generation run 2026-04-24
67 min completedmodel pipeline-v5plan not recordedrun/68703491…Selection
Verification
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The model's own caveats
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Reproduce
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- 29 source keys (listed under Sources)
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- not recorded — template version, prompt hash and git SHA are written from 2026-09 onward
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- none — agent transcripts are persisted from 2026-09 onward
27 searches — query, source, results, what was kept and why
| # | source | query | seen | kept | rationale |
|---|---|---|---|---|---|
| 1 | PubMed | methylenedioxyamphetamine metabolism neurotoxicity role | 2 | 2 | — |
| 2 | PubMed · absence | MDA MDMA serotonin syndrome drug interaction tramadol | 0 | — | — |
| 3 | PubChem | CID 1614 | 1 | 1 | — |
| 4 | PubChem · absence | MDA 3,4-methylenedioxyamphetamine | 0 | 1 | — |
| 5 | PubMed | MDA 3,4-methylenedioxyamphetamine pharmacology receptor binding | 8 | 3 | — |
| 6 | PubMed | MDA methylenedioxyamphetamine serotonin transporter monoamine release Ki | 1 | 1 | — |
| 7 | PubMed | methylenedioxyamphetamine neurotoxicity serotonin dopamine | 10 | 1 | — |
| 8 | PubMed | MDA methylenedioxyamphetamine hyperthermia overdose death case report | 1 | 1 | — |
| 9 | PubMed | MDA methylenedioxyamphetamine human pharmacokinetics half-life urine | 4 | 2 | — |
| 10 | PubMed | MDA methylenedioxyamphetamine cardiovascular blood pressure heart rate | 7 | 4 | — |
| 11 | OpenAlex | MDA methylenedioxyamphetamine neurotoxicity serotonin axon terminal (citation-sorted) | 8 | 2 | — |
| 12 | PubMed | MDA methylenedioxyamphetamine 5-HT2A agonist psychedelic mechanism | 1 | 1 | — |
| 13 | PubMed | MDA drug discrimination amphetamine LSD | 1 | 1 | — |
| 14 | PubMed · absence | MDA MDMA serotonin syndrome lethal interaction opioid | 0 | — | — |
| 15 | PubMed | Nichols entactogen MDMA MBDB pharmacology class | 1 | 1 | — |
| 16 | OpenAlex | MDA 3,4-methylenedioxyamphetamine pharmacology (citation-sorted) | 10 | 1 | — |
| 17 | PubMed | PMID 40999236 (Straumann 2026 MDA vs MDMA RCT) | 1 | 1 | — |
| 18 | ClinicalTrials.gov | methylenedioxyamphetamine MDA | 10 | 1 | — |
| 19 | WebSearch | MDA 3,4-methylenedioxyamphetamine Schedule I DEA 1970 legal history scheduling | 10 | 1 | — |
| 20 | OpenAlex | tramadol serotonin syndrome interaction amphetamine MDMA pharmacodynamic | 5 | 1 | — |
| 21 | WebFetch | Wikidoc MDA page | 1 | 3 | — |
| 22 | WebSearch | MDA UK Canada Australia legal status Misuse of Drugs Act | 10 | 3 | — |
| 23 | WebSearch | MDA methylenedioxyamphetamine synthesis history 1910 Mannich patent | 10 | 1 | — |
| 24 | OpenAlex | MDA methylenedioxyamphetamine human study subjective effects entactogen (citation-sorted) | 8 | 0 | — |
| 25 | PLoS ONE (WebFetch) | Baggott 2010 MDA RCT full data | 1 | 1 | — |
| 26 | PubMed + OpenAlex · absence | Multiple final searches for tolerance, dependence, harm reduction MDA-specific | 0 | 0 | — |
| 27 | PubMed | Straumann 2025 2026 MDA MDMA lysine prodrug crossover NCT04847206 | 1 | 1 | — |
86 claims by section — every cited sentence, checked against its source
safety22 · 22 ok
The landmark preclinical study by O'Hearn et al. (1988) demonstrated that MDA (20 mg/kg s.c., twice daily for 4 days) caused profound and selective loss of serotonergic (5-HT) axon terminals throughout the rat forebrain, while completely sparing catecholamine axons. MDA produced a greater reduction of 5-HT axons than MDMA at the same dosage — establishing that MDA is more neurotoxic than MDMA on a per-dose basissupported
MDA/MDMA cause selective serotonergic axon terminal ablation in rat forebrain. MDA more neurotoxic than MDMA at same dose. Catecholamine axons completely spared. pmid:2457659
The mechanism is metabolic, not direct: MDA undergoes CYP2D6-mediated O-demethylenation to alpha-methyldopamine (alpha-MeDA), which oxidizes to an ortho-quinone and conjugates with glutathione to form thioether adductssupported
Neither MDA nor MDMA produces neurotoxicity when injected directly into brain. Alpha-methyldopamine (alpha-MeDA)...their thioether conjugates...produce long-term depletions in serotonin concentrations. pmid:15228153
