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 effectively counters Experimental Autoimmune Encephalomyelitis (EAE) and suppresses deleterious T cell immune responses, primarily through direct action on myeloid Antigen-Presenting Cells (APC). It modifies myeloid APC subsets, curbing the polarization of Th1 and Th17 in myelin-specific T cells, and induces type II (M2) monocytes which reverse established EAE [1]. Additionally, Laquinimod modulates both the phenotype of B cells in healthy donors and the expression of regulatory markers in B cells of patients with Relapsing-Remitting Multiple Sclerosis (RRMS), alongside reducing IFNγ cytokine levels in CD4+ T cells [2].

Laquinimod sodium treatment suppresses the ability of donor myelin-specific T cells to transfer Experimental Autoimmune Encephalomyelitis (EAE) to naive recipient mice. It also modifies myeloid antigen-presenting cell (APC) subpopulations in vivo, characterized by reduced numbers of CD11c+ CD11b+ CD4+ dendritic cells (DC) and increased levels of CD11b hi Gr1 hi monocytes [1].