Good afternoon, everyone, and thank you for standing by and welcome to the Corvus Pharmaceuticals Fourth Quarter and Full Year 2025 Business Update and Financial Results Conference Call. At this time, all participants are in listen-only mode. Later, we will conduct a question- and- answer session and instructions will follow at that time. It is now my pleasure to turn the call over to Mr. Zack Kubow from Real Chemistry. Please go ahead, sir. Thank you, operator, and good afternoon, everyone. Thanks for joining us for the Corvus Pharmaceuticals Fourth Quarter and Full Year 2025 Business Update and Financial Results Conference Call. On the call to discuss the results and business updates are Richard Miller, Chief Executive Officer, Leiv Lea, Chief Financial Officer, Jeff Arcara, Chief Business Officer, and Ben Jones, Senior Vice President of Regulatory and Pharmaceutical Sciences. The executive team will open the call with some prepared remarks, followed by a question and answer period. I would like to remind everyone that comments made by management today and answers to questions will include forward-looking statements. Forward-looking statements are based on estimates and assumptions as of today and are subject to risks and uncertainties that may cause actual results to differ materially from those expressed or implied by those statements, including the risks and uncertainties described in Corvus's annual report on Form 10-K for the year ended December 31, 2025, and other filings the company makes with the SEC from time to time. The company undertakes no obligation to publicly update or revise any forward-looking statements except as required by law. With that, I'd like to turn the call over to Leiv. Thank you, Zach. I will begin with a brief overview of our fourth quarter and full year 2025 financials and then turn the call over to Richard for a business update. Research and development expenses in the fourth quarter 2025 totaled $9.9 million compared to $6 million for the same period in 2024. R&D expenses for the full year 2025 totaled $33.7 million compared to $19.4 million for the full year 2024. For both the fourth quarter and full year 2025, the increases in R&D expenses were primarily due to higher clinical trial and manufacturing costs associated with the development of soquelitinib, as well as an increase in personnel costs. Net loss for the fourth quarter 2025 was $12.3 million compared to a net loss of $12.1 million for the same period in 2024. Included in the net loss for the fourth quarter of 2025 and 2024 were non-cash losses of $0.7 million and $2.2 million, respectively, from Corvus's equity method investment in Angel Pharmaceuticals and a non-cash loss of $2.3 million in the fourth quarter of 2024 associated with the change in fair value of the company's warrant liability. Total stock compensation expense for the three months ended December 31, 2025 was $1.6 million compared to $0.8 million for the same period in 2024. As of December 31, 2025, Corvus had cash equivalents, and marketable securities totaling $56.8 million compared to $52 million at December 31, 2024. In January, we closed an upsized underwritten public offering that included a premier group of biotech investors and generated net proceeds of $189 million. Including the net proceeds from this financing, pro forma cash at December 31, 2025 was approximately $246 million, extending our cash runway into the second quarter of 2028. I will now turn the call over to Richard, who will discuss our clinical progress and elaborate on our strategy and plans. Thank you, Leiv, and good afternoon, everyone. Thank you for joining us today for our update call. In 2025, we made significant progress advancing the development of soquelitinib, our first-in-class selective ITK inhibitor that is designed to rebalance or reset the immune system. This was highlighted by the presentation of final results from our phase I/I-B trial in peripheral T-cell lymphoma in an oral session at the ASH annual meeting and the recent announcement of data from cohort 4 of our phase I atopic dermatitis trial, which showed that soquelitinib could become a leading therapy for atopic dermatitis and potentially other inflammatory diseases. Shortly after the data announcement, we completed a $200 million financing, reflecting high investor interest in the opportunity for soquelitinib and ITK inhibition, given our strong data to date, its unique mechanism of action, and its broad potential to help patients across multiple areas of medicine. As a result, we are entering 2026 in a position of strength with ongoing enrollment in our phase III PTCL trial, our recently initiated phase II atopic dermatitis trial, and the opportunity to expand into mid-stage trials for other important inflammatory diseases such as hidradenitis suppurativa and asthma later this year. Based on our current plans and anticipated timelines, our cash runway extends beyond key data readouts for all of these programs. On today's call, I will recap the highlights from our cohort 4 data announcement, share the latest on our plans to present additional data from the trial at an upcoming medical meeting, and provide an update on our phase II trial. I will also review our pipeline expansion plans and key upcoming milestones. The results from cohort 4 and the full phase I trial show that soquelitinib's emerging clinical profile appears to provide substantial advantages in the treatment landscape for atopic dermatitis. 