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5-MeO-DiPT
5-methoxy-N,N-diisopropyltryptamine
5-MeO-DiPT (5-methoxy-N,N-diisopropyltryptamine) — Foxy, Foxy Methoxy — is a synthetic psychedelic of the tryptamine class. It is a close relative of 5-MeO-MiPT, set apart by its emphasis on tactile and auditory effects over visual distortion. It blocks serotonin reuptake and directly activates serotonin receptors, producing a profile that blends psychedelic and empathogenic qualities.[1][2][3]
5-MeO-DiPT (5-methoxy-N,N-diisopropyltryptamine) — Foxy, Foxy Methoxy — is a synthetic psychedelic of the tryptamine class. It is a close structural relative of 5-MeO-MiPT, distinguished by prominent tactile and auditory effects over visual distortion. 5-MeO-DiPT is a 5-HT₂A receptor agonist that also inhibits serotonin reuptake, producing its effects through dual serotonergic activation.[1][2][3]
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psilocybin, LSD, DMT +2 morepsilocybin, LSD, DMT, mescaline, 5-MeO-DMT show less
Alexander Shulgin and Michael Carter first synthesized it in 1980, reporting it as an orally active psychedelic tryptamine.[4] It spread through internet vendors from around 1999 under the name "Foxy" and was permanently placed into Schedule I by the DEA in 2004.[5][6] Today it is controlled in the United States and Japan, with no approved medical use.
Subjective effects include tactile enhancement, auditory distortion, physical stimulation, euphoria, and heightened sexual arousal.[7] The experience is distinctly body-centered — more warmth and stimulation than visual immersion, closer to an empathogen than a classical psychedelic. Nausea, diarrhea, and anxious overstimulation are characteristic unwanted effects.
5-MeO-DiPT produces no physical dependence, and no lethal dose has been established — though animal studies document DNA damage and brain changes at high doses.[8][9] Combining it with MAOIs is potentially fatal: they block serotonin breakdown, and together with the drug's dual serotonergic action, the result can be dangerous overload.[10][11] No controlled human studies have been conducted — knowledge rests on animal research, case reports, and self-experimentation.
History[edit]
Discovery
5-MeO-DiPT was first synthesized by Alexander Shulgin and Michael Carter in 1980, reported alongside DiPT as orally active tryptamine analogs.[4] Shulgin later documented extended self-experimentation in TiHKAL: Tryptamines I Have Known and Loved (1997), which remains the most detailed early account of its effects in humans.
Prohibition and modern use
5-MeO-DiPT surfaced as a street drug around 1999, sold through internet vendors under the names "Foxy" and "Foxy Methoxy".[5] By 2003 the DEA had documented seizures across twelve US states and temporarily placed it into Schedule I; permanent scheduling followed in 2004.[12][6] Japan restricted it in April 2005 following abuse reports and a violent incident linked to combined tryptamine use.[13]
The street names "Foxy" and "Foxy Methoxy" reflected the compound's reputation as a sexually enhancing psychedelic. Epidemiological data from East Asia document significant use among men who have sex with men: a 2018 survey in Qingdao, China found that 66.8% of MSM drug users had used 5-MeO-DiPT in the preceding six months, with sexual enhancement as the primary motivator.[14] Similar patterns were reported among HIV-positive males in Japan.[15]
Chemistry[edit]
Structural class
5-MeO-DiPT belongs to the substituted tryptamine family, sharing the indole backbone found in psilocin, DMT, and 5-MeO-DMT.[16] Two modifications define it: a methoxy group at the 5-position of the indole ring, and two isopropyl groups on the nitrogen.[16]
Its molecular formula is C₁₇H₂₆N₂O (molecular weight 274.40 g/mol), and its moderate lipophilicity allows efficient passage across cell membranes.[17]
Molecular properties
| Molecular formula | C₁₇H₂₆N₂O |
| Molecular weight | 274.40 g/mol |
Pharmacology[edit]
Mechanism of action
5-MeO-DiPT raises serotonin levels in the synapse by blocking reuptake, and simultaneously activates two types of serotonin receptors.[1][2] The psychedelic effects depend on one of those receptor activations specifically — blocking it in animal tests eliminates the hallucinogenic response.[2][3] In behavioral tests it partially substituted for LSD, placing it pharmacologically close to classical psychedelics but not identical.[2]
Downstream effects
In animal studies, 5-MeO-DiPT also raises dopamine and glutamate levels across brain regions including the cortex and striatum.[8][18] The dopamine rise likely drives the stimulant and euphoric qualities; the glutamate release follows from serotonin receptor activation and is shared with other serotonergic psychedelics.
Metabolism
The liver breaks down 5-MeO-DiPT primarily via the CYP2D6 enzyme, producing a bufotenin-like metabolite;[11] an N-oxide metabolite has also been identified in human urine.[19] People who metabolize CYP2D6 slowly — genetically or due to fluoxetine, paroxetine, or bupropion — experience significantly higher drug exposure from the same dose.[10][11]
Neuroscience[edit]
Where it acts
In animal studies, 5-MeO-DiPT simultaneously raises serotonin, dopamine, and glutamate levels in the frontal cortex, striatum, and nucleus accumbens.[8] These regions govern sensory processing, reward, and decision-making — their concurrent activation likely underlies the blend of perceptual distortion, physical stimulation, and mood elevation.[18] No human neuroimaging studies have been published.
