Psychedex is in open beta. We are still fine-tuning the generation and review process. Please double-check sources.
+1 more
Serotonin receptor ligandpsilocybin, psilocin, LSD +4 morepsilocybin, psilocin, LSD, mescaline, 4-AcO-DMT, 4-HO-MET, 4-HO-MiPT show less
4-AcO-DiPT
4-acetoxy-N,N-diisopropyltryptamine
4-AcO-DiPT (4-acetoxy-N,N-diisopropyltryptamine) — Ipracetin, Aces — is a synthetic psychedelic of the tryptamine class. It is a prodrug of 4-OH-DiPT,[1] its pharmacologically active metabolite. It activates serotonin receptors and serotonin transporters,[2][3] producing both psychedelic and empathogenic effects.
4-AcO-DiPT (4-acetoxy-N,N-diisopropyltryptamine) — Ipracetin, Aces — is a synthetic psychedelic of the tryptamine class. It is a prodrug of 4-OH-DiPT,[1] distinguished by its short duration among 4-substituted tryptamines.[2] 4-AcO-DiPT's active metabolite is a near-full 5-HT₂A receptor agonist with additional SERT activity, producing its effects through both receptor activation and monoamine modulation.[3][4]
Psychedex is in open beta. We are still fine-tuning the generation and review process. Please double-check sources.
+1 more
Serotonin receptor ligandpsilocybin, psilocin, LSD +4 morepsilocybin, psilocin, LSD, mescaline, 4-AcO-DMT, 4-HO-MET, 4-HO-MiPT show less
4-OH-DiPT was synthesized in 1977[4] and its human effects documented by Shulgin in 1997.[5] The acetate ester prodrug appeared on grey markets around 2005,[6] circulating as a short-duration psychedelic. It remains unscheduled under U.S. federal law as of April 2026; a related clinical compound, RE104, has completed Phase 2 trials for postpartum depression.[7][8]
Subjective effects include visual distortion, mood elevation, empathogenic warmth, stimulation, and introspective depth. The experience is a compressed hybrid — intense psychedelic and empathogenic qualities packed into a few hours, more stimulating than 4-AcO-DMT and carrying an emotional warmth its close relatives lack.[5] Physical tremors, anxiety, and challenging psychological states are characteristic unwanted effects.
4-AcO-DiPT produces no physical dependence and carries low abuse liability.[9] The main danger is psychological — panic and distress that scale with dose — and combining it with MAOIs can trigger a potentially fatal serotonin overload; frequent use poses an unstudied cardiovascular risk.[2] No human toxicity or pharmacokinetic studies exist; what is known derives from analogy to related tryptamines.
History[edit]
Discovery
4-OH-DiPT, the active form of 4-AcO-DiPT, was first synthesized in 1977 by Repke, Ferguson, and Bates as part of a series of psilocin analogs.[4] No human effects were reported at the time. Twenty years later, Alexander Shulgin documented those effects in TiHKAL — describing rapid onset, brief duration, stimulation, and elation.[5]
Grey-market emergence
The acetate ester prodrug appeared on grey markets around 2005.[6] Chapman (2017) confirmed grey-market samples were correctly identified — none were misrepresented.[10] In 2022 the U.S. DEA proposed scheduling 4-OH-DiPT under Schedule I, then withdrew the proposal in July of that year pending further evaluation.[11]
Modern clinical development
Reunion Neuroscience created RE104 — a different ester prodrug of 4-OH-DiPT — and showed antidepressant-like effects in animal models.[8] RE104 has completed Phase 2 trials for postpartum depression,[7] with additional trials in adjustment disorder[12] and generalized anxiety disorder underway.
The name Ipracetin follows systematic prodrug nomenclature: ipr- from isopropyl, -acet- from acetate. The street name Aces likely derives from the AcO (acetoxy) abbreviation. Within research chemical communities, 4-AcO-DiPT is valued for its compressed timeline relative to psilocybin or LSD, and noted for an empathogenic warmth unusual in its chemical family.
Chemistry[edit]
Structural class
4-AcO-DiPT belongs to the 4-substituted tryptamine family. It is an acetate ester prodrug — the body converts it to the active compound 4-OH-DiPT,[1] which produces all its effects. Its molecular formula is C₁₈H₂₆N₂O₂ (molecular weight 302.4 g/mol).
This prodrug relationship parallels psilocybin, which the body similarly converts to its active form psilocin.
Pharmacology[edit]
Mechanism of action
4-AcO-DiPT is a prodrug. Esterase enzymes in the liver release 4-OH-DiPT, the pharmacologically active compound.[1] All effects come from this conversion.
4-OH-DiPT primarily targets the serotonin receptor responsible for the effects of psilocybin and LSD.[2] Unusually for a classical psychedelic, it also interacts with serotonin and norepinephrine transporters — a profile closer to MDMA than to LSD or mescaline.[3] This transporter activity likely contributes the empathogenic warmth that sets it apart from other tryptamines.
Pharmacokinetics
No human pharmacokinetic studies exist for 4-AcO-DiPT. Shulgin reported 4-OH-DiPT lasting 2–3 hours orally;[5] the slightly longer duration of 4-AcO-DiPT reflects the added time required for prodrug conversion.[8][13] DiPT-class compounds also inhibit a liver enzyme (CYP2D6) in laboratory studies,[14] which could alter the metabolism of many antidepressants and opioids when combined.
