Ivabradine 2.5mg tablets
Requires a prescription from a doctor or prescriber
Ivabradine is a novel heart rate lowering medicine for the symptomatic management of stable angina pectoralis and symptomatic chronic heart failure.
Safety information for pregnancy and breastfeeding
Pregnancy
Always consult your doctor or midwife before taking any medicine during pregnancy or while breastfeeding. Source: DrugBank (CC BY-NC 4.0).
Official documents, adverse reaction reporting, and safety monitoring
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Official medicine documents
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Drug safety updates
MHRA alerts for Ivabradine
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 Ivabradine
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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 Ivabradine
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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.
7 branded products available
MHRA licensed products
View all licensed products for Ivabradine on the MHRA register
Ivabradine 2.5mg tablets
Ivabradine 2.5mg tablets
Ivabradine 2.5mg tablets
Ivabradine 2.5mg tablets
Ivabradine 2.5mg tablets
Ivabradine 2.5mg 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)
10 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(7)
Ivabradine for treating chronic heart failure (TA267)
Stable angina (QS21)
Stable angina: management (CG126)
Dapagliflozin for treating chronic heart failure with reduced ejection fraction (TA679)
Chronic heart failure in adults: diagnosis and management (NG106)
Chronic heart failure in adults (QS9)
Sacubitril valsartan for treating symptomatic chronic heart failure with reduced ejection fraction (TA388)
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: 24 · Randomised trials: 23 · 2003–2026
Showing the 50 most relevant studies, sorted by most relevant.
M. Komajda, R. Isnard, A. Cohen-Solal, et al.
European Journal of Heart Failure, 2017
Kim Fox, Ian Ford, P Gabriel Steg, et al.
The Lancet, 2008
J.-C. Tardif, P. Ponikowski, T. Kahan
European Heart Journal, 2009
K. Fox, I. Ford, Ph. G. Steg, et al.
European Heart Journal, 2009
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
Calabrò LA, Pasetto M, Scolletta S, et al.
2025
- Shock, Septic
- Shock, Cardiogenic
- Cardiovascular Agents
IntroductionIn patients with acute illness, compensatory tachycardia initially serves to maintain adequate cardiac output, oxygen delivery and tissue oxygenation but may persist despite appropriate fluid and vasopressor resuscitation or may be secondary to inotropic therapy. Sustained tachycardia is a predictor of adverse outcomes in critical illness. Ivabradine, a highly selective inhibitor of the sinoatrial node's pacemaker current (If or "funny" current), mitigates tachycardia by modulating diastolic depolarization slope without affecting contractility.AimTo report the existing evidence on the use of ivabradine in critically ill patients and assess its effect on rate control.MethodsA systematic literature search was performed up to May 2024 in the MEDLINE/PubMed®, Cochrane Controlled Clinical Trial register, EMBASE® and Scopus® databases. The search included: P- only original studies conducted in humans admitted to the Intensive Care Unit (ICU); I - when ivabradine administration was tested; C - in presence or absence of a control group; O - for any outcome; S - including case reports, randomized and observational trials, published in English in peer-reviewed journals.ResultsAfter the first screening, 39 studies were assessed for eligibility on a total of 682 records identified. Among those, 29 were excluded; 10 studies (4 randomized controlled trial, 5 case report/series, 1 prospective observational), including a total of 243 patients, were included in the qualitative analysis, 6 studies were included in the quantitative analysis. The use of ivabradine resulted in a pooled mean heart rate reduction of 18.70 [12.70-24.80] bpm (p ConclusionsIvabradine may be a useful alternative to beta-blocker in the management of inappropriate sinus tachycardia. Yet, evidence is limited and inconsistent. Larger randomized trials are needed to investigate the potential benefits or hazards of ivabradine use on hemodynamics and long-term outcomes.
Abstract licence: CC BY-NC-ND
Kwok CS, Gillespie D, Ur Rehman Qazi N, et al.
2026
- Cardiovascular Agents
- Heart Rate
- Postural Orthostatic Tachycardia Syndrome
Bokhari SFH, Mushtaq MM, Mushtaq M, et al.