The mechanism is metabolic, not direct: MDA undergoes CYP2D6-mediated O-demethylenation to alpha-methyldopamine (alpha-MeDA), which oxidizes to an ortho-quinone and conjugates with glutathione to form thioether adductssupported
MDMA and MDA are O-demethylenated to N-Me-alpha-MeDA and alpha-MeDA (catechols) which oxidize to ortho-quinones and conjugate with glutathione. pmid:17467183
MDA injected directly into the brain does not produce neurotoxicity, confirming the requirement for peripheral metabolism.supported
Neither MDA nor MDMA produces neurotoxicity when injected directly into brain. pmid:15228153
Temperature dependence: Malberg and Seiden (1998) demonstrated that small (2°C) changes in ambient temperature produce large changes in MDMA/MDA-induced serotonin neurotoxicity in ratssupported
Small (2°C) changes in ambient temperature produce large changes in MDMA neurotoxicity and core temperature. jneurosci.18-13-05086.1998
Bexis and Docherty (2006) compared cardiovascular effects of MDMA, MDA, and MDEA in freely moving rats using radiotelemetrysupported
MDMA and MDA produced prolonged increases in blood and diastolic pressures; MDA caused the most marked rise. pmid:16491100
The pressor effect is mediated by alpha-1A and alpha-1D adrenoceptor agonism — MDA is the most potent alpha-1 agonist in the MDxx series.supported
MDA most potent at alpha1-adrenoceptors. pmid:16491100
In mice, MDA produced potent hyperthermia partially antagonized by bretylium and blocked by haloperidol, implicating both noradrenergic and dopaminergic mechanisms.supported
MDA had potent hyperthermic effect in mice partially antagonized by bretylium, blocked by haloperidol. pmid:1174022
The intravenous LD50 in dogs is 8.1 mg/kg (95% CI: 7.0–9.4 mg/kg), with LD1 ≈ 5 mg/kg and LD99 ≈ 14 mg/kgsupported
LD50 and 95% CI: 8.1 (7.0-9.4) mg/kg IV. LD1 approx 5 mg/kg, LD99 approx 14 mg/kg. pmid:3753103
At lethal IV doses, death was preceded by hyperthermia, tachycardia, and hypertension progressing to cardiovascular depression and respiratory failuresupported
High IV dose of MDA (20 mg/kg) in dogs elevated body temperature, heart rate, blood pressure initially then depression and death. pmid:3699443
Chlorpromazine (10 mg/kg IV) administered after MDA overdose led to stabilization and 48-hour survival in dogs.supported
Chlorpromazine (10 mg/kg IV) after MDA showed stabilization and 48h survival. pmid:3699443
De Letter et al. (2006) reviewed amphetamine-related fatalities in Ghent, Belgium from 1976–2004supported
In 34 fatalities, amphetamines were involved (including MDA). pmid:16454462
The Straumann et al. (2026) RCT documented significantly greater "fear" and "bad drug effects" with MDA compared to MDMA at equimolar dosessupported
MDA induced greater stimulant effects, more bad drug effects, more fear, more visual alterations. s41386-025-02248-3
MDA's greater stimulant and adverse effect burden compared to MDMA suggests that compulsive use patterns are pharmacologically plausible via dopaminergic reinforcement, but the elevated fear and dysphoria may paradoxically limit compulsive redosingsupported
MDA induced greater stimulant effects, more bad drug effects, more fear, more visual alterations. s41386-025-02248-3
In severe cases, serotonin syndrome manifests as hyperthermia, muscle rigidity, clonus, autonomic instability, and multiple organ failure.supported
Serotonin toxicity characterised by neuromuscular excitation (clonus, hyperreflexia, myoclonus, rigidity), autonomic stimulation (hyperthermia, tachycardia, diaphoresis). j.1326-5377.2007.tb01282.x
Tramadol: Tramadol inhibits SERT and NET at clinically relevant concentrationssupported
Opioids may inhibit the SERT and NET. Tramadol SERT inhibition may contribute to serotonin syndrome risk. bph.14105
Fluoxetine, paroxetine, quinidine, bupropion, and other CYP2D6 inhibitors reduce MDA metabolism, substantially increasing plasma MDA concentrations and toxicity risksupported
MDMA is a potent mechanism-based inhibitor (MBI) of CYP2D6...CYP2D6 inactivation relevant to MDA metabolism. pmid:16478752
The norepinephrine transporter inhibitor reboxetine reduces MDMA's cardiovascular and stimulant effects by blocking NET-mediated norepinephrine releasesupported
