Welcome to Evommune's EVO301 Topline phase 2a Results Conference Call. All participants will be in listen-only mode until the question-and-answer session begins. As a reminder, this conference call is being recorded. If you have any objections, please disconnect at this time. I would now like to turn the call over to Paul Leyland, a communications consultant at Evommune. Good morning, everyone. Thank you for joining us on today's webcast to review positive topline data from our phase 2A proof-of-concept trial of EVO301 in atopic dermatitis. We will leave time at the end of the call for questions. Before we begin, I'll remind everyone that today's Evommune's team will be making forward-looking statements. Actual results may differ materially from those indicated in these statements, and we encourage you to review the risk factors described in our SEC filings and the forward-looking statements on this slide in detail. On today's call, we will hear from Luis Peña, co-founder, president, and CEO of Evommune, and Dr. Mark Jackson, senior vice president of clinical development. I will now turn it over to Luis. Thank you, Paul. This is an important day for Evommune, and we are very pleased to report unequivocally positive data that validate IL-18 inhibition and show significant activity of EVO301 in moderate to severe atopic dermatitis patients. Let me start with a brief overview of Evommune and describe how EVO301 fits within our broader strategy to address chronic inflammatory diseases. Chronic inflammation is a major global health challenge contributing to a significant share of mortality and healthcare costs worldwide. Current therapies help many patients, but a large portion still experience inadequate disease control, tolerability issues, or treatment fatigue. Over time, this raises the risk of multiple serious comorbidities that can limit our lifespan. We are advancing a portfolio of differentiated product candidates, including EVO756 and EVO301, that together give us multiple ways to intervene in chronic inflammatory pathways. On this slide, you can see how EVO301 fits within our broader portfolio. EVO756, our oral small molecule MRGPRX2 antagonist, has already shown proof of concept in chronic inducible urticaria and is currently being evaluated in two phase 2b trials in chronic spontaneous urticaria and atopic dermatitis. We are excited to have those two datasets later this year, as promised, and also to expand into additional indications where migraine has become our focus for the next study planned to initiate in the second half of 2026. EVO301 complements that program as a biologic targeting a distinct inflammatory pathway. EVO301 is designed as a long-acting fusion protein that neutralizes IL-18, an important mediator capable of driving multiple inflammatory responses, including TH1, TH2, TH17, TH22, and innate pathways. This upstream position is crucial for treating conditions where heterogeneous inflammation, where targeting a single pathway may not be optimal. We believe EVO301 has the potential to become a first-line therapy for patients with moderate to severe atopic dermatitis, a disease that is still underserved despite existence of approved therapies targeting alternative mechanisms of action. The key takeaway before we go into more detail on the mechanism and the data are that EVO301 phase 2A proof-of-concept trial met its primary endpoint and did so in a decisive way while also displaying a very clean safety profile. These data make us very confident that IL-18 is a clinically relevant new target in AD and that EVO301's unique approach to IL-18 neutralization can potentially drive even more activity in disease as we dose-optimize in a phase 2B study, considering we only administer doses at day 1 and 28 in this phase 2A study. I will now pass it over to Mark to review the EVO301 program and the clinical data. Mark? Thanks, Luis. IL-18 is a well-characterized inflammatory cytokine, which plays a key role in various immune processes and acts as a key therapeutic target for atopic dermatitis and other chronic inflammatory diseases. IL-18 also acts as a general amplifier of inflammation, capable of driving multiple inflammatory responses, including TH1, TH2, TH17, and TH22, along with innate pathways. Broadly impacting these pathways is crucial for treating conditions with heterogeneous inflammation where targeting a single pathway may not be optimal. When the IL-18 pathway is upregulated in a chronic and cyclical fashion, it can trigger a cascade of inflammatory mediators that ultimately lead to tissue damage and disease manifestations, including those that we see in atopic dermatitis. IL-18 also directly disrupts essential skin barrier functions, positioning it as a pivotal pathogenic factor. Targeting IL-18 offers broader therapeutic utility with a novel approach, simultaneously reducing inflammation and restoring tissue integrity for patients with complex inflammatory conditions. EVO301 is a long-acting injectable SAFA