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PsychedeliaDokholyan Laboratory
Plate 380 of 545Verified

Lisuride

Also known asLysuride · Lisurida · Lisuridum · Dopergin · Methylergol Carbamide · Lysurid · Mesylate, Lisuride · Carbamide, Methylergol

3-[(6aR,9S)-7-methyl-6,6a,8,9-tetrahydro-4H-indolo[4,3-fg]quinolin-9-yl]-1,1-diethylurea

PubChem CID
28864
Measurements
94
InChIKey
BKRGVLQUQGGVSM-KBXCAEBGSA-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

  • Lisuride is a monocarboxylic acid amide. It has a role as a serotonergic agonist, an antiparkinson drug, a dopamine agonist and an antidyskinesia agent. It derives from a hydride of an ergoline.

    ChEBI

  • An ergot derivative that acts as an agonist at dopamine D2 receptors (dopamine agonists). It may also act as an antagonist at dopamine D1 receptors, and as an agonist at some serotonin receptors (serotonin agonists).

    DrugBank

  • An ergot derivative that acts as an agonist at dopamine D2 receptors (DOPAMINE AGONISTS). It may also act as an antagonist at dopamine D1 receptors, and as an agonist at some serotonin receptors (SEROTONIN RECEPTOR AGONISTS).

    Medical Subject Headings (MeSH)

  • See also: Carbidopa (related); Cabergoline (related); Pergolide (related) ... View More ...

    PubChem

How it acts

  • Lisuride is an anti-Parkinson drug chemically related to the dopaminergic ergoline Parkinson's drugs. Lisuride binds to the 5-HT(1A) and 5-HT(2A/2C) receptors. It is also thought to bind to the dopamine receptor and to act as a dopamine agonist. Evidence has also emerged that Lisuride also binds to the Histamine H1 receptor.

    DrugBank

  • There is evidence that lisuride lowers prolactin levels and, in low doses, prevents migraine attacks.

    DrugBank

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

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 Lisuride 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 Lisuride 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 — 94 measurements in this archive, equilibrium constants kept apart from functional readouts.
  • Toxicology — nothing published for Lisuride. 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 Lisuride 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 Lisuride
Depiction served by PubChem for CID 28864. Not redrawn here, so the picture and the identity come from the same record.
Formula
C20H26N4OR
Molecular weight
338.46g/molR
Exact mass
338.2107DaR
cLogP
2.84R
TPSA
51.4ŲR
H-bond donors
2R
H-bond acceptors
2R
Rotatable bonds
3R
Aromatic rings
2R
Heavy atoms
25R
Fraction sp³
0.450R
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

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.

Mechanism, as published

Quoted verbatim from the database named after each passage, never summarized.

  • Lisuride is an anti-Parkinson drug chemically related to the dopaminergic ergoline Parkinson's drugs. Lisuride binds to the 5-HT(1A) and 5-HT(2A/2C) receptors. It is also thought to bind to the dopamine receptor and to act as a dopamine agonist. Evidence has also emerged that Lisuride also binds to the Histamine H1 receptor.
    DrugBank
  • There is evidence that lisuride lowers prolactin levels and, in low doses, prevents migraine attacks.
    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.

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 2 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, ADRA1B, ADRB1cerebellum — 5.8 nTPM, from ADRA2A, HTR5A, DRD4hippocampal formation — 6.1 nTPM, from HTR1A, ADRA1D, ADRA2Camygdala — 6.4 nTPM, from ADRA2C, ADRA1B, ADRB1hypothalamus — 12.6 nTPM, from HTR2C, DRD2, ADRA2Athalamus — no resolved target expressed herebasal ganglia — 62.0 nTPM, from DRD2, HTR2C, 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 2.2.

