DOM
2,5-dimethoxy-4-methylamphetamine
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DOM (2,5-dimethoxy-4-methylamphetamine) — also known as STP — is a synthetic psychedelic of the phenethylamine class. It is the founding member of the DOx amphetamine series, distinguished by exceptional duration and intermediate potency.[1] DOM is a full agonist at 5-HT₂A receptors, producing its effects by activating serotonin signalling on cortical neurons.[2][3]
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LSD, psilocybin, mescaline +3 moreLSD, psilocybin, mescaline, DOI, DOB, DPT show less
Synthesized by Alexander Shulgin at Dow Chemical in 1963–1964, DOM was the first phenethylamine psychedelic to reach wide distribution.[4] In 1967, thousands of high-dose tablets flooded San Francisco's Summer of Love, triggering a mass medical crisis that accelerated federal scheduling.[4] It is Schedule I internationally and has largely disappeared from illicit markets, persisting primarily as a reference compound in preclinical pharmacology.[1]
Subjective effects include colour intensification, geometric visual patterns, time alteration, emotional enhancement, and introspective ideation.[5] The experience is defined by its slow-building persistence — a sustained, body-present plateau with somatic stimulation characteristic of the phenethylamine scaffold, distinct from the wave-like intensity cycling of tryptamine psychedelics.[6] Anxiety during the prolonged onset, physical tension, and difficulty sleeping through the extended tail are common unsought effects.
DOM produces no physical dependence and has no established lethal dose in any species.[6]safety citation needed The primary risk is psychological: the exceptionally long duration creates extended exposure to altered states, and the slow onset has historically led to dangerous redosing by users expecting faster effects.[4] Only one controlled human study has been published, and basic pharmacokinetic parameters remain entirely uncharacterized.[7][4]
History[edit]
Discovery
Shulgin synthesized DOM at Dow Chemical in 1963–1964 under the internal code K-61,082.[4] His first self-experiment took place on January 4, 1964, at 1 mg; colleague Thornton Sargent documented the compound's hallucinogenic properties a month later at 2.3 mg.[4] The only controlled human study — by Snyder, Faillace, and Hollister — appeared in Science in 1967, establishing DOM as approximately 100 times more potent than mescaline and one-thirtieth the potency of LSD.[7]
The 1967 Crisis
On the 1967 summer solstice, Augustus Owsley Stanley III distributed approximately 5,000 tablets of DOM in San Francisco's Golden Gate Park, each containing 10–20 mg — far exceeding the common dose range of 3–10 mg.[5] The slow onset led users to redose, compounding the effects dramatically. The Haight-Ashbury Free Medical Clinic treated dozens of patients; physicians who administered chlorpromazine — then standard for LSD crises — found it worsened the response, a finding that reshaped emergency protocols for psychedelic adverse reactions.[4]
Scheduling and Modern Legacy
The crisis accelerated regulatory action: DOM was placed in Schedule I in the United States in 1970 and under the UN Convention on Psychotropic Substances in 1971, after which it largely vanished from illicit circulation.[4] Its modern significance is preclinical — DOM remains the standard training compound in animal drug discrimination studies and the founding member of the DOx structure-activity series.[3][1]
The acronym "DOM" was coined by Shulgin. The street name "STP" — popularly glossed as "Serenity, Tranquility, Peace" — was applied during the compound's brief period of illicit circulation in 1967. Shulgin documented DOM as entry #68 in PiHKAL (1991).[5]
Chemistry[edit]
Structural Class
DOM is a substituted amphetamine belonging to the DOx series — a family defined by methoxy groups at positions 2 and 5 of the aromatic ring and a variable substituent at position 4. In DOM, that variable element is a methyl group, making it the simplest 4-alkyl member of the series.[2] The 2,5-dimethoxy pattern is essential for psychedelic activity.[8]
Molecular Properties
| Molecular formula | C₁₂H₁₉NO₂ |
| Molecular weight | 209.28 g/mol |
The molecule consists of a 1,4-disubstituted benzene ring bearing methoxy groups at positions 2 and 5, a methyl group at position 4, and an aminopropyl side chain. The α-methyl group on the side chain — inherited from the amphetamine scaffold — confers metabolic stability relative to the corresponding phenethylamine (2C-D) and contributes to DOM's extended duration of action.
