2,5-DMA
2,5-dimethoxyamphetamine
Studies and references cited across this article, graded by evidence strength.
Data points an editor reviewed and accepted for publication.
Value Provenance
Dosing
oraltrace
| Field | Published | AI Proposed | Confidence |
|---|---|---|---|
| Threshold | 10 mg | 10 mg | medium |
| Low | 40–80 mg | 40–80 mg | medium |
| Common | 80–160 mg | 80–160 mg | medium |
| Strong | 160–200 mg | 160–200 mg | medium |
| Heavy | 200+ mg | 200+ mg | medium |
| Editorial | Common (moderate) range of 80–160 mg from PiHKAL #54 (Shulgin 1991) — the only published human dose reference. Light range revised upward from DB's 10–40 mg to 40–80 mg based on PiHKAL characterization of sub-active doses. Threshold of 10 mg retained from existing DB but has no primary source support. Strong (high) range of 160–200 mg inferred from PiHKAL upper range. Heavy 200+ mg has no primary source. ⚠️ DOSE RANGE FLAG: Existing DB 'Common' of 40–80 mg is substantially lower than PiHKAL's 80–160 mg. PiHKAL is treated as primary. | ||
ReasoningReasoningCommon (moderate) range of 80–160 mg from PiHKAL #54 (Shulgin 1991) — the only published human dose reference. Light range revised upward from DB's 10–40 mg to 40–80 mg based on PiHKAL characterization of sub-active doses. Threshold of 10 mg retained from existing DB but has no primary source support. Strong (high) range of 160–200 mg inferred from PiHKAL upper range. Heavy 200+ mg has no primary source. ⚠️ DOSE RANGE FLAG: Existing DB 'Common' of 40–80 mg is substantially lower than PiHKAL's 80–160 mg. PiHKAL is treated as primary. Evidence basis: community_consensus_large | |||
Duration
oral
| Field | Published | AI Proposed | Confidence |
|---|---|---|---|
| Onsettrace | 30–60 minutes | 30–60 minutes | low |
| Editorial | No published onset data for 2,5-DMA. Inferred from DOx class oral onset times. Reference compounds: DOI, DOM. | ||
ReasoningReasoningNo published onset data for 2,5-DMA. Inferred from DOx class oral onset times. Reference compounds: DOI, DOM. Evidence basis: structural_analogy | |||
| Peaktrace | 2–4 hours | 2–4 hours | low |
| Editorial | No published peak duration data for 2,5-DMA. Inferred from total duration of 6–8 hours minus estimated onset and resolution phases. Stimulant arc pattern assumed. | ||
ReasoningReasoningNo published peak duration data for 2,5-DMA. Inferred from total duration of 6–8 hours minus estimated onset and resolution phases. Stimulant arc pattern assumed. Evidence basis: structural_analogy | |||
| Offsettrace | 2–3 hours | 2–3 hours | low |
| Editorial | No published offset data for 2,5-DMA. Inferred from total 6–8 hours minus onset (0.5–1h) and peak (2–4h). Gradual stimulant resolution pattern. | ||
ReasoningReasoningNo published offset data for 2,5-DMA. Inferred from total 6–8 hours minus onset (0.5–1h) and peak (2–4h). Gradual stimulant resolution pattern. Evidence basis: structural_analogy | |||
| Totaltrace | 6–8 hours | 6–8 hours | medium |
| Editorial | Confirmed by PiHKAL #54 (Shulgin 1991). The only published duration value for 2,5-DMA. | ||
ReasoningReasoningConfirmed by PiHKAL #54 (Shulgin 1991). The only published duration value for 2,5-DMA. Evidence basis: community_consensus_large | |||
Safety
Toxicity Profiletrace
| Field | Published | AI Proposed | Confidence |
|---|---|---|---|
| Acute | low | low | low |
| Chronic | low | low | low |
| Organs Affected | cardiovascular | cardiovascular | low |
| Editorial | Acute 'low' reflects absence of adverse event reports and weak receptor activity, but is entirely class-inferred from DOx/25I-NBOMe sympathomimetic toxidrome data — no substance-specific toxicity data exist. Chronic 'low' (downgraded from work-notes 'no data' to lowest assignable level) is structural analogy from DOI/DOM with evidence discount applied. Reference compounds: DOI, DOM, 25I-NBOMe (Hieger et al. 2015). | ||
ReasoningReasoningAcute 'low' reflects absence of adverse event reports and weak receptor activity, but is entirely class-inferred from DOx/25I-NBOMe sympathomimetic toxidrome data — no substance-specific toxicity data exist. Chronic 'low' (downgraded from work-notes 'no data' to lowest assignable level) is structural analogy from DOI/DOM with evidence discount applied. Reference compounds: DOI, DOM, 25I-NBOMe (Hieger et al. 2015). Evidence basis: structural_analogy | |||
Dependence Profiletrace
| Field | Published | AI Proposed | Confidence |
|---|---|---|---|
| Physical | none | none | medium |
| Psychological | negligible | negligible | medium |
| Compulsive Redosing | negligible | negligible | medium |
