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Identification
Name Selegiline
Accession Number DB01037 (APRD00525)
Type small molecule
Groups approved
Description

A selective, irreversible inhibitor of Type B monoamine oxidase. It is used in newly diagnosed patients with Parkinson’s disease. It may slow progression of the clinical disease and delay the requirement for levodopa therapy. It also may be given with levodopa upon onset of disability. (From AMA Drug Evaluations Annual, 1994, p385) The compound without isomeric designation is Deprenyl. [PubChem]
Structure Thumb
Download: MOL | SDF | SMILES | InChI
Display: 2D Structure | 3D Structure
Synonyms
L-Deprenalin
Selegeline Hcl
Selegilina [INN-Spanish]
Selegilinum [INN-Latin]
Salts Not Available
Brand names
Name Company
Apo-Selegiline
Carbex
Eldepryl
Emsam
Gen-Selegiline
Jumex
Novo-Selegiline
Nu-Selegiline
Sd Deprenyl
Zelapar
Brand mixtures Not Available
Categories
  • Central Nervous System Agents
  • Antiparkinson Agents
  • Antidyskinetics
  • Neuroprotective Agents
  • Monoamine Oxidase Inhibitors
  • Dopaminergics
CAS number 14611-51-9
Weight Average: 187.2808
Monoisotopic: 187.136099549
Chemical Formula C13H17N
InChI Key InChIKey=MEZLKOACVSPNER-UHFFFAOYSA-N
InChI
InChI=1S/C13H17N/c1-4-10-14(3)12(2)11-13-8-6-5-7-9-13/h1,5-9,12H,10-11H2,2-3H3
Plain Text
IUPAC Name
methyl(1-phenylpropan-2-yl)(prop-2-yn-1-yl)amine
SMILES
CC(CC1=CC=CC=C1)N(C)CC#C
Plain Text
Mass Spec Not Available
Taxonomy
Kingdom Not Available
Classes Not Available
Substructures Not Available
Pharmacology
Indication Monotherapy for initial treatment of Parkinson's disease, as well as an adjunct therapy in patients with a decreased response to levodopa/carbadopa. Also used for the palliative treatment of mild to moderate Alzheimer's disease and at higher doses, for the treatment of depression.
Pharmacodynamics Dopamine is an essential chemical that occurs in many parts of the body. It is the premature degradation of dopamine that results in the symptoms of Parkinson's disease. Monoamine oxidase (MAO) is an enzyme which accelerates the breakdown of dopamine. Selegiline can prolong the effects of dopamine in the brain by preventing its breakdown through seletively blocking MAO-B. It also may prevent the removal of dopamine between nerve endings and enhance release of dopamine from nerve cells.
Mechanism of action Although the mechanisms for selegiline's beneficial action in the treatment of Parkinson's disease are not fully understood, the selective, irreversible inhibition of monoamine oxidase type B (MAO-B) is thought to be of primary importance. MAO-B is involved in the oxidative deamination of dopamine in the brain. Selegiline binds to MAO-B within the nigrostriatal pathways in the central nervous system, thus blocking microsomal metabolism of dopamine and enhancing the dopaminergic activity in the substantial nigra. Selegiline may also increase dopaminergic activity through mechanisms other than inhibition of MAO-B. At higher doses, selegiline can also inhibit monozmine oxidase type A (MAO-A), allowing it to be used for the treatment of depression.
Absorption Rapidly absorbed from the gastrointestinal tract.
Volume of distribution Not Available
Protein binding > 99.5%
Metabolism Not Available
Route of elimination Not Available
Half life 1.2-2 hours
Clearance Not Available
Toxicity LD50=63 mg/kg (rats, IV)
Affected organisms
  • Humans and other mammals
Pathways Not Available
Pharmacoeconomics
Manufacturers
  • Somerset pharmaceuticals inc
  • Aaipharma llc
  • Apotex inc
  • Dava pharmaceuticals inc
