Back سيليجيلين Arabic سلژیلین AZB Selegilin Welsh Selegilin German Selegilina Spanish سلژیلین Persian Selegiliini Finnish Sélégiline French סלג'ילין HE Szelegilin Hungarian

Selegiline

Selegiline
Clinical data
Pronunciation/səˈlɛdʒɪliːn/ sə-LEJ-i-leen ("seh-LEH-ji-leen")[1][2]
Trade namesEldepryl, Jumex, Zelapar, Emsam, Anipryl, others[3]
Other namesL-Deprenyl; L-Deprenil; L-Deprenalin; L-Deprenaline; L-E-250; L-Phenylisopropylmethylpropinylamine; (R)-(–)-N,α-Dimethyl-N-2-propynylphenethylamine; (R)-(–)-N-Methyl-N-2-propynylamphetamine; (R)-(–)-N-2-Propynylmethamphetamine; N-Propargyl-L-methamphetamine
AHFS/Drugs.comMonograph
MedlinePlusa697046
License data
Pregnancy
category
  • AU: B2
Routes of
administration		• Oral (tablet, capsule)[4][5]
• Buccal (ODTTooltip orally disintegrating tablet)[6][7]
• Transdermal (patch)[8][9]
Drug classMonoamine oxidase inhibitor; Catecholaminergic activity enhancer; Norepinephrine releasing agent; Antiparkinsonian; Antidepressant; Neuroprotective
ATC code
Legal status
Legal status
Pharmacokinetic data
BioavailabilityOral: 4–10%[5][11][12]
ODT: ~5–8× oral[13][7][14]
Patch: 75%[9]
Protein binding85–90%[9][8][6]
MetabolismLiver, other tissues (CYP2B6, CYP2C19, others)[5][18][9][19]
Metabolites• Desmethylselegiline (DMS)
• Levomethamphetamine (L-MA)
• Levoamphetamine (L-A)
Elimination half-lifeOral:
• S (single): 1.2–3.5 h[5]
• S (multi): 7.7–9.7 h[5][12]
• DMS (single): 2.2–3.8 h[5]
• DMS (multi): 9.5 h[5]
• L-MA: 14–21 h[5][7]
• L-A: 16–18 h[5][7]
ODT:
• S (single): 1.3 h[6]
• S (multi): 10 h[6]
Patch:
• S: 20 h[12][8]
ExcretionUrine (87%):[15][16][7][5][17]
• L-MA: 20–63%
• L-A: 9–26%
• DMS: 1%
• S: 0.01–0.03%
Feces: 15%[15][7]
Identifiers
  • (R)-N-methyl-N-(1-phenylpropan-2-yl)prop-3-yn-1-amine
CAS Number
PubChem CID
IUPHAR/BPS
DrugBank
ChemSpider
UNII
KEGG
ChEBI
ChEMBL
CompTox Dashboard (EPA)
ECHA InfoCard100.109.269 Edit this at Wikidata
Chemical and physical data
FormulaC13H17N
Molar mass187.286 g·mol−1
3D model (JSmol)
ChiralityLevorotatory enantiomer
  • C#CCN([C@@H](Cc1ccccc1)C)C
  • 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 checkY
  • Key:MEZLKOACVSPNER-GFCCVEGCSA-N checkY
  (verify)

Selegiline, also known as L-deprenyl and sold under the brand names Eldepryl, Zelapar, and Emsam among others, is a medication which is used in the treatment of Parkinson's disease and major depressive disorder.[4][6][8][3] It has also been studied for a variety of other indications, but has not been formally approved for any other use.[20][21] The medication in the form licensed for depression has modest effectiveness for this condition that is similar to that of other antidepressants.[21][22][23] Selegiline is provided as a swallowed tablet or capsule[4][5] or an orally disintegrating tablet (ODT)[6][7] for Parkinson's disease and as a patch applied to skin for depression.[8][9]

Side effects of selegiline occurring more often than with placebo include insomnia, dry mouth, dizziness, nervousness, abnormal dreams, and application site reactions (with the patch form), among others.[21][22][24][4][8] At high doses, selegiline has the potential for dangerous food and drug interactions, such as the tyramine-related "cheese reaction" or hypertensive crisis and risk of serotonin syndrome.[9][25][5] However, doses within the approved clinical range appear to have little to no risk of these interactions.[9][25][5] In addition, the ODT and transdermal patch forms of selegiline have reduced risks of such interactions compared to the conventional oral form.[7][9] Selegiline has no known misuse potential or dependence liability and is not a controlled substance.[26][27][28][29][8]

Selegiline acts as a monoamine oxidase inhibitor (MAOI) and thereby increases levels of monoamine neurotransmitters in the brain.[30][11][25][5] At typical clinical doses used for Parkinson's disease, selegiline is a selective and irreversible inhibitor of monoamine oxidase B (MAO-B), increasing brain levels of dopamine.[30][11][25][5] At higher doses, it loses its specificity for MAO-B and also inhibits monoamine oxidase A (MAO-A), which increases serotonin and norepinephrine levels in the brain as well.[30][11][25][5] In addition to its MAOI activity, selegiline is a catecholaminergic activity enhancer (CAE) and enhances the impulse-mediated release of norepinephrine and dopamine in the brain.[31][32][33][34][25] This action may be mediated by TAAR1 agonism.[35][36][37] After administration, selegiline partially metabolizes into levomethamphetamine and levoamphetamine, which act as norepinephrine releasing agents (NRAs) and may contribute to its therapeutic and adverse effects.[38][28][39] The levels of these metabolites are much lower with the ODT and transdermal patch forms of selegiline.[7][9] Chemically, selegiline is a substituted amphetamine,[40] a derivative of methamphetamine,[40] and the purified levorotatory enantiomer of deprenyl (the racemic form).[41][20]

Deprenyl was discovered and studied in the early 1960s.[41][20] Subsequently, selegiline was purified from deprenyl and was studied and developed itself.[41] Selegiline was first introduced for medical use in Hungary in 1977.[42] It was subsequently approved in the United Kingdom in 1982 and in the United States in 1989.[42][43] The ODT was approved in the United States in 2006 and in the European Union in 2010, while the patch was introduced in the United States in 2006.[42][20] Selegiline was the first selective MAO-B inhibitor to be discovered and marketed.[13][44][45] In addition to its medical use, there has been interest in selegiline as a potential anti-aging drug and nootropic.[46][47][48] However, effects of this sort are controversial and uncertain.[46][49][50][51] Generic versions of selegiline are available in the case of the conventional oral form but not in the case of the ODT or transdermal patch forms.[52][53]

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