Milrinone 30mg/50ml solution for infusion pre-filled syringes
Requires a prescription from a doctor or prescriber
Heart failure is a multifactorial condition that affects roughly 1-2% of the adult population.
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1 branded products available
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.
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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: 20 · Randomised trials: 27 · 1991–2026
Showing the 50 most relevant studies, sorted by most relevant.
M. Cuffe, R. Califf, K. Adams, et al.
JAMA, 2002
Kavanagh T, Kilpatrick T, Hardy B, et al.
2025
- Hypertension, Pulmonary
- Milrinone
- Vasodilator Agents
To summarize the evidence on the hemodynamic effects and vasopressor requirements of adult patients with known pulmonary hypertension (PH) undergoing cardiac surgery treated with intravenous and inhaled milrinone. A total of 400 patients in 5 prospective (4 RCT) studies were included for pooled analysis. There was no significant difference in the primary outcome; mean pulmonary artery pressure (MPAP) between groups (MD: -4.80, 95% CI -10.57 to 0.98). Inhaled milrinone was associated with a greater systemic vascular resistance index (SVRI) (MD: 259.21, 95% CI 168.70 to 349.72) and reduction in pulmonary capillary wedge pressure (MD: -4.64, 95% CI -5.47 to -3.81). There were no observable differences in mean arterial pressure, pulmonary vascular resistance, cardiac index, or central venous pressure. All studies included were assessed to be moderate/some concern risk of bias. Inhaled milrinone has not been shown to have a significant beneficial effect on MPAP and SVR when compared to intravenous milrinone in patients with known PH undergoing cardiac surgery. However, it has shown some benefits in maintaining MAP and improving oxygenation in this patient cohort. The study is limited by the bias of the included studies and the variability of inhaled drug dosage and administration timing, further well-powered randomized controlled trials are required.
Abstract licence: CC BY-NC-SA
Emara A, Ellebedy M, Aboeldahab H, et al.
2026
- Milrinone
- Cardiotonic Agents
- Cardiac Surgical Procedures
Yamamoto M, Hosoya Y, Hanada H, et al.
2025
BackgroundInotropes play a significant role in the treatment of cardiogenic shock (CS). Phosphodiesterase 3 inhibitors (PDE3i) are being used with increasing frequency, despite limited supporting evidence.Methods and resultsWe performed a systematic review to assess the clinical importance of PDE3i in CS. The search included studies that compared the effect of 'PDE3i with or without inotropes' with 'No PDE3i with or without inotropes' in patients with cardiogenic shock. Early death, cardiac arrest, and initiation of renal replacement therapy were assessed as outcomes. We identified 2 randomized controlled trials (RCT) with a total of 224 patients who met the eligibility requirements from the PubMed, Web of Science, and CENTRAL databases, up until October 31, 2024. One RCT compared milrinone with dobutamine (DOB), and another compared enoximone with levosimendan. Meta-analysis revealed that PDE3i were neither superior nor inferior for the outcomes in the total cohort (odds ratio [OR] 1.47, 95% confidence interval [CI] 0.35-6.26 for early deaths; OR 1.14, 95% CI 0.42-3.14 for cardiac arrest; OR 1.53, 95% CI 0.80-2.92 for the initiation of renal replacement therapy).ConclusionsThe present systematic review revealed no difference in outcomes, early deaths, cardiac arrest and initiation of renal replacement therapy when using PDE3i in patients with CS treated with or without other inotropes.
Abstract licence: CC BY-NC-ND
William Bahagia
Majalah Kardiologi Indonesia, 2023
Daniyal Rashid, Shamyl Zehra
Annals of Cardiac Anaesthesia, 2026
Omar Abdel-Razek, MD, MSc, Pietro Di Santo, MD, Richard G. Jung, MD, PhD, et al.
Critical Care Explorations, 2023
Adji AS, Wardahni RK, Maulidah I, et al.