Stereochemistry
DOM has one chirality centre at the α-carbon, producing (R)- and (S)-enantiomers. The (R)-(−)-enantiomer is the more pharmacologically active form and is preferentially metabolised by hepatic enzymes.[9][10] Commercially and illicitly available preparations are racemic mixture.
Structure-Activity Relationships
Within the DOx series, the 4-position substituent determines potency and selectivity. Extending the methyl group to an ethyl, iodine (→ DOI), or bromine (→ DOB) alters receptor affinity and duration.[2][1] Removing the α-methyl group converts DOM to 2C-D, a shorter-acting and less potent compound.
Pharmacology[edit]
Mechanism of Action
DOM acts as a full agonist at serotonin 5-HT₂A and 5-HT₂C receptors.[6] The psychedelic effects are driven by 5-HT₂A activation on cortical pyramidal neurons. Multiple lines of evidence confirm this target: selective 5-HT₂A antagonists competitively block DOM's effects in animal models,[3] while dopamine antagonists have no blocking effect.[10]
The 5-HT₂C receptor contributes meaningfully to the overall response. SSRIs such as citalopram amplify DOM's effects through a 5-HT₂C-dependent mechanism — elevated synaptic serotonin from reuptake inhibitor enhances tonic 5-HT₂C activation, potentiating rather than blunting the experience.[11]
DOM is not a monoamine releasing agent despite its amphetamine-derived structure. It has no meaningful affinity for the SERT,[11] does not substitute for amphetamine or methylphenidate in discrimination studies,[10] and its cardiovascular effects are centrally mediated through serotonin receptors rather than catecholamine release.[12] Its mechanism is direct receptor agonism, not transporter-mediated release.
Pharmacokinetics
Human pharmacokinetic data for DOM are essentially absent — the compound was scheduled before basic parameters could be established.[4]
Onset is slow, requiring 30 minutes to 2 hours for full effects after oral administration.[5] This delayed onset was the critical factor in the 1967 overdose crisis. Total duration is dose-dependent: approximately 8 hours near the psychedelic threshold versus 14–20 hours at common doses.[7][5]
Hepatic metabolism proceeds through stereoselective N-oxidation, with the (R)-enantiomer preferentially oxidised. The (R)-enantiomer may inhibit its own metabolising enzyme through mechanism-based inactivation, which could contribute to the extended duration.[9] Bioavailability, plasma half-life, and other standard pharmacokinetic values have not been characterised in humans.
Neuroscience[edit]
Where It Acts
DOM activates 5-HT₂A receptors on layer V pyramidal neurons of the prefrontal cortex, the same cellular trigger that initiates psychedelic states with LSD and psilocybin.[6] This activation is expected to disrupt default mode network integrity, destabilise thalamocortical gating, and increase global functional connectivity — though no neuroimaging studies of DOM in humans have been conducted.
Chronic administration in rats produces region-selective decreases in 5-HT₂A/₂C receptor density, with the olfactory nucleus showing the most pronounced downregulation.[13] This regional pattern suggests tolerance to DOM may not develop uniformly across the brain.
Why It Matters
Under the relaxed beliefs under psychedelics (REBUS) framework, DOM's potent 5-HT₂A agonism would flatten the brain's energy landscape, loosening the grip of prior beliefs and enabling freer information flow.[6] The exceptionally long duration may extend this window of cognitive flexibility far beyond what shorter-acting psychedelics provide.[5]
Serotonergic psychedelics as a class promote structural neuroplasticity — dendritic growth and new synaptic connections — via 5-HT₂A-dependent signalling pathways.[6] Whether DOM specifically induces these changes has not been tested. Rapid receptor desensitisation within 2 hours in vitro[14] suggests the neuroplasticity window may be temporally constrained even during the extended experience.
- Does DOM promote neuroplastic changes comparable to those documented for LSD and psilocybin?
- What explains the large dose-dependent variation in duration (8 hours near threshold vs. 14–20 hours at common doses)? Mechanism-based enzyme inhibition by the (R)-enantiomer[9] is one candidate, but this has not been confirmed.
- Would human neuroimaging during DOM reveal the same network disruption patterns seen with other serotonergic psychedelics, or does the phenethylamine scaffold produce a distinct signature?
Subjective Effects[edit]
DOM produces an experience marked by slow assembly and remarkable endurance. The gradual onset demands patience uncommon among classical psychedelics — full effects may take two hours to arrive — and the resulting plateau is characteristically stable, resisting the wave-like intensity cycling typical of LSD.[5] The qualitative character shifts meaningfully with dose: lower ranges produce perceptual brightening and gentle cognitive shifts, while common to strong doses bring immersive visual and introspective territory that the extended duration forces the user to inhabit fully. Set and setting carry particular weight — the sheer length of the experience means environmental and psychological conditions at onset shape many hours of unfolding effects.
