Skip to content
PsychedeliaDokholyan Laboratory
Plate 333 of 545Verified

Ergotamine

Also known asErgotamin · Ergonsvine · Ergotamina · ergotaminum · Ergo Kranit · Mono, Ergodryl · N02CA02 · Gynergen

(6aR,9R)-N-[(1S,2S,4R,7S)-7-benzyl-2-hydroxy-4-methyl-5,8-dioxo-3-oxa-6,9-diazatricyclo[7.3.0.02,6]dodecan-4-yl]-7-methyl-6,6a,8,9-tetrahydro-4H-indolo[4,3-fg]quinoline-9-carboxamide

PubChem CID
8223
ChEMBL
CHEMBL442
Measurements
130
InChIKey
XCGSFFUVFURLIX-VFGNJEKYSA-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

  • Ergotamine Tartrate can cause developmental toxicity according to state or federal government labeling requirements.

    California Office of Environmental Health Hazard Assessment (OEHHA)

  • Ergotamine is a peptide ergot alkaloid that is dihydroergotamine in which a double bond replaces the single bond between positions 9 and 10. It has a role as a mycotoxin, a non-narcotic analgesic, an alpha-adrenergic agonist, a serotonergic agonist, an oxytocic and a vasoconstrictor agent. It is a conjugate base of an ergotamine(1+).

    ChEBI

  • A vasoconstrictor found in ergot of Central Europe. It is an alpha-1 selective adrenergic agonist and is commonly used in the treatment of migraine disorders.

    DrugBank

  • ergotamine has been reported in Festuca ovina, Festuca rubra, and other organisms with data available.

    LOTUS - the natural products occurrence database

Recognized use

  • Oxytocics; Vasoconstrictor Agents; Serotonin Receptor Agonists; Analgesics, Non-Narcotic; Adrenergic alpha-1 Receptor Agonists

    Therapeutic Uses

    Hazardous Substances Data Bank (HSDB)National Library of Medicine's Medical Subject Headings. Chloramphenicol. Online file (MeSH, 2017). Available from, as of May 8, 2017: https://www.nlm.nih.gov/mesh/2017/mesh_browser/MBrowser.html

  • /CLINICAL TRIALS/ ClinicalTrials.gov is a registry and results database of publicly and privately supported clinical studies of human participants conducted around the world. The Web site is maintained by the National Library of Medicine (NLM) and the National Institutes of Health (NIH). Each ClinicalTrials.gov record presents summary information about a study protocol and includes the following: Disease or condition; Intervention (for example, the medical product, behavior, or procedure being studied); Title, description, and design of the study; Requirements for participation (eligibility criteria); Locations where the study is being conducted; Contact information for the study locations;…

    Therapeutic Uses

    Hazardous Substances Data Bank (HSDB)NIH/NLM; ClinicalTrials.Gov. Available from, as of May 8, 2017: https://clinicaltrials.gov/

  • Ergomar is indicated as therapy to abort or prevent vascular headache, e.g., migraine, migraine variants or a so-called "histaminic cephalalgia". /Included in US product label/

    Therapeutic Uses

    Hazardous Substances Data Bank (HSDB)NIH; DailyMed. Current Medication Information for Ergomar Sublingual (Ergotamine Tartrate) Tablet (Updated: December 2016). Available from, as of May 9, 2017: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=dac9637f-3326-4f25-b7b9-f9f54b738232

  • Because of the likelihood of adverse effects, ergotamine generally should not be used for prophylactic management of migraine headaches. /Not included in US product label/

    Therapeutic Uses

    Hazardous Substances Data Bank (HSDB)American Society of Health-System Pharmacists 2017; Drug Information 2017. Bethesda, MD. 2017

  • For use as therapy to abort or prevent vascular headache, e.g., migraine, migraine variants, or so called "histaminic cephalalgia".

    Drug Indication

    DrugBank

  • Ergot lysergic acid alkaloid produced by Claviceps species (fungal pathogens) commonly found on various grasses; Used to treat migraines (in pure form); [Reference #1] An alkaloid produced by fungi growing on rye; [Hawley]

    Use Classification

    Haz-Map, Information on Hazardous Chemicals and Occupational DiseasesHawley - Lewis RJ. _Hawley's Condensed Chemical Dictionary, _15th Ed. New York: John Wiley & Sons, 2007.

  • For use as therapy to abort or prevent vascular headache, e.g., migraine, migraine variants, or so called "histaminic cephalalgia". Ergotamine is a secondary metabolite (natural product) and principal alkaloid of the ergot fungus, Claviceps purpurea, and related fungi in the family Clavicipitaceae. It is used medicinally for treatment of acute migraine attacks (sometimes in combination with caffeine), and to induce childbirth and prevent post-partum haemorrhage. (L1927)

    Use Classification

    Toxin and Toxin Target Database (T3DB)

How it acts

  • Ergotamine acts on migraine by one of two proposed mechanisms: 1) activation of 5-HT1D receptors located on intracranial blood vessels, including those on arterio-venous anastomoses, leads to vasoconstriction, which correlates with the relief of migraine headache, and 2) activation of 5-HT1D receptors on sensory nerve endings of the trigeminal system results in the inhibition of pro-inflammatory neuropeptide release.

