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Digoxin | CAS No: 20830-75-5 | GMP-certified suppliers
A medication that supports treatment of mild to moderate heart failure and chronic atrial fibrillation by improving cardiac function and controlling ventricular rate.
Therapeutic categories
Primary indications
- Digoxin is indicated in the following conditions: 1) For the treatment of mild to moderate heart failure in adult patients
- 2) To increase myocardial contraction in children diagnosed with heart failure
- 3) To maintain control ventricular rate in adult patients diagnosed with chronic atrial fibrillation
Product Snapshot
- Digoxin is available as oral tablets and injectable solutions, representing oral small molecule and parenteral formulations
- It is primarily used for the management of mild to moderate heart failure and control of ventricular rate in chronic atrial fibrillation
- Digoxin is approved for use in key regulatory markets including the United States and Canada
Clinical Overview
Clinically, digoxin is indicated for the treatment of mild to moderate heart failure in adults and to increase myocardial contractility in pediatric patients with heart failure. It is also used to control the ventricular rate in adults with chronic atrial fibrillation. In adults, optimal heart failure management with digoxin typically involves co-administration with diuretics and angiotensin-converting enzyme (ACE) inhibitors.
Pharmacodynamically, digoxin exhibits positive inotropic effects by increasing myocardial contractility and negative chronotropic effects by reducing heart rate. These actions help improve cardiac output and reduce symptoms related to heart failure, such as exercise intolerance and hospitalization rates. The therapeutic mechanism primarily involves reversible inhibition of the Na-K ATPase pump in cardiac myocytes, leading to increased intracellular sodium and secondary elevation of intracellular calcium. The augmented calcium concentration enhances contractile force and improves left ventricular ejection fraction. Additionally, digoxin enhances parasympathetic tone via vagal stimulation, resulting in decreased sinoatrial and atrioventricular nodal conduction and heart rate reduction.
Absorption, distribution, metabolism, and excretion (ADME) properties of digoxin include renal elimination as a primary clearance route, with known involvement of transport proteins such as P-glycoprotein. Digoxin has a narrow therapeutic window, requiring careful dose titration and monitoring to avoid toxicity. Safety concerns include the risk of severe cardiac arrhythmias, notably ventricular fibrillation in patients with accessory atrioventricular pathways and exacerbation of heart block in those with pre-existing conduction system disease. Monitoring for signs of digoxin toxicity and electrolyte imbalances, particularly hyperkalemia, is critical during therapy.
Notable brand names for digoxin include Lanoxin among others, and the drug remains a standard pharmacological option for specific heart failure and arrhythmia indications worldwide.
Regarding API sourcing, digoxin requires high purity with stringent control of glycosidic composition and potency due to its narrow therapeutic index. Suppliers must ensure compliance with regulatory standards such as those outlined by pharmacopoeias (e.g., USP, EP). Stability and batch-to-batch consistency are critical factors when procuring digoxin API for pharmaceutical formulation.
