Hello. Thank you for joining us to discuss the top-line results from the third cohort of the phase IIa open-label study evaluating vilobelimab in patients with pyoderma gangrenosum. For those participating via conference call, we have made the slides available via webcast. A replay of this call will also be available on our website following the call. Before I begin, I'd like to point out that we will be making forward-looking statements that are based on our current expectations and beliefs. These beliefs are subject to certain risks and uncertainties, and our actual results may differ materially. I encourage you to consult the risk factors discussed in our SEC filings for additional details. With me on the call presenting the data is Professor Niels Riedemann, our CEO and founder, along with Dr. Hoda Tawfik, our Senior Program Director of Dermatology. Our Chief Clinical Development Officer, Dr. Korinna Pilz, and our CFO, Dr. Thomas Taapken, will join the Q&A section at the end of the call. Now I'll turn the call over to Niels. Yes. Thank you very much, Jordan. It's my pleasure to welcome everyone on this call today. Our team is very excited to share these data with you today on today's call. I would like to first direct you to the agenda of today's call. We will have an overview of the pyoderma gangrenosum and the measure of the PGA score, which is used for measuring efficacy of this disease. We'll then be presenting the study results and the design of the study, and we'll also guide you through three case studies selected for you. Pyoderma gangrenosum, we start on page five, is a very debilitating skin disease. The clinical features of this disease, which is a rare disease, can be potentially life-threatening. Usually this disease leads to chronic and highly painful and difficult to treat wounds and ulcers. Many PG patients also suffer from other autoimmune disorders. On the top of the list is ulcerative colitis, but there are also others like rheumatoid arthritis and also hematological diseases and disorders. Patients suffer from severe pain, long healing times, and frequent relapses of these ulcers. Sometimes this can even lead to amputation of extremities. The incidence is rare. We estimate, upon data research, up to 50,000 patients total in the U.S. and Europe together. The current treatment options are limited. There are no drugs approved for this disease. For less severe cases, usually topical and intralesional treatments can be used. For more severe cases, which usually end up in larger dermatological practices or clinics, the use of different types of immunosuppressants have been suggested, like corticosteroids, high-dose treatment, but also cyclosporine and other anti-inflammatory or immunosuppressive agents. The reports about efficacy are mixed, and these are usually very long treatment durations, and the relapses are frequently. The reason why we got interested in this disease is really for the mode of action, because this is one of the so-called neutrophilic skin diseases, meaning these ulcers are usually surrounded and infiltrated by a large amount of neutrophils that are activated, and that may have to do with the disease not being able to heal properly when being activated at site. You can find these neutrophils infiltrating the skin and affecting these areas. We believe that C5a, as a strong agent to attract neutrophils and to excite neutrophils, potentially, is involved in the disease progression and this is why we started this trial. Now, on page six, I would like to briefly introduce you into the measure of efficacy, which is the Physician Global Assessment score, or PGA score. Now I'd like to direct your attention first to the right side of this picture. PGA score measures a difference and a change from baseline. So if there's no change, your score will remain on a 5. If it's worsened, you will get a 6. So starting with the number 4, you see a slight improvement, which can be up to 50% of the ulcer size reduction. However, usually at that stage, you still have significant remaining disease. Now, we qualified a score of 3 or less as a responder, where you have over 50% reduction in the ulcer size. We qualified a score of 1 or 0 as remission or also called closure of target ulcer in this case. Now, there seems to be a certain contradiction because as you can see, when you score 1, you may have remnants of dusky erythema or very small alterations which sometimes happens if the clusters break off, et cetera. Even though that may seem contradictive, you will see from some of the examples we have in the slide deck later today why this is considered the full wound closure, full ulcer closure. It is my great pleasure to hand over this presentation now. I would like to very briefly introduce our clinical team. With us on the call is Korinna Pilz, our Chief Clinical Development Officer with many years of experience in drug development and successful experience even bringing drugs to market. She has done an amazing job in building this team and also oversees all parts of development within the clinical area, and we are on track with all developments, and this is remarkable. Korinna will be joining the Q&A session. Now it's my special pleasure to introduce Dr. Hoda Tawfik to you. She has extensive experience as well in drug development and brings