Digoxin 62.5microgram tablets
Prescription only
Requires a prescription from a doctor or prescriber
Tablet
Oral
Positive inotropic drugs
Active ingredients:
Digoxin
No active safety alerts
Official documents, adverse reaction reporting, and safety monitoring
Report a side effect
Submit a Yellow Card report to the MHRA
Official medicine documents
Source: MHRA Products DatabaseOGL 3.0
Updated 3 months ago(16 Jan 2026)Safety monitoring data
Yellow Card reports
MHRA
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.
View Drug Analysis Profile
Suspected adverse reactions reported for Digoxin
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
EMA
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 Digoxin
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.
19 branded products available
Show details
Part of the Lanoxin brand family (generic: Digoxin)
19 products
MHRA licensed products
View all licensed products for Digoxin on the MHRA register
Digoxin 62.5microgram tablets
Digoxin 62.5microgram tablets
Digoxin 62.5microgram tablets
Digoxin 62.5microgram tablets
Digoxin 62.5microgram tablets
Digoxin 62.5microgram tablets
Digoxin 62.5microgram tablets
Digoxin 62.5microgram tablets
Show details
£1.03indicative price
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)
250 microgram
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 NHS dm+d BNF mapping files. Contains public sector information licensed under the Open Government Licence v3.0.
Therapeutically similar medicines
Show details
Digoxin 50micrograms/1ml solution for injection ampoules
Injection
1ml
Same therapeutic group
Digoxin 125micrograms/5ml oral suspension
Oral suspension
5ml
Same therapeutic group
Digoxin 125micrograms/5ml oral solution
Oral solution
5ml
Same therapeutic group
Digoxin 250micrograms/5ml oral suspension
Oral suspension
5ml
Same therapeutic group
Digoxin 250micrograms/5ml oral solution
Oral solution
5ml
Same therapeutic group
Similarity based on WHO Anatomical Therapeutic Chemical (ATC) classification and NHS BNF section grouping. Source data: NHS dm+d via TRUD (OGL v3.0), WHO ATC/DDD Index.
NHS prescribing volume and spending trends
Show details
Loading prescribing data...
Clinical guidelines and formulary information
British National Formulary
Digoxin
BNF
Drug monograph — bnf.nice.org.ukSource: British National Formulary, NICE. Joint Formulary Committee. Contains public sector information licensed under the Open Government Licence v3.0.
NICE clinical guidance(9)
Atrial fibrillation: diagnosis and management (NG196)
NG196
NICE guideline
Updated Jun 2021Chronic heart failure in adults: diagnosis and management (NG106)
NG106
NICE guideline
Updated Sept 2025Dapagliflozin for treating chronic heart failure with reduced ejection fraction (TA679)
TA679
Technology appraisal
Updated Feb 2021Ivabradine for treating chronic heart failure (TA267)
TA267
Technology appraisal
Updated Nov 2012Partial left ventriculectomy (the Batista procedure) (HTG19)
HTG19
Guidance
Updated Feb 2004Chronic heart failure in adults (QS9)
QS9
Quality standard
Updated Sept 2025Gastroparesis in adults: oral erythromycin (ESUOM13)
ESUOM13
Evidence summary
Updated Jun 2013Abortion care (NG140)
NG140
NICE guideline
Updated May 2025Lead-I ECG devices for detecting symptomatic atrial fibrillation using single time point testing in primary care (HTG508)
HTG508
Guidance
Updated May 2019Source: 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
Show details
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 & product information
Official product databases and supply status monitoring
Pharmacy links redirect to the retailer's own search and do not represent real-time stock levels. emc (electronic medicines compendium) is operated by Datapharm Ltd. Shortage information sourced from NHS Specialist Pharmacy Service (SPS), sps.nhs.uk.
Codes for healthcare professionals and prescribing systems
Show details
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. BNF codes from NHS Business Services Authority (NHSBSA). ATC codes from the WHO Collaborating Centre for Drug Statistics Methodology (whocc.no).
Active and completed clinical studies from ClinicalTrials.gov
Show details
Searching UK clinical trials...
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.
Pharmacology and chemical data from DrugBank
Key facts
Drug status
Approved
Major interactions
2 found
Half-life
1.5-2 days
Mechanism
Digoxin exerts hemodynamic, electrophysiologic, and neurohormonal effects on the cardiovascular system.
Food interactions
4 warnings
Human targets
7 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
70-80%
Digoxin is approximately 70-80% absorbed in the first part of the small bowel.
[A178228]…
[A178228]…
Half-life
1.5-2 days
Digoxin has a half-life of 1.5-2 days in healthy subjects.
[L9143]
The half-life in patients who do not pass urine, usually due to renal failure, is prolonged to 3.5-5…
[L9143]
The half-life in patients who do not pass urine, usually due to renal failure, is prolonged to 3.5-5…
Protein binding
25%
Digoxin protein binding is approximately 25%.
[L9143]
It is mainly bound to albumin.
[A178228]
[L9143]
It is mainly bound to albumin.
[A178228]
Volume of distribution
475-500 L
This drug is widely distributed in the body, and is known to cross the blood-brain barrier and the placenta.
[L9143][A178228]…
[L9143][A178228]…
Metabolism
13%
About 13% of a digoxin dose is found to be metabolized in healthy subjects.…
Elimination
50-70%
The elimination of digoxin is proportional to the total dose, following first order kinetics.…
Clearance
44ml/min
The clearance of digoxin closely correlates to creatinine clearance, and does not depend on urinary flow.…
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Status:
Approved
Investigational
Small molecule
About this compound
Digoxin is one of the oldest cardiovascular medications used today.[A178225] It is a common agent used to manage atrial fibrillation and the symptoms of heart failure.[A178234] Digoxin is classified as a cardiac glycoside and was initially approved by the FDA in 1954.[L9143]
This drug originates from the foxglove plant, also known as the Digitalis plantT610, studied by William Withering, an English physician and botanist in the 1780s.[A178237][A178240] Prior to this, a Welsh family, historically referred to as the Physicians of Myddvai, formulated drugs from this plant. They were one of the first to prescribe cardiac glycosides, according to ancient literature dating as early as the 1250s.[A178240]
This drug originates from the foxglove plant, also known as the Digitalis plantT610, studied by William Withering, an English physician and botanist in the 1780s.[A178237][A178240] Prior to this, a Welsh family, historically referred to as the Physicians of Myddvai, formulated drugs from this plant. They were one of the first to prescribe cardiac glycosides, according to ancient literature dating as early as the 1250s.[A178240]
Properties:
solid
Avg. mass: 780.94 Da
DrugBank indication
Digoxin is indicated in the following conditions: 1) For the treatment of mild to moderate heart failure in adult patients.
[L9143]
2) To increase myocardial contraction in children diagnosed with heart failure.
