Corvus Pharmaceuticals, Inc. ($CRVS)

Okay. We'll continue with the next session. Thank you for joining us. I'm Paul Choi, and I cover the SMID-cap 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. Yes. 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, soquelitinib is our lead program. It's in a Phase III registrational trial for peripheral T-cell lymphoma, which is a really tough cancer as well as we're in a Phase II trial for moderate to severe atopic dermatitis and that's called the SIERRA1 trial. And both of those trials are enrolling as we speak. Based on soquelitinib'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 II asthma study as well as a proof-of-concept study in HS. Just of note, we have really good composition of matter protection on soquelitinib. So we have protection through November of '37, and that doesn't include any pharmaceutical extensions, which could be an additional 5 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 maybe 3 things I can think of is 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 at 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 and bringing those to market. Does that make sense?

Yes, it does. So 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 what is the rationale, I guess, to go from a Phase III program in a blood cancer into I&I? And more specifically, atopic derm. Can you walk us through what was sort of the background behind that?

Sure. So rationale for AD. So first of all, we follow the science. So essentially, how soquelitinib works is that we block Th2 and Th17 in their respective cytokines. So you think about we block Th2, we block IL-4 and 13, just like DUPIXENT, 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 18-year-olds with eczema. One thing that's 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 that's targeted and selective for ITK. So therefore, we think we'll have limited off-target effects. So I think that's important. And then finally, I think in terms of 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 lebri and nemo, all injectables. So I think we have more patient preferred and with an oral product. Now of course, there is Rinvoq, right, which is an oral tablet, but it is -- 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, very dense, very competitive, which I think is a fair assessment. But can you maybe talk about how soquelitinib differs versus some of the other AD0 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?

Sure. 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 subcu. And when you look at the pipeline for novel drugs, novel oral drugs, it's actually fairly limited. I mean, you've got us an ITK inhibitor, of course, there's STAT6 that you brought up. There's also IRAK-4 that's in development. 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 we -- 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. I think the other thing that is unique about our mechanism of action is that we not only block cytokines, but we also believe that we're modulating for rebalancing the immune system. And what do I mean by that? So not only we block Th17 and the respective cytokines style 17, but we've actually shown to be able to shift or switch Th17 to become active T reg 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 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 on 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. What sort of -- you talked a little bit about the population, roughly 1/3 of them were patients who have previously failed a 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?

Yes. So we're -- we think we have pretty compelling clinical data. When you look at EASI-75 and IGA 0/1, we're somewhere between a biologic and JAK level of efficacy. So EASI-75 is actually comparable to a JAK placebo adjusted and IGA 0/1 comparable to a biologic. So we're pretty excited about what we've seen so far, and we hope that we can replicate that in our Phase II trial, which is ongoing the SIERRA1 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. So can you maybe tell us what that data looks like and then just how do physicians and KOLs you've spoken with since you've released said data view this result?

Yes. Yes. So it is interesting data to see this kind of follow-up post stopping the drug. Maybe what I would say first is that our plan is to bring soquelitinib 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 ICOTYDE, 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 -- soquelitinib market quickly in AD. Now to your point, in the SIERRA1 trial, we are going to follow patients longer term. So it will be a SIERRA1 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 lifecycle management strategy. Does that make sense?

Yes. And then maybe physician feedback on the response or duration of response off treatment. What have doctors said about this?

Yes. I mean they're encouraged. I think just in general, physicians are looking for more durable treatment and treatments with less treatment burden. But I will say efficacy is still #1 as it is for any drug. So I think they're excited to see the EASI-75 response and the IgA-0 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 soquelitinib in AD, is there a particular group or aspect or subgroup of the population or part of the population that you think makes most sense for the target and the mechanism of action here?

Yes. Yes. It's a good question because we work more upstream because we blocked Th2 and Th17 we brought -- 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 patients that have actually failed a prior systemic therapy I think, obviously, 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 II and that can inform some of these commercial strategy decisions.

