Head-to-head clinical analysis & difference comparison: details on mechanism of action, dosing, half-life, interactions, and maternal-fetal safety.
KETOPROFEN vs ACTRON
Clinician-reviewed, head-to-head comparison of mechanism, dosing, pharmacokinetics, and safety profiles.
Last clinically reviewed: July 2026 · OpiCalc Medical Review Team
Non-selective cyclooxygenase (COX-1 and COX-2) inhibitor, reducing prostaglandin synthesis; also inhibits leukotriene synthesis and has direct membrane-stabilizing effects.
Acetaminophen (paracetamol) is a non-opioid analgesic and antipyretic. Its mechanism is not fully understood but involves inhibition of cyclooxygenase (COX) enzymes in the central nervous system, reducing prostaglandin synthesis. It also modulates the endocannabinoid system and serotonergic pathways.
Rheumatoid arthritis,Osteoarthritis,Ankylosing spondylitis,Mild to moderate pain,Dysmenorrhea,Acute gouty arthritis (off-label)
Mild to moderate pain,Fever
Oral: 75 mg three times daily or 50 mg four times daily; maximum 300 mg/day. Intravenous: 100 mg every 12-24 hours, infused over 15-30 minutes.
Oral: 400 mg every 4-6 hours as needed for pain; maximum 1200 mg/day.
Terminal elimination half-life: 2-4 hours; clinical context: short half-life allows for quick drug clearance but requires frequent dosing; may be prolonged in elderly or renal impairment.
Terminal elimination half-life 2-4 hours; prolonged to 6-12 hours in elderly or renal impairment (Cr Cl <30 m L/min).
Hepatic metabolism via cytochrome P450 (CYP) enzymes, primarily CYP3A4 and CYP2C9; conjugation with glucuronic acid; minor hydrolysis to metabolites.
Primarily metabolized in the liver via glucuronidation (UGT1A1, UGT1A6, UGT1A9), sulfation (SULT1A1, SULT1A3), and oxidation (CYP2E1, CYP3A4) to form the toxic metabolite N-acetyl-p-benzoquinone imine (NAPQI), which is detoxified by glutathione.
Renal: ~80% (60% as glucuronide conjugates, 20% as unchanged drug); Biliary/Fecal: ~20% via bile.
Renal: 90% as unchanged drug; biliary/fecal: 10% as metabolites.
99% bound, primarily to albumin; free fraction increases in hypoalbuminemia.
>99% bound to albumin.
0.1-0.2 L/kg; clinical meaning: low Vd indicates limited tissue distribution, primarily confined to plasma and extracellular fluid; higher in elderly due to increased body fat.
0.1-0.2 L/kg; indicates limited extravascular distribution.
Oral: ~90% (capsules); Topical: 5-10% (systemic absorption); Rectal: ~80%; Intramuscular: ~100%.
Oral: 70-90% (first-pass metabolism minimal); IV: 100%.
Cr Cl >50 m L/min: no adjustment. Cr Cl 25-50 m L/min: reduce dose to 50% of normal. Cr Cl <25 m L/min: avoid use or maximum 50 mg twice daily.
GFR <30 m L/min: Avoid use. GFR 30-50 m L/min: Reduce dose to 50% of normal, maximum 600 mg/day.
Child-Pugh A: no adjustment. Child-Pugh B: reduce dose by 50%. Child-Pugh C: avoid use.
Child-Pugh Class B: Reduce dose by 50%; maximum 600 mg/day. Child-Pugh Class C: Contraindicated.
Children ≥6 months: oral 1-2 mg/kg/day divided every 6-8 hours; maximum 4 mg/kg/day. Not to exceed adult maximum.
Children ≥12 years: 400 mg orally every 6-8 hours as needed; maximum 1200 mg/day. Children <12 years: Not recommended.
Initiate at lowest effective dose (e.g., 50 mg twice daily); use short duration; monitor renal function, GI bleeding, and cardiovascular risk.
Initiate at 200 mg every 6-8 hours; maximum 600 mg/day due to increased risk of gastrointestinal bleeding and renal impairment.