Neuroscience[edit]
Where it acts
The most detailed brain data come from mice. In the amygdala — the brain's threat-detection center — 4-OH-DiPT activates cells that quiet fear-signaling neurons.[2] This dampening of fear output may underlie the emotional openness and reduced anxiety the experience produces.
The compound's interactions with serotonin and norepinephrine transporters[3][15] may layer an empathogenic, emotionally open quality on top of the standard psychedelic perceptual changes.
Why it matters
One week after a single dose of the related compound RE104, rats still showed antidepressant-like effects.[8] This points to lasting structural changes in the brain — not just an acute drug response — consistent with evidence that serotonin-agonist psychedelics promote new neural connections.
Does 4-OH-DiPT promote new neural connections via the same pathways as other serotonin-agonist psychedelics? No direct evidence exists. Does its short duration compress the window of brain plasticity compared to longer compounds like psilocybin or LSD? And why did female mice show greater fear-extinction effects than male mice[2]? These remain open questions.
Subjective Effects[edit]
4-AcO-DiPT delivers a hybrid of psychedelic and empathogenic experience compressed into a few hours. Visual changes and introspective depth arrive alongside a warmth and emotional openness that most tryptamines don't produce. The combination of stimulation and empathogenic quality gives it a distinct character — neither pure psychedelic nor pure entactogen, but both simultaneously.
Compared to 4-AcO-DMT, it is more stimulating and carries an empathogenic dimension its dimethyl relative lacks. Relative to 4-HO-MET, it is deeper and more emotionally intense. Among 4-substituted tryptamines, it occupies a unique position at the intersection of a psychedelic and a mild entactogen.
4-OH-DiPT was first synthesized in 1977 by Repke, Ferguson, and Bates as part of a series of psilocin analogs;[5] Shulgin documented its human effects two decades later in TiHKAL.[2] The acetate ester prodrug appeared on grey markets around 2005,[6] and a related prodrug — RE104 — has since completed Phase 2 clinical trials in postpartum depression.[7][8] 4-AcO-DiPT remains unscheduled under U.S. federal law as of April 2026.
Subjective effects include visual alteration, empathy enhancement, stimulation, and introspective states. The experience is a compressed hybrid of psychedelic and empathogenic qualities — rapid onset gives way to high-intensity effects that resolve within hours, producing a character distinct from the gentler arc of 4-AcO-DMT.[2] Physical tremors, anxiety, and challenging psychological experiences are characteristic unsought effects.
4-AcO-DiPT produces no physical dependence, and the tryptamine psychedelic class carries low abuse liability overall.[9] The primary risk is psychological — acute distress scales with dose and predisposition — while 4-OH-DiPT's strong serotonin₂B agonism[3] represents an unstudied cardiovascular concern under frequent use. No clinical trials, controlled toxicity data, or human pharmacokinetic studies have been conducted on 4-AcO-DiPT itself.
History[edit]
Discovery
4-OH-DiPT, the pharmacologically active form of 4-AcO-DiPT, was first synthesized in 1977 by David B. Repke, William J. Ferguson, and David K. Bates as part of a series of psilocin analogs.[5] The original publication reported only the chemical synthesis — no pharmacological or human data were included. Twenty years later, Alexander Shulgin documented 4-OH-DiPT's human effects in TiHKAL (1997), reporting rapid onset, brief duration, and a phenomenology marked by stimulation, elation, and introspection.[2]
Grey-market emergence
4-AcO-DiPT — the acetate ester prodrug — appeared on grey markets as a novel designer drug around 2005.[6] Chapman (2017) confirmed structural identity of grey-market tryptamine samples, including 4-AcO-DiPT, via NMR spectroscopy; none were found to be misrepresented.[10] In January 2022 the U.S. DEA proposed scheduling 4-OH-DiPT under Schedule I, but withdrew the rule in July 2022 pending further evaluation.[11]
Modern clinical development
The 4-OH-DiPT pharmacological class entered clinical development through Reunion Neuroscience, which created RE104 — a glutarate ester prodrug distinct from the acetate ester in 4-AcO-DiPT. RE104 produced antidepressant-like effects in animal models[8] and has completed Phase 2 trials in postpartum depression,[7] with additional trials in adjustment disorder[12] and generalized anxiety disorder underway.
The name Ipracetin follows systematic prodrug nomenclature: ipr- from isopropyl, -acet- from acetate, -in as a tryptamine suffix. The street name Aces likely derives from the AcO (acetoxy) abbreviation. Within research chemical communities, 4-AcO-DiPT occupies a niche reputation as a short-duration psychedelic — valued for its compressed timeline relative to psilocybin or LSD and noted for an empathogenic warmth unusual in the 4-substituted tryptamine series.
Chemistry[edit]
Structural class
4-AcO-DiPT belongs to the 4-substituted tryptamine family — specifically the acetate ester prodrugs of 4-hydroxyindole psychedelics. The indole ring system bears an aminoethyl chain at position 3 and an acetoxy group at position 4. The N,N-diisopropyl substitution differentiates it from 4-AcO-DMT (N,N-dimethyl) and 4-AcO-MET (N-methyl-N-ethyl).
As an acetate ester, 4-AcO-DiPT is hydrolyzed in vivo to yield 4-OH-DiPT — the pharmacologically active metabolite.[1] This prodrug relationship parallels that of psilocybin to psilocin and 4-AcO-DMT to psilocin.
