Fingolimod does not promote remyelination

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Fingolimod has been shown to work in animal models of MS, and has been approved as a treatment for relapsing-remitting MS.

There is controversy in the literature regarding the contribution of fingolimod to myelin repair. 
In this study the investigators looked at the effect of fingolimod on myelin repair in two models of demyelination that have a minimal inflammation.
Fingolimod failed to promote remyelination in either animal model. 
These studies suggest that while fingolimod may be effective at modulating inflammation in MS, it is unlikely to affect the process of remyelination.
“These results are disappointing as previous studies have suggested that fingolimod may enhance remyelination. Hence the trial of this drug in PPMS.”

“Please note that this study was done by scientists working at Biogen-Idec, the company that makes Avonex and Tysabri and who are developing anti-Lingo. Biogen-Idec are therefore competitors of Novartis, the company that makes fingolimod. These results should therefore be reproduced by another group or groups of scientists.”

“Science is all about reproducing results; if we all accepted this mantra we would not be in the pickle we’ve gotten ourselves into with CCSVI.”
Extra reading: fingolimod, myelin, CCSVI
Other posts on this blog on fingolimod:
08 Jul 2011
What exactly are you planning on doing to change that Prof G? Having seen the Fingolimod corporate advert extolling its excellence I have to ask that if it is so effective why it is only approved for RRMS patients? 
03 Jun 2011
What exactly are you planning on doing to change that Prof G? Having seen the Fingolimod corporate advert extolling its excellence I have to ask that if it is so effective why it is only approved for RRMS patients? 
30 Apr 2011
In addition to its immune effects Fingolimod readily penetrates the CNS and may have direct effects on neural cells. This central mechanism of action distinguishes Fingolimod from other immunosuppressive drugs and may 
02 May 2011
Fingolimod: brain volume data. As a follow-up to my comment on a previous posting; I predict that if the PPMS trial is positive Fingolimod will be the first drug to be licensed as a neuroprotective therapy in MS. 
Etc. 
Search terms used: fingolimod

About the author

Prof G

Professor of Neurology, Barts & The London. MS & Preventive Neurology thinker, blogger, runner, vegetable gardener, husband, father, cook and wine & food lover.

6 comments

  • How did the previous results indicate Fingolimod may enhance remyelination? I thought it was just a potassium channel blocker.

  • Re: "How did the previous results indicate Fingolimod may enhance remyelination? I thought it was just a potassium channel blocker."

    Fingolimod is a sphingosine phosphate-1 receptor modulator. The potassium channel blocker is Fampridine, which is licensed for improving walking speed in subjects with walking difficulties.

  • So maybe the scientists actually discovered that Fingolimod does not help remyelination, or maybe they are dishonest.
    Researchers who deliberately mis-design or mis-report studies should be penalised for confusing people and wasting everybody's time. (Fined, suspended, de-licenced, jailed?)

  • Re: "or maybe they are dishonest."

    Nobody is suggesting they are dishonest. All you need to know is that they have a conflict of interest and as always this may affect the way scientists interpret their results.

    In my opinion, conflict of interests are fine provided they are declared so that the reader can factor them into their interpretation of the results. This is why this work needs to be reproduced by a second, and possibly third, group before I accept them as definite.

  • I was (by mistake probably) in an FTY720 trial for a year and a half even though I think an objective observer would have had a hard time arguing that I was not progressive when I started the trial. I was really counting on the neuroprotective potential, but so far as I could tell FTY720 had no effect whatsoever (good or bad). I'm pretty sure I was on the real drug as my WBC was so low my PCP was trying to figure out how to ask me to consider an AIDS test and it was normal within 10 days of being out of the trial. Of course, I'm a data point of one and I hope it works out better for the people in the PPMS trial.

  • Re: "I'm a data point of one and I hope it works out better for the people in the PPMS trial."

    Thanks for sharing this with us. Unfortunately, MS is such a difficult disease to monitor that we really need to see the results of the PPMS trial before we make any call. The impact fingolimod may not be big; for example even if it only slows down disease progression in PPMS by say 20%, this should be viewed as being good news. At least it will be start and something to build on. In addition, headline trial results report the average effect; some MS'ers do better than others. This is the so called responder vs. non-responder debate that continues to be discussed at meetings. You may be a non-responder, whilst someone else may respond very well.

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