関: deprenyl、selegiline、selegiline hydrochloride

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2016/07/04 23:03:29」(JST)

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Selegiline, also known as L-deprenyl is a substituted phenethylamine that at normal clinical doses it is a selective irreversible MAO-B inhibitor. In larger doses it loses its specificity and also inhibits MAO-A. It is available in pill form under many brand names^[1] and is used to reduce symptoms in early-stage Parkinson's disease. A transdermal patch (brand name, Emsam) is used to treat depression.

1 Medical uses
- 1.1 Parkinson's disease
- 1.2 Depression
- 1.3 Veterinary use
2 Adverse effects
- 2.1 Interactions
3 Pharmacology
- 3.1 Protein binding
- 3.2 Pharmacokinetics of the pill form
- 3.3 Pharmacokinetics of the patch form
- 3.4 Metabolites
  - 3.4.1 Desmethylselegiline
  - 3.4.2 Levoamphetamine and levomethamphetamine
4 Chemistry
5 History
6 Research
7 Society and culture
8 See also
9 References

Medical uses

For all human uses and all forms, selegiline is Pregnancy Category C,^[2]^[3] meaning that caution is in order because studies in pregnant laboratory animals have shown an adverse effect on the fetus and there are no adequate and well-controlled studies in humans, but that the drug's potential benefits may nonetheless warrant use of the drug in some pregnant women.

Parkinson's disease

In its pill form, selegiline is used to treat symptoms of Parkinson's disease.^[2] It can be used on its own or in a combination with another agent, most often L-DOPA.^[4]

Selegiline delays the time point when the L-DOPA (levodopa) treatment becomes necessary from about 11 months to about 18 months after diagnosis,^[5] which is beneficial despite not being definitive evidence of neuroprotection. The rationale for adding selegiline to levodopa is to decrease the required dose of levodopa and thus reduce the motor complications of levodopa therapy.^[6]

Depression

Selegiline is also delivered via a transdermal patch; in this form it is used as a treatment for major depressive disorder.^[3]^[7]

A quantitative review published in 2015 found that for the pooled results of the pivotal trials, the number needed to treat (a sign of effect size, so a low number is better) for the patch for symptom reduction was 11, and for remission, was 9.^[7] The number needed to harm (inverse of the NNT, a high number here is better) ranged from 387 for sexual side effects to 7 for application site reaction.^[7] With regard to the likelihood to be helped or harmed (LHH), the analysis showed that the selegiline patch was 3.6 times as likely to lead to a remission vs. a discontinuation due to side effects; the LHH for remission vs. incidence of insomnia was 2.1; the LHH for remission vs. discontinuation due to insomnia was 32.7. The LHH for remission vs insomnia and sexual dysfunction were both very low.^[7]

Veterinary use

Selegiline (brand name Anipryl) is also used (at extremely high dosages relative to humans) in veterinary medicine to treat the symptoms of Cushing's disease and cognitive dysfunction (Canine Cognitive Dysfunction)^[8]^[9] in dogs.^[10]^[11]^[12]

Adverse effects

Side effects of the pill form include, in decreasing order of frequency, nausea, hallucinations, confusion, depression, loss of balance, insomnia, low blood pressure, increased involuntary movements, agitation, arrhythmia, slow heart rate, delusions, hypertension, new or increased angina pectoris, and syncope.^[2]

The main side effects of the patch form for depression included application site reactions, insomnia, diarrhea, and sore throat.^[3]

The selegiline transdermal patch for depression carries a black box warning about the risk of suicide, especially for young people,^[3] as do all antidepressants since 2007.^[13]

Interactions

Both forms of the drug carry warnings about combining selegiline with drugs that could produce serotonin syndrome.^[2]^[3] However, the risk of a serotonin syndrome with SSRIs and selegiline is quite low, and the combination can be taken together if caution is used.^{[citation needed]} However, combination of selegiline with fluoxetine can lead to severe reactions.^[14] Selegiline in combination with pethidine is not recommended as it can lead to severe adverse effects.^[14]

