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PsychedeliaDokholyan Laboratory
Plate 531 of 545Verified

UCD0076

PubChem records this structure as [2-(1H-indol-4-yl)ethyl]dimethylamine.

Also known as4-(2-di-methylaminoethyl) indole

2-(1H-indol-4-yl)-N,N-dimethylethanamine

PubChem CID
12825951
ChEMBL
— not recorded in the archive
Measurements
9
InChIKey
CUMMXOMCIOVFBY-UHFFFAOYSA-N

Admitted on a publication

This compound is in the archive because a named paper characterized it. Basargin, Domokosa, Hennessey et al., Proceedings of the National Academy of Sciences 2026 prints it as UCD0076 (PMID 42709856). It reports Ki at psychLight2 (Table S1, Fig. 2A); EC50 and Emax of Gq activation at 5-HT2A, 5-HT2B and 5-HT2C (Table S2, Figs. 3-5), where the 5-HT2A readout is ND; beta-arrestin2 recruitment at 5-HT2A (Table S3), also ND; EC50 and Emax of GoB activation at D2 (Table S4, Fig. S15); potency and efficacy across nine further serotonin receptors (Table S5, Fig. 8F); the psychLight antagonist experiment (Fig. 8A); suppression of 5-MeO-DMT-induced head twitch (Fig. 8B); and dose-dependent attenuation of amphetamine-induced hyperlocomotion (Figs. 8C-E). This is the compound the paper's abstract singles out as preferring 5-HT2C over the other 5-HT2 receptors and producing antipsychotic-like properties in mice.

ChEMBL holds no molecule whose InChIKey skeleton matches CUMMXOMCIOVFBY, so it holds no measurement for this compound and cannot be its source. The paper is the only source there is, which is the case this door was cut for.

Identity The SI names the freebase '2-(1H-indol-4-yl)-N,N-dimethylethan-1-amine' (Experimental Procedures for the Synthesis of UCD0076, p. S46), and the article describes the same compound as carrying 'the pyrrole-fused phenethylamine motif of LSD'. PubChem CID 12825951 lists '2-(1H-indol-4-yl)-N,N-dimethylethanamine' verbatim — the same name without the '-1-' locant — with the CAS index form '1H-Indole-4-ethanamine, N,N-dimethyl-' and CAS 84401-01-4; formula C12H16N2. The paper's material is the hemifumarate and this record is the free base. The molecule is achiral, so no stereochemical question arises.

Read Two files, both read in full. The article as published (PNAS 2026;123(38):e2603412123, open access under CC BY): Significance, abstract, Introduction, all of Results, Discussion, Methods, the captions of Figs. 1-8, and the reference list. And the Supporting Information (Appendix 01, pnas.2603412123.sapp.pdf, 144 pp., retrieved from PNAS on 2026-09-09): the synthetic schemes S1-S9 and S12, the Experimental Procedures section carrying the systematic name, salt form, NMR, LC-MS, HRMS, IR and UHPLC purity for every ergolog, Tables S1-S5, and the pharmacology methods 'Radioligand Binding Assays', '5-HT2 Gq dissociation BRET Assays' and 'beta-Arrestin2 Recruitment BRET Assays'. The SI is what fixes each of the paper's compound codes to a molecule, and without it none of this would be admissible.

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.

— No descriptive record. PubChem holds no attributed passage about UCD0076 under any heading this site reads, and ChEMBL curates no mechanism for it. That is the common case for the research chemicals in this archive: they have structures and binding measurements, and nobody has written a monograph. The measurements are still on the plates that follow.

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 UCD0076 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 UCD0076 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 — 9 measurements in this archive, equilibrium constants kept apart from functional readouts.
  • Toxicology — nothing published for UCD0076. An absent record is an absence of study, not evidence of safety.
  • 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 UCD0076 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 UCD0076
Depiction served by PubChem for CID 12825951. 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

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, HTR1A, HTR1Ecerebellum — 1.0 nTPM, from HTR1E, DRD2, HTR2Ahippocampal formation — 6.1 nTPM, from HTR1A, HTR2A, HTR2Camygdala — 3.5 nTPM, from HTR2A, DRD2, HTR2Chypothalamus — 12.6 nTPM, from HTR2C, DRD2, HTR2Athalamus — no resolved target expressed herebasal ganglia — 62.0 nTPM, from DRD2, HTR2C, HTR1Dmedulla 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: pituitary gland 56.6, midbrain 23.4, retina 10.8, spinal cord 1.0.

