Citation noticeOur citation system is being overhauled
References and citation markers may currently be incomplete, mismatched, or incorrect. This system is being rebuilt and reviewed before the full site launch.
ET
ET is a substituted tryptamine1 with reported entactogen and stimulant effects2. It was first described in 19471 and later developed by Upjohn as the antidepressant Monase before being withdrawn because of toxicity1. Unlike related tryptamines, it is not reported to produce psychedelic effects and is described as less stimulating than MDMA. Reported adverse outcomes include idiosyncratic agranulocytosis3, and deaths reported with recreational use2.
Dosage & Duration
Dosage
Doses are population estimates that vary widely between individuals.
Duration
Subjective Effects
Pharmacology
Pharmacodynamics
α-Ethyltryptamine acts primarily as a serotonin, norepinephrine, and dopamine releasing agent, with serotonin release predominating. It is about 10-fold more potent at inducing serotonin release than dopamine release and about 28-fold more potent than norepinephrine release; the (+)-enantiomer shows a more balanced serotonin-dopamine releasing profile. α-Ethyltryptamine is also a weak partial agonist at 5-HT2A receptors in its (+)-enantiomeric form, with marked enantiomeric differences4, and has weak affinity for several other serotonin receptor subtypes. It selectively and reversibly inhibits monoamine oxidase A, although this weak activity has been considered unlikely by some sources to account for its main psychoactive effects.
Pharmacokinetics
Absorption appears rapid, and α-ethyltryptamine has a relatively large volume of distribution. It undergoes hydroxylation and is eliminated primarily in urine, with most of a dose excreted within 12-24 hours. The elimination half-life is approximately 8 hours.
Interactions
An unlisted combination is an unknown one, not a safe one. Check a dedicated combination chart before mixing.
Tolerance
Tolerance timelines are rules of thumb, not exact schedules, and vary widely between individuals and use patterns.
Harm Potential
Toxicity
Recreational use has been linked to several deaths. In one report, a roughly 700 mg dose, though not confirmed, was followed by fatal agitated delirium with hyperthermia.
ET may cause MDMA-like serotonergic neurotoxicity. Rat studies have reported persistent decreases in serotonin, 5-HIAA, and serotonin transporter binding sites in the hippocampus and frontal cortex.
Agranulocytosis is a rare but serious side effect that has occurred with prolonged administration at antidepressant doses and has resulted in several cases and/or deaths; this was the primary reason for withdrawal from commercial development.
Marked hyperthermia, including cases that may be life-threatening, can occur, especially with excessive dosing.
Psychosis Risk
Agitated delirium has been reported in at least one fatal overdose case.
History & Culture
Early scientific description
α-Ethyltryptamine was first described in the scientific literature in 1947. Its enantiomers were later described individually in 1970.5
Legality
References
Citations
Further Reading
Article Status
Step 1 · Automated synthesisAn autonomous workflow built by Josie Kins compiled this article's foundation from information published across the web.
- Step 2 · First-pass reviewPending
Not yet reviewed: this article is pending editorial review by Lyrea.
- Step 3 · Citation reviewPending
No one has reviewed this article's citations yet. That second pass checks each claim against the source it cites.
Suggest an edit
Spotted a mistake, an outdated claim, or something missing from the ET article? Send the editors a private note. Feedback lands in a moderation queue and is never shown on the site.
Wish to give generalised feedback? You can do so here.