Corvus Pharmaceuticals - Earnings Call - Q4 2024

Executive Summary

• Q4 2024 GAAP net loss was $12.1M (vs. $6.7M YoY), with GAAP EPS of $(0.18); cash, cash equivalents and marketable securities ended at $52.0M, supporting runway into Q1 2026.
• On S&P Global consensus, “Primary EPS” actual was $(0.14)* vs. $(0.12)* estimated (slight miss), and revenue was immaterial/zero versus a $0 consensus estimate*, consistent with the company’s pre‑revenue stage.
• Pipeline execution advanced: AD Phase 1 Cohort 1–2 showed positive efficacy/safety; Cohort 3 nearing completion with data from Cohorts 1–3 planned in May 2025; ALPS Phase 2 initiated with NIAID; PTCL Phase 3 enrollment ongoing; solid tumor Phase 2 start guided to Q3 2025.
• Non‑cash fair value changes in warrant liability ($2.3M loss in Q4) and Angel Pharma equity method losses ($2.2M in Q4) impacted GAAP results; early warrant exercises in Q4 delivered $18.6M cash, with ~$41M additional potential if remaining warrants are exercised.

What Went Well and What Went Wrong

• What Went Well

  • Positive AD signal and clean safety at low doses: 26% IGA 0/1 and 37% EASI‑75 across Cohorts 1–2 at 28 days; no significant safety or lab abnormalities; no IGA 0/1 or EASI‑75 in placebo.
  • Management confidence on ITK mechanism breadth and durability across immune diseases and cancer; clear plan to present Cohorts 1–3 in May and full dataset in Q3 2025.
  • Liquidity strengthened: $52.0M year‑end cash and $18.6M from early warrant exercise; runway into Q1 2026 provides time for key 2025–2026 readouts.

• What Went Wrong

  • Slight EPS miss vs S&P consensus on “Primary EPS” (actual $(0.14)* vs $(0.12)*) despite GAAP EPS of $(0.18); non‑cash items (warrant fair value loss $2.3M; Angel equity loss $2.2M) weighed on results.
  • Some program timelines pushed: solid tumor Phase 2 now Q3 2025 (was early 2025); AD full dataset now guided to Q3 2025 (was 1H25).
  • R&D spending rose with soquelitinib trials (Q4 R&D $6.0M vs $4.0M YoY), increasing quarterly cash burn as programs scale.

Transcript

Speaker 2

Good afternoon, everyone. Thank you for standing by, and welcome to the Corvus Pharmaceuticals fourth quarter and full year 2024 business update and financial results conference call. At this time, all participants are in a 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 of Real Chemistry. Thank you. Please go ahead, sir.

Speaker 3

Thank you, Operator, and good afternoon, everyone. Thanks for joining us for the Corvus Pharmaceuticals' fourth quarter and full year 2024 business update and financial results conference call. On the call to discuss the results and business updates are Richard Miller, Chief Executive Officer; Leif 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, 2024, that was filed today, 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 Leif Lea. Leif?

Speaker 1

Thank you, Zack. Excuse me. I will begin with a quick overview of our fourth quarter and full year 2024 financials and then turn the call over to Richard for a business update. Research and development expenses in the fourth quarter of 2024 total $6 million, compared to $4 million for the same period in 2023. The $2 million increase was primarily due to an increase in soquelitinib clinical trial expenses. R&D expenses for the full year 2024 totaled $19.4 million, compared to $16.5 million for the full year 2023. For the full year 2024, the increase of approximately $2.9 million was primarily due to higher clinical trial costs associated with the development of soquelitinib. The net loss for the fourth quarter 2024 was $12.1 million, including a non-cash loss of $2.2 million related to Angel Pharmaceuticals, our partner in China.

In addition, we recorded a non-cash loss of $2.3 million from the change in fair value of Corvus' warrant liability during the fourth quarter of 2024. This compares to a net loss of $6.7 million for the same period in 2023, which included a $1.4 million non-cash loss related to Angel Pharmaceuticals. The net loss for the full year 2024 was $63.3 million, including a $3.2 million non-cash loss related to Angel and a non-cash loss of $33.4 million from the change in fair value of Corvus' warrant liability during the year. This compares to a, excuse me, this compares to a net loss of $27.0 million, including a $5.3 million non-cash loss related to Angel for the full year 2023.