1, it is an oral medication. 2, it has a novel mechanism of action that combines tissue-selective and target-specific precision with ability to affect multiple inflammatory signaling pathways. 3, it appears safe and effective in a broad range of patients, including those who have received prior systemic therapies. 4, it produces durable responses with no disease rebound. Based on our market research, this profile would be considered a significant advancement for patients with atopic dermatitis. We are excited that soquelitinib data further elevates its profile and potential. It shows one of the strongest EASI 75 results at only 8 weeks of therapy, and the durability of responses with no disease rebound may provide the opportunity for new approaches to therapy of immune diseases, including the potential for soquelitinib to be an intermittent therapy. Overall, if the current profile continues to be supported by larger clinical trials, we believe soquelitinib will be very well-positioned to be among the leading options for the treatment of patients with moderate to severe atopic dermatitis. I will now review key highlights from our recent data announcement. First highlight, efficacy. For cohort four, which was designed as a randomized placebo-controlled trial with drug given over an eight-week treatment period, the mean percent reduction in EASI was 72% versus 40% for placebo that was statistically significant at 0.035. 75% of patients, 9 of 12, achieved EASI 75, and one additional patient was an EASI 74. 25% of patients achieved EASI 90, and 33% achieved IGA 0 or 1. 11 of 12 patients achieved EASI 50. The only non-responder was a patient who was refractory to previous therapy with both DUPIXENT and RINVOQ. Two of the EASI 90 patients were resistant or non-responsive to prior systemic therapies. 20% of placebo patients achieved EASI 75, or 17% if you include two patients that missed the day 56 evaluation and on later evaluation never reached EASI 75. In addition, two placebos required rescue medication due to disease flares versus none in the active group. The two placebo patients who were EASI 75 were both patients who had not received prior systemic therapies. None of seven placebo patients who received prior systemic therapy achieved EASI 75, whereas 3 of 5 active patients who received prior systemic therapies achieved EASI 75. The cohort 4 results confirm our hypothesis from cohorts 1 through 3, which is that extending the treatment duration would deepen responses. The data also show that soquelitinib is superior to placebo in every efficacy endpoint evaluated. When compared to other agents, we believe the results obtained so far for soquelitinib place it among the most active agents, oral or injectable, approved or under development for atopic dermatitis. Second highlight, durability. Starting with cohort 3, we took a more systematic approach to measuring the remission duration with a longer blinded post-treatment follow-up period of 90 days compared to 30 days tracked for cohorts 1 and 2. The cohort 3 data show that responses observed at day 28, the last day of treatment, were maintained or slightly improved out to 118 days or 90 days without therapy. This compares to other systemic therapies for atopic dermatitis, which all show a rapid rebound in disease that starts as soon as 1 week after stopping therapy. We see no rebound phenomenon with soquelitinib both in cohorts 3 and 4. We believe that the induction of T-regulatory cells by soquelitinib could be responsible for this durable suppression of inflammation and sustained disease remission. We have seen this in preclinical experiments, and biomarker data shows an increase in circulating Tregs in cohort 3 patients. The demonstration of circulating Tregs is quite remarkable, as usually these cells are very rarely found in the blood. It is likely that these cells are migrating to and concentrating in sites of disease, as we have found in our animal models. Third highlight, broad applicability. 