Good morning everyone. Welcome to the next session at the Cantor Global Healthcare Conference. I'm Steve Seedaus. Thanks to everyone on the webcast and in the room for joining us and really privileged to welcome the next participating company at the conference, InflaRx. I'm joined on stage by CEO Niels Reidemann, CFO Thomas Tapkin and Head of IR, John Medina. Really, thanks so much for being here and would love to just open it up, maybe pass it to you Niels to just give us current state of affairs and at InflowRx, the outlook for the rest of the year and just how you're viewing the positioning of the company, and then we'll get right into Q and A thereafter. Yeah. First of all, thanks so much for having us. I really appreciate being in this conference. Yes, so we are it's going be an exciting year for us because as you know we have an interesting asset that we've produced very interesting phase one data about a year ago, which is a small oral RavA receptor antagonist and we have upcoming data here, you know, in the timeframe September, beginning November, so you know, roughly say October is gonna be likely of, know, for data in two very interesting indications, hetero-ninety superativa, there are other interesting readouts coming our way here and also chronic spontaneous urticaria. So that's a differentiated molecule in terms of could be best in class as much as far as the phase one data go, happy to speak to that a little bit. So this is an upcoming readout. We also have an antibody drug addressing not the receptor but the ligand C5a that has commercial angle in The U. S. Under an emergency use authorization and in Europe under an approval in the ARDS space in Europe, and that that's, you know, that speaks to the to the pathway in and of itself, like, to be lifesaving in very diseased COVID patients in this in this case that that require life support. So from that angle, we also are working on PG aftermath. We had a trial that was pulled because we hit futility as you know, but we're going to work on that as well. So there might still be residual potential upside for the future, maybe with a partner, we're going to speak about that. So this is on the map, but key focus of the company is the small molecule that could be a differentiated mechanism in the markets. And maybe just can you recap what it is about 09/2004, this C5a receptor inhibitor, the molecular design and what was evidenced by the Phase I data ultimately that makes this so much more bio available than the first generation of this class and what you think has set it apart. Think the key to recap some of the chemistry and pharmacology there. Yes. So first of all, it new is chemical entity and has an entirely new patent coverage with issued patents in The US and elsewhere in the world. But it has the same allosteric binding site that was discovered back then by ChemoCentryx, now Amgen owns the drug. And we worked a lot on this molecule in order to give it a different PK, bring it to a situation where you cannot only maybe 50% block the pathway, but come to 90% to 100% at any dose you wanted to choose for treatment and then also to be able from there on to up dose which may be important for skin diseases. We have a very differentiated molecule but also a different formulation that allows us to pack it more densely and to like to go to higher doses with the formulation. And last but not least, we also designed it in a way that it has much less inhibition or pretty much very low to no contact with the CYP3A4 liver detoxifying enzyme apparatus. That is important because you don't want to have drug drug interaction issues or liver tox issues. So from multiple angles this is a differentiated molecule and the phase one has really shown that at the equivalent dose you can see a 10x area under the curve increase and 3x peak and what that translates to in easier words is you can reach therapeutic exposure if need be on day one. But certainly within the first week or so with doses that are equivalent and you can up dose quite a bit. Why is this important? Last sentence here is because that probably allows you to explore the full potential of blocking the pathway without having to compromise to say maybe I block 50% or so. The idea is like in all like best case scenarios I can block 100% even in a tissue like the skin. Important also the onset of action just given the fact this basket study that you're running obviously is four week efficacy look in these two indications you mentioned, HS and CSU. But maybe help frame what would be a win from that study? I mean, are you looking to show in four weeks in either indication and just help frame the objectives. Sure, yes. So for us, this is short term dosing open label clear but since it's an important trial because we designed this to say look with everything we have hand ideally we can make the statement this is an active drug and deserves to be put forward as a new differentiated oral mechanism. For us a win, to say it in simple words, is, if we, produce data that are clearly away from like with the common endpoints used and also you know more differentiated in the different diseases away from what has been reported for placebo and in line with successful drugs at four weeks or even later stage to say look if we reach therapeutic levels very early, maybe we can produce already in four weeks a significant response that you probably only see later. So like to set the stage, we want to be differentiated from anything that has reported