Phenylethylamine (PEA)

Endogenous trace amine, structural cousin of amphetamine, found in chocolate and produced from L-phenylalanine in the brain. Acts as a TAAR1 agonist and monoamine releaser, but is cleared by MAO-B within minutes. Standalone oral PEA is a 5-15 minute "rush" with negligible sustained effect. Useful only when paired with a MAO-B inhibitor (selegiline) or a competitive MAO-B substrate like hordenine to extend duration.

Phenylethylamine is the parent skeleton of all phenethylamines (which includes amphetamine, methamphetamine, MDMA, mescaline, dopamine itself, etc.). The non-substituted parent compound:

• TAAR1 agonist: Trace amine-associated receptor 1 is a Gs/Gq-coupled GPCR enriched in monoaminergic neurons. TAAR1 activation modulates DA and 5-HT firing. PEA is the prototypical endogenous TAAR1 agonist.
• Monoamine release: Like amphetamine, PEA reverses VMAT2 and DAT/NET function to release dopamine and norepinephrine into the synapse, with weaker 5-HT release.
• Mild reuptake inhibition: At higher concentrations PEA inhibits DAT/NET reuptake.
• Rapid MAO-B clearance: This is the dominant pharmacokinetic fact. PEA is the preferred substrate of MAO-B and is metabolized within ~5-15 minutes of oral ingestion. Brain levels peak and crash on the same time scale.

Net subjective effect: a brief amphetamine-like surge that vanishes before you finish noticing it.