35% of all patients enrolled in the phase I trial had received prior systemic therapies, including 50% of patients in cohort 4. dupilumab was the most commonly used prior therapy, followed by JAK inhibitors, and some patients received multiple prior therapies. This includes patients who were resistant to their last systemic therapy. In other words, they were non-responsive to their prior treatment. Typically, patients that are treatment resistant or who have gone through multiple prior therapies are more challenging, and this was confirmed when looking at the placebo patients in the trial. The response curve data showed that placebo patients who received prior systemic therapies do worse than those who did not receive prior therapies, indicating that prior systemic therapy is an unfavorable characteristic. However, the response curves for patients receiving soquelitinib are very similar across these groups, indicating that soquelitinib is not affected by prior systemic therapy experience. Together with our baseline patient characteristics, this also indicates that the patient population treated on our protocol was more unfavorable than those reported in most atopic dermatitis clinical trials. As noted above, in patients who received prior systemic therapies, the EASI-75 was 0% for placebo, 0 out of seven, versus 60%, three of five, seen in patients who received soquelitinib. In terms of patient indications, our conclusions are that soquelitinib is active in patients who have received prior systemic therapies with outcomes no different than naive patients, despite these patients having more unfavorable disease. Responses were observed in patients who are refractory to their prior systemic therapy. This supports our hypothesis regarding the novel mechanism of action for soquelitinib and the lack of resistance due to prior therapy experience. Fourth highlight, safety. No new safety signals were seen in cohort 4 with a longer 8-week treatment duration. In cohort 4 and the full phase I trial, re-reported adverse events are similar in both placebo and active groups. No significant lab abnormalities were observed. There were no hepatic abnormalities, no changes in liver function tests. Infections were similar in treated and placebos and were minor. I'd like to make some additional comments on infection. We have received questions from investors regarding the potential for EBV viral reactivation. These questions are based on very rare reports in the literature of EBV infection in babies born with germline mutations in ITK. In a neonate, the immune system is primitive, as T and B cells have not yet formed. Immune system maturation occurs during development and exposure to antigens. A germline mutation in ITK in the primitive developing immune system is completely different than transiently blocking the kinase domain of ITK with a small molecule drug in an individual with a mature immune system. We have seen no serious infections of any kind in more than 150 patients treated with soquelitinib across our lymphoma, atopic dermatitis, and ALPS trials to date. This involves over 14,000 patient days of treatment, with some patients on therapy for more than two years. In PTCL, most patients harbor EBV and other viruses such as CMV. In our phase I lymphoma study, we identified over 30 patients with EBV virus detectable at baseline, that is before therapy, in their blood, measured using a PCR technique, that is they are viremic. None of these patients or any other patient had any evidence of EBV reactivation or related illness during the treatment, which in some cases lasted over two years. Recall, these patients are extremely immunocompromised. One other thing to note, ITK inhibition spares TH1 cells, also known as TH1 skewing. TH1 cells are the cells responsible for eliminating viruses. Now, beyond clinical results, biomarkers have been identified that support the novel mechanism of action with ITK inhibition that leads to immune rebalancing. Some of these biomarkers represent new discoveries. Briefly, the data show a decrease in IL-4, IL-5, and IL-17 cytokines, a small reduction in TARC, a reduction in Th2 cells, and an increase in Tregs. In ongoing work, we're also finding very significant and interesting changes in the JAK-STAT signaling pathways that will be reported on later. With the additional information that is emerging, both from the clinic and our biomarker analysis, such as induction of Tregs, we believe that soquelitinib's novel mechanism of action and safety will allow for its utility in diverse indications in immune inflammatory diseases and in cancers. Our soquelitinib abstract was accepted for oral presentation at the Society for Investigative Dermatology, or SID annual meeting, which takes place in mid-May. We plan to present the phase I clinical data, expanding our safety and durability data. We will also focus on our biomarker results in this presentation, which we believe will provide novel ideas regarding control of immune diseases. Our late breaker abstract was not selected for presentation at AAD, which typically favors later-stage trials. Angel Pharmaceuticals, our partner in China, is enrolling their phase Ib/2 trial in atopic dermatitis. This is a blinded, placebo-controlled trial that is evaluating a 12-week treatment regimen in 48 patients with soquelitinib doses of 100 milligrams BID, 200 milligrams QD, 200 milligrams BID, and 400 milligrams QD. The patient eligibility and endpoints are the same as was used by Corvus. Depending on the results from the phase I portion, an additional 60-90 patients will be enrolled in the phase II portion of the study. This trial is open at leading centers in China that are very experienced in performing these types of trials. The