Ladies and gentlemen, thank you for standing by. Welcome, and thank you for joining InflaRx's conference call to discuss the results announced today from the phase I study with INF904. During today's presentation, all participants will be in a listen-only mode. Please note that today's call is being recorded. The presentation will be followed by a Q&A session, where you may ask written or audio questions. Please note that you can ask questions only online. I would now like to turn the call over to Dr. Niels Riedemann, CEO and founder of InflaRx. Niels, please go ahead. Yes, thank you so much, Laurie. Good morning, everyone on this call. It's our great pleasure to represent to present to you today the results from our single-ascending dose phase I study of our new oral C5a receptor inhibitor. Before I go into it, I would like to direct your attention on the next two slides briefly to our corporate disclaimers. We will be making forward-looking statement and also have some comparisons to published data from other drugs. So please take note of the disclaimer, and then I would like to continue the next slide, please. One more. So with me today representing InflaRx, I have our C-suite team. It's my great pleasure to flag you also that we have our new Chief Medical Officer, Camilla Chong, on the call with us for the first time. Camilla brings a lot of industry experience from large and also small biotech and pharma into the company. With me as well is our valued Chief Financial Officer, Thomas Taapken, and my business partner and co-founder of the company, our Chief Scientific Officer, Renfeng Guo. Next slide, please. So this is the agenda of today, and we want to give you a bit of the background to make it a bit clearer why this company put so much effort into developing this drug. Next slide, please. So we'll start with the background. Yes, one more. We'll start with the background, and we would first like to introduce a bit about this target. C5a receptor is a G protein-coupled receptor It's very much expressed on neutrophils in the blood, but also on macrophages, many other cells, and it can be induced in various epithelial cells during inflammation. So it is a major mediator of the C5a pathophysiology in so many different disease settings as it relates to preclinical and sometimes also already clinical studies. So these studies showed a strong anti-inflammatory effect in different models, and C5aR antagonists can be expected to be a standalone or even also adjunct treatment in various diseases. There is a currently marketed inhibitor which may be improved based on the published data on its properties, and that's where we are coming in with this drug. Now, on the right side, you see all these disease areas, and certainly there's a lot of work in immunology, rheumatology, nephrology, ophthalmology. There's a lot of new work in dermatology as it relates to immunodermatological diseases, and then in other chronic settings, including neurology, pulmonology, and also inflammation-related diseases. So outside the well-researched, acute, life-threatening inflammation, where C5a, C5aR interaction plays a key role, there are numerous chronic disease settings where we see a potential application of the drug. Next slide, please. So when we're talking about potential improvement, what is it really that we're talking about? We're talking about, especially about the PK properties. So the plasma presence over time is something that may be important to also have good control over the blocking activity delivered. Now, we believe that the blocking activity is particularly important at levels of C5a that are disease-relevant and that are observed in human diseases, and we have ample experience as a company in that. So we want to have a near complete inhibition during settings that we believe are relevant to human diseases. And then also there may be a different drug strength that may make application and administration a bit more convenient for the patient. On the right side here, you see a publication from the marketed competitor, avacopan, which is their phase I publication. In this case, it's multiple ascending dose data. And I want to introduce you into what we believe could be improved. And we've modified this picture by putting in these zones, but also the red marked arrows and also wording. So this is a so-called CD11b, which measures a very sensitive marker on neutrophils that shows neutrophil activation, especially upon C5a engagement with neutrophils, 'cause they have a very high density of the C5a receptor. And here, patients were, in this case, healthy humans were dosed for seven days, in this case at 30 milligrams twice a day, and then at 12 hours, always before the next dosing. And please keep in mind, 12 hours. At 12 hours, blood was taken. Here, I wanna take your--draw your attention to the blue dotted line. The drug was taken, the blood was taken ex vivo, and different doses of C5a were administered to see whether neutrophils would get excited. And you see that at doses of C5a, around 10 nanomolar, which is certainly something you see in disease settings like hidradenitis suppurativa, or in other diseases, the neutrophil activation came back to up to almost 50%. So that is, in our eyes, not ideal. So ideally, you would have an inhibitor that shifts this curve so that in this yellow space, you get an inhibition of maybe 80% or higher. So you want to cover the signal in human plasma. Why? Because this is where neutrophils start