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PsychedeliaDokholyan Laboratory
Plate 384 of 545Verified

Lysergic acid amide (LSA)

PubChem records this structure as Lysergic acid amide.

Also known asLysergic acid amide · Ergine · D-Lysergic acid amide · (+)-Lysergamide · d-Lyergic acid amide · LYSERGAMIDE [MI] · Ergine (Lysergic acid amide)

(6aR,9R)-7-methyl-6,6a,8,9-tetrahydro-4H-indolo[4,3-fg]quinoline-9-carboxamide

PubChem CID
442072
Measurements
2
InChIKey
GENAHGKEFJLNJB-QMTHXVAHSA-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

  • Lysergamide is an ergoline alkaloid comprising ergoline lacking hydrogens at positions 9 and 10 and also having a methyl group attached to the piperidine nitrogen. It derives from a hydride of an ergoline.

    ChEBI

  • Lysergic acid amide is a DEA Schedule III controlled substance. Substances in the DEA Schedule III have a potential for abuse less than substances in Schedules I or II and abuse may lead to moderate or low physical dependence or high psychological dependence. It is a Depressants substance.

    Drug Enforcement Administration (DEA)

  • ergine has been reported in Ipomoea corymbosa, Stictocardia tiliifolia, and other organisms with data available.

    LOTUS - the natural products occurrence database

  • A 2025 systematic review of Lysergic Acid Amide noted a potential therapeutic application for cluster headaches.

    Pertti (Bert) Hakkinen's Toxicology and Other Annotationsdoi:doi.org/10.3390/pharmacy13040098

Recognized use

  • Ergoline alkaloids occur in various species of vines of the Convolvulaceae (morning glory) family and in some species of lower fungi. Ergine is the dominant alkaloid in the hallucinogenic seeds of Rivea corymbosa, Argyreia nervosa (Hawaiian baby woodrose) and Ipomoea tricolor (morning glory), and may be responsible for their psychedelic activity, though this has not been proven. (L1918, L1919)

    Toxin and Toxin Target Database (T3DB)

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 Lysergic acid amide (LSA) 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 Lysergic acid amide (LSA) 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 — 2 measurements in this archive, equilibrium constants kept apart from functional readouts.
  • Toxicology — 2 published passages, plus any assay in this archive bearing on toxicity.
  • Legal — DEA Schedule III, 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 Lysergic acid amide (LSA) 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 LSA
Depiction served by PubChem for CID 442072. Not redrawn here, so the picture and the identity come from the same record.
Formula
C16H17N3OR
Molecular weight
267.33g/molR
Exact mass
267.1372DaR
cLogP
1.52R
TPSA
62.1ŲR
H-bond donors
2R
H-bond acceptors
2R
Rotatable bonds
1R
Aromatic rings
2R
Heavy atoms
20R
Fraction sp³
0.312R
Formal charge
0R

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

Bemis–Murcko scaffold

C1=C2c3cccc4[nH]cc(c34)C[C@H]2NCC1

Shared with 1B-LSD, 1DD-LSD, 1H-LSD, 1P-AL-LAD, 1P-ETH-LAD, 1P-LSD and 23 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 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.

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.

Affect0Mood1Perception2Cognition0Thought process0Thought content0Psychomotor activity0Insight and judgment0
This measures the literature, not the compound. Each spoke counts how many of the 2 records this archive holds for this compound say something under that domain — 2 at the widest ring. A long spoke means the subject has been written about, not that the effect is strong, and a spoke at the center means nothing here discusses it rather than that nothing happens. The terms behind each domain are listed in the method.
Mood 1
matched on “euphoria” · in Toxicology: Pertti (Bert) Hakkinen's Toxicology and Other Annotations
Perception 2
matched on “hallucinat” · in Toxicology: Pertti (Bert) Hakkinen's Toxicology and Other Annotations; Toxicology: Toxin and Toxin Target Database (T3DB)

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 — 4.6 nTPM, from DRD1, DRD2cerebellum — 0.8 nTPM, from DRD2, DRD1hippocampal formation — 2.1 nTPM, from DRD2, DRD1amygdala — 3.4 nTPM, from DRD2, DRD1hypothalamus — 10.8 nTPM, from DRD2, DRD1thalamus — no resolved target expressed herebasal ganglia — 62.0 nTPM, from DRD2, DRD1medulla 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 0.8.