Among classical psychedelics, DOM occupies a middle ground in potency — far more active than mescaline by weight but substantially less so than LSD.[7] Its character is distinctly phenethylamine: more body-present and somatically energising than tryptamine psychedelics, with a physical aliveness underlying the cognitive and visual dimensions.[6]
Effect Grid
At common oral doses (3–5 mg), the full psychedelic experience manifests: pronounced visual enhancement with colour intensification, geometric patterning overlaying surfaces, and drifting or morphing of objects. Closed-eye imagery becomes vivid and may synchronise with music. Time distortion is significant. Thought connectivity increases dramatically, producing introspective insights and novel conceptual associations. Emotional responses intensify — music, nature, and interpersonal interactions carry heightened meaning.
Physically, mydriasis, tachycardia, dry mouth, jaw tension, and body tremors may appear. Thirst increases while urination diminishes. The experience demands commitment: effects build slowly over 1–2 hours and persist for 14–20 hours at this dose range. Sleep is impossible for the duration. Functional impairment is substantial.
Modeled from the effect's dose-dependence curve — not per-substance measurements.
Tracers · Brightness alteration · Music enhancement · Environmental patterning · Visual breathing · Visual morphing · Depth perception distortion · Perspective distortion · After-images · Visual diffraction · Auditory enhancement · Light sensitivity · Visual melting · Visual acuity enhancement · Holotropic state · Auditory distortion · Touch enhancement · Peripheral vision distortion · Sound sensitivity · Spatial disorientation · Vestibular distortion · Auditory misinterpretation · Proprioceptive distortion · Visual haze / noise · Visual processing acceleration · Synesthesia · Flashbacks · Object transformations · Environmental orbism / cubism · External hallucinations · Object activation · Visual recursion · Internal hallucinations · Visual scenery slicing · Auditory hallucinations · Perspective hallucinations · Persisting hallucinations
Visual breathing · Visual morphing · Depth perception distortion · Perspective distortion · After-images · Visual diffraction · Auditory enhancement · Light sensitivity · Visual melting · Visual acuity enhancement · Holotropic state · Auditory distortion · Touch enhancement · Peripheral vision distortion · Sound sensitivity · Spatial disorientation · Vestibular distortion · Auditory misinterpretation · Proprioceptive distortion · Visual haze / noise · Visual processing acceleration · Synesthesia · Flashbacks · Object transformations · Environmental orbism / cubism · External hallucinations · Object activation · Visual recursion · Internal hallucinations · Visual scenery slicing · Auditory hallucinations · Perspective hallucinations · Persisting hallucinations
Stimulation · Insomnia · Body high · Dry mouth · Spontaneous body sensations · Excessive sweating · Muscle tension · Nausea · Dehydration sensation · Heart rate perception changes · Physical fatigue · Restlessness · Motor control impairment · Tingling / electric sensations · Vibrations / buzzing · Bruxism · Bodily pressures · Body schema distortion · Dizziness · Headache · Laughter fits · Tactile euphoria · Diarrhea · Involuntary body movements · Bodily lightness · Breathing alteration · Nystagmus (eye wobbles) · Sexual arousal enhancement · Trembling · Abnormal heartbeat · Vomiting · Motor control enhancement · Salivation · Tactile hallucination
Dry mouth · Spontaneous body sensations · Excessive sweating · Muscle tension · Nausea · Dehydration sensation · Heart rate perception changes · Physical fatigue · Restlessness · Tingling / electric sensations · Vibrations / buzzing · Bruxism · Bodily pressures · Body schema distortion · Dizziness · Headache · Laughter fits · Tactile euphoria · Diarrhea · Involuntary body movements · Bodily lightness · Breathing alteration · Nystagmus (eye wobbles) · Sexual arousal enhancement · Trembling · Abnormal heartbeat · Vomiting · Motor control enhancement · Salivation · Tactile hallucination
Novelty enhancement · Aesthetic enhancement · Openness enhancement · Immersion enhancement · Thought acceleration · Cognitive flexibility · Introspection enhancement · Multiple thought streams · Creativity enhancement · Memory suppression · Cognitive euphoria · Cognitive fatigue · Increased nature relatedness · Analysis enhancement · Cognitive impairment · Humor enhancement · Memory fragmentation · Motivation enhancement · Synchronicity · Thought loops · Focus enhancement · Information processing enhancement · Confusion · Focus suppression · Information processing suppression · Memory replays · Thought disorganization · Cognitive dysphoria
