Mechanism of action<unk>  works by reversibly inhibiting both the COX-1 and COX-2 enzymes as a non-selective coxib. This results in the inhibition of prostaglandin synthesis. Prostaglandins act as signaling molecules in the body, inducing inflammation. Thus, by inhibiting COX-1/2,<unk>  induces an anti-inflammatory effect. Pharmacokinetics<unk>  is a minor substrate of CYP1A2 and CYP2C9. It is extensively metabolized in the liver to 6-O-desmethylnaproxen, and both the parent drug and the desmethyl metabolite undergo further metabolism to their respective acylglucuronide conjugated metabolites. An analysis of two clinical trials shows that<unk> 's time to peak plasma concentration occurs between 2–4 hours after oral administration, though<unk>  sodium reaches peak plasma concentrations within 1–2 hours. Pharmacogenetics The pharmacogenetics of<unk>  has been studied in an effort to better understand its adverse effects. In 1998, a small pharmacokinetic (PK) study failed to show that differences in a patient's ability to clear<unk>  from the body could account for differences in a patient's risk of experiencing the adverse effect of a serious gastrointestinal bleed while taking<unk> . However, the study failed to account for differences in the activity of CYP2C9, a drug-metabolizing enzyme that is necessary for clearing<unk> . Studies on the relationship between CYP2C9 genotype and NSAID-induced gastrointestinal bleeds have shown that genetic variants in CYP2C9 that reduce the clearance of major CYP2C9 substrates (like<unk>  increase the risk of NSAID-induced gastrointestinal bleeds, especially for homozygous defective variants. , there were no recommendations for routine CYP2C9 testing for<unk> .
Naproxen
Celecoxib
Ibuprofen
Fenoprofen
Ketoprofen
Aceclofenac
Loxoprofen
Lornoxicam