Both forms of the drug carry warnings about food restrictions, to avoid hypertensive crisis that are associated with MAO inhibitors.^[2]^[3] The patch form of the drug was created in part to overcome the issues with food restrictions: the clinical trials did not include food restrictions, and no hypertensive crisis during the course of them. Additionally, in post-marketing surveillance from April 2006 to October 2010, only 13 self-reports of possible hypertensive events or hypertension were made out of 29,141 exposures to the drug, and none were accompanied by objective clinical data.^[7] Nonetheless, selegiline in either form, and whether in combination with the older non-selective MAOIs or in combination with the reversible MAO-A inhibitor moclobemide, requires a low tyramine diet.^[14]

Pharmacology

Protein binding

Selegiline is a selective inhibitor of MAO-B; MAO-B metabolizes dopamine and phenylethylamine.^[15]

Selegiline also inhibits CYP2A6 and can increase the effects of nicotine as a result.^[16] Selegiline appears to activate sigma-1 receptors with a relatively high affinity of approximately 400nM.^[17]^[18]

Pharmacokinetics of the pill form

Selegiline has a low oral bioavailability, which increases to moderate when ingested together with a high-fat meal, the molecule being fat soluble.^[19]

Selegiline's oral bioavailability is drastically increased in females taking oral contraceptives (10- to 20-fold).^[20] This could lead to loss of MAO-B selectivity, with inhibition of both MAO-A and MAO-B, which would make patients susceptible to the usual risks of unselective MAOIs such as tyramine-induced hypertensive crisis and serotonin toxicity when combined with serotonergics such as SSRIs.^[20]

Pharmacokinetics of the patch form

Following application of the patch to humans, 25% to 30% of the selegiline content on average is delivered systemically over 24 hours (range approximately 10% to 40%). Transdermal dosing results in significantly higher exposure to selegiline with significantly lower exposure for all metabolites when compared to oral dosing, due to extensive first-pass metabolism for the pill form and low first-pass metabolism for the patch form. The site of application is not a significant factor in how the drug is distributed. In humans, selegiline does not accumulate in the skin nor is it metabolized in the skin.^[3]

When radiolabeled selegiline is given transdermally to laboratory animals, the drug is rapidly distributed to all body tissues and rapidly penetrates the blood-brain barrier.^[3]

Metabolites

Desmethylselegiline

N-Desmethylselegiline may have neuroprotective antiapoptotic properties. A large multicenter study suggests a decrease in the disease progression of Parkinsonism but may have reflected other symptomatic response.^[15] Desmethylselegiline is metabolized by CYP2C19.^[21]

Levoamphetamine and levomethamphetamine

Selegiline is partly metabolized to levomethamphetamine (l-methamphetamine), one of the two enantiomers of methamphetamine, in vivo.^[22]^[23] While these metabolites may contribute to the drug's ability to inhibit reuptake of the neurotransmitters dopamine and norepinephrine, they have also been associated with orthostatic hypotension and hallucinations in some people.^[23]^[24]^[25] A newer antiparkinson MAO-B inhibitor, rasagiline, metabolizes into 1(R)-aminoindan which has no amphetamine-like characteristics.^[26]

This metabolic pathway may cause persons taking selegiline to test positive for amphetamine or methamphetamine on drug screening tests.^[27]

Chemistry

Selegiline belongs to a class of drugs called phenethylamines. Selegiline is a levomethamphetamine derivative with a propargyl group attached to the nitrogen atom. This detail is borrowed from pargyline, an older phenethylamine MAO-B inhibitor.^[28]

Selegiline, N-methyl-N-(2-propynyl)-2-methyl-1-phenylethyl-2-amine, is synthesized by the alkylation of (–)-methamphetamine using propargyl bromide.^[29]^[30]^[31]^[32]

History

Following the discovery that the tuberculosis drug iproniazid elevated the mood of people taking it for TB, and the subsequent discovery that the effect was likely due to inhibition of MAO, many people and companies started trying to discover MAO inhibitors to use as antidepressants. Selegiline was discovered by Z. Ecseri at the Hungarian drug company, Chinoin (part of Sanofi since 1993^[33]), which they called E-250.^[34]^:66–67 Chinoin received a patent on the drug in 1962 and the compound was first published in the scientific literature in English in 1965.^[34]^:67^[35] Work on the biology and effects of E-250 in animals and humans was conducted by a group led by József Knoll at Semmelweis University which was also in Budapest.^[34]^:67

Deprenyl is a racemic compound, a mixture of two isomers called enantiomers. Further work determined that the levorotatory enantiomer was a more potent MAO-inhibitor, which was published in 1967, and subsequent work was done with that recemically pure compound, L-deprenyl.^[34]^:67^[36]^[37]

