Mefenamic acid is a member of the anthranilic acid derivatives (or fenamate) class of NSAID drugs, and is used to treat mild to moderate pain, including menstrual pain, and is sometimes used to prevent migraines associated with menstruation.

Its name derives from its systematic name, dimethylphenylaminobenzoic acid. It was discovered and brought to market by Parke-Davis in the 1960s. It became generic in the 1980s and is available worldwide under many brand names.

Scientists led by Claude Winder from Parke-Davis invented mefenamic acid in 1961, along with fellow members of the class of anthranilic acid derivatives, flufenamic acid in 1963 and meclofenamate sodium in 1964.


Non-steroidal anti-inflammatory drug


Reversibly inhibits cyclooxygenase 1 and 2 (COX 1 and 2) enzymes, which results in decreased prostaglandin
precursors; has anti-pyretic, analgesic and anti-inflammatory properties. Other proposed mechanisms not
fully elucidated (and possibly contributing to the anti-inflammatory effect to varying degrees)
include inhibiting chemotaxis, altering lymphocyte activity, inhibiting neutrophil aggregation/activation and decreasing pro-cytokine activation levels. Mefenamic inhibits the synthesis of prostangladins at the central nervous system and peripherally blocks pain impulse generation; also produces antipyresis effect from inhibition of hypothalamic heat regulating center.


Absorption: Mefenamic acid is absorbed from the gastrointestinal tract. Peak levels of 10mg/l occur after 2 hours of the administration of 1g oral dose to adults.

Distribution: Mefenamic acid has been reported as being greater than 90% bound to albumin. Apparent volume of distribution is 1.06 l/kg.

Metabolism and Excretion: Mefenamic acid is predominantly metabolized by 3 cytochrome P450 enzyme CYP2C9 in the liver, first to a hydroxymethyl derivative (metabolite 1) and then a 3 caboxyl derivative (Metabolite 2). Both metabolites undergo secondary conjugation to form glucunonides. 52% of the dose is recovered in urine, 6% as Mefenamic acid, 25% as metabolite 1 and 25% as metabolite 2. The fecal route of elimination accounts for up to 20% of the dose; mainly in the form of unconjugated 3 carboxymefenamic acid. The plasma levels of unconjugated Mefenamic acid decline with a half-life of approximately 2 hours.


  • Pain and Inflammation in rheumatoid arthritis and osteoarthritis and osteoarthritis
  • Post-operative pain
  • Mild to moderate pain
  • Dysmenorrhea and menorrhagia


  • Hypersensitivity to Mefenamic acid or any other ingredients
  • Inflammatory bowel syndrome
  • Severe heart failure, hepatic failure and renal failure
  • It is contra-indicated in patients with active gastrointestinal ulceration or bleeding. It is contra-indicated in patients with a history recurrent gastro-intestinal ulceration or hemorrhage (two distinct episodes) and in patients with a history of gastrointestinal bleeding or perforation related to previous NSAID therapy. Because the potential exists for cross sensitivity to aspirin, ibuprofen or any other NSAID drugs, Mefenamic acid should not be given to patients who have previously should hypersensitivity reaction to any NSAID. Eg asthma, bronchospasm, rhinitis, angioedema and urticarial) to these medicines.
  • During the last trimester of pregnancy
  • Treatment of pain after coronary artery by-pass graft (CABG) Surgery.


  • Elderly: The elderly has an increased frequency of adverse reactions to NSAIDs especially gastrointestinal bleeding and perforation which may be fatal
  • Respiratory disorders: Caution is required if administered to patients suffering from or previous history of bronchial asthma since NSAIDs have been shown to precipitate bronchospasm in such patients.
  • Hepatic impairment: It should be used with caution in patients with hepatic impairment. There is increased risk of gastrointestinal bleeding and fluid retention. It should be avoided in severe liver disease.
  • Renal Impairment. It should be avoided if possible or used with caution in patients with renal impairment. The lowest effective dose should be used for the shortest time possible. And renal function should be monitored. Sodium and water retention may occur and renal function mat deteriorate, possibly leading to renal failure. Deterioration in renal function has also been reported in after topical use.
  • Cardiovascular and cerebrovascular effects: It should be used with caution in patients with history of cardiac failure, left ventricular dysfunction, hypertension, left ventricular dysfunction, ischaemic heart disease, peripheral arterial disease, cerebrovascular disease, in patients with oedema from any other reasons, in patients with other risks for cardiovascular events.
  • Gastrointestinal bleeding, ulceration and perforation: GI bleeding, ulceration or perforation which can be fatal has been reported with all NSAIDs at any time of treatment, with or without warning symptoms or a previous event of serious GI events. Smoking and alcohol use are added risk factors. The relative risk increases with the dose used in patients with a history of ulcers, particularly if complicated with a type of hemorrhage or perforation and the elderly, fragile, low body weight. Mefenamic acid should be administered with caution and under close supervision in patients in patients with a history of gastrointestinal disease (ulcerative colitis, Crohn’s disease), due to the risk of worsening the disease.
  • SLE and Mixed connective tissue disease: In patients with Systemic lupus erythematosus (SLE) and mixed connective tissue disorders there may be an increased risk of aseptic meningitis.
  • Skin Effects: Serious skin reactions, some of them fatal including exfoliative dermatitis, syndromes Stevens-Johnson syndrome and toxic epidermal necrolysis have been reported very rarely during NSAID therapy.
  • Epilepsy: Caution should be excised in patients with epilepsy
  • Pregnancy: Avoiding use of NSAIDs during pregnancy or avoiding them unless the potential benefit outweighs the risk. NSAIDs should be avoided with use especially in the third trimester because it is associated with a risk of closure of fetal ductus arteriosus in utero and possibly persistent pulmonary hypertension of the newborn. In addition, the onset of labour may be delayed and its duration increased.
  • Lactation: Trace amounts of Mefenamic acid may be present in breast milk and transmitted to the nursing infant. Therefore, Mefenamic acid should be avoided in the nursing infant.