[L9143]
3) To maintain control ventricular rate in adult patients diagnosed with chronic atrial fibrillation.
[L9143]
In adults with heart failure, when it is clinically possible, digoxin should be administered in conjunction with a diuretic and an angiotensin-converting enzyme (ACE) inhibitor for optimum effects.
[L9143]
[L9143]
2) To increase myocardial contraction in children diagnosed with heart failure.
[L9143]
3) To maintain control ventricular rate in adult patients diagnosed with chronic atrial fibrillation.
[L9143]
In adults with heart failure, when it is clinically possible, digoxin should be administered in conjunction with a diuretic and an angiotensin-converting enzyme (ACE) inhibitor for optimum effects.
[L9143]
Also known as(85)
12β-hydroxydigitoxin
Digossina
Digoxin
Digoxina
Digoxine
Digoxinum
7.2.2.13
Na(+)/K(+) ATPase alpha-1 subunit
Dosage forms(61)
Injection, solution (Parenteral) — 0.1 MG/ML
Injection, solution (Parenteral) — 0.25 MG/ML
Injection (Intramuscular; Intravenous) — 0.25 mg/1mL
Injection (Intramuscular; Intravenous) — 0.25 mg/1.0mL
Injection, solution (Intramuscular; Intravenous; Parenteral) — 250 ug/1mL
Solution (Oral) — 0.05 mg/1mL
Tablet (Oral)
Tablet (Oral) — 0.125 mg/301
Molecular properties(19)
Drug interactions(1702)
Known interactions with other medications. Always consult a healthcare professional.
Cyclosporine
Unknown severity
The serum concentration of Digoxin can be increased when it is combined with Cyclosporine.
Digoxin may increase the bradycardic activities of Ceritinib.
Ruxolitinib
Moderate
Ruxolitinib may increase the bradycardic activities of Digoxin.
The serum concentration of Digoxin can be decreased when it is combined with Acarbose.
Icosapent may decrease the excretion rate of Digoxin which could result in a higher serum level.
Mesalazine
Moderate
Mesalazine may decrease the excretion rate of Digoxin which could result in a higher serum level.
Nabumetone
Moderate
Nabumetone may decrease the excretion rate of Digoxin which could result in a higher serum level.
Ketorolac may decrease the excretion rate of Digoxin which could result in a higher serum level.
Tenoxicam may decrease the excretion rate of Digoxin which could result in a higher serum level.
Celecoxib may decrease the excretion rate of Digoxin which could result in a higher serum level.
Tolmetin may decrease the excretion rate of Digoxin which could result in a higher serum level.
Rofecoxib may decrease the excretion rate of Digoxin which could result in a higher serum level.
Piroxicam may decrease the excretion rate of Digoxin which could result in a higher serum level.
Fenoprofen
Moderate
Fenoprofen may decrease the excretion rate of Digoxin which could result in a higher serum level.
Valdecoxib
Moderate
Valdecoxib may decrease the excretion rate of Digoxin which could result in a higher serum level.
Sulindac may decrease the excretion rate of Digoxin which could result in a higher serum level.
Flurbiprofen
Moderate
Flurbiprofen may decrease the excretion rate of Digoxin which could result in a higher serum level.
Etodolac may decrease the excretion rate of Digoxin which could result in a higher serum level.
Mefenamic acid
Moderate
Mefenamic acid may decrease the excretion rate of Digoxin which could result in a higher serum level.
Naproxen may decrease the excretion rate of Digoxin which could result in a higher serum level.
Phenylbutazone
Moderate
Phenylbutazone may decrease the excretion rate of Digoxin which could result in a higher serum level.
Carprofen may decrease the excretion rate of Digoxin which could result in a higher serum level.
Diflunisal
Moderate
Diflunisal may decrease the excretion rate of Digoxin which could result in a higher serum level.
Salicylic acid
Moderate
Salicylic acid may decrease the excretion rate of Digoxin which could result in a higher serum level.
Meclofenamic acid
Moderate
Meclofenamic acid may decrease the excretion rate of Digoxin which could result in a higher serum level.
Oxaprozin may decrease the excretion rate of Digoxin which could result in a higher serum level.
Ketoprofen
Moderate
Ketoprofen may decrease the excretion rate of Digoxin which could result in a higher serum level.
Balsalazide
Moderate
Balsalazide may decrease the excretion rate of Digoxin which could result in a higher serum level.
Olsalazine
Moderate
Olsalazine may decrease the excretion rate of Digoxin which could result in a higher serum level.
Lumiracoxib
Moderate
Lumiracoxib may decrease the excretion rate of Digoxin which could result in a higher serum level.
Magnesium salicylate
Moderate
Magnesium salicylate may decrease the excretion rate of Digoxin which could result in a higher serum level.
Salsalate may decrease the excretion rate of Digoxin which could result in a higher serum level.
Choline magnesium trisalicylate may decrease the excretion rate of Digoxin which could result in a higher serum level.
Antrafenine
Moderate
Antrafenine may decrease the excretion rate of Digoxin which could result in a higher serum level.
Aminophenazone
Moderate
Aminophenazone may decrease the excretion rate of Digoxin which could result in a higher serum level.
Antipyrine
Moderate
Antipyrine may decrease the excretion rate of Digoxin which could result in a higher serum level.
Tiaprofenic acid
Moderate
Tiaprofenic acid may decrease the excretion rate of Digoxin which could result in a higher serum level.
Etoricoxib
Moderate
Etoricoxib may decrease the excretion rate of Digoxin which could result in a higher serum level.
Taxifolin may decrease the excretion rate of Digoxin which could result in a higher serum level.
Oxyphenbutazone
Moderate
Oxyphenbutazone may decrease the excretion rate of Digoxin which could result in a higher serum level.
Licofelone
Moderate
Licofelone may decrease the excretion rate of Digoxin which could result in a higher serum level.
Nimesulide
Moderate
Nimesulide may decrease the excretion rate of Digoxin which could result in a higher serum level.
Benoxaprofen
Moderate
Benoxaprofen may decrease the excretion rate of Digoxin which could result in a higher serum level.
Metamizole
Moderate
Metamizole may decrease the excretion rate of Digoxin which could result in a higher serum level.
Zomepirac may decrease the excretion rate of Digoxin which could result in a higher serum level.
Cimicoxib may decrease the excretion rate of Digoxin which could result in a higher serum level.
Lornoxicam
Moderate
Lornoxicam may decrease the excretion rate of Digoxin which could result in a higher serum level.
Aceclofenac
Moderate
Aceclofenac may decrease the excretion rate of Digoxin which could result in a higher serum level.
Zaltoprofen
Moderate
Zaltoprofen may decrease the excretion rate of Digoxin which could result in a higher serum level.
