CYP2D6

Human liver enzyme

CYP2D6

| Available structures

PDB| Human UniProt search: PDBe RCSB
| List of PDB id codes

2F9Q, 3QM4, 3TBG, 3TDA, 4WNT, 4WNU, 4WNV, 4WNW, 4XRY, 4XRZ

Identifiers
Aliases| CYP2D6, CPD6, CYP2D, CYP2D7AP, CYP2D7BP, CYP2D7P2, CYP2D8P2, CYP2DL1, CYPIID6, P450-DB1, P450C2D, P450DB1, cytochrome P450 family 2 subfamily D member 6, Cytochrome P450 2D6
External IDs| OMIM: 124030 HomoloGene: 133550 GeneCards: CYP2D6
| Gene location (Human)

Chr.| Chromosome 22 (human)[1]

Band| 22q13.2| Start| 42,126,499 bp[1]
End| 42,130,865 bp[1]
| RNA expression pattern

Bgee| | Human| Mouse (ortholog)

|

| Top expressed in

* right lobe of liver

* duodenum

* sural nerve

* right uterine tube

* pituitary gland

* right lobe of thyroid gland

* left lobe of thyroid gland

* nucleus accumbens

* anterior pituitary

* putamen

n/a

More reference expression data
BioGPS| |

More reference expression data
| Gene ontology

Molecular function|

* iron ion binding
* metal ion binding
* heme binding
* oxidoreductase activity, acting on paired donors, with incorporation or reduction of molecular oxygen
* oxidoreductase activity
* aromatase activity
* oxidoreductase activity, acting on paired donors, with incorporation or reduction of molecular oxygen, reduced flavin or flavoprotein as one donor, and incorporation of one atom of oxygen
* steroid hydroxylase activity
* monooxygenase activity

Cellular component|

* organelle membrane
* endoplasmic reticulum membrane
* membrane
* intracellular membrane-bounded organelle
* endoplasmic reticulum
* mitochondrion
* cytoplasm

Biological process|

* steroid metabolic process
* alkaloid metabolic process
* coumarin metabolic process
* lipid metabolism
* isoquinoline alkaloid metabolic process
* alkaloid catabolic process
* oxidative demethylation
* heterocycle metabolic process
* negative regulation of binding
* monoterpenoid metabolic process
* xenobiotic metabolic process
* arachidonic acid metabolic process
* negative regulation of cellular organofluorine metabolic process
* long-chain fatty acid biosynthetic process
* organic acid metabolic process

Sources:Amigo / QuickGO
| Orthologs

Species| Human| Mouse
Entrez| |

1565

n/a

Ensembl| | ENSG00000100197
ENSG00000275211
ENSG00000280905
ENSG00000282966
ENSG00000283284

ENSG00000272532

n/a

UniProt| |

P10635

n/a

RefSeq (mRNA)| |

NM_000106
NM_001025161

n/a

RefSeq (protein)| |

NP_000097
NP_001020332

n/a

Location (UCSC)| Chr 22: 42.13 – 42.13 Mb| n/a
PubMed search| [2]| n/a
Wikidata
| View/Edit Human|

|

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.[3] CYP2D6 also activates some prodrugs. This enzyme also metabolizes several endogenous substances, such as hydroxytryptamines, neurosteroids, and both m-tyramine and p-tyramine which CYP2D6 metabolizes into dopamine in the brain and liver.[3][4]

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.[5] 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.[6] Individuals who have ultrarapid polymorphism, however, may metabolize prodrugs, such as codeine or tramadol, to potentially fatal levels either through breast milk[7][8][9] such as treating post-cesarian section pain. These drugs may also cause serious toxicity in ultrarapid metabolizer patients when used to treat other post-operative pain, such as after tonsillectomy.[10][11][12] 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.[5]

## Gene[edit]

The gene is located on chromosome 22q13.1. near two cytochrome P450 pseudogenes (CYP2D7P and CYP2D8P).[13] Among them, CYP2D7P originated from CYP2D6 in a stem lineage of great apes and humans,[14] the CYP2D8P originated from CYP2D6 in a stem lineage of Catarrhine and New World monkeys' stem lineage.[15] Alternatively spliced transcript variants encoding different isoforms have been found for this gene.[16]