IL-18 fusion binding protein designed to neutralize upregulated IL-18. The molecule is unique in that it combines native human IL-18 binding protein with a serum albumin binding domain. This design is intended to improve tissue distribution, extend half-life, maintain high affinity, and selectively bind to IL-18. We believe this approach offers advantages over traditional monoclonal antibodies that have attempted to antagonize IL-18, including the smaller molecular weight and improved penetration into inflamed tissues. By efficiently neutralizing IL-18, where it is really driving disease, EVO301 aims to address the root cause of inflammatory signaling rather than only treating downstream symptoms such as itch or visible lesions. We also see important complementarity between EVO301 and EVO756, giving us multiple upstream levers across chronic inflammatory diseases. A primary reason we like the IL-18 target is that it impacts biology beyond just TH2. We believe this is key in a very heterogeneous disease such as atopic dermatitis and may lead to better disease resolution for patients. This broad impact across inflammatory pathways is a key differentiator of the IL-18 target in AD. Let me start with the topline takeaways before we go into more detail on the data the program has generated. First, and most importantly, the study met its primary endpoint and did so as early as week four. The Bayesian success criteria was defined as a posterior probability of 75% or greater that the true difference between EVO301 and placebo in the percent change from baseline at EASI was at least 8%. At week 12, we observed a Bayesian posterior probability of 99.76% that the true difference between EVO301 and placebo is at least 8%, unequivocally meeting our primary endpoint in this trial. Second, we also met our secondary efficacy endpoint of percent change from baseline in EASI when analyzed under the more commonly utilized frequentist method. Here, we showed highly statistically significant improvement versus placebo at weeks 4, 8, and 12 with 34% and 33% placebo-adjusted improvement in EASI at week 8 and 12, respectively. Third, we observed 23% of patients achieved an IGA of 0 or 1 versus 0% in placebo. Fourth, EVO301 was well-tolerated in this study population. We didn't observe any related serious or severe adverse events, and the safety profile of EVO301 is very clean as we would expect by targeting this mechanism. Fifth, we observed corresponding reductions across secondary endpoints as well as a reduction in key TH2 and non-TH2 cytokines. These signals reinforce that the effect of EVO301 extended across multiple clinically relevant domains. Finally, the pharmacokinetic data show EVO301 achieved robust and sustained IL-18 neutralization at the dose tested, with exposure consistent with a long-acting profile supporting a Q4 week dosing regimen moving forward. Taken together, these data provide clear clinical validation for IL-18 neutralization in a very robust trial in atopic dermatitis and support our plans to move EVO301 into a full-dose ranging Phase 2B program. A special thanks must go to all of the study participants: our investigators, our CRO partner Novotech, AprilBio, and our statistical analysis partner Brad Carlin and the team at Phase V. Let's turn now to the trial design. We initiated this study after a successful phase 1 trial where EVO301 demonstrated favorable safety, tolerability, and PK consistent with Q4 week dosing. This phase 2A trial was a randomized double-blind placebo-controlled study conducted in adult patients with moderate to severe atopic dermatitis. The design optimized for early clinical signal detection utilizing a Bayesian analysis on the primary endpoint to allow greater power with smaller sample size and provide a clear basis for advancing the program. We enrolled 70 patients at 12 sites in Australia and New Zealand. All patients had disease that warranted systemic therapy. Participants were randomized to receive EVO301 with doses of 5 milligrams per kilogram administered IV on day 1 and day 28. This is important to note as we only administered two doses of EVO301 during this 12-week study. The primary endpoint was percentage change from baseline in Eczema Area and Severity Index, or EASI, at week 12. Secondary endpoints included the Investigator Global Assessment and pruritus numeric rating scale, all evaluated at week 12. We also collected pharmacokinetic and pharmacodynamic data to understand exposure, target engagement, as well as the relationship between IL-18 neutralization and clinical responses, along with a standard safety assessment. Of the 70 patients we enrolled and treated, 48 in the active arm and 22 in the placebo group, 65 completed the trial, with 45 in the active and 20 in the placebo. The terminations in the active arm were subjects lost to follow-up, and the terminations in the placebo arm were lost to follow-up and subject withdrawal. No subject discontinued the study due to adverse events. We enrolled