| Dose Escalation | negligible | negligible | medium |
| Editorial | Class-level evidence for 5-HT2A agonist non-dependence is strong (Halberstadt & Geyer 2011). Substance-specific dependence data absent, but the absence of monoamine transporter activity (Kolaczynska et al. 2019) and weak 5-HT2A partial agonism make dependence formation implausible. | ||
ReasoningReasoningClass-level evidence for 5-HT2A agonist non-dependence is strong (Halberstadt & Geyer 2011). Substance-specific dependence data absent, but the absence of monoamine transporter activity (Kolaczynska et al. 2019) and weak 5-HT2A partial agonism make dependence formation implausible. Evidence basis: structural_analogy | |||
Withdrawal Profiletrace
| Field | Published | AI Proposed | Confidence |
|---|---|---|---|
| Severity | none | none | medium |
| Symptoms | — | — | medium |
| Fatal | No | No | medium |
| Medical Supervision | Not required | Not required | medium |
| Editorial | No withdrawal syndrome documented for any 5-HT2A agonist. Class-level evidence strongly supports absence of withdrawal. | ||
ReasoningReasoningNo withdrawal syndrome documented for any 5-HT2A agonist. Class-level evidence strongly supports absence of withdrawal. Evidence basis: structural_analogy | |||
Tolerance Profiletrace
| Field | Published | AI Proposed | Confidence |
|---|---|---|---|
| Buildup | rapid | rapid | low |
| Half-life | 4 days | 4 days | low |
| Full Reset | 8.5 days | 8.5 days | low |
| Cross-tolerances | DOI, DOB, DOM, DOC, LSD, psilocybin, mescaline | DOI, DOB, DOM, DOC, LSD, psilocybin, mescaline | low |
| Editorial | Tolerance data from DOI (de la Fuente Revenga et al. 2022) and DOI/2C-T-7 cross-tolerance (Smith et al. 2014). Half-life and full reset values carried from existing DB (class-inferred from psychedelic 5-HT2A agonist cross-tolerance data). NOT substance-specific PK. | ||
ReasoningReasoningTolerance data from DOI (de la Fuente Revenga et al. 2022) and DOI/2C-T-7 cross-tolerance (Smith et al. 2014). Half-life and full reset values carried from existing DB (class-inferred from psychedelic 5-HT2A agonist cross-tolerance data). NOT substance-specific PK. Evidence basis: structural_analogy | |||
Effects & Profile
Contraindications
| Field | Published | AI Proposed | Confidence |
|---|---|---|---|
| cardiovascular Cardiovascular diseasetrace | absolute | absolute | low |
| Editorial | Class-inferred from DOx sympathomimetic profile; Shulgin directly documents cardiovascular stimulation at active doses. No substance-specific contraindication studies exist. | ||
ReasoningReasoningClass-inferred from DOx sympathomimetic profile; Shulgin directly documents cardiovascular stimulation at active doses. No substance-specific contraindication studies exist. | |||
| cardiovascular Pre-existing hypertensiontrace | absolute | absolute | low |
| Editorial | Class-inferred from sympathomimetic amphetamine/DOx profile. Shulgin documents cardiovascular stimulation as primary effect at active doses. | ||
ReasoningReasoningClass-inferred from sympathomimetic amphetamine/DOx profile. Shulgin documents cardiovascular stimulation as primary effect at active doses. | |||
| cardiovascular Cardiac arrhythmiastrace | absolute | absolute | low |
| Editorial | Class-inferred from DOx/sympathomimetic stimulant profile. Abnormal heartbeat is a seeded effect in the DB for this substance. | ||
ReasoningReasoningClass-inferred from DOx/sympathomimetic stimulant profile. Abnormal heartbeat is a seeded effect in the DB for this substance. | |||
| neurological Seizure disorderstrace | relative | relative | low |
| Editorial | Class-inferred from sympathomimetic stimulant profile and 25I-NBOMe case series showing seizures. Reference compound: 25I-NBOMe (structurally related 2,5-dimethoxyphenyl compound). | ||
ReasoningReasoningClass-inferred from sympathomimetic stimulant profile and 25I-NBOMe case series showing seizures. Reference compound: 25I-NBOMe (structurally related 2,5-dimethoxyphenyl compound). | |||
| other Concurrent MAOI usetrace | absolute | absolute | low |
| Editorial | Class-inferred from 5-HT2A agonist/MAOI interaction pattern and CYP2D6 metabolism pathway (Ewald & Maurer 2008). | ||
ReasoningReasoningClass-inferred from 5-HT2A agonist/MAOI interaction pattern and CYP2D6 metabolism pathway (Ewald & Maurer 2008). | |||
| other Concurrent SSRI/SNRI usetrace | relative | relative | low |
| Editorial | Class-inferred from serotonergic psychedelic interaction pattern. 2,5-DMA's weak receptor affinity may reduce but not eliminate this risk. | ||
