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unsatisfactory; "a poor light for reading"; "poor morale"; "expectations were poor"
characterized by or indicating poverty; "the country had a poor economy"; "they lived in the poor section of town"
having little money or few possessions; "deplored the gap between rich and poor countries"; "the proverbial poor artist living in a garret"
lacking in specific resources, qualities or substances; "a poor land"; "the area was poor in timber and coal"; "food poor in nutritive value"
produce by metabolism (同)metabolise

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『貧乏な,貧しい』 / 『貧相な』,みすぼらしい / (一定規準よりも)劣る,落ちる / 《名詞の前にのみ用いて》哀れな,不運な,かわいそうな / 《名詞の前にのみ用いて》故人となった,なくなった / 《名詞の前にのみ用いて》《謙そん,またはおどけて》つまらない,取るに足らない / 《the~》《名詞的に》《複数扱い》貧しい人々;かわいそうな人々
= poo-poo・（幼児語）うんち・うんちをする

Wikipedia preview

出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2013/10/11 11:11:18」(JST)

wiki en

Cytochrome P450 2D6 is an enzyme that in humans is encoded by the CYP2D6 gene. CYP2D6 is primarily expressed in the liver.

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.^[1] This enzyme also metabolizes several endogenous substances such as hydroxytryptamines and neurosteroids.^[1]

There is considerable variation 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 (extensive 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.^[2] Hence the dose of the drug may have to be adjusted to take into account of the speed at which it is metabolized by CYP2D6.^[3]

In addition, 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 a second drug who is a CYP2D6 substrate, the first drug may affect the elimination rate of the second through what is known as a drug-drug interaction.^[2]

Gene[edit]

The gene is located near two cytochrome P450 pseudogenes on chromosome 22q13.1. Alternatively spliced transcript variants encoding different isoforms have been found for this gene.^[4]

Genotype/phenotype variability[edit]

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.

The CYP2D6 function in any particular subject may be described as one of the following:^[5]

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, and therefore greater-than-normal CYP2D6 function

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).^[6]

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 extensive metabolizers (strong CYP2D6 function) will have an exaggerated response to the drug and stronger side-effects.^[7]

Genetic basis of variability[edit]

The genetic basis for extensive and poor metaboliser variability is the CYP2D6 allele, located on chromosome 22. Subjects possessing certain allelic variants will show normal, decreased, or no CYP2D6 function, depending on the allele.

CYP2D6 allele and enzyme activity^[8]
Allele	CYP2D6 activity
CYP2D61*	normal
CYP2D62*	increased
CYP2D63*	none
CYP2D64*	none
CYP2D65*	none
CYP2D69*	decreased
CYP2D610*	decreased
CYP2D617*	decreased

Ethnic factors in variability[edit]

Ethnicity is a factor in the occurrence of CYP2D6 variability. The prevalence of CYP2D6 poor metabolizers is approximately 6–10% in white populations, but is lower in most other ethnic groups such as Asians (2%).^[9] In blacks, the frequency of poor metabolizers is greater than for whites.^[10] The occurrence of CYP2D6 ultrarapid metabolizers appears to be greater among Middle Eastern and North African populations.^[11]

This variability is accounted for by the differences in the prevalence of various CYP2D6 alleles among the populations–approximately 10% of whites are intermediate metabolzers, due to decreased CYP2D6 function, because they appear to have the non-functional CYP2D6*4 allele,^[8] while approximately 50% of Asians possess the decreased functioning CYP2D6*10 allele.^[8]

Ligands[edit]

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, or more than 80% decrease in clearance.^[12]
Moderate inhibitor being one that causes at least a 2-fold increase in the plasma AUC values, or 50-80% decrease in clearance.^[12]
Weak inhibitor being one that causes at least a 1.25-fold but less than 2-fold increase in the plasma AUC values, or 20-50% decrease in clearance.^[12]

