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PsychedeliaDokholyan Laboratory
Plate 272 of 545Verified

Bromocriptine

Also known asBromoergocryptine · Bromocriptin · Bromoergocriptine · Bromergocryptine · 2-Bromo-alpha-ergocryptine · Bromocriptina · 2-Bromo-alpha-ergokryptin · 2-Bromo-alpha-ergokryptine

(6aR,9R)-5-bromo-N-[(1S,2S,4R,7S)-2-hydroxy-7-(2-methylpropyl)-5,8-dioxo-4-propan-2-yl-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
31101
ChEMBL
CHEMBL493
Measurements
129
InChIKey
OZVBMTJYIDMWIL-AYFBDAFISA-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

  • Bromocriptine is an indole alkaloid. It has a role as an antiparkinson drug, a hormone antagonist, a dopamine agonist and an antidyskinesia agent. It derives from a hydride of an ergotaman.

    ChEBI

  • Bromocriptine mesylate is a semisynthetic ergot alkaloid derivative with potent dopaminergic activity. It inhibits prolactin secretion and may be used to treat dysfunctions associated with hyperprolactinemia. Bromocriptine is also indicated for the management of signs and symptoms of Parkinsonian Syndrome, as well as the treatment of acromegaly. Bromocriptine has been associated with pulmonary fibrosis, and can also cause sustained suppression of somatotropin (growth hormone) secretion in some patients with acromegaly. In 1995, the FDA withdrew the approval of bromocriptine mesylate for the prevention of physiological lactation after finding that bromocriptine was not shown to be safe for u…

    DrugBank

  • Bromocriptine is an oral dopamine receptor agonist used predominantly in the therapy of Parkinson disease, but which has other activities including inhibition of prolactin and growth hormone release which has led to its use in acromegaly, infertility and galactorrhea. Bromocriptine therapy is associated with low rate of transient serum enzyme elevations during treatment and has been implicated in rare cases of acute liver injury.

    LiverTox

  • Bromocriptine is a semisynthetic, ergot alkaloid with antiparkinson and lactation inhibitory activities. Bromocriptine selectively binds to and activates the postsynaptic dopamine D2-like receptors in the corpus striatum of the central nervous system (CNS). D2-like receptors are coupled to inhibitory G-proteins, which inhibit adenylyl cyclase, thereby preventing signal transduction mediated via cAMP and leading to an inhibitory effect on neurotransmission. This improves Parkinson symptoms, such as dyskinesia. Bromocriptine also has an inhibitory effect on the anterior pituitary gland, which results in blockage of prolactin secretion, thereby suppressing lactation.

    NCI Thesaurus (NCIt)

Recognized use

  • For the treatment of galactorrhea due to hyperprolactinemia, prolactin-dependent menstrual disorders and infertility, prolactin-secreting adenomas, prolactin-dependent male hypogonadism, as adjunct therapy to surgery or radiotherapy for acromegaly or as monotherapy is special cases, as monotherapy in early Parksinsonian Syndrome or as an adjunct with levodopa in advanced cases with motor complications. Bromocriptine has also been used off-label to treat restless legs syndrome and neuroleptic malignant syndrome.

    DrugBank

  • Bromocriptine is an ergot alkaloid derivative in the dopamine D2 agonist class of drugs used to manage various conditions, including type 2 diabetes, Parkinson disease, acromegaly, and pituitary prolactinomas.

    StatPearls

How it acts

  • The dopamine D2 receptor is a 7-transmembrane G-protein coupled receptor associated with Gi proteins. In lactotrophs, stimulation of dopamine D2 receptor causes inhibition of adenylyl cyclase, which decreases intracellular cAMP concentrations and blocks IP3-dependent release of Ca2+ from intracellular stores. Decreases in intracellular calcium levels may also be brought about via inhibition of calcium influx through voltage-gated calcium channels, rather than via inhibition of adenylyl cyclase. Additionally, receptor activation blocks phosphorylation of p42/p44 MAPK and decreases MAPK/ERK kinase phosphorylation. Inhibition of MAPK appears to be mediated by c-Raf and B-Raf-dependent inhibitio……

    DrugBank

  • Bromocriptine stimulates centrally-located dopaminergic receptors resulting in a number of pharmacologic effects. Five dopamine receptor types from two dopaminergic subfamilies have been identified. The dopaminergic D1 receptor subfamily consists of D1 and D5 subreceptors, which are associated with dyskinesias. The dopaminergic D2 receptor subfamily consists of D2, D3 and D4 subreceptors, which are associated with improvement of symptoms of movement disorders. Thus, agonist activity specific for D2 subfamily receptors, primarily D2 and D3 receptor subtypes, are the primary targets of dopaminergic antiparkinsonian agents. It is thought that postsynaptic D2 stimulation is primarily responsible……

    DrugBank

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

In the body

  • Approximately 28% of the oral dose is absorbed; however due to a substantial first pass effect, only 6% of the oral dose reaches the systemic circulation unchanged. Bromocriptine and its metabolites appear in the blood as early as 10 minutes following oral administration and peak plasma concentration are reached within 1-1.5 hours. Serum prolactin may be decreased within 2 hours or oral administration with a maximal effect achieved after 8 hours. Growth hormone concentrations in patients with acromegaly is reduced within 1-2 hours with a single oral dose of 2.5 mg and decreased growth hormone concentrations persist for at least 4-5 hours.

