| Indication |
For the treatment of osteoarthritis and dysmenorrhoea |
| Pharmacodynamics |
Valdecoxib, a selective cyclooxygenase-2 (COX-2) inhibitor, is
classified as a nonsteroidal anti-inflammatory drug (NSAID). Valdecoxib
is used for its anti-inflammatory, analgesic, and antipyretic activities
in the management of osteoarthritis (OA) and for the treatment of
dysmenorrhea or acute pain. Unlike celecoxib, valdecoxib lacks a
sulfonamide chain and does not require CYP450 enzymes for metabolism. |
| Mechanism of action |
Both COX-1 and COX-2 catalyze the conversion of arachidonic acid
to prostaglandin (PG) H2, the precursor of PGs and thromboxane.
Valdecoxib selectively inhibits the cyclooxygenase-2 (COX-2) enzyme,
important for the mediation of inflammation and pain. Unlike
non-selective NSAIDs, valdecoxib does not inhibit platelet aggregation. |
| Absorption |
Oral bioavailability is 83%. |
| Volume of distribution |
|
| Protein binding |
98% |
| Metabolism |
Hepatic (involves CYP3A4 and 2C9) |
| Route of elimination |
Valdecoxib is eliminated predominantly via hepatic metabolism with
less than 5% of the dose excreted unchanged in the urine and feces.
About 70% of the dose is excreted in the urine as metabolites, and about
20% as valdecoxib N-glucuronide. |
| Half life |
8-11 hours |
| Clearance |
- oral cl=6 L/h
- 6 – 7 L/h [In patients undergoing hemodialysis]
- 6 – 7 L/h [healthy elderly subjects]
|
| Toxicity |
Symptoms following acute NSAID overdoses are usually limited to
lethargy, drowsiness, nausea, vomiting, and epigastric pain, which are
generally reversible with supportive care. Gastrointestinal bleeding can
occur. Hypertension, acute renal failure, respiratory depression and
coma may occur, but are rare. |