  • Valeant pharmaceuticals international
  • Apotex inc etobicoke site
  • Endo pharmaceuticals inc
  • Ivax pharmaceuticals inc sub teva pharmaceuticals usa
  • Mylan pharmaceuticals inc
  • Siegfried ltd
  • Stason industrial corp
  • Teva pharmaceuticals usa inc
Packagers
Dosage forms
Form Route Strength
Tablet Oral
Prices
Unit description Cost Unit
Emsam 30 12 mg/24hr Patches Box 627.1 USD box
Emsam 30 6 mg/24hr Patches Box 627.1 USD box
Emsam 30 9 mg/24hr Patches Box 627.1 USD box
Selegiline hcl powder 127.3 USD g
Eldepryl 30 5 mg capsule Box 89.55 USD box
Emsam 12 mg/24 hours patch 20.1 USD patch
Emsam 6 mg/24 hours patch 20.1 USD patch
Emsam 9 mg/24 hours patch 20.1 USD patch
Zelapar 1.25 mg odt tablet 8.33 USD tablet
Selegiline HCl 5 mg capsule 2.4 USD capsule
Selegiline hcl 5 mg tablet 2.1 USD tablet
Apo-Selegiline 5 mg Tablet 1.33 USD tablet
Mylan-Selegiline 5 mg Tablet 1.33 USD tablet
Novo-Selegiline 5 mg Tablet 1.33 USD tablet
Nu-Selegiline 5 mg Tablet 1.33 USD tablet
Pms-Selegiline 5 mg Tablet 1.33 USD tablet
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DrugBank does not sell nor buy drugs. Pricing information is supplied for informational purposes only.
Patents
Country Patent Number Approved Expires (estimated)
United States 7150881 1998-06-12 2018-06-12
United States 5648093 1994-07-15 2014-07-15
Properties
State solid
Experimental Properties
Property Value Source
melting point 141-142 °C Not Available
logP 2.7 Not Available
Predicted Properties
Property Value Source
water solubility 2.54e-02 g/l ALOGPS
logP 3.08 ALOGPS
logP 2.85 ChemAxon
logS -3.9 ALOGPS
pKa (strongest basic) 8.67 ChemAxon
physiological charge 1 ChemAxon
hydrogen acceptor count 1 ChemAxon
hydrogen donor count 0 ChemAxon
polar surface area 3.24 ChemAxon
rotatable bond count 4 ChemAxon
refractivity 61.35 ChemAxon
polarizability 22.48 ChemAxon
References
Synthesis Reference Not Available
General Reference
  1. Engberg G, Elebring T, Nissbrandt H: Deprenyl (selegiline), a selective MAO-B inhibitor with active metabolites; effects on locomotor activity, dopaminergic neurotransmission and firing rate of nigral dopamine neurons. J Pharmacol Exp Ther. 1991 Nov;259(2):841-7. Pubmed
  2. Macleod AD, Counsell CE, Ives N, Stowe R: Monoamine oxidase B inhibitors for early Parkinson’s disease. Cochrane Database Syst Rev. 2005 Jul 20;(3):CD004898. Pubmed# Magyar K, Tothfalusi L: Pharmacokinetic aspects of deprenyl effects. Pol J Pharmacol Pharm. 1984 Jul-Aug;36(4):373-84. Pubmed
  3. Heinonen EH, Anttila MI, Lammintausta RA: Pharmacokinetic aspects of l-deprenyl (selegiline) and its metabolites. Clin Pharmacol Ther. 1994 Dec;56(6 Pt 2):742-9. Pubmed
  4. Deleu D, Northway MG, Hanssens Y: Clinical pharmacokinetic and pharmacodynamic properties of drugs used in the treatment of Parkinson’s disease. Clin Pharmacokinet. 2002;41(4):261-309. Pubmed
  5. Culpepper L, Kovalick LJ: A review of the literature on the selegiline transdermal system: an effective and well-tolerated monoamine oxidase inhibitor for the treatment of depression. Prim Care Companion J Clin Psychiatry. 2008;10(1):25-30. Pubmed
  6. Lee KC, Chen JJ: Transdermal selegiline for the treatment of major depressive disorder. Neuropsychiatr Dis Treat. 2007;3(5):527-37. Pubmed
External Links
Resource Link
KEGG Drug D03731 Link_out
KEGG Compound C07245 Link_out
BindingDB 15579 Link_out
ChEBI 50217 Link_out
ChEMBL 50217 Link_out
Therapeutic Targets Database DAP000579 Link_out
PharmGKB PA451316 Link_out
Drug Product Database 2238340 Link_out
RxList http://www.rxlist.com/cgi/generic/seleg.htm Link_out