Why it matters
5-MeO-DiPT disrupts normal sensory filtering by activating serotonin receptors on cortical neurons, triggering glutamate release.citation needed The additional serotonin reuptake blockade raises synaptic serotonin — engaging reward and social bonding circuits in a way that partially resembles MDMA, though through a different mechanism.
Whether 5-MeO-DiPT promotes the growth of new neural connections — as other serotonergic psychedelics appear to — has not been tested. The dose threshold for brain damage in humans is unknown; rodent damage occurs at doses far exceeding typical human use,[8] but the safety margin has not been characterized.
Subjective Effects[edit]
5-MeO-DiPT produces a body-centered psychedelic experience dominated by tactile intensification, auditory distortion, and physical stimulation. Visual effects are notably subdued compared to most tryptamines. At lower doses the mood is socially engaging and euphorically warm; the same dose can shift toward restless anxiety depending on context.
Within the tryptamine class, it sits between psilocybin (more visual, less stimulating) and MDMA (shared tactile warmth and mood lift, different mechanism). The closest comparator is 5-MeO-MiPT, which shares the tactile emphasis and 5-methoxy character but differs in potency and duration.
Alexander Shulgin and Michael Carter first synthesized 5-MeO-DiPT in 1980.[4] It circulated as a "research chemical" from approximately 1999 before the US Drug Enforcement Administration placed it into Schedule I — temporarily in 2003 and permanently in 2004.[5][6] It remains a controlled substance in the United States and Japan, with no approved clinical applications.
Subjective effects include tactile enhancement, auditory distortion, physical stimulation, and sexual arousal enhancement.[7] The experience is distinctly body-centered — more tactile and socially engaging than visually immersive, placing it closer to an empathogenic tryptamine than a classical psychedelic. Nausea, diarrhea, and anxious overstimulation are characteristic unsought effects.
5-MeO-DiPT produces no physical dependence, and no lethal dose has been established — though rodent studies document persistent DNA damage and dopaminergic changes at high doses.[8][9] The combination of serotonin reuptake inhibitor and direct receptor agonism creates compounded serotonin syndrome risk, particularly with MAOIs, while genetic variation in CYP2D6 introduces unpredictable differences in drug exposure.[10][11] No controlled human studies have been conducted; the current understanding rests on animal research, case reports, and uncontrolled self-experimentation.
History[edit]
Discovery
5-MeO-DiPT was first synthesized by Alexander Shulgin and Michael Carter in 1980 and reported alongside DiPT as orally active tryptamine analogs with central nervous system activity.[4] Shulgin later included an extended self-experimentation account in his 1997 book TiHKAL: Tryptamines I Have Known and Loved, which remains the most detailed early description of the compound's effects in humans — though it constitutes an unverifiable primary source.
Prohibition and modern use
5-MeO-DiPT surfaced as a street drug around 1999, sold through internet vendors under the label "research chemical" and known by the names "Foxy" and "Foxy Methoxy".[5] By 2003 the DEA had documented seizures or abuse reports across twelve US states and temporarily placed it into Schedule I; permanent scheduling followed in 2004.[12][6] Japan restricted the compound in April 2005 following abuse reports and a violent incident attributed to combined tryptamine use.[13]
The street names "Foxy" and "Foxy Methoxy" reflect the compound's reputation as a sexually enhancing psychedelic — a characterization that shaped its user base and cultural niche. Epidemiological data from East Asia document significant prevalence among men who have sex with men: a 2018 survey in Qingdao, China found that 66.8% of MSM drug users sampled had used 5-MeO-DiPT in the preceding six months, with sexual enhancement as the primary motivator.[14] Similar use patterns were reported among HIV-positive males in Japan.[15]
Chemistry[edit]
Structural class
5-MeO-DiPT belongs to the substituted tryptamine family, sharing the indole-ethylamine backbone common to psilocin, DMT, and 5-MeO-DMT. Two structural modifications define the compound: a methoxy group at the 5-position of the indole ring and two isopropyl groups on the terminal nitrogen. The 5-methoxy substitution favors serotonin receptor binding, while the bulky diisopropyl groups increase lipophilicity and shape the compound's distinctive receptor and transporter interactions.[16]
Molecular properties
| Molecular formula | C₁₇H₂₆N₂O |
| Molecular weight | 274.40 g/mol |
The molecule consists of a methoxy-substituted indole ring connected via a two-carbon bridge to the diisopropylamino group, giving it a calculated LogP of 3.73 — indicating moderate lipophilicity and efficient membrane permeability.[17]
Stereochemistry
5-MeO-DiPT is achiral — the molecule contains no stereocenters, and no active isomers exist.[18]
Physical properties
5-MeO-DiPT is a crystalline powder with a melting point of 181°C.[17] Predicted boiling point is 411.3 ± 35.0°C at 760 mmHg with a density of 1.0 ± 0.1 g/cm³.[17] No published data on solubility, storage stability, or degradation pathways are available.