a very robust patient population who had significant baseline EASI scores and a meaningful itch burden at baseline, reflecting a real-world disease severity and activity. Baseline demographics and disease characteristics were generally well-balanced across both active and placebo arms, supporting a relevant comparison between EVO301 and placebo. Finally, the population did not include any patients with prior exposure to biologic therapies, given the general lack of access to biologics in Australia and New Zealand, though they would have not been excluded, and clinically, we would not anticipate any differences in results in those patients. The trial clearly met its primary endpoint, a Bayesian success criterion related to the difference between active and placebo in the percent improvement in baseline and EASI. While the success criterion required at least 75% of this posterior distribution to be an improvement of at least 8% over placebo at week 12, the results of this study demonstrated 99.76% of the posterior distribution met that threshold. That is a dramatic win on the primary endpoint. This also gives us tremendous confidence that EVO301 is a highly active and relevant drug in atopic dermatitis. While we clearly met the Bayesian primary endpoint, we have also achieved statistical significance at weeks 4, 8, and 12 at p < 0.01 when analyzed by the more commonly used frequentist method. This slide shows the percent change from baseline in EASI at weeks 4, 8, and 12. With only two doses of EVO301 administered at day 1 and 28, we believe these are remarkable efficacy data. Patients who received EVO301 experienced a 41%, 50%, and 55% mean reduction in EASI at weeks 4, 8, and 12, respectively, as compared with 18%, 16%, and 22% on placebo at weeks 4, 8, and 12. We observe statistically significant separation from placebo emerging as early as week 4 and maintain that through week 12, consistent with the expected onset and durability of effect for a long-acting biologic. Importantly, the confidence intervals and p-value demonstrate that this is not only clinically meaningful but also statistically robust. These results support the central hypothesis that neutralizing IL-18 can meaningfully reduce the signs and symptoms of atopic dermatitis and has the potential for frontline therapy in AD as we move forward into a Phase 2B, where we will deliver more doses of EVO301 in the treatment period. This slide shows visual representations of the previous data while plotting the curves over time. Given our experience in history developing biologics, these data exceeded our expectations in this study. The rapid onset of statistically significant and clinically meaningful separation from placebo that maintained throughout the study duration is very notable after just 2 doses of EVO301 at day 1 and day 28. While cross-trial comparisons are challenging and no head-to-head comparisons are available, at the 12-week time point, after only 2 doses, EVO301 demonstrated similar improvement in EASI from baseline to that of other approved biologics at week 16 targeting alternative mechanisms, with each having significantly more dose-optimized regimens. A really exciting part of the EVO301 story is that we only administered 2 single doses at day 1 and 28 in this phase 2A study and saw a rapid onset of meaningful efficacy at week 4 that continued through week 12. We have no safety concerns around the target or molecule and plan to be aggressive with our dosing in the phase 2B program to drive as much additional efficacy as possible for these patients. As we advance EVO301 into a phase 2B sub-Q study in atopic dermatitis, we will leverage the insights from this study and our experience with biologic dosing in the past, such as lebrikizumab, now Ebglyss, which Luis and the team developed at Dermira, to add several more doses during a traditional 16-week study. This would deliver significant additional drug than this phase 2A study did and potentially drive even greater efficacy than the already robust responses we have seen in this study. As you can see here, 23% of EVO301 patients achieved an IGA 0 or 1 at week 12 versus 0% in the placebo group. Again, these results are very impressive when you consider that we only administered two doses of EVO301 at day 1 and 28 and saw IGA 0 or 1 improvement continuing eight weeks after patients had received their last dose of EVO301. We're encouraged by the durability of this activity and look forward to seeing how we could potentially deliver further improvement in a fully dose-optimized phase 2B study. Here we summarize some of the additional endpoint and target engagement findings. EVO301 showed dose-proportional and predictable pharmacokinetics with levels consistent with a long-acting agent and continues to support a Q4 week dosing regimen. We saw corresponding reductions in secondary endpoints and in line with what we were hoping for in this study. We observed clear target engagement with evidence of sustained IL-18 