**Selected inducers, inhibitors and substrates of CYP2D6**
Substrates ↑ = bioactivation by CYP2D6	Inhibitors	Inducers
All^[13] tricyclic antidepressants, e.g. imipramine^[12] amitriptyline^[12] etc. Most^[13] SSRIs (antidepressant), e.g. fluoxetine^[12] paroxetine^[12] fluvoxamine^[12] venlafaxine^[12]^[13] (SNRI antidepressant) mianserin^[13] (tetracyclic antidepressant) opioids codeine^[12]^[13] ↑^[14] into morphine tramadol^[12]^[13] ↑^[14] oxycodone ^[12] hydrocodone ↑^[15] antipsychotics, e.g. haloperidol^[12]^[13] risperidone^[12]^[13] perphenazine^[12]^[13] thioridazine^[12]^[13] zuclopenthixol^[12]^[13] iloperidone^[12]^[13] aripiprazole^[12]^[13] chlorpromazine^[12]^[13] levomepromazine^[13] remoxipride^[13] minaprine^[12] (RIMA antidepressant) tamoxifen^[12]^[13] ↑^[16] (SERM) beta-blockers metoprolol^[12]^[13] timolol^[12]^[13] alprenolol^[12]^[13] carvedilol^[12] bufuralol^[12] nebivolol^[12] propranolol^[12] debrisoquine^[12] (antihypertensive) Class I antiarrhythmics flecainide^[12]^[13] propafenone^[12]^[13] encainide^[12]^[13] mexiletine^[12]^[13] lidocaine^[12] sparteine^[12] ondansetron^[12]^[13] (antiemetic) donepezil^[12]^[13] (acetylcholinesterase inhibitor) phenformin^[12]^[13] (antidiabetic) tropisetron^[13] (5-HT3 receptor antagonist) amphetamine^[12] (in ADHD, narcolepsy) atomoxetine^[12] (in ADHD) chlorphenamine^[12] (antihistamine) dexfenfluramine^[12] (serotoninergic anorectic) dextromethorphan^[12] (antitussive) into psychoactive dextrorphan duloxetine^[12] (SNRI) metoclopramide^[12] (dopamine antagonist) Methoxyamphetamine^[12] perhexiline^[12] (antianginal agent) phenacetin^[12] (analgesic) promethazine^[12] (antihistamine antiemetic)	strong: SSRIs fluoxetine^[12]^[13] paroxetine^[12]^[13] bupropion^[12] (non-SSRI antidepressant) quinidine^[12]^[13] (class I antiarrhythmic agent) cinacalcet^[12] (calcimimetic) ritonavir^[13] (antiretroviral) Moderate sertraline^[12] (SSRI) duloxetine^[12] (SNRI) terbinafine^[12] (antifungal) weak: buprenorphine^[17] (in opioid addiction) amiodarone^[12] (antiarrhythmic) cimetidine^[12] (H2-receptor antagonist) unspecified potency: antipsychotics haloperidol^[18]^[12] perphenazine^[12]^[18] thioridazine^[18] zuclopenthixol^[18] risperidone^[18] chlorpromazine^[12] bicalutamide^[19] hyperforin (St. Johns Wort)^[20] antihistamines (H1-receptor antagonists) Promethazine^[21] chlorphenamine^[12] diphenhydramine^[12] hydroxyzine^[12] tripelennamine^[12] some SSRI antidepressants citalopram^[12] escitalopram^[12] clemastine^[12] (antihistamine and anticholinergic) celecoxib^[12] (NSAID) clomipramine^[12] (tricyclic antidepressant) cocaine^[12] (stimulant) doxorubicin^[12] (chemotherapeutic) metoclopramide^[12] (antiemetic, prokinetic) methadone^[12] (analgesic and anti-addictive) moclobemide^[12] (antidepressant) ranitidine^[12] (H2-receptor antagonist) doxepin^[12] (tricyclic antidepressant, anxiolytic) halofantrine^[12] (in malaria) levomepromazine^[12] (antipsychotic) mibefradil^[12] (calcium channel blocker) midodrine^[12] (α₁ agonist) ticlopidine^[12] (antiplatelet)	dexamethasone^[12] (glucocorticoid) rifampicin^[12] (bactericidal) strong: glutethimide (hypnotic sedative)