Drugs.com http://www.drugs.com/cdi/selegiline.html Link_out
Wikipedia http://en.wikipedia.org/wiki/Selegiline Link_out
ATC Codes
  • N04BD01
AHFS Codes
  • 92:00.00
  • 28:92.00
PDB Entries
FDA label show (189 KB)
MSDS show (73.9 KB)
Interactions
Drug Interactions
Drug Interaction
Bezafibrate MAO Inhibitors may enhance the adverse/toxic effect of Bezafibrate. Avoid concomitant use of bezafibrate with monoamine oxidase inhibitors (MAOIs) like selegiline.
Brimonidine MAO Inhibitors like selegiline may enhance the hypertensive effect of Alpha2-Agonists (Ophthalmic). The concomitant use of monoamine oxidase inhibitors and ophthalmic alpha2 agonists is contraindicated.
Buprenorphine Buprenorphine may enhance the adverse/toxic effect of MAO Inhibitors like selegiline. When possible, avoid use of buprenorphine in patients who have used a monoamine oxidase inhibitor within the past 14 days due to possible severe adverse effects.
Citalopram Possible severe adverse reaction with this combination
Desvenlafaxine Increased risk of serotonin syndrome. Ensure adequate washout period between therapies to avoid toxicity. Concurrent therapy should be avoided.
Dextromethorphan Combination associated with possible serotoninergic syndrome
Escitalopram Possible severe adverse reaction with this combination
Fluoxetine Possible severe adverse reaction with this combination
Fluvoxamine Possible severe adverse reaction with this combination
Meperidine Potentially fatal adverse effects
Moclobemide Decrease in selectivity
Paroxetine Possible severe adverse reaction with this combination
Tapentadol Increases the toxicity of tapentadol by unknown mechanism. Discontinue selegiline at least 14 days prior to tapentadol administration.
Tetrabenazine Tetrabenazine may increase the adverse/toxic effects of Selegiline. Concomitant therapy is contraindicated.
Thiotepa Thiotepa, a strong CYP2B6 inhibitor, may decrease the metabolism and clearance of Selegiline, a CYP2B6 substrate. Consider alternate therapy or monitor for changes in the therapeutic and adverse effects of Selegiline if Thiotepa is initiated, discontinued or dose changed.
Tolcapone Tolcapone and Selegiline decrease the metabolism of endogenous catecholamines. Concomitant therapy may result in increased catecholamine effects. Consider alternate therapy or use cautiously and monitor for increased catecholamine effects.
Tramadol Tramadol increases the risk of serotonin syndrome and seizure induction by the MAO inhibitor, Selegiline.
Tranylcypromine Increased risk of serotonin syndrome. Use caution during concomitant therapy and monitor for symptoms of serotonin syndrome.
Trazodone Increased risk of serotonin syndrome. Monitor for symptoms of serotonin syndrome.
Trimipramine Increased risk of serotonin syndrome. Ensure adequate washout period between therapies to avoid toxicity. Avoid combination or monitor for symptoms of serotonin syndrome and/or hypertensive crisis.
Venlafaxine Increased risk of serotonin syndrome. Ensure adequate washout period between therapies to avoid toxicity. Concurrent therapy should be avoided.
Vilazodone MAO Inhibitors may enhance the serotonergic effect of Selective Serotonin Reuptake Inhibitors. This may cause serotonin syndrome. Avoid combination.
Zolmitriptan The MAO inhibitor, selegiline, may increase the serum concentration of zolmitriptan by decreasing its metabolism. Concomitant therapy and use of zolmitriptan within two weeks of discontinuing selegiline are contraindicated.
Food Interactions
  • Food increases the oral bioavailability by 3-5 fold.
Targets

