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Y0000775

Benzbromarone

European Pharmacopoeia (EP) Reference Standard

Synonym(s):

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

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About This Item

Empirical Formula (Hill Notation):
C17H12Br2O3
CAS Number:
3562-84-3
Molecular Weight:
424.08
MDL number:
MFCD00078962
UNSPSC Code:
41116107
PubChem Substance ID:
329831145
NACRES:
NA.24

grade

pharmaceutical primary standard

API family

benzbromarone

manufacturer/tradename

EDQM

application(s)

pharmaceutical (small molecule)

format

neat

storage temp.

2-8°C

SMILES string

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

InChI key

WHQCHUCQKNIQEC-UHFFFAOYSA-N

Gene Information

human ... SLC22A12(116085)

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General description

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.

Packaging

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

Other Notes

Sales restrictions may apply.

Pictograms

Skull and crossbones
GHS06

Signal Word

Danger

Hazard Statements

H301

Precautionary Statements

P301 + P310 + P330

Hazard Classifications

Acute Tox. 3 Oral

Storage Class Code

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

WGK

WGK 3

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable

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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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