years of drug development experience in oncology and dermatological area with her, including phase III trials and market approvals. She's been in a C-suite role in different companies, at last for many years in a public company. She got very interested in the mode of action, and she agreed to take over the role of the Immunoderm Senior Director. We feel very privileged and honored that she works with us on this role, and she does it out of passion, and you will see that this comes across, hopefully also in the presentation. Hoda, without further noting, the floor is yours, and you will please now introduce us into the trial, the results. Thank you. Thank you very much, Niels, for this nice introduction, and I'm happy to present the outcome of the study so far. This slide shows the study design, which is already published in ClinicalTrials.gov. I don't want to go into details for that. This study is in two cohorts, three cohorts. The first two cohorts were published, 800 mg and 1600 mg. The third cohort with the 2400 mg is what we want to concentrate on today. The two first cohorts are completed and the observation of the last cohort is ongoing. Just to highlight that the investigator had the chance to uptitrate a patient from one dose to the higher one on day 57 of treatment if there is no improvement of the target ulcer, and at least five patients treated with the current lower dose showed no safety issues. The next slide shows at a glance the key eligibility criteria also published on ClinicalTrials.gov. The only thing which I would like to mention is that it is allowed to give the patients up to 10 mg prednisolone during the study. This dose is a common practice for pain control in pyoderma gangrenosum, and it is not the treating dose. On the next slide, we can see the results of the group one. Again, we already announced these results. We have two patients achieved remission. One patient achieved a clinical response, and also one with a fluctuating PG score. What I would like to highlight here or to raise your attention is this visual impression of response that it is fluctuating on this group. Some patients terminated early the trial, and the reason of that is the start of the pandemic situation and the closure of one of our sites due to the moving of one investigator to a new site to the Mayo Clinic in the U.S. One patient in this cohort was uptitrated to 1600. The next slide shows the second cohort, again, also announced. One of the treated patients, the red one, showed a complete remission. This patient is good to note that this patient was uptitrated to 2400 mg on day 57. Two patients terminated very early. One of them terminated because of the hypersensitivity reaction, and the other one terminated because of personal reasons. The next slide shows group 3 on which we want to concentrate today. We can see here that 6 of the 7 enrolled patients showed remission with PGA score of 1 or less. Patient number 18, who did not show remission, but slight improvement from the PGA score. Nevertheless, when we looked to the ulcer area, the ulcer area decreased by more than 50%. I would like to raise your attention to the visual impression of the response here on this graph. If you look to that, you can see that the improvements, there is a continuous improvement in the target lesion, and this improvement is consistent. That means that there is no visual impression of fluctuation. I would like to flag two patients. It's patient 19. This patient is a complicated case. The patient had a pre-existing diabetes and a pre-existing infection in the area surrounding, the large area surrounding the target ulcer in the beginning of day one. The investigator decided during the study to treat the infection with broad-spectrum antibiotic and with cyclosporine A. Cyclosporine A is not allowed in the study, so definitely the patient is a protocol violation. Nevertheless, we could see a remarkable improvement till remission with this patient. The other patient I want to flag is the patient number 16. This patient is the only patient in the study who got 10 mg prednisolone started during the study. It is allowed, but again, just wanted to highlight, and it is, as I said, previously, it is a common practice for pain control in PG. Another patient which I would like to mention is the patient number 13. The patient terminated early the treatment because of a delayed information out of the TB, tuberculosis test, which was done in baseline, but it was delayed information from the lab. As soon as we got this information from the investigator, we of course withdrew the patient from the study due to safety reasons. However, this patient showed a very good response, and I will get back to this patient later in the examples. The next slide shows the C5a levels in group 1 and 2. It was already announced that our drug showed an effect in reduction of C5a, compared to baseline. This was also confirmed in the next slide on, in group 3. Next. Here we can see also the good reduction of the C5a level under treatment with our drug. Please note that these C5a levels are measured in plasma and not in skin, so it doesn't reflect what is happening in the skin from a C5a level concern. The next slide summarize what I tried to show you in the previous slides. From the safety point of view, we didn't see any infusion-related reactions. We had two patients with related serious adverse event reported by the investigators, already published and announced. One of these is SAEs, the rash, which is already announced, as I said, the delayed hypersensitivity. The other one is erysipelas, leading to hospitalization. This case was judged by InflaRx as not related to the drug as this infection is a very common and well-known complication of the disease, pyoderma gangrenosum. There was no dose-related adverse events, and the observed adverse events profile was in line with the patient's underlying disease. Concluding the clinical response, 17 patients were evaluable for clinical response at end of treatment visit or at the day of last administration. 