1. Amine oxidase [flavin-containing] B

Pharmacological action: yes
Actions: inhibitor

Catalyzes the oxidative deamination of biogenic and xenobiotic amines and has important functions in the metabolism of neuroactive and vasoactive amines in the central nervous system and peripheral tissues. MAOB preferentially degrades benzylamine and phenylethylamine

Organism class: human
UniProt ID: P27338 Link_out
Gene: MAOB Link_out
Protein Sequence: FASTA
Gene Sequence: FASTA
SNPs: SNPJam Report Link_out

References:
  1. Chen X, Ji ZL, Chen YZ: TTD: Therapeutic Target Database. Nucleic Acids Res. 2002 Jan 1;30(1):412-5. Pubmed
  2. Chrisp P, Mammen GJ, Sorkin EM: Selegiline. A review of its pharmacology, symptomatic benefits and protective potential in Parkinson’s disease. Drugs Aging. 1991 May;1(3):228-48. Pubmed
  3. Heinonen EH, Myllyla V: Safety of selegiline (deprenyl) in the treatment of Parkinson’s disease. Drug Saf. 1998 Jul;19(1):11-22. Pubmed
  4. Selegiline: a second look. Six years later: too risky in Parkinson’s disease. Prescrire Int. 2002 Aug;11(60):108-11. Pubmed
  5. Macleod AD, Counsell CE, Ives N, Stowe R: Monoamine oxidase B inhibitors for early Parkinson’s disease. Cochrane Database Syst Rev. 2005 Jul 20;(3):CD004898. Pubmed# Magyar K, Tothfalusi L: Pharmacokinetic aspects of deprenyl effects. Pol J Pharmacol Pharm. 1984 Jul-Aug;36(4):373-84. Pubmed
  6. Heinonen EH, Anttila MI, Lammintausta RA: Pharmacokinetic aspects of l-deprenyl (selegiline) and its metabolites. Clin Pharmacol Ther. 1994 Dec;56(6 Pt 2):742-9. Pubmed
  7. Deleu D, Northway MG, Hanssens Y: Clinical pharmacokinetic and pharmacodynamic properties of drugs used in the treatment of Parkinson’s disease. Clin Pharmacokinet. 2002;41(4):261-309. Pubmed
  8. Patkar AA, Pae CU, Masand PS: Transdermal selegiline: the new generation of monoamine oxidase inhibitors. CNS Spectr. 2006 May;11(5):363-75. Pubmed
  9. Azzaro AJ, Ziemniak J, Kemper E, Campbell BJ, VanDenBerg C: Pharmacokinetics and absolute bioavailability of selegiline following treatment of healthy subjects with the selegiline transdermal system (6 mg/24 h): a comparison with oral selegiline capsules. J Clin Pharmacol. 2007 Oct;47(10):1256-67. Epub 2007 Aug 22. Pubmed
  10. Lee KC, Chen JJ: Transdermal selegiline for the treatment of major depressive disorder. Neuropsychiatr Dis Treat. 2007;3(5):527-37. Pubmed
  11. Baker GB, Sowa B, Todd KG: Amine oxidases and their inhibitors: what can they tell us about neuroprotection and the development of drugs for neuropsychiatric disorders? J Psychiatry Neurosci. 2007 Sep;32(5):313-5. Pubmed

2. Amine oxidase [flavin-containing] A

Pharmacological action: no
Actions: inhibitor

Catalyzes the oxidative deamination of biogenic and xenobiotic amines and has important functions in the metabolism of neuroactive and vasoactive amines in the central nervous system and peripheral tissues. MAOA preferentially oxidizes biogenic amines such as 5-hydroxytryptamine (5-HT), norepinephrine and epinephrine

Organism class: human
UniProt ID: P21397 Link_out
Gene: MAOA Link_out
Protein Sequence: FASTA
Gene Sequence: FASTA
SNPs: SNPJam Report Link_out

