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PsychedeliaDokholyan Laboratory
Plate 313 of 545Verified

Dimethyltryptamine (DMT)

PubChem records this structure as N,N-Dimethyltryptamine.

Also known asN,N-Dimethyltryptamine · Dimethyltryptamine · 2-(3-Indolyl)ethyldimethylamine · 3-(2-Dimethylaminoethyl)indole · 3-[2-(dimethylamino)ethyl]indole · 3-(2-(DIMETHYLAMINO)ETHYL)INDOLE · N,N Dimethyltryptamine · (2-Indol-3-ylethyl)dimethylamine

2-(1H-indol-3-yl)-N,N-dimethylethanamine

PubChem CID
6089
Measurements
56
InChIKey
DMULVCHRPCFFGV-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.

Synthesized summary

written by this site — every other word below is quoted

DMT is a tryptamine bearing two N-methyl groups on the side chain 1, reported from plants including Acacia confusa and Anadenanthera peregrina 8, and used as a hallucinogen by many indigenous peoples of tropical South America, most commonly in Amazonian Peru and Bolivia 3. Two things in this record set it apart from everything else in the archive. The first is that it is endogenous: the sources describe it in mammalian brain, blood and urine, and one study found it in the twenty-four-hour urine of nineteen normal human subjects at a mean of 386 ng, with diet and intestinal flora excluded as the source 2,4. The second is that route decides whether it works at all — it is cleared chiefly by monoamine oxidase rather than by hepatic microsomal enzymes 6, which is what makes the orally active preparation ayahuasca, where harmala alkaloids inhibit that enzyme 7. Even then most of the dose appears as the N-oxide and very little parent compound reaches urine 7. In a controlled study of oral ayahuasca the subjective peak fell between 1.5 and 2 hours and coincided with peak plasma DMT 5. Its receptor action is given as mixed rather than uniform: agonist at some serotonin receptors, antagonist at others 2. It is Schedule I 9.

Drawn only from the passages printed below, so every claim above can be checked against material on this page. The numbers are those passages. Synthesized by Claude Opus 5 (claude-opus-5), via Claude Code on 2026-08-27.

What it is

  • 1cited by the summary above

    N,N-dimethyltryptamine is a tryptamine derivative having two N-methyl substituents on the side-chain. It is a member of tryptamines and a tryptamine alkaloid. It is functionally related to a tryptamine. It is a conjugate base of a N,N-dimethyltryptaminium.

    ChEBI

  • Dimethyltryptamine is a DEA Schedule I controlled substance. Substances in the DEA Schedule I have no currently accepted medical use in the United States, a lack of accepted safety for use under medical supervision, and a high potential for abuse. It is a Hallucinogenic substances substance.

    Drug Enforcement Administration (DEA)

  • 2cited by the summary above

    An N-methylated indoleamine derivative, a serotonergic hallucinogen found in several plants, especially Prestonia amazonica (Apocynaceae) and in mammalian brain, blood, and urine. It apparently acts as an agonist at some types of serotonin receptors and an antagonist at others.

    DrugBank

  • 8cited by the summary above

    dimethyltryptamine has been reported in Acacia confusa, Anadenanthera peregrina, and other organisms with data available.

    LOTUS - the natural products occurrence database

Recognized use

  • Some people use this compound as a psychedelic inducing agent.

    Drug Indication

    DrugBank

  • 9cited by the summary above

    Dimethyltryptamine (DEA Code Number: 7435) /is a Schedule I controlled substance/.

    Use Classification

    Hazardous Substances Data Bank (HSDB)21 CFR 1308.11(d) (USFDA); U.S. National Archives and Records Administration's Electronic Code of Federal Regulations. Available from, as of March 8, 2012: https://www.ecfr.gov

  • 3cited by the summary above

    Hallucinogen used by many indigenous peoples of tropical South America, most commonly Amazonian Peru and Boliva

    Use Classification

    Hazardous Substances Data Bank (HSDB)Blackledge RD, Taylor CM; Psychotria viridis - A botanical source of dimethyltryptamine (DMT). US DEA; Microgram. Volume 1, 2003. Available from, as of Feb 9, 2012: https://www.justice.gov/dea/programs/forensicsci/microgram/journal_v1/2003_1-2.pdf

How it acts

  • DMT acts as a non-selective agonist at most or all of the serotonin receptors.

    DrugBank

  • N,N-dimethyltryptamine (DMT) is a hallucinogen found endogenously in human brain that is commonly recognized to target the 5-hydroxytryptamine 2A receptor or the trace amine-associated receptor to exert its psychedelic effect. DMT has been recently shown to bind sigma-1 receptors, which are ligand-regulated molecular chaperones whose function includes inhibiting various voltage-sensitive ion channels. Thus, it is possible that the psychedelic action of DMT might be mediated in part through sigma-1 receptors. ...