Identification & chemistry
| Generic name | Digoxin |
|---|---|
| Molecule type | Small molecule |
| CAS | 20830-75-5 |
| UNII | 73K4184T59 |
| DrugBank ID | DB00390 |
Pharmacology
| Summary | Digoxin acts primarily by reversibly inhibiting the sodium/potassium-transporting ATPase enzyme (sodium pump) in myocardial cells, leading to increased intracellular calcium and enhanced cardiac contractility. It also modulates autonomic control by stimulating the parasympathetic nervous system, resulting in decreased heart rate via effects on the sinoatrial and atrioventricular nodes. These combined pharmacodynamic actions provide positive inotropic and negative chronotropic effects, supporting its use in heart failure and rate control in atrial fibrillation. |
|---|---|
| Mechanism of action | Digoxin exerts hemodynamic, electrophysiologic, and neurohormonal effects on the cardiovascular system. 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_. 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. This improves the left ventricular ejection fraction (EF), an important measure of cardiac function. Digoxin also stimulates the parasympathetic nervous system via the vagus nerve leading to sinoatrial (SA) and atrioventricular (AV) node effects, decreasing the heart rate. 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. |
| Pharmacodynamics | Digoxin is a positive inotropic and negative chronotropic drug, meaning that it increases the force of the heartbeat and decreases the heart rate. The decrease in heart rate is particularly useful in cases of atrial fibrillation, a condition characterized by a fast and irregular heartbeat. 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. Digoxin has a narrow therapeutic window. **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. 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. |
Targets
| Target | Organism | Actions |
|---|---|---|
| Sodium/potassium-transporting ATPase subunit alpha-1 | Humans | inhibitor |
ADME / PK
| Absorption | Digoxin is approximately 70-80% absorbed in the first part of the small bowel. The bioavailability of an oral dose varies from 50-90%, however, oral gelatinized capsules of digoxin are reported to have a bioavailability of 100%. 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. 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. 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. **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. **A note on malabsorption** Patients with malabsorption due to a variety of causes may have a decreased ability to absorb digoxin. 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. |
|---|---|
| Half-life | Digoxin has a half-life of 1.5-2 days in healthy subjects. 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. |
| Protein binding | Digoxin protein binding is approximately 25%. It is mainly bound to albumin. |
| 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. |
| 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. 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. |
| Volume of distribution | This drug is widely distributed in the body, and is known to cross the blood-brain barrier and the placenta. The apparent volume of distribution of digoxin is 475-500 L. A large portion of digoxin is distributed in the skeletal muscle followed by the heart and kidneys. It is important to note that the elderly population, generally having a decreased muscle mass, may show a lower volume of digoxin distribution. |
| 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. One pharmacokinetic study measured the mean body clearance of intravenous digoxin to be 88 ± 44ml/min/l.73 m². 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. |
Formulation & handling
- Digoxin is administered via both oral and parenteral routes, including intravenous and intramuscular injections, requiring formulation versatility.
- As a small molecule cardenolide glycoside, it exhibits low water solubility (~0.127 g/L) and moderate lipophilicity (LogP 2.37), impacting formulation strategies.
- Concomitant administration with multivalent ions, potassium, high fiber foods, or St. John’s Wort should be avoided due to significant effects on absorption and drug levels.
Regulatory status
| Lifecycle | The API is currently marketed in Canada and the US, with key patents having expired or nearing expiry, indicating a mature market with increasing generic availability. Ongoing regulatory and competitive dynamics continue to influence product lifecycle management in these regions. |
|---|
| Markets | Canada, US |
|---|
Supply Chain
| Supply chain summary | The manufacturing landscape for digoxin involves multiple originator and generic pharmaceutical companies, reflecting a competitive supply environment. Branded products such as Digitek and Apo-digoxin have a global presence primarily in the US and Canada. Given that digoxin is widely available from numerous manufacturers and packagers, patent expiry has likely led to existing generic competition across these markets. |
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Safety
| Toxicity | Oral TDLO (human female): 100 ug/kg, Oral TDLO (human male): 75 ug/kg, Oral LD50 (rat): 28270 ug/kg[MSDS] Digoxin toxicity can occur in cases of supratherapeutic dose ingestion or as a result of chronic overexposure. 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. |
|---|
- Exposure to digoxin at or above 75-100 µg/kg orally may result in toxic effects
- Cumulative exposure increases risk
- Signs of toxicity include gastrointestinal disturbances and cardiac arrhythmias
Digoxin is a type of Cardiac glycosides
Cardiac glycosides are a vital subcategory of pharmaceutical active pharmaceutical ingredients (APIs) with significant therapeutic value. These compounds, derived from various plant sources, are known for their potent cardiovascular effects, making them valuable in the treatment of heart-related disorders.
Cardiac glycosides, such as digoxin and digitoxin, exert their pharmacological action by inhibiting the sodium-potassium ATPase pump in cardiac cells. This inhibition leads to an increase in intracellular calcium levels, resulting in enhanced contractility of the heart muscles. By strengthening the heart's pumping action, these glycosides are highly effective in treating conditions like congestive heart failure, atrial fibrillation, and certain types of arrhythmias.