In 1971, Knoll showed that selegiline selectively inhibits the B-isoform of monoamine oxidase (MAO-B) and proposed that it is unlikely to cause the infamous "cheese effect" (hypertensive crisis resulting from consuming foods containing tyramine) that occurs with non-selective MAO inhibitors. A few years later, two Parkinson's disease researchers based in Vienna, Peter Riederer and Walther Birkmayer, realized that selegiline could be useful in Parkinson's disease. One of their colleagues, Prof. Moussa B.H. Youdim, visited Knoll in Budapest and took selegiline from him to Vienna. In 1975, Birkmayer's group published the first paper on the effect of selegiline in Parkinson's disease.^[37]^[38]

The discovery that selegiline seemed to have a neuroprotection effect in Parkinson's disease led to widespread speculation in the 1970s that it could be useful as an anti-aging drug.^[39]

In 1987 Somerset Pharmaceuticals in New Jersey, which had acquired the US rights to develop selegiline, filed a new drug application (NDA) with the FDA to market the drug for PD in the US.^[40] While the NDA was under review, Somerset was acquired in a joint venture by two generic drug companies, Mylan and Bolan Pharmaceuticals.^[40] Selegiline was approved for Parkinson's disease by the FDA in 1989.^[40]

6mg/24hr dose

In the 1990s, J. Alexander Bodkin at McLean Hospital, an affiliate of Harvard Medical School, began a collaboration with Somerset to develop delivery of selegiline via a transdermal patch in order to avoid the well known dietary restrictions of MAO inhibitors.^[39]^[41]^[42] Somerset obtained FDA approval to market the patch in 2006.^[43]

Research

A selegiline transdermal patch was tested for its effectiveness in treating ADHD.^[44]

Selegiline's effectiveness in helping people stop smoking tobacco or cannabis has been studied.^[45]^[46]

Society and culture

Due to the structural similarity to amphetamine, selegiline has been classified as a controlled substance in Japan and thus can only be obtained with a prescription or special government license. Amphetamine and methamphetamine are illegal in the country.

In E for Ecstasy^[47] (a book examining the uses of the street drug ecstasy in the UK) the writer, activist and ecstasy advocate Nicholas Saunders highlighted test results showing that certain consignments of the drug also contained selegiline. Consignments of ecstasy known as "Strawberry" contained what Saunders described as a "potentially dangerous combination of ketamine, ephedrine and selegiline," as did a consignment of "Sitting Duck" Ecstasy tablets.^[48]

In the US, Selegiline is available by prescription but is not scheduled as a controlled substance.