    Hazardous Substances Data Bank (HSDB)PMID 19278957Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3155724

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

In the body

  • (14)C-DMT accumulates in rat brain cortical slices incubated at 37 °C. ... Most of the accumulated (14)C-DMT was associated with the cytoplasmic fraction. Of the portion associated with the crude mitochondrial fraction, 54.4% was associated with nerve-ending fraction.

    Absorption, Distribution and Excretion

    Hazardous Substances Data Bank (HSDB)PMID 41604Sangiah et al; Biol Psychiatry 14 (6): 925-36 (1979)

  • 4cited by the summary above

    The hallucinogenic substance N',N'-dimethyltryptamine and its precursor N-methyltryptamine were found in 24-hr specimens of urine from 19 normal human subjects; the mean excretion rates were 386 ng 24 hr(-1) and 856 ng 24 hr(-1) respectively. The urinary excretion of both compounds was unrelated to age, sex, urinary volume, or creatinine, nor was any consistent diurnal pattern observed. Rates for the mono and dimethylated compounds were not correlated. Diet and the intestinal flora were excluded as a source of urinary dimethyltryptamine. Administration to 4 subjects of sufficient ammonium chloride to /decrease/ the /pH/ of the urine caused a transient increase in dimethyltryptamine excretion…

    Absorption, Distribution and Excretion

    Hazardous Substances Data Bank (HSDB)PMID 22091Oon MC et al; Psychopharmacology (Berl) 54 (2): 171-5 (1977)

  • 5cited by the summary above

    ... Eighteen volunteers with prior experience in the use of psychedelics received single oral doses of encapsulated freeze-dried ayahuasca (0.6 and 0.85 mg of DMT/kg of body weight) and placebo. Ayahuasca produced significant subjective effects, peaking between 1.5 and 2 hr, involving perceptual modifications and increases in ratings of positive mood and activation. ...Cmax values for DMT after the low and high ayahuasca doses were 12.14 ng/mL and 17.44 ng/mL, respectively. Tmax (median) was observed at 1.5 hr after both doses. The Tmax for DMT coincided with the peak of subjective effects. ...

    Absorption, Distribution and Excretion

    Hazardous Substances Data Bank (HSDB)PMID 12660312Riba J et al; J Pharmacol Exp Ther 306 (1): 73-83 (2003)

  • The endogenous hallucinogen, N,N-dimethyltryptamine (DMT), was labeled with (11)C and its regional distribution in rat brain studied. (11)C-DMT showed higher accumulation in the cerebral cortex, caudate putamen, and amygdaloid nuclei. Studies of the subcellular distribution of (11)C-DMT revealed the specific localization in the fractions enriched with serotonin receptors only when a very low dose was injected into rats. ...

    Absorption, Distribution and Excretion

    Hazardous Substances Data Bank (HSDB)PMID 3489620Yanai K et al; Eur J Nucl Med 12 (3): 141-6 (1986)

  • Following intraperitoneal administration, 5-methoxy-N,N-dimethyltryptamine and N,N-dimethyltryptamine are subject to both a very rapid uptake into, and clearance from, all tissues examined. The current studies in vivo confirm previous in vitro observations that the routes involved in the metabolism of these compounds include oxidative deamination, N-demethylation, O-demethylation, and N-oxidation. The analysis of metabolic profiles in various tissues led to the identification of the N-oxides as major metabolites...

    Metabolism/Metabolites

    Hazardous Substances Data Bank (HSDB)PMID 3472526Sitaram BR et al; Biochem Pharmacol 36 (9): 1509-12 (1987)

  • 7cited by the summary above

    ... /From/ ... urine samples collected from three individuals that were administered ayahuasca ... /authors/ show that the major metabolite of the hallucinogenic component of ayahuasca, N,N-dimethyltryptamine (DMT), is the corresponding N-oxide... Further, very little DMT was detected in urine, despite the inhibition of monoamine oxidase afforded by the presence of the harmala alkaloids in ayahuasca. ...

    Metabolism/Metabolites

    Hazardous Substances Data Bank (HSDB)PMID 21058415McIlhenny EH et al; Biomed Chromatogr 25 (9): 970-84 (2011)

  • 6cited by the summary above

    Behavioral aspects and metabolic fate of N,N-dimethyltryptamine (DMT) were studied in mice pretreated with beta-diethylaminoethyl-diphenylpropylacetate (SKF 525-A), iproniazid or chlorpromazine (CPZ.). ... Dose-dependent increases with rapid uptake and disappearance in the brain, plasma and hepatic levels of DMT were measured with doses of 10 and 25 mg/kg DMT. ... It is concluded that DMT is metabolized chiefly by monoamine oxidase rather than by drug-metabolizing hepatic microsomal enzymes and that DMT-induced behavioral effects are due to the parent compound rather than its metabolite.

