Head-to-head clinical analysis & difference comparison: details on mechanism of action, dosing, half-life, interactions, and maternal-fetal safety.
ACYLANID 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
Acylanid is a cardiac glycoside that inhibits the Na+/K+-ATPase pump, leading to increased intracellular sodium and calcium concentrations, which enhances myocardial contractility.
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,Atrial fibrillation,Atrial flutter
Heart failure (FDA-approved for pediatric patients with heart failure),Atrial fibrillation (off-label for rate control in pediatric patients)
0.1 mg IV bolus over 5 minutes, followed by 0.1 mg IV after 1 hour if needed; then 0.1-0.2 mg orally every 6-8 hours for maintenance. Maximum cumulative dose: 0.4 mg IV.
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 half-life 33–36 hours (anuric patients up to 110 hours); requires dose adjustment in renal impairment.
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.
Hepatic metabolism via hydrolysis and conjugation; not significantly metabolized by CYP enzymes.
Primarily renally excreted unchanged; minimal hepatic metabolism (mostly via reduction, hydrolysis, and conjugation in older children).
Renal (≈70% as unchanged drug), biliary/fecal (≈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.
25–30% bound to albumin.
25% bound to serum albumin; binding decreases in uremia and hyperbilirubinemia.
7.5–10 L/kg; wide distribution indicating extensive tissue binding.
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: 70–85% (variable, dependent on gastrointestinal absorption).
Oral: 60-80% (elixir 70-85%, tablets 60-75%); IM: 70-85% (but erratic absorption and pain limit use); IV: 100%.
GFR <30 m L/min: reduce dose by 50% and extend dosing interval to every 12-24 hours. GFR 30-50 m L/min: consider 25% dose reduction. Monitor digoxin levels.
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.
Child-Pugh Class B: reduce dose by 25-50%. Child-Pugh Class C: use with caution, reduce dose by 50% and monitor levels. Not recommended in severe hepatic impairment.
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.
Loading dose: 10-15 mcg/kg IV over 5 minutes. Maintenance: 5-10 mcg/kg orally every 8-12 hours. Maximum daily dose: 250 mcg in children <2 years, 500 mcg in older children.
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.
Initiate with 50% of usual adult dose due to reduced renal function and increased sensitivity. Maximum loading dose: 0.2 mg IV. Maintenance: 0.1 mg every 12 hours. Monitor electrolytes and ECG.
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.
None.
Toxicity can be life-threatening. Use caution in renal impairment, electrolyte disturbances (hypokalemia, hypomagnesemia, hypercalcemia). Narrow therapeutic index requires monitoring.
Risk of digitalis toxicity; monitor renal function and electrolytes; caution in hypokalemia, hypomagnesemia, and hypercalcemia.
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 cardiac glycosides,Digitalis toxicity
Ventricular fibrillation, hypersensitivity to digitalis preparations, hypokalemia (uncorrected), hypercalcemia (uncorrected), AV block (second or third degree) unless pacemaker present.
Avoid high-potassium foods (bananas, oranges, spinach) unless directed; hypokalemia increases toxicity. Take with food to reduce GI upset. Do not take with high-fiber meals as may reduce absorption.
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.
Acylanid is a cardiac glycoside with limited data in pregnancy. First trimester: No specific malformations reported, but potential for fetal cardiac effects due to mechanism. Second and third trimesters: Maternal toxicity (arrhythmias, electrolyte disturbances) may cause fetal hypoxia or growth restriction. Avoid toxicity. Category C.
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.
Acylanid is excreted into breast milk in low amounts (M/P ratio not established; estimated <1% of maternal dose). No adverse effects reported in nursing infants. Use with caution, monitor infant for bradycardia or arrhythmias.
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 reduce serum levels; monitor drug levels and adjust dose to maintain therapeutic range (0.5-2 ng/m L). Start at lower doses if hypokalemia or preeclampsia present.
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.
Acylanid (lanatoside C) is a digitalis glycoside with rapid onset (IV 10-30 min) and moderate duration; use in atrial fibrillation with rapid ventricular response, especially in acute settings. Monitor renal function due to renal elimination; toxicity risk increases with hypokalemia, hypomagnesemia, hypercalcemia. Adjust dose in renal impairment (Cr Cl <50 m L/min). Therapeutic drug monitoring: target serum level 0.5-2 ng/m L (drawn >6-8 hours post-dose).
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 skip doses or double up. Missed dose: take if within 12 hours, otherwise skip.,Monitor for signs of toxicity: nausea, vomiting, diarrhea, visual disturbances (yellow-green halos, blurred vision), confusion, irregular heartbeat.,Avoid OTC medications without consulting prescriber, especially antacids, laxatives, and antiarrhythmics.,Keep regular appointments for blood tests (digoxin level, kidney function, electrolytes).,Report weight gain >2 lbs/day, swelling, shortness of breath, or palpitations.
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 ACYLANID vs DIGOXIN PEDIATRIC, answered by our medical review team.
ACYLANID is a Cardiac Glycoside that works by Acylanid is a cardiac glycoside that inhibits the Na+/K+-ATPase pump, leading to increased intracellular sodium and calcium concentrations, which enhances myocardial contractility.. 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 ACYLANID 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 ACYLANID is: 0.1 mg IV bolus over 5 minutes, followed by 0.1 mg IV after 1 hour if needed; then 0.1-0.2 mg orally every 6-8 hours for maintenance. Maximum cumulative dose: 0.4 mg IV.. 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 ACYLANID 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. ACYLANID is classified as Category C. Acylanid is a cardiac glycoside with limited data in pregnancy. First trimester: No specific malformations reported, but potential for fetal cardiac effects due to mechanism. Secon. 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.