Head-to-head clinical analysis & difference comparison: details on mechanism of action, dosing, half-life, interactions, and maternal-fetal safety.
ACYLANID vs CRYSTODIGIN
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.
Cardiac glycoside that inhibits the Na+/K+-ATPase pump, leading to increased intracellular sodium, which in turn promotes calcium influx via the Na+/Ca2+ exchanger, resulting in increased myocardial contractility (positive inotropy). It also has negative chronotropic and dromotropic effects via vagomimetic action.
Heart failure,Atrial fibrillation,Atrial flutter
Treatment of heart failure with reduced ejection fraction (FDA-approved),Control of ventricular response in atrial fibrillation and atrial flutter (FDA-approved)
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.
0.5 mg intravenously over 2-4 hours, then 0.25 mg every 6 hours as needed up to a total of 1.5 mg in 24 hours.
Terminal half-life 33–36 hours (anuric patients up to 110 hours); requires dose adjustment in renal impairment.
Terminal elimination half-life approximately 1.6–1.9 days (38–45 hours) in patients with normal renal function; prolonged in renal impairment.
Hepatic metabolism via hydrolysis and conjugation; not significantly metabolized by CYP enzymes.
Primarily renal excretion; minimal hepatic metabolism. Not significantly metabolized by cytochrome P450 enzymes.
Renal (≈70% as unchanged drug), biliary/fecal (≈30%)
Primarily renal excretion of unchanged drug; ~80-90% eliminated in urine, ~10-20% in feces via biliary excretion.
25–30% bound to albumin.
~20–25% bound to plasma proteins, primarily albumin.
7.5–10 L/kg; wide distribution indicating extensive tissue binding.
Vd approximately 5–10 L/kg, indicating extensive tissue distribution; clinical significance: large Vd means low plasma concentration relative to total body load, necessitating loading doses.
Oral: 70–85% (variable, dependent on gastrointestinal absorption).
Oral: 60–80% (variable, depends on formulation and gastrointestinal factors); Intravenous: 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.
Cr Cl 10-50 m L/min: reduce dose by 25-50%; Cr Cl <10 m L/min: reduce dose by 50-75% or use alternative.
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.
Child-Pugh class B: reduce dose by 50%; Child-Pugh class C: avoid use.
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.
Loading dose: 10-20 mcg/kg intravenously over 2-4 hours; maintenance: 5-10 mcg/kg every 6 hours as needed.
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.
Start at lower end of dosing range (0.25 mg intravenously), adjust based on renal function and response, monitor for toxicity.
None.
None.
Risk of digitalis toxicity; monitor renal function and electrolytes; caution in hypokalemia, hypomagnesemia, and hypercalcemia.
Narrow therapeutic index; toxicity can be life-threatening.,Hypokalemia, hypomagnesemia, and hypercalcemia increase risk of digoxin toxicity.,Electrolyte monitoring and dose adjustment in renal impairment.,Patients with acute myocardial infarction, myocarditis, or severe pulmonary disease may be at increased risk of arrhythmias.
Ventricular fibrillation,Hypersensitivity to cardiac glycosides,Digitalis toxicity
Ventricular fibrillation,Known hypersensitivity to digoxin or other digitalis glycosides,Hypercalcemia,Hypokalemia (uncorrected),Atrioventricular block (second- or third-degree) unless a pacemaker is present,Hypertrophic obstructive cardiomyopathy (relative contraindication)
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.
Avoid high-fiber foods and large amounts of bran or pectin, as they may reduce absorption. Grapefruit juice may increase blood levels; limit consumption. Consistent dietary potassium intake is important; extremes (high or low) can affect drug action.
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.
Pregnancy Category C. First trimester: Association with fetal cardiac glycoside toxicity and malformations in animal studies; limited human data. Second trimester: Potential for fetal bradycardia and hypoxia due to placental transfer. Third trimester: Risk of neonatal digitalis toxicity, including arrhythmias and heart block.
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.
Excreted in breast milk in low concentrations (M/P ratio approximately 0.75-1.0). Considered compatible with breastfeeding; monitor infant for signs of toxicity (bradycardia, vomiting).
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.
Increased volume of distribution and renal clearance in second and third trimesters may necessitate dose increases. Monitor serum digoxin levels and adjust to maintain therapeutic range (0.5-1.0 ng/m L).
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).
Crystodigin (digitoxin) has a very long half-life (~5-7 days) requiring careful monitoring to avoid accumulation. Unlike digoxin, it is primarily hepatically metabolized, so renal impairment has less impact on dosing. Always check for drug interactions with CYP3A4 inducers/inhibitors. Therapeutic monitoring of serum levels is essential (target 15-25 ng/m L).
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 miss doses or double up.,Report any symptoms of toxicity: nausea, vomiting, visual disturbances (yellow-green halos), or irregular heartbeat.,Avoid over-the-counter medications without consulting your doctor, especially antacids and laxatives.,Keep regular appointments for blood tests to monitor drug levels and kidney function.,Do not stop suddenly; withdrawal can worsen heart condition.
No interactions on record
No interactions on record
Explore head-to-head clinical comparisons of other medications in the same therapeutic classes.
Common clinical questions about ACYLANID vs CRYSTODIGIN, 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.. CRYSTODIGIN is a Cardiac Glycoside that works by Cardiac glycoside that inhibits the Na+/K+-ATPase pump, leading to increased intracellular sodium, which in turn promotes calcium influx via the Na+/Ca2+ exchanger, resulting in increased myocardial contractility (positive inotropy). It also has negative chronotropic and dromotropic effects via vagomimetic action.. They differ in pharmacokinetic profiles, FDA-approved indications, and side effect profiles.
Potency comparisons between ACYLANID and CRYSTODIGIN 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 CRYSTODIGIN is: 0.5 mg intravenously over 2-4 hours, then 0.25 mg every 6 hours as needed up to a total of 1.5 mg in 24 hours.. 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 CRYSTODIGIN 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. CRYSTODIGIN is classified as Category C. Pregnancy Category C. First trimester: Association with fetal cardiac glycoside toxicity and malformations in animal studies; limited human data. Second trimester: Potential for fe. Always consult a maternal-fetal medicine specialist before taking either drug during pregnancy or lactation.