Mirabegron is not an inducer or a mechanism-based inhibitor of CYP 3A4, CYP 2C9 or 2C19.

Mirabegron is a beta-3 adrenergic receptor agonist.

Mirabegron is used in the symptomatic treatment of urgency, increased micturition frequency and/or urgency incontinence as may occur in adult patients with overactive bladder (OAB) syndrome.

Mirabegron is metabolized to pharmacologically inactive glucuronides via multiple pathways, with only minimal involvement of CYP 2D6 and CYP 3A4 (Lee 2013, Krauwinkel 2012). Elimination half-life is approximately 50 hours. Based on in vitro studies, mirabegron is unlikely to inhibit the metabolism of co-administered medicinal products metabolized by the following cytochrome P450 enzymes: CYP1A2, CYP2B6, CYP2C8, CYP2C9, CYP2C19 and CYP2E1, because mirabegron did not inhibit the activity of these enzymes at clinically relevant concentrations. Studies of mirabegron using human liver microsomes and recombinant human CYP enzymes showed that mirabegron is a moderate and time-dependent inhibitor of CYP2D6 and a weak inhibitor of CYP3A (SPC, Takusagawa 2012). The relative abundance of CYP2D6 in the liver is less than 5 per cent of the total CYP isoforms (Mouly 2009 and Pelkonen 2008). The mechanism-based inhibition of CYP2D6 may lead to increased de novo synthesis of CYP2D6, but with the very low relative abundance of CYP2D6 the potential effect on the total heme biosynthetic flux is expected to be minimal. The use of mirabegron is therefore not expected to significantly influence the level of ALA and PGB in patients with an acute porphyria.