    DrugBank

  • Ergotamine has complex pharmacologic effects. In therapeutic doses, ergotamine causes peripheral vasoconstriction (if the vascular tone is low) primarily by stimulating alpha-adrenergic receptors; however, the drug causes vasodilation in very hypertonic vessels. With higher doses, ergotamine is also a competitive alpha-adrenergic blocker, but this effect is somewhat masked by the drug's alpha-adrenergic agonist activity. With therapeutic doses, ergotamine also inhibits reuptake of norepinephrine, thereby maintaining a high concentration of circulating norepinephrine and increasing ergotamine's vasoconstrictor action. Ergotamine has greater vasoconstrictor activity than the other ergot alkalo…

    Hazardous Substances Data Bank (HSDB)American Society of Health-System Pharmacists 2017; Drug Information 2017. Bethesda, MD. 2017

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

In the body

  • The bioavailability of sublingually administered ergotamine has not been determined.

    Absorption, Distribution and Excretion

    DrugBank

  • Following oral administration, absorption of ergotamine tartrate is quite variable; peak plasma concentrations are attained within 0.5-3 hours. Orally administered ergotamine tartrate undergoes first-pass metabolism.

    Absorption, Distribution and Excretion

    Hazardous Substances Data Bank (HSDB)American Society of Health-System Pharmacists 2017; Drug Information 2017. Bethesda, MD. 2017

  • The unchanged drug is erratically secreted in the saliva and only traces of unchanged drug are excreted in urine and feces. Following a single oral dose of ergotamine in individuals with normal renal and hepatic function in one study, only about 4% of the dose was excreted in urine within 96 hours; the remainder of the dose was presumably excreted in feces. Ergotamine is eliminated by dialysis.

    Absorption, Distribution and Excretion

    Hazardous Substances Data Bank (HSDB)American Society of Health-System Pharmacists 2017; Drug Information 2017. Bethesda, MD. 2017

  • For more Absorption, Distribution and Excretion (Complete) data for Ergotamine (10 total), please visit the HSDB record page.

    Absorption, Distribution and Excretion

    Hazardous Substances Data Bank (HSDB)

  • Hepatic. Ergotamine is metabolized by the liver by largely undefined pathways, and 90% of the metabolites are excreted in the bile.

    Metabolism/Metabolites

    DrugBank

  • Ergotamine, particularly the peptide portion of the molecule, is extensively metabolized in the liver by the cytochrome P-450 (CYP) enzyme system, mainly by the 3A4 isoenzyme; 90% of the metabolites are excreted in bile.

    Metabolism/Metabolites

    Hazardous Substances Data Bank (HSDB)American Society of Health-System Pharmacists 2017; Drug Information 2017. Bethesda, MD. 2017

  • This study investigated if genetic differences exhibited in endophyte-resistant and -susceptible mouse lines had persisted after 13 generations in which the integrity of lines was maintained yet selection ceased. Experimental groups were mouse lines fed an endophyte-free (E-) or -infected (E+) diet. The in vitro metabolism of the ergot alkaloid ergotamine in mouse liver microsomes was characterized by LC-MS/MS and compared between both lines before and after exposure to E+ feed. ... Microsomal incubations produced nine predominate peaks in the HPLC assay. The peaks were confirmed by LC-MS/MS to be ergotamine, ergotamine epimer, monohydroxylated metabolites (M1, M2, M1e, M2e) and dihydroxylat…

    Metabolism/Metabolites

    Hazardous Substances Data Bank (HSDB)PMID 16192106Duringer JM et al; Xenobiotica 35 (6): 531-48 (2005)

  • Ergotamine is metabolized by the liver by largely undefined pathways, and 90% of the metabolites are excreted in the bile. (A1497) Half Life: 2 hours

    Metabolism/Metabolites

    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 Ergotamine 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 Ergotamine 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 — 130 measurements in this archive, equilibrium constants kept apart from functional readouts.
  • Toxicology — 12 published passages, plus any assay in this archive bearing on toxicity.
  • Legal — listed by the DEA among its drugs of concern, with no schedule stated in the record held here.
  • 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 Ergotamine 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 Ergotamine
Depiction served by PubChem for CID 8223. Not redrawn here, so the picture and the identity come from the same record.
Formula
C33H35N5O5R
Molecular weight
581.67g/molR
Exact mass
581.2638DaR
cLogP
1.99R
TPSA
118.2ŲR
H-bond donors
3R
H-bond acceptors
6R
Rotatable bonds
4R
Aromatic rings
3R
Heavy atoms
43R
Fraction sp³
0.424R
Formal charge
0R

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

Bemis–Murcko scaffold

O=C(NC1OC2[C@@H]3CCCN3C(=O)[C@H](Cc3ccccc3)N2C1=O)[C@@H]1C=C2c3cccc4[nH]cc(c34)C[C@H]2NC1

Shared with Ergocristine. 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.

2–2.5 h

“The elimination of half-life is 2 to 2.5 hours and clearance is about 0.68 L/h/kg”
Perrin VL, Clinical pharmacokinetics 1985. PMID 3899452

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.

