I'm Dr. Mark Jackson, Vice President of Clinical Development at Evommune. Thank you for tuning into this webcast to review the full dataset from our U.S. multicenter phase II trial of EVO756 in adults with chronic inducible urticaria. This data was presented today, September 19th, as a late-breaker oral presentation at the European Academy of Dermatology and Venereology 2025 Congress in Paris. As you can see on this disclaimer slide, some of what we present today include forward-looking statements. Chronic inflammation is a global healthcare crisis, and we at Evommune are trying to create solutions for this problem. We know that chronic inflammation destroys lives, contributing to three out of five deaths worldwide, and creates a substantial burden to the healthcare system. We also know that many patients continue to be underserved by current therapies. We have an experienced team that is evaluating distinct mechanisms to bring solutions to those patients. We have multiple near-term clinical milestones with our most advanced program, EVO756. We are moving forward with the phase II-B program in chronic spontaneous urticaria, with data expected in the first half of 2026. We are also actively enrolling in our phase II-B multidose trial for atopic dermatitis, with phase II-B data expected in the second half of 2026, and we are also evaluating other indications. We have encouraging data in two trials to date. One, our proof of concept trial in 132 healthy volunteers demonstrated good tolerability at doses from one to 500 mgs across all doses, was well tolerated, demonstrated clear target engagement, and dose-proportional PK. Our Phase II trial in chronic inducible urticaria was also well tolerated across all doses. Complete responses were noted as early as week one, and our proof of concept achieved after just four weeks of dosing, and as mentioned, we are actively enrolling in our phase II-B in CSU and atopic dermatitis. Today, I'd like to introduce you to our guest speaker, Dr. Ted Lain, who is a board-certified dermatologist, clinical investigator, chief medical officer at Sanova Dermatology, a well-known KOL in the field of dermatology, and an active participant in our phase II trial in inducible urticaria. Thanks for joining us today, Dr. Lain. Thank you so much, Mark. And hello, everybody. My name is Ted Lain, as Mark mentioned. I'm a dermatologist in Austin, Texas, and I run a robust clinical trial center. We have been lucky enough to be involved in the Evommune study for chronic inducible urticaria, and I'm happy to share the results as well as my own experience with this trial. Note that this is a small-molecule inhibitor of the MRGPRX2 receptor. And from here on, I'll just be calling it the X2 receptor for the sake of brevity. So in terms of the background for this condition, chronic inducible urticaria, we in dermatology call it CIndU, is considered a subtype of chronic spontaneous urticaria. It affects about 0.5% of the population, and it tends to last longer than chronic spontaneous urticaria. CSU, in particular, tends to run a course of months to years, whereas CIndU can take a much longer course. About 35% of spontaneous urticaria patients have concomitant dermatographism, so it's not uncommon for us to see someone with a history of spontaneous hives, and then when we do a test for dermatographism, we do a scratch test on their back, we find they also have that condition as well. The subtypes of dermatographism, excuse me, of CIndU include dermatographism, cold urticaria, heat urticaria. You can see we split them into physical and non-physical subtypes. In this trial, in the phase II trial, we looked at patients with CIndU that had two types of physical CIndU, including dermatographism and cold urticaria. We know the pathogenesis likely is an autoallergenic IgE-mediated mast cell activation, where you see mast cells or MC in this presentation. That stands for mast cells. Mast cells are tissue-bound. They are in the area in which the hives are located. We'll also talk about basophils, which are considered circulating mast cells. They're in the circulation, but they can target the tissue as well. There is an IgE receptor called the Fc epsilon RI receptor, which is present both on mast cells and basophils, and it looks to be at an overexpressed state, much like we see in CSU. So the expression of the IgE receptor is elevated in both basophils and mast cells in both CIndU and CSU. I think of these two conditions as cousins. We see that there's a high majority, or excuse me, there's a high minority of patients with CSU that have concomitant CIndU, and therefore I think of them as closely linked conditions. Next slide, please. So the treatment landscape for CIndU is, of course, avoidance of triggers. That's easier said than done, isn't it? Especially when there's dermatographism involved. It's just a scratch or pressure urticaria as well, for example. Here in Austin, avoiding cold urticaria isn't a problem, but certainly in other areas of the nation