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A7154

Sigma-Aldrich

Adenosine, periodate oxidized

≥93%

Synonym(s):

ADOX, Adenosine-2′,3′-dialdehyde

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25 MG
$106.25
100 MG
$328.95

About This Item

Empirical Formula (Hill Notation):
C10H11N5O4
CAS Number:
Molecular Weight:
265.23
MDL number:
UNSPSC Code:
41106305
PubChem Substance ID:
NACRES:
NA.51

$106.25

List Price$125.00Save 15%
Web-Only Promotion

Available to ship onMay 01, 2025Details


biological source

synthetic (organic)

Quality Level

assay

≥93%

form

powder

solubility

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

storage temp.

−20°C

SMILES string

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

Application

Adenosine, periodate oxidized has been used:
  • as a methylarginine transferase inhibitor in the human embryonic kidney (HEK)-293 T cells[1]
  • as a methylase inhibitor in H4 neuroglioma[2]
  • as a broad inhibitor of S-adenosylmethionine (AdoMet)-dependent methyltransferases in mouse embryo fibroblast NIH3T3 cells[3]

Biochem/physiol Actions

Adenosine, periodate oxidized (Adox) is a protein arginine methyltransferases (PRMTs) inhibitor.[4] It also inhibits the enzyme S-adenosylhomocysteine hydrolase and induces apoptosis.[5] Its inhibitory effect on histone methyltransferases prevents histone methylation.[6] Adox also elicits intrinsic cytotoxic properties.[1]

Storage Class

11 - Combustible Solids

wgk_germany

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable

ppe

Eyeshields, Faceshields, Gloves, type N95 (US)


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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
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
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
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

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