Corvus Pharmaceuticals, Inc. (NASDAQ:CRVS) Q3 2025 Earnings Call Transcript

Corvus Pharmaceuticals, Inc. (NASDAQ:CRVS) Q3 2025 Earnings Call Transcript November 4, 2025

Corvus Pharmaceuticals, Inc. beats earnings expectations. Reported EPS is $-0.12, expectations were $-0.14.

Operator: Good afternoon, everyone. Thank you for standing by, and welcome to the Corvus Pharmaceuticals Third Quarter 2025 Business Update and Financial Results Conference Call. [Operator Instructions] It is now my pleasure to turn the call over to Zack Kubow of Real Chemistry. Please go ahead, sir.

Zack Kubow: Thank you, operator, and good afternoon, everyone. Thanks for joining us for the Corvus Pharmaceuticals Third Quarter 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’ quarterly report on Form 10-Q for the quarter ended September 30, 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 Lea. Leiv?

Leiv Lea: Thank you, Zack. I will begin with a brief overview of our third quarter 2025 financials and then turn the call over to Richard for a business update. Research and development expenses in the third quarter of 2025 totaled $8.5 million, compared to $5.2 million for the same period in 2024. The $3.3 million increase was primarily due to higher clinical trial and manufacturing costs associated with the development of soquelitinib as well as an increase in personnel-related costs. The net loss for the third quarter of 2025 was $10.2 million, including a noncash loss of $300,000 related to Angel Pharmaceuticals, our partner in China. This compares to a net loss of $40.2 million for the same period in 2024, which included a $32.8 million noncash loss related to the change in fair value of Corvus’ warrant liability and a $700,000 noncash loss related to Angel Pharmaceuticals.

Total stock compensation expense for the third quarter of 2025 was $1.2 million, compared to $700,000 in the same period in 2024. As of September 30, 2025, Corvus had cash, cash equivalents and marketable securities totaling $65.7 million, as compared to $52 million at December 31, 2024. Consistent with our last quarter, we expect our current cash to fund operations into the fourth quarter of 2026. I will now turn the call over to Richard, who will discuss our clinical progress and elaborate on our strategy and plans.

Richard Miller: Thank you, Leiv, and good afternoon, everyone. Thank you for joining us today for our update call. Our primary focus continues to be on the development of soquelitinib for both atopic dermatitis and T cell lymphomas, and we have several important milestones upcoming for these programs. First, we have completed enrollment in the extension Cohort 4 of our Phase I trial, and we expect to have the results of the full data set in late December. Given the proximity to the holidays, we plan to report results in January. Second, the initiation of our Phase II atopic dermatitis trial is on track for early Q1 2026. We believe soquelitinib is strongly positioned as an oral medication with a novel mechanism of action that so far has shown favorable safety and efficacy profile.

There has been increasing interest in drugs with novel mechanisms to address atopic dermatitis and other inflammatory diseases. Our confidence in soquelitinib is bolstered by our belief that the data to date not only stands up favorably against recent data sets from other approaches, but indicates that we have the potential to be a leader in this space. We are also encouraged that the clinical evidence obtained to date with soquelitinib in both atopic dermatitis and in T cell lymphoma bode well for the potential of ITK inhibition in a broad range of immunology and inflammatory indications, and we continue to explore potential next opportunities for our platform. On today’s call, I will provide an overview of extension Cohort 4 and our plans for reporting this data, and the status of our planned Phase II trial in atopic dermatitis.

I will also discuss the relevance of our soquelitinib ASH oral presentation for our Phase III peripheral T cell lymphoma trial and its implications for I&I indications, including atopic dermatitis. And I will provide a brief recap of other operational progress and updates. Let me start with a reminder of the key data reported to date for soquelitinib in atopic dermatitis. In June, we reported data from Cohort 3 of the Phase I trial evaluating a 200-milligram twice-per-day oral dose for 28 days of treatment, building on the encouraging results we had already reported with a lower dose level from cohorts 1 and 2. All of the treatment cohorts demonstrated a favorable safety and efficacy profile compared to placebo. The Cohort 3 efficacy data was especially remarkable, demonstrating earlier and deeper responses compared to cohorts 1 and 2.

