Earnings Call Transcript - CRVS Q4 2025

Operator, Operator

Good afternoon, everyone, and thank you for joining us for the Corvus Pharmaceuticals Fourth Quarter and Full Year 2025 Business Update and Financial Results Conference Call. It is now my pleasure to turn the call over to Mr. Zack Kubow from Real Chemistry. Please proceed.

Zack Kubow, Event Host

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' 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.

Leiv Lea, CFO

Thank you, Zack. 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 of 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 of 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 noncash losses of $0.7 million and $2.2 million, respectively, from Corvus' equity method investment in Angel Pharmaceuticals, and a noncash 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 3 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, 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, '25, 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.

Richard Miller, CEO

Thank you, Leiv, and good afternoon, everyone. Thank you for joining us today for our update call. In 2025, we made significant progress in developing soquelitinib, our first-in-class selective ITK inhibitor aimed at rebalancing the immune system. This was showcased by the presentation of final results from our Phase I/Ib trial in peripheral T-cell lymphoma at the ASH Annual Meeting, along with recent data from cohort 4 of our Phase I atopic dermatitis trial, indicating that soquelitinib may become a leading therapy for atopic dermatitis and potentially other inflammatory diseases. Following this data announcement, we successfully completed a $200 million financing, reflecting high investor interest in soquelitinib and ITK inhibition, supported by our robust data, its unique mechanism of action, and its potential to benefit patients across various medical fields. As we approach 2026, we are well-positioned with ongoing enrollment in our Phase III PTCL trial, our recently started Phase II atopic dermatitis trial, and plans to expand into mid-stage trials for other critical inflammatory diseases, including hidradenitis suppurativa and asthma later this year. Our cash runway extends beyond key data readouts for all these programs, based on our current plans and anticipated timelines. In today’s call, I will summarize the key takeaways from our cohort 4 data announcement, outline our plans to present additional data at an upcoming medical meeting, and provide an update on our Phase II trial. I will also discuss our pipeline expansion plans and upcoming milestones. The results from cohort 4 and the entire Phase I trial suggest that soquelitinib's clinical profile offers significant benefits in the treatment of atopic dermatitis. First, it's an oral medication. Second, it features a novel action mechanism that combines tissue selectivity and target specificity while influencing multiple inflammatory signaling pathways. Third, it appears to be safe and effective across a broad patient range, including those who have experienced previous systemic therapies. Lastly, it produces lasting responses with no disease rebound. Our market research indicates that this profile represents a substantial improvement for patients with atopic dermatitis. We are excited that recent data further enhances soquelitinib’s profile and potential. It demonstrated one of the strongest EASI 75 results after just 8 weeks of treatment, and the lasting responses without disease rebound may open new avenues for treating immune diseases, including intermittent therapy with soquelitinib. If the current profile continues to hold up in larger clinical trials, we believe soquelitinib will be strategically positioned among the top options for treating moderate-to-severe atopic dermatitis. I will now discuss key highlights from our latest data announcement. First, regarding efficacy, in cohort 4—a randomized placebo-controlled trial over an 8-week treatment period—the mean percent reduction in EASI was 72% compared to 40% for placebo, which was statistically significant at 0.035. Seventy-five percent of patients, or 9 of 12, achieved EASI 75, with one additional patient at EASI 74. Twenty-five percent of patients achieved EASI 90, and 33% recorded IGA 0/1, while 11 of 12 patients reached EASI 50. The only non-responder was a patient who did not respond to prior treatments with Dupixent and Rinvoq. Among EASI 90 patients, two had previously been unresponsive to systemic therapies. Meanwhile, 20% of placebo patients reached EASI 75, or 17% if we include two patients who missed the day 56 evaluation and never reached EASI 75 later on. Additionally, two individuals in the placebo group needed rescue medication due to disease flares, unlike the active group. Of the two placebo patients who achieved EASI 75, both had not undergone prior systemic therapies; none of the seven placebo patients with previous systemic therapy managed to achieve EASI 75, while three out of five active patients with prior treatments did reach that benchmark. The results from cohort 4 corroborate our earlier hypotheses from cohorts 1 through 3, which suggested that extending treatment duration would enhance responses. The