Dolfenal Mechanism of Action

250 mg: This product contains mefenamic acid which belongs to a group of medicines called non-steroidal anti-inflammatory drugs (NSAIDs). Like other NSAIDs, mefenamic acid works by changing the body's chemical response to pain, swelling and fever, resulting in relief of symptoms of inflammation (e.g., swelling, redness) and relief of pain.
500mg: Pharmacology: Pharmacodynamics: Mefenamic acid exhibits anti-inflammatory, analgesic and antipyretic activities. It inhibits cyclooxygenase (COX)-1 and COX-2 isoenzymes, thus inhibiting prostaglandin synthesis in body tissues. Prostaglandins sensitize pain receptors to mechanical stimulation and to other chemical mediators (e.g., bradykinin, histamine).
Unlike other nonsteroidal anti-inflammatory drugs (NSAIDs), mefenamic acid appears to compete with prostaglandins for binding at the prostaglandin receptor site and thus potentially affect prostaglandins that have already been formed.
The anti-inflammatory, analgesic and antipyretic effects of mefenamic acid appear to result from inhibition of prostaglandin synthesis. These effects appear to be mediated principally through inhibition of COX-2 isoenzymes at inflammation sites.
Pharmacokinetics: Mefenamic acid is rapidly absorbed after oral administration. Peak plasma concentrations of approximately 10 to 20 mcg/mL are readied in 2 to 4 hours.
Mefenamic acid is extensively bound to plasma proteins (>90%). The volume of distribution is 1.06 L/kg, following a 500 mg oral dose. It is not known if the drug or its metabolites cross the placenta. The drug is distributed into milk in very small amounts.
Mefenamic acid has a plasma half-life of two hours. Mefenamic acid is metabolized extensively in the aver by cytochrome P-450 (CYP) isoenzyme 2C9 to 3'-hydroxymethyl mefenamic acid; further oxidation to 3'-carboxyl-mefenamic acid may occur. Glucuronic acid conjugates of the drug and its metabolites are also formed.
About 52% of a dose of mefenamic acid is excreted in urine as glucuronic acid conjugates of the drug and its metabolites. About 20% of a dose is excreted in feces. Mefenamic acid is apparently not dialyzable.
Special Populations: Hepatic Insufficiency: Hepatic metabolism is the significant pathway of mefenamic acid elimination; patients with acute and chronic hepatic disease may require reduced doses of mefenamic acid compared to patients with normal hepatic function.
Renal Insufficiency: Since mefenamic acid, its metabolites and conjugates are primarily excreted by the kidneys, the potential exists for mefenamic acid metabolites to accumulate. Mefenamic acid should not be given to patients with preexisting renal disease or in patients with significantly impaired renal function.
Poor CYP2C9 Metabolizers: In patients who are known or suspected to be poor CYP2C9 metabolizers based on previous history or experience with other CYP2C9 substrates, mefenamic acid should be administered with caution as they may have abnormally high plasma levels due to reduced metabolic clearance.