Okay. We'll continue with the next session. Thank you for joining us. I'm Paul Choi, and I cover the SmidCat biotech sector here at the firm. It's my pleasure to have Corvus Pharmaceuticals here for our next session. My immediate left here is Jeff, who is the CBO of Corvus. Maybe what we'll do is let Jeff kick it off with some high-level comments on sort of what are the company's priorities for the remainder of 2026 and going into 2027, and then we'll go
into questions after that. Sure, sure. Yeah, so maybe I can give a little bit of an overview of the company and talk about some of our competencies and priorities. So Corvus is a clinical stage company. We're developing novel immune therapies for the treatment of cancer and immune diseases. Socolitinib is our lead program. It's in a phase three registrational trial for peripheral T-cell lymphoma, which is a really tough cancer, as well as we're in a phase two trial for moderate to severe atopic dermatitis, and that's called the CR1 trial. And both of those trials are enrolling as we speak. You know, based on socolitinib's target and mechanism of action, we think it's got a pipeline and a product opportunity. So in the second half of this year, we'll be starting an asthma study, a phase two asthma study, as well as a proof of concept study in HS. Just of note, we have really good composition of matter protection on socolitinib. So we have protection through November of 37, and that doesn't include any pharmaceutical extensions, which could be an additional five years. And then ITK represents a platform technology for us. We have a number of next generation and backup compounds in development. So in terms of like our focus, I think like maybe three things I could think of is, you know, we're really good at developing novel science, ITK, which stands for interleukin-2 inducible T-cell kinase. It's involved in T-cell receptor signaling and differentiation. We're really good chemistry so we can make very targeted and selective drugs and that's important not only for efficacy but also for safety and we've gotten a very experienced management team that's done this before developing drugs like ibrutinib and rituxan bringing those to market does that make
sense yes it does um but maybe you know if we think about it this way an investor might look at your company and say wait you're developing the same drug for a blood cancer and also in the dermatology space, how does that work potentially? And, you know, what was the rationale, I guess, to, you know, go from a phase three program in a blood cancer into INI and more specifically atopic derm, excuse me. Can you walk us through, you know, what was sort of the background behind
that? Sure. So rationale for AD. So, you know, first of all, we follow the science. So essentially how Sokolet works is that we block Th2 and Th17 in their respective cytokines. So you think about when we block TH2, we block IL-4 and 13, just like Dupixin, which of course is approved for atopic dermatitis. In addition, we block TH17, so therefore we block IL-17, which is also involved in atopic dermatitis as well as other immune diseases. So the biology and the target made sense. In addition for atopic dermatitis, any new therapy safety is absolutely required because you're actually treating, you know, 18-year-olds with eczema. One thing is really interesting about ITK is ITK has very limited tissue distribution. It is only found on NK cells and T cells. And we have a drug targeted and selected for ITK, so therefore we think we'll have limited off-target effects. So I think, you know, that's important. And then finally, I think in terms of, you know, the current standard of care, we have an oral product, right? And so I think that's a big differentiation. Obviously, you've got Dupixent, you've got Lebry and Nemo, all injectable. So I think we have more patient-preferred with an oral product. Now, of course, there is Rinvoke, right, which is an oral tablet. But, you know, it does have the label, has the safety warning in the label, as well as it requires monitoring. So we're hoping to improve on that as well. So that's the rationale for AD.
You touched on this a little bit, but with respect to the AD landscape, it's very, very dense, very competitive, which I think is a fair assessment. But can you maybe talk about how socolitinib differs versus some of the other AD drugs that are either commercially approved or in clinical development? Then also on the oral side, there are some other oral programs that are out there on the JAK side and STAT6 programs. So maybe can you just walk us through the landscape there?
