Good afternoon, everyone, and welcome to the Jefferies Healthcare Conference. My name is Xander Guarna. I'm from the investment banking team at Jefferies, and it's my pleasure to introduce Daniel Vitt, the CEO of Immunic. Yeah, thank you for having us here today. Please consider our cautionary note regarding forward-looking statements during the presentation. Happy to introduce Immunic today. Immunic is a clinical-stage company focusing on new oral treatments for chronic inflammation, autoimmune diseases, and specifically with a focus on multiple sclerosis. With pretty new data. T his morning we published another update on very interesting, exciting data from our phase 2 study in progressive MS patients. With our portfolio, we are targeting a large commercial opportunity of several- billion- dollars peak sales potential for vidofludimus calcium. Also to add on that, we just recently completed a secondary offering for $65 million. Our pipeline consists of a couple of products, most advanced vidofludimus calcium in phase 3 in relapsing MS. As I said, just recently brand hot data from our progressive MS CALLIPER study. On top of that, we also run a second clinical stage program, IMU-856, targeting gastrointestinal diseases, specifically celiac disease. Also here, we recently published some interesting additional data specifically on the effect on integrins. Let me start with more details on our vidofludimus calcium program, which is quite, could be a very transformative new treatment for multiple sclerosis. Vidofludimus calcium is an oral new drug, which is designed to combine the best of two worlds: Neuroprotection on the one hand and relapse prevention on the other one. It is doing this by having a dual mode of action on the one hand, a very potent inhibitor of an established target, DHODH, which is a very nice way to smooth an overshooting immunity by really leveling down the inflammatory activity in multiple sclerosis. On top of that, the drug is a very potent activator of NURR1. NURR1 is a nuclear receptor which is involved in protection of neurons from cell death. As I said, it's an oral drug, and it has an outstanding good safety and tolerability profile. We think it's the perfect benefit-risk profile for treating multiple sclerosis. If you look on current treatments and the medical need in multiple sclerosis, clearly the key unmet medical need, the elephant in the room for patients with multiple sclerosis, is disability progression. The ultimate purpose of developing new drugs in MS is really to stop or slow down disability worsening. The main reason why the current treatments really did not so far really deliver something substantial on that, specifically if it comes to disability progression, which is independent of relapse activity, is that most drugs are really focusing on just systemic inflammation. I think it's important to have a look on the different roles of inflammation and neurodegeneration in the different forms of multiple sclerosis. On the left, you see in relapsing MS, the main symptoms are really coming from relapses, which are obvious. Whereas on the right side in progressive MS, the main clinical progression is really seen in disability worsening over time. Ultimately, in all forms of multiple sclerosis, this motoring disease or neurodegeneration plays an important role. In relapsing MS, we call this PIRA. In the progressive forms, this is just the progression we measure in clinical trials. In progressive MS, we have basically two forms of PMS. One is secondary progressive MS, where patients progressed from relapsing MS into a stage where relapses go away, but disability is still worsening over time. Whereas in primary progressive MS, these patients never had clinical manifestation of relapses, but are progressing more or less from the very beginning of diagnosis. Globally, or maybe in the seven biggest markets, the number of eligible patients for multiple sclerosis is 1.2 billion, with 900,000 in relapsing MS, 175,000 in non-active SPMS, and around about 120,000 patients with PPMS. Our product is, as I said, in phase -3 testing for RMS and just completed phase 2 study for both forms of progressive MS. With the number of patients and also the high number of patients which are currently not on a treatment, we project the peak sales potential of the drug to be all in all $3 billion-$7 billion in all of the different forms of MS. Where did it start and why are we testing it in all the different forms of MS? It goes back to a phase- 2 study we performed in 2019 and 2020 in patients with relapsing MS, the EMphASIS study. That study was very successful. I'll show you some data in a minute. Based on the outcome of that study, we decided to, on the one hand, continue the drug in relapsing MS in the so-called ENSURE-1 and ENSURE-2 studies. I'm very happy to announce that we announced today that we fully enrolled both studies and are now waiting to read out top line data from the study at the end of 2026. Based on some interesting results from the EMPhASIS phase two study, we also have seen hints of neuroprotection at that time. From there, we decided to test