Good morning, everyone. My name is Yatin Suneja. Welcome to Google and I'm Second Annual Healthcare Innovation Conference. Our first presenting company here with us is Corvus. From the company, we have the Chief Business Officer, Jeffrey Arcara. Jeff, why don't you maybe make some opening comment? Just tell us a little bit about Corvus, what are some of the upcoming catalysts that we should be focusing on, and then we'll go into this next 15 minutes Q&A session. Sure, sure. First, thanks for hosting us. I appreciate the opportunity to tell the story. Corvus, we're a clinical stage company. We are focused on developing first-in-class immune modulators for the treatment of cancer and immune disease. Our lead program is soquelitinib. That is a novel oral targeted therapy that selectively inhibits ITK. ITK stands for interleukin-2-inducible T-cell kinase. It's involved in T-cell receptor signaling. We are actually in a phase III registrational trial for peripheral T-cell lymphoma, in addition to a phase Ib trial and soon-to-be phase II trial in moderate to severe atopic dermatitis. Our programs are backed up with strong IP. We have issued composition of matter patents out through 2037, and that does not include any pharmaceutical extensions. The FDA can give you, I think, up to five years of additional exclusivity for time and development. ITK is a platform technology for Corvus, so we have a number of backups and next-generation inhibitors in development. Got it. Very good. Very helpful. I think the company has generated some data in atopic dermatitis. That was a phase I data, 28-day worth of data. There is a lot of focus from investors there, more on the atopic dermatitis side than on the PTCL side. Could you just put in perspective what exactly you have generated across the three cohorts where you've tested the molecule? Yeah, yeah. First, maybe the rationale might make sense if we can talk about ITK and AD. First of all, we follow the science, right? AD is a Th2-driven disease. We block Th2 and Th17 in the respective cytokines, so think IL-4, IL-17, similar or same as Dupixent. In addition, because we work upstream, we inhibit the pathways. We actually block a broader set of cytokines, so think IL-17, which is relevant for AD, as well as other INI diseases. In addition, and this is important, ITK has very limited tissue distribution. It is only found on T cells and NK cells. We are very specific for ITK. With that, we expect limited off-target effects and hopefully a good safety profile. In AD, it is very important to have a good safety profile. Physicians actually choose their therapies based on the safety. In terms of your question about what have we learned so far in terms of the 28-day data, I think what we've seen so far and what it's suggested is that we have a safe drug, we have an active drug, and we have a drug potentially with a prolonged effect. In terms of safety, we see very similar, if not the same, as placebo in terms of safety profile. In terms of efficacy, when you look at the first three cohorts, we actually show a statistical separation from placebo at 28 days at 0.036. In terms of durability of effect, after we stopped treatment at 28 days and we followed them out to day 56, we actually saw the curves continue to stay separated. We're wondering if we have a remissive effect. That is something we're looking at in clinical trials now. Does that make sense? Got it. Yeah, very helpful. Since you touched on the mechanism, are there any key biomarkers that you think are either relative to the mechanism or to the disease that you or the company talks about? Yeah. So I think a couple of things. In terms of, I mentioned a remissive effect or a durable effect, we've actually seen that we increased Tregs in our AD patients in our clinical trials. In terms of Th2 and Th17, we've shown a decrease in IL-5, a decrease in IL-17, IL-31, which of course is involved in itch, as well as TSLP. Keep in mind, this is all in serum. We have not done skin biopsies yet. It's something we plan to do, at least in a subset of patients in our phase II trial. There are a number of cytokines like IL-4, for example, that actually are very almost undetectable in serum, and they have very fast turnover. That's just some of the limitations that we have. Got it. Got it. Very helpful. Going back on the data, again, the data are very, very intriguing, the 28 data that you have generated. Can you just talk about the onset, like why we are seeing the effect in such a short duration of time? If you can then just go into the cohort four, because I think last week on the earnings call, you mentioned that the data most likely going to come in January. How are those cohorts? How are they differentiated from the first three cohorts and the dosing? Yeah, yeah. The onset is actually similar to what you see in the other drugs, other competitive drugs in the market. I do think the cohort four, as you bring up, is the current stage of our current program that we're in. Maybe just to base that, our current program is a prospective randomized placebo-controlled trial, and we're studying four cohorts. The first three cohorts we just talked about. The fourth cohort is the same dose as cohort three, so it's 200 mg b.i.d. What we're looking at is we're looking at two months or 56 days of efficacy. The reason for that is that when you look at the kinetics of our curves and you look at the slopes of our curves, at 28 days, those curves are still pointing down. Our thinking is that if we continue to treat longer, that we could pick up some incremental efficacy. Does that make sense? Yeah, yeah. In terms of how are you benchmarking against other AD data, what exactly in this cohort four you would like to see, or how does the success look like? Yeah, yeah. In terms of benchmarking, as I mentioned, we are competitive in terms of our current cohort three data with the existing therapies that are on the market and even the therapies that are in development. When you look at our cohort three data, for example, when you look at placebo-adjusted EASI-75, we're actually similar to the JAKs. When you look at placebo-adjusted IGA 0/1, we're similar to Dupixent. Your question is, what does success