Pharmacodynamics<unk> , being similar to amphetamine in its action at their common biomolecular targets, releases norepinephrine and dopamine.<unk>  also appears to induce acetylcholine release via a glutamate-mediated mechanism.<unk>  has been shown to bind to human trace amine-associated receptor 1 (hTAAR1) as an agonist. Pharmacokinetics By oral route,<unk> 's half-life is minutes; endogenously produced<unk>  in catecholamine neurons has a half-life of roughly 30 seconds. In humans,<unk>  is metabolized by phenylethanolamine N-methyltransferase (PNMT), monoamine oxidase A (), monoamine oxidase B (), the semicarbazide-sensitive amine oxidases (SSAOs) AOC2 and AOC3, flavin-containing monooxygenase 3 (FMO3), and aralkylamine N-acetyltransferase (AANAT). , an isomer of amphetamine, is produced in humans via the metabolism of<unk>  by PNMT. β-Phenylacetic acid is the primary urinary metabolite of<unk>  and is produced via monoamine oxidase metabolism and subsequent aldehyde dehydrogenase metabolism. Phenylacetaldehyde is the intermediate product which is produced by monoamine oxidase and then further metabolized into β-phenylacetic acid by aldehyde dehydrogenase. When the initial phenylethylamine concentration in the brain is low, brain levels can be increased when taking a monoamine oxidase inhibitor (MAOI), particularly a MAO-B inhibitor, and by times when the initial concentration is high.
Phenethylamine
Chlorphenamine
Methoxyphenamine
Phenoxyethanol
Pseudophenmetrazine
Trimethobenzamide
Carctol
Triprolidine