Body

heart — 20.3 nTPM, from ADRB1, ADRA2B, ADRA2Csmooth muscle — 15.7 nTPM, from HTR2B, ADRB2, ADRA1Alung — 18.4 nTPM, from ADRB2, ADRB1, ADRA2Aliver — 56.2 nTPM, from ADRA1A, ADRB2, ADRA1Bkidney — 33.4 nTPM, from ADRA2C, ADRA2B, ADRA2Astomach — 7.1 nTPM, from ADRB2, HTR1B, HTR2Bduodenum — 9.4 nTPM, from ADRA2A, HTR1D, ADRB2small intestine — 7.1 nTPM, from HTR1D, HTR2B, ADRA2Acolon — 8.5 nTPM, from HTR2B, ADRA2A, ADRB2adrenal gland — 17.2 nTPM, from HTR2B, DRD2, ADRA2Cthyroid gland — 8.7 nTPM, from ADRA2A, HTR2B, ADRB2pancreas — 28.8 nTPM, from ADRA2A, ADRA2C, DRD4urinary bladder — 14.8 nTPM, from ADRA2A, ADRB2, ADRA2Cskeletal muscle — 10.9 nTPM, from ADRB2, ADRA2B, ADRA2Cspleen — 20.8 nTPM, from ADRA2C, ADRA2A, ADRA1Bsalivary gland — 11.3 nTPM, from DRD2, ADRB2, ADRA2A
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. amygdala

    6.4 nTPM

  8. hippocampal formation

    6.1 nTPM

  9. cerebellum

    5.8 nTPM

  10. spinal cord

    2.2 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. kidney

    33.4 nTPM

  3. pancreas

    28.8 nTPM

  4. spleen

    20.8 nTPM

  5. heart muscle

    20.3 nTPM

  6. lung

    18.4 nTPM

  7. adrenal gland

    17.2 nTPM

  8. smooth muscle

    15.7 nTPM

  9. urinary bladder

    14.8 nTPM

  10. salivary gland

    11.3 nTPM

  11. skeletal muscle

    10.9 nTPM

  12. duodenum

    9.4 nTPM

  13. thyroid gland

    8.7 nTPM

  14. colon

    8.5 nTPM

  15. small intestine

    7.1 nTPM

  16. stomach 1

    7.1 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 23 molecular targets. Cell-line and whole-organism screens are excluded here — they carry no affinity — and appear in the table below.

5-HT1A — Ki 10.10 pX5-HT7 — Ki 9.30 pX5-HT2A — Ki 9.13 pX5-HT1D — Ki 9.01 pX5-HT2B — Ki 8.97 pX5-HT5A — Ki 8.51 pX5-HT6 — Ki 8.28 pX5-HT2C — Ki 8.28 pX5-HT1B — Ki 7.80 pX5-HT1E — Ki 7.35 pXD2 — Ki 9.74 pXD3 — Ki 9.55 pXD5 — Ki 8.45 pXD4 — Ki 8.42 pXD1 — Ki 7.19 pXAlpha2A — Ki 10.26 pXAlpha2B — Ki 9.87 pXAlpha2C — Ki 9.40 pXAlpha1D — Ki 8.53 pXAlpha1A — Ki 8.26 pXBeta2 — Ki 8.10 pXBeta1 — Ki 8.09 pXAlpha1B — Ki 7.78 pX5-HT1A5-HT75-HT2A5-HT1D5-HT2B5-HT5A5-HT65-HT2C5-HT1B5-HT1ED2D3D5D4D1Alpha2AAlpha2BAlpha2CAlpha1DAlpha1ABeta2Beta1Alpha1B579
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 Lisuride in this archive.

Published toxicology

— None. The toxicology databases this site reads — HSDB, RTECS and LiverTox, by way of PubChem — hold no record for Lisuride. 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 94