getting activated, moving into the tissue and doing damage. Okay, so next slide, please. So let's look at the preclinical properties and also some of the data summarized that we have gathered with our new drug. It is a new chemical entity. We have issued a U.S., uh-... Patent, and we are issuing patents in other countries. It is a novel Markush structure, and it binds to a well-defined allosteric binding site. Now, in the preclinical work, there were no obvious toxicity findings up to the highest dose groups in rat and monkey, up to 300 milligrams per kilogram. The drug showed a very good in vitro potency, as expected, but it also showed very strong plasma presence, even in one-to-one comparative studies in animals with avacopan, which we synthesized ourselves. And, it showed also an increased efficacy in a head-to-head model, which I will introduce you on the next slide in a second. But then also we had first signs of efficacy in therapeutic effects in preclinical disease models, for example, in renal models and certain peritonitis models. So overall, the preclinical work was very promising and suggested that there is a best-in-class potential for this drug. Next slide. So I want to give you this one head-to-head study that we did in a hamster model. And what was done here is the animals were dosed either with INF904 in blue or with avacopan, which we synthesized ourselves at the exact same dosing, 10 mg per kilogram, orally administered. And then the animals were challenged with C5a, recombinant C5a. And when that was done, neutrophils get activated in the blood immediately, and they start sticking to the endothelial cell wall. When you draw blood at that time point, it looks like you have a neutropenia because the neutrophils are sticking to the cell wall. However, if inhibited, if C5a receptors are fully covered, you will have no inhibition, meaning, no, no sticking of the neutrophils to the endothelial cell wall, so you inhibit that sticking to 100%. And you see that here, there's almost a doubling of the effect, when you do this head-to-head. And I also want to draw your attention to the plasma levels down there that are taken at eight hours, where you see that INF904 had a much higher plasma level, roughly four to four point something higher than avacopan, which we again, synthesized for this experiment. So this was very encouraging, and now I want to move into the phase I data together with you. Next slide, please. I want to briefly show you the study design. This is, next slide, please. A classical, single ascending dose on the left side that is now completed. We enrolled 62 patients at different dosing levels. The three, 10, and 30 mg were taken purposely to give a comparison to the published phase one data of the existing competitor. But then we also dosed higher, up to 240 milligrams, and you see how the patients here are distributed. You will note that at 60 mg, there were a lot more patients dosed. That is because we tested different drug strength and different ways of formulating the drug. On the right-hand side, you see the multiple ascending dose study that is still enrolling, so that is not completed, and we expect data towards the end of the year, which we may present early 2024. Next slide, please. So to the safety outcome, next slide, please. We... The INF904 drug was well tolerated. We had the treated volunteers with no safety signal of concern up to in the entire dose range up to 240 mg. Overall, the percentage of adverse events in the placebo group was higher than in the actively treated subjects with INF904. You see the AE severity. There were mild adverse events, one and moderate, nine, and there was no severe adverse event. There was one moderate AE that was related, possibly related, judged by the investigator, but that was a placebo patient, and there was one withdrawn subject for an unrelated AE and finding. So overall, it really confirmed the absolute great safety profile that we saw in the animal tox studies here in this first exposure in humans. Next slide, please. So now we come to the PK outcome. Next slide. So this is an exciting slide because this is about plasma presence of the drug. You see here, the plasma concentration of 904 at different doses, up to 240 milligrams. You see that you reach very high peaks, a very good, nearly dose proportional exposure. And you see that the peak in all these curves is around six hours, with a very good plasma presence over time. Now, for orientation purposes only, we did a superimposed, and in here, data published for avacopan. This was not a head-to-head study. I want to flag that this is just for orientation, and we did use their 30-milligram data, and we also put our 30-milligram data here in the lighter blue to give you a good visual sense of the difference. So you see, not only is the peak a different one, instead of two hours, more towards 6 hours with 904, but also you have a very different plasma presence. On the right-hand side, you see a few data for the comparable doses here, which is 3 milligrams, 10, and 30 milligrams. And you see that the area in the curve, but also is quite different and not just the Cmax, but especially also the systemic exposure is up to 10-fold higher, across the board for the comparable doses. So that really confirmed the animal data when it comes to the PK profile, and it made us look very positively into the future of this drug, because not only did we see no safety signals of concern and a good tolerability, but also