  • Sumatriptan, dihydroergotamine and methysergide inhibit 1% formalin-induced nociception by activation of peripheral 5-HT1B/1D receptors. This study set out to investigate the pharmacological profile of the antinociception produced by intrathecal and intraplantar administration of ergotamine (a 5-HT1B/1D and 5-HT5A/5B receptor agonist) and…
    Hazardous Substances Data Bank (HSDB)PMID 27068146Vidal-Cantu GC et al; Eur J Pharmacol 781: 109-16 (2016)
  • It has previously been suggested that ergotamine produces external carotid vasoconstriction in vagosympathectomised dogs via 5-HT1B/1D receptors and alpha2-adrenoceptors. The present study has reanalyzed this suggestion by using more selective antagonists alone and in combination. Fifty-two anesthetized dogs were prepared for ultrasonic m…
    Hazardous Substances Data Bank (HSDB)PMID 15224175Valdivia LF et al; Naunyn Schmiedebergs Arch Pharmacol 370 (1): 46-53 (2004)
  • Ergotamine acts on migraine by one of two proposed mechanisms: 1) activation of 5-HT1D receptors located on intracranial blood vessels, including those on arterio-venous anastomoses, leads to vasoconstriction, which correlates with the relief of migraine headache, and 2) activation of 5-HT1D receptors on sensory nerve endings of the trige…
    DrugBank
  • Ergotamine has complex pharmacologic effects. In therapeutic doses, ergotamine causes peripheral vasoconstriction (if the vascular tone is low) primarily by stimulating alpha-adrenergic receptors; however, the drug causes vasodilation in very hypertonic vessels. With higher doses, ergotamine is also a competitive alpha-adrenergic blocker,…
    Hazardous Substances Data Bank (HSDB)American Society of Health-System Pharmacists 2017; Drug Information 2017. Bethesda, MD. 2017
  • Ergotamine is a vasoconstrictor and alpha adrenoreceptor antagonist. The pharmacological properties of ergotamine are extremely complex; some of its actions are unrelated to each other, and even mutually antagonistic. The drug has partial agonist and/or antagonist activity against tryptaminergic, dopaminergic and alpha adrenergic receptor…
    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.

Affect0Mood2Perception1Cognition5Thought process0Thought content0Psychomotor activity1Insight and judgment0
This measures the literature, not the compound. Each spoke counts how many of the 22 records this archive holds for this compound say something under that domain — 5 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 2
matched on “depression” · in Pharmacology: Pharmacodynamics; Toxicology: Hazardous Substances Data Bank (HSDB)
Perception 1
matched on “hallucinat” · in Toxicology: Toxin and Toxin Target Database (T3DB)
Cognition 5
matched on “concentrat”, “confus” · in Pharmacology: Mechanism of Action; Pharmacology: Biological Half-Life; PMID 3899452; Toxicology: Hazardous Substances Data Bank (HSDB); PMID 3917386
Psychomotor activity 1
matched on “stupor” · in 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 — 21.1 nTPM, from CCKBR, CNR1, HTR2Acerebellum — 18.3 nTPM, from CNR1, CCKBR, ADRA2Ahippocampal formation — 13.2 nTPM, from CNR1, HTR1A, ADRA1Damygdala — 13.3 nTPM, from CNR1, CCKBR, ADRA2Chypothalamus — 12.6 nTPM, from HTR2C, DRD2, CNR1thalamus — 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 — 41.3 nTPM, from CCKBR, ADRB2, HTR1Bduodenum — 9.4 nTPM, from ADRA2A, HTR1D, HTR4small intestine — 8.5 nTPM, from HTR4, CNR1, HTR1Dcolon — 10.0 nTPM, from CNR1, HTR2B, ADRA2Aadrenal gland — 17.2 nTPM, from HTR2B, DRD2, CNR1thyroid gland — 8.7 nTPM, from ADRA2A, CNR1, HTR2Bpancreas — 28.8 nTPM, from ADRA2A, CCKBR, ADRA2Curinary 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
    • D2DRD28.7 pX56.6
    • CB1CNR18.4 pX17.3
    • Alpha2CADRA2C8.7 pX4.7
    • Alpha2AADRA2A7.0 pX2.2
    • Gastrin/cholecystokinin type B receptorCCKBR4.8 pX0.8
    • and 16 more

  3. midbrain

    23.4 nTPM

  4. cerebral cortex

    21.1 nTPM
    • Gastrin/cholecystokinin type B receptorCCKBR4.8 pX21.1
    • CB1CNR18.4 pX18.6
    • 5-HT2AHTR2A9.2 pX18.2
    • Alpha1BADRA1B8.3 pX9.1
    • Beta1ADRB15.6 pX7.9
    • and 20 more

  5. cerebellum

    18.3 nTPM
    • CB1CNR18.4 pX18.3
    • Gastrin/cholecystokinin type B receptorCCKBR4.8 pX16.4
    • Alpha2AADRA2A7.0 pX5.8
    • 5-HT5AHTR5A8.4 pX4.0
    • Alpha2CADRA2C8.7 pX2.2
    • and 11 more

  6. amygdala

    13.3 nTPM
    • CB1CNR18.4 pX13.3
    • Gastrin/cholecystokinin type B receptorCCKBR4.8 pX9.7
    • Alpha2CADRA2C8.7 pX6.4
    • Alpha1BADRA1B8.3 pX3.9
    • Beta1ADRB15.6 pX3.7
    • and 20 more

