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CYP2D6

From Wikipedia, the free encyclopedia

CYP2D6
Available structures
PDBOrtholog search: PDBe RCSB
Identifiers
AliasesCYP2D6, CPD6, CYP2D, CYP2D7AP, CYP2D7BP, CYP2D7P2, CYP2D8P2, CYP2DL1, CYPIID6, P450-DB1, P450C2D, P450DB1, cytochrome P450 family 2 subfamily D member 6, Cytochrome P450 2D6
External IDsOMIM: 124030; MGI: 1929474; HomoloGene: 133550; GeneCards: CYP2D6; OMA:CYP2D6 - orthologs
Orthologs
SpeciesHumanMouse
Entrez

1565

56448

Ensembl

ENSMUSG00000061740

UniProt

P10635

Q9JKY7

RefSeq (mRNA)

NM_000106
NM_001025161

NM_001163472
NM_019823

RefSeq (protein)

NP_000097
NP_001020332

NP_001156944
NP_062797

Location (UCSC)Chr 22: 42.13 – 42.13 MbChr 15: 82.25 – 82.26 Mb
PubMed search[3][4]
Wikidata
View/Edit HumanView/Edit Mouse

Cytochrome P450 2D6 (CYP2D6) is an enzyme that in humans is encoded by the CYP2D6 gene. CYP2D6 is primarily expressed in the liver. It is also highly expressed in areas of the central nervous system, including the substantia nigra.

CYP2D6, a member of the cytochrome P450 mixed-function oxidase system, is one of the most important enzymes involved in the metabolism of xenobiotics in the body. In particular, CYP2D6 is responsible for the metabolism and elimination of approximately 25% of clinically used drugs, via the addition or removal of certain functional groups – specifically, hydroxylation, demethylation, and dealkylation.[5] CYP2D6 also activates some prodrugs. This enzyme also metabolizes several endogenous substances, such as N,N-Dimethyltryptamine, hydroxytryptamines, neurosteroids, and both m-tyramine and p-tyramine which CYP2D6 metabolizes into dopamine in the brain and liver.[5][6][7]

Considerable variation exists in the efficiency and amount of CYP2D6 enzyme produced between individuals. Hence, for drugs that are metabolized by CYP2D6 (that is, are CYP2D6 substrates), certain individuals will eliminate these drugs quickly (ultrarapid metabolizers) while others slowly (poor metabolizers). If a drug is metabolized too quickly, it may decrease the drug's efficacy while if the drug is metabolized too slowly, toxicity may result.[8] So, the dose of the drug may have to be adjusted to take into account of the speed at which it is metabolized by CYP2D6.[9] Individuals who exhibit an ultrarapid metabolizer phenotype, metabolize prodrugs, such as codeine or tramadol, more rapidly, leading to higher than therapeutic levels.[10][11] A case study of the death of an infant breastfed by an ultrarapid metabolizer mother taking codeine impacted postnatal pain relief clinical practices, but was later debunked.[12] These drugs may also cause serious toxicity in ultrarapid metabolizer patients when used to treat other post-operative pain, such as after tonsillectomy.[13][14][15] Other drugs may function as inhibitors of CYP2D6 activity or inducers of CYP2D6 enzyme expression that will lead to decreased or increased CYP2D6 activity respectively. If such a drug is taken at the same time as a second drug that is a CYP2D6 substrate, the first drug may affect the elimination rate of the second through what is known as a drug-drug interaction.[8]

Gene

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The gene is located on chromosome 22q13.1. near two cytochrome P450 pseudogenes (CYP2D7P and CYP2D8P).[16] Among them, CYP2D7P originated from CYP2D6 in a stem lineage of great apes and humans,[17] the CYP2D8P originated from CYP2D6 in a stem lineage of Catarrhine and New World monkeys' stem lineage.[18] Alternatively spliced transcript variants encoding different isoforms have been found for this gene.[19]

Genotype/phenotype variability

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CYP2D6 shows the largest phenotypical variability among the CYPs, largely due to genetic polymorphism. The genotype accounts for normal, reduced, and non-existent CYP2D6 function in subjects. Pharmacogenomic tests are now available to identify patients with variations in the CYP2D6 allele and have been shown to have widespread use in clinical practice.[20] The CYP2D6 function in any particular subject may be described as one of the following:[21]

