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Y0000775

Benzbromarone

European Pharmacopoeia (EP) Reference Standard

Synonyme(s) :

3-(3,5-Dibromo-4-hydroxybenzoyl)-2-ethylbenzofuran

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About This Item

Formule empirique (notation de Hill):
C17H12Br2O3
Numéro CAS:
Poids moléculaire :
424.08
Numéro MDL:
Code UNSPSC :
41116107
ID de substance PubChem :
Nomenclature NACRES :
NA.24

Qualité

pharmaceutical primary standard

Famille d'API

benzbromarone

Fabricant/nom de marque

EDQM

Application(s)

pharmaceutical (small molecule)

Format

neat

Température de stockage

2-8°C

Chaîne SMILES 

CCc1oc2ccccc2c1C(=O)c3cc(Br)c(O)c(Br)c3

InChI

1S/C17H12Br2O3/c1-2-13-15(10-5-3-4-6-14(10)22-13)16(20)9-7-11(18)17(21)12(19)8-9/h3-8,21H,2H2,1H3

Clé InChI

WHQCHUCQKNIQEC-UHFFFAOYSA-N

Informations sur le gène

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Description générale

This product is provided as delivered and specified by the issuing Pharmacopoeia. All information provided in support of this product, including SDS and any product information leaflets have been developed and issued under the Authority of the Issuing Pharmacopoeia. For further information and support please go to the website of the issuing Pharmacopoeia.

Application

Benzbromarone EP Reference standard, intended for use in laboratory tests only as specifically prescribed in the European Pharmacopoeia.

Conditionnement

The product is delivered as supplied by the issuing Pharmacopoeia. For the current unit quantity, please visit the EDQM reference substance catalogue.

Autres remarques

Sales restrictions may apply.

Pictogrammes

Skull and crossbones

Mention d'avertissement

Danger

Mentions de danger

Conseils de prudence

Classification des risques

Acute Tox. 3 Oral

Code de la classe de stockage

6.1C - Combustible acute toxic Cat.3 / toxic compounds or compounds which causing chronic effects

Classe de danger pour l'eau (WGK)

WGK 3

Point d'éclair (°F)

Not applicable

Point d'éclair (°C)

Not applicable


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Certificats d'analyse (COA)

Lot/Batch Number

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Dingyu Wang et al.
Cardiovascular toxicology, 21(3), 192-205 (2020-10-26)
High levels of serum uric acid is closely associated with atrial fibrillation (AF); nonetheless, the detailed mechanisms remain unknown. Therefore, this work examined the intricate mechanisms of AF triggered by hyperuricemia and the impact of the uricosuric agent benzbromarone on
Tip W Loo et al.
Biochemistry, 50(21), 4393-4395 (2011-04-28)
Deletion of Phe508 from the first nucleotide-binding domain of the CFTR chloride channel causes cystic fibrosis because it inhibits protein folding. Indirect approaches such as incubation at low temperatures can partially rescue ΔF508 CFTR, but the protein is unstable at
Atsushi Iwamura et al.
Drug metabolism and disposition: the biological fate of chemicals, 39(5), 838-846 (2011-02-16)
Drug-induced hepatotoxicity is a major problem in drug development, and reactive metabolites generated by cytochrome P450s are suggested to be one of the causes. CYP2C9 is one of the major enzymes in hepatic drug metabolism. In the present study, we
Fernanda Cristina Mazali et al.
Nephron. Experimental nephrology, 120(1), e12-e19 (2011-12-01)
Hyperuricemia frequently complicates cyclosporine (CsA) therapy. Previous studies have shown that hyperuricemia exacerbates interstitial and vascular lesions in the cyclosporine model. We tested the hypothesis that normalization of uric acid could prevent the development of cyclosporine toxicity. CsA nephropathy was
Tip W Loo et al.
Biochemical pharmacology, 83(3), 345-354 (2011-12-06)
The most common cause of cystic fibrosis is deletion of Phe508 in the first nucleotide-binding domain (NBD) of the CFTR chloride channel, which inhibits protein folding. ΔF508 CFTR can be rescued by indirect approaches such as low temperature but the

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