References:
  1. Patkar AA, Pae CU, Masand PS: Transdermal selegiline: the new generation of monoamine oxidase inhibitors. CNS Spectr. 2006 May;11(5):363-75. Pubmed
  2. Azzaro AJ, Ziemniak J, Kemper E, Campbell BJ, VanDenBerg C: Pharmacokinetics and absolute bioavailability of selegiline following treatment of healthy subjects with the selegiline transdermal system (6 mg/24 h): a comparison with oral selegiline capsules. J Clin Pharmacol. 2007 Oct;47(10):1256-67. Epub 2007 Aug 22. Pubmed
  3. Lee KC, Chen JJ: Transdermal selegiline for the treatment of major depressive disorder. Neuropsychiatr Dis Treat. 2007;3(5):527-37. Pubmed
  4. Baker GB, Sowa B, Todd KG: Amine oxidases and their inhibitors: what can they tell us about neuroprotection and the development of drugs for neuropsychiatric disorders? J Psychiatry Neurosci. 2007 Sep;32(5):313-5. Pubmed
Enzymes

1. Cytochrome P450 2B6

Actions: substrate

Cytochromes P450 are a group of heme-thiolate monooxygenases. In liver microsomes, this enzyme is involved in an NADPH-dependent electron transport pathway. It oxidizes a variety of structurally unrelated compounds, including steroids, fatty acids, and xenobiotics

UniProt ID: P20813 Link_out
Gene: CYP2B6 Link_out
Protein Sequence: FASTA
Gene Sequence: FASTA
SNPs: SNPJam Report Link_out

References:
  1. Culpepper L, Kovalick LJ: A review of the literature on the selegiline transdermal system: an effective and well-tolerated monoamine oxidase inhibitor for the treatment of depression. Prim Care Companion J Clin Psychiatry. 2008;10(1):25-30. Pubmed
  2. Lee KC, Chen JJ: Transdermal selegiline for the treatment of major depressive disorder. Neuropsychiatr Dis Treat. 2007;3(5):527-37. Pubmed
  3. Benetton SA, Fang C, Yang YO, Alok R, Year M, Lin CC, Yeh LT: P450 phenotyping of the metabolism of selegiline to desmethylselegiline and methamphetamine. Drug Metab Pharmacokinet. 2007 Apr;22(2):78-87. Pubmed
  4. Walsky RL, Astuccio AV, Obach RS: Evaluation of 227 drugs for in vitro inhibition of cytochrome P450 2B6. J Clin Pharmacol. 2006 Dec;46(12):1426-38. Pubmed
  5. Preissner S, Kroll K, Dunkel M, Senger C, Goldsobel G, Kuzman D, Guenther S, Winnenburg R, Schroeder M, Preissner R: SuperCYP: a comprehensive database on Cytochrome P450 enzymes including a tool for analysis of CYP-drug interactions. Nucleic Acids Res. 2010 Jan;38(Database issue):D237-43. Epub 2009 Nov 24. Pubmed

2. Cytochrome P450 3A4

Actions: substrate

Cytochromes P450 are a group of heme-thiolate monooxygenases. In liver microsomes, this enzyme is involved in an NADPH-dependent electron transport pathway. It performs a variety of oxidation reactions (e.g. caffeine 8-oxidation, omeprazole sulphoxidation, midazolam 1'-hydroxylation and midazolam 4- hydroxylation) of structurally unrelated compounds, including steroids, fatty acids, and xenobiotics. The enzyme also hydroxylates etoposide

UniProt ID: P08684 Link_out
Gene: CYP3A4
Protein Sequence: FASTA
Gene Sequence: FASTA
SNPs: SNPJam Report Link_out

References:
  1. Benetton SA, Fang C, Yang YO, Alok R, Year M, Lin CC, Yeh LT: P450 phenotyping of the metabolism of selegiline to desmethylselegiline and methamphetamine. Drug Metab Pharmacokinet. 2007 Apr;22(2):78-87. Pubmed

