PT  - JOURNAL ARTICLE
AU  - Shin, Ho-Sang
TI  - Metabolism of Selegiline in Humans
DP  - 1997 Jun 01
TA  - Drug Metabolism and Disposition
PG  - 657--662
VI  - 25
IP  - 6
4099  - http://dmd.aspetjournals.org/content/25/6/657.short
4100  - http://dmd.aspetjournals.org/content/25/6/657.full
SO  - Drug Metab Dispos1997 Jun 01; 25
AB  - Nine urinary metabolites of selegiline hydrochloride [N-methyl-N-propargyl(2-phenyl-1-methyl)ethylammonium chloride], a monoamine oxidase inhibitor, after administration to humans were identified. Their identities were confirmed by comparison of the spectra from GC/MS of peaks with those of authentic compounds. The following metabolites and unchanged drug (selegiline) were detected in urine: (R)-desmethylselegiline, (R)-methamphetamine, (R)-amphetamine, (1S,2R)-norephedrine, (1R,2R)-norpseudoephedrine, (1S,2R)-ephedrine, (1R,2R)-pseudoephedrine, (R)-p-hydroxyamphetamine, and (R)-p-hydroxymethamphetamine. The metabolites excreted 2 days after administration of 2.5–10 mg of selegiline hydrochloride amounted to 44–58% of the dose. Selegiline was metabolized by three distinct pathways: N-dealkylation, β-carbon hydroxylation, and ring-hydroxylation. The major metabolite was (R)-methamphetamine. During metabolism, no racemic transformation occurred and β-carbon hydroxylation showed apparently product stereoselectivity. The American Society for Pharmacology and Experimental Therapeutics