DOI
2,5-dimethoxy-4-iodoamphetamine
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DOI (2,5-dimethoxy-4-iodoamphetamine) is a synthetic psychedelic of the phenethylamine class. It is the most potent member of the DOx amphetamine series, distinguished by an exceptionally long duration of action. DOI is a full agonist at 5-HT₂A receptors, producing its effects through non-canonical Gᵢ signalling that disrupts normal sensory filtering.[1]
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LSD, psilocybin, mescaline +3 moreLSD, psilocybin, mescaline, DMT, DOB, DOC show less
First synthesized in 1973 as part of a structure-activity study of DOM analogs,[2] DOI achieved its primary significance not as a recreational drug but as the field-standard pharmacological tool for 5-HT₂A receptor research — its radioiodinated form became the prototypical radioligand in the late 1980s.[3] It remains largely confined to laboratory use, with minimal recreational adoption due to its extreme duration and body load.
Subjective effects include geometric visual patterns, color enhancement, stimulation, empathy enhancement, and time alteration. The experience is defined by its sheer temporal scale — a 16–30 hour arc that passes through multiple psychological states and energy levels, accompanied by a pronounced physical stimulation that distinguishes it from tryptamine psychedelics.[4] Vasoconstriction, muscle tension, and physical exhaustion from extended wakefulness are characteristic unsought effects.
DOI produces no physical dependence, and no confirmed human fatalities from pure DOI have been published.[5] The primary risks are cardiovascular stress from sustained vasoconstriction over 16–30 hours and psychological distress during an experience too long to simply wait out — compounded by the danger of misidentification when DOx compounds are sold as LSD on blotter.[6] Human pharmacokinetic data remain entirely absent; the current understanding rests on decades of animal research and limited self-report data.
History[edit]
Discovery
DOI was first synthesized in 1973 by R.T. Coutts and J.M. Malicky at the University of Alberta as part of a systematic exploration of 4-substituted analogs of DOM.[2] Alexander Shulgin later characterized the compound through personal bioassays, documenting the 1.5–3 mg active dose range and 16–30 hour duration that remain the primary human reference.[4]
Scientific Significance
DOI's transformation from research curiosity to indispensable tool occurred in the late 1980s when the radioiodinated form [¹²⁵I]-R-(−)-DOI was developed, becoming the prototypical 5-HT₂A radioligand.[3] By the 1990s it served simultaneously as a radioligand for receptor binding studies, a reference agonist for functional assays, and the primary stimulus in the head-twitch response model of hallucinogenesis.[5] Contemporary research has extended into anti-inflammatory applications[7][8] and non-hallucinogenic derivative development.[1]
Recreational Context
DOI has seen negligible recreational adoption — its extreme duration, significant body load, and availability of more manageable alternatives limit appeal. The primary harm concern is misidentification: DOx compounds have appeared on blotter paper sold as LSD at music festivals, documented by drug checking services at the 2014 Boom Festival in Portugal.[6]
The name "DOI" follows DOx series nomenclature: Dimethoxy (the 2,5-dimethoxy pharmacophore), O (denoting the oxygen-bearing substitution pattern), and I (iodine at position 4). The compound holds almost no street reputation — it exists primarily in the cultural awareness of psychedelic researchers and a small circle of experienced psychonauts who regard it as an endurance test rather than a recreational choice.
Chemistry[edit]
Structural Class
DOI belongs to the DOx series of substituted amphetamines — a family of 2,5-dimethoxy-4-substituted phenylisopropylamine psychedelics derived from DOM.[9] The defining structural features are a phenyl ring with methoxy groups at positions 2 and 5 (the pharmacophore required for high-affinity serotonin receptor binding), an iodine atom at position 4, and a 2-aminopropyl side chain.