3. Cytochrome P450 2A6

Actions: substrate

Exhibits a high coumarin 7-hydroxylase activity. Can act in the hydroxylation of the anti-cancer drugs cyclophosphamide and ifosphamide. Competent in the metabolic activation of aflatoxin B1. Constitutes the major nicotine C-oxidase

UniProt ID: P11509 Link_out
Gene: CYP2A6
Protein Sequence: FASTA
Gene Sequence: FASTA
SNPs: SNPJam Report Link_out

References:
  1. Lee KC, Chen JJ: Transdermal selegiline for the treatment of major depressive disorder. Neuropsychiatr Dis Treat. 2007;3(5):527-37. Pubmed
  2. Benetton SA, Fang C, Yang YO, Alok R, Year M, Lin CC, Yeh LT: P450 phenotyping of the metabolism of selegiline to desmethylselegiline and methamphetamine. Drug Metab Pharmacokinet. 2007 Apr;22(2):78-87. Pubmed
  3. Preissner S, Kroll K, Dunkel M, Senger C, Goldsobel G, Kuzman D, Guenther S, Winnenburg R, Schroeder M, Preissner R: SuperCYP: a comprehensive database on Cytochrome P450 enzymes including a tool for analysis of CYP-drug interactions. Nucleic Acids Res. 2010 Jan;38(Database issue):D237-43. Epub 2009 Nov 24. Pubmed

4. Cytochrome P450 1A2

Actions: substrate, inhibitor

Cytochromes P450 are a group of heme-thiolate monooxygenases. In liver microsomes, this enzyme is involved in an NADPH-dependent electron transport pathway. It oxidizes a variety of structurally unrelated compounds, including steroids, fatty acids, and xenobiotics. Most active in catalyzing 2-hydroxylation. Caffeine is metabolized primarily by cytochrome CYP1A2 in the liver through an initial N3-demethylation. Also acts in the metabolism of aflatoxin B1 and acetaminophen

UniProt ID: P05177 Link_out
Gene: CYP1A2
Protein Sequence: FASTA
Gene Sequence: FASTA
SNPs: SNPJam Report Link_out

References:
  1. Preissner S, Kroll K, Dunkel M, Senger C, Goldsobel G, Kuzman D, Guenther S, Winnenburg R, Schroeder M, Preissner R: SuperCYP: a comprehensive database on Cytochrome P450 enzymes including a tool for analysis of CYP-drug interactions. Nucleic Acids Res. 2010 Jan;38(Database issue):D237-43. Epub 2009 Nov 24. Pubmed

5. Cytochrome P450 2C19

Actions: substrate

Responsible for the metabolism of a number of therapeutic agents such as the anticonvulsant drug S-mephenytoin, omeprazole, proguanil, certain barbiturates, diazepam, propranolol, citalopram and imipramine

UniProt ID: P33261 Link_out
Gene: CYP2C19 Link_out
Protein Sequence: FASTA
Gene Sequence: FASTA
SNPs: SNPJam Report Link_out

References:
  1. Preissner S, Kroll K, Dunkel M, Senger C, Goldsobel G, Kuzman D, Guenther S, Winnenburg R, Schroeder M, Preissner R: SuperCYP: a comprehensive database on Cytochrome P450 enzymes including a tool for analysis of CYP-drug interactions. Nucleic Acids Res. 2010 Jan;38(Database issue):D237-43. Epub 2009 Nov 24. Pubmed

6. Cytochrome P450 2C8

Actions: substrate

Cytochromes P450 are a group of heme-thiolate monooxygenases. In liver microsomes, this enzyme is involved in an NADPH-dependent electron transport pathway. It oxidizes a variety of structurally unrelated compounds, including steroids, fatty acids, and xenobiotics. In the epoxidation of arachidonic acid it generates only 14,15- and 11,12-cis-epoxyeicosatrienoic acids. It is the principal enzyme responsible for the metabolism the anti- cancer drug paclitaxel (taxol)

UniProt ID: P10632 Link_out
Gene: CYP2C8
Protein Sequence: FASTA
Gene Sequence: FASTA
SNPs: SNPJam Report Link_out