Reboxetine reduced MDMA effects including elevations in plasma NE, blood pressure and heart rate, drug high, stimulation...NE transporter-mediated NE release has critical role in cardiovascular and stimulant-like effects of MDMA. clpt.2011.78
Cardiovascular disease and hypertension: MDA is the most potent pressor agent in the MDxx seriessupported
MDA caused the most marked rise. MDA most potent at alpha1-adrenoceptors. pmid:16491100
Hepatic impairment: MDA metabolism is CYP2D6/CYP3A4 dependentsupported
demethylenation (CYP2D6 or CYP3A2/4) pmid:10720722
Mechanistic basis for lethal serotonin toxicity is established.supported
Tramadol SERT inhibition may contribute to serotonin syndrome risk. bph.14105
Mechanistic basis for lethal serotonin toxicity is established.supported
Severe serotonin toxicity only occurs with combinations of drugs acting at different sites. j.1326-5377.2007.tb01282.x
pharmacology19 · 15 ok
Claim in pharmacology — not_supportednot supportedworking →
Claim in pharmacology — inconclusiveinconclusiveworking →
Kolaczynska et al. (2022) established that MDA inhibits NET with the greatest potency among the three transporters and preferentially inhibits serotonin over dopamine uptakesupported
MDA, its fluorinated analogs...inhibited NET with the greatest potency and preferentially inhibited 5-HT vs. dopamine uptake. j.euroneuro.2022.03.006
The potency order for dopamine release from striatal synaptosomes is MDA > MDMA > MDEA = MDBA, while MDA and MDMA are equipotent at inducing serotonin release from cortical and hippocampal preparationssupported
MDA, MDMA and MDEA were equipotent at inducing [3H]5-HT release from frontal cortex/hippocampal synaptosomes...The potency order for inducing [3H]DA release from striatal synaptosomes was MDA > MDMA > MDEA = MDBA. pmid:11371001
The potency order for dopamine release from striatal synaptosomes is MDA > MDMA > MDEA = MDBA, while MDA and MDMA are equipotent at inducing serotonin release from cortical and hippocampal preparationssupported
MDA, MDMA and MDEA were equipotent at inducing [3H]5-HT release...The potency order for inducing [3H]DA release from striatal synaptosomes was MDA > MDMA > MDEA = MDBA. pmid:11371001
This greater dopaminergic releasing activity underlies MDA's more pronounced stimulant profile relative to MDMA, a difference confirmed in human subjects.supported
MDA induced greater stimulant effects, more bad drug effects, more fear, more visual alterations. s41386-025-02248-3
Unlike MDMA, MDA also binds and activates the 5-HT₂A receptor directly, with affinity in the low-micromolar range (Ki ≤ 10 µM in radioligand binding assays; partial or full agonist in functional activation assays)supported
Most compounds bound to 5-HT2A and 5-HT2C receptors (Ki ≤ 10 μM) and several substances activated the 5-HT2A and 5-HT2B receptor as partial or full agonists. j.euroneuro.2022.03.006
Drug discrimination studies confirm this dual character: MDA substitutes for both LSD and amphetamine in trained animals, while MDMA is primarily amphetamine-like at typical dosessupported
MDMA is apparently 'amphetamine-like' and not 'LSD-like' while MDA is apparently both 'LSD-like' and 'amphetamine-like.' pmid:1979215
The MDMA discriminative cue generalizes completely to MDA, confirming shared entactogen-class properties.supported
MDMA cue completely generalized to MDA but not to LSD or DOM. pmid:2898791
Claim in pharmacology — inconclusiveinconclusiveworking →
Plasma elimination half-life (geometric mean) is 8.4 hours, measured in the same crossover RCT at 92 mg oral (for comparison, MDMA half-life was 7.3 hours under identical conditions)supported
Plasma half-life: MDMA 7.3h, MDA 8.4h. s41386-025-02248-3
MDA undergoes hepatic metabolism through two primary pathways:supported
demethylenation (CYP2D6 or CYP3A2/4) followed by COMT methylation and/or glucuronide/sulfate conjugation; N-dealkylation and deamination to benzoic acid derivatives. pmid:10720722
Claim in pharmacology — inconclusiveinconclusiveworking →
Poor CYP2D6 metabolizers and individuals taking CYP2D6 inhibitors (fluoxetine, paroxetine, quinidine) will experience elevated MDA plasma concentrations and increased toxicity risksupported