Azapropazone
Moderate
Azapropazone may decrease the excretion rate of Digoxin which could result in a higher serum level.
Showing 50 of 1702 interactions
Food & lifestyle interactions
Advice
Avoid multivalent ions. Calcium and aluminum containing products (including kaolin-pectin) may interfere with absorption) and digoxin administration must be separated by several hours.
Advice
Avoid potassium-containing products. They may cause arrhythmias when given with digoxin.
Advice
Avoid St. John's Wort. This drug can decrease digoxin levels.
Advice
Do not take with bran and high fiber foods. Separate administration of bran and high fiber foods from medication by at least 2 hours.
Toxicity & overdose
Oral TDLO (human female): 100 ug/kg, Oral TDLO (human male): 75 ug/kg, Oral LD50 (rat): 28270 ug/kgMSDS
Digoxin toxicity can occur in cases of supratherapeutic dose ingestion or as a result of chronic overexposure.T607 Digoxin toxicity may be manifested by symptoms of nausea, vomiting, visual changes, in addition to arrhythmia. Older age, lower body weight, and decreased renal function or electrolyte abnormalities lead to an increased risk of digoxin toxicity.
[L9143]
Digoxin toxicity can occur in cases of supratherapeutic dose ingestion or as a result of chronic overexposure.T607 Digoxin toxicity may be manifested by symptoms of nausea, vomiting, visual changes, in addition to arrhythmia. Older age, lower body weight, and decreased renal function or electrolyte abnormalities lead to an increased risk of digoxin toxicity.
[L9143]
How it works
Mechanism of action
Digoxin exerts hemodynamic, electrophysiologic, and neurohormonal effects on the cardiovascular system.[A178234] It reversibly inhibits the Na-K ATPase enzyme, leading to various beneficial effects. The Na-K ATPase enzyme functions to maintain the intracellular environment by regulating the entry and exit of sodium, potassium, and calcium (indirectly). Na-K ATPase is also known as the sodium pump[L9143]. The inhibition of the sodium pump by digoxin increases intracellular sodium and increases the calcium level in the myocardial cells, causing an increased contractile force of the heart.[L9143][A178264] This improves the left ventricular ejection fraction (EF), an important measure of cardiac function.[A178234,T613]
Digoxin also stimulates the parasympathetic nervous system via the vagus nerveT607 leading to sinoatrial (SA) and atrioventricular (AV) node effects, decreasing the heart rate.[L9143][A178234] Part of the pathophysiology of heart failure includes neurohormonal activation, leading to an increase in norepinephrine. Digoxin helps to decrease norepinephrine levels through activation of the parasympathetic nervous system.[A178234]
Digoxin also stimulates the parasympathetic nervous system via the vagus nerveT607 leading to sinoatrial (SA) and atrioventricular (AV) node effects, decreasing the heart rate.[L9143][A178234] Part of the pathophysiology of heart failure includes neurohormonal activation, leading to an increase in norepinephrine. Digoxin helps to decrease norepinephrine levels through activation of the parasympathetic nervous system.[A178234]
Pharmacodynamics
Digoxin is a positive inotropic and negative chronotropic drug[A178234], meaning that it increases the force of the heartbeat and decreases the heart rate.[L6253] The decrease in heart rate is particularly useful in cases of atrial fibrillation, a condition characterized by a fast and irregular heartbeat.[A178282] The relief of heart failure symptoms during digoxin therapy has been demonstrated in clinical studies by increased exercise capacity and reduced hospitalization due to heart failure and reduced heart failure-related emergency medical visits.[L9143] Digoxin has a narrow therapeutic window.[L9143]
A note on cardiovascular risk
Digoxin poses a risk of rapid ventricular response that can cause ventricular fibrillation in patients with an accessory atrioventricular (AV) pathway. Cardiac arrest as a result of ventricular fibrillation is fatal.[L9143] An increased risk of fatal severe or complete heart block is present in individuals with pre-existing sinus node disease and AV block who take digoxin.[L9143]
A note on cardiovascular risk
Digoxin poses a risk of rapid ventricular response that can cause ventricular fibrillation in patients with an accessory atrioventricular (AV) pathway. Cardiac arrest as a result of ventricular fibrillation is fatal.[L9143] An increased risk of fatal severe or complete heart block is present in individuals with pre-existing sinus node disease and AV block who take digoxin.[L9143]
Pharmacokinetics
How the body processes this drug — absorption, distribution, metabolism, and elimination
Absorption
Digoxin is approximately 70-80% absorbed in the first part of the small bowel.
[A178228]
The bioavailability of an oral dose varies from 50-90%, however, oral gelatinized capsules of digoxin are reported to have a bioavailability of 100%.
[A178252]
Tmax, or the time to reach the maximum concentration of digoxin was measured to be 1.0 h in one clinical study of healthy patients taking 0.25 mg of digoxin with a placebo.
[A178369]
Cmax, or maximum concentration, was 1.32 ± 0.18 ng/ml−1 in the same study, and AUC (area under the curve) was 12.5 ± 2.38 ng/ml−1.
[A178369]
If digoxin is ingested after a meal, absorption is slowed but this does not change the total amount of absorbed drug. If digoxin is taken with meals that are in fiber, absorption may be decreased.
[L6274]
A note on gut bacteria
An oral dose of digoxin may be transformed into pharmacologically inactive products by bacteria in the colon. Studies have indicated that 10% of patients receiving digoxin tablets will experience the degradation of at least 40% of an ingested dose of digoxin by gut bacteria.
Several antibiotics may increase the absorption of digoxin in these patients, due to the elimination of gut bacteria, which normally cause digoxin degradation.
[L9143]
A note on malabsorption
Patients with malabsorption due to a variety of causes may have a decreased ability to absorb digoxin.
[L9143]
P-glycoprotein, located on cells in the intestine, may interfere with digoxin pharmacokinetics, as it is a substrate of this efflux transporter. P-glycoprotein can be induced by other drugs, therefore reducing the effects of digoxin by increasing its efflux in the intestine.
[L9143]
[A178228]
The bioavailability of an oral dose varies from 50-90%, however, oral gelatinized capsules of digoxin are reported to have a bioavailability of 100%.
[A178252]
Tmax, or the time to reach the maximum concentration of digoxin was measured to be 1.0 h in one clinical study of healthy patients taking 0.25 mg of digoxin with a placebo.
[A178369]
Cmax, or maximum concentration, was 1.32 ± 0.18 ng/ml−1 in the same study, and AUC (area under the curve) was 12.5 ± 2.38 ng/ml−1.
[A178369]
If digoxin is ingested after a meal, absorption is slowed but this does not change the total amount of absorbed drug. If digoxin is taken with meals that are in fiber, absorption may be decreased.
