FTY720 on the way from the base camp to the summit of the mountain: relevance for remyelination

Author:

Kipp M12,Amor S23

Affiliation:

1. Institute of Neuroanatomy, Faculty of Medicine, RWTH Aachen University, Germany

2. Department of Pathology, VU University Medical Center, Amsterdam, Netherlands

3. Neuroimmunology Unit, Queen Mary University of London, Neuroscience Centre, Blizard Institute of Cell and Molecular Science, Barts and The London School of Medicine and Dentistry, UK

Abstract

FTY720 (fingolimod; Gilenya®), a sphingosine 1-phosphate (S1P) receptor modulator, is the first oral disease-modifying therapy to be approved for the treatment of relapsing–remitting multiple sclerosis. FTY720 is rapidly converted in vivo to the active S-fingolimod-phosphate, which binds to S1P receptors. This action inhibits egress of lymphocytes from the lymph nodes, preventing entry into the blood and thus infiltration into the central nervous system. More recent studies, however, convincingly show that FTY720 crosses the blood–brain barrier, where it is thought to act on S1P receptors on cells within the central nervous system, such as astrocytes, oligodendrocytes or microglia. Here we discuss the evidence showing that FTY720 also plays a role in remyelination and repair within the brain. While the mechanisms of action still require firm elucidation, it is clear that FTY720 could also be reparative, extending its therapeutic potential for multiple sclerosis.

Publisher

SAGE Publications

Subject

Neurology (clinical),Neurology

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