Head-to-head clinical analysis & difference comparison: details on mechanism of action, dosing, half-life, interactions, and maternal-fetal safety.
ADALAT CC 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
Nifedipine, a dihydropyridine calcium channel blocker, inhibits calcium ion influx across cardiac and smooth muscle cell membranes, leading to vasodilation and decreased 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.
Hypertension,Chronic stable angina,Vasospastic angina (Prinzmetal's angina)
Heart failure (FDA-approved for pediatric patients with heart failure),Atrial fibrillation (off-label for rate control in pediatric patients)
30 mg orally once daily; may titrate to 60 mg or 90 mg once daily based on response and tolerability.
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: 7-10 hours; clinical context: sustained-release formulation provides therapeutic concentrations over 24 hours with once-daily dosing, but half-life does not directly reflect drug effect duration due to slow absorption.
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 CYP3A4; nifedipine is converted to inactive metabolites.
Primarily renally excreted unchanged; minimal hepatic metabolism (mostly via reduction, hydrolysis, and conjugation in older children).
Renal: 70-80% as metabolites, fecal: 15-20% as metabolites, biliary: minimal (<5% unchanged).
Renal excretion accounts for 50-70% of elimination as unchanged drug; biliary/fecal excretion accounts for 30-40%, primarily as metabolites; enterohepatic recirculation occurs.
92-98% bound primarily to albumin.
25% bound to serum albumin; binding decreases in uremia and hyperbilirubinemia.
1.2-1.6 L/kg; clinical meaning: indicates extensive tissue distribution, with higher concentrations in organs such as liver and kidney, and lower in brain due to P-glycoprotein efflux.
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).
65-90% after oral administration; absolute bioavailability of nifedipine in ADALAT CC: approximately 65% due to first-pass metabolism in liver and gut wall.
Oral: 60-80% (elixir 70-85%, tablets 60-75%); IM: 70-85% (but erratic absorption and pain limit use); IV: 100%.
No dose adjustment required for mild to moderate renal impairment. For severe renal impairment (Cr Cl <30 m L/min), start at 30 mg once daily and titrate cautiously.
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.
For mild to moderate hepatic impairment (Child-Pugh A or B), reduce initial dose to 30 mg once daily; for severe impairment (Child-Pugh C), contraindicated or use with extreme caution.
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.
Safety and efficacy not established; use is not recommended in pediatric patients.
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 at 30 mg once daily; titrate slowly due to increased risk of hypotension and higher drug exposure. Monitor closely.
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.
No FDA black box warning.
Toxicity can be life-threatening. Use caution in renal impairment, electrolyte disturbances (hypokalemia, hypomagnesemia, hypercalcemia). Narrow therapeutic index requires monitoring.
Beta-blocker withdrawal: taper if discontinuing; exacerbation of angina,Heart failure: use caution in patients with severe left ventricular dysfunction,Hepatic impairment: reduce dose,Peripheral edema: may occur; differentiate from worsening heart failure,Monitor blood pressure during initiation and titration
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.
Hypersensitivity to nifedipine or any component,Cardiogenic shock,Concurrent use with strong CYP3A4 inducers (e.g., rifampin)
Ventricular fibrillation, hypersensitivity to digitalis preparations, hypokalemia (uncorrected), hypercalcemia (uncorrected), AV block (second or third degree) unless pacemaker present.
Avoid grapefruit and grapefruit juice as they inhibit CYP3A4 metabolism, raising nifedipine levels and risk of toxicity. High-fat meals may increase absorption; take consistently with respect to meals. Avoid alcohol as it may exacerbate hypotension.
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.
Adalat CC (nifedipine) is an extended-release formulation of nifedipine, a dihydropyridine calcium channel blocker. In animal studies, nifedipine has been associated with embryotoxicity, fetotoxicity, and teratogenicity (e.g., digital anomalies, cleft palate) at doses several times the maximum recommended human dose. In humans, data are limited but there is no clear evidence of a significant increase in major congenital malformations. First trimester exposure is not strongly associated with major defects; however, some studies suggest a possible small increase in oral clefts. Second and third trimester use may cause maternal hypotension and subsequent fetal distress (e.g., reduced uteroplacental perfusion). Use near term may theoretically inhibit labor, but nifedipine is used as a tocolytic for preterm labor. Overall, the risk is considered low; however, fetal monitoring is recommended if used in pregnancy. FDA Pregnancy Category C (prior to 2015 categorization).
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.
Nifedipine is excreted into human breast milk in small amounts. The milk-to-plasma (M/P) ratio is approximately 0.56 to 1.0 based on limited data. The estimated daily infant dose via milk is less than 5% of the maternal weight-adjusted dose, which is considered clinically insignificant. No adverse effects have been reported in breastfed infants. However, caution is advised, especially with high maternal doses or prolonged use. The American Academy of Pediatrics considers nifedipine compatible with breastfeeding.
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.
Pregnancy may alter the pharmacokinetics of nifedipine due to increased plasma volume and altered hepatic metabolism. However, specific dosing adjustments for Adalat CC in pregnancy are not well established. In clinical practice, dosing for hypertension in pregnancy (e.g., preeclampsia) often uses immediate-release nifedipine, not extended-release. For Adalat CC, the same dosing as in non-pregnant adults (30-90 mg once daily) is typically used, but titration should be cautious to avoid maternal hypotension. No formal dose adjustment is recommended, but careful monitoring and individualized titration are advised.
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.
Adalat CC (nifedipine extended-release) is a dihydropyridine calcium channel blocker used primarily for hypertension. Avoid in patients with unstable angina or within 4 weeks of myocardial infarction due to reflex tachycardia risk. May cause peripheral edema, especially in higher doses; consider adding an ACE inhibitor if edema is problematic. CYP3A4 inhibitors (e.g., grapefruit juice, macrolides, azole antifungals) significantly increase nifedipine levels; avoid coadministration. Tablet shell may appear intact in stool; this is normal.
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.
Swallow the tablet whole; do not crush or chew.,Do not consume grapefruit or grapefruit juice while taking this medication.,May cause dizziness or lightheadedness; avoid driving if affected.,Notify your doctor if you experience rapid heartbeat, swelling in the ankles or feet, or prolonged erections.,Take exactly as prescribed; do not skip doses or stop abruptly without consulting your doctor.
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 ADALAT CC vs DIGOXIN PEDIATRIC, answered by our medical review team.
ADALAT CC is a Calcium Channel Blocker that works by Nifedipine, a dihydropyridine calcium channel blocker, inhibits calcium ion influx across cardiac and smooth muscle cell membranes, leading to vasodilation and decreased 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 ADALAT CC and DIGOXIN PEDIATRIC depend on the specific clinical indication. These are agents from distinct pharmacological classes and are not directly interchangeable by dose. A physician or clinical pharmacist should guide any therapeutic switching decisions.
The standard adult dose of ADALAT CC is: 30 mg orally once daily; may titrate to 60 mg or 90 mg once daily based on response and tolerability.. 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 ADALAT CC 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. ADALAT CC is classified as Category C. Adalat CC (nifedipine) is an extended-release formulation of nifedipine, a dihydropyridine calcium channel blocker. In animal studies, nifedipine has been associated with embryotox. 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.