data confirm that soquelitinib outperformed placebo across all efficacy endpoints evaluated. Furthermore, in comparison to other agents, we believe the results obtained so far position soquelitinib among the most active agents, whether oral or injectable, approved or in development for atopic dermatitis. Second, in terms of durability, beginning with cohort 3, we adopted a more structured approach to measuring remission duration with a longer blinded post-treatment follow-up of 90 days, compared to the 30 days tracked for cohorts 1 and 2. The data from cohort 3 demonstrate that responses observed at day 28, the final day of treatment, were either maintained or slightly improved at 118 days or 90 days without therapy. This stands in contrast to other systemic therapies for atopic dermatitis, which typically exhibit a rapid disease rebound starting just one week after stopping treatment. No rebound was observed with soquelitinib in cohorts 3 and 4. We believe the induction of T regulatory cells by soquelitinib may account for this durable inflammation suppression and sustained disease remission. This finding aligns with our preclinical experiments and biomarker data indicating an increase in circulating Tregs in cohort 3 patients. The presence of circulating Tregs is noteworthy, as these cells are usually very rare in blood. They likely migrate and concentrate in disease sites, as shown in our animal models. Thirdly, our findings indicate broad applicability. Thirty-five percent of all patients in the Phase I trial had experienced prior systemic therapies, with 50% in cohort 4. The most common prior treatment was Dupilumab, followed by JAK inhibitors, and some patients had undergone multiple previous therapies. This included individuals who were resistant to their last systemic therapy. Typically, treatment-resistant patients who have been through multiple therapies are more difficult to treat, and this was validated by analyzing the placebo patients in the trial. The response curve data revealed that placebo patients with previous systemic therapies fared worse than those without prior therapies, indicating that previous treatment is a disadvantage. However, the response curves for patients taking soquelitinib were quite similar across these groups, suggesting that soquelitinib’s efficacy is not influenced by prior systemic therapy experiences. Our baseline patient characteristics also indicate that those treated under our protocol were less favorable than those in most atopic dermatitis clinical trials. In patients who received previous systemic therapies, EASI 75 was 0% for placebo patients (0 out of 7) compared to 60% (3 of 5) for those receiving soquelitinib. Therefore, we conclude that soquelitinib is effective in patients who have undergone prior systemic therapies, with results comparable to treatment-naive patients, despite these prior patients having more severe disease. Responses were noted in patients unresponsive to their initial systemic therapy, supporting our hypothesis about the novel mechanism of action for soquelitinib and the absence of resistance stemming from prior therapy experiences. Fourth, regarding safety, no new safety concerns were observed in cohort 4 following the extended 8-week treatment duration. In both cohort 4 and the entire Phase I trial, the reported adverse events were similar between the placebo and treatment groups, with no significant lab abnormalities detected. No hepatic issues or changes in liver function tests were reported, and infections were consistent across treated and placebo patients, mostly minor. I'd like to address some investor inquiries regarding the risk of EBV viral reactivation. These concerns stem primarily from rare literature reports about EBV infections in infants born with germline mutations in ITK. In neonates, the immune system is not fully developed, as T and B cells have not yet matured. Immune system development occurs over time through exposure to antigens. Germline mutations in ITK in a developing immune system differ greatly from the temporary inhibition of the ITK kinase domain using a small molecule drug in mature immune systems. To date, we have seen no serious infections in more than 150 patients treated with soquelitinib across our lymphoma, atopic dermatitis, and ALPS trials, totaling over 14,000 patient days of treatment, with some individuals on therapy for more than two years. In the PTCL study, most participants had detectable EBV and other viruses like CMV prior to therapy. In our Phase I lymphoma study, we found over 30 patients with detectable EBV in their blood before starting treatment. None of these patients or any others showed signs of EBV reactivation or related illnesses during treatment, which in some cases extended for over two years, despite the fact these patients were highly immunocompromised. Additionally, it's worth noting that ITK inhibition preserves Th1 cells, which are critical for eliminating viruses. Beyond clinical results, biomarkers supporting the unique action mechanism of ITK inhibition leading to immune rebalancing have been identified, with some being novel discoveries. In summary, the data indicates a decrease in IL-4, IL-5, and IL-17 cytokines, a slight reduction