[L6274]
A note on gut bacteria
An oral dose of digoxin may be transformed into pharmacologically inactive products by bacteria in the colon. Studies have indicated that 10% of patients receiving digoxin tablets will experience the degradation of at least 40% of an ingested dose of digoxin by gut bacteria.
Several antibiotics may increase the absorption of digoxin in these patients, due to the elimination of gut bacteria, which normally cause digoxin degradation.
[L9143]
A note on malabsorption
Patients with malabsorption due to a variety of causes may have a decreased ability to absorb digoxin.
[L9143]
P-glycoprotein, located on cells in the intestine, may interfere with digoxin pharmacokinetics, as it is a substrate of this efflux transporter. P-glycoprotein can be induced by other drugs, therefore reducing the effects of digoxin by increasing its efflux in the intestine.
[L9143]
Half-life
Digoxin has a half-life of 1.5-2 days in healthy subjects.
[L9143]
The half-life in patients who do not pass urine, usually due to renal failure, is prolonged to 3.5-5 days. Since most of the drug is distributed extravascularly, dialysis and exchange transfusion are not optimal methods for the removal of digoxin.
[L9143]
[L9143]
The half-life in patients who do not pass urine, usually due to renal failure, is prolonged to 3.5-5 days. Since most of the drug is distributed extravascularly, dialysis and exchange transfusion are not optimal methods for the removal of digoxin.
[L9143]
Protein binding
Digoxin protein binding is approximately 25%.
[L9143]
It is mainly bound to albumin.
[A178228]
[L9143]
It is mainly bound to albumin.
[A178228]
Volume of distribution
This drug is widely distributed in the body, and is known to cross the blood-brain barrier and the placenta.
[L9143][A178228]
The apparent volume of distribution of digoxin is 475-500 L.
[L9143]
A large portion of digoxin is distributed in the skeletal muscle followed by the heart and kidneys.
[A178228]
It is important to note that the elderly population, generally having a decreased muscle mass, may show a lower volume of digoxin distribution.
[L9143]
[L9143][A178228]
The apparent volume of distribution of digoxin is 475-500 L.
[L9143]
A large portion of digoxin is distributed in the skeletal muscle followed by the heart and kidneys.
[A178228]
It is important to note that the elderly population, generally having a decreased muscle mass, may show a lower volume of digoxin distribution.
[L9143]
Metabolism
About 13% of a digoxin dose is found to be metabolized in healthy subjects. Several urinary metabolites of digoxin exist, including dihydrodigoxin and digoxigenin bisdigitoxoside. Their glucuronidated and sulfated conjugates are thought to be produced through the process of hydrolysis, oxidation, and additionally, conjugation.
The cytochrome P-450 system does not play a major role in digoxin metabolism, nor does this drug induce or inhibit the enzymes in this system.
[L9143]
The cytochrome P-450 system does not play a major role in digoxin metabolism, nor does this drug induce or inhibit the enzymes in this system.
[L9143]
Route of elimination
The elimination of digoxin is proportional to the total dose, following first order kinetics. After intravenous (IV) administration to healthy subjects, 50-70% of the dose is measured excreted as unchanged digoxin in the urine. Approximately 25 to 28% of digoxin is eliminated outside of the kidney. Biliary excretion appears to be of much less importance than renal excretion.
[A178228]
Digoxin is not effectively removed from the body by dialysis, exchange transfusion, or during cardiopulmonary bypass because most of the drug is bound to extravascular tissues.
[L9143]
[A178228]
Digoxin is not effectively removed from the body by dialysis, exchange transfusion, or during cardiopulmonary bypass because most of the drug is bound to extravascular tissues.
[L9143]
Clearance
The clearance of digoxin closely correlates to creatinine clearance, and does not depend on urinary flow. Individuals with renal impairment or failure may exhibit extensively prolonged half-lives. It is therefore important to titrate the dose accordingly and regularly monitor serum digoxin levels.
[L9143]
One pharmacokinetic study measured the mean body clearance of intravenous digoxin to be 88 ± 44ml/min/l.73 m².
[A178324]
Another study provided mean clearance values of 53 ml/min/1.73 m² in men aged 73-81 and 83 ml/min/1.73 m² in men aged 20-33 years old after an intravenous digoxin dose.
[A178318]
[L9143]
One pharmacokinetic study measured the mean body clearance of intravenous digoxin to be 88 ± 44ml/min/l.73 m².
[A178324]
Another study provided mean clearance values of 53 ml/min/1.73 m² in men aged 73-81 and 83 ml/min/1.73 m² in men aged 20-33 years old after an intravenous digoxin dose.
[A178318]
Drug targets(7)
Proteins and enzymes this drug interacts with in the body
Sodium/potassium-transporting ATPase subunit alpha-1
ATP1A1
inhibitor
Specific functionATP binding
Cellular location
Cell membrane
General function & pharmacology
This is the catalytic component of the active enzyme, which catalyzes the hydrolysis of ATP coupled with the exchange of sodium and potassium ions across the plasma membrane. This action creates the electrochemical gradient of sodium and potassium ions, providing the energy for active transport of various nutrients .
PMID:29499166 PMID:30388404
Could also be part of an osmosensory signaling pathway that senses body-fluid sodium levels and controls salt intake behavior as well as voluntary water intake to regulate sodium homeostasis (By similarity)
PMID:29499166 PMID:30388404
Could also be part of an osmosensory signaling pathway that senses body-fluid sodium levels and controls salt intake behavior as well as voluntary water intake to regulate sodium homeostasis (By similarity)
Sodium/potassium-transporting ATPase subunit beta-3
ATP1B3
inhibitor
Specific functionATPase activator activity
Cellular location
Apical cell membrane
General function & pharmacology
This is the non-catalytic component of the active enzyme, which catalyzes the hydrolysis of ATP coupled with the exchange of Na(+) and K(+) ions across the plasma membrane. The exact function of the beta-3 subunit is not known
Sodium/potassium-transporting ATPase subunit beta-2
ATP1B2
inhibitor
Specific functionATPase activator activity
Cellular location
Cell membrane
General function & pharmacology
This is the non-catalytic component of the active enzyme, which catalyzes the hydrolysis of ATP coupled with the exchange of Na(+) and K(+) ions across the plasma membrane. The exact function of the beta-2 subunit is not known
Sodium/potassium-transporting ATPase subunit beta-1
ATP1B1
inhibitor
Specific functionATPase activator activity
Cellular location
Cell membrane
General function & pharmacology
This is the non-catalytic component of the active enzyme, which catalyzes the hydrolysis of ATP coupled with the exchange of Na(+) and K(+) ions across the plasma membrane. The beta subunit regulates, through assembly of alpha/beta heterodimers, the number of sodium pumps transported to the plasma membrane .