Pharmacology[edit]
Mechanism of action
5-MeO-DiPT acts through three simultaneous serotonergic mechanisms: it blocks the SERT (preventing reuptake), activates 5-HT₁A receptors, and activates 5-HT₂A receptors.[1][2] Despite binding more strongly to 5-HT₁A than 5-HT₂A in laboratory assays, its hallucinogenic effects depend on 5-HT₂A activation — selective blockade of this receptor abolishes the hallucination-associated behavioral response in mice.[2][3]
This dual action — transporter inhibition plus direct receptor activation — places 5-MeO-DiPT in a hybrid pharmacological position.[1] The transporter blockade raises serotonin levels in the synapse, while direct agonism activates postsynaptic receptors independently. The result is a serotonergic profile more complex than classical psychedelics like psilocybin or LSD, which act primarily through direct receptor binding.
In drug discrimination tests, 5-MeO-DiPT partially substituted for LSD (75% generalization), confirming pharmacological overlap with classical psychedelics but not identity.[2] Whether 5-MeO-DiPT also causes direct serotonin release (as MDMA does) remains unresolved — data from the related compound DiPT suggest this is plausible,[19] but no specific releasing assay data have been published for 5-MeO-DiPT itself.
Downstream effects
Beyond serotonin, 5-MeO-DiPT increases dopamine and glutamate levels across multiple brain regions in animal studies.[8][20] The dopamine elevation likely contributes to the stimulant and euphoric qualities of the experience, while glutamate release — a downstream consequence of 5-HT₂A activation on cortical neurons — is a mechanism shared with other serotonergic psychedelics.
Metabolism
No human pharmacokinetic studies have been published — bioavailability, peak concentration, and half-life remain unknown in humans. Liver enzyme studies identify two primary metabolic pathways[11]:
- O-demethylation, primarily carried out by the CYP2D6 enzyme, producing a bufotenin-like metabolite
- N-deisopropylation, carried out by multiple enzymes including CYP1A2, CYP2C8, and CYP3A4
An additional N-oxide metabolite has been identified in human urine.[21]
CYP2D6 is the critical variable. Individuals who are poor metabolizers of CYP2D6 — whether genetically or due to medications that inhibit the enzyme (fluoxetine, paroxetine, bupropion) — may experience significantly higher drug exposure and prolonged effects from the same dose.[10][11] Standard immunoassay drug screens do not detect 5-MeO-DiPT; confirmation requires specialized mass spectrometry methods.[21]
Neuroscience[edit]
Where it acts
No human neuroimaging studies of 5-MeO-DiPT have been published. Animal neurochemistry reveals simultaneous increases in serotonin, dopamine, and glutamate across the frontal cortex, striatum, and nucleus accumbens.[8] These regions govern sensory processing, reward, and executive function — their concurrent activation likely underlies the compound's characteristic blend of perceptual distortion, physical stimulation, and mood elevation. Differential monoamine changes across the prefrontal cortex, striatum, and hippocampus further suggest region-specific effects on cognition and memory.[20]
Why it matters
As a confirmed serotonin 2A receptor agonist, 5-MeO-DiPT engages the same cortical disruption mechanism described for classical psychedelics: activation of 5-HT₂A receptors on cortical neurons triggers glutamate release, disrupting the brain's default filtering of sensory and cognitive information.citation needed The additional SERT inhibition introduces an empathogenic dimension — elevated synaptic serotonin engages reward and social bonding circuits in a manner partially analogous to MDMA, though through a different mechanism.
Whether 5-MeO-DiPT promotes neuroplasticity (new neural connections) as other serotonergic psychedelics do remains untested. The dose threshold for neurotoxicity in humans is unknown — rodent damage occurs at doses far exceeding typical human use,[8] but the safety margin has not been characterized.
Subjective Effects[edit]
5-MeO-DiPT produces a body-centered psychedelic experience dominated by tactile intensification, auditory distortion, and physical stimulation — with visual effects notably subdued compared to most tryptamines. At lower doses the experience tends toward sociable euphoria and sensory sharpening; higher doses bring stronger perceptual distortion, more pronounced gastrointestinal discomfort, and greater risk of anxious overstimulation. Set and setting modulate the emotional character substantially: the same dose can produce warm sociability or restless anxiety depending on context.
Within the tryptamine class, 5-MeO-DiPT occupies a hybrid position between psilocybin (more visual, less stimulating) and MDMA (shared tactile warmth and mood elevation, different mechanism). The closest experiential comparator is 5-MeO-MiPT, which shares the tactile emphasis and 5-methoxy substitution but differs in potency and duration.
Effect Grid
At common doses (10–15 mg oral), the characteristic 5-MeO-DiPT profile fully manifests. Tactile enhancement becomes pronounced — skin sensitivity, body warmth, and sexual arousal intensify markedly. Auditory distortion emerges: pitch shifting, enhanced music appreciation, and novel auditory texturing. Visual effects remain moderate relative to other tryptamine psychedelics: mild open-eye patterning, color saturation, movement trails, and surface drifting. Mood elevation and euphoria are prominent. Thought connectivity increases, sometimes producing rapid ideation.
Physically, stimulation is notable — restlessness, jaw tension, and increased heart rate are common. Nausea and diarrhea are among the most frequently reported adverse effects at this range. Pupil dilation is evident. The experience demands 4–6 hours of commitment, with residual stimulation potentially extending several hours beyond.
