Although it sounds like a character out of Gladiator III….Vidofludimus (calcium) is not a Russel Crowe look alike…but it is a teriflunomide look alike. It is not a generic of teriflunomide but works in the same way.
Teriflunomide is the active breakdown product of leflunomide which is used in rheumatoid arthritus. So would leflunomide work in MS, yep it would because you give leflunomide and within a few minutes/hours the body turns it in teriflunomide. The Boffins thought let’s cut out the middleman/woman and simply give the active compound. This can be patented and allows the companies to grease their palms. As teriflunomides patent runs out you could make a generic or do something to give a patent so you can make more money if you can make improvements over the former compound. We have seen this over and over again…You can adapt the original drug either manipulate it to give a different does or route Copaxone daily to become three times a week and then as a depot once a month (Remember it is a random mix of amino acids and each batch is different)…..Avonex beta interferon-1a once a week to become plegridy (pegylated avonex beta interferfon-1a with anti-freeze i.e polyethylene glycol) once every two weeks, natalizumab gives way to subcutaneous natalizumab, ocrelizumab becomes subcutaneous ocrelizumab (Ocrevus zunovo), alemtuzumab become…nothing because it has collected too much baggage and it is hardly used so it was probably not considered worth it to develop a me too. An alternative is to develop another agent that works in the same way as the originator fingolimod targets sphingosine-1-phopshate as a mechanism of action in MS so does siponimod, ozanimod and ponsesimod, dimethyl fumarate works because it is degraded into monomethyl fumarate so alternative is make a drug that is monomethyl fumarate or another one diroximel fumarate that also breaks down to monmethyl fumarate and guess what pharma has been inventive and made a molecule that blocks dihydroorotate dehydrogenase just like teriflunomide and may be more effective on the target and so it will have a similar side effect potential and will be anti-proliferative. It make not target some of the off-target effects of teriflunomide but it also activates nuclear receptor-related 1 (Nurr1), a neuroprotective transcription factor and emerging target for neurodegenerative diseases. Activation of Nurr1 is associated with neuroprotective effects.
Data from a early trial in progressive MS is presenteted at ACTRIMS 2026 but it has been trialed in relapsing MS the (CALLIPER trial). A weird name. Is it after a device that gives precision to measuring things but it is also another name for a brace/orthoses for spastic legs. Phase III trials have been done ENSURE I & II NCT05201638/NCT05134441. Let’s see where they go will they be better than whats out there. It is suggested that it is an EBV inhibitor presented at ACTRIMS2026. This has been suggested previously for teriflunomide. I would say it has to be a weak inhibitor because we know that you can do better as teriflunomide is not a high efficacy treatment.
Me COI: Non-relevant
Disclaimer: My views
Source: multiple-sclerosis-research.org