    Metabolism/Metabolites

    Hazardous Substances Data Bank (HSDB)PMID 276891Shah NS, Hedden MP; Pharmacol Biochem Behav 8 (4): 351-6 (1978)

  • Studies were conducted using tritiated DMT and DMT-N-oxide (DMT-NO), and metabolites were identified and quantified using thin-layer chromatography and liquid scintillation counting techniques. Metabolite confirmation was obtained by incubation of alpha,alpha,beta,beta-tetradeutero-DMT (DDMT) with whole brain homogenate followed by combined gas chromatographic/mass spectrometric analyses. The metabolites of DMT were identified as indoleacetic acid (IAA), DMT-NO, N-methyltryptamine (NMT), 2-methyl-1,2,3,4-tetrahydro-beta-carboline (2-MTHBC), tryptamine (TA) and 1,2,3,4- tetrahydro-beta-carboline (THBC). DMT-NO was metabolized to give DMT, NMT, IAA and 2-MTHBC. Formation of these metabolites f…

    Metabolism/Metabolites

    Hazardous Substances Data Bank (HSDB)PMID 6770869Barker et al; Biochem Pharmacol 29 (7): 1049-57 (1980)

History, discovery and cultural use

Written by this site · every claim referenced

DMT is a hallucinogen used by many indigenous peoples of tropical South America, most commonly in Amazonian Peru and Bolivia 1. It is not active by mouth on its own, and the Amazonian preparations that carry it combine it with plants supplying β-carbolines such as harmine 2.

  1. 1Hazardous Substances Data Bank (HSDB), via PubChem
  2. 2Medical Subject Headings (MeSH), via PubChem MeSH's harmine record describes the western Amazonian hallucinogenic drinks and the identity of harmine with banisterine.

Ref 1 is the HSDB use-class passage held in this archive. The second sentence's link between DMT and the β-carboline-bearing preparations is supported by the MeSH harmine record, also held here; the pharmacological reason it matters is not asserted beyond what those records state. Nothing above is quoted from Dimethyltryptamine (DMT)’s own database records; those appear as quotations elsewhere on this plate.

Histories of this field

Scholarship on psychedelics generally, not on Dimethyltryptamine (DMT) 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 — 56 measurements in this archive, equilibrium constants kept apart from functional readouts.
  • Toxicology — 7 published passages, plus any assay in this archive bearing on toxicity.
  • Legal — DEA Schedule I, with the passage it was read from.
  • 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 Dimethyltryptamine (DMT) 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 DMT
Depiction served by PubChem for CID 6089. Not redrawn here, so the picture and the identity come from the same record.
Formula
C12H16N2R
Molecular weight
188.27g/molR
Exact mass
188.1313DaR
cLogP
2.27R
TPSA
19.0ŲR
H-bond donors
1R
H-bond acceptors
1R
Rotatable bonds
3R
Aromatic rings
2R
Heavy atoms
14R
Fraction sp³
0.333R
Formal charge
0R

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

Bemis–Murcko scaffold

c1ccc2[nH]ccc2c1

Shared with 1-Acetyl-5-MeO-DMT, 1-Methylpsilocin, 2-Me-DET, 2-Methyltryptamine, 2,N,N-TMT, 4-AcO-DALT and 81 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

resolved by ~30 min

intravenous, dose-response study in experienced volunteers

“Psychological effects of IV DMT began almost immediately after administration, peaked at 90 to 120 seconds, and were almost completely resolved by 30 minutes”
Strassman RJ et al., Archives of general psychiatry 1994. PMID 8297217

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.

9–12 min

“DMT was rapidly cleared for all doses: mean elimination half-life was 9-12 min”
Good M et al., European journal of drug metabolism and pharmacokinetics 2023. PMID 37086340

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.

  • N,N-dimethyltryptamine (DMT) is a hallucinogen found endogenously in human brain that is commonly recognized to target the 5-hydroxytryptamine 2A receptor or the trace amine-associated receptor to exert its psychedelic effect. DMT has been recently shown to bind sigma-1 receptors, which are ligand-regulated molecular chaperones whose func…
    Hazardous Substances Data Bank (HSDB)PMID 19278957Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3155724
  • The psychotomimetic agent dimethyltryptamine (DMT) has been identified as an endogenous compound in the central nervous system of rodents using a sensitive electron capture gas chromatographic technique. DMT along with its proposed precursor, tryptamine, were identified and quantitated as the heptafluorobutyryl derivatives. A specific hig…
    Hazardous Substances Data Bank (HSDB)PMID 20877Christian ST et al; Biochem Med 18(2) : 164-83 (1977)
  • The interactions of the indolealkylamine N,N-dimethyltryptamine (DMT) with 5-hydroxytryptamine1A (5-HT1A) and 5-HT2 receptors in rat brain were analyzed using radioligand binding techniques and biochemical functional assays. The affinity of DMT for 5-HT1A sites labeled by (3)H-8-hydroxy-2-(di-n-propylamino)tetralin (3)H-8-OH-DPAT) was dec…
    Hazardous Substances Data Bank (HSDB)PMID 1828347Deliganis AV et al; Biochem Pharmacol 41 (11): 1739-44 (1991)
  • DMT acts as a non-selective agonist at most or all of the serotonin receptors.
    DrugBank

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.