Body

heart — 4.6 nTPM, from HTR2B, HTR2A, HTR1Fsmooth muscle — 15.7 nTPM, from HTR2B, HTR2A, DRD2lung — 0.8 nTPM, from HTR2B, HTR2A, HTR1Fliver — 3.3 nTPM, from HTR2B, HTR2Akidney — 3.1 nTPM, from HTR2B, DRD2, HTR1Bstomach — 4.7 nTPM, from HTR1B, HTR2B, HTR1Eduodenum — 8.0 nTPM, from HTR1D, HTR2B, HTR2Asmall intestine — 7.1 nTPM, from HTR1D, HTR2B, HTR2Acolon — 8.5 nTPM, from HTR2B, HTR2A, DRD2adrenal gland — 17.2 nTPM, from HTR2B, DRD2, HTR1Bthyroid gland — 3.2 nTPM, from HTR2B, HTR1E, HTR1Fpancreas — 0.2 nTPM, from HTR1D, HTR1F, DRD2urinary bladder — 2.0 nTPM, from HTR2B, HTR1B, HTR2Askeletal muscle — 0.8 nTPM, from DRD2, HTR2A, HTR1Fspleen — 0.6 nTPM, from HTR1F, HTR2Bsalivary gland — 11.3 nTPM, from DRD2, HTR2B, HTR1B
062 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

    62.0 nTPM

  2. pituitary gland

    56.6 nTPM

  3. midbrain

    23.4 nTPM

  4. cerebral cortex

    18.2 nTPM

  5. hypothalamus

    12.6 nTPM

  6. retina

    10.8 nTPM

  7. hippocampal formation

    6.1 nTPM

  8. amygdala

    3.5 nTPM

  9. spinal cord

    1.0 nTPM

  10. cerebellum

    1.0 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. salivary gland

    11.3 nTPM

  4. colon

    8.5 nTPM

  5. duodenum

    8.0 nTPM

  6. small intestine

    7.1 nTPM

  7. stomach 1

    4.7 nTPM

  8. heart muscle

    4.6 nTPM

  9. liver

    3.3 nTPM

  10. thyroid gland

    3.2 nTPM

  11. kidney

    3.1 nTPM

  12. urinary bladder

    2.0 nTPM

  13. lung

    0.8 nTPM

  14. skeletal muscle

    0.8 nTPM

  15. spleen

    0.6 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.

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

5-HT1D — EC50 6.87 pX5-HT2C — EC50 6.48 pX5-HT1F — EC50 6.31 pX5-HT1E — EC50 6.22 pX5-HT1B — EC50 6.10 pX5-HT1A — EC50 6.08 pX5-HT2B — EC50 5.79 pX5-HT2A — Ki 5.71 pXD2 — EC50 6.23 pX5-HT1D5-HT2C5-HT1F5-HT1E5-HT1B5-HT1A5-HT2B5-HT2AD2579
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 UCD0076 in this archive.

Published toxicology

— None. The toxicology databases this site reads — HSDB, RTECS and LiverTox, by way of PubChem — hold no record for UCD0076. 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 1

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

TargetClassTypeValue (nM)pXOrganismAssay
5-HT2ASerotonin receptorsKi1,9685.71— organism not recordedPMID 42709856

Functional readouts 8

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

TargetClassTypeValue (nM)pXOrganismAssay
5-HT1DSerotonin receptorsEC501346.87— organism not recordedPMID 42709856
5-HT2CSerotonin receptorsEC503346.48— organism not recordedPMID 42709856
5-HT1FSerotonin receptorsEC504886.31— organism not recordedPMID 42709856
D2Dopamine receptorsEC505876.23— organism not recordedPMID 42709856
5-HT1ESerotonin receptorsEC506076.22— organism not recordedPMID 42709856
5-HT1BSerotonin receptorsEC507876.10— organism not recordedPMID 42709856
5-HT1ASerotonin receptorsEC508306.08— organism not recordedPMID 42709856
5-HT2BSerotonin receptorsEC501,6295.79— organism not recordedPMID 42709856
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 UCD0076 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 UCD0076 · 2-(1H-indol-4-yl)-N,N-dimethylethan-1-amine · 2-(1H-indol-4-yl)-N,N-dimethylethanamine. 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 UCD0076 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

    Deconstruction of lysergic acid diethylamide

    Basargin AG, Domokosa A, Hennessey JJ et al. · Proceedings of the National Academy of Sciences of the United States of America 2026

    • · 9 measurements at 9 targets (EC50, Ki), strongest 5-HT1D at 6.87 pX

    PMID 42709856