Immunic at Jefferies Conference: Promising MS Drug Insights

On Thursday, 05 June 2025, Immunic Inc (NASDAQ:IMUX) presented at the Jefferies Global Healthcare Conference 2025, showcasing its strategic focus on novel treatments for multiple sclerosis (MS) and gastrointestinal diseases. The company highlighted promising clinical trial results and outlined ambitious financial goals, though it faces challenges in a competitive market.

Key Takeaways

• Immunic’s lead drug, edifumumab calcium, showed positive results in Phase 2 trials for progressive MS, reducing disability worsening.
• Phase 3 trials for relapsing MS are underway, with results expected by the end of 2026.
• IMU-856 demonstrated potential in restoring gut health and managing weight gain in preclinical and clinical studies.
• A recent $65 million secondary offering supports ongoing research and development efforts.
• Immunic projects peak sales potential for edifumumab calcium between $3 billion and $7 billion across all forms of MS.

Financial Results

• Completed a secondary offering, raising $65 million to fund clinical programs.

Pipeline Update

edifumumab calcium

• Phase 3 trials ENSURE-1 and ENSURE-2 are fully enrolled, involving approximately 1,100 patients in each arm.
• Phase 2 CALIPER study showed a significant reduction in disability progression in progressive MS.
• EMPHASIS phase 2 study in relapsing MS demonstrated a 76% reduction in active lesions and a 78% reduction in gadolinium-enhancing lesions.

IMU-856

• Phase 1b study in celiac disease patients showed significant protection of gut villi and improved vitamin B12 uptake.
• Preclinical studies in rats indicated a dose-dependent reduction in body weight gain by up to 40%.

Operational Updates

• Phase 3 trials ENSURE-1 and ENSURE-2 are fully enrolled, with topline data expected by the end of 2026.
• The CALIPER study has been completed.
• Potential NDA submission for edifumumab calcium in 2027, pending successful trial outcomes.

Future Outlook

• Immunic aims to submit an NDA for edifumumab calcium in 2027, contingent on positive Phase 3 results.
• Continued exploration of IMU-856 for weight management and gastrointestinal disorders.
• Focused on advancing the clinical pipeline to address unmet needs in MS and gastrointestinal diseases.

Readers are encouraged to refer to the full transcript for more comprehensive insights.

Full transcript - Jefferies Global Healthcare Conference 2025:

Xander Guarna, Investment Banking Team, Jefferies: 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 Witt, the CEO of Munich.

Daniel Witt, CEO, Munich: Yeah. Thank you for having us here today, and please consider our cautionary note of regarding forward looking statements during the presentation. So happy to introduce Immuniq, today. So Immuniq is a clinical stage company focusing on new oral treatments for chronic inflammation, autoimmune disease, and specifically with a focus on multiple sclerosis with pretty new data. This morning we published another update on very interesting, exciting data from our phase two study in progressive MS patients.

With with our portfolio, we are targeting a large commercial opportunity of several billion dollars peak sales potential for video fullness calcium. And and also to to add on that, we just recently completed a secondary offering for $65,000,000. Our pipeline consists a couple of products. Most advanced beta thalamus calcium in phase three in relapsing MS. And as I said, just recently, brand hot data from our progressive MS CALIPER study.

On top of that, we also run a second clinical stage program IMU eight five six targeting gastrointestinal diseases, specifically celiac disease. And also here, we recently published some interesting additional data specifically on the effect on integrins. So let me start with more details on our beta thalamus calcium program, which is a quite could be a very transformative new treatment for multiple sclerosis. Beta frutimous 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. And it’s 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 to smoothen overshooting immunity by really leveling down the the anti inflammatory the anti the inflammatory activity in myelofibrosis.

On top of that, the drug is a very potent activator of NurOwn. NurOwn 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. So we think it’s the perfect the perfect benefit risk profile for treating myelofibrosis. But if you look on current treatments and the medical need in multiple sclerosis, clearly, the key unmet medical need, so the elephant in the room for patients with multiple sclerosis is disability progression.