At day 28, Cohort 3 showed a mean percent reduction of EASI score of 64.8%, compared to 54.6% for the combined cohorts 1 and 2 and 34% for placebo. In Cohort 3, 50% of patients achieved EASI 75, 8% achieved EASI 90 and 25% achieved IGA 0 or 1. No placebo patients achieved EASI 75 or IGA 0/1. We also saw an impact on itch with a number of Cohort 3 patients reporting steep drops in patient-reported PP-NRS score beginning at day 8. In terms of the kinetics of response, Cohort 3 showed earlier and deeper separation from placebo starting at day 8, compared to cohorts 1 and 2, with the EASI score improvement continuing through day 15 and 28. The continuous downward slope of the curve suggests that longer treatment duration could potentially deepen responses further, which we are now exploring with the extension Cohort 4.

We have completed enrollment in the extension Cohort 4 of the Phase I trial, which is evaluating 24 patients at the Cohort 3 dose of 200 milligrams twice per day given for 8 weeks, with an additional 30-day follow-up without therapy. The 24 patients were randomized in a blinded fashion 1-to-1 with placebo, 12 active and 12 placebo. As mentioned earlier, we plan to report the 8-week data set on 24 patients in January. Our objective with this additional data is to confirm the results obtained in our earlier cohorts in a larger number of patients and to determine if the longer treatment duration of 8 weeks leads to better efficacy. The second upcoming milestone for soquelitinib in atopic dermatitis is the initiation of our planned Phase II clinical trial, which we anticipate will begin early Q1 2026.

The trial will be randomized, placebo-controlled and double-blinded, involving approximately 70 clinical trial sites globally. The trial was designed to enroll approximately 200 patients with moderate to severe atopic dermatitis that have failed at least 1 prior topical or systemic therapy. I would like to emphasize that we are including patients who have failed previous systemic therapies, such as Dupixent or JAK inhibitors. We are interested in this population of patients because soquelitinib has a mechanism of action that is different than currently available agents and prior use of these agents would not be expected to lead to resistance to soquelitinib. The patients will be randomized equally into 4 cohorts, 50 patients each, receiving soquelitinib 200 milligrams once per day, 200 milligrams twice per day, 400 milligrams once per day, or placebo.

The treatment duration will be 12 weeks and patients will be followed for an additional 90 days without therapy. The primary endpoint will be the mean percent reduction in EASI score from baseline to week 12. This is the typical endpoint for Phase II clinical trials in atopic dermatitis. Secondary endpoints will include the percent of patients achieving EASI 75 or IGA 0/1 at week 12, impact on itch measured by the percent of patients achieving greater than or equal to 4-point decrease in PP-NRS at week 12, and safety. Photographic documentation of disease at baseline and response to therapy will be mandated on the study and reviewed by independent experts. In oncology, we continue to enroll patients in our registrational Phase III trial of soquelitinib in patients with relapsed PTCL, driving towards interim data in late 2026.

In addition, we are pleased to report that the final results from our Phase I/Ib clinical trial of soquelitinib for the treatment of relapsed/refractory T cell lymphomas will be presented in an oral session at the Annual Meeting of the American Society of Hematology meeting in December. This presentation will report on the clinical data and supporting preclinical work that drives us to continue advancing the program for PTCL, as well as providing the rationale and safety information motivating us to focus on immune and inflammatory diseases. In particular, we will report on the durability of progression-free and overall survival. We believe the presentation at ASH adds to the growing clinical evidence that soquelitinib is a safe and active agent working through a mechanism that supports its utility in both T cell lymphoma and immune-mediated diseases.

As a reminder, some patients in the Phase I trial were treated beyond 2 years in the same daily dose range as is being studied in atopic dermatitis. And complete durable tumor responses were seen in patients with highly aggressive tumors. We also have a growing body of preclinical data supporting the potential of ITK inhibition in a broad range of additional indications across dermatology, rheumatology, pulmonary medicine, solid cancers and other diseases. Briefly on other operational updates. In October, we appointed Mr. David Moore to our Board of Directors, building on the addition of Richard van den Broek in April. David is Executive Vice President, U.S. Operations, at Novo Nordisk and President at Novo Nordisk. His experience leading one of the most successful GLP-1 franchises, along with his broad expertise across strategy, commercial, market access, business development and investing, is anticipated to be an important strategic resource as we work to maximize the potential of our ITK inhibitor platform.

In closing, we remain very optimistic about the potential of soquelitinib in atopic dermatitis. In addition, the knowledge and experience from our current trial motivates us to think beyond atopic dermatitis, to a broad range of other immune diseases. We believe we may have the opportunity to establish selective blockade of ITK as a new therapeutic approach to autoimmune inflammatory diseases based on modulation or rebalancing of cellular immunity. We look forward to providing soquelitinib updates in the coming months. First, at ASH for our T cell lymphoma program, and then in January for the extension Cohort 4 data for our atopic dermatitis program. Combined with the planned initiation of our Phase II atopic dermatitis trial in early Q1 2026 and the ongoing enrollment in our Phase III PTCL trial, we are building significant momentum for soquelitinib coming into the new year.