9 out of these 17 patients showed clinical remission. That means PG score 1 or 0, PGA score 1 or 0. An additional patient showed at that time a clinical response. That means PG score at least 3. The other seven patients showed slight improvement of PGA score 4. The highest rate of target ulcer closure and clinical remission was observed with the high-dose group with 2,400 mg. In one sentence, we can say that vilobelimab bi-weekly given showed a good safety and tolerability profile, and we could observe evidence for a dose-dependent drug activity in PG. Getting all these data, the next step will be to go to the FDA and discuss with the regulatory bodies the next steps for the development in this PG. Please allow me to say that my team and I are really very excited about these results and are very excited to discuss these with the FDA. We come with the next slide to the patient case studies. Here are some examples. This is patient 10, a patient enrolled in the cohort 2, 1600 mg and uptitrated to 2400 mg at day 57. This patient had a previous history of PG medication and did not heal or show improvement under the previous medication. The patient was enrolled in the study, and if you look to the very left, you can see the ulcer in baseline, which is pretty large. On the very right picture, you can see the improvement and the healing of the target lesion with the area of zero with a PGA score of 1. The next case is patient number 14. Patient enrolled in the third cohort, 2400 mg. The patient had a history of treatment for PG and failed on the previous treatment, but enrolled in our study, and we can see how the lesion from baseline improved from baseline till end of treatment on the very right. The third case, again, on the very left, a big ulcer. Within the study the patient was treated, and we could see that the wound was improving and closing till day 80, 98, end of treatment visit, where the PGA score was 1, almost closure. We already have information about this patient that is even after end of treatment in the later observation, the wound completely closed, PG score 0, and complete remission. I have an important note for this patient, is that this patient is that one which I mentioned earlier, you know, if you remember, with the turquoise line. This patient was treated with adalimumab for psoriasis many years before the study start and continued with this treatment. During the course of the treatment of adalimumab for psoriasis, the PG pyoderma, not PGA, pyoderma gangrenosum developed and the wound opened. Therefore, the patient was enrolled in the study, and we can see that under the treatment with the vilobelimab, his pyoderma gangrenosum improved very good. Unfortunately, this is the patient who was withdrawn from the study because of the delayed tuberculosis test. Nevertheless, we could see the closure of the wound after end of treatment and even better after the observation, you know, the observation visit. These were the three cases I've chosen just to give you a flavor of how the development of the disease upon treatment with vilobelimab. Thank you very much. Now I hand over to Jordan for the Q&A session. Thank you, Hoda. Fantastic presentation. Operator, please start the first Q&A question. Ladies and gentlemen, at this time, we will begin the question and answer session. Anyone who wishes to ask a telephone question may press star followed by one on their touch tone telephone. If you wish to remove yourself from the question queue, you may press star followed by two. If you're using speaker equipment today, please lift the handset before making your selections. Anyone who has a telephone question may press star followed by one at this time. If you would like to ask a web question, please write your question into the ask a question box in the webcast. One moment for the first telephone question, please. First question comes from the line of Steven Seedhouse from Raymond James. Please go ahead. Hi. Good morning. Good afternoon, Niels. Thanks for hosting this call. Really interesting data. I think one of the hypotheses emerging from the SHINE study that you ran previously in HS was maybe IFX-1 was underdosed. I know you commented on antibody turnover in HS maybe being different than expected. Here you've doubled the dose in the third cohort relative to the high dose there and it, I mean, it's a pretty substantial signal. The C5a data at 2400 mg certainly looks very clean and compelling. I'm just wondering what you make of that, what you make of dose in general here, what you're learning about PK and certainly what