Dimethyl fumarate

Dimethyl fumarate (DMF) is an orally active and brain-penetrant Nrf2 activator and induces upregulation of antioxidant gene expression. Dimethyl fumarate induces necroptosis in colon cancer cells through GSH depletion/ROS increase/MAPKs activation pathway, and also induces cell autophagy. Dimethyl fumarate can be used for multiple sclerosis research^[1][2]. In Vitro: Dimethyl fumarate (DMF; 20-200 μM; 24 hours) treatment dose-dependently reduces the viability of SGC-7901, HT29, HCT116 and CT26 cancer cells^[1].
Dimethyl fumarate (DMF; 100 μM; 3-24 hours) significantly activates JNK, p38 and ERK in CT26 cells^[1].
Dimethyl fumarate induces necroptosis in colon cancer cells and the mechanism involves GSH depletion, an increase in ROS and activation of MAPKs-mediated signalling^[1].
Dimethyl fumarate inhibits dendritic cell (DC) maturation by reducing inflammatory cytokine production (IL-12 and IL-6) and the expression of MHC class II, CD80, and CD86. Dimethyl fumarate impairs NF-κB signaling via reduced p65 nuclear translocalization and phosphorylation. Dimethyl fumarate inhibits maturation of DCs and subsequently Th1 and Th17 cell differentiation by suppression of both NF-κB and ERK1/2-MSK1 signaling^[2].
Dimethyl fumarate (DMF), an immune modulator and inducer of the antioxidant response, suppresses HIV replication and neurotoxin release^[3]. In Vivo: Dimethyl fumarate (DMF; 50 mg/kg; oral gavage; daily; for 7 days) treatment is shown to upregulate the mRNA and protein levels of Nrf2 and Nrf2-regulated cytoprotective genes, attenuate 6-OHDA induced striatal oxidative stress and inflammation in C57BL/6 mice^[4].