Beta-blocker metabolised by CYP 2D6. Vast clinical experience, and several references, point to non-porphyrinogenicity. The observation of mechanism-based CYP 2D inactivation is a putative alarming one, but the abundance of clinical observation of non-porphyrinogenicity suggests that propranolol is safe to use in acute porphyria.

Beta-receptor blocking agent. Metbolized in the liver by CYP2D6. Possibly also acting as a CYP inhibitor. Frequently used under attacks of acute porphyria. A beneficial effect is believed to be the result of an increase in the amount of heme in the hepatic free regulatory heme-pool. Based on observations in rat liver microsomes some authors suggest that a propranol metabolite causes mechanism-based inactivation of CYPs of the 2D family, the mechanism being binding of the reactive species to an amino acid residue of the active site of the enzyme. Thunell, patient report (n=3): tolerated. Andersson, patient report (n=26): tolerated.

Uneventful use reported in 44 patients with acute porphyria.