I mean, it is a crowded landscape, but it's going to be a huge market, right? It's a big market now, and it's projected to go to $30 billion and maybe even $50 billion by 2030 or 32. So significant opportunity. Now, there's a lot of drugs in development that are sub-Q. When you look at the pipeline for novel drugs, novel oral drugs, it's actually fairly limited. I mean, you've got us as an ITK inhibitor. Of course, there's STAT6 that you brought up. There's also IRAC4 that's in development. and I think Sanofi has a program there, but that actually, there's been some negative data in AD in the past. So I would say novel oral, not as competitive, but still competitive. So the question is, how would we differentiate from other orals? I think first, the target that we just talked about, so we could be potentially first in class, selective ITK inhibitor coming to market. I mentioned the limited tissue distribution. One thing, they tend to be expressed in a broader set of cells and tissues. So you can find them in the skin, in the lungs, in the GI tract, where again, we have this limited tissue distribution. So we think clinically that should support a good safety profile. You know, I think the other thing is unique about our mechanism of action is that we not only block cytokines, but we also believe that we're modulating or rebalancing the immune system. And what do I mean by that? So not only we block TH17 and the respective cytokines like IL-17, but we've actually shown to be able to shift or switch TH17 cells to become active Treg cells. So in some ways, we're kind of taking our foot off the gas and also strengthening the brakes at the same time. And I think that leads to a third point of potential differentiation. You know, based on working more upstream and this mechanism of action, we actually think we could work in a broader set of patients. And I think there's an example of that in our January data when we released. We had about, I think it was 35% of our patients were on a prior systemic therapy. And actually, we worked very good in those patients and even in patients that had failed prior systemic therapy. So I think we might be able to work in a broader set of AD patients and in a broader set of illnesses and indications as well. That's a number of characteristics of how we could differentiate.
Since you brought it up, maybe you can recap for us your recent data. You talked a little bit about the population. Roughly a third of them were patients who previously failed the systemic therapy. But can you maybe just compare and contrast how your recent data looks compared to the current standard of care and some of the existing therapies?
So we think we have pretty compelling clinical data. You know, when you look at EZ75 and IGA01, we're somewhere between a biologic and JAK level of efficacy. So EZ75 is actually comparable to a JAK placebo-adjusted and IGA01 comparable to a biologic. So we're pretty excited about what we've seen so far, and we hope that we can, you know, replicate that in our phase two trial, which is ongoing, the CR1 trial.
Great. Another aspect of the data that you presented was patient follow-up through 90 days off treatment. Can you maybe recapitulate that for us? This is something that's kind of not typically followed in AD development, and so can you maybe tell us what that data looked like and then just how do physicians and KOLs you've spoken with since you've released that data view this result?
Yeah, so it is interesting data to see this kind of follow-up post-stopping the drug. Maybe what I would say first is that, you know, our plan is to bring socolitinib to market as quickly as possible, and we'll do that through standard continuous dosing first. And so just like what J&J just did with Icotide, right, which was just approved for psoriasis, that's basically one pill once a day, and that's simple. So that's our plan. So we're going to follow the typical clinical development and regulatory path that's already been paid for us to bring the market to market quickly in AD. Now, to your point, in the Sierra One trial, we are going to follow patients longer term. So Sierra One trial is a 12-week study for efficacy for treatment, and then we'll have a 90-day follow-up off drug. So we'll see what that looks like. If we continue to see that durable effect, we'll continue to study it in future trials and likely it will be part of our life cycle management strategy. Does that make sense?
And then maybe physician feedback on the response or duration of response off treatment. What have doctors said about this?
Yeah, I mean, they're encouraged. I think just in general, you know, physicians are looking for more durable treatment and treatments with less treatment burden. But I will say efficacy is still number one as it is for any drug. So I think they're excited to see the ED75 response response and the IgA0 response, which is what we've shown just with continuous daily dosing, which is why we'll pursue that for the initial indication.
Based on your data to date, as you think about socolitinib and AD, is there a particular group or aspect or subgroup of the population or part of the population that you think make most sense for the target and the mechanism of action here?
Yeah. Yeah, it's a good question. Because we work more upstream, because we block TH2 and TH17, we block a broader set of cytokines. We actually think we're going to work on a broader set of patients. And I think that actually aligns us up for actually like a first line treatment, actually. And again, I mentioned that we've shown that we can work in, you know, patients that have actually failed a prior systemic therapy. You know, I think obviously, you know, in terms of making decisions about positioning and segmentation, it's really going to be driven by the target product profile. So we'll see what that looks like after the phase two and that can inform some of these, you know, commercial strategy decisions.
