Laquinimod (ABR-215062) sodium is a carboxamide derivative administered orally that serves as a powerful immunomodulator, designed to prevent inflammation and neurodegeneration within the central nervous system. This compound effectively diminishes the activation of astrocytic NF-κB, offering protection against Cuprizone-induced demyelination. It shows promise for the treatment of both relapsing-remitting (RR) and chronic progressive (CP) forms of multiple sclerosis (MS; RRMS or CPMS), in addition to its potential applications in the study of neurodegenerative diseases [1] [2] [3] [4].

Laquinimod sodium reverses EAE and inhibits pathogenic T cell immune responses. Laquinimod reverses RR-EAE and inhibits inflammatory T cell responses via a direct effect on myeloid APC. Laquinimod alters myeloid APC subsets and inhibits Th1 and Th17 polarization of myelin-specific T cells. Laquinimod-induced type II (M2) monocytes reverse established EAE [1]. Laquinimod modulates the phenotype of B cells of healthy donors. Laquinimod modulates expression of markers related to regulatory capacity in B cells of RRMS patients. Laquinimod reduces IFNγ cytokine expression in CD4 + T cells [2].

Laquinimod sodium treatment inhibits donor myelin-specific T cells from transferring EAE to naive recipient mice. In vivo laquinimod treatment alters subpopulations of myeloid antigen presenting cells (APC) that include a decrease in CD11c + CD11b + CD4 + dendritic cells (DC) and an elevation of CD11b hi Gr1 hi monocytes [1].