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Serotonin receptor ligandpsilocybin, psilocin, lsd +4 morepsilocybin, psilocin, lsd, dmt, mescaline, 4-aco-dmt, 4-ho-met show less
4-HO-DiPT
4-hydroxy-N,N-diisopropyltryptamine
4-HO-DiPT (4-hydroxy-N,N-diisopropyltryptamine) is a synthetic psychedelic of the tryptamine class. It is a close structural analog of psilocin, the primary psychoactive molecule in psilocybin mushrooms. It activates serotonin receptors in the brain and also slows serotonin reuptake,[1] producing the visual and cognitive shifts characteristic of classical psychedelics.[2]
4-HO-DiPT (4-hydroxy-N,N-diisopropyltryptamine) is a synthetic psychedelic of the tryptamine class. It is a close structural analog of psilocin, distinguished by its exceptionally short duration of action. 4-HO-DiPT is a 5-HT₂A receptor agonist that also inhibits serotonin reuptake,[1] producing its effects by disrupting serotonergic filtering of sensory and cognitive input.[2]
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First synthesized in 1977 as part of a systematic study of psilocin analogs,[3] 4-HO-DiPT was documented for human use by Alexander Shulgin in TiHKAL in 1997.[4] A pharmaceutical company later developed it into the prodrug luvesilocin (RE104),[5] which received FDA Breakthrough Therapy Designation for postpartum depression in February 2026.[6] It remains unscheduled at the US federal level, though several countries control it under broad psychoactive substance laws.
Subjective effects include color enhancement, mild visual distortion, introspective thought, time compression, and heightened body awareness. The experience is defined by its brevity — a full psychedelic state that arrives fast and ends well before a psilocybin trip would peak, with lighter visuals and closer in character to smoked DMT than to oral mushrooms. Leg tremors, muscle tension, nausea, and elevated heart rate are characteristic unwanted effects.[7]
4-HO-DiPT does not produce physical dependence, and no lethal dose has been established.safety citation needed The primary danger is the steep dose-response curve — a modest increase in dose can shift the experience from mild to overwhelming, making precise measurement critical;[4] combining it with MAOIs or tramadol risks dangerous overloading of the serotonin system. What is known comes from preclinical studies, one prodrug clinical trial, and user reports — controlled human toxicity data for the free compound do not exist.safety citation needed
History[edit]
Discovery
4-HO-DiPT was first synthesized in 1977 by David Repke and colleagues as part of a systematic study of psilocin analogs.[3] No human testing followed the original publication. Alexander Shulgin documented the compound's human effects twenty years later as entry #17 in TiHKAL (1997), describing it as unmatched among oral psychedelics for speed and brevity.[4]
Clinical development
Reunion Neuroscience developed luvesilocin (RE104), a subcutaneous prodrug form of 4-HO-DiPT designed for controlled clinical use.[5] A Phase 2 trial in 84 patients with postpartum depression met its primary endpoint.[8] The FDA granted Breakthrough Therapy Designation in February 2026.[6]
Regulatory history
The DEA proposed placing 4-HO-DiPT in Schedule I in January 2022, then withdrew the proposal in July 2022 pending further scientific review from the Department of Health and Human Services.[9] The compound remains unscheduled federally but may be prosecuted as a structural analog of Psilocin under the Federal Analogue Act.
The name iprocin — a contraction of "isopropyl" and "psilocin" — follows the Shulgin-era naming convention for tryptamine analogs. 4-HO-DiPT first appeared on European research chemical markets around 2005,[10] earning a niche reputation for its unusually short duration, though it never achieved the recognition of psilocybin or LSD.
Chemistry[edit]
4-HO-DiPT belongs to the tryptamine family — the same chemical class as psilocin, DMT, and serotonin itself. It is a direct structural analog of psilocin, with the nitrogen-methyl groups replaced by bulkier isopropyl groups — a change that shifts receptor binding while preserving psychedelic activity.[11]
Its molecular formula is C₁₆H₂₄N₂O. It is also the active compound released when the pharmaceutical prodrug luvesilocin (RE104) is metabolized in the body.[5]
Pharmacology[edit]
Mechanism of action
4-HO-DiPT produces psychedelic effects primarily by activating serotonin receptors. Blocking this activation eliminates psychedelic-like behavior in animals.[11][2] It also slows the brain's serotonin reuptake process,[1] placing its pharmacological profile closer to psilocin than to LSD or mescaline.
Pharmacokinetics
No human pharmacokinetic study has been published for oral 4-HO-DiPT. In rats given the prodrug RE104, the compound had a plasma half-life of roughly 40 minutes, with blood concentration tracking directly with behavioral intensity.[5] This short half-life is consistent with the brief total duration reported in human accounts.[4]
Metabolism
Most metabolic data come from studies of 4-AcO-DiPT, which rapidly converts to 4-HO-DiPT in the body.[12] The primary breakdown enzyme is CYP2D6.[13][14] People who metabolize drugs slowly through this enzyme may experience stronger or more prolonged effects.[15]
Neuroscience[edit]
Where it acts
4-HO-DiPT activates serotonin receptors[2] and is expected to trigger activity in frontal brain regions — disrupting the normal filtering of sensory information and producing the characteristic expansion of awareness.inferred Preclinical work also shows it activates inhibitory neurons in the amygdala — the brain's fear-processing center — dampening conditioned fear responses.[2]
Why it matters
Despite its brief duration, 4-HO-DiPT produced antidepressant-like effects in animals that lasted a week after a single dose.[5] The RECONNECT clinical trial showed sustained improvement at four weeks from a single short session.[6] This supports the idea that psychedelics trigger structural brain changes — new connections, new growth — that outlast the drug itself.[16]
Key unknowns include whether 4-HO-DiPT promotes neuroplasticity through pathways independent of serotonin receptors (as psilocin does via the TrkB/BDNF pathway[16]), whether its short duration limits or preserves therapeutic benefit compared to longer-acting psychedelics, and how genetic variation in CYP2D6 metabolism affects both the experience and the therapeutic response.