You did present 90-day off-treatment data for cohort three, but you decided in your most recent update not to present that for cohort four, excuse me. Can you walk us through the rationale behind that and just was it protocol driven or just was there anything else behind it?
Yeah, I think two things. I think, you know, first of all, you know, cohort four was meant to look at two months of efficacy, you know, dosing. And that was the purpose of cohort four. It actually wasn't to follow for off-treatment derailability. So just as a reminder, cohorts one through three were only four weeks of treatment. And when you looked at those curves, you actually saw the kinetics of those curves still pointing down. So we saw that, boy, if we kept treating, we might get deeper responses. So that was the purpose of Cohort 4, to see what a depth of response that we could get. And we absolutely did see that. And that was important because we needed to design the Phase 2 trial and start the Phase 2 trial. We want to move forward as quickly as possible. So that was the purpose of Cohort 4. In addition, we were already enrolling Cohort 4 before we actually saw the 90-day Cohort 3 data. So we would have actually had to amend the protocol. We would have had to go back to the RRB sites. It didn't really make sense from a standpoint, from a time and money standpoint. So we decided it was just best to move forward. The purpose of that trial was a proof-of-concept trial to support the moving into Phase 2. We felt like we accomplished that and wanted to move quickly.
Does that make sense?
Yes, it does.
You guys are working on prosecuting, developing the socolitinib here in the U.S., but you've also engaged with a partner for ex-US markets, specifically ANGEL in China.
You maybe remind us of
what is their clinical development plan, how does that trial look like compared to yours, and then when might we potentially see some data from your partner in China?
Sure. So ANGEL is our partner in China. They have the rights to socolitinib and are developing it there. Corvus owns 46% of ANGEL, as you know, and they are running a very similar program to your point. So they're running a phase 1B program that will lead into a phase 2B trial in atopic dermatitis. So they have two cohorts. Cohort 1 is low dose, and that's a QD versus BID. And then cohort 2 is a higher dose, QD versus BID. And then based on the results of those two cohorts, that will inform the dosing for the phase 2 portion. So by the end of the year, we should see cohort one, which that will give us 12 weeks of dosing, which we don't have yet, so that'll be interesting, as well as we'll be able to see what the effect is at the low dose for a QD. So that's what we'll have at the end
of the year from Angel. One of the big obsessions of Wall Street biotech investors is the difference in translatability of drugs in development in different geographic populations. Can you maybe just briefly recap for us how the treatment paradigm in China might differ, and also any other sort of clinical differences between the Chinese population and the U.S. or Western population?
Yeah, it's a good question, right? And I think that's one of the reasons we're starting with a lower-dose cohort, because we're studying in a Chinese population, so we want to be careful, right, and study it You know, one thing that's interesting that Richard talked about is actually there was a study that showed that Chinese patients actually have higher incidence of IL-17, TH17 and IL-17, for atopic dermatitis. So with the fact that we blocked both TH2 and TH17, it will be interesting to see what the effect is, you know, in this Asian population. But otherwise, all else is going to be the same in terms of enrollment criteria, easy score, endpoints, you know, easy score, primary endpoint is easy score reduction, secondary endpoints will be IGA01 and EZ75.
Maybe turning back to your program and your Phase 2 CR1 study, can you walk us through the trial design and just how you think about prosecuting that and what timelines might be both to enroll and potentially timelines to data.
So we're enrolling Sierra One now. It's a global study. We'll have about 70 plus sites in North America and Europe. It's a 200 patient study, and this is very similar to all the other programs like Labrie, Nemo, did a similar size study. So 200 patients.
We have four dosing arms.
So we have a placebo, and then we have a low-dose, again, QD, and then we have the two high doses, QID versus BID. And so it's a 12-week study, as I mentioned, and then we have the 90-day follow-up. And so we will look to read out that data in Q3 of 2027.