Non-steroidal anti-inflammatory drugs (NSAIDs) cause an increased risk of serious cardiovascular thrombotic events, including myocardial infarction and stroke, which can be fatal. This risk may increase with duration of use. Patients with cardiovascular disease or risk factors may be at greater risk. NSAIDs are contraindicated for treatment of perioperative pain in the setting of coronary artery bypass graft (CABG) surgery.
Acetaminophen has been associated with cases of acute liver failure, sometimes resulting in liver transplant and death. Most cases involve use of acetaminophen at doses exceeding 4000 mg per day, often involving more than one acetaminophen-containing product.
Cardiovascular thrombotic events; gastrointestinal bleeding, ulceration, and perforation; hypertension; congestive heart failure; renal toxicity; anaphylactoid reactions; serious skin reactions; hematologic toxicity; hepatic toxicity; use with caution in patients with asthma or history of GI bleeding.
Hepatotoxicity: risk increased with chronic alcohol use, liver disease, or use of other acetaminophen-containing products. Avoid exceeding 4000 mg/day. Severe skin reactions: Stevens-Johnson syndrome, toxic epidermal necrolysis, acute generalized exanthematous pustulosis. Hypersensitivity reactions: anaphylaxis.
History of hypersensitivity to ketoprofen, aspirin, or other NSAIDs; active peptic ulcer disease; history of gastrointestinal bleeding or perforation; severe renal impairment; severe hepatic impairment; during perioperative pain in CABG surgery.
Severe hepatic impairment or active liver disease. Known hypersensitivity to acetaminophen or any component of the formulation.
Avoid alcohol as it increases the risk of GI bleeding. Taking with food may reduce gastrointestinal irritation but delays absorption.
Avoid alcohol; may increase risk of GI bleeding. No specific food restrictions, but taking with food can reduce gastrointestinal irritation. Maintain adequate hydration to prevent renal impairment.
First trimester: Avoid due to risk of spontaneous abortion and major congenital malformations (cardiac, gastroschisis). Second trimester: Avoid if possible; associated with oligohydramnios, constriction of ductus arteriosus. Third trimester: Contraindicated due to risk of premature closure of ductus arteriosus, oligohydramnios, fetal nephrotoxicity, and periventricular hemorrhage.
First trimester: Based on animal studies and limited human data, possible increased risk of cardiovascular and neural tube defects. Second/third trimester: Risk of premature closure of ductus arteriosus and oligohydramnios with prolonged use. Avoid after 30 weeks gestation.
Compatible with caution. Small amounts excreted in breast milk (M/P ratio ~0.01-0.1). Due to risk of infant toxicity (e.g., gastrointestinal effects, renal impairment), consider alternative analgesics. Monitor infant for drowsiness, poor feeding, or rash.
Excreted in breast milk; M/P ratio 0.15. Low oral bioavailability to infant; considered compatible with breastfeeding. Monitor infant for sedation or feeding problems.
No specific dose adjustments recommended; use lowest effective dose for shortest duration. Increased clearance in pregnancy may necessitate dose adjustment, but avoid in third trimester. Use with caution in first and second trimesters due to maternal volume expansion and increased renal clearance.
Dose adjustment not typically required; however, due to increased renal clearance and volume of distribution in pregnancy, higher doses may be needed to achieve therapeutic effect. Use lowest effective dose for shortest duration.
Maximum analgesic effect occurs at 50 mg oral doses; higher doses increase GI toxicity without additional pain relief. Use with caution in patients with renal impairment as ketoprofen decreases renal blood flow. Avoid use with other NSAIDs, including aspirin, due to increased ulcer risk. Ketoprofen is highly protein-bound; monitor for displacement interactions with warfarin and oral hypoglycemics.
ACTRON (ketorolac tromethamine) is a nonsteroidal anti-inflammatory drug (NSAID) for short-term management of moderate to severe acute pain, typically not exceeding 5 days due to risk of GI bleeding, renal impairment, and cardiovascular events. Avoid in patients with active peptic ulcer disease, bleeding diathesis, or advanced renal disease. Monitor renal function and signs of bleeding. Use lowest effective dose for shortest duration. May cause bronchospasm in aspirin-sensitive asthma.