Subjective Effects[edit]
The 4-HO-DiPT experience is defined by compression. A full psychedelic state arrives quickly and recedes within a couple of hours — intense, direct, and physically grounded. Characteristic leg tremors and a heightened sense of the body run throughout, anchoring an otherwise perceptual experience.
Compared to psilocybin, the experience is faster, shorter, and visually lighter, with a more prominent body load. Relative to smoked DMT, it is more navigable — similar in intensity but gentler in entry and long enough to orient.
First synthesized in 1977 as part of a systematic study of psilocin analogs,[3] 4-HO-DiPT was characterized for human use by Alexander Shulgin in TiHKAL (1997).[4] The compound entered clinical development as the prodrug luvesilocin (RE104),[5] which received FDA Breakthrough Therapy Designation for postpartum depression in February 2026.[6] It remains unscheduled at the US federal level, though it is controlled in several other jurisdictions.
Subjective effects include color enhancement, mild visual distortion, introspective thought, and time compression. The experience is defined by its brevity and speed — a full-intensity psychedelic state compressed into a timeframe closer to smoked DMT than oral psilocybin, with a lighter visual signature and more pronounced body awareness. Leg tremors, muscle tension, nausea, and elevated heart rate are characteristic unsought effects.[7]
4-HO-DiPT produces no physical dependence and has no established lethal dose — rapid tolerance after a single use makes compulsive redosing self-limiting.inferred The primary risk is the steep dose-response curve: a small increase in dose produces a disproportionate jump in intensity, making precise measurement critical.[4] No controlled human toxicity data exist for the free compound, and the current understanding rests on limited preclinical studies, one Phase 2 trial of a prodrug formulation, and user reports.safety citation needed
History[edit]
Discovery
4-HO-DiPT was first synthesized in 1977 by David Repke, William Ferguson, and David Bates at the University of Kansas as part of a systematic investigation of psilocin analogs.[3] No human pharmacological evaluation accompanied the original publication. Twenty years later, Alexander Shulgin documented the compound's synthesis and human effects as entry #17 in TiHKAL (1997), describing it as unmatched among oral psychedelics for speed, intensity, and brevity.[4]
Clinical development
4-HO-DiPT entered formal pharmaceutical development when Reunion Neuroscience created luvesilocin (RE104), a subcutaneous prodrug designed for controlled clinical delivery.[5] The Phase 2 RECONNECT trial enrolled 84 patients with postpartum depression and met its primary endpoint (p = 0.0094).[8][6] The FDA granted Breakthrough Therapy Designation to luvesilocin in February 2026.[6]
Regulatory history
In January 2022, the DEA proposed placing 4-HO-DiPT and four other tryptamines in Schedule I of the Controlled Substances Act.[9] Following public comment and multiple hearing requests, the DEA withdrew the proposal in July 2022, citing the need for an updated scientific evaluation from the Department of Health and Human Services.[9] The compound remains unscheduled at the federal level but may be prosecuted under the Federal Analogue Act as a structural analog of Psilocin.
The name iprocin — a contraction of "isopropyl" and "psilocin" — follows the Shulgin-era naming convention for tryptamine analogs. 4-HO-DiPT first appeared on European research chemical markets around 2005,[10] where its unusually short duration earned it a niche reputation among psychonauts, though it never achieved the mainstream recognition of psilocybin or LSD.
Chemistry[edit]
Structural class
4-HO-DiPT belongs to the substituted tryptamine family, sharing the 2-aminoethylindole backbone common to psilocin, DMT, and serotonin itself. It is a direct structural analog of psilocin (4-HO-DMT), with both N-methyl groups replaced by bulkier isopropyl groups on the terminal amine. This substitution alters the compound's receptor selectivity while preserving psychedelic activity.[11]
The compound is the active metabolite of 4-AcO-DiPT (released by hydrolysis of the acetoxy ester at the 4-position) and of the clinical prodrug luvesilocin (RE104), a glutarate ester designed for subcutaneous administration.[5]
Molecular properties
| Molecular formula | C₁₆H₂₄N₂O |
| Molecular weight | 260.37 g/mol |
The molecular structure features an indole ring system with a hydroxyl group at the 4-position, a two-carbon ethylamine side chain at the 3-position, and two isopropyl groups on the terminal nitrogen. The 4-hydroxyl group is the critical pharmacophore for serotonin receptor binding, mimicking the hydroxyl of serotonin shifted to the indole 4-position — a feature shared across all 4-substituted tryptamine psychedelics. The compound contains no chirality centres and exists as a single stereoisomeric form.
Physical properties
The free base appears as a white powder.[12] The hydrochloride salt melts at 263°C.[4] No published experimental solubility or stability data exist for either form. Like other 4-hydroxytryptamines, the phenolic hydroxyl group is susceptible to oxidative degradation, particularly under alkaline conditions and UV exposure.
