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PsychedeliaDokholyan Laboratory
Plate 167 of 545Verified

5-MeO-DALT

Also known asN,N-Diallyl-5-methoxytryptamine · 5-methoxy DALT · 5-methoxy-N,N-diallyltryptamine · 5-METHOXY-DALT · 5-MEO DALT · 5-Methoxy-diallyltryptamine · N,N-DI ALLYL-5-METHOXY TRYPTAMINE

N-[2-(5-methoxy-1H-indol-3-yl)ethyl]-N-prop-2-enylprop-2-en-1-amine

PubChem CID
50878551
Measurements
45
InChIKey
HGRHWEAUHXYNNP-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

  • 1h-indole-3-ethanamine, 5-methoxy-n,n-di-2-propen-1-yl- is a member of tryptamines.

    ChEBI

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 5-MeO-DALT 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 5-MeO-DALT 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 — 45 measurements in this archive, equilibrium constants kept apart from functional readouts.
  • Toxicology — nothing published for 5-MeO-DALT. An absent record is an absence of study, not evidence of safety.
  • Legal — no DEA record is held here — which is not a finding that this compound is uncontrolled.
  • 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 5-MeO-DALT 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 5-MeO-DALT
Depiction served by PubChem for CID 50878551. Not redrawn here, so the picture and the identity come from the same record.
Formula
C17H22N2OR
Molecular weight
270.38g/molR
Exact mass
270.1732DaR
cLogP
3.39R
TPSA
28.3ŲR
H-bond donors
1R
H-bond acceptors
2R
Rotatable bonds
8R
Aromatic rings
2R
Heavy atoms
20R
Fraction sp³
0.294R
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

MeSH indexes no pharmacological class for this compound.

Duration of acute subjective effects

—

No controlled human trial reporting a duration for this compound is cited here. The archive holds no other record of one either. 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.

Nothing about this compound’s pharmacology is published with a citation in the sources this site reads. The measured binding data below is what the archive can show.

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.

No diagnostic chapter is shown for this compound. Either PubChem records no MeSH pharmacological class for it, or the class it records is not one of the substance classes ICD-11 gives a chapter to. Inferring a chapter from the compound’s name or its binding profile would be a diagnosis this archive is in no position to make.

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.

None of the 0 records this archive holds for this compound uses a term from any of the clinical domains. That is a statement about the literature recorded here, not about the compound.

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, ADRA2C, HTR1Acerebellum — 5.8 nTPM, from ADRA2A, HTR5A, ADRA2Chippocampal formation — 6.1 nTPM, from HTR1A, ADRA2C, HTR2Aamygdala — 6.4 nTPM, from ADRA2C, HTR2A, HTR2Chypothalamus — 12.6 nTPM, from HTR2C, ADRA2A, ADRA2Cthalamus — no resolved target expressed herebasal ganglia — 28.2 nTPM, from HTR2C, ADRA2C, HTR6medulla 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, pituitary gland 4.7, spinal cord 1.4, retina 0.7.

Body

heart — 9.4 nTPM, from ADRA2B, ADRA2C, HTR2Bsmooth muscle — 15.7 nTPM, from HTR2B, ADRA2A, HTR2Alung — 27.2 nTPM, from SLC6A4, ADRA2A, ADRA2Cliver — 6.3 nTPM, from ADRA2B, HTR2B, ADRA2Akidney — 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, ADRA2Bsalivary gland — 6.5 nTPM, from ADRA2A, ADRA2B, ADRA2C
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

    6.4 nTPM

  6. hippocampal formation

    6.1 nTPM

  7. cerebellum

    5.8 nTPM

  8. pituitary gland

    4.7 nTPM

  9. spinal cord

    1.4 nTPM

  10. retina

    0.7 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. kidney

    33.4 nTPM

  3. pancreas

    28.8 nTPM

  4. lung

    27.2 nTPM

  5. spleen

    20.8 nTPM

  6. adrenal gland

    17.2 nTPM

  7. smooth muscle

    15.7 nTPM

  8. urinary bladder

    14.8 nTPM

  9. duodenum

    9.7 nTPM

  10. heart muscle

    9.4 nTPM

  11. thyroid gland

    8.7 nTPM

  12. colon

    8.5 nTPM

  13. salivary gland

    6.5 nTPM

  14. liver

    6.3 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.

2 of this compound’s targets could not be resolved to a gene and are absent from both columns: Sigma 1, Sigma 2.

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

5-HT1A — Ki 7.72 pX5-HT2B — Ki 7.23 pX5-HT7 — Ki 7.05 pX5-HT1D — Ki 7.00 pX5-HT6 — Ki 6.82 pX5-HT2A — Ki 6.66 pX5-HT2C — Ki 6.34 pX5-HT1E — Ki 6.30 pX5-HT1B — Ki 6.13 pX5-HT5A — Ki 5.48 pXAlpha2A — Ki 6.67 pXAlpha2B — Ki 6.14 pXAlpha2C — Ki 5.83 pXKOR — Ki 5.95 pXSigma 2 — Ki 6.60 pXSigma 1 — Ki 6.52 pXSERT — Ki 6.30 pXDAT — Ki 5.50 pX5-HT1A5-HT2B5-HT75-HT1D5-HT65-HT2A5-HT2C5-HT1E5-HT1B5-HT5AAlpha2AAlpha2BAlpha2CKORSigma 2Sigma 1SERTDAT579
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 5-MeO-DALT in this archive.