  • poor metabolizer – little or no CYP2D6 function
  • intermediate metabolizers – metabolize drugs at a rate somewhere between the poor and extensive metabolizers
  • extensive metabolizer – normal CYP2D6 function
  • ultrarapid metabolizer – multiple copies of the CYP2D6 gene are expressed, so greater-than-normal CYP2D6 function occurs

A patient's CYP2D6 phenotype is often clinically determined via the administration of debrisoquine (a selective CYP2D6 substrate) and subsequent plasma concentration assay of the debrisoquine metabolite (4-hydroxydebrisoquine).[22]

The type of CYP2D6 function of an individual may influence the person's response to different doses of drugs that CYP2D6 metabolizes. The nature of the effect on the drug response depends not only on the type of CYP2D6 function, but also on the extent to which processing of the drug by CYP2D6 results in a chemical that has an effect that is similar, stronger, or weaker than the original drug, or no effect at all. For example, if CYP2D6 converts a drug that has a strong effect into a substance that has a weaker effect, then poor metabolizers (weak CYP2D6 function) will have an exaggerated response to the drug and stronger side-effects; conversely, if CYP2D6 converts a different drug into a substance that has a greater effect than its parent chemical, then ultrarapid metabolizers (strong CYP2D6 function) will have an exaggerated response to the drug and stronger side-effects.[23] Information about how human genetic variation of CYP2D6 affects response to medications can be found in databases such PharmGKB,[24] Clinical Pharmacogenetics Implementation Consortium (CPIC).[25]

Genetic basis of variability

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The variability in metabolism is due to multiple different polymorphisms of the CYP2D6 allele, located on chromosome 22. Subjects possessing certain allelic variants will show normal, decreased, or no CYP2D6 function, depending on the allele. Pharmacogenomic tests are now available to identify patients with variations in the CYP2D6 allele and have been shown to have widespread use in clinical practice.[20] The current known alleles of CYP2D6 and their clinical function can be found in databases such as PharmVar.[26]

Ethnic factors in variability

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Ethnicity is a factor in the occurrence of CYP2D6 variability. The reduction of the liver cytochrome CYP2D6 enzyme occurs approximately in 7–10% in white populations, and is lower in most other ethnic groups such as Asians and African-Americans at 2% each. A complete lack of CYP2D6 enzyme activity, wherein the individual has two copies of the polymorphisms that result in no CYP2D6 activity at all, is said to be about 1-2% of the population.[27] The occurrence of CYP2D6 ultrarapid metabolizers appears to be greater among Middle Eastern and North African populations.[28][29]

Caucasians with European descent predominantly (around 71%) have the functional group of CYP2D6 alleles, producing extensive metabolism, while functional alleles represent only around 50% of the allele frequency in populations of Asian descent.[30]

This variability is accounted for by the differences in the prevalence of various CYP2D6 alleles among the populations–approximately 10% of whites are intermediate metabolizers, due to decreased CYP2D6 function, because they appear to have the one (heterozygous) non-functional CYP2D6*4 allele,[31] while approximately 50% of Asians possess the decreased functioning CYP2D6*10 allele.[31]

Ligands

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Following is a table of selected substrates, inducers and inhibitors of CYP2D6. Where classes of agents are listed, there may be exceptions within the class.

Inhibitors of CYP2D6 can be classified by their potency, such as:

  • Strong inhibitor being one that causes at least a 5-fold increase in the plasma AUC values of sensitive substrates metabolized through CYP2D6, or more than 80% decrease in clearance thereof.[32]
  • Moderate inhibitor being one that causes at least a 2-fold increase in the plasma AUC values of sensitive substrates metabolized through CYP2D6, or 50-80% decrease in clearance thereof.[32]
  • Weak inhibitor being one that causes at least a 1.25-fold but less than 2-fold increase in the plasma AUC values of sensitive substrates metabolized through CYP2D6, or 20-50% decrease in clearance thereof.[32]
Selected inducers, inhibitors and substrates of CYP2D6
Substrates
↑ = bioactivation by CYP2D6		 Inhibitors Inducers