  7. hippocampal formation

    13.2 nTPM
    • CB1CNR18.4 pX13.2
    • 5-HT1AHTR1A9.8 pX6.1
    • Alpha1DADRA1D7.6 pX6.1
    • Alpha2CADRA2C8.7 pX4.6
    • Gastrin/cholecystokinin type B receptorCCKBR4.8 pX4.6
    • and 20 more

  8. hypothalamus

    12.6 nTPM

  9. retina

    10.8 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. stomach 1

    41.3 nTPM
    • Gastrin/cholecystokinin type B receptorCCKBR4.8 pX41.3
    • Beta2ADRB25.7 pX7.1
    • 5-HT1BHTR1B10.5 pX4.7
    • 5-HT2BHTR2B8.9 pX4.4
    • D5DRD56.8 pX4.2
    • and 14 more

  3. kidney

    33.4 nTPM

  4. pancreas

    28.8 nTPM
    • Alpha2AADRA2A7.0 pX28.8
    • Gastrin/cholecystokinin type B receptorCCKBR4.8 pX25.5
    • Alpha2CADRA2C8.7 pX3.6
    • Beta1ADRB15.6 pX1.3
    • CB1CNR18.4 pX1.2
    • and 11 more

  5. spleen

    20.8 nTPM

  6. heart muscle

    20.3 nTPM

  7. lung

    18.4 nTPM

  8. adrenal gland

    17.2 nTPM

  9. smooth muscle

    15.7 nTPM

  10. urinary bladder

    14.8 nTPM

  11. salivary gland

    11.3 nTPM

  12. skeletal muscle

    10.9 nTPM

  13. colon

    10.0 nTPM

  14. duodenum

    9.4 nTPM

  15. thyroid gland

    8.7 nTPM

  16. small intestine

    8.5 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-HT5B, Adenylate cyclase, Cholecystokinin receptor type A.

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

5-HT1B — Ki 10.52 pX5-HT1D — Ki 10.15 pX5-HT1A — Ki 9.77 pX5-HT2A — Ki 9.19 pX5-HT6 — Ki 9.02 pX5-HT2B — Ki 8.89 pX5-HT2C — Ki 8.72 pX5-HT5B — Ki 8.50 pX5-HT5A — Ki 8.40 pX5-HT7 — Ki 7.77 pX5-HT1E — Ki 7.72 pX5-HT1F — Ki 7.30 pX5-HT4 — Ki 6.58 pXD2 — Ki 8.84 pXD3 — Ki 8.83 pXD1 — Ki 7.52 pXD5 — Ki 6.77 pXAlpha2A — Ki 9.10 pXAlpha2B — Ki 8.76 pXAlpha2C — Ki 8.74 pXAlpha1A — Ki 8.49 pXAlpha1B — Ki 8.34 pXAlpha1D — Ki 7.62 pXBeta2 — Ki 5.72 pXBeta1 — Ki 5.62 pXCB1 — Ki 8.40 pX5-HT1B5-HT1D5-HT1A5-HT2A5-HT65-HT2B5-HT2C5-HT5B5-HT5A5-HT75-HT1E5-HT1F5-HT4D2D3D1D5Alpha2AAlpha2BAlpha2CAlpha1AAlpha1BAlpha1DBeta2Beta1CB1579
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 Ergotamine 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 Rabbit iv 100 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. 1594

  • LD50 Mouse iv 62 mg/kg

    Hazardous Substances Data Bank (HSDB)O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. Cambridge, UK: Royal Society of Chemistry, 2013., p. 678

  • LD50 Rabbit iv 3 mg/kg

    Hazardous Substances Data Bank (HSDB)O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. Cambridge, UK: Royal Society of Chemistry, 2013., p. 678

  • LD50 Rat iv 80 mg/kg

    Hazardous Substances Data Bank (HSDB)O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. Cambridge, UK: Royal Society of Chemistry, 2013., p. 678

  • LD50 Cat sc 11 mg/kg

    Hazardous Substances Data Bank (HSDB)O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. Cambridge, UK: Royal Society of Chemistry, 2013., p. 678

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

  • IDENTIFICATION AND USE: Ergotamine tartrate is used to prevent or abort vascular headaches, including migraine and cluster headaches. It is also used in veterinary medicine. HUMAN STUDIES: There have been reports of drug abuse and psychological dependence in patients on ergotamine tartrate therapy. In addition to the adverse effects which may occur with usual doses or prolonged administration of high doses (especiall…

    Hazardous Substances Data Bank (HSDB)

  • 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)

Human Toxicity Excerpts

  • /HUMAN EXPOSURE STUDIES/ Ergotamine tartrate (0.5 mg) was injected intramuscularly into 10 subjects with migraine. The effect on peripheral arteries, measured as a decrease in toe-arm systolic gradients, developed slowly and was well sustained after 29 hr. In contrast, ergotamine was quickly absorbed (half-life = 3 min) and plasma levels (measured by HPLC) declined, with a biologic half-life of 2.5 hr. A hypothetic e…

    Hazardous Substances Data Bank (HSDB)PMID 3917386Tfelt-Hansen P, Paalzow L; Clin Pharmacol Ther 37 (Jan): 29-35 (1985)

  • /SIGNS AND SYMPTOMS/ There is a wide variation in sensitivity to the vasoconstrictor effects of ergotamine and, although adverse effects are most common with long-term therapy using higher than usual doses, vasospasm also has occurred rarely with short-term therapy or usual doses of the drug. Vasoconstriction may cause coronary insufficiency with precipitation or aggravation of angina pectoris and possibly myocardial…