for placebo and in at least in line with successful drugs in And the if that's the case, we play the card that this is an oral, there's no known safety issue on the mechanism. Everything we have including the extensive now by now extensive tox package including nine months monkey studies have not produced any signal of safety concerns. So you know having an oral with a very differentiated mechanism carries a lot of potential upside and that's what we're open for. Yeah. I think in CSU, I mean, should be able to look at UAS, UAS seven I guess and it would be sort of like the traditional endpoint. Even at four weeks, it could be informative. In HS, I'm not sure what you think. I mean, it is it could like probably too early for a high score 75 or a high score 50 sort of read that's instructive. But maybe if you look at lesions and, you know that would be maybe IHS, but talk to me about your perspective there. Yeah. So HS it's interesting because certainly there are lesion movements like you see ideally the lesion reduction in all three lesions that's been reported in other studies. There's not that much data on four week data because most of them look at twelve or sixteen weeks as you know for high score. But you know if the drugs works as we believe it should work, you should reductions and we're going to report this in line with what other coms have produced. Now I want to point out one thing that because as we all know in HS the abscess and nodules fluctuate, right. So it's not an easy thing to look at and make definitive statements on on small datasets. But there is a lesion, the draining tunnels that don't show traditionally in all the report studies much of or any placebo response. So if you had a clear response or a clear reduction there, could anchor around saying look this is nothing that has ever produced a placebo response. So there's a higher conviction level that what you see is real activity of the drug. And then you mentioned high score. Yes, there are data reported for high score at week four. As you know, high score depends extremely on your baseline depending on how sick your baseline is. You have it easier to show the 50 end count reduction already at week four or not. But yeah, we will have all this data available and also then the comps around it but focus will be lesion reductions of all three lesions and then we comp that and show you why we believe it's active or, you know, or not if we don't have the data, but certainly that's what we will do. And draining tunnels specifically, I don't think it's as well appreciated as it should be with this particular mechanism. I mean, the mode of action should be on neutrophils and neutrophil recruitment to the site of the lesion and vis a vis draining tunnels, right, that's where you should see like a huge reduction in pus and a conversion from draining to non draining and you might expect to see early activity specifically there uniquely for this mechanism. So I mean, is am I correct there? Am I missing anything? Yeah. No. Absolutely. Give you a bit more color like one of the big things in HS is durability and response. We're not there yet ideally with the mechanisms addressed so far and the other thing is like reliable deep reduction of drainage which is kind of the most bearing socially bearing thing on these patients. You have to understand like the draining tunnels are, we call them draining tunnels but that's basically the opening to the outside that you see but if a tunnel drains, there's a deep seated large inflammatory area constantly produces pus. Now that needs to be reduced for it to stop draining. And so there's a lot happening in the deeper skin and you're right, C. V. A receptor has been found in different cell types, particularly neutrophils and others around all three lesions at all levels of the disease but particularly strongly in and around draining tunnels. So yeah, we believe there could be a fast onset there. Obviously I would always still and that all data show that belief that if you treat longer than four weeks you will see further deepening of the response. And then are you keeping your option open to advance into Phase II for both indications if you see good efficacy in both? And maybe Tom, for you, I mean, just in terms of the balance sheet, I mean, have you budgeted for both Phase IIs? Would you have to triage? How much cash would you need to complete both Phase IIs, maybe you can both comment on how you're thinking about that as a company. Yeah, I mean the outcome of the trials will of course determine what is appropriate in terms of design and size of Phase II trials and which indications we want to carry the drug forward with. And we are of course first having to do a thorough analysis here to be able to judge what is exactly the cash need in order to carry out these studies. There there's going to be two sources for that. I mean, we have not only investors interested in the data, we have also some large pharma companies that have expressed interest in seeing the data. And we could imagine that, you know, partnerships could help address some of the cash need for future activities. But it's certainly going to be substantial if we decide to move forward in both indications with large Phase 2b trials, that's going to be a significant amount. Would you prioritize one or the other in terms of keeping wholly owned by Influrax or I guess you just Well I think I would even go further. In terms of the potential of the drug, we see areas of interest