Affect0Mood0Perception4Cognition2Thought process0Thought content0Psychomotor activity0Insight and judgment0
This measures the literature, not the compound. Each spoke counts how many of the 13 records this archive holds for this compound say something under that domain — 4 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 4
matched on “hallucinogen” · in PMID 19278957; PMID 16123739; PMID 8297217; PMID 8297216
Cognition 2
matched on “concentrat” · in PMID 20877; PMID 329291

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, ADRA1B, ADRA2Ccerebellum — 5.8 nTPM, from ADRA2A, HTR5A, ADRA2Chippocampal formation — 6.1 nTPM, from HTR1A, ADRA2C, ADRA1Bamygdala — 6.4 nTPM, from ADRA2C, ADRA1B, HTR2Ahypothalamus — 12.6 nTPM, from HTR2C, ADRA2A, ADRA1Bthalamus — no resolved target expressed herebasal ganglia — 28.2 nTPM, from HTR2C, DRD1, ADRA2Cmedulla 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: retina 7.8, pituitary gland 4.7, midbrain 2.5, spinal cord 1.4.

Body

heart — 9.4 nTPM, from ADRA2B, ADRA2C, ADRA1Asmooth muscle — 15.7 nTPM, from HTR2B, ADRA1A, ADRA2Alung — 27.2 nTPM, from SLC6A4, ADRA2A, ADRA2Cliver — 56.2 nTPM, from ADRA1A, ADRA1B, ADRA2Bkidney — 33.4 nTPM, from ADRA2C, ADRA2B, ADRA2Astomach — 4.7 nTPM, from HTR1B, HTR2B, ADRA2Aduodenum — 9.7 nTPM, from SLC6A4, ADRA2A, HTR1Dsmall intestine — 38.0 nTPM, from SLC6A4, HTR1D, HTR2Bcolon — 8.5 nTPM, from HTR2B, ADRA2A, ADRA2Cadrenal gland — 17.2 nTPM, from HTR2B, ADRA2C, ADRA2Bthyroid gland — 8.7 nTPM, from ADRA2A, HTR2B, ADRA2Cpancreas — 28.8 nTPM, from ADRA2A, ADRA2C, SLC6A4urinary bladder — 14.8 nTPM, from ADRA2A, ADRA2C, ADRA2Bskeletal muscle — 6.0 nTPM, from ADRA2B, ADRA2C, ADRA2Aspleen — 20.8 nTPM, from ADRA2C, ADRA2A, ADRA1Bsalivary gland — 6.5 nTPM, from ADRA2A, ADRA1A, ADRA2B
056 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. basal ganglia

    28.2 nTPM

  2. cerebral cortex

    18.2 nTPM

  3. hypothalamus

    12.6 nTPM

  4. retina

    7.8 nTPM

  5. amygdala

    6.4 nTPM

  6. hippocampal formation

    6.1 nTPM

  7. cerebellum

    5.8 nTPM

  8. pituitary gland

    4.7 nTPM

  9. midbrain

    2.5 nTPM

  10. spinal cord

    1.4 nTPM

Peripheral & autonomic

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

  1. liver

    56.2 nTPM

  2. small intestine

    38.0 nTPM

  3. kidney

    33.4 nTPM

  4. pancreas

    28.8 nTPM

  5. lung

    27.2 nTPM

  6. spleen

    20.8 nTPM

  7. adrenal gland

    17.2 nTPM

  8. smooth muscle

    15.7 nTPM

  9. urinary bladder

    14.8 nTPM

  10. duodenum

    9.7 nTPM

  11. heart muscle

    9.4 nTPM

  12. thyroid gland

    8.7 nTPM

  13. colon

    8.5 nTPM

  14. salivary gland

    6.5 nTPM

  15. skeletal muscle

    6.0 nTPM

  16. stomach 1

    4.7 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.

3 of this compound’s targets could not be resolved to a gene and are absent from both columns: 5-HT1, Serotonin (5-HT) receptor, Sigma 1.

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 20 molecular targets. Cell-line and whole-organism screens are excluded here — they carry no affinity — and appear in the table below.

5-HT2C — Ki 7.48 pX5-HT2A — Ki 7.38 pX5-HT2B — Ki 7.35 pX5-HT6 — Ki 7.17 pX5-HT1D — Ki 7.15 pX5-HT7 — Ki 7.06 pX5-HT1A — Ki 6.92 pX5-HT1E — Ki 6.34 pX5-HT5A — Ki 6.21 pX5-HT1 — Kd 6.00 pXSerotonin (5-HT) receptor — Kd 6.00 pX5-HT1B — Ki 5.66 pXD1 — Ki 6.57 pXAlpha2B — Ki 6.59 pXAlpha2C — Ki 6.59 pXAlpha1B — Ki 6.01 pXAlpha2A — Ki 5.81 pXAlpha1A — Ki 5.76 pXSigma 1 — Ki 5.28 pXSERT — Ki 5.43 pX5-HT2C5-HT2A5-HT2B5-HT65-HT1D5-HT75-HT1A5-HT1E5-HT5A5-HT1Serotonin (5-HT)…5-HT1BD1Alpha2BAlpha2CAlpha1BAlpha2AAlpha1ASigma 1SERT579
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 Dimethyltryptamine (DMT) 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 iv 32 mg/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. 1383