    Hazardous Substances Data Bank (HSDB)American Society of Health-System Pharmacists 2017; Drug Information 2017. Bethesda, MD. 2017

  • /SIGNS AND SYMPTOMS/ In addition to the adverse effects which may occur with usual doses or prolonged administration of high doses (especially adverse vasospastic effects, nausea, and vomiting), acute overdosage of ergotamine may cause lassitude, impaired mental function, confusion, depression, drowsiness, delirium, severe dyspnea, hypotension, hypertension, rapid and weak pulse, unconsciousness, spasms of the limbs,…

    Hazardous Substances Data Bank (HSDB)American Society of Health-System Pharmacists 2017; Drug Information 2017. Bethesda, MD. 2017

  • /SIGNS AND SYMPTOMS/ Symptoms /of overdose/ include vomiting, numbness, tingling, pain and cyanosis of the extremities associated with diminished or absent peripheral pulses; hypertension or hypotension; drowsiness, stupor, coma, convulsions and shock.

    Hazardous Substances Data Bank (HSDB)NIH; DailyMed. Current Medication Information for Ergomar Sublingual (Ergotamine Tartrate) Tablet (Updated: December 2016). Available from, as of May 9, 2017: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=dac9637f-3326-4f25-b7b9-f9f54b738232

  • For more Human Toxicity Excerpts (Complete) data for Ergotamine (37 total), please visit the HSDB record page.

    Hazardous Substances Data Bank (HSDB)

