Good morning, everyone, and welcome back to Oppenheimer's 35th Annual Healthcare Conference. I am delighted to welcome Corvus Pharmaceuticals and Chief Business Officer Jeff Arcara. Jeff, in the interest of time, I will let you take it away to talk about the Corvus story. Okay, thank you, Jeff, for the invitation to present today at the Oppenheimer Healthcare Conference. My name is Jeff Arcara. I'm Chief Business Officer for Corvus Pharmaceuticals, and we'll spend today providing an overview of the company, as well as reviewing where we are with the development of our pipeline, and specifically our lead program, Soquelitinib. So on the screen is our safe harbor and forward-looking statement, which can be found and reviewed on our presentation deck at the Corvus website. So who is Corvus? What do we do? And most importantly, what do we do differently? So Corvus is a clinical stage company developing first-in-class immune modulators with broad opportunity in cancer and immune diseases. Our lead program is Soquelitinib, which is currently in a phase III registrational trial in peripheral T- cell lymphoma, as well as a phase I trial in atopic dermatitis. We're excited about the opportunity for Soquelitinib as a novel oral and convenient therapy that so far has a very attractive safety and tolerability profile and experience in over 100 patients. On the right-hand side of the screen, you can see we have a strong IP position with an issued composition of patent through November 2037, and that doesn't include any pharmaceutical extensions, and we're also developing next-generation ITK inhibitors that will allow us to expand and leverage our ITK pipeline in a platform opportunity to other diseases and indications, so looking a little deeper at our pipeline, as I mentioned, our phase III registrational trial in lymphoma is ongoing, and data expected by mid-year 2026. We'll also be starting a solid tumor study specifically in renal cell carcinoma in Q2 of this year, with data expected also in the first half of 2026. The atopic dermatitis trial is ongoing. This is a prospective randomized placebo-controlled trial with full data readout in Q2 of 2025. And finally, we're about to start a collaboration with NIAID, which is the National Institute of Allergy and Infectious Diseases, studying a rare disease called ALPS, which is autoimmune lymphoproliferative syndrome, which is basically a very, very bad autoimmune disease that affects adults and children. And that study is actually being run and funded by NIAID. So the Corvus team has always been interested in the intersection between lymphoma and immune diseases, as lymphomas are essentially cancers of the immune system. And what you can learn in lymphoma can actually be applied to autoimmune disease. As an example, rituximab, which was developed by the Corvus team, was approved quickly for lymphomas and then went on to receive approval in autoimmune diseases like rheumatoid arthritis and other diseases. Ibrutinib is another example, also worked on by the Corvus team, which is a BTK inhibitor. It also started in lymphoma, is now being studied in numerous autoimmune diseases. And so we think the same could be true for Soquelitinib, but here we focus on T- cells, T- cell lymphoma, and T- cell diseases of the immune system. So how does Soquelitinib and target ITK inhibition work? So this is precision medicine where Soquelitinib selectively inhibits ITK. ITK stands for interleukin-2 inducible T- cell kinase, which is involved in T- cell receptor signaling, as you can see in the cartoon. Genetic studies have shown that if you precisely knock out the ITK gene and nothing else, that you inhibit Th2 and Th17 cells and the resulting cytokines that come from those cells. Those are well-known cytokines, as you can see on the bottom right-hand side of the slide, IL-4, IL-5, IL-9, IL-13, IL-17. Many of them are involved in autoimmune, inflammatory, fibrotic, and allergic diseases. With that, we still permit the differentiation and skewing of Th1 cells. So the Th1 cells can help fight cancer as well as fight and reject off virally infected cells. It is important to note that you only want to block ITK and not inhibit RLK, which has never really been done before Corvus. You don't want to inhibit RLK, which stands for resting lymphocyte kinase, because if you do, you can actually cause T- cell dysfunction. So the story and the science has gotten a little interesting over the last few months. A few different laboratories have now shown that if you block ITK, you not only get Th1 skewing, but you also get a shift from pro-inflammatory Th17 cells into Treg cells. And why is that important? Because possibly that could be the holy