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CYP2D6  -  cytochrome P450, family 2, subfamily D,...

Homo sapiens

Synonyms: CPD6, CYP2D, CYP2D7AP, CYP2D7BP, CYP2D7P2, ...
 
 
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Disease relevance of CYP2D6

 

Psychiatry related information on CYP2D6

 

High impact information on CYP2D6

  • Drugs for which there is a potential case for prospective testing include warfarin (CYP2C9), perhexiline (CYP2D6), and perhaps the proton pump inhibitors (CYP2C19) [13].
  • CONCLUSIONS: This study finds that the levels of two different carcinogen-DNA adducts vary in lung tissue (an important target tissue) in association with three separate genetic polymorphisms (i.e., CYP2D6, CYP2E1, and GSTM1) [14].
  • RESULTS: Higher 7-methyl-dGMP adduct levels were associated with CYP2D6 genotypes (P = .01), consistent with the reports of the increased risk of lung cancer associated with this genotype [14].
  • Genetic basis for a lower prevalence of deficient CYP2D6 oxidative drug metabolism phenotypes in black Americans [15].
  • To determine the genetic basis for this difference, inactivating CYP2D6 mutations were assessed by allele-specific PCR amplification and RFLP analyses of genomic DNA from 126 unrelated whites and 127 unrelated blacks [15].
 

Chemical compound and disease context of CYP2D6

 

Biological context of CYP2D6

  • The normal CYP2D6 gene was isolated; was completely sequenced, including 1,531 and 3,522 bp of 5' and 3' flanking DNA, respectively; and was found to contain nine exons within 4,378 bp [21].
  • We have constructed a genomic library from lymphocyte DNA of an EM positively identified by pedigree analysis to be homozygous for the normal CYP2D6 allele [21].
  • A hypothesis is presented that the presence of a pseudogene within the CYP2D subfamily transfers detrimental mutations via gene conversions into the CYP2D6 gene, thus accounting for the high frequency of mutations observed in the CYP2D6 gene in humans [21].
  • The CYP2D6 (-) "poor metabolizer " and the NQO1 (-) "defective" genotypes were not clearly associated with a higher risk of RCC [22].
  • CYP2D6 activity was rejected as a risk factor by phenotyping and by detailed molecular genetic analyses [23].
 

Anatomical context of CYP2D6

  • In contrast, neither in vector-infected NIH/3T3 cells nor in CYP2D6- and CYP2E1-expressing cells was an increase of mutation frequency observed [24].
  • Experiments performed with these enzyme expression systems indicated that the highest formation rate of N-hydroxyprocainamide was observed in the presence of CYP2D6 enriched microsomes [25].
  • Using a simplified non-extractive reversed-phase HPLC assay with fluorescence detection, biphasic Michaelis-Menten kinetics were obtained for formation of all three dihydroxyamphetamines in liver microsomes from a CYP2D6 extensive metabolizer subject [26].
  • CYP2D6 is the major target autoantigen of LKM-1 and expressed on plasma membrane (PM) of hepatocytes, suggesting a pathogenic role for anti-LKM-1 in liver injury as a trigger [27].
  • As expected, the effect of fluoxetine on CYP2D6 in hepatocytes was consistent with potent yet reversible inhibition [28].
 

Associations of CYP2D6 with chemical compounds

 

Physical interactions of CYP2D6

  • All 16 sera from AIH-2 patients strongly bound to this CYP2D6 antigen [34].
 

Enzymatic interactions of CYP2D6

 

Co-localisations of CYP2D6

 

Regulatory relationships of CYP2D6

  • CYP2C9 and CYP2C19 provided enhanced formation of R-EDDP and CYP2D6 incubation resulted in the preferential conversion to S-EDDP [40].
  • However, the Km values of the expressed CYP1A2 (approximately 15 microM) were almost identical with those of the expressed CYP2D6 (approximately 22 microM) and human liver microsomes [41].
  • CYP2D6 possessed highest intrinsic (-)-OSU6162 N-depropylase activity when compared with a battery of recombinant heterologously expressed human p450 enzymes [42].
  • CYP2D6 catalyzed desalkyl delavirdine formation was linear with time (up to 30 min) but when catalyzed by cDNA expressed CYP3A4 or human liver microsomes the reaction rate declined progressively with time [43].
  • 4. This work suggests that quinidine is a non-classical inhibitor of CYP1A1 and that it is not as highly specific at inhibiting CYP2D6 as previously thought [44].
 

