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PsychedeliaDokholyan Laboratory
Plate 395 of 545Verified

MDA

PubChem records this structure as 3,4-Methylenedioxyamphetamine.

Also known as3,4-Methylenedioxyamphetamine · Tenamfetamine · Methylenedioxyamphetamine · Tenamfetaminum · Love · methylene dioxyamphetamine · Tenanfetamina · 3,4 Methylenedioxyamphetamine

1-(1,3-benzodioxol-5-yl)propan-2-amine

PubChem CID
1614
Measurements
15
InChIKey
NGBBVGZWCFBOGO-UHFFFAOYSA-N

I · Summary

What is known

Published passages, each quoted whole and attributed to the database that published it. Two blocks are written here rather than quoted, and both say so where they stand: the synthesized summary at the top, which may draw only on the passages beneath it, and the history note, which cites the works it came from. Every claim in either carries a marker to its source.

What it is

  • An amphetamine derivative that inhibits uptake of catecholamine neurotransmitters. It is a hallucinogen. It is less toxic than its methylated derivative but in sufficient doses may still destroy serotonergic neurons and has been used for that purpose experimentally.

    Medical Subject Headings (MeSH)

Recognized use

  • Adrenergic Uptake Inhibitors; Hallucinogens; Serotonin Agents

    Therapeutic Uses

    Hazardous Substances Data Bank (HSDB)National Library of Medicine's Medical Subject Headings online file (MeSH, 1999)

  • ... Destroys serotonergic neurons and has been used for that purpose experimentally.

    Use Classification

    Hazardous Substances Data Bank (HSDB)Wishart DS et al; DrugBank: a comprehensive resource for in silico drug discovery and exploration. Nucleic Acids Res. 2006 1;34. Available from, as of Feb 11, 2008: https://redpoll.pharmacy.ualberta.ca/drugbank/

  • Pharmaceuticals -> Illicit drugs and related compounds -> Transformation products

    Use Classification

    NORMAN Suspect List ExchangeS66 | EAWAGTPS | Parent-Transformation Product Pairs from Eawag | DOI:10.5281/zenodo.3754448

How it acts

  • Phenylethylamines act on the peripheral and central nervous system by alpha- and beta-adrenergic stimulation. These compounds may also have varying degrees of serotonergic and dopaminergic activity, depending on structural similarity to mescaline. /Phenylethylamines/

    Hazardous Substances Data Bank (HSDB)Haddad, L.M. (Ed). Clinical Management of Poisoning and Drug Overdose 3rd Edition. Saunders, Philadelphia, PA. 1998., p. 574

  • The effect of various analogues of the neurotoxic amphetamine derivative, MDA (3,4-methylenedioxyamphetamine) on carrier-mediated, calcium-independent release of 3H-5-HT and 3H-DA from rat brain synaptosomes was investigated. Both enantiomers of the neurotoxic analogues MDA and MDMA (3,4-methylenedioxymethamphetamine) induce synaptosomal release of 3H-5-HT and 3H-DA in vitro. The release of 3H-5-HT induced by MDMA is partially blocked by 10(-6) M fluoxetine. The (+) enantiomers of both MDA and MDMA are more potent than the (-) enantiomers as releasers of both 3H-5-HT and 3H-DA. ... Possible long-term serotonergic neurotoxicity was assessed by quantifying the density of 5-HT uptake sites in r…

    Hazardous Substances Data Bank (HSDB)PMID 1829838McKenna DJ et al; Pharmacol Biochem Behav 38 (3): 505-12 (1991)

Behavior carries the pharmacological classes and the acute-effect durations, with plasma half-life kept separate from duration of effect.

In the body

  • ... This paper describes for the first time an evaluation of the concentrations of methylenedioxymethamphetamine (MDMA) and 3,4-methylenedioxyamphetamine (MDA) found in five fatalities admitted to hospital where both antemortem and postmortem blood samples were available. Admission MDMA and MDA concentrations ranged between 0.55 and 4.33 mg/L and 0 and 0.10 mg/L, respectively, in antemortem serum/plasma. Postmortem blood MDMA and MDA concentrations ranged between 0.47 and 28.39 mg/L and 0.02 and 1.33 mg/L, respectively. Postmortem concentrations were higher than corresponding antemortem concentrations in all 5 cases with postmortem/antemortem ratios between 1.1 and 6.6 for MDMA and 1.5 and 1…

    Absorption, Distribution and Excretion

    Hazardous Substances Data Bank (HSDB)PMID 16105252Elliott SP; J Anal Toxicol 29 (5): 296-300 (2005)

