Bromocriptine 10mg/5ml oral suspension
Requires a prescription from a doctor or prescriber
Bromocriptine mesylate is a semisynthetic ergot alkaloid derivative with potent dopaminergic activity.
Official documents, adverse reaction reporting, and safety monitoring
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Official medicine documents
Yellow Card
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Drug safety updates
MHRA alerts for Bromocriptine
Safety monitoring data
Yellow Card reports
The MHRA Yellow Card scheme collects reports of suspected side effects from healthcare professionals and patients. View the Drug Analysis Profile (iDAP) for real-world adverse reaction data.
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Suspected adverse reactions reported for Bromocriptine
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Submit a Yellow Card report to the MHRA
Data from the MHRA Yellow Card scheme. A reported reaction does not necessarily mean the medicine caused it. Contains public sector information licensed under the Open Government Licence v3.0.
EudraVigilance
The European Medicines Agency (EMA) collects suspected adverse reaction reports from across the EU/EEA through the EudraVigilance system. Search for safety data on this medicine.
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Suspected adverse reactions reported for Bromocriptine
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Learn about EU pharmacovigilance and safety monitoring
EudraVigilance data is published by the European Medicines Agency (EMA). A suspected adverse reaction is not necessarily caused by the medicine.
1 branded products available
WHO defined daily dose (DDD)
5 mg
Not a recommended dose. The DDD is the assumed average maintenance dose per day for a drug used for its main indication in adults. It is a statistical measure used for research and comparison purposes only.
Source: WHO Collaborating Centre for Drug Statistics Methodology, distributed via the NHS dm+d supplementary mapping files (NHSBSA). Contains public sector information licensed under the Open Government Licence v3.0.
Therapeutically similar medicines
Similarity is based on WHO Anatomical Therapeutic Chemical (ATC) classification and on a factual NHS dm+d therapeutic-grouping code prefix. Source data: NHS dm+d via TRUD (OGL v3.0), WHO ATC/DDD Index.
NHS prescribing volume and spending trends
Guidelines from the National Institute for Health and Care Excellence
NICE clinical guidance(1)
Source: National Institute for Health and Care Excellence (NICE). Contains public sector information licensed under the Open Government Licence v3.0.
Check stock at pharmacies and supply information
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Supply & safety information
Official UK regulator monitoring and safety alerts
Pharmacy links redirect to the retailer's own search and do not represent real-time stock levels. Shortage and safety information sourced from MHRA drug safety updates (gov.uk, Crown Copyright under OGL v3.0).
Codes for healthcare professionals and prescribing systems
These codes are used by healthcare IT systems and prescribers to identify this medicine.
NHS UK identifiers
Browse tools
SNOMED CT and dm+d codes from NHS TRUD (Technology Reference data Update Distribution), licensed under the Open Government Licence v3.0. ATC codes from the WHO Collaborating Centre for Drug Statistics Methodology (whocc.no).
Active and completed clinical studies from ClinicalTrials.gov
Source: ClinicalTrials.gov, a database of the U.S. National Library of Medicine (NLM), National Institutes of Health (NIH). Data accessed via ClinicalTrials.gov API v2. Trial information is provided for research purposes and does not constitute medical advice.
Academic studies and reviews for this medicine's active substance
Showing the 50 most relevant studies.
Reviews & meta-analyses: 11 · Randomised trials: 10 · 1974–2026
Showing the 50 most relevant studies, sorted by most relevant.
J. Gaziano, A. Cincotta, C. O'connor, et al.
Diabetes Care, 2010
A. Walters, W. Hening, N. Kavey, et al.
Annals of Neurology, 1988
Amos D. Korczyn, E. Brunt, J. P. Larsen, et al.
Neurology, 1999
Attachaipanich T, Attachaipanich S, Kaewboot K
2025
- Pregnancy Complications, Cardiovascular
- Puerperal Disorders
- Cardiomyopathies
Dara T, Zabihi M, Hoseinzade F, et al.