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 108

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

TargetClassTypeValue (nM)pXOrganismAssay
5-HT1BSerotonin receptorsKi0.03010.52RATPMID 19912901
5-HT1BSerotonin receptorsKi0.03010.52RATPMID 7984267
5-HT1DSerotonin receptorsKi0.07010.15RATPMID 7984267
5-HT1DSerotonin receptorsKi0.07010.15RATPMID 19912901
5-HT1BSerotonin receptorsKi0.09110.04Rattus norvegicusCHEMBL1909210
5-HT1ASerotonin receptorsKi0.1709.77HUMANPDSP
5-HT1ASerotonin receptorsKi0.1709.77testPMID 28792478
5-HT1BSerotonin receptorsKi0.3009.52testPMID 28792478
5-HT1DSerotonin receptorsKi0.3009.52testPMID 28792478
5-HT1ASerotonin receptorsKi0.4439.35Rattus norvegicusCHEMBL1909209
5-HT2ASerotonin receptorsKi0.6409.19HUMANPMID 9225287
Alpha2AAdrenergic receptorsKi0.7969.10Homo sapiensCHEMBL1909088
5-HT1DSerotonin receptorsKi0.8009.10Homo sapiensCHEMBL616927
5-HT1DSerotonin receptorsKi0.9009.05BOVINEPMID 2664084
5-HT6Serotonin receptorsKi0.9489.02Homo sapiensCHEMBL1909108
5-HT2ASerotonin receptorsKi0.9779.01HUMANPMID 15322733
5-HT1DSerotonin receptorsKi1.009.00HUMANPDSP
5-HT2BSerotonin receptorsKi1.298.89HUMANPMID 15322733
5-HT2ASerotonin receptorsKi1.418.85RATPMID 9225287
D2Dopamine receptorsKi1.438.84Homo sapiensCHEMBL1909140
5-HT2ASerotonin receptorsKi1.458.84RATPDSP
D3Dopamine receptorsKi1.468.83Homo sapiensCHEMBL1909141
Alpha2BAdrenergic receptorsKi1.758.76Homo sapiensCHEMBL1909089
D2Dopamine receptorsKi1.808.74CALFPMID 995128
Alpha2CAdrenergic receptorsKi1.818.74Homo sapiensCHEMBL1909090
5-HT2ASerotonin receptorsKi1.858.73Homo sapiensCHEMBL1909211
5-HT2BSerotonin receptorsKi1.908.72testPMID 28792478
5-HT2BSerotonin receptorsKi1.908.72HUMANPDSP
5-HT2CSerotonin receptorsKi1.918.72HUMANPMID 15322733
5-HT1DSerotonin receptorsKi1.948.71DogPMID 7984267
5-HT1BSerotonin receptorsKi2.048.69RATPDSP
5-HT1DSerotonin receptorsKi2.208.66Homo sapiensCHEMBL3106305
5-HT2BSerotonin receptorsKi2.208.66Homo sapiensCHEMBL1909104
5-HT6Serotonin receptorsKi2.348.63RATPMID 9225298
UncheckedUnclassifiedKi2.438.61— organism not recordedCHEMBL1909159
5-HT2CSerotonin receptorsKi2.458.61RATPMID 9225287
5-HT1DSerotonin receptorsKi2.638.58Homo sapiensCHEMBL3106305
5-HT1ASerotonin receptorsKi3.008.52RATPMID 8398139
5-HT2BSerotonin receptorsKi3.008.52HUMANPMID 11104741
5-HT1BSerotonin receptorsKi3.028.52Homo sapiensCHEMBL3106304
5-HT1BSerotonin receptorsKi3.108.51Homo sapiensCHEMBL3106304
5-HT5BSerotonin receptorsKi3.168.50MOUSEPMID 8450829
5-HT5BSerotonin receptorsKi3.168.50MOUSEPMID 7984267
Alpha1AAdrenergic receptorsKi3.268.49Rattus norvegicusCHEMBL1909085
5-HT2BSerotonin receptorsKi3.548.45HUMANPMID 9225287
5-HT5ASerotonin receptorsKi3.988.40MOUSEPMID 8450829
5-HT5ASerotonin receptorsKi3.988.40MOUSEPMID 7984267
CB1Cannabinoid receptorsKi3.988.40MOUSEPMID 1464308
Alpha1BAdrenergic receptorsKi4.558.34Rattus norvegicusCHEMBL1909086
5-HT1BSerotonin receptorsKi4.708.33HUMANPDSP
5-HT1DSerotonin receptorsKi6.008.22HUMANPMID 21907583
5-HT1DSerotonin receptorsKi6.008.22Homo sapiensCHEMBL1831560
5-HT5ASerotonin receptorsKi6.308.20RATPMID 7984267
5-HT5ASerotonin receptorsKi6.308.20MOUSEPMID 7984267
5-HT5BSerotonin receptorsKi6.308.20RATPMID 7682702
5-HT2ASerotonin receptorsKi9.008.05RATPDSP
5-HT2ASerotonin receptorsKi9.008.05RATPMID 11104741
5-HT2CSerotonin receptorsKi9.778.01HUMANPMID 9225287
5-HT2CSerotonin receptorsKi12.007.92RATPMID 11104741
5-HT2CSerotonin receptorsKi12.007.92RATPDSP
5-HT6Serotonin receptorsKi12.007.92HUMANPDSP
5-HT6Serotonin receptorsKi12.007.92testPMID 28792478
5-HT5ASerotonin receptorsKi14.007.85HUMANPMID 21907583
5-HT5ASerotonin receptorsKi14.007.85Homo sapiensCHEMBL1831564
5-HT5ASerotonin receptorsKi15.497.81Homo sapiensCHEMBL3106135
5-HT5ASerotonin receptorsKi15.707.80RATPMID 7682702
5-HT5BSerotonin receptorsKi15.847.80RATPMID 7984267
5-HT5ASerotonin receptorsKi16.007.80Homo sapiensCHEMBL3106135
5-HT7Serotonin receptorsKi17.007.77RATPMID 8398139
5-HT7Serotonin receptorsKi17.377.76RATPMID 7984267
5-HT1ESerotonin receptorsKi19.007.72testPMID 28792478
5-HT1ESerotonin receptorsKi19.007.72HUMANPDSP
5-HT2ASerotonin receptorsKi20.407.69RATPDSP
5-HT5ASerotonin receptorsKi22.007.66Homo sapiensCHEMBL618072
Alpha1DAdrenergic receptorsKi24.007.62Homo sapiensCHEMBL1909087
5-HT2CSerotonin receptorsKi29.007.54Homo sapiensCHEMBL1909105
D1Dopamine receptorsKi30.007.52CALFPMID 995128
5-HT5ASerotonin receptorsKi38.007.42MOUSEPMID 8549774
5-HT5ASerotonin receptorsKi40.007.40Homo sapiensCHEMBL618085
5-HT2BSerotonin receptorsKi44.677.35HUMANPMID 23519215
5-HT7Serotonin receptorsKi48.977.31GUINEA PIGPMID 7647964
5-HT2CSerotonin receptorsKi50.007.30PIGPDSP
5-HT1FSerotonin receptorsKi50.117.30MOUSEPMID 7984267
5-HT6Serotonin receptorsKi50.117.30MOUSEPMID 8394987
5-HT7Serotonin receptorsKi50.117.30MOUSEPMID 7984267
5-HT1FSerotonin receptorsKi52.487.28RATPMID 7984267
5-HT2CSerotonin receptorsKi56.207.25PIGPDSP
Alpha2BAdrenergic receptorsKi88.307.05HUMANPDSP
Alpha2AAdrenergic receptorsKi1066.97HUMANPDSP
5-HT6Serotonin receptorsKi1076.97RATPMID 9225298
5-HT7Serotonin receptorsKi1386.86GUINEA PIGPMID 7647964
5-HT1ESerotonin receptorsKi1556.81HUMANPMID 2664084
5-HT1FSerotonin receptorsKi1706.77HUMANPMID 7984267
D5Dopamine receptorsKi1706.77HUMANPDSP
5-HT1FSerotonin receptorsKi1716.77HUMANPMID 8380639
5-HT4Serotonin receptorsKi2646.58Cavia porcellusCHEMBL1909107
5-HT1ESerotonin receptorsKi5376.27HUMANPMID 7984267
5-HT1ESerotonin receptorsKi5756.24HUMANPMID 7984267
5-HT1ESerotonin receptorsKi5996.22HUMANPMID 1513320
5-HT1ESerotonin receptorsKi6006.22RATPMID 8384716
5-HT1ESerotonin receptorsKi6036.22HUMANPMID 7984267
M1UnclassifiedKi8626.06HUMANPDSP
D1Dopamine receptorsKi8646.06Homo sapiensCHEMBL1909139
M2UnclassifiedKi9116.04HUMANPDSP
5-HT7Serotonin receptorsKi1,2915.89HUMANPDSP
5-HT7Serotonin receptorsKi1,2915.89testPMID 28792478
Beta2Adrenergic receptorsKi1,8985.72Homo sapiensCHEMBL1909092
Beta1Adrenergic receptorsKi2,3925.62Homo sapiensCHEMBL1909091