Molecular properties
| Molecular formula | C₁₈H₂₆N₂O₂ |
| Molecular weight | 302.4 g/mol |
The two isopropyl groups on the amine nitrogen create significant steric bulk compared to smaller N-alkyl tryptamines, reducing receptor binding potency relative to dimethyl and diethyl analogs.[13][14]
Stereochemistry
4-AcO-DiPT contains no chirality centers. The sp³ nitrogen bearing two isopropyl groups undergoes rapid pyramidal inversion; the compound exists as a single constitutional isomer without enantiomeric or diastereomeric forms.
Physical properties
No published characterization of the melting point, solubility, or stability parameters exists in peer-reviewed literature. Chapman (2017) confirmed structural identity of grey-market samples via NMR but did not report physical constants.[10] The acetate ester is expected to hydrolyze under acidic or basic aqueous conditions and in the presence of esterases, consistent with its prodrug function.
Pharmacology[edit]
Mechanism of action
4-AcO-DiPT is a prodrug: hepatic esterases cleave the acetate group to release 4-OH-DiPT, the pharmacologically active metabolite.[1] All psychoactive effects stem from this conversion.
4-OH-DiPT's primary target is the 5-HT₂A receptor, where it acts as a near-full agonist — the same receptor responsible for the effects of psilocybin and LSD. It also activates serotonin₂B and 5-HT₂C receptors with comparable potency at both mouse and human receptor forms.[3]
Unusually for a classical psychedelic, 4-OH-DiPT also interacts with the SERT (SERT) and NET (NET) — a transporter profile more similar to MDMA than to LSD or mescaline.[4] The related compound DiPT acts as a SERT substrate rather than a blocker, meaning it may accumulate within serotonergic neurons.[15]
Pharmacokinetics
No human pharmacokinetic studies exist for 4-AcO-DiPT. Oral bioavailability has not been measured, though acetate ester prodrugs of tryptamines are generally assumed to improve oral absorption relative to free hydroxy forms.
In rats, 4-OH-DiPT showed a plasma half-life of approximately 40 minutes after subcutaneous administration of a related prodrug (RE104).[8] Shulgin reported 4-OH-DiPT duration as 2–3 hours oral;[2] the 3–4 hour total duration observed with 4-AcO-DiPT is consistent with additional time required for prodrug conversion.[8][16]
DiPT-class compounds inhibit CYP2D6 in laboratory studies,[17] which is potentially relevant when combined with medications metabolized by this enzyme — including many antidepressants and opioids. Clinical significance has not been confirmed in humans.
Neuroscience[edit]
Where it acts
The most detailed neural data for 4-AcO-DiPT come from studies of its active metabolite in mice. 4-OH-DiPT activates inhibitory interneurons in the basolateral amygdala (BLA) via 5-HT₂A receptors, suppressing the output of fear-signaling neurons.[3] This interneuron-mediated inhibition reduced freezing in fear extinction paradigms, with greater potency in female than male mice — consistent with broader evidence that serotonergic psychedelics dampen amygdala reactivity.
The additional SERT and NET interactions[4][15] may contribute entactogenic-type neural effects — enhanced emotional openness and reduced threat sensitivity — layered on top of classical psychedelic perceptual changes.
Why it matters
The amygdala data fit the REBUS (Relaxed Beliefs Under Psychedelics) model: by inhibiting fear-circuit output, 4-OH-DiPT may loosen the brain's weighting of threat-related expectations, facilitating the extinction of maladaptive fear responses. The antidepressant-like effects of RE104 persisting one week after administration in rats[8] are consistent with lasting structural brain changes (neuroplasticity) rather than acute drug action alone.
Does 4-OH-DiPT promote the growth of new neural connections via the same signaling pathways demonstrated for other 5-HT₂A agonists? No direct neuroplasticity data exist. What role does the unusual SERT substrate activity play in shaping the experience — and does it produce brain-network signatures distinct from classical psychedelics?
Subjective Effects[edit]
4-AcO-DiPT produces a hybrid of psychedelic and empathogenic qualities. 5-HT₂A agonism drives classical perceptual shifts — geometric visuals, altered thought flow, introspective depth — while SERT activity contributes an empathogenic warmth and stimulant energy unusual for a 4-substituted tryptamine. At lower doses the experience tilts toward sociable warmth and mild visual enhancement; at higher doses, deep introspection and intense perceptual alteration dominate. Set and setting strongly modulate both character and intensity.
Compared to 4-AcO-DMT, 4-AcO-DiPT is more stimulating and carries a distinct empathogenic dimension that its dimethyl cousin lacks. Relative to 4-HO-MET, it is deeper, more emotionally intense, and less recreationally light.
Effect Grid
At common doses (15–30 mg oral), the full psychedelic experience manifests: pronounced color alteration and saturation, visual drifting and morphing of surfaces, tracers behind moving objects, and emerging geometric patterns. Cognitive effects include novelty enhancement, immersion enhancement, and increased introspective depth. Empathy enhancement and emotional openness become prominent — consistent with the DiPT class's SERT substrate activity contributing entactogenic qualities alongside classical psychedelia.
Physically, stimulation is moderate to strong, accompanied by bodily lightness, spontaneous body sensations, and muscle tension. Nausea is possible during onset but typically transient. Pupil dilation is pronounced. Temperature dysregulation and occasional abnormal heartbeat sensation may occur.
The experience peaks within 1–2 hours of onset and resolves within 3–4 hours total. Functional impairment is significant during the peak; plan for the full duration plus aftereffects.
