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    Phenethylamine molecular structure

    Phenethylamine Stats & Data

    Pea Benzeneethanamine Beta-phenylethylamine
    NPS DataHub
    MW121.18
    FormulaC8H11N
    CAS64-04-0
    LD50300.0 mg/kg (Rat 300 mg/kg; Merck)
    IUPAC2-phenylethanamine
    SMILESNCCc1ccccc1
    InChIKeyBHHGXPLMPWCGHP-UHFFFAOYSA-N
    Phenethylamines
    Chemical Class Phenethylamine
    Psychoactive Class Stimulant

    Pharmacology

    DrugBank
    State Solid

    Description

    Pea allergenic extract is used in allergenic testing.

    Receptor Profile

    Receptor Actions

    Agonists
    TAAR1 agonist (trace amine-associated receptor 1)
    Inhibitors
    VMAT2 inhibitor (vesicular monoamine transporter 2)

    Measured Affinities

    Guide to PHARMACOLOGY

    Measured binding and functional data for β-phenylethylamine, curated by the IUPHAR/BPS Guide to PHARMACOLOGY. Each row cites the paper it came from. Lower concentrations mean tighter binding — a value in the sub-nanomolar range indicates a very potent interaction.

    Target Action Measure Value Concentration Species Source
    TAAR4P Taar4 Agonist pEC50 6 1,000 nM Mouse PMID 16878137
    TA1 receptor TAAR1 Full agonist pEC50 — — Human —
    TA1 receptor Taar1 Full agonist pEC50 — — Mouse —
    TA1 receptor Taar1 Full agonist pEC50 — — Rat —
    TAAR4P Taar4 Partial agonist - — — Rat PMID 20559446

    Reading this. pKi, pEC50 and pIC50 are negative log molar values, so a higher number means a tighter interaction; the concentration column converts them for you. Values from non-human species are laboratory measurements and do not translate directly to human effect. Receptor affinity is not a dose — it describes what a molecule binds, not how much of it is safe to take.

    Receptor data from the IUPHAR/BPS Guide to PHARMACOLOGY (v2026.2), licensed CC BY-SA 4.0. Matched to this substance by InChIKey.

    History & Culture

    Phenethylamine has long held a special place in psychopharmacological research due to its status as the simplest member of the phenethylamine chemical class. Its clean molecular structure, natural presence in human tissues and bodily fluids, and close chemical relationship to both amphetamine and endogenous neurotransmitters have made it a subject of sustained scientific interest. The compound occurs widely throughout nature in both plants and animals, produced as a metabolic byproduct during the bacterial decomposition of phenylalanine in tissue. Multiple synthetic routes for phenethylamine were established in the mid-twentieth century. In 1948, R. F. Nystrom and W. G. Brown first reported a convenient synthesis involving the reduction of ω-nitrostyrene using lithium aluminium hydride in ether. An alternative method was later published in 1955 by J. C. Robinson and H. R. Snyder in Organic Syntheses, which employed the reduction of benzyl cyanide with hydrogen in liquid ammonia using a Raney-Nickel catalyst under high temperature and pressure conditions. Phenethylamine gained popular attention through its association with chocolate, where it occurs as a significant component, particularly following microbial fermentation. This led to its characterization in mainstream media as "the love-sickness chemical," spawning a popular myth that individuals experiencing heartbreak compulsively consume chocolate to replenish depleted phenethylamine levels. While some researchers have speculated that phenethylamine may play a role in romantic affection, these claims have not been substantiated by direct experimental evidence. The compound has also been implicated in the euphoric effects of vigorous physical activity; research has demonstrated that thirty minutes of moderate- to high-intensity exercise significantly elevates urinary levels of phenylacetic acid, the primary metabolite of phenethylamine. Similar increases have been observed following skydiving, suggesting phenethylamine may contribute to the subjective pleasure associated with intense physical exertion.

    Toxicity

    PubChem

    PEA poisonings may be severe in young and healthy individuals. The most frequently reported symptoms included anxiety and hallucinations (49%), mydriasis and headache (41%), tachycardia (40%) and hypertension (15%).

    Effect Profile

    Curated + 5 Reports
    Stimulant 5.6

    Moderate euphoria and focus with strong anxiety/jitters, mild stimulation

    Stimulation / Energy×3
    5
    Euphoria / Mood Lift×2
    7
    Focus / Productivity×2
    7
    Anxiety / Jitters×1
    8

    Tolerance & Pharmacokinetics

    drugs.wiki
    Half-Life
    Minutes (very short; dominated by rapid MAO-B metabolism).
    Addiction Potential
    Low physiological dependence potential; however, the very short duration can promote binge/redose patterns in some individuals, particularly when potentiated by MAO-B inhibitors.

    Tolerance Decay

    Full tolerance 1d Half tolerance 3d Baseline ~18d

    Data are anecdotal; users frequently report rapid loss of effect with repeated dosing in a session and partial return to baseline sensitivity after several days to a week.