the neuroprotective features of the drug by just going into a set of patients which are not suffering from relapses. There is no overlay of the two signals, but really to focus on reducing disability progression. That was done in a phase-2 study, so-called CALLIPER study. Before going there, let me first start with a summary of the mode of action. As I said, on the one end, the drug targets DHODH on the right here, which makes it a very potent drug to stop inflammation or overshooting inflammation on the one hand, but also to reduce or to prevent reactivation of viruses. As I said, the unique thing about this drug is that we have found that the drug is an activator of nuclear receptor- related 1, and NURR1 activation was found to be an important regulator for protecting neurons from cell death in several settings. As I said, it first started with a phase-2 study, the EMPhaSIS study in patients with relapsing MS. This was a pretty successful study, 268 patients randomized. We tested three different doses, 10, 30, and 45 mg against placebo. The primary endpoint of the study was reduction of inflammatory lesions in the MRI. That was pretty successful. We have seen a 76% reduction of cumulated active lesions after 24 weeks of treatment compared with placebo, and a reduction of 78% of gadolinium-enhancing lesions at week 24 with high statistical significance. That is just checking the box. The drug confirms the expected anti-inflammatory effect. What was a little bit surprising was to see that after 24 weeks already, we have seen a quite remarkable lower rate of confirmed disability worsening with the drug comparing the treatment arms with the placebo arms. That was more or less the reason why we decided to further investigate the neuroprotective features of the drug. We followed up those patients after the double-blind placebo-controlled part of the study in an open- label extension. In these two years after completion of the main study period, after two years, still 94.2% of patients were free of confirmed disability worsening. That was a quite promising thing. Therefore, now I'm happy to, in a minute, show you data from the progressive MS studies. Another important aspect, and it's somehow often underestimated, is safety and tolerability. I think we have a couple of good drugs today available for patients with MS. I think if you are newly diagnosed, maybe at the age of 25 to 30, and you still want to continue a normal life, safety is an important feature. We think that our safety profile we have generated so far is pretty promising and would be a very attractive profile for patients with MS. Based on all of that, we then started the phase-3 clinical development of vidofludimus calcium in relapsing MS in the ENSURE studies. In these studies, which, as I said, was just right now completely enrolled, we are testing separately around about 1,100 patients in each study against around about 550 in each arm, 35 mg of vidofludimus calcium against placebo. The primary endpoint of the study is time to first relapse. The studies are expected to read our top line data end of 2026. An important piece is here that we predefined that we can pool the data from both studies together to read out a secondary endpoint of the study, which is confirmed disability worsening again, because we also want to demonstrate that the drug has an advantage in reducing the progression independent of relapse activity in the RMS patient population tested here. Switching over to progressive MS. As I said, this is an indication of high unmet medical needs. So far, there is only one drug approved for treating one of the forms of progressive MS, which is primary progressive MS. The approved drug is Ocrevus from Roche, and 120,000 patients are diagnosed in the U.S. and the EU5 countries. Interestingly, really only 45% of patients are on active disease-modifying therapy. Also, on top of that, the indication is highly underdiagnosed. There's, I think, a hidden bigger chunk of patients which need treatments in the future. We decided to not jump immediately into a phase-3 study, but really to do a scientifically driven phase-2 study and testing the effect of the drug in different forms of MS in this study. Based on the data I've shown you earlier, we decided that to really have the maximum effect possible, we decided to go for 45 mg. We're testing 45 mg against placebo in 467 patients randomized. We also allowed patients of an age from 18 up to 65 years to be part of the study. We enrolled patients with primary and secondary progressive MS. The study duration was at minimum 72 weeks for patients and up to 120 weeks follow-up time. An important thing is here the different sub-indications. We have 32% of patients with primary progressive MS, 57% of patients with non-active SPMS, and 10% of patients with active SPMS. On the right, you see the baseline characteristics. The median age was 51 years. An important piece is on the bottom of that table is that we had a quite low number of patients with active gadolinium-enhancing lesions at baseline of 16.3%. That means this patient population is pretty advanced and has