that we are not pursuing ourselves because we don't have the means to do that and if you go and look into the broad spectrum of what the drug could potentially do, we feel that there is certain pharma companies that fully understand and we could imagine even going beyond the two indications that we have initially targeted. So it will depend very much on the quality of the data and the way we're able to convince anybody about what is appropriate to move the drug forward. Yeah, mean obviously Avacopan is approved for ANCA vasculitis, which is and there's been other data from even your own antibody and your partner in China in ANCA vasculase and that a couple years into launch, mean, that drug's annualizing close to half a billion. That that alone would be maybe one possible opportunity there. Absolutely. Can you just make in CSU it's fascinating and just the origin of this program and how you got involved here and the conviction that this mechanism c five a r and that signaling access is is involved. What do we know about that and and how did this become, you know, one of one of the focuses for this molecule. Yes, so it's interesting, like about forty, fifty years ago when CFA was discovered, the original name was anaphylatoxin, realizing that you can induce anaphylactic shock reactions and death because of anaphylactic reactions through histamine release. So in of itself that's not a new story and it's been described that there's a dose dependent, c. V. V. Dependent histamine release in basophils. It's suggested for mast cells that start carrying the receptor in the skin in CSU patients. So there's a lot of research going on into this that this could be an IgE kind of cross linking independent way for these cells to degranulate and to produce histamine. It's never been tested in the human setting although it's almost textbook knowledge. It was brought to us by a friend that unfortunately is no longer with us, Markus Mauer, lived about a two hour drive away from me in Germany and he's been doing great work with other drugs in the field and really progressed the field together with others of course. And so we, you know, we here run the first human experiment. It it we are, you know, we are quite we got quite interested in the research that he brought to us and did our own kind of studies. We're still working with that in the lab and, you know, can confirm that, you know, basophils have this ability. We showed some data already publicly that to put out histamine in a dose dependent manner to a substantial amount. So I would say the research is all there but it's never been addressed with a drug on the complement angle in human disease. You know, in a way, so it's the first study around that mechanism in the disease. This mechanism, I mean, it seems like in CSU it would be almost pleiotropic or at least sort of multiple mechanisms that you're blocking basophil mediated histamine release, I think, but maybe also directly impacting mast cells and That's it. Is there any other mechanism that's comparable here or is this unique amid the competitive landscape? I don't think there's another mechanism in CSU that's comparable. I would I would compare it a bit like from my understanding, there's another indication called Sindu, like the inducible form of this urticaria where certain neurotransmitters play a role and there's like the like people call it the X2 receptor that that has been shown to play a role there. So I'd say there's like parallel situations of other receptors that funnel into the histamine release. But when it comes to CSU, don't know if there's any other shown like clear independent way produce histamine. Quite unique, if it works, it'd be something that could go broader in other kind of allergic diseases probably. Do you think four weeks is going to be sufficient to maybe also establish some safety tolerability advantages of this mechanism versus some of the drugs that have promising efficacy in CSU I think have some drawbacks on that front? Yeah, what we'd like to compare ourselves with is primarily on the first level with other orals, right? There's more orals coming, like, and we all know it's been the JAKs and and BTKs and, you know, they all kind of carry their little packages of history of causing infection or other side effects and that could be an advantage. Obviously four weeks is too short to make a definitive statement. Just want to be also realistic. But the advantage is that blocking that mechanism, we have done that with the antibody to the ligand, avacopan has done that with receptor, has not produced these types of signals like increased infection risk or anything like that. So there is no known safety issue on the mechanism in and of itself Provided the drug itself is safe, that could be a huge advantage. And maybe to add to that, I mean this is obviously knowledge, but we have released also now that we have the long term tox data in non human primates for example, nine month data, etcetera. So we have safety data on the drug itself that is really quite convincing and encouraging for longer term dosing now. And just on the HS cohort, anything to note on the patient demographics there, early stage two, early stage three? You've got a lot of experience obviously, multiple studies in HS. Have you been able to apply any of that to sort of maybe optimize that cohort for success? Yes. So we are interested to have at least x amount of patients with who carry draining active draining tunnels just to make a