Strong

Moderate

Weak

Unspecified potency

Strong

Unspecified potency

Dopamine biosynthesis

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Biosynthetic pathways for catecholamines and trace amines in the human brain[70][71][41]
The image above contains clickable links
In humans, catecholamines and phenethylaminergic trace amines are derived from the amino acid phenylalanine. It is well established that dopamine is produced from L-tyrosine via L-dopa; however, recent evidence has shown that CYP2D6 is expressed in the human brain and catalyzes the biosynthesis of dopamine from L-tyrosine via p-tyramine.[41] Similarly, CYP2D6 also metabolizes m-tyramine into dopamine.[41]


References

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  1. ^ a b c ENSG00000275211, ENSG00000280905, ENSG00000282966, ENSG00000283284, ENSG00000272532 GRCh38: Ensembl release 89: ENSG00000100197, ENSG00000275211, ENSG00000280905, ENSG00000282966, ENSG00000283284, ENSG00000272532 – Ensembl, May 2017
  2. ^ a b c GRCm38: Ensembl release 89: ENSMUSG00000061740 – Ensembl, May 2017
  3. ^ "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  4. ^ "Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  5. ^ a b Wang B, Yang LP, Zhang XZ, Huang SQ, Bartlam M, Zhou SF (2009). "New insights into the structural characteristics and functional relevance of the human cytochrome P450 2D6 enzyme". Drug Metabolism Reviews. 41 (4): 573–643. doi:10.1080/03602530903118729. PMID 19645588. S2CID 41857580.
  6. ^ Wang X, Li J, Dong G, Yue J (February 2014). "The endogenous substrates of brain CYP2D". European Journal of Pharmacology. 724: 211–218. doi:10.1016/j.ejphar.2013.12.025. PMID 24374199.
  7. ^ Good M, Joel Z, Benway T, Routledge C, Timmermann C, Erritzoe D, et al. (22 April 2023). "Pharmacokinetics of N,N-dimethyltryptamine in Humans". European Journal of Drug Metabolism and Pharmaco Kinetics. 48 (3): 311–327. doi:10.1007/s13318-023-00822-y. PMC 10122081. PMID 37086340.
  8. ^ a b Teh LK, Bertilsson L (2012). "Pharmacogenomics of CYP2D6: molecular genetics, interethnic differences and clinical importance". Drug Metabolism and Pharmacokinetics. 27 (1): 55–67. doi:10.2133/dmpk.DMPK-11-RV-121. PMID 22185816.
  9. ^ Walko CM, McLeod H (April 2012). "Use of CYP2D6 genotyping in practice: tamoxifen dose adjustment". Pharmacogenomics. 13 (6): 691–697. doi:10.2217/pgs.12.27. PMID 22515611.
  10. ^ Pratt VM, Scott SA, Pirmohamed M, Esquivel B, Kattman BL, Malheiro AJ, et al. (2012). Tramadol Therapy and CYP2D6 Genotype. PMID 28520365.
  11. ^ Pratt VM, Scott SA, Pirmohamed M, Esquivel B, Kattman BL, Malheiro AJ, et al. (2012). Codeine Therapy and CYP2D6 Genotype. PMID 28520350.
  12. ^ Zipursky J, Juurlink DN (November 2020). "The Implausibility of Neonatal Opioid Toxicity from Breastfeeding". Clinical Pharmacology and Therapeutics. 108 (5): 964–970. doi:10.1002/cpt.1882. PMID 32378749. S2CID 218535295.
  13. ^ Sadhasivam S, Myer CM (July 2012). "Preventing opioid-related deaths in children undergoing surgery". Pain Medicine. 13 (7): 982–3, author reply 984. doi:10.1111/j.1526-4637.2012.01419.x. PMID 22694279.
  14. ^ Kelly LE, Rieder M, van den Anker J, Malkin B, Ross C, Neely MN, et al. (May 2012). "More codeine fatalities after tonsillectomy in North American children" (PDF). Pediatrics. 129 (5): e1343–e1347. doi:10.1542/peds.2011-2538. PMID 22492761. S2CID 14167063. Archived (PDF) from the original on 2 February 2024. Retrieved 2 February 2024.