## 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. 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.[17] The CYP2D6 function in any particular subject may be described as one of the following:[18]

* 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).[19]

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.[20] Information about how human genetic variation of CYP2D6 affects response to medications can be found in databases such PharmGKB,[21] Clinical Pharmacogenetics Implementation Consortium (CPIC).[22]

## Genetic basis of variability[edit]

The genetic basis for CYP2D6-mediated metabolic 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. 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.[17] The current known alleles of CYP2D6 and their clinical function can be found in databases such as PharmVar.[23]

CYP2D6 enzyme activity for selected alleles[24][23]

Allele  | CYP2D6 activity
CYP2D6*1 | normal
CYP2D6*2 | normal
CYP2D6*3 | none
CYP2D6*4 | none
CYP2D6*5 | none
CYP2D6*6 | none
CYP2D6*7 | none
CYP2D6*8 | none
CYP2D6*9 | decreased
CYP2D6*10 | decreased
CYP2D6*11 | none
CYP2D6*12 | none
CYP2D6*13 | none
CYP2D6*14 | none
CYP2D6*15 | none
CYP2D6*17 | decreased
CYP2D6*19 | none
CYP2D6*20 | none
CYP2D6*21 | none
CYP2D6*29 | decreased
CYP2D6*31 | none
CYP2D6*38 | none
CYP2D6*40 | none
CYP2D6*41 | decreased
CYP2D6*42 | none
CYP2D6*44 | none
CYP2D6*47 | none
CYP2D6*50 | decreased
CYP2D6*51 | none
CYP2D6*68 | none
CYP2D6*92 | none
CYP2D6*100 | none
CYP2D6*101 | none
CYP2D6 duplication | increased

## Ethnic factors in variability[edit]

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.[25] The occurrence of CYP2D6 ultrarapid metabolizers appears to be greater among Middle Eastern and North African populations.[26][27]

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.[28]

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,[24] while approximately 50% of Asians possess the decreased functioning CYP2D6*10 allele.[24]

## 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 of sensitive substrates metabolized through CYP2D6, or more than 80% decrease in clearance thereof.[29]
* 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.[29]
* 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.[29]

Selected inducers, inhibitors and substrates of CYP2D6 Substrates
↑ = bioactivation by CYP2D6 | Inhibitors | Inducers

|
|

* All[30] tricyclic antidepressants, e.g.
* imipramine[29]
* amitriptyline[29]
* etc.
* Most[30] SSRIs (antidepressant), e.g.
* fluoxetine[29]
* paroxetine[29]
* fluvoxamine[29]
* venlafaxine[29][30] (SNRI antidepressant)
* duloxetine[29] (SNRI, moderate sensitive substrates of CYP2D6[29])
* mianserin[30] (tetracyclic antidepressant)
* mirtazapine[30] (antidepressant)
* opioids
* codeine[29][30] ↑ [into morphine][31]
* tramadol[29][30] ↑ [into O-desmethyltramadol][31]
* N-desmethyltramadol [inactive] ↑ [into N,O-didesmethyltramadol]
* oxycodone[29]
* hydrocodone ↑ [into hydromorphone][32]
* tapentadol
* antipsychotics, e.g.
* haloperidol[29][30]
* risperidone[29][30]
* perphenazine[29][30]
* thioridazine[29][30]
* zuclopenthixol[29][30]
* iloperidone[29][30]
* aripiprazole[29][30]
* chlorpromazine[29][30]
* levomepromazine[30]
* remoxipride[30]
* minaprine[29] (RIMA antidepressant)
* tamoxifen[29][30] ↑ [into hydroxytamoxifen][33] (SERM)
* beta-blockers
* metoprolol[29][30]
* timolol[29][30]
* alprenolol[29][30]
* carvedilol[29]
* bufuralol[29]
* nebivolol[29]
* propranolol[29]
* debrisoquine[29] (antihypertensive)
* Class I antiarrhythmics
* flecainide[29][30]
* propafenone[29][30]
* encainide[29][30]
* mexiletine[29][30]
* lidocaine[29]
* sparteine[29]
* ondansetron[29][30] (antiemetic)
* donepezil[29][30] (acetylcholinesterase inhibitor)
* phenformin[29][30] (antidiabetic)
* tropisetron[30] (5-HT3 receptor antagonist)
* stimulants
* amphetamine[29]
* methoxyamphetamine[29]
* dextromethamphetamine[29]
* Lisdexamfetamine
* NRI
* atomoxetine (Sensitive substrate of CYP2D6) [29]
* H3 receptor antagonist/inverse agonist
* pitolisant[34]
* chlorphenamine[29] (antihistamine)
* dexfenfluramine[29] (serotoninergic anorectic)
* dextromethorphan[29] ↑ [into dextrorphan] (antitussive)
* metoclopramide[29] (dopamine antagonist)
* perhexiline[29] (antianginal agent)
* phenacetin[29] (analgesic)
* promethazine[29] (antihistamine antiemetic)
* m-tyramine[35]
* p-tyramine[35]
* Lysergic acid diethylamide (LSD)[36]
* 5-methoxy-N,N-dimethyltryptamine[37]
* Calcium channel blocker
* diltiazem (minor/moderate sensitive substrate) [38]
* nifedipine (minor/moderate sensitive substrate)[39]