PMID:19694409
Plays a role in innate immunity by enhancing virus-triggered induction of interferons (IFNs) and interferon stimulated genes (ISGs). Mechanistically, enhances the ubiquitination of TRAF3 and TRAF6 as well as the phosphorylation of TAK1 and TBK1 PMID:34011520
PMID:19694409
Plays a role in innate immunity by enhancing virus-triggered induction of interferons (IFNs) and interferon stimulated genes (ISGs). Mechanistically, enhances the ubiquitination of TRAF3 and TRAF6 as well as the phosphorylation of TAK1 and TBK1 PMID:34011520
Sodium/potassium-transporting ATPase subunit alpha-3
ATP1A3
inhibitor
Specific functionamyloid-beta binding
Cellular location
Cell membrane
General function & pharmacology
This is the catalytic component of the active enzyme, which catalyzes the hydrolysis of ATP coupled with the exchange of sodium and potassium ions across the plasma membrane. This action creates the electrochemical gradient of sodium and potassium ions, providing the energy for active transport of various nutrients
Metabolizing enzymes(1)
Enzymes involved in drug metabolism — important for understanding drug interactions
Enzyme activity key
substrate
inhibitor
inducer
CYP11A1Cholesterol side-chain cleavage enzyme, mitochondrial
inhibitor
Transporters(7)
Proteins that transport this drug across cell membranes
ATP-dependent translocase ABCB1
ABCB1
substrate
inhibitor
inducer
Specific functionABC-type xenobiotic transporter activity
Cellular location
Cell membrane
General function & pharmacology
Translocates drugs and phospholipids across the membrane .
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
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
Solute carrier organic anion transporter family member 4C1
SLCO4C1
substrate
Specific functionorganic anion transmembrane transporter activity
Cellular location
Basolateral cell membrane
General function & pharmacology
Mediates the transport of organic anions such as steroids (estrone 3-sulfate, chenodeoxycholate, glycocholate) and thyroid hormones (3,3',5-triiodo-L-thyronine (T3), L-thyroxine (T4)), in the kidney .
PMID:14993604 PMID:19129463 PMID:20610891
Capable of transporting cAMP and pharmacological substances such as digoxin, ouabain and methotrexate .
PMID:14993604
Transport is independent of sodium, chloride ion, and ATP .
PMID:14993604
Transport activity is stimulated by an acidic extracellular environment due to increased substrate affinity to the transporter .
PMID:19129463
The driving force for this transport activity is currently not known (By similarity). The role of hydrogencarbonate (HCO3(-), bicarbonate) as the probable counteranion that exchanges for organic anions is still not well defined .
PMID:19129463
Functions as an uptake transporter at the apical membrane, suggesting a role in renal reabsorption (By similarity). Involved in the renal secretion of the uremic toxin ADMA (N(omega),N(omega)-dimethyl-L-arginine or asymmetrical dimethylarginine), which is associated to cardiovascular events and mortality, and the structurally related amino acids L-arginine and L-homoarginine (a cardioprotective biomarker) .
PMID:30865704
Can act bidirectionally, suggesting a dual protective role of this transport protein; exporting L-homoarginine after being synthesized in proximal tubule cells, and mediating uptake of ADMA from the blood into proximal tubule cells where it is degraded by the enzyme dimethylarginine dimethylaminohydrolase 1 (DDAH1) .
PMID:30865704 PMID:32642843
May be involved in sperm maturation by enabling directed movement of organic anions and compounds within or between cells (By similarity).
This ion-transporting process is important to maintain the strict epididymal homeostasis necessary for sperm maturation (By similarity). May have a role in secretory functions since seminal vesicle epithelial cells are assumed to secrete proteins involved in decapacitation by modifying surface proteins to facilitate the acquisition of the ability to fertilize the egg (By similarity)
PMID:14993604 PMID:19129463 PMID:20610891
Capable of transporting cAMP and pharmacological substances such as digoxin, ouabain and methotrexate .
PMID:14993604
Transport is independent of sodium, chloride ion, and ATP .
PMID:14993604
Transport activity is stimulated by an acidic extracellular environment due to increased substrate affinity to the transporter .
PMID:19129463
The driving force for this transport activity is currently not known (By similarity). The role of hydrogencarbonate (HCO3(-), bicarbonate) as the probable counteranion that exchanges for organic anions is still not well defined .
PMID:19129463
Functions as an uptake transporter at the apical membrane, suggesting a role in renal reabsorption (By similarity). Involved in the renal secretion of the uremic toxin ADMA (N(omega),N(omega)-dimethyl-L-arginine or asymmetrical dimethylarginine), which is associated to cardiovascular events and mortality, and the structurally related amino acids L-arginine and L-homoarginine (a cardioprotective biomarker) .
PMID:30865704
Can act bidirectionally, suggesting a dual protective role of this transport protein; exporting L-homoarginine after being synthesized in proximal tubule cells, and mediating uptake of ADMA from the blood into proximal tubule cells where it is degraded by the enzyme dimethylarginine dimethylaminohydrolase 1 (DDAH1) .
PMID:30865704 PMID:32642843
May be involved in sperm maturation by enabling directed movement of organic anions and compounds within or between cells (By similarity).
This ion-transporting process is important to maintain the strict epididymal homeostasis necessary for sperm maturation (By similarity). May have a role in secretory functions since seminal vesicle epithelial cells are assumed to secrete proteins involved in decapacitation by modifying surface proteins to facilitate the acquisition of the ability to fertilize the egg (By similarity)
Bile salt export pump
ABCB11
substrate
Specific functionABC-type bile acid transporter activity
Cellular location
Apical cell membrane
General function & pharmacology
Catalyzes the transport of the major hydrophobic bile salts, such as taurine and glycine-conjugated cholic acid across the canalicular membrane of hepatocytes in an ATP-dependent manner, therefore participates in hepatic bile acid homeostasis and consequently to lipid homeostasis through regulation of biliary lipid secretion in a bile salts dependent manner .
PMID:15791618 PMID:16332456 PMID:18985798 PMID:19228692 PMID:20010382 PMID:20398791 PMID:22262466 PMID:24711118 PMID:29507376 PMID:32203132
Transports taurine-conjugated bile salts more rapidly than glycine-conjugated bile salts .
PMID:16332456
Also transports non-bile acid compounds, such as pravastatin and fexofenadine in an ATP-dependent manner and may be involved in their biliary excretion PMID:15901796 PMID:18245269
PMID:15791618 PMID:16332456 PMID:18985798 PMID:19228692 PMID:20010382 PMID:20398791 PMID:22262466 PMID:24711118 PMID:29507376 PMID:32203132
Transports taurine-conjugated bile salts more rapidly than glycine-conjugated bile salts .