  15. ^ Prows CA, Zhang X, Huth MM, Zhang K, Saldaña SN, Daraiseh NM, et al. (May 2014). "Codeine-related adverse drug reactions in children following tonsillectomy: a prospective study". The Laryngoscope. 124 (5): 1242–1250. doi:10.1002/lary.24455. PMID 24122716. S2CID 5326129.
  16. ^ Ahmad HI, Afzal G, Jamal A, Kiran S, Khan MA, Mehmood K, et al. (2021). "In Silico Structural, Functional, and Phylogenetic Analysis of Cytochrome (CYPD) Protein Family". BioMed Research International. 2021: 5574789. doi:10.1155/2021/5574789. PMC 8128545. PMID 34046497.
  17. ^ Wang H, Tompkins LM (September 2008). "CYP2B6: new insights into a historically overlooked cytochrome P450 isozyme". Current Drug Metabolism. 9 (7): 598–610. doi:10.2174/138920008785821710. PMC 2605793. PMID 18781911.
  18. ^ Yasukochi Y, Satta Y (2011). "Evolution of the CYP2D gene cluster in humans and four non-human primates". Genes & Genetic Systems. 86 (2): 109–116. doi:10.1266/ggs.86.109. PMID 21670550.
  19. ^ "Entrez Gene: CYP2D6 cytochrome P450, family 2, subfamily D, polypeptide 6". Archived from the original on 8 March 2010. Retrieved 3 November 2017.
  20. ^ a b Dinama O, Warren AM, Kulkarni J (August 2014). "The role of pharmacogenomic testing in psychiatry: Real world examples". The Australian and New Zealand Journal of Psychiatry. 48 (8): 778. doi:10.1177/0004867413520050. PMID 24413808. S2CID 206399446.
  21. ^ Bertilsson L, Dahl ML, Dalén P, Al-Shurbaji A (February 2002). "Molecular genetics of CYP2D6: clinical relevance with focus on psychotropic drugs". British Journal of Clinical Pharmacology. 53 (2): 111–122. doi:10.1046/j.0306-5251.2001.01548.x. PMC 1874287. PMID 11851634.
  22. ^ Llerena A, Dorado P, Peñas-Lledó EM (January 2009). "Pharmacogenetics of debrisoquine and its use as a marker for CYP2D6 hydroxylation capacity". Pharmacogenomics. 10 (1): 17–28. doi:10.2217/14622416.10.1.17. PMID 19102711.
  23. ^ Lynch T, Price A (August 2007). "The effect of cytochrome P450 metabolism on drug response, interactions, and adverse effects". American Family Physician. 76 (3): 391–396. PMID 17708140.
  24. ^ "PharmGKB". PharmGKB. Archived from the original on 3 October 2022. Retrieved 3 October 2022.
  25. ^ "CYP2D6 CPIC guidelines". cpicpgx.org. Archived from the original on 3 October 2022. Retrieved 3 October 2022.
  26. ^ "PharmVar". www.pharmvar.org. Archived from the original on 19 May 2020. Retrieved 15 February 2024.
  27. ^ Lilley LL, Harrington S, Snyder JS, Swart B (2007). Pharmacology and the Nursing Process. Toronto: Mosby Elsevier. p. 25. ISBN 9780779699711.
  28. ^ McLellan RA, Oscarson M, Seidegård J, Evans DA, Ingelman-Sundberg M (June 1997). "Frequent occurrence of CYP2D6 gene duplication in Saudi Arabians". Pharmacogenetics. 7 (3): 187–191. doi:10.1097/00008571-199706000-00003. PMID 9241658.
  29. ^ Owen RP, Sangkuhl K, Klein TE, Altman RB (July 2009). "Cytochrome P450 2D6". Pharmacogenetics and Genomics. 19 (7): 559–562. doi:10.1097/FPC.0b013e32832e0e97. PMC 4373606. PMID 19512959.
  30. ^ Bradford LD (March 2002). "CYP2D6 allele frequency in European Caucasians, Asians, Africans and their descendants". Pharmacogenomics. 3 (2): 229–243. doi:10.1517/14622416.3.2.229. PMID 11972444.