References[edit]

^ ^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 Metab. Rev. 41 (4): 573–643. doi:10.1080/03602530903118729. PMID 19645588.
^ ^a ^b Teh LK, Bertilsson L (2012). "Pharmacogenomics of CYP2D6: molecular genetics, interethnic differences and clinical importance". Drug Metab. Pharmacokinet. 27 (1): 55–67. doi:10.2133/dmpk.DMPK-11-RV-121. PMID 22185816.
^ Walko CM, McLeod H (April 2012). "Use of CYP2D6 genotyping in practice: tamoxifen dose adjustment". Pharmacogenomics 13 (6): 691–7. doi:10.2217/pgs.12.27. PMID 22515611.
^ "Entrez Gene: CYP2D6 cytochrome P450, family 2, subfamily D, polypeptide 6".
^ Bertilsson L, Dahl ML, Dalén P, Al-Shurbaji A (February 2002). "Molecular genetics of CYP2D6: clinical relevance with focus on psychotropic drugs". Br J Clin Pharmacol 53 (2): 111–22. doi:10.1046/j.0306-5251.2001.01548.x. PMC 1874287. PMID 11851634.
^ 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.
^ Lynch T, Price A (August 2007). "The effect of cytochrome P450 metabolism on drug response, interactions, and adverse effects". Am Fam Physician 76 (3): 391–6. PMID 17708140.
^ ^a ^b ^c Droll K, Bruce-Mensah K, Otton SV, Gaedigk A, Sellers EM, Tyndale RF (1998). "Comparison of three CYP2D6 probe substrates and genotype in Ghanaians, Chinese and Caucasians". Pharmacogenetics 8 (4): 325–33. doi:10.1097/00008571-199808000-00006. PMID 9731719.
^ Australian Medicines Handbook (AMH) 2004. ISBN 0-9578521-4-2
^ Gaedigk A, Bradford LD, Marcucci KA, Leeder JS (2002). "Unique CYP2D6 activity distribution and genotype-phenotype discordance in black Americans". Clin. Pharmacol. Ther. 72 (1): 76–89. doi:10.1067/mcp.2002.125783. PMID 12152006.
^ 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): 187–91. doi:10.1097/00008571-199706000-00003. PMID 9241658.
^ ^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 ^ch Flockhart DA (2007). "Drug Interactions: Cytochrome P₄₅₀ Drug Interaction Table". Indiana University School of Medicine. Retrieved on July 2011
^ ^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 FASS (drug formulary): Swedish environmental classification of pharmaceuticals Facts for prescribers (Fakta för förskrivare), retrieved July 2011
^ ^a ^b PHARMACOGENETICS AND PHARMACOGENOMICS. J. Steven Leeder PharmD, PhD Pediatric Clinics of North America - Volume 48, Issue 3 (June 2001). doi:10.1016/S0031-3955%2805%2970338-2.
^ "Hydrocodone". Drugbank. Retrieved 14 June 2011.
^ Hoskins JM, Carey LA, McLeod HL (August 2009). "CYP2D6 and tamoxifen: DNA matters in breast cancer". Nat. Rev. Cancer 9 (8): 576–86. doi:10.1038/nrc2683. PMID 19629072.
^ Zhang W, Ramamoorthy Y, Tyndale RF, Sellers EM (June 2003). "Interaction of buprenorphine and its metabolite norbuprenorphine with cytochromes p450 in vitro". Drug Metab. Dispos. 31 (6): 768–72. doi:10.1124/dmd.31.6.768. PMID 12756210.
^ ^a ^b ^c ^d ^e FASS, The Swedish official drug catalog > Kodein Recip Last reviewed 2008-04-08
^ Cockshott ID (2004). "Bicalutamide: clinical pharmacokinetics and metabolism". Clin Pharmacokinet 43 (13): 855–78. doi:10.2165/00003088-200443130-00003. PMID 15509184.
^ Foster BC, Sockovie ER, Vandenhoek S, Bellefeuille N, Drouin CE, Krantis A, Budzinski JW, Livesey J, and Arnason JT (2004). "In Vitro Activity of St. John's Wort Against Cytochrome P450 Isozymes and P-Glycoprotein ". Pharmaceutical Biology 42 (2): 159–169. doi:10.1080/13880200490512034.
^ 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". Eur. J. Clin. Pharmacol. 57 (12): 847–51. doi:10.1007/s00228-001-0399-0. PMID 11936702.

