Head-to-head clinical analysis & difference comparison: details on mechanism of action, dosing, half-life, interactions, and maternal-fetal safety.
DIGOXIN PEDIATRIC vs LANOXIN PEDIATRIC
Clinician-reviewed, head-to-head comparison of mechanism, dosing, pharmacokinetics, and safety profiles.
Last clinically reviewed: July 2026 · OpiCalc Medical Review Team
Inhibits sodium-potassium ATPase, increasing intracellular sodium, which promotes calcium influx via sodium-calcium exchanger, enhancing cardiac contractility. Also increases vagal tone, slowing AV conduction.
Inhibition of Na+/K+ ATPase leading to increased intracellular calcium and positive inotropy.
Heart failure (FDA-approved for pediatric patients with heart failure),Atrial fibrillation (off-label for rate control in pediatric patients)
Heart failure,Atrial fibrillation,Atrial flutter
For pediatric patients, digoxin pediatric dosing is weight-based; no standard adult dose. Typical pediatric loading dose: 10-12 mcg/kg orally divided every 6-8 hours, with maintenance: 5-10 mcg/kg/day divided every 12 hours. For infants <1 month, loading: 10-15 mcg/kg, maintenance: 4-6 mcg/kg/day. For children 1-24 months, loading: 15-20 mcg/kg, maintenance: 5-8 mcg/kg/day. For children >2 years, loading: 10-15 mcg/kg, maintenance: 3-5 mcg/kg/day.
Adult: Oral loading dose 0.75-1.5 mg in divided doses over 24-48 hours. Maintenance: 0.125-0.5 mg once daily. Intravenous: Loading dose 0.5-1 mg over 10-20 minutes, then maintenance 0.125-0.5 mg once daily.
Terminal elimination half-life in neonates is 35-70 hours, infants 18-30 hours, children 12-30 hours, and adults 36-48 hours; prolonged in renal impairment and hypothyroidism.
Terminal elimination half-life is 36-48 hours in adults with normal renal function; prolonged to 3.5-5 days in anephric patients due to reduced renal clearance.
Primarily renally excreted unchanged; minimal hepatic metabolism (mostly via reduction, hydrolysis, and conjugation in older children).
Hepatic via glucuronidation; substrate of P-glycoprotein; renal excretion of unchanged drug.
Renal excretion accounts for 50-70% of elimination as unchanged drug; biliary/fecal excretion accounts for 30-40%, primarily as metabolites; enterohepatic recirculation occurs.
Renal excretion of unchanged drug accounts for 60-80% of elimination; nonrenal clearance is 20-40% (biliary/fecal).
25% bound to serum albumin; binding decreases in uremia and hyperbilirubinemia.
20-30% bound to plasma proteins, primarily albumin.
Vd: 6-10 L/kg in infants and children, 5-7 L/kg in adults; large Vd indicates extensive tissue binding, particularly to cardiac muscle (Na+/K+-ATPase).
Vd is 5-10 L/kg in adults, indicating extensive tissue binding; higher in infants (up to 16 L/kg) with reduced protein binding.
Oral: 60-80% (elixir 70-85%, tablets 60-75%); IM: 70-85% (but erratic absorption and pain limit use); IV: 100%.
Oral: 60-80% (Lanoxin Pediatric elixir 70-85%); variable due to first-pass metabolism and P-glycoprotein effects.
Digoxin is primarily renally excreted. For pediatric patients, if GFR <30 m L/min/1.73m2, reduce maintenance dose by 50% and monitor serum levels. For GFR 30-60, reduce dose by 25-50%. In neonates with renal impairment, dose reduction proportional to creatinine clearance.
GFR >50 m L/min: no adjustment; GFR 10-50 m L/min: reduce dose by 25-50%; GFR <10 m L/min: reduce dose by 50-75% or consider alternative.
Digoxin is minimally hepatically metabolized; no dose adjustment required for hepatic impairment. However, in Child-Pugh class C, monitor levels due to potential altered distribution.
Child-Pugh A: no adjustment; Child-Pugh B: reduce dose by 25-50%; Child-Pugh C: avoid use or reduce dose by 50-75% with monitoring.
See standard_dosing. Weight-based dosing: total digitalizing dose (TDD) and maintenance as above. For premature infants, TDD 10-15 mcg/kg, maintenance 3-5 mcg/kg/day divided q12h. For full term neonates, TDD 15-20 mcg/kg, maintenance 5-7 mcg/kg/day. For infants 1-24 months, TDD 20-25 mcg/kg, maintenance 7-10 mcg/kg/day. For children 2-10 years, TDD 10-15 mcg/kg, maintenance 5-7 mcg/kg/day. For children >10 years, TDD 10-15 mcg/kg, maintenance 3-5 mcg/kg/day. Divide TDD into 3-4 doses every 6-8 hours. Maintenance started 12 hours after last loading dose.