Modeled from the effect's dose-dependence curve — not per-substance measurements.
Tracers · Brightness alteration · Geometry · Light sensitivity · Sound sensitivity · Touch enhancement · Visual breathing · Depth perception distortion · Perspective distortion · After-images · Auditory enhancement · Auditory misinterpretation · Visual morphing · Symmetrical texture repetition · Visual diffraction · Proprioceptive distortion · Spatial disorientation · Vestibular distortion · Visual acuity enhancement · Synesthesia · Object transformations · Internal hallucinations · Auditory hallucinations · External hallucinations
Sound sensitivity · Touch enhancement · Visual breathing · Depth perception distortion · Perspective distortion · After-images · Auditory enhancement · Auditory misinterpretation · Visual morphing · Symmetrical texture repetition · Visual diffraction · Proprioceptive distortion · Spatial disorientation · Vestibular distortion · Visual acuity enhancement · Synesthesia · Object transformations · Internal hallucinations · Auditory hallucinations · External hallucinations
Spontaneous body sensations · Diarrhea · Sexual arousal enhancement · Tactile euphoria · Nausea · Muscle tension · Restlessness · Wakefulness · Dehydration sensation · Appetite suppression · Dizziness · Dry mouth · Heart rate perception changes · Insomnia · Physical fatigue · Tingling / electric sensations · Vibrations / buzzing · Bodily pressures · Headache · Bodily lightness · Excessive sweating · Motor control impairment · Temperature dysregulation · Trembling · Vomiting
Tactile euphoria · Nausea · Muscle tension · Restlessness · Wakefulness · Dehydration sensation · Appetite suppression · Dizziness · Dry mouth · Heart rate perception changes · Insomnia · Physical fatigue · Tingling / electric sensations · Vibrations / buzzing · Bodily pressures · Headache · Bodily lightness · Excessive sweating · Temperature dysregulation · Trembling · Vomiting
Pattern recognition enhancement · Conceptual thinking · Immersion enhancement · Memory suppression · Cognitive impairment · Focus suppression · Introspection enhancement · Thought acceleration · Thought connectivity · Thought loops · Confusion · Information processing suppression · Memory fragmentation · Thought disorganization · Delusions
Memory suppression · Cognitive impairment · Focus suppression · Introspection enhancement · Thought acceleration · Thought connectivity · Thought loops · Confusion · Information processing suppression · Memory fragmentation · Thought disorganization
Anxiety
Sociability enhancement · Derealization · Emotional susceptibility · Depersonalization · Boundary dissolution · Ego dissolution
Boundary dissolution · Ego dissolution
Timeline
First alerts appear as subtle body awareness shift, mild warmth, and faint tactile sensitivity. Gastrointestinal unease (mild nausea) may begin before perceptual effects emerge.
Effects build noticeably: tactile sensitivity sharpens, auditory perception begins to shift, and stimulation increases. Nausea typically peaks during this phase. Mood elevation and body buzz emerge.
Full effect intensity reached approximately 60–90 minutes post-ingestion. Tactile enhancement, auditory distortion, visual effects, and cognitive shifts are at maximum. Sexual arousal enhancement is most pronounced.
Effects plateau at reduced intensity after peak. Perceptual distortions persist but feel more manageable. Stimulation remains prominent.
Gradual return toward baseline. Perceptual effects diminish progressively, though residual stimulation and tactile sensitivity may linger. Cognitive clarity returns.
Residual stimulation, mild mood elevation, and subtle body awareness may persist for several hours. Some individuals report stimulation lasting 10–14 hours post-ingestion, likely reflecting CYP2D6 metabolizer variability.
⚠ Do not drive or operate machinery until all residual stimulation has fully resolved and a full night of sleep has been obtained.
Safety[edit]
- Acute toxicity
- Low
- Chronic toxicity
- Moderate
- Withdrawal
- None
- Tolerance buildup
- rapid
- Tolerance reset
- 7 days
- Physical
- None
- Psychological
- Low
- Compulsive redosing
- Negligible
- Dose escalation
- Negligible
- Cross-tol.
- psilo · LSD · DMT
Toxicity
Acute toxicity
No lethal dose has been established in any species, and no human death attributed solely to 5-MeO-DiPT has been published.[3] The toxic dose in humans is unknown.safety citation needed
Reported acute adverse effects include[7][21][22][23]:
- Gastrointestinal: nausea, vomiting, and diarrhea — the most consistently reported adverse effects
- Cardiovascular: Rapid heart rate and elevated blood pressure
- Neurological: headache; possible seizures at high doses
- Autonomic: Dilated pupils, elevated body temperature
Animal neurotoxicity
Rodent studies at high doses document DNA damage lasting up to 60 days, decreased dopamine-related neurochemicals, and markers of cell death in brain tissue.[8][9] Repeated exposure during adolescence impaired learning and memory in adulthood.[24]
These doses substantially exceed typical human psychoactive doses. Direct extrapolation to human neurotoxicity is not warranted, but the concern cannot be dismissed.