    Absorption, Distribution and Excretion

    DrugBank

  • Parent drug and metabolites are almost completely excreted via the liver, and only 6% eliminated via the kidney.

    Absorption, Distribution and Excretion

    DrugBank

  • Completely metabolized by the liver, primarily by hydrolysis of the amide bond to produce lysergic acid and a peptide fragment, both inactive and non-toxic. Bromocriptine is metabolized by cytochrome P450 3A4 and excreted primarily in the feces via biliary secretion.

    Metabolism/Metabolites

    DrugBank

  • Bromocriptine has known human metabolites that include 5-bromo-N-[2,11-dihydroxy-7-(2-methylpropyl)-5,8-dioxo-4-propan-2-yl-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 and 5-bromo-N-[2,10-dihydroxy-7-(2-methylpropyl)-5,8-dioxo-4-propan-2-yl-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.

    Metabolism/Metabolites

    NORMAN Suspect List ExchangeS73 | METXBIODB | Metabolite Reaction Database from BioTransformer | DOI:10.5281/zenodo.4056560

  • Completely metabolized by the liver, primarily by hydrolysis of the amide bond to produce lysergic acid and a peptide fragment, both inactive and non-toxic. Bromocriptine is metabolized by cytochrome P450 3A4 and excreted primarily in the feces via biliary secretion. Route of Elimination: Parent drug and metabolites are almost completely excreted via the liver, and only 6% eliminated via the kidney. Half Life: 2-8 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 Bromocriptine 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 Bromocriptine 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 — 129 measurements in this archive, equilibrium constants kept apart from functional readouts.
  • Toxicology — 3 published passages, plus any assay in this archive bearing on toxicity.
  • 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 Bromocriptine 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 Bromocriptine
Depiction served by PubChem for CID 31101. Not redrawn here, so the picture and the identity come from the same record.
Formula
C32H40BrN5O5R
Molecular weight
654.61g/molR
Exact mass
653.2213DaR
cLogP
3.19R
TPSA
118.2ŲR
H-bond donors
3R
H-bond acceptors
6R
Rotatable bonds
5R
Aromatic rings
2R
Heavy atoms
43R
Fraction sp³
0.594R
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)CN2C1=O)[C@@H]1C=C2c3cccc4[nH]cc(c34)C[C@H]2NC1

No other compound in this archive shares it. 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.

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.

  • The dopamine D2 receptor is a 7-transmembrane G-protein coupled receptor associated with Gi proteins. In lactotrophs, stimulation of dopamine D2 receptor causes inhibition of adenylyl cyclase, which decreases intracellular cAMP concentrations and blocks IP3-dependent release of Ca2+ from intracellular stores. Decreases in intracellular ca……
    DrugBank
  • Bromocriptine stimulates centrally-located dopaminergic receptors resulting in a number of pharmacologic effects. Five dopamine receptor types from two dopaminergic subfamilies have been identified. The dopaminergic D1 receptor subfamily consists of D1 and D5 subreceptors, which are associated with dyskinesias. The dopaminergic D2 recepto……
    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.

Affect0Mood0Perception0Cognition2Thought process0Thought content0Psychomotor activity0Insight and judgment0
This measures the literature, not the compound. Each spoke counts how many of the 6 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.
Cognition 2
matched on “concentrat” · in Pharmacology: Mechanism of Action; 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 — 18.2 nTPM, from HTR2A, ADRA1B, ADRB1cerebellum — 5.8 nTPM, from ADRA2A, DRD4, ADRA2Chippocampal formation — 6.1 nTPM, from ADRA1D, HTR1A, 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, AR, ADRB2lung — 18.4 nTPM, from ADRB2, ADRB1, ADRA2Aliver — 3367.1 nTPM, from CYP3A4, ADRA1A, ARkidney — 33.4 nTPM, from ADRA2C, ADRA2B, ADRA2Astomach — 7.1 nTPM, from ADRB2, HTR1B, HTR2Bduodenum — 713.0 nTPM, from CYP3A4, ADRA2A, HTR1Dsmall intestine — 754.5 nTPM, from CYP3A4, HTR1D, HTR2Bcolon — 8.5 nTPM, from HTR2B, ADRA2A, ADRB2adrenal gland — 17.2 nTPM, from HTR2B, DRD2, ADRA2Cthyroid gland — 8.7 nTPM, from ADRA2A, HTR2B, ARpancreas — 28.8 nTPM, from ADRA2A, CYP3A4, ADRA2Curinary bladder — 14.8 nTPM, from ADRA2A, ADRB2, ADRA2Cskeletal muscle — 13.0 nTPM, from AR, ADRB2, ADRA2Bspleen — 20.8 nTPM, from ADRA2C, ADRA2A, ADRA1Bsalivary gland — 11.3 nTPM, from DRD2, ADRB2, ADRA2A
03367 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
    • D2DRD29.2 pX56.6
    • Alpha2CADRA2C7.6 pX4.7
    • D4DRD46.5 pX3.9
    • Alpha2AADRA2A8.0 pX2.2
    • Androgen receptorAR5.8 pX1.0
    • and 14 more