Modeled from the effect's dose-dependence curve — not per-substance measurements.
Visual breathing · Color alteration · Tracers · Auditory enhancement · Brightness alteration · Auditory distortion · Depth perception distortion · Environmental patterning · Light sensitivity · Perspective distortion · Sound sensitivity · Spatial disorientation · Visual morphing · Visual acuity enhancement · After-images · Dreaming enhancement · Peripheral vision distortion · Proprioceptive distortion · Sleep-transition hallucinations · Symmetrical texture repetition · Synesthesia · Vestibular distortion · Visual diffraction · Visual haze / noise · Visual melting · Auditory misinterpretation · Peripheral misidentification · Visual magnification · Olfactory enhancement · Taste enhancement · Visual processing acceleration · Tinnitus · Flashbacks · Internal hallucinations · Object transformations · Object activation · Visual recursion · External hallucinations · Perspective hallucinations · Auditory hallucinations · Visual flipping · Visual scenery slicing · Persisting hallucinations
Brightness alteration · Auditory distortion · Depth perception distortion · Environmental patterning · Light sensitivity · Perspective distortion · Sound sensitivity · Spatial disorientation · Visual morphing · Visual acuity enhancement · After-images · Dreaming enhancement · Peripheral vision distortion · Proprioceptive distortion · Sleep-transition hallucinations · Symmetrical texture repetition · Synesthesia · Vestibular distortion · Visual diffraction · Visual haze / noise · Visual melting · Auditory misinterpretation · Peripheral misidentification · Visual magnification · Olfactory enhancement · Taste enhancement · Visual processing acceleration · Tinnitus · Flashbacks · Internal hallucinations · Object transformations · Object activation · Visual recursion · External hallucinations · Perspective hallucinations · Auditory hallucinations · Visual flipping · Visual scenery slicing · Persisting hallucinations
Stimulation · Sexual arousal enhancement · Tactile euphoria · Tingling / electric sensations · Bodily lightness · Body schema distortion · Nausea · Laughter fits · Appetite suppression · Insomnia · Physical fatigue · Vibrations / buzzing · Muscle relaxation · Muscle tension · Restlessness · Bodily pressures · Dizziness · Dry mouth · Heart rate perception changes · Sedation · Wakefulness · Yawning · Watery eyes · Bodily heaviness · Excessive sweating · Kundalini-like energy · Pain suppression · Vasoconstriction · Abnormal heartbeat · Bruxism · Diarrhea · Headache · Involuntary body movements · Trembling · Vomiting · Seizure threshold reduction · Bodily dissociation · Tactile hallucination
Tingling / electric sensations · Bodily lightness · Body schema distortion · Nausea · Laughter fits · Appetite suppression · Insomnia · Physical fatigue · Vibrations / buzzing · Muscle relaxation · Muscle tension · Restlessness · Bodily pressures · Dizziness · Dry mouth · Heart rate perception changes · Sedation · Wakefulness · Yawning · Watery eyes · Bodily heaviness · Excessive sweating · Kundalini-like energy · Pain suppression · Abnormal heartbeat · Bruxism · Diarrhea · Headache · Involuntary body movements · Trembling · Vomiting · Seizure threshold reduction · Bodily dissociation · Tactile hallucination
Cognitive euphoria · Introspection enhancement · Openness enhancement · Cognitive flexibility · Conceptual thinking · Pattern recognition enhancement · Thought connectivity · Humor enhancement · Multiple thought streams · Cognitive impairment · Creativity enhancement · Increased nature relatedness · Synchronicity · Thought acceleration · Analysis enhancement · Information processing enhancement · Compulsive redosing urge · Analysis suppression · Cognitive fatigue · Confusion · Focus suppression · Information processing suppression · Memory fragmentation · Memory replays · Memory suppression · Thought disorganization · Thought loops · Focus enhancement · Language enhancement · Motivation enhancement · Motivation suppression · Cognitive dysphoria · Language suppression · Thought deceleration · Thought organization · Amnesia · Delusions
Cognitive flexibility · Conceptual thinking · Pattern recognition enhancement · Thought connectivity · Humor enhancement · Multiple thought streams · Cognitive impairment · Creativity enhancement · Increased nature relatedness · Synchronicity · Thought acceleration · Analysis enhancement · Information processing enhancement · Analysis suppression · Cognitive fatigue · Confusion · Focus suppression · Information processing suppression · Memory fragmentation · Memory replays · Memory suppression · Thought disorganization · Thought loops · Focus enhancement · Language enhancement · Motivation enhancement · Motivation suppression · Cognitive dysphoria · Language suppression · Thought deceleration · Thought organization · Amnesia · Delusions
Anxiety suppression · Emotional lability · Simultaneous emotions · Anxiety · Catharsis · Dysphoria · Irritability · Mania
Anxiety · Catharsis · Dysphoria · Irritability
Emotional susceptibility · Sociability enhancement · Trust enhancement · Communication enhancement · Automaticity · Depersonalization · Flow state · Compulsive behavior reduction · Craving · Ego inflation · Social disconnection · Boundary dissolution · Cognitive disconnection · Ego dissolution · Identity alteration · Telepathic feelings
Automaticity · Depersonalization · Flow state · Compulsive behavior reduction · Craving · Ego inflation · Social disconnection · Boundary dissolution · Cognitive disconnection · Ego dissolution · Identity alteration · Telepathic feelings
Time cessation
Death-rebirth sequence · Entity contact · Non-dual awareness · Transpersonal memory access · Cessation · Near-death experience · Voidness
Cessation · Near-death experience · Voidness
Cognitive dissonance · Recursive awareness
Timeline
First alerts appear as subtle mood shift, mild sensory brightening, and a faint body awareness. Onset is notably rapid for a 4-substituted tryptamine — Shulgin reported 15–20 minutes for 4-OH-DiPT; the prodrug adds slight delay.
