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PsychedeliaDokholyan Laboratory
Plate 320 of 545Verified

DOM

PubChem records this structure as 2,5-Dimethoxy-4-Methylamphetamine.

Also known as2,5-Dimethoxy-4-Methylamphetamine · STP (hallucinogen) · (RS)-DOM · 2,5-Dimethoxymethylamphetamine · 4-Methyl-2,5-dimethoxyamphetamine · (+-)-DOM · Racemic DOM · DOM [MI]

1-(2,5-dimethoxy-4-methylphenyl)propan-2-amine

PubChem CID
85875
Measurements
26
InChIKey
NTJQREUGJKIARY-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

  • 4-methyl-2,5-dimethoxy-amphetamine 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)

  • A psychedelic phenyl isopropylamine derivative, commonly called DOM, whose mood-altering effects and mechanism of action may be similar to those of LSD.

    DrugBank

How it acts

  • Alterations in brain serotonergic function have been implicated in the mechanism of action of LSD, mescaline, and other similarly acting hallucinogenic drugs of abuse such as STP (2,5-dimethoxyphenylisopropylamine; DOM). In order to test the hypothesis that the mechanism of action of LSD and phenylisopropylamine hallucinogens is through stimulation of a specific brain serotonin receptor sub-type, the affinities of these compounds for radiolabelled 5-HT2, 5-HT1A, 5-HT1B, and 5-HT1C receptors have been determined using recently developed in vitro radioligand binding methodologies. The 5-HT2 receptor was labelled with the agonist/hallucinogen radioligand 3H-DOB (4-bromo-2,5-dimethoxyphenylisopr…

    Hazardous Substances Data Bank (HSDB)PMID 3127847Titeler M et al; Psychopharmacology (Berl) 94 (2): 213-6 (1988)

  • 2,5-Dimethoxy-4-methylamphetamine (DOM, "STP") is a potent hallucinogen, proposed to be a serotonin receptor agonist. Its effects have not previously been tested upon central neurons where serotonin is excitatory and serotonin antagonists are effective. Extracellular single unit recordings were obtained from facial motoneurons in anesthetized rats, and drugs were applied from five-barrelled micropipettes by iontophoresis. Facial motoneurons were commonly silent. During subthreshold application of glutamate, firing could be induced by dopamine and DOM. As reported by others, serotonin and noradrenaline also excited facial motoneurons under these conditions. Methysergide antagonized responses…

    Hazardous Substances Data Bank (HSDB)PMID 3801984Penington NJ, Reiffenstein RJ; Can J Physiol Pharmacol 64 (10): 1302-9 (1986)

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

In the body

  • DOM produces effects within 1 to 2 hours of ingestion of doses ranging from 2 to 14 mg. Twenty percent of an ingested dose appears unchanged in the urine within 24 hours.

    Absorption, Distribution and Excretion

    Hazardous Substances Data Bank (HSDB)Haddad, L.M. (Ed). Clinical Management of Poisoning and Drug Overdose 3rd Edition. Saunders, Philadelphia, PA. 1998., p. 573

  • In an effort to more fully characterize the metabolic fate of the psychotomimetic amine (1-(2, 5-dimethoxy-4-methylpheny)-2-aminopropane (DOM, STP), the formation of the two possible monophenols and the p-hydroquinone metabolites of the parent drug by 10,000 X g supernatent fractions of rabbit liver homogenates has been investigated. All three metabolites have been fully characterized and quantitatively estimated by chemical ionization mass spectrometry with the aid of deuterium enriched compounds. The stereochemical course of the mono-O-demethylation reactions has been shown to proceed with enantiomeric enrichment of the S-aminophenols. The mechanistic implications concerning the mode of ac…

    Metabolism/Metabolites

    Hazardous Substances Data Bank (HSDB)PMID 1224005Zwieg JS, Castagnoli N Jr; Psychopharmacol Commun 1 (4): 359-71 (1975)

  • The possible relationship between metabolism and psychotomimetic activity among the methoxylated 1-phenyl-2-aminopropanes led to our investigation of the in vitro O-demethylation of 1-(2,5-dimethoxy-4-methylphenyl)-2-aminopropane (1, DOM, STP). Employing a sensitive and highly selective stable isotope dilution assay, we observed that rabbit liver homogenates biotransform the amine 1 to its 2-O-demethyl, 5-O-demethyl, and bis (O-demethyl) metabolite metabolites. Both monophenolic metabolites are enriched in their S enantiomers. The bis(O-demethyl) metabolite has structural, chemical, and electrochemical similarities to the sympatholytic agent "6-hydroxydopamine". The possible significance of…

    Metabolism/Metabolites

    Hazardous Substances Data Bank (HSDB)PMID 845874Zweig JS, Castagnoli N Jr; J Med Chem 20 (3): 414-21(1977)