  • LD50 Mouse ip 47 mg/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. 1383

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

  • /HUMAN EXPOSURE STUDIES/ In a controlled study on 38 volunteers the effects of 250 ug/kg N,N-dimethyltryptamine (DMT) i.m. on objective and performance tests measuring psychoticism according to Eysenck were assessed. The hypothesis was tested that subjects treated with DMT (N = 26) differ from those receiving placebo (N = 12) in the same way as endogenous psychotics differ from normals. Confirmation was obtained in 7…

    Hazardous Substances Data Bank (HSDB)PMID 329291Bickel P et al; Pharmakopsychiatr Neuropsychopharmakol 10 (1): 10-4 (1977)

  • /HUMAN EXPOSURE STUDIES/ ... A total of 15 healthy volunteers participated in a randomized, double-blind, crossover study with a low and a high dose of /dimethyltryptamine (DMT)/ and S-ketamine, which elicited subtle 'prepsychotic' or full-blown psychotic symptoms (low and high dose, respectively). Nine subjects completed both experimental days with the two doses of both drugs. Overall, both hallucinogens slowed down…

    Hazardous Substances Data Bank (HSDB)PMID 16123739Gouzoulis-Mayfrank E et al; Neuropsychopharmacology 31(2): 431-41 (2006)

  • /HUMAN EXPOSURE STUDIES/ /Investigators/ describe the subjective effects of graded doses of N,N-dimethyltryptamine (DMT), an endogenous hallucinogen and drug of abuse, in a group of experienced hallucinogen users. ... Twelve highly motivated volunteers received two doses (0.04 and 0.4 mg/kg) of intravenous (IV) dimethyltryptamine fumarate "nonblind," before entering a double-blind, saline placebo-controlled, randomiz…

    Hazardous Substances Data Bank (HSDB)PMID 8297217Strassman RJ, Qualls CR; Arch Gen Psychiatry 51 (2): 98-108 (1994)

  • /HUMAN EXPOSURE STUDIES/ To begin applying basic neuropharmacological hypotheses of hallucinogenic drug actions to humans, /the authors/ generated dose-response data for intravenously administered dimethyltryptamine fumarate's (DMT) neuroendocrine, cardiovascular, autonomic, and subjective effects in a group of experienced hallucinogen users. Dimethyltryptamine, an endogenous mammalian hallucinogen and drug of abuse,…

    Hazardous Substances Data Bank (HSDB)PMID 8297216Strassman RJ, Qualls CR; Arch Gen Psychiatry 51 (2): 85-97 (1994)

  • For more Human Toxicity Excerpts (Complete) data for N,N-Dimethyltryptamine (9 total), please visit the HSDB record page.

    Hazardous Substances Data Bank (HSDB)

