All right. Hey, good morning, everyone. Welcome to Oppenheimer's 36th Annual Healthcare Life Sciences Conference. My name is Andreas Argyrides. I'm one of the senior biotech analysts at Oppenheimer, and today I have the pleasure to be joined by Niels C. Riedemann, CEO, and Jan Medina, IR. InflaRx is a biopharmaceutical company focused on applying its proprietary anti-C5a and C5a inhibitors to the treatment of inflammatory diseases such as hidradenitis suppurativa and chronic. Great to have you today, Niels and Jan. With that, I'll let you take it away with the presentation, and we'll have some time at the end for some Q&A. Thank you so much, Andreas. Thanks also for inviting us. We're happy to be here today. I'm happy to guide you through the presentation. Let's go right at it. Please make sure to take note of our forward-looking statement that we will be making and the disclosures here, since we're a public company. We will be presenting also reported data from other drugs and compiled data for orientational purposes only. Please take note that that is important for us. As Andreas, as you put this already quite rightly into words, we are focusing on the terminal complement pathway with inhibitors for C5a, C5aAR, and we are very excited about our new oral inhibitor, izicopan, that blocks the C5a receptor 1, and has just recently shown biologic-like efficacy in HS and also efficacy in CSU. You know, what we love about this mechanism and this drug is a few things. First of all, it is really showing a high potency on its target engagement, and therefore, you know, it's a very well-known target in the I&I space, so probably this has large potential, as we believe, to be transformative, even in some anti-inflammatory diseases or in various diseases, being a pipeline and a product. At the same time, there's a market comparator, and we have clearly shown best-in-class potential here from our studies, and I will go through this in a bit more detail. We have recently streamlined our corporate strategy really towards the development of this drug in the broader I&I space. I will talk to that as well. We are right now cash funded with operations into mid-2027, and we have various exciting potential next steps in front of us. We have a very strong I.P. position with just recently issued I.P. in the U.S., but also elsewhere on this new molecule with a broad portfolio, also on C5a inhibitors in general. Let's talk about terminal complement inhibition, just very briefly. As you know, we're targeting C5a or C5aR. I've been talking about C5aR1 here with izicopan, our new small oral inhibitor, but we also have a very active, very potent monoclonal IV-infused antibody, which is vilobelimab, that targets the ligand C5a. This pathway is important because it really translates all sorts of signals of inflammation, danger signals, into the cellular immune response, particularly of neutrophils, macrophages, monocytes. It's the innate immune side of things that when you have flares, for example, in chronic diseases, get very damaging, you know, tissue damage, driving disease progression. We believe that this drug can really exert an effect by really preventing this tissue damage. Why not use upstream inhibitors? That's a question we frequently get, and the answer is: just because upstream inhibitors are not potently inhibiting this terminal complement pathway. Why is this? Because there's two different ways to generate C5a and interact with C5aR. One is through the upstream pathways, through the so-called C5 convertases. This is like the blue side of things on the left side here. The other one is all sorts of different enzymes, even those produced by monocytic cells like macrophages and neutrophils, can cleave C5 directly with a different mechanism, directly at the cis side bonds, where it's attached to the mother molecule. This mechanism is not inhibited at all, not even by C5 inhibitors that you may know that are approved for various diseases. Long story short, you can't fully block C5a. You can't even get significant control over this pathway, other than through going through the ligand or to the receptor with highly potent drugs like we have. Let's take a look at our pipeline. We recently completed a phase II study in HS and CSU, as Andreas already alluded to at the beginning, and we'll be sharing some of the data with you today. We are very interested in other immuno-dermatology, but also broader I&I space, and we'll be talking about that in the next slide. Now, just to mention that this pathway is validated already with our Gohibic drug, our vilobelimab antibody that has gotten an U.S. Emergency Use Authorization and an approval in Europe for SARS-CoV-2-induced moderate to severe ARDS in Europe. You know, that is interesting because it has shown life-saving potential, and there is the potential to develop this in broader ARDS. We're running a phase II study selected by the U.S. government, by BARDA, in one of the largest ARDS trials, which is currently ongoing. That's just as a teaser here, but we will be talking and spending time today on izicopan. Why is this interesting? It holds the potential to develop in various different areas, as depicted on this slide. Our initial focus with HS here clearly is the immuno-dermatology space and beyond HS. There are other spaces, particularly in the I&I space, the renal space, and others that we want to be talking about. One of the indications we're very seriously investigating right now into a future potential development is ANCA-associated vasculitis. Why is this the case? Because as you may know, there's a marketed comparator that has been approved for ANCA-associated vasculitis and has been commercially so far very successful. There have been recent news from the FDA related to that have prompted us to say, "Let's take