we have a plasma presence that probably allows you to reach very different tissue and plasma levels over time, and hopefully a very good control over the signaling. Next slide, please. So this is just a summary of what we have just shown you. The Tmax is at six hours, and systemic exposure in the dose range was really dose proportional, and we had a very good systemic exposure over time for the comparable doses. Next slide. So how does it relate to the pharmacodynamic, the blocking activity? On the next slide, you see a slide that looks familiar to you already, even though this is, of course, new data. This is only INF904 data, and this is after single exposure. I want to draw your attention, this is again the CD11b assay, so the neutrophil excitation assay. It's done in a comparative manner, so we have taken blood from these healthy volunteers after single-dose exposure. But here we did not take blood after 12 hours, and I want to flag that this is after 24 hours. You see that at doses of 30 mg and higher, we already reach a blocking activity of over 90% across the board at a exposure of C5a of 12.6 nanomolar. Now, that has to do with the dilution in the assay, but these are pretty high levels, but levels you see in disease settings. And you see that, we have a very nice, right shift accomplished just as we set out to do. And I want to flag also that the published data of our comparator really showed that they only reached 50%, but that was at 12 hours. So again, more than 90% at 24 hours. So that gives us a very strong confidence that the drug could perform really well in future studies. Next slide. So I'm coming to the summary. Next slide, please. So the key outcomes, INF904, was well tolerated in treated healthy volunteers. It resulted in no safety signals of concern, in the dose range-finding study. In the dose range study of 30 milligram to 240 milligram, INF904 demonstrated a favorable PK profile. It also demonstrated a strong C5a blocking potential. And, and we also, this is data we haven't here shown in detail, but we also were able to formulate in different drug strengths, up to 30 mg per capsule, which would also be a convenience advantage if taken forward into into further development. So all in all, this confirms the best-in-class potential that we have seen already in the preclinical work, and, you can, certainly see a very happy team about this work. And the last slide, what are the next steps? Next steps, the multiple ascending dose study is going on. We expect the data to be available towards the end of the year, maybe presented early in, in Q1 2024. We have ongoing scientific and strategic work within selected disease areas for the future development. As you know, we've been always very interested in also exploring settings of that, like, the immunoderm space and like other spaces where complement hasn't been extensively researched before. Work ongoing is also here to optimize the formulation for ideal manufacturing and drug convenience. And we are also preparing for next clinical development steps, obviously, and that also includes some preclinical work still, like the chronic toxicology study, which will allow us long-term dosing for the drug. So overall, we believe that these data, for us, are very positive, and that they really support the further development of INF904. So with that, I come to the end of the presentation. I hand back over to Laurie. Our team will be more than happy to answer some questions. Thank you. Thank you, everyone. This concludes the formal presentation. We will now open the call to questions. You can ask questions in one of two ways. You can submit a question in writing via the Q&A button below the presentation window. I'll then read the question aloud. Or you can ask a question using the Raise Hand icon under the presentation window. We will call on each person in turn. Just give us a moment, please, while we collect the first questions. Our first question is from Evan Tadeo with Guggenheim. Please unmute your line. Sorry, they were typed in. Let me read them. How comparable are the neutrophil activation data with avacopan, given that this is not a head-to-head comparison? Yes, thank you so much, Evan, for this great question. I will hand this over to our CSO, who's been an expert in developing these assays. Renfeng, will you tackle that? Yeah, sure. Thank you. Yeah, that's a very good question. I think that it's not 100%, comparable, of course, because if you don't do a head-to-head. However, when you are familiar with these assays, you would know that, you know, you have a standard curve, and you also have a placebo. So you will know that, you know, how much C5a activate a neutrophil and you have with the standard curve. So that's as a reference standard, and you always have a pretreatment dose and to compare with what's reacted, the effect after dosing. So that's... So every data we got is relative data, so that's why I think it's not 100%, but you do have a good reference to understand on the such amount of a C5a, what blocking activity that you would see. So I would say this is actually relatively pretty good comparison. He had another question: What work still needs to be done on the formulation? ... Yeah, that's again another question. Very good. So as you'll see that we have did a lot of work on the formulation, mainly because we want to address the question that what the strengths, how high the strengths we can go. As you'll see that in one of the group, we did a lot of