References

^ ^a ^b Drugs.com international listings for selegiline Page accessed Feb 7, 2016]
^ ^a ^b ^c ^d ^e Selegiline oral label. Updated Dec 31, 2008
^ ^a ^b ^c ^d ^e ^f ^g ^h Emsam label Last revised Sept 2014. Index page at FDA
^ Riederer P, Lachenmayer L, Laux G (August 2004). "Clinical applications of MAO-inhibitors". Curr. Med. Chem. 11 (15): 2033–43. doi:10.2174/0929867043364775. PMID 15279566.
^ Riederer P, Lachenmayer L (November 2003). "Selegiline's neuroprotective capacity revisited". J Neural Transm 110 (11): 1273–8. doi:10.1007/s00702-003-0083-x. PMID 14628191.
^ Ives NJ, Stowe RL, Marro J, et al. (September 2004). "Monoamine oxidase type B inhibitors in early Parkinson's disease: meta-analysis of 17 randomised trials involving 3525 patients". BMJ 329 (7466): 593. doi:10.1136/bmj.38184.606169.AE. PMC 516655. PMID 15310558.
^ ^a ^b ^c ^d ^e Citrome L, Goldberg JF, Portland KB. Placing transdermal selegiline for major depressive disorder into clinical context: number needed to treat, number needed to harm, and likelihood to be helped or harmed. J Affect Disord. 2013 Nov;151(2):409-17. Review. PMID 23890583
^ Lundgren, Becky. "Canine Cognitive Dysfunction". Veterinary Partner. Retrieved April 8, 2011.
^ "Cognitive Dysfunction Syndrome". Long Beach Animal Hospital. Retrieved April 8, 2011.
^ http://www.petplace.com/drug-library/selegiline-hcl-anipryl/page1.aspx
^ "Anipryl consumer information". Drugs.com Vet. Retrieved April 3, 2011.
^ Braddock JA, Church DB, Robertson ID (2004). "Selegiline Treatment of Canine Pituitary-Dependent Hyperadrenocorticism" (PDF). Australian Veterinary Journal. Retrieved April 8, 2011. (PDF)
^ Friedman RA, Leon AC (2007). "Expanding the black box – depression, antidepressants, and the risk of suicide". N. Engl. J. Med. 356 (23): 2343–6. doi:10.1056/NEJMp078015. PMID 17485726.
^ ^a ^b ^c Heinonen EH, Myllylä V (July 1998). "Safety of selegiline (deprenyl) in the treatment of Parkinson's disease". Drug Saf 19 (1): 11–22. doi:10.2165/00002018-199819010-00002. PMID 9673855.
^ ^a ^b Katzung, Bertram G. Basic & Clinical Pharmacology. 9th Edition. 2004. page 453. Lange Medical Books - McGraw Hill Publishers.
^ Siu, E. C.; Tyndale, R. F. (2008). "Selegiline is a mechanism-based inactivator of CYP2A6 inhibiting nicotine metabolism in humans and mice". Journal of Pharmacology and Experimental Therapeutics 324 (3): 992–9. doi:10.1124/jpet.107.133900. PMID 18065502.
^ Itzhak, Yossef (1994). Sigma Receptors. Academic press. p. 84. ISBN 978-0-12-376350-1.
^ Stone, T. W. (1993). Acetylcholine, Sigma Receptors, CCK and Eicosanoids, Neurotoxins. Taylor & Francis. p. 124. ISBN 978-0-7484-0063-8.
^ Barrett, Jeffrey S.; Szego, Peter; Rohatagi, Shashank; Morales, Richard J.; Dewitt, Kimberly E.; Rajewski, Gregory; Ireland, Joyce (1996). "Absorption and presystemic metabolism of selegiline hydrochloride at different regions in the gastrointestinal tract in healthy males". Pharmaceutical Research 13 (10): 1535–40. doi:10.1023/A:1016035730754. PMID 8899847.
^ ^a ^b Laine, Kari; Anttila, Markku; Helminen, Antti; Karnani, Hari; Huupponen, Risto (2001). "Dose linearity study of selegiline pharmacokinetics after oral administration: Evidence for strong drug interaction with female sex steroids". British Journal of Clinical Pharmacology 47 (3): 249–54. doi:10.1046/j.1365-2125.1999.00891.x. PMC 2014223. PMID 10215747.
^ Taavitsainen, Paivi; Anttila, Markku; Nyman, Leena; Karnani, Hari; Salonen, Jarmo S.; Pelkonen, Olavi (2000). "Selegiline Metabolism and Cytochrome P450 Enzymes:In vitro Study in Human Liver Microsomes*". Pharmacology and Toxicology 86 (5): 215–21. doi:10.1034/j.1600-0773.2000.d01-38.x. PMID 10862503.
^ Engberg, G; Elebring, T; Nissbrandt, H (1991). "Deprenyl (selegiline), a selective MAO-B inhibitor with active metabolites; effects on locomotor activity, dopaminergic neurotransmission and firing rate of nigral dopamine neurons". The Journal of Pharmacology and Experimental Therapeutics 259 (2): 841–7. PMID 1658311.
^ ^a ^b Lemke, Thomas L.; Williams, David A, eds. (2012). Foye's Principles of Medicinal Chemistry. Lippincott Williams & Wilkins. p. 434. ISBN 1609133455.
^ Bar Am, Orit; Amit, Tamar; Youdim, Moussa B. H. (2004-01-30). "Contrasting neuroprotective and neurotoxic actions of respective metabolites of anti-Parkinson drugs rasagiline and selegiline". Neuroscience Letters 355 (3): 169–172. doi:10.1016/j.neulet.2003.10.067. ISSN 0304-3940. PMID 14732458.