statement on that lesion and because you know we spoke about already the meaning of that lesion that doesn't have placebo response as much. So that's that's what we did but I think what I can observe like being in that field for a while now that by now if you go to the classical big bigger centers that enroll patients in HS trials, you have a lot of patients that have biologic experience, mostly of course anti TNFs, not just Humira also others off label and then anti IL-17s by now. So as patients progress and that's something I've heard also from experts again and again and kind of start getting refractory or progress under these treatments, their phenotype seems to become very severe and they're quite desperate for new mechanisms. So this is because they don't have the best durability these drugs or HS is so variable that it just almost like gets around it somehow. There's huge need for differentiated mechanisms. So we see more patients that have even double exposure to biologics also in their Certainly looking forward to that data here that's I guess I could say weeks away maybe is is accurate which exciting. I wanna also cover Vilabelumab. Mean, obviously, this is a long development history here and the most recent readout was in PG but this is also an antibody that's approved as Cohibic for COVID. So I I wanna cover sort of all this. And then of course the partner in China that's using I think the cell line to leverage this this antibody essentially, you had some recent promising data in ANCA vasculitis and you have some economic exposure there as well. It could be favorable for Inflorex. So maybe we'll just rapid fire through all that. I don't I don't even know where to start. Maybe let's start with COVID. I mean, the the so you're on market there. I mean, obviously, there hasn't been much sales to speak of historically just because, you know, ventilated COVID patients, right, fortunately for all of us, not so prevalent as they once were. But there's been some recent changes. I mean, EUAs are getting revoked. They're being replaced by full approvals. I mean, are you sensing anything is changing here and for GoHibix specifically? Is there anything to say about the regulatory status and what you might expect going forward? Yes, happy to cover that. So in The U. S, I have to say we've been finding a very supportive and collaborative FDA division here that really wants to collaborate with us on a broader label and make that like very vocal to us because there's a huge need for like an ARDS drug. I always keep using the term like if you had an off the shelf host directed threat agnostic therapy, that will be a big thing for pandemic preparedness. So there is interest from different sides of the government agencies that are in this field that these types of drugs get progressed into potentially approval situation one day that would require additional studies. But there's a lot of support. We're not running these studies currently on our own behalf because we don't have the funds to do that. I would say if you had a full label in the ARDS space, you can apply for extra payments outside the DRG frame. That actually lifts the problem in the hospitals that if they apply a drug that is expensive like life saving drug that they're actually losing money on it even if it makes the patient survive. So it's the system that works against it but for that you can apply for NTAP payments and if you have that for life saving drugs that's typically a reason to apply Then the hospital doesn't have that barrier anymore to give the drug because it gets it separately reimbursed. So there are potential upsides. We're not there yet, but we're running the BARDA study. We've been selected by the US government BARDA agency, one of the largest ARDS trials in history here in The US. And that study is enrolling, so there is potential for huge upside. Nothing on the near horizon, so I don't want to oversell here, but it is a meaningful mechanism. In Europe, we have an approval that's a bit different, so we're trying actively to find a partner. Even though COVID induced ARDS, we get requests, can we use a drug for ARDS? I have a patient. It's not on the market because we wouldn't commercialize that on our own. We need a partner in Europe. You have a partner in China, not for COVID, but I mentioned this is had some recent clinical success. What's the timeline for that? I mean, we hear a lot about China these days in biotech and everything's accelerated there. And this asset in particular looks like it's moving pretty swiftly through the clinic. What's Influorx's sort of economic share there? What do you expect in terms of timeline of development? What's the opportunity for ANCA vasculitis in China? Yeah. So we also it also blows my mind when I see how how fast they get these studies done. And in ANCA vasculitis, we've been probing this with them a bit because, you know, as you know, there's an oral drug here, you know, approved in Europe and in The US with abacopan. But they're running these studies in a fraction of the time. I mean, there are centers that are seeing twenty, thirty patients a month and then these are huge centers because it's so centralized to see to enroll 10 patients in a center in one month, you probably need to open twenty, thirty, 40 centers in Europe or in The US to get that. So there's a huge dimension to it. The data that they produced was very successful showing similar to what we showed with our antibody before that you can reduce and