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 56

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

TargetClassTypeValue (nM)pXOrganismAssay
5-HT2CSerotonin receptorsKi33.007.48Homo sapiensCHEMBL617282
5-HT2ASerotonin receptorsKi42.007.38RATPMID 2795135
5-HT2BSerotonin receptorsKi44.477.35Homo sapiensCHEMBL6114542
5-HT2ASerotonin receptorsKi53.007.28HUMANPMID 24488404
5-HT2ASerotonin receptorsKi65.007.19Homo sapiensCHEMBL615729
5-HT6Serotonin receptorsKi68.007.17HUMANPMID 8522988
5-HT1DSerotonin receptorsKi71.387.15COWPDSP
5-HT7Serotonin receptorsKi87.507.06HUMANPMID 20126400
5-HT1DSerotonin receptorsKi93.007.03HUMANPMID 20126400
5-HT2BSerotonin receptorsKi1017.00Homo sapiensCHEMBL617410
5-HT2BSerotonin receptorsKi1086.97HUMANPMID 20126400
5-HT1ASerotonin receptorsKi1206.92HUMANPDSP
5-HT1ASerotonin receptorsKi1286.89— organism not recordedPMID 41120735
5-HT1ASerotonin receptorsKi1416.85BOVINEPDSP
5-HT2CSerotonin receptorsKi1666.78HUMANPMID 24488404
5-HT2ASerotonin receptorsKi1756.76HUMANPMID 24488404
5-HT2ASerotonin receptorsKi1866.73Homo sapiensCHEMBL6114541
5-HT1DSerotonin receptorsKi1906.72BOVINEPDSP
5-HT2ASerotonin receptorsKi2106.68HUMANPMID 24488404
5-HT2ASerotonin receptorsKi2306.64HUMANPDSP
5-HT1ASerotonin receptorsKi2456.61RATPDSP
5-HT2CSerotonin receptorsKi2546.60— organism not recordedPMID 41120735
Alpha2BAdrenergic receptorsKi2586.59HUMANPMID 20126400
Alpha2CAdrenergic receptorsKi2596.59HUMANPMID 20126400
5-HT1ASerotonin receptorsKi2596.59Rattus norvegicusCHEMBL616115
5-HT2ASerotonin receptorsKi2596.59— organism not recordedPMID 41120735
5-HT1DSerotonin receptorsKi2706.57HUMANPDSP
D1Dopamine receptorsKi2716.57HUMANPMID 20126400
5-HT2CSerotonin receptorsKi3356.48HUMANPMID 20126400
5-HT1DSerotonin receptorsKi3436.46BOVINEPDSP
5-HT1ASerotonin receptorsKi4106.39Homo sapiensCHEMBL993916
5-HT1ASerotonin receptorsKi4506.35HUMANPMID 24488404
5-HT1ESerotonin receptorsKi4566.34HUMANPMID 20126400
5-HT2ASerotonin receptorsKi4626.34HUMANPDSP
5-HT6Serotonin receptorsKi4876.31HUMANPMID 20126400
5-HT2BSerotonin receptorsKi5506.26BOVINEPMID 2795135
5-HT2ASerotonin receptorsKi5586.25RATPDSP
5-HT5ASerotonin receptorsKi6116.21HUMANPMID 20126400
Alpha1BAdrenergic receptorsKi9746.01HUMANPMID 20126400
5-HT2BSerotonin receptorsKi9756.01— organism not recordedPMID 41120735
5-HT1Serotonin receptorsKd1,0006.00Rattus norvegicusCHEMBL3258848
5-HT2BSerotonin receptorsKd1,0006.00Rattus norvegicusCHEMBL617633
Serotonin (5-HT) receptorSerotonin receptorsKd1,0006.00Rattus norvegicusCHEMBL3279114
Serotonin (5-HT) receptorSerotonin receptorsKd1,0006.00Rattus norvegicusCHEMBL619183
5-HT2ASerotonin receptorsKi1,1835.93RATPDSP
5-HT2ASerotonin receptorsKi1,2005.92RATPDSP
5-HT2ASerotonin receptorsKi1,2005.92RATPDSP
Alpha2AAdrenergic receptorsKi1,5615.81HUMANPMID 20126400
5-HT2ASerotonin receptorsKi1,6365.79Rattus norvegicusCHEMBL980603
Alpha1AAdrenergic receptorsKi1,7455.76HUMANPMID 20126400
5-HT1BSerotonin receptorsKi2,2005.66RATPDSP
5-HT2ASerotonin receptorsKi2,3235.63HUMANPMID 20126400
SERTMonoamine transportersKi3,7425.43HUMANPMID 20126400
SERTMonoamine transportersKi4,2205.37— organism not recordedPMID 41120735
Sigma 1Sigma receptorsKi5,2095.28HUMANPMID 20126400
Sigma 1Sigma receptorsKi15,0004.82Cavia porcellusCHEMBL1780499
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.

17T

Registered studies

7T

Open or ongoing

17T

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.

  • Early phase 12
  • Phase 112
  • Phase 22
  • 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.

  • Completed10
  • Recruiting4
  • Active, not recruiting2
  • Not yet recruiting1

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.

  • NCT07693257Not yet recruiting · Phase 1

    Neural Effects of Intravenous N,N-dimethyltryptamine (DMT)

    Enrollment
    20Testimated
    Started
    2026-09-01
    Sponsor
    Jon Dean

    Conditions Healthy Participants Study

    Matched “N,N-Dimethyltryptamine” in the study’s intervention “N,N-Dimethyltryptamine (15 mg)”

  • NCT07562191Recruiting · Phase 2

    Inhaled DMT for Major Depressive Disorder

    Enrollment
    140Testimated
    Started
    2026-08-01
    Sponsor
    Universidade Federal do Rio Grande do Norte

    Conditions MDD · Major Depressive Disorder (MDD) · Major Depression · Suicidal Ideation · Suicide

    Matched “N,N-Dimethyltryptamine” in the study’s intervention “N,N-Dimethyltryptamine (15 mg + 60 mg)”

  • NCT06927076Recruiting · Not applicable

    Antidepressant Response of DMT Masked With Propofol

    Enrollment
    112Testimated
    Started
    2025-08-05
    Sponsor
    University Hospital, Basel, Switzerland

    Conditions Major Depressive Disorder · Psychedelic Experiences

    Matched “N,N-Dimethyltryptamine” in the study’s intervention “N,N-Dimethyltryptamine”

  • NCT06070649Recruiting · Phase 1

    The Potential Therapeutic Effects of Psychedelic, N, N-dimethyltryptamine (DMT), on Alcohol Use Disorder (AUD)

    Enrollment
    63Testimated
    Started
    2025-08-04
    Sponsor
    Yale University