The iodine substituent distinguishes DOI from other DOx members (DOB: bromine; DOC: chlorine; DOM: methyl) and confers the highest serotonin receptor binding affinity within the series. As the heaviest halogen used in the DOx family, iodine contributes substantial molecular weight and influences the electronic character of the ring.
| Molecular formula | C₁₁H₁₆INO₂ |
| Molecular weight | 321.15 g/mol (free base) |
Structure-Activity Relationships
The amphetamine backbone (alpha-methyl group on the side chain) differentiates DOx compounds from the related 2C-x phenethylamine series and confers increased metabolic stability, oral bioavailability, and dramatically extended duration of action. Where 2C-I (the phenethylamine equivalent lacking the alpha-methyl) lasts 6–10 hours, DOI's additional methyl group extends activity to 16–30 hours by resisting enzymatic breakdown.
The 2,5-dimethoxy pattern is essential — removal or repositioning of either methoxy group abolishes high-affinity serotonin receptor binding.[9] The 4-position substituent modulates potency and duration across the series.
Stereochemistry
DOI has one chirality center at the alpha-carbon, yielding R and S enantiomers. The R-(−) enantiomer is the pharmacologically active form, as demonstrated by its exclusive use in radioligand studies[3] and anti-inflammatory research.[7][8] Most published research and all known recreational material uses the racemic mixture (±)-DOI. DOI is commercially available as the hydrochloride salt.[10]
Pharmacology[edit]
Mechanism of Action
DOI is a potent, direct full agonist at serotonin 5-HT₂A and 5-HT₂C receptors.[11] Despite its amphetamine scaffold, DOI does not release monoamines — it has no significant affinity at dopamine, serotonin, or norepinephrine transporters.[12] Its psychedelic effects arise entirely from direct receptor activation.
The hallucinogenic activity specifically requires non-canonical Gᵢ signalling at 5-HT₂A, rather than the classical Gq pathway that drives phospholipase C activation.[1] This discovery resolved a longstanding puzzle about why some potent 5-HT₂A agonists (like lisuride) lack hallucinogenic effects. DOI simultaneously engages the Gq pathway, which drives expression of plasticity-related genes in the cortex.[13]
The full behavioral response to DOI requires the 5-HT₂A–mGluR2 receptor complex. In animals lacking mGluR2, the characteristic head-twitch response is abolished and hallucinogen-specific gene activation does not occur.[14]
DOI also enhances dopamine D2 signalling through D2–5-HT₂A receptor complexes in the striatum — an effect shared with LSD but absent for non-hallucinogenic 5-HT₂A agonists.[15] At the hormonal level, DOI stimulates release of stress hormones, oxytocin, and prolactin.[16]
Pharmacokinetics
No controlled human pharmacokinetic studies have been published for DOI. All temporal parameters derive from self-report data.[4]
Onset occurs 1–2 hours after oral ingestion, with total duration extending 16–30 hours. Plasma half-life, bioavailability, and metabolic pathways have not been determined in humans. As a substituted amphetamine, DOI is likely subject to liver enzyme-mediated breakdown, but the 4-iodo substituent may resist metabolic removal — potentially contributing to the extreme duration.inferred
The duration substantially exceeds that of structurally related 2C-I (6–10 hours), attributable to the alpha-methyl group conferring resistance to enzymatic degradation.
Neuroscience[edit]
Where It Acts
DOI activates 5-HT₂A receptors concentrated on layer V pyramidal neurons in the neocortex, triggering expression of plasticity-associated genes including BDNF and Arc.[13] A single dose produces measurable increases in brain volume across sensory and association cortical areas within 24 hours, accompanied by improved cognitive flexibility persisting at least one week.[17]
In the claustrum — a thin brain structure proposed as a consciousness integration hub — DOI's effects are unexpectedly mediated by 5-HT₂C rather than 5-HT₂A receptors.[18] This suggests the psychedelic experience emerges from circuit-specific receptor engagement rather than uniform activation of a single receptor type.