Psychological risks
Anxiety, paranoia, and psychosis can occur — particularly at higher doses or in predisposed individuals.[23][7] A separate case in Japan documented a homicide during psychosis attributed to combined use of 5-MeO-DiPT and 5-MeO-MiPT.[13]
One documented case describes a delusional state lasting two months in a person with no prior psychiatric history, later re-triggered by an unrelated aromatic substance.[20] This pattern — sensitization — means prior 5-MeO-DiPT use may lower the threshold for future psychosis from later exposures. No data on HPPD specific to 5-MeO-DiPT have been published.
Tolerance & dependence
Tolerance develops rapidly through serotonin downregulation, consistent with other serotonergic psychedelics. Cross-tolerance with psilocybin, LSD, and DMT is expected. No physical dependence or withdrawal has been documented.
Paradoxically, while short-term tolerance to psychedelic effects builds quickly, repeated use may produce long-term sensitization to psychosis — a reverse tolerance operating on a different axis.[20] DiPT, a related compound, showed hallucinogen-like stimulus effects in rats,[25] suggesting behavioral abuse potential without evidence of compulsive use.
Drug Interactions
The combination of serotonin reuptake inhibitor and direct receptor activation creates compounded overload risk with other serotonergic substances.
- MAOIs block serotonin breakdown; combined with 5-MeO-DiPT's dual serotonergic action, this creates potentially fatal overactivation.[10][26] This applies to irreversible MAOIs (phenelzine, tranylcypromine) and reversible MAOIs (moclobemide, harmine/harmaline in ayahuasca)
- MDMA forces serotonin release through the same transporter 5-MeO-DiPT blocks, creating dual-mechanism overload[27]
- Tramadol adds serotonin and norepinephrine reuptake inhibition and lowers the seizure threshold[10]
- CYP2D6 inhibitors (fluoxetine, paroxetine, bupropion) impair metabolism, increasing drug exposure[11][10]
- Cocaine combines dopaminergic and serotonergic enhancement, increasing cardiovascular stress and body temperature risk[8]
Contraindications
7 knownPersonal or family history of psychotic disorders is the most significant psychiatric contraindication, given documented prolonged psychosis and sensitization.[20] Heart conditions increase risk from elevated heart rate and blood pressure.
CYP2D6 poor metabolizer status — genetic or medication-induced — increases exposure and toxicity risk.[11][10] Prior 5-MeO-DiPT use itself is a risk factor: sensitization may leave prior users vulnerable to psychotic episodes from subsequent exposures.[20] Pregnancy and breastfeeding are absolute contraindications given absent reproductive safety data and documented genotoxicity in animals.[8]
Harm Reduction[edit]
Forms & Identification
5-MeO-DiPT typically circulates as a powder or pressed into tablets. It is active at low milligram doses, so accurate measurement requires a milligram-precision scale — estimating by eye is dangerous. Reagent testing can distinguish it from other tryptamines but cannot confirm purity or dose.
CYP2D6 metabolism varies significantly between individuals. Two people taking identical measured doses may experience substantially different intensities and durations.
Guidelines
- Test all material with reagent kits before use
- Weigh doses with a milligram-precision scale — never estimate
- Start with the lowest effective dose, especially if CYP2D6 metabolizer status is unknown
- Allow at least 90 minutes before considering any redose — onset can be slow and variable
- Eat lightly or not at all in the 2–3 hours before dosing to reduce nausea
- Have a sober sitter present, especially at higher doses or for first experiences
- Keep the environment calm and controllable — have a quiet space available for retreat
- Stay hydrated but avoid excessive water intake
Set & Setting
The body-centered, socially engaging character of the experience makes environment particularly influential. A familiar, comfortable setting with trusted company reduces the likelihood of anxious overstimulation. Gastrointestinal effects are common — access to a bathroom and eating lightly before dosing are practical considerations.
First experiences should include an experienced, sober companion present.
Aftercare & integration. The body load and gastrointestinal effects can leave users physically drained. Rest, gentle nutrition, and hydration in the hours after support recovery. If the experience involved significant anxiety, unexpected emotional intensity, or perceptual disturbance, journaling or talking it through can help.
If unusual perceptual changes, anxiety, or mood disturbance persist beyond 48 hours, consult a healthcare professional. The documented risk of sensitization means lingering psychological effects after 5-MeO-DiPT use warrant more caution than after other psychedelics.
Recovery & Support
5-MeO-DiPT does not produce physical dependence, and compulsive use is rare in the serotonergic psychedelic class. If use has become a recurring pattern connected to sexual activity or social settings, addressing the underlying motivation may be more useful than focusing on the substance itself. Psychedelic integration therapists, harm reduction organizations, and peer support communities can provide nonjudgmental guidance.
For individuals experiencing lasting psychological effects — particularly sensitization-related psychotic symptoms — psychiatric evaluation is appropriate.
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Recognizing an emergency: Severe nausea with inability to keep fluids down, chest pain, rapid or irregular heartbeat, dangerously elevated body temperature, seizures, loss of consciousness, or complete disconnection from reality with self-harm risk.
Immediate steps:
- 1. Call emergency services if the person is unconscious, seizing, overheating, or showing signs of serotonin overload — rigid muscles, rapid heart rate, high temperature, agitation
- 2. Do not leave the person alone
- 3. Move them to a cool, quiet environment
- 4. If unconscious but breathing, place in the recovery position
- 5. Do not induce vomiting
- 6. Do not restrain unless there is immediate danger of self-harm
What to tell the dispatcher: Name the substance (5-MeO-DiPT / "Foxy"), estimated amount taken, time of ingestion, and current symptoms. Good Samaritan laws in many jurisdictions protect callers who report drug-related emergencies.