Pharmacology[edit]
Mechanism of action
4-HO-DiPT produces psychedelic effects primarily through activation of the 5-HT₂A receptor. Blocking this receptor with selective antagonists eliminates psychedelic-like behaviour in animal models.[11][2] The compound is classified as a near-full agonist at 5-HT₂A, serotonin₂B, and 5-HT₂C receptors, with female mice showing greater sensitivity than males.[2]
Beyond direct receptor activation, 4-HO-DiPT also inhibits the SERT (SERT) and partially inhibits the NET (NET).[1] This dual action — receptor agonism combined with reuptake inhibitor — places its pharmacological profile closer to psilocin than to LSD or mescaline, and may contribute to its rapid onset and distinctive subjective character.
Preclinical research has demonstrated that 4-HO-DiPT enhances fear extinction in mice through 5-HT₂A-dependent activation of inhibitory neurons in the amygdala.[2] This mechanism offers a cellular-level explanation for the potential therapeutic use of short-acting psychedelics in anxiety- and trauma-related conditions.
Pharmacokinetics
No human pharmacokinetic study has been published for orally administered 4-HO-DiPT. All available data derive from preclinical studies of the prodrug RE104 (luvesilocin).
In rats receiving subcutaneous RE104, 4-HO-DiPT showed a plasma half-life of approximately 40 minutes, with plasma concentration tracking directly with behavioural intensity.[5] This short half-life is consistent with the 2–3 hour total duration reported in humans.[4] Oral bioavailability has not been measured in any species.
Metabolism
Metabolic data come primarily from human liver cell studies of 4-AcO-DiPT, which is rapidly converted to 4-HO-DiPT by ester hydrolysis.[13] The principal metabolic pathways include glucuronidation of the 4-hydroxyl group (the primary elimination route), removal of one isopropyl group to yield the active metabolite 4-HO-NiPT,[14] oxidation of the terminal amine, and sulfate conjugation.
The liver enzyme CYP2D6 is the most potently inhibited by the compound.[12] By structural analogy with related diisopropyltryptamines, CYP2D6 and CYP3A4 are likely the primary enzymes responsible for breaking down the compound.[15] Individuals who metabolize drugs slowly through CYP2D6 (poor metabolizers) may experience altered drug exposure.[16]
Neuroscience[edit]
Where it acts
As a near-full serotonin 2A receptor agonist,[2] 4-HO-DiPT is expected to activate deep-layer neurons in the prefrontal cortex — the primary trigger for psychedelic effects across the serotonergic class.inferred This activation is predicted to increase neural complexity, disrupt the brain's default mode network, and loosen the filtering of sensory and associative information, producing the characteristic expansion of awareness reported by users. No direct neuroimaging data have been published for this compound.
The most substance-specific finding comes from preclinical work showing that 4-HO-DiPT activates inhibitory neurons in the amygdala's fear-processing circuit, dampening fear-conditioned responses in a dose-dependent and sex-dependent manner.[2]
Why it matters
4-HO-DiPT's short duration poses a compelling test of the REBUS framework, which proposes that psychedelics work by temporarily loosening rigid belief patterns. The RECONNECT trial — showing sustained improvement at Day 28 from a single short session — suggests that the duration of belief relaxation may matter less than its intensity.[6]
The compound's sustained antidepressant-like effects in rodents — persisting one week after a single dose despite a 40-minute half-life[5] — support the psychoplastogen hypothesis: that psychedelics trigger rapid structural brain changes (new connections, dendritic growth) that outlast the drug's presence.[17]
Key unknowns include whether 4-HO-DiPT directly promotes neuroplasticity through mechanisms independent of 5-HT₂A (as psilocin does via the TrkB/BDNF receptor[17]), whether the short duration limits or preserves therapeutic benefit compared to longer-acting psychedelics, and how genetic variation in CYP2D6 metabolism affects both the experience and therapeutic response.
Subjective Effects[edit]
The 4-HO-DiPT experience is defined by compression: a full-spectrum psychedelic state delivered within a 2–3 hour window, with an onset speed that feels closer to vaporized tryptamines than to oral psilocybin. The steep dose-response curve — where a roughly 30% dose increase produces a qualitative shift from mild to overwhelming — makes precise measurement and cautious titration unusually consequential. Set and setting exert their typical strong influence, amplified by the speed at which the experience reaches full intensity.
Compared to psilocybin, the experience is faster-onset and shorter, with a lighter visual signature and a more prominent body load featuring characteristic leg tremors. Relative to smoked DMT, it offers a more grounded and navigable state, with oral dosing allowing a gentler entry into the psychedelic space.
Effect Grid
At common doses (15–20 mg oral), the full psychedelic experience unfolds rapidly. Colour enhancement becomes pronounced, objects may exhibit mild drifting and morphing, and rainbow halos or tracers appear around light sources. Closed-eye visuals remain modest compared to psilocin. Thought connectivity increases significantly, often producing introspective insights and novel personal perspectives. Cognitive euphoria ranges from mild to strong.
Physically, leg tremors, muscle loosening, mild stimulation, and elevated heart rate are commonly reported. A vague body malaise and chill-like sensations may occur. Nausea is possible but less prominent than with psilocybin.