External links[edit]

Flockhart Lab Cyp2D6 Substrates Page at IUPUI
PharmGKB: Annotated PGx Gene Information for CYP2D6

UpToDate Contents

全文を閲覧するには購読必要です。 To read the full text you will need to subscribe.

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English Journal

Impact of CYP2C19 gene polymorphism on warfarin maintenance doses in patients with non-valvular atrial fibrillation.

Zhang H1, Ma K1, Liu W1, Yang F1, Liu J1, Zhou H2.
Gene.Gene.2016 Oct 10;591(1):80-4. doi: 10.1016/j.gene.2016.06.046. Epub 2016 Jun 26.
BACKGROUND: Pharmacogenetics has provided compelling evidence towards the influence of gene polymorphisms on warfarin therapies. This study aimed to determine the impact of CYP2C19 gene polymorphism on warfarin maintenance doses in patients with non-valvular atrial fibrillation for the progress in o
PMID 27356304

The Use of In Vitro Data and Physiologically-Based Pharmacokinetic Modeling to Predict Drug Metabolite Exposure: Desipramine Exposure in Cytochrome P4502D6 Extensive and Poor Metabolizers Following Administration of Imipramine.

Nguyen HQ1, Callegari E2, Obach RS2.
Drug metabolism and disposition: the biological fate of chemicals.Drug Metab Dispos.2016 Oct;44(10):1569-78. doi: 10.1124/dmd.116.071639. Epub 2016 Jul 20.
Major circulating drug metabolites can be as important as the drugs themselves in efficacy and safety, so establishing methods whereby exposure to major metabolites following administration of parent drug can be predicted is important. In this study, imipramine, a tricyclic antidepressant, and its m
PMID 27440861

Effect of cytochrome P450 2C19 polymorphisms on the clinical outcomes of voriconazole: a systematic review and meta-analysis.

Li X1,2, Yu C1,3, Wang T4, Chen K1, Zhai S1, Tang H5.
European journal of clinical pharmacology.Eur J Clin Pharmacol.2016 Oct;72(10):1185-93. doi: 10.1007/s00228-016-2089-y. Epub 2016 Jul 8.
BACKGROUND: Genetic polymorphisms of cytochrome P450 enzymes, especially CYP2C19, could influence voriconazole pharmacokinetics. The association between CYP2C19 polymorphisms and voriconazole clinical outcomes is not well established. The aim of this meta-analysis was to evaluate the effect of CYP2C
PMID 27388292

Japanese Journal

Characterization of Patients With Angioscopically-Detected In-Stent Mural Thrombi:– Genetics of Clopidogrel Responsiveness and Generations of Drug-Eluting Stents –

Ichikawa Minoru,Takei Yoshizumi,Hamasaki Toshimitsu,Kijima Yoshiyuki
Circulation Journal, 2014
… A poor metabolizer (PM) of clopidogrel was defined as a homozygote of CYP2C19 loss-of-function alleles. …
NAID 130004701551