Oral loading: 10-20 mcg/kg in divided doses over 24 hours; maintenance: 5-10 mcg/kg once daily. IV loading: 10-15 mcg/kg; maintenance: 4-8 mcg/kg once daily. Monitor levels.
Not applicable for pediatric formulation. For elderly, use adult digoxin dosing with caution: reduced renal function may require lower maintenance doses. Typical adult maintenance: 0.0625-0.25 mg daily based on renal function and lean body mass.
Reduced dose: initial maintenance 0.0625-0.125 mg once daily due to age-related renal impairment and increased sensitivity. Monitor renal function and serum digoxin levels.
Toxicity can be life-threatening. Use caution in renal impairment, electrolyte disturbances (hypokalemia, hypomagnesemia, hypercalcemia). Narrow therapeutic index requires monitoring.
Digitalis toxicity can cause severe arrhythmias; monitoring of serum digoxin levels required.
Monitor serum digoxin levels, renal function, electrolytes (potassium, magnesium, calcium). Risk of arrhythmias (including ventricular fibrillation, bradycardia, AV block). Use with caution in patients with thyroid disease, acute myocardial infarction, or myocarditis.
Risk of toxicity in renal impairment, electrolyte disturbances, and drug interactions; monitor digoxin levels and ECG.
Ventricular fibrillation, hypersensitivity to digitalis preparations, hypokalemia (uncorrected), hypercalcemia (uncorrected), AV block (second or third degree) unless pacemaker present.
Hypersensitivity to digoxin, ventricular fibrillation, digitalis toxicity.
High-fiber foods may decrease absorption; take digoxin 1 hour before or 2 hours after meals. Avoid natural licorice, which can cause hypokalemia and increase toxicity. Maintain consistent dietary potassium intake.
Avoid concurrent ingestion of high-fiber foods, as they may reduce absorption. Separate dosing by at least 2 hours from meals rich in bran, oats, or other fiber. Maintain consistent dietary potassium intake; both low and high potassium can affect digoxin toxicity. Grapefruit juice may increase absorption; avoid excessive consumption.
Digoxin crosses the placenta. First trimester: No increased risk of major malformations reported in human studies. Second/third trimester: Potential for fetal toxicity (e.g., bradycardia, cardiac arrhythmias) at maternal toxic doses. No known teratogenicity at therapeutic doses.
First trimester: No evidence of increased risk of major malformations. Second/third trimester: Potential for fetal bradycardia, cardiac arrhythmias, and intrauterine growth restriction due to transplacental transfer and maternal hemodynamic changes.
Digoxin is excreted into breast milk in low concentrations. M/P ratio approximately 0.6–0.9. Infant dose via milk is <1% of maternal weight-adjusted dose, unlikely to cause adverse effects in term infants. Caution in preterm or neonates with renal impairment.
Digoxin is excreted into breast milk with an M/P ratio of approximately 0.6–0.9. Levels are low (typically <1 ng/m L) and considered compatible with breastfeeding; however, monitor infant for signs of toxicity including bradycardia and feeding difficulties.
During pregnancy, increased volume of distribution and renal clearance may reduce serum digoxin levels. Dose adjustments may be required based on therapeutic drug monitoring; typical dose increase of 20–30% in third trimester. Postpartum, reduce dose to prepregnancy level to avoid toxicity.
Due to increased volume of distribution and renal clearance in pregnancy, higher doses (up to 30–50% increase) may be required to maintain therapeutic serum levels. Monitor serum digoxin concentrations and titrate to therapeutic range (0.5–0.9 ng/m L in heart failure; 0.8–2.0 ng/m L for arrhythmias).
Monitor serum digoxin levels (therapeutic range 0.5-2 ng/m L) and renal function, especially in neonates. Correct hypokalemia, hypomagnesemia, and hypercalcemia before administration to reduce toxicity risk. Use with caution in patients with WPW, hypertrophic cardiomyopathy, or incomplete heart block. Dosing in infants and children is based on weight and renal function.
Lanoxin Pediatric (digoxin) requires monitoring of renal function and serum electrolytes (especially potassium and magnesium) due to narrow therapeutic index. Check digoxin levels 6-8 hours after dose; therapeutic range 0.8-2.0 ng/m L. Avoid concurrent use with drugs that affect renal function or electrolyte balance.
Take exactly as prescribed; do not double up doses.,Monitor for signs of toxicity: nausea, vomiting, vision changes (yellow-green halos), arrhythmias.,Keep medication out of reach of children; immediate medical attention if overdose suspected.,Do not stop abruptly without consulting healthcare provider.,Inform healthcare provider of all medications, including OTC and herbal supplements.