Total stock compensation expense for the fourth quarter and full year 2024 was $0.8 million and $3 million, respectively, compared to $0.6 million and $2.1 million for the same periods in 2023. As of December 31, 2024, Corvus had cash, cash equivalents, and marketable securities totaling $52 million, as compared to $27.1 million at December 31, 2023. Of note, associated with our financing in May 2024, we also sold common stock warrants that have an exercise price of $3.50 and expire on June 30, 2025. Two investors early exercised their warrants during the fourth quarter of 2024, resulting in $18.6 million in cash to the company. If all the remaining warrants are exercised, we will receive approximately $41 million in additional cash. Based on our current plans, we anticipate our cash provides runway into the first 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.

Speaker 0

Thanks, Leif, and good afternoon, everyone. Thank you for joining us today for our business update call. As we look into 2025, we remain optimistic on the potential for soquelitinib to provide a powerful new approach for the treatment of a broad range of immune diseases and cancer. Soquelitinib is well-positioned as a first-in-class oral therapy that selectively inhibits ITK to modulate and control parallel signaling pathways in the immune system. Our confidence is backed by a strong and growing body of evidence, both from our clinical efforts and preclinical research conducted by us and others. First, we have reported a 39% objective response rate from our phase one trial of soquelitinib in patients with relapsed T-cell lymphoma. This included a 26% complete response rate, which is more than double the rate seen with standard chemotherapies.

Based on this data, we are enrolling a registrational phase 3 trial of soquelitinib in patients with relapsed peripheral T-cell lymphoma, and we have gained a significant amount of experience that we are applying to our other soquelitinib programs. Second, we observed a favorable safety and efficacy profile from interim data from our phase 1 trial of soquelitinib in patients with moderate to severe atopic dermatitis. This includes significant responses in the soquelitinib treatment groups compared to placebo for the clinically significant endpoints of Investigator Global Assessment, or IGA-0/1, and Eczema Area and Severity Index, or EASI-75. Third, preclinical data supports the potential of ITK inhibition in a broad range of indications, including solid tumors, immune conditions such as autoimmune lymphoproliferative syndrome, or ALPS, systemic sclerosis, pulmonary fibrosis, and graft versus host disease, and inflammatory conditions such as asthma, psoriasis, and inflammatory bowel disease.

The data also highlights its mechanism of action, skewing differentiation to Th1 cells, reducing Th2 and Th17 cells and their downstream cytokines, and promoting a switch to T regulatory cells that suppress inflammation. Given the broad applicability of its mechanism of action, we view the potential of ITK inhibition as analogous to BTK inhibition, a category that members of the Corvus team, including myself, helped to develop. BTK inhibitors were first approved for B-cell malignancies and then expanded into autoimmune conditions. Today, I will recap our previously reported data in atopic dermatitis and next steps for the trial, share some detail on the recently initiated NIH trial in ALPS, and highlight the upcoming milestones for soquelitinib. In January, we reported interim data from the phase one trial of soquelitinib in patients with moderate to severe atopic dermatitis.

The trial includes four cohorts that are enrolling 16 subjects each at a three-to-one ratio of active to placebo, 12 active four placebo. The trial is double-blind, meaning the patient and the doctor do not know what they're taking. The active medicine and placebo are indistinguishable tablets. The company and the data review committee are not blinded. The treatment period is 28 days, and then we follow patients off therapy for another 30 days. The 28-day treatment period is relatively short compared to later-stage atopic dermatitis studies with other agents, which typically treat up to 16 weeks or longer. The primary endpoint is safety and tolerability. Secondary endpoints measure based on IGA and EASI scores, along with patient-reported measures of itch and biomarkers. The first two cohorts received soquelitinib doses of 100 milligrams twice a day and 200 milligrams once per day.

The same total dose of drug was used in the first two cohorts. Based on our lymphoma studies, we know that 100 milligrams will provide 50%-80% occupancy of the target, and 200 milligrams will provide about 80%-100% occupancy. In January, we reported data from 16 patients in cohort one and 10 patients in cohort two, for which 28 days of treatment had been completed. In total, from the combined cohort one and two, this included 19 patients treated with soquelitinib and seven patients treated with placebo. In the soquelitinib group, 26% achieved IGA-0/1, and 37% achieved EASI-75. Recall, these have been accepted as measures of clinical benefit and have been used as the basis for regulatory approval for several approved treatments for atopic dermatitis. In the placebo group, no patients achieved IGA-0/1 or EASI-75.