and the world, it is. The second-generation H1 antihistamines, the non-sedating antihistamines, are considered part of the current treatment landscape, much like they are for CSU, and we dose up to four times the current recommended dosing on label. But 20% of CIndU patients are on these second-generation H1 antihistamines and yet still have symptoms. Then, of course, there's Omalizumab, which targets IgE as an IgE antibody. But this would be considered off-label use because Omalizumab is really only indicated for CSU. Next slide, please. The X2 receptor is located on mast cells, but notably, it's located on sensory neurons as well. When we think about the sensation of our urticaria patients, there's certainly itch, right, which is associated with both the inflammation, the tissue expansion of that inflammation, but that sensory neurons, as we know from atopic dermatitis and prurigo nodularis and other inflammatory diseases in the skin, sensory neurons absolutely play a role. This targeting the X2 receptor, therefore, makes a lot of sense pathophysiologically, and really this is the only treatment which can target both the mast cell and the sensory neuron for CIndU. Now, it's important to understand the X2 receptor is on both, but also important to show that the mast cells and the nerve cells are in close proximity to each other. Next slide, I just want to show you why that's important. Mast cell degranulation has mediators that lead to sensory neuron activation, including ligands for the X2 receptor, as shown in this graphic here, so having them in close proximity to each other, therefore, means to me, at least, that the mast cell mediators are highly likely to activate the X2 receptor and lead to a greater sensation of itch, which is why targeting the X2 receptor, again, because of the pathogenesis of this disease process, makes a lot of sense clinically. Now, as with most aspects of the body, there are closely linked pathways between different body systems, so we've got the neuronal system, which is activated by the mast cell degranulation, which, of course, is part of the immune system, then we've got the vascular system involved as well with vasodilation, extravasation of immune cells, and therefore release of inflammatory cytokines as well. So this just shows you what we know in terms of almost all inflammatory disease, that different body systems have crosstalk and sometimes positive feedback between them. And that's certainly what we're seeing here between the mast cells and the sensory neurons. Next slide, please. Luckily, EVO756 is an oral small molecule that competitively inhibits the X2 receptor, and by doing that, it blocks the effects of multiple ligands, and those are listed here. Cathelicidin LL-37 is an interesting ligand. We see that in rosacea as well. Peptide hormones are listed there. Neuropeptides, including cortistatin, for example, substance P, is one that we commonly think of that causes pain and itch. By being able to block the effect or the binding of multiple ligands to the X2 receptor on both mast cells as well as sensory neurons, we alleviate, in my view, many of the causes of CIndU at the cellular level. Next slide, please. Let's go into the phase II study, and we'll talk about the results as well. Patients were enrolled in this open-label trial, multiple-dose trial. We had a 300 mg QD dosing and a 50 mg BID dosing cohort. Week four was where we measured the primary efficacy endpoint. Now, notably, there's no placebo because we weren't sure which dose was going to work. There is no animal model for X2 receptors. In fact, X2 receptors are only found in humans. So Evommune did its best with other preclinical work to understand the dosing range, which is in this 50- 300 mg, excuse me, this 50 BID to 300 mg dose, but weren't sure exactly which one would be the most effective. And that's why you see that wide range there. The primary endpoint, it's a phase II trial. So the primary endpoint was safety, but the efficacy measures were there as well. And we looked at this via the Fric score, which is a pressure score. And I'll show you what that is. It's a paddle with four different-lengthed prongs. And when we scrape that on the skin, for patients with dermatographism, we saw the urticarial lines that happen. And if we could reduce that Fric score by at least two lines, that would be considered a response. A complete response, of course, is no lines with the FricTest. We also looked at change from baseline and pruritus numerical rating score. That's a zero- 10 Likert scale where we asked patients over the last 24 hours what their peak itch score was. That's how we captured the pruritus NRS. We also looked at patient subtyping via IgE presence, whether high or low IgE presence in the serum. Then pharmacodynamics, of course, and disease severity. After week four, we stopped dosing, and there was a two-week follow-up to the end of the trial being at week six. Okay, let's go on to the next trial. Of note, patients were 18-65 years of