    Cross-Tolerances

    Other stimulants (indirect sympathomimetics)

    Experience Report Analysis

    Erowid
    13 Reports
    5 Single-substance
    2008–2024 Date Range
    11 With Age Data
    4 Effects Detected

    Demographics

    Gender Distribution

    Too few reports for a chart: gender is known from 13 reports, and a split is drawn only from 20 reports or more. Counts are shown instead. Why 20?

    • Male 12 of 13
    • Female 1 of 13

    Age Distribution

    Reports Over Time

    Effect Analysis

    Erowid

    Effects aggregated from 5 experience reports (5 single-substance Erowid)

    5 Reports
    4 Effects Detected
    3 Positive
    1 Adverse
    0 Neutral

    Effect Sentiment Distribution

    Confidence Distribution

    Each bar is the share of reports mentioning the effect; its whisker, and the band on the rows below, is the 95% interval: where the share could plausibly be with other reports of the same kind.

    Too few reports for bars: these effects come from 5 single-substance Erowid reports, and a bar is drawn only from 20 reports or more. With fewer, a percentage cannot tell a common effect from a rare one. Counts are shown instead. Why 20?

    Positive Effects 3

    Euphoria 4 of 5 70%
    Tactile Enhancement 4 of 5 70%
    Empathy 3 of 5 70%

    Adverse Effects 1

    Confusion 3 of 5 70%

    Also reported in combinations. In the 8 Phenethylamine reports where another drug was taken too, 1 mentions hospital, emergency services or an overdose, 0 a seizure and 0 psychosis (too few reports for percentages). In the 5 single-substance reports: 0, 0 and 0. These are not in the figures above: they cannot be put down to Phenethylamine alone, and a mention is not always something that happened to the writer.

    Real-World Dose Distribution

    Erowid

    From 11 of 19 recorded dose entries: those that state a weight (mg, g or µg), in routes with at least five of them. Values above Q3 + 3×IQR, far above what people typically take, are left out; they can include real heavy doses and overdoses, not only mistakes.

    Oral (n=10)

    Median: 1000.0mg 25th: 425.0mg 75th: 1237.5mg 90th: 3100.0mg

    Common Combinations

    Most co-occurring substances, as a share of all 13 reports filed under Phenethylamine

    Too few reports for bars: these combinations come from 13 reports, and a bar is drawn only from 20 reports or more. With fewer, a percentage cannot tell a common effect from a rare one. Counts are shown instead. Why 20?

    • Selegiline 3 of 13

    Form / Preparation

    Most common forms and preparations, as a share of the 5 reports that give one

    Too few reports for bars: these forms come from 5 reports, and a bar is drawn only from 20 reports or more. With fewer, a percentage cannot tell a common effect from a rare one. Counts are shown instead. Why 20?

    • Capsule 3 of 5
    • Powder / Crystals 2 of 5

    Harm Reduction

    drugs.wiki

    - PEA is preferentially metabolized by monoamine oxidase-B (MAO-B), leading to a very short duration and low oral bioavailability; any MAO-B inhibition can dramatically increase exposure and physiological impact. This is the central harm-reduction issue: avoid all MAOIs (including Parkinson’s drugs and the antibiotic linezolid).

    - Selective MAO-B inhibitors (selegiline, rasagiline, safinamide) and nonselective/irreversible MAOIs (phenelzine, tranylcypromine, isocarboxazid) can potentiate PEA to a degree that risks severe hypertension, hyperthermia, or cerebrovascular events; this risk exists even at small PEA doses when MAO is inhibited.

    - Linezolid is a reversible, nonselective MAOI used as an antibiotic; combining PEA with linezolid can precipitate dangerous pressor responses and should be strictly avoided.

    - Because the psychoactive window is brief, some users escalate to gram-level oral doses or engage in frequent redosing cycles; harm-reduction priorities include not stacking stimulants, monitoring blood pressure/heart rate, maintaining hydration, and stopping at the first signs of severe headache, chest pain, or marked flushing. These redosing patterns are consistently reported in harm-reduction forums and align with the known indirect sympathomimetic profile of PEA.

    - PEA primarily acts as an endogenous trace amine/TAAR1 agonist and an indirect sympathomimetic (catecholamine-releasing); expect tachycardia, blood pressure elevation, and anxiety at higher doses, especially with co-stimulants. Individuals with cardiovascular disease should avoid use.

    - Food-derived/background PEA (e.g., chocolate) is trivial compared to supplemental doses; however, in the presence of MAOI therapy even trace amines can become clinically significant, reinforcing the strict MAOI-avoidance guidance.

    - Urine drug testing: cross-reactivity data indicate β-phenethylamine can interfere with some assays; although not usually targeted, unexpected results should be confirmed with specific methods (e.g., GC/MS).

    - There is no established therapeutic dosing for psychoactive purposes. If an individual nevertheless chooses to experiment, conservative spacing (weeks) and strict avoidance of MAOIs and stimulant stacks are critical to reduce cumulative cardiovascular strain and compulsive redosing risk.

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