2026
Background: Cardiogenic shock (CS) is a life-threatening condition requiring timely pharmacological support. Dobutamine and milrinone are commonly used inotropes, yet their comparative efficacy and safety in CS management remain uncertain. This systematic review and meta-analysis aims to evaluate the outcomes associated with dobutamine versus milrinone in CS patients. Methods: A thorough literature search was conducted across databases including MEDLINE (via PubMed), CENTRAL (Cochrane Central Register of Controlled Trials), and Scopus, spanning publications up to February 2025. Randomized controlled trials and observational studies comparing dobutamine and milrinone in adult patients diagnosed with CS were incorporated. Statistical analyses were performed employing a random-effects model. Effect measures comprised odds ratios (OR) for binary outcomes and standardized mean differences (SMD) for continuous outcomes, accompanied by 95% confidence intervals (CI), with heterogeneity evaluated using I 2 statistics. Results: Dobutamine was associated with higher in-hospital mortality (OR 1.56, 95% CI 1.01-2.39; I 2 = 93%; p = 0.04), which was non-significant in RCTs (OR 1.24, 95% CI 0.70-2.19; I 2 = 0%; p = 0.46; moderate certainty) but significant in observational studies (OR 1.63, 95% CI 1.02-2.59; I 2 = 94%; p = 0.04; very low certainty). Mortality was markedly increased in ICU settings (OR 2.85, 95% CI 1.42-5.69; I 2 = 93%; p I 2 = 84%; low certainty). Overall all-cause mortality was also higher with dobutamine (OR 1.54, 95% CI 1.07-2.21; I 2 = 87%; p = 0.02), remaining non-significant in RCT data (OR 1.30, 95% CI 0.73-2.32; moderate certainty) but significant in observational data (OR 1.58, 95% CI 1.06-2.35; I 2 = 89%; low certainty). No significant differences were observed in ICU length of stay (SMD -0.13, 95% CI -0.99 to 0.73; I 2 = 93%) or hospital length of stay (SMD -0.69, 95% CI -4.49 to 3.11; I 2 = 98%), and significant arrhythmias were comparable (OR 0.88, 95% CI 0.40-1.93; I 2 = 76%). However, acute renal failure was significantly more frequent with dobutamine (OR 1.22, 95% CI 1.01-1.47; I 2 = 0%; p = 0.03). Conclusion: Dobutamine is associated with increased mortality particularly in ICU patients and a higher risk of acute renal failure compared with milrinone, with evidence certainty ranging from moderate to very low and substantial heterogeneity across mortality outcomes.
Abstract licence: CC BY
Cadd M
2026
Albedaiwi M, Gharaibeh K, Ali A, et al.
2025
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
4 found
Half-life
2.3 hours
Mechanism
Heart failure is a condition characterized by the heart's inability to provide a…
Food interactions
None known
Human targets
1 target
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
10-100 μg/k
[A228333]
…
Half-life
2.3 hours
Protein binding
70%
[L31483]
Volume of distribution
0.38 L/kg
Metabolism
Elimination
60%
Clearance
0.13 L/kg
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Milrinone was originally synthesized at the Sterling Winthrop Research Institute in the 1980s.[A228333] It was approved by the FDA on December 31, 1987, and was marketed under the trademark PRIMACOR® by Sanofi-Aventis US before being discontinued.[L31483]
[L31483]
Known interactions with other medicines. Always consult a healthcare professional.
Showing 50 of 736 interactions
[L31483]
Milrinone is a partial competitive inhibitor of phosphodiesterase III (PDE-III), with a measured IC50 value of between 0.66 and 1.3 μM.[A228338][A11759] As a PDE-III inhibitor, milrinone results in an increase in intracellular cAMP, responsible for its pharmacological effects, including positive inotropy, positive lusitropy, and vasodilation.[A228323][A228333][A228348] As milrinone affects cAMP levels through PDE-III and not through β-adrenergic receptors, it is effective in patients who have downregulated or otherwise desensitized β-adrenergic receptors and can be administered together with β-agonists/antagonists.[A228353][A228358]
How the body processes this drug — absorption, distribution, metabolism, and elimination
[A228333]
The plasma AUC is significantly dose-dependent.
[L31483]
[L31483]
[L31483]
[L31483]
[A228333][L31483]
[A228333][A228358][L31483]
[L31483]
Proteins and enzymes this drug interacts with in the body
PMID:1315035 PMID:25961942 PMID:8155697 PMID:8695850
Also has activity toward cUMP .
PMID:27975297
Independently of its catalytic activity it is part of an E2/17beta-estradiol-induced pro-apoptotic signaling pathway. E2 stabilizes the PDE3A/SLFN12 complex in the cytosol, promoting the dephosphorylation of SLFN12 and activating its pro-apoptotic ribosomal RNA/rRNA ribonuclease activity. This apoptotic pathway might be relevant in tissues with high concentration of E2 and be for instance involved in placenta remodeling PMID:31420216 PMID:34707099
ATC C01CE02
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)
Milrinone
Additional database identifiers
Drugs Product Database (DPD)
1216
ChemSpider
4052
BindingDB
15296
PDB
MIL
ZINC
ZINC000009224016
HUGO Gene Nomenclature Committee (HGNC)
HGNC:8778
GenAtlas
PDE3A
GeneCards
PDE3A
GenBank Gene Database
M91667
GenBank Protein Database
38201493
Guide to Pharmacology
1298
UniProt Accession
PDE3A_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