Corvus Pharmaceuticals, Inc. Q3 FY2025 earnings call

• Research and development expenses in Q3 2025 were $8.5M, up from $5.2M in 2024, driven by higher clinical trial, manufacturing, and personnel costs.
• Net loss in Q3 2025 was $10.2M vs $40.2M in 2024.
• Completed enrollment in extension Cohort 4 of Phase I trial for soquelitinib, expecting results in Jan 2026.
• Phase II atopic dermatitis trial to start early Q1 2026.
• ASH presentation on soquelitinib for T cell lymphomas, highlighting durable responses and immunology relevance.
• Appointed David Moore to Board of Directors in Oct 2025.

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 net loss for the third quarter of 2025 was $10.2 million, including a noncash loss of $300,000 related to Angel Pharmaceuticals. This compares to a net loss of $40.2 million for 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.

• Current cash expected to fund operations into Q4 2026.
• Plan to report 8-week data set from extension Cohort 4 in Jan 2026.
• Phase II atopic dermatitis trial to begin early Q1 2026.
• Upcoming ASH presentation for T cell lymphoma program.

• Forward-looking statements are subject to risks and uncertainties described in Corvus' quarterly report on Form 10-Q for the quarter ended September 30, 2025 and other SEC filings. The company undertakes no obligation to publicly update or revise any forward-looking statements except as required by law.

Q: Congrats on the progress in the quarter. 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.

A: 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.

Q: 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?

A: 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.

Q: 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?

A: 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.

Q: 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.

A: 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.

Q: 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?

A: 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?

Q: 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?

A: 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.

Q: 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.

A: 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.

Q: 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?

A: 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.