    Conditions Alcohol Use Disorder (AUD) · Alcohol-Related Disorders · Alcohol Use

    Matched “Dimethyltryptamine” in the study’s intervention “0.3mg/kg/min Dimethyltryptamine + Normal Saline infusion”

  • NCT06772753Recruiting · Phase 1

    Investigation of Psychedelic Effects in Psychoactive Substances

    Enrollment
    50Testimated
    Started
    2025-02-05
    Sponsor
    Johns Hopkins University

    Conditions Psychedelic Effects in Healthy Volunteers

    Matched “Dimethyltryptamine(DMT)” in the study’s intervention “Dimethyltryptamine (DMT)”

  • NCT05695495Completed · Phase 1

    Acute Dose-dependent Effects of DMT-bolus Applications in Healthy Subjects (DMT BDR-Study)

    Enrollment
    36Tactual
    Started
    2024-06-12
    Sponsor
    University Hospital, Basel, Switzerland

    Conditions Healthy

    Matched “N,N-Dimethyltryptamine” in the study’s intervention “N,N-Dimethyltryptamine (5mg)”

  • NCT06252506Completed · Phase 1

    Molecular Imaging Study of Harmine/DMT: a Basic Research Approach

    Enrollment
    17Tactual
    Started
    2024-01-22
    Sponsor
    Insel Gruppe AG, University Hospital Bern

    Conditions Neuropharmacological Investigation of Ayahuasca Constituents DMT and Harmine

    Matched “N,N-Dimethyltryptamine” in the study’s intervention “N,N-dimethyltryptamine (DMT) + harmine”

  • NCT06094907Completed · Phase 2

    Safety, Tolerability and Antidepressant Effects of DMT in Patients With Depression

    Enrollment
    14Tactual
    Started
    2023-10-09
    Sponsor
    Universidade Federal do Rio Grande do Norte

    Conditions Depressive Disorder · Depression, Unipolar

    Matched “N,N-Dimethyltryptamine” in the study’s intervention “N,N-Dimethyltryptamine”

  • NCT05829603Completed · Phase 1

    Dose-finding Study for the Combination of DMT and Harmine in Healthy Subjects

    Enrollment
    16Tactual
    Started
    2023-05-05
    Sponsor
    Reconnect Labs

    Conditions Healthy

    Matched “DMT” in the study’s intervention “Dimethyltryptamin (DMT) & Harmine”

  • NCT05901012Completed · Phase 1

    Safety and Tolerability of DMT in Healthy Adults

    Enrollment
    25Tactual
    Started
    2023-04-26
    Sponsor
    Universidade Federal do Rio Grande do Norte

    Conditions Safety Issues · Healthy Volunteers

    Matched “N,N-Dimethyltryptamine” in the study’s intervention “N,N-Dimethyltryptamine”

  • NCT05780216Completed · Early phase 1

    Mindfulness and Psychedelics

    Enrollment
    40Tactual
    Started
    2023-02-20
    Sponsor
    Milan Scheidegger

    Conditions Healthy Participants

    Matched “DMT” in the study’s intervention “DMT + harmine”

  • NCT05559931Active, not recruiting · Phase 1

    Single and Repeat Doses of DMT in Healthy Subjects

    Enrollment
    60Testimated
    Started
    2023-01-13
    Sponsor
    Algernon Pharmaceuticals

    Conditions Stroke

    Matched “N,N-Dimethyltryptamine” in the study’s intervention “N,N-Dimethyltryptamine”

  • NCT05384678Completed · Phase 1

    Acute Dose-dependent Effects of DMT in Healthy Subjects

    Enrollment
    24Tactual
    Started
    2022-11-15
    Sponsor
    University Hospital, Basel, Switzerland

    Conditions Healthy

    Matched “N,N-Dimethyltryptamine” in the study’s intervention “N,N-Dimethyltryptamine (54 mg)”

  • NCT05573568Completed · Phase 1

    Clinical Study of DMT in Healthy Adults

    Enrollment
    27Tactual
    Started
    2022-06-01
    Sponsor
    Biomind Labs Inc.

    Conditions Healthy Volunteers

    Matched “N,N-Dimethyltryptamine” in the study’s intervention “N,N-Dimethyltryptamine”

  • NCT04353024Completed · Phase 1

    Effects of Dimethyltryptamine in Healthy Subjects

    Enrollment
    31Tactual
    Started
    2021-06-18
    Sponsor
    University Hospital, Basel, Switzerland

    Conditions Healthy

    Matched “Dimethyltryptamine(DMT)” in the study’s intervention “Dimethyltryptamine (DMT)”

  • NCT04711915Active, not recruiting · Phase 1

    Fixed Order, Open-Label, Dose-Escalation Study of DMT in Humans

    Enrollment
    30Testimated
    Started
    2021-03-17
    Sponsor
    Yale University

