Ketoprofen is a substrate of CYP2C9. It is not listed as a mechanism-based inhibitor or inducer of any CYP enzymes and is therefore regarded as probably not porphyrinogenic. This classification is supported by 45 clinical reports of uneventful use. Risk for gastrointestinal adverse events in the form of nausea, vomiting, abdominal pain, diarrhoea and dyspepsia motivates vigilance against insufficient intake of food, especially of carbohydrate.

Dexketoprofen is the S-(+)-enantiomer of ketoprofen.

Dexketoprofen is indicated for the treatment of symptomatic treatment of pain of mild to moderate intensity, such as musculoskeletal pain, dysmenorrhoea and dental pain. Common side effects that can be potentially porphyrinogenic through reduction in carbohydrate intake and that also can be confused with an acute porphyria attack are nausea, vomiting, abdominal pain, diarrhoea and dyspepsia.

Ketoprofen exhibits little stereoselectivity in its pharmacokinetics. The data generated using non-stereospecific assays may therefore be used to explain the pharmacokinetics of individual enantiomers (Jamali 1990). Ketoprofen is listed as a substrate of CYP2C9 (Holstein 2012 and Zhou 2009). Dexketoprofen is not bioinverted to R-(-)-ketoprofen in humans (Baranoj 2001). Ketoprofen is glucuroconjugated and excreted in urine (Jamali 1990). Half-life elimination is 1.5-4 hours.

Ketoprofen (the racemate mixture with R- and dexketoprofen) is listed as thought to be safe for use in acute porphyria (Moore 1997).

Ketoprofen (the racemate mixture with R- and dexketoprofen): uneventful use reported in 45 patients with acute porphyria.