age in this trial. So the mean age for the 300 QD and the 50 BID was in the mid- to late 40s. The majority of patients were female, more in the 50 BID trial than the 300 mg QD. That mimics the overall incidence of this disease, which is higher in females. The mean weight is listed there in kgs. We limited the percentage of high IgE in this trial, and you could see it's about 20%-27%. The baseline FricTest score was between three and four, and the baseline pruritus NRS was four to five. Now, it's interesting to note about that pruritus score, right? When you're thinking about itch, we often think this is a very itchy disease, but with CIndU, you're talking about localized itch. And so a lot of patients will not consider that as itchy as you would think of for an atopic dermatitis, where you have more generalized itch. So I'm not surprised at the mean baseline NRS being in the four to five range. In terms of patient disposition, on the right of the slide, you can see enrolled is about 11 in the 300 mg cohort. 50 BID had about 19 patients. 10 and 17 completed. One patient in the 50 BID arm missed the week four visit, which decreased the total number of participants available for efficacy there. And then the unavailable, loss to follow-up is listed there, one and two in the 300 and the 50 BID cohort groups. Next slide, please. All right, let's talk about efficacy. All right, so again, the number of 300 mg patients were 10. Complete response seen in about 30% of those. What about a partial response? So one patient had at least a two-point decrease, and two patients had a one-point decrease. Although clinically, we think of clinical efficacy as at least a two-point decrease. I can tell you as someone who myself has dealt with chronic spontaneous urticaria, and I did have concomitant CIndU as well with dermatographism, this is when I was a young man, that any kind of decrease in CIndU is very helpful and clinically meaningful to the patient. Four patients had no response, therefore, in the 300 mg QD arm. In the 50 BID arm, we saw some very similar, if not better results, actually. Complete response in about 30% of patients again. Two-point decrease in 12%, but a one-point decrease in 35%. So in total, you can see on the far right of the trial, we had about 30% of patients have a complete response, with another 40% having at least a two-point or one-point response there, and no response only in 30%. In terms of the IgE categorization, those with high IgE, 50% of the complete responders were those with high IgEs. We think about those with high IgEs as more of that type one autoimmunity. And so usually you think about those as Omalizumab, for example, would have a much greater chance of achieving efficacy with the high IgE as a monoclonal IgE antibody. With this type of treatment, though, a small molecule targeting the X2 receptor present on the mast cells and the sensory neurons, we shouldn't see difference, in my view, between high and low IgE, and indeed we really didn't. Okay, next slide. This is showing you FricTest scores by subject in the higher dosing cohort, the 300 mg cohort, and then the 50 mg BID cohort. And you could see there's really not much difference between them, right? It didn't really change between the two doses. Now, based on pharmacokinetics, actually, the 50 mg BID dose, if we look at area under the curve, is about a quarter of the dose of the 300 mg QD cohort. So we are looking at quite a difference in the dosing there, but not much difference in the efficacy at all. So it makes sense to move forward with a lower dose, and there's some other aspects to the lower dose that make sense as well. We could see 70% of patients had at least a one-point improvement. 41% had a two-point improvement. That's a clinically relevant improvement, excuse me, and then 30% had a complete response when we look at the trial as a whole. Next slide, please. Now, when we look at this over time, over the weeks, right? And again, small number of patients, so take the up and down of the graph a little bit with a grain of salt, because even one patient can change the average Fric score with such a small number of patients. But I think the trend is telling that we see with greater exposure to this drug in terms of length of time, we see continued improvement. And so while four weeks was considered the end of the trial for this phase II trial, as we tried to determine which dosing was the right dose for the patient, certainly one would imagine with the slope going downwards that with prolonged exposure, longer number of weeks, a higher number of weeks, we would continue to get better and better efficacy. That's my thought process as to what's going on with these patients. Also, from my experience in the clinical trials, we saw patients in whom, you know, it's interesting in the clinical trials, actually, because we saw some patients whose dermatographic hives, for example, didn't necessarily change with the FricTest, but they did talk about reduction in itch. And we see