  • Data ... reported /here/ include postmortem distribution of methylenedioxymethamphetamine (MDMA) and methylenedioxyamphetamine (MDA) in heart blood, gastric content, urine, and bile specimens from 20 fatal cases; other drugs found in the heart blood from these 20 cases; and the distribution of MDMA and MDA in 25 antemortem urine and 6 hair specimens. The MDA/MDMA concentration ratio observed in a limited number of hair specimens (n=6) are consistent and appear to be higher than those found in other specimens. Compared to other commonly abused drugs (e.g., cocaine and heroin), the "drug/metabolite" concentration ratio (MDMA/MDA) in hair is not significantly different from the ratios derived f…

    Absorption, Distribution and Excretion

    Hazardous Substances Data Bank (HSDB)PMID 16105252Liu RH et al; J Anal Toxicol 30 (8): 545-50 (2006)

  • The phase I and II metabolites of the designer drugs methylenedioxyamphetamine (MDA), R,S-methylenedioxymethamphetamine (MDMA), R,S-methylenedioxyethylamphetamine (MDE), R, S-benzodioxazolylbutanamine (BDB) and R, S-N-methyl-benzodioxazolylbutanamine (MBDB) were identified by gas chromatography-mass spectrometry (GC-MS) or liquid chromotography-mass spectrometry (LC-MS) in urine and liver microsomes of humans and rats. Two overlapping pathways could be postulated: (1) demethylenation followed by catechol-O-methyl-transferase (COMT) catalyzed methylation and/or glucuronidation/sulfatation; (2) N-dealkylation, deamination and only for MDA, MDMA, MDE oxidation to the corresponding benzoic acid…

    Metabolism/Metabolites

    Hazardous Substances Data Bank (HSDB)PMID 10720722Maurer HH et al; Toxicol Lett 112-113: 133-42 (2000)

  • The two major metabolites of (+/-)3,4-methylenedioxyamphetamine (MDA), alpha-methyldopamine (alpha-MeDA) and 3-O-methyl-alpha-methyldopamine (3-O-Me-alpha-MeDA), were administered to rats intracerebroventricularly and into brain parenchyma. In addition, their precursors, (alpha-MeDOPA and 3-O-Me-alpha-MeDOPA, respectively) were administered systemically, individually and in combination. None of these treatments produced a lasting depletion of brain serotonin (5-HT). These findings suggest that neither of MDA's major metabolites mediate its toxic effects on 5-HT neurons and that either a minor metabolite is responsible or that alternate mechanisms are involved.

    Metabolism/Metabolites

    Hazardous Substances Data Bank (HSDB)PMID 1860050McCann UD, Ricaurte GA; Brain Res 545 (1-2): 279-82 (1991)

  • 3,4-Methylenedioxyamphetamine (MDA) and 3,4-methylenedioxymethamphetamine (MDMA, ecstasy) are ring-substituted amphetamine derivatives with stimulant and hallucinogenic properties. The recreational use of these amphetamines, especially MDMA, is prevalent despite warnings of irreversible damage to the central nervous system. MDA and MDMA are primarily serotonergic neurotoxicants. Because (1) neither MDA nor MDMA produces neurotoxicity when injected directly into brain, (2) intracerebroventricular (i.c.v.) administration of some major metabolites of MDA and MDMA fails to reproduce their neurotoxicity, (3) alpha-methyldopamine (alpha-MeDA) and N-methyl-alpha-MeDA are metabolites of both MDA and…

    Metabolism/Metabolites

    Hazardous Substances Data Bank (HSDB)PMID 15228153Momks TJ et al; Ther Drug Monit 26 (2): 132-6 (2004)

  • 3,4-Methylenedioxyamphetamine (MDA) and 3,4-methyl-enedioxymethamphetamine (MDMA, ecstasy) are widely abused amphetamine derivatives that target the serotonin system. The serotonergic neurotoxicity of MDA and MDMA seems dependent on their systemic metabolism. 5-(Glutathion-S-yl)-alpha-methyldopamine [5-(GSyl)-alpha-MeDA] and 2,5-bis(glutathion-S-yl)-alpha-methyldopamine [2,5-bis(GSyl)-alpha-MeDA], metabolites of MDA and MDMA, are also selective serotonergic neurotoxicants and produce behavioral and neurochemical changes similar to those seen with MDA and MDMA. 5-(GSyl)-alpha-MeDA and 2,5-bis(GSyl)-alpha-MeDA are more potent than MDA and MDMA (K(i) = 69, 50, 107, and 102 microM, respectively)…

    Metabolism/Metabolites

    Hazardous Substances Data Bank (HSDB)PMID 15169827Jones DC et al; J Pharmacol Exp Ther 311 (1): 298-306 (2004)

History, discovery and cultural use

— Not in this archive. PubChem, ChEMBL and the Human Protein Atlas publish pharmacology, regulation and toxicology, and none of them publishes a heading for when MDA was first made, by whom, or how it has been used. That is a gap in the databases this site reads and not a gap in the literature — the history of these compounds is written, at length and under peer review, in the works below. This site does not summarize them; it says where they are. Where a published passage above happens to touch origin or traditional use, it appears inside the entry that carries it.