And just in terms of endpoints, any differences versus what you've done in your phase two? Or should investors also look towards EZ75 and IGA01?
Yeah, for the most part, it's the same endpoints. You know, EZ-75, IG-01, TPNRS, pretty much the same. I want to turn back to a moment towards efficacy
and thinking about sort of treatment options for patients who have been on prior therapies, and you presented efficacy there. Can you remind us in Sierra, too, you know, what portion of patients might be on, have been on prior therapies? and maybe starting there?
Yeah, so as I mentioned, in the Phase I trial, we had about 35% of patients on prior systemic therapies. In the Sierra I trial, the Phase II trial that's going on right now, we can have up to 40% patients on a prior systemic therapy. So we'll continue to look at that, and I think it's interesting. Of course, from a positioning standpoint and interest in the drug, being an oral drug, most physicians as well ourselves, we see this as a frontline drug, as a first-line drug, you know, prior to the injectable. But it's interesting to see this effect in, you know, prior systemic treated patients. So it gives you some optionality as well, you know, for future life cycle decisions. So, you know, again, we'll be able to see that data and look at that. We can have no more than 40% in the Sierra One trial.
So we don't really know what percentage of patients that we'll see. I want to double-click on that a little more because as you're, you know, running a trial with both frontline and treatment experience patients, this could have downstream implications to your point to how the drug is used, whether as you envision it as a frontline trial or as a drug for refractory patients. Does that also think about your pivotal trial development down the road? Would you similarly pursue a mixed population? I don't know. We'll have to see
in the phase two trial. Again, being a novel oral safe product. I think most physicians and ourselves see this as a frontline drug in front of the injectables. But I will say, you know, you have to also look out five to 10 years, right? And if in five or seven years, you have a biosimilar dupixent, and it's priced at $4,000 a year, you may have payers requiring you to step through some of these therapies. So if you do know you work in these, say, refractory patients or prior early treated patients, that's a benefit. But right now, I think if we're novel oral safe, we probably see it more positioned as a frontline
Does that make sense? Yes, it does. Maybe sticking on CR1 and your Phase 2 program, can you maybe lay out how you're thinking about the differences between your dosing arm, specifically your 200-mig BID versus your 400-mig QD dosing? Are you expecting daylight between the two to be similar than different? How do you think about it?
B versus BID. Maybe a couple of things, so first it's important to note that socolitinib is a covalent drug. So once we attach to the target, we stay on the target and this target of course is the ITK protein. The ITK protein has a half-life of 12 hours in terms of its turnover. So we'll stay on the target longer than the drug will stay in the plasma. As a reminder, cohort one and cohort two were the low doses but it was QD versus BID. And both those doses were effective. They separated from placebo, but remember, it was only a four-week study. So, you know, with a 12-week study, you know, we hope to see that the QD dose will be as effective, you know, as a treatment, because our target is to have a QD dose. And, you know, that doesn't include any sort of formulation options you have as well. I mean, actually, RINVOC is actually a long-acting formulation, but our target is to have a QD drug. So we hope to see that in the CR1 trial, actually, and in the ANGEL trial as well.
I want to turn for a moment to your oncology program because sometimes that gets overlooked. You're actually in Phase 3 already and relatively far along here. Can you remind us first what is the status of that study in PTCL?
So we're in a registrational Phase 3 trial for PTCL. That trial is enrolling 150 patients in about 40 centers, and enrollment is on track. the primary endpoint for that is PFS and that's versus current standard of care which is Blinistat or Prelotrexate at least in the United States and unfortunately they're not very effective drugs so there's a very, very high on that need in PTC so our plan for that is that by the end of the year we're looking to have a futility analysis so it's just essentially a go, no-go look at the data and that should be out by the end of the year and actually by the time we enroll for the futility analysis or have enough events for the futility analysis will probably have actually enrolled the entire study, so most likely we'll just finish up the study and then submit the package, because our goal is to have a full approval for the drug, where the current therapies,
they're under accelerated approval only. Can you just remind me if the futility analysis will be done on a blinded or unblinded basis, and if not, is there any statistical penalty from doing this?