grail of autoimmune therapy, right? If you could potentially induce a lasting remissive effect on autoimmune diseases by inducing these Treg suppressor cells. So what makes Corvus and Soquelitinib so unique? Really, it's our chemistry, which is focused on covalency and ITK selectivity. We try to create highly differentiated and unique drug properties. This data was published last month in Drug Discovery. And as you can see in the table in the center of the slide, as well as in the chemokine tree on the very right-hand side, we are very specific for ITK, and we spare other kinases such as RLK or BTK. This is not only important for efficacy, but it's important for safety. And why do I say that? So first, we have a target in ITK that's very restricted to the tissue distribution, found only in Tregs and NK cells. Second, we have a drug that's very specific to that target, so off-target cross-reactivity is minimized. And third, we have a drug with rapid clearance, so it's eliminated pretty quickly from the body like in a day. So speaking of an unmet need for new and effective therapies, we are in phase III for relapsed and refractory T-cell lymphoma. You can see on the left-hand side, T-cell lymphoma is a very difficult cancer with a very low five-year survival rate. There are no fully FDA-approved treatments for relapsed PTCL, which is why the NCCN guidelines actually recommend going into a clinical trial in patients that relapsed. The current standard of care doesn't work that well. Most patients will get chemotherapy and respond to chemotherapy, but then relapse. Then once a patient relapses, you have a very low six-month survival rate, as you can see on that curve on the right-hand side. Based on that unmet need, we were very encouraged by our phase I data results where we're seeing durable and complete responses. From our phase I data set, we've demonstrated an ORR of approximately 40% with progression-free survival of greater than six months. That's versus approximately one and a half to three and a half months with belinostat or pralatrexate. Of the 23 patients that were treated monotherapy with our dose of 200 milligrams b.i.d., we had nine out of 23 responders by Lugano criteria, which is that 40% ORR. Of those nine patients, we actually had six with complete responses, which is rare in this disease. Many of these CRs are lasting for two years. Based on these results, we met with FDA and came to an agreement on a phase III registrational trial. The study is in 150 patients in five subtypes, which you can see on the left-hand side of the screen. These subtypes make up about 70%-80% of PTCL patients. To be eligible, you'll have to have failed no more than three prior therapies. Patients are randomized on a one-to-one to either Soquelitinib 200 milligrams b.i.d. or standard of care agents, which is physician's choice between belinostat and Pralotrexate, which are basically chemotherapy drugs. PFS is the primary endpoint, including multiple secondary endpoints such as overall survival and duration of response. So speaking of duration of response, here is a patient from our phase I study. She was diagnosed with PTCL NOS, and as you can see on that photo there, she has a football-sized tumor on the side of her abdomen. She failed four prior therapies, started Soquelitinib, and had a very quick response by day 15, and a complete response, a CR, for over two years now on Soquelitinib. And actually, when she came off therapy, that tumor actually came back. So in addition to looking at tumor response, we can also look at tissue samples in these patients. And we can see mechanistically the potential application for ITK in both cancer and immunology. At the top left, you can see an increase in Th1 cells. This is in blood. And you can also see a reduction in Th17 cells. You can see the same in the upper right-hand corner where you see a reduction in IL-5, which is, of course, a Th2 cytokine, as well as you can see a reduction in eosinophils, and we've gone here from 17,000 down to 1,000, which is a pretty significant reduction. Here's another example of a patient with cutaneous T- cell lymphoma. This lymphoma originates in the skin. It's Th2-driven and actually has similar immune characteristics as atopic dermatitis. As you can see, she had extensive disease, extensive plaque that responded well to Soquelitinib therapy. She was a PR at nine months, or excuse me, at nine weeks, and actually continues to slowly improve while she's on therapy, and she's coming up on two years of therapy on Soquelitinib. Oftentimes, physicians believe and misdiagnose CTCL as atopic dermatitis. They get treated for atopic dermatitis, except with this disease, of course, it gets