  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

    3367.1 nTPM
    • Cytochrome P450 3A4CYP3A45.5 pX3367.1
    • Alpha1AADRA1A8.4 pX56.2
    • Androgen receptorAR5.8 pX35.8
    • Beta2ADRB26.1 pX13.3
    • Alpha1BADRA1B8.9 pX11.4
    • and 10 more

  2. small intestine

    754.5 nTPM

  3. duodenum

    713.0 nTPM

  4. kidney

    33.4 nTPM

  5. pancreas

    28.8 nTPM

  6. spleen

    20.8 nTPM

  7. heart muscle

    20.3 nTPM

  8. lung

    18.4 nTPM

  9. adrenal gland

    17.2 nTPM

  10. smooth muscle

    15.7 nTPM
    • 5-HT2BHTR2B7.3 pX15.7
    • Androgen receptorAR5.8 pX8.8
    • Beta2ADRB26.1 pX3.5
    • Alpha1AADRA1A8.4 pX2.7
    • Alpha2AADRA2A8.0 pX2.6
    • and 10 more

  11. urinary bladder

    14.8 nTPM
    • Alpha2AADRA2A8.0 pX14.8
    • Beta2ADRB26.1 pX6.4
    • Alpha2CADRA2C7.6 pX4.0
    • Alpha2BADRA2B7.5 pX3.2
    • Androgen receptorAR5.8 pX2.7
    • and 12 more

  12. skeletal muscle

    13.0 nTPM
    • Androgen receptorAR5.8 pX13.0
    • Beta2ADRB26.1 pX10.9
    • Alpha2BADRA2B7.5 pX6.0
    • Alpha2CADRA2C7.6 pX3.3
    • Beta1ADRB16.2 pX2.2
    • and 10 more

  13. salivary gland

    11.3 nTPM

  14. thyroid gland

    8.7 nTPM
    • Alpha2AADRA2A8.0 pX8.7
    • 5-HT2BHTR2B7.3 pX3.2
    • Androgen receptorAR5.8 pX2.0
    • Beta2ADRB26.1 pX1.8
    • D4DRD46.5 pX1.7
    • and 10 more

  15. colon

    8.5 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.

2 of this compound’s targets could not be resolved to a gene and are absent from both columns: Adrenergic receptor alpha-2, Dopamine receptor.

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

5-HT1A — Ki 8.49 pX5-HT2B — Ki 8.28 pX5-HT1D — Ki 8.00 pX5-HT2A — Ki 8.00 pX5-HT6 — Ki 8.00 pX5-HT7 — Ki 7.97 pX5-HT1B — Ki 7.33 pX5-HT2C — Ki 6.70 pXD3 — Ki 9.69 pXD2 — Ki 9.28 pXDopamine receptor — IC50 7.55 pXD1 — Ki 6.97 pXD4 — Ki 6.55 pXD5 — Ki 6.34 pXAlpha1D — Ki 8.95 pXAlpha1B — Ki 8.86 pXAlpha1A — Ki 8.55 pXAlpha2A — Ki 8.26 pXAlpha2B — Ki 7.80 pXAlpha2C — Ki 7.55 pXAdrenergic receptor alpha-2 — IC50 6.29 pXBeta1 — Ki 6.23 pXBeta2 — Ki 6.13 pXAndrogen receptor — Ki 5.82 pXCytochrome P450 3A4 — IC50 5.52 pX5-HT1A5-HT2B5-HT1D5-HT2A5-HT65-HT75-HT1B5-HT2CD3D2Dopamine receptorD1D4D5Alpha1DAlpha1BAlpha1AAlpha2AAlpha2BAlpha2CAdrenergic recep…Beta1Beta2Androgen receptorCytochrome P450 …579
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.

Cytochrome P450 inhibition 1

Inhibition of a drug-metabolising enzyme, which is how interactions arise — the harmala alkaloids' MAO inhibition is the same kind of fact, and appears with the measurements above.

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

  • Signs and Symptoms of Overdose

    StatPearls

  • The dopamine D2 receptor is a 7-transmembrane G-protein coupled receptor associated with Gi proteins. In lactotrophs, stimulation of dopamine D2 receptor causes inhibition of adenylyl cyclase, which decreases intracellular cAMP concentrations and blocks IP3-dependent release of Ca2+ from intracellular stores. Decreases in intracellular calcium levels may also be brought about via inhibition of calcium influx through……

    Toxin and Toxin Target Database (T3DB)

Hepatotoxicity

  • Bromocriptine has been reported to cause serum aminotransferase elevations in a small proportion of patients, but these abnormalities are usually mild, asymptomatic and self-limiting even without dose adjustment. In rare instances, more marked elevations occur that may require dose modification or discontinuation and which can recur with rechallenge. In addition, bromocriptine has been implicated in a small number of…