study is conducted in close collaboration with the Corvus team. Results from the initial cohorts are expected late this year. Now I would like to discuss our phase II randomized placebo-controlled trial in atopic dermatitis. We announced today that the trial has been initiated. This trial is planned to enroll 200 patients with moderate to severe disease, randomized into one of four cohorts with 50 patients in each cohort. We will allow patients who have received prior systemic therapies. Doses of 200 milligrams QD, 200 milligrams BID, and 400 milligrams QD will be examined along with placebo. The treatment duration is 12 weeks with an off-treatment follow-up period of 90 days. The primary endpoint is median percent reduction in the EASI at 12 weeks, a typical endpoint for phase II studies in atopic dermatitis. Other endpoints include EASI-75, EASI-90, IGA, PP-NRS, and others. This will be an international study. We anticipate the data from this trial will be available in mid-2027. Outside of atopic dermatitis, we continue to enroll patients in our phase III registration PTCL trial with an interim analysis expected later this year. We recently conducted a planned meeting of our outside independent data safety monitoring board. No safety signals were observed, and the study continues as planned. In December, at the American Society of Hematology, or ASH, annual meeting, we presented the final data from our phase I/I-B clinical trial evaluating soquelitinib in patients with T-cell lymphoma. The data are supportive of the ongoing phase III program, showing that patients in the 200 milligram BID cohort, the same dose being studied in phase III, had a median progression-free survival of 6.2 months and a median overall survival of 28 months, comparing favorably, very favorably to results with other therapies. For example, median survivals with chemotherapy are less than one year, and PFSs are less than three and a half months. The data presented at ASH also shows soquelitinib's immunobiological effects and its mechanism of action of affecting T-cell differentiation via ITK inhibition. These data support its potential in atopic dermatitis and a much broader range of immune and inflammatory diseases. We also continue to collect very exciting data from our ALPS, or autoimmune lymphoproliferative syndrome, clinical trial, with three patients now on therapy for close to a year. We continue to collaborate with the team at NIAID, and our current plan is to submit data for a potential presentation on the study at the ASH meeting in December. In terms of upcoming clinical trials, we plan to initiate a phase two trial of soquelitinib for hidradenitis suppurativa and asthma later this year. There is strong scientific rationale for evaluating soquelitinib in HS, which is an IL-17-driven disease. In both in vitro and in vivo animal models, soquelitinib is a potent inhibitor of Th17 cells and reduces IL-17 production. Our trial design for HS is further along. At a high level, we are planning to enroll about 60 total patients with moderate to severe HS into three arms: 200 milligram BID, 400 milligram QD, and placebo. The treatment period will be 12 weeks, and the primary endpoints are safety and efficacy measured by HiSCR50, HiSCR75. The asthma study design is emerging and will likely involve about 150 patients treated for three months. In closing, our confidence continues to grow in the long-term potential for soquelitinib in atopic dermatitis, peripheral T-cell lymphoma, and a broad range of additional inflammatory diseases. We are only beginning to unlock the full potential of ITK inhibition and immunomodulation, which could lead to new and better therapies for inflammatory, autoimmune, and fibrotic diseases and cancers. We are building strong momentum with soquelitinib and our ITK platform, and we look forward to updating you on our progress throughout the year. I will now turn the call over to the operator for the question and answer period. Operator? Thank you. Ladies and gentlemen, we'll now begin the question-and-answer session. Should you have a question, please press the star followed by the one on your touchtone phone. You will then hear a prompt that your hand has been raised. Should you wish to decline from the polling process, please press the star followed by the two. Again, if you are using a speakerphone, please lift the handset before pressing any keys. One moment please for your first question. Your first question comes from Roger Song from Jefferies. Please go ahead. Great. Thanks for taking our question, and congrats for all the progress you have made. Mm-hmm. Richard, maybe just one question related to the results from the data readout you will have before the phase II, the global interim in the United States mid-next year. You will have a PTCL potential data and then also the China twelve-week study data. How should we think about the results from those data readouts to the phase II AD, maybe from the efficacy and then the safety perspective, particularly on the high dose 400 milligram QD. Thank you. Okay. We