No specific reversal agent exists for 5-MeO-DiPT. Treatment is supportive.
Legal Status[edit]
5-MeO-DiPT is a controlled substance in the United States, Japan, and Australia, and is regulated as a new psychoactive substance in the United Kingdom.
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| United States | Schedule I (Controlled Substances Act) | Temporarily placed April 4, 2003 as imminent hazard;[12] permanently scheduled 2004[6] |
| Japan | Controlled (Narcotics and Psychotropics Control Law) | Restricted April 2005 following abuse reports and violent incidents[13] |
| United Kingdom | Psychoactive Substances Act 2016 | Illegal to produce, supply, or import; simple possession not criminalized. Not controlled under the Misuse of Drugs Act 1971 (unlike 5-MeO-DMT, which is Class A)[28] |
| Australia | Illegal (Poisons Standard) | Controlled substance; specific scheduling details not confirmed from primary sourcescitation needed |
| Canada | Not confirmed | Not explicitly listed in CDSA schedules; may fall under analog provisionscitation needed |
| Germany / EU | Varies by member state | Not confirmed; NPS legislative approaches differ across EU member statescitation needed |
In the UK, the distinction between the Psychoactive Substances Act and the Misuse of Drugs Act carries practical significance: PSA offences carry lower maximum penalties, and simple possession is not criminalized.[28]
Legal status varies by jurisdiction and changes over time. This information is not legal advice — verify current status in any relevant jurisdiction before acting.
Safety[edit]
- Acute toxicity
- Low
- Chronic toxicity
- Moderate
- Withdrawal
- None
- Tolerance buildup
- rapid
- Tolerance reset
- 7 days
- Physical
- None
- Psychological
- Low
- Compulsive redosing
- Negligible
- Dose escalation
- Negligible
- Cross-tol.
- psilo · LSD · DMT
Toxicity
Acute toxicity
No lethal dose has been established for 5-MeO-DiPT in any species, and no human fatalities attributed solely to the compound have been published.[3] The toxic dose in humans is unknown.safety citation needed
Reported acute adverse effects include[7][23][24][25]:
- Gastrointestinal: nausea, vomiting, and diarrhea — the most consistently reported adverse effects
- Cardiovascular: Rapid heart rate and elevated blood pressure
- Neurological: headache; possible seizures at high doses
- Autonomic: Dilated pupils, elevated body temperature
Animal neurotoxicity
Rodent studies at 5–20 mg/kg document DNA damage persisting up to 60 days, decreased dopamine-related neurochemicals, and markers of cell death in brain tissue.[8][9] Repeated adolescent exposure impaired learning and memory in adulthood.[26]
These doses substantially exceed typical human psychoactive doses on a mg/kg basis. Direct extrapolation to human neurotoxicity is not warranted, but the findings identify a genuine concern that cannot be dismissed.
Psychological risks
Anxiety, paranoia, and psychosis can occur — particularly at higher doses or in predisposed individuals.[25][7]
A documented case describes a prolonged delusional state lasting two months in a 30-year-old male with no prior psychiatric history, which was subsequently re-triggered by an unrelated aromatic substance.[22] The authors proposed sensitization — prior exposure lowering the threshold for future drug-induced psychosis. This carries clinical significance: individuals with a history of 5-MeO-DiPT use may be vulnerable to psychotic episodes from later psychoactive exposures.
A separate case documented a homicide in Japan committed during severe psychosis attributed to combined use of 5-MeO-DiPT and 5-MeO-MiPT.[13]
No data on HPPD (HPPD) specific to 5-MeO-DiPT have been published.
Tolerance & dependence
Tolerance develops rapidly through 5-HT₂A downregulation, consistent with the pattern seen across serotonergic psychedelics. Cross-tolerance with psilocybin, LSD, and DMT is expected. No 5-MeO-DiPT-specific tolerance studies in humans exist.
Paradoxically, while short-term tolerance to psychedelic effects develops quickly, repeated use may produce long-term sensitization of the neural substrate for psychosis — a reverse tolerance effect operating on a different neurobiological axis.[22]
No physical dependence or withdrawal has been documented. No animal self-administration studies have been conducted. DiPT showed hallucinogen-like discriminative stimulus effects in rats,[27] establishing behavioral abuse liability potential without addressing compulsive use.
Drug Interactions
The combination of serotonin reuptake inhibitor and direct receptor agonism creates compounded serotonin syndrome risk.
MAOIs are the most dangerous interaction. They block serotonin breakdown; combined with 5-MeO-DiPT's reuptake inhibition and direct receptor activation, this creates a three-mechanism convergence on serotonergic overactivation that is potentially fatal.[10][28] This applies to irreversible MAOIs (phenelzine, tranylcypromine) and reversible MAOIs (moclobemide, harmine/harmaline in ayahuasca preparations).