readthrough that might have to your HS study designs going forward. Yes. Thank you. Thank you, Steve. It's a great question. Obviously, dosing has been, as you mentioned, clearly on our minds since we got the HS results. In HS, we did extensive modeling, PK/PD modeling, as well as a physiologically-based PK modeling to assess not only what we could learn from the plasma doses, but also to model how that would relate to a tissue dose and tissue coverage of the signal. What we learned in HS, and here again, I think the overall learning is that in skin diseases, you need a lot more dosing, even though I would say if you just look at plasma levels, you can certainly reduce C5a extremely well to below normal levels already with lower doses. However, as Hoda pointed out, it may not reflect what's going on in the skin. Now, in HS, we did extensive modeling, and we found that a slightly higher dose than what we chose, the highest dose back then we chose was 1200 mg every other week. We found that a higher dose would result in better coverage in the tissue coverage model that we put together with experts in the physiologically-based PK modeling. Now, I think this is somewhat reconfirmed here, even though I have to caution, of course, PG is a quite different animal compared to HS. I'm saying that because PG seems to be extraordinarily difficult to treat and it's known that vast amount of neutrophils get activated in the skin, and so you may need an even higher dose in PG. Certainly, what we take from this is that dosing in skin diseases, especially here with our antibody, seems to be an extremely important topic when looking at efficacy. I think the most important point we want to make really is that even though from C5a levels, all of the test doses were clearly giving C5a levels below normal or on the lower range of normal plasma levels, you see that the clinical picture at the lower dose was quite off. I would say visual impression of fluctuation, but in the high dose, you really saw continuous improvement over time. Thanks for that question. Dosing is important, and we have done a lot of modeling. We know that in HS, we need to go higher than where we were before, and this has been confirmed with authorities already because we have agreement on the primary dose we're gonna use in a phase III trial. In PG, clearly, we're even a bit higher here with that dose, but obviously with these results, we would move forward with the highest dose tested in PG. Great. Okay, thanks. I mean, I'm just looking here at the plot for the high dose again, and I know you flagged patient 13—or excuse me, patient 19, and patient 16, who sort of started some concomitant medicines and that maybe contributed to some of their response. For the others, sounds like no, and the kinetics there are. I mean, patients are responding immediately, basically, so in three or four of these other patients. I wanted to ask about the kinetics at study entry. I mean, were these target lesions they need to be sort of stable or persistent at study entry. Do you know anything about sort of what was happening with these lesions before they went on IFX-1 treatment? Yeah. That's a great question. We wanted to have a longer lasting diagnosis, but we, in our exclusion criteria, we didn't want to have ulcers that already existed longer than three years because it's believed that the ulcers may change and get into an anergic state. We certainly learned a huge amount about the type of patients you can enroll that have a chance to heal. We haven't gone into all details, and we will do that within medical conferences in the time to follow. Obviously, we have also enrolled some patients with even much larger damage than you've seen here. As you can imagine, if you imagine a patient that has a circumferential skin loss, that was a patient we talked about earlier in press releases and also in conferences on the low-dose group. You can imagine that you need some healthy skin to heal from. If the damage is too large, you may not qualify for the drug to heal you completely, even though you may find a better ground. I mentioned that some of these patients get even amputated or transplanted. I think the ideal situation is to go to an active ulcer that is already there for longer. It doesn't seem to matter whether the ulcer has been treated before with high-dose corticosteroids or cyclosporine or whether it's the first treatment attempt. We don't see that there is a difference in whether you had pre-existing treatment attempt or not at this point, but the patient numbers are really low. Certainly, we noticed that when you exceed a certain damage, it's becoming unlikely to heal a wound in six months in this disease. I wanna flag again, Hoda has taken over the Immunoderm program last year, and she and her team under the lead of Korinna, they've done a fantastic job in delineating and working this out with the investigators for each separate case enrolled. The high-dose group really reflects also a learning within our team and within the study. Target ulcer size is very important. We certainly don't have a case where the ulcer was just appearing in the last month or two. All these patients, you can see from the medical history, had it for at least a year or longer, I would say. Some of them had the PG diagnosis longer, but we