    LiverTox

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 102

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

TargetClassTypeValue (nM)pXOrganismAssay
D3Dopamine receptorsKi0.2029.69Homo sapiensCHEMBL1909141
D2Dopamine receptorsKi0.5279.28Homo sapiensCHEMBL1909140
D2Dopamine receptorsKi0.6209.21HUMANPMID 8301582
D2Dopamine receptorsKi0.6209.21Homo sapiensCHEMBL5346625
D2Dopamine receptorsKi0.6909.16MOUSEPMID 2017157
Alpha1DAdrenergic receptorsKi1.128.95HUMANPMID 12388666
Alpha1BAdrenergic receptorsKi1.388.86HUMANPMID 12388666
D2Dopamine receptorsKi1.808.74HUMANPMID 7756621
Alpha1BAdrenergic receptorsKi1.968.71Rattus norvegicusCHEMBL1909086
D2Dopamine receptorsKi2.008.70HUMANPMID 9577836
D2Dopamine receptorsKi2.008.70HUMANPMID 21143431
D3Dopamine receptorsKi2.108.68HUMANPMID 8301582
D2Dopamine receptorsKi2.508.60CALFPMID 995128
D2Dopamine receptorsKi2.808.55HUMANPMID 21143431
Alpha1AAdrenergic receptorsKi2.828.55Rattus norvegicusCHEMBL1909085
D2Dopamine receptorsKi3.008.52HUMANPMID 19925619
5-HT1ASerotonin receptorsKi3.228.49Rattus norvegicusCHEMBL1909209
Alpha1AAdrenergic receptorsKi4.178.38HUMANPMID 12388666
D2Dopamine receptorsKi5.008.30HUMANPMID 21143431
D2Dopamine receptorsKi5.018.30HUMANPMID 12388666
5-HT2BSerotonin receptorsKi5.298.28Homo sapiensCHEMBL1909104
D2Dopamine receptorsKi5.308.28RATPMID 1975644
D2Dopamine receptorsKi5.308.28RATPMID 1840645
D2Dopamine receptorsKi5.308.28HUMANPMID 7756621
Alpha2AAdrenergic receptorsKi5.538.26Homo sapiensCHEMBL1909088
D3Dopamine receptorsKi6.768.17HUMANPMID 12388666
D3Dopamine receptorsKi7.108.15HUMANPMID 9686407
D3Dopamine receptorsKi7.408.13HUMANPMID 7756621
D3Dopamine receptorsKi7.408.13RATPMID 1975644
D2Dopamine receptorsKi8.208.09HUMANPMID 9686407
D2Dopamine receptorsKi9.008.05HUMANPMID 21143431
5-HT1ASerotonin receptorsKi10.008.00HUMANPMID 19925619
5-HT1DSerotonin receptorsKi10.008.00HUMANPMID 19925619
5-HT2ASerotonin receptorsKi10.008.00Homo sapiensCHEMBL1909211
5-HT6Serotonin receptorsKi10.008.00Homo sapiensCHEMBL1909108
D2Dopamine receptorsKi10.008.00Homo sapiensCHEMBL5527105
D2Dopamine receptorsKi10.008.00Homo sapiensCHEMBL672313
5-HT7Serotonin receptorsKi10.707.97RATPMID 8394362
5-HT7Serotonin receptorsKi10.717.97RATPMID 7984267
5-HT1DSerotonin receptorsKi10.727.97HUMANPMID 12388666
Alpha2AAdrenergic receptorsKi10.967.96HUMANPMID 12388666
D3Dopamine receptorsKi12.007.92HUMANPMID 7756621
D2Dopamine receptorsKi12.607.90HUMANPMID 1840645
5-HT1ASerotonin receptorsKi12.887.89HUMANPMID 12388666
5-HT1ASerotonin receptorsKi12.907.89HUMANPMID 16051647
D2Dopamine receptorsKi14.797.83HUMANPMID 12388666
Alpha1DAdrenergic receptorsKi15.007.82Homo sapiensCHEMBL1909087
Alpha2BAdrenergic receptorsKi16.007.80Homo sapiensCHEMBL1909089
Alpha1AAdrenergic receptorsKi18.007.74Homo sapiensCHEMBL5527115
D2Dopamine receptorsKi19.007.72HUMANPMID 8097160
5-HT1ASerotonin receptorsKi24.007.62Homo sapiensCHEMBL5527111
5-HT1ASerotonin receptorsKi24.007.62Homo sapiensCHEMBL616370
5-HT1ASerotonin receptorsKi25.007.60HUMANPMID 9686407
5-HT1ASerotonin receptorsKi25.707.59PIGPDSP
Alpha2AAdrenergic receptorsKi26.007.59Homo sapiensCHEMBL5527118
Alpha2CAdrenergic receptorsKi28.187.55HUMANPMID 12388666
5-HT6Serotonin receptorsKi33.007.48HUMANPMID 8522988
Alpha2BAdrenergic receptorsKi34.677.46HUMANPMID 12388666
UncheckedUnclassifiedKi35.007.46— organism not recordedCHEMBL1909159
5-HT1BSerotonin receptorsKi47.007.33Rattus norvegicusCHEMBL1909210
5-HT7Serotonin receptorsKi48.807.31RATPMID 8394362
5-HT7Serotonin receptorsKi48.977.31RATPMID 7984267
D2Dopamine receptorsKi54.007.27RATPMID 1356154
5-HT2BSerotonin receptorsKi56.237.25HUMANPMID 12388666
D2Dopamine receptorsKi68.007.17RATPMID 9021894
Alpha2CAdrenergic receptorsKi76.007.12Homo sapiensCHEMBL1909090
D2Dopamine receptorsKi83.007.08RATPMID 1356154
D3Dopamine receptorsKi87.007.06Homo sapiensCHEMBL5527106
D3Dopamine receptorsKi87.007.06Homo sapiensCHEMBL673828
D1Dopamine receptorsKi1066.97CALFPMID 995128
5-HT2ASerotonin receptorsKi1076.97HUMANPMID 16051647
5-HT2ASerotonin receptorsKi1076.97HUMANPMID 12388666
D2Dopamine receptorsKi1106.96HUMANPMID 9021894
5-HT1BSerotonin receptorsKi1126.95RATPDSP
5-HT2ASerotonin receptorsKi1126.95RATPDSP
5-HT2ASerotonin receptorsKi1176.93RATPMID 9686407
5-HT2ASerotonin receptorsKi1196.92Homo sapiensCHEMBL5527108
5-HT6Serotonin receptorsKi1266.90MOUSEPMID 8394987
5-HT7Serotonin receptorsKi1266.90MOUSEPMID 7984267
5-HT2CSerotonin receptorsKi2006.70PIGPDSP
5-HT2CSerotonin receptorsKi2096.68PIGPDSP
5-HT2CSerotonin receptorsKi2786.56Homo sapiensCHEMBL1909105
D4Dopamine receptorsKi2856.55HUMANPMID 8097160
D4Dopamine receptorsKi3406.47RATPMID 1840645
5-HT1BSerotonin receptorsKi3556.45HUMANPMID 12388666
D4Dopamine receptorsKi3726.43HUMANPMID 12388666
D4Dopamine receptorsKi3736.43Homo sapiensCHEMBL5527107
D5Dopamine receptorsKi4546.34HUMANPMID 1826762
D5Dopamine receptorsKi5376.27HUMANPMID 12388666
Beta1Adrenergic receptorsKi5896.23HUMANPMID 12388666
D1Dopamine receptorsKi6726.17HUMANPMID 1826762
D1Dopamine receptorsKi6926.16HUMANPMID 12388666
5-HT2CSerotonin receptorsKi7416.13HUMANPMID 12388666
Beta2Adrenergic receptorsKi7416.13HUMANPMID 12388666
D4Dopamine receptorsKi1,0006.00HUMANPMID 9223553
Beta1Adrenergic receptorsKi1,3865.86Homo sapiensCHEMBL1909091
D1Dopamine receptorsKi1,4445.84Homo sapiensCHEMBL1909139
Androgen receptorNuclear receptorsKi1,5215.82Rattus norvegicusCHEMBL1909115
D1Dopamine receptorsKi2,0705.68HUMANPMID 9686407
D1Dopamine receptorsKi3,4185.47Homo sapiensCHEMBL5527104
5-HT2CSerotonin receptorsKi4,6745.33RATPMID 9686407
UncheckedUnclassifiedKi6,1055.21— organism not recordedCHEMBL1909112