Tramadol adds serotonin and norepinephrine reuptake inhibition to 5-MeO-DiPT's existing serotonergic load and also lowers seizure threshold.[10]
MDMA and other serotonin releasing agents create dual-mechanism overload: 5-MeO-DiPT blocks the SERT while MDMA forces serotonin release through it.[29]
CYP2D6 inhibitors — including fluoxetine, paroxetine, and bupropion — impair metabolism of 5-MeO-DiPT, effectively increasing drug exposure.[11][10]
Cocaine combines dopaminergic and serotonergic enhancement, creating cardiovascular stress and elevated body temperature risk.[8]
Contraindications
7 knownPersonal or family history of psychotic disorders is the most significant psychiatric contraindication, given documented prolonged psychosis and sensitization.[22]
CYP2D6 poor metabolizer status — genetic or medication-induced — increases exposure and toxicity risk.[11][10]
Prior 5-MeO-DiPT use itself constitutes a risk factor: sensitization may leave prior users vulnerable to psychotic episodes from subsequent psychoactive exposures at otherwise sub-threshold doses.[22]
Heart conditions increase risk from elevated heart rate and blood pressure effects. Pregnancy and breastfeeding are absolute contraindications given absent reproductive safety data and documented genotoxicity in animals.[8]
Harm Reduction[edit]
Forms & Identification
5-MeO-DiPT typically circulates as a powder or pressed into tablets. Because it is active at low milligram doses, accurate measurement requires a milligram-precision scale — volumetric estimation or eyeballing is dangerous. Reagent testing can help distinguish it from other tryptamines but cannot confirm purity or dose. Given the compound's sensitivity to CYP2D6 metabolism, two individuals taking identical measured doses may experience substantially different intensities and durations.
Guidelines
- Test all material with reagent kits before use
- Weigh doses with a milligram-precision scale — never estimate
- Start with the lowest effective dose, especially if CYP2D6 metabolizer status is unknown
- Allow at least 90 minutes before considering any redose — onset can be slow and variable
- Eat lightly or not at all in the 2–3 hours before dosing to reduce nausea
- Have a sober sitter present, especially at higher doses or for first experiences
- Keep the environment calm and controllable — have a quiet space available for retreat
- Stay hydrated but avoid excessive water intake
Set & Setting
The body-centered, socially engaging nature of the 5-MeO-DiPT experience makes environmental context particularly influential. A familiar, comfortable environment with trusted company reduces the likelihood of anxious overstimulation. Because gastrointestinal effects are common, access to a bathroom and a light stomach before dosing are practical considerations. First-time users should have an experienced, sober companion present.
Aftercare & integration. The body load and gastrointestinal effects of 5-MeO-DiPT can leave users physically drained. Rest, gentle nutrition, and hydration in the hours after the experience support recovery. If the experience involved significant psychological content — anxiety, unexpected emotional intensity, or perceptual disturbance — journaling or discussing the experience with a trusted person can help process it.
If unusual perceptual changes, anxiety, or mood disturbance persist beyond 48 hours, consult a healthcare professional. The documented risk of sensitization means that lingering psychological effects after 5-MeO-DiPT use warrant more caution than they might after other psychedelics.
Recovery & Support
5-MeO-DiPT does not produce physical dependence, and compulsive use patterns are rare for the serotonergic psychedelic class. If use has become a recurring pattern connected to sexual activity or social settings, addressing the underlying motivation may be more useful than focusing on the substance itself. Psychedelic integration therapists, harm reduction organizations, and peer support communities can provide nonjudgmental guidance.
For individuals experiencing lasting psychological effects — particularly the sensitization-related psychotic symptoms documented in clinical literature — psychiatric evaluation is appropriate.
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Recognizing an emergency: Severe nausea with inability to keep fluids down, chest pain, rapid or irregular heartbeat, body temperature that feels dangerously elevated through clothing, seizures, loss of consciousness, or complete disconnection from reality with self-harm risk.
Immediate steps:
- 1. Call emergency services if the person is unconscious, seizing, hyperthermic, or showing signs of serotonin syndrome (rigid muscles, tachycardia, high temperature, agitation)
- 2. Do not leave the person alone
- 3. Move them to a cool, quiet environment
- 4. If unconscious but breathing, place in the recovery position
- 5. Do not induce vomiting
- 6. Do not restrain unless there is immediate danger of self-harm
What to tell the dispatcher: Name the substance (5-MeO-DiPT / "Foxy"), estimated amount taken, time of ingestion, and current symptoms. Good Samaritan laws in many jurisdictions protect callers who report drug-related emergencies.
No specific reversal agent exists for 5-MeO-DiPT. Treatment is supportive.
Legal Status[edit]
5-MeO-DiPT is a controlled substance in the United States, Japan, and Australia, and is regulated as a new psychoactive substance in the United Kingdom. No international treaty specifically lists it; control has been implemented through national legislation.
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| United States | Schedule I (Controlled Substances Act) | Temporarily placed April 4, 2003 as imminent hazard;[12] permanently scheduled 2004[6] |
| Japan | Controlled (Narcotics and Psychotropics Control Law) | Restricted April 2005 following abuse reports and violent incidents[13] |
| United Kingdom | Psychoactive Substances Act 2016 | Illegal to produce, supply, or import; simple possession not criminalized. Not controlled under the Misuse of Drugs Act 1971 (unlike 5-MeO-DMT, which is Class A)[30] |
| Australia | Illegal (Poisons Standard) | Controlled substance; specific scheduling details not confirmed from primary sourcescitation needed |
| Canada | Not confirmed | Not explicitly listed in CDSA schedules; may fall under analog provisionscitation needed |
| Germany / EU | Varies by member state | Not confirmed; NPS legislative approaches differ across EU member statescitation needed |
The distinction between UK classification under the Psychoactive Substances Act versus the Misuse of Drugs Act carries practical significance: PSA offences carry lower maximum penalties, and simple possession is not criminalized.[30]
Frequently asked questions
How long does 5-MeO-DiPT last?
