birth defects research. Part A, Clinical and molecular teratology, 82(10), 676-683 (2008-10-22)
An impaired DNA methylation has been suggested to underlie the complex etiology of neural tube defects (NTDs). Previously, we have demonstrated that inhibition of methylation by periodate oxidized adenosine (Adox) results in a widening of the anterior neuropore (ANP) in
Rita Castro et al.
Journal of molecular medicine (Berlin, Germany), 83(10), 831-836 (2005-06-25)
Hyperhomocysteinemia is a risk factor for atherosclerosis and vascular disease; however, the mechanism underlying this association remains poorly understood. Increased levels of intracellular S-adenosylhomocysteine (AdoHcy), secondary to homocysteine-mediated reversal of the AdoHcy hydrolase reaction, have been associated with reduced DNA
Jessica A Sipkens et al.
Atherosclerosis, 221(1), 48-54 (2011-12-30)
We have previously shown that homocysteine (Hcy) induces phosphatidylserine (PS) exposure, apoptosis and necrosis in human endothelial cells. Since it has been suggested that S-adenosylhomocysteine (SAH) is the main causative factor in Hcy-induced pathogenesis of cardiovascular disease, we evaluate here

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