Intra-gastric pH following single oral administrations of rabeprazole and esomeprazole: double-blind cross-over comparison

, , , , , , , , , , , , , , , , , , , , , , ,
Journal of Clinical Biochemistry and Nutrition 55(3), 178-183, 2014
… In poor metabolizer, both of the drugs showed stronger acid inhibition. …
NAID 130004694546

開心術後 Warfarin と PPI の相互作用による合併症回避のためのリスクマネージメントを目標としたゲノム解析

木村玄,秦光賢,塩野元美,関野久邦
日本心臓血管外科学会雑誌 43(4), 163-169, 2014
… 過程を共有するため，INR（International Normalizing Ratio）が急上昇し出血合併症のリスクとなる．［対象］CYP2C19の遺伝子亜型は代謝の早いEM（Extensive Metabolizer）型，遅いPM（Poor Metabolizer）型，中間のIM（Intermediate Metabolizer）型の3種が存在するが，WF，PPIの競合作用における遺伝子の関与については不明である．［結果］われわれは，PPIの種類とCYP2C19遺伝子亜型によ …
NAID 130004679591

Related Pictures

★リンクテーブル★

リンク元	「ultra-rapid metabolizers」
関連記事	「poor」「metabolize」

「ultra-rapid metabolizers」

Cytochrome P450, family 2, subfamily D, polypeptide 6
	; PDB rendering based on 2f9q.
Available structures
PDB	Ortholog search: PDBe, RCSB
List of PDB id codes
	2F9Q, 3QM4, 3TBG, 3TDA
Identifiers
Symbols	CYP2D6; CPD6; CYP2D; CYP2D7AP; CYP2D7BP; CYP2D7P2; CYP2D8P2; CYP2DL1; CYPIID6; P450-DB1; P450C2D; P450DB1
External IDs	OMIM: 124030 MGI: 1929474 HomoloGene: 86099 GeneCards: CYP2D6 Gene
EC number	1.14.14.1
Gene Ontology
Molecular function	• monooxygenase activity; • iron ion binding; • drug binding; • electron carrier activity; • oxidoreductase activity; • heme binding; • aromatase activity;
Cellular component	• mitochondrion; • endoplasmic reticulum; • endoplasmic reticulum membrane;
Biological process	• xenobiotic metabolic process; • steroid metabolic process; • coumarin metabolic process; • alkaloid metabolic process; • alkaloid catabolic process; • monoterpenoid metabolic process; • drug metabolic process; • isoquinoline alkaloid metabolic process; • drug catabolic process; • small molecule metabolic process; • heterocycle metabolic process; • negative regulation of binding; • oxidation-reduction process; • oxidative demethylation; • negative regulation of cellular organofluorine metabolic process;
	Sources: Amigo / QuickGO
RNA expression pattern
	More reference expression data
Orthologs
	This box: view; talk; edit;

　　[★]

同: UM
関: extensive metabolizer EM, poor metabolizer PM, inter-mediate metabolizer, IM

特定の薬物の代謝が異常に早い人

「poor」

　　[★]

adj.

乏しい

関: scant、scanty、short

「metabolize」

　　[★]

vt.

新陳代謝させる

vi.

新陳代謝する

関: metabolism

[pmid19645588-1] 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 Metab. Rev. 41 (4): 573–643. doi:10.1080/03602530903118729. PMID 19645588.

[pmid22185816-2] Teh LK, Bertilsson L (2012). "Pharmacogenomics of CYP2D6: molecular genetics, interethnic differences and clinical importance". Drug Metab. Pharmacokinet. 27 (1): 55–67. doi:10.2133/dmpk.DMPK-11-RV-121. PMID 22185816.

[pmid22515611-3] Walko CM, McLeod H (April 2012). "Use of CYP2D6 genotyping in practice: tamoxifen dose adjustment". Pharmacogenomics 13 (6): 691–7. doi:10.2217/pgs.12.27. PMID 22515611.