little remaining inflammatory activity. More difficult to treat with any current drugs. Main conclusions from the study are that CALLIPER successfully demonstrated the neuroprotective potential of vidofludimus calcium in progressive MS. Secondly, we have seen a clinically meaningful risk reduction of confirmed disability of 24% in the overall study and 33% in the PPMS, primary progressive MS subpopulation of the study. As I said, just fresh from the press, our data on time to 24- week confirmed disability worsening. This is, by the way, the endpoint, which likely will be the endpoint of any future phase-3 study in PPMS or SPMS. Overall, we have seen a 24.1% reduction of risk on time to 24- week confirmed disability worsening. In the PPMS, primary progressive MS population, it was 32.5%, a pretty remarkably high number of re duction; in non-active SPMS, almost 20%; and in the active SPMS subset, 33.7%. We also have followed up as a secondary endpoint the change of EDSS, or the disability score from baseline. What you see in this graph is that for the treated patients, it's almost a flat line. A very small increase or marginal increase on EDSS and average over time, whereas the placebo group really increases all the time on EDSS. Starting from week 60, this difference got statistically significant on the difference between placebo and active. How to position the data? What does it tell us? I think if you look back on the, I mentioned the only approved drug, Ocrevus, the baseline characteristics between CALLIPER subset of PPMS and the ORATORIO study was pretty similar: age, baseline EDSS, and so forth. Maybe the most remarkable difference was that in the ORATORIO study, they had around about 26% of patients with active inflammation, so baseline gadolinium-enhancing lesions, whereas our activity here was 17.8% only. We have seen on a numerical level a quite high rate of risk reduction here compared also to ORATORIO. The question was, how does vidofludimus calcium perform in the patients which are free of gadolinium lesions, so which do not have this remaining activity? We know that for Ocrevus, for example, the activity of risk reduction was really less pronounced in patients without inflammation. Surprisingly, we have seen a very, very strong activity in those patients, 391 atients were free of baseline gadolinium-enhancing lesions, and we have seen a 34% reduction of time to 24- week confirmed disability worsening. That comes from both subgroups, from PPMS and non-active SPMS populations, with 35% for PPMS and almost 30% for non-active SPMS. Maybe to point to that a little bit, this is, I think, key data showing how good the drug differentiates from what is currently available. We think this is a key feature of vidofludimus calcium, which really underlines the benefit of the drug and the potential to differentiate from all other current treatments available for treating MS. I mentioned earlier that safety and tolerability is also an important endpoint, and I'm very glad that the top line data confirmed the favorable safety and tolerability profile of vidofludimus calcium with no new findings on the safety side. I think the occurrence of treatment-emerging adverse events and SAEs with similar frequency in both treatment arms, as shown here on the tables. In summary, we believe that we have a quite unique molecule for treating progressive multiple sclerosis with clinically meaningful reduction of disability worsening, a remarkable 34% reduction of 24-w eek confirmed disability worsening in the patients without baseline inflammatory lesions. All in all, a pretty attractive result from that study. What's next? With this wonderful data, we're now heading towards the readout of the ENSURE phase-3 studies towards the end of next year, which in a positive outcome case would allow us to submit an NDA in 2027. That was the summary of vidofludimus calcium in multiple sclerosis. Let's switch over to our second asset, IMU-856. As I said, this is a program which is targeting gastrointestinal diseases. The concept here is that we want to restore a healthy gut through renewal of the bowel wall, the epithelial layer of the bowel wall, basically. This is a completely new approach. This molecule is a Sirtuin 6 selective, Sirtuin 6 modulator, and with that targeting the epithelial regeneration and the gut cell function. It can, in principle, because it's an approach which is not immunosuppressive, it can be applied, in principle, to a very broad set of GI disorders and by leveraging its physiological intestinal epithelial regeneration, including the production of natural hormones in the gut wall. That looks pretty simple. If we could fix these damaged cells here, I think you can achieve a lot of things. I think the most important thing is that you restore a proper barrier function in the gut wall. Secondly, renewal of healthy cells also allows the proper uptake of nutrients from the gut into the blood system and block, for example, allergens or other antigens to then be recognized by the immune system. More or less, it's a defense against the root cause of a couple of GI disorders. Before coming