Open Access Short Communication

Future Insight to Mannuronic Acid (M2000) in Treatment of Neurodegenerative Diseases

Soheil Najafi and Abbas Mirshafiey*

Department of Immunology, Tehran University of Medical Sciences, Iran

Corresponding Author

Received Date: December 16, 2019;  Published Date: January 06, 2020


The β-D-Mannuronic acid (M2000) as a novel immunosuppressive drug, patented (PCT/EP2017/067920), has immunosuppressive effects. M2000 has shown a notable efficacy in experimental models of multiple sclerosis (MS), rheumatoid arthritis, and nephrotic syndrome. The influence of M2000 on myelin basic protein (MBP) induced experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis, was evaluated. The results of this study demonstrated that the treatment of EAE with M2000 could significantly decline disease development both prophylactically and therapeutically. The onset and symptoms of EAE in Lewis rats could be suppressed following the administration of M2000. In another study, the effect of M2000 on the treatment of Alzheimer’s disease (AD) was performed by Morris water maze experiment, and the immunological evaluations were performed by Western blot, apoptosis (procaspase-3, Bax/Bcl2, P53), enzymatic (superoxide dismutase [SOD]), and nonenzymatic oxidative stress (malondialdehyde [MDA]) tests. Our data showed that M2000 can reduce the amount of Bax/Bcl2, P53, MDA, and SOD, as well as it normalized the level of procaspase 3. Also, in a clinical trial, we assessed the efficacy and safety outcomes in MS treated patients with mannuronic acid compared to the conventional drug. As compared with the conventional drug, mannuronic acid (M2000) improved the risk of disability progression (based on MRI and EDSS assessment). This clinical trial demonstrated the efficacy and safety of mannuronic acid in patients with MS. Our results suggest M2000 is a potential therapeutic agent for the treatment of MS and AD.

Keywords: M2000; Mannuronic acid; Multiple sclerosis; Alzheimer’s disease; EAE

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