^ Yasar, S.; Goldberg, J. P.; Goldberg, S. R. (1996-01-01). "Are metabolites of l-deprenyl (selegiline) useful or harmful? Indications from preclinical research". Journal of Neural Transmission. Supplementum 48: 61–73. ISSN 0303-6995. PMID 8988462.
^ Chen JJ, Swope DM (2005). "Clinical pharmacology of rasagiline: a novel, second-generation propargylamine for the treatment of Parkinson disease". J Clin Pharmacol 45 (8): 878–94. doi:10.1177/0091270005277935. PMID 16027398.
^ Romberg, R. W.; Needleman, S. B.; Snyder, J. J.; Greedan, A. (1995-11-01). "Methamphetamine and amphetamine derived from the metabolism of selegiline". Journal of Forensic Sciences 40 (6): 1100–1102. ISSN 0022-1198. PMID 8522918.
^ Miklya, Ildiko (13 March 2014). "The History of Selegiline/(-)-Deprenyl the First Selective Inhibitor of B-Type Monoamine Oxidase and The First Synthetic Catecholaminergic Activity Enhancer Substance". International Network for the History of Neuropsychopharmacology. Retrieved 7 January 2016.
^ J. Knoll, E. Sanfai, DE 1568277 (1966).
^ J. Hermann Nee Voeroes, Z. Ecsery, G. Sabo, L. Arvai, L. Nagi, O. Orban, E. Sanfai, U.S. Patent 4,564,706 (1986)
^ B. Brunova, M. Ferenc, EP 344675 (1989)
^ Fowler, Joanna S. (1977). "2-Methyl-3-butyn-2-ol as an acetylene precursor in the Mannich reaction. A new synthesis of suicide inactivators of monoamine oxidase". The Journal of Organic Chemistry 42 (15): 2637–7. doi:10.1021/jo00435a026. PMID 874623.
^ Staff, The Pharma Letter. Sept 20, 1993 Sanofi Extends Holding in Chinoin
^ ^a ^b ^c ^d Kalman Magyar. The pharmacology of selegiline. Chapter 4 in Monoamine Oxidases and their Inhibitors. Volume 100 of International Review of Neurobiology. Eds Moussa Youdim, Peter Riederer. Academic Press, 2011. ISBN 9780123864680
^ Knoll J, Ecseri Z, Kelemen K, Nievel J, Knoll B. Phenylisopropylmethylpropinylamine (E-250), a new spectrum psychic energizer. Arch Int Pharmacodyn Ther. 1965 May;155(1):154-64. PMID 4378644
^ Magyar K, Vizi ES, Ecseri Z, Knoll J.Comparative pharmacological analysis of the optical isomers of phenyl-isopropyl-methyl-propinylamine (E-250). Acta Physiol Acad Sci Hung. 1967;32(4):377-87. PMID 5595908
^ ^a ^b Healy, David (2000). "The psychopharmacology of life and death. Interview with Joseph Knoll.". The Psychopharmacologists, Vol. III: Interviews. London: Arnold. pp. 81–110. ISBN 0-340-76110-5.
^ Birkmayer W, Riederer P, Youdim MB, Linauer W (1975). "The potentiation of the anti akinetic effect after L-dopa treatment by an inhibitor of MAO-B, Deprenil". J. Neural Transm. 36 (3–4): 303–26. doi:10.1007/BF01253131. PMID 1172524.
^ ^a ^b William J. Cromie (2002-11-07). "Bodkin is Patching up Depression". Harvard University Gazette. Retrieved 2007-09-08.
^ ^a ^b ^c John T. Seaman, John T. Landry. Mylan: 50 Years of Unconventional Success : Making Quality Medicine Affordable and Accessible. UPNE, 2012. ISBN 9781611682700. Page 50
^ Frampton, JE; Plosker, GL (2007). "Selegiline transdermal system: in the treatment of major depressive disorder". Drugs 67 (2): 257–67, discussion 266–7. PMID 17284087.
^ Mary Duffy for the New York Times. December 3, 2002 Patch Raises New Hope For Beating Depression
^ Cascade EF, Kalali AH, Preskorn SH. Emsam: the first year. Psychiatry (Edgmont). 2007 Jun;4(6):19-21. PMID 20711332 Free full text
^ Akhondzadeh, Shahin; Tavakolian, Reza; Davari-Ashtiani, Rozita; Arabgol, Fariba; Amini, Homayoun (1 August 2003). "Selegiline in the treatment of attention deficit hyperactivity disorder in children: a double blind and randomized trial". Progress in Neuro-Psychopharmacology & Biological Psychiatry 27 (5): 841–845. doi:10.1016/S0278-5846(03)00117-9. ISSN 0278-5846. PMID 12921918.
^ "Effectiveness of Selegiline in Treating Marijuana Dependent Individuals". ClinicalTrials.gov. National Institute on Drug Abuse. March 2005. Retrieved February 16, 2007.
^ "Usefulness of Selegiline as an Aid to Quit Smoking". ClinicalTrials.gov. National Institute on Drug Abuse. July 2004. Retrieved February 16, 2007.
^ Saunders, N., & Heron, L., (1993) E for Ecstasy (Paperback), N. Saunders, London. (ISBN 0950162884)^{[page needed]}
^ See: [1] for details online.