The experience peaks within 20–30 minutes of onset and resolves to baseline within approximately 2–3 hours. The steep dose-response curve means that 15 mg produces a mild-to-moderate experience while 20 mg can reach full intensity.
Modeled from the effect's dose-dependence curve — not per-substance measurements.
Color enhancement · Geometry · Brightness alteration · Music enhancement · Holotropic state · Visual morphing · Symmetrical texture repetition · Tracers · Auditory enhancement · Auditory misinterpretation · Environmental patterning · Light sensitivity · Sound sensitivity · Touch enhancement · Vestibular distortion · Visual haze / noise · Visual melting · Depth perception distortion · Perspective distortion · After-images · Ganzfeld effect · Peripheral vision distortion · Proprioceptive distortion · Spatial disorientation · Visual acuity enhancement · Synesthesia · Visual diffraction · Dreaming enhancement · Peripheral misidentification · Tinnitus · Visual acuity suppression · Visual magnification · Visual processing acceleration · Flashbacks · Object transformations · Internal hallucinations · Visual recursion · Auditory hallucinations · Environmental orbism / cubism · External hallucinations · Object activation · Perspective hallucinations · Shadow people · Persisting hallucinations
Holotropic state · Visual morphing · Symmetrical texture repetition · Tracers · Auditory enhancement · Auditory misinterpretation · Environmental patterning · Light sensitivity · Sound sensitivity · Touch enhancement · Vestibular distortion · Visual haze / noise · Visual melting · Depth perception distortion · Perspective distortion · After-images · Ganzfeld effect · Peripheral vision distortion · Proprioceptive distortion · Spatial disorientation · Visual acuity enhancement · Synesthesia · Visual diffraction · Dreaming enhancement · Peripheral misidentification · Tinnitus · Visual acuity suppression · Visual magnification · Visual processing acceleration · Flashbacks · Object transformations · Internal hallucinations · Visual recursion · Auditory hallucinations · Environmental orbism / cubism · External hallucinations · Object activation · Perspective hallucinations · Shadow people · Persisting hallucinations
Spontaneous body sensations · Appetite suppression · Stimulation · Physical fatigue · Tactile euphoria · Tingling / electric sensations · Wakefulness · Bodily heaviness · Bodily pressures · Body schema distortion · Breathing alteration · Dizziness · Dry mouth · Heart rate perception changes · Insomnia · Nausea · Laughter fits · Muscle tension · Vibrations / buzzing · Bodily lightness · Excessive sweating · Headache · Muscle relaxation · Restlessness · Dehydration sensation · Diarrhea · Involuntary body movements · Abnormal heartbeat · Pain suppression · Respiratory stimulation · Sedation · Sexual arousal enhancement · Trembling · Vasoconstriction · Yawning · Nystagmus (eye wobbles) · Vomiting · Bodily dissociation · Tactile hallucination
Physical fatigue · Tactile euphoria · Tingling / electric sensations · Wakefulness · Bodily heaviness · Bodily pressures · Body schema distortion · Breathing alteration · Dizziness · Dry mouth · Heart rate perception changes · Insomnia · Nausea · Laughter fits · Muscle tension · Vibrations / buzzing · Bodily lightness · Excessive sweating · Headache · Muscle relaxation · Restlessness · Dehydration sensation · Diarrhea · Involuntary body movements · Pain suppression · Respiratory stimulation · Sedation · Sexual arousal enhancement · Trembling · Vasoconstriction · Yawning · Nystagmus (eye wobbles) · Vomiting · Bodily dissociation · Tactile hallucination
Introspection enhancement · Openness enhancement · Pattern recognition enhancement · Cognitive euphoria · Immersion enhancement · Cognitive flexibility · Increased nature relatedness · Thought connectivity · Creativity enhancement · Memory suppression · Thought loops · Cognitive fatigue · Cognitive impairment · Focus suppression · Information processing suppression · Memory fragmentation · Multiple thought streams · Thought acceleration · Analysis enhancement · Humor enhancement · Analysis suppression · Confusion · Motivation suppression · Synchronicity · Thought disorganization · Information processing enhancement · Motivation enhancement · Cognitive dysphoria · Language suppression · Memory replays · Focus enhancement · Language enhancement · Thought organization · Memory enhancement · Delusions
Cognitive euphoria · Immersion enhancement · Cognitive flexibility · Increased nature relatedness · Thought connectivity · Creativity enhancement · Memory suppression · Thought loops · Cognitive fatigue · Cognitive impairment · Focus suppression · Information processing suppression · Memory fragmentation · Multiple thought streams · Thought acceleration · Analysis enhancement · Humor enhancement · Analysis suppression · Confusion · Motivation suppression · Synchronicity · Thought disorganization · Information processing enhancement · Motivation enhancement · Cognitive dysphoria · Language suppression · Memory replays · Focus enhancement · Language enhancement · Thought organization · Memory enhancement
Anxiety · Empathy enhancement · Catharsis · Anxiety suppression · Dysphoria · Irritability
Dysphoria · Irritability
Trust enhancement · Sociability enhancement · Communication enhancement · Flow state · Automaticity · Communication suppression · Sociability suppression · Social disconnection · Boundary dissolution · Ego dissolution · Cognitive disconnection · Identity alteration · Telepathic feelings
Automaticity · Communication suppression · Sociability suppression · Social disconnection · Boundary dissolution · Ego dissolution · Cognitive disconnection · Identity alteration · Telepathic feelings
Time cessation
Transpersonal visions · Entity contact · Transpersonal memory access · Cessation · Death-rebirth sequence · Near-death experience · Voidness
Death-rebirth sequence · Near-death experience · Voidness
Recursive awareness
Timeline
First alerts within 10–20 minutes: subtle mood shift, mild visual brightening, and a growing sense of bodily awareness. The rapid onset is a defining feature of 4-HO-DiPT.
