Comparative Pharmacology
Head-to-head clinical analysis: ALEVE D SINUS COLD versus SULINDAC.
Peer-Reviewed Evidence
Head-to-head clinical analysis: ALEVE D SINUS COLD versus SULINDAC.
ALEVE-D SINUS & COLD vs SULINDAC
Comparing the clinical profiles, pharmacokinetic behaviors, and safety indices of these two therapeutic agents.
Naproxen is a nonsteroidal anti-inflammatory drug (NSAID) that inhibits cyclooxygenase (COX-1 and COX-2), reducing prostaglandin synthesis. Pseudoephedrine is a sympathomimetic amine that acts as a decongestant via alpha-adrenergic receptor agonism in the nasal mucosa.
Non-selective cyclooxygenase (COX-1 and COX-2) inhibitor, reducing prostaglandin synthesis. Prodrug converted to active sulfide metabolite which inhibits COX enzymes.
Naproxen 220 mg (as naproxen sodium) and pseudoephedrine HCl 120 mg orally every 12 hours; maximum 2 doses per 24 hours.
150-200 mg orally twice daily, with maximum daily dose 400 mg.
None Documented
None Documented
Clinical Note
moderateSulindac + Digitoxin
"Sulindac may decrease the cardiotoxic activities of Digitoxin."
Clinical Note
moderateSulindac + Deslanoside
"Sulindac may decrease the cardiotoxic activities of Deslanoside."
Clinical Note
moderateSulindac + Acetyldigitoxin
"Sulindac may decrease the cardiotoxic activities of Acetyldigitoxin."
Clinical Note
moderateSulindac + Ouabain
"Sulindac may decrease the cardiotoxic activities of Ouabain."
Naproxen: 12-17 hours (clinical: twice daily dosing); pseudoephedrine: 4-6 hours (clinical: every 4-6 hours).
14 hours (sulfide active metabolite); 3-4 hours (parent sulindac). Steady-state attained in 3-4 days.
Renal elimination: naproxen ~95% (mostly as unconjugated naproxen and 6-O-desmethyl naproxen), pseudoephedrine ~70-90% unchanged. Biliary/fecal: minor (<5% for each).
Primarily renal (about 50% as glucuronide conjugates, 25-30% as sulfide and sulfone metabolites); biliary/fecal elimination accounts for approximately 25-30%.
Category C
Category D/X
NSAID/Decongestant Combination
NSAID