Head-to-head clinical analysis & difference comparison: details on mechanism of action, dosing, half-life, interactions, and maternal-fetal safety.
LANOXICAPS vs DIGOXIN PEDIATRIC
Clinician-reviewed, head-to-head comparison of mechanism, dosing, pharmacokinetics, and safety profiles.
Last clinically reviewed: July 2026 · OpiCalc Medical Review Team
Inhibition of Na+/K+-ATPase pump, leading to increased intracellular sodium and calcium, positive inotropy, and increased vagal tone.
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.
Heart failure (NYHA class II-IV) with reduced ejection fraction,Atrial fibrillation (rate control)
Heart failure (FDA-approved for pediatric patients with heart failure),Atrial fibrillation (off-label for rate control in pediatric patients)
0.125-0.25 mg orally daily, initially 0.25 mg daily in divided doses 3-4 times daily, maintenance 0.125-0.25 mg daily.
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.
Terminal elimination half-life is approximately 5-7 days (120-168 hours) in patients with normal renal function; prolonged in renal impairment, necessitating dose adjustment.
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.
Primarily renal excretion as unchanged drug; minor hepatic metabolism via CYP3A4 and glucuronidation.
Primarily renally excreted unchanged; minimal hepatic metabolism (mostly via reduction, hydrolysis, and conjugation in older children).
Digitoxin is primarily excreted via the kidneys (approx. 70-80%) as unchanged drug and metabolites; the remainder undergoes biliary/fecal elimination (approx. 20-30%).
Renal excretion accounts for 50-70% of elimination as unchanged drug; biliary/fecal excretion accounts for 30-40%, primarily as metabolites; enterohepatic recirculation occurs.
Digitoxin is approximately 90-97% bound to serum proteins, primarily albumin.
25% bound to serum albumin; binding decreases in uremia and hyperbilirubinemia.
Volume of distribution is approximately 0.6 L/kg, indicating extensive tissue binding and distribution; the large Vd reflects accumulation in tissues like myocardium and skeletal muscle.
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).
Oral bioavailability is virtually 100% (90-100%) for Lanoxicaps (digitoxin), with consistent absorption from the gastrointestinal tract.
Oral: 60-80% (elixir 70-85%, tablets 60-75%); IM: 70-85% (but erratic absorption and pain limit use); IV: 100%.
For e GFR <50 m L/min, reduce dose by 50% or extend dosing interval: e GFR 35-50 m L/min: 0.125 mg every 24-48 hours; e GFR 10-34 m L/min: 0.125 mg every 48-72 hours; e GFR <10 m L/min: 0.125 mg every 72-96 hours.
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.
Severe hepatic impairment (Child-Pugh class C) requires dose reduction by 50-75%; monitor digoxin levels. Avoid in fulminant hepatitis.
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.
Neonates: 4-6 mcg/kg/day; Infants: 6-10 mcg/kg/day; Children 1-5 years: 10-15 mcg/kg/day; Children 6-12 years: 8-10 mcg/kg/day; Adolescents: 3-5 mcg/kg/day. All doses given orally.
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.
Start at lower dose (0.0625-0.125 mg daily) due to reduced renal function and lean body mass; monitor serum creatinine and digoxin 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.
Toxicity: Narrow therapeutic index; monitor serum levels; avoid in patients with ventricular fibrillation or outflow obstruction.
Toxicity can be life-threatening. Use caution in renal impairment, electrolyte disturbances (hypokalemia, hypomagnesemia, hypercalcemia). Narrow therapeutic index requires monitoring.
Monitor for digitalis toxicity (anorexia, nausea, visual disturbances, arrhythmias). Adjust dose in renal impairment, hypokalemia, hypomagnesemia, hypercalcemia, and hypothyroidism.
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.