I will now turn the call over to the operator for questions and answer period. Operator?

Q&A Session

Operator: [Operator Instructions] Your first question comes from the line of Graig Suvannavejh from Mizuho.

Graig Suvannavejh: Congratulations on the progress in the quarter. I had a couple of questions. First, on your ASH abstract and the data that you will be presenting next month. I’m wondering, we saw very impressive OS data, and with that in mind, with other information that was in that abstract, could you perhaps put in context the comparability that obviously leads to your enthusiasm for the prospects of soquelitinib in peripheral T cell lymphoma? And I’ll come back with a second question.

Richard Miller: First of all, the PFS and OS being presented at ASH meeting is quite impressive, the — especially when you consider this is a Phase I trial using an agent that was not previously tested in this disease. As you all know, T cell lymphoma is a very bad disease with a median survival usually of about 6 months in relapsed. We have far better results than that and we’re excited about that. The reason that we’re also excited is we’ve learned so much from that trial in terms of immunobiology, safety, pharmacokinetics, pharmacodynamics, mechanisms of action that pertain to — that are very pertinent with regard to immune diseases. One of the things I talk about in the ASH abstract, and we’ll elaborate on at the meeting, is the fact that we’re seeing responses in T cell lymphomas that are so-called GATA3-positive.

Now GATA3 is a transcription factor that is also known as the master regulator of Th2 function. Th2 cells are the cells of interest in a variety of immune diseases, including atopic dermatitis. So putting all that information together we feel bodes well, not just for the T cell lymphoma program, but for a range of immune diseases. It’s confirming and consistent with our belief that we have a drug with a really new novel mechanism of action, it’s oral, it appears very safe. And we are seeing really significant signals of activity in patients who have a cancer of their immune system that involves the very same cells that are involved in all these other immune diseases. I hope I answered that question.

Graig Suvannavejh: You did. And then if I could just go to soquelitinib and your atopic dermatitis readout that’s coming in the early part of the year. As you have expanded the treatment duration and as you’ve expanded the number of patients, is it fair for us to assume that what you saw previously will have an improvement on the efficacy that you saw? And if you don’t see an improvement versus what you saw previously, does that change in any way your enthusiasm for the prospects of soquelitinib in atopic dermatitis?

Richard Miller: So first of all, we feel, and so do many of our outside experts feel, that the data that we generated in Cohort 3 with 28 days of treatment was quite good. It was safe and it was quite active in that. What we aim to show — and as you recall, the reduction in EASI scores were continuing to go down for the last few weeks of therapy. So with the expanded cohort, we really are looking for 2 things. Number one, we want to show consistency. We want to show — confirm what we showed before in a larger set of patients with more placebos and more patients getting active drug. Placebos, I don’t have to tell you folks, placebos are very important in evaluating these diseases. The second thing we’re looking for is: does the extension of the treatment duration improve the results further?

So those 2 concepts. I want to see consistency of the data from what we did earlier, and yes, we’d like to see an improvement as we go beyond 28 days. And of course, we want to confirm safety and the other things as well. So that would be what to expect as we look at the data that comes out in January.

Operator: Your next question comes from the line of Jeff Jones from Oppenheimer.

Jeffrey Jones: Congrats on the real progress you’re making here. One on soquelitinib. Richard, as you mentioned, you’ve seen and been generating data in a number of other indications in the I&I space. What are your plans to take soquelitinib forward in other indications at this point, sort of indications and timing?

Richard Miller: Okay. So just to be clear, Jeff, soquelitinib in humans is being studied in the registration Phase III trial and, of course, in our Phase II atopic dermatitis trial. We also have a trial in lymphoproliferative disease called ALPS that you know about. Now we have many preclinical models that we’ve evaluated soquelitinib, everything from asthma, atopic dermatitis, psoriasis, scleroderma, systemic sclerosis, et cetera. We are making definite plans to move into other immune-related diseases. I’ll be talking more about that early next year. The key diseases for us now appear to be asthma, and probably another dermatologic condition, yet to be defined.

Jeffrey Jones: Great. Appreciate that. And then you — or the Kidney Cancer Research Consortium reported an update on the cifo trial at ESMO. Just curious as to the next steps there. The trial is still ongoing, there are still patients on follow-up. How are you thinking about ciforadenant in the context of renal cell and beyond?