  • Adult over 18 years: 500mg 3 times daily
  • Child 12-18 years: Acute pain including dysmenorrhea, menorrhagia, 500mg 3 times daily.
  • Child under 12 years. Not recommended.
  • Elderly (over 65 years) Refer to adult dosing.


  • Gastrointestinal disturbances including discomfort, nausea, diarrhea and occasionally bleeding and ulceration.
  • Paresthesia and fatigue
  • Rarely hypotension
  • Palpitation
  • Glucose intolerance
  • Thrombocytopenia
  • Haemolytic anaemia
  • Aplastic anaemia
  • Hypersensitivity reactions
  • Headache, dizziness,
  • Nervousness
  • Depression
  • Drowsiness
  • Insomnia
  • Vertigo
  • Hearing disturbance such as tinnitus
  • Photosensitivity
  • Haematuria.
  • Fluid retention may occur.


  • Anti-coagulants: It may precipitate the effects of anticoagulants such as heparin.
  • Lithium. Reduce in renal lithium clearance and elevation in plasma lithium levels.
  • Other analgesics including cyclogenase-2 selective inhibitors: Avoid concomitant use of two or more NSAIDs (including aspirin) as this may increase risk of adverse effects.
  • Selective Serotonin Re-Uptake Inhibitors (SSRIs). Increased risk of gastrointestinal bleeding.
  • Anti-hypertensives and diuretics. A reduction in hypertensive and diuretic effect has been observed
  • Aminoglycosides: reduction in renal function in susceptible individuals, decreased elimination of aminoglycoside and increased plasma concentrations.
  • Anti-platelet agents: increased risk of gastro-intestinal ulceration and bleeding.
  • Cardiac Glycosides: NSAIDs may exacerbate cardiac failure, reduce GFR and increase cardiac glycoside levels.
  • Ciclosporin: Risk of nephrotoxicity with Ciclosporin maybe increased with NSAIDs.
  • Corticosteroids: Increased risk of gastrointestinal bleeding or ulceration.
  • Oral Hypoglycemic agents: Inhibition of metabolism of sulfonylurea drugs, prolonged half-life and increased risk of hypoglycaemia.
  • Methotrexate: elimination of the drug can be reduced, resulting increased plasma levels.
  • Mifepristone: NSAIDs should not be taken 8 – 10 days after mifepristone. NSAIDs can reduce the effects of mifepristone.
  • Probenecid: Reduction in metabolism and elimination of NSAIDs and metabolites.
  • Quinolone antibiotics: Patients taking NSAIDs and quinolones may have increased risk of developing convulsions.
  • Tacrolimus. Possible increased risk of nephrotoxicity when NSAIDs given with tacrolimus.
  • Zidovudine. Increased risk of haematological toxicity when NSAIDs given with zidovudine.


Symptoms: These include headache, nausea, vomiting, epigastric pain, gastrointestinal bleeding, rarely diarrhea, disorientation, excitation, coma, drowsiness, tinnitus, fainting, occasionally convulsions. In cases of significant poisoning acute renal failure and renal damage may be possible.


  • Should be treated symptomatically as required.
  • Within one hour of ingestion of a potentially toxic amount, activated charcoal should be considered. Alternatively, in adults, gastric lavage should be considered within one hour of ingestion of a potentially life-threatening overdose.
  • Good urine output should be ensured.
  • Renal and liver function should be closely monitored; patients should be observed for at least four hours for potentially toxic amounts.
  • Frequent prolonged convulsions should be treated with intravenous diazepam.
  • Other measures maybe indicated by the patients’ clinical condition.
  • Haemodialysis is of little value since Mefenamic acid and its metabolites are firmly bound to plasma proteins.