No significant safety issues were observed, and no clinically significant laboratory abnormalities were seen. Cohort three of the trial, which administers a dose of 200 milligrams twice a day, that is twice the total daily dose we used in the earlier cohorts, is nearing completion of enrollment, and some patients have already reached the 28-day follow-up period. The efficacy results so far in the trial, including full cohort one and two and the initial experience in cohort three, have been positive and consistent with what we have reported to date. No patients in the active treatment groups received concomitant topical steroids or required rescue medications. One patient in the placebo group did receive concomitant topical corticosteroids.

In cohorts one and two, two placebos experienced flares in their disease during the 28-day treatment period, whereas no disease flares were seen in the patients receiving active drug during the 28-day treatment period, as well as the follow-up period off treatment. Soquelitinib has been very safe to date as well, with no patients requiring interruption of therapy. We now have experience in over 100 patients with lymphoma and atopic dermatitis, representing more than 9,000 patient days of treatment, including patients with lymphoma on therapy for up to two years. We continue to believe that soquelitinib is an active medicine for atopic dermatitis, with several advantages: oral route of administration, attractive safety profile, a novel mechanism of action with an opportunity for unique positioning, including the potential to bridge between topical therapies and systemic injectables.

We plan to report data covering the first three cohorts at the Society for Investigative Dermatology meeting taking place May 7 to 10 in San Diego. Our abstract has already been accepted for an oral and poster presentation at this meeting. Outside of atopic dermatitis, we continue to enroll patients in our registrational phase three trial of soquelitinib in patients with relapsed PTCL. Recently, we presented updated data from our phase one trial at the T-cell lymphoma forum, with longer follow-up showing that the median progression-free survival is 6.2 months and the 18-month progression-free survival is 30%. The median duration of response was 17.2 months. PFS, or progression-free survival, is the primary endpoint of our phase three trial, which is comparing soquelitinib to either belinostat or pralatrexate, the standard of care agents, with reported median PFSs of about three months and 18-month PFSs of under 20%.

We also have recently announced the initiation of enrollment in a phase two trial of soquelitinib in patients with ALPS, autoimmune lymphoproliferative syndrome. This study not only addresses a disease with unmet need, but will also provide additional information on the activity of selective ITK inhibition in a serious autoimmune disease. ALPS patients are born with a genetic mutation in FAS signaling that results in lymphoproliferation and a myriad of autoimmune problems such as anemia, neutropenia, thrombocytopenia, and others. Some of these patients go on to also develop malignant lymphomas. The ALPS trial is being conducted under a clinical research and development agreement with the National Institute of Allergy and Infectious Diseases at NIH. It will enroll up to 30 patients aged 16 years or older with confirmed ALPS based on genetic testing.

There will be two dosing cohorts, 200 milligrams or 400 milligrams of soquelitinib twice per day for a period of up to 360 days. The primary endpoint of the trial is efficacy, determined by reductions in spleen and lymph node volumes as measured by CT scans. In addition, improvements in cytopenias, or lowered blood cell levels, will be assessed by complete blood counts. Improvements in cytopenias can improve quality of life and overall health and serve as a biomarker associated with ALPS disease activity, including autoantibody levels that are reactive with red cells, white cells, and/or platelets. Secondary endpoints include safety and tolerability. We are also planning a single-agent soquelitinib solid tumor trial in relapsed renal cell cancer, or RCC, representing a new approach to immunotherapy of this disease. We plan to initiate this trial during the third quarter of 2025.

Outside of soquelitinib, we also continue to advance our other clinical stage development programs. We have been one of the leaders in the development of adenosine A2A receptor antagonists for the treatment of cancer with ciforadenant. This includes our phase one B2 clinical trial that is being conducted in collaboration with the Kidney Cancer Research Consortium. The trial is evaluating ciforadenant, or ciforadenant, as a potential first-line therapy for metastatic renal cell cancer in combination with ipilimumab and nivolumab. The study has reached full enrollment of 60 patients at sites, including MD Anderson, Vanderbilt, Duke, and the University of Pennsylvania. The patients are being followed, and we anticipate our partners at the Kidney Cancer Research Consortium will present data from the trial sometime later in 2025. Finally, I should mention that we are advancing several second and third-generation ITK selective inhibitors designed to preferentially affect particular ITK signaling pathways.

Summarizing the outlook for the remainder of 2025, we remain focused on advancing the broad opportunity for soquelitinib, which has several potential upcoming catalysts. This includes, number one, additional data from the phase one trial in atopic dermatitis in May at the Society for Investigative Dermatology meeting. Number two, full data from the phase one trial in atopic dermatitis in the third quarter. Number three, initiating a phase two clinical trial with soquelitinib in solid tumors in the third quarter of 2025, with initial data anticipated in the first half of 2026. Number four, initiating a phase two atopic dermatitis trial in late 2025. Number five, continuing to activate sites and drive enrollment in the registrational phase three trial of soquelitinib in PTCL, driving towards interim data in late 2026.