Histories of this field

Scholarship on psychedelics generally, not on MDA specifically. Whether any of these treats this compound is a question for the book, not for this page.

  • Mescaline: A Global History of the First Psychedelic

    Traces mescaline and the peyote and San Pedro cacti from pre-Columbian ritual use through nineteenth-century chemistry to twentieth-century psychiatry and the counterculture.

    Jay M. Mescaline: A Global History of the First Psychedelic. Yale University Press, New Haven and London; 2019. ISBN 9780300231076.

  • Expanding Mindscapes: A Global History of Psychedelicsopen access

    Essays on the international and cross-cultural history of psychedelic science, deliberately decentring the standard North American and European account.

    Dyck E, Elcock C, editors. Expanding Mindscapes: A Global History of Psychedelics. The MIT Press, Cambridge MA; 2023. ISBN 9780262546935 (paper), 9780262376891 (open access). doi:10.7551/mitpress/14417.001.0001.

  • Plants of the Gods: Their Sacred, Healing, and Hallucinogenic Powers

    Botany, ethnography and chemistry of the principal hallucinogenic plants, by the founder of modern ethnobotany and the chemist who first synthesized LSD.

    Schultes RE, Hofmann A, Rätsch C. Plants of the Gods: Their Sacred, Healing, and Hallucinogenic Powers. 2nd ed. Healing Arts Press, Rochester VT; 2001. ISBN 9780892819799.

  • Psychonauts: Drugs and the Making of the Modern Mind

    The tradition of scientific self-experimentation with psychoactive drugs, and its part in the emergence of psychology and of modernism.

    Jay M. Psychonauts: Drugs and the Making of the Modern Mind. Yale University Press, New Haven; 2023. ISBN 9780300257946.

  • Ancient Psychoactive Substances

    Archaeological and bioarchaeological evidence for psychoactive plant use across the ancient world.

    Fitzpatrick SM, editor. Ancient Psychoactive Substances. University Press of Florida, Gainesville; 2018. ISBN 9780813056708.

  • History and Current Status of Psychedelics and Entactogens for the Treatment of Psychiatric Disorders

    A chapter tracing psychedelic and entactogen research from earlier ritual use through the mid-century research period to current clinical trials.

    Stroud C, Posey Norris SM, Matney C, editors. History and Current Status of Psychedelics and Entactogens for the Treatment of Psychiatric Disorders. In: Exploring Psychedelics and Entactogens as Treatments for Psychiatric Disorders: Proceedings of a Workshop. National Academies Press, Washington DC; 2022. NBK587225.

    Workshop proceedings record what participants said; they are not a consensus statement of the National Academies.

  • Pharmacokinetic and Pharmacodynamic Aspects of Peyote and Mescaline: Clinical and Forensic Repercussions

    Peer-reviewed review covering the isolation, synthesis, pharmacology and ritual use of peyote and mescaline.

    Dinis-Oliveira RJ, Pereira CL, da Silva DD. Pharmacokinetic and Pharmacodynamic Aspects of Peyote and Mescaline: Clinical and Forensic Repercussions. Current Molecular Pharmacology 12(3):184–194; 2019. doi:10.2174/1874467211666181010154139.

Institutional archives

  • Heffter Research Institute Funds and coordinates clinical research on psilocybin, and keeps records of the studies it has supported since 1993. Sponsors the research it archives.
  • Multidisciplinary Association for Psychedelic Studies (MAPS) Sponsors clinical research, chiefly on MDMA-assisted therapy, and publishes an archive of historical and contemporary documents. A sponsor and an advocacy organization, not a disinterested archive; its clinical programme has a commercial arm.

The rest of this dossier

  • Affinity — 15 measurements in this archive, equilibrium constants kept apart from functional readouts.
  • Toxicology — 10 published passages, plus any assay in this archive bearing on toxicity.
  • Legal — listed by the DEA among its drugs of concern, with no schedule stated in the record held here.
  • Systems — where this compound’s targets are transcribed, by brain region and tissue.