Why It Matters
DOI qualifies as a psychoplastogen — a compound that promotes structural and functional neural reorganization.[19] The documented gene expression changes[13] and brain volume increases[17] support this classification. The 2026 discovery that hallucinogenic effects require Gᵢ signalling while plasticity operates through the Gq pathway[1] opens the possibility of separating therapeutic benefits from hallucinogenic effects — a central goal of modern psychedelic drug development.
The mechanistic basis for DOI's 16–30 hour duration remains unknown — it could reflect slow elimination, persistent receptor occupancy, or sustained downstream signalling cascades. Whether the structural brain changes observed in animals translate to humans is unconfirmed. The relative contribution of 5-HT₂C (versus 5-HT₂A) to human subjective experience remains an open question raised by the claustrum findings.[18]
Subjective Effects[edit]
DOI produces a psychedelic experience defined by temporal endurance and physical activation. The 16–30 hour arc passes through distinct phases — a slow-building onset gives way to a plateau that can sustain for 8–12 hours before a protracted descent. Set and setting exert powerful influence, and the sheer length of the experience means multiple environments, moods, and energy states will be traversed regardless of preparation.
Compared to LSD, DOI is reported as more physically stimulating with greater body load (vasoconstriction, muscle tension) and a less intricate cognitive headspace. Where LSD's 8–12 hours demand a committed day, DOI demands surrender of an entire waking cycle — a fundamentally different level of temporal commitment that limits the experience to those willing to plan around it.
Effect Grid
At common doses (1.5–2.5 mg oral), the full psychedelic experience manifests: pronounced visual drifting, color alteration and enhancement, symmetrical texture repetition, after-images and tracers, and object transformations. Thought connectivity increases substantially — novel conceptual associations, pattern recognition enhancement, and analysis enhancement dominate the cognitive space. Emotional enhancement and empathy enhancement are prominent. Time alteration becomes significant.
Physically, vasoconstriction intensifies (cold hands and feet), muscle tension becomes persistent, bruxism may appear, and appetite is fully suppressed. Stimulation and wakefulness are pronounced throughout. Nausea is possible during the extended come-up.
The total experience spans 16–24 hours. Sleep is impossible for the first 12–16 hours. A full-day and overnight commitment in a safe environment is required.
Modeled from the effect's dose-dependence curve — not per-substance measurements.
Visual drifting · Music enhancement · Visual breathing · Perspective distortion · Symmetrical texture repetition · Tracers · Depth perception distortion · Auditory enhancement · Environmental patterning · Light sensitivity · Visual morphing · Holotropic state · After-images · Visual diffraction · Touch enhancement · Auditory distortion · Dreaming suppression · Peripheral vision distortion · Sound sensitivity · Spatial disorientation · Visual melting · Visual acuity enhancement · Auditory misinterpretation · Ganzfeld effect · Peripheral misidentification · Proprioceptive distortion · Sleep-transition hallucinations · Vestibular distortion · Visual haze / noise · Visual processing acceleration · Synesthesia · Visual magnification · Flashbacks · Object transformations · External hallucinations · Visual recursion · Internal hallucinations · Object activation · Perspective hallucinations · Auditory hallucinations · Environmental orbism / cubism · Visual flipping · Visual scenery slicing · Persisting hallucinations
Symmetrical texture repetition · Tracers · Depth perception distortion · Auditory enhancement · Environmental patterning · Light sensitivity · Visual morphing · Holotropic state · After-images · Visual diffraction · Touch enhancement · Auditory distortion · Dreaming suppression · Peripheral vision distortion · Sound sensitivity · Spatial disorientation · Visual melting · Visual acuity enhancement · Auditory misinterpretation · Ganzfeld effect · Peripheral misidentification · Proprioceptive distortion · Sleep-transition hallucinations · Vestibular distortion · Visual haze / noise · Visual processing acceleration · Synesthesia · Visual magnification · Flashbacks · Object transformations · External hallucinations · Visual recursion · Internal hallucinations · Object activation · Perspective hallucinations · Auditory hallucinations · Environmental orbism / cubism · Visual flipping · Visual scenery slicing · Persisting hallucinations