Functional readouts 27

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

TargetClassTypeValue (nM)pXOrganismAssay
D3Dopamine receptorsIC500.5969.22Homo sapiensCHEMBL1909141
D2Dopamine receptorsIC501.588.80Homo sapiensCHEMBL1909140
Alpha1BAdrenergic receptorsIC503.558.45Rattus norvegicusCHEMBL1909086
5-HT1ASerotonin receptorsIC505.638.25Rattus norvegicusCHEMBL1909209
Alpha1AAdrenergic receptorsIC506.968.16Rattus norvegicusCHEMBL1909085
5-HT2BSerotonin receptorsIC508.328.08Homo sapiensCHEMBL1909104
Alpha2AAdrenergic receptorsIC5015.007.82Homo sapiensCHEMBL1909088
5-HT6Serotonin receptorsIC5022.007.66Homo sapiensCHEMBL1909108
Dopamine receptorDopamine receptorsIC5027.907.55Rattus norvegicusCHEMBL675834
Dopamine receptorDopamine receptorsIC5027.907.55Rattus norvegicusCHEMBL673002
Alpha1DAdrenergic receptorsIC5030.007.52Homo sapiensCHEMBL1909087
Alpha2BAdrenergic receptorsIC5035.007.46Homo sapiensCHEMBL1909089
5-HT2ASerotonin receptorsIC5036.007.44Homo sapiensCHEMBL1909211
UncheckedUnclassifiedIC5053.007.28— organism not recordedCHEMBL1909159
5-HT1BSerotonin receptorsIC501036.99Rattus norvegicusCHEMBL1909210
Adrenergic receptor alpha-2Adrenergic receptorsIC505146.29Rattus norvegicusCHEMBL647559
Alpha2CAdrenergic receptorsIC505206.28Homo sapiensCHEMBL1909090
5-HT2CSerotonin receptorsIC505326.27Homo sapiensCHEMBL1909105
Androgen receptorNuclear receptorsIC502,2815.64Rattus norvegicusCHEMBL1909115
Beta1Adrenergic receptorsIC502,4005.62Homo sapiensCHEMBL1909091
D1Dopamine receptorsIC502,8895.54Homo sapiensCHEMBL1909139
Cytochrome P450 3A4EnzymesIC502,9995.52Homo sapiensCHEMBL1063294
UncheckedUnclassifiedIC506,6925.17— organism not recordedCHEMBL1909112
Nonstructural protein 3UnclassifiedIC5013,0404.88Zika virusCHEMBL4407774
Nonstructural protein 3UnclassifiedIC5021,6004.67Zika virusCHEMBL4619845
Alpha-synucleinUnclassifiedIC5024,7004.61Homo sapiensCHEMBL4700553
UncheckedUnclassifiedPotency25,1194.60— organism not recordedCHEMBL3215169
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.

