A7154
Adenosine, periodate oxidized
≥93%, synthetic, Powder
Synonym(s):
ADOX, Adenosine-2′,3′-dialdehyde
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About This Item
Empirical Formula (Hill Notation):
C10H11N5O4
CAS Number:
Molecular Weight:
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
Product Name
Adenosine, periodate oxidized, ≥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
Adenosine, periodate oxidized has been used:
- as a methylarginine transferase inhibitor in the human embryonic kidney (HEK)-293 T cells
- as a methylase inhibitor in H4 neuroglioma
- as a broad inhibitor of S-adenosylmethionine (AdoMet)-dependent methyltransferases in mouse embryo fibroblast NIH3T3 cells
Biochem/physiol Actions
Adenosine, periodate oxidized (Adox) is a protein arginine methyltransferases (PRMTs) inhibitor. It also inhibits the enzyme S-adenosylhomocysteine hydrolase and induces apoptosis. Its inhibitory effect on histone methyltransferases prevents histone methylation. Adox also elicits intrinsic cytotoxic properties.
Storage Class
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
ppe
Eyeshields, Faceshields, Gloves, type N95 (US)
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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
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
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
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
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