work with the crossover and with 10-30 mg different strengths, and we're very happy to see the result at a 30 mg strength, that I see a pretty good result. And currently, we are trying to improve stability of this formulation, and we still have, you know, because first, as you know, that, for the, you know, the first clinical study, you really, you just go with the best possible formulation, and then you want—you would like to increase the ability for the commercial formulation. That's what we're looking for at the moment. I think our team is pretty confident that we're going to move to the next stage with the formulation work. Okay. Our next questions are from Steve Seedhouse with Raymond James. Please unmute your line. Yeah, thanks so much for taking the question and for hosting the call and, and going through the data. I wanted to ask just first, presumably you'd be trying to develop a once daily regimen as opposed to BID, but I just wanted to confirm that. And then also maybe if you could talk a little bit about dose selection in the MAD. The paper that you walked through for avacopan, I think they achieved ultimately 94% inhibition in reading that paper with the thirty mg BID dosing that they ultimately settled on for clinical development. So are you looking to test doses basically that do better than that, quite simply? Or are you trying to maximize, like getting to 98%, 99% inhibition based on the SAD data? Yeah. Thanks, Steve. Thanks so much for joining in, but also for the question. So I think then when you're looking at the inhibition data, it's very important not just to look at what's the maximum inhibition you achieve, 'cause if that's 94 or 97, I don't think that's necessarily relevant. The question is, how does your inhibition look over time, for example, at trough level? So for avacopan, that would be when they dose the next dosing. And the data that I have shown at the beginning, these were the multiple dosing data after 7 days dosing and reaching trough. So at trough level, if you then only have 50% inhibition, then you can calculate the time over which you don't have good control of the signal. So our goal is not to say we can make 99% on one shot. We may or may not, but the goal is to say we maintain an inhibitory potential of maybe 90%, at least 80% and more over time, also at trough, before you get the next dose. To your first question, that was ultimately the convenience. Yes, of course, if possible, a single dosing per day is something that would be ideal. We don't think that twice per day is necessarily a killer. That can also be done. But of course, if you had twice per day, it would be ideal to have one pill and not necessarily three, for example, right? So there are convenience levels that we want to look at as well, and we may or may not be able to dose once daily or twice daily at a better strength. So that's a bit too early. We will look at that when we have the MAD data at hand. But I would say our key objective is really that what I mentioned before, is to maintain the blocking activity as much as possible over time, and that means also before you get the next dose. I hope that answers the questions. Yeah. No, no, it does. Thanks, Niels. I also wanted to ask just on the preclinical tox work that you indicated you'll be starting for to enable chronic dosing. Could you start, of course, after you find your optimal dose in the MAD study, could you still start, like, a three or a six-month phase II study? And is that something that you plan on doing, or are you going to wait until you have the chronic tox, preclinical tox data in hand before moving ahead into phase II development? And then in talking about phase II, I know you haven't really disclosed indications, but maybe generally speaking, can you just update sort of how you're thinking about the strategy and the type of indications that make most sense for this pretty interesting molecule? Yeah, absolutely. I mean, I'm happy to hand the strategy question also a bit over to Camilla in a second here. But on your first question is really like the question whether or not you bring this drug into a shorter time dosing in the meantime is not fully decided yet. Right now, our preclinical program would support a dosing of up to a month, and we could do that after we finish this study. But the chronic tox we're gearing up here, which also includes large animals, would then be one for small molecules. So that means it's a pretty long tox, which would allow you, hopefully infinite dosing with the drug. So your question was, are we anticipating that we do, in the meantime, a study where we first expose, for example, certain diseased humans to a shorter time exposure? And that is certainly something we're looking into as a company. Obviously, what we're trying to do here is if we are doing that, it would be of interest to see can we gather first signals of efficacy of this drug? And that means we have to also be mindful about what are we clinically looking at, so it becomes a credible proposition of activity. And that's something we are actively exploring with experts right now. And maybe, Camilla, I hand over to you here for, you know, giving a bit more perspective on how we think about where the drug could be put in the future. Yeah, please, Camilla. ... I, thank you. Thank you for the question. You know, just to reiterate, so right now, we have animal toxicity study that will allow us to dose up to four weeks in human. And while that's happening, you