Comparative Pharmacology
Head-to-head clinical analysis: IBUPROFEN versus INDOCIN.
Head-to-head clinical analysis: IBUPROFEN versus INDOCIN.
Ibuprofen vs INDOCIN
Comparing the clinical profiles, pharmacokinetic behaviors, and safety indices of these two therapeutic agents.
Non-selective inhibition of cyclooxygenase (COX-1 and COX-2), reducing prostaglandin synthesis, leading to anti-inflammatory, analgesic, and antipyretic effects.
Indomethacin is a nonsteroidal anti-inflammatory drug (NSAID) that inhibits cyclooxygenase (COX-1 and COX-2) enzymes, thereby reducing prostaglandin synthesis, which mediates inflammation, pain, and fever. It also decreases renal blood flow and may cause ductus arteriosus closure.
200-800 mg orally every 6-8 hours; maximum 3200 mg/day.
25 mg orally 2-3 times daily; maximum 200 mg/day. Intravenous: 0.5-1 mg/kg as single dose for ductus arteriosus closure.
None Documented
None Documented
Clinical Note
moderateIbuprofen + Gatifloxacin
"Ibuprofen may increase the neuroexcitatory activities of Gatifloxacin."
Clinical Note
moderateIbuprofen + Rosoxacin
"Ibuprofen may increase the neuroexcitatory activities of Rosoxacin."
Clinical Note
moderateIbuprofen + Levofloxacin
"Ibuprofen may increase the neuroexcitatory activities of Levofloxacin."
Clinical Note
moderateIbuprofen + Trovafloxacin
"Ibuprofen may increase the neuroexcitatory activities of Trovafloxacin."
Terminal elimination half-life is 2-4 hours; no accumulation with repeated dosing in normal renal function.
Terminal elimination half-life approximately 4.5 hours (range 2.6–11.2 hours); prolonged in elderly and patients with hepatic impairment.
Renal excretion of conjugated metabolites (about 90% as glucuronide and sulfate conjugates, <10% as unchanged drug); minor biliary/fecal elimination (<5%).
Renal (60% as unchanged drug and glucuronide conjugates), biliary/fecal (33% via enterohepatic circulation).
Category D/X
Category C
NSAID
NSAID