Newsflash new addition for secondary progressive MS


Treatment arrives for secondary progressive MS. Siponimod has been approved by the FDA in the US.

This can be used from clinically.isolated syndrome onwards.

So why would you want fingolimod?

I wonder. They work the same way but siponimod may have lesser side effects.

What will NICE do? keep it second.line like fingolimod or.give it a first line licence. I guess it depends on what the EMA say

Biologically there has never been a reason for this. Likewise if it works for spms it should work for ppms, but is licenced for spms

Fingo has little patent life left I wonder if this was pulled could the generics arrive?

The mod wars have begun expect more …imods to come your way

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  • Mayzent® (siponimod) is indicated for the treatment of adults with relapsing forms of multiple sclerosis, including secondary progressive multiple sclerosis (SPMS) with active disease, relapsing-remitting multiple sclerosis (RRMS) and clinically isolated syndrome (CIS).

    • Hopefully NICE and EMA can read through the non sense of this grossly overpriced ineffective drug for SPMS as did the FDA. It is only slightly effective for “active” SPMS at 21% over 3 whopping months and 26% in 6 months.

      “However, according to an FDA press announcement, “in the subgroup of patients with non-active SPMS, the results were not statistically significant.” People with non-active SPMS experience disability progression but without relapses”

  • So what will this mean for ocrelizumab if that gets approved for progressive?

    How does siponimod compare to Ocrelizumab with regards to data side effects and how it works?

    How does siponimod compare to cladribine again with regards to data side-effects and how it works?

  • “Little patent life” is likely why siponimod was created and the fingolimod progressive trials were aborted abruptly by Novartis. I would imagine if a trial were run head to head that their results would be identical. Just another example of Pharma slightly changing a drug to extend profits, not results.

    While it is about bloody time that a drug was created for SPMS, its results are extremely underwhelming compared to even placebo. You will get to the same horrible endpoint as taking no medication at all, just slightly slower (an underwhelming 21% over a whopping 3 months in the EXPAND trial).

    Its results pale in comparison to results from ibudilast or even early trials with alpha lipoic acid. When are researchers going to stop having such tunnel vision as to B-cells and T-cells in progressive MS? It should focus on neurodegeneration (hot microglia, mitochondrial dysfunction, neuron apoptosis, A1 astrocytes), remyelination and neurorestoration.

  • Would it be possible to use this press release as an occasion to provide a simple overview of the current Novartis S1P Receptor Modulator Pipeline (i.e. Fingolimod, Siponimod, Ponesimod, and Ozanimod)?

    What is the benefit of bringing four nearly identical products to market and is it really such a big deal if a therapy targets e.g. S1P4 or S1P5 receptors or not?

    Does this really mean that one therapy works for progressive forms while the other doesn’t?

  • Great news! Officially the first licensed dmt for those in the SPMS box. Won’t do much, but we knew that. This is for everyone who missed out on the days of early treatment. Been a long time, what say EMA? #unmet need

  • Important to note that the FDA approval is for active SPMS only. Meaning SPMS that still has relapses and/or enhancing lesions.

    I believe this is an important distinction to be made for all drugs regarding progressive ms. I remain unconvinced that ocrelizumab does much good for PPMSer’s with” inactive” disease, as it still strikes me quite odd that Genentech did not set up their study to be sufficiently powered to differentiate between active and inactive people with progressive ms.

    It’s also odd that Novartis seems to be producing a line of drugs that will directly compete with each other. Any thoughts on this? Is it simply patent protection? Or are there indications that these drugs may offer differing benefits?

  • Right so if you fail Fingolimod being spms, are you magically be better of with siponimod? I am being a bit cinical. What are the magic benefits for spms?

  • In real life, SPMS patients who still had relapses were labeled as RRMS in order to be on a DMT. Little difference will this drug have to Tysabri or Ocrevus (if these last are not even better).

  • ‘In real life, SPMS patients who still had relapses were labeled as RRMS in order to be on a DMT’
    Good where it happens. In the UK I know several people SPMS with occasional relapses and no DMT. No MRIs either, so who’s to know if any new or expanding* lesions to tick the active box?
    Contrast that with France where I have another friend SPMS still on fingolimod and has yearly MRI amongst other things to monitor (gotta love French healthcare!)

    *Do slow expanding lesions count as active?

    • UK second from bottom of western countries with access to DMT, Australia number 1. They have a different culture…They can read and learn:-(

  • The price of Mayzent

    “Indeed, Costello said the NMSS has “long called for a reversal in the upward trajectory” of expensive MS medications, and criticized Novartis for pricing Mayzent at $88,500 a year — especially after the Boston-based Institute for Clinical and Economic Review (ICER) determined that to hit a cost-effectiveness threshold of $150,000 per added year of health, the therapy should cost no more than $12,000 a year, according to a March 27 report by Bloomberg.

    That’s almost 87 percent cheaper than the price Novartis has established.”

    • Anyone else get the feeling that pricing is done on the basis of what the market will stand, rather than reflecting the true costs incurred and a reasonable profit margin? This is after all a me-too on the back of Fingolimod.

      • And it is not even a cure…. for that price it better deliver on substantial benefits…..which I doubt…more of the same.

      • “Novartis considered many factors in determining the price of Mayzent,” the company said in a statement sent to NMSS. “As the first oral drug to delay disability progression in RRMS, CIS, and active SPMS, Mayzent is poised to substantially reduce the burden of the condition on patients, caregivers, employers, insurers, and the healthcare system and society as a whole.”

        The price is not based on the costs of the trials in accordance to the proportion of the patients with the disease plus the normal profit. They estimate how much a national health care sytem would lose in insurance payments and how much would be needed for caregiving, and they take that money instead. It’s not about -mods, its about Mobs 😉

          • Novartis is disgusting. At least the FDA read through their nonsense on this ineffective ripoff fingolimod clone drug aimed to profit off of desperate progressiveSPMS population, in which majority are not “active”:

            “in the subgroup of patients with non-active SPMS, the results were not statistically significant.”

  • Lots of negative and interrogative comments on siponimod with very few answers or opinions. Why?
    People want advice as to whether to ignore this new drug or push their neurologist for it.

      • Can you remind me what the comparable improvements were to rrms patients taking fingolimod and spms patients taking siponimod

        Also if it is not yet clear what drives progressive then siponimod will not have the answer so I assume it really is renamed fingolimod?

        • Siponimod versus placebo in secondary progressive multiple sclerosis (EXPAND): a double-blind, randomised, phase 3 study.
          Kappos L, Bar-Or A, Cree BAC, Fox RJ, Giovannoni G, Gold R, Vermersch P, Arnold DL, Arnould S, Scherz T, Wolf C, Wallström E, Dahlke F; EXPAND Clinical Investigators.
          Lancet. 2018 Mar 31;391(10127):1263-1273.

          It is surely a ProfG post as one of the authors…I will just say it is “fingolimod with more of a patent life:-(“..with fewer (SP13 & S1P4) targets. The driver of the effect may well be new lesion formation and this was massively reduced by siponimod but the efffect on progression not massive. ProfG may also like to address why siponimod was not that effective on slowing loss of hand function loss…Is this a problem for his #thinkhand approach. Effect on EDSS and not hand function?

          Because of action of S1P5 there is a hope that it affects glial responses.

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