that sometimes in eczema as well, where we see the erythema and the scale persist, but the itch reduces. And it's been my experience that patients in whom the phenotype of the disease maybe doesn't change, but the itch does change, the symptom of the disease change, they're quite happy because that itch is really driving them crazy. So important to show here, yes, we see a reduction in the FricTest score, but that itch reduction may be even more important to the patients. Although overall, we see a slope going downwards, and it's my conclusion here that if we extended this trial, we'd probably see better and better results. Next slide, please. This is what I'm talking about regarding itch. We see reduction in itch that is concomitant with the reduction in the FricTest score. So that's really nice to see. Although, as I mentioned, anecdotally, I did see some patients, even who were not considered responders, who did have an itch reduction as well. So really good results for those patients as well. Next slide, please. All right, let's talk about safety. So we see here in the 300 mg QD dose, we had two patients with ALT/AST increases. That cohort was filled first. Again, not sure when we started the phase II trial which dosing we were going to do. There was a planned data review at the end of the completion of this cohort. Two patients did have asymptomatic ALT/AST increases. Both of these patients had concomitant issues that may have explained the elevations in LFTs versus the IP. You could see the disparity in the numbers is because of that planned data review at the end of enrollment of the 300 mg arm. In addition, we had small numbers of patients, one patient in both arms that had gastroenteritis, one patient in each arm that had pruritus. Certainly, the gastroenteritis, I'd be very suspect, is related to the IP. Then the pruritus is part of the disease process. So not surprising that somebody with dermatographic urticaria might complain of an increase in pruritus as an AE. Otherwise, the EVO756 was pretty darn well tolerated. No serious adverse events and no treatment discontinuations due to adverse events either. Next slide, please. So when we think about these CIndU results, as I mentioned, 35% of CSU patients have CIndU. So when we see these kinds of results in CIndU, we think about the opportunity to treat CSU patients via the same mechanism of action. We could see here for those other drugs that have had a positive response in CIndU, they've worked well with CSU as well. Omalizumab, the anti-KIT antibody, Barzolvolumab has both. And then the BTK, the covalent highly specific BTK molecule, Remibrutinib, has shown efficacy in CSU. CIndU trials, we don't have the results read out for those. And then in terms of the IL-4 and 13, while it does show efficacy in CSU, although one of the trials for Omalizumab failed, cold urticaria and the other urticaria have failed for the IL-4 and 13 inhibitor that is Dupilumab. Okay, next slide, please. So as a summary here, we have the trial that achieved key objectives, robust efficacy in both arms, rapid onset of improvements in both the pruritus NRS and FricTest scores at one week, as I showed you in those graphs, with continued improvement over time such that we had a downward slope in terms of reduction in FricTest and pruritus through week four. And as I mentioned, 50% of the patients who were complete responders were in the high IgE group. So we don't think that efficacy is just limited to IgE low subjects at all. I believe there is opportunity for more improvement with continued dosing beyond four weeks. Otherwise, the efficacy, 93% demonstrated improvement at just four weeks in either Fric test or pruritus NRS. Both are important for patients. 70% demonstrated improvement in the Fric test at just four weeks, with 30% achieving complete response. As I mentioned, 50% of the complete responders were in that high IgE group. In terms of reduction of itch, 78% of patients demonstrated improvement at week four, with over 40% demonstrating at least a four-point reduction. That's with those who had at least a grade of four in their NRS at baseline. That four-point reduction by the agency is considered clinically relevant. CIndU results support translatable clinical applicability to CSU. Safety, there were no serious AEs, no discontinuation due to AEs, and otherwise it was well tolerated. Even in those patients with elevated LFTs, they were completely asymptomatic. Thank you, Dr. Lain, for your presentation. We appreciate you joining us today, as well as to those of you who have listened in. Before we wrap up, I want to conclude by saying that there are numerous potential opportunities to address the needs of underserved patients in a multitude of inflammatory diseases with 756. We hope we were able to demonstrate how we believe we can impact the underlying disease and look forward to the upcoming data readouts that are anticipated next year in both CSU and AD. That concludes our webcast. Thanks again for joining in.