know, clearly we, we are embarking on the sort of longer-term animal tox study in order to allow us to do chronic to chronic dosing in chronic conditions in humans. So while that's happening, I guess, you know, as Niels have said already, we're trying to think about potentially either some immunodermatological conditions whereby we can dose for up to four weeks to have a look, a quick look-see of efficacy signals in humans. You know, and clearly this is not just restricted to immunodermatological conditions. There could potentially be other inflammatory areas that we could also take a quick look-see. So without, you know, being any more specific than that, I just wanted to tell you that, you know, we're definitely looking into this in a highly prioritized area, to see whether, you know, there are some other clinical biomarkers that could actually show us, you know, the efficacy with dosing up to four weeks in human. So I hope that addresses your question, Steve. Yeah, it does. Thanks. Thanks so much. Our next call, questions are from Will Soghikian with Leerink. Please accept the request to unmute your line. Great. Please go ahead. Hi, all. Yeah, congrats on the progress today, and thanks for taking our questions here. So two from us. First, just kind of drilling down a bit more on the toxicology studies. You know, what are the gating factors to getting this started, and how quickly can you, you guys get these up on the ground running? And are these typically going to be six to nine months, or are you looking at a little bit of a longer duration? Yeah, Renfeng, do you want to tackle this? I'm not fully understand the question, but if your question is, what's the duration of the talks, usually for monkey, it's nine months, and six months rodent. That's a standard package that's required for the regulatory. Great, thanks. Then quick question for Thomas. You know, given the company has many interesting opportunities ongoing here, you know, we have the COVID-19 launch and the PG study getting underway. You know, are you still guiding, thinking about cash runway into 2026, or has this been adjusted now with the INF904 studies? Thank you. Yeah, great question, Will. Also, thanks for joining on my end before I forget. I hand over to Tom for that question. Sure. Thank you. Yeah, so when we guided the markets, in terms of our cash reach, we were assuming, of course, that we would continue the development of 904. So at this point, we're not changing the guidance. As Niels said, the planning is still a bit fluid in terms of whether or not we might want to do additional studies, immediately, let's say, short-term dosing studies, with nine oh four. That is, yet still to be decided, but it will not have a huge impact. No matter what we do in the next, you know, 12-24 months, it will not have a huge impact right now, as we see it. So the last cash position was $115.2 million, and we're still comfortable with that to be funded into 2026. Excellent. Thank you, guys, again, and congrats on the progress. Thank you. Thank you. Thanks. Our next question comes from Sam Slutsky with Life Sci Capital. Please accept the request to unmute. Go ahead. Hey, everyone. Good morning. Thanks for the questions, and congrats on the update. Just a couple from me. You know, as you think about C5a signaling and inhibition at this point, I guess, what's your thoughts on C5aR versus C5L2, and do you miss anything on efficacy from just going after C5aR? Yeah, that's a really great question. First of all, thanks for joining, Sam. I appreciate your question. So, the question of what role does C5L2 play into certain diseases is, of course, a much under-researched area. That has also to be, to do with the fact that C5L2 has been first reported as G protein-coupled signaling receptor, then that was kind of revoked. And so in the history, Renfeng and I are well aware because we were postdocs in the laboratory of P. Ward at the University of Michigan, when the whole thing was started with the Gerard group in Boston and others. And so the question that. The way we see C5L2 is when you look at the high-quality studies, that means studies, for example, from AstraZeneca group and others, where they have good tools, for example, antibodies that really selectively block C5L2. Which is a very different thing from looking at a C5L2 knockout study, where the animal doesn't have that receptor. So if you look at studies that are more specific, they actually confirm that C5L2 has a certain pro-inflammatory role in certain settings. So especially when you look at life-threatening diseases like ANCA-associated vasculitis flares or maybe also the sepsis setting, the ARDS setting, the COVID setting, the immune response setting, you may want to prefer to go to C5a as your target, to be, I would say, covering any potential additional in signaling. Now, as it relates to the chronic side of things, when you look at data published for C5aR, and there's, as I mentioned, literally thousands of publications on the role of C5aR, they always point towards a clear benefit signal when blocking this receptor in tissue. So the one thing, for example, we noted is that C5L2 is way lower expressed in certain tissues. Interestingly, it's a bit higher expressed in liver, but in neutrophils, low expression. In many tissues, very low expression, hard to find the receptor, and again, it has different ligands. So I would say for the chronic disease setting, C5aR is our preferred target. I don't think there would