So the ultimate purpose of developing new drugs in MS is really to stop or slow down disability worsening. And main reason why the the current treatmentsreally.net did not so far really deliver something substantial on that and specifically if it comes to disability progression, which is independent of relapse activity, is that most drugs really focusing on on just systemic inflammation. And I think it’s important to have a look on the different roles of inflammation and neurodegeneration in the different forms of multiple sclerosis. So on the left, you see in relapsing MS, the main 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 in disability worsening over time.

But ultimately, in all forms of multiple sclerosis, this motoring disease or neurodegeneration plays an important role. In relapsing MS, we call this PERA. In the progressive forms, this is just a progression we measure in in clinical trials. In progressive MS, we have basically two forms of 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 of diagnosis. Globally or or maybe in the in the in the seven biggest markets, the the number of eligible patients for multiple sclerosis is one point two billion with nine hundred thousand in relapsing MS, hundred and seventy five thousand in non active SPMS, and roundabout a hundred twenty thousand patients with PPMS. And our product is, as I said, in phase three testing for RMS and just completed phase two study for both forms of progressive MS. With the number of patients and also the the high number of patients which are currently not on a treatment, we project the the peak sales potential of the drug to be all in all 3 to 7,000,000,000 in all of the the different forms of of MS. So where did it start and and why are we testing it in all the different forms of progressive of MS?

So it goes back to a phase two study we performed in ’9 ’2 thousand ’19 and ’20 ’20 in patients with relapsing MS, the EMPHASIS study. And that study was very successful, and I’ll show you some data in a minute. And based on the outcome of that study, we decided to, on the one hand, continue the drug in relapsing MS, the so called ensure one and ensure two studies. And I’m very happy to to announce that that we announced today that we fully enrolled both studies and now waiting to read out top line data from the study at the end of twenty twenty six. Based on some interesting results from the EMPHASIS phase two study, we also have seen hints of neuroprotection at that time.

And 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, so there is no overlay of the two signals, but really to focus on reducing disability progression. And that was done in the phase two study, so called CALIPR study. But before going there, let me first start with a summary of the the mode of action. So as I said, on the one end, the drug targets d h o d h 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 one, and no one activation was found to be an important regulator for protecting neurons from cell death in in several settings.

So as I said, it first started with a phase two study, the emphasis study in patients with relapsing MS. And this is a this was a pretty successful study. Two hundred sixty eight patients randomized. We tested three different doses, ten, thirty, and forty five milligram against placebo. And the primary endpoint of the study was reduction of inflammatory lesions in the MRI.

And that was pretty successful. So we have seen a seventy six percent reduction of accumulated active lesions after twenty four week of treatment compared with placebo. A reduction of seventy eight percent of gadolinium enhancing lesions at week twenty four with high statistically significance. So that’s just checking the box of drug confirms the expected anti inflammatory effect. What was a little bit surprising was to see that that after twenty four 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.

And that that was more or less the reason why we decided to further investigate the neuroprotective features of the drug. And also we followed up those patients after the double blind placebo controlled part of the study in an open label extension. And in these two years after after completion of the the main study period, after two years, still ninety four point two percent of patients were free of confirmed disability worsening. It was a quite promising thing, and therefore, now I’m happy to, in in a minute, to 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. So 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. So based on all of that, we then started phase three clinical development of ediformis calcium in relapsing MS in the INSURE studies. In these studies, which as I said was just right now and completely enrolled, we are testing separately roundabout 1,100 patients in each study against roundabout 550 in each arm, thirty five milligram of edifameless calcium against placebo.

And the primary endpoint of the study is time to first relapse. The studies are expected to to read our top line data end of twenty twenty six. An important piece is here that we we predefined that we can pull 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 a indication of high unmet medical needs.

So far, there’s only one drug approved for treating one of the forms of prime of progressive MS, which is primary progressive MS, and the approved drug is subgrievous from Roche. And hundred and twenty thousand patients are diagnosed in US and The U Five countries. And interestingly, really, only forty five percent of patients are on active deceit modifying therapy. Also, on top of that, the indication is highly underdiagnosed. So there’s a, I think, a hidden bigger chunk of patients which which need treatments in the future.