Passages via PubChem descriptive sections, aggregating DrugBank, LiverTox, FDA, DEA, HSDB, EPA. Each is quoted whole and attributed to the database that published it. The only prose written here about MDA is the history note, which says so on its face and carries a reference for every claim in it.

II · Identity

Structure and descriptors

Descriptors are computed here with RDKit from the structure PubChem returns — not from the archive's stored copy, so an edited local structure cannot reach this table.

2D structural depiction of MDA
Depiction served by PubChem for CID 1614. Not redrawn here, so the picture and the identity come from the same record.
Formula
C10H13NO2R
Molecular weight
179.22g/molR
Exact mass
179.0946DaR
cLogP
1.30R
TPSA
44.5ŲR
H-bond donors
1R
H-bond acceptors
3R
Rotatable bonds
2R
Aromatic rings
1R
Heavy atoms
13R
Fraction sp³
0.400R
Formal charge
0R

Computed with RDKit 2025.09.2 from the SMILES returned by PubChem. Audit run 26/09/2026.

Bemis–Murcko scaffold

c1ccc2c(c1)OCO2

Shared with 1,3-Benzodioxolyl-N-ethylbutanamine, 1,3-Benzodioxolyl-N-ethylpentanamine, 1,3-Benzodioxolyl-N-methylpentanamine, 1,3-Benzodioxolylbutanamine, 2-Bromo-4,5-methylenedioxyamphetamine, 2,3-Dimethoxy-4,5-methylenedioxyamphetamine and 31 more. All families

III · Behavior

Behavioral summary

Class, mechanism, and the duration of acute effects — each quoted from the record or trial that publishes it. Duration of effects and plasma half-life are shown separately, because they are different quantities and diverge by a factor of three or four.

Classification

Duration of acute subjective effects

6.1 ± 0.5 h

125 mg, oral

“MDA produced stronger and longer-lasting subjective "any drug effects" compared with MDMA, with effect durations of (mean ± SEM) 6.1 ± 0.5 vs 4.1 ± 0.4 h, respectively”
Straumann I et al., Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology 2026. PMID 40999236

Plasma elimination half-life

How fast the body clears the drug — not how long the effects last. The two diverge sharply: LSD is cleared with a half-life of about 2.6 h while its subjective effects run 8–12 h.

No half-life is published for this compound in the sources this site reads.

Primary pharmacological drivers

ChEMBL holds no curated mechanism-of-action record for this compound. The measured affinities below are the evidence this archive has for what it binds.

Mechanism, as published

Quoted verbatim from the database named after each passage, never summarized.

  • The effect of various analogues of the neurotoxic amphetamine derivative, MDA (3,4-methylenedioxyamphetamine) on carrier-mediated, calcium-independent release of 3H-5-HT and 3H-DA from rat brain synaptosomes was investigated. Both enantiomers of the neurotoxic analogues MDA and MDMA (3,4-methylenedioxymethamphetamine) induce synaptosomal…
    Hazardous Substances Data Bank (HSDB)PMID 1829838McKenna DJ et al; Pharmacol Biochem Behav 38 (3): 505-12 (1991)
  • The effect of the R(-) and S(+) isomers of 3,4-methylenedioxyamphetamine (MDA) and its N-methyl analog 3,4-methylenedioxymethamphetamine (MDMA) on [3H]inositol monophosphate accumulation was studied in cells expressing either 5-HT2A or 5-HT2C receptors. The isomers of MDA produced a concentration dependent increase in phosphatidyl inosito…
    Hazardous Substances Data Bank (HSDB)PMID 7824160Nash JF et al; Neurosci Lett 177 (1-2): 111-5 (1994)
  • Phenylethylamines act on the peripheral and central nervous system by alpha- and beta-adrenergic stimulation. These compounds may also have varying degrees of serotonergic and dopaminergic activity, depending on structural similarity to mescaline. /Phenylethylamines/
    Hazardous Substances Data Bank (HSDB)Haddad, L.M. (Ed). Clinical Management of Poisoning and Drug Overdose 3rd Edition. Saunders, Philadelphia, PA. 1998., p. 574

IV · Clinical

Clinical description

Where this compound's substance class sits in ICD-11 and DSM-5-TR, and how much of the recorded literature speaks to each domain of a mental status examination.

Filed under Hallucinogens

  • 6C49Disorders due to use of hallucinogens

Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, Text Revision (DSM-5-TR): Hallucinogen-Related Disorders. Category names only — the manual is in copyright and no diagnostic criterion is reproduced here.