in TARC, a reduction in Th2 cells, and an increase in Tregs. Ongoing research is also uncovering noteworthy changes in JAK/STAT signaling pathways that will be shared in future reports. With the emerging information from both our clinical trials and biomarker analysis, especially regarding Treg induction, we believe soquelitinib's novel mechanism and safety profile will allow its application in a variety of immune inflammatory diseases and cancers. Our soquelitinib abstract has been accepted for an oral presentation at the Society for Investigative Dermatology Annual Meeting, scheduled for mid-May, where we will share Phase I clinical data, including safety and durability results and new biomarker findings suggesting innovative strategies for managing immune diseases. Unfortunately, our late-breaker abstract was not selected for the AAD presentation, which generally favors trials in later stages. Angel Pharmaceuticals, our partner in China, is enrolling in a Phase Ib/II trial in atopic dermatitis, a blinded placebo-controlled study assessing a 12-week treatment regimen for 48 patients with various soquelitinib dosages. The patient eligibility criteria and endpoints align with those established by Corvus. Depending on the results from the Phase I portion of the study, an additional 60 to 90 patients will be included in the Phase II component. This trial is being conducted at leading centers in China, which have extensive experience in executing similar studies, and is in close collaboration with the Corvus team. We expect initial cohort results to be available later this year. Moving on to our recently initiated Phase II randomized placebo-controlled trial in atopic dermatitis, this study aims to enroll 200 patients with moderate to severe disease, who will be random to one of four cohorts, each with 50 patients. We will include individuals who have previously been treated with systemic therapies. We will explore dosing of 200 milligrams QD, 200 milligrams BID, and 400 milligrams QD alongside a placebo group. The treatment period will last 12 weeks, followed by a 90-day off-treatment follow-up. The primary endpoint is the median percent reduction in EASI at 12 weeks, in line with standard Phase II study endpoints for atopic dermatitis. Other endpoints will include EASI 75, EASI 90, IGA, PP-NRS, and additional measures. This study will be conducted internationally, with data anticipated by mid-2027. Additionally, we continue to enroll patients in our Phase III registration trial for PTCL, with an interim analysis planned for later this year. Recently, we held a scheduled meeting with our independent Data Safety Monitoring Board, which reported no safety concerns, allowing the study to proceed as planned. In December, we presented final data from our Phase I/Ib clinical trial evaluating soquelitinib for T-cell lymphoma at the ASH Annual Meeting. The findings support our ongoing Phase III program, showing that patients in the 200-milligram BID cohort, the same dose being analyzed in Phase III, experienced a median progression-free survival of 6.2 months and a median overall survival of 28 months, which is favorable when compared to other treatments. For instance, median survivals with chemotherapy are under 1 year, while PFSs are less than 3.5 months. The ASH data also highlight soquelitinib's immunobiological effects and its mechanism of affecting T cell differentiation through ITK inhibition. These findings indicate potential for soquelitinib in atopic dermatitis and a wider spectrum of immune and inflammatory diseases. We're also gathering exciting data from our ALPS clinical trial, with three patients on therapy for almost a year now. We aim to submit data for potential presentation at the ASH meeting in December, in collaboration with the NIAID team. Looking ahead to upcoming clinical trials, we plan to initiate a Phase II trial of soquelitinib for hidradenitis suppurativa and asthma later this year. There exists a strong scientific basis for assessing soquelitinib in HS, as it is an IL-17-driven disease. In both in vitro and in vivo models, soquelitinib has proven to be an effective inhibitor of Th17 cells, reducing IL-17 production. Our trial design for HS is advancing, with plans to enroll around 60 patients with moderate to severe HS in three arms: 200 milligrams BID, 400 milligrams QD, and placebo, over a treatment duration of 12 weeks. Primary endpoints will focus on safety and efficacy, measured by HiSCR 50 and HiSCR 75. The asthma study design is also developing, likely involving approximately 150 patients treated for three months. In conclusion, our confidence in the long-term potential of soquelitinib for atopic dermatitis, peripheral T-cell lymphoma, and a wide array of additional inflammatory diseases continues to strengthen. We are just beginning to uncover the full scope of ITK inhibition and immunomodulation, which could lead to innovative and improved therapies for inflammatory, autoimmune, fibrotic diseases, and cancers. We are building strong momentum with soquelitinib and our ITK platform, and we look forward to keeping you updated on our progress throughout the upcoming year. Now, I will turn the call over to the operator for the questions-and-answer period.

