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经验公式(希尔记法):
C10H11N5O4
化学文摘社编号:
分子量:
265.23
UNSPSC Code:
41106305
PubChem Substance ID:
NACRES:
NA.51
MDL number:
Assay:
≥93%
Biological source:
synthetic (organic)
Form:
powder
Solubility:
0.2 M HCl: 50 mg/mL, clear, colorless to faintly yellow
Storage temp.:
−20°C
产品名称
氧化高碘酸腺苷, ≥93%
SMILES string
Nc1ncnc2n(cnc12)C(OC(CO)C=O)C=O
InChI key
ILMNSCQOSGKTNZ-UHFFFAOYSA-N
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)
biological source
synthetic (organic)
assay
≥93%
form
powder
solubility
0.2 M HCl: 50 mg/mL, clear, colorless to faintly yellow
storage temp.
−20°C
Quality Level
Application
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
Biochem/physiol Actions
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。
存储类别
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
ppe
Eyeshields, Faceshields, Gloves, type N95 (US)
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
Björn Hultberg
Clinica chimica acta; international journal of clinical chemistry, 356(1-2), 117-124 (2005-05-05)
Many clinical and epidemiological studies show that mild hyperhomocysteinemia is associated with premature vascular disease. Information about the metabolism of homocysteine is therefore essential for an understanding of its role in atherogenesis, thereby enabling a modulation of that risk. In
H S Kim et al.
Experimental & molecular medicine, 32(4), 197-203 (2001-02-24)
3-Deazaadenosine (DZA), one of the potent inhibitors of S-adenosylhomocysteine hydrolase, is known to possess several biological properties including an induction of apoptosis. To evaluate a possibility that DZA may be utilized for the treatment of human leukemia, we studied molecular
Regulation of arginine methylation in endothelial cells: role in premature senescence and apoptosis.
Alla Polotskaia et al.
Cell cycle (Georgetown, Tex.), 6(20), 2524-2530 (2007-08-30)
With the recent characterization of enzymes responsible for protein arginine methylation and demonstration that catabolic products of arginine methylation, such as asymmetric dimethylarginine (ADMA), are among the most powerful mechanisms of atherogenesis, developing endothelial dysfunction and cardiovascular complications in a
Christian Schwerk et al.
Oncogene, 24(47), 7002-7011 (2005-07-12)
We have analysed the importance of proper substrate methylation by S-adenosylmethionine-dependent methyltransferases for cell survival and cell cycle progression. We show that treatment of cells with the methyltransferase inhibitor adenosine dialdehyde (AdOx) causes cell cycle arrest and death in different
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