Other interactions of CYP2D6

  • The measured CYP3A4 and CYP2D6 activities also failed to predict the susceptible patients [45].
  • There was strong evidence against linkage for the remaining loci in all families analyzed individually, except for TH, which was uninformative in Families A and B, and CYP2D6, which gave slightly positive pairwise lod scores in Family A [46].
  • Phenotypic measurements were in concordance with the subject's CYP2C9, CYP2C19, and CYP2D6 genotypes [47].
  • No significant changes in either CYP1A2 or CYP2D6 activities were observed between placebo and treatment arms of the study [48].
  • METHODS: Twenty-four healthy heterozygous or homozygous carriers of the CYP2C9 variants Arg144Cys (*2) and Ile359Leu (*3) and 2 individuals with the deficient CYP2D6 genotype *4/*4 took 40 mg racemic fluvastatin daily for 14 days [49].
 

Analytical, diagnostic and therapeutic context of CYP2D6

  • RESULTS: The CYP2D6 poor metabolizers, who are enzyme deficient (2/13 in the case series and 3/20 in the case-control study), did not appear to tolerate risperidone well [50].
  • Multiple sequence alignment of CYPs identified CYP2C9 Asp(293) as corresponding to Asp(301) of CYP2D6, which has been suggested to play a role in the binding of basic substrates to the latter enzyme [51].
  • A western blot of microsomes prepared from yeast transformed with pELT1 were probed with a monoclonal antibody to CYP2D6 and revealed a strong band with a molecular mass consistent with that of CYP2D6 from human liver microsomes [52].
  • There was a significant correlation between the quantity of immunoreactive CYP2D6 as determined by immunoblotting with anti-peptide 2 antiserum and dextromethorphan O-demethylation in a panel of 10 human liver microsomes (r = 0.95) [53].
  • The cis-, trans1-, and trans2-4-monohydroxylation rates of (+)- and (-)-PHX by human liver microsomes from three extensive metabolizers (EMs), two intermediate metabolizers (IMs), and two poor metabolizers (PMs) of CYP2D6 were measured with a high-performance liquid chromatography assay [54].
  • It is hypothesised that CYP2D6 gene variants result in poor metabolism of tamoxifen and reduce its efficacy. However, the absence of an association of CYP2D6 variants with breast cancer specific survival (BCSS) in tamoxifen-treated patients questions the validity of the reported association between CYP2D6 genotype and treatment response in breast cancer. Until larger, prospective studies confirming any associations are available, routine pre-treatment CYP2D6 genetic testing should not be used in the clinical setting [55].

 

 

References

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  19. QTc interval lengthening is related to CYP2D6 hydroxylation capacity and plasma concentration of thioridazine in patients. LLerena, A., Berecz, R., de la Rubia, A., Dorado, P. J. Psychopharmacol. (Oxford) (2002) [Pubmed]
  20. Metabolism of delavirdine, a human immunodeficiency virus type-1 reverse transcriptase inhibitor, by microsomal cytochrome P450 in humans, rats, and other species: probable involvement of CYP2D6 and CYP3A. Voorman, R.L., Maio, S.M., Hauer, M.J., Sanders, P.E., Payne, N.A., Ackland, M.J. Drug Metab. Dispos. (1998) [Pubmed]
  21. The human debrisoquine 4-hydroxylase (CYP2D) locus: sequence and identification of the polymorphic CYP2D6 gene, a related gene, and a pseudogene. Kimura, S., Umeno, M., Skoda, R.C., Meyer, U.A., Gonzalez, F.J. Am. J. Hum. Genet. (1989) [Pubmed]
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