2025
BackgroundCongenital junctional ectopic tachycardia (CJET) is a rare but life-threatening arrhythmia in neonates and infants, often refractory to conventional antiarrhythmic therapy. Ivabradine, a selective inhibitor of hyperpolarization-activated cyclic nucleotide-gated channels, has emerged as a promising drug for CJET management.AimTo evaluate the efficacy and safety of ivabradine in the management of CJET. Specifically, this study aims to analyze the dosing strategies, treatment outcomes, and the role of ivabradine as monotherapy or adjunct therapy in patients who have previously received other antiarrhythmic medications. Additionally, this review seeks to assess the impact of ivabradine on heart rate (HR) control, rhythm conversion, and its overall safety profile to provide evidence-based insights into its clinical use for CJET management.MethodsThis systematic review aims to evaluate the outcomes of ivabradine, either as monotherapy or as an adjunctive therapy, in the treatment of CJET. A comprehensive literature search was conducted across multiple electronic databases to identify relevant studies investigating the use of ivabradine in CJET. Stringent inclusion and exclusion criteria were applied to ensure the inclusion of high-quality, peer-reviewed studies. Data extraction and quality assessment were performed independently by two reviewers.ResultsTen studies, comprising 6 case reports, 3 case series, and 1 cohort study, met the inclusion criteria. Ivabradine doses ranged from 0.025 to 0.28 mg/kg/dose, administered either as monotherapy or in combination with various antiarrhythmic medications. Overall, ivabradine demonstrated promising results in achieving HR control, conversion to sinus rhythm, or stabilization of junctional rhythm. No significant adverse effects related to ivabradine were reported.ConclusionThe available evidence suggests that ivabradine may be an effective adjunctive therapy or, in some cases, a potential monotherapy for the management of CJET, particularly in cases refractory to traditional antiarrhythmic medications. However, the current evidence is limited by the small sample sizes and retrospective nature of the included studies. Well-designed prospective studies with larger cohorts and longer follow-up periods are warranted to further elucidate the role of ivabradine in CJET management.
Abstract licence: CC BY-NC
Melo APG, Moretti MA, Chagas ACP
2025
- Cardiovascular Agents
- Postural Orthostatic Tachycardia Syndrome
- Ivabradine
BackgroundPostural Orthostatic Tachycardia Syndrome (POTS) is an autonomic dysfunction characterized by symptoms of orthostatic intolerance, associated with an increase in heart rate within 10 minutes of assuming an upright position or head-up tilt, in the absence of hypotension. There are three phenotypes of POTS - neuropathic, hypovolemic, and hyperadrenergic - and all result in tachycardia and altered cerebral perfusion. Pharmacological therapy is indicated in certain cases; however, no specific medication has yet been approved for this condition. Some studies have shown that ivabradine may be beneficial, as it reduces heart rate without affecting blood pressure.ObjectivesTo evaluate the efficacy and safety of ivabradine in the treatment of POTS.MethodSystematic review using the descriptors "Ivabradine" and "Postural Orthostatic Tachycardia Syndrome" in the PubMed, Scielo, LILACS, and Google Scholar databases. Articles were grouped and assessed using the PICO strategy.ResultsA total of 52 articles were identified, of which seven were included in the review - three prospective and four retrospective studies. In total, 203 patients were evaluated, the majority of whom were female. All studies reported a significant reduction in heart rate and improvement in symptoms of orthostatic intolerance, with most patients not reporting adverse effects, regardless of their POTS phenotype.ConclusionIvabradine proved to be effective and safe in the treatment of patients with POTS.
Abstract licence: CC BY
Umar M, Ali A, Guha A, et al.
2026
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
None known
Half-life
2 hours
Mechanism
Ivabradine lowers heart rate by selectively inhibiting If channels ("funny chann…
Food interactions
1 warning
Human targets
1 target
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
1 hour
Half-life
2 hours
Protein binding
70%
Volume of distribution
100 L
Metabolism
Elimination
Clearance
400ml/min
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Known interactions with other medicines. Always consult a healthcare professional.
Showing 50 of 553 interactions
How the body processes this drug — absorption, distribution, metabolism, and elimination
Proteins and enzymes this drug interacts with in the body
PMID:10228147 PMID:22006928
Contributes to the native pacemaker currents in heart (If) and in neurons (Ih) .
PMID:10228147 PMID:10524219
Can also transport ammonium in the distal nephron (By similarity). Involved in the initiation of neuropathic pain in sensory neurons (By similarity)
Enzymes involved in drug metabolism — important for understanding drug interactions
ATC C01EB17
ATC C07FX05
ATC C07FX06
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)
Ivabradine
Additional database identifiers
Drugs Product Database (DPD)
22836
ChemSpider
117373
BindingDB
50326992
PDB
VNZ
ZINC
ZINC000003805768
HUGO Gene Nomenclature Committee (HGNC)
HGNC:4846
GeneCards
HCN2
Guide to Pharmacology
401
UniProt Accession
HCN2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2637
GenAtlas
CYP3A4
GeneCards
CYP3A4
GenBank Gene Database
M18907
Guide to Pharmacology
1337
UniProt Accession
CP3A4_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