A7154
氧化高碘酸腺苷
≥93%, synthetic, Powder
别名:
抗氧化剂, 腺苷-2′，3′-二醛
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关于此项目
经验公式（希尔记法）:
C10H11N5O4
化学文摘社编号:
分子量:
265.23
MDL编号:
UNSPSC代码:
41106305
PubChem化学物质编号:
NACRES:
NA.51
产品名称
氧化高碘酸腺苷, ≥93%
生物来源
synthetic (organic)
质量水平
方案
≥93%
表单
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。
储存分类代码
11 - Combustible Solids
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)
历史批次信息供参考:
分析证书(COA)
Lot/Batch Number
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
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
Francois H T Duong et al.
Hepatology (Baltimore, Md.), 43(4), 796-806 (2006-03-25)
Hepatitis C virus (HCV) infection is an important cause of chronic liver disease. Standard therapy, pegylated interferon alpha (pegIFNalpha) combined with ribavirin, results in a sustained response rate in approximately half of patients. The cause of treatment failure in 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
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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