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

TargetClassTypeValue (nM)pXOrganismAssay
Alpha2AAdrenergic receptorsKi0.05510.26HUMANPMID 12388666
5-HT1ASerotonin receptorsKi0.08010.10RATPDSP
Alpha2BAdrenergic receptorsKi0.1359.87HUMANPMID 12388666
5-HT1ASerotonin receptorsKi0.1489.83HUMANPMID 12388666
D2Dopamine receptorsKi0.1809.74HUMANPMID 7756621
D3Dopamine receptorsKi0.2829.55HUMANPMID 12388666
5-HT1ASerotonin receptorsKi0.3009.52HUMANPMID 20126400
D2Dopamine receptorsKi0.3399.47HUMANPMID 12388666
D3Dopamine receptorsKi0.3909.41HUMANPMID 7756621
5-HT1ASerotonin receptorsKi0.4009.40HUMANPMID 7984267
Alpha2CAdrenergic receptorsKi0.4009.40HUMANPMID 20126400
5-HT1ASerotonin receptorsKi0.4109.39HUMANPMID 8461029
Alpha2BAdrenergic receptorsKi0.5009.30HUMANPMID 20126400
5-HT7Serotonin receptorsKi0.5019.30RATPMID 9149537
5-HT7Serotonin receptorsKi0.5209.28RATPMID 8394362
5-HT7Serotonin receptorsKi0.5209.28RATPMID 7984267
D2Dopamine receptorsKi0.6619.18HUMANPMID 12388666
5-HT2ASerotonin receptorsKi0.7409.13HUMANPMID 9225287
5-HT1ASerotonin receptorsKi0.7609.12PIGPDSP
5-HT7Serotonin receptorsKi0.8909.05RATPMID 8394362
5-HT7Serotonin receptorsKi0.8909.05RATPMID 7984267
5-HT1DSerotonin receptorsKi0.9779.01HUMANPMID 12388666
5-HT2BSerotonin receptorsKi1.078.97HUMANPMID 9225287
5-HT2BSerotonin receptorsKi1.328.88HUMANPMID 12388666
5-HT2BSerotonin receptorsKi1.388.86HUMANPMID 11882920
5-HT2ASerotonin receptorsKi1.408.85HUMANPMID 10611640
D2Dopamine receptorsKi1.408.85HUMANPMID 7756621
D3Dopamine receptorsKi1.708.77HUMANPMID 7756621
Alpha2AAdrenergic receptorsKi1.808.74HUMANPMID 20126400
5-HT2ASerotonin receptorsKi2.048.69RATPMID 9225287
5-HT1ASerotonin receptorsKi2.598.59RATPDSP
5-HT1ASerotonin receptorsKi2.688.57RATPDSP
5-HT2ASerotonin receptorsKi2.758.56HUMANPMID 12388666
5-HT2BSerotonin receptorsKi2.908.54HUMANPMID 20126400
5-HT7Serotonin receptorsKi2.958.53GUINEA PIGPMID 7647964
Alpha1DAdrenergic receptorsKi2.958.53HUMANPMID 12388666
5-HT5ASerotonin receptorsKi3.108.51HUMANPMID 20126400
5-HT7Serotonin receptorsKi3.168.50GUINEA PIGPMID 9149537
D5Dopamine receptorsKi3.558.45HUMANPMID 12388666
D4Dopamine receptorsKi3.808.42HUMANPMID 20126400
D4Dopamine receptorsKi4.578.34HUMANPMID 12388666
D4Dopamine receptorsKi4.748.32HUMANPMID 9223553
5-HT2ASerotonin receptorsKi5.208.28HUMANPMID 10611640
5-HT6Serotonin receptorsKi5.248.28RATPMID 7984267
5-HT2CSerotonin receptorsKi5.308.28RATPMID 10611640
5-HT6Serotonin receptorsKi5.308.28RATPMID 7680751
5-HT2ASerotonin receptorsKi5.408.27HUMANPMID 20126400
Alpha1AAdrenergic receptorsKi5.508.26HUMANPMID 12388666
5-HT2ASerotonin receptorsKi5.508.26RATPDSP
5-HT2ASerotonin receptorsKi5.508.26RATPDSP
5-HT2CSerotonin receptorsKi5.888.23HUMANPMID 9225287
5-HT7Serotonin receptorsKi6.308.20RATPMID 7984267
5-HT7Serotonin receptorsKi6.308.20RATPMID 8397408
5-HT7Serotonin receptorsKi6.318.20RATPMID 9149537
5-HT2CSerotonin receptorsKi6.468.19HUMANPMID 11882920
5-HT2CSerotonin receptorsKi6.618.18HUMANPMID 12388666
D2Dopamine receptorsKi6.708.17HUMANPMID 20126400
D4Dopamine receptorsKi6.778.17HUMANPMID 9223553
5-HT7Serotonin receptorsKi6.808.17HUMANPMID 20126400
5-HT1ASerotonin receptorsKi6.908.16HUMANPMID 8461029
5-HT1ASerotonin receptorsKi6.918.16HUMANPMID 7984267
5-HT6Serotonin receptorsKi7.248.14RATPMID 9225298
5-HT6Serotonin receptorsKi7.308.14HUMANPMID 20126400
Beta2Adrenergic receptorsKi7.948.10HUMANPMID 12388666
5-HT6Serotonin receptorsKi8.128.09RATPMID 7984267
5-HT6Serotonin receptorsKi8.198.09RATPMID 7680751
Beta1Adrenergic receptorsKi8.208.09HUMANPMID 20126400
5-HT2CSerotonin receptorsKi11.007.96RATPMID 10611640
5-HT2CSerotonin receptorsKi15.847.80RATPMID 9225287
5-HT1BSerotonin receptorsKi16.007.80HUMANPMID 20126400
Alpha1BAdrenergic receptorsKi16.607.78HUMANPMID 12388666
5-HT7Serotonin receptorsKi18.627.73GUINEA PIGPMID 7647964
5-HT1BSerotonin receptorsKi18.627.73HUMANPMID 12388666
5-HT2CSerotonin receptorsKi19.507.71PIGPDSP
5-HT2CSerotonin receptorsKi19.507.71PIGPDSP
5-HT2CSerotonin receptorsKi20.007.70PIGPDSP
Alpha1AAdrenergic receptorsKi24.607.61HUMANPMID 20126400
5-HT1DSerotonin receptorsKi25.707.59PIGPDSP
5-HT6Serotonin receptorsKi30.197.52RATPMID 9225298
5-HT1DSerotonin receptorsKi30.907.51CALFPDSP
5-HT1DSerotonin receptorsKi30.907.51CALFPDSP
5-HT1DSerotonin receptorsKi30.907.51COWPDSP
5-HT1DSerotonin receptorsKi31.607.50CALFPDSP
H1UnclassifiedKi34.677.46GUINEA PIGPMID 12388666
Beta2Adrenergic receptorsKi35.307.45HUMANPMID 20126400
5-HT1ESerotonin receptorsKi44.307.35HUMANPMID 20126400
D1Dopamine receptorsKi64.577.19HUMANPMID 12388666
Beta1Adrenergic receptorsKi67.617.17HUMANPMID 12388666
D5Dopamine receptorsKi77.007.11HUMANPMID 20126400
5-HT1DSerotonin receptorsKi1146.94HUMANPMID 20126400
D3Dopamine receptorsKi1366.87HUMANPMID 20126400
5-HT1BSerotonin receptorsKi2246.65RATPDSP
5-HT1BSerotonin receptorsKi2246.65RATPDSP
Alpha1BAdrenergic receptorsKi2516.60HUMANPMID 20126400
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.

