Common adverse reactions of ticagrelor that can be confused with symptoms of an acute porphyric attack are nausea and constipation.

Ticagrelor is metabolized by CYP 3A4, and has potential for modulating the activity of both CYP 3A4 and CYP 2C9 by mechanisms including activation and inhibition. The inhibition of CYP 3A4 is possibly the most pronounced effect, but this is not a mechanism-based inhibition. The activating effect of CYP 3A4 is not due to induction according to in vitro findings. Ticagrelor has shown in vitro to be a CYP 2C9 inhibitor and activator, but these effects are very weak, and not shown in vivo. Ticagrelors interactions with CYP enzymes are not considered to have porphyrinogenic potential.

Ticagrelor is a cyclopentyltriazolopyrimidine.

Ticagrelor is a platelet aggregation inhibitor that is co-administered with acetylsalicylic acid for the prevention of atherothrombotic events in adult patients. It is administered orally.

Ticagrelor is mainly metabolized by CYP 3A4. The major metabolite of ticagrelor is AR-C124910XX, which is also active as assessed by in vitro binding to the platelet P2Y12 ADP-receptor. The systemic exposure to the active metabolite is approximately 30-40% of that obtained for ticagrelor. Ticagrelor has a half-life of 7 hours, while its active metabolite has a half-life of 9 hours. Ticagrelor is a mild inhibitor and activator of CYP 3A4 (SPC, EMA assessment report). In a drug-drug interaction study the AUC of the CYP 3A4 substrate simvastatin was increased by 56% and the Cmax by 81%, indicating that ticagrelor is a mild inhibitor of CYP 3A4 (Teng 2013a). In vitro studies using preincubation methods showed that the inhibition of CYP 3A4 is not mechanism-based. (Zhou 2011). In an in-vivo study ticagrelor was found to be a week activator (and inhibitor) of the metabolism of midazolam (Teng 2013b). However, the activation of CYP 3A4 is shown in vitro not to be caused by induction (Zhou 2011). Zhou et al (2011) also found ticagrelor to be a weak inducer of CYP 2B6 and 2C9, but the induction was only observed at concentrations 13 times above therapeutic Cmax. In the same study modest inhibition of CYP 2C9 was also reported. In a study with healthy volunteers ticagrelor did not alter the metabolism of the CYP 2C9 substrate tolbutamide, and it is not expected that ticagrelor has interaction potential with drugs metabolized by CYP 2C9 (Teng 2013c).