a look at this market." Because we believe we have a differentiated molecule that can be differentiated on its potential to influence or not influence, in this case, drug-drug interactions, because we have a better profile there. Also, we have a pretty potent drug that's differently formulated. I will be speaking about the differentiation in the next slide, but this is an area where we get a lot of recent questions. We have been interested in ANCA-associated vasculitis for a long time. We've been conducting two studies that successfully concluded some years ago with the antibody, so we principally know the space quite well. Now that this market has become very real in terms of commercial opportunity, with a $1 billion + opportunity depicted by current sales of the market comparator, at peak, I should say. They're not there yet, but, you know, that's the peak prediction here. For us, this creates potential opportunities, we're evaluating this. Beyond that, there's also interesting other areas. I mentioned the proven pathway already in some of the life-threatening diseases, with the immune response playing a big role in that. Let's look at the differentiation to the marketed comparator, which you can see quite visually here on the upper right side. This is just reported data for avacopan, which is the name of that comparator, at 30 mg, which is the approved dose, and you see in blue lines here, different doses of our drug. Again, this was not head-to-head, but you can see that the 30 mg dose, which is kind of above the red, shows a very differentiated profile already. We have a 10x increase of area under the curve, a 3x higher peak, and just a very different plasma distribution. Plus, we could dose safely up to 240 mg. Now, why is this important to have such a differentiated PK? Because we believe you need that to significantly block this pathway, not just in human blood, where we have shown that in the picture below. We have super nice, 90%-100% inhibitory potential at all different doses tested above 30 mg, really great outcome. That has not been the case in the reported data of avacopan, where they only reached about 50% blocking activity. Also in the tissue, right? You wanna have a high plasma and high tissue presence. Long story short, we believe it is the PK differentiation that allows us to reach plasma levels much earlier. Avacopan takes 30 weeks to reach steady state in ANCA-associated vasculitis. We can reach multiples of that steady state plasma levels already in the first days or week. That's really the one thing. The other thing is we have also a safety differentiation. We have a 36-fold less engagement with the CYP3A4/5 inhibition, liver enzymatic apparatus that builds down, for example, corticosteroids, but also all sorts of drugs and toxins. You don't wanna touch that too much, because that can induce LiverTox signals. We haven't seen such signals, and we have a very clean safety profile so far. We have over 100 up, 80 human subjects dosed so far, up to four weeks, maximum, I should say. But so far, we have not seen any signals of safety concern. Last but not least, we have 30 mg formulated in one capsule, not in three, like avacopan, and we have the potential to up dose, and the potential, which still has to be shown and fully worked out, of QD dosing in the future. Long story short, we're very differentiated. We've worked many, many years on creating a potential best-in-class drug. We believe we have a drug with this potential in our hands. This is just one illustration of why that makes sense, because this was a real head-to-head experiment with avacopan in a in vivo system in hamster. Don't want to go into details, just saying at the same 10 mg, you see again, a very different plasma presence here on the right side of the graph. Again, the like 3.5x already right away, and you see almost a doubling of the inhibitory potential of the drug in plasma, which has to do with the PK. I do wanna mention that in vitro, the IC50 of these two drugs are very similar, almost identical. It really is the different structure of the molecule and the different PK and formulation that was a huge challenge over the years to solve, to really get to this high potency in the in vivo system. This just illustrates from the phase II some of the initial considerations, I should say. On the right graph, you see avacopan posted, we plotted the data that were reported for avacopan in ANCA-associated vasculitis, so different disease takes 13 weeks to reach steady state, and you see that in our phase II study here in HS and also in CSU, we reach a multiple already on day 1, so to speak, after the first tablets. We have really therapeutic exposures as we believe already right away in the first days or week or so. That's a huge outcome for us. It's exactly what we had hoped to see, and I would like to now go into the data that we generated. Before I do that, last comment here on my end, we have more data on the differentiation of these two molecules that we put in the public domain. You'll find that in the full slide deck, also on our website. That's interesting because it's not just the CYP3A4/5, it's also the fact that our drug has a different structure, chemical structure. It has three chiral centers, not two, like avacopan, and it is more stable in in vitro studies, creating a significantly less metabolite formation and being a differentiated drug with a differentiated feature. Take a look if you're interested. Let's go to HS. It's a very interesting disease, and we have here taken a four-week study. The results we posted so far is from 29 patients that were evaluable. We also had a four-week follow-up period without dosing and visit, where we had 25 patients. I will speak to that a little bit, so take a note. There were two additional patients, not in