be an area where you have an effect that you get with a C5a inhibitor, like vilobelimab, which you could not get with a C5aR inhibitor if that C5aR inhibitor is able to block the signal completely. The one thing, though, that may be a big differentiator, and that is when you look at tissue presence and how well do you cover the receptor, which can be greatly induced in tissue and inflammation, in all sorts of epithelial cells, you know, lung, liver, kidney, et cetera. With a small molecule, do you have a better penetration? Do you have a better coverage? That is what we believe may happen. So for that, for these particular reasons, we see C5aR an ideal target for the chronic inflammatory settings. Got it. Super helpful. And just one more for me. You know, obviously, a lot of the data in here is in comparison to avacopan, which obviously is approved for ANCA-associated vasculitis. I guess, with that in mind, would you consider going into AAV to compete with avacopan, or would you likely look to other indications outside of AAV? So that's a very good question. So we do have, of course, data with vilobelimab suggesting that when you have a strong inhibitor, that that may be helpful in ANCA-associated vasculitis. You know, I would say at this stage, we're not excluding anything in the future, but it's certainly not our current priority to think that we want to compete in ANCA-associated vasculitis with this molecule. We think this molecule is, for us, very exciting. We think there may be areas that we would prefer over going after ANCA-associated vasculitis. Well, we do get the beauty of going after the same indication as it relates to risk. But then also, as you know, the regulatory path for approval for avacopan was, I would say, pretty bumpy, to say the least. And so it's not a no-brainer in terms of what do you actually try to achieve in ANCA-associated vasculitis. So I wouldn't exclude that we come to this at one point in time, maybe also if it becomes a really attractive market, which currently we don't see strong signs for that yet, but at this point in time, it's not our focus. And here, I really also defer to Camilla. Camilla, do you think I adequately reflected that from your perspective as well? Yes, Niels, you know, nothing more to add on my end. You know, I mean, clearly, we're watching very closely in terms of the FDA's acceptance of potentially, you know, not a totally new pathway for this indication, but I think some of the endpoints, you know, we're watching the evolution to see whether there are some, let's put it, more realistic endpoints that, you know, we can try and strive for, basically. Yeah. Got it. Okay. Thanks, everyone. Thank you. Our next question comes from Yatin Suneja with Guggenheim. Please accept the request to unmute your line, and please go ahead. Perfect. Can you hear me? Yes. Yes. Hi, Yatin. Hi, beautiful. Hey, everyone. Thank you for the presentation and all the details. Just one from me. I don't know if this was answered. So one of the issues with avacopan is its interaction with steroids. It does increase the exposure to steroids. So I'm just curious, your comment on 904, what you have to do to tease that out and how clean it is. And then, you know, from the DDI requirement, like, what sort of work you would be doing as you move from MAD to clinical studies? Yeah, absolutely. Well, first of all, thanks for joining, Yatin. Great questions. I'll probably hand them over to Renfeng, and I'm happy to cover some of that as well. I do want to mention before I hand over to Renfeng that we have mentioned before that we have seen in preclinical studies a strong difference in the CYP3A4 inhibition, which is, you know, the enzyme that metabolizes prednisone, where there were questions during the approval process for avacopan whether that inhibition could have led to higher plasma levels of corticosteroids because they were not necessarily measured in phase III. So there is a very clear differentiation, but of course, it's always difficult to predict how it then in the end looks when you take it to the patients you want to take it to. But at least from the preclinical end, the molecule is very differentiated. Renfeng, I hand over to you also for the second part of the question, but I'm sure you have maybe more to add. Yeah. So yeah, thanks for that question. Yeah, just try to re-elaborate a little bit on the CYP inhibition part. From preclinical study with data, that enzymatic study, and showing that there have a different profile, as you'll see that from the published data, that from avacopan is a pretty strong inhibitor for CYP, and well, data on INF904 that show a pretty weak inhibition. So from that end, we actually have a better feel that about the, you know, the CYP CYP inhibition aspect, especially towards the glucocorticoid metabolism. So but, you know, in the end, you have to do the DDI study and try to understand that what would the influence, what would be the endogenous corticosteroid accumulation. I think that will be our focus in the DDI study. We're not there yet, and we're definitely going to start the DDI study or the phase study. So, in the near future, because this is actually really important to guide through in the clinical trial, because as you said, one of the issue that avacopan has, it did not get rid of the steroid sparing. So that, I think that could be a potential future clinical action to towards. So it's, yeah, it's a good question. That's definitely think into it. Got