Still 11:30 A.M. Okay, good morning everyone. Yatin Suneja from Guggenheim. Welcome to Guggenheim Outlook, Biotech Summit 2026. Pleasure to welcome our next presenting company, InflaRx. From the company we have two executives here. We have Thomas Taapken, who is the Chief Financial Officer, and then we have Jan Medina, who's on the IR side. Gentlemen, thank you so much for your time. We appreciate it. Tom, why don't you make some opening comment, tell us the story of InflaRx, what are some of the upcoming milestones, and then we'll go into some of the Q&A that I have prepared for you. Thank you very much, Yatin, for having us, first of all, and good morning everybody. Happy to be here again, and, yeah, be happy to say a few words about, InflaRx, for those who don't know us. We're a company based in, Germany and in the U.S., been around for a while, listed, did an IPO here on NASDAQ in 2017, and, you know, have been developing drugs in the area of, terminal complement, inhibition of C5a, through an antibody called vilobelimab, and now also inhibition of the C5a receptor 1, which we are addressing with a new small molecule called izicopan. So that's been in development now for a while and has recently completed its first, proof of concept, phase IIA study with, results that we deem to be quite, quite positive. Got it. So let's, I'll come back to I think you're going to do a Capital Markets Day, but I think I'm going to come back to that later. So let's just focus on the main molecule, oral C5aR receptor antagonist, izicopan that you have. How differentiated that molecule is, in your view, relative to what is out there? Amgen has a drug approved. There is some stuff going on there. We'll discuss that. But just articulate for us the properties of the molecule, at least, on a pharmacological level. Sure. Happy to do that. So, the inhibition of C5aR has been something that a lot of pharma companies have been working on for a long time, and it has been very challenging, and so far, very few have been successful in developing molecules that have the right pharmacological parameters and also the right safety and efficacy. So the first molecule in this area was avacopan from a company called ChemoCentryx that subsequently was acquired by Amgen. Avacopan was ultimately approved for the treatment of ANCA-associated vasculitis, and for us, it really was also a little bit of the blueprint for our own discovery efforts. So we looked at the same kind of area. We looked at molecules that were binders of the specific region in the receptor that avacopan is also targeting, and we developed, or tried to develop and then successfully developed izicopan, which is a molecule that has comparable chemical properties, comparable receptor binding, high receptor binding as avacopan has, but it has significantly improved pharmacological properties. And these include, for example, you know, significantly higher availability and bioavailability of the molecule. We have significantly higher plasma levels at same dosing. We see the more rapid onset of receptor inhibition. So within very few days, we reach our peak levels, and at steady state, which for avacopan takes significantly longer. Actually, it's in the range of three months or so, I think 13 weeks, for them. What is also important on the safety side, the inhibition of CYP3A4, which is part of the cytochrome P450 liver clearance mechanism, is significantly lower in our case. So we do have a 36 times lower inhibition, which leads to potentially less significant issues going forward with drug-drug interactions and things like that. So we feel we have a safer molecule, a molecule that is more stable as well, and a molecule that reaches you know therapeutic levels in lower doses much faster than avacopan. Got it, got it. So clearly a differentiated molecule, right, higher bioavailability, you get faster peak, no DDIs. But I think the one thing that we are recently picking up is, and I want you to sort of opine on that, this hepatotoxicity that we see with the avacopan. Is that, in your view, a molecule-specific issue because that molecule doesn't have the clean DDI, or is a target issue in what you might have seen in any of your patients that have been dosed with your drug? Now, so far we are absolutely clean. We have not seen any toxicity issues that would relate to the molecule itself or to the pathway. So what we believe it to be the case for avacopan is clearly molecule-related and not pathway-related. So our molecule has a very clean safety profile, and it's very important to mention this. We have treated now, I think, in the range of 200 patients, and all of them have shown no signals at different doses, even high doses, no signals of hepatotoxicity. We associate the observed and reported hepatotoxicity of avacopan in certain Japanese patients that has been published to the, you know, the inhibition of the liver enzymes and the accumulation of other drugs because these patients have received, of course, significant amounts of glucocorticosteroids, but also some other drugs that are cleared through the liver. So we believe there could be an association of the high CYP3A4 binding and the observed hepatotoxicity. Got it. But we don't know. It's speculative. As Tom said, I think, you know, in terms of the biologic, the pathway seems clean from a liver tox. So it's more. Got it, got it. So I know you guys are going into more