38T

Registered studies

5T

Open or ongoing

38T

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.

  • Early phase 11
  • Phase 17
  • Phase 210
  • Phase 310
  • Phase 47
  • Not applicable7

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.

  • Completed21
  • Unknown status6
  • Recruiting3
  • Withdrawn3
  • Not yet recruiting2
  • Terminated2
  • Suspended1

The 25 most recently started, of 38

Newest first by start date. Each identifier opens the registry record it came from; the title is the sponsor’s own, quoted.

  • NCT03575000Not yet recruiting · Phase 4

    Bromocriptine for Patients With Schizophrenia and Prediabetes

    Enrollment
    15Testimated
    Started
    2026-01-01
    Sponsor
    VA Pittsburgh Healthcare System

    Conditions Schizophrenia · PreDiabetes

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

  • NCT07124221Recruiting · Phase 3

    A Phase III Clinical Study of Cabergoline Tablets Compared With Bromocriptine Mesylate Tablets

    Enrollment
    382Testimated
    Started
    2025-09-12
    Sponsor
    Changchun GeneScience Pharmaceutical Co., Ltd.

    Conditions Hyperprolactinemia

    Matched “Bromocriptine” in the study’s intervention “Bromocriptine mesylate tablets”

  • NCT06250257Recruiting · Phase 3

    Bromocriptine in Dilated Cardiomyopathy Among Women of Reproductive Age

    Enrollment
    112Testimated
    Started
    2024-10-21
    Sponsor
    Jimma University

    Conditions Dilated Cardiomyopathy

    Matched “Bromocriptine” in the study’s intervention “Bromocriptine mesylate plus standard GDMT”

  • NCT06556186Not yet recruiting · Not applicable

    Surgical and Pharmacological Efficacy of Knosp Grade 0-2 Prolactinoma

    Enrollment
    600Testimated
    Started
    2024-10-01
    Sponsor
    Second Affiliated Hospital, Zhejiang University, School of Medicine

    Conditions Pituitary Tumor

    Matched “Bromocriptin” in the study’s intervention “Bromocriptin 2.5mg, 2-3 times a day”

  • NCT05180773Recruiting · Phase 4

    Impact of Bromocriptine on Clinical Outcomes for Peripartum Cardiomyopathy

    Enrollment
    250Testimated
    Started
    2022-07-27
    Sponsor
    Dennis M. McNamara, MD, MS

    Conditions Peripartum Cardiomyopathy, Postpartum

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

  • NCT04674670Completed · Not applicable

    Psychobiological Mechanisms Underlying Chronic Pain

    Enrollment
    48Tactual
    Started
    2021-11-01
    Sponsor
    susanne becker

    Conditions Fibromyalgia · Pain, Chronic · Chronic Pain, Widespread

    Matched “Bromocriptine” in the study’s intervention “Bromocriptine Mesylate Capsules”

  • NCT04128683Completed · Early phase 1

    Dopamine Receptor Contributions to Prediction Error and Reversal Learning in Anorexia Nervosa

    Enrollment
    31Tactual
    Started
    2020-10-20
    Sponsor
    University of California, San Diego

    Conditions Anorexia Nervosa

    Matched “Bromocriptine” in the study’s intervention “bromocriptine”

  • NCT04413344Completed · Phase 1 / Phase 2

    Repurposing Bromocriptine for Abeta Metabolism in Alzheimer's Disease

    Enrollment
    8Tactual
    Started
    2020-06-05
    Sponsor
    Kyoto University

    Conditions Familial Alzheimer Disease (FAD) · PSEN1 Mutation

    Matched “Bromocriptine” in the study’s intervention “Bromocriptine Mesilate”

  • NCT04038749Unknown status · Not applicable

    Satisfaction of Patients With the Chosen Method of Inhibition of Lactation

    Enrollment
    90Testimated
    Started
    2019-06-16
    Sponsor
    Żelazna Medical Centre, LLC

    Conditions Lactation Suppressed

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

  • NCT04351126Completed · Phase 2

    Management of Ovarian Hyperstimulation Syndrome as a State of Defective Mineralocorticoid Response

    Enrollment
    107Tactual
    Started
    2019-04-01
    Sponsor
    Ganin Fertility Center

    Conditions Ovarian Hyperstimulation Syndrome

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

  • NCT04181385Unknown status · Phase 2 / Phase 3

    Acute Olanzapine and Lipid Response

    Enrollment
    15Testimated
    Started
    2019-01-01
    Sponsor
    University Health Network, Toronto