are anticipating that Angel Pharmaceuticals, who is conducting a placebo randomized trial and looking at different doses, will have some data from their initial couple of cohorts later this year. That would be the first data readout. That's gonna be looking at 100 milligrams BID and 200 milligrams QD. Recall, they're going for 12 weeks. They're treating for 12 weeks. We've only gone up to 8 weeks. You know, that'll be very important information for us. That data is unblinded. They look at that. We can report that. The next part of the study will look at 200 milligrams BID and 400 QD. That'll be probably middle of 2027. Okay? We'll get some data on more patients and things. Now, in total, after that, Angel goes on and does 40 or 50, 60 or 60 to 90 patients in a phase II study, rolls right into that. In total, you're looking at around 140 patients or so, and that, well, yeah, 130, 140 patients. That's, you know, totally completed by mid-2027 or early 2027. We'll have some data from them late this year, more data in first half of 2027. The PTCL trial will have an interim formal review in later this year. That has a futility analysis as part of it, so, and safety analysis. But the complete trial results are expected in late 2027. Okay? Now, what I talked about on the call was we do have also periodic safety outside independent safety reviews on the phase III PTCL trial. We had one of those very recently and everything looked good, as I mentioned. Thank you. Okay. Thank you. Your next question comes from Li Watsek from Cantor. Please go ahead. Hey, guys. Thanks for taking my questions too from us. If you just first on the data that you're going to present at the SID meeting in May. Richard talked about, you know, biomarker and durability data before. Can you just maybe, you know, set expectations for us? Yeah. Well, I can set expectations. The durability continues to look great. In terms of biomarkers, the things I've mentioned previously, but we have discovered some new biomarkers, which is gonna be probably the main part of the SID presentation. Fascinating work around the T-regulatory cells and some of the JAK-STAT signaling. The key message there is that you're affecting different multiple cytokine pathways. Even though you're targeting a very specific enzyme restricted to T cells, that can affect several different cytokines, all of which are important in inflammatory diseases like IL-5 and IL-4 and IL-17, et cetera. Plus we'll update the clinical data with the durability and a few other things. My second question. All right. Sorry. My second question is on the phase II trial in HS. You know, just wondering, you know, what the benchmark that you're looking at, especially, you know, relative to the approved agents like IL-17 in the space. Do you think, you know, in terms of efficacy, you have to match the biologics? Well, first of all, we have to find the optimum dose, which we're gonna look at a couple of different doses. Of course, the AD study informs us as well as the T-cell lymphoma study informs us on the HS trial. I would expect efficacy as good or better than what's out there. Which is what the corrected HiSCR scores are, what? 25% or so. Thank you. Your next question comes from Graig Suvannavejh from Mizuho. Please go ahead. Good afternoon, Richard. Congrats on the great progress we're seeing with soquelitinib across multiple indications, and thanks for taking my questions. I just wanted to maybe touch upon a couple of things. First, just on your next data presentations, you did mention that maybe you did apply for a late breaker abstract to AAD. I think you gave us a reason why perhaps your abstract was not accepted. Although I do think that Kymera does have a late breaker. I don't know their dataset very well, as I don't cover it, and so it's not at the top of or the tip of my tongue. Any thoughts on whether it is perhaps they had a bigger database? 'Cause I do think that their a bstract is. Just curious if you had any thoughts there? Well, Graig, what gets accepted, abstracts that get accepted or even publications that get accepted, this is a capricious process. There are a lot of factors. I don't know why they accept some and not others. I personally am shocked that the Kymera with no placebo and an interesting study, for sure, but you know, I don't have an explanation for it. There may not be a good one. I just thought I'd speculate. Have you speculated at all? You know, I wouldn't get too worried about that. I mean, I've had some really, really good papers get accepted at journals and be rejected at others. You know, it is at the end of the day, it's you know, one or two guys read some abstracts. I used to do it myself. You get a few hundred to review, and you know, you decide what looks good, you know, whatever. So I don't know if I'd focus too much on any reasons on that. We're not very active in AAD. We've never done anything there. We don't have booths. We don't, you know, subscribe to their journals. I think you know, that's another factor. Could be another factor. Not sure. Anyway. Okay. SID