excluded patients where the target ulcer was older than three years. That's all. I wanna mention that. That's great. Just last question, it's a technical one. I just wanna clarify. The dots on all of these line graphs are in fact observed visits with measurements of the lesion. There's nothing imputed or carried forward here in these dots? Yes, that's correct. Hoda, you correct me if I'm saying something wrong here, but to my information, these dots reflect actual patient visits, PGA scores. Exactly, yes. Yes. Since we allowed for the later visits, always plus minus a few days, for convenience purposes, they may not always be exactly on the same line, but they actually reflect the actual date and measurement. Yeah. That's great. Thanks so much for taking the questions. Appreciate you guys hosting the call. Of course. Thanks for the great questions. Thanks, Pete. Next question is from the line of Yatin Suneja from Guggenheim Securities. Please go ahead. Hey, guys. This is Evan on for Yatin. Congrats on the data, and thanks for taking our questions. Two-part question from our side. Patient 18 developed new ulcers despite a robust reduction in C5a levels. I'm just wondering, you know, what else could be driving new ulcer formation in the absence of C5a? And then kind of as a part two to this question, how different are plasma versus skin C5a levels in PG? And are there any correlations between the two? Evan, thanks for this great question. These are two questions. I'm gonna take the first question first myself, and then maybe have Hoda answer the second or help me answer the second question. Or vice versa. First, let's go in the C5a levels first. We have not found, and I don't think there exists a credible way to measure skin levels of C5a. Those need to be modeled and assumed. Plasma C5a levels, you can assume that C5a can be carried over into the plasma to a certain extent, but it never will reflect exactly what's going on in and at the skin site. That's why we caution saying, yes, we see that, and you're completely right. We have patients where we have a great suppression of C5a levels, but we don't see a response. Now, hopefully that answers the first question. We cannot yet measure skin C5a. We can model that. The question is, why does not each and every single patient respond when you block it in the plasma completely. You can assume it's nicely blocked in the skin as well. Now, of course, we cannot, and that really was the first part of your question, sorry for confusing that. We cannot make a definitive statement on that. I do wanna flag and then hand over to Hoda that PG is a very complex dermatological disease. Some people call it the holy grail of treating patients because it's basically a diagnosis that usually comes through exclusion. Oftentimes, these patients are treated first with antibiotics for having an infection or an ulcer, and then people see it's not getting better. Eventually, you move through a few diagnoses until you say, "Okay, this must be PG. It's not responding to the usual treatment of an ulcer." Having said that, these patients are, some of them have concomitant diseases, sometimes diabetic skin diseases. They also oftentimes have concomitant infections or can develop infections. We've learned that from the one very complex case that we flagged that had a protocol violation getting on cyclosporine A. This was a case with a dramatic wound infection at baseline. Now, in that infected area, later on, you know, new ulcers developed that were then also going away. That is something where you can never know whether such a phenomenon is really PG progression. Hard to believe because it's happening very fast. My guess is that additional infections in the skin can also cause skin alterations. If you think about an infection in diabetic skin, you may see something at the site of where your main ulcer is that looks like an ulcer, and it could be PG, but it could also be just an infection. To delineate it or to differentiate it is like from a physical point of view as a medical doctor, and we spoke personally to the person with that complicated case, to the medical director there. It is a very difficult task to differentiate. When new PG. By the way, this happens in very few cases. The vast majority, if not almost all of them, develop no new PG lesions. They really heal the entire disease. I think that knowing what an additional ulcer is caused by is very difficult in this disease. I hand over to Hoda if she may have something to add to this because clearly this is the best I can answer the question. Niels, I agree with you 100%, and especially you mentioned this patient, which I already highlighted in my presentation, the patient with a very complicated disease course, having a pre-existing diabetes and wound infection. This is a really challenging case. Although it was such a challenging case, the patient responded and had a remission. From the other patients who did not show remission, in the earlier cohorts, we also had some patients which were from the entire condition of their health situation. They were very challenging, as you said, for example, transplantation or also infections. All this makes it a very, very difficult to manage the disease. Pyoderma gangrenosum is, in general, a very, very challenging disease. I would say even more