Thought acceleration · Cognitive flexibility · Introspection enhancement · Multiple thought streams · Creativity enhancement · Memory suppression · Cognitive euphoria · Cognitive fatigue · Increased nature relatedness · Analysis enhancement · Cognitive impairment · Humor enhancement · Memory fragmentation · Motivation enhancement · Synchronicity · Thought loops · Focus enhancement · Information processing enhancement · Confusion · Focus suppression · Information processing suppression · Memory replays · Thought disorganization · Cognitive dysphoria
Empathy enhancement · Anxiety · Catharsis · Irritability · Anhedonia · Dysphoria
Anhedonia · Dysphoria
Social connection · Sociability enhancement · Depersonalization · Trust enhancement · Flow state · Ego inflation · Social disconnection · Boundary dissolution · Identity alteration · Ego dissolution
Flow state · Ego inflation · Social disconnection · Boundary dissolution · Identity alteration · Ego dissolution
Non-dual awareness · Transpersonal visions · Death-rebirth sequence
Recursive awareness
Timeline
First alerts emerge subtly — mild perceptual brightening, a faint body awareness, slight mood shift. Effects are easily overlooked at this stage, which historically led to dangerous redosing.
Perceptual changes gradually intensify: colours deepen, surfaces begin to shimmer, and body stimulation builds. Emotional tone shifts become more apparent. The come-up is notably gradual compared to tryptamine psychedelics.
Full psychedelic immersion: vivid colour enhancement, geometric patterning, closed-eye imagery, time dilation, emotional amplification, and introspective depth. Physical effects (mydriasis, tachycardia, jaw tension) are maximal. The peak is sustained and broad — a defining feature of DOM.
Intensity gradually diminishes but perceptual and cognitive effects remain clearly present. Waves of renewed intensity may occur. Emotional processing continues.
Effects progressively fade toward baseline. Perceptual distortions become intermittent. Cognitive clarity returns incrementally.
Residual mood elevation, reflective thought patterns, and mild perceptual sensitivity may persist for 4–16 hours after the primary experience resolves. Sleep quality may be affected for the following night.
⚠ Do not drive or operate machinery until after a full night's sleep following the resolution of all perceptual effects — DOM's extended duration means residual impairment can persist well into the next day.
Safety[edit]
- Acute toxicity
- Low
- Chronic toxicity
- Low
- Withdrawal
- None
- Tolerance buildup
- rapid
- Tolerance reset
- 7 days
- Physical
- None
- Psychological
- Negligible
- Compulsive redosing
- Negligible
- Dose escalation
- Negligible
- Cross-tol.
- LSD · psilo · mesc
Toxicity
Acute Toxicity
No lethal dose has been established for DOM in any species, and no fatal overdoses appear in the published literature.safety citation needed The 1967 mass exposure event — in which hundreds of users ingested 10–20 mg, three to seven times the common dose — did not produce reported fatalities.[4]
At those high doses, documented effects included severe anxiety, panic, confusion, delusional and sometimes violent behaviour, amnesia, and seizures.[4] Heart rate and blood pressure increases are centrally generated through serotonin receptors.[12]
Heart and Circulation
DOM produces blood pressure and heart rate increases mediated by central serotonin receptors, with tolerance developing rapidly to repeated cardiovascular stimulation.[12] Chronic activation of 5-HT₂B receptors by DOx compounds raises a theoretical risk of heart valve damage, though no DOM-specific data exist on this endpoint.citation needed
Neurotoxicity
No neurotoxicity data exist for DOM. Despite its amphetamine backbone, DOM does not release monoamines — the mechanism responsible for the brain toxicity associated with MDMA and MDA.[11][10]
Psychological Risks
The psychological risks mirror those of serotonergic psychedelics as a class but are amplified by duration. At common to strong doses, the 14–20 hour experience window[5] creates prolonged exposure to altered perception and cognition, increasing cumulative risk of panic, acute distress, and transient psychotic symptoms.