Richard Miller: So as you know, the cifo trial was done in collaboration with the Kidney Cancer Consortium, who pay for most of the trial. I don’t think we have any other expenses related to that. There were 19 patients still on treatment and on follow-up, 19 out of 50, 40% or so almost. So we’re going to continue to follow those people, and we’ll decide what to do once we see how the rest of the data evolves. But that’s our current plan for that.

Operator: Your next question comes from the line of Li Watsek from Cantor.

Li Wang Watsek: Congrats on the progress. I have a couple of questions here. First, maybe just in terms of baseline characteristics of the Cohort 4 versus prior 3 cohorts. Is it reasonable for us to assume they’re pretty similar to Cohort 3? Or is there any difference that we should keep in mind? And I have a follow-up.

Richard Miller: It is very reasonable for you to assume that the characteristics are very similar to Cohort 3. And to elaborate on that, the enrollment in the trial is 17 centers, all U.S. centers, the same centers that were utilized for the first 3 cohorts. None of the criteria for eligibility have been changed. And yes, we know the demographics already of our patients, very, very similar to those of Cohort 3.

Li Wang Watsek: Okay. Great. And then for the Phase II trial, just given the patient population that you’ll be enrolling, it sounds like the patients can be exposed to JAK inhibitors and Dupi. So just given this demographic, what should be the bar for the EASI score?

Richard Miller: Okay. So first of all, when we go to Phase II, of course, it’s a larger trial, 200 patients, it would be very difficult, would take a long time to enroll that solely in the U.S. So there is going to be a heavy reliance on sites outside United States, particularly in Europe, which is what most companies are doing now. I think that we’re somewhat unique in that we’re allowing patients who failed Dupi and JAK and other systemic therapies — within reason. I mean you can’t fail 10 therapies. But — now the reason we’re doing that is that we have some patients that we’ve seen in cohorts 1, 2, 3 and now even in the fourth cohort that have failed those systemic therapies, and they’re responding to our drug. So I don’t know what the final numbers are going to be on that yet, whether it’s identical to first-line therapies or somewhat not identical.

So it’s a little bit hard for me to say what the bar is. First of all, I’m not aware of any data that has specifically been published on the response of a drug to somebody who’s failed the JAK inhibitor or Dupi. Now those studies do, I know, recycle patients. They take patients who are EASI 50s and they treat them again for longer periods of time. But that’s really kind of a different kind of experiment. So look, I think it’s a little early to set a bar for the Phase II. Let’s get our Phase I results. Let’s take a look at the Dupi failures and the JAK failures, and then we can talk more about that. But I think it is an important point, I’m glad you asked the question, that the Corvus patient population is a little bit different. Now we’re doing that deliberately.

We want these failures because we think that we have a drug with a mechanism of action that is going to — where the mechanism of resistance to a Dupi or a JAK is really — may not really be pertinent or relevant for our mechanism. And then we need to learn that. So the good news here is that it expands the potential use of our drug. We feel that it potentially could be used first line or it could be used in the relapsed situation.

Operator: Your next question comes from the line of Aydin Huseynov from Ladenburg.

Aydin Huseynov: Congrats on the progress this quarter, and appreciate taking questions, I got a couple. So Richard, so you’re already running a trial in atopic dermatitis, and I was curious to hear any thoughts on potential other dermatologic indications such as either hidradenitis suppurativa, vitiligo, psoriasis or anything else. And can you run several trials simultaneously — several dermatologic trials simultaneously? Just wanted to get your thoughts on this.

Richard Miller: Okay. So the preclinical models and the data we have in the lab tells us that asthma should be a very good indication for us. We also think that a disease like hidradenitis suppurativa would be a very good disease for us. It’s in the dermatology space and that’s a disease that’s both Th2 and Th17 driven. So let’s think about that a little bit. A Dupixent, for example, or a STAT6 inhibitor or whatever, is going to get your Th2-type cytokines, but it’s not getting Th17 because that doesn’t signal through STAT6. So we think we have a distinct advantage here for a disease like HS because we hit 17 and Th2. There are other reasons as well. So other diseases we’re thinking about are prurigo nodularis, that’s a Th2 and Th17 disease as well.