is a good meeting. If anything, scientifically more rigorous. It is the meeting for early stage and translational biology and research. We ended up, I think, in a very good place. Okay, great. If I could ask just on the phase II trial in AD, that you did start, and congratulations there. I think you mentioned that data would be available in middle of 2027, and just trying to get a sense of, in between now and mid-2027, will there be an opportunity for the company to provide some kind of update? Just trying to get a sense of news flow from that trial from now until mid-2027. That phase II trial is placebo-controlled, randomized, and blinded. No, we will not see that data until it's completed. As I mentioned, the Angel trial is underway. That's also blinded and placebo-controlled, but they can look at the data after each cohort, similar to what we did in our phase I. There will be a news flow from that in terms of the AD stuff. Okay. Okay? Last question, if I could, just on hidradenitis suppurativa, just given coverage of some other companies that I have. I'm under the view that there are not very good preclinical models of HS. That's correct. Just wondering then how do you handicap success in HS when perhaps there are not very well-established or good predictive models in HS? Thanks. You are correct. There are not good animal models for HS. It's pretty clear in the human studies that IL-17 is very important. Th17 and IL-17 are very important. In fact, IL-17s are approved to treat it. I think there's proof of principle already that if you can block IL-17, it should work. We block IL-17 among the many other cytokines that we block. Hidradenitis suppurativa has a lot of different inflammatory cells, T cells, neutrophils, B cells, for example. Again, I think the advantage of soquelitinib is that since you're blocking multiple cytokine pathways, you actually affect many lineages, many different lineages, and I think that's gonna be important. Because when you look at the sites of disease, even in atopic dermatitis, you see, you know, you just don't see Th2 cells, you see a lot of different cells. Thank you. I think that I mean, I would say the best explanation for that is, "Hey, anti-IL-17 works in that disease, and we block it even better. Thank you very much. Thank you. Your next question comes from Jeff Jones from Oppenheimer. Please go ahead. Good afternoon, guys, and thanks for taking the question. Since I think we've beaten HS to death, maybe talk about AD and how you guys are. This is a different disease and indication than the dermatological ones. How are you thinking about dosing in your strategy there? I think you mean asthma probably. Asthma. I'm sorry. Yeah, yeah. You mentioned AD. Well, as you know, atopic dermatitis and asthma frequently go together, and drugs that work in one often work in the other. They seem to be part of the atopic syndromes. We have several, and now that's one where we do have several animal models, and our drug works really well in those asthma models. Four or five different models, soquelitinib works beautifully. In terms of dosing, I think it's the same dosing that we've talked about. The AD and PTCL studies inform the asthma. The asthma study used pretty much the same dosing regimens. There'd be no reason to change that. Okay. One question on Just to elaborate. Remember, we have the best biomarker in the world, which is that, and we've been doing this for years. You can give the drug, you take out the T-cells from the patient, either in the blood or the sites of disease, and you can measure quite accurately the drug sitting in the target. It is a clean quantitative assay. It blocks the function of that enzyme. That's a biomarker. We know that when you give a 200 milligram dose, you pretty much completely block that. Sorry, Jeff. Appreciate that, Richard. On the ALPS trial, which you're doing with the NIH, can you maybe comment on how the outcome of that might impact how you think about other indications or inform what you guys are doing? ALPS is a disease where you have such an overreactive autoimmune response to so many different things. They have antibodies to red cells and white cells and platelets and other things. In ALPS and lymphocyte proliferation, abnormal lymphocytes. We have seen really interesting results in our patients. I think that what we're learning there, similar to what we learned in lymphoma, is that the drug is very active, it's safe, and it's interfering with the signaling pathways that we would predict. Now, I'm not sure I can say, "Okay, if it works in ALPS, it's gonna work in lupus," even though the ALPS mouse equivalent is a model for SLE. I don't think we're thinking of it that way. We're thinking of it as an indicator that we're affecting aberrant autoinflammatory responses in a disease where there's you know you know no good treatments, really. It's kind of a model, if you will, but it's a human model. It is an orphan disease. There's no good therapies. Could you get approval for ALPS? Yes, you could. It's more of a childhood disease. We've been