The 1967 crisis demonstrated that high-dose DOM (10–20 mg) can produce frank psychosis, delusional behaviour, amnesia, and violent agitation.[4] At common doses, risk is dose-dependent and strongly shaped by set and setting.
No published data exist on DOM-specific risk of HPPD (HPPD) or lasting psychotic disorders. Class-level evidence indicates these risks are rare but real, particularly in individuals with personal or family histories of psychotic spectrum conditions.[6]
Tolerance and Dependence
Tolerance develops with exceptional speed. In laboratory conditions, near-complete receptor desensitisation occurs within 2 hours of DOM exposure.[14] Recovery takes 5–12.5 hours depending on the length of exposure.[14] In the only human tolerance data available, volunteers receiving 6 mg daily showed diminished response by the third day.[5]
Cross-tolerance extends to LSD, psilocybin, and mescaline through shared 5-HT₂A downregulation.[15][16][6]
DOM does not produce physical dependence. Serotonergic psychedelics as a class do not lead to dependence or addiction.[6] DOM does not function as a positive reinforcer in self-administration studies.[17]
Drug Interactions
SSRIs/SNRIs
SSRIs potentiate DOM rather than blunting it. Citalopram amplifies DOM's effects through a 5-HT₂C-dependent mechanism — the opposite of what users may expect from experience with tryptamine psychedelics.[11]
Phenothiazine Antipsychotics
Chlorpromazine and other phenothiazine antipsychotics are clinically contraindicated for DOM adverse reactions. During the 1967 crisis, chlorpromazine worsened rather than improved the clinical picture.[4] Benzodiazepines are the preferred pharmacological intervention for DOM-related agitation.
Tramadol
Combining DOM with tramadol carries serotonin syndrome risk from additive serotonergic effects: tramadol inhibits serotonin reuptake while DOM directly activates serotonin receptors.safety citation needed
5-HT₁A Agonists
Buspirone and related serotonin 1A receptor agonists reduce DOM's effects in primates but not in rodents.[18] No human data exist on this interaction.
Lithium
No DOM-specific data exist. Class-level concern for seizure risk exists with the combination of lithium and serotonergic psychedelics.safety citation needed
MAOIs
No published interaction data exist for DOM and MAOIs. Given DOM's direct serotonin receptor agonism and the potential for MAOIs to elevate serotonin levels, the combination carries theoretical serotonin syndrome risk.
Contraindications
Phenothiazine Antipsychotic Use
Chlorpromazine and related phenothiazines are absolutely contraindicated as interventions for DOM adverse reactions, based on clinical documentation from the 1967 mass exposure.[4]
Psychotic Spectrum Disorders
Personal or family history of psychotic disorders constitutes a strong contraindication. 5-HT₂A agonism can trigger or worsen psychotic episodes.[6]
Cardiovascular Conditions
DOM produces centrally mediated increases in heart rate and blood pressure.[12] Individuals with uncontrolled blood pressure, irregular heart rhythms, or structural heart conditions face elevated risk.
Serotonergic Co-medication
Concurrent use of SSRIs, SNRIs, MAOIs, or tramadol elevates serotonin syndrome risk when combined with DOM's direct serotonin receptor agonism.
Harm Reduction[edit]
Forms & Identification
DOM most commonly appears as tablets or capsules, though powder and blotter forms have been reported. The critical identification concern is dose accuracy: DOM is active in the low milligram range, and the difference between a common dose and a dangerous one is small. Volumetric dosing or a verified milligram-precision scale is essential for powder forms.
The slow onset is a safety-critical characteristic — users unfamiliar with DOM's 1–2 hour build have historically redosed, believing the initial amount was inactive, with dangerous cumulative results.[4]
Guidelines
- Verify substance identity with reagent testing before use
- Use a milligram-precision scale for powder forms — never estimate doses in the single-milligram range
- Start at the low end of the common dose range on a first experience
- Do not redose. The onset takes up to 2 hours — wait at least 3 hours before concluding the dose was insufficient
- Clear the full day and following morning — plan for up to 20 hours of effects plus recovery time
- Eat a light meal 2–3 hours before; have water and light snacks available throughout
- Keep a benzodiazepine accessible in case of severe anxiety (the preferred intervention over antipsychotics)
- Ensure at least one sober person is present who understands the timeline
- Avoid combining with SSRIs, which potentiate rather than blunt DOM's effects[11]
Set & Setting
DOM demands more environmental planning than most psychedelics. The 14–20 hour duration at common doses means the setting must remain safe and comfortable across an entire waking day and potentially through the night.[5]
A trusted, sober sitter is strongly recommended, particularly for first experiences. The sitter should be briefed on the timeline: effects build slowly over 1–2 hours, plateau for many hours, and resolve gradually. The extended commitment makes mid-experience location changes difficult — choose a setting that will remain available and comfortable for at least 20 hours.