challenging than hidradenitis, for example. You cannot choose the optimum patient because it is a very, very severe disease and associated with other conditions which makes the life of the patient very difficult and also of the treatment very difficult. Okay, that's my time. Got it. Thank you. Next question is from the line of Joseph Schwartz from Leerink Partners. Please go ahead. Great, thanks. Congratulations on the data. I was wondering if you could talk about what placebo response would you expect from the types of patients who were treated in this study? How replicable do you think these responses would be in a placebo-controlled study that would be done in many more patients at multiple centers? Can you compare these findings in any way to what you saw in HS in an open label setting, when that wasn't later confirmed in a placebo-controlled setting? Yeah. Thanks, Joseph. This is a great question. I'm gonna hand the question over to Hoda. The question was, Hoda, how, you know, can we make a suggestion or can we guess how placebo response rate would look like, knowing that there are very few randomized controlled trials in this? And then also, the question is there evidence how this what you can find in such a trial reflects later on in a larger study, maybe controlled study? Hoda. Thank you, Niels. Of course, to suggest or to guess what is the potential response of placebo, this is really very difficult. If you look even for the clinical trials, for example, the clinical trial of adalimumab, which led to the approval in Japan, it was a single-arm study and not versus control versus placebo. The reason why it was not or it is not done versus placebo, because again, it is a very severe disease, and it is the question if we can afford or a developer can afford to enter in a study and give the patient just placebo. It is really hard to predict what is the placebo effect in this pyoderma disease. This is my guess. From the literature, there is no real placebo or there is no placebo-controlled studies. Okay. That's helpful. Thanks. And then? We- Sorry, Niels. Go ahead. Yeah, maybe just to add to this, I think there was one phase III attempt in the U.S. with an IL-1β antagonist, and that was prematurely stopped for futility, so we don't know more about details of that trial. Just to reiterate or to also emphasize what Hoda said, you know, we spoke to a few investigators, and some feel that a placebo-controlled trial would be unethical because these patients are in dramatic pain and suffering. To say, "I'm gonna take a six-month endpoint and let you run against placebo," is difficult unless you offer a clear scheme on what rescue would look like and then how do you compare that. It is a challenge, but there's a very high unmet medical need. I can confirm, and that's something we have said when the first cohort was released. I think it was actually in one of your conferences, Joseph, that we had spoken to an investigator where we saw the two remarkable first responses that we had published from the low-dose group, that the investigator felt that it's very rare that these ulcers heal by themselves. She couldn't give a number, but she said they need treatment, and oftentimes treatment is not of a lasting effect. This was kind of the rough, you know, answer you get. In the end, there's no full answer to your question, but I would say if you don't do anything to these wounds, just regular wound care, it is not expected that many of these patients would even heal. Exactly. Right. Can you talk a little bit more about the PGA score and whether, you know, do you think that could be used as a valid endpoint for regulators? You know, how well does it capture the array of features in PG, do you think, according to regulators? Yes. Thanks for that question. That's of course a question that's on our mind, the team, and I will be happy to have also Korinna chime in here. I give you my first two cents on it. But I think that the PGA score has been used in some trials. The phase III trial attempt I mentioned, I think had target ulcer closure, so very similar to what we did here as primary endpoint, and we assume it has been pre-discussed with the FDA 'cause they also got an orphan designation. I think the PGA score is the only one established instrument used so far, next to ulcer healing times, ulcer size reduction. In the end, we will have to go to the FDA and go to the regulators and have that discussion. I would think that the way we have applied it here, at least in our view, makes a certain sense as a valid endpoint. Maybe Korinna, do you have other thoughts? Yeah. Actually, I agree, Niels, that the PGA score for pyoderma is really the most important assessment tool that has been used in many case studies and also the small trials that were done in the past. What also is often used, and you might have seen that also, it's remarked in our presentation before that, is a photographic measurement of the wound area, which then can contribute and give some numbers to the PGA score in addition. That's helpful. Maybe I can just ask one follow-up. At what point do you feel like you're ready to go to the FDA and EMA and get alignment on what you can use in a phase III? Yeah. Great question. I mean, obviously, this is an open label study. We're now just waiting for the last few patients