Wakefulness · Body scan awareness · Spontaneous body sensations · Body high · Insomnia · Muscle tension · Physical fatigue · Dehydration sensation · Dry mouth · Heart rate perception changes · Restlessness · Tingling / electric sensations · Nausea · Excessive sweating · Bodily pressures · Body schema distortion · Breathing alteration · Dizziness · Motor control impairment · Tactile euphoria · Vibrations / buzzing · Abnormal heartbeat · Involuntary body movements · Diarrhea · Sexual arousal enhancement · Bruxism · Headache · Laughter fits · Nasal congestion · Nystagmus (eye wobbles) · Trembling · Salivation · Vomiting · Motor control enhancement · Seizure threshold reduction · Bodily dissociation · Tactile hallucination
Body high · Insomnia · Muscle tension · Physical fatigue · Dehydration sensation · Dry mouth · Heart rate perception changes · Restlessness · Tingling / electric sensations · Nausea · Excessive sweating · Bodily pressures · Body schema distortion · Breathing alteration · Dizziness · Tactile euphoria · Vibrations / buzzing · Abnormal heartbeat · Involuntary body movements · Diarrhea · Sexual arousal enhancement · Bruxism · Headache · Laughter fits · Nasal congestion · Nystagmus (eye wobbles) · Trembling · Salivation · Vomiting · Motor control enhancement · Seizure threshold reduction · Bodily dissociation · Tactile hallucination
Pattern recognition enhancement · Immersion enhancement · Aesthetic enhancement · Introspection enhancement · Openness enhancement · Thought acceleration · Cognitive euphoria · Memory suppression · Cognitive flexibility · Cognitive impairment · Multiple thought streams · Creativity enhancement · Thought loops · Analysis enhancement · Cognitive fatigue · Confusion · Focus suppression · Increased nature relatedness · Information processing suppression · Memory fragmentation · Thought disorganization · Humor enhancement · Focus enhancement · Information processing enhancement · Motivation enhancement · Analysis suppression · Cognitive dysphoria · Memory replays · Motivation suppression · Synchronicity · Language suppression · Delusions · Amnesia · Delirium
Introspection enhancement · Openness enhancement · Thought acceleration · Cognitive euphoria · Memory suppression · Cognitive flexibility · Cognitive impairment · Multiple thought streams · Creativity enhancement · Thought loops · Analysis enhancement · Cognitive fatigue · Confusion · Focus suppression · Increased nature relatedness · Information processing suppression · Memory fragmentation · Thought disorganization · Humor enhancement · Focus enhancement · Information processing enhancement · Motivation enhancement · Analysis suppression · Cognitive dysphoria · Memory replays · Motivation suppression · Synchronicity · Language suppression · Amnesia · Delirium
Simultaneous emotions · Empathy enhancement · Euphoria · Irritability · Catharsis · Dysphoria
Catharsis · Dysphoria
Disinhibition · Communication suppression · Social connection · Trust enhancement · Flow state · Sociability enhancement · Automaticity · Ego inflation · Social disconnection · Boundary dissolution · Cognitive disconnection · Ego dissolution · Identity alteration
Flow state · Sociability enhancement · Automaticity · Ego inflation · Social disconnection · Boundary dissolution · Cognitive disconnection · Ego dissolution · Identity alteration
Time cessation
Transpersonal memory access · Transpersonal visions · Death-rebirth sequence · Voidness
Recursive awareness
Timeline
First alerts emerge 1–2 hours after ingestion: subtle mood shift, mild stimulation, slight color brightening. Easily mistaken for placebo at this stage.
Effects build gradually over 1. 5–3 hours. Visual enhancement, body load (vasoconstriction, muscle tension), and thought acceleration emerge progressively.