ReasoningReasoningClass-inferred from serotonergic psychedelic interaction pattern. 2,5-DMA's weak receptor affinity may reduce but not eliminate this risk. | |||
| other Concurrent tramadol usetrace | absolute | absolute | low |
| Editorial | Class-inferred from general serotonergic psychedelic–tramadol interaction pattern. DB lists tramadol interaction as 'dangerous' but no primary source was found. Flagged for editorial review. | ||
ReasoningReasoningClass-inferred from general serotonergic psychedelic–tramadol interaction pattern. DB lists tramadol interaction as 'dangerous' but no primary source was found. Flagged for editorial review. | |||
| pregnancy breastfeeding Pregnancy and lactationtrace | absolute | absolute | low |
| Editorial | Precautionary contraindication due to absence of any reproductive safety data for 2,5-DMA or closely related DOx compounds. | ||
ReasoningReasoningPrecautionary contraindication due to absence of any reproductive safety data for 2,5-DMA or closely related DOx compounds. | |||
Timeline Phases
oral
| Field | Published | AI Proposed | Confidence |
|---|---|---|---|
| Onsettrace | 1800–3600 sec(i=0.20) | 1800–3600 sec(i=0.20) | low |
| Editorial | Only the total duration (6–8 hours, PiHKAL #54) is published. Individual phase timings are inferred from DOx class oral pharmacokinetics and the simple stimulant arc described by Shulgin. Come_up, ascent, plateau, and afterglow phases are not distinctly documented — the experience appears to have a simple onset/peak/resolution structure without the complex phase profile of psychedelic DOx compounds. | ||
ReasoningReasoningOnly the total duration (6–8 hours, PiHKAL #54) is published. Individual phase timings are inferred from DOx class oral pharmacokinetics and the simple stimulant arc described by Shulgin. Come_up, ascent, plateau, and afterglow phases are not distinctly documented — the experience appears to have a simple onset/peak/resolution structure without the complex phase profile of psychedelic DOx compounds. Evidence basis: structural_analogy | |||
| Peaktrace | 7200–14400 sec(i=1.00) | 7200–14400 sec(i=1.00) | low |
| Editorial | Only the total duration (6–8 hours, PiHKAL #54) is published. Individual phase timings are inferred from DOx class oral pharmacokinetics and the simple stimulant arc described by Shulgin. Come_up, ascent, plateau, and afterglow phases are not distinctly documented — the experience appears to have a simple onset/peak/resolution structure without the complex phase profile of psychedelic DOx compounds. | ||
ReasoningReasoningOnly the total duration (6–8 hours, PiHKAL #54) is published. Individual phase timings are inferred from DOx class oral pharmacokinetics and the simple stimulant arc described by Shulgin. Come_up, ascent, plateau, and afterglow phases are not distinctly documented — the experience appears to have a simple onset/peak/resolution structure without the complex phase profile of psychedelic DOx compounds. Evidence basis: structural_analogy | |||
| Resolutiontrace | 7200–10800 sec(i=0.40) | 7200–10800 sec(i=0.40) | low |
| Editorial | Only the total duration (6–8 hours, PiHKAL #54) is published. Individual phase timings are inferred from DOx class oral pharmacokinetics and the simple stimulant arc described by Shulgin. Come_up, ascent, plateau, and afterglow phases are not distinctly documented — the experience appears to have a simple onset/peak/resolution structure without the complex phase profile of psychedelic DOx compounds. | ||
ReasoningReasoningOnly the total duration (6–8 hours, PiHKAL #54) is published. Individual phase timings are inferred from DOx class oral pharmacokinetics and the simple stimulant arc described by Shulgin. Come_up, ascent, plateau, and afterglow phases are not distinctly documented — the experience appears to have a simple onset/peak/resolution structure without the complex phase profile of psychedelic DOx compounds. Evidence basis: structural_analogy | |||
Dose Tier Summaries
No primary source establishes a threshold dose for 2,5-DMA. The existing value of approximately 10 mg is unverifiable. At this level, effects — if present — would be sub-perceptual, limited to possible mild physiological awareness such as a faint increase in heart rate or subtle alertness. Physical effects are minimal to absent. No cognitive, perceptual, or emotional changes are expected. The user may not be certain whether any effect has occurred. No published report documents effects at this dose. Functional impairment is not expected, though individual sensitivity varies.