neutralization over the dosing interval. We also observed corresponding reduction of key inflammatory cytokines, both TH2-associated, such as CCL17 and CCL22, and non-TH2-associated, such as IL-22. This supports our thesis that IL-18 modulates pathways more broadly than just TH2 alone. Early exploratory analyses suggest a relationship between exposure, IL-18 pathway modulation, and clinical response, which will inform dose selection for Phase 2B. These PK/PD results, combined with the clinical data, support our confidence in both the mechanism and the dosing strategy we plan to take forward. Full results from the Phase 2A trial will be presented at a future scientific conference. Turning to the safety, EVO301 was very well-tolerated in this Phase 2A trial, which is what we expected targeting this mechanism and from the Phase 1 study in healthy volunteers who were dosed up to 10 mg/kg intravenously. We did not observe any serious or severe adverse events assessed as related to study drug, and there were no discontinuations due to treatment-related adverse events. There were also no meaningful differences in safety events between active and placebo groups. Importantly, there were no observed cases of conjunctivitis, which is a key differentiator versus other biologics in atopic dermatitis. There's nothing noted that would prevent us from dosing higher or more frequently in further development. Overall, we're very pleased with the safety profile in this study and believe that this is a differentiator for this target and molecule. At this time, I will turn it back over to Luis to review the AD landscape and wrap up the call. Thanks, Mark. Now let's look into the context of the broader atopic dermatitis landscape. It is important to factor in the burden of moderate to severe atopic dermatitis, which affects about 13 million Americans. This isn't just a skin disease. It's a chronic systemic inflammatory disease. If left untreated, it may also limit your lifespan. Even with today's advanced therapies, we're not where we need to be. Around 40% of patients are still not adequately controlled, which tells you the unmet need remains real. That's why the opportunity here matters. There is a clear need for broad, safe treatment options that can consistently control disease over time. Over the past several years, we've seen some important advances in atopic dermatitis treatment, including multiple biologics. However, a substantial number of patients remain uncontrolled, cycle through multiple therapies, or discontinue due to tolerability or convenience issues. We believe EVO301 is differentiated by its mechanism and design. By targeting IL-18, we are going upstream to an inflammatory driver that may contribute to disease persistence and tissue damage. If the profile continues to hold in larger trials, this drug could offer an attractive option for patients who have inadequate response to existing therapies or who are seeking a therapy that addresses the underlying inflammatory signaling more directly. So to summarize and wrap up, based on these top-line findings from our POC study, we plan to advance EVO301 into a phase 2B study in atopic dermatitis with dosing regimens leveraging insights from this phase 2A study and our experience with biologic dosing in the past, such as lebrikizumab, now Ebglyss, which our team developed as members at Dermira. We are underway in our phase 2B planning with a subcutaneous formulation subject to ongoing regulatory and operational planning. In parallel, we are also evaluating additional indications where IL-18 is believed to play a key role, including ulcerative colitis and other chronic inflammatory diseases. Detailed results from the phase 2A study will be submitted for presentation at an upcoming scientific congress, ensuring the dermatology community can fully review and interpret the data. I want to thank our amazing Evommune team. Following our IPO last year, we had a really important 2026 lined up with three key value inflection points. We have now had the readout on IL-18, and we are unequivocally thrilled with the outcome of that study, which now gives us two validated mechanisms in the immunology space. Thank you all for your time today. Again, thank you to our supporters and all those who contributed to the study and their outcomes, which are very much a team effort. We can now turn the presentation over to the moderator for Q&A. Thank you. At this time, if you'd like to ask a question, please click on the raise hand button, which can be found on the black bar at the bottom of your screen. When it is your turn, you will receive a message on your screen from the host allowing you to talk, and then you'll hear your name called. Please accept, unmute your audio, and ask your question. At this time, we ask that you limit to one question and a related follow-up. We'll wait one moment to allow the queue to form. Our first question will come from Judah Frommer with Morgan Stanley. Please, you may unmute your audio