Functional readouts 22

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

TargetClassTypeValue (nM)pXOrganismAssay
5-HT1BSerotonin receptorsIC500.2019.70Rattus norvegicusCHEMBL1909210
5-HT1ASerotonin receptorsIC500.7749.11Rattus norvegicusCHEMBL1909209
5-HT6Serotonin receptorsIC502.048.69Homo sapiensCHEMBL1909108
Alpha2AAdrenergic receptorsIC502.128.67Homo sapiensCHEMBL1909088
5-HT2BSerotonin receptorsIC503.468.46Homo sapiensCHEMBL1909104
UncheckedUnclassifiedIC503.658.44— organism not recordedCHEMBL1909159
Alpha2BAdrenergic receptorsIC503.848.42Homo sapiensCHEMBL1909089
D2Dopamine receptorsIC504.308.37Homo sapiensCHEMBL1909140
D3Dopamine receptorsIC504.318.37Homo sapiensCHEMBL1909141
5-HT2ASerotonin receptorsIC506.498.19Homo sapiensCHEMBL1909211
Alpha1AAdrenergic receptorsIC508.068.09Rattus norvegicusCHEMBL1909085
Alpha1BAdrenergic receptorsIC508.218.09Rattus norvegicusCHEMBL1909086
Alpha2CAdrenergic receptorsIC5012.007.92Homo sapiensCHEMBL1909090
Alpha1DAdrenergic receptorsIC5049.007.31Homo sapiensCHEMBL1909087
5-HT2CSerotonin receptorsIC5056.007.25Homo sapiensCHEMBL1909105
5-HT4Serotonin receptorsIC501,5845.80Cavia porcellusCHEMBL1909107
D1Dopamine receptorsIC501,7285.76Homo sapiensCHEMBL1909139
Beta2Adrenergic receptorsIC502,7615.56Homo sapiensCHEMBL1909092
Beta1Adrenergic receptorsIC504,1425.38Homo sapiensCHEMBL1909091
Gastrin/cholecystokinin type B receptorOther named receptorsIC5017,0004.77Mus musculusCHEMBL652241
Cholecystokinin receptor type AOther named receptorsIC5034,0004.47Mus musculusCHEMBL651446
Adenylate cyclaseEnzymesIC5070,0004.15Arthrospira platensisCHEMBL979110
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.

1T

Registered studies

0T

Open or ongoing

1T

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

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.

  • Completed1

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.

  • NCT00223691Completed · Phase 1

    Treatment of Orthostatic Hypotension in Autonomic Failure

    Enrollment
    389Tactual
    Started
    2002-03
    Sponsor
    Vanderbilt University

    Conditions Autonomic Failure · Orthostatic Hypotension

    Matched “Ergotamine” in the study’s intervention “Ergotamine/ Caffeine”

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 Ergotamine · Ergonsvine · Ergotamina. 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 Ergotamine 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

    Molecular biology of 5-HT receptors

    Boess FG, Martin IL · Neuropharmacology 1994

    • · 16 measurements at 7 targets (Ki), strongest 5-HT1B at 10.52 pX

    PMID 7984267

  2. 02

    Marine Inspired 2-(5-Halo-1H-indol-3-yl)-N,N-dimethylethanamines as Modulators of Serotonin Receptors: An Example Illustrating the Power of Bromine as Part of the Uniquely Marine Chemical Space

    Ibrahim MA, El-Alfy AT, Ezel K et al. · Marine drugs 2017

    • · 7 measurements at 7 targets (Ki), strongest 5-HT1A at 9.77 pX

    PMID 28792478

  3. 03

    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 9.19 pX

    PMID 9225287

  4. 04

    Pharmacological characterisation of the agonist radioligand binding site of 5-HT(2A), 5-HT(2B) and 5-HT(2C) receptors

    Knight AR, Misra A, Quirk K et al. · Naunyn-Schmiedeberg's archives of pharmacology 2004

    • · 3 measurements at 3 targets (Ki), strongest 5-HT2A at 9.01 pX

    PMID 15322733

  5. 05

    Evidence for possible involvement of 5-HT(2B) receptors in the cardiac valvulopathy associated with fenfluramine and other serotonergic medications

    Rothman RB, Baumann MH, Savage JE et al. · Circulation 2000

    • · 3 measurements at 3 targets (Ki), strongest 5-HT2B at 8.52 pX

    PMID 11104741

  6. 06

    CNS and antimalarial activity of synthetic meridianin and psammopemmin analogs

    Lebar MD, Hahn KN, Mutka T et al. · Bioorganic & medicinal chemistry 2011

    • · 2 measurements at 2 targets (Ki), strongest 5-HT1D at 8.22 pX

    PMID 21907583

  7. 07

    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 8.63 pX

    PMID 9225298

  8. 08

    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 7.31 pX

    PMID 7647964

  9. 09

    A novel adenylyl cyclase-activating serotonin receptor (5-HT7) implicated in the regulation of mammalian circadian rhythms