Work-notes specify no primary source for threshold. DB value of 10 mg retained with low confidence. Description inferred from sub-active dose characterization in PiHKAL.
ReasoningReasoning
Work-notes specify no primary source for threshold. DB value of 10 mg retained with low confidence. Description inferred from sub-active dose characterization in PiHKAL.
Evidence basis: community_consensus_large
Mild sympathomimetic activation begins — slight cardiovascular awareness with possible increase in heart rate and blood pressure. Wakefulness and a subtle increase in environmental interest may emerge. No perceptual or sensory changes occur at this dose range. Physical effects are the dominant experience: mild stimulation, possible faint muscle tension or restlessness. Appetite suppression may begin. These effects are qualitatively similar to a low dose of amphetamine. Duration is expected to track the 6–8 hour range. Sleep may be delayed if taken in the evening. Functional impairment is minimal.
Work-notes describe light tier as mild sympathomimetic activation with physical effects only, based on PiHKAL characterization of sub-active doses. Revised upward to 40–80 mg per work-notes.
ReasoningReasoning
Work-notes describe light tier as mild sympathomimetic activation with physical effects only, based on PiHKAL characterization of sub-active doses. Revised upward to 40–80 mg per work-notes.
Evidence basis: community_consensus_large
The core 2,5-DMA experience. Cardiovascular stimulation becomes prominent — increased heart rate and blood pressure are clearly noticeable. Tremor, muscle tension, and sustained wakefulness define the physical profile. Shulgin described 80 mg as 'totally a physical trip' with 'nothing of a sensory nature.' Cognitive effects are limited to enhanced interest in surroundings and mild cognitive euphoria. The experience is 'largely pleasant' but lacks any visual, auditory, or perceptual alterations. No psychedelic phenomenology occurs despite 2,5-DMA's structural relationship to the DOx series. Duration is 6–8 hours. Appetite suppression and insomnia are likely. Temperature dysregulation and excessive sweating may occur.
Directly sourced from PiHKAL #54 (Shulgin 1991), the only published human dose reference. Common range revised to 80–160 mg per work-notes, matching PiHKAL.
ReasoningReasoning
Directly sourced from PiHKAL #54 (Shulgin 1991), the only published human dose reference. Common range revised to 80–160 mg per work-notes, matching PiHKAL.
Evidence basis: community_consensus_large
Intensified stimulant effects dominate — pronounced tachycardia, blood pressure elevation, tremor, and temperature dysregulation. The amphetamine-like character becomes more apparent at the upper end of the dose range, as noted by the WHO ECDD's characterization of high-dose effects as similar to amphetamine. Physical discomfort may become the primary experience. Restlessness, anxiety, and muscle tension can reach uncomfortable levels. Excessive sweating and vasoconstriction are more likely. Whether any weak perceptual effects emerge at these doses has not been documented. The cardiovascular load at this tier warrants particular caution. Pre-existing cardiovascular conditions are an absolute contraindication.
Work-notes describe intensified stimulant effects with pronounced sympathomimetic activation. ECDD characterization of amphetamine-like high-dose effects supports this description. No direct human dose-escalation data exist beyond PiHKAL's 80 mg observation.
ReasoningReasoning
Work-notes describe intensified stimulant effects with pronounced sympathomimetic activation. ECDD characterization of amphetamine-like high-dose effects supports this description. No direct human dose-escalation data exist beyond PiHKAL's 80 mg observation.
Evidence basis: structural_analogy
Doses exceeding 200 mg are undocumented in published literature. No human experience reports exist at this level. The expected profile is severe sympathomimetic activation — significant cardiovascular strain including dangerous tachycardia and hypertension, potential hyperthermia, and pronounced tremor. Whether psychedelic or perceptual effects emerge at extreme doses is unknown. The risk of serious adverse cardiovascular events increases substantially. Anxiety, agitation, and paranoia are plausible based on stimulant class pharmacology. This dose range carries meaningful risk of medical emergency. No data exist to characterize the upper safety boundary. The toxic dose of 2,5-DMA is completely unknown.