Effects build quickly with emerging color enhancement, body stimulation, and increasing emotional openness. Nausea, if present, typically manifests during this phase and resolves before peak. The rapid escalation can feel abrupt compared to psilocybin.
Maximum intensity across perceptual, cognitive, and emotional domains. Visual effects, empathy enhancement, and introspective depth reach their zenith. Physical stimulation and muscle tension are most pronounced.
Effects recede relatively quickly. Perceptual distortions diminish, cognitive clarity returns, and physical stimulation fades. Mood remains elevated.
Residual mood elevation, mild sensory enhancement, and reflective states may persist for several hours. Physical baseline is largely restored. Fatigue or mild headache is occasionally reported.
Safety[edit]
- Acute toxicity
- Low
- Chronic toxicity
- Moderate
- Withdrawal
- None
- Tolerance buildup
- rapid
- Tolerance reset
- 7 days
- Physical
- None
- Psychological
- Low
- Compulsive redosing
- Low
- Dose escalation
- Low
- Cross-tol.
- psilo · psilocin · LSD
Toxicity
No lethal dose data exist for 4-AcO-DiPT or 4-OH-DiPT in any species. No case reports of overdose or fatality have been identified.[16] The toxic dose is unknown.
Heart and circulation
4-OH-DiPT strongly activates a serotonin receptor — 5-HT₂B — that other drugs have been shown to damage heart valves through.[2] No cardiac safety data exist for 4-AcO-DiPT. This is an unstudied risk that may be particularly relevant with frequent use. safety citation needed
Distinction from 5-MeO-DiPT
5-MeO-DiPT — a different compound with a similar name — damages nerve cells in rats through potent serotonin-releasing activity.[17] 4-AcO-DiPT has a different mechanism: weaker transporter interaction[3] and primary action through receptor activation rather than serotonin release. Those neurotoxicity findings do not automatically apply here.
Psychological risks
Panic, paranoia, and challenging experiences occur with all serotonin-agonist psychedelics and scale with dose, predisposition, and setting. Persistent visual disturbances after the experience have been documented for the psychedelic class,[18][19] though no substance-specific data exist for 4-AcO-DiPT. Those with personal or family history of psychotic disorders face elevated risk.
Tolerance and dependence
Tolerance develops through downregulation of serotonin receptors.[20] Unusually, the backbone compound DiPT does not develop tolerance to psychedelic-like responses with daily dosing in mice,[21] suggesting tolerance in this series may build more slowly than commonly assumed.
Cross-tolerance with psilocybin, LSD, and mescaline is expected from shared receptor mechanisms.[20][21] The tryptamine class carries low abuse liability overall.[9]
Drug Interactions
Serotonin syndrome risk
Combining 4-AcO-DiPT with MAOIs dramatically amplifies serotonin levels,[15][3] risking a potentially fatal response involving high body temperature, muscle rigidity, and cardiovascular crisis. safety citation needed
Tramadol raises the same risk through its own serotonergic action.[22] safety citation needed SSRIs and SNRIs add serotonergic load; chronic SSRI use typically blunts psychedelic effects, but the transporter interaction in the DiPT class adds complexity.[15]
CYP2D6 interactions
DiPT-class compounds inhibit a liver enzyme (CYP2D6) in laboratory studies.[14] This may alter the metabolism of codeine, tramadol, many antidepressants, and several antipsychotics when combined.
Lithium
Lithium combined with serotonergic psychedelics carries seizure risk at the class level. No substance-specific data exist for 4-AcO-DiPT. safety citation needed
Contraindications
8 knownAbsolute contraindications (inferred from class pharmacology):
- Psychotic disorders or family history of psychosis — serotonin-agonist psychedelics may trigger or worsen psychotic episodes.
- Concurrent MAOI use — critical serotonin overload risk given transporter properties of the DiPT class.[15]
- Concurrent lithium use — class-level seizure risk. safety citation needed
Relative contraindications:
- Bipolar disorder — risk of manic episode.
- Heart conditions — the active metabolite's serotonin receptor action[2] represents an unstudied risk for those with pre-existing valve disease.
- Pregnancy and breastfeeding — no reproductive safety data exist.
Harm Reduction[edit]
Forms & Identification
4-AcO-DiPT circulates primarily as a powder or pressed pellet from grey-market research chemical vendors. No pharmaceutical-grade product exists. Purity varies between batches and sources.
Reagent testing confirms the tryptamine class but cannot distinguish 4-AcO-DiPT from closely related 4-substituted tryptamines. The dose range is narrow enough that estimating by volume introduces meaningful overdose risk — milligram-precision weighing is essential.
Guidelines
- Test every batch with a reagent kit before use.
- Weigh doses on a milligram-precision scale — never estimate from volume or appearance.
- Start at the low end of the common range if unfamiliar with the batch or the substance.
- Eat lightly 2–3 hours before dosing to reduce nausea without an empty stomach.