2025
BackgroundType 2 diabetes mellitus is a chronic condition driven by insulin resistance and impaired beta-cell function. As beta cells gradually lose function, blood glucose levels rise, leading to clinical diabetes. This condition also elevates the risk of cardiovascular complications. Treatment typically requires multiple medications with different mechanisms of action. Recent developments include bromocriptine, a dopamine agonist approved by the Food and Drug Administration (FDA) for type 2 diabetes, which has been shown to reduce plasma glucose, triglycerides, and free fatty acid levels. To deepen our understanding of type 2 diabetes and refine treatment approaches, a comprehensive analysis of clinical studies and related data is essential.MethodsThis systematic review and meta-analysis investigated the efficacy of bromocriptine in diabetes outcomes by analyzing randomized clinical trials (RCTs) in English up to November 25, 2024. The comprehensive search spanned Scopus, PubMed, and Web of Science, with additional studies identified through supplementary web searches and reference list checks. Inclusion criteria required clinical trials with clear methodologies and defined drug dosages. Data extraction gathered information on study design, outcomes, and intervention specifics, with quality assessment using the JADAD scoring system. Statistical analysis focused on standard mean difference (SMD), while the I2 statistic measured study heterogeneity. A funnel plot analysis was employed to identify publication bias, with all analyses conducted using Comprehensive Meta-Analysis and Stata software.ResultsEighteen RCTs were conducted, revealing that dopamine D2 agonists have a relatively strong impact on reducing Hemoglobin A1C (HbA1c) and fasting blood sugar (FBS). However, with I2 values of 96% for HbA1c and 99% for FBS, the results show high heterogeneity among the studies.ConclusionsBromocriptine presents a promising alternative for individuals with diabetes who cannot tolerate conventional medications. Its unique mechanism of action might offer relief to those who suffer from side effects associated with standard treatments, providing a novel way to manage blood sugar levels.
Abstract licence: CC BY-NC-ND
Adamu UG, Mojela K, Karaye KM, et al.
2025
- Pregnancy Complications, Cardiovascular
- Puerperal Disorders
- Cardiomyopathies
Bromocriptine has been proposed as a disease-modifying therapy for peripartum cardiomyopathy (PPCM). The long-term outcomes of bromocriptine use remain uncertain. We conducted a systematic review, meta-analysis and trial sequential analysis (TSA) to assess the long-term efficacy and safety of bromocriptine in combination with standard care versus standard care alone in patients with PPCM. We systematically searched PubMed, Embase and Cochrane up until March 2025 for published studies comparing bromocriptine plus standard care with standard care alone in patients with PPCM. The outcomes included changes in left ventricular (LV) ejection fraction, LV end-systolic and end-diastolic dimensions, major adverse cardiovascular events (MACE), all-cause mortality and rehospitalization. We computed mean differences (MDs) for continuous outcomes and odds ratios (ORs) for binary endpoints with 95% confidence intervals (CIs). We used TSA to assess the conclusiveness of the available evidence. A total of 12 studies [2 randomized controlled trials (RCTs) and 10 observational studies] and 1765 patients (age range 29-33.8 years) were included, of whom 474 (26.9%) received bromocriptine with standard care and 1291 (73.1%) received standard care alone. Compared with standard care alone, bromocriptine with standard care was associated with a significant improvement in LV ejection fraction (MD 9.98%; 95% CI: 2.86 to 17.10; P < 0.001), LV end-diastolic diameter (MD -2.51 cm; 95% CI: -4.23 to -0.79; P = 0.004), and LV end-systolic diameter (MD -5.61 cm; 95% CI: -10.03 to -1.18; P = 0.010). The proportion of patients with improved LV function was higher in those who received bromocriptine with standard care than in those who received standard care alone (OR 0.35; 95% CI: 0.16 to 0.75; P = 0.007). There were no significant differences between groups regarding the incidence of MACE, all-cause mortality or heart failure rehospitalization. The TSA showed that LV ejection fraction and diastolic dimension reached the required information size (RIS); however, only LV ejection fraction crossed the monitoring boundary before the full sample size was achieved. In this meta-analysis with TSA, the use of bromocriptine with standard care was associated with improved LV function and remodelling in patients with PPCM compared with standard care alone, with a similar effect on mortality and re-hospitalization. TSA indicated that current evidence is promising, but larger and adequately powered randomized trials are needed to confirm bromocriptine's cardioprotective effects.
Abstract licence: CC BY-NC
Mulualem Tesfaye Birhan, Teklie Mengie Ayele, Fikire Wondimu Abebe, et al.
Diabetology & Metabolic Syndrome, 2023
Bieś R, Krzystanek M, Górski M, et al.
2025
Patel P, Adusumilli A, Hari Narayanan D, et al.
2025
R. DeFronzo
Diabetes Care, 2011
Sources: aggregated from Europe PMC (EMBL-EBI), OpenAlex, Crossref, PubMed and other open scholarly databases. Retracted articles are excluded. Study information is provided for research purposes and does not constitute medical advice.
Pharmacology and chemical data from DrugBank
Key facts
Drug status
Approved
Major interactions
13 found
Half-life
2-8 hours
Mechanism
The dopamine D2 receptor is a 7-transmembrane G-protein coupled receptor associated with Gi proteins.
Food interactions
2 warnings
Human targets
18 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
28%
Half-life
2-8 hours
Protein binding
90-96%
Metabolism
Elimination
6%
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
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 use.[L43942][L43947] It continues to be used for the indications mentioned above.
Known interactions with other medicines. Always consult a healthcare professional.
