Oxybutynin is not an inducer or mechanism-based inhibitor of any major CYP enzymes, and therefore no pharmacokinetic porphyrinogenic effects are suspected.

Oxybutynin is an anticholinergic spasmolytic used in the treatment of urinary incontinence, urgency and frequency in unstable bladder conditions. It may also be used in the treatment of hyperhidrosis. It may be administered by the oral, rectal, transdermal or intravesical route.

Oxybutynin is metabolized primarily by CYP3A4. It undergoes extensive first pass gastric and hepatic metabolism and the bioavailability of oxybutynin from orally administered preparations is about 6 %. The plasma level of the pharmacologically active metabolite, desethyloxybutynin, is about 5 to 12 times greater than oxybutynin following oral ingestion (Kennelly 2010 FDA label, SPC). The half-life of oxybutynin is approximately 2 to 3 hours. In an in vitro study oxybutynin was found not to inhibit major human CYPs at clinically relevant concentrations. This study also concluded that oxybutynin is not a time-dependent inhibitor. (Dahlinger 2017). In another in vitro study it was observed a 50% reduction in CYP3A4 activity at oxybutynin concentrations that might theoretically occur in the gut wall from orally administered preparations (Lukkari 1998).

Uneventful use reported in 3 patients with acute porphyria.