    Conditions Major Depressive Disorder · Depression

    Matched “Dimethyltryptamine(DMT)” in the study’s intervention “0.1 mg/kg Dimethyltryptamine (DMT)”

  • NCT04716335Completed · Early phase 1

    Neurodynamics of Prosocial Emotional Processing Following Serotonergic Stimulation With N,N-Dimethyltryptamine (DMT) and Harmine in Healthy Subjects

    Enrollment
    34Tactual
    Started
    2020-12-01
    Sponsor
    Psychiatric University Hospital, Zurich

    Conditions Emotions · Mood · Cognitive Function 1, Social · Empathy

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

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 N,N-Dimethyltryptamine · Dimethyltryptamine · 2-(3-Indolyl)ethyldimethylamine. 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 Dimethyltryptamine (DMT) 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

    Psychedelics and the human receptorome

    Ray TS · PloS one 2010

    • · 16 measurements at 16 targets (Ki), strongest 5-HT7 at 7.06 pX

    PMID 20126400

  2. 02

    Neuropharmacology of halogenated DMT analogs: psychoplastogenic and antidepressant properties of 5-Br-DMT, a psychedelic derivative with low hallucinogenic potential

    Puigseslloses P, Nadal-Gratacós N, Fumàs B et al. · Molecular psychiatry 2026

    • · 5 measurements at 5 targets (Ki), strongest 5-HT1A at 6.89 pX

    PMID 41120735

  3. 03

    Mefloquine and psychotomimetics share neurotransmitter receptor and transporter interactions in vitro

    Janowsky A, Eshleman AJ, Johnson RA et al. · Psychopharmacology 2014

    • · 5 measurements at 3 targets (Ki), strongest 5-HT2A at 7.28 pX

    PMID 24488404

  4. 04

    Differentiation of 5-hydroxytryptamine2 receptor subtypes using 125I-R-(-)2,5-dimethoxy-4-iodo-phenylisopropylamine and 3H-ketanserin

    McKenna DJ, Peroutka SJ · The Journal of neuroscience : the official journal of the Society for Neuroscience 1989

    • · 2 measurements at 2 targets (Ki), strongest 5-HT2A at 7.38 pX

    PMID 2795135

  5. 05

    Cloning, characterization, and chromosomal localization of a human 5-HT6 serotonin receptor

    Kohen R, Metcalf MA, Khan N et al. · Journal of neurochemistry 1996

    • · 1 measurement at 1 target (Ki), strongest 5-HT6 at 7.17 pX

    PMID 8522988

  6. 06

    Acute effects of intravenous DMT in a randomized placebo-controlled study in healthy participants

    Vogt SB, Ley L, Erne L et al. · Translational psychiatry 2023

    • · 4 timed observations on the simulation plate

    PMID 37221177

  7. 07

    Pharmacokinetics of N,N-dimethyltryptamine in Humans

    Good M, Joel Z, Benway T et al. · European journal of drug metabolism and pharmacokinetics 2023

    • · Plasma elimination half-life

    PMID 37086340

  8. 08

    When the endogenous hallucinogenic trace amine N,N-dimethyltryptamine meets the sigma-1 receptor

    Su TP, Hayashi T, Vaupel DB · Science signaling 2009

    • · Mechanism of Action

    PMID 19278957

  9. 09

    Inhibition of return in the human 5HT2A agonist and NMDA antagonist model of psychosis

    Gouzoulis-Mayfrank E, Heekeren K, Neukirch A et al. · Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology 2006

    • · Human Toxicity Excerpts

    PMID 16123739

  10. 10

    Dose-response study of N,N-dimethyltryptamine in humans. I. Neuroendocrine, autonomic, and cardiovascular effects

    Strassman RJ, Qualls CR · Archives of general psychiatry 1994

    • · Human Toxicity Excerpts

    PMID 8297216

  11. 11

    Dose-response study of N,N-dimethyltryptamine in humans. II. Subjective effects and preliminary results of a new rating scale

    Strassman RJ, Qualls CR, Uhlenhuth EH et al. · Archives of general psychiatry 1994

    • · Duration of acute subjective effects
    • · Human Toxicity Excerpts

    PMID 8297217

  12. 12

    Differential interactions of dimethyltryptamine (DMT) with 5-HT1A and 5-HT2 receptors

    Deliganis AV, Pierce PA, Peroutka SJ · Biochemical pharmacology 1991

    • · Mechanism of Action

    PMID 1828347

  13. 13

    [Effects of N,N-dimethyltryptamine (DMT) on tests of psychoticism (author's transl)]

    Bickel P, Dittrich A, Schöpf J · Pharmakopsychiatrie, Neuro-Psychopharmakologie 1977

    • · Human Toxicity Excerpts

    PMID 329291

  14. 14

    The in vitro identification of dimethyltryptamine (DMT) in mammalian brain and its characterization as a possible endogenous neuroregulatory agent

    Christian ST, Harrison R, Quayle E et al. · Biochemical medicine 1977

    • · Mechanism of Action

    PMID 20877