- Prepare the environment in advance: comfortable space, trusted company, no obligations for the following hours.
- Have a sober sitter present, especially at higher doses.
- Keep water accessible and stay hydrated throughout.
- Avoid redosing during the experience — the short duration can tempt early redosing before the first dose has fully resolved, risking unexpectedly intense effects.
Set & Setting
The rapid onset leaves little gradual come-up to ease into the experience. A calm, familiar environment with trusted company and no time pressure provides the strongest foundation. Physical comfort and stable mood both matter.
A sober sitter is advisable, particularly at higher doses or for those unfamiliar with the substance.
Aftercare & integration. The compressed timeline means aftereffects often arrive the same day as the experience. Allow several hours of unstructured time after resolution — emotional and cognitive residue can be significant even after acute effects pass. Journaling within 24 hours helps capture insights before they fade.
If the experience was challenging, process it with a trusted person or an integration-focused therapist. Persistent distress, mood changes, or visual disturbances lasting beyond a few days warrant professional consultation.
Recovery & Support
Compulsive use of tryptamine psychedelics is rare. If use is becoming a coping mechanism or increasing in frequency, peer support communities and harm-reduction organizations offer confidential guidance. Professional therapists with psychedelic experience can help address underlying patterns without judgment.
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Recognizing an emergency: uncomfortable anxiety and body load are common and usually self-limiting. Seek immediate help for: self-harm attempts or expressed intent, complete disconnection from reality with inability to communicate, seizures, chest pain, or sustained high body temperature.
Immediate steps:
- Move the person to a quiet, safe space away from stimulation.
- Speak calmly and reassure them that the effects are temporary and will pass within hours.
- If they are unresponsive or seizing, place them in the recovery position and call emergency services immediately.
- Do not restrain them unless they pose immediate danger to themselves or others.
- Do not induce vomiting.
What to tell the dispatcher: name the substance (4-AcO-DiPT, a tryptamine psychedelic), the estimated dose and time taken, and current symptoms. Good Samaritan laws in many jurisdictions protect people who call for help during a drug emergency.
Legal Status[edit]
4-AcO-DiPT occupies an ambiguous legal position in most jurisdictions — not specifically scheduled in many countries, but potentially covered by structural analog legislation or prodrug provisions. Legal status varies significantly and is subject to change.
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| United States | Unscheduled (federal) | DEA proposed Schedule I for 4-OH-DiPT in January 2022 (87 FR 2376); rule withdrawn July 27, 2022.[11] Federal Analogue Act (21 U.S.C. § 813) may apply if intended for human consumption. |
| United Kingdom | Class A | Controlled as an ester of 4-HO-DiPT under the Misuse of Drugs Act 1971.[13] citation needed |
| Germany | Controlled | Covered under Neue-psychoaktive-Stoffe-Gesetz (NpSG), effective July 18, 2019.[13] |
| Sweden | Controlled (illegal) | Classified under the Narcotics Act.[13] |
| Japan | Controlled | Designated as a controlled substance.[23][13] |
| Canada | Likely unscheduled | No confirmed scheduling found; similar 4-AcO compounds are not specifically listed. citation needed |
| Australia | Unclear | Possible Schedule 9 by psilocin analog argument; not confirmed. citation needed |
Analog and prodrug considerations
In jurisdictions with analog laws — notably the U.S. Federal Analogue Act — 4-AcO-DiPT's structural similarity to controlled tryptamines and its prodrug relationship to 4-OH-DiPT may make it legally equivalent to a Schedule I substance when intended for human consumption. The withdrawn 2022 DEA proposal to schedule 4-OH-DiPT, and its subsequent withdrawal pending further evaluation, leaves both compounds in regulatory limbo as of April 2026.[11]
Legal status changes frequently and varies by jurisdiction. This information is not legal advice.
Safety[edit]
- Acute toxicity
- Low
- Chronic toxicity
- Moderate
- Withdrawal
- None
- Tolerance buildup
- rapid
- Tolerance reset
- 7 days
- Physical
- None
- Psychological
- Low
- Compulsive redosing
- Low
- Dose escalation
- Low
- Cross-tol.
- psilo · psilocin · LSD
Toxicity
No lethal dose data have been published for 4-AcO-DiPT or 4-OH-DiPT in any species. No case reports of adverse events, overdose, or fatalities specifically involving 4-AcO-DiPT have been identified.[18] The toxic dose is unknown.
Heart and circulation
4-OH-DiPT strongly activates serotonin₂B receptors.[3] Chronic activation of this receptor by other drugs (fenfluramine, methysergide) has caused heart valve damage in humans. No cardiac safety data exist for 4-AcO-DiPT, making this an unstudied risk — particularly with patterns of frequent use. safety citation needed
Distinction from 5-MeO-DiPT
5-MeO-DiPT, a structurally related but pharmacologically distinct compound, causes nerve cell damage in rats at moderate doses through potent serotonin-releasing activity.[19] 4-AcO-DiPT has a different profile: weaker SERT interaction[4] and primary action through 5-HT₂A agonism rather than serotonin release. The neurotoxicity findings for 5-MeO-DiPT should not be assumed to apply to 4-AcO-DiPT without further study.
Psychological risks
No controlled studies have assessed psychological risks specific to 4-AcO-DiPT. Risks are inferred from the serotonergic psychedelic class:
- Acute psychological distress — anxiety, panic, paranoia, and challenging experiences occur with all 5-HT₂A agonist psychedelics and scale with dose, predisposition, and setting.