That’s not as common, but there’s even more of an unmet need there. Alopecia areata, we’ve considered. It’s a very competitive space. JAK inhibitors work well. But that’s still on our list and we’re still doing some work on that. Now your question, can we run more trials? We intend to run multiple trials in immune disease. We intend to push this drug in multiple areas, as I mentioned on my talk, not just in dermatology, pulmonary medicine, oncology, rheumatology, et cetera, et cetera. Now of course, we know at some point here, we’re going to have to raise some money to do that. And we’re optimistic that with the data that we have coming out, that we’ll be in a position to raise money to fund those activities.

Aydin Huseynov: Very helpful, Richard. One more question I have regarding Phase II registration trial. I just wanted to better understand the time lines, the potential readout, and hopefully, the potential launch of the drug. So given so many developments with soquelitinib, I guess this is the first indication — that’s the first indication you’re going to launch the drug. And I just wanted to get a better sense of immediate commercial opportunity and the time lines in PTCL for soquelitinib.

Richard Miller: Yes. So well, our time line is a futility interim analysis at the end of 2026, probably finished, full data by end of 2027. Launch would be, I think, relatively quick for this. One of the beauties of this trial is that it’s a single registration, randomized trial that could lead to full approval should you meet your endpoints. And it’s 150 patients, relatively small trial, with relatively short endpoints. The control — the chemotherapy control arm is expected median PFS, which is the primary endpoint of, what, 3 months, 2 months. So we’re excited about it. I’m an oncologist and lymphoma is my expertise, as you know, and I ran a clinic at Stanford for 25 years or more taking care of lymphoma patients, there is no treatment, no good treatment for this disease.

There is no competition at this point. Even in the research stages, I mean, really there’s nothing new in this area. So we think we have the potential should this drug be approved, where it will be used immediately in all T cell lymphomas, frontline, late line, you name it, because really there isn’t anything else. I mean we have a ways to go before we can figure all that out, but the opportunity here, we think, is much larger than people recognize. Now it’s not atopic dermatitis in terms of the number of patients, of course, but it also doesn’t have the competition and it also doesn’t have the very long time lines to approval. All right?

Operator: Your next question comes from the line of Etzer Darout from Barclays.

Jordan Becker: This is Jordan Becker on for Etzer Darout. Thanks for taking our questions and congrats on the updates. Two questions. You alluded to it, but I just want to double-click on this. Do you plan to do any post hoc analysis following the Cohort 4 completion to look at efficacy in Dupi and JAK-naive and refractory populations? And then two, can we expect a similar analysis in terms of biomarker correlates of clinical efficacy with the updated data?

Richard Miller: The answer is yes and yes, Jordan. Thanks for the question. We, of course, will be doing post hoc analysis trying to figure out how the drug is working, how to make it work better, all sorts of things. So clearly, looking at the effects of prior therapy, prior systemic therapies, all those clinical variables will be evaluated. We do have a pretty aggressive biomarker program. We’re minimizing biopsies of the lesions on patients only because that does hurt enrollment, and we don’t want to do that. But we have a pretty extensive program now looking at single-cell RNA sequencing of blood, and that’s revealing a lot of interesting things. I mean there’s a lot of new things that are coming out on this. I think the same old, same old look at IL-13 or whatever, that’s going to go bye bye, TARC, et cetera.

Those are not good biomarkers, everybody knows that. The best biomarkers for these diseases are yet to be defined because they’re heterogeneous diseases and we don’t really know what the cause is. So we’re looking at a lot of that. We’ll report on what we find. The biomarker game is a tough game. There’s a lot of variables to look at, and hard to make much of anything when you have a small number of patients. But we certainly will hope to get clues and signals that we can validate in larger trials. Okay?

Operator: Your next question comes from the line of Sean Lee from H.C. Wainwright.

Xun Lee: I just have a couple of quick ones on the design of the upcoming Phase II AD study. So what’s the reasoning behind the settling on a 12-week duration treatment rather than the 8 weeks that you’re testing in the Cohort 4? And are there any notable differences between the enrollment criteria of the Phase II compared to the patients that you’re enrolling in Phase I?

Richard Miller: So far, the eligibility criteria are pretty much identical. The reason we’re going to 12 weeks is we’re going to examine that. Most therapies are out at 16 weeks now. But if you look at the data from most studies, you’ll see that most of the separation, most of the efficacy is obtained in the first 12 weeks. You don’t really gain that much more by treating longer. So that’s the reason for our 12-week study. Look, I’m trying to make this a shorter treatment, not a longer treatment, okay? I don’t know any patient, and I’ve been, as I mentioned earlier, running a clinic for over 30 years, I don’t know any patient who wants more medicine to take longer. So I’m trying to see if we can go shorter, not longer. But of course, we want to maximize — both are important.