Body

heart — 0.1 nTPM, from DRD2smooth muscle — 1.4 nTPM, from DRD2, DRD1lung — 0.7 nTPM, from DRD1, DRD2liver — 1.0 nTPM, from DRD1kidney — 1.2 nTPM, from DRD2, DRD1stomach — 0.2 nTPM, from DRD1, DRD2duodenum — 0.1 nTPM, from DRD1small intestine — 0.3 nTPM, from DRD1, DRD2colon — 0.4 nTPM, from DRD2, DRD1adrenal gland — 7.9 nTPM, from DRD2, DRD1thyroid gland — 0.1 nTPM, from DRD1pancreas — 0.2 nTPM, from DRD2urinary bladder — 0.7 nTPM, from DRD1, DRD2skeletal muscle — 0.8 nTPM, from DRD2spleen — 0.1 nTPM, from DRD1salivary gland — 11.3 nTPM, from DRD2
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. retina

    10.8 nTPM

  5. hypothalamus

    10.8 nTPM

  6. cerebral cortex

    4.6 nTPM

  7. amygdala

    3.4 nTPM

  8. hippocampal formation

    2.1 nTPM

  9. cerebellum

    0.8 nTPM

  10. spinal cord

    0.8 nTPM

Peripheral & autonomic

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

  1. salivary gland

    11.3 nTPM

  2. adrenal gland

    7.9 nTPM

  3. smooth muscle

    1.4 nTPM

  4. kidney

    1.2 nTPM

  5. liver

    1.0 nTPM

  6. skeletal muscle

    0.8 nTPM

  7. lung

    0.7 nTPM

  8. urinary bladder

    0.7 nTPM

  9. colon

    0.4 nTPM

  10. small intestine

    0.3 nTPM

  11. stomach 1

    0.2 nTPM

  12. pancreas

    0.2 nTPM

  13. duodenum

    0.1 nTPM

  14. thyroid gland

    0.1 nTPM

  15. spleen

    0.1 nTPM

  16. heart muscle

    0.1 nTPM

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

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

D1 — Ki 6.74 pXD2 — Ki 6.41 pXD1D2579
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 Lysergic acid amide (LSA) in this archive.

As published

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

Toxicity Summary

  • A 2025 systematic review of Lysergic Acid Amide noted that the reported effects include euphoria, hallucinations, nausea, and anxiety, while severe adverse outcomes included psychosis, hypertension, and hospitalization. This review also stated that Lysergic Acid Amide appears to have a lower potential for abuse than Lysergic Acid Diethylamide, primarily due to its milder psychotomimetic effects and more pronounced au…

    Pertti (Bert) Hakkinen's Toxicology and Other Annotationsdoi:doi.org/10.3390/pharmacy13040098

  • Ergoline alkaloids tend to act as a group, producing complex and variable effects of partial agonism or antagonism at adrenergic, dopaminergic, and serotonergic receptors. Variables relating to these effects are influenced by the agent, dosage, species, tissue, physiological, and endocrinological state, and experimental conditions. In particular, ergoline alkaloids have been shown to have the significant affinity tow…

    Toxin and Toxin Target Database (T3DB)

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 2

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

TargetClassTypeValue (nM)pXOrganismAssay
D1Dopamine receptorsKi1806.74CALFPMID 995128
D2Dopamine receptorsKi3906.41CALFPMID 995128
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 Lysergic acid amide (LSA) 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 Lysergic acid amide · D-Lysergic acid amide · (+)-Lysergamide. 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 Lysergic acid amide (LSA) 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

    Properties of [3H]haloperidol and [3H]dopamine binding associated with dopamine receptors in calf brain membranes

    Burt DR, Creese I, Snyder SH · Molecular pharmacology 1976

    • · 2 measurements at 2 targets (Ki), strongest D1 at 6.74 pX

    PMID 995128