PMID:16332456
Also transports non-bile acid compounds, such as pravastatin and fexofenadine in an ATP-dependent manner and may be involved in their biliary excretion PMID:15901796 PMID:18245269
Solute carrier organic anion transporter family member 1A2
SLCO1A2
substrate
Specific functionbile acid transmembrane transporter activity
Cellular location
Cell membrane
General function & pharmacology
Na(+)-independent transporter that mediates the cellular uptake of a broad range of organic anions such as the endogenous bile salts cholate and deoxycholate, either in their unconjugated or conjugated forms (taurocholate and glycocholate), at the plasmam membrane .
PMID:19129463 PMID:7557095
Responsible for intestinal absorption of bile acids (By similarity). Transports dehydroepiandrosterone 3-sulfate (DHEAS), a major circulating steroid secreted by the adrenal cortex, as well as estrone 3-sulfate and 17beta-estradiol 17-O-(beta-D-glucuronate) .
PMID:11159893 PMID:12568656 PMID:19129463 PMID:23918469 PMID:25560245 PMID:9539145
Mediates apical uptake of all-trans-retinol (atROL) across human retinal pigment epithelium, which is essential to maintaining the integrity of the visual cycle and thus vision .
PMID:25560245
Involved in the uptake of clinically used drugs .
PMID:17301733 PMID:20686826 PMID:27777271
Capable of thyroid hormone transport (both T3 or 3,3',5'-triiodo-L-thyronine, and T4 or L-tyroxine) .
PMID:19129463 PMID:20358049
Also transports prostaglandin E2 .
PMID:19129463
Plays roles in blood-brain and -cerebrospinal fluid barrier transport of organic anions and signal mediators, and in hormone uptake by neural cells (By similarity). May also play a role in the reuptake of neuropeptides such as substance P/TAC1 and vasoactive intestinal peptide/VIP released from retinal neurons .
PMID:25132355
May play an important role in plasma and tissue distribution of the structurally diverse chemotherapeutic drugs methotrexate and paclitaxel .
PMID:23243220
Shows a pH-sensitive substrate specificity which may be ascribed to the protonation state of the binding site and leads to a stimulation of substrate transport in an acidic microenvironment .
PMID:19129463
Hydrogencarbonate/HCO3(-) acts as the probable counteranion that exchanges for organic anions .
PMID:19129463
May contribute to regulate the transport of organic compounds in testis across the blood-testis-barrier (Probable)
PMID:19129463 PMID:7557095
Responsible for intestinal absorption of bile acids (By similarity). Transports dehydroepiandrosterone 3-sulfate (DHEAS), a major circulating steroid secreted by the adrenal cortex, as well as estrone 3-sulfate and 17beta-estradiol 17-O-(beta-D-glucuronate) .
PMID:11159893 PMID:12568656 PMID:19129463 PMID:23918469 PMID:25560245 PMID:9539145
Mediates apical uptake of all-trans-retinol (atROL) across human retinal pigment epithelium, which is essential to maintaining the integrity of the visual cycle and thus vision .
PMID:25560245
Involved in the uptake of clinically used drugs .
PMID:17301733 PMID:20686826 PMID:27777271
Capable of thyroid hormone transport (both T3 or 3,3',5'-triiodo-L-thyronine, and T4 or L-tyroxine) .
PMID:19129463 PMID:20358049
Also transports prostaglandin E2 .
PMID:19129463
Plays roles in blood-brain and -cerebrospinal fluid barrier transport of organic anions and signal mediators, and in hormone uptake by neural cells (By similarity). May also play a role in the reuptake of neuropeptides such as substance P/TAC1 and vasoactive intestinal peptide/VIP released from retinal neurons .
PMID:25132355
May play an important role in plasma and tissue distribution of the structurally diverse chemotherapeutic drugs methotrexate and paclitaxel .
PMID:23243220
Shows a pH-sensitive substrate specificity which may be ascribed to the protonation state of the binding site and leads to a stimulation of substrate transport in an acidic microenvironment .
PMID:19129463
Hydrogencarbonate/HCO3(-) acts as the probable counteranion that exchanges for organic anions .
PMID:19129463
May contribute to regulate the transport of organic compounds in testis across the blood-testis-barrier (Probable)
Organic solute transporter subunit alpha
SLC51A
substrate
Specific functionbile acid transmembrane transporter activity
Cellular location
Cell membrane
General function & pharmacology
Essential component of the Ost-alpha/Ost-beta complex, a heterodimer that acts as the intestinal basolateral transporter responsible for bile acid export from enterocytes into portal blood .
PMID:16317684
Efficiently transports the major species of bile acids (taurocholate) .
PMID:16317684
Taurine conjugates are transported more efficiently across the basolateral membrane than glycine-conjugated bile acids (By similarity). Can also transport steroids such as estrone 3-sulfate and dehydroepiandrosterone 3-sulfate, therefore playing a role in the enterohepatic circulation of sterols .
PMID:16317684
Able to transport eicosanoids such as prostaglandin E2 (By similarity)
PMID:16317684
Efficiently transports the major species of bile acids (taurocholate) .
PMID:16317684
Taurine conjugates are transported more efficiently across the basolateral membrane than glycine-conjugated bile acids (By similarity). Can also transport steroids such as estrone 3-sulfate and dehydroepiandrosterone 3-sulfate, therefore playing a role in the enterohepatic circulation of sterols .
PMID:16317684
Able to transport eicosanoids such as prostaglandin E2 (By similarity)
Organic solute transporter subunit beta
SLC51B
substrate
Specific functionbile acid transmembrane transporter activity
Cellular location
Cell membrane
General function & pharmacology
Essential component of the Ost-alpha/Ost-beta complex, a heterodimer that acts as the intestinal basolateral transporter responsible for bile acid export from enterocytes into portal blood .
PMID:16317684
Modulates SLC51A glycosylation, membrane trafficking and stability activities .
PMID:16317684
The Ost-alpha/Ost-beta complex efficiently transports the major species of bile acids (taurocholate) .
PMID:16317684
Taurine conjugates are transported more efficiently across the basolateral membrane than glycine-conjugated bile acids (By similarity). Can also transport steroids such as estrone 3-sulfate and dehydroepiandrosterone 3-sulfate, therefore playing a role in the enterohepatic circulation of sterols .
PMID:16317684
Able to transport eicosanoids such as prostaglandin E2 (By similarity)
PMID:16317684
Modulates SLC51A glycosylation, membrane trafficking and stability activities .
PMID:16317684
The Ost-alpha/Ost-beta complex efficiently transports the major species of bile acids (taurocholate) .
PMID:16317684
Taurine conjugates are transported more efficiently across the basolateral membrane than glycine-conjugated bile acids (By similarity). Can also transport steroids such as estrone 3-sulfate and dehydroepiandrosterone 3-sulfate, therefore playing a role in the enterohepatic circulation of sterols .