Strong

* Certain SSRIs
* fluoxetine[29][30]
* paroxetine[29][30]
* bupropion[29][40] (non-SSRI antidepressant)
* quinidine[29][30] (class I antiarrhythmic agent)
* quinine[41]
* cinacalcet[29] (calcimimetic)
* ritonavir[30] (antiretroviral)
* cannabidiol[42]

Moderate

* duloxetine[29] (SNRI)
* terbinafine[29] (antifungal)

Weak

* amiodarone[29] (antiarrhythmic)
* berberine[43][44][45] (an alkaloid found in plants like berberis)
* buprenorphine[46] (in opioid addiction)
* cimetidine[29] (H2-receptor antagonist)
* citalopram[29][47] (SSRI)
* escitalopram[29][47][48] (SSRI)
* fluvoxamine[49] (SSRI)
* methylphenidate[50]
* diltiazem[38]
* felodipine[51][52][53]
* mirtazapine[54]
* sertraline[49] (SSRI)

Unspecified potency

* antipsychotics
* haloperidol[55][29]
* perphenazine[29][55]
* thioridazine[55]
* zuclopenthixol[55]
* chlorpromazine[29]
* antihistamines (H1-receptor antagonists)
* promethazine[56] (antipsychotic)
* chlorphenamine[29]
* diphenhydramine[29]
* hydroxyzine[29]
* tripelennamine[29]
* celecoxib[29] (NSAID)
* clemastine[29] (antihistamine and anticholinergic)
* clomipramine[29] (tricyclic antidepressant)
* cocaine[29] (stimulant)
* doxepin[29] (tricyclic antidepressant, anxiolytic)
* doxorubicin[29] (chemotherapeutic)
* halofantrine[29] (in malaria)
* hyperforin (St. Johns Wort)[57]
* levomepromazine[29] (antipsychotic)
* methadone[29] (analgesic and anti-addictive)
* metoclopramide[29] (antiemetic, prokinetic)
* mibefradil[29] (calcium channel blocker)
* midodrine[29] (α1 agonist)
* moclobemide[29] (antidepressant)
* niacin[58] (nicotinic acid) and its form – niacinamide (nicotinamide), collectively called as vitamin B3
* sesame[59] (seeds, oil)
* ticlopidine[29] (antiplatelet)

Strong

* glutethimide (hypnotic sedative)

Unspecified potency

* haloperidol[60] (typical antipsychotic)

### Dopamine biosynthesis[edit]

Biosynthetic pathways for catecholamines and trace amines in the human brain[61][62][35]

L-Phenylalanine

L-Tyrosine

L-DOPA

Epinephrine

Phenethylamine

p-Tyramine

Dopamine

Norepinephrine

N-Methylphenethylamine

N-Methyltyramine

p-Octopamine

Synephrine

3-Methoxytyramine

AADC

AADC

AADC

primary
pathway

PNMT

PNMT

PNMT

PNMT

AAAH

AAAH

brain
CYP2D6

minor
pathway

COMT

DBH

DBH

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.[35] Similarly, CYP2D6 also metabolizes m-tyramine into dopamine.[35]

