Midodrine 10mg tablets
Requires a prescription from a doctor or prescriber
An ethanolamine derivative that is an adrenergic alpha agonist.
Official documents, adverse reaction reporting, and safety monitoring
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Official medicine documents
Yellow Card
Report side effects (MHRA)
Drug safety updates
MHRA alerts for Midodrine
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 Midodrine
Browse all iDAP reports
Interactive Drug Analysis Profiles for all medicines
Report a side effect
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.
View EudraVigilance report
Suspected adverse reactions reported for Midodrine
About EudraVigilance
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.
3 branded products available
MHRA licensed products
View all licensed products for Midodrine on the MHRA register
Bramox 10mg tablets
Midodrine 10mg tablets
Midodrine 10mg tablets
This is the NHS Drug Tariff indicative price used for reimbursement purposes. It may not reflect the price paid by patients or pharmacies.
View full Drug TariffSource: NHS Drug Tariff via NHSBSA. Derived from dm+d VMPP (Virtual Medicinal Product Pack) pricing data. Contains public sector information licensed under the Open Government Licence v3.0.
WHO defined daily dose (DDD)
30 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(2)
Orthostatic hypotension due to autonomic dysfunction: midodrine (ESNM61)
Parkinson's disease in adults (NG71)
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
Pharmacy stock checkers
Search for this medicine at major UK pharmacy chains. These links open the retailer's own website — results depend on their current online catalogue.
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: 16 · Randomised trials: 34 · 2018–2026
Showing the 50 most relevant studies, sorted by most relevant.
E. Solà, C. Solé, M. Simón-Talero, et al.
Journal of hepatology, 2018
Mohamed Hamed, S. Elseidy, Ahmed Elkheshen, et al.
Cardiology and Therapy, 2023
S. Kilcommons, Fadi Hammal, Mostafa Kamaleldin, et al.
Critical Care Medicine, 2024
- Shock
- Midodrine
- Vasoconstrictor Agents
Qian He, Xiaokang Xing, T-Q Wang, et al.
European review for medical and pharmacological sciences, 2023
Schiweck N, Langer K, Maier A, et al.
2026
- Postural Orthostatic Tachycardia Syndrome
Postural orthostatic tachycardia syndrome (POTS) is a condition defined by symptoms of orthostatic intolerance and a sustained heart rate (HR) increment of ≥ 30 beats per minute (bpm) upon postural change to the upright position in the absence of orthostatic hypotension, defined as a sustained decrease in systolic blood pressure (SBP) of ≥ 20 mmHg or a decrease in diastolic blood pressure (DBP) of ≥ 10 mmHg within 3 min of standing. In children, a sustained HR increment of at least 40 bpm is required for diagnosis of POTS. POTS is a common condition in adults and children suffering from myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). In daily clinical practice, therapeutic recommendations are rare and evidence is missing. The objective of this review is to present the current knowledge on non-pharmacological and pharmacological approaches in POTS with a special focus on POTS therapy in children and people with ME/CFS. Of 3853 studies, 45 studies were included in the systematic review. Evidence on therapy in POTS is rare and large randomized controlled trials (RCT) on single interventions are needed. Non-pharmacological approaches such as the use of compression garments, physical training, salt supplementation and transdermal vagal nerve stimulation could be possible treatment options in POTS because they are easy to implement as first-line therapeutic measures in clinical practice. For pharmaceuticals, several studies showed significant effects following therapy with ivabradine and β-adrenergic blocking agents. There are single studies which imply that midodrine (hydrochloride) and pyridostigmine seem to have a beneficial effect on hemodynamics in POTS.
Abstract licence: CC BY
Prem Balaji Reddy Lankapothu, Shrinidhi B., Satish Kumar M., et al.
Romanian Medical Journal, 2024
Kwok CS, Lee S, Afzal A, et al.
2026
Pavic N, Zhang S, Zhou E, et al.
2026
- Midodrine
- Vasoconstrictor Agents
- Stroke Volume
Verma A, Saraya E, Haque MS, et al.