of the autoimmune indications like HS and urticaria. There you have a plan. But let's say if Amgen were to pull the drug from the market, avacopan, is that an indication? Does that open up new opportunities for you because your molecule is so clean and very, very differentiated? No, absolutely. We, you know, saw the news, as you all have seen it, in the last couple of weeks, and we were very surprised and, of course, immediately saw this as an opportunity to consider. We have initiated conversations with our key opinion leaders and are preparing ourselves to position ourselves. But you know, at this point, it's too premature to make any decisions. We'll see how this all unfolds and develops, but we believe that there is certainly a potentially interesting opportunity that could open up very quickly. Got it. Then, for the HS, hidradenitis suppurativa, you conducted a study there. Just can you review for us, like, what exactly did you see, how what type of doses you have seen there? I know it was a 28-day or four-week study, but I think the signal was there. So just articulate for us, like, what exactly in the key learnings. Yeah, as I said earlier, this is really the first proof of concept studies in patients that we did. It was a basket study in HS patients and CSU in different doses. We only could dose for four weeks at that time because when we initiated the study, our long-term tox data was not ready yet, but we still wanted to do this as a signal-finding study. What we saw there was actually quite remarkable. We compared the data that we generated to all the published phase II and phase III conducted HS trials, and we could see very clear, you know, in-line, if not better, responses after four weeks compared to all other molecules that have been developed in HS. So for us, it's early data, of course, and it's not placebo-controlled. However, it is a very encouraging signal that we have seen. There are two elements that are especially remarkable. One is the reduction of draining tunnels, which we feel is a unique feature of the drug that has really been shown very clearly even after that short treatment period across all doses, but especially in the high dose that we tried. The second element was the reduction of pain, which was also very remarkable compared to what other drugs have shown after four weeks. This is a very clear indicator for the reduction of the inflammation in the deep skin. We feel that these two things are, in fact, correlated and could potentially hint at a differentiated mechanism that has great advantages to what others have been doing in this field. Got it. It really drives to a consistency of the mechanism, the pathology of the disease, and then the data that we saw is all very, very consistent, and makes sense. I mean, yeah, it's not just you because I think the similar mechanism with avacopan has been evaluated. So it's a second independent study where there was a sort of a clear signal that the pathway is active. Yeah, the avacopan data actually is interesting in the sense that at that time, when we looked at it, it looked like, okay, it is not a particularly strong drug. But looking at the pharmacokinetic properties of the drug, one could see that you see initial signals of efficacy towards the end of the dosing period. What we could not understand at the time, of course, is related to the fact that only steady state is only reached at a very late stage in the dosing. And we have this data already available that we see that, you know, we see full exposure after a few days, and that gives us an opportunity to dose, you know, by significantly lower dosage, having still the very good effect. Got it. So, I think you tested three doses there, right? Do you have a good handle on the dose, going forward? What are your plans, after this? Where are you, in terms of the tox work also that enables long-term dosing? So to start with the latter one, tox for long-term dosing is available. We have completed all the experiments, and they're all clean and allow us to go into indefinite dosing, basically. So this was the 9-month non-human primate data that was missing at the time we started this study, and that's all available now, and we're clear and good to go from that perspective. In terms of doses for the next phase II study, for the phase IIB study, we're still discussing this internally and also with the FDA because we think that what we saw at that time when we did the phase IIA is maybe a little bit early in terms of being able to come up with conclusive views on the dose and the appropriate dose. So we are doing, you know, additional PK simulation studies and additional work that will guide us to find the appropriate doses. We would be interested to test as many doses as possible on one side. On the other side, you want to be, of course, conscious of time and money that you spend on this study, so that's why we're balancing and trying to elucidate what the right, the right doses would be for. Got it. And then the next step would be what? Just to go into a phase II, or you do go directly into a phase III? Like, what, how are you thinking about the development plan? No, we will have to go and do a phase IIB study. That would be a requirement because this four-week trial will not allow us to go straight into a pivotal trial. That's pretty sure. Yes. Okay. And then, you are hosting this Capital Markets Day. Do we know when? I