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4-AcO-DET (4-acetoxy-N,N-diethyltryptamine) is a synthetic tryptamine, the acetate ester of 4-HO-DET and the diethyl homolog of psilacetin. It is generally regarded as a prodrug that is hydrolyzed in the body to the active phenol 4-HO-DET, an agonist at the 5-HT2A serotonin receptor; in rodent drug-discrimination testing it and its 4-hydroxy metabolite fully substitute for the classic hallucinogen DOM, consistent with a psilocybin-like mechanism. Structure-activity studies indicate that O-acetylation lowers intrinsic 5-HT2A potency while preserving efficacy, supporting the view that in vivo activity depends on deacetylation. In vitro toxicology has flagged potential cardiac liabilities, including hERG potassium-channel inhibition and QT prolongation, and the compound has been identified in forensic casework. Controlled human pharmacology remains sparsely documented.
- Psilocin-like headspace
- Visual and emotional changes
- Moderate duration
- Prodrug yielding a psilocin-like 5-HT2A psychedelic
- Nausea and stomach upset
- Anxiety or confusion
Mechanism
4-AcO-DET carries an acetyl group at the 4-position that is cleaved in the body to yield 4-HO-DET, the active compound; this parallels how psilocybin converts to psilocin. The active form is an at the receptor, the core of the classic psychedelic state, with additional activity at other serotonin receptors such as and 5-HT2C. The result is altered perception, mood, and cognition driven by serotonergic signaling.
receptor fingerprint
receptoragonist (via active metabolite)
receptoragonist
5-HT2C receptoragonist
Safetyrisks and cautions, not medical advice
As a substituted tryptamine, 4-AcO-DET is expected to be relatively low in physiological toxicity but psychologically intense, and it is poorly studied, so margins are uncertain. It can cause anxiety, nausea, and disorientation, and should be avoided by anyone with a personal or family history of psychosis or bipolar disorder; combining it with MAOIs or other strongly serotonergic drugs risks serotonin toxicity. Not medical advice.
Subjective profileweighing the evidence above
Chemically sensible and probably low in physical toxicity, but poorly studied, with margins inferred from its relatives rather than measured. If a psilocin-like experience is the goal, the better-characterized tryptamines are the sane choice, and anyone with a psychosis or bipolar history should skip it entirely.
Resources
This entry is here for reference.
Research
- 2020first citedDiscriminative Stimulus Effects of Substituted Tryptamines in Rats
- 2023most recentA Fatal Case Report Resulting from the Abuse of the Designer Benzodiazepines Clonazolam and Flu…
- 1.Discriminative Stimulus Effects of Substituted Tryptamines in Rats
- 2.Investigation of the Structure-Activity Relationships of Psilocybin Analogues
- 3.Cardiotoxic effects of [3-[2-(diethylamino)ethyl]-1H-indol-4-yl] acetate and 3-[2-[ethyl(methyl)amino]ethyl]-1H-indol-4-ol.
- 4.A Fatal Case Report Resulting from the Abuse of the Designer Benzodiazepines Clonazolam and Flualprazolam in Conjunction with Dried Opium Poppy Pods.
4 listed here; entry last updated August 2026
Reviews
My notesprivate to this device
FAQ
Is 4-AcO-DET a prodrug?
Largely yes; it is thought to be deacetylated in the body to 4-HO-DET, much like psilocybin converts to psilocin.
How does it feel compared to psilocybin?
Broadly psilocin-like as a diethyl tryptamine, though it is far less studied and experiences vary.
What is the main mechanism?
Its active form agonizes the 5-HT2A serotonin receptor, the core of classic psychedelics.
Limitations of the evidence
- Limited safety data
Adverse effects
- Nausea and stomach upset
- Anxiety or confusion
Notes and cautions
- Pupil dilation