Effects build quickly over 10–20 minutes. Colour enhancement sharpens, body load manifests as leg restlessness or tremor, and thought patterns begin to shift. The transition from first alerts to approaching peak can feel abrupt.
Full psychedelic intensity lasts 45–90 minutes. Visual effects, introspective cognition, and emotional amplification reach maximum. The steep dose-response curve means peak intensity is highly dose-sensitive.
Effects diminish steadily over 30–60 minutes. Visual distortion fades, cognitive clarity returns, and body load eases. Most users feel substantially baseline by this phase.
Mild residual mood elevation and subtle sensory enhancement may persist for 1–3 hours after primary effects resolve. Cognitive function is largely restored but subtle perceptual shifts remain.
⚠ Do not drive or operate machinery for the remainder of the day following a 4-HO-DiPT experience.
Safety[edit]
- Acute toxicity
- Low
- Chronic toxicity
- Negligible
- Withdrawal
- None
- Tolerance buildup
- rapid
- Tolerance reset
- 7 days
- Physical
- None
- Psychological
- Negligible
- Compulsive redosing
- Negligible
- Dose escalation
- Negligible
- Cross-tol.
- psilo · psilocin · lsd
Toxicity
Acute toxicity
No lethal dose has been established in any species, and no hospitalization or death has been reported from the compound.safety citation needed In a Phase 2 trial of the prodrug luvesilocin (84 patients, subcutaneous — not directly comparable to oral free base), the most common side effects were nausea (43.9%) and headache (34.1%), both mild to moderate.[8] No serious adverse events occurred, and preclinical studies showed no organ toxicity.[5]
User reports describe leg tremors, muscle tension, body malaise, and elevated heart rate, though none have been measured under controlled conditions.[7]
Chronic toxicity
No chronic toxicity data exist. The compound is used episodically, and no repeat-dosing studies have been published.
Dose-response sensitivity
The steep dose-response curve is the primary substance-specific safety concern.[4] At 15 mg oral, effects are mild; at 20 mg, they reach full psychedelic intensity — a roughly 30% dose increase that produces a disproportionate intensity jump. Without precise weighing equipment, accidental overdose is a real risk.
Psychological risks
As a serotonergic psychedelic, 4-HO-DiPT can produce acute anxiety, panic, paranoia, dysphoria, and perceptual disturbance. The steep dose-response curve amplifies this — small weighing errors can shift the experience from mild to overwhelming.
The short duration means adverse effects resolve faster than with psilocybin or LSD. Cannabis co-administration can unpredictably amplify effects, increasing panic and paranoia risk.[7] No compound-specific data exist on persistent perceptual disturbance or psychosis precipitation, though both are recognized risks of the serotonergic psychedelic class.inferred
Tolerance and dependence
4-HO-DiPT is not habit-forming. Tolerance develops rapidly after a single dose through downregulation — the same mechanism shared by all serotonergic psychedelics. Cross-tolerance exists with psilocin, LSD, DMT, and mescaline,inferred and sensitivity is estimated to reset within approximately 7 days.inferred
Drug Interactions
Serotonergic interactions
4-HO-DiPT both activates serotonin receptors and slows serotonin reuptake,[1] making it unusually vulnerable to serotonin overload when combined with other serotonergic agents.
Tramadol adds further serotonin activity on top of 4-HO-DiPT's own load, creating a dangerous additive effect.[17][18]
MAO inhibitors block the enzymatic breakdown of serotonin. Combined with a substance that both activates serotonin receptors and slows reuptake, this can trigger severe serotonin syndrome — a potentially life-threatening response involving high fever, muscle rigidity, and seizures.[15][19]
SSRIs and SNRIs may blunt psychedelic effects through chronic receptor adaptation, while acute combination risks serotonin toxicity.inferred
Other interactions
Cannabis can unpredictably amplify psychedelic effects, significantly increasing the risk of adverse psychological reactions.[7]
Lithium carries a class-based seizure risk when combined with serotonergic psychedelics.safety citation needed
4-HO-DiPT inhibits the liver enzyme CYP2D6,[13] which may affect the breakdown of drugs processed by this enzyme — including codeine, tamoxifen, and many antidepressants. Clinical significance at typical doses has not been studied.
Contraindications
7 knownAbsolute contraindications
- Concurrent MAOI use — severe serotonin toxicity risk[19]
- Concurrent tramadol use — dangerous additive serotonergic mechanism[17]
Relative contraindications
- Personal or family history of psychotic disorders — serotonergic psychedelics can trigger or worsen psychosis in vulnerable individualsinferred
- Bipolar disorder with psychotic features — risk of manic or psychotic episodeinferred
- Concurrent lithium use — seizure risksafety citation needed
- Concurrent SSRI/SNRI use — blunted efficacy or serotonin toxicity riskinferred
- Pregnancy and breastfeeding — no reproductive toxicity data existsafety citation needed
Harm Reduction[edit]
Forms & Identification
4-HO-DiPT is sold primarily as a powder — free base or hydrochloride salt — and occasionally as pellets. Established reagent test profiles for this compound are limited, making visual identification unreliable.
