Alme MN, Nystad AE, Bø L, Myhr KM, Vedeler CA, Wergeland S, Torkildsen Ø. Fingolimod does not enhance cerebellar remyelination in the cuprizone model. J Neuroimmunol. 2015 15;285:180-6.Fingolimod (FTY720) is approved for treatment of relapsing-remitting multiple sclerosis. In vitro studies have found that fingolimod stimulates remyelination in cerebellar slices, but in vivo animal studies have not detected any positive effect on cerebral remyelination. The discrepant findings could be a result of different mechanisms underlying cerebral and cerebellar remyelination. The cuprizone model for de- and remyelination was used to evaluate whether fingolimod had an impact on cerebellar remyelination in vivo. We found that fingolimod did not have any effect on cerebellar remyelination, number of mature oligodendrocytes, microglia or astrocytes when fed after cuprizone exposure.
Fingolimod is a sphingosine -1 -phosphate receptor modulator. It stops white blood cells by modulating the S1P1 receptor. But S1P5 is expresse by glial cells and Novaritis would have it that fingolimod was going to induce remyelination. However as a spoiler Biogen sponsored a study to show no remyelination potential. Novartis have sponsored a study and now found the same thing, so maybe time to put this to bed. This may be part of the reason why fingolimod did not stop progressive MS