## References[edit]

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46. ^ 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): 768–72. doi:10.1124/dmd.31.6.768. PMID 12756210.
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## Further reading[edit]

* Smith G, Stubbins MJ, Harries LW, Wolf CR (December 1998). "Molecular genetics of the human cytochrome P450 monooxygenase superfamily". Xenobiotica; the Fate of Foreign Compounds in Biological Systems. 28 (12): 1129–65. doi:10.1080/004982598238868. PMID 9890157.
* Wolf CR, Smith G (1999). "Cytochrome P450 CYP2D6". IARC Scientific Publications (148): 209–29. PMID 10493260.
* Ding X, Kaminsky LS (2003). "Human extrahepatic cytochromes P450: function in xenobiotic metabolism and tissue-selective chemical toxicity in the respiratory and gastrointestinal tracts". Annual Review of Pharmacology and Toxicology. 43: 149–73. doi:10.1146/annurev.pharmtox.43.100901.140251. PMID 12171978.
* Lilienfeld S (2006). "Galantamine--a novel cholinergic drug with a unique dual mode of action for the treatment of patients with Alzheimer's disease". CNS Drug Reviews. 8 (2): 159–76. doi:10.1111/j.1527-3458.2002.tb00221.x. PMC 6741688. PMID 12177686.
* Yu AM, Idle JR, Gonzalez FJ (May 2004). "Polymorphic cytochrome P450 2D6: humanized mouse model and endogenous substrates". Drug Metabolism Reviews. 36 (2): 243–77. doi:10.1081/DMR-120034000. PMID 15237854. S2CID 11330784.
* Abraham JE, Maranian MJ, Driver KE, Platte R, Kalmyrzaev B, Baynes C, et al. (2010). "CYP2D6 gene variants: association with breast cancer specific survival in a cohort of breast cancer patients from the United Kingdom treated with adjuvant tamoxifen". Breast Cancer Research. 12 (4): R64. doi:10.1186/bcr2629. PMC 2949659. PMID 20731819.
* Abraham JE, Maranian MJ, Driver KE, Platte R, Kalmyrzaev B, Baynes C, et al. (June 2011). "CYP2D6 gene variants and their association with breast cancer susceptibility". Cancer Epidemiology, Biomarkers & Prevention. 20 (6): 1255–8. doi:10.1158/1055-9965.EPI-11-0321. PMID 21527579. S2CID 32846974.

## External links[edit]

* Flockhart Lab Cyp2D6 Substrates Page at IUPUI
* PharmGKB: Annotated PGx Gene Information for CYP2D6
* Human CYP2D6 genome location and CYP2D6 gene details page in the UCSC Genome Browser.
* Overview of all the structural information available in the PDB for UniProt: P10635 (Cytochrome P450 2D6) at the PDBe-KB.

* v
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PDB gallery

* 2f9q: Crystal Structure of Human Cytochrome P450 2D6

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Cytochromes, oxygenases: cytochrome P450 (Most belong to EC 1.14)

CYP1|

* A1
* A2
* A5
* B1

CYP2|

* A6
* A7
* A13
* B6
* C8
* C9
* C18
* C19
* D6
* E1
* F1
* J2
* R1
* S1
* U1
* W1

CYP3 (CYP3A)|

* A4
* A5
* A7
* A37
* A43

CYP4|

* A11
* A22
* B1
* F2
* F3
* F8
* F11
* F12
* F22
* V2
* X1
* Z1

CYP5-20|

* CYP5 (A1)
* CYP6 (G1, M2)
* CYP7 (A1, B1)
* CYP8 (A1, B1)
* CYP9
* CYP10
* CYP11 (A1, A2, B1, B2, B3, C1)
* CYP12
* CYP13
* CYP14
* CYP15
* CYP16
* CYP17 (A1)
* CYP18
* CYP19 (A1)
* CYP20 (A1)