to complete the observational time period. I don't think anything would hold us back to start this process ASAP. Obviously, we will also do some internal validation work and thinking on what we can propose. Again, this is a high unmet medical need area with nothing approved in the U.S. or in Europe. We see a chance of being a first mover. This is always, at the same time, an advantage, but also at the same time a challenge. We understand that. I don't think anything holds us up to get the data in the right format, present it, and have at least an end-of-phase II or at least a scientific discussion with the FDA and seek advice on how to move into a pivotal program. Very helpful. Thanks. Next question comes from the line of Anupam Rama from J.P. Morgan. Please go ahead. Hey, guys. Thanks so much for taking the question. With some of the high-dose data that you have at this point, is there a rationale for starting at 2400 mg initiation and just keeping that dose for the maintenance phase just for simplicity purposes? Or is there a rationale in later stage trials to test sort of dosing optionality to give physicians in the clinic and in practice in the real world more dosing options? Thanks so much. Thanks, Anupam, and great that you joined. Yes, absolutely. That's a great question, and we've been discussing this question before. As you can see, in almost all of our trials, we have used this three times 800 mg introduction dose or basically we do that on day one, day four, day eight, and then coming week, we start on biweekly treatment. We've had very good safety experience, and so we haven't changed it to be consistent. We know from all of our trials and PK/PD modeling exactly what this first three shots, 800 do. Of course, with the 2,400 showing really no safety concerns here in this trial for us, it's a completely valid question. Why not just directly start with the first shot of 2,400? I think the development team and also our PK/PD specialists are already looking into this, and I don't think that there's a, I would say, a technical hurdle to that. Got it. Thanks so much for taking our question. Absolutely. Next question is from the line of Edward White from H.C. Wainwright. Please go ahead. Good morning. Congratulations on the data. Thanks, Edward. I have another question on dosing. Since we are seeing excellent data with the 2400 dose, are you thinking of looking at even higher doses, in particular, maybe not starting the patients off at the 2400 as you just discussed, but up dosing patients who have somewhat of response like patient number 18, but didn't get a full response? Yeah, that's a great question, Edward. Thanks for joining the call. You know, for our drug, 2400 is a very, very high dose. We in other diseases would never imagine to go that high because we know we have a very good serum level controlled C5a with other doses as well already. However, as we had already discussed earlier for another question, I mean, skin disease, it seems to be a game of dosing, and you need to have high enough dosing to cover that large organ. We have not made that decision yet, whether we put in an even higher dose in a future endeavor. I think it's a pretty rare disease considering it took quite a while for these 19 patients to be enrolled. It's also a feasible question, how long can you play with even higher doses? Now, we may think of such an option for non-responders in the future, but we have not made that decision yet. Because this is relatively hot off the press here, and we felt it's meaningful because, and to say that in general here, it's meaningful because this is a very tough to treat disease, and we saw some really great responses. I was very stunned personally about the case that we presented that had for years adalimumab and developed PG ulcers under adalimumab and then responded to our treatment. It is a high unmet need area. We also felt it's meaningful data because you know that we are now for a while in immunodermatology. We are planning a big endeavor in hidradenitis suppurativa, which is another neutrophilic skin disease, obviously with a different phenotype and with a different disease pattern. I think it's another evidence that our drug has clear activity, and in this case we've seen even dose-dependent activity. Coming back to your question, I think this is an option we may need to consider for future trials, even though we feel that obviously given these data, the 2400 mg for PG could be an ideal dose moving forward. Building in an opportunity to even go higher, especially for such a rare disease, may be something we will be considering, of course. Okay, thank you. Regarding patients that received prednisolone, it appeared that patient number 16, looking at the graph, responded better after receiving the dose of prednisolone. I was just wondering if any future studies will stratify patients results for those getting prednisolone. Finally, my last question would just be on timing. We had mentioned before about meeting with the FDA. Just your thoughts. You did have, as you mentioned, trouble enrolling patients due to the small patient size. How should we be thinking about perhaps the size of a pivotal study and your thoughts on how long a pivotal study might take to enroll? Thank you. Yes, thanks, Edward. With regards to pivotal, it's clearly