MDMA is a potent mechanism-based inhibitor (MBI) of CYP2D6...CYP2D6 inactivation relevant to MDA metabolism. pmid:16478752
These thioether metabolites cross the blood-brain barrier, stimulate acute monoamine release, and cause long-term serotonergic neuronal death, elevated GFAP expression (an astrogliosis marker), and microglial activationsupported
their thioether conjugates stimulate acute release of serotonin, dopamine, and norepinephrine and produce long-term depletions in serotonin concentrations, elevations in GFAP expression, and activation of microglial cells. pmid:15228153
These thioether metabolites cross the blood-brain barrier, stimulate acute monoamine release, and cause long-term serotonergic neuronal death, elevated GFAP expression (an astrogliosis marker), and microglial activationsupported
Thioether MDMA metabolites are strong neurotoxins, significantly more than their parent catechols...Hyperthermia (40°C) accelerated neuronal death. pmid:17467183
Critically, MDA does not produce neurotoxicity when injected directly into the brain — only when administered peripherally, demonstrating that hepatic metabolism to these reactive intermediates is required for neurotoxicitysupported
Neither MDA nor MDMA produces neurotoxicity when injected directly into brain. pmid:15228153
Alpha-MeDA is more neurotoxic than MDA itself, and the glutathione-thioether conjugates are the most toxic species in the pathway.partially supported
Thioether MDMA metabolites are strong neurotoxins, significantly more than their parent catechols. N-Me-alpha-MeDA and alpha-MeDA are more neurotoxic than MDMA. pmid:17467183
MDA is produced in vivo by N-demethylation of MDMA at a plasma ratio of approximately 3–5:100 (MDA:MDMA)supported
MDMA biotransformed into MDA; plasma MDA:MDMA ratio 3-5/100 in monkeys, similar to humans. pmid:15999148
summary13 · 11 ok
It produces stimulant, entactogenic, and psychedelic effects over a total duration of approximately 5–8 hours (mean 6.1 ± 0.5 hours at 92 mg oral), placing it at the intersection of three pharmacological classes — a profile shared by few other compounds.supported
MDA produced stronger/longer-lasting effects (6.1±0.5h vs 4.1±0.4h). MDA induced greater stimulant effects...more visual alterations. s41386-025-02248-3
It served as a conceptual anchor for David Nichols' 1986 coinage of the term "entactogen"supported
Seminal paper coining the term 'entactogen' for a new pharmacological class including MDA and MDMA, distinguishing them from classic hallucinogens and stimulants. pmid:2880944
No clinical trials have investigated MDA as a primary therapeutic agent; the compound's current research significance lies in comparative pharmacology with mdma, where a 2026 head-to-head RCT established MDA's distinct psychedelic and adverse-effect profile.supported
MDA (92mg) vs MDMA (100mg) equimolar crossover. MDA induced greater stimulant effects, more bad drug effects, more fear, more visual alterations. NCT04847206. s41386-025-02248-3
MDA acts as a substrate-type releaser at the serotonin, dopamine, and norepinephrine transporters, with greatest potency at NET and greater dopaminergic releasing activity than MDMApartially supported
MDA, its fluorinated analogs...inhibited NET with the greatest potency and preferentially inhibited 5-HT vs. dopamine uptake. j.euroneuro.2022.03.006
MDA acts as a substrate-type releaser at the serotonin, dopamine, and norepinephrine transporters, with greatest potency at NET and greater dopaminergic releasing activity than MDMApartially supported
The potency order for inducing [3H]DA release from striatal synaptosomes was MDA > MDMA > MDEA = MDBA. pmid:11371001
Claim in summary — not_supportednot supportedworking →
Claim in summary — inconclusiveinconclusiveworking →
Set and setting modulate the balance between prosocial warmth and anxiety, a dynamic confirmed by the elevated "fear" and "bad drug effects" scores reported under controlled conditions.supported
MDA induced greater stimulant effects, more bad drug effects, more fear, more visual alterations. s41386-025-02248-3
In preclinical models, it produces greater selective serotonergic axon terminal ablation at equivalent doses, mediated by neurotoxic thioether metabolites of alpha-methyldopamine formed via CYP2D6supported