Showing 50 of 1722 interactions
How the body processes this drug — absorption, distribution, metabolism, and elimination
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.
Proteins and enzymes this drug interacts with in the body
PMID:21645528
Positively regulates postnatal regression of retinal hyaloid vessels via suppression of VEGFR2/KDR activity, downstream of OPN5 (By similarity)
PMID:10452531 PMID:1565658 PMID:1652050 PMID:33762731
Also functions as a receptor for ergot alkaloid derivatives, various anxiolytic and antidepressant drugs and other psychoactive substances .
PMID:10452531 PMID:1565658 PMID:1652050 PMID:33762731
Ligand binding causes a conformation change that triggers signaling via guanine nucleotide-binding proteins (G proteins) and modulates the activity of downstream effectors, such as adenylate cyclase .
PMID:10452531 PMID:1565658 PMID:1652050 PMID:33762731
HTR1D is coupled to G(i)/G(o) G alpha proteins and mediates inhibitory neurotransmission by inhibiting adenylate cyclase activity .
PMID:33762731
Regulates the release of 5-hydroxytryptamine in the brain, and thereby affects neural activity .
PMID:18476671 PMID:20945968
May also play a role in regulating the release of other neurotransmitters .
PMID:18476671 PMID:20945968
May play a role in vasoconstriction PMID:18476671 PMID:20945968
PMID:22957663 PMID:3138543 PMID:33762731 PMID:37935376 PMID:37935377 PMID:8138923 PMID:8393041
Also functions as a receptor for various drugs and psychoactive substances .
PMID:22957663 PMID:3138543 PMID:33762731 PMID:38552625 PMID:8138923 PMID:8393041
Ligand binding causes a conformation change that triggers signaling via guanine nucleotide-binding proteins (G proteins) and modulates the activity of downstream effectors, such as adenylate cyclase .
PMID:22957663 PMID:3138543 PMID:33762731 PMID:8138923 PMID:8393041
HTR1A is coupled to G(i)/G(o) G alpha proteins and mediates inhibitory neurotransmission: signaling inhibits adenylate cyclase activity and activates a phosphatidylinositol-calcium second messenger system that regulates the release of Ca(2+) ions from intracellular stores .
PMID:33762731 PMID:35610220
Beta-arrestin family members regulate signaling by mediating both receptor desensitization and resensitization processes .
PMID:18476671 PMID:20363322 PMID:20945968
Plays a role in the regulation of 5-hydroxytryptamine release and in the regulation of dopamine and 5-hydroxytryptamine metabolism .
PMID:18476671 PMID:20363322 PMID:20945968
Plays a role in the regulation of dopamine and 5-hydroxytryptamine levels in the brain, and thereby affects neural activity, mood and behavior .
PMID:18476671 PMID:20363322 PMID:20945968
Plays a role in the response to anxiogenic stimuli PMID:18476671 PMID:20363322 PMID:20945968
Enzymes involved in drug metabolism — important for understanding drug interactions
Proteins that transport this drug across cell membranes
PMID:2897240 PMID:35970996 PMID:8898203 PMID:9038218 PMID:35507548
Catalyzes the flop of phospholipids from the cytoplasmic to the exoplasmic leaflet of the apical membrane. Participates mainly to the flop of phosphatidylcholine, phosphatidylethanolamine, beta-D-glucosylceramides and sphingomyelins .