You did present a 90-day off-treatment data for cohort 3, but you decided in your most recent update not to present that for code for Cohort 4, excuse me, can you walk us through the rationale behind that? And just was that protocol-driven or just was there anything else behind it?

Yes. I think 2 things. I think first of all Cohort 4 was meant to look at 2 months of efficacy dosing. And that was the purpose of Cohort 4. It actually wasn't to follow for off-treatment durability. So just as a reminder, cohorts 1 through 3, we're only 4 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 a 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 II trial and start the Phase III trial, and 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 RV 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 II. And we felt like we accomplished that and we wanted to move quickly. Does that make sense?

Yes, it does. You guys are working on prosecuting development of soquelitinib here in the U.S., but you've also engaged with a partner for ex U.S. markets, specifically Angel in China. Can 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 right to soquelitinib 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 Ib program that will lead into a Phase IIb trial in atopic dermatitis. So they have 2 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 2 cohorts, that will inform the dosing for the Phase II portion. So by the end of the year, we should see Cohort 1, which -- that will give us 12 weeks of dosing, which we don't have yet. So that will be interesting as well as we'll be able to see what the effect is at the low dose for 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 in the U.S. or Western population?

Yes, 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 thoroughly. 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 in this Asian population. So -- but otherwise, all else is going to be the same in terms of enrollment criteria, EASI score, end points, EASI score -- primary endpoint is EASI score reduction, secondary points will be IGA 0/1, and EASI-75.

Great. Maybe turning back to your program and your Phase II SIERRA1 study. Can you walk us through the trial design and just how are you thinking about prosecuting that and what time lines might be both to enroll and potentially time lines to data?

Sure. So we're enrolling SIERRA1 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 lebri, nemo, did a similar size study. So 200 patients. We have 4 dosing arms. So we have a placebo and then we have a low dose, again, QD, and then we have the 2 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.

Okay. And just in terms of end points, any differences versus what you've done in your Phase II or should investors also look towards EASI-75 and IGA 0/1?

Yes, most part, it's the same endpoints. EASI-75, IGA 0/1, PNRS pretty much the same.

Okay. 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 present efficacy there. Can you remind us in SIERRA too, what portion of patients might be on -- have been on prior therapies? And do you -- maybe starting there?

Yes. Yes. So as I mentioned, in the Phase I trial, we had about 35% of patients on prior systemic therapies. In the SIERRA1 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 prior to the injectable. But it's interesting to see this effect in prior systemic treated patients. So it gives you some optionality as well for future life cycle decisions. So again, we'll be able to see that data and look at that. We can have no more than 40% in the SIERRA1 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 running a trial with both frontline and treatment-experienced patients, this could have downstream implications for how 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 from the Phase II 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 have to also look out 5 to 10 years, right? And if in 5 or 7 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 priorly 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 front line. Does that make sense?

Yes, it does. Maybe sticking on CR1 and your Phase II program. Can you maybe lay out how you're thinking about the differences between your dosing arm, specifically your 200 mg BID versus your 400 mg QD dosing? Are you expecting daylight between the [indiscernible] to be similar than different? Just how do you think [indiscernible]

[indiscernible] versus BID. Maybe a couple of things. So first, it's important to note that soquelitinib is a covalent drug, right? 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 1 and Cohort 2 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 4-week study. So with a 12-week study, we hope to see that the Q QD dose will be as effective as a treatment because our target is to have a QD dose. And that doesn't include any sort of formulation options you have as well. I mean, actually, Rinvoq is actually a long-acting -- but our target is to have a QD drug. So we hope to see that in the SERA01 trial, actually and in the Angel trial as well.

Yes. I want to turn for a moment to your oncology program because sometimes it gets overlooked. You're actually in Phase III already and relatively far along here. So can you remind us, first, what is the status of that study in PTCL?

Sure. So we're in a registrational Phase III 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 belinostat or palatrexate, at least in the United States. And unfortunately, they're not very effective drugs. So there's a very, very high unmet