treating adults. We do intend to increase the number of sites, and we do intend to move down in age into children over the next year or so. We've been talking about that with NIH. It's another indication, and it happens to be an autoimmune disease. All right. Appreciate that. Thank you, guys. Thank you. Your next question comes from Aydin Huseynov from Ladenburg Thalmann. Please go ahead. Hi, Richard, congratulations for the tremendous progress so far this quarter in your pipeline in the drug soquelitinib. I got a couple of questions. First, I wanted to ask about the near-term focused near-term phase III readout, interim analysis, from the trial in PTCL. I was curious to hear any comments you may provide regarding the enrollment process so far. You know, what types of PTCL you actually enrolling? Is it NOS? Is it ALCL, follicular, cutaneous? And what the physicians are using as standard of care. Is it preferred belinostat or pralatrexate? Just curious to hear overall dynamics of the trial. Okay. Let's take that question first. The trial is enrolling, and it's going perfectly according to plan. Patients get randomized into either soquelitinib monotherapy, 200 milligrams BID, versus the investigator's choice of either belinostat or pralatrexate. Now, recall belinostat and pralatrexate are received conditional approval, accelerated approval, oh, maybe 15 years ago or so, based on response rate in patients with relapsed PTCL. In our discussions with FDA, that was the logical control arm. Soquelitinib versus those agents. Now, it's not a blinded trial 'cause you can't. Well, first of all, we don't usually do that in cancer, but you can't blind soquelitinib's oral, right, as we know. belinostat and pralatrexate are given intravenously and have associated usual toxicities of chemotherapy, mucositis, blood count problems, you know, things like that. So far the trial is, you know, is enrolling. We had our first safety monitoring board and, you know, there were no new safety or different safety signals with regard to soquelitinib. Obviously, it's much safer than chemotherapy, you know, we win on every count on that. Now the types of patients that are enrolled are, as stated in the protocol, PTCL NOS. That's the most common one. We do allow anaplastic lymphomas that are ALK-positive. The other big category would be what's called T follicular helper, which used to be what's called AITL, angioimmunoblastic lymphoma. It's not CTCL. CTCL really is a little bit more of a chronic disease and is treated differently so that's the reason not to include that in this trial. It's pretty typical. These are the most common peripheral T-cell lymphomas. Now, peripheral T-cell lymphoma, again, just to remind people, there is no fully approved treatment for relapsed disease. It has a you know median PFS. belinostat median PFS is 1.7 months. Pralatrexate is 3 months. OSs are under a year. Those are really bad. These are really bad disease. These are sick patients. I can tell you that we are very, very happy with the way the trial is going. I think it could represent a very important breakthrough in hematology if we finish the trial and get the results that we're expecting. Does that answer your question? What- Yeah. Yeah. Thanks so much. Yeah. Appreciate that. Yeah. I got another one for asthma, if you don't mind. Sure. Regarding the upcoming trial design in asthma, do you plan to have a cohort with patients who may have both asthma and atopic dermatitis? In your opinion, is there any accelerated path with small pivotal trial for patients with two diseases simultaneously? Essentially that would allow soquelitinib to cure two diseases at the same time. Mm-hmm. As we know, DUPIXENT is the only drug that treats both diseases. Yeah Maybe you can have it in one shot. Well, that'd be great, but I don't know. First of all, trying to get two indications on one, that's really very difficult. You know, you can get anecdotal information. I know some people report that. We've had some anecdotal information about that. The problem is you don't know how many patients are gonna have both diseases concomitantly, how severe it is, what measurements you're gonna use, and how you power the study statistically for each disease. It's really hard to do that. You know, anecdotally, it's something you would look at. You have to do a separate trial. Even DUPIXENT was, you know, separate trials for asthma and eosinophilic esophagitis and COPD and all those things. It requires a separate trial. Now one thing we are considering is, we're really very interested in, I would say two things. One is this durability of response is quite interesting. We think we have explanation for it. I think we have a very good immunologic explanation for it. It's very elegant, and compatible with what's known about the immune responses and so forth. We also are very struck by the activity we see in patients who failed previous therapies. And I talked about that in my discussion here. We are allowing, and I don't know if I mentioned it, patients who have failed prior therapies in our phase II