look like? We've talked to a number of the top KOLs. We've done primary market research. We've done TPP market research looking at different efficacy levels. What we've seen is that if we just reproduce the existing data that we have from cohort three, so Dupixent-like level of efficacy, we'll have a significant drug. Got it. So basically, DUPI is the benchmark. And the duration of cohort four? It's two months? It's 56 days for efficacy, and then we have a 30-day follow-up. When you announce the data, would you just give us the 56-day or two-month cutoff, or will you have maybe three months for all these patients so that we can see durability? Yeah, we'll see how much we have. As Richard just mentioned on the last call, we finished enrollment in the study. Of course, based on that last patient in, we'll have to follow that patient out for the two months plus the 30 days. We'll have, of course, all the efficacy data, and I'm sure we'll at least have a subset of some of that longer-term safety data. Yeah. Could you talk a little bit about the placebo or just the clinical study execution, especially in atopic dermatitis and some of these diseases, atopic diseases? You do have very high placebo responses. In your first study, in the first three cohorts, the placebo response was very low. How should we think about placebo performance in the cohort four? What are your expectations and what you have done to sort of manage that? Yeah. So I think when you look at cohorts one and three or one through three, excuse me, as you mentioned, we did not have much of a placebo response. I think that is part of it because we are only looking at 28 days. I think if we treat longer, you will start to see a placebo response. Of course, in cohort four, we are treating longer. We will see what we learn in terms of placebo response. When you look historically at Dupixent, Rinvoq, lebrikizumab, nemolizumab, and you look at their clinical studies, they typically have a placebo response in the 10%-15% range. That is something that we will also take into consideration for our phase II trial. Got it. And that's for EASI-75? Correct. Yeah. OK. And then. Just easy reduction. Just EASI reduction, yeah. Percentage EASI. OK. And then you are going into a, I think that's also as an announcement, right? You're moving into phase II. Just talk about what type of study, how you're thinking about the design, and then the fact that you announced that you're going to go into phase II sort of gives at least some people comfort that you might be seeing something in the phase I that is helping you to move forward. Yeah. Richard, I think, talked a little bit about the phase II design on the earnings call. It'll be a global study in North America and Europe, 70 sites, 200 patients, four arms. We have three active arms and one placebo. We are going to study a low-dose arm again. We have a 200 milligram QD dose. Part of that was actually when you looked at the cohort three data, when you looked at those lower-dose arms, they were continuing to slope downward. Part of our question is, could the lower dose still be effective if we just studied it in a longer treatment effect? We have the low-dose arm. We'll have the 200 milligram b.i.d., which is our current dose. We have the 400 milligram QD, and then we'll have placebo. That'll be a 12-week study, and the primary endpoint is EASI reduction. Easy reduction. In cohort four, sorry, I'm jumping back and forth. Would you expect bio-experienced patients, and how are you thinking about enrolling bio-experienced in the phase II study? Yeah. So what I can say is that we are going to stratify by prior systemic therapies. We can have up to, I believe, up to 40% of our patients can be bio-experienced. We'll have to see what the current data looks like in cohort four to see what we can learn in terms of their response rates. We are encouraged so far. We've had a number of patients that have failed Dupixent and have failed Rinvoq that have responded really well to soquelitinib, so similar to bio-naive patients. It seems like the consistency of the efficacy is there irrespective of the prior failures, right? So the drug effect. Yeah. OK. What will be the enrollment time frame for AD for the second study? Yeah. From the start of the study, it should be about 18 months till we report out data. OK. So most likely in 2027. OK. Can you put in perspective the commercial opportunity in AD? What is feedback that you are getting? Again, anything, at least for Th2 diseases, there is not much, or there is no oral option. So there is a lot of excitement around oral. So what are you hearing from physicians and what work you've done? Yeah. So in terms of the commercial opportunity, I mean, first, there's still a high unmet need for safe and effective therapies in AD. There's an even higher unmet need for orals, as you point out. Each 1% market share in AD is worth $1 billion. So you do not need a large market share to have a significant product. In terms of where the drug might be used, for example, positioning, again, we've talked to KOLs. We've done primary market research. The feedback is if we have a safe oral drug, they would like to use it first line. But whether it's used first line or second line or a combination of both, again, still a significant opportunity. Keep in mind, you're talking about 30 million patients, 3 million patients with moderate severe, and only about a 15% penetration rate with advanced therapies. So big market opportunity. Significant. Can you talk also about where else you are going with this asset? How is the biology in other areas? Yeah. We talked a little bit about this on the earnings call. We plan to do an asthma study and start that study in this year, 2026. Again, we'll follow the science. Asthma is a Th2-driven disease. We've shown in patients that we reduce IL-5 as well as eosinophils. Obviously, when you look at drugs, IL-5 drugs like Nucala and Fasenra, these are very successful drugs. You look at DUPI. DUPI is indicated for AD as well as asthma and COPD. It just makes a lot of sense for us to go there. In addition, about 25% of asthma patients or AD patients will have asthma, and that's about 40% in children. That is that atopic