PMID:8898203
Energy-dependent efflux pump responsible for decreased drug accumulation in multidrug-resistant cells PMID:2897240 PMID:35970996 PMID:9038218
ATC N04BC01
ATC G02CB01
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
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Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Linked compound data from DrugBank Open Data (CC BY-NC 4.0)
Bromocriptine
Additional database identifiers
Drugs Product Database (DPD)
11220
ChemSpider
28858
BindingDB
81993
PDB
08Y
ZINC
ZINC000053683151
HUGO Gene Nomenclature Committee (HGNC)
HGNC:3023
GenAtlas
DRD2
GeneCards
DRD2
GenBank Gene Database
M30625
GenBank Protein Database
181432
Guide to Pharmacology
215
UniProt Accession
DRD2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:3024
GenAtlas
DRD3
GeneCards
DRD3
GenBank Gene Database
U32499
GenBank Protein Database
927342
Guide to Pharmacology
216
UniProt Accession
DRD3_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:5289
GenAtlas
HTR1D
GeneCards
HTR1D
GenBank Gene Database
M89955
GenBank Protein Database
177772
Guide to Pharmacology
3
UniProt Accession
5HT1D_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:281
GenAtlas
ADRA2A
GeneCards
ADRA2A
GenBank Gene Database
M23533
GenBank Protein Database
178196
Guide to Pharmacology
25
UniProt Accession
ADA2A_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:5286
GenAtlas
HTR1A
GeneCards
HTR1A
GenBank Gene Database
M28269
GenBank Protein Database
189928
Guide to Pharmacology
1
UniProt Accession
5HT1A_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:283
GenAtlas
ADRA2C
GeneCards
ADRA2C
GenBank Gene Database
J03853
GenBank Protein Database
178194
Guide to Pharmacology
27
UniProt Accession
ADA2C_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:282
GenAtlas
ADRA2B
GeneCards
ADRA2B
GenBank Gene Database
M34041
GenBank Protein Database
178198
Guide to Pharmacology
26
UniProt Accession
ADA2B_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:5294
GenAtlas
HTR2B
GeneCards
HTR2B
GenBank Gene Database
X77307
GenBank Protein Database
475198
Guide to Pharmacology
7
UniProt Accession
5HT2B_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:3025
GenAtlas
DRD4
GeneCards
DRD4
GenBank Gene Database
L12398
GenBank Protein Database
291946
Guide to Pharmacology
217
UniProt Accession
DRD4_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:5293
GenAtlas
HTR2A
GeneCards
HTR2A
GenBank Gene Database
S42168
GenBank Protein Database
36431
Guide to Pharmacology
6
UniProt Accession
5HT2A_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:5287
GenAtlas
HTR1B
GeneCards
HTR1B
GenBank Gene Database
D10995
GenBank Protein Database
219679
Guide to Pharmacology
2
UniProt Accession
5HT1B_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:5295
GenAtlas
HTR2C
GeneCards
HTR2C
GenBank Gene Database
M81778
GenBank Protein Database
338028
Guide to Pharmacology
8
UniProt Accession
5HT2C_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:3026
GenAtlas
DRD5
GeneCards
DRD5
GenBank Gene Database
X58454
GenBank Protein Database
32049
Guide to Pharmacology
218
UniProt Accession
DRD5_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:3020
GenAtlas
DRD1
GeneCards
DRD1
GenBank Gene Database
X55760
GenBank Protein Database
30397
Guide to Pharmacology
214
UniProt Accession
DRD1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:277
GenAtlas
ADRA1A
GeneCards
ADRA1A
GenBank Gene Database
D25235
GenBank Protein Database
433201
Guide to Pharmacology
22
UniProt Accession
ADA1A_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:278
GenAtlas
ADRA1B
GeneCards
ADRA1B
GenBank Gene Database
M99589
Guide to Pharmacology
23
UniProt Accession
ADA1B_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:280
GenAtlas
ADRA1D
GeneCards
ADRA1D
GenBank Gene Database
M76446
GenBank Protein Database
177807
Guide to Pharmacology
24
UniProt Accession
ADA1D_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:5302
GenAtlas
HTR7
GeneCards
HTR7
GenBank Gene Database
U68487
GenBank Protein Database
1857143
Guide to Pharmacology
12
UniProt Accession
5HT7R_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2637
GenAtlas
CYP3A4
GeneCards
CYP3A4
GenBank Gene Database
M18907
Guide to Pharmacology
1337
UniProt Accession
CP3A4_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:40
GenAtlas
ABCB1
GeneCards
ABCB1
GenBank Gene Database
M14758
GenBank Protein Database
307180
Guide to Pharmacology
768
UniProt Accession
MDR1_HUMAN
DrugBank citations
If you use DrugBank data in your research, please cite:
- DrugBank 6.02024Recommended citationKnox C., Wilson M., Klinger C.M., et alDrugBank 6.0: the DrugBank Knowledgebase for 2024Nucleic Acids Res. 2024 Jan 552(D1):D1265-D1275
- DrugBank 5.02018Wishart D.S., Feunang Y.D., Guo A.C., et alDrugBank 5.0: a major update to the DrugBank database for 2018Nucleic Acids Res. 2017 Nov 846(D1):D1074-D1082
- DrugBank 4.02014Law V., Knox C., Djoumbou Y., et alDrugBank 4.0: shedding new light on drug metabolismNucleic Acids Res. 2014 Jan 142(1):D1091-7
- DrugBank 3.02011Knox C., Law V., Jewison T., et alDrugBank 3.0: a comprehensive resource for 'omics' research on drugsNucleic Acids Res. 2011 Jan39(Database issue):D1035-41
- DrugBank 2.02008Wishart D.S., Knox C., Guo A.C., et alDrugBank: a knowledgebase for drugs, drug actions and drug targets.Nucleic Acids Research2008 Jan36(Database issue):D901-6
- DrugBank 1.02006Wishart D.S., Knox C., Guo A.C., et alDrugBank: a comprehensive resource for in silico drug discovery and exploration.Nucleic Acids Research2006 Jan 134(Database issue):D668-72