Dexibuprofen

Dexibuprofen (= S(+)-ibuprofen) is considered to be the pharmacologically active enantiomer of racemic ibuprofen. Racemic ibuprofen is a non-steroidal substance with antiinflammatory and analgesic effects. Its mechanism of action is thought to be due to inhibition of prostaglandin synthesis.

Bridging studies in order to compare the efficacy of racemic ibuprofen and dexibuprofen in osteoarthritis over a treatment period of 15 days and in dysmenorrhea, including symptoms of pain, have demonstrated at least non-inferiority of dexibuprofen versus racemic ibuprofen at the recommended dosage.

Dexibuprofen is absorbed primarily from the small intestine. After metabolic transformation in the liver (hydroxylation, carboxylation), the pharmacologically inactive metabolites are completely excreted, mainly by the kidneys (90%), but also in the bile. The elimination half-life is 1.8–3.5 hours; the plasma protein binding is about 99%. Maximum plasma levels are reached about 2 hours after oral administration.

The administration of dexibuprofen with a meal delays the time to reach maximum concentrations (from 2.1 hours after fasting conditions to 2.8 hours after non-fasting conditions) and decreases the maximum plasma concentrations (from 20.6 to 18.1 μg/ml, which is of no clinical relevance), but has no effect on the extent of absorption.

Bridging studies on single and repeated dose toxicity, reproduction toxicity and mutagenicity have shown that the toxicological profile of dexibuprofen is comparable to that of racemic ibuprofen.

Racemic ibuprofen inhibited ovulation in the rabbit and impaired implantation in different animal species (rabbit, rat, mouse). Administration of prostaglandin synthesis inhibitors including ibuprofen (mostly in doses higher than used therapeutically) to pregnant animals has been shown to result in increased pre- and postimplantation loss, embryo-fetal lethality and increased incidences of malformations.