How much has been written about each domain

The clinical domains, and how many of the records this archive holds for this compound say something under each. What the terms mean, and the word list behind every spoke, are set out in the method.

Affect0Mood0Perception2Cognition2Thought process0Thought content0Psychomotor activity2Insight and judgment0
This measures the literature, not the compound. Each spoke counts how many of the 14 records this archive holds for this compound say something under that domain — 2 at the widest ring. A long spoke means the subject has been written about, not that the effect is strong, and a spoke at the center means nothing here discusses it rather than that nothing happens. The terms behind each domain are listed in the method.
Perception 2
matched on “altered perception”, “hallucinogen” · in Toxicology: Hazardous Substances Data Bank (HSDB); PMID 7283563
Cognition 2
matched on “attention”, “concentrat” · in PMID 7824160; PMID 3285124
Psychomotor activity 2
matched on “agitat” · in PMID 3285124; Toxicology: Hazardous Substances Data Bank (HSDB)

V · Systems

Systems physiology

Where the targets this compound binds are transcribed — brain regions on the left, peripheral and autonomic tissues on the right. A join of two measurements, not a claim about what the compound does to either.

Brain

cerebral cortex — 18.2 nTPM, from HTR2A, HTR2C, SLC6A3cerebellum — 0.2 nTPM, from HTR2A, SLC6A4hippocampal formation — 2.7 nTPM, from HTR2A, HTR2Camygdala — 3.5 nTPM, from HTR2A, HTR2C, SLC6A3hypothalamus — 12.6 nTPM, from HTR2C, HTR2A, SLC6A3thalamus — no resolved target expressed herebasal ganglia — 28.2 nTPM, from HTR2C, HTR2Amedulla oblongata — no resolved target expressed here

basal ganglia: drawn as the caudate nucleus, putamen and globus pallidus.

Measured but not drawn — this anatomogram has no outline for them: midbrain 92.9, spinal cord 1.0, retina 0.7, pituitary gland 0.4.

Body

heart — 0.9 nTPM, from SLC6A4, HTR2Asmooth muscle — 2.4 nTPM, from HTR2A, SLC6A2lung — 27.2 nTPM, from SLC6A4, HTR2A, SLC6A3liver — 0.2 nTPM, from SLC6A2, HTR2Akidney — 0.5 nTPM, from SLC6A3, SLC6A4, HTR2Astomach — 0.8 nTPM, from SLC6A4, HTR2A, SLC6A3duodenum — 9.7 nTPM, from SLC6A4, HTR2Asmall intestine — 38.0 nTPM, from SLC6A4, HTR2A, SLC6A2colon — 0.5 nTPM, from HTR2A, SLC6A4adrenal gland — 9.9 nTPM, from SLC6A2, HTR2A, SLC6A4thyroid gland — 0.7 nTPM, from SLC6A3, SLC6A4, HTR2Apancreas — 1.3 nTPM, from SLC6A4urinary bladder — 0.8 nTPM, from HTR2A, SLC6A3, SLC6A2skeletal muscle — 0.3 nTPM, from HTR2Aspleen — 0.1 nTPM, from SLC6A4salivary gland — 1.1 nTPM, from SLC6A2, SLC6A4, HTR2A
093 nTPM

Square-root ramp · shared scale across both plates

Shading is transcript level — not affinity, and not affinity combined with expression. Outlined but unshaded organs hold none of this compound’s resolved targets above the atlas’s detection threshold. Anatomy from EMBL-EBI Anatomogram (Apache License 2.0); regions identified by Uberon (uberon.org), CC BY 3.0.

Brain regions

Regions where this compound's measured targets are transcribed. Linked from the plate above.

  1. midbrain

    92.9 nTPM

  2. basal ganglia

    28.2 nTPM

  3. cerebral cortex

    18.2 nTPM

  4. hypothalamus

    12.6 nTPM

  5. amygdala

    3.5 nTPM

  6. hippocampal formation

    2.7 nTPM

  7. spinal cord

    1.0 nTPM

  8. retina

    0.7 nTPM

  9. pituitary gland

    0.4 nTPM

  10. cerebellum

    0.2 nTPM

Peripheral & autonomic

Tissues outside the CNS expressing the same targets — where a compound's bodily effects become possible.