PMID:16317684
Able to transport eicosanoids such as prostaglandin E2 (By similarity)
Solute carrier organic anion transporter family member 1B1
SLCO1B1
substrate
inhibitor
Specific functionbile acid transmembrane transporter activity
Cellular location
Basolateral cell membrane
General function & pharmacology
Mediates the Na(+)-independent uptake of organic anions .
PMID:10358072 PMID:15159445 PMID:17412826
Shows broad substrate specificity, can transport both organic anions such as bile acid taurocholate (cholyltaurine) and conjugated steroids (dehydroepiandrosterone 3-sulfate, 17-beta-glucuronosyl estradiol, and estrone 3-sulfate), as well as eicosanoids (prostaglandin E2, thromboxane B2, leukotriene C4, and leukotriene E4), and thyroid hormones (T4/L-thyroxine, and T3/3,3',5'-triiodo-L-thyronine) .
PMID:10358072 PMID:10601278 PMID:10873595 PMID:11159893 PMID:12196548 PMID:12568656 PMID:15159445 PMID:15970799 PMID:16627748 PMID:17412826 PMID:19129463 PMID:26979622
Can take up bilirubin glucuronides from plasma into the liver, contributing to the detoxification-enhancing liver-blood shuttling loop .
PMID:22232210
Involved in the clearance of endogenous and exogenous substrates from the liver .
PMID:10358072 PMID:10601278
Transports coproporphyrin I and III, by-products of heme synthesis, and may be involved in their hepatic disposition .
PMID:26383540
May contribute to regulate the transport of organic compounds in testes across the blood-testis-barrier (Probable). Can transport HMG-CoA reductase inhibitors (also known as statins), such as pravastatin and pitavastatin, a clinically important class of hypolipidemic drugs .
PMID:10601278 PMID:15159445 PMID:15970799
May play an important role in plasma and tissue distribution of the structurally diverse chemotherapeutic drug methotrexate .
PMID:23243220
May also transport antihypertension agents, such as the angiotensin-converting enzyme (ACE) inhibitor prodrug enalapril, and the highly selective angiotensin II AT1-receptor antagonist valsartan, in the liver .
PMID:16624871 PMID:16627748
Shows a pH-sensitive substrate specificity towards prostaglandin E2 and T4 which may be ascribed to the protonation state of the binding site and leads to a stimulation of substrate transport in an acidic microenvironment .
PMID:19129463
Hydrogencarbonate/HCO3(-) acts as the probable counteranion that exchanges for organic anions PMID:19129463
PMID:10358072 PMID:15159445 PMID:17412826
Shows broad substrate specificity, can transport both organic anions such as bile acid taurocholate (cholyltaurine) and conjugated steroids (dehydroepiandrosterone 3-sulfate, 17-beta-glucuronosyl estradiol, and estrone 3-sulfate), as well as eicosanoids (prostaglandin E2, thromboxane B2, leukotriene C4, and leukotriene E4), and thyroid hormones (T4/L-thyroxine, and T3/3,3',5'-triiodo-L-thyronine) .
PMID:10358072 PMID:10601278 PMID:10873595 PMID:11159893 PMID:12196548 PMID:12568656 PMID:15159445 PMID:15970799 PMID:16627748 PMID:17412826 PMID:19129463 PMID:26979622
Can take up bilirubin glucuronides from plasma into the liver, contributing to the detoxification-enhancing liver-blood shuttling loop .
PMID:22232210
Involved in the clearance of endogenous and exogenous substrates from the liver .
PMID:10358072 PMID:10601278
Transports coproporphyrin I and III, by-products of heme synthesis, and may be involved in their hepatic disposition .
PMID:26383540
May contribute to regulate the transport of organic compounds in testes across the blood-testis-barrier (Probable). Can transport HMG-CoA reductase inhibitors (also known as statins), such as pravastatin and pitavastatin, a clinically important class of hypolipidemic drugs .
PMID:10601278 PMID:15159445 PMID:15970799
May play an important role in plasma and tissue distribution of the structurally diverse chemotherapeutic drug methotrexate .
PMID:23243220
May also transport antihypertension agents, such as the angiotensin-converting enzyme (ACE) inhibitor prodrug enalapril, and the highly selective angiotensin II AT1-receptor antagonist valsartan, in the liver .
PMID:16624871 PMID:16627748
Shows a pH-sensitive substrate specificity towards prostaglandin E2 and T4 which may be ascribed to the protonation state of the binding site and leads to a stimulation of substrate transport in an acidic microenvironment .
PMID:19129463
Hydrogencarbonate/HCO3(-) acts as the probable counteranion that exchanges for organic anions PMID:19129463
Scientific references(19)
Thompson D.F., Carter J.R.
Drug‐Induced Gynecomastia.
Pharmacotherapy: The Journal of Human Pharmacology and Drug Therapy
199313(1):37-45. doi: 10.1002/j.1875-9114.1993.tb02688.x
Doering W., Konig E., Sturm W.
Digitalis Intoxication: Specificity of Clinical and Electrocardiographic Signs. International Boehringer Mannheim Symposia. 1978;:358-366.
doi: 10
1007/978-3-642-66904-0_31
Kaplanski J., Weinhouse E., Topaz M., Genchik G.
Mechanisms of Digoxin-Amiodarone Interaction in the Rat.
Experimental Biology and Medicine
1988188(1):96-102. doi: 10.3181/00379727-188-42713
Flanagan R.J., Jones A.L.
Fab Antibody Fragments.
Drug Safety
200427(14):1115-1133. doi: 10.2165/00002018-200427140-00004
MacLeod-Glover N., Mink M., Yarema M., Chuang R.
Digoxin interaction.
Reactions Weekly
1997&NA;(673):8. doi: 10.2165/00128415-199706730-00017
Iisalo E.
Clinical pharmacokinetics of digoxin.
Clinical Pharmacokinetics
1977 Jan-Feb2(1):1-16. doi: 10.2165/00003088-197702010-00001
Ziff O.J., Kotecha D.
Digoxin: The good and the bad.
Trends Cardiovasc Medicine
2016 Oct26(7):585-95. doi: 10.1016/j.tcm.2016.03.011. Epub 2016 Mar 31
Whayne TF Jr
Clinical Use of Digitalis: A State of the Art Review.
American Journal Cardiovasc Drugs
2018 Dec18(6):427-440. doi: 10.1007/s40256-018-0292-1
Norn S., Kruse P.R.
Foxglove, Cardiac Glycosides, and Congestive Heart Failure. Pharmacodynamic Basis of Herbal Medicine. 2006;:419-434.
doi: 10
1201/9781420006452-42
Currie G.M., Wheat J.M., Kiat H.
Pharmacokinetic considerations for digoxin in older people.
Open Cardiovasc Medicine Journal
20115:130-5. doi: 10.2174/1874192401105010130. Epub 2011 Jun 15
Mangoni M.E., Nargeot J.