    Conditions Healthy

    Matched “Bromocriptine” in the study’s intervention “Bromocriptine 5 milligram”

  • NCT03496545Completed · Phase 1 / Phase 2

    Efficacy of Bromocriptine For Fever Reduction in Acute Neurologic Injury

    Enrollment
    47Tactual
    Started
    2018-11-30
    Sponsor
    University of California, San Francisco

    Conditions Subarachnoid Hemorrhage · Subdural Hematoma · Traumatic Brain Injury · Ischemic Stroke · Fever · Intracerebral Hemorrhage

    Matched “Bromocriptine” in the study’s intervention “Bromocriptine 5 MG”

  • NCT03525002Completed · Phase 2

    Dopamine Action on Metabolism in Relation to Genotype

    Enrollment
    120Tactual
    Started
    2018-05-03
    Sponsor
    University Hospital Tuebingen

    Conditions Obesity

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

  • NCT03384524Withdrawn · Phase 1 / Phase 2

    Evaluation of Bromocriptine, Metoprolol and Tamsulosin in Eyes With Non-Central DME

    Enrollment
    0Tactual
    Started
    2018-03
    Sponsor
    Andrew Moshfeghi, MD, MBA

    Conditions Diabetic Macular Edema

    Matched “Bromocriptine” in the study’s intervention “Bromocriptine 2.5 MG”

  • NCT05405244Completed · Phase 3

    Examination of Bromocriptine on Homeostatic and Hedonic Mechanisms of Food Intake in Individuals at High Risk for T2DM

    Enrollment
    55Tactual
    Started
    2017-09-19
    Sponsor
    University of North Carolina, Chapel Hill

    Conditions Overweight and Obesity · Eating Behavior

    Matched “Bromocriptine” in the study’s intervention “Bromocriptine-QR”

  • NCT02590601Withdrawn · Phase 3

    Bromocriptine in the Treatment of Peripartum Cardiomyopathy

    Enrollment
    0Tactual
    Started
    2017-01-01
    Sponsor
    Montreal Heart Institute

    Conditions Peripartum Cardiomyopathy

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

  • NCT02846493Unknown status · Phase 2

    Efficacy and Safety of Dexamethasone Prevention for Patients of Ovarian Hyperstimulation Syndrome

    Enrollment
    200Testimated
    Started
    2016-08
    Sponsor
    Sun Yat-sen University

    Conditions Ovarian Hyperstimulation Syndrome

    Matched “Bromocriptine” in the study’s intervention “bromocriptine”

  • NCT02544321Completed · Phase 2

    Bromocriptine Quick Release (BCQR) as Adjunct Therapy in Type 1 Diabetes

    Enrollment
    108Tactual
    Started
    2015-09
    Sponsor
    University of Colorado, Denver

    Conditions Type 1 Diabetes

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

  • NCT02428946Completed · Not applicable

    Bromocriptine and Insulin Sensitivity

    Enrollment
    15Tactual
    Started
    2014-10
    Sponsor
    Academisch Medisch Centrum - Universiteit van Amsterdam (AMC-UvA)

    Conditions Insulin Sensitivity

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

  • NCT02133755Unknown status · Phase 3

    Effect of Bromocriptine on Insulin Resistance in Polycystic Ovarian Syndrome - A Pilot Study

    Enrollment
    60Testimated
    Started
    2014-07
    Sponsor
    IWK Health Centre

    Conditions PCOS · Insulin Resistance

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

  • NCT02078440Completed · Phase 1

    Pharmacokinetic Study of CYCLOSET ® 0.8 mg Tablets in Children and Adolescent Type 2 Diabetes Mellitus Subjects

    Enrollment
    18Tactual
    Started
    2014-01
    Sponsor
    VeroScience

    Conditions Type 2 Diabetes

    Matched “Bromocriptine” in the study’s intervention “Bromocriptine mesylate”

  • NCT02265484Completed · Not applicable

    To Study the Efficacy of Bromocriptine in Patients With Hepatic/Cirrhosis Related Parkinsonism

    Enrollment
    50Tactual
    Started
    2013-11
    Sponsor
    Institute of Liver and Biliary Sciences, India

    Conditions Cirrhosis Related Parkinsonism

    Matched “Bromocriptine” in the study’s intervention “Lactulose+Rifaximin +Bromocriptine”

  • NCT02428933Completed · Not applicable

    Dopaminergic Effects on Brown Adipose Tissue

    Enrollment
    8Tactual
    Started
    2013-10
    Sponsor
    Academisch Medisch Centrum - Universiteit van Amsterdam (AMC-UvA)

    Conditions Obesity

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

  • NCT02929485Withdrawn · Phase 4

    Dopaminergic Modulation of Frontostriatal Function With a Dopamine Agonist and COMT Inhibitor

    Enrollment
    0Tactual
    Started
    2013-07
    Sponsor
    University of California, Berkeley

    Conditions Addiction

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

  • NCT01821001Completed · Phase 1

    Vaginal Bromocriptine for Treatment of Adenomyosis

    Enrollment
    1Tactual
    Started
    2013-03
    Sponsor
    Mayo Clinic

    Conditions Adenomyosis

    Matched “Bromocriptine” in the study’s intervention “Vaginal Bromocriptine”

