Source of information: Drugbank (External Link). Last updated on: 3rd July 18
*Trade Name used in the content below may not be the same as the HSA-registered product.
Active Ingredient / Synonyms
2-(3-Benzoylphenyl)propionic acid | 3-Benzoyl-alpha-methylbenzeneacetic acid | 3-Benzoyl-α-methylbenzeneacetic acid | 3-Benzoylhydratropic acid | Ketoprofen | L'Acide (benzoyl-3-phenyl)-2-propionique | m-Benzoylhydratropic acid | Orudis (tn) | Ketoprofen |
Ketoprofen, a propionic acid derivative, is a nonsteroidal anti-inflammatory agent (NSAIA) with analgesic and antipyretic properties.
For symptomatic treatment of acute and chronic rheumatoid arthritis, osteoarthritis, ankylosing spondylitis, primary dysmenorrhea and mild to moderate pain associated with musculotendinous trauma (sprains and strains), postoperative (including dental surgery) or postpartum pain.
Mechanism of Action
The anti-inflammatory effects of ketoprofen are believed to be due to inhibition cylooxygenase-2 (COX-2), an enzyme involved in prostaglandin synthesis via the arachidonic acid pathway. This results in decreased levels of prostaglandins that mediate pain, fever and inflammation. Ketoprofen is a non-specific cyclooxygenase inhibitor and inhibition of COX-1 is thought to confer some of its side effects, such as GI upset and ulceration. Ketoprofen is thought to have anti-bradykinin activity, as well as lysosomal membrane-stabilizing action. Antipyretic effects may be due to action on the hypothalamus, resulting in an increased peripheral blood flow, vasodilation, and subsequent heat dissipation.
Ketoprofen is a nonsteroidal anti-inflammatory agent (NSAIA) with analgesic and antipyretic properties. Ketoprofen has pharmacologic actions similar to those of other prototypical NSAIDs, which inhibit prostaglandin synthesis. Ketoprofen is used to treat rheumatoid arthritis, osteoarthritis, dysmenorrhea, and alleviate moderate pain.
Ketoprofen is rapidly and well-absorbed orally, with peak plasma levels occurring within 0.5 to 2 hours.
Rapidly and extensively metabolized in the liver, primarily via conjugation to glucuronic acid. No active metabolites have been identified.
In a 24 hour period, approximately 80% of an administered dose of ketoprofen is excreted in the urine, primarily as the glucuronide metabolite.
Conventional capsules: 1.1-4 hours
Extended release capsules: 5.4 hours due to delayed absorption (intrinsic clearance is same as conventional capsules)
* Oral-dose cl=6.9 +/- 0.8 L/h [Ketoprofen Immediate-release capsules (4 × 50 mg)] * Oral-dose cl=6.8 +/- 1.8 L/h [Ketoprofen Extended-release capsules (1 × 200 mg)] * 0.08 L/kg/h * 0.7 L/kg/h [alcoholic cirrhosis patients]
LD50=62.4 mg/kg (rat, oral).
Symptoms of overdose include drowsiness, vomiting and abdominal pain.
Side effects are usually mild and mainly involved the GI tract. Most common adverse GI effect is dyspepsia (11% of patients). May cause nausea, diarrhea, abdominal pain, constipation and flatulence in greater than 3% of patients.
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