  1. small intestine

    38.0 nTPM

  2. lung

    27.2 nTPM

  3. adrenal gland

    9.9 nTPM

  4. duodenum

    9.7 nTPM

  5. smooth muscle

    2.4 nTPM

  6. pancreas

    1.3 nTPM

  7. salivary gland

    1.1 nTPM

  8. heart muscle

    0.9 nTPM

  9. urinary bladder

    0.8 nTPM

  10. stomach 1

    0.8 nTPM

  11. thyroid gland

    0.7 nTPM

  12. colon

    0.5 nTPM

  13. kidney

    0.5 nTPM

  14. skeletal muscle

    0.3 nTPM

  15. liver

    0.2 nTPM

  16. spleen

    0.1 nTPM

Each row joins two published measurements and nothing else: the affinity this archive holds for the compound at that target, and the transcript level the Human Protein Atlas reports for that target’s gene in that region. Bars scale with expression only. Expression is not activation — a receptor transcribed in a region is a receptor available to be bound there, which is a weaker and more defensible claim than saying the region is affected.

2 of this compound’s targets could not be resolved to a gene and are absent from both columns: 5-HT2, Serotonin (5-HT) receptor.

Expression data from Human Protein Atlas (CC BY-SA 3.0), RNA expression, nTPM (normalized transcripts per million), consensus tissue dataset. Uhlén M, et al. Tissue-based map of the human proteome. Science. 2015;347(6220):1260419.

VI · Profile

Affinity rosette

The strongest measurement at each of 7 molecular targets. Cell-line and whole-organism screens are excluded here — they carry no affinity — and appear in the table below.

Serotonin (5-HT) receptor — Kd 6.45 pX5-HT2A — Ki 6.41 pX5-HT2C — Ki 5.68 pX5-HT2 — Ki 5.66 pXNET — IC50 6.58 pXSERT — IC50 6.32 pXDAT — IC50 6.05 pXSerotonin (5-HT)…5-HT2A5-HT2C5-HT2NETSERTDAT579
Fig. Radius is pX = −log₁₀(value in M), that is 9 − log₁₀(value in nM), computed from the normalized measurement. Hatched wedges are equilibrium binding constants (Ki, Kd); dashed outlines are functional readouts (IC₅₀, EC₅₀, AC₅₀, potency), which answer a different question and are not pooled with them. Rings mark whole pX units from 5 to 10, labeled every second ring in the gutter at the top. Where a target carries several measurements, the strongest is drawn.

VII · Toxicology

Toxicological profile

What has been measured, and what has been published — kept apart, and neither scored. There is no risk rating on this page; the archive once carried one, identical for every compound, produced by a stub.

Measured in this archive

Assays that bear on toxicity, drawn from the same ChEMBL records as everything else on this page. They are measurements of what a compound binds or does to cells — not verdicts about what it does to a person.

No hERG, cytochrome, cytotoxicity or transport measurement exists for MDA in this archive.

Lethal-dose values — animal studies

These are not human doses. An LD50 is the dose killing half of a group of animals of one species by one route, and it is a poor predictor of human risk for these compounds. Each value is printed whole, with the species and route it was measured in, because a lethal dose separated from those two facts is worse than no figure at all. Nothing here supports inferring a safe dose for anyone.

  • LD50 Mouse oral 13,300 ug/kg

    Hazardous Substances Data Bank (HSDB)Lewis, R.J. Sr. (ed) Sax's Dangerous Properties of Industrial Materials. 11th Edition. Wiley-Interscience, Wiley & Sons, Inc. Hoboken, NJ. 2004., p. 2438

  • LD50 Mouse ip 82,300 ug/kg

    Hazardous Substances Data Bank (HSDB)Lewis, R.J. Sr. (ed) Sax's Dangerous Properties of Industrial Materials. 11th Edition. Wiley-Interscience, Wiley & Sons, Inc. Hoboken, NJ. 2004., p. 2438

  • LD50 Mouse ip 68 mg/kg /hydrochloride/

    Hazardous Substances Data Bank (HSDB)O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. Whitehouse Station, NJ: Merck and Co., Inc., 2006., p. 996

  • LD50 Mouse iv 31,100 ug/kg

    Hazardous Substances Data Bank (HSDB)Lewis, R.J. Sr. (ed) Sax's Dangerous Properties of Industrial Materials. 11th Edition. Wiley-Interscience, Wiley & Sons, Inc. Hoboken, NJ. 2004., p. 2438

  • For more Non-Human Toxicity Values (Complete) data for 3,4-METHYLENEDIOXYAMPHETAMINE (7 total), please visit the HSDB record page.

    Hazardous Substances Data Bank (HSDB)

As published

Quoted verbatim from the database named after each passage, never summarized — a summary of a toxicology statement is a new claim.

