Related Experiment Video
Updated: Oct 27, 2025

Synthesis and Characterization of an Aspirin-fumarate Prodrug that Inhibits NFκB Activity and Breast Cancer Stem Cells
Published on: January 18, 2017
A comparison study between dimethyl itaconate and dimethyl fumarate in electrophilicity, Nrf2 activation, and
Yong Zhang1, Yu-Jun Zhou1, Jing-Shu Tang1
1State Key Laboratory of Bioactive Substances and Functions of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100050, China.
Abstract:
Dimethyl itaconate (DMI) is an analog of dimethyl fumarate (DMF), an approved NF-E2-related Factor 2 (Nrf2) activator for multiple sclerosis. This study evaluated the potential of DMI as an anti-inflammatory agent by comparing DMI with DMF in electrophilicity, Nrf2 activation, and anti-inflammation in vitro. The results showed that DMI was less electrophilic but better at inducing a durable activation of Nrf2 when compared with DMF. However, DMI demonstrated poor anti-inflammatory effects in Jurkat cells, bone marrow-derived dendritic cells, and RAW264.7 cells. Our study suggested that DMI was a potent electrophilic Nrf2 activator but was probably not a promising anti-inflammatory agent.

