A7154
Adenosine, periodate oxidized
≥93%
Synonym(s):
ADOX, Adenosine-2′,3′-dialdehyde
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All Photos(2)
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
Recommended Products
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
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
- 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 Code
11 - Combustible Solids
WGK
WGK 3
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Personal Protective Equipment
dust mask type N95 (US), Eyeshields, Gloves
Certificates of Analysis (COA)
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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
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
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
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
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