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Key Documents

D1306

Sigma-Aldrich

Debrisoquine sulfate

powder, ≥98% (TLC)

Sinônimo(s):

3,4-Dihydro-2(1H)-isoquinolinecarboximidamide, Debrisoquin sulfate, Ro 5-33071

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About This Item

Fórmula linear:
C20H26N6 · H2SO4
Número CAS:
Peso molecular:
448.54
Número CE:
Número MDL:
Código UNSPSC:
12352204
ID de substância PubChem:
NACRES:
NA.32

product name

Debrisoquine sulfate,

Ensaio

≥98% (TLC)

Nível de qualidade

forma

powder

pf

285 °C

solubilidade

H2O: 20 mg/mL (with heat)

temperatura de armazenamento

room temp

cadeia de caracteres SMILES

OS(O)(=O)=O.NC(=N)N1CCc2ccccc2C1.NC(=N)N3CCc4ccccc4C3

InChI

1S/2C10H13N3.H2O4S/c2*11-10(12)13-6-5-8-3-1-2-4-9(8)7-13;1-5(2,3)4/h2*1-4H,5-7H2,(H3,11,12);(H2,1,2,3,4)

chave InChI

CAYGYVYWRIHZCQ-UHFFFAOYSA-N

Informações sobre genes

human ... SLC6A2(6530)

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Ações bioquímicas/fisiológicas

Debrisoquine is an anti-hypertensive agent. It is metabolized by cytochrome P4502D6.

Substratos

A substrate for cytochrome P450 CYP2D6; an indicator for genetic polymorphism in cytochrome P450.

Pictogramas

Exclamation mark

Palavra indicadora

Warning

Frases de perigo

Declarações de precaução

Classificações de perigo

Acute Tox. 4 Oral

Código de classe de armazenamento

11 - Combustible Solids

Classe de risco de água (WGK)

WGK 3

Ponto de fulgor (°F)

Not applicable

Ponto de fulgor (°C)

Not applicable

Equipamento de proteção individual

dust mask type N95 (US), Eyeshields, Gloves


Certificados de análise (COA)

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Visite a Biblioteca de Documentos

E Jacqz-Aigrain et al.
Biochemical pharmacology, 41(11), 1657-1663 (1991-06-01)
Interindividual variations of debrisoquine metabolism was recently identified in non-human primates tested in vivo. The catalytical and immunological characterization of cytochrome P450IID subfamily was undertaken in hepatic microsomes from extensive metabolizer primates. The NADPH/O2 mediated metabolism of debrisoquine, dextromethorphan and
N E Caporaso et al.
Environmental health perspectives, 98, 101-105 (1992-11-01)
Debrisoquine is an antihypertensive drug that is metabolized by cytochrome P4502D6. Deficient metabolism is inherited as an autosomal recessive condition. We previously reported in a case-control study that extensive metabolizers of debrisoquine were at greater risk of lung cancer compared
J W Ho et al.
Analytical biochemistry, 203(2), 348-351 (1992-06-01)
Debrisoquine and sparteine are prototype substrates of a genetic deficiency in cytochrome P450-dependent drug metabolism. Sensitive assays of in vitro oxidation of sparteine and debrisoquine are required for evaluation of this polymorphism. The activities were measured by quantitative analysis of
The debrisoquine metabolic phenotype and DNA-based assays: implications of misclassification for the association of lung cancer and the debrisoquine metabolic phenotype.
Caporaso N E, et al.
Environmental Health Perspectives, 98, 101-105 (1992)
B Clement et al.
Biochemical pharmacology, 46(12), 2249-2267 (1993-12-14)
The microsomal N-hydroxylation of the strongly basic guanidinium group (debrisoquine) to N-hydroxyguanidine (N-hydroxydebrisoquine) and the retroreduction of the N-hydroxyguanidine are demonstrated for the first time. The reduction of the N-hydroxyguanidine by liver homogenates and hepatocytes is catalysed by a microsomal

Artigos

Phase I biotransformation reactions introduce or expose functional groups on the drug with the goal of increasing the polarity of the compound. Although Phase I drug metabolism occurs in most tissues, the primary and first pass site of metabolism occurs during hepatic circulation.

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