  • Metabolites of STP have been synthesized and identified in rat urine and feces. A 4-hydroxymethyl compound which resulted from hydroxylation of the 4-methyl group of STP accounted for half of the total amount of the metabolites isolated in the 24 hour urine. The further oxidation product of the 4-hydroxymethyl compound, the 4-carboxy metabolite and unchanged STP were present in a ratio of 2 to 7. A trace amount of the ketone, derived from oxidation of the side-chain of STP, was also detected. The feces at the same time interval contained almost exclusively the 4-carboxy metabolite, with the 4-hydroxymethyl metabolite and a relatively small quantity of unchanged STP amounting to less than 7%.…

    Metabolism/Metabolites

    Hazardous Substances Data Bank (HSDB)PMID 4998281Ho BT et al; Brain Res 29 (1): 166-9 (1971)

  • The designer drug 2,5-dimethoxy-4-methyl-amphetamine (DOM, STP) is known to be extensively metabolized in various species. The current study showed that cytochrome P450 2D6 was the only isoenzyme involved in formation of the main metabolite hydroxy DOM. In addition, the authors' systematic toxicological analysis (STA) procedure using full-scan GC-MS was suitable to prove an intake of a common drug users' dose of DOM by detection of hydroxy DOM in rat urine. Assuming similar metabolism, the described STA procedure should be suitable for proof of an intake of DOM in human urine. However, DOM and/or other metabolites such as deamino-oxo-hydroxy DOM might be the target analyte in urine of CYP2D6…

    Metabolism/Metabolites

    Hazardous Substances Data Bank (HSDB)PMID 18155651Ewald AH et al; J Chromatogr B Analyt Technol Biomed Life Sci 862 (1-2): 252-6 (2008)

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 DOM 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 DOM 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 — 26 measurements in this archive, equilibrium constants kept apart from functional readouts.
  • Toxicology — 5 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 DOM 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 DOM
Depiction served by PubChem for CID 85875. Not redrawn here, so the picture and the identity come from the same record.
Formula
C12H19NO2R
Molecular weight
209.29g/molR
Exact mass
209.1416DaR
cLogP
1.90R
TPSA
44.5ŲR
H-bond donors
1R
H-bond acceptors
3R
Rotatable bonds
4R
Aromatic rings
1R
Heavy atoms
15R
Fraction sp³
0.500R
Formal charge
0R

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

Bemis–Murcko scaffold

c1ccccc1

Shared with 2-Bromomescaline, 2-TOET, 2-TOM, 2,3,4,5-Tetramethoxyamphetamine, 2,4-dimethoxyamphetamine, 2,5-Dimethoxy-4-(2-fluoroethyl)amphetamine and 129 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

—

No controlled human trial reporting a duration for this compound is cited here. The archive does hold onset and duration ranges for it, inherited from an earlier build, but their source column is empty and so they cannot be shown. A duration is not inferred from a chemical relative.

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.

  • Alterations in brain serotonergic function have been implicated in the mechanism of action of LSD, mescaline, and other similarly acting hallucinogenic drugs of abuse such as STP (2,5-dimethoxyphenylisopropylamine; DOM). In order to test the hypothesis that the mechanism of action of LSD and phenylisopropylamine hallucinogens is through s…
    Hazardous Substances Data Bank (HSDB)PMID 3127847Titeler M et al; Psychopharmacology (Berl) 94 (2): 213-6 (1988)
  • 2,5-Dimethoxy-4-methylamphetamine (DOM, "STP") is a potent hallucinogen, proposed to be a serotonin receptor agonist. Its effects have not previously been tested upon central neurons where serotonin is excitatory and serotonin antagonists are effective. Extracellular single unit recordings were obtained from facial motoneurons in anesthet…
    Hazardous Substances Data Bank (HSDB)PMID 3801984Penington NJ, Reiffenstein RJ; Can J Physiol Pharmacol 64 (10): 1302-9 (1986)
  • ... In perfused dog forelimb DOM produced a vasodilation followed by a vasoconstriction. The vasoconstriction produced by DOM was not blocked by phentolamine but was antagonized by methysergide. In isolated superfused vascular strips of dog dorsal metatarsal vein, DOM elicited a muscle contraction which was not blocked by phentolamine or…
    Hazardous Substances Data Bank (HSDB)PMID 4719787Cheng HC et al; J Pharmacol Exp Ther 186 (2): 345-54 (1973)

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.