march. Again, that is a very large market. You're talking about 60 million patients, 10 million moderate severe. Again, if we have a novel safe oral drug, especially in that T2 moderate to severe patient population, it's a significant commercial opportunity. Got it. What would be the size and scope of the asthma study? That's being designed as we speak now. More to come there. OK. Do we know about the dosing? Do we need to go high on the dose, or are you getting sort of enough coverage at 400 dose? Yeah. Right now, we think it's similar or same doses that we have now. And keep in mind, we have data that we look at receptor occupancy. So we know that with the current dose, like 200 mg b.i.d., we are covering 80%-100% of the receptors. So the question is, how much do you really need to cover to see an effect? But right now, it could be the same dose, but we'll continue to look at that as we design the study. Got it. I'm going to go back to your biomarker comment. I think a couple of times you mentioned IL-5 that you were able to reduce and also some of the other biomarker. What about TARC? I think that's one biomarker that we and investors sort of focus on. Do you have any view on TARC? Is that a mechanism? Is that a biomarker that should be reduced with your mechanism? Yeah. We have seen a small trend in reduction in TARC when you look at our responding patients versus non-responding patients. Keep in mind, again, this is small numbers. It is also only 28 days. The question is, if you treat longer, will you see a greater response? Keep in mind, there has actually been some data with the JAKs that have actually shown that they have increased TARC and still have a response. With that, we will continue to look at TARC as well as the other biomarkers with the existing cohort four. As I mentioned, again, we are also going to do skin biopsies, at least in a subset of patients in our phase II trial. Got it. Got it. When you announce the data, will we get, even in January, are you planning to disclose data on biomarker and all these biopsy results? Yeah. We should continue to have additional data for you. It might be a little bit delayed. Part of the challenge is that you have to collect the serum and get the samples in. It takes sometimes a month or so to get all these biomarker analysis done. We will report out the data. The timing will be, we'll have to figure that out. Got it. So then I think if you can also put in perspective the commercial dynamic, I think there are other companies that are thinking of going into a similar mechanism with ITK inhibition. And you are also working, I think, on a next generation or a backup. Can you just talk about how are you differentiated or where the competition is and what you are trying to improve with the next generation asset? Yeah. So a couple of things. I think in terms of the competitive set, there are a number of programs in development. Most of them are injectables. There really are not a lot of novel oral products in development. Of course, you have got STAT6. You have got IRAK4. And there are a number of STAT6s. I think there are 12 of them now that are in development. As far as we know, there has been no real clinical data in terms of efficacy and safety with STAT6. IRAK4, I believe there was some data a few years ago, which I do not think was successful in terms of efficacy or biomarkers. Really, in terms of competition, there is not a lot of novel products in development. I think in terms of differentiation, of cours`e, first of all, our target, right? We have the potential to be the first in class selective ITK inhibitor in AD. We also talked about upstream pathways. Potentially, we'll work on a broader set of patients, potentially in the systemic failures. Of course, we're an oral tablet, so that's patient preferred, as well as you have good compliance. Keep in mind that we actually have demonstrated safety and efficacy in over 150 patients to date. We already know that we have an active drug. Finally, again, this prolonged durable effect with these Tregs, that's something that we'll continue to look at in our clinical trials. Got it. Very helpful. Then how big of a focus is the PTCL study? It's phase III, right? How is the company thinking between an oncology indication and a broader INI indication? Yeah. At this point, first of all, it's a good problem to have, right? We've got an active drug that works in oncology and immunology. We're seeing this more and more like with the BTK inhibitors. The target and mechanism just makes sense in terms of both cancer and immunology. We are in a phase III program. It is a registrational trial. I think at this point, we're going to push on all cylinders. We have the phase III program going. We have the phase II atopic dermatitis trial that will kick off. As you're pointing out, we actually have a number of next generation ITK inhibitors that are in development. They're about 12-15 months from the market. We'll look at pushing forward in all three levers, and we'll make some commercial assessments as we go forward and see what we learn. First, we have to show success in these trials first. Got it. Anything on the competitive front that we need to keep an eye on that might be reading out? I think also you also have a partnership with Angelini Pharma. I do not know if there is any readout from Angelini that we need to. Yeah. So I think in terms of Angel, so they're our partner in China. So Corvus owns 49% of Angel. Richard, our CEO, and Leif, our CFO, sit on the board. To your point, they're actually doing a phase II atopic dermatitis trial as well with soquelitinib. We'll get the benefit of learning from them. They're actually just starting that trial now. OK. What is the duration of that study? I think it's the same as our current trial, 12 weeks. 12 weeks. OK. Then maybe the final question, how is the balance sheet looking right now? Yeah. As of September 30, we have $65 million in cash. That gives us runway through Q4 of 2026. Very good. Jeff, I think that's all I had for you. Thank you. Thank you so much. We're looking forward to the data in January. Great. Thank you. Thank you. This presentation has now finished. Please check back shortly for the archive.