Maximum intensity sustained for 4–6 hours. Full visual phenomena, profound thought connectivity, emotional enhancement, and significant body load. The extended peak is DOI's defining temporal characteristic.
Effects diminish gradually but remain clearly perceptible for 4–7 hours. Visual phenomena recede before cognitive and stimulant effects. Body load persists.
Residual stimulation, mild visual enhancement, and wakefulness persist 2–4 hours beyond subjective plateau. Muscle tension and appetite suppression continue.
Residual mood alteration, mild cognitive fatigue, and physical recovery extend 8–24 hours post-resolution. Sleep quality may remain disrupted for 1–2 nights.
⚠ Do not drive or operate machinery until after a full night of restorative sleep following complete resolution of all effects.
Safety[edit]
- Acute toxicity
- Low
- Chronic toxicity
- Negligible
- Withdrawal
- None
- Tolerance buildup
- rapid
- Tolerance reset
- 12 days
- Physical
- None
- Psychological
- Negligible
- Compulsive redosing
- Negligible
- Dose escalation
- Negligible
- Cross-tol.
- LSD · psilo · mesc
Toxicity
No lethal dose has been established for DOI in any species, and no confirmed human fatalities from pure DOI ingestion have been published. In animal research, DOI has been administered across hundreds of experiments without reported mortality.[5]
Cardiovascular Effects
DOI produces vasoconstriction through 5-HT₂A activation in blood vessel walls.[20] Given the 16–30 hour duration, this represents sustained cardiovascular stress — elevated blood pressure and reduced peripheral blood flow persisting far longer than most psychedelics. No published case reports document DOI-specific cardiovascular events, but the mechanism predicts meaningful risk for anyone with pre-existing heart or blood pressure conditions.
Adulteration Risk
The most dangerous real-world toxicity scenario involves misidentification. DOx compounds have been distributed on blotter paper as LSD.[6] A user expecting LSD's 100–200 µg active range and 8–12 hour duration may redose when DOI's slower onset creates the impression of an inactive tab, potentially reaching dangerous doses. Related N-benzyl derivatives (25I-NBOMe) have caused fatalities, though these are pharmacologically distinct from DOI.[21]
Psychological Risks
The extreme duration is DOI's defining psychological hazard. A difficult experience cannot be waited out in a few hours — distress may persist for 16–30 hours with no option for rapid resolution. Specific risks include sustained anxiety and paranoia, physical and cognitive exhaustion from extended wakefulness, escalation of psychological crisis over many hours, and sleep deprivation compounding emotional distress.
No cases of Hallucinogen Persisting Perception Disorder (HPPD) specific to DOI have been published. No DOI-specific data exist on triggering psychotic episodes, though serotonin receptor activation as a class carries this risk in predisposed individuals.inferred
Tolerance & Dependence
Tolerance develops within 24 hours of a single dose, mediated by downregulation in frontal cortex.[22] In animal studies, daily dosing produces progressive tolerance, while 48-hour spacing allows full recovery.[23]
Full cross-tolerance exists between DOI and LSD. The non-hallucinogenic 5-HT₂A agonist lisuride does not produce cross-tolerance with DOI, suggesting tolerance is specific to the hallucinogenic signalling pathway.[22]
No evidence of physical dependence, withdrawal, or compulsive use has been published. The extreme duration and significant body load make repeated use inherently aversive.
Drug Interactions
Serotonergic Combinations
Tramadol is classified as dangerous in combination with DOI. The dual serotonergic action creates significant risk of serotonin syndrome — characterized by dangerously elevated body temperature, rapid heart rate, high blood pressure, muscle jerking, and seizures.safety citation needed
MAOIs (both irreversible and reversible) represent the highest theoretical risk. By blocking the breakdown of serotonin, MAOIs dramatically potentiate any serotonergic compound. No specific DOI + MAOI case exists, but the mechanism-based risk is severe.safety citation needed
SSRIs and SNRIs increase baseline serotonin levels. Chronic SSRI use may blunt DOI's effects through receptor adaptation; acute combinations carry additive serotonergic risk.
