Patients on immunosuppressive therapy have an increased risk of infections. Since infections have a potential to trigger acute porphyric attacks vigilance is motivated regarding signs or symptoms of infection and/or possible symptoms of a porphyric attack. Side effects like nausea and vomiting may potentially be porphyrinogenic through reduction in carbohydrate intake.

Infections are common in patients using immunosuppressants and since infections might trigger an acute porphyric attack, vigilance regarding signs and symptoms of an infection and/ or a porphyric attack is recommended. Common adverse reactions of teriflunomide that can be confused with an acute porphyric attack are nausea and vomiting. These side effects may potentially be porphyrinogenic if leading to a decrease in carbohydrate intake.

Teriflunomide is only to a minor or negligible degree metabolized by CYP-enzymes. Some inhibitory potential on CYP 3A4 and CYP 2C9 cannot be ruled out, however the effect on CYP is probably week, and there are no indications of irreversible inhibition.

Teriflunomide is the active metabolite of leflunomide, and is an open-ring cyanoacetic acid metabolite.

Teriflunomide is indicated for the treatment of adult patients with relapsing remitting multiple sclerosis. It acts as an immunomodulatory agent by inhibiting pyrimidine synthesis. It is administered orally.

Teriflunomide is excreted in the gastrointestinal tract mainly through the bile as unchanged drug. In vivo studies suggest that teriflunomide is a week inhibitor of CYP 2C8, and a week inducer of CYP 1A2. Also, a small increase in plasma concentration of ethinyl estradiol and levonorgestrel (CYP 34A substrates) was shown in an in vivo study, but no mechanism was proposed. Two case reports of bleeding and increased INR when leflunomide (prodrug to teriflunomide) was administered concomitantly with warfarin, suggests possible inhibitory effects of leflunomide and/or teriflunomide on CYP 2C9. (Chonlahan 2006, Lim 2002). However, no alterations on the pharmacokinetics of warfarin by teriflunomid were seen in an in vivo study described in the SPC and it is proposed that teriflunomide is not an inducer or inhibitor of 2C9.