References:
  1. Preissner S, Kroll K, Dunkel M, Senger C, Goldsobel G, Kuzman D, Guenther S, Winnenburg R, Schroeder M, Preissner R: SuperCYP: a comprehensive database on Cytochrome P450 enzymes including a tool for analysis of CYP-drug interactions. Nucleic Acids Res. 2010 Jan;38(Database issue):D237-43. Epub 2009 Nov 24. Pubmed

7. Cytochrome P450 2C9

Actions: substrate, inhibitor

Cytochromes P450 are a group of heme-thiolate monooxygenases. In liver microsomes, this enzyme is involved in an NADPH-dependent electron transport pathway. It oxidizes a variety of structurally unrelated compounds, including steroids, fatty acids, and xenobiotics. This enzyme contributes to the wide pharmacokinetics variability of the metabolism of drugs such as S- warfarin, diclofenac, phenytoin, tolbutamide and losartan

UniProt ID: P11712 Link_out
Gene: CYP2C9
Protein Sequence: FASTA
Gene Sequence: FASTA
SNPs: SNPJam Report Link_out

References:
  1. Preissner S, Kroll K, Dunkel M, Senger C, Goldsobel G, Kuzman D, Guenther S, Winnenburg R, Schroeder M, Preissner R: SuperCYP: a comprehensive database on Cytochrome P450 enzymes including a tool for analysis of CYP-drug interactions. Nucleic Acids Res. 2010 Jan;38(Database issue):D237-43. Epub 2009 Nov 24. Pubmed

8. Cytochrome P450 2D6

Actions: inhibitor

Responsible for the metabolism of many drugs and environmental chemicals that it oxidizes. It is involved in the metabolism of drugs such as antiarrhythmics, adrenoceptor antagonists, and tricyclic antidepressants

UniProt ID: P10635 Link_out
Gene: CYP2D6 Link_out
Protein Sequence: FASTA
Gene Sequence: FASTA
SNPs: SNPJam Report Link_out

References:
  1. Preissner S, Kroll K, Dunkel M, Senger C, Goldsobel G, Kuzman D, Guenther S, Winnenburg R, Schroeder M, Preissner R: SuperCYP: a comprehensive database on Cytochrome P450 enzymes including a tool for analysis of CYP-drug interactions. Nucleic Acids Res. 2010 Jan;38(Database issue):D237-43. Epub 2009 Nov 24. Pubmed

9. Cytochrome P450 2E1

Actions: inhibitor

Metabolizes several precarcinogens, drugs, and solvents to reactive metabolites. Inactivates a number of drugs and xenobiotics and also bioactivates many xenobiotic substrates to their hepatotoxic or carcinogenic forms

UniProt ID: P05181 Link_out
Gene: CYP2E1 Link_out
Protein Sequence: FASTA
Gene Sequence: FASTA
SNPs: SNPJam Report Link_out

References:
  1. Preissner S, Kroll K, Dunkel M, Senger C, Goldsobel G, Kuzman D, Guenther S, Winnenburg R, Schroeder M, Preissner R: SuperCYP: a comprehensive database on Cytochrome P450 enzymes including a tool for analysis of CYP-drug interactions. Nucleic Acids Res. 2010 Jan;38(Database issue):D237-43. Epub 2009 Nov 24. Pubmed
Transporters

1. Multidrug resistance protein 1

Actions: inhibitor

Energy-dependent efflux pump responsible for decreased drug accumulation in multidrug-resistant cells

UniProt ID: P08183 Link_out
Gene: ABCB1 Link_out
Protein Sequence: FASTA
Gene Sequence: FASTA
SNPs: SNPJam Report Link_out

References:
  1. Mahar Doan KM, Humphreys JE, Webster LO, Wring SA, Shampine LJ, Serabjit-Singh CJ, Adkison KK, Polli JW: Passive permeability and P-glycoprotein-mediated efflux differentiate central nervous system (CNS) and non-CNS marketed drugs. J Pharmacol Exp Ther. 2002 Dec;303(3):1029-37. Pubmed
Comments
Drug created on June 13, 2005 07:24 / Updated on February 08, 2013 16:19