CYP21-49|

* CYP21 (A2)
* CYP22 (A1)
* CYP23
* CYP24 (A1)
* CYP25
* CYP26 (A1, B1, C1)
* CYP27 (A1, B1, C1)
* CYP28 (A1)
* CYP29
* CYP35 (B1)
* CYP39 (A1)
* CYP46 (A1)

CYP51-69|

* CYP51 (A1, F1)
* CYP52
* CYP53 (A1)
* CYP55
* CYP56A1
* CYP61

CYP71-99|

* CYP71 (C1, C2, C3, C4, Z6, AJ4, AV1, BA1)
* CYP72A1
* CYP73A1
* CYP74 (D1)
* CYP75 (A1, B1)
* CYP76 (B6, M7)
* CYP79 (A1, A2, B1, B2, B3, D1, D2, D3, D4)
* CYP80 (A1, B1, G2)
* CYP81 (E1, E3, E7, E9)
* CYP88D6
* CYP90C1
* CYP93E1
* CYP97C1
* CYP99A3

CYP101-281|

* CYP101A1
* CYP102A1
* CYP105
* A1
* D7
* CYP106A2
* CYP107
* A1
* G1
* CYP109
* B1
* E1
* CYP111
* CYP113A1
* CYP119A1
* CYP123
* CYP125A1
* CYP139
* CYP152
* A1
* B1
* CYP154C3
* CYP158A
* CYP161C
* CYP170
* A1
* B1
* CYP176A1
* CYP183A
* CYP199A2
* CYP255A

CYP301-499|

* CYP303A1
* CYP305
* M2
* Halloween genes ( CYP302A1, CYP306A1, CYP307A1, CYP307A2, CYP314A1, CYP315A1)
* CYP318A1

CYP501-699|

* CYP503
* CYP504B1

CYP701-999|

* CYP710
* CYP720A1

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Oxidoreductases: dioxygenases, including steroid hydroxylases (EC 1.14)

1.14.11: 2-oxoglutarate|

* Prolyl hydroxylase
* HIF prolyl-hydroxylase
* EGLN1
* EGLN2
* EGLN3
* P4HTM
* Lysyl hydroxylase
* AlkB
* ALKBH1
* FTO

1.14.13: NADH or NADPH|

* Flavin-containing monooxygenase
* FMO1
* FMO2
* FMO3
* FMO4
* FMO5
* Nitric oxide synthase
* NOS1
* NOS2
* NOS3
* Cholesterol 7 alpha-hydroxylase
* Methane monooxygenase
* 3A4
* 14α-demethylase
* 24-hydroxycholesterol 7α-hydroxylase

1.14.14: reduced flavin or flavoprotein|

* 19A1
* 2D6
* 2E1

1.14.15: reduced iron–sulfur protein|

* 11B1
* 11B2
* 11A1

1.14.16: reduced pteridine (BH4 dependent)|

* Phenylalanine hydroxylase
* Tyrosine hydroxylase
* Tryptophan hydroxylase

1.14.17: reduced ascorbate|

* Dopamine beta-hydroxylase

1.14.18-19: other|

* Tyrosinase
* Stearoyl-CoA desaturase-1

1.14.99 \- miscellaneous|

* Cyclooxygenase
* Heme oxygenase (HMOX1)
* Squalene monooxygenase
* 17A1
* 21A2
* Ecdysone 20-monooxygenase
* Deoxyhypusine monooxygenase

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Enzymes

Activity|

* Active site
* Binding site
* Catalytic triad
* Oxyanion hole
* Enzyme promiscuity
* Diffusion-limited enzyme
* Cofactor
* Enzyme catalysis

Regulation|

* Allosteric regulation
* Cooperativity
* Enzyme inhibitor
* Enzyme activator

Classification|

* EC number
* Enzyme superfamily
* Enzyme family
* List of enzymes

Kinetics|

* Enzyme kinetics
* Eadie–Hofstee diagram
* Hanes–Woolf plot
* Lineweaver–Burk plot
* Michaelis–Menten kinetics

Types|

* EC1 Oxidoreductases (list)
* EC2 Transferases (list)
* EC3 Hydrolases (list)
* EC4 Lyases (list)
* EC5 Isomerases (list)
* EC6 Ligases (list)
* EC7 Translocases (list)

Portal:

* Biology

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