  31. ^ a b Droll K, Bruce-Mensah K, Otton SV, Gaedigk A, Sellers EM, Tyndale RF (August 1998). "Comparison of three CYP2D6 probe substrates and genotype in Ghanaians, Chinese and Caucasians". Pharmacogenetics. 8 (4): 325–333. doi:10.1097/00008571-199808000-00006. PMID 9731719.
  32. ^ a b c d e f g h i j k l m n o p q r s t u v w x y z aa ab ac ad ae af ag ah ai aj ak al am an ao ap aq ar as at au av aw ax ay az ba bb bc bd be bf bg bh bi bj bk bl bm bn bo bp bq br bs bt bu bv bw bx by bz ca cb cc cd ce cf cg "Drug Interactions: Cytochrome P450 Drug Interaction Table". Indiana University School of Medicine. 2007. Archived from the original on 10 October 2007. Retrieved 25 July 2010. Retrieved in July 2011
  33. ^ a b c d e f g h i j k l m n o p q r s t u v w x y z aa ab ac ad ae af ag ah FASS (drug formulary): Swedish environmental classification of pharmaceuticals Archived 11 June 2002 at the Wayback Machine Facts for prescribers (Fakta för förskrivare), retrieved July 2011
  34. ^ a b Leeder JS (June 2001). "Pharmacogenetics and pharmacogenomics". Pediatric Clinics of North America. 48 (3): 765–781. doi:10.1016/S0031-3955(05)70338-2. PMID 11411304.
  35. ^ "Hydrocodone". Drugbank. Archived from the original on 6 September 2011. Retrieved 14 June 2011.
  36. ^ Davies SJ, Westin AA, Castberg I, Lewis G, Lennard MS, Taylor S, et al. (2010). "Characterisation of zuclopenthixol metabolism by in vitro and therapeutic drug monitoring studies". Acta Psychiatrica Scandinavica. 122 (6): 444–453. doi:10.1111/j.1600-0447.2010.01619.x. PMID 20946203.
  37. ^ Hoskins JM, Carey LA, McLeod HL (August 2009). "CYP2D6 and tamoxifen: DNA matters in breast cancer". Nature Reviews. Cancer. 9 (8): 576–586. doi:10.1038/nrc2683. PMID 19629072. S2CID 19501089.
  38. ^ Dean L (29 June 2020). "Atomoxetine Therapy and CYP2D6 Genotype". National Center for Biotechnology Information (US). PMID 28520366. Retrieved 24 April 2024.
  39. ^ Brown JT, Abdel-Rahman SM, van Haandel L, Gaedigk A, Lin YS, Leeder JS (June 2016). "Single dose, CYP2D6 genotype-stratified pharmacokinetic study of atomoxetine in children with ADHD". Clinical Pharmacology and Therapeutics. 99 (6): 642–650. doi:10.1002/cpt.319. PMC 4862932. PMID 26660002.
  40. ^ "Wakix pitolisant tablets Prescribing Information" (PDF). Wakix HCP. Archived (PDF) from the original on 11 January 2023. Retrieved 11 January 2023.
  41. ^ a b c d e Wang X, Li J, Dong G, Yue J (February 2014). "The endogenous substrates of brain CYP2D". European Journal of Pharmacology. 724: 211–218. doi:10.1016/j.ejphar.2013.12.025. PMID 24374199.
  42. ^ Vizeli P, Straumann I, Holze F, Schmid Y, Dolder PC, Liechti ME (May 2021). "Genetic influence of CYP2D6 on pharmacokinetics and acute subjective effects of LSD in a pooled analysis". Scientific Reports. 11 (1): 10851. Bibcode:2021NatSR..1110851V. doi:10.1038/s41598-021-90343-y. PMC 8149637. PMID 34035391.
  43. ^ Shen HW, Jiang XL, Winter JC, Yu AM (October 2010). "Psychedelic 5-methoxy-N,N-dimethyltryptamine: metabolism, pharmacokinetics, drug interactions, and pharmacological actions". Current Drug Metabolism. 11 (8): 659–666. doi:10.2174/138920010794233495. PMC 3028383. PMID 20942780.
  44. ^ a b "DILTIAZEM HCL CD- diltiazem hydrochloride capsule, coated, extended release". DailyMed. 1 February 2017. Archived from the original on 31 January 2019. Retrieved 31 January 2019.