too early to give you a size indication. I can tell you that the one study that I mentioned earlier on the call that was a phase II or marked as a phase III study in the U.S. was in the range of 60-80 patients, if I recall correctly. It wasn't an awfully huge endeavor, but it was large considering that's a pretty rare disease. Now, we started in several centers here within Canada and in the U.S., and then enlarged the study to be more international also to Europe. Actually we ran into the start of the pandemic with the study, so it's hard for us to differentiate whether it's been tough generally speaking. I would say once the sites here in Europe were open, where the pandemic was at that time well controlled, we saw a good enrollment, the last cohort really enrolled well. We are confident that this is an area where you can find patients. Obviously it is a rare disease and it's hard for us to predict how long such a study would take. In terms of size, again, this really depends on the endpoint, on the statistics and also on the advice we get from the FDA. I must ask for some patience until we have had such discussions. Obviously, flagging that the former phase III endeavor from a biotech in the U.S. was not very large either. I hope that covers that part of your question. Then you had also mentioned, okay, patient 16, which we flagged, which was the only patient who got started on 10 mg low dose prednisolone during the trial, really showed responding later. That's why we flagged it because, for us it's, you know, starting it while you have IFX-1 doesn't make too much sense. Again, I think Hoda's team spoke to the investigator why he felt like starting it. Obviously, he showed some response but not sufficient to be happy at that point in time, but he also suffered from a pretty substantial pain. As Hoda mentioned, and you see that we have several patients that have either for years or many months prior to enrollment in our study are on 10 mg per day prednisolone just because investigators feel this can handle the disease better, maybe also handle the pain better. Now, there's not much literature about that, but I would say local guidelines and expert opinions that recommend corticosteroids for treatment of PG really recommend much higher doses. On the low end, 0.5, on the high end, 2-3 mg/ kg body weight per day. Some even say you should start with 1 g for five days consecutive pulse dosing. The treatment recommendation of corticosteroids for this disease are much above the low-dose 10 mg level. However, we need to consider. I think it's common practice, and Hoda mentioned it in the adalimumab trial in Japan. This was also allowed to have 10 mg prednisolone. So it's kind of almost common practice even though these trials are rare. We may wanna consider if we allow starting patients on it if they're not already on it in the future. That's certainly something we need to consider. Okay, thank you. Congratulations again. Thanks. Thanks, Edward. Next question is from the line of Rami Katkhuda from LifeSci Capital. Please go ahead. Morning, everyone. This is Rami on for Sam. Thanks for taking our questions. Just a couple quick ones from me. Were patients enrolled in cohort three required to have the elevated C5a levels at baseline, or did these patients just have the elevated levels given its role in the disease? Yeah. Thanks, Rami. Thanks for the question. Very good question. I hand this over to Hoda. Could you repeat the question again, please? Yeah, of course. Just basically, were patients enrolled in cohort three required to have elevated levels of C5a? Did that just happen because there's the role of that C5a in the disease? Actually, the C5a level in baseline was elevated, of course, because of the disease and the underlying condition. What we could see in the slide where I showed that under treatment with vilobelimab, the C5a level was markedly reduced and also the effect on the ulcer and the target ulcer was seen. We can see that the re- Hoda, I think. Sorry for interrupting. I think the question was it a prerequisite for them to start with? No, no. It was not a prerequisite. No, it wasn't. Got it. It wasn't a prerequisite. Makes sense. Thank you. Just quickly, across cohorts, what was kind of the remission rate for patients with these elevated C5a levels? Hoda, will you be able to comment to that? Thank you. Go ahead. Sorry. Yeah, no. I just wanted to hand the question to you. Sorry for that. If you look to the C5a level which was reduced, it is of course in parallel to the remission in the different cohorts. We can see that the reduction of the C5a level in cohort 3, where we could see the highest number of remission, was higher and was more significant than that which we saw in the first 2 cohorts. We can say that there is a certain parallel development between the reduction of the C5a level and the effect on the target ulcers and the remission. Got it. That makes a lot of sense. Thank you. Thank you. There are no further questions at this time, and I would like to hand back to Jordan Zwick. Please go ahead. Thank you. It seems that the written questions most of them have all been answered. I think we can close the call at this time. Thank you very much everyone for joining, and any additional questions, please reach out to us directly. We're happy to