The demand for cardiac glycosides has been driven by the rising prevalence of cardiovascular diseases worldwide. As the population ages and risk factors such as obesity and sedentary lifestyles increase, the need for effective cardiac medications becomes more crucial.
Pharmaceutical companies invest in research and development to improve the synthesis, purification, and formulation processes of cardiac glycosides. This ensures the production of high-quality APIs that comply with stringent regulatory standards. Additionally, advanced extraction techniques and modern analytical methods are employed to ensure the purity, potency, and safety of these APIs.
In conclusion, cardiac glycosides represent a valuable subcategory of pharmaceutical APIs that play a crucial role in the treatment of cardiovascular disorders. With their potent cardiac effects and increasing prevalence of heart-related diseases, the demand for these APIs is expected to remain high. The pharmaceutical industry continues to focus on optimizing the production and quality control processes to ensure the availability of safe and effective cardiac glycoside medications.
Digoxin (Cardiac glycosides), classified under Anti-arrhythmics
Anti-arrhythmics belong to the pharmaceutical API category designed to treat irregular heart rhythms, also known as arrhythmias. These medications work by targeting the electrical signals in the heart, helping to regulate the heart's rhythm and restore it to a normal, steady beat.
Anti-arrhythmics are crucial in managing various types of arrhythmias, such as atrial fibrillation, ventricular tachycardia, and supraventricular tachycardia. These conditions can pose serious risks, including an increased likelihood of stroke or heart failure. Hence, anti-arrhythmics play a vital role in improving patient outcomes and reducing these associated risks.
Pharmaceutical companies develop anti-arrhythmic APIs, which are the active ingredients used to formulate the final medications. These APIs undergo rigorous testing and quality control measures to ensure their safety, efficacy, and consistent performance. They are manufactured in accordance with Good Manufacturing Practices (GMP) guidelines to meet the highest quality standards.
Healthcare professionals prescribe anti-arrhythmics based on the specific arrhythmia type, severity, and individual patient factors. These APIs can be formulated into different dosage forms, including tablets, capsules, or intravenous solutions, depending on the desired route of administration and patient requirements.
It is important to note that anti-arrhythmics are prescription-only medications and should only be used under medical supervision. Patients using these medications must follow their healthcare provider's instructions and regularly monitor their heart rhythm to ensure optimal treatment effectiveness and minimize potential side effects.
In conclusion, anti-arrhythmics are a crucial category of pharmaceutical APIs used to treat various types of irregular heart rhythms. They are formulated into medications that help regulate the heart's electrical signals, reduce associated risks, and improve patient outcomes.
Digoxin API manufacturers & distributors
Compare qualified Digoxin API suppliers worldwide. We currently have 7 companies offering Digoxin API, with manufacturing taking place in 3 different countries. Use the table below to review supplier type, countries of origin, certifications, product portfolio and GMP audit availability.
| Supplier | Type | Country | Product origin | Certifications | Portfolio |
|---|---|---|---|---|---|
| Alkaloids Corporation | Producer | India | India | CEP, CoA, FDA, GMP, USDMF, WC, WHO-GMP | 11 products |
| Boehringer Ingelheim | Producer | Germany | Unknown | CEP, CoA, FDA, GMP, JDMF, USDMF | 35 products |
| Chr. Olesen Group | Distributor | Denmark | India | CEP, CoA, USDMF | 252 products |
| Danashmand | Producer | India | India | CoA, WC | 3 products |
| Nobilus Ent | Producer | Poland | Poland | CEP, CoA, FDA, GMP, JDMF, USDMF | 5 products |
| Tenatra Exports Private L... | Distributor | India | India | BSE/TSE, CoA, FDA, GMP, MSDS | 263 products |
| Vital Laboratories Pvt. L... | Producer | India | India | CoA, USDMF, WC | 22 products |
When sending a request, specify which Digoxin API quality you need: for example EP (Ph. Eur.), USP, JP, BP, or another pharmacopoeial standard, as well as the required grade (base, salt, micronised, specific purity, etc.).
Use the list above to find high-quality Digoxin API suppliers. For example, you can select GMP, FDA or ISO certified suppliers. Visit our help page to learn more about sourcing APIs via Pharmaoffer.
