| Indication |
For the treatment of rheumatoid arthritis, osteoarthritis, dysmenorrhea, and mild to moderate pain, inflammation, and fever. |
| Pharmacodynamics |
Mefenamic acid, an anthranilic acid derivative, is a member of
the fenamate group of nonsteroidal anti-inflammatory drugs (NSAIDs). It
exhibits anti-inflammatory, analgesic, and antipyretic activities.
Similar to other NSAIDs, mefenamic acid inhibits prostaglandin
synthetase. |
| Mechanism of action |
Mefenamic acid binds the prostaglandin synthetase receptors COX-1
and COX-2, inhibiting the action of prostaglandin synthetase. As these
receptors have a role as a major mediator of inflammation and/or a role
for prostanoid signaling in activity-dependent plasticity, the symptoms
of pain are temporarily reduced. |
| Absorption |
Mefenamic acid is rapidly absorbed after oral administration. |
| Volume of distribution |
- 1.06 L/kg [Normal Healthy Adults (18-45 yr)]
|
| Protein binding |
90% |
| Metabolism |
Mefenamic acid undergoes metabolism by CYP2C9 to 3-hydroxymethyl
mefenamic acid, and further oxidation to a 3-carboxymefenamic acid may
occur. The activity of these metabolites has not been studied. Mefenamic
acid is also glucuronidated directly. |
| Route of elimination |
The fecal route of elimination accounts for up to 20% of the dose,
mainly in the form of unconjugated 3-carboxymefenamic acid.3 The
elimination half-life of mefenamic acid is approximately two hours.
Mefenamic acid, its metabolites and conjugates are primarily excreted by
the kidneys. Both renal and hepatic excretion are significant pathways
of elimination. |
| Half life |
2 hours |
| Clearance |
- Oral cl=21.23 L/hr [Healthy adults (18-45 yrs)]
|
| Toxicity |
Oral, rat LD50: 740 mg/kg. Symptoms of overdose may
include severe stomach pain, coffee ground-like vomit, dark stool,
ringing in the ears, change in amount of urine, unusually fast or slow
heartbeat, muscle weakness, slow or shallow breathing, confusion, severe
headache or loss of consciousness. |