MDA/MDMA cause selective serotonergic axon terminal ablation in rat forebrain. MDA more neurotoxic than MDMA at same dose. Catecholamine axons completely spared. pmid:2457659
In preclinical models, it produces greater selective serotonergic axon terminal ablation at equivalent doses, mediated by neurotoxic thioether metabolites of alpha-methyldopamine formed via CYP2D6supported
Alpha-methyldopamine (alpha-MeDA) and N-methyl-alpha-MeDA are metabolites of both MDA and MDMA; their thioether conjugates...produce long-term depletions in serotonin concentrations, elevations in GFAP expression. pmid:15228153
In preclinical models, it produces greater selective serotonergic axon terminal ablation at equivalent doses, mediated by neurotoxic thioether metabolites of alpha-methyldopamine formed via CYP2D6supported
MDMA and MDA are O-demethylenated to N-Me-alpha-MeDA and alpha-MeDA (catechols) which oxidize to ortho-quinones and conjugate with glutathione. Thioether MDMA metabolites are strong neurotoxins. pmid:17467183
Cardiovascular risk is elevated: MDA is the most potent pressor agent among the MDxx compounds, acting through alpha-1 adrenoceptor agonismsupported
MDA caused the most marked rise [in blood pressure]. MDA most potent at alpha1-adrenoceptors. pmid:16491100
Ambient temperature strongly modulates neurotoxicity — small increases in environmental heat dramatically amplify serotonergic damagesupported
Small (2°C) changes in ambient temperature produce large changes in MDMA neurotoxicity and core temperature. jneurosci.18-13-05086.1998
receptor-pharmacology9 · 8 ok
Kolaczynska et al. (2022) characterized the transporter potency profile: MDA inhibits NET with the greatest potency, followed by SERT, with DAT inhibition being weakestsupported
MDA...inhibited NET with the greatest potency and preferentially inhibited 5-HT vs. dopamine uptake. j.euroneuro.2022.03.006
This triple-releasing profile is shared across the MDxx series, but MDA's relative dopaminergic potency exceeds that of MDMA: the rank order for dopamine release from striatal synaptosomes is MDA > MDMA > MDEA.supported
The potency order for inducing [3H]DA release from striatal synaptosomes was MDA > MDMA > MDEA = MDBA. pmid:11371001
Kolaczynska et al. (2022) reported Ki ≤ 10 µM in radioligand binding and partial-to-full agonist activity in functional assayssupported
Most compounds bound to 5-HT2A and 5-HT2C receptors (Ki ≤ 10 μM) and several substances activated the 5-HT2A and 5-HT2B receptor as partial or full agonists. j.euroneuro.2022.03.006
This 5-HT₂A agonism is pharmacologically confirmed in vivo: Teitler et al. (1990) demonstrated that MDA is both "LSD-like" and "amphetamine-like" in drug discrimination paradigms, a dual substitution pattern that requires 5-HT₂A activation (for the LSD cue) in addition to monoamine release (for the amphetamine cue)supported
MDA is apparently both 'LSD-like' and 'amphetamine-like'...The data...strongly implicate the brain 5HT2 receptor as the site-of-action of the hallucinogenic PIAs and LSD. pmid:1979215
MDA binds the 5-HT₂C receptor (Ki ≤ 10 µM) and activates it as a partial or full agonist. 5-HT₂C activation generally opposes dopaminergic transmission in mesolimbic circuits and may contribute to appetite suppression and anxiogenic effects.partially supported
Most compounds bound to 5-HT2A and 5-HT2C receptors (Ki ≤ 10 μM) and several substances activated the 5-HT2A and 5-HT2B receptor as partial or full agonists. j.euroneuro.2022.03.006
MDA is the most potent compound among the MDxx series at alpha-1A and alpha-1D adrenoceptorssupported
MDA most potent at alpha1-adrenoceptors. pmid:16491100
This alpha-1 agonism is the primary mechanism for MDA's pressor effects — the most marked blood pressure elevation among MDMA, MDA, and MDEA in radiotelemetry studiessupported
MDMA and MDA produced prolonged increases in blood and diastolic pressures; MDA caused the most marked rise. MDA most potent at alpha1-adrenoceptors. pmid:16491100
Claim in receptor-pharmacology — inconclusiveinconclusiveworking →
MDA modulates human GABA-A receptors (α₁β₂γ₂ subunit composition) in a bidirectional, occupancy-dependent manner: inhibition at low receptor occupancy and potentiation at high occupancysupported
