Vimirogant hydrobromide

Vimirogant (p.o.) hydrobromide (VTP-43742 hydrobromide) significantly inhibits clinical symptoms, demyelination, and mRNA expression of multiple inflammatory markers in the spinal cord of MOG35-55/CFA-immunized EAE mice^[3].
Vimirogant (prophylactic administration; 11 days) hydrobromide dose-dependently inhibits CD4⁺IL-17⁺IFNγ⁻ and CD4⁺IL-17⁺IFNγ⁺ T cells in the spleen and draining lymph nodes of MOG35-55/CFA-immunized EAE mice; following ex vivo restimulation of splenocytes obtained from treated mice with MOG35-55, Th17-derived cytokines are specifically suppressed^[4].
Vimirogant (high dose; prophylactic administration) hydrobromide completely suppresses EAE clinical scores in chronic EAE studies, with a greater degree of suppression than MM17F3; it also inhibits Th17-related markers in the spinal cord and reduces demyelination and inflammatory cell infiltration^[4].
Vimirogant (30 μg/kg; p.o.; 7 days) hydrobromide reduces M1 macrophage polarization in the colonic mucosa of DSS-induced colitis mice and alleviates colitis-associated inflammatory injury; the main text states that IL-17a expression does not change under this condition^[5].
Vimirogant (30 μg/kg; intragastric administration; 7 days; combined with SYD 2.50 g/kg) hydrobromide inhibits colonic mucosal inflammatory injury in DSS-induced colitis mice more strongly than SYD alone^[5].