Human Toxicity Excerpts

  • /SIGNS AND SYMPTOMS/ ... In overdose the differences between methamphetamine, 3,4-methylenedioxyamphetamine (MDA), and 3,4-methylenedioxymethamphetamine (MDMA) blur and the clinical presentation is similar to that of amphetamine overdose characterized by tachycardia, hypertension, hyperthermia, diaphoresis, mydriasis, agitation, muscle rigidity, and hyper-reflexia. Death usually results from arrhythmias, hyperthermia…

    Hazardous Substances Data Bank (HSDB)PMID 3285124Buchanan JF, Brown CR; Med Toxicol Adverse Drug Exp 3 (1): 1-17 (1988)

  • /SIGNS AND SYMPTOMS/ Central nervous system effects may be secondary to both sympathetic stimulation and altered perception. Therapeutic or recreational doses may induce feelings of warmth and are purported to promote communication and empathy. Higher doses may induce hallucinations, agitation, delirium, hyperreflexia, or rigidity. Seizures may occur and can reflect either direct CNS stimulation or hypertension induc…

    Hazardous Substances Data Bank (HSDB)Haddad, L.M. (Ed). Clinical Management of Poisoning and Drug Overdose 3rd Edition. Saunders, Philadelphia, PA. 1998., p. 574

  • /SIGNS AND SYMPTOMS/ Cardiovascular effects generally reflect sympathetic stimulation. Systolic and diastolic hypertension can be seen. Plus can be variably affected. Tachycardia can be seen; however if alpha-adrenergic effects predominate, hypertension with reflex bradycardia can occur. /Phenylethylamines/

    Hazardous Substances Data Bank (HSDB)Haddad, L.M. (Ed). Clinical Management of Poisoning and Drug Overdose 3rd Edition. Saunders, Philadelphia, PA. 1998., p. 574

  • /CASE REPORTS/ ... In this case /investigators/ detail a divided dose of 850 mg of MDA ingested within 2 hr and 15 min /which/ was sufficient to cause the death of a 24-year-old male, 4 hr after the final dose. The symptoms of MDA intoxication exhibited by the decedent prior to death closely mimic those of acute amphetamine poisoning: profuse sweating, violent and irrational behavior, and stereotypically compulsive b…

    Hazardous Substances Data Bank (HSDB)PMID 512617Poklis A et al; J Forensic Sci 24 (1): 70-5 (1979)

  • /CASE REPORTS/ ...The following symptoms were found in a patient /following Methylenedioxyamphetamine exposure/: sympathomimetic effects, coma, seizures, hyperreflexia, and hyperthermia. The patient's condition was initially stabilized and then deteriorated with uncontrollable hyperthermia, hematologic abnormalities, and coma that culminated in death. ... The concept that this drug is primarily a hallucinogen with mi…

    Hazardous Substances Data Bank (HSDB)PMID 7283563Simpson DL, Rumack BH; Arch Intern Med 141 (11): 1507-9 (1981)

Published passages via PubChem toxicology sections, aggregating Hazardous Substances Data Bank (HSDB), RTECS, LiverTox. No figure on this page is scored, ranked or combined into a risk level.

VIII · Evidence

Every measurement

One row per published value. The identifier in the last column resolves to the ChEMBL assay record it was read from.

Equilibrium binding constants 10

Ki and Kd — a concentration at equilibrium. Directly comparable across rows at the same target.

TargetClassTypeValue (nM)pXOrganismAssay
Serotonin (5-HT) receptorSerotonin receptorsKd3556.45Rattus norvegicusCHEMBL3279114
Serotonin (5-HT) receptorSerotonin receptorsKd3556.45Rattus norvegicusCHEMBL619177
5-HT2ASerotonin receptorsKi3876.41Rattus norvegicusCHEMBL4009965
5-HT2CSerotonin receptorsKi2,1005.68Rattus norvegicusCHEMBL616834
5-HT2Serotonin receptorsKi2,1905.66Rattus norvegicusCHEMBL617438
5-HT2CSerotonin receptorsKi2,2905.64Rattus norvegicusCHEMBL616832
5-HT2CSerotonin receptorsKi2,9325.53PIGPDSP
5-HT2Serotonin receptorsKi3,4255.47Rattus norvegicusCHEMBL617438
5-HT2ASerotonin receptorsKi5,3305.27RATPDSP
5-HT2ASerotonin receptorsKi8,3405.08HUMANPDSP

Functional readouts 5

IC₅₀, EC₅₀, AC₅₀ and potency. Assay-dependent, and not interchangeable with a binding constant.

