DET
DET is a synthetic psychedelic of the tryptamine class, first synthesized by Stephen Szára in 1956.1 A close structural analog of DMT, it is distinguished by its oral activity, which results from increased resistance to monoamine oxidase metabolism.2 DET produces effects similar to DMT, including intense hallucinations and profound alterations in consciousness.2 It remains extremely uncommon with little history of human usage, and has no known natural sources.
Dosage & Duration
Dosage
Doses are population estimates that vary widely between individuals.
2C-B exhibits a notably steep dose-response relationship, particularly within the 12–24 mg range, where differences of just 2 mg can substantially alter both the intensity and qualitative nature of the experience. Careful, incremental dosing is recommended when establishing individual sensitivity.
Subjective Effects
DET produces a psychedelic experience frequently compared to DMT in the character of its illusions and hallucinations, but one that is active orally and unfolds over a much longer, gentler arc, with effects often described as following a wave-like time course. Oral onset is slow, sometimes taking an hour or more to become undeniable, with peak intensity from roughly the first through third hour and full resolution by around five hours; smoked onset arrives within about five minutes and is notably gentle, euphoric, and empathogenic. The experience is strongly shaped by set and setting — favorable environments yield profound aesthetic, emotional, and philosophical states, while unfavorable ones or excessive doses can produce anxiety, paranoia, perplexity, and social withdrawal. A pleasant afterglow is commonly reported the following day, though higher doses can instead leave a hangover of lassitude and blunted, fuzzy thinking.
Physical
Body effects resemble the autonomic symptoms of DMT: sweating of the hands and feet, pupil dilation, pronounced tachycardia, and a hollowness in the chest, with dizziness, vertigo, paleness, shakiness, fine muscle tremor, athetoid movements, and occasional nausea or vomiting at stronger doses. Injected routes can produce a slight burning and numbness of the hands and feet during onset.
Autonomic
Cardiovascular
Stimulation
Mental and physical stimulation with restlessness is typical, and insomnia can follow.
Uncomfortable
Early physical symptoms tend to appear during onset and fade as the experience develops; DMT-like vegetative or autonomic symptoms are characteristic.
Cognitive
The headspace combines euphoria, empathy, and emotional insight with a sense of heightened meaning — objects can feel newly significant, and users describe perceiving the world anew like a small child, alongside cosmic, mystical, and philosophical currents of thought. This coexists with genuine impairment: drifting thoughts, difficulty concentrating, confusion, and an alcohol-like or stoned quality, and at anxious moments a peculiar double orientation in which the ordinary and the hallucinated world are held as real simultaneously.
Emotional
The emotional tone is typically euphoric, empathic, and open, but is highly dependent on set and setting; unfavorable conditions or excessive doses can invert it into anxiety and paranoia.
Enhancements
Suppressions
Transpersonal
Visual
Visual effects range from color intensification and closed-eye patterning at lighter doses to DMT-like illusions and hallucinations, with both closed- and open-eye visuals reported.
Hallucinatory States
Auditory
Music is enhanced and can contribute powerfully to the experience; auditory hallucinations have also been reported.
Tactile
Tactile sensation is enhanced, and physical touch can feel unusually rewarding and socially bonding.
Olfactory
Olfactory hallucinations have been reported.
Multisensory
Pharmacology
Pharmacodynamics
DET acts as a non-selective serotonin receptor agonist, with activity at the 5-HT2A, 5-HT2B, and 5-HT2C receptors.5 At the 5-HT2A receptor, it activates Gq-mediated signaling with an Emax exceeding 70% and produces the head-twitch response in rodents, a behavioral proxy for psychedelic-like activity.6 The substance also exhibits very weak reversible monoamine oxidase inhibitory activity and may act as a serotonin reuptake inhibitor with low affinity but moderate potency,5 while showing no activity at the norepinephrine or dopamine transporters.5
Pharmacokinetics
DET demonstrates significant resistance to monoamine oxidase metabolism, which may be attributable to the steric bulk of its N-ethyl substituents providing sufficient metabolic stability for oral activity.7 The substance is rapidly distributed through plasma, liver, and brain following administration, with most of the compound cleared from these tissues within 30 minutes, though it remains detectable in the brain at 60 minutes.7 DET is metabolized primarily through 6-hydroxylation of the indole ring and N-dealkylation, with approximately 20% of the administered dose excreted in urine as glucuronide conjugates.8 Repeated administration results in decreased excretion of unchanged drug and increased metabolite output.2
Tolerance
Tolerance timelines are rules of thumb, not exact schedules, and vary widely between individuals and use patterns.