Affect0Mood1Perception3Cognition0Thought process0Thought content0Psychomotor activity0Insight and judgment0
This measures the literature, not the compound. Each spoke counts how many of the 8 records this archive holds for this compound say something under that domain — 3 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.
Mood 1
matched on “euphoria” · in Toxicology: Hazardous Substances Data Bank (HSDB)
Perception 3
matched on “hallucinogen”, “perceptu” · in PMID 3127847; PMID 3801984; 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, HTR1A, HTR2Ccerebellum — 0.2 nTPM, from HTR2A, HTR2B, HTR1Bhippocampal formation — 6.1 nTPM, from HTR1A, HTR2A, HTR2Camygdala — 3.5 nTPM, from HTR2A, HTR2C, HTR1Ahypothalamus — 12.6 nTPM, from HTR2C, HTR2A, HTR1Athalamus — no resolved target expressed herebasal ganglia — 28.2 nTPM, from HTR2C, HTR2A, HTR1Bmedulla 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 2.2, spinal cord 1.0, retina 0.7, pituitary gland 0.4.

Body

heart — 4.6 nTPM, from HTR2B, HTR2A, HTR1Asmooth muscle — 15.7 nTPM, from HTR2B, HTR2A, HTR1Blung — 0.8 nTPM, from HTR2B, HTR2A, HTR1Bliver — 3.3 nTPM, from HTR2B, HTR2Akidney — 3.1 nTPM, from HTR2B, HTR1B, HTR2Astomach — 4.7 nTPM, from HTR1B, HTR2B, HTR2Aduodenum — 1.4 nTPM, from HTR2B, HTR2A, HTR1Bsmall intestine — 5.0 nTPM, from HTR2B, HTR2A, HTR1Bcolon — 8.5 nTPM, from HTR2B, HTR2A, HTR1Badrenal gland — 17.2 nTPM, from HTR2B, HTR1B, HTR2Athyroid gland — 3.2 nTPM, from HTR2B, HTR2A, HTR1Bpancreas — 0.2 nTPM, from HTR2B, HTR1Burinary bladder — 2.0 nTPM, from HTR2B, HTR1B, HTR2Askeletal muscle — 0.3 nTPM, from HTR2A, HTR2Bspleen — 0.4 nTPM, from HTR2Bsalivary gland — 0.4 nTPM, from HTR2B, HTR1B, HTR2A
028 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. hippocampal formation

    6.1 nTPM

  5. amygdala

    3.5 nTPM

  6. midbrain

    2.2 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. adrenal gland

    17.2 nTPM

  2. smooth muscle

    15.7 nTPM

  3. colon

    8.5 nTPM

  4. small intestine

    5.0 nTPM

  5. stomach 1

    4.7 nTPM

  6. heart muscle

    4.6 nTPM

  7. liver

    3.3 nTPM

  8. thyroid gland

    3.2 nTPM

  9. kidney

    3.1 nTPM

  10. urinary bladder

    2.0 nTPM

  11. duodenum

    1.4 nTPM

  12. lung

    0.8 nTPM

  13. salivary gland

    0.4 nTPM

  14. spleen

    0.4 nTPM

  15. skeletal muscle

    0.3 nTPM

  16. pancreas

    0.2 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, 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 8 molecular targets. Cell-line and whole-organism screens are excluded here — they carry no affinity — and appear in the table below.

5-HT2A — Ki 8.69 pX5-HT2C — Ki 7.59 pXSerotonin (5-HT) receptor — Kd 7.13 pX5-HT2 — Ki 7.00 pX5-HT2B — Ki 6.40 pX5-HT1B — Ki 5.74 pX5-HT1 — Ki 5.54 pX5-HT1A — Ki 5.14 pX5-HT2A5-HT2CSerotonin (5-HT)…5-HT25-HT2B5-HT1B5-HT15-HT1A579
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 DOM 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 ip 89 + or -4.2 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. 577

  • LD50 Mouse ip 94 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. 3304

  • LD50 Rabbit oral 200 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. 3304

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

  • /OTHER TOXICITY INFORMATION/ DOM /(4-methyl-2,5-dimethoxyamphetamine)/ ... is particularly interesting because at low doses /it/ produces mild euphoria and enhanced self-awearness without perceptual distortion or hallucinogenic effects. At higher doses DOM has typical psychedelic activity.