UpToDate Contents

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1. パーキンソン病に対する神経保護療法 neuroprotective therapy for parkinson disease
2. 成人の注意欠陥多動性障害（ADHD）に対する薬物療法 pharmacotherapy for adult attention deficit hyperactivity disorder
3. パーキンソン病における症状の変動およびジスキネジア motor fluctuations and dyskinesia in parkinson disease

English Journal

(E)-3-Heteroarylidenechroman-4-ones as potent and selective monoamine oxidase-B inhibitors.

Desideri N1, Proietti Monaco L2, Fioravanti R2, Biava M2, Yáñez M3, Alcaro S4, Ortuso F4.
European journal of medicinal chemistry.Eur J Med Chem.2016 Jul 19;117:292-300. doi: 10.1016/j.ejmech.2016.03.081. Epub 2016 Mar 29.
A series of (E)-3-heteroarylidenechroman-4-ones (1a-r) was designed, synthesized and investigated in vitro for their ability to inhibit the enzymatic activity of both human monoamine oxidase (hMAO) isoforms, hMAO-A and hMAO-B. All the compounds were found to be selective hMAO-B inhibitors showing I
PMID 27135371

The effect of R-(-)-deprenyl administration on antioxidant enzymes in rat testis.

Horváthová F1, Danielisová V2, Domoráková I3, Solár P4, Rybárová S1, Hodorová I1, Mihalik J5.
European journal of pharmacology.Eur J Pharmacol.2016 Jun 9;788:21-28. doi: 10.1016/j.ejphar.2016.06.015. [Epub ahead of print]
The aim of the study was to investigate the effect of R-(-)-deprenyl administration on the activity and localization of superoxide dismutases (SODs) and catalase (CAT) in rat testis. After 30 days of intraperitoneal administration of either saline (control) or R-(-)-deprenyl dissolved in saline at c
PMID 27292162

3,4-Dihydroxyphenylethanol (Hydroxytyrosol) Mitigates the Increase in Spontaneous Oxidation of Dopamine During Monoamine Oxidase Inhibition in PC12 Cells.

Goldstein DS1, Jinsmaa Y2, Sullivan P2, Holmes C2, Kopin IJ2, Sharabi Y2,3.
Neurochemical research.Neurochem Res.2016 May 25. [Epub ahead of print]
The catecholaldehyde hypothesis predicts that monoamine oxidase (MAO) inhibition should slow the progression of Parkinson's disease, by decreasing production of the autotoxic dopamine metabolite 3,4-dihydroxyphenylacetaldehyde (DOPAL). Inhibiting MAO, however, diverts the fate of cytoplasmic dopamin
PMID 27220335

Japanese Journal

Paraquat induces long-lasting dopamine overflow through the excitotoxic pathway in the striatum of freely moving rats

BRAIN RESEARCH 976(2), 243-252, 2003-27-Jun
NAID 120001024640

Paraquat leads to dopaminergic neural vulnerability in organotypic midbrain culture

Neuroscience research : the official journal of the Japan Neuroscience Society 46(4), 523-532, 2003-08-01
NAID 10016207557

l-Deprenyl metabolism by cytochrome P450 system in monkey (Cercopithecus aethips) liver microsome

Xenobiotica 33, 181-195, 2003
NAID 30016795338

Related Pictures

11 C]L-Deprenyl and [ 11270 Systematic ( IUPAC ) name Deprenyl HCL - Jumex Selegiline/l-Deprenyl Selegiline (L-Deprenyl) for ADHD - Reviews deprenyl (veterinary trade name, Anipryl Suchanfragen zu Deprenyl selegiline buy l - d e p r e n y l