Ventricular fibrillation,Hypersensitivity to digitalis glycosides,Wolff-Parkinson-White syndrome with atrial fibrillation,Second- or third-degree AV block (without pacemaker),Hypertrophic obstructive cardiomyopathy
Ventricular fibrillation, hypersensitivity to digitalis preparations, hypokalemia (uncorrected), hypercalcemia (uncorrected), AV block (second or third degree) unless pacemaker present.
High-fiber foods (bran, oats) and certain foods containing pectin can reduce digoxin absorption; take Lanoxicaps on an empty stomach or at least 1 hour before or 2 hours after meals. St. John's Wort may decrease digoxin levels. Avoid licorice root, which can cause hypokalemia and increase toxicity. Consistent dietary potassium intake is important; avoid potassium supplements unless directed.
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.
FDA Pregnancy Category C. First trimester: digitalis glycosides cross placenta; animal studies show fetotoxicity, but no adequate human data. Second/third trimester: risk of fetal bradycardia, low birth weight; therapeutic levels near toxic for fetus. Use only if maternal benefit outweighs risk.
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.
Digoxin is excreted into breast milk at low levels (M/P ratio ~0.6–0.9); infant exposure is subtherapeutic. Considered compatible with breastfeeding, but monitor infant for signs of digoxin toxicity (e.g., arrhythmias, nausea).
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.
Increased volume of distribution and renal clearance in pregnancy may lower digoxin levels; dose adjustment often needed in third trimester. Monitor levels frequently and increase dose if subtherapeutic. Postpartum, reduce dose as clearance normalizes.
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.
Lanoxicaps (digoxin) has a high bioavailability (90-100%) compared to standard digoxin tablets; adjust dose when switching formulations to avoid toxicity. Monitor renal function and electrolytes (especially potassium, magnesium, calcium) closely; hypokalemia increases digoxin toxicity risk. Digoxin toxicity can present with arrhythmias (e.g., bidirectional ventricular tachycardia, atrial tachycardia with block) and visual disturbances (yellow-green halos). Use digoxin-specific Fab fragments for life-threatening toxicity. Therapeutic drug monitoring: draw levels at least 6-8 hours after dose; target 0.5-0.9 ng/m L for heart failure, 0.8-2.0 ng/m L for atrial fibrillation.
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.
Take exactly as prescribed; do not miss doses or double up. If a dose is missed, skip it unless close to next dose.,Do not switch between Lanoxicaps and standard digoxin tablets without your doctor's approval due to different absorption.,Report symptoms of toxicity: nausea, vomiting, diarrhea, confusion, visual changes (blurred vision, yellow-green halos), or irregular heartbeat.,Keep regular appointments for blood tests to monitor digoxin levels, kidney function, and electrolytes.,Avoid over-the-counter medications, especially antacids, kaolin-pectin, and some laxatives, which can affect absorption.,Maintain consistent dietary intake of potassium-rich foods (bananas, oranges) and avoid extreme changes in diet.
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.
No interactions on record
"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."
Explore head-to-head clinical comparisons of other medications in the same therapeutic classes.
Common clinical questions about LANOXICAPS vs DIGOXIN PEDIATRIC, answered by our medical review team.
LANOXICAPS is a Cardiac Glycoside that works by Inhibition of Na+/K+-ATPase pump, leading to increased intracellular sodium and calcium, positive inotropy, and increased vagal tone.. 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.. They differ in pharmacokinetic profiles, FDA-approved indications, and side effect profiles.
Potency comparisons between LANOXICAPS and DIGOXIN 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 LANOXICAPS is: 0.125-0.25 mg orally daily, initially 0.25 mg daily in divided doses 3-4 times daily, maintenance 0.125-0.25 mg daily.. 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.. 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 LANOXICAPS and DIGOXIN 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. LANOXICAPS is classified as Category C. FDA Pregnancy Category C. First trimester: digitalis glycosides cross placenta; animal studies show fetotoxicity, but no adequate human data. Second/third trimester: risk of fetal . 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. Always consult a maternal-fetal medicine specialist before taking either drug during pregnancy or lactation.