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D1306

Sigma-Aldrich

Debrisoquine sulfate

powder, ≥98% (TLC)

Synonym(e):

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

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About This Item

Lineare Formel:
C20H26N6 · H2SO4
CAS-Nummer:
581-88-4
Molekulargewicht:
448.54
EG-Nummer:
209-472-4
MDL-Nummer:
MFCD00153791
UNSPSC-Code:
12352204
PubChem Substanz-ID:
24277710
NACRES:
NA.32

Produktbezeichnung

Debrisoquine sulfate,

Assay

≥98% (TLC)

Qualitätsniveau

200

Form

powder

mp (Schmelzpunkt)

285 °C

Löslichkeit

H2O: 20 mg/mL (with heat)

Lagertemp.

room temp

SMILES String

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)

InChIKey

CAYGYVYWRIHZCQ-UHFFFAOYSA-N

Angaben zum Gen

human ... SLC6A2(6530)

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Biochem./physiol. Wirkung

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

Substrate

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

Piktogramme

Exclamation mark
GHS07

Signalwort

Warning

H-Sätze

H302

Gefahreneinstufungen

Acute Tox. 4 Oral

Lagerklassenschlüssel

11 - Combustible Solids

WGK

WGK 3

Flammpunkt (°F)

Not applicable

Flammpunkt (°C)

Not applicable

Persönliche Schutzausrüstung

dust mask type N95 (US), Eyeshields, Gloves

Hier finden Sie alle aktuellen Versionen:

Analysenzertifikate (COA)

Lot/Batch Number
117M4067V
13170606
086M4151V
085M4015V
123M4110V

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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
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Artikel

Phase I Drug Metabolism

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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