the high-dose group that was completed, but in the low and medium-dose group that we're still missing in this analysis, and we will show these data in due course in the conference. I'm not gonna introduce in the long fashion the disease HS. I think by now it's very well known in the field. Let me just say that it is probably more common than originally thought. There's a lot of patients suffering from this disease. It's a living nightmare. These patients develop different lesions, particularly three inflammatory lesions, the inflammatory nodules that are deep-seated in the skin and very painful. They can ripen into real abscesses that become very painful and can release lots of pus at once when they break open. Then the most chronic form, the so-called draining tunnels, that can drain up to 1 liter of pus per tunnel per day, and unfortunately, they usually are under the armpits or in the groin areas, genital areas. They have a huge social impact on social life, on odor, on pus formation, on just daily activity. It's a nightmare disease. There's approved drugs. It's a huge market opportunity, there's no drug that caters to the exact same mechanism like our drug, and I want to show you why this is important. This is why. There's now more and more evidence on the role of C5a, C5aR, particularly, the role of the cells that C5aR activation attracts, namely neutrophils and monocytic cells, into and around the lesions. You see that beautifully here in the upper middle picture, where all these brown-stained C5a receptors, these are all on neutrophils and monocytic cells and giant cells. Guess what? They gather around the draining tunnels. They are very similar pictures, how they gather around abscesses and in the lesional skin or surrounding these lesions, but particularly strongly in and around draining tunnels. Why is this important? Neutrophils, when they engage with C5a through C5aR, they undergo NETosis. NETosis has been described as one of the key drivers of sheath formation and tunnel formation in the deep skin. There are numerous review articles speaking to that, and, you know, we started this several years ago, and by now it's accepted that complement may play a big role, and it may play also a role by combining the idea that super infections that can engage C5a activation strongly, leads to strong flares and chronicity of the disease. There's multiple angles why this makes sense, and I speak about the data we generated here in the short-term exposure. The reason we only did four weeks open label is back then, we only had four weeks tox coverage. By now, we have completed the entire tox package, including months months non-human primate tox, without signals of safety concern. Back then, we only had the four-week coverage, so we did 60 mixed BID, 90 mixed BID, and 120 mixed BID for four weeks. As you can see, after the baseline visit, we had four treatment visits, even though patients took the tablets every day. At week four, we stopped dosing. We visited them, or we had them come back for a visit, the patients, one more time at week eight. In between, there was no dosing and no visits. Let's look at the lesions that I mentioned. The AN count is very important because it goes into the currently used score, the high score, and AN count means abscess and inflammatory nodules. You see on the left side how these three groups were composed, the green line will always show you the average of all doses together. The first thing you see is that already at week one, throughout the four weeks, you see a consistent improvement at all doses over time. Obviously, the most prominent in the high-dose group here, with a pretty remarkable reduction of abscess and nodules. I did not show you the baseline here, this was the group with by far the highest AN count at baseline. A more severe, like a severe disease population with a higher severity score, HS 4 score, a clearly impressive reduction. Now, how does it compare. Sorry, how does it compare here to the approved drugs, which are depicted in blue and the placebo in dotted blue, versus also phase II here, izicopan in gray and the placebo of it in the dotted gray? You see that the AN count reduction to this reported, pooled reported data, you find all the data going into this analysis underneath the slide. We are right on it, on the successful, like, drug curve, when it comes to the pooling, but the red group, so the 120 mg group, clearly exceeded that, you know, that average. Now comes a very meaningful point, the draining tunnels. You can see all the draining tunnels were reduced as well. There's always a bit of variability, but consistently, all three dose groups had a effect on draining tunnels, particularly strong, again, on the 120 mg group. On the right side, you see those patients that had draining tunnels, how many of those were at zero tunnel at week four already? That was 50% in the high-dose group, the average, close to 30%. Why is this meaningful? Draining tunnels take usually a long time to heal. That's a meaningful early notion. That's a big medical need for these patients 'cause there are no known drugs that sufficiently and significantly reduce drainage to this extent, at least. You know, normally, people would be happy to have such a readout at week 16. We have this at week four, by it being open label, we really like the data. This is how it compares to the published, completed, successful phase III studies. They compile sometimes analysis of all patients or those that only have draining tunnels at baseline, so we show you here both. However, that we depicted, it clearly is a very early deep signal. Interesting fun fact, placebo has hardly any any effect on draining tunnels throughout all these trials in average. So very unlikely that a -0.2 move on draining tunnels is a placebo effect in