Corvus Pharmaceuticals, Inc. Q4 FY2024 earnings call

• Financials: Q4 2024 R&D expenses $5.2M vs $3.2M in 2023; full year 2024 R&D $19.4M vs $16.5M in 2023. Q4 2024 net loss $12.1M vs $6.7M in 2023; full year 2024 net loss $63.3M vs $27.0M in 2023. Cash, cash equivalents, and marketable securities at 2024 end $52M vs $27.1M in 2023.
• Clinical progress: Socalitinib Phase 1 trial in relapsed T-cell lymphoma had 39% objective response rate. Phase 1 trial in atopic dermatitis showed favorable safety and efficacy. Preclinical data supports broad indications. Initiated Phase 2 trial in ALPS and planning solid tumor trial in RCC. Advancing adenosine A2A receptor antagonists with ciforadenant.

No distinct product segments with financial performance and revenue contribution discussed in detail.

• Anticipate cash runway into Q1 2026.
• Upcoming milestones: Data from AD Phase 1 in May, full AD Phase 1 data in Q3, initiate solid tumor trial in Q3 2025, initiate AD Phase 2 in late 2025, continue enrollment in PTCL Phase 3, potential data from ALPS Phase 2 in late 2025/early 2026.

Forward-looking statements subject to risks and uncertainties described in Corvus's annual report on Form 10-K for the year ended December 31, 2024, and other SEC filings.

Q: 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, will the what would should we expect full data on cohorts three as well as additional patients on cohort two? And then as you think about the efficacy hurdle there, what do you guys have in your head to move this ahead in the Phase 2a that you just mentioned? Or, you know, in just competitiveness in the field.

A: Okay. So 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 gonna have additional one-month follow-up beyond that. So we'll have the full data for cohort one, two, and three, I also expect to have biomarker data for those first three cohorts as well.

Q: Okay. Great. And then just in terms of the success hurdles and efficacy bar that you guys are looking at?

A: Well, first of all, we're pretty pleased with the efficacy we saw in cohort one and two. Let me remind you of you know, that's twenty-eight days of treatment. We see, what, a thirty percent difference in some of these twenty-five, thirty-five percent difference between placebo, which was zero in cohort one and two, and our actives, that's a pretty good number. And, you know, that number sustained or improved would be, you know, would be very good. In our opinion. Now, of course, many people are asking about what would happen if we increase the duration of therapy, and that's something that we're thinking about and will come in time. So 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 study, the design of our study was really intended to determine whether or not selective inhibition of ITK had some role in immune diseases. Is there some signal, some indication of efficacy in an autoimmune disease? And I think we've got that. Now, of course, as we think about Phase 2 trials and beyond, we'll begin to think about, you know, what it what's required for registration, etcetera. But 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. And so I think we're, you know, in pretty good shape on this.

Q: Hi. Good afternoon, everyone. Richard, congratulations with the progress this quarter. I got a couple of questions here. So regarding the potential cohort four, so could you clarify your plans for cohort four, whether you still would like to enroll in four hundred milligrams? And just if you could give us, like, a general idea what is the difference in terms of the doses. I mean, why would you why would you like four hundred milligram dose? As compared to the oncology trial where your optimal dose was just two hundred milligram.

A: Thank you, Aydin. Good question. So just for the benefit of everyone else, cohort one was a hundred milligrams, BID, cohort two was the same total dose, two hundred milligrams once a day. Cohort three, two hundred milligrams twice a day. And cohort four, as you indicate, would be four hundred milligrams at the same total dose, one time. So before deciding whether we're gonna do cohort four, that is the plan, but, you know, we wanna 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 the duration of treatment. You know, each of the doses, one hundred, two hundred, four hundred, is very good occupancy of the receptor. And of course, as I've indicated in previous calls, we don't really know what it takes to get a clinical effect or a biologic effect in atopic dermatitis, whether you really need a hundred percent occupancy. But even at our starting dose of one hundred, there's pretty good occupancy. So right now, the plan is to do cohort four. But before we decide, you know, definitively on that, we want to look at our data.

Q: Okay. Understood. And regarding the prior therapies, I know that many of those patients previously failed DUPIXENT. First two cohorts. How about the cohort three? Did you see the patients Sorry. Sorry. They're DUPIXENT naive, sorry, the first cohort. So is the cohort three also sort of mostly DUPIXENT naive patients?

A: We have deliberately searched for sicker patients in cohort three. So 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. So we'll have to look at that, and we'll see how, you know, how that turns out. Whether there's an, you know, whether there's a particularly good or effect in the DUPIXENT failures, we don't know yet. We don't really know how that variable fits in yet.

Q: Okay. Understood. And the last one, is the biomarker question. I think you mentioned that you will be talking about biomarkers in May. So could you elaborate a little bit on that? What kind of biomarkers are out there for atopic dermatitis?

A: Well, 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. You know, 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. And I mean, it's a small dataset. It's very early. But it's also very provocative at this point.

