Novartis maybe now believes Biogen. Fingolimod does not promote remyelination

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

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  • You do know they've spent $1 billion to confirm this lousy basic science assumption regarding fingolimod's remyelination fallacy? That is ONE BILLION DOLLARES!

    No wonder MS drugs are so expensive.

  • Would it be possible to do a piece on remyelination? One or Prof G's presentations liste 5 or 6 agents which were being tested, but they never seem to report. I found the anti-lingo antibody results most dissapointing.

    • Until the trials report there is little to report of interest except the ongoing studies and the pre-clinical data.

      Not sure why you should be disappointed they apparently now have a positive as they have obviously fiddled with the data between the Biogen announcement and ECTRIMS and they started dosing probably weeks too late. It is a start.

  • Mouse,

    Thanks. My disappointment is the strategy for the remyelination is focused on remyelination shortly after a relapse / active inflammation. I was hoping remyelination would focus on progressive disease to stop further degeneration. Repairing damage to those with established disability must be the holy grail.

    • Dont be dispondent. People do the remyelination just after relapse because that is all they can do. However we can look at the remyelination potential in the post relapsing situation. We havent done this because becuase this has not been our focus because we only have too hands howevet this aspect can be tested and then we will find that some ideas are put to the sword but others wont be.

    • on the plus point. Using these easy models in relapse then it is used fo justify a study in non relapsing ms. it would take longer to do the animal experiments in the non relapsinv situation.

  • We know that the key is to remyelinate old lesions because that is the most dificult. experimentally the experiment is to remyinate something faster than would remyelinate naturally. There are the chemical demyelinatio. models which make a point and then the EAE studies that are largely uninterpretable because of the way they are done. (personal opinion). This creates expectations and tells us little of what will happen. Why arent the right experiments done….fear of failure and laziness and cost

    • I've always wondered why Dr Franklinstein has never done the obvious experiment.
      I suspect option A.

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