an open label study. Now we are talking about high score. High score is the currently used score that shows a very large variability due to various reasons that I'm not gonna get into today, but if you're interested, reach out to us. We're happy to educate a bit further on this. However, high score is something that, of course, you want to show because it makes it all comparable, and you see that there, despite some zigzagging, which is very normal, between tri dates on small data sets, we see a 38% on the high-dose group and the average of around 28%, which is, you know, clearly differentiated from placebo. The interesting part comes when we stop the drug. We looked at week eight, as I mentioned, and we saw a continued deepening of the effect. The high-dose group is completed here with these eight patients and went up to 63%, and the average went to 44%. That's great because that shows that we see continuous improvement with this mechanism after we take drug off. I should mention that we measure drug samples, initial drug samples at week eight, and they were still active drug levels, maybe not 200% blocking, but significantly blocking active levels, up to, for example, where avacopan accumulates to those types of levels, up to 200 nanogram per ml. We are happy about that. We also show on the right side how the different high-score brackets move, meaning as the time passes, we see more patients coming from a high score, 30% - 40% - 50%, which is a darker blue, to high score, 75%. It is a measure of time. Even though the effect may not be immediately strongest on nodules, they kick in after time and show impressive improvements. How does it compare? Altogether, we're right on the successful drug trial curve for phase III completed drugs. Again, the red curve, the high-dose group exceeds that a bit. Again, there's a large variability in HiSCR, so take it with a grain of salt, but we still wanted to show the data. The most meaningful data of all that we have gathered from discussing this with experts around the world, from Australia to U.K. to U.S., of course, is really the skin pain change over time. You see that within the four weeks, the two-point, sorry, the NRS30, meaning 30% improvement on the numeric rating scale of skin pain from 0 - 10, and at least two-point reduction has produced already up to 75% and an average of 66%. Is this meaningful? You see it on the right side. It is really exceeding reported data at early time points on pain. Does it make sense? Yes, it makes complete sense because a lot of the pain that these patients suffer from comes from the deep-seated formation of pus, the tissue tension in the draining tunnels and in the abscesses. If you have a drug that has an early impact on draining tunnels, you should see pain improvements, and we saw pretty remarkable pain improvements, and they were very consistent in the three dose groups. That's really something that we think makes a lot of sense together with the draining tunnel data and the overall data we've seen on all lesion reductions. Last but not least, a brief comparator analysis. Avacopan has been tested with its 30 mix, which is the approved dose in ANCA vasculitis. It has been tested in HS. They reported over time data on draining tunnels for whatever reason in ClinicalTrials.gov. You see how we compare here. On the right side, that's an apple and pear comparison, is izicopan four weeks versus avacopan 12-week data. You see that we reach already in average what they reach with their 30 mix. Clearly exceeding that with 120 mix at already four weeks, which bodes well with our theory that this is a PK game and a matter of how much you can block the pathway. The skin pain below also speaks to that. Long story short, we are very happy with these results. Even though it's just a four-week study, we feel this is biologic-like efficacy we see. We have a further deepening after we take the drug off here on the HiSCR, but also on other lesions. That data is not yet in here. Fast and deep reductions in draining tunnels, which is very remarkable, consistent with the skin pain I just showed you, and of course, other parameters we measured, like the Dermatology Life Quality Index. There were no signals of safety concern. I haven't gone through the safety data for time reasons, but really no signal that we spotted as a safety concern. Overall, clearly differentiated mechanism. We're really excited to work out the path, how we can further this with the FDA currently, and we're in active discussions as we have made public, and we will share that within the Capital Markets Day, come spring, and hopefully, we can point to a development path that excites the field as we bring a new mechanism to life here for this very, very devastating disease. Just a few words on Chronic Spontaneous Urticaria. We have tested also 30 patients only on two doses. We just tested them on 60 and 120 mix here. You see that, we also did a very similar trial setup, and I wanted to show you just a few patient data. This is a bit of a different angle. These patients suffer from histamine release of mast cells and basophils, and it's known that TVV can induce histamine release in these cells. There's a certain rational angle on testing C5aR inhibition here in this disease, but also there's a neutrophil angle that drives the chronic more, let's say, more severe inflammation scene. There's more and more mechanistic knowledge coming to life on the role of neutrophils. I just want to reiterate, while there's active drugs, there's anti-IgE approaches. Of course, there's antihistamine, but usually, if patients don't respond to antihistamines, they need special drug treatment. For example, omalizumab, anti-IgE, and new anti-IgEs, and patients respond well, but there's still a significant need in 30%-60% of these patients