A milligram-precision scale (0.001 g) is essential. The steep dose-response curve means 2–3 mg of error can dramatically alter the experience. Volumetric dosing — dissolving a weighed amount in a measured volume of liquid — offers the most reliable accuracy at low doses.
Guidelines
- Start at the low end of the dose range (15 mg or below). Do not redose — the experience will end naturally within a few hours.
- Use a milligram-precision scale. Volumetric dosing is strongly recommended for doses under 20 mg.
- Set up the environment fully before dosing: music, lighting, water, blankets, phone silenced.
- Have a sober sitter present, especially for first experiences or doses above 15 mg.
- Avoid a heavy meal within 2 hours of dosing to reduce nausea.
- Wait at least 7 days between experiences to allow full sensitivity reset.
Set & Setting
The fast onset leaves little transition time between baseline and full effect. The environment should be fully arranged before dosing — music, lighting, water, and a clear physical space all in place.
A calm, familiar, private setting with a sober sitter present is strongly recommended, especially for first experiences or higher doses. The short total duration makes structured sessions practical, but the speed of onset can catch an unprepared person off guard.
Aftercare & integration. The return to baseline is rapid, but the psychological content of the experience can still carry weight. Allow the rest of the day for quiet recovery — avoid demanding tasks or social obligations.
Journaling within the first few hours captures insights before they fade. If the experience was emotionally intense or disturbing, discussing it with a trusted person or integration-trained therapist within the first week supports processing. Persistent anxiety, mood changes, or intrusive thoughts lasting more than a few days warrant professional consultation.
Recovery & Support
4-HO-DiPT does not produce physical dependence, and compulsive use is rare across the psychedelic class. If psychedelic use is becoming avoidance rather than engagement, or if experiences are causing more distress than insight, a pause and professional support are warranted. Resources include the Fireside Project (psychedelic peer support line), MAPS integration therapist directory, and local harm reduction organisations.
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Recognizing an emergency: Most uncomfortable experiences resolve within a few hours without medical intervention. Seek immediate help if the person shows signs of self-harm intent, complete disconnection from reality (unable to recognize people or surroundings), seizure activity, severe chest pain, or loss of consciousness.
Immediate steps:
- Stay with the person. Speak in calm, short sentences.
- If conscious and distressed, move to a quiet, low-stimulation space.
- If unconscious or seizing, place in the recovery position (on their side, airway clear) and call emergency services immediately.
- Do not restrain unless there is immediate danger of self-harm or harm to others.
- Do not attempt to induce vomiting.
What to tell the dispatcher: Name the substance (4-HO-DiPT, a tryptamine psychedelic), the approximate amount taken, the time of ingestion, and current symptoms. Good Samaritan laws in many jurisdictions protect people who call for help during a drug-related emergency.
Legal Status[edit]
As of April 2026, 4-HO-DiPT is unscheduled at the US federal level but occupies legally ambiguous territory in most countries — its structural similarity to psilocin exposes it to structural analog drug laws in jurisdictions that employ them.
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| United States (federal) | Not scheduled | DEA proposed Schedule I placement Jan 2022; withdrew proposal Jul 2022 pending HHS re-evaluation.[9] May be prosecuted under Federal Analogue Act as a structural analog of psilocin. |
| United States (Florida) | Schedule I | Specifically scheduled at state level.[7] |
| United Kingdom | Class A | Controlled under Misuse of Drugs Act 1971 via generic tryptamine clause. Possession: up to 7 years; supply/production: up to life imprisonment.[7] |
| Canada | Not controlled | Not listed in the Controlled Drugs and Substances Act as of 2025.[7] |
| Germany | NpSG | Controlled under the Neue-Psychoaktive-Stoffe-Gesetz (New Psychoactive Substances Act). Use permitted only for industrial and scientific purposes.[7] |
| Australia | Uncertain | Not explicitly listed in the Poisons Standard. May be captured as an analog of psilocin under Criminal Code Regulations.citation needed |
Legal status changes frequently and varies by jurisdiction. This information is not legal advice. Always verify current local law before relying on it.
Analog and prodrug considerations
The Federal Analogue Act potentially applies to 4-HO-DiPT as a structural analog of Psilocin, provided it is intended for human consumption. The clinical prodrug luvesilocin (RE104) is under FDA Investigational New Drug authorization, which covers the clinical trial but does not change the scheduling status of the parent compound.
Safety[edit]
- Acute toxicity
- Low
- Chronic toxicity
- Negligible
- Withdrawal
- None
- Tolerance buildup
- rapid
- Tolerance reset
- 7 days
- Physical
- None
- Psychological
- Negligible
- Compulsive redosing
- Negligible
- Dose escalation
- Negligible
- Cross-tol.
- psilo · psilocin · lsd
Toxicity
Acute toxicity
No lethal dose has been established for 4-HO-DiPT in any species, and no published case reports describe hospitalization or death from the compound.safety citation needed The best available acute safety data come from the RECONNECT Phase 2 trial of the prodrug luvesilocin (RE104, subcutaneous injection — not directly comparable to oral free base). In that trial (n = 84), the most common side effects were nausea (43.9%) and headache (34.1%), both mild to moderate.[8] No serious adverse events occurred.
