text: Parecoxib sodium is a water-soluble inactive ester amide prodrug of valdecoxib, a novel second-generation COX-2-specific inhibitor and the first such agent to be developed for injectable use. It is rapidly converted by hepatic enzymatic hydrolysis to the active form valdecoxib. The compound then undergoes another conversion, which involves both cytochrome P450-mediated pathway (CYP2C9, CYP3A4) and non-cytochrome P450-mediated pathway, to hydroxylated metabolite and glucuronide metabolite. The hydroxylated metabolite, that also has weak COX-2-specific inhibitory properties, is then further metabolized by non-cytochrome P450 pathway to a glucuronide metabolite. These metabolites are excreted in the urine.
  After intra-muscular administration of Parecoxib sodium peak plasma concentration is reached within 15 minutes. The plasma concentration decreases rapidly after administration because of a rather short serum half-life, which is about 15–52 minutes. This can be explained by the rapid formation of Valdecoxib. In contrast to the rapid clearance of Parecoxib, plasma concentration of Valdecoxib declines slowly because of a longer half-life. On the other hand, when Valdecoxib is taken orally it is absorbed rapidly (1–2 hours), but presence of food can delay peak serum concentration. It then undergoes the same metabolism that is described above. It is extensively protein-bound (98%), and the plasma half-life is about 7–8 hours. Note that the half-life can be significantly prolonged in the elderly or those with hepatic impairment, and can lead to drug accumulation.
  The hydroxyl metabolite reaches its highest mean plasma concentration within 3 to 4 hours from administration, but it is considerably lower than of Valdecoxib or about 1/10 of the plasma levels of Valdecoxib.