We decided to not jump immediately into a phase three study, but really to do a a scientifically driven phase two study and testing the effect of the drug in the 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 forty five milligrams. So we’re testing forty five milligram against placebo in four hundred sixty seven patients randomized. We also allowed patients of an age from 18 up to 65 years to be part of the study, and we enrolled patients with primary and secondary progressive MS. The study duration was at minimum seventy two weeks for patients and up to a hundred and twenty weeks follow-up time.

An important thing is here the different sub indications. So we have thirty two percent of patients with primary progressive MS, fifty seven percent of patients with non active SPMS, and ten percent of patients with active SPMS. On the right, you see the baseline characteristics. So the median age was 51 years. An important piece is on the bottom of the table is that we had a quite low number of patients with active gadolinium enhancing lesions at baseline of sixteen point three percent.

So that means this patient population is pretty advanced and has little remaining inflammatory activity, so more difficult to treat with any current drugs. Main conclusions from the study are Caliper successfully demonstrated the neuroprotective potential of edifluminous calcium in progressive MS. And secondly, we have seen a clinically meaningful risk reduction of confirmed disability of twenty four percent in the overall study and thirty three percent in the PPMS primary progressive MS subpopulation study. And as I said, just fresh from the press, our our data on time to ’24, we confirmed disability worsening. This is, by the way, the endpoint which likely will be the endpoint of any future phase three study in PPMS or SPMS.

So in overall, we have seen a twenty four point one percent reduction of risk on time to twenty four week confirmed disability worsening. And in the PPMS, primary progressive MS population, it was thirty two point five percent, a pretty remarkably high number of reduction. In non active SPMS, almost twenty percent. And in the active SPMS subset, thirty three point seven percent. We also have follow-up as a secondary endpoint, the change of EDSS or the disability score from baseline.

And what you see in this graph is that for the treated patients, it’s almost a flat line. So very small increase or marginal increase on EDSS and average over time. Whereas the placebo group really increases all the time on EDSS. And starting from week 60, this difference got statistically significant on the difference between placebo and active. So how to position the data?

What does it tell us? I think if you look back on the I mentioned the only approved doc or crevasse, the baseline characteristics between CALIPER subset of PPMS and the AUTORIO study was pretty similar, age, baseline EDSS and SURPHY. Maybe the most remarkable difference was that, you know, in the aurorio study, they had around about twenty six percent of patients with active inflammation. So baseline gadolinium enhancing lesions, whereas our our activity here was seventeen point eight percent only. But we have seen on a numerical level a quite high rate of risk reduction here compared also to to Arterio.

And so the question was, how does beta frutimous calcium perform in in the patients which are free of gadolinium lesions, so which don’t have this remaining activity. We know that that for for or previous, for example, the activity of risk reduction was really less pronounced in patients without inflammation. And surprisingly, we have seen a very, very strong activity in those patients. So three hundred ninety one patients were free of baseline gadolinium enhancing lesions and we’ve seen a thirty four percent reduction of ten to twenty four week confirmed disability worsening. And that comes from both subgroups from PPMS and non active SPMS populations.

With thirty five percent for PPMS and almost thirty percent for non active SPMS. Maybe to to point to that a little bit, this is, I think, key data showing how good the drug differentiates from what’s currently available. And we think this is a key feature of beta thalamus 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 important endpoint and I’m very glad that the top line data confirmed the favorable safety and tolerability profile of edifumumab calcium with no new findings on the safety side. And I think the occurrence of treatment emerging adverse events and SAEs with similar frequency in both treatment arms as shown here on the tables.

So 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 thirty four percent reduction of twenty four week confirmed disability worsening in the patients without baseline inflammatory lesions. So all in all, a pretty attractive result from that study. So what’s next? So with this wonderful data, we’re now heading towards the readout of the ENDSURE phase three studies towards end of next year, which in in a positive outcome case would allow us to submit an NDA in 2027. So that was the summary of beautiful miss calcium in multiple sclerosis.