think you've said spring. Would you set the stage for us? What should we expect? It seems like there should be some disclosure around HS there. Yes, absolutely. I mean, what I hinted to is that the fact that we're still working on trial design, on the number of arms and the endpoints, the doses that we're going to use. And that's all subject of discussions with regulators, key opinion leaders, and internal deliberations. And once we have all that cleared out, we will be hosting that Capital Markets Day, hopefully, you know, sooner than later, but we're still. Yeah, in the spring. I think we'd also like to talk a little bit about the indications we'd be looking at outside HS or CSU, whether it's AAV or we've talked a lot about really looking at the pipeline in a product and, you know, with new options today than we did. Yeah. I think if you look at the HS space, there is a lot of white space for orals. Obviously, the JAKs are there. We're going to get there with izicopan. How do you see the landscape? What is there a relative bar that you hear from physicians? I think for monoclonal antibodies, we hear it's about 20% delta. Everybody talks about from placebo-adjusted HiSCR. But how are you looking at the commercial side for HS from oral drug perspective? Well, a couple of things here. Obviously, we need to have convincing biologic-like activity, which we believe we have already seen in this short 4-week treatment study. So that is one of the bars that we need certainly to reach. We cannot be significantly worse than the injectables out there. However, safety is going to be a very important issue around the orals, especially. And some of the oral PO molecules out there are in classes that potentially might have some safety issues. So it's not clear that everybody will have that, but that will have to be watched very carefully. And we believe with our safety profile so far, we are in a very good position to really have potentially a best-in-class molecule. The treatment of draining tunnels remains one of the major unmet needs. And, you know, if you look at the results we had in our short trial and the pain reduction, we believe that this will be a very clear differentiating factor. In terms of differentiation from HiSCR, I believe here, you know, you know our views about HiSCR and how HiSCR is not maybe an ideal endpoint. And if you ask key opinion leaders, nobody is really using HiSCR in order to assess his or her patients. This is a clinical trial endpoint rather than a true, you know, measure of severity of disease for patients. So we will have to work that out, and we'll have to show, of course, this convincing efficacy. But we feel that, you know, this will be also part of, by the way, of the regulatory discussions we're having to define the right way of showing these effects on draining tunnels that we are seeing and how to include this in a potential endpoint for a phase III and then, of course, at some point into the label. Got it. With regard to the CSU or chronic spontaneous urticaria study, what are the plans in urticaria? Is that something you could still pursue, or that's or HS is the key focus right now? Well, I mean, of course, as a relatively small company, we have to focus, and for us, HS is the primary focus. However, the data that we generated in CSU, we feel, is quite encouraging, and we have looked into the data now in more and more detail also with some external key opinion leaders. And we got a lot of encouragement that this is data that is certainly worth pursuing in additional clinical trials. So, you know, given unlimited resources, we certainly would also look into this. Or in the context of potential partnerships going forward, this could be something in an area in which we would be able to expand very easily. We have, you know, initial data. We have physicians that believe that this is a mechanism that could play a significant role in CSU. We have a drug that we feel, even in this competitive landscape, is quite unique and could differentiate itself very well from the competitors. Got it. We saw some particularly good data in some of the subset of patients in terms of more severe CSU or CSU patients with angioedema. Small numbers, but still large parts of the CSU population that we could potentially consider phase IIB. So that's indication seems like is on the cards provided funding, I mean, if you have the resources. It's not that you're not. Okay. How is the financial position? I think you guys recently, you know, reduced some expenses. Like, what part of the operations are being deprioritized? Like, how are you optimizing the company? Well, as you know, we had, still, significant amount of activities around vilobelimab and the development there. We, unfortunately had to stop a phase III study in 2025. And, you know, with the deprioritization of, vilobelimab as a development asset and also as a commercial opportunity, for COVID, which was anyway a very niche market and a relatively small activity, we had to take all that out of the equation. So in the end, we were able to reduce our fixed cost basis by roughly 30%, including personnel, but also other ongoing expenses in that area. Got it. Got it. Yeah. Well, very good. I think looking forward to the Capital Markets Day, hopefully in spring relatively soon. But yeah, thank you so much. Thank you very much, Yatin. Thank you. How are we? Thanks. Looking forward. Bye now.