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Dimethyl fumarate (TECFIDERA) is an orally administered fumarate ester recently FDA approved for first-line monotherapy of multiple sclerosis. Because it is rapidly and completely hydrolyzed by esterases before reaching the systemic circulation, the pharmacologic activity of dimethyl fumarate is due to its active metabolite, monomethyl fumarate.^[1] Although the precise mechanism of action is incompletely characterized, monomethyl fumarate is thought to exert neuroprotective effects in patients with multiple sclerosis by activating the nuclear erythroid 2-related factor 2 (nuclear factor erythroid-derived 2-like 2; Nrf2)^[2] transcriptional pathway.^[1,3,4,5] Using a model of endogenous neuronal oxidative stress, Albrecht, et al., studied time- and concentration-dependent effects of dimethyl fumarate and monomethyl fumarate and concluded that dimethyl fumarate causes a brief period of oxidative stress that results in the intraneuronal synthesis of the antioxidant glutathione (GSH) mediated through the Nrf2 pathway (see Figure 1).^[6] Others have proposed additional immunomodulatory actions for dimethyl fumarate mediated through nitric oxide, interleukins, tumor necrosis factor (TNF-α), or other cytokines.

dimethyl fumarate administered at a dose of 240 mg twice daily by mouth over a period of 2 years were associated with a statistically significant reduction in clinical disease exacerbations (the primary efficacy endpoint), a reduction in the necessity for rescue therapy with intravenous corticosteroids, and improvements in other indicators of disease progression, including MRI images of brain lesions (see Table 1 ). To date studies have been insufficiently powered to detect a consistent effect on disability progression,^[5] but quality of life assessments are expected as a secondary outcome

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