Serotonergic psychedelics
Harm Potential
Addiction & Dependence
Psychological
Extremely LowDET is believed to be non-habit-forming, and the desire to use it may actually decrease with continued use, consistent with the typical profile of classic psychedelics.910
Physical
Extremely LowNo physical dependence or withdrawal syndrome has been documented. Rapid tolerance development naturally limits frequent use patterns.9
Psychosis Risk
Like other classic psychedelics, DET can produce acute psychotic-like symptoms including delusions, paranoia, and perceptual disturbances during intoxication. Early research explored DET as a psychotomimetic model, though this framework has since been largely dismissed by researchers. Risk may be elevated in predisposed individuals.9
Seizure Risk
No direct seizure risk documented for DET alone. As with other psychedelics, it may act as a seizure trigger in predisposed individuals, particularly when combined with substances that lower seizure threshold.
History & Culture
DET was first synthesized in 1956 by Hungarian chemist Stephen Szára, with his findings published the following year.11 More systematic studies were subsequently conducted by Szára and colleagues,2 as well as independently by Böszörményi and…
Legality
International
DET (N,N-diethyltryptamine) is listed in Schedule I of the 1971 Convention on Psychotropic Substances. It is not listed in the schedules to the 1961 Single Convention on Narcotic Drugs or in Tables I and II of the 1988 Convention against Illicit Traffic in Narcotic Drugs and Psychotropic Substances.
By Country
References
Source Pages
Citations
- Z. Böszörményi, P. Dér, & T. Nagy. (1959). Observations on the Psychotogenic Effect of N-N Diethyltryptamine, a New Tryptamine Derivative. Journal of Mental Science, 105(438), 171-181. https://www.cambridge.org/core/journals/journal-of-mental-science/article/observations-on-the-psychotogenic-effect-of-nn-diethyltryptamine-a-new-tryptamine-derivative/50B67E1D3E6BABF8D4957E550B6C85731
- Szara, S., Rockland, L. H., Rosenthal, D., & Handlon, J. H.. (1966). Psychological effects and metabolism of N,N-diethyltryptamine in man. Archives of General Psychiatry, 15(3), 320–329. https://doi.org/10.1001/archpsyc.1966.017301500960141234
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- Shulgin, Alexander, & Shulgin, Ann. (1997). TiHKAL: The Continuation. Transform Press. https://www.erowid.org/library/books_online/tihkal/tihkal03.shtml123
- Blough BE, Landavazo A, Decker AM, Partilla JS, Baumann MH, & Rothman RB. (2014). Interaction of psychoactive tryptamines with biogenic amine transporters and serotonin receptor subtypes. Psychopharmacology (Berl), 231(21), 4135-4144. https://doi.org/10.1007/s00213-014-3557-7123
- Wallach J, Cao AB, Calkins MM, Heim AJ, Lanham JK, Bonniwell EM, Hennessey JJ, Bock HA, Anderson EI, Sherwood AM, Morris H, de Klein R, Klein AK, Cuccurazzu B, Gamrat J, Fannana T, Zauhar R, Halberstadt AL, & McCorvy JD. (2023). Identification of 5-HT2A receptor signaling pathways associated with psychedelic potential. Nature Communications. https://doi.org/10.1038/s41467-023-44016-11
- Klemens Egger, Helena D. Aicher, Paul Cumming, & Milan Scheidegger. (2024). Neurobiological research on N,N-dimethyltryptamine (DMT) and its potentiation by monoamine oxidase (MAO) inhibition: from ayahuasca to synthetic combinations of DMT and MAO inhibitors. https://doi.org/10.1007/s00018-024-05353-612
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- Cunningham, K.A., & Anastasio, N.C.. (2014). The serotonin 5-HT2C receptor and the non-addictive nature of classic hallucinogens. Neuropharmacology. https://doi.org/10.1016/j.neuropharm.2014.04.0161
- Szára, S.. (1957). The comparison of the psychotic effect of tryptamine derivatives with the effects of mescaline and LSD-25 in self-experiments. Psychotropic Drugs, 460–467. https://www.erowid.org/references/refs_view.php?ID=16671
- Böszörményi, Z., Dér, P., & Nagy, T.. (1959). Observations on the Psychotogenic Effect of N-N Diethyltryptamine, a New Tryptamine Derivative. Journal of Mental Science, 105(438), 171–181. https://doi.org/10.1192/bjp.105.438.1711
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