4T

Registered studies

0T

Open or ongoing

4T

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.

  • Phase 11
  • Phase 21
  • Phase 32

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.

  • Completed3
  • Unknown status1

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.

  • NCT00408915Completed · Phase 3

    Continuous Application of Lisuride in Parkinson's Disease by Subcutaneous Infusion

    Enrollment
    60Testimated
    Started
    2006-07
    Sponsor
    Axxonis Pharma AG

    Conditions Parkinson's Disease

    Matched “Lisuride” in the study’s intervention “Continuous Subcutaneous Lisuride Infusion”

  • NCT00089622Completed · Phase 2

    Lisuride Patch to Treat Parkinson's Disease

    Enrollment
    40Tnot qualified
    Started
    2004-08-04
    Sponsor
    National Institute of Neurological Disorders and Stroke (NINDS)

    Conditions Parkinson Disease

    Matched “Lisuride” in the study’s intervention “Lisuride Transdermal System”

  • NCT00000338Unknown status · Phase 1

    Infusion Laboratory: Protocol 2 (Lisuride) - 3

    Enrollment
    2Tnot qualified
    Started
    1996-03
    Sponsor
    National Institute on Drug Abuse (NIDA)

    Conditions Cocaine-Related Disorders

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

  • NCT00367822Completed · Phase 3

    Transdermal Lisuride: a Trial for the Treatment of Patients With Restless Legs Syndrome (RLS)

    Enrollment
    300Tnot qualified
    Started
    — no start date recorded
    Sponsor
    Axxonis Pharma AG

    Conditions Restless Legs Syndrome

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

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 Lisuride · Methylergol Carbamide · Mesylate, Lisuride. 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 Lisuride 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

    • · 20 measurements at 20 targets (Ki), strongest 5-HT1A at 9.52 pX

    PMID 20126400

  2. 02

    Differential actions of antiparkinson agents at multiple classes of monoaminergic receptor. I. A multivariate analysis of the binding profiles of 14 drugs at 21 native and cloned human receptor subtypes

    Millan MJ, Maiofiss L, Cussac D et al. · The Journal of pharmacology and experimental therapeutics 2002