2025
Orthostatic hypotension (OH), defined as a sustained drop in systolic (≥20 mmHg) or diastolic (≥10 mmHg) blood pressure upon standing, is a debilitating condition prevalent in older adults and individuals with neurodegenerative disorders. It significantly impacts quality of life, leading to dizziness, falls, and syncope, and is associated with increased morbidity and mortality. This systematic review evaluates the efficacy and safety of pharmacological treatments for OH. Following the PRISMA 2020 guidelines, 25 studies, including randomized (RCTs) and non-randomized controlled trials (NRCTs), were analyzed. Study quality was assessed using the Cochrane Risk of Bias 2 (ROB 2) tool, the Joanna Briggs Institute (JBI) Checklist, and the Newcastle-Ottawa Scale (NOS). The Grading of Recommendations, Assessment, Development and Evaluation (GRADE) framework was applied to evaluate the certainty of evidence across key outcomes. Drugs approved by the U.S. Food and Drug Administration (FDA), such as droxidopa and midodrine, consistently improve orthostatic symptoms and are recommended as first-line therapies. Atomoxetine and fludrocortisone showed moderate efficacy, while pyridostigmine in combination therapies provided additional benefits. Octreotide demonstrated potential for refractory OH but lacked robust evidence. Adverse effects, including supine hypertension, dizziness, gastrointestinal disturbances, and fatigue, highlight the need for personalized therapy to balance efficacy and tolerability. While pharmacological treatments show promise, further comparative and long-term studies are necessary to refine therapeutic strategies and improve patient outcomes.
Abstract licence: CC BY
Ahmed A, Singla S, Singla B, et al.
2025
This systematic review evaluated the role of human albumin infusion in patients with decompensated cirrhosis, refractory ascites, acute-on-chronic liver failure (ACLF), and hepatorenal syndrome type 1 (HRS-1). A total of 398 studies were screened, with 125 excluded for not meeting eligibility criteria, and the final selection comprised randomized controlled trials and clinically relevant post hoc analyses published between 2016 and 2024. The findings suggest that albumin infusion confers significant benefits in reducing the incidence of post-paracentesis circulatory dysfunction (PICD), acute kidney injury (AKI), and hyponatremia, while also improving survival in selected patient populations. Comparative trials demonstrated that albumin may outperform standard care and support vasoconstrictor-based regimens, though cost-effectiveness concerns remain when compared to alternatives such as midodrine. The evidence base is strengthened by large multicenter trials with objective outcomes, though limitations include small pilot studies, post hoc subgroup analyses, and heterogeneity in dosing strategies. Overall, albumin infusion appears to be a clinically valuable intervention in the management of advanced cirrhosis, but further trials are warranted to clarify its long-term effects, particularly on hepatocellular carcinoma progression and optimal treatment regimens.
Abstract licence: CC BY
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
1 found
Half-life
3 to 4 hours
Mechanism
Midodrine undergoes metabolism to form its pharmacologically active metabolite, desglymidodrine.
Food interactions
1 warning
Human targets
3 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
1 to 2 hours
Half-life
3 to 4 hours
Metabolism
Clearance
385 mL/min
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Known interactions with other medicines. Always consult a healthcare professional.
Showing 50 of 829 interactions
Desglymidodrine is dialyzable.
How the body processes this drug — absorption, distribution, metabolism, and elimination
The absolute bioavailability of midodrine (measured as desglymidodrine) is 93% and is not affected by food. As desglymidodrine displays poor diffusibility across the blood-brain barrier, it is expected to have minimal effects on the central nervous system.
Proteins and enzymes this drug interacts with in the body
Enzymes involved in drug metabolism — important for understanding drug interactions
Proteins that transport this drug across cell membranes
PMID:15521010 PMID:18367661 PMID:19685173 PMID:26320580 PMID:7896779 PMID:8914574 PMID:9835627
Primarily responsible for the absorption of dietary di- and tripeptides from the small intestinal lumen (By similarity). Mediates transepithelial transport of muramyl and N-formylated bacterial dipeptides contributing to recognition of pathogenic bacteria by the mucosal immune system PMID:15521010 PMID:9835627
ATC C01CA17
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Show
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Linked compound data from DrugBank Open Data (CC BY-NC 4.0)
Midodrine
Additional database identifiers
Drugs Product Database (DPD)
918
ChemSpider
4050
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:2625
GenAtlas
CYP2D6
GeneCards
CYP2D6
GenBank Gene Database
M20403
GenBank Protein Database
181350
Guide to Pharmacology
1329
UniProt Accession
CP2D6_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10920
GenAtlas
SLC15A1
GeneCards
SLC15A1
GenBank Gene Database
U13173
GenBank Protein Database
773588
Guide to Pharmacology
984
UniProt Accession
S15A1_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