And the second one is more dedicated to CALLIPER and to trial design and NfL, but no really new data. But it’s important to put that in context. We figured out that the market is maybe not fully up to speed on the link between NfL and future disability progression. And we therefore think we want to come into this casual with doctors on this more specifically and to also talk about Nurr1 activation and the way this has the neuroprotective potentially. Because this could really change the way we treat the disease and could be a major, major impact for the whole MS market if the data reads out in a positive way next April.
William Wood: Got it. And thank you for correcting me there. It definitely is CALLIPER interim results. And then lastly, just if I may, could you discuss how or possibly what the current learnings for vidofludimus calcium, the differentiated MOA position it in relation to other anti-CD20, or actually just anti-CD20 antibodies, and even emerging excitement sort of in regards to the CD19 CAR-T space?
Daniel Vitt: I think the bigger difference is that Nurr1 is not targeting focal classical inflammation signals, which is different from basically all of the other approaches. And that makes it unique in a way that it may — and we’ve seen that in the NfL data, but we may see also this in clinical outcomes, starting with the CALLIPER study, that vidofludimus calcium can have a beneficial effect in patients which are not benefiting or not enough benefiting from immunosuppressive therapies like anti-CD20s, anti-CD19 or whatever you use there because it is just something different, an orthogonal mode of action to these. The good thing about vidofludimus is that on the other hand, we also inhibit DHODH which also, on top of this potential neuroprotective effect, also is anti-inflammatory.
So then we — if you’re focused on the key unmet medical need, which is really preventing and slowing down disability worsening in MS patients of all kind, that we target both. So the more relapse-related and the relapse-independent worsening of progression in the patients. And that would be I think the best differentiator you can have and also the best news for patients suffering from these indications like primary progressive and secondary progressive MS specifically.
William Wood: Got it. Very helpful. And thank you for taking our questions and congratulations again.
Daniel Vitt: Yes. Thank you, William.
Jessica Breu: Thank you, William. I actually have another question here on the Nurr1 target in the Q&A tool. In case of Nurr1 activation confirmation, do you see further benefits of vidofludimus in the future for other neuromuscular disorders such as Parkinson’s disease or even Alzheimer’s?
Daniel Vitt: A simple answer, yes. So, very clear, this is something, it was a breakthrough finding when we, together with our collaborators at University here in Munich around Daniel Murak, found that vidofludimus calcium is such a good activator of Nurr1. And most of the historic research on therapeutic use of Nurr1 has been performed in the area of Parkinson’s disease. So this was the original main focus of researchers in the world. And I think Nurr1 still is on the top of the list of hope for potential targets for Parkinson’s disease. Therefore, this primes, of course, our vidofludimus to be tested there. But we have more molecules. We have a bunch of derivatives. We have molecules with different properties, maybe priming molecules for different, for example, CMS penetration and so forth.
So there may be the potential to start other independent developments with our molecules in such indications with very specific target profiles. So we see a huge potential there. But once again, currently, the focus is delivering data for MS. And therefore, we will not use huge amounts of our budget for these highly innovative new things. But we are also considering collaborations there as well to boost things in parallel to our current MS activities.
Jessica Breu: I have another question here in writing. Are there any plans for the vidofludimus UC program, given the stronger maintenance phase data?
Daniel Vitt: Yes, that’s the money question right now again. So I would love to continue with the Phase III directly in that indication. Once again and that was the reason why we kicked off a new program called IMU-381. We have molecules which are maybe from their tissue distribution profile better suited for GI penetration, but using our mode of action and our proof-of-concept from the CALLIPER studies. So yes, in principle, yes. But once again, something we would likely more likely separate in a different development track.
Jessica Breu: Thanks, Daniel. Final question I currently have may be a good chance for you to summarize the status quo and upcoming milestones for vido. What are the updates regarding IMU-856 — IMU-838, I’m sorry.
Daniel Vitt: Well, more or less the summary of what we spoke about. I think we were intrigued by the data of last year, specifically the NfL data giving us a very nice signal and really increasing the likelihood of success for the clinical outcomes of the CALLIPER study with a readout in April 25. This would make the drug a very huge also commercial opportunity, I think. This is a very huge potential for vidofludimus calcium. That’s I think maybe the main driving force here right now. In parallel, we have that rock solid ENSURE program in relapsing MS ongoing, which is more or less just based on our very good Phase II data for that molecule we obtained from the EMPhASIS study, which allows us a low risk way forward towards approval and data readout in 2026.
So these are the key driving forces for the vidofludimus program. But to reiterate — I don’t want to talk too long here, but to reiterate, we also had this positive readout on GI, on UC study on the maintenance data, which is more or less boosting other molecule developments in that space. And also the Nurr1 potential beyond just multiple sclerosis and other related neurological indications, also something where we think this has another huge potential. And we will definitely also look into these things.
Jessica Breu: Very good. This concludes our question-and-answer session today. I would like to turn the conference back over to Daniel for any closing remarks.