and ask your question. Yeah. Hi, good morning, guys. Thanks for taking the questions and congrats on the update here. Maybe can you just help us with how you're thinking about dosing heading into the Phase 2B? I think you did dose higher in the MAD portion of the Phase 1. So how are you thinking about kind of going potentially above 5 mg per kg versus potentially loading doses, the frequency of dosing in the Phase 2B? Can you remind us what you've done in terms of bridging from the IV to the sub-Q? And then just a related question, which we continue to get today: how do you think about 756 versus 301 in AD after these data? Thanks. Good morning, and thank you for the congratulations. Yeah, I mean, I think you nailed it. We have several opportunities, either going up in dose above 5 mg per kg, given that the molecule so far is just so well-tolerated, or increasing frequency and doses, or both. So there's an opportunity here. Given the safety profile of the molecule, the opportunity is for us to drive up efficacy. And because AD is such a heterogeneous disease and because we really have largely not had a molecule that's had great efficacy, or we've had Dupixent, lebrikizumab with the best efficacy, I should say, but we've seen nothing like psoriasis. Pushing for better efficacy is always key. So we will definitely do that. We will give guidance later in terms of what a phase 2B program would look like, but likely it will have more doses administered. It'll likely go out to 16 weeks. We definitely know that we have the ability to go Q4 week, but certainly can push the dose in the initial 16 weeks and then go Q4 week in the maintenance, or even Q8 week, really, from what we've seen of the durability of response that we had from finishing dosing at week 4 all the way to week 12. So the options are there for us. We will likely explore many of them with the ability to push the efficacy while maintaining a good safety profile. And sorry, finishing up on 756. It's a landscape that needs many, many therapies. Talking to Dr. Lebwohl just recently, one of the best dermatologists in the world, his belief is only about a quarter of the 80% patients right now are well-served, and we need many more treatments. From our perspective, the patients can have many more biologics available to them. We know that they cycle through them. We've seen that with the mature biologic markets. We would like to have certainly more mechanisms in terms of orals for these patients. We like both programs. I've said before, if we had more biologics and orals, we'd probably advance those. We're very happy with these two mechanisms that are differentiated and seem to have great potential in AD. Thanks. Our next question comes from Thomas Smith with Leerink Partners. You may now unmute your audio and ask your question. Hey, guys. Good morning. Congrats on these impressive results, and thanks for taking our questions. One on safety. I didn't see it on the safety table, and obviously, there weren't any treatment-related discontinuations. But can you comment on whether you saw any incidents of injection site reactions? And then as a follow-up, I know you're saving some of the detailed data here, but given the impact on TH2 and non-TH2 biomarkers, can you just describe a little bit more about what you're seeing on those non-TH2 biomarkers and how you're thinking about potential read-through from this dataset to your plans in ulcerative colitis? Thanks so much. Yeah, sure. So we gave this IV, which is pretty common for proof-of-concept studies at this point. We have been developing a sub-Q formulation and are quite aware that it is key for these formulations to be well-tolerable. So as we develop that formulation, we're going to be really focused on having components that aren't painful. And we think we have a pretty good handle on the history of doing that. So the expectation as we move forward with the sub-Q formulation is that that won't happen. And so we'll see as they go forward. But this as an IV was very well-tolerated. We were very excited about both secondary endpoints and biomarkers. We withheld that, and we had planned that in advance so that we can be on the podium, hopefully as a late breaker at one of the major meetings. But they're very much in line with what we expected, not only in terms of hitting the innate pathways but having an impact on the TH2 side. So that seems to be playing out, and that's going to be critical for us. So the initial read on those is it looks good. We're having an impact on both sides, and that should play out well for the mechanism in this heterogeneous disease. Super helpful. Thanks for the caller, and congrats again on the data. Sure. Thank you. Our next question comes from Gavin Clark-Gartner with Evercore ISI. You may now unmute your audio and ask your question. Hey, guys. It's Gavin here for myself and Umer. Congrats on the really great data. What were the discontinuations for any reason in the trial, and how did you handle that data? And