worse and can eventually kill you. And we do see responses in this disease. So coming back to the mechanism of action specifically for immune diseases, again, a key difference versus standard of care agents is that we work upstream. So Soquelitinib blocks Th2 and Th17, which produce these multiple cytokines, versus standard of care, which are blocking one or two cytokines at the receptor level. So what does that mean? Essentially, we have potential then for broad application and opportunity in multiple immune diseases, Th2 diseases like atopic dermatitis and asthma, IL-17-driven diseases like psoriasis, IL-5-driven diseases or allergic diseases driven by eosinophilic inflammation, and fibrotic diseases, which are primarily Th2-driven, such as scleroderma, which is systemic sclerosis, pulmonary fibrosis, and also inflammatory bowel disease. With all these diseases, why did we start in atopic dermatitis? First, we follow the science. AD, of course, is a Th2-driven disease. Second, there's a significant market opportunity and a high unmet need for a novel oral and safe and effective AD treatment. There's not a lot of novel oral treatments actually in the pipeline. There are approximately 30 million patients diagnosed with AD in the G7. That market is projected to grow from $12 billion-$27 billion by 2030. In the target patients, you see about 40%-50% of moderate to severe disease. That's about three million target patients, of which right now only about 10% are treated with advanced therapy. We see a significant commercial opportunity and upside. So with that, we are conducting a prospective randomized double-blind placebo-controlled trial, a phase I trial in moderate to severe atopic dermatitis patients. The plan is to enroll on the left-hand side. You can see 64 patients. These patients will have failed at least one prior topical or systemic therapy. There are four cohorts. They're sequentially enrolled. Each cohort is 16 subjects on a three-to-one ratio, active to placebo. So we'll have 12 active and four placebos. The primary endpoint, as you can see on the right-hand side, is safety. But we are treating patients for 28 days. And we actually have follow-up with patients that are off drug for 30 days. The efficacy endpoints are the EASI scores and the IgA. In regards to dose, so the cohorts are 100 milligrams b.i.d., and then we go to 200 milligrams q.d. That's the same total daily dose, but given at one time, so you get higher peak concentrations. We finished enrolling those cohorts one and two, and we're now enrolling cohort three. Cohorts three and four. This is the first time that we're actually going up in dose. We'll go to 200 milligrams b.i.d., which is currently our oncology dose. Then cohort four, we'll go to 400 milligrams q.d. How do we come up with these doses? The lower cohort doses, one and two, those will give you about 50%-80% occupancy of the target based on our work we've done in lymphoma. Cohorts three and four should give you about 100% occupancy of the target. Now, we don't know if we need 100% occupancy to be effective, but that's the experience from our oncology dosing. The reasons we're testing these different doses is that we know we have a covalent drug. And with a covalent drug, since it binds, it irreversibly sticks to that target. So we have information, as others do, that the Cmax, the maximum concentration may be more important than steady state. But that's what we'll see when we see the results from cohort three and cohort four. So these are the patient characteristics from cohort one and cohort two. As of the data cutoff, we have 24 treated with Soquelitinib and eight on placebo. We had very small numbers of placebos by design and a three-to-one ratio. We wanted to get more data on the active therapy. The patient characteristics in cohort one and two are basically the same, so we combined them for this slide. These patients are fairly standard for what you see these days in these trials. A couple of things to point out. We have a higher proportion of African Americans, as we mentioned back in December. African Americans can have underappreciated and potentially worse disease, so it can make treatment a little more difficult. As you can see in the center of the slide, the baseline EASI score is 19.9 versus 17.8, a little bit better for the placebo, which may potentially work against us. EASI scores have come down over the past decade with greater access to treatment, better treatments. I think Jonathan Silverberg actually published a paper about this on lower EASI score trends over time. Regarding prior therapies, none of the patients on the active Soquelitinib arm were on concomitant topical steroids. They were