Operator, Operator

And your first question comes from Roger Song from Jefferies.

Jiale Song, Analyst

Congrats for all the progress you have made. Richard, maybe just one question related to the read-through from the data readout you will have before the Phase II, the global atopic dermatitis data mid next year. So you will have a PTCL potentially data and then also the China 12-week study data. So how should we think about the read-through 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?

Richard Miller, CEO

We expect that Angel Pharmaceuticals will provide data from their initial cohorts of a placebo-randomized trial later this year, focusing on doses of 100 milligrams BID and 200 milligrams QD over a 12-week treatment period. This will be important as we've only tested up to 8 weeks. Once the data is unblinded, we can share the results, and the study will then proceed to evaluate doses of 200 milligrams BID and 400 milligrams QD, with results anticipated around mid-2027. In total, Angel will be conducting a Phase II study on approximately 130 to 140 patients, which will conclude by early to mid-2027. We will have some preliminary data by late this year and further insights in the first half of 2027. Additionally, the PTCL trial is set for an interim formal review later this year, which will include futility and safety analyses, with complete results expected in late 2027. I also mentioned that we have ongoing independent safety reviews for the Phase III PTCL trial, the most recent of which indicated positive results.

Operator, Operator

And your next question comes from Li Watsek from Cantor.

Li Wang Watsek, Analyst

Two from us. Maybe just first on the data that you're going to present at the SID meeting in May. Rich, you talked about biomarker and durability data before. Can you just maybe set expectations for us?

Richard Miller, CEO

Yes. Well, I can set expectations. The durability continues to look great. And in terms of biomarkers, the things I've mentioned previously, but we have discovered some new biomarkers, which is going to be probably the main part of the SID presentation, fascinating work around the T regulatory cells and some of the JAK-STAT signaling. And 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 17, et cetera. So plus we'll update the clinical data with the durability and a few other things.

Li Wang Watsek, Analyst

And then sorry, my second question is on the Phase II trial in HS. Just wondering what the benchmark that you're looking at, especially relative to the approved agents like IL-17 in the space, do you think in terms of efficacy you have to match the biologics?

Richard Miller, CEO

Well, first of all, we have to find the optimum dose, which we're going to look at a couple of different doses. But 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.

Operator, Operator

And your next question comes from Graig Suvannavejh from Mizuho.

Graig Suvannavejh, Analyst

Richard, congratulations on the impressive progress we’re witnessing with soquelitinib across various indications. I wanted to address a few points. First, regarding your upcoming data presentations, you mentioned that you applied for a late-breaking abstract to AAD. You provided some insight into why your abstract may not have been accepted, but I noticed that Kymera does have a late-breaking abstract. I’m not very familiar with their data set since I don’t cover it, so it’s not at the forefront of my mind. I’m curious if they might have a larger database, and I’d like to hear any thoughts you have on that.

Richard Miller, CEO

Well, Graig, what gets accepted abstracts that get accepted or even publications that get accepted? This is a capricious process, and there are a lot of factors. I don't know why they accept some and not others. I personally am shocked that Kymera has no placebo and an interesting study for sure. But I don't have an explanation for it.

Graig Suvannavejh, Analyst

There may not be a good one. I just thought I'd speculate...

Richard Miller, CEO

I wouldn't worry too much about that. I've had some really good papers accepted by certain journals while being rejected by others. Ultimately, it's just a few individuals reviewing some abstracts. I used to do it myself, and you end up with a few hundred to go through and decide what seems promising. So, I don’t think it's worth focusing too much on any specific reasons for that. We're not particularly active in AAD. We've never participated there, we don't have booths, and we don't subscribe to their journals. I think that could be another factor, but I'm not certain. Regardless, SID is a great meeting. Scientifically, it's even more rigorous and is the primary event for early-stage and translational biology and research. So, I believe we’re in a very good position.

Graig Suvannavejh, Analyst

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 the 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?

Richard Miller, CEO

So that Phase II trial is placebo-controlled, randomized, and blinded. No, we will not see that data until it's completed. And 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. So there will be a news flow from that in terms of the AD stuff.

Operator, Operator

Okay. And 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 and just wondering then how do you handicap success in HS when perhaps there are not very well established or good predictive models in HS?

Richard Miller, CEO

You are correct; there are not good animal models for hidradenitis suppurativa, but studies in humans clearly indicate that IL-17 is crucial. Th17 and IL-17 are very significant, and in fact, IL-17s have been approved for treatment. This suggests that blocking IL-17 should be effective, and we do block IL-17 along with many other cytokines. Hidradenitis suppurativa involves various inflammatory cells, including T cells, neutrophils, and B cells. The advantage of soquelitinib is that by blocking multiple cytokine pathways, it impacts various cell lineages. This is important because, when examining disease sites, even in atopic dermatitis, one can observe a variety of cells rather than just Th2 cells. Therefore, a strong explanation for this phenomenon is that anti-IL-17 is effective in that condition. We enhance this effect even further.