Published toxicology

— None. The toxicology databases this site reads — HSDB, RTECS and LiverTox, by way of PubChem — hold no record for 5-MeO-DALT. They index compounds that have been studied for decades, so most of this archive has no entry. An absent record is an absence of study, not evidence of safety.

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 45

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

TargetClassTypeValue (nM)pXOrganismAssay
5-HT1ASerotonin receptorsKi19.007.72Homo sapiensCHEMBL3756275
5-HT1ASerotonin receptorsKi19.007.72HUMANPMID 29499272
5-HT1ASerotonin receptorsKi19.957.70Homo sapiensCHEMBL3756275
5-HT2BSerotonin receptorsKi58.887.23Homo sapiensCHEMBL3756280
5-HT2BSerotonin receptorsKi59.007.23HUMANPMID 29499272
5-HT7Serotonin receptorsKi89.137.05Homo sapiensCHEMBL3756284
5-HT7Serotonin receptorsKi90.007.05HUMANPMID 29499272
5-HT1DSerotonin receptorsKi1007.00Homo sapiensCHEMBL3756277
5-HT1DSerotonin receptorsKi1076.97HUMANPMID 29499272
5-HT1DSerotonin receptorsKi1506.82Homo sapiensCHEMBL3756277
5-HT6Serotonin receptorsKi1536.82HUMANPMID 29499272
5-HT6Serotonin receptorsKi1556.81Homo sapiensCHEMBL3756283
Alpha2AAdrenergic receptorsKi2146.67Homo sapiensCHEMBL3756288
Alpha2AAdrenergic receptorsKi2156.67HUMANPMID 29499272
5-HT2ASerotonin receptorsKi2186.66Homo sapiensCHEMBL3756279
5-HT2ASerotonin receptorsKi2186.66HUMANPMID 29499272
5-HT2ASerotonin receptorsKi2196.66Homo sapiensCHEMBL3756279
UncheckedUnclassifiedKi2516.60— organism not recordedCHEMBL3756497
Sigma 2Sigma receptorsKi2536.60RATPMID 29499272
Sigma 1Sigma receptorsKi3016.52RATPMID 29499272
Sigma 1Sigma receptorsKi3026.52Homo sapiensCHEMBL3756496
Sigma 1Sigma receptorsKi3986.40Cavia porcellusCHEMBL2395634
Sigma 1Sigma receptorsKi4006.40Cavia porcellusCHEMBL2395634
5-HT2CSerotonin receptorsKi4566.34HUMANPMID 29499272
5-HT2CSerotonin receptorsKi4576.34Homo sapiensCHEMBL3756281
SERTMonoamine transportersKi4996.30HUMANPMID 29499272
5-HT1ESerotonin receptorsKi5006.30HUMANPMID 29499272
5-HT1ESerotonin receptorsKi5016.30Homo sapiensCHEMBL3756278
H1UnclassifiedKi5016.30Homo sapiensCHEMBL3756492
SERTMonoamine transportersKi5016.30Homo sapiensCHEMBL3756500
H1UnclassifiedKi5056.30HUMANPMID 29499272
Alpha2BAdrenergic receptorsKi7246.14Homo sapiensCHEMBL3756488
Alpha2BAdrenergic receptorsKi7266.14HUMANPMID 29499272
5-HT1BSerotonin receptorsKi7356.13HUMANPMID 29499272
5-HT1BSerotonin receptorsKi7416.13Homo sapiensCHEMBL3756276
KOROpioid receptorsKi1,1225.95Homo sapiensCHEMBL3756494
KOROpioid receptorsKi1,1325.95HUMANPMID 29499272
Alpha2CAdrenergic receptorsKi1,4675.83HUMANPMID 29499272
Alpha2CAdrenergic receptorsKi1,4795.83Homo sapiensCHEMBL3756489
H3UnclassifiedKi1,6985.77Homo sapiensCHEMBL3756493
H3UnclassifiedKi1,7125.77GUINEA PIGPMID 29499272
DATMonoamine transportersKi3,1625.50Homo sapiensCHEMBL3756498
5-HT5ASerotonin receptorsKi3,3115.48Homo sapiensCHEMBL3756282
5-HT5ASerotonin receptorsKi3,3125.48HUMANPMID 29499272
DATMonoamine transportersKi3,3785.47HUMANPMID 29499272
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 5-MeO-DALT 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 5-MeO-DALT · N,N-Diallyl-5-methoxytryptamine · 5-methoxy DALT. 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 5-MeO-DALT 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

    Receptor binding profiles and behavioral pharmacology of ring-substituted N,N-diallyltryptamine analogs

    Klein LM, Cozzi NV, Daley PF et al. · Neuropharmacology 2018

    • · 20 measurements at 20 targets (Ki), strongest 5-HT1A at 7.72 pX

    PMID 29499272