Depending on enrollment trends, it's possible we could see initial data from the phase two ALPS study in late 2025 or early 2026. Our current cash gives us runway into the first quarter of 2026, allowing us to execute on these important milestones and further demonstrate the value of our programs, and in particular, the significant opportunity for ITK inhibition in immunology and cancer. We look forward to providing updates on our programs in the coming quarters. I will now turn the call over to the operator for a question and answer period. Operator. Thank you. Ladies and gentlemen, we will now begin the question and answer session. Should you have a question, please press star followed by the one on your telephone keypad. Should you wish to cancel your request, please press star followed by the two.

If you're using a speakerphone, please lift the handset before pressing any keys. One moment, please, for your first question. Thank you. Your first question comes from the line of Jeff Jones from Oppenheimer. Please go ahead. Good afternoon, guys, and thanks for taking the question. Lots of data updates to come, so really exciting time for you guys. I guess starting out on the AD front and the update in May, should we expect full data on cohort three as well as additional patients on cohort two? As you think about the efficacy hurdle there, what do you guys have in your head to move this ahead into the phase 2A that you just mentioned, or in just competitiveness in the field? Okay.

Jeff, the meeting in May, the Society of Investigative Dermatology, we intend to report the full dataset on cohort one, the full dataset on cohort two. We've already completed enrollment and follow-up in those two cohorts. Cohort three is almost completed enrollment. Twenty-eight-day follow-up is coming in on patients now. We're also going to have additional one-month follow-up beyond that. We will have the full data for cohort one, two, and three. I also expect to have biomarker data for those first three cohorts as well. Okay. Great. And then just in terms of the success hurdles and efficacy bar that you guys are looking at. First of all, we're pretty pleased with the efficacy we saw in cohort one and two. Let me remind you, that's 28 days of treatment.

We see what a 30% difference in some of these, 25-35% difference between placebo, which was zero in cohort one and two, and our actives. That's a pretty good number. That number sustained or improved would be very good, in our opinion. Of course, many people are asking about what would happen if we increase the duration of therapy. That's something that we're thinking about, and will come in time. We're pretty pleased with the efficacy results we have to date. In terms of a competitive landscape, of course, we're oral. We have a different mechanism of action. Safety looks really good so far. Convenience. The design of our study was really intended to determine whether or not selective inhibition of ITK had some role in immune disease. Is there some signal, some indication of efficacy in an autoimmune disease?

I think we've got that. Now, of course, as we think about phase two trials and beyond, we'll begin to think about what's required for registration, etc. I think from a competitive standpoint, to my knowledge, we're the only selective ITK inhibitor. I know there are some other companies that have ITK inhibitors and are talking about it now, but they're not selective, and we view that as critical in the biology. I think we're in pretty good shape on this. Great. Thanks, Richard. I'll hop back in queue. Thank you. Your next question comes from the line of Aydin Huseynov from Ladenburg Thalmann. Please go ahead. Hi. Good afternoon, everyone. Richard, congratulations with the progress this quarter. I've got a couple of questions here.

Regarding the potential cohort four, could you clarify your plans for cohort four, whether you still would like to enroll in 400 milligrams? If you could give us a general idea, what is the difference in terms of the doses? I mean, why would you like 400 milligram doses as compared to the oncology trial where your optimal dose is just 200 milligram? Thank you, Aydin. Good question. Just for the benefit of everyone else, cohort one was 100 milligrams b.i.d. Cohort two was same total dose, 200 milligrams once a day. Cohort three, 200 milligrams twice a day. Cohort four, as you indicate, would be 400 milligrams. That is same total dose one time. Before deciding whether we're going to do cohort four, that is the plan, but we want to look at the full dataset from cohort three.

We already have cohort one and two. We'll look at the data from cohort three, and then we'll decide whether we would do that or not. Right now, the plan is to do that, although we are thinking about other possibilities like extending duration of therapy. Each of the doses, 100, 200, 400, give very good occupancy of the receptor. Of course, as I've indicated in previous calls, we don't really know what it takes to get a clinical effect or biologic effect in atopic dermatitis, whether you really need 100% occupancy. Even at our starting dose of 100, there's pretty good occupancy. Right now, the plan is to do cohort four, but before we decide definitively on that, we want to look at our data. That makes sense. Regarding the prior therapies, I know that many of those patients previously failed Dupixent, first took cohorts.

