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Adenosine, periodate oxidized

Name: Adenosine, periodate oxidized
Brand: SIGMA

≥93%, synthetic, Powder

Synonym(s):

ADOX, Adenosine-2′,3′-dialdehyde

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About This Item

Empirical Formula (Hill Notation):

C₁₀H₁₁N₅O₄

CAS Number:

34240-05-6

Molecular Weight:

265.23

UNSPSC Code:

41106305

PubChem Substance ID:

24891180

NACRES:

NA.51

MDL number:

MFCD00056960

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

Pricing and availability is not currently available.

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Properties

Product Name

Adenosine, periodate oxidized, ≥93%

biological source

synthetic (organic)

Quality Level

200

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

Description

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]

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This Item	A6779	A9376	A6904
Sigma-Aldrich A7154 Adenosine, periodate oxidized	Sigma-Aldrich A6779 Adenosine 5′-triphosphate, periodate oxidized sodium salt	Sigma-Aldrich A9376 Adenosine 2′:3′-cyclic monophosphate sodium salt	Sigma-Aldrich A6904 Adenosine 5′-diphosphate, periodate oxidized sodium salt
biological source synthetic (organic)	biological source bacterial (corynebacterium sp)	biological source synthetic (organic)	biological source -
Quality Level 200	Quality Level 200	Quality Level 200	Quality Level 200
form powder	form powder	form powder	form solid
assay ≥93%	assay ≥97%	assay ≥93%	assay 90-95%
solubility 0.2 M HCl: 50 mg/mL, clear, colorless to faintly yellow	solubility -	solubility water: 50 mg/mL, clear, colorless	solubility -
storage temp. −20°C	storage temp. −20°C	storage temp. −20°C	storage temp. −20°C

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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The polyphenol quercetin strongly increases homocysteine production in a human hepatoma (Hep G2) cell line.

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

Inhibition of methylation and changes in gene expression in relation to neural tube defects.

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

Intracellular S-adenosylhomocysteine increased levels are associated with DNA hypomethylation in HUVEC.

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