Desmethylselegiline

Desmethylselegiline
Clinical data
Other namesDMS; N-Desmethylselegiline; Norselegiline; L-Desmethyldeprenyl; L-DD; R-(–)-N-Desmethyldeprenyl; L-Nordeprenyl; N-Propargyl-L-amphetamine
Routes of
administration		By mouth[1][2][3]
Drug classMonoamine oxidase inhibitor; Catecholaminergic activity enhancer; Norepinephrine–dopamine releasing agent
Pharmacokinetic data
Metabolites• Levoamphetamine[4][1][3]
Identifiers
IUPAC name
  • 1-Phenyl-N-prop-2-ynylpropan-2-amine
CAS Number
PubChem CID
ChemSpider
ChEMBL
CompTox Dashboard (EPA)
Chemical and physical data
FormulaC12H15N
Molar mass173.259 g·mol−1
3D model (JSmol)
SMILES
  • CC(CC1=CC=CC=C1)NCC#C
InChI
  • InChI=1S/C12H15N/c1-3-9-13-11(2)10-12-7-5-4-6-8-12/h1,4-8,11,13H,9-10H2,2H3
  • Key:UUFAJPMQSFXDFR-UHFFFAOYSA-N

Desmethylselegiline (DMS), also known as norselegiline or as N-propargyl-L-amphetamine, is an active metabolite of selegiline, a medication used in the treatment of Parkinson's disease and depression.[4][1][2][3]

Like selegiline, DMS is a monoamine oxidase inhibitor (MAOI); specifically, it is a selective and irreversible inhibitor of monoamine oxidase B (MAO-B).[1][2][3] In addition, it is a catecholaminergic activity enhancer (CAE) similarly to selegiline.[5][6] The drug also produces levoamphetamine as an active metabolite, which is a norepinephrine–dopamine releasing agent with sympathomimetic and psychostimulant effects.[1][7][8]

DMS has been studied much less extensively than selegiline and has not been developed or approved for medical use.[9]

  1. ^ a b c d e Mahmood I (August 1997). "Clinical pharmacokinetics and pharmacodynamics of selegiline. An update". Clinical Pharmacokinetics. 33 (2): 91–102. doi:10.2165/00003088-199733020-00002. PMID 9260033.
  2. ^ a b c Heinonen EH, Anttila MI, Lammintausta RA (December 1994). "Pharmacokinetic aspects of l-deprenyl (selegiline) and its metabolites". Clinical Pharmacology and Therapeutics. 56 (6 Pt 2): 742–749. doi:10.1038/clpt.1994.204. PMID 7995016.
  3. ^ a b c d Heinonen EH, Anttila MI, Karnani HL, Nyman LM, Vuorinen JA, Pyykkö KA, et al. (July 1997). "Desmethylselegiline, a metabolite of selegiline, is an irreversible inhibitor of monoamine oxidase type B in humans". Journal of Clinical Pharmacology. 37 (7): 602–609. doi:10.1002/j.1552-4604.1997.tb04342.x. PMID 9243353.
  4. ^ a b Tábi T, Vécsei L, Youdim MB, Riederer P, Szökő É (May 2020). "Selegiline: a molecule with innovative potential". Journal of Neural Transmission. 127 (5): 831–842. doi:10.1007/s00702-019-02082-0. PMC 7242272. PMID 31562557.
  5. ^ Miklya I (June 2014). "Essential difference between the pharmacological spectrum of (-)-deprenyl and rasagiline". Pharmacological Reports. 66 (3): 453–458. doi:10.1016/j.pharep.2013.11.003. PMID 24905523.
  6. ^ Miklya I (March 2008). "(-)-deprenil, az N-metilprogargilamin-1-aminoindan (J-508) és a J-508 dezmetil analógjának (rasagilin) összehasonlító farmakológiai analízise" [A comparison of the pharmacology of (-)-deprenyl to N-methylpropargylamine-1-aminoindane (J-508) and rasagiline, the desmethyl-analogue of J-508] (PDF). Neuropsychopharmacologia Hungarica (in Hungarian). 10 (1): 15–22. PMID 18771016.
  7. ^ Cite error: The named reference HealSmithGosden2013 was invoked but never defined (see the help page).
  8. ^ Cite error: The named reference SmithDavis1977 was invoked but never defined (see the help page).
  9. ^ Cite error: The named reference HeinonenLammintausta1991 was invoked but never defined (see the help page).
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