Vasoconstrictive Combinations
DOI's vasoconstriction[20] is compounded by co-administration of triptans, ergotamines, or high-dose stimulants. The 16–30 hour duration means vascular stress accumulates over an extended period.
Cannabis
No published data exist on DOI + cannabis interaction. Both compounds carry anxiety-amplifying potential at high doses; additive distress is plausible but unconfirmed.
Contraindications
No published contraindication data specific to DOI exist. The following are inferred from mechanism:
- Heart or blood pressure conditions: sustained vasoconstriction and stimulation over 16–30 hours pose meaningful cardiovascular risk
- Personal or family history of psychotic disorders: serotonin receptor activation can trigger psychotic episodes in predisposed individuals
- Seizure disorders: serotonin receptor activation may lower seizure threshold
- Concurrent serotonergic medication: SSRIs, SNRIs, MAOIs, tramadol — serotonin syndrome risk
- Pregnancy: vasoconstriction poses theoretical risk to placental blood flow; no reproductive toxicity data exist
Harm Reduction[edit]
Forms & Identification
DOI's primary identification challenge is distinguishing it from LSD when encountered on blotter paper. Both are active at microgram-to-low-milligram doses and can be laid on identical carrier media. The critical differentiator is taste: DOI on blotter often produces a noticeable bitter or metallic flavor, while LSD is tasteless. However, taste alone is not a reliable identification method.
Reagent testing provides important but incomplete information. An Ehrlich test that produces no reaction suggests the substance is not an indole (ruling out LSD), which should raise immediate suspicion if the material was sold as LSD. Quantitative testing through drug checking services is the only way to confirm identity and dose.
Guidelines
- Test all material with reagent kits before ingestion — verify it is not a more dangerous NBOMe compound
- Start at the low end of the dose range; the extremely long duration makes titration impractical once committed
- Clear a full 36-hour window: 24 hours for the experience plus 12 hours for sleep recovery
- Prepare food, water, and comfortable clothing in advance — appetite may be suppressed but hydration and nutrition matter over 20+ hours
- Keep the environment temperature-controlled; vasoconstriction can make cold feel more intense
- Have a trusted person aware of your timeline who can check in periodically
- Do not redose if effects haven't appeared within 2 hours — onset can be slow
- Avoid physical exertion during the experience; vasoconstriction increases cardiovascular demands
Set & Setting
DOI's 16–30 hour duration demands a fundamentally different level of preparation than shorter psychedelics. A full day and night must be cleared of obligations, with no driving, work, or childcare responsibilities for at least 24 hours. The setting must remain safe and accessible for the entire duration — a location that feels comfortable at 2 AM after 18 hours of continuous altered consciousness.
A trusted sitter who understands the timeline is strongly recommended. The sitter should be prepared for shifts, or multiple sitters should be arranged, since no single person can maintain attentive presence for 20+ hours. Mental preparation should include explicit acceptance that the experience cannot be shortened once begun.
Aftercare & integration. The primary aftercare need following DOI is physical recovery. Sleep is the first priority — the body has been awake and stimulated for 16–30 hours under vasoconstriction and elevated stress hormones. Do not attempt to process the experience intellectually until adequate rest has been obtained.
In the 48 hours following, expect fatigue, emotional sensitivity, and possible low mood as neurotransmitter systems rebalance. Light meals, hydration, gentle movement, and contact with trusted people support recovery. Journaling or integration conversations are best deferred 2–3 days until cognitive baseline returns.
If distressing psychological content persists beyond one week, or if perceptual disturbances do not fully resolve, consult a mental health professional experienced with psychedelic experiences.
Recovery & Support
DOI does not produce physical dependence or withdrawal. Compulsive use patterns are essentially unknown due to the aversive duration and body load. If repeated use is occurring despite negative consequences, the underlying motivation is more likely psychological avoidance or compulsive novelty-seeking than pharmacological dependence.