then secondly, maybe you could just discuss how quickly you can move into one or multiple phase 2Bs and kind of more granularly what the next steps are. Thank you. Okay. Mark, why don't you talk about the discontinuations, and I'll talk about moving into phase 2B. Thanks, Gavin, for the congrats, and thanks for being on today. We had five discontinuations. None of those due to adverse events, two in the active group and three in the placebo group. And as I said, none of these were related to any issues. It was withdrawal of consent in those situations, and it was an MMRM dataset carrying forward. But again, none of those appeared to have any relationship to drug or issue. And as Lewis said, we were very encouraged by the safety profile we saw, which is as expected from our Healthy Volunteer trial. Yeah. And as it relates to moving into phase 2B, we're not giving guidance on that now. We have some manufacturing to do in order to prepare for that. I'd likely talk to the agency as well. We have been making great progress on a sub-Q formulation and are already in the range of where we need to be, but we certainly need to manufacture more. But are definitely looking to move as aggressively as we can in phase 2B. So stay tuned in the future for more guidance on that. And as was mentioned earlier, the potential for other indications, I think, is quite high. If you look at IL-18, it's elevated in a number of diseases. We really like the potential in IBD, and it is possible that we would initiate a proof of concept sooner than later, especially with this validation of its activity right now. But in terms of how we move forward, please stay tuned on that. We'll give guidance likely Q2. Great. Thanks, guys. Thank you, Gavin. Our next question comes from Matt Phipps with William Blair. You may now unmute yourself and ask your question. Good morning, team. Thanks for taking my question. Congrats on this dataset here. Just wondering, were there any cases of rescue medications and maybe how those were treated, particularly in the frequentist analysis? And then for a phase 2B, do you think you would try to explicitly enroll cohorts of biologic-experienced patients, just given how much of an unmet need there is in that patient population? Thank you. Sure. Thanks, Matt. All right. Mark, you want to talk about rescue medications? Sure. Thanks, Matt. So we did allow for mild potency topical steroids in the trial along with moisturizers. We did a censoring evaluation, and we had a pre-data review analysis of what we would do, and we pre-specified that. And there were visits that were censored in any patients that used moderate to more potent topical steroids, and we censored those visits to exclude them from the analysis. But mild potency topical steroids were allowed. We just had the investigators use them as little as possible. And when evaluating the trial and looking at the dataset in general, there was really very little use of that at all. So we're hopeful that that means that the patients were doing well. And we also allowed them to use a moisturizer coming in. So they did have a skin regimen washing in and during the trial. Yeah. As it relates to patients without biologics, we had none in this trial. We didn't exclude any, but we were in New Zealand and Australia, and there's just not much biologic use down there. But our expectation would be that we will work quite well in those patients. While we're on the subject of talking about New Zealand and Australia, I just want to say kudos to those investigators. We went down there when we initiated the phase 3 studies for lebrikizumab, and they do a tremendous job. I think the study was well-controlled. We saw the placebo rates were low and the outcome unequivocal. It looks like we have a very nice mechanism here, but it is important to run these studies at sites that are very experienced. These investigators did a very nice job. Our next question comes from Prakhar Agrawal with Cantor. You may now unmute your audio and ask your question. Hi. Thank you for taking my questions, and congratulations on this really strong data. So maybe just a couple. We haven't talked about the EASI 50-75 responder rates, and we've gotten some investor questions on this. So if you could qualitatively tell how it's tracking versus other biologics. And maybe just on the PK/PD and the exposure data that you saw in the trial, could you just talk about that and what gives you confidence that giving more drug in the induction phase will lead to even better efficacy? And lastly, just a quick follow-up. How was missing data handled in the frequentist analysis? Thank you and congrats again. All right. Thanks, Prakhar. Why don't we go with Jigar on PKPD, Mark on missing data, and then I'll finish on secondary endpoints? Yeah. Absolutely. Thanks for the question, Prakhar. So as you know, this is a half-life extended serum albumin Fab that allows us to dose on up to kind of an every 4-week schedule based on PK and PKPD. We are able to