Take exactly as prescribed at the same time each day. Do not double the dose if you miss one.,Do not stop taking without consulting your doctor. Sudden withdrawal may worsen heart condition.,Watch for signs of toxicity: nausea, vomiting, diarrhea, vision changes (blurring, yellow-green halos), confusion, irregular heartbeat.,Keep all appointments for blood tests to monitor levels and kidney function.,Contact your doctor before taking any new medications, including over-the-counter drugs and supplements.,Limit alcohol and avoid potassium-sparing diuretics unless prescribed. Maintain consistent dietary intake of potassium-rich foods.
"Eflornithine, an ornithine decarboxylase inhibitor used in the treatment of African trypanosomiasis and hirsutism, may reduce the therapeutic efficacy of digoxin, a cardiotonic glycoside used for heart failure and atrial fibrillation. The proposed mechanism involves eflornithine-induced alterations in gastrointestinal motility or absorption, potentially decreasing digoxin bioavailability. This could lead to subtherapeutic digoxin levels, diminished inotropic and chronotropic effects, and increased risk of arrhythmias or worsening heart failure."
"Osimertinib, a tyrosine kinase inhibitor used in non-small cell lung cancer, can inhibit P-glycoprotein (P-gp) transport in the gastrointestinal tract and kidneys, leading to increased absorption and reduced renal clearance of digoxin. This elevation in serum digoxin concentration heightens the risk of digoxin toxicity, including cardiac arrhythmias (e.g., bradycardia, atrial tachycardia with block) and gastrointestinal symptoms such as nausea and vomiting. Clinical monitoring for digoxin toxicity is warranted, especially when initiating or adjusting osimertinib therapy."
"Lenvatinib, a tyrosine kinase inhibitor, may reduce the therapeutic efficacy of digoxin by interfering with its cardiotonic effects. This interaction could lead to decreased inotropic support in patients with heart failure, potentially worsening cardiac function and clinical outcomes. The clinical consequence is a possible loss of rate control in atrial fibrillation or diminished contractility in systolic dysfunction."
No interactions on record
Explore head-to-head clinical comparisons of other medications in the same therapeutic classes.
Common clinical questions about DIGOXIN PEDIATRIC vs LANOXIN PEDIATRIC, answered by our medical review team.
DIGOXIN PEDIATRIC is a Cardiac Glycoside that works by Inhibits sodium-potassium ATPase, increasing intracellular sodium, which promotes calcium influx via sodium-calcium exchanger, enhancing cardiac contractility. Also increases vagal tone, slowing AV conduction.. LANOXIN PEDIATRIC is a Cardiac Glycoside that works by Inhibition of Na+/K+ ATPase leading to increased intracellular calcium and positive inotropy.. They differ in pharmacokinetic profiles, FDA-approved indications, and side effect profiles.
Potency comparisons between DIGOXIN PEDIATRIC and LANOXIN PEDIATRIC depend on the specific clinical indication. These are both Cardiac Glycoside agents and are not directly interchangeable by dose. A physician or clinical pharmacist should guide any therapeutic switching decisions.
The standard adult dose of DIGOXIN PEDIATRIC is: For pediatric patients, digoxin pediatric dosing is weight-based; no standard adult dose. Typical pediatric loading dose: 10-12 mcg/kg orally divided every 6-8 hours, with maintenance: 5-10 mcg/kg/day divided every 12 hours. For infants <1 month, loading: 10-15 mcg/kg, maintenance: 4-6 mcg/kg/day. For children 1-24 months, loading: 15-20 mcg/kg, maintenance: 5-8 mcg/kg/day. For children >2 years, loading: 10-15 mcg/kg, maintenance: 3-5 mcg/kg/day.. The standard adult dose of LANOXIN PEDIATRIC is: Adult: Oral loading dose 0.75-1.5 mg in divided doses over 24-48 hours. Maintenance: 0.125-0.5 mg once daily. Intravenous: Loading dose 0.5-1 mg over 10-20 minutes, then maintenance 0.125-0.5 mg once daily.. Dosing should always be individualized based on indication, renal and hepatic function, age, and other patient factors.
No direct drug-drug interaction has been formally documented between DIGOXIN PEDIATRIC and LANOXIN PEDIATRIC in current clinical databases. However, individual patient risk factors including other medications, organ function, and comorbidities should always be evaluated by a qualified healthcare provider.
The maternal-fetal safety profiles differ. DIGOXIN PEDIATRIC is classified as Category A/B. Digoxin crosses the placenta. First trimester: No increased risk of major malformations reported in human studies. Second/third trimester: Potential for fetal toxicity (e.g., brady. LANOXIN PEDIATRIC is classified as Category C. First trimester: No evidence of increased risk of major malformations. Second/third trimester: Potential for fetal bradycardia, cardiac arrhythmias, and intrauterine growth restric. Always consult a maternal-fetal medicine specialist before taking either drug during pregnancy or lactation.