Support resources for problematic psychedelic use include the Fireside Project (62-FIRESIDE / 623-473-7433), MAPS integration therapist directory, and local harm reduction organizations. Psychedelic integration circles — peer support groups focused on processing difficult experiences — are available in many cities and online.
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Recognizing an emergency: Distinguish discomfort from danger. Anxiety, restlessness, and unpleasant body sensations are expected and not emergencies. Seek immediate help for: chest pain or pressure, numbness or discoloration in extremities (suggesting severe vasoconstriction), seizure activity, complete disconnection from reality with self-harm risk, or expressed suicidal intent.
Immediate steps:
- Move the person to a calm, safe environment
- Speak in short, reassuring sentences — remind them what they took and that it will end
- If chest pain or extremity numbness is present, call emergency services immediately
- Do not physically restrain unless there is immediate danger of self-harm
- Monitor breathing and consciousness
What to tell the dispatcher: Name the substance (DOI or "a DOx amphetamine psychedelic"), approximate dose if known, time of ingestion, and current symptoms. Good Samaritan laws in many jurisdictions protect callers from drug-related prosecution when seeking medical help.
Legal Status[edit]
DOI occupies an unusual regulatory position: despite decades of use as a research tool and potent psychoactive properties, it remains unscheduled in several major jurisdictions as of May 2026. It is not among the sixteen phenethylamines controlled under the UN 1971 Convention on Psychotropic Substances, leaving regulation to national legislation.
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| United States | Currently unscheduled (federal) | DEA proposed Schedule I placement April 2022;[24] ALJ hearing stayed June 2024 pending district court matter.[25] May trigger Federal Analogue Act if intended for human consumption. |
| United Kingdom | Controlled (Class A equivalent) | Scheduled under Misuse of Drugs Act 1971 phenethylamine catch-all clause.[26] Additionally covered by Psychoactive Substances Act 2016. |
| Canada | Schedule III (CDSA) | Controlled as amphetamine analogue under the Controlled Drugs and Substances Actcitation needed |
| Sweden | Schedule I (Förteckning I) | Classified as narcotics effective August 30, 2007citation needed |
| Finland | Banned from consumer market | Classified as psychoactive substance prohibited from consumer salecitation needed |
| Australia | Tentatively unscheduled | Not listed in SUSMP as of available data; requires verification against current schedulecitation needed |
The dynamic US regulatory situation warrants monitoring: scheduling proceedings were stayed in June 2024, and the final outcome will determine DOI's availability for both research and potential clinical development.
references
- [1] ^abcdXu Z, Wang H, Yu J et al. (2026) Psychedelics elicit their effects by 5-HT2A receptor-mediated Gi signalling — Nature doi:10.1038/s41586-025-10061-7
- [2] ^abCoutts RT, Malicky JL (1973) The Synthesis of Some Analogs of the Hallucinogen 1-(2,5-Dimethoxy-4-methylphenyl)-2-aminopropane (DOM). — Canadian Journal of Chemistry doi:10.1139/v73-210
- [3] ^abcMcKenna DJ, Peroutka SJ (1989) Differentiation of 5-hydroxytryptamine2 receptor subtypes using 125I-R-(-)2,5-dimethoxy-4-iodo-phenylisopropylamine and 3H-ketanserin. — Journal of Neuroscience PMID:2795135
- [4]
- [5] ^abcCanal CE, Morgan D (2012) Head-twitch response in rodents induced by the hallucinogen 2,5-dimethoxy-4-iodoamphetamine: a comprehensive history, a re-evaluation of mechanisms, and its utility as a model — Drug Testing and Analysis doi:10.1002/dta.1333
- [6] ^abcMartins D, Barratt MJ, Pires CV et al. (2017) The detection and prevention of unintentional consumption of DOx and 25x-NBOMe at Portugal's Boom Festival — Human Psychopharmacology doi:10.1002/hup.2608