    Lovenberg TW, Baron BM, de Lecea L et al. · Neuron 1993

    • · 2 measurements at 2 targets (Ki), strongest 5-HT1A at 8.52 pX

    PMID 8398139

  10. 10

    Mouse 5-hydroxytryptamine5A and 5-hydroxytryptamine5B receptors define a new family of serotonin receptors: cloning, functional expression, and chromosomal localization

    Matthes H, Boschert U, Amlaiky N et al. · Molecular pharmacology 1993

    • · 2 measurements at 2 targets (Ki), strongest 5-HT5B at 8.50 pX

    PMID 8450829

  11. 11

    Two members of a distinct subfamily of 5-hydroxytryptamine receptors differentially expressed in rat brain

    Erlander MG, Lovenberg TW, Baron BM et al. · Proceedings of the National Academy of Sciences of the United States of America 1993

    • · 2 measurements at 2 targets (Ki), strongest 5-HT5B at 8.20 pX

    PMID 7682702

  12. 12

    Distinct 5-HT(1B) and 5-HT(1D) serotonin receptors in rat: Structural and pharmacological comparison of the two cloned receptors

    Hamblin MW, McGuffin RW, Metcalf MA et al. · Molecular and cellular neurosciences 1992

    • · 2 measurements at 2 targets (Ki), strongest 5-HT1B at 10.52 pX

    PMID 19912901

  13. 13

    Detection of a novel serotonin receptor subtype (5-HT1E) in human brain: interaction with a GTP-binding protein

    Leonhardt S, Herrick-Davis K, Titeler M · Journal of neurochemistry 1989

    • · 2 measurements at 2 targets (Ki), strongest 5-HT1D at 9.05 pX

    PMID 2664084

  14. 14

    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 D2 at 8.74 pX

    PMID 995128

  15. 15

    Structural features for functional selectivity at serotonin receptors

    Wacker D, Wang C, Katritch V et al. · Science (New York, N.Y.) 2013

    • · 1 measurement at 1 target (Ki), strongest 5-HT2B at 7.35 pX

    PMID 23519215

  16. 16

    Expression of functional mouse 5-HT5A serotonin receptor in the methylotrophic yeast Pichia pastoris: pharmacological characterization and localization

    Weiss HM, Haase W, Michel H et al. · FEBS letters 1995

    • · 1 measurement at 1 target (Ki), strongest 5-HT5A at 7.42 pX

    PMID 8549774

  17. 17

    Cloning of another human serotonin receptor (5-HT1F): a fifth 5-HT1 receptor subtype coupled to the inhibition of adenylate cyclase

    Adham N, Kao HT, Schecter LE et al. · Proceedings of the National Academy of Sciences of the United States of America 1993

    • · 1 measurement at 1 target (Ki), strongest 5-HT1F at 6.77 pX

    PMID 8380639

  18. 18

    Molecular cloning and functional expression of 5-HT1E-like rat and human 5-hydroxytryptamine receptor genes

    Lovenberg TW, Erlander MG, Baron BM et al. · Proceedings of the National Academy of Sciences of the United States of America 1993

    • · 1 measurement at 1 target (Ki), strongest 5-HT1E at 6.22 pX

    PMID 8384716

  19. 19

    Molecular cloning of a mammalian serotonin receptor that activates adenylate cyclase

    Plassat JL, Amlaiky N, Hen R · Molecular pharmacology 1993

    • · 1 measurement at 1 target (Ki), strongest 5-HT6 at 7.30 pX

    PMID 8394987

  20. 20

    Human gene S31 encodes the pharmacologically defined serotonin 5-hydroxytryptamine1E receptor

    Zgombick JM, Schechter LE, Macchi M et al. · Molecular pharmacology 1992

    • · 1 measurement at 1 target (Ki), strongest 5-HT1E at 6.22 pX

    PMID 1513320

  21. 21

    The mouse 5HT5 receptor reveals a remarkable heterogeneity within the 5HT1D receptor family

    Plassat JL, Boschert U, Amlaiky N et al. · The EMBO journal 1992

    • · 1 measurement at 1 target (Ki), strongest CB1 at 8.40 pX

    PMID 1464308

  22. 22

    Role of 5-HT5A and 5-HT1B/1D receptors in the antinociception produced by ergotamine and valerenic acid in the rat formalin test

    Vidal-Cantú GC, Jiménez-Hernández M, Rocha-González HI et al. · European journal of pharmacology 2016

    • · Mechanism of Action

    PMID 27068146

  23. 23

    5-HT1B receptors, alpha2A/2C- and, to a lesser extent, alpha1-adrenoceptors mediate the external carotid vasoconstriction to ergotamine in vagosympathectomised dogs

    Valdivia LF, Centurión D, Arulmani U et al. · Naunyn-Schmiedeberg's archives of pharmacology 2004

    • · Mechanism of Action

    PMID 15224175

  24. 24

    Clinical pharmacokinetics of ergotamine in migraine and cluster headache

    Perrin VL · Clinical pharmacokinetics 1985

    • · Biological Half-Life
    • · Plasma elimination half-life

    PMID 3899452

  25. 25

    Intramuscular ergotamine: plasma levels and dynamic activity

    Tfelt-Hansen P, Paalzow L · Clinical pharmacology and therapeutics 1985

    • · Human Toxicity Excerpts

    PMID 3917386