  45. ^ "NIFEDIPINE EXTENDED RELEASE- nifedipine tablet, extended release". DailyMed. 29 November 2012. Archived from the original on 31 January 2022. Retrieved 1 February 2019.
  46. ^ Kotlyar M, Brauer LH, Tracy TS, Hatsukami DK, Harris J, Bronars CA, et al. (June 2005). "Inhibition of CYP2D6 activity by bupropion". Journal of Clinical Psychopharmacology. 25 (3): 226–229. doi:10.1097/01.jcp.0000162805.46453.e3. PMID 15876900. S2CID 24591644.
  47. ^ Fasinu PS, Tekwani BL, Avula B, Chaurasiya ND, Nanayakkara NP, Wang YH, et al. (September 2016). "Pathway-specific inhibition of primaquine metabolism by chloroquine/quinine". Malaria Journal. 15 (1): 466. doi:10.1186/s12936-016-1509-x. PMC 5020452. PMID 27618912.
  48. ^ "Medical Cannabis Adverse Effects & Drug Interactions" (PDF). Archived (PDF) from the original on 14 December 2019. Retrieved 28 October 2019.
  49. ^ Zhao Y, Hellum BH, Liang A, Nilsen OG (June 2015). "Inhibitory Mechanisms of Human CYPs by Three Alkaloids Isolated from Traditional Chinese Herbs". Phytotherapy Research. 29 (6): 825–834. doi:10.1002/ptr.5285. PMID 25640685. S2CID 24002845.
  50. ^ Hermann R, von Richter O (September 2012). "Clinical evidence of herbal drugs as perpetrators of pharmacokinetic drug interactions". Planta Medica. 78 (13): 1458–1477. doi:10.1055/s-0032-1315117. PMID 22855269.
  51. ^ Feng P, Zhao L, Guo F, Zhang B, Fang L, Zhan G, et al. (September 2018). "The enhancement of cardiotoxicity that results from inhibiton of CYP 3A4 activity and hERG channel by berberine in combination with statins". Chemico-Biological Interactions. 293: 115–123. Bibcode:2018CBI...293..115F. doi:10.1016/j.cbi.2018.07.022. PMID 30086269. S2CID 206489481.
  52. ^ Zhang W, Ramamoorthy Y, Tyndale RF, Sellers EM (June 2003). "Interaction of buprenorphine and its metabolite norbuprenorphine with cytochromes p450 in vitro". Drug Metabolism and Disposition. 31 (6): 768–772. doi:10.1124/dmd.31.6.768. PMID 12756210.
  53. ^ a b "Citalopram Oral Solution". Drugs.com. Archived from the original on 8 February 2018. Retrieved 23 January 2018.
  54. ^ "Escitalopram-drug-information". UpToDate. Archived from the original on 28 October 2020. Retrieved 22 May 2019.
  55. ^ a b "Drug Development and Drug Interactions: Table of Substrates, Inhibitors and Inducers". FDA. 26 May 2021. Archived from the original on 4 November 2020. Retrieved 21 June 2020.
  56. ^ Nevels RM, Weiss NH, Killebrew AE, Gontkovsky ST (July 2013). "Methylphenidate and Its Under-recognized, Under- explained, and Serious Drug Interactions: A Review of the Literature with Heightened Concerns" (PDF). German Journal of Psychiatry: 29–42. Archived from the original (PDF) on 9 April 2018. Retrieved 31 August 2016.
  57. ^ Bailey DG, Bend JR, Arnold JM, Tran LT, Spence JD (July 1996). "Erythromycin-felodipine interaction: magnitude, mechanism, and comparison with grapefruit juice". Clinical Pharmacology and Therapeutics. 60 (1): 25–33. doi:10.1016/s0009-9236(96)90163-0. PMID 8689808. S2CID 1246705.
  58. ^ Lown KS, Bailey DG, Fontana RJ, Janardan SK, Adair CH, Fortlage LA, et al. (May 1997). "Grapefruit juice increases felodipine oral availability in humans by decreasing intestinal CYP3A protein expression". The Journal of Clinical Investigation. 99 (10): 2545–2553. doi:10.1172/jci119439. PMC 508096. PMID 9153299.
