2 sources
Collated from TripSit, Pharmacology. Where sources differ (e.g. dosing), Compare shows them side by side.
Also known as peaTS
Organic compound, which is a name of a class of chemicals that are quite well known for psychoactive and/or stimulant effects. Normally not used as a supplement as it is rapidly broken down into inactive compounds. Is found in many foods.TS
Oral
Route dataTripSit
| Threshold | Light | Common | Strong | Heavy |
|---|---|---|---|---|
| — | — | 300–500 mg | — | —+ |
| Onset | 15–30 minutes |
|---|---|
| Total | 1–4 hours |
| After-effects | 10–60 minutes |
🧬 Receptor activityPH
| Target | Action | Affinity | Source | |
|---|---|---|---|---|
| Unchecked | — | Ki 4000 nM | CHEMBL | TargetUnchecked Action— AffinityKi 4000 nM SourceCHEMBL |
| 5-hydroxytryptamine receptor 2A | — | Ki 10000 nM | CHEMBL | Target5-hydroxytryptamine receptor 2A Action— AffinityKi 10000 nM SourceCHEMBL |
| Serine protease 1 | — | Ki 11000 nM | CHEMBL | TargetSerine protease 1 Action— AffinityKi 11000 nM SourceCHEMBL |
| Phenylethanolamine N-methyltransferase | — | Ki 220000 nM | CHEMBL | TargetPhenylethanolamine N-methyltransferase Action— AffinityKi 220000 nM SourceCHEMBL |
| Glutamate NMDA receptor | — | Ki 753000 nM | CHEMBL | TargetGlutamate NMDA receptor Action— AffinityKi 753000 nM SourceCHEMBL |
Pharmacokinetics
Half-lifePH
Plasma pharmacokinetics of PEA could be described by 1st-order kinetics with estimated t/2 of approx 5-10 min.
AbsorptionPH
This study was performed to characterize the intestinal transport of beta-phenylethylamine (PEA). Uptake of [(14)C]PEA into Caco-2 cells was Na(+)-independent but strongly stimulated by an outside directed H(+) gradient. At extracellular pH 7.5, the concentration-dependent uptake of PEA was saturable with kinetic parameters of 2.6 mM (K(t)) and 96.2 nmol/min per mg of protein (V(max)). Several biogenic amines such as harmaline and N-methylphenylethylamine as well as cationic drugs such as phenelzine, tranylcypromine, d,l-amphetamine, methadone, chlorphenamine, diphenhydramine and promethazine strongly inhibited the [(14)C]PEA uptake with K(i) values around 1 mM. Tetraethylammonium, N-methyl-4-phenylpyridinium and choline had no effect. We also studied the bidirectional transepithelial transport of [(14)C]PEA at cell monolayers cultured on permeable filters. Net transepithelial flux of [(14)C]PEA from apical-to-basolateral side exceeded basolateral-to-apical flux 5-fold. We conclude that PEA is transported into Caco-2 cells by a highly active, saturable, H(+)-dependent (antiport) process. The transport characteristics do not correspond to those of the known carriers for organic cations of the SLC22, SLC44, SLC47 and other families.
Phenylethylamine was found in cervical spinal cord dorsal and ventral horns, zona intermedia, and lumbar cord dorsal and ventral horns of rats in concentrations of 114-238 pg/mg protein. Values found in caudate nucleus (218 pg/mg) and cerebellum (73 pg/mg). Repeated treatment with amphetamine for 10 days increased levels in both brain and spinal cord.
Specific binding of tritiated beta-phenylethylamine to rat forebrain membranes was saturable; the apparent dissociation constant was 55 nmol and the density of binding sites was approx 1078 pmol/mg protein. Highest binding was observed in hypothalamus and striatum.
The urinary excretion rate of the endogenous, amphetamine-like substance beta-phenethylamine was markedly elevated in human subjects in association with an initial parachuting experience. The increases were delayed in most subjects and were not correlated with changes in urinary pH or creatinine excretion. The data suggest a stress-related role for beta-phenethylamine.
Found in normal human urine (about 30 ug/L).
MetabolismPH
Free 2-phenylethylamine excretion was ... significantly elevated ... in phenylketonuric adults and children receiving a normal or a slightly restricted intake of phenylalanine. Urinary 2-phenylethylamine was also significantly increased in phenylketonuric children receiving low phenylalaine dietary therapy. Conjugated 2-phenylethylamine excretion was ... not ... increased above normal.
2-Phenylethylamine is an endogenous constituent of human brain and is implicated in cerebral transmission. It is also found in certain foodstuffs and may cause toxic side-effects in susceptible individuals. Metabolism of 2-phenylethylamine to phenylacetaldehyde is catalyzed by monoamine oxidase and the oxidation of the reactive aldehyde to its acid derivative is catalyzed mainly by aldehyde dehydrogenase and perhaps aldehyde oxidase, with xanthine oxidase having minimal transformation. The present investigation examines the metabolism of 2-phenylethylamine to phenylacetaldehyde in liver slices and compares the relative contribution of aldehyde oxidase, xanthine oxidase and aldehyde dehydrogenase activity in the oxidation of phenylacetaldehyde with precision-cut fresh liver slices in the presence/absence of specific inhibitors of each enzyme. In liver slices, phenylacetaldehyde was rapidly converted to phenylacetic acid. Phenylacetic acid was the main metabolite of 2-phenylethylamine, via the intermediate phenylacetaldehyde. Phenylacetic acid formation was completely inhibited by disulfiram (specific inhibitor of aldehyde dehydrogenase), whereas isovanillin (specific inhibitor of aldehyde oxidase) inhibited acid formation to a lesser extent and allopurinol (specific inhibitor of xanthine oxidase) had little or no effect. Therefore, in liver slices, phenylacetaldehyde is rapidly oxidized by aldehyde dehydrogenase and aldehyde oxidase with little or no contribution from xanthine oxidase.
We report here very high urinary phenylethylamine level in a phenylketonuric newborn and variable phenylethylamine levels in phenylketonuric patients with similar phenylalanine levels. As phenylethylamine, a very toxic metabolite of phenylalanine, is rapidly degraded by monoamine oxydase type B, an enzyme that has a very low activity in neonates, these results are consistent with those of the hypothesis of MAO-B acting as a modifying gene in phenylketonuria.
Incubation of phenylethylamine with rabbit liver microsomes, divalent MN and NADPH generating system leads to formation of azoxy-2-phenylethane (a mutagen). 38 nmol of azoxy-2-phenylethane is formed from 10 umol of phenylethylamine during 30 min incubation. Metabolism to azoxy-2-phenylamine appears completely dependent on the presence of divalent MN.
For more Metabolism/Metabolites (Complete) data for 2-Phenylethylamine (9 total), please visit the HSDB record page.
Plan a dose of Phenethylamine
Loading the fact-sheet…
Logging a dose needs somewhere to keep it. Start a free session — no signup; it and everything in it expire in 7 days.
External links
Fact-sheets from PsychonautWiki. Harm-reduction reference only — not medical advice.