    Hazardous Substances Data Bank (HSDB)Gilman, A.G., T.W. Rall, A.S. Nies and P. Taylor (eds.). Goodman and Gilman's The Pharmacological Basis of Therapeutics. 8th ed. New York, NY. Pergamon Press, 1990., p. 556

  • /OTHER TOXICITY INFORMATION/ Psychosis is common with derivatives of amphetamine that are hallucinogens, such as mescaline, DOM, MDA, p-methoxyamphetamine, and MDMA. /Amphetamines/

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

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 26

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

TargetClassTypeValue (nM)pXOrganismAssay
5-HT2ASerotonin receptorsKi2.068.69HUMANPMID 24488404
5-HT2ASerotonin receptorsKi4.308.37HUMANPMID 24488404
5-HT2ASerotonin receptorsKi4.808.32RATPMID 2795135
5-HT2ASerotonin receptorsKi13.707.86HUMANPMID 24488404
5-HT2ASerotonin receptorsKi21.007.68HUMANPMID 10611640
5-HT2CSerotonin receptorsKi25.707.59HUMANPMID 24488404
5-HT2CSerotonin receptorsKi41.687.38RATPMID 7984267
Serotonin (5-HT) receptorSerotonin receptorsKd74.137.13Rattus norvegicusCHEMBL619176
Serotonin (5-HT) receptorSerotonin receptorsKd75.867.12Rattus norvegicusCHEMBL3279114
Serotonin (5-HT) receptorSerotonin receptorsKd75.867.12Rattus norvegicusCHEMBL619177
5-HT2CSerotonin receptorsKi94.007.03PIGPDSP
5-HT2Serotonin receptorsKi1007.00Rattus norvegicusCHEMBL617444
5-HT2Serotonin receptorsKi1007.00Rattus norvegicusCHEMBL617438
5-HT2ASerotonin receptorsKi1007.00Rattus norvegicusCHEMBL980602
5-HT2ASerotonin receptorsKi1007.00RATPDSP
5-HT2ASerotonin receptorsKi1007.00RATPDSP
5-HT2ASerotonin receptorsKi1626.79HUMANPDSP
5-HT2CSerotonin receptorsKi1936.71Rattus norvegicusCHEMBL616834
5-HT2CSerotonin receptorsKi1936.71PIGPDSP
5-HT2ASerotonin receptorsKi3066.51HUMANPMID 10611640
5-HT2CSerotonin receptorsKi3726.43RATPMID 7984267
5-HT2BSerotonin receptorsKi4006.40BOVINEPMID 2795135
5-HT1BSerotonin receptorsKi1,8405.74RATPDSP
5-HT1BSerotonin receptorsKi2,0635.69RATPDSP
5-HT1Serotonin receptorsKi2,8905.54Rattus norvegicusCHEMBL615400
5-HT1ASerotonin receptorsKi7,2675.14HUMANPMID 8382063
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.

— No registered study names DOM as an intervention. That is an absence of registered research, not evidence about the compound. Most of this archive has never been the subject of a registered trial.

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 2,5-Dimethoxy-4-Methylamphetamine · STP (hallucinogen) · 2,5-Dimethoxymethylamphetamine. Run this search at the registry.

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

    Mefloquine and psychotomimetics share neurotransmitter receptor and transporter interactions in vitro

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

    • · 4 measurements at 2 targets (Ki), strongest 5-HT2A at 8.69 pX

    PMID 24488404

  2. 02

    Agonist high and low affinity state ratios predict drug intrinsic activity and a revised ternary complex mechanism at serotonin 5-HT(2A) and 5-HT(2C) receptors

    Egan C, Grinde E, Dupre A et al. · Synapse (New York, N.Y.) 2000

    • · 2 measurements at 1 target (Ki), strongest 5-HT2A at 7.68 pX

    PMID 10611640

  3. 03

    Molecular biology of 5-HT receptors

    Boess FG, Martin IL · Neuropharmacology 1994

    • · 2 measurements at 1 target (Ki), strongest 5-HT2C at 7.38 pX

    PMID 7984267

  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 8.32 pX

    PMID 2795135

  5. 05

    Activity of serotonin (5-HT) receptor agonists, partial agonists and antagonists at cloned human 5-HT1A receptors that are negatively coupled to adenylate cyclase in permanently transfected HeLa cells

    Pauwels PJ, Van Gompel P, Leysen JE · Biochemical pharmacology 1993

    • · 1 measurement at 1 target (Ki), strongest 5-HT1A at 5.14 pX

    PMID 8382063

  6. 06

    Radioligand binding evidence implicates the brain 5-HT2 receptor as a site of action for LSD and phenylisopropylamine hallucinogens

    Titeler M, Lyon RA, Glennon RA · Psychopharmacology 1988

    • · Mechanism of Action

    PMID 3127847

  7. 07

    Possible involvement of serotonin receptors in the facilitatory effect of a hallucinogenic phenethylamine on single facial motoneurons

    Penington NJ, Reiffenstein RJ · Canadian journal of physiology and pharmacology 1986

    • · Mechanism of Action

    PMID 3801984

  8. 08

    Cardiovascular effects of 2, 5-dimethoxy-4-methylamphetamine (DOM, STP)

    Cheng HC, Long JP, Barfknecht CF et al. · The Journal of pharmacology and experimental therapeutics 1973

    • · Mechanism of Action

    PMID 4719787