off, I think, at least three or four weeks before they had, since they had their last dose of steroid. One in the placebo patient did have concomitant corticosteroids, and none of the patients in this study so far have had any breakthrough medications, so this data is from cohort one, and we showed this last month. This is the four and eight-week data. First, looking at the EASI mean reduction percentage, that top row there, the placebo was 27%. The active was 55%. That's approximately a 30% difference, and again, this is at four-week dosing. If you look to the right of that, the eight-week dose, the data changes a little. The placebo EASI change was 19% at day 58, and the active was 69%. That's about a 50-point difference, which is a pretty significant difference. Now, looking at EASI 75, 90, and IgA 0 and 1, we saw no response in placebos. Just to make the point, these are the regulatory approval endpoints, so the bar is much higher. You're less likely to see a placebo response in these endpoints. As you can see, we had zero placebo response in those endpoints versus active. Now, if we look at this updated data that we have from cohorts one and cohorts two, again, focusing on the regulatory endpoints of IgA 0 and 1 and EASI 75, we have seven actives and three placebos from cohort two that have been through 28 days of data as of the cutoff, which was January 5th of 2025. We've had, again, no placebo responses in these endpoints. Typically, when you see these larger trials, you might see a response rate of 10%-15% in these endpoints. We haven't seen any response so far in this data set. Again, we're still looking at the data. Again, from cohort one, we saw around 25% in both the IgA 0 and 1 and EASI 75. If you look in the center of the slide, you can see cohort two, 200 milligram q.d. dose. We saw 29% in IgA 0, 1, and 50% EASI 75 in the Soquelitinib. Then when you combine them, you can see on the right-hand side, cohorts one and two together. We see a response rate of about 26% and 37%. Again, this is at 28 days of treatment. In addition to efficacy, what does the safety look like? So far, we have a very safe and well-tolerated drug. In the Soquelitinib arm, we've had three subjects with AEs. We had a nausea that was reported in one patient, and that, I think, was just with the morning dose. We had a COVID patient on day 27, and we had a grade 1 headache on day 57. As a reminder, they weren't even on Soquelitinib at that time. They were off drug. We had one AE in the placebo, which was a grade 1 upper respiratory tract infection. Overall, our safety continues to look really good. Again, when you're comparing to other agents, and again, this comes back to our novel mechanism of blocking upstream Th2 and Th17, you can see on this slide, we block a number of cytokines from Th2 and Th17, but we also have an increase in Treg and may have an impact on ILC2s, which we haven't discussed today. You can compare that to the current treatments on the market, like Dupixent and Ebglyss and Nemo. And so what this means, again, is that we think we have application in a broad number of immune diseases that we could potentially treat with Soquelitinib and ITK inhibition. So in summary, with these results so far, we have an oral administration with a novel OA. We've seen really good safety so far in both lymphoma and AD patients. We have pretty good efficacy. We have preliminary efficacy so far from cohorts one and two that looks pretty encouraging. And we see a difference from placebo in IgA 0, 1 and EASI 75. And we have durable responses and, again, potential for application in broad indications. And of course, dose optimization continues. So we're starting cohort three, as I mentioned, now in terms of dosing. So what are our couple of milestones that we'll be looking at in 2025? So from an atopic dermatitis standpoint, again, we have the full data readout coming up in next quarter, Q2 2025. I also mentioned that we have two studies that we'll be starting up. We'll have the ALPS study, which will start in a phase II trial next month, as well as we'll initiate a solid tumor trial. That trial initially is going to be in RCC, renal cell carcinoma. And then finally, in the second half of 2025, we'll start initiating our phase II trial for atopic dermatitis and then looking at a second indication. So we are already planning the phase II AD trial with Soquelitinib. So with that, I'll stop there. And thank you for your time to allow me to present today and your interest in Corvus. Thank you very much, Jeff. Looks like we've got a few minutes for questions. So I guess one that's come in over the lines is for Soquelitinib, as you think about PTCL, how do you think about