The precise mechanisms by which teriflunomide exerts its clinical effects in MS are incompletely understood. Teriflunomide acts primarily as an inhibitor of dihydroorotate-dehydrogenase (DHODH), a key mitochondrial enzyme involved in the de novo synthesis of pyrimidines in proliferating cells. Teriflunomide thus reduces the activity of proliferating T lymphocytes and B lymphocytes, resulting in anti-inflammatory effects. Importantly, teriflunomide does not affect resting or homeostatically proliferating hematopoietic cell lines, since the necessary cellular pyrimidine pools can be generated through an alternate “salvage pathway,” which is independent of the DHODH. Teriflunomide is thus considered a cytostatic drug to leukocytes, rather than cytotoxic. In addition to DNA and RNA synthesis, teriflunomide’s effects on pyrimidine synthesis result in modulation of a variety of cellular functions, including phospholipid synthesis, protein and lipid glycosylation and DNA strand repair, which together lead to a variety of downstream immunomodulatory effects.
Teriflunomide may decrease the risk of infections compared to chemotherapy-like drugs because of its more-limited effects on the immune system. It has been found that teriflunomide blocks the transcription factor NF-κB. It also inhibits tyrosine kinase enzymes, but only in high doses not clinically used.
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