TargetClassTypeValue (nM)pXOrganismAssay
NETMonoamine transportersIC502666.58Homo sapiensCHEMBL1169103
NETMonoamine transportersIC502666.58Homo sapiensCHEMBL1116588
SERTMonoamine transportersIC504786.32Homo sapiensCHEMBL1169102
DATMonoamine transportersIC508906.05Homo sapiensCHEMBL1169104
DATMonoamine transportersIC508906.05Homo sapiensCHEMBL1116589
P
PubChem
C
ChEMBL
R
Computed here with RDKit
D
Derived here from the stored measurement

IX · Trials

Registered clinical trials

Studies filed with ClinicalTrials.gov that name this compound as an intervention. A registered trial is a protocol, not a result — status and enrollment are printed beside every row, and withdrawn studies are counted rather than hidden.

2T

Registered studies

0T

Open or ongoing

2T

With a phase recorded

By phase

A study may carry two phase codes at once, so these count studies bearing each phase and do not sum to the total.

  • Phase 11
  • Not applicable1

By status

The registry’s own status for each record. Withdrawn and terminated studies are counted here rather than hidden — a stopped trial is part of what is known.

  • Completed2

Every matched study

Newest first by start date. Each identifier opens the registry record it came from; the title is the sponsor’s own, quoted.

  • NCT04847206Completed · Phase 1

    Effects of MDMA-like Substances in Healthy Subjects

    Enrollment
    23Tactual
    Started
    2021-12-01
    Sponsor
    University Hospital, Basel, Switzerland

    Conditions Healthy

    Matched “3,4-Methylenedioxyamphetamine” in the study’s intervention “3,4-methylenedioxyamphetamine”

  • NCT00823407Completed · Not applicable

    Clinical Pharmacology of MDA [3,4-methylenedioxyamphetamine]

    Enrollment
    12Tactual
    Started
    2009-01
    Sponsor
    California Pacific Medical Center Research Institute

    Conditions Healthy

    Matched “MDA” in the study’s intervention “MDA”

Records from ClinicalTrials.gov (U.S. National Library of Medicine, NIH), API v2. A study is listed against a compound only when a verified name for that compound appears as a whole word in one of the study's own intervention names. A short code must appear as written, and a name the registry uses for something else (Aleph, a vaccine maker) is not matched. Title matches are not accepted. The matched name and the intervention text it matched are shown with every row.

Searched as 3,4-Methylenedioxyamphetamine · Tenamfetamine · Methylenedioxyamphetamine. Run this search at the registry — it returns the unfiltered result, including studies this page rejected as belonging to a different molecule.

A registered trial is a protocol somebody filed with the registry. It is not a result, and nothing on this plate says whether MDA worked.

XI · Literature

Sources behind this dossier

The papers this compound's values were read from, ranked by what each contributed. Not a review of the field.

Every paper below is one some value on this page came from — a binding constant, a passage of pharmacology or toxicology, or a measured duration. Each entry says what this archive took from it. Nothing else is claimed about any of them: the title is the study’s own account of itself, and a summary written here would be an assertion with no source behind it.

  1. 01

    Acute effects of MDMA, MDA, lysine-MDMA, and lysine-MDA in a randomized, double-blind, placebo-controlled, crossover trial in healthy participants

    Straumann I, Vizeli P, Avedisian I et al. · Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology 2026

    • · Duration of acute subjective effects

    PMID 40999236

  2. 02

    Effect of the R(-) and S(+) isomers of MDA and MDMA on phosphatidyl inositol turnover in cultured cells expressing 5-HT2A or 5-HT2C receptors

    Nash JF, Roth BL, Brodkin JD et al. · Neuroscience letters 1994

    • · Mechanism of Action

    PMID 7824160

  3. 03

    3,4-Methylenedioxyamphetamine (MDA) analogues exhibit differential effects on synaptosomal release of 3H-dopamine and 3H-5-hydroxytryptamine

    McKenna DJ, Guan XM, Shulgin AT · Pharmacology, biochemistry, and behavior 1991

    • · Mechanism of Action

    PMID 1829838

  4. 04

    'Designer drugs'. A problem in clinical toxicology

    Buchanan JF, Brown CR · Medical toxicology and adverse drug experience 1988

    • · Human Toxicity Excerpts

    PMID 3285124

  5. 05

    Methylenedioxyamphetamine. Clinical description of overdose, death, and review of pharmacology

    Simpson DL, Rumack BH · Archives of internal medicine 1981

    • · Human Toxicity Excerpts

    PMID 7283563

  6. 06

    Fatal intoxication from 3,4-methylenedioxyamphetamine

    Poklis A, Mackell MA, Drake WK · Journal of forensic sciences 1979

    • · Human Toxicity Excerpts

    PMID 512617