Work-notes specify no published documentation at 200+ mg. Description reflects expected severe sympathomimetic toxicity risk from class inference. All claims are speculative.
ReasoningReasoning
Work-notes specify no published documentation at 200+ mg. Description reflects expected severe sympathomimetic toxicity risk from class inference. All claims are speculative.
Evidence basis: structural_analogy
History
publish Oct 2, 2026 · by agent-psx
backfill Jun 4, 2026
Historical versions do not record which reviewer approved them; editorial accountability is recorded per value in the database and in the publication ledger going forward.
Sources
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- [2]weakAmines related to 2,5-dimethoxyphenethylamineBaltzly R, Buck JS · 1940 · Journal of the American Chemical Societylinkno claims checked
- [3]insufficient
- [4]weakCritical Review Report: 2,5-Dimethoxyamphetamine (DMA)WHO Expert Committee on Drug Dependence · 1985linkno claims checked
- [5]moderateMultiple receptors contribute to the behavioral effects of indoleamine hallucinogensHalberstadt AL, Geyer MA · 2011 · Neuropharmacology
- [6]weak2,5-DMA - ECDD Information RepositoryWHO Expert Committee on Drug Dependence · 1985linkno claims checked
- [7]moderateReceptor Interaction Profiles of 4-Alkoxy-Substituted 2,5-Dimethoxyphenethylamines and Related Amphetamines.Kolaczynska KE, Luethi D, Trachsel D, Hoener MC, Liechti ME · 2019 · Frontiers in Pharmacology
- [8]moderateTolerance and Cross-Tolerance among Psychedelic and Nonpsychedelic 5-HT2A Receptor Agonists in Micede la Fuente Revenga M, Jaster AM, McGinn J, Silva G, Saha S, Gonzalez-Maeso J · 2022 · ACS Chemical Neuroscience
- [9]moderate1-(2,5-Dimethoxy-4-iodophenyl)-2-aminopropane (DOI): From an Obscure to Pivotal Member of the DOX Family of Serotonergic Psychedelic Agents - A Review.Glennon RA, Dukat M · 2024 · ACS Pharmacology & Translational Science
- [10]weak
- [11]strongThe 4-alkyl chain length of 2,5-dimethoxyamphetamines differentially affects in vitro serotonin receptor actions versus in vivo psychedelic-like effectsLuethi D et al. · 2026 · Molecular Psychiatry
- [12]moderateEffect of a chiral 4-alkyl substituent in hallucinogenic amphetamines.Oberlender R, Ramachandran PV, Johnson MP, Huang X, Nichols DE · 1995 · Journal of Medicinal Chemistrypubmed 7658446no claims checked
- [13]weak2,5-DMA (2,5-Dimethoxyamphetamine) - Chemical IdentityCAS Common Chemistry, PubChem · 2024linkno claims checked
- [14]moderate5-HT1 and 5-HT2 binding properties of derivatives of the hallucinogen 1-(2,5-dimethoxyphenyl)-2-aminopropane (2,5-DMA)Shannon M, Battaglia G, Glennon RA, Titeler M · 1984 · European Journal of Pharmacologypubmed 6479216no claims checked
- [15]moderate2,5-Dimethoxyamphetamine-derived designer drugs: studies on the identification of cytochrome P450 (CYP) isoenzymes involved in formation of their main metabolites and on their capability to inhibit CYP2D6.Ewald AH, Maurer HH · 2008 · Toxicology Letters
- [16]moderateLC-MS/MS screening method for designer amphetamines, tryptamines, and piperazines in serumWohlfarth A, Weinmann W, Dresen S · 2010 · Analytical and Bioanalytical Chemistry
- [17]moderateAnalysis of 2,5-dimethoxy-amphetamines and 2,5-dimethoxy-phenethylamines aiming their determination in biological matrices: a review.Nieddu M, Baralla E, Sodano F, Boatto G · 2023 · Forensic Toxicology
- [18]moderateComparison of the behavioral effects of mescaline analogs using the head twitch response in miceHalberstadt AL, Chatha M, Chapman SJ, Brandt SD · 2019 · Journal of Psychopharmacology
- [19]weakSevere poisoning after self-reported use of 25-I-NBOME: a case seriesHieger MA, Rose SR, Cumpston KL, Stromberg PE, Miller S, Wills BK · 2015 · American Journal of Emergency Medicine
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Claim Verification
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