Anti-CYP2D6 monoclonal antibody

Name: Anti-CYP2D6 monoclonal antibody
SKU: DCABH-9726
Rating: 5 (1 reviews)

Mouse anti-Human CYP2D6 monoclonal antibody for ELISA, WB

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COA

SDS

Datasheet

Summary

Specifications

Antibody Isotype

IgG2a

Species Reactivity

Human

Immunogen

Recombinant fragment: LVTHGEDTAD RPPVPITQIL GFGPRSQGVF LARYGPAWRE QRRFSVSTLR NLGLGKKSLE QWVTEEAACL CAAFANHSGR PFRPNGLLDK AVSNVIASLT, corresponding to amino acids 91-190 of Human Cytochrome P450 2D6, with tag.

Conjugate

Unconjugated

Applications

Application Notes

WB: 1 - 5 μg/ml

Target

Alternative Names

CYP2D6; cytochrome P450, family 2, subfamily D, polypeptide 6; CYP2D7AP, CYP2D7BP, CYP2D7P2, CYP2D8P2, CYP2DL1, cytochrome P450, family 2, subfamily D, polypeptide 7 pseudogene 2 , cytochrome P450, family 2, subfamily D, polypeptide 8 pseudogene 2 , cy

Entrez Gene ID

1565

UniProt ID

C1ID52

Product Background

Antigen Description

Cytochrome P450 2D6 is a member of the cytochrome P450 superfamily of enzymes. The cytochrome P450 proteins are monooxygenases which catalyze many reactions involved in drug metabolism and synthesis of cholesterol, steroids and other lipids. This protein localizes to the endoplasmic reticulum and is known to metabolize as many as 20% of commonly prescribed drugs. Its substrates include debrisoquine, an adrenergic-blocking drug; sparteine and propafenone, both anti-arrythmic drugs; and amitryptiline, an anti-depressant. The gene is highly polymorphic in the population; certain alleles result in the poor metabolizer phenotype, characterized by a decreased ability to metabolize the enzymes substrates. Cytochrome P450 2D6 is the molecular target of autoantibodies against the "liver kidney microsomal antigen 1" (LKM 1).

Pathway

Biological oxidations, organism-specific biosystem; Codeine and morphine metabolism, organism-specific biosystem; Cytochrome P450 - arranged by substrate type, organism-specific biosystem; Drug metabolism - cytochrome P450, organism-specific biosystem; Drug metabolism - cytochrome P450, conserved biosystem; Fatty Acid Omega Oxidation, organism-specific biosystem; Metabolism, organism-specific biosystem;

Citations

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Documents

pdf COA

pdf SDS

pdf Datasheet

QA & Reviews

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References

Inhibitory Effect of Myricetin on the Pharmacokinetics of Aripiprazole In Vivo and In Vitro

LATIN AMERICAN JOURNAL OF PHARMACY

Authors: Zhan, Yun-yun; Wu, Jiao-fen; Zhang, Wei; Wu, Zhuo-chao; Chen, Xu-hui; Hu, Guo-xin; Wang, Ying

Abstract

The aim of this study was to explore the impact of myricetin on the metabolism of aripiprazole both in vivo and in vitro. Fourteen healthy male SD rats were randomly divided into two groups: A group (control group) and B group (a single dose of 80 mg/kg myricetin). A single dose of 3 mg/kg aripiprazole wasadministered orally 30 min after administration of myricetin. Aripiprazole plasma levels were measured by UPLC-MS/MS, and pharmacokinetic parameters were calculated by DAS 3.0 software. The single dose of 80 mg/kg myricetin significantly (p < 0.05) increased the AUC, t(1/)(2) and C(max)( )of aripiprazole and decreased the T-max and CL. Also, different concentrations of myricetin together incubation with aripiprazole in CYP3A4*1, CYP2D6*1, human and rat microsomes, the 1050 values was 20.25, 95.54, 25.33, and 73.65 mu mol/L, respectively. This result indicated that myricetin could significantly inhibit the metabolism of aripiprazole both in vivo and in vitro.

Precision dosing-based optimisation of paroxetine during pregnancy for poor and ultrarapid CYP2D6 metabolisers: a virtual clinical trial pharmacokinetics study

JOURNAL OF PHARMACY AND PHARMACOLOGY

Authors: Almurjan, Aminah; Macfarlane, Hannah; Badhan, Raj K. S.

Abstract

Background Paroxetine has been demonstrated to undergo gestation-related reductions in plasma concentrations, to an extent which is dictated by the polymorphic state of CYP 2D6. However, knowledge of appropriate dose titrations is lacking. Methods A pharmacokinetic modelling approach was applied to examine gestational changes in trough plasma concentrations for CYP 2D6 phenotypes, followed by necessary dose adjustment strategies to maintain paroxetine levels within a therapeutic range of 20-60 ng/ml. Key findings A decrease in trough plasma concentrations was simulated throughout gestation for all phenotypes. A significant number of ultrarapid (UM) phenotype subjects possessed trough levels below 20 ng/ml (73-76%) compared to extensive metabolisers (EM) (51-53%). Conclusions For all phenotypes studied, there was a requirement for daily doses in excess of the standard 20 mg dose throughout gestation. For EM, a dose of 30 mg daily in trimester 1 followed by 40 mg daily in trimesters 2 and 3 is suggested to be optimal. For poor metabolisers (PM), a 20 mg daily dose in trimester 1 followed by 30 mg daily in trimesters 2 and 3 is suggested to be optimal. For UM, a 40 mg daily dose throughout gestation is suggested to be optimal.