Aftercare & integration. The extended duration of DOM means the experience may still be processing well after effects have faded. Allow at least one full rest day afterward — fatigue, residual mood shifts, and mild perceptual afterglow are normal in the 24–48 hours following a session.
Journaling or structured reflection within a few days helps consolidate insights before they fade. If the experience was difficult or raised persistent psychological distress, seek support from a therapist familiar with psychedelic experiences. Integration circles and peer support communities can also provide useful context.
Recovery & Support
DOM does not produce physical dependence, and compulsive use patterns are rare among serotonergic psychedelics.[6] However, repeated use of any psychedelic can become psychologically habitual, and difficult experiences may leave lasting distress.
If use has become a concern, peer support communities and psychedelic integration services can provide non-judgmental guidance. For persistent psychological difficulties following DOM use — including ongoing anxiety, depersonalisation, or perceptual disturbances — professional mental health support is recommended.
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Recognising an emergency: Uncomfortable anxiety during a long psychedelic experience is common and usually manageable. Seek immediate help if any of the following occur: violent or self-harming behaviour, complete loss of contact with reality, seizures, chest pain, or loss of consciousness.
Immediate steps:
- 1. Stay with the person. Speak calmly and simply.
- 2. Move them to a quiet, low-stimulation environment if safely possible.
- 3. Do not administer chlorpromazine or other phenothiazine antipsychotics — these have been documented to worsen DOM reactions.[4]
- 4. A benzodiazepine (diazepam, lorazepam) may be given for severe agitation if available.
- 5. If symptoms include seizures, chest pain, or loss of consciousness, call emergency services immediately.
- 6. Place an unconscious person in the recovery position.
What to tell the dispatcher: Name the substance (DOM / STP), the estimated dose and time of ingestion, and current symptoms. Good Samaritan laws in many jurisdictions protect callers from drug-related prosecution.
Legal Status[edit]
DOM is among the most broadly controlled psychedelic substances internationally. Following the 1967 distribution crisis in San Francisco, it was rapidly scheduled in the United States and subsequently listed under the United Nations Convention on Psychotropic Substances (1971), obligating signatory nations to implement domestic controls.
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| United States | Schedule I (Controlled Substances Act, 1970) | No accepted medical use; high abuse potential classification. Federally controlled since 1970. |
| United Nations | Schedule I (Convention on Psychotropic Substances, 1971) | International control obligating domestic scheduling by signatory nations. |
| United Kingdom | Class A (Misuse of Drugs Act 1971), Schedule 1 | Maximum penalty for supply: life imprisonment. Research licence required for possession. |
| Canada | Schedule I (Controlled Drugs and Substances Act) | Prohibited substance; no medical exemptions currently issued. |
| Australia | Schedule 9 (Poisons Standard) | Prohibited substance — available only for approved research. |
| Germany | Controlled (BtMG)citation needed | Specific scheduling classification not confirmed in primary legal sources accessed. |
As a substituted amphetamine, DOM may fall within the scope of structural analog legislation in jurisdictions with such provisions, though its explicit scheduling renders analog provisions redundant in most cases.
references
- [1] ^abcdGlennon RA, Dukat M (2024) 1-(2,5-Dimethoxy-4-iodophenyl)-2-aminopropane (DOI): From an Obscure to Pivotal Member of the DOX Family of Serotonergic Psychedelic Agents - A Review. — ACS Pharmacology & Translational Science doi:10.1021/acsptsci.4c00157
- [2] ^abcLuethi D et al. (2026) The 4-alkyl chain length of 2,5-dimethoxyamphetamines differentially affects in vitro serotonin receptor actions versus in vivo psychedelic-like effects — Molecular Psychiatry doi:10.1038/s41380-025-03325-1
- [3] ^abcLi JX, Rice KC, France CP (2009) Discriminative stimulus effects of 1-(2,5-dimethoxy-4-methylphenyl)-2-aminopropane in rhesus monkeys: antagonism and apparent pA2 analyses. — Journal of pharmacology and experimental therapeutics doi:10.1124/jpet.108.145458
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- [6]