- Hallucinogen persisting perception disorder (HPPD) — persistent visual disturbances following psychedelic use have been documented for the broader class.[20][21] No substance-specific data exist for 4-AcO-DiPT.
- Psychosis precipitation — individuals with personal or family history of psychotic disorders face elevated risk from 5-HT₂A agonist psychedelics.
Tolerance and dependence
Tolerance develops through downregulation of the 5-HT₂A receptor.[22] Notably, DiPT — the backbone compound of 4-AcO-DiPT — does not develop tolerance to psychedelic-like responses with daily dosing in mice, unlike phenethylamine hallucinogens.[23] This suggests tolerance development in the DiPT series may be less robust than commonly assumed.
Cross-tolerance with other serotonergic psychedelics (psilocybin, LSD, mescaline) is expected based on shared 5-HT₂A receptor downregulation.[22][23] The tryptamine psychedelic class is considered to carry low abuse liability.[9]
Drug Interactions
Serotonin syndrome risk
Combination with monoamine oxidase inhibitors (MAOIs) carries critical risk. Given DiPT's documented serotonin transporter substrate activity,[15][4] co-administration with MAOIs could dramatically increase serotonin levels and trigger serotonin syndrome — a potentially fatal condition involving high body temperature, muscle rigidity, and cardiovascular instability. safety citation needed
Tramadol elevates serotonin syndrome risk through its own serotonergic activity.[24] No published study has directly tested this combination with 4-AcO-DiPT; the severity rating is class-based. safety citation needed
SSRIs and SNRIs increase serotonergic load when combined with 5-HT₂A agonist tryptamines. Chronic SSRI use typically blunts psychedelic effects, but the SERT substrate properties of the DiPT class add complexity: SSRIs block the transporter through which DiPT-class compounds enter neurons.[15]
CYP2D6 interactions
DiPT-class compounds inhibit the CYP2D6 liver enzyme in laboratory studies.[17] Combination with drugs metabolized by CYP2D6 — including codeine, tramadol, many antidepressants, and several antipsychotics — may alter metabolism of both drugs.
Contraindications
8 knownAbsolute contraindications (inferred from class pharmacology):
- Psychotic disorders or family history of psychosis — 5-HT₂A agonist psychedelics may trigger or worsen psychotic episodes.
- Concurrent MAOI use — critical serotonin syndrome risk given SERT substrate properties of the DiPT class.[15]
- Concurrent lithium use — class-level seizure risk. safety citation needed
Relative contraindications:
- Bipolar disorder — risk of manic episode.
- Heart conditions — 4-OH-DiPT's 5-HT₂B agonism[3] represents an unstudied risk for individuals with pre-existing valve disease.
- Pregnancy and breastfeeding — no reproductive safety data exist.
Harm Reduction[edit]
Forms & Identification
4-AcO-DiPT circulates primarily as a powder or pressed pellet from grey-market research chemical vendors. Because no pharmaceutical-grade product exists, purity varies between batches and sources. Reagent testing confirms the tryptamine class but cannot distinguish 4-AcO-DiPT from closely related 4-substituted tryptamines — a limitation worth understanding when interpreting results. The common dose range is narrow enough that estimating by eye introduces meaningful overdose risk; milligram-precision weighing is essential.
Guidelines
- Test every batch with a reagent kit before use.
- Weigh doses on a milligram-precision scale — never estimate from volume or appearance.
- Start at the low end of the common range if unfamiliar with the batch or the substance.
- Eat lightly 2–3 hours before dosing to reduce nausea without an empty stomach.
- Prepare the environment in advance: comfortable space, trusted company, no obligations for the following hours.
- Have a sober sitter present, especially at higher doses.
- Keep water accessible and stay hydrated throughout.
- Avoid redosing during the experience — the short duration can tempt early redosing before the first dose has fully resolved, risking unexpectedly intense effects.
Set & Setting
4-AcO-DiPT's rapid onset and compressed timeline make preparation especially important — there is little gradual come-up to ease into the experience. A calm, familiar environment with trusted company and no time pressure provides the strongest foundation. Physical comfort (temperature, lighting, access to water) and psychological readiness (stable mood, no unresolved acute distress) both matter. A sober sitter is advisable, particularly at higher doses or for those unfamiliar with the substance.
Aftercare & integration. The compressed timeline of 4-AcO-DiPT means aftereffects often arrive the same day as the experience itself. Allow several hours of unstructured time after resolution — the emotional and cognitive residue can be significant even after acute effects have passed. Journaling within 24 hours helps capture insights before they fade.
If the experience was challenging, talk it through with a trusted person or an integration-focused therapist. Intense emotional material, particularly from introspective or empathogenic states, benefits from conscious processing rather than suppression. Persistent distress, mood changes, or visual disturbances lasting beyond a few days warrant professional consultation.
Recovery & Support
Compulsive use of tryptamine psychedelics is rare, but patterns of frequent use — particularly as emotional self-medication — can develop. If 4-AcO-DiPT use is becoming a coping mechanism or increasing in frequency, peer support communities and harm-reduction organizations offer confidential guidance. Professional therapists with psychedelic experience can help address underlying patterns without judgment.
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Recognizing an emergency: uncomfortable anxiety and body load are common and usually self-limiting. Seek immediate help for: self-harm attempts or expressed intent, complete disconnection from reality with inability to communicate, seizures, chest pain, or sustained high body temperature.