Preclinical studies showed no evidence of organ toxicity.[5] User reports describe leg tremors, muscle tension, body malaise, and elevated heart rate, though none have been measured under controlled conditions.[7]
Chronic toxicity
No data on chronic toxicity exist. The compound is used episodically rather than daily, and no repeat-dosing studies have been published.
Dose-response sensitivity
The steep dose-response curve is the primary substance-specific safety concern.[4] At 15 mg oral, effects are mild; at 20 mg, effects reach full psychedelic intensity. This approximately 30% dose increment produces a disproportionate intensity increase, creating high risk of accidental overdose without precise weighing equipment.
Psychological risks
As a serotonergic psychedelic, 4-HO-DiPT carries the class-typical psychological risk profile: acute anxiety, panic, paranoia, dysphoria, and perceptual disturbance under adverse conditions. The steep dose-response curve amplifies this risk, as small weighing errors can shift the experience from mild to overwhelming.
No compound-specific data exist on HPPD (HPPD) or psychosis precipitation, though both are recognised risks of the serotonergic psychedelic class.inferred
The short duration (2–3 hours) is a partial mitigating factor: adverse psychological experiences resolve more rapidly than with psilocybin (4–6 hours) or LSD (8–12 hours).
Cannabis co-administration has been reported to amplify effects unpredictably, increasing the risk of anxiety, paranoia, and panic.[7]
Tolerance and dependence
4-HO-DiPT is not considered habit-forming. No evidence of physical dependence, withdrawal, or compulsive redosing has been reported. Tolerance develops rapidly after a single dose through downregulation — the same mechanism shared by all serotonergic psychedelics. Cross-tolerance exists with psilocin, LSD, DMT, and mescaline.inferred
Full sensitivity is estimated to reset within approximately 7 days by class inference, though this has not been verified for 4-HO-DiPT specifically.inferred
Drug Interactions
Serotonergic interactions
4-HO-DiPT both activates serotonin receptors and inhibits serotonin reuptake,[1] creating a dual serotonergic mechanism that increases vulnerability to serotonin syndrome when combined with other serotonergic agents.
Tramadol presents a dangerous interaction by adding further serotonin reuptake inhibitor and receptor activity atop 4-HO-DiPT's own serotonergic load.[18][19]
MAO inhibitors represent a potentially life-threatening combination. By blocking the enzymatic breakdown of serotonin, MAOIs combined with a direct serotonin agonist and reuptake inhibitor create severe serotonin toxicity risk.[16][20]
SSRIs and SNRIs interact bidirectionally: chronic use may blunt psychedelic effects through receptor adaptation, while acute combination risks serotonin toxicity.inferred
Other interactions
Cannabis can unpredictably amplify psychedelic effects, significantly increasing the risk of adverse psychological reactions.[7]
Lithium carries a class-based risk of seizures when combined with serotonergic psychedelics.safety citation needed
4-HO-DiPT inhibits the liver enzyme CYP2D6,[12] raising the possibility of interactions with drugs processed by this enzyme (including codeine, tamoxifen, and many antidepressants). The clinical significance at typical doses has not been studied.
Contraindications
7 knownAbsolute contraindications
- Concurrent MAOI use — severe serotonin toxicity risk[20]
- Concurrent tramadol use — dangerous additive serotonergic mechanism[18]
Relative contraindications
- Personal or family history of psychotic disorders — serotonergic psychedelics can trigger or worsen psychosis in vulnerable individualsinferred
- Bipolar disorder with psychotic features — risk of manic or psychotic episodeinferred
- Concurrent lithium use — seizure risksafety citation needed
- Concurrent SSRI/SNRI use — blunted efficacy or serotonin toxicity riskinferred
- Pregnancy and breastfeeding — no reproductive toxicity data existsafety citation needed
Harm Reduction[edit]
Forms & Identification
4-HO-DiPT circulates primarily as a powder (free base or hydrochloride salt), occasionally pressed into pellets. The lack of widely established reagent test profiles for this specific compound makes identification more challenging than for common tryptamines. A milligram-precision scale (0.001 g) is essential given the steep dose-response curve — even 2–3 mg of error can dramatically alter the experience. Volumetric dosing (dissolving a known quantity in a measured volume of liquid) offers the most reliable way to achieve accurate doses in this range.
Guidelines
- Start at the low end of the dose range (15 mg or below) and do not redose during the experience — the short duration means the experience will end naturally within 2–3 hours.
- Use a milligram-precision scale. Volumetric dosing is strongly recommended for doses under 20 mg.
- Ensure the setting is fully prepared before ingestion: music, lighting, water, blankets, phone silenced.
- Have a sober sitter present, especially for first experiences or doses above 15 mg.
- Avoid eating a heavy meal within 2 hours of dosing to reduce nausea.
- Wait a minimum of 7 days between experiences to allow full sensitivity reset.
Set & Setting
The rapid onset (15–20 minutes) and compressed duration demand particular attention to preparation. The environment should be fully established before dosing — there is little transition time between baseline and altered states. A calm, familiar, private space with a trusted sitter is recommended, especially at higher doses or for first experiences. The short total duration makes this compound practical for structured sessions, but the speed of onset can catch unprepared users off guard.
Aftercare & integration. The compressed timeline of 4-HO-DiPT means the return to baseline is rapid, but the psychological content of the experience can still carry significant weight. Allow the rest of the day for quiet recovery — avoid demanding tasks or social obligations.