Oh, like alpha? Yeah, no alpha penalty.
No alpha penalty, okay. You referenced currently available treatment options, including Bluenosat, and can you maybe just refresh us on one of these available options shown in PTCL in terms of the standard of care, and how do you think about, based on your prior data, what socolitinib might do in terms of improving on efficacy here?
Yeah, yeah. So unfortunately, they don't work very well. These drugs were approved a long time ago. So in fact, I think the FDA has got their eye on these drugs because they haven't done the pivotal drugs or pivotal studies. You know, you see anywhere from, unfortunately, like one and a half to three months, you know, PFS for these drugs. So most patients are going to come off these drugs due to toxicity or to just lack of efficacy. And in our PTCL trial, we actually have a crossover. So if patients fail on either bolinostat or prolatrexate, they can cross over to socolitinib. So unfortunately, just still a high-endment need in terms of current standard of care.
Just on that crossover arm part, can you just maybe walk us through how that might, down the road, affect a potential OS analysis? How do you think about that? And just sort of the implications there.
Yeah, so the primary endpoint is PFS, and I think we're looking at just under five months PFS, basically doubling what is currently there. And we've already had discussions with the FDA. We have an approvable for one trial. But look, I mean, our OS, I think, if I remember right at the ASH meeting, is I think almost 28 months. So very different. So we are seeing, you know, an effect on these patients. And again, to keep it, it's a novel oral drug, which is also a big advantage for these patients.
You mentioned this briefly earlier, but just on the registrational path within PTCL, how do you think about this? Is there a way to fast track it for either regular approval or are you thinking about more of an accelerated approval with a final approval
downstream? So we have fast track status today for socalitinib. There's a high eminent need that we just talked about. So assuming the data is supportive, we will and can talked to the FDA about a regulatory path, so potentially an accelerated approval or breakthrough
therapy designation. I want to give the audience a moment to ask any questions. If they have any, happy to pass around a mic if necessary. Just raise your hands and we'll be happy to get a mic to you. But in the meantime, can you just sort of remind us of how prevalent PT sale is and how you think about the commercial opportunities there.
So prevalence is about 70,000 patients globally. In the U.S., it's about 10,000 patient prevalence, EU 15,000 prevalence, and the rest, the balance is Asia. It's more prevalent in Asia because it's actually, a lot of it is driven by EBV and the virus. So in the U.S., the incidence is around 3,300. And unfortunately, most patients get chemotherapy, But unfortunately, most patients fail. So they're going to pass down to the refractory patient population, which is where we're studying it right now. So look, I think with a high unmet need and a small orphan in terms of the size of the market, it's a significant opportunity for us. It's probably underlooked.
Can you remind us, you have fast-track status for Cucolitinib here in PTCL. But if you are successful here with your clinical trial and theoretically get an approval, can you walk us through what the exclusivity implications might be from getting an approval here? You talked earlier about composition matter going to 2037 with the possibility of extensions there, but just maybe sort of what are the exclusivity implications from getting maybe the first new drug approved for PTCL in a long time.
Sure. Yeah, absolutely. And so we also have orphan designations. So obviously, assuming a successful approval in the U.S. that gets you seven years of exclusivity and in Europe it can get you 10 years of exclusivity as well. So that would give us some additional protections in addition to the composition of matter patents that we have.
You know, maybe turning back to ITK biology, I think you and I and Richard have talked about its applications potentially in other non-other therapeutic categories outside of AD and also PTCL. Can you maybe talk about where you are investigating socolitinib currently beyond those two lead indications and where you think ITK biology might be applicable?