Q: Hi. This is Sam on for Graig. 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, like, the addressable patient population that you guys are kind of a due diligence and also, you know, what if there's a subset of patients that would be ideal candidates for socalitinib among people with ALPS? Thank you.

A: Okay. So in the United States, ALPS or ALTS, 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. They at around age two, they start to develop anemia and dysplains and lymphadenopathy. Infections, and they get a diagnosis made, of course. And then they're on lifelong, immunosuppressive therapies, chemo cyclophosphamide, steroids, mTOR inhibitors, things like that, and they can be on that a long time. The disease is not curable, and they'll have waxing and waning, adenopathy, and cytopenias, anemia, neutropenia, thrombocytopenia. Can live thirty, forty, fifty years old now. But they're, you know, they suffer a lot of the complications. They have massive splenomegaly. That's another problem they have, which sometimes can rupture. A subset of these patients, maybe ten, twenty percent go on to develop malignant lymphomas. Usually, they're B-cell lymphomas. But the abnormal cell in ALPS is a T-cell. It's an abnormal T-cell. Called the 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. And in our work looking at the effect of socalitinib in various murine autoimmune models, we found that the same there's a strain of mouse called the MRLLPR negative negative mouse that has the very same mutation that you see in these patients. Same disease, basically, genetically. And when we treated animals with our drug, it was dramatically effective. Really dramatically effective. Cytopenias go reverse and become normal, splenomegaly, lymphopenia, all that thing. Basically, these animals become normal. And so that prompted us to say hey. Let's go treat the human genetic, you know, identical genetic disease in humans. And that led us to the NIAID that has a very big collection of these patients. Now most pediatric hospitals have patients like this, and you asked about the market. There are about two thousand five hundred patients with this disease in the United States. Currently. They live a long time. They live to be age forty fifty, 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. So I just, you know, we just don't know. Sometimes there are slightly different mutations in patients. But the main problem in the mouse and in the human beings is that their cells, their lymphocytes do not undergo apoptosis. Now there's a very strong connection between T-cell receptor signaling and apoptosis. Think about it. When there's 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. And when you block ITK, you restore apoptosis to these cells. And so that's the rationale for this. So, basically, this is a treatment that I think you would take for a long time. And, you know, given the safety we've seen so far, I think this could be very important. Now, also from a regulatory standpoint, this is not a disease, I don't think, where you're gonna be asked to do big randomized clinical trials. So that's something else to think about. We're very excited and interested in this disease. You can tell by my long-winded answer. And then 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.

Q: 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 demographic insights, that would be great.

A: Well, 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. Don't know if I would require I mean, baseline EASI scores to be moderate are sixteen or greater. So I don't think we would have any requirements beyond that. You know, I think a typical study would be look at two different dose levels plus a placebo. So probably a three-arm study maybe around two hundred patients total. But, you know, that's an s you know, kind of an approximate answer at this point. But that's all pretty standard. Okay. Sounds good. And the endpoint would be either EASI 75 those who achieve EASI-seventy-five. Or IGA zero one. That's pretty standard endpoint now.

Q: Hi, team. This is Daniel Bronder on for Li. I have a question about the prioritizing of opportunities for socalitinib in oncology versus inflammatory disease and how you look at it as you move into later stage trials.

A: Okay. Well, right now, we have socalitinib in a phase three registration trial that could produce data in less than two years. And so we're pushing on all fronts as aggressively as we can. So the idea, the strategy is to try to get an approval in lymphoma. Try to get an approval or in an immune disease. Now we are aware of some of the issues with having a similar same drug for autoimmune and cancer. We have a very aggressive program in second and third-generation compounds. We also think that the dosing and duration of are gonna be very different in oncology versus immunology. A very good example would be Rituxan, for example, which came out of my lab at IDAC. Rituxan is approved for lymphomas, as you know. It's also approved for rheumatoid arthritis, pemphigus, ITP, and probably a few more autoimmune diseases. And there is not really no issue with pricing because the treatment regimens are such that on a per milligram basis, it turns out to be pretty similar. So our strategy now is to push forward on all these fronts and, you know, get deeper and deeper into the pipeline and, you know, at some point, of course, we recognize that autoimmune diseases is a vast undertaking. There's many different diseases and competitive areas, and of course, we would at the right time, consider some sort of a collaboration or partnership.

Q: 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 socalitinib or will it be just a general basket study? And also, would you need to do a dose escalation again, or would you start with the PTCL dose? Thanks.

A: So the first part of the question, which tumors? I would start with的 we will start with the immune responses tumors. So 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, you know, adequately somewhat adequately treated by other treatments. So I would say, you know, 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. But would probably want to look at different doses. But we have a pretty good handle now on, you know, the dose, and we have a very good pharmacodynamic marker, which is we know what it takes to saturate the ITK target. So, you know, one hundred, two hundred, three hundred, four hundred, we're all in the same ballpark. They're all gonna give you pretty much the same similar findings.