You want to maximize responses. You want to hopefully shoot for total clearance of disease, that is EASI 100%, that’s what you want. And that’s what we’ll try to do. But that’s — if you look at most studies, you don’t gain much by going from 12 weeks to 16 weeks. Now some people are going to 6 months, 1 year. I mean, great, if you’re willing to take a drug for that long, for an incremental benefit that’s marginal.

Operator: Your next question comes from the line of Cha Cha Yang from Jefferies.

Cha Cha Yang: This is Cha Cha on for Roger Song. I was hoping that you could give us some color on any of your plans for potential partnerships or licensing deals for soquelitinib in the coming future, or if you plan to raise money and take this forward yourselves in either AD and oncology.

Richard Miller: Okay. So thanks for the question, Cha Cha. I can tell you that ITK as a target is on the radar of every major company that works in this area. I know that because we’re talking to them. We’ll evaluate partnering opportunities as they arise, whether it be in oncology or immune diseases. At this time, however, we’re pushing forward with our cancer program and our immunology program. We, as I mentioned just a few minutes ago, we do recognize that we’re going to have to raise more money to maximally develop all these programs. We’re optimistic about our data and we think there will be ample opportunity to raise funding, whether it be through offering stock or partnerships at the appropriate time.

Operator: Next question is from the line of Graig Suvannavejh from Mizuho.

Graig Suvannavejh: I was very curious, as you think about your ITK portfolio and comments around potentially advancing next-generation ITK, I was wondering, Richard, if you could share kind of the vision or strategy around the potential of adding another indication for soquelitinib versus moving forward with a next-generation ITK inhibitor with perhaps a similar indication in mind. Just how do you balance that kind of strategy?

Richard Miller: Well, that’s a — thank you for the question. That’s a good question. Obviously, pushing forward with soquelitinib, which now has a wealth of safety and efficacy data in hundreds of patients, is — will move faster than bringing along one of our backup compounds, which, of course, still have to go through IND-enabling studies. And then if you go in the immunology space, don’t forget you need to do normal volunteer single-dose, normal volunteer multi-dose. So that takes time. But we are going to consider all that. Right now, we’re pushing forward in the PTCL, atopic dermatitis and soon other immune diseases. We’re also considering other dosage forms and formulations of soquelitinib. We’re working on that now. We also are looking at soquelitinib-like ITK degraders.

We’ve made some of those. We’re looking at those in the laboratory. Interestingly, it turns out that soquelitinib, a covalent drug, leads to degradation of the ITK target to a certain extent. We’ve learned that. That’s really interesting. I don’t think anyone has known that before. So we’re looking at any and all of that stuff. But certainly pushing forward with our lead compound, that’s going to be the fastest.

Operator: Your last question is from the line of Jeff Jones from Oppenheimer.

Jeffrey Jones: Just a quick one. Digging a little bit deeper into the Dupi and JAK-exposed patients that could be enrolled in the Phase II study. Would you guys be powering the study to really do a subgroup analysis that could be statistically significant again and separate those systemically exposed patients versus systemic therapy naive patients?

Richard Miller: No, we would not be doing that. I mean that’s — I mean, we don’t have enough information yet, Jeff, to make a commitment like that. But one thing is for sure, we will stratify the studies to look at that subgroup. So what I mean by that is that will be a defined subgroup. We will stratify randomization based on whether you fail this — a prior systemic therapy or not. You want those equally distributed in your placebo and in your active arm. But without really knowing the efficacy signal yet we would expect in that, it’s a little hard to power how many patients you would need and what effect you’re looking for. I think that would be going pretty far. I’m not sure you’d want to do that at this stage. I’d rather do a study, include everyone — the best outcome, do a study, include those people, have a positive study in your predefined endpoint. You get approval, I mean if it were Phase III, you get approval for everyone.

Jeffrey Jones: Yes. No, great. And the other way to look at that would be stratifying. So really appreciate the clarity.

Richard Miller: Thanks, Jeff.

Operator: Thank you very much. As there are no further questions at this time. I would like to turn the call back to Mr. Richard Miller for closing comments. Sir, please go ahead.

Richard Miller: Thank you very much, operator. Thank you, everyone, for participating in this call. We look forward to advancing the soquelitinib programs and our other programs. And we look forward to updating you on our progress as we move forward into 2026 and beyond. Thank you very much.

Operator: Ladies and gentlemen, this concludes today’s conference call. Thank you very much for your participation. You may now disconnect.