it. Yeah. Maybe two more questions, if I can. So this one is regarding the formulation. So what exactly was the formulation used here? Do you use the tablet? Are you sort of optimizing the tablet or are you working on, let's say, an extended release type formulation? So that's one. Yeah. The second one I have is, you talked about, you know, immunoderm indications. So that, you know, many companies have been very successful with fast follower, you know, best-in-class assets. So would you go after Amgen is already approved, and/or avacopan is already approved, and Amgen is going, or would you carve out some sort of new indication for this asset? Thank you. Yeah, I'll probably take this one, Niels. Maybe you can take the second one. Sure. For the formulation. As you see, this is a highly, both avacopan INF904, they have lipophilic compounds, so therefore, the base formulation is the preferred choice. Currently, it's actually in the liquid, so very similar to the avacopan formulation. And this is a lipophilic formulation. But I think the differentiation factor that we found is the strength, right? We try to really increase the strength for that. And another important probably, you see in the presentation, one thing that is not striking, but it's definitely important, is the DS, the DS drug, DS chemistry, which is amorphous on INF904. So I think that's also very important to note for the chemist that this could be the potential reason that we have a very good exposure in. I hope that addressed your question for the formulation part. Yes. So maybe also one thing to add to Yatin's question. I think also to note, the slow release thoughts, I think that's less in our immediate attention because we see such a good PK profile. For us, it's more like to optimize, as you mentioned, the strength, right? And to optimize things that have to do with larger scale manufacturing in the future as well. So it's an ongoing constant effort. As you know, for small molecules, you never stop during with the first human exposure. But I think it's fair to say that currently used in this SAD study is very similar, as you mentioned, to avacopan, right? We basically went with very similar structure. Right. Different component, of course, but the same idea, lipophilic. Yeah, yeah. And then for the second question was, which was more like fast follower, et cetera. I think, maybe, you, you were not on, on, on the call already, but, we, we covered that partially in the last, one of the last questions, that we are looking clearly at, at avacopan in terms of what are the end, how the endpoints developing, how is the regulatory, and also how successful is avacopan overall, in ANCA-associated vasculitis. We would assume that patient or their doctors give the drug, maybe even, to lower cholesterol, even if it's not on the label. But that's a guess. We don't know that. We are certainly, and Camilla, just the end, but we are certainly interested in where Amgen takes the drug elsewhere and following that very well. But I mentioned before, there's a certain hesitation to right away go into ANCA-associated vasculitis for various reasons. It is a molecule that is not building the market. It's a very small market. Unless we know it's a very good market, the attraction may not be as high. And then also the regulatory path is very, has been very bumpy for avacopan, and so we would have to really take a like, I would say, a differentiated approach, but we would certainly face similar, similar obstacles that they faced. Maybe, Camilla, if you had additional thoughts related to following Amgen's steps with the lead molecule, avacopan. Yeah, I mean, just, just to build on that, right? The phase one data which you've seen today are very compelling. And clearly, you know, the application of that in terms of the different indications are vast. You know, we could follow the same path that avacopan has, or we could also explore other areas. Mm-hmm. You know, and certainly we already have some experiences in immunoderm, and even within the immunoderm space, you know, we've already explored HS and PG. So there are other possibilities where, you know, immunoinflammation, which involves the C5a receptor inhibition path, can play a critical role. So that's just one area that you probably are aware, you know, there are other applications in kidney diseases and so on. So I would say at the moment, you know, early days to hone in on exactly where and what path we want to take. But, you know, we're definitely thinking about this very carefully. We're definitely having, you know, strategic discussions to ensure that, you know, we come up with the right prioritization, right? Because, you know, it's very tempting to be able to go into all sorts of potential indications, which was also a possibility. But, but we need to be focused here, and we're certainly taking this in, certainly right now, you know, as our next step, to consider these strategic questions into which indications and what should we look at very, very, very carefully. So. Good. Excellent, thanks. Thank you. There are no further questions, so I'll turn the call back over to Dr. Riedemann for closing remarks. Niels? Yes, thank you, Laurie. Just nothing much to add other than thanking the team for being here with me, but also thanking everyone that joined and is interested in this drug. Last sentence, yes, I think we're really all very excited about this drug and its future potential. With that, thanks for joining, and have a great day.