Operator, Operator

And your next question comes from Jeff Jones from Oppenheimer.

Jeffrey Jones, Analyst

Since we've covered HS extensively, could you discuss AD and how your approach differs given this is a different disease and indication compared to dermatological conditions? What are your thoughts on dosing and your overall strategy?

Richard Miller, CEO

I think you mean asthma probably.

Jeffrey Jones, Analyst

Asthma, I'm sorry.

Richard Miller, CEO

Yes, you mentioned atopic dermatitis. As you know, atopic dermatitis and asthma often occur together, and treatments that are effective for one tend to be effective for the other. They appear to be part of the same atopic syndromes. We have multiple animal models for this condition, and our drug performs exceptionally well in those asthma models. Soquelitinib shows great results. Regarding dosing, I believe we will use the same dosing regimens that we have previously discussed. The studies for atopic dermatitis and peripheral T-cell lymphoma provide insights for the asthma study. The dosing for the asthma study will be largely identical, and there is no reason to modify that.

Jeffrey Jones, Analyst

Okay. And then one...

Richard Miller, CEO

Sorry, just to elaborate, we have the best biomarker in the world, which we've been using for years. You can administer the drug, extract the T cells from the patient, either from the blood or the disease sites, and measure the drug in the target accurately. It is a clean quantitative assay. It inhibits the function of that enzyme. That's a biomarker. We know that when you administer a 200-milligram dose, it nearly completely blocks that. Sorry, Jeff.

Jeffrey Jones, Analyst

I appreciate that, Richard. Regarding the ALPS trial you're conducting with the NIH, can you comment on how the outcome of that might influence your thinking about other indications or inform your current strategies?

Richard Miller, CEO

ALPS is a condition characterized by an excessive autoimmune response to various stimuli. Patients have antibodies against red blood cells, white blood cells, platelets, and other elements, along with abnormal lymphocyte activity. We've observed fascinating results in our patients. What we're learning in this context is reminiscent of our findings in lymphoma: the drug is highly active, safe, and it modifies the predicted signaling pathways. However, I'm hesitant to conclude that success in ALPS would guarantee similar results in lupus, even though the equivalent mouse model for ALPS does serve as a reference for systemic lupus erythematosus. Our focus is on understanding that we are addressing abnormal auto-inflammatory processes in a condition that currently lacks effective treatments. Essentially, it acts as a model—albeit a human one—for an orphan disease with no established therapies. Approval for ALPS is feasible, as it primarily affects children, although we've been treating adults. We plan to expand the number of treatment sites and to include younger patients within the next year. Discussions with the NIH are ongoing in this regard. This represents another indication within the realm of autoimmune diseases.

Operator, Operator

And your next question comes from Aydin Huseynov from Ladenburg.

Aydin Huseynov, Analyst

Richard, congratulations for the tremendous progress so far this quarter in your pipeline in the drug soquelitinib. I got a couple of questions. So first, I wanted to ask about the near-term focus 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? What types of PTCL you're actually enrolling? Is it NIS? Is it ALCL, follicular cutaneous? And what the physicians are using a standard of care prefer belinostat and pralatrexate? Just curious to hear the overall dynamic of the trial.

Richard Miller, CEO

The trial is currently enrolling participants and proceeding as planned. Patients are being randomized to receive either soquelitinib monotherapy at a dosage of 200 milligrams twice daily or the investigator's choice between belinostat and pralatrexate. It's worth noting that belinostat and pralatrexate gained conditional and accelerated approval around 15 years ago based on their response rates in patients with relapsed peripheral T-cell lymphoma (PTCL). Based on our discussions with the FDA, these agents were chosen as the logical control arm for comparison with soquelitinib. The trial is not blinded because, in cancer trials, it's typically not done, and it's particularly challenging in this case since soquelitinib is an oral medication while belinostat and pralatrexate are administered intravenously and come with the usual side effects associated with chemotherapy, such as mucositis and blood count issues. So far, the enrollment is going well, and the initial safety monitoring board found no new safety signals related to soquelitinib. Clearly, it appears to be much safer than chemotherapy, which is a significant advantage. The patient types included in the trial are aligned with the protocol; the most common is PTCL not otherwise specified (NOS), and we are accepting anaplastic lymphomas that are ALK positive. Another significant group involved is termed T follicular helper, previously known as angioimmunoblastic lymphoma. We opted not to include cutaneous T-cell lymphoma (CTCL) since it tends to be more chronic and is treated differently. These are typical cases for peripheral T-cell lymphomas. It’s important to emphasize that there is currently no fully approved treatment for relapsed PTCL, with the median progression-free survival (PFS) for belinostat being 1.7 months, pralatrexate at 3 months, and overall survivals being under a year for these patients, indicating a very serious condition. We are very pleased with the trial's progress and believe it has the potential to represent a significant breakthrough in hematology if we complete the trial and achieve the expected results.