★リンクテーブル★

リンク元	「selegiline hydrochloride」「L-デプレニル」
関連記事	「L」

「selegiline hydrochloride」

Selegiline
Systematic (IUPAC) name
	(R)-N-methyl-N-(1-phenylpropan-2-yl)prop-1-yn-3-amine
Clinical data
Trade names	Pill form is generic and available under many brand names; transdermal patch is called Emsam
AHFS/Drugs.com	Monograph
MedlinePlus	a697046
License data	US FDA: Selegiline;
Pregnancy; category	AU: B2; US: C (Risk not ruled out); ;
Routes of; administration	Oral, transdermal, buccal
Legal status
Legal status	AU: S4 (Prescription only); CA: ℞-only; UK: POM (Prescription only); US: ℞-only;
Pharmacokinetic data
Bioavailability	4.4% (oral, fasted), 20% (oral, after food), 73% (patch)
Protein binding	90%
Metabolism	liver
Biological half-life	10 hours (oral), 18-25 hours (transdermal)
Excretion	urine
Identifiers
CAS Number	14611-51-9 ; 14611-52-0 (HCl)
ATC code	N04BD01 (WHO) QN06AX90 (WHO)
PubChem	CID 26757
IUPHAR/BPS	6639
DrugBank	DB01037
ChemSpider	24930
UNII	2K1V7GP655
KEGG	D03731
ChEBI	CHEBI:9086
ChEMBL	CHEMBL972
Chemical data
Formula	C13H17N
Molar mass	187.281 g/mol
	SMILES C#CCN([C@@H](Cc1ccccc1)C)C ;
	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/t12-/m1/s1 ; Key:MEZLKOACVSPNER-GFCCVEGCSA-N ;
(verify)

　　[★]

塩酸セレギリン、セレギリン塩酸塩

関: deprenyl、L-deprenyl、selegiline

「L-デプレニル」

　　[★]

英: L-deprenyl
関: デプレニル、セレギリン、塩酸セレギリン

「L」

　　[★]

[DrugNames-1] Drugs.com international listings for selegiline Page accessed Feb 7, 2016]

[PillLabel-2] Selegiline oral label. Updated Dec 31, 2008

[PatchLabel-3] ^ ^a ^b ^c ^d ^e ^f ^g ^h Emsam label Last revised Sept 2014. Index page at FDA

[pmid15279566-4] Riederer P, Lachenmayer L, Laux G (August 2004). "Clinical applications of MAO-inhibitors". Curr. Med. Chem. 11 (15): 2033–43. doi:10.2174/0929867043364775. PMID 15279566.

[pmid14628191-5] Riederer P, Lachenmayer L (November 2003). "Selegiline's neuroprotective capacity revisited". J Neural Transm 110 (11): 1273–8. doi:10.1007/s00702-003-0083-x. PMID 14628191.

[pmid15310558-6] Ives NJ, Stowe RL, Marro J, et al. (September 2004). "Monoamine oxidase type B inhibitors in early Parkinson's disease: meta-analysis of 17 randomised trials involving 3525 patients". BMJ 329 (7466): 593. doi:10.1136/bmj.38184.606169.AE. PMC 516655. PMID 15310558.

[QuantRev2013-7] Citrome L, Goldberg JF, Portland KB. Placing transdermal selegiline for major depressive disorder into clinical context: number needed to treat, number needed to harm, and likelihood to be helped or harmed. J Affect Disord. 2013 Nov;151(2):409-17. Review. PMID 23890583

[8] Lundgren, Becky. "Canine Cognitive Dysfunction". Veterinary Partner. Retrieved April 8, 2011.

[9] "Cognitive Dysfunction Syndrome". Long Beach Animal Hospital. Retrieved April 8, 2011.

[10] ttp://www.petplace.com/drug-library/selegiline-hcl-anipryl/page1.aspx

[11] "Anipryl consumer information". Drugs.com Vet. Retrieved April 3, 2011.

[12] Braddock JA, Church DB, Robertson ID (2004). "Selegiline Treatment of Canine Pituitary-Dependent Hyperadrenocorticism" (PDF). Australian Veterinary Journal. Retrieved April 8, 2011. (PDF)

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[48] See: [1] for details online.

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L-deprenyl