Genesis and regulation of the heart automaticity.
Physiology Review
2008 Jul88(3):919-82. doi: 10.1152/physrev.00018.2007
Vincent J.L.
Understanding cardiac output.
Crit Care
200812(4):174. doi: 10.1186/cc6975. Epub 2008 Aug 22
Gutierrez C., Blanchard D.G.
Anticoagulation in patients with nonvalvular atrial fibrillation.
Canadian Family Physician
202369(6):381.1-381. doi: 10.46747/cfp.6906381
Virgadamo S., Charnigo R., Darrat Y., Morales G., Elayi C.S.
Digoxin: A systematic review in atrial fibrillation, congestive heart failure and post myocardial infarction.
World Journal Cardiology
2015 Nov 267(11):808-16. doi: 10.4330/wjc.v7.i11.808
Ewy G.A., Kapadia G.G., Yao L., Lullin M., Marcus F.I.
Digoxin Metabolism in the Elderly.
Circulation
196939(4):449-453. doi: 10.1161/01.cir.39.4.449
Koup J.R., Jusko W.J., Elwood C.M., Kohli R.K.
Digoxin pharmacokinetics: role of renal failure in dosage regimen design.
Clinical Pharmacology Therapeutics
1975 Jul18(1):9-21. doi: 10.1002/cpt19751819
Schmidt T.A., Bundgaard H., Olesen H.L., Secher N.H., Kjeldsen K.
Digoxin affects potassium homeostasis during exercise in patients with heart failure.
Cardiovascular Research
199529(4):506-511. doi: 10.1016/s0008-6363(96)88526-9
Watanabe Y., Okumura K., Hashimoto H., Ito T., Ogawa K., Satake T.
Effects of Digoxin on Acetylcholine and Norepinephrine Concentrations in Rat Myocardium.
Journal of Cardiovascular Pharmacology
198913(5):702-708. doi: 10.1097/00005344-198913050-00004
Schwartz J.I., Agrawal N.G., Wehling M., Musser B.J., Gumbs C.P., Michiels N., De Smet M., Wagner J.A.
Evaluation of the pharmacokinetics of digoxin in healthy subjects receiving etoricoxib.
British Journal of Clinical Pharmacology
2008 Dec66(6):811-7. doi: 10.1111/j.1365-2125.2008.03285.x. Epub 2008 Sep 24
ATC classification(1 code)
ATC C01AA05
Affected organisms(1)
Humans and other mammals
International brands(17)
Experimental properties(5)
Commercial products(238)
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)
Digoxin
Additional database identifiers
Drugs Product Database (DPD)
6731
ChemSpider
2006532
BindingDB
46355
PDB
DGX
ZINC
ZINC000242548690
HUGO Gene Nomenclature Committee (HGNC)
HGNC:799
GenAtlas
ATP1A1
GeneCards
ATP1A1
GenBank Gene Database
D00099
GenBank Protein Database
219942
UniProt Accession
AT1A1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:806
GeneCards
ATP1B3
UniProt Accession
AT1B3_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:805
GeneCards
ATP1B2
UniProt Accession
AT1B2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:804
GeneCards
ATP1B1
UniProt Accession
AT1B1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:801
GeneCards
ATP1A3
UniProt Accession
AT1A3_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:800
GeneCards
ATP1A2
UniProt Accession
AT1A2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:23612
GeneCards
SLCO4C1
GenBank Gene Database
AF401643
GenBank Protein Database
33308060
UniProt Accession
SO4C1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2590
GeneCards
CYP11A1
GenBank Gene Database
M14565
GenBank Protein Database
181376
Guide to Pharmacology
1358
UniProt Accession
CP11A_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
HUGO Gene Nomenclature Committee (HGNC)
HGNC:23612
GeneCards
SLCO4C1
GenBank Gene Database
AF401643
GenBank Protein Database
33308060
UniProt Accession
SO4C1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:42
GenAtlas
ABCB11
GeneCards
ABCB11
GenBank Gene Database
AF091582
GenBank Protein Database
3873243
Guide to Pharmacology
778
UniProt Accession
ABCBB_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10956
GeneCards
SLCO1A2
GenBank Gene Database
U21943
GenBank Protein Database
885978
Guide to Pharmacology
1219
UniProt Accession
SO1A2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:29955
GeneCards
SLC51A
GenBank Gene Database
AY194243
GenBank Protein Database
30348899
UniProt Accession
OSTA_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:29956
GeneCards
SLC51B
GenBank Gene Database
AY194242
GenBank Protein Database
30348897
UniProt Accession
OSTB_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10959
GenAtlas
SLCO1B1
GeneCards
SLCO1B1
GenBank Gene Database
AF060500
GenBank Protein Database
5051630
Guide to Pharmacology
1220
UniProt Accession
SO1B1_HUMAN
International reference pricing
25 formulations
Reference pricing from DrugBank. Prices are indicative and may not reflect current UK costs.
From $0.22/tablet
To $727.91/vial
Digoxin 125 mcg tablet
$0.22/tablet
Digoxin 250 mcg tablet
$0.22/tablet
Toloxin 0.0625 mg Tablet
$0.27/tablet
Toloxin 0.125 mg Tablet
$0.27/tablet
Toloxin 0.25 mg Tablet
$0.27/tablet
Source: DrugBank. Used under CC BY-NC 4.0 academic licence for non-commercial purposes.
DrugBank citations
If you use DrugBank data in your research, please cite the following publications:
Knox C., Wilson M., Klinger C.M., et al
DrugBank 6.
0: the DrugBank Knowledgebase for 2024
Nucleic Acids Res. 2024 Jan 552(D1):D1265-D1275
Wishart D.S., Feunang Y.D., Guo A.C., et al
DrugBank 5.
0: a major update to the DrugBank database for 2018
Nucleic Acids Res. 2017 Nov 846(D1):D1074-D1082
Show earlier publications
Law V., Knox C., Djoumbou Y., et al
DrugBank 4.
0: shedding new light on drug metabolism
Nucleic Acids Res. 2014 Jan 142(1):D1091-7
Knox C., Law V., Jewison T., et al
DrugBank 3.
0: a comprehensive resource for 'omics' research on drugs
Nucleic Acids Res. 2011 Jan39(Database issue):D1035-41
Wishart D.S., Knox C., Guo A.C., et al
DrugBank: a knowledgebase for drugs, drug actions and drug targets.
Nucleic Acids Research
2008 Jan36(Database issue):D901-6
Wishart D.S., Knox C., Guo A.C., et al
DrugBank: a comprehensive resource for in silico drug discovery and exploration.
Nucleic Acids Research
2006 Jan 134(Database issue):D668-72
Source: go.drugbank.comCC BY-NC 4.0
Updated 26 days ago(8 Mar 2026)