Aydin Huseynov, Analyst

Appreciate that. I got another one for asthma, if you don't mind.

Richard Miller, CEO

Sure.

Aydin Huseynov, Analyst

So yes, so regarding the upcoming trial design in asthma, do you plan to have a cohort with patients who may have both asthma and atopic dermatitis? And in your opinion, is there any accelerated path with small pivotal trial with patients with 2 diseases simultaneously? So essentially, that would allow soquelitinib to cure 2 diseases at the same time. And as we know, Dupixent is the only drug that treats both diseases, but maybe you can have it in one shot.

Richard Miller, CEO

It would be ideal, but obtaining two indications is quite challenging. Anecdotal information exists, but it's difficult to determine how many patients will have both conditions at once, their severity, the measurements required, and the statistical power needed for each disease. Conducting a separate trial is necessary, similar to how Dupixent had separate trials for its indications. We are particularly interested in the durability of response, which we believe we can explain quite well based on immunologic principles. Additionally, we are intrigued by the response in patients who have not responded to previous therapies; this has been a point of discussion. In our Phase II atopic dermatitis study, we are including patients who have previously failed treatments. Many investors have suggested that we conduct a separate study focused on these resistant patients, and that's something we're considering. Such a trial could be smaller since we might see a greater difference in outcomes due to the poor performance of placebos. However, we are currently enrolling both naive and experienced patients in our Phase II study, which we plan to continue into Phase III to ensure a comprehensive patient population. As more treatments are introduced for atopic dermatitis, the number of treatment-experienced patients is rising, while the number of treatment-naive patients is likely decreasing. Therefore, this resistant patient population is becoming increasingly appealing. There are many aspects of soquelitinib that excite us; it's oral and safe, but its durability of response may significantly change our approach to the disease. It opens up the possibility for frontline therapy, addressing relapsed cases, multiple therapies, and intermittent treatments. This reflects our overall perspective on the issue.

Xun Lee, Analyst

To touch upon the durability a bit more. I think in the previous Phase I study, you guys followed the patients for up to 3 months. How long are you following these patients in Phase II? And is the study powering any way to really make a differentiation on the durability of this response?

Richard Miller, CEO

So the Phase II trial has built in continued blinding of the trial out to 90 days beyond the therapy. So 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 sort of atypical. Now I think that in the future, this issue of how durable the responses are is something that you might study separately. But I think it stands to reason. I mean, we'll talk more about this, but we have over 90% of our patients don't relapse and 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, dupi, STAT6, 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 a shorter treatment duration. Disease goes away, you don't need to take your drug again for a long time, if at all, hopefully, but that's asking a lot. So the durability is important because it's important to understand why it's happening and does it pertain to other inflammatory diseases? In other words, how broad is that going to be? Is that unique to atopic dermatitis? Or is that something that you could think about for other autoimmune diseases? And that's why we're excited about that. But 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 12 weeks.

Sean Lee, Analyst

For the second question about the asthma study, will the upcoming study focus on eosinophilic asthma with the Th2 high subtype, or will it also target the more challenging Th17 driven population?

Richard Miller, CEO

We're discussing various options right now, and we are inclined to include everyone. I'm glad you brought that up because there's a misconception that we only treat Th2 disease. I’m not sure where that idea comes from. Some people assume that we're only selecting Th2 patients with atopic dermatitis. First of all, I don’t even know how to do that. We're not doing that. Our atopic dermatitis patients are typical patients from U.S. centers. They must meet the necessary eligibility criteria, but we haven’t specifically targeted any patient population. Most of our atopic dermatitis patients do not have eosinophilia; their eosinophil counts are normal or low. Therefore, I don’t think we will limit it to high eosinophil asthma. However, I should mention that the asthma study protocol has not been finalized and is still under discussion. Alright. 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.

Operator, Operator

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.