This report evaluates the therapeutic effects of CIC-39 in the experimental autoimmune encephalomyelitis (EAE) mouse model of multiple sclerosis. In vivo administration of CIC-39 (60 mg/kg for 15 days) effectively halted disease progression and significantly reduced the expression of the pro-inflammatory cytokines IL-17 and IFN-γ, key mediators of pathogenic Th17 and Th1 responses. These anti-inflammatory effects were achieved without altering immune cell differentiation or disrupting overall immune homeostasis, indicating a targeted immunomodulatory action. Collectively, the findings highlight CIC-39 as a promising candidate for further development as a selective and safe therapeutic approach for multiple sclerosis.
Giuseppe Cappellano (Thu,) studied this question.