replace corticosteroids. It's a part that's not in the label of Avacopan for reasons that you probably know back then. Interesting discussions around that. And so, yeah, so the upside is a single digit royalty that we carry. We we own all rights outside China. They cannot take the drug outside unless we want them to and and have even a higher royalty there or we can do it ourselves. So we we own all rights to it. They've been a great partner, Statsun. They also produced data in the ARDS space lately, which significantly moved their stock. So they continue to confirm the mechanism with, in this case, an ANCA vasculitis with a licensed drug from us. There's potential of huge upsides. The interesting part is whatever they venture outside ANCA is also, you know, we're also owning that outside China and can use it with our drug or even use their drug, which is essentially the same drug produced from the same cell line under a separate watch, so to speak, you know. And The United States did indicate they'd be starting Phase III in AAV. Yep, okay. Let's talk about PG. I mean, I know you were planning obviously that study unfortunately didn't meet the continuing criteria at the interim analysis and we don't really know the details yet, but I know you're looking to analyze that. I think you mentioned it and maybe even planning to meet with the FDA to discuss the data endpoints maybe future, you know, for posterity if not for your own future in this indication. Maybe update us on have you met with the FDA or do you have that scheduled and just what the path forward is here, like what you're hoping to learn and accomplish? So, yes, thanks for that question. Appreciate that. The order of things will be we're going to unblind the data soon. We wanted to watch GCP requirements, not violate the protocol for the required safety watch after you stop dosing. We put the dosing, but we still needed to apply the X month of safety watch to not be uncompliant with the protocol. That's important if you ever want to use the data as supportive element in your submissions. So we we that's the reason why we haven't already un blinded it. So that's coming up, then we will look at it. We also by the way, while we're still blinded trying to adjudicate all the baseline data with independent experts to say is this really PG to your opinion because that we know there are sometimes misdiagnosis. So we're trying to do every work around and then look at our secondary efficacy measures as well like pain is a big one, but also fifty percent reduction of the total wound size which is like again and again voiced to us from investigators as being very meaningful for larger also. Just to remind people, complete wound closure was the primary endpoint. But fifty percent wound reduction obviously you'd be interested in Exactly. And you know that the FURIDILIA was done only on thirty patients reaching the full kind of treatment paradigm. We enrolled a total of 54, not all of them reached the six month because we put the study but we will be looking at more substantial data set than the 30 patients, right? Yeah. So in other words, we will also look at the primary endpoint. That's a pretty high bar fifty four patients, you have more data rates. Right. We will have more data and you know, depending on what we see then, first of all, we are doing all this because we have also interest from potential strategic partners that want us to do this and want to look at this. Because they think it's a very attractive indication to get in the market. And if we do see interesting signals with them, we'll plan and go back to the FDA and discuss. And if you unblinded it and the 54 there's a nominal p value even though there was zero? Yeah, those things happen in clinical trials and that make always makes the person running the study a bit look silly, but you know, I mean this like, kidding aside, this is a huge unmet medical need. I think it's a real market. So delivering a drug there probably we see a lot with the new administration, a lot of efforts to like approve drugs in the rare disease space. This is a clear high unmet need rare disease situation. So we will explore it if we have enough signals that we feel is worth putting it forward. And you know, the upside is if we have enough signals, will also publish this then maybe we can push this forward with a partner. We are currently focusing on nine zero four, that's where we put our money. Yeah. But if there is upside, are we gonna explore potential partnerships? What about nine zero four in PG, if you see the mechanism as maybe there's an interesting signal there? True. But that would be development wise quite a bit like years away. Yeah. So if we could bring an IV drug, in this case every two or three weeks delivered, it's not a big issue. The the patients will do everything if if it closes these wounds. That could be attractive like, know, also from a pricing issue. Yeah. It's a pretty rare disease, so you want a high price to make worth efforts. But yes, theoretically you could then also treat it with the C. Va receptor antagonist. That's maybe theoretical but down the you obviously have the data coming up here in weeks as I mere weeks as I mentioned and we're looking forward to that Hoping for a good outcome there. And thanks so much for joining us at the Cantor conference. Thanks to everyone in the room and on the webcast for listening and Thank you for having us. You bet. Thanks for having us. Thanks, Steve. Thanks. Thank you.