  59. ^ Guengerich FP, Brian WR, Iwasaki M, Sari MA, Bäärnhielm C, Berntsson P (June 1991). "Oxidation of dihydropyridine calcium channel blockers and analogues by human liver cytochrome P-450 IIIA4". Journal of Medicinal Chemistry. 34 (6): 1838–1844. doi:10.1021/jm00110a012. PMID 2061924.
  60. ^ Owen JR, Nemeroff CB (30 May 1998). "New antidepressants and the cytochrome P450 system: focus on venlafaxine, nefazodone, and mirtazapine". Depression and Anxiety. 7 (Suppl 1): 24–32. doi:10.1002/(SICI)1520-6394(1998)7:1+<24::AID-DA7>3.0.CO;2-F. PMID 9597349. S2CID 34832618. Archived from the original on 1 November 2019. Retrieved 1 November 2019.
  61. ^ Spina E, D'Arrigo C, Migliardi G, Morgante L, Zoccali R, Ancione M, et al. (August 2004). "Plasma risperidone concentrations during combined treatment with sertraline". Therapeutic Drug Monitoring. 26 (4): 386–390. doi:10.1097/00007691-200408000-00008. PMID 15257068.
  62. ^ Sproule BA, Otton SV, Cheung SW, Zhong XH, Romach MK, Sellers EM (April 1997). "CYP2D6 inhibition in patients treated with sertraline". Journal of Clinical Psychopharmacology. 17 (2): 102–106. doi:10.1097/00004714-199704000-00007. PMID 10950472.
  63. ^ a b c d FASS, The Swedish official drug catalog > Kodein Recip Archived 19 July 2011 at the Wayback Machine Last reviewed 8 April 2008
  64. ^ Shin JG, Kane K, Flockhart DA (January 2001). "Potent inhibition of CYP2D6 by haloperidol metabolites: stereoselective inhibition by reduced haloperidol". British Journal of Clinical Pharmacology. 51 (1): 45–52. doi:10.1046/j.1365-2125.2001.01313.x. PMC 2014431. PMID 11167668.
  65. ^ He N, Zhang WQ, Shockley D, Edeki T (February 2002). "Inhibitory effects of H1-antihistamines on CYP2D6- and CYP2C9-mediated drug metabolic reactions in human liver microsomes". European Journal of Clinical Pharmacology. 57 (12): 847–851. doi:10.1007/s00228-001-0399-0. PMID 11936702. S2CID 601644.
  66. ^ Foster BC, Sockovie ER, Vandenhoek S, Bellefeuille N, Drouin CE, Krantis A, et al. (2008). "In Vitro Activity of St. John's Wort Against Cytochrome P450 Isozymes and P-Glycoprotein". Pharmaceutical Biology. 42 (2): 159–69. doi:10.1080/13880200490512034. S2CID 2366709.
  67. ^ Gaudineau C, Auclair K (May 2004). "Inhibition of human P450 enzymes by nicotinic acid and nicotinamide". Biochemical and Biophysical Research Communications. 317 (3): 950–956. doi:10.1016/j.bbrc.2004.03.137. PMID 15081432.
  68. ^ Briguglio M, Hrelia S, Malaguti M, Serpe L, Canaparo R, Dell'Osso B, et al. (December 2018). "Food Bioactive Compounds and Their Interference in Drug Pharmacokinetic/Pharmacodynamic Profiles". Pharmaceutics. 10 (4): 277. doi:10.3390/pharmaceutics10040277. PMC 6321138. PMID 30558213.
  69. ^ Kudo S, Ishizaki T (December 1999). "Pharmacokinetics of haloperidol: an update". Clinical Pharmacokinetics. 37 (6): 435–456. doi:10.2165/00003088-199937060-00001. PMID 10628896. S2CID 71360020.
  70. ^ Broadley KJ (March 2010). "The vascular effects of trace amines and amphetamines". Pharmacology & Therapeutics. 125 (3): 363–375. doi:10.1016/j.pharmthera.2009.11.005. PMID 19948186.
  71. ^ Lindemann L, Hoener MC (May 2005). "A renaissance in trace amines inspired by a novel GPCR family". Trends in Pharmacological Sciences. 26 (5): 274–281. doi:10.1016/j.tips.2005.03.007. PMID 15860375.

Further reading

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