cover the target sufficiently in that duration. However, obviously, the magnitude of engagement could change with the level of exposure that you have overall. The other variable here is obviously duration of treatment and the kind of time to disease resolution. Those are two other variables that we will continue to explore in the phase 2B study. But we're very happy with the level of target engagement and the durations that we saw efficacy in this phase 2A study. As I highlighted earlier, we saw engagement of the target as well as disease resolution beyond the dosing period that we dosed. We only dosed 2 doses but still continued to demonstrate activity. And so that kind of highlights the level of activity and engagement that we had. Loading doses do provide some advantages that we will continue to explore in phase 2B. They allow you to get to higher levels early on. We know the early disease resolution is important, and so we want to at least extract some of that data as well. Mark, missing data? Yeah. Missing data was handled with the MMRM technique, and we just inputted the data based on anticipated values. Yeah. And then as it relates to secondary endpoints, again, I want to state that we had planned to withhold some of them, including the biomarkers, so that we can get on the podium at a major meeting. But we put the IGA 0/1 as an indicator that even though we did not power for those endpoints and we powered for the percent EASI change, they're all directionally positive. So I think the IGA 0/1 is a pretty good indicator, and it looks a lot like lebrikizumab did when we first licensed that at Dermira from Genentech, where it's very promising, but we know that we can definitely improve on the efficacy by what has been noted earlier, either increase in dose, giving more doses, or both. And so that's very encouraging. But every secondary endpoint and all the biomarkers that we read were consistent with the activity that was shown with the primary endpoint. Thank you. Our next question comes from Martin Auster with Raymond James. Please unmute your audio to ask your question. Great. Hey, good morning. This is Thomas from Leerink. Congrats on the really strong data this morning, and thanks for taking our question as well. Most of ours have been asked, maybe two quick ones. Curious if you can give any more color on kind of potential venues for a more fulsome presentation of these results. I assume this missed kind of the late-breaking deadline for AAD, so should we be looking somewhere kind of later in the calendar year? That's the first one. And then just curious if you can remind us on the license agreement for 301, are there any milestones here that become payable as you move either ahead in AD to a larger phase 2B or potentially as you expand indications? Thanks very much. Yeah. Thank you. Yeah. I mean, I think that the venue that we're looking at, obviously, the biggest podium would be the best. We're likely looking at EADV. Unfortunately, it's all the way in September, but we just missed the late breaker for the AAD here in the United States. So the EADV is a pretty data-centric big meeting, and we think that that's going to be a good venue for us. As it relates to the license agreement, Greg, why don't you comment? Sure. I think the best way to answer that question is we've negotiated a very on-market and competitive license agreement, and there's nothing abnormal or unusual in our upstream license obligations. So as development continues, we will owe kind of standard traditional milestones, but they're all baked into our use of proceeds and nothing that you would consider off-market. Got it. Makes sense. Yeah. I would add very modest for the development stage molecule. That's true. Yep. Okay. Thanks and congrats again. Yeah. Thank you. Our next question comes from Andreas Argyrides with Oppenheimer. Please unmute yourself to ask your question. Great. Good morning. And thanks for taking our question, and congrats on these really strong results. Just a couple of questions here, as most have been asked as well. So just can you provide additional color on how these data position 301 as a potential best-in-class IL-18 given the competitive landscape? How does the impact on pruritus add to differentiation? And then can you talk more about the pipeline and the pill potential under the indications that you mentioned, like IBD? Thank you. Sure. Yeah. I mean, we really like this molecule. I mean, one of the things that caught our eye was that first, it's a naturally occurring binding protein of IL-18, and so that we think could be a great benefit. But also the fact that it was bound to this fab that not only increased the half-life of the molecule, but it actually helps it to penetrate inflamed tissue. And as we saw with 756, where we had 70% of the drug delivered to the skin when we measured interstitial fluid, it's a benefit. It's a benefit to get the drug to the target. And the construct of this biologic, we believe, actually allows it