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]
^Cite error: The named reference Parkinsons.org2018 was invoked but never defined (see the help page).
^Cite error: The named reference Acosta2020 was invoked but never defined (see the help page).
^ abcPae CU, Lim HK, Han C, Neena A, Lee C, Patkar AA (August 2007). "Selegiline transdermal system: current awareness and promise". Prog Neuropsychopharmacol Biol Psychiatry. 31 (6): 1153–1163. doi:10.1016/j.pnpbp.2007.04.020. PMID17614182.
^ abLöhle M, Storch A (November 2008). "Orally disintegrating selegiline for the treatment of Parkinson's disease". Expert Opin Pharmacother. 9 (16): 2881–2891. doi:10.1517/14656566.9.16.2881. PMID18937619.
^Clarke A, Brewer F, Johnson ES, Mallard N, Hartig F, Taylor S, et al. (November 2003). "A new formulation of selegiline: improved bioavailability and selectivity for MAO-B inhibition". Journal of Neural Transmission. 110 (11): 1241–1255. doi:10.1007/s00702-003-0036-4. PMID14628189. S2CID711419.
^ abHeinonen EH, Anttila MI, Lammintausta RA (December 1994). "Pharmacokinetic aspects of l-deprenyl (selegiline) and its metabolites". Clin Pharmacol Ther. 56 (6 Pt 2): 742–749. doi:10.1038/clpt.1994.204. PMID7995016.
^Heinonen EH, Myllylä V, Sotaniemi K, Lamintausta R, Salonen JS, Anttila M, et al. (November 1989). "Pharmacokinetics and metabolism of selegiline". Acta Neurologica Scandinavica. Supplementum. 126: 93–99. doi:10.1111/j.1600-0404.1989.tb01788.x. PMID2515726. S2CID221440315.
^Chrisp P, Mammen GJ, Sorkin EM (May 1991). "Selegiline: A Review of its Pharmacology, Symptomatic Benefits and Protective Potential in Parkinson's Disease". Drugs Aging. 1 (3): 228–248. doi:10.2165/00002512-199101030-00006. PMID1794016.
^Cite error: The named reference FinbergRabey2016 was invoked but never defined (see the help page).
^Cite error: The named reference FabbriniAbbruzzeseMarconi2012 was invoked but never defined (see the help page).
^ abYasar S, Goldberg JP, Goldberg SR (January 1, 1996). "Are metabolites of l-deprenyl (Selegiline) useful or harmful? Indications from preclinical research". Deprenyl — Past and Future. Journal of Neural Transmission. Supplementum. Vol. 48. pp. 61–73. doi:10.1007/978-3-7091-7494-4_6. ISBN978-3-211-82891-5. PMID8988462.
^Cite error: The named reference NickelSzelenyiSchulze1994 was invoked but never defined (see the help page).
^Shimazu S, Miklya I (May 2004). "Pharmacological studies with endogenous enhancer substances: β-phenylethylamine, tryptamine, and their synthetic derivatives". Prog Neuropsychopharmacol Biol Psychiatry. 28 (3): 421–427. doi:10.1016/j.pnpbp.2003.11.016. PMID15093948.
^Berry MD (January 2007). "The potential of trace amines and their receptors for treating neurological and psychiatric diseases". Rev Recent Clin Trials. 2 (1): 3–19. doi:10.2174/157488707779318107. PMID18473983.
^Gerlach M, Reichmann H, Riederer P (2012). "A critical review of evidence for preclinical differences between rasagiline and selegiline". Basal Ganglia. 2 (4): S9–S15. doi:10.1016/j.baga.2012.04.032.
^ abKraemer T, Maurer HH (April 2002). "Toxicokinetics of amphetamines: metabolism and toxicokinetic data of designer drugs, amphetamine, methamphetamine, and their N-alkyl derivatives". Ther Drug Monit. 24 (2): 277–289. doi:10.1097/00007691-200204000-00009. PMID11897973.
^ abcParnham MJ (1993). "The History of l-Deprenyl". Inhibitors of Monoamine Oxidase B: Pharmacology and Clinical Use in Neurodegenerative Disorders. Milestones in Drug Therapy. Basel: Birkhäuser Basel. pp. 237–251. doi:10.1007/978-3-0348-6348-3_12. ISBN978-3-0348-6349-0.
^Finberg JP (April 2019). "Inhibitors of MAO-B and COMT: their effects on brain dopamine levels and uses in Parkinson's disease". Journal of Neural Transmission. 126 (4): 433–448. doi:10.1007/s00702-018-1952-7. PMID30386930.
^Cite error: The named reference Drugs@FDA was invoked but never defined (see the help page).
^Cite error: The named reference AsnisHenderson2014 was invoked but never defined (see the help page).