Take with food or milk to reduce stomach upset.,Do not exceed recommended dose; taking more does not provide extra pain relief.,Avoid alcohol while taking this medication.,Contact your doctor immediately if you experience black or bloody stools, chest pain, or signs of an allergic reaction.,Do not take with other NSAIDs or aspirin without consulting your healthcare provider.
Take with food or milk to reduce stomach upset.,Do not take for more than 5 days as prescribed; longer use increases risk of serious side effects.,Avoid alcohol while taking this medication to lower risk of stomach bleeding.,Report any signs of bleeding (e.g., black stools, vomiting blood), unusual bruising, or decreased urination.,Do not take with other NSAIDs (e.g., ibuprofen, naproxen) or aspirin without consulting your doctor.,Inform your doctor about all medications, especially blood thinners (e.g., warfarin) and diuretics.,If you have asthma, be aware of potential bronchospasm; seek immediate help if you have breathing trouble.,Not recommended during pregnancy, especially in the third trimester.
"The concurrent use of ketoprofen, a nonsteroidal anti-inflammatory drug (NSAID), with gemeprost, a synthetic prostaglandin E1 analogue used for cervical ripening and induction of labor, may antagonize the therapeutic effects of gemeprost. Ketoprofen inhibits cyclooxygenase (COX) enzymes, reducing prostaglandin synthesis, which directly opposes the prostaglandin-mediated actions of gemeprost, such as cervical softening and uterine contraction. This pharmacodynamic antagonism can lead to decreased efficacy of gemeprost in achieving cervical ripening or inducing labor, potentially prolonging the induction-to-delivery interval or necessitating alternative interventions."
"Amodiaquine inhibits CYP2C9, the primary enzyme responsible for metabolizing ketoprofen. This results in decreased clearance and elevated plasma concentrations of ketoprofen, increasing the risk of dose-dependent adverse effects such as gastrointestinal bleeding, renal impairment, and central nervous system toxicity. Clinically, patients may experience heightened analgesic and anti-inflammatory effects, but also a greater propensity for NSAID-related toxicity."
"Lumacaftor, a strong cytochrome P450 (CYP) 3A4 inducer, significantly decreases the systemic exposure of ketoprofen, a CYP3A4 substrate, by increasing its hepatic metabolism. This interaction can lead to reduced ketoprofen plasma concentrations, potentially compromising its analgesic and anti-inflammatory efficacy. Clinically, patients may experience suboptimal pain relief or require alternative pain management strategies."
No interactions on record
Explore head-to-head clinical comparisons of other medications in the same therapeutic classes.
Common clinical questions about KETOPROFEN vs ACTRON, answered by our medical review team.
KETOPROFEN is a NSAID that works by Non-selective cyclooxygenase (COX-1 and COX-2) inhibitor, reducing prostaglandin synthesis; also inhibits leukotriene synthesis and has direct membrane-stabilizing effects.. ACTRON is a NSAID that works by Acetaminophen (paracetamol) is a non-opioid analgesic and antipyretic. Its mechanism is not fully understood but involves inhibition of cyclooxygenase (COX) enzymes in the central nervous system, reducing prostaglandin synthesis. It also modulates the endocannabinoid system and serotonergic pathways.. They differ in pharmacokinetic profiles, FDA-approved indications, and side effect profiles.
Potency comparisons between KETOPROFEN and ACTRON depend on the specific clinical indication. These are both NSAID agents and are not directly interchangeable by dose. A physician or clinical pharmacist should guide any therapeutic switching decisions.
The standard adult dose of KETOPROFEN is: Oral: 75 mg three times daily or 50 mg four times daily; maximum 300 mg/day. Intravenous: 100 mg every 12-24 hours, infused over 15-30 minutes.. The standard adult dose of ACTRON is: Oral: 400 mg every 4-6 hours as needed for pain; maximum 1200 mg/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 KETOPROFEN and ACTRON 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. KETOPROFEN is classified as Category D/X. First trimester: Avoid due to risk of spontaneous abortion and major congenital malformations (cardiac, gastroschisis). Second trimester: Avoid if possible; associated with oligohy. ACTRON is classified as Category C. First trimester: Based on animal studies and limited human data, possible increased risk of cardiovascular and neural tube defects. Second/third trimester: Risk of premature closur. Always consult a maternal-fetal medicine specialist before taking either drug during pregnancy or lactation.