Let’s switch over to our second asset, IMU eight five six. And as I said, this is a program which is targeting gastrointestinal diseases. And the the concept here is that we want to restore a healthy gut through renewal of the the bowel wall, the epithelial layer of the bowel wall, basically. This is a completely new approach. This molecule is a sertoin six selective sertoin six modulator.

And with that, targeting the epithelial regeneration and the the gut cell function. It can, in principle, because it’s a it’s an approach which is not immunosuppressive, it can be applied, in principle, 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. So 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. So more or less, it’s a it’s a defense against the the root cause of a couple of GI disorders. Before coming to the clinical part, we have done as part of our phase one study where we tested also on top of safety and tolerability the effect in patients with celiac disease. And 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 of specifically of enteroendocrine cells or l cells in the gut is to produce incretins. And the incretins are important messengers of, for example, of food uptake and stop of hunger and so forth. And that’s a natural control mechanism. And and therefore a very important system to control weight gain and gut health in general. We have, as I said, we have performed a phase one clinical study with IMU856 where we tested several doses of the drug against placebo, But also we have performed the long term chronic tox studies including a six month study in rats, where we tested a couple of different dose things of the molecule.

And we have seen very interesting results from both studies, from the clinical and the preclinical studies. And let me start with the preclinical data. For for the for the treatment here in in in rats, I think we have seen a very nice dose dependent effect on body weight gain. And this was linked to the food consumptions in the study and affected males and females. So the conclusion here from that preclinical work was that IMU eight fifty six efficiently reduced the body weight gain in a in a dose dependent fashion of up to 40.

So this was not a weight reduction, but a prevention of weight gain experiment. So we we’ve we said, okay. We still have the clinical samples of our celiac disease patients. So we we went back and looked on the changes of of incretins and specifically GLP one. We were surprised to see that we see here at the specifically at the hundred sixty milligram dose group, a up to 250% increase of baseline GLP one levels in the patient samples.

That’s another confirmation of the role of the gut cells in producing these things, and we will further investigate to what extent IMU eight fifty six could be a quite unique, new, and differentiated approach to manage weight gain in humans. But coming back to the initial idea of gut health and a proof of concept study we have done in a in a phase one b study. And we decided to choose celiac disease as an important indication with no approved drug for proof of concept here. And it’s important to to notice that there are millions of people which are suffering from from celiac disease. And most importantly, among those patients, have twenty four to forty seven percent of patients which have ongoing active disease despite being on gluten free diet.

And this is most people aren’t aware of that high high number of patients which are really having suffering from symptoms of celiac disease despite really sticking to a very rigid gluten free diet. And so far, as I said, there is no therapeutic approach. So the only approach right now is to really stay away from gluten for lifelong gluten free diet. So this study was a two was a four week study where the first two weeks were just dosing either the active agent of eight five six or or placebo. And then in the second two weeks of the study, we also added six gram daily gluten to the diet.

And so the concept here was first to give the patients time so that the drug works and can restore the epithelial layer in the gut. And then for the next two weeks to observe to what extent can we protect the patients from damage of the gut wall. And for doing that, we did histological assessments at baseline and after four weeks of treatment. We tested eighty, one hundred and sixty milligram of the dose against placebo as pretty small studies, but despite only having eleven, thirteen and thirteen patients in the different dose groups, we have seen a statistically significant protection of the the villi in the gut over the twenty nine day observation period. So pretty amazing data for that short time frame.

Another question, a functional question, and maybe more links to the GLP one data I’ve shown before was, can we improve the function of the gut again? So remember the the on the the challenge of active transport of nutrients. And interestingly, you see on the left side that the drug was able in this short time frame to restore the uptake of vitamin b twelve 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. So let me summarize immunoSEQ in general.

So we have with vitreous calcium, we have a derisked near term commercial opportunity in active phase three testing in relapsing MS and with a wonderful differentiated profile and unique dataset from our recently completed phase two study in progressive MS. And 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 they are their progression is independent of relapses and independent of active inflammation. And 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. And we think that vitreiformis 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. And with that, I want to conclude my presentation.

Thank you for for being here on the last presentation of the conference.

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