moving that from relapse refractory to frontline? And what might that take? Yeah. Yeah. I mean, it's a good question. It's a logical question to ask. I think we just talked about in the slides, there's a significant unmet need in this disease. Most patients who get chemotherapy will fail. So we already have our investigators talking to us about frontline. We've already been looking at designing that study. One of the positives that we have is that we have an oral, so far, a very safe drug. So it can be easily combined with frontline treatments. And it's got the profile of what you'd want for a maintenance drug, right? It's an oral product, safe and well-tolerated. So it's a logical extension to go from relapse refractory up to frontline therapy with Soquelitinib. Okay. And And I guess staying on the oncology side, and as you mentioned, you're doing renal as your first solid, as your next study in solid tumors. What's your sort of process for selecting your next oncology indications? Yeah. So as you mentioned, we are studying or starting our RCC trial next quarter. Our process is probably what you'd expect. Number one, we start with the science, where we think the drug, the target, and mechanism will work. Then we look at the current unmet need, which means we'll look at the current standard of care and how well it works and what the unmet need is there. And then, of course, we'll look at our target product profile and see what it looks like and where we could help in those diseases. And this goes the same for oncology diseases or immunology diseases. Does that make sense? Yep. And I guess shifting over to AD, as you think about where you guys sit currently, reporting out this quarter some of the data on additional cohorts. You're in cohort three now. I guess Richard has talked a little bit about anticipating cohort three, that 200 mg b.i.d. being your likely target dose for the next clinical study. Is that being driven by target occupancy or something else? Yeah. I think that's right. We've been able to learn from our lymphoma studies and look at the target occupancy. And just as a reminder, and I think Richard covered this in previous presentations, cohorts one and two at that 200 milligram dose will get anywhere from a 50%-80% occupancy level. Going up in cohorts three and four, this is, again, our oncology dose. We see occupancy level up to 100%. So we don't know, again, if we need 100% for treatment for atopic dermatitis, but that is potentially one of the rationales for looking at those higher doses. Okay, and a question coming in in the atopic derm space and thinking about, as you and I were talking a little bit before we started, Soquelitinib versus some of these next-generation ITK molecules that you guys have. How are you thinking about those next-generation programs? Would these be how rapidly do you advance them? Do you think about those for some of these other immunological indications that you were referencing? Yeah. So for Soquelitinib, we're pushing forward in both oncology and immunology. As I mentioned, we are now designing a trial, a phase II trial for atopic dermatitis with Soquelitinib. First of all, hopefully, we're showing positive response in both oncology and immunology, which is a good thing. In atopic dermatitis, as we talked about, there's a very high unmet need for a novel oral safe drug. So with that, we are going to go forward with Soquelitinib and continue to go forward in both oncology and immunology. We're designing the phase II trial right now for Soquelitinib in AD. The next-generation ITK inhibitors, they're about 12 to 15 months from the clinic, and we can look at those, of course, for other immune diseases, as you mentioned. And then it's been interesting, well, step back. The AD, obviously a really competitive space, dominated by Dupy. How are you thinking about where Soquelitinib would fit here and how it's differentiated? Yeah. Yeah. So as you mentioned, it is a competitive space. Dupy does dominate atopic dermatitis. But I think a couple of things. When you look at the pipeline, there aren't a lot of novel oral drugs in development for atopic dermatitis. And if you just look at the parallels between psoriasis market and AD, you see that the psoriasis market grew incredibly, and there's now eight blockbuster drugs that are used in psoriasis. So I think there's plenty of room for novel agents. But specifically, when you have a novel oral agent, I think we'll be positioned very well in terms of the opportunity for Soquelitinib. I think we are up on time. So Jeff, thank you very much for presenting the Corvus story. Have a great rest of the day with your one-on-ones, and look forward to hearing more. Thank you.