Immediate steps:
- Move the person to a quiet, safe space away from stimulation.
- Speak calmly and reassure them that the effects are temporary and will pass within hours.
- If they are unresponsive or seizing, place them in the recovery position and call emergency services immediately.
- Do not restrain them unless they pose immediate danger to themselves or others.
- Do not induce vomiting.
What to tell the dispatcher: name the substance (4-AcO-DiPT, a tryptamine psychedelic), the estimated dose and time taken, and current symptoms. Good Samaritan laws in many jurisdictions protect people who call for help during a drug emergency.
Legal Status[edit]
4-AcO-DiPT occupies an ambiguous legal position in most jurisdictions. It is not specifically scheduled under many national drug control frameworks, but its status as an ester of 4-OH-DiPT — or as a structural analog of controlled tryptamines — may bring it within scope of analog or blanket ban legislation. Legal status varies significantly by jurisdiction and is subject to change.
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| United States | Unscheduled (federal) | DEA proposed Schedule I for 4-OH-DiPT in January 2022 (87 FR 2376); rule withdrawn July 27, 2022.[11] Federal Analogue Act (21 U.S.C. § 813) may apply if intended for human consumption. |
| United Kingdom | Class A | Controlled as an ester of 4-HO-DiPT under the Misuse of Drugs Act 1971.[16] citation needed |
| Germany | Controlled | Covered under Neue-psychoaktive-Stoffe-Gesetz (NpSG), effective July 18, 2019.[16] |
| Sweden | Controlled (illegal) | Classified under the Narcotics Act.[16] |
| Japan | Controlled | Designated as a controlled substance.[25][16] |
| Canada | Likely unscheduled | No confirmed scheduling found; similar 4-AcO compounds are not specifically listed. citation needed |
| Australia | Unclear | Possible Schedule 9 by psilocin analog argument; not confirmed. citation needed |
Analog and prodrug considerations
In jurisdictions with analog legislation — notably the U.S. Federal Analogue Act (21 U.S.C. § 813) — 4-AcO-DiPT's structural similarity to scheduled tryptamines and its prodrug relationship to 4-OH-DiPT may render it legally equivalent to a Schedule I substance when intended for human consumption. The withdrawn 2022 DEA proposal to schedule 4-OH-DiPT directly, and its subsequent withdrawal pending further evaluation, leaves both compounds in regulatory limbo as of April 2026.[11]
Frequently asked questions
What is 4-AcO-DiPT?
4-AcO-DiPT is a synthetic substituted tryptamine psychedelic and acetate ester prodrug of 4-OH-DiPT. It appeared on grey markets around 2005; its active metabolite is under clinical investigation as RE104 for postpartum depression.
How long does 4-AcO-DiPT last?
Total duration by route of administration — Oral: 3 – 4 hours. Ranges vary with dose and individual factors; see the duration table for onset, peak, and after-effect phases.
Where can I find dosage information for 4-AcO-DiPT?
Psychedex publishes a dosage table for 4-AcO-DiPT on this page covering these routes of administration: oral. Dose values are presented only in that table, always alongside their route of administration.
What are dangerous combinations with 4-AcO-DiPT?
The highest-severity documented interactions for 4-AcO-DiPT: MAOIs (Lethal), Dopamine agonists (Dangerous), GHB, Baclofen (Dangerous), GHB, GBL (Dangerous), Ibogaine (Dangerous). See the interactions section for the full list with mechanisms and severity levels.
Is 4-AcO-DiPT addictive?
Psychedex records tolerance and dependence data rather than a yes/no rating. Recorded tolerance indicators for 4-AcO-DiPT: tolerance builds rapid; full reset takes 7 days; cross-tolerance develops with psilocybin, psilocin, LSD, mescaline, 4-AcO-DMT, 4-HO-MET, 4-HO-MiPT. See the article's dependence and safety sections for recorded dependence data.
experience reports
No experience reports yet. Be the first to contribute.
First-person accounts of subjective effects, timing, and outcomes — submitted for harm reduction.
references
- [1] ^abcMalaca S, Huestis MA, Lattanzio L, Marsella LT, Tagliabracci A, Carlier J, Busardo FP (2022) Human Hepatocyte 4-Acetoxy-N,N-Diisopropyltryptamine Metabolite Profiling by LC-HRMS/MS — Metabolites doi:10.3390/metabo12080705
- [2]
- [3]
- [4] ^abRepke D, Ferguson W, Bates D (1977) Psilocin analogs. 1. Synthesis of 3-[2-(dialkylamino)ethyl]-and 3-[2-(cycloalkylamino)ethyl] indol-4-ols — Journal of Heterocyclic Chemistry doi:10.1002/jhet.5570140113
- [5]
- [6]
references
- [1] ^abcMalaca S, Huestis MA, Lattanzio L, Marsella LT, Tagliabracci A, Carlier J, Busardo FP (2022) Human Hepatocyte 4-Acetoxy-N,N-Diisopropyltryptamine Metabolite Profiling by LC-HRMS/MS — Metabolites doi:10.3390/metabo12080705
- [2]
- [3]
- [4]
- [5] ^abRepke D, Ferguson W, Bates D (1977) Psilocin analogs. 1. Synthesis of 3-[2-(dialkylamino)ethyl]-and 3-[2-(cycloalkylamino)ethyl] indol-4-ols — Journal of Heterocyclic Chemistry doi:10.1002/jhet.5570140113
- [6]