[4] "Entrez Gene: CYP2D6 cytochrome P450, family 2, subfamily D, polypeptide 6".

[pmid11851634-5] Bertilsson L, Dahl ML, Dalén P, Al-Shurbaji A (February 2002). "Molecular genetics of CYP2D6: clinical relevance with focus on psychotropic drugs". Br J Clin Pharmacol 53 (2): 111–22. doi:10.1046/j.0306-5251.2001.01548.x. PMC 1874287. PMID 11851634.

[pmid19102711-6] 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.

[pmid17708140-7] Lynch T, Price A (August 2007). "The effect of cytochrome P450 metabolism on drug response, interactions, and adverse effects". Am Fam Physician 76 (3): 391–6. PMID 17708140.

[Droll_1998-8] Droll K, Bruce-Mensah K, Otton SV, Gaedigk A, Sellers EM, Tyndale RF (1998). "Comparison of three CYP2D6 probe substrates and genotype in Ghanaians, Chinese and Caucasians". Pharmacogenetics 8 (4): 325–33. doi:10.1097/00008571-199808000-00006. PMID 9731719.

[9] Australian Medicines Handbook (AMH) 2004. ISBN 0-9578521-4-2

[10] Gaedigk A, Bradford LD, Marcucci KA, Leeder JS (2002). "Unique CYP2D6 activity distribution and genotype-phenotype discordance in black Americans". Clin. Pharmacol. Ther. 72 (1): 76–89. doi:10.1067/mcp.2002.125783. PMID 12152006.

[pmid9241658-11] 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): 187–91. doi:10.1097/00008571-199706000-00003. PMID 9241658.

[Flockhart-12] ^ ^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 ^ch Flockhart DA (2007). "Drug Interactions: Cytochrome P₄₅₀ Drug Interaction Table". Indiana University School of Medicine. Retrieved on July 2011

[FASS-13] ^ ^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 FASS (drug formulary): Swedish environmental classification of pharmaceuticals Facts for prescribers (Fakta för förskrivare), retrieved July 2011

[Leeder-14] PHARMACOGENETICS AND PHARMACOGENOMICS. J. Steven Leeder PharmD, PhD Pediatric Clinics of North America - Volume 48, Issue 3 (June 2001). doi:10.1016/S0031-3955%2805%2970338-2.

[15] "Hydrocodone". Drugbank. Retrieved 14 June 2011.

[pmid19629072-16] Hoskins JM, Carey LA, McLeod HL (August 2009). "CYP2D6 and tamoxifen: DNA matters in breast cancer". Nat. Rev. Cancer 9 (8): 576–86. doi:10.1038/nrc2683. PMID 19629072.

[pmid12756210-17] Zhang W, Ramamoorthy Y, Tyndale RF, Sellers EM (June 2003). "Interaction of buprenorphine and its metabolite norbuprenorphine with cytochromes p450 in vitro". Drug Metab. Dispos. 31 (6): 768–72. doi:10.1124/dmd.31.6.768. PMID 12756210.

[fass-codeine-18] FASS, The Swedish official drug catalog > Kodein Recip Last reviewed 2008-04-08

[pmid15509184-19] Cockshott ID (2004). "Bicalutamide: clinical pharmacokinetics and metabolism". Clin Pharmacokinet 43 (13): 855–78. doi:10.2165/00003088-200443130-00003. PMID 15509184.

[20] Foster BC, Sockovie ER, Vandenhoek S, Bellefeuille N, Drouin CE, Krantis A, Budzinski JW, Livesey J, and Arnason JT (2004). "In Vitro Activity of St. John's Wort Against Cytochrome P450 Isozymes and P-Glycoprotein ". Pharmaceutical Biology 42 (2): 159–169. doi:10.1080/13880200490512034.

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poor metabolizer