How about the cohort three? Did you see the patients? Sorry, the Dupixent naive, sorry, the first cohort. Is the cohort three also sort of mostly Dupixent naive patients? We have deliberately searched for sicker patients in cohort three. We do have more Dupixent and systemic treatment failures in cohort three. We also have, so far, I mean, we're not done with the cohort. We do appear to have higher baseline EASI scores. We will have to look at that, and we will see how that turns out. Whether there is a particularly good effect in the Dupixent failures, we do not know yet. We do not really know how that variable fits in yet. Okay. Understood. The last one is the biomarker question. I think you mentioned that you will be talking about biomarkers in May. Could you elaborate a little bit on that?

What kind of biomarkers are out there for atopic dermatitis? I would say that some of the work that we presented back in January on biomarkers or in December is being confirmed in our ongoing studies. In addition, we've picked up a couple of other things that I think are quite interesting. I've been talking about, we've been talking and studying these T regulatory suppressor cells and other cells, and I think those are turning out to be extremely interesting. We continue to see a very durable effect of our treatment in patients who receive the drug. I mean, it's a small dataset. It's very early, but it's also very provocative at this point. Okay. Understood. Thanks so much. Thank you. Your next question comes from the line of Greg Subanave from Zero Securities. Please go ahead. Hi. This is Sam on for Greg.

Thanks for taking our questions. Maybe one on ALPS, just given that it's a new indication. Can you just tell us in terms of the addressable patient population that you guys are kind of due diligence and also if there's a subset of patients that would be ideal candidates for soquelitinib among people with ALPS? Thank you. Okay. ALPS, or autoimmune lymphoproliferative syndrome, is a genetic disease. You're born with it. I'll give you a little background on the disease. Babies are born with it. At around age two, they start to develop anemia and big spleens and lymphadenopathy infections, and they get a diagnosis made, of course. They're on lifelong immunosuppressive therapies, cyclophosphamide, steroids, mTOR inhibitors, things like that. They can be on that a long time. The disease is not curable. They'll have waxing and waning adenopathy and cytopenias, anemia, neutropenia, thrombocytopenia.

They can live 30, 40, 50 years old now, but they suffer a lot of the complications. They have massive splenomegaly as another problem they have which sometimes can rupture. A subset of these patients, maybe 10-20%, go on to develop malignant lymphomas. Usually, they're B-cell lymphomas. The abnormal cell in ALPS is a T-cell. It's an abnormal T-cell called a double negative T-cell that does not have CD8 or CD4. I won't go into the biology of it, but it has a lot of ITK expression. In our work looking at the effect of soquelitinib in various murine autoimmune models, we found that there's a strain of mouse called the MRL LPR negative negative mouse that has the very same mutation that you see in these patients. Same disease, basically, genetically.

When we treated animals with our drug, it was dramatically effective, really dramatically effective. Cytopenias go reverse and become normal. Splenomegaly, lymphadenopathy, all that thing. Basically, these animals become normal. That prompted us to say, "Hey, let's go treat the human identical genetic disease in humans." That led us to the NIAID that has a very big collection of these patients. Most pediatric hospitals have patients like this. You asked about the market. There are about 2,500 patients with this disease in the United States currently. They live a long time. They live to be aged 40, 50, as I said. Some die sooner, but that, in general, is their lifespan. I don't think there's any particular subset that would be, not to our knowledge now, that would be more or less amenable to this therapy. We just don't know.

Sometimes there are slightly different mutations in patients. The main problem in the mouse and in the human beings is that their cells, their lymphocytes, do not undergo apoptosis. Now, there is a very strong connection between T-cell receptor signaling and apoptosis. Think about it. When there is antigen or you have an infection, you want your T-cells to proliferate, kill off the infection, but then you want those T-cells to go away when the infection is eliminated. That requires apoptosis. That is regulated by ITK. ITK has many roles in various signaling pathways. When you block ITK, you restore apoptosis to these cells. That is the rationale for this. Basically, this is a treatment that I think you would take for a long time. Given the safety we have seen so far, we think this could be very important.