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 Bromocriptine · Bromoergocryptine · Bromocriptin. 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 Bromocriptine 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

    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 Alpha1D at 8.95 pX

    PMID 12388666

  2. 02

    Standard binding and functional assays related to medications development division testing for potential cocaine and opiate narcotic treatment medications

    Toll L, Berzetei-Gurske IP, Polgar WE et al. · NIDA research monograph 1998

    • · 6 measurements at 6 targets (Ki), strongest D3 at 8.15 pX

    PMID 9686407

  3. 03

    Antipsychotic occupancy of dopamine receptors in schizophrenia

    Nord M, Farde L · CNS neuroscience & therapeutics 2011

    • · 4 measurements at 1 target (Ki), strongest D2 at 8.70 pX

    PMID 21143431

  4. 04

    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 8.74 pX

    PMID 7756621

  5. 05

    Triptans, serotonin agonists, and serotonin syndrome (serotonin toxicity): a review

    Gillman PK · Headache 2010

    • · 3 measurements at 3 targets (Ki), strongest D2 at 8.52 pX

    PMID 19925619

  6. 06

    Molecular biology of 5-HT receptors

    Boess FG, Martin IL · Neuropharmacology 1994

    • · 3 measurements at 1 target (Ki), strongest 5-HT7 at 7.97 pX

    PMID 7984267

  7. 07

    Cloning of the gene for a human dopamine D4 receptor with high affinity for the antipsychotic clozapine

    Van Tol HH, Bunzow JR, Guan HC et al. · Nature 1991

    • · 3 measurements at 2 targets (Ki), strongest D2 at 8.28 pX

    PMID 1840645

  8. 08

    Monoamine oxidase inhibitors, opioid analgesics and serotonin toxicity

    Gillman PK · British journal of anaesthesia 2005

    • · 2 measurements at 2 targets (Ki), strongest 5-HT1A at 7.89 pX

    PMID 16051647

  9. 09

    Dopamine D2-like sites in schizophrenia, but not in Alzheimer's, Huntington's, or control brains, for [3H]benzquinoline

    Seeman P, Guan HC, Nobrega J et al. · Synapse (New York, N.Y.) 1997

    • · 2 measurements at 1 target (Ki), strongest D2 at 7.17 pX

    PMID 9021894

  10. 10

    Expression and pharmacological characterization of the human D3 dopamine receptor

    Freedman SB, Patel S, Marwood R et al. · The Journal of pharmacology and experimental therapeutics 1994

    • · 2 measurements at 2 targets (Ki), strongest D2 at 9.21 pX

    PMID 8301582

  11. 11

    Dopamine D4 receptors bind inactive (+)-aporphines, suggesting neuroleptic role. Sulpiride not stereoselective

    Seeman P, Van Tol HH · European journal of pharmacology 1993

    • · 2 measurements at 2 targets (Ki), strongest D2 at 7.72 pX

    PMID 8097160

  12. 12

    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 7.97 pX

    PMID 8394362

  13. 13

    Characterization of [3H]quinpirole binding to D2-like dopamine receptors in rat brain

    Levant B, Grigoriadis DE, DeSouza EB · The Journal of pharmacology and experimental therapeutics 1992

    • · 2 measurements at 1 target (Ki), strongest D2 at 7.27 pX

    PMID 1356154

  14. 14

    Cloning of the gene for a human dopamine D5 receptor with higher affinity for dopamine than D1

    Sunahara RK, Guan HC, O'Dowd BF et al. · Nature 1991

    • · 2 measurements at 2 targets (Ki), strongest D5 at 6.34 pX

    PMID 1826762

  15. 15

    Molecular cloning and characterization of a novel dopamine receptor (D3) as a target for neuroleptics

    Sokoloff P, Giros B, Martres MP et al. · Nature 1990

    • · 2 measurements at 2 targets (Ki), strongest D2 at 8.28 pX

    PMID 1975644

  16. 16

    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 8.60 pX

    PMID 995128

  17. 17

    Antipsychotic drugs which elicit little or no parkinsonism bind more loosely than dopamine to brain D2 receptors, yet occupy high levels of these receptors

    Seeman P, Tallerico T · Molecular psychiatry 1998

    • · 1 measurement at 1 target (Ki), strongest D2 at 8.70 pX

    PMID 9577836

  18. 18

    [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

    • · 1 measurement at 1 target (Ki), strongest D4 at 6.00 pX

    PMID 9223553

  19. 19

    Cloning, characterization, and chromosomal localization of a human 5-HT6 serotonin receptor

    Kohen R, Metcalf MA, Khan N et al. · Journal of neurochemistry 1996

    • · 1 measurement at 1 target (Ki), strongest 5-HT6 at 7.48 pX

    PMID 8522988

  20. 20

    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 6.90 pX

    PMID 8394987

  21. 21

    Regulation of dopamine D2 receptors by sodium and pH

    Neve KA · Molecular pharmacology 1991

    • · 1 measurement at 1 target (Ki), strongest D2 at 9.16 pX

    PMID 2017157