MDMA and its metabolite MDA both inhibited the GABA-evoked current at low receptor occupancy. However...MDA induced a potentiation. j.neuro.2011.05.016
neuroscience6 · 2 ok
MDA's equipotent serotonin release relative to MDMA suggests comparable engagement of these circuits, though the simultaneous 5-HT₂A agonism may modulate the qualitative character of the experience.supported
MDA, MDMA and MDEA were equipotent at inducing [3H]5-HT release from frontal cortex/hippocampal synaptosomes. pmid:11371001
Claim in neuroscience — inconclusiveinconclusiveworking →
Claim in neuroscience — inconclusiveinconclusiveworking →
Claim in neuroscience — inconclusiveinconclusiveworking →
The greater stimulant effects of MDA relative to MDMA in human subjects reflect this enhanced catecholaminergic profile.supported
MDA induced greater stimulant effects, more bad drug effects, more fear, more visual alterations. s41386-025-02248-3
Claim in neuroscience — inconclusiveinconclusiveworking →
pharmacokinetic-detail5 · 2 ok
Claim in pharmacokinetic-detail — inconclusiveinconclusiveworking →
Claim in pharmacokinetic-detail — inconclusiveinconclusiveworking →
Like MDMA, MDA is expected to exhibit mechanism-based (irreversible) inhibition of CYP2D6, meaning the enzyme that metabolizes MDA is destroyed in the processsupported
MDMA is a potent mechanism-based inhibitor (MBI) of CYP2D6, causing quasi-irreversible inhibition in vitro...CYP2D6 inactivation relevant to MDA metabolism. pmid:16478752
Phase I metabolism proceeds through two principal routes:supported
Phase I and II metabolites of MDA identified in human urine: demethylenation (CYP2D6 or CYP3A2/4)...N-dealkylation and deamination to benzoic acid derivatives. pmid:10720722
Claim in pharmacokinetic-detail — inconclusiveinconclusiveworking →
clinical-evidence3 · 2 ok
The only published RCT specifically designed around MDA's psychedelic properties:supported
RCT investigating mechanisms of drug-induced visions using MDA in humans. Very few serotonergic hallucinogens have been studied in humans in decades. journal.pone.0014074
Claim in clinical-evidence — inconclusiveinconclusiveworking →
The definitive comparative human pharmacology study:supported
N=23 healthy participants. MDA (92mg) vs MDMA (100mg) equimolar crossover...Plasma half-life: MDMA 7.3h, MDA 8.4h. s41386-025-02248-3
comparative-pharmacology3 · 2 ok
In the dopamine release rank order, MDEA = MDBA and both fall below MDMA, which falls below MDAsupported
The potency order for inducing [3H]DA release from striatal synaptosomes was MDA > MDMA > MDEA = MDBA. pmid:11371001
Claim in comparative-pharmacology — inconclusiveinconclusiveworking →
Schindler et al. (2014) demonstrated that MDA is a cardiovascular-active MDMA metabolite, contributing to the pressor and tachycardic effects observed during MDMA sessionssupported
Cardiovascular effects of MDMA and its metabolites in conscious rats. Metabolites including MDA contribute to cardiovascular effects of MDMA. bph.12423
chemistry2 · 0 ok
history2 · 2 ok
In 1986, David Nichols published a landmark paper coining the term "entactogen" — literally "touching within" — to describe a novel pharmacological class encompassing MDA, MDMA, and MBDB, distinguished from both classical hallucinogens and amphetamine-type stimulantssupported
Seminal paper coining the term 'entactogen' for a new pharmacological class including MDA and MDMA, distinguishing them from classic hallucinogens and stimulants. pmid:2880944
The most significant modern study is a Phase 1 trial at the University Hospital Basel (NCT04847206, completed) that included MDA as a comparator arm alongside MDMA and their lysine prodrugs, generating the definitive head-to-head human data published by Straumann et al. in 2026supported
N=23 healthy participants. MDA (92mg) vs MDMA (100mg) equimolar crossover...NCT04847206. s41386-025-02248-3
effects-overview1 · 1 ok
The anxiogenic potential is higher than with MDMA — fear and dysphoria are reported even in controlled settings — making psychological preparation and environment more consequential.supported
MDA induced greater stimulant effects, more bad drug effects, more fear, more visual alterations. s41386-025-02248-3
legal-status1 · 0 ok
Claim in legal-status — inconclusiveinconclusiveworking →