    • · 20 measurements at 19 targets (Ki), strongest Alpha2A at 10.26 pX

    PMID 12388666

  3. 03

    Molecular biology of 5-HT receptors

    Boess FG, Martin IL · Neuropharmacology 1994

    • · 7 measurements at 3 targets (Ki), strongest 5-HT1A at 9.40 pX

    PMID 7984267

  4. 04

    RS-102221: a novel high affinity and selective, 5-HT2C receptor antagonist

    Bonhaus DW, Weinhardt KK, Taylor M et al. · Neuropharmacology 1997

    • · 5 measurements at 3 targets (Ki), strongest 5-HT2A at 9.13 pX

    PMID 9225287

  5. 05

    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

    • · 4 measurements at 2 targets (Ki), strongest 5-HT2A at 8.85 pX

    PMID 10611640

  6. 06

    A functional test identifies dopamine agonists selective for D3 versus D2 receptors

    Sautel F, Griffon N, Lévesque D et al. · Neuroreport 1995

    • · 4 measurements at 2 targets (Ki), strongest D2 at 9.74 pX

    PMID 7756621

  7. 07

    The 5-HT7 receptor: orphan found

    Eglen RM, Jasper JR, Chang DJ et al. · Trends in pharmacological sciences 1997

    • · 3 measurements at 1 target (Ki), strongest 5-HT7 at 9.30 pX

    PMID 9149537

  8. 08

    Characterization of phospholipase C activity at h5-HT2C compared with h5-HT2B receptors: influence of novel ligands upon membrane-bound levels of [3H]phosphatidylinositols

    Cussac D, Newman-Tancredi A, Quentric Y et al. · Naunyn-Schmiedeberg's archives of pharmacology 2002

    • · 2 measurements at 2 targets (Ki), strongest 5-HT2B at 8.86 pX

    PMID 11882920

  9. 09

    [35S]Guanosine-5'-O-(3-thio)triphosphate binding as a measure of efficacy at human recombinant dopamine D4.4 receptors: actions of antiparkinsonian and antipsychotic agents

    Newman-Tancredi A, Audinot V, Chaput C et al. · The Journal of pharmacology and experimental therapeutics 1997

    • · 2 measurements at 1 target (Ki), strongest D4 at 8.32 pX

    PMID 9223553

  10. 10

    Functional and radioligand binding characterization of rat 5-HT6 receptors stably expressed in HEK293 cells

    Boess FG, Monsma FJ Jr, Carolo C et al. · Neuropharmacology 1997

    • · 2 measurements at 1 target (Ki), strongest 5-HT6 at 8.14 pX

    PMID 9225298

  11. 11

    Characterization and distribution of putative 5-ht7 receptors in guinea-pig brain

    To ZP, Bonhaus DW, Eglen RM et al. · British journal of pharmacology 1995

    • · 2 measurements at 1 target (Ki), strongest 5-HT7 at 8.53 pX

    PMID 7647964

  12. 12

    Characterization of recombinant human serotonin 5HT1A receptors expressed in Chinese hamster ovary cells. [3H]spiperone discriminates between the G-protein-coupled and -uncoupled forms

    Sundaram H, Newman-Tancredi A, Strange PG · Biochemical pharmacology 1993

    • · 2 measurements at 1 target (Ki), strongest 5-HT1A at 9.39 pX

    PMID 8461029

  13. 13

    Cloning and expression of a novel serotonin receptor with high affinity for tricyclic psychotropic drugs

    Monsma FJ Jr, Shen Y, Ward RP et al. · Molecular pharmacology 1993

    • · 2 measurements at 1 target (Ki), strongest 5-HT6 at 8.28 pX

    PMID 7680751

  14. 14

    Molecular cloning and expression of a 5-hydroxytryptamine7 serotonin receptor subtype

    Shen Y, Monsma FJ Jr, Metcalf MA et al. · The Journal of biological chemistry 1993

    • · 2 measurements at 1 target (Ki), strongest 5-HT7 at 9.28 pX

    PMID 8394362

  15. 15

    Molecular cloning, characterization, and localization of a high-affinity serotonin receptor (5-HT7) activating cAMP formation

    Ruat M, Traiffort E, Leurs R et al. · Proceedings of the National Academy of Sciences of the United States of America 1993

    • · 1 measurement at 1 target (Ki), strongest 5-HT7 at 8.20 pX

    PMID 8397408