Journaling within the first few hours of return can capture insights before they fade. If the experience was emotionally intense or disturbing, discussing it with a trusted person or integration-trained therapist within the first week supports processing. Persistent anxiety, mood changes, or intrusive thoughts lasting more than a few days warrant professional consultation.
Recovery & Support
4-HO-DiPT does not produce physical dependence, and compulsive use patterns are rare across the psychedelic class. If psychedelic use is becoming a way to avoid processing difficult emotions rather than engage with them, or if experiences are causing more distress than insight, a pause and professional support are warranted. Resources include the Fireside Project (psychedelic peer support line), MAPS integration therapist directory, and local harm reduction organisations.
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Recognizing an emergency: Most uncomfortable 4-HO-DiPT experiences resolve within 2–3 hours without medical intervention. Seek immediate help if the person shows signs of self-harm intent, complete disconnection from reality (unable to recognise people or surroundings), seizure activity, severe chest pain, or loss of consciousness.
Immediate steps:
- Stay with the person. Speak in calm, short sentences.
- If they are conscious and distressed, move them to a quiet, low-stimulation space.
- If unconscious or seizing, place them in the recovery position (on their side, airway clear) and call emergency services immediately.
- Do not restrain them unless there is immediate danger of self-harm or harm to others.
- Do not attempt to induce vomiting.
What to tell the dispatcher: Name the substance (4-HO-DiPT, a tryptamine psychedelic), the approximate amount taken, the time of ingestion, and current symptoms. Good Samaritan laws in many jurisdictions protect people who call for help during a drug-related emergency.
Legal Status[edit]
As of April 2026, 4-HO-DiPT occupies a legally ambiguous position in most jurisdictions. It is not scheduled at the United States federal level following the DEA's withdrawal of its proposed Schedule I placement in 2022, though several countries classify it under broad tryptamine or novel psychoactive substance provisions. Its structural relationship to psilocin (a Schedule I substance in the US and controlled internationally) exposes it to structural analog drug laws in jurisdictions that employ them.
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| United States (federal) | Not scheduled | DEA proposed Schedule I placement Jan 2022; withdrew proposal Jul 2022 pending HHS re-evaluation.[9] May be prosecuted under Federal Analogue Act as a structural analog of psilocin. |
| United States (Florida) | Schedule I | Specifically scheduled at state level.[7] |
| United Kingdom | Class A | Controlled under Misuse of Drugs Act 1971 via generic tryptamine clause. Possession: up to 7 years; supply/production: up to life imprisonment.[7] |
| Canada | Not controlled | Not listed in the Controlled Drugs and Substances Act as of 2025.[7] |
| Germany | NpSG | Controlled under the Neue-Psychoaktive-Stoffe-Gesetz (New Psychoactive Substances Act). Use permitted only for industrial and scientific purposes.[7] |
| Australia | Uncertain | Not explicitly listed in the Poisons Standard. May be captured as an analog of psilocin under Criminal Code Regulations.citation needed |
Analog and prodrug considerations
The Federal Analogue Act (21 U.S.C. § 813) potentially applies to 4-HO-DiPT as a structural analog of Psilocin, provided the substance is intended for human consumption. The clinical prodrug luvesilocin (RE104) is under FDA Investigational New Drug authorisation, which provides legal protection within the registered clinical trial but does not change the scheduling status of the parent compound.
Frequently asked questions
What is 4-HO-DiPT?
4-HO-DiPT is a synthetic substituted tryptamine psychedelic distinguished by its short oral duration of 2–3 hours and steep dose-response curve. Its prodrug luvesilocin (RE104) received FDA Breakthrough Therapy Designation for postpartum depression in 2026.
How long does 4-HO-DiPT last?
Total duration by route of administration — Oral: 2 – 3 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-HO-DiPT?
Psychedex publishes a dosage table for 4-HO-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-HO-DiPT?
The highest-severity documented interactions for 4-HO-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-HO-DiPT addictive?
Psychedex records tolerance and dependence data rather than a yes/no rating. Recorded tolerance indicators for 4-HO-DiPT: tolerance builds rapid; full reset takes 7 days; cross-tolerance develops with psilocybin, psilocin, lsd, dmt, mescaline, 4-aco-dmt, 4-ho-met. See the article's dependence and safety sections for recorded dependence data.
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First-person accounts of subjective effects, timing, and outcomes — submitted for harm reduction.
references
- [1] ^abcRickli A, Moning OD, Hoener MC, Liechti ME (2016) Receptor interaction profiles of novel psychoactive tryptamines compared with classic hallucinogens — European Neuropsychopharmacology doi:10.1016/j.euroneuro.2016.05.001
- [2] ^abcdKelly TJ, Bonniwell EM, Mu L, Liu X, Hu Y, Friedman V, Yu H, Su W, McCorvy JD, Liu QS (2024) Psilocybin analog 4-OH-DiPT enhances fear extinction and GABAergic inhibition of principal neurons in the basolateral amygdala — Neuropsychopharmacology doi:10.1038/s41386-023-01744-8
- [3] ^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
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references
- [1] ^abcRickli A, Moning OD, Hoener MC, Liechti ME (2016) Receptor interaction profiles of novel psychoactive tryptamines compared with classic hallucinogens — European Neuropsychopharmacology doi:10.1016/j.euroneuro.2016.05.001
- [2]
- [3] ^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
- [4]
- [5]
- [6]