Total duration by route of administration — Oral: 3 – 8 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 5-MeO-DiPT?
Psychedex publishes a dosage table for 5-MeO-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 5-MeO-DiPT?
The highest-severity documented interactions for 5-MeO-DiPT: MAOIs (Lethal), 5-HTP, Tryptophan (Dangerous), Alpha-2 adrenergic receptor antagonist (Dangerous), Amphetamines (Dangerous), Anticholinergics (Dangerous). See the interactions section for the full list with mechanisms and severity levels.
Is 5-MeO-DiPT addictive?
Psychedex records tolerance and dependence data rather than a yes/no rating. Recorded tolerance indicators for 5-MeO-DiPT: tolerance builds rapid; full reset takes 7 days; cross-tolerance develops with psilocybin, LSD, DMT, mescaline, 5-MeO-DMT. See the article's dependence and safety sections for recorded dependence data.
experience reports
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First-person accounts of subjective effects, timing, and outcomes — submitted for harm reduction.
references
- [1] ^abHagino Y, Hall FS, Uhl GR, Sora I, Ikeda K (2021) Dual actions of 5-MeO-DIPT at the serotonin transporter and serotonin 5-HT1A receptor in the mouse striatum and prefrontal cortex. — Neuropsychopharmacology Reports doi:10.1002/npr2.12161
- [2] ^abcdFantegrossi WE, Harrington AW, Kiessel CL, Eckler JR, Rabin RA, Winter JC, Coop A, Rice KC, Woods JH (2006) Hallucinogen-like actions of 5-methoxy-N,N-diisopropyltryptamine in mice and rats. — Pharmacology, Biochemistry, and Behavior PMID:16460788
- [3] ^abcLi K, Li N, Chen Y, Li X, Qiao Y, Wang D, Di B, Xu P (2025) Effects of three tryptamines: alpha-methyltryptamine, 5-methoxy-alpha-methyltryptamine, and 5-methoxy-N,N-diisopropyltryptamine on acute toxicity, locomotor activity, and hallucinogenic behavior in mice. — Behavioural pharmacology doi:10.1097/fbp.0000000000000841
- [4] ^abShulgin AT, Carter MF (1980) N,N-Diisopropyltryptamine (DIPT) and 5-methoxy-N,N-diisopropyltryptamine (5-MeO-DIPT). Two orally active tryptamine analogs with CNS activity. — Communications in Psychopharmacology PMID:6949674
- [5] ^abSmolinske SC, Rastogi R, Schenkel S (2005) Foxy methoxy: a new drug of abuse. — Journal of Medical Toxicology PMID:18072099
- [6] ^abcDEA Deputy Administrator (2004) Schedules of controlled substances: placement of alpha-methyltryptamine and 5-methoxy-N,N-diisopropyltryptamine into schedule I of the Controlled Substances Act. Final rule. — Federal Register PMID:15455477
references
- [1] ^abcHagino Y, Hall FS, Uhl GR, Sora I, Ikeda K (2021) Dual actions of 5-MeO-DIPT at the serotonin transporter and serotonin 5-HT1A receptor in the mouse striatum and prefrontal cortex. — Neuropsychopharmacology Reports doi:10.1002/npr2.12161
- [2] ^abcdFantegrossi WE, Harrington AW, Kiessel CL, Eckler JR, Rabin RA, Winter JC, Coop A, Rice KC, Woods JH (2006) Hallucinogen-like actions of 5-methoxy-N,N-diisopropyltryptamine in mice and rats. — Pharmacology, Biochemistry, and Behavior PMID:16460788
- [3] ^abcLi K, Li N, Chen Y, Li X, Qiao Y, Wang D, Di B, Xu P (2025) Effects of three tryptamines: alpha-methyltryptamine, 5-methoxy-alpha-methyltryptamine, and 5-methoxy-N,N-diisopropyltryptamine on acute toxicity, locomotor activity, and hallucinogenic behavior in mice. — Behavioural pharmacology doi:10.1097/fbp.0000000000000841
- [4] ^abShulgin AT, Carter MF (1980) N,N-Diisopropyltryptamine (DIPT) and 5-methoxy-N,N-diisopropyltryptamine (5-MeO-DIPT). Two orally active tryptamine analogs with CNS activity. — Communications in Psychopharmacology PMID:6949674
- [5] ^abSmolinske SC, Rastogi R, Schenkel S (2005) Foxy methoxy: a new drug of abuse. — Journal of Medical Toxicology PMID:18072099
- [6] ^abcDEA Deputy Administrator (2004) Schedules of controlled substances: placement of alpha-methyltryptamine and 5-methoxy-N,N-diisopropyltryptamine into schedule I of the Controlled Substances Act. Final rule. — Federal Register PMID:15455477