So as I mentioned, in the second half of the year, we'll start a phase two trial on asthma as well as a proof-of-concept trial in HS. So like I mentioned at the front end, we follow the science. So asthma is a TH2-driven disease, very much similar as to AD. In fact, the overlap, I think, is about 25% of adults and up to 40% of children have concomitant disease. So we're following the science with asthma. Still an unmet need for oral tablets in general for most I&I diseases. It's the same in asthma. Also, there's some efficacy opportunity as well. About 25% of patients in asthma, you know, don't respond to current, you know, therapies. And you're talking about a very large market there, 60 million patients in the G7, 10 million patients moderate to severe. So it makes a lot of sense from the biology and from the market opportunity and our profile to look at asthma. HS is really interesting, right? That's primarily a Th17-driven disease. and we've shown clinically that we can actually really impact and lower TH or IL-17. You know, Vimzelex was recently approved. That's been a very successful drug, and that blocks IL-17A and F. So we think the biology makes sense there, at least for socolitinib. That's about 1.2 million patients in the G7, about 700,000 patients that are moderate to severe. And actually, I was just looking at Evaluate Pharma, and they actually now have that projected to be an $8 billion opportunity starting out at $500 million. So I think it's going to grow. So I think both opportunities are significant for socolitinib. Maybe just sticking with the asthma, advancing socolitinib, can you talk about which in terms
You talked about moderate and severe patients, but is there a particular group within that, whether it's, you know, EOE-driven disease, other areas that make most sense for you to
investigate first? Yeah, obviously EOE makes sense. You know, in addition to blocking aisle 4 and 13, we block aisle 5, right? And so obviously you've got the Senra, you've got Nicala, which are very successful drugs. They're a couple billion dollars each, and they're effective in asthma. You know, it's an interesting point you bring up. Obviously the larger portion of the market is T2 disease. So that's 70% of the market. But the subset of non-T2, there's a subset that's actually driven by IL-17. And because we block both Th2 and Th17, we could potentially work in the non-T2, obviously, with drugs like Tespire that are approved there. So we're still designing the phase two protocol for asthma, but that's something we're considering is could we actually maybe include at least a segment of non-T2 as well that could expand the market
opportunity for us. Great. And then on the HS side, you know, typically patients go through Humira, which is approved for that, but clinical development in HS has been a bit of a landmine, minefield, excuse me, for clinical stage drugs. Can you maybe talk to, you know, what your learnings are from competitor programs that have had some stumbles recently as you think about
developing a clinical program in HS? Yeah, I mean, we're, so we're talking to our KOLs right now. So we are very cognizant of what you're bringing up, and I think that's why we're doing a proof of concept study in H.S. versus saying a phase two trial in asthma. So I think we want to be, you know, have a definitive answer in terms of the study design, but we also want to make sure we're managing our resources. And there's a number of things that we're looking at in terms of endpoints and how you manage placebos and how you're measuring. Some of these endpoints are still being discussed, and so it's an evolving field. But, you know, you do have a pathway now with BIMZELX. There's other drugs in development. So we are looking at a number of protocols to make sure we kind of optimize the HS protocol. And we're working with, you know, some of the KOLs now to finalize.
Maybe looking a little bit into the future after asthma and HS, you've talked about historically about a range of diseases that might also be subject to ITK biology. Maybe what would sort of be the focus areas for investors down the road as we think about development?
Yeah, I think in our slide deck we have a slide that kind of talks about, you know, the diseases by biology. So TH2, TH17, fibrotic diseases, IL-5. So, you know, I think it's interesting as IBD. I think IBD is very interesting, right? And we have a number of really good animal models that show that we're pretty, that we can impact the biology of IBD. So I think that's something we'll consider and look at. And again, I think obviously we've got socolitinib that's in the clinic, so we may do a number of these proof-of-concept studies with socolitinib, but then the question might be, would it make sense maybe to switch to a next-generation ITK inhibitor just to maximize the opportunity in terms of patents and Inflation Reduction Act and that sort of thing.
Can you remind us what your cash position is currently and what your cash runway takes you to in terms of prosecuting your current programs in the clinic and just how you think about needs for your pivotal trial program, pivotal stage programs.
Sure. So in January, we raised $200 million. Our balance sheet as of March 31st is $237 million. And what that buys us is that we have money to complete the Phase III PTCL study, the Phase II atopic dermatitis study, the CR1, as well as the asthma and the HS study. And that gives us a runway into mid-2028.
There are no questions from the audience. I think we'll end it there. Thanks to Jeff and Corvus for joining us today.