Now, also from a regulatory standpoint, this is not a disease, I do not think, where you are going to be asked to do big randomized clinical trials. That is something else to think about. We are very excited and interested in this disease. You can tell by my long-winded answer. Finally, what this does is, I mean, this is really an opportunity to look at the effect of our drug on all sorts of autoimmune manifestations: anti-red cell antibodies, anti-platelet antibodies, all that sort of stuff, which we think will have important relevance to other autoimmune diseases. Does that answer your question? Probably. Definitely. Very insightful. Thanks so much, Richard, for taking our question. Thank you. Your next question comes from the line of Roger Song from Jefferies. Please go ahead. Hi. This is Cha Cha Yang on for Roger.

I'm looking towards your phase two for AD, and I'm wondering if you can give some color on what subpopulations within the disease you're hoping to target. More specifically, if you could talk about aspects like prior medication use, baseline EASI scores, and then any geography and demographics insights, that would be great. That's a pretty tough question considering we haven't finished phase one yet, but moderate to severe atopic dermatitis, failed topical corticosteroids, or systemic therapy, very similar to the criteria we're using now. I don't know if I would require, I mean, baseline EASI scores to be moderate or 16 or greater. I don't think we would have any requirements beyond that. I think a typical study would be look at two different dose levels plus a placebo, so probably a three-arm study, maybe around 200 patients total.

That is kind of an approximate answer at this point. That is all pretty standard. Okay. Sounds good. The endpoint would be either EASI-75, those who achieve EASI-75, or IGA-0/1. That is a pretty standard endpoint now. Great. Thank you for that. Thank you. Your next question comes from the line of Lee Watsek from Cantor. Please go ahead. Hi, team. This is Daniel Bronder on for Lee. I have a question about the prioritizing of opportunities for soquelitinib in oncology versus inflammatory disease and how you look at it as you move into later stage trials. Okay. Right now, we have soquelitinib in a phase 3 registration trial that could produce data in less than two years. We are pushing on all fronts as aggressively as we can.

The strategy is try to get an approval in lymphoma, try to get an approval in an immune disease. Now, we are aware of some of the issues with having the same drug for autoimmune disease and cancer. We have a very aggressive program in second and third-generation compounds. We also think that the dosing and duration of therapy are going to be very different in oncology versus immunology. A very good example would be Rituxan, for example, which came out of my lab at IDEC. Rituxan is approved for lymphomas, as you know. It's also approved for rheumatoid arthritis, pemphigus, ITP, and probably a few more autoimmune diseases. There's really no issue with pricing because the treatment regimens are such that on a per-milligram basis, it turns out to be pretty similar.

Our strategy now is push forward on all these fronts and get deeper and deeper into the pipeline. At some point, of course, we recognize that autoimmune diseases is a vast undertaking. There are many different diseases and competitive areas. Of course, we would, at the right time, consider some sort of a collaboration or partnership. Okay. Cool. Thank you so much for that detailed answer. The other question we were wondering about is you alluded to earlier a little bit. The delay in the presentation of cohort four, is that more driven by your waiting and seeing of cohort three results, or has there been a delay in enrollment more generally? No delay in enrollment. We are waiting to see the data from cohort three, and we will make a decision about proceeding with cohort four or maybe expand one of the other cohorts. Okay. Cool.

Thank you so much. Thank you. Your next question comes from the line of Sean Lee from H.C. Wainwright. Please go ahead. Hi. Good afternoon, and thanks for taking my question. I just have one on the upcoming solid tumor study that's been planned. I was wondering whether there are specific indications that you feel are most suitable for soquelitinib, or would it be just a general basket study? Also, would you need to do a dose escalation again, or would you start with the PTCL dose? Thanks. The first part of the question, which tumors? I would start with the we will start with the immune-responsive tumors. What are those? Those are renal cell cancer. Lung cancer would be good. Those would be probably the top choices to start because you want tumors where you think there's some evidence for immunotherapeutic effects.

Melanoma might be another one, although that's a much less common disease and is somewhat adequately treated by other treatments. I would say renal, lung. I don't think we need to do a dose escalation, but certainly, you would want to do different doses. You'd want to look at different doses. It wouldn't be a dose escalation in the usual sense that you're thinking of like a phase one oncology study. You would probably want to look at different doses. We have a pretty good handle now on the dose, and we have a very good pharmacodynamic marker, which is we know what it takes to saturate the ITK target. 100, 200, 300, or 400, we're all in the same ballpark. They're all going to give you pretty much similar findings. Great. Thanks for that. Thank you.

If there are no further questions at this time, I would now hand the call back to Mr. Richard Miller for any closing remarks. Okay. I want to thank everyone for participating in the call, and we look forward to additional updates in the future. Thank you very much. Thank you. This concludes today's call. Thank you for participating. You may all disconnect.