atopic dermatitis study. Some people, many investors have been asking me, "Why don't you do a separate study in the resistant patients with atopic dermatitis?" That is something we are thinking about. You know, that could be a smaller trial because the efficacy and placebo do so poorly, you would presumably show a bigger difference with a fewer number of patients. But we are including both naive and experienced patients in our phase II. I would do that in phase III as well, which would enable you to get the total population of patients. There's no doubt that with more and more therapies coming out in atopic dermatitis, the proportion of patients that are not treatment naive, that is, that have failed the prior therapies, that pool of patients is increasing. The pool of patients that is naive is gonna decrease proportionally. Okay. That the resistant patient becomes, I think, very attractive. I mean, we have a lot of things that we're excited about with soquelitinib. It's oral and it's safe and all that other stuff. The durability is, I think, a game changer, changes how you approach the disease. I think the fact that, you know, you can think about frontline therapy or relapsed disease or multiple therapies, you know, intermittent therapy. That's our, you know, it's the way we think about it. Makes sense. Yeah. Thanks so much. Very helpful, and congrats with the results. Thank you. Your last question comes from Sean Lee from H.C. Wainwright & Co. Please go ahead. Hey, good afternoon, guys, and thanks for taking our questions. To touch upon the durability a bit more, I think in the previous phase one study, you guys followed the patients for up to three months. How long are you following these patients in phase two? Is the study powered in any way to really make a differentiation on the durability of this response? The phase II trial has built-in continued blinding of the trial out to 90 days beyond the therapy. It's 12 weeks of therapy plus the 90 follow-up. That's baked into the protocol. However, the endpoint is the EASI score compared to placebo at 12 weeks, and that's the typical endpoint. To do something different would be, you know, sort of atypical. I think that in the future this issue of how durable the responses are is something that you might, you know, study separately. I think it stands to reason. I mean, we'll talk more about this, but, you know, we have over 90% of our patients don't relapse. In follow-up now out to 3 months beyond the last dose, over 90% of patients, disease just doesn't come back. Now, you look at other agents, DUPIXENT, STAT6, STAT whatever, the IL-13s, IL-2s, whatever, these diseases come back pretty quickly. In my view, that's not a very good therapy. Best therapy is, you know, a shorter treatment duration. Disease goes away, you don't need to take your drug again for a long time, if at all. Hopefully. That's asking a lot. The durability is important because it's important to understand why it's happening. Does it pertain to other inflammatory diseases? In other words, how broad is that gonna be? Is that unique to atopic dermatitis, or is that something that you could think about for other autoimmune diseases? You know, that's why we're excited about that. Anyway, the answer to your question is in the phase II, it is part of the formal follow-up is blinded, but it's not part of the statistical endpoint. The statistical endpoint is the typical one, which is EASI score at the 12 weeks. Okay. Got it. Thanks for that. Touching on the asthma study for our second question, as the upcoming study, will you be focusing on eosinophilic asthma with the Th2 high, or are you targeting the more difficult to treat the Th17-driven population as well? Those are some of the things we're discussing now. We're leaning to taking everybody. I see. For the upcoming I'm actually, Sean, glad you brought that up because there's something. Some people say, "Well, we only treat Th2 disease." I don't know where that comes from. Some people say, "Oh, you're only selecting patients with atopic dermatitis that are Th2." First of all, I don't even know how to do that. If we're not doing that. Our atopic dermatitis patients are, you know, run-of-the-mill patients from U.S. centers. You know, they have to have the necessary eligibility criteria, but we didn't enrich for any patient population. Most of our, by the way, AD patients do not have eosinophilia. Their eosinophil counts are normal or low. I don't think we're gonna restrict it to the high EO asthma. Although I have to say, the asthma study protocol has not yet been finalized and that's still under discussion. Okay. Got it. Yeah, that's very helpful. Thanks again for taking our questions. All right. Okay, well, first of all, thank you everyone for participating in our call. We look forward to updating you throughout the rest of the year and beyond. Appreciate everybody's interest. Thank you. Ladies and gentlemen, this does conclude your conference call for today. We thank you very much for your participation, and you may now disconnect. Have a great day.