to get to the target. And so that is a benefit that it looks like it's playing out, and we're excited to see as we continue to dose optimize in phase 2B. The drug did well in pruritus. The overall pruritus scores in Australia and New Zealand, even though the severity of the patients was very high, was a little bit lower. And we have seen regionally where that can happen, where it's slightly lower. And so as we move these trials into broader populations in the U.S., we think the pruritus baseline score is going to move up, and the drug should do well in pruritus. But we saw certainly an improvement in pruritus over placebo, but definitely the major improvement was in inflammation. Can you repeat the IBD question? I didn't quite get it. It seems like, given the mechanism, that there's read-through to a couple of other indications. So maybe 301 has a pipeline and a pill potential. So just maybe your thoughts on expanding into other indications such as IBD. Yeah. No, no question. Yeah. Thanks for bringing that up. Yeah. I mean, we're excited about that. I remember when we were doing the first diligence on the molecule. And by the way, kudos to the team. We have an incredible small molecule drug discovery team. That is one of our superpowers, is that we have amazing medicinal chemists. But again, this shows our ability when we do have a gap between programs is that we can go out and find great molecules. So kudos to the team for identifying this molecule. But I do remember when we were first getting up to speed in IL-18, we were quite impressed about how it's elevated in so many different inflammatory diseases. So there is no question that there may be a pipeline in a molecule here. We like IBD as the initial second indication. It is an area where it's competitive in terms of all the trials that are going on, and investigators are pretty reluctant to start working with the molecule unless they know that it has good anti-inflammatory activity. And this certainly opens the door for us now that we've proven the concept in atopic dermatitis patients, and we can go to them with this dataset and I think be pretty compelling in terms of going into that space. So I would say the probability that we would go into IBD first is higher right now than any other indications. But as we have done with 756, and we're excited to give more details in the second quarter of expanding that program, not only in CSU and AD, but also into migraine, which we think the data may be even most compelling, we will do the same for IL-18. Okay. Great. Thanks for taking my questions and congrats again on the data. Thank you. Our final question will come from Mitchell Kapoor with H.C. Wainwright. Please unmute your audio to ask your question. Hey, good morning. This is Katie on from Mitchell. Congratulations on the fantastic data. I think the last question that I had was kind of a nitty-gritty one on what flexibility do you have in the sub-Q formulations? With your safety, you have some room to dose up, but do you actually have the ability to formulate higher doses? I know a lot of the traditional biologics get stuck where they can't go any higher. Do you have extra flexibility because of the fusion protein that you're using? Great. Thank you, Katie. Appreciate it. Yeah. I mean, traditionally, these formulations have been in the range of 120-150 milligrams per mL. We're already there and are making sure, as I mentioned earlier, that the components of that formulation are such that you can have injection sites stinging. There are certainly some components we've seen in previous formulations that certainly are guilty of doing that. When we picked the 5 milligrams per kg dose, keeping in mind that we would go to a sub-Q in the future, that put us, from our calculation, somewhere around 2 to 2.5 mL. And so there's certainly the prospect in loading doses of going up, and we will definitely be looking at that. Then I think the nice thing is if we can do that early and we've shown we certainly have, but others have shown that with biologic development, the faster you get to steady state, the more aggressive you are initially with your dosing, which we certainly have the room to do here, the better outcome there is for patients long-term. So we're quite excited at the prospect of pushing the dose, especially in the first 16 weeks, and then with then going to maintenance doses of Q4 and Q8 week. And not only looking at a 5 mg/kg formulation, but also maybe pushing that a bit. So there is flexibility there. We will certainly do everything within our power to push the dose. But we're also, as I think you're alluding to here, cognizant that there is a limitation to how many or how much drug and how much drug volume you can get. But I think given the safety of the molecule currently and where we are with the sub-Q formulation, we think we have nice flexibility there. Perfect. Thank you. Thank you, Katie. This concludes the question-and-answer session and today's call. You may now disconnect.