to the clinical part, we have done as part of our phase-1 study where we tested also on top of safety and tolerability the effect in patients with celiac disease. I want to show you some recent data we have found by diving deeper into the data. If we talk about gut health, an important function of cells, specifically of enteroendocrine cells or L- cells in the gut, is to produce incretins. The incretins are important messengers of, for example, food uptake and stop of hunger and so forth. That is a natural control mechanism and therefore a very important system to control weight gain and gut health in general. We have, as I said, performed a phase one clinical study with IMU-856, where we tested several doses of the drug against placebo. We have performed the long-term chronic tox studies, including a six-month study in rats, where we tested a couple of different dose strengths of the molecule. We have seen very interesting results from both studies, from the clinical and the preclinical studies. Let me start with the preclinical data. For the treatment here in rats, I think we have seen a very nice dose-dependent effect on body weight gain. This was linked to the food consumptions in the study and affected males and females. The conclusion here from that preclinical work was that IMU-856 efficiently reduced the body weight gain in a dose-dependent fashion of up to 40%. This was not a weight reduction, but a prevention of weight gain experiment. We said, okay, we still have the clinical samples of our celiac disease patients. We went back and looked on the changes of incretins and specifically GLP-1. We were surprised to see that we see here at the specifically at the 160- mg- dose group, an up to 250% increase of baseline GLP-1 levels in the patient samples. That is another confirmation of the role of the gut cells in producing these things. We will further investigate to what extent IMU-856 could be a quite unique, new, and differentiated approach to manage weight gain in humans. Coming back to the initial idea of gut health and a proof of concept study we have done in a phase- 1B study. We decided to choose celiac disease as an important indication with no approved drug for proof of concept here. It is important to notice that there are millions of people which are suffering from celiac disease. Most importantly, among those patients, we have 24%-47% of the patients which have ongoing active disease despite being on a gluten-free diet. This is most people not aware of that high number of patients which are really suffering from symptoms of celiac disease despite really sticking to a very rigid gluten-free diet. So far, as I said, there is no therapeutic approach. The only approach right now is to really stay away from gluten for a lifelong gluten-free diet. This study was a four-week study where the first two weeks were just dosing either the active agent of 856 or placebo. In the second two weeks of the study, we also added 6- g daily gluten to the diet. The concept here was first to give the patients time so that the drug works and can restore the epithelial layer in the gut. For the next two weeks, to observe to what extent can we protect the patients from damage of the gut wall. For doing that, we did histological assessments at baseline and after four weeks of treatment. We tested 80 mg, 160 milligrams of the dose against placebo as pretty small studies. Despite only having 11, 13, and 13 patients in the different dose groups, we have seen a statistically significant protection of the villi in the gut over the 29-day observation period. Pretty amazing data for that short time frame. Another question, a functional question, and maybe more links to the GLP-1 data I've shown before, was can we improve the function of the gut again? Remember the challenge of active transport of nutrients. Interestingly, you see on the left side that the drug was able in this short time frame to restore the uptake of vitamin B12 in a dose-dependent fashion and also to a quite substantial quantitative level here. On the right, you see that's also true for zinc, and we have also positive data for other nutrients measured in the study. Let me summarize Immunic in general. We have with vidofludimus calcium, we have a de-risk near-term commercial opportunity in active phase-3 testing in relapsing MS and with a wonderful differentiated profile and unique data set from our recently completed phase-2 study in progressive MS. I think the most remarkable data point for me and for the company was really to see that the drug works in patients which have no treatment option because their progression is independent of relapses and independent of active inflammation. We think that this drug, therefore, has the potential to be a game changer in treating multiple sclerosis abroad from relapsing MS to progressive MS. We think that vidofludimus calcium could be the only oral option in the next couple of years available for the holistic MS landscape from RMS to all forms of progressive MS. With that, I want to conclude my presentation. Thank you for being here on the last presentation of the conference.