that remain symptomatic. Not surprisingly, there's lots of developments, and if we think there's a clear market opportunity here, that is meaningful with $1 billion estimated with our external research. Just to give you an illustration of what we mean here, our red is the high dose, yellow is the 60 mix, which has shown pretty good plasma levels already. Now, this is a very small dataset. One hiccup of one patient, for example, in the red arm here, can already like create a dent. Overall speaking, at week four, we're already at a meaningful Urticaria Activity Score 7 reduction. This is the endpoint used for approval of drugs. This was the more severe patient population, meaning those that had a high UAS7 at baseline of 28 or higher. We also reported on initial three, and we will report on a bit more here soon. Patients with concomitant angioedema that showed a very remarkable response on the UAS7, and also not on the slide here, on the angioedema score of concern. Here's a bit more what we've seen throughout our analysis. Overall, we reach about - 15, and in the more severe subgroup, up to - 18.7 on this reduction. We feel there is merit in a potentially safe oral drug for the future here, but it isn't put to our highest priority level right now, where we develop in HS. With that, I want to conclude. I want to thank you guys for listening in, and I hand back over to Andreas for potential additional questions. Thank you, guys. Yeah. Thanks, Nils. Very, you know, progress that you guys have made, and I'm looking forward to the update in HS. I think you said around the springtime, so I think that's gonna be a very highly anticipated catalyst. We like to see, you know, HS, as you mentioned, is a very hot area. Maybe just two questions here. If you can, you know, for the sake of time, maybe just additional thoughts on the potential in ANCA-associated vasculitis, given the Tavneos situation. Yeah, thanks for this question. Great question. I think, you know, we see a potential. Maybe let's start there. First of all, about a year ago, we didn't have that type of oral drug with this profile in our hands that has shown efficacy in phase II, even in phase IIa. People question: Is this market real? Will it still grow? I think the numbers that we've seen, this is a big market. For a rare disease, this could be clearly a $1 billion+, maybe up to one and a half. I don't know, this is guessing, but I think the current all-in is around $700 million global sales already that we've seen last year from the reports, and around $600 million alone in the U.S. Altogether, I think exciting market. That's the first case. Why do we think this has promise? If you look at the current label of the marketed comparator, it doesn't say corticosteroid-sparing because it inhibits CYP3A4/5, and the FDA was relatively clear that with this inhibition, and you haven't shown plasma levels, you may lower corticosteroids, but they may still be high in plasma levels, right? With that, we see an opportunity to get a differentiated label to, for example, say corticosteroid-sparing. We did develop in this area before. We have shown that we can go to real corticosteroid-sparing with the antibody. Back then, in our trials, we showed a GC toxicity index of zero in average, 0.8, which I think nobody has ever shown before. We have licensed that cell line technology of ours from in China to our partner, STS. They've produced phenomenal phase II data as well, showed them to the Chinese FDA, showed that they could replace corticosteroids literally, and are now in a running phase III with that mechanism. Long story short, C5AC inhibition seems to be validated on numerous levels. We have a drug that doesn't show the CYP345 inhibition. We believe we can get to a differentiated label, and the best part of it is, if you don't block the liver enzymatic activity and you have a more stable drug, you may see less, or no LiverTox issues at all, and that would differentiate the drug on various levels. Last but not least, if you can go to QD dosing or only need one pill or twice a day, that's also an advantage. Multiple advantages, and at the end, we may be, you know, really playing our best-in-class potential and see if this drug could get more market share. These are the thoughts. As I said, we haven't decided to kick off development, but we're deeply assessing it right now. All right. I know we're a little over time, but just, I think, an important question here. you know, MoonLake Immunotherapeutics had talked about differentiating their assets on the sonelokimab via the PRO, like pain. How are you thinking about that vis-a-vis for izicopan, the data that you showed? We were very excited about MoonLake Immunotherapeutics talking about that because I think we have produced really, really exciting early data on pain reduction alongside with draining tunnels. I think it is real because this is what matters to patients, right? Pain is a very frequent symptom, especially when you have progressed disease. If you have and you deliver a safe oral, for example, drug, in our case, that has this opportunity to show it a relatively fast, immediate, steep improvement in pain and in pus formation, this is exactly how we try to differentiate our drug as well. We have a mechanism that is so differentiated that we, like, caters to it. We're excited about that. This is exactly the route we're thinking of going to, and our data compare really favorably to any other reported pain dataset yet. Good. Great. Sorry, we're getting told that we gotta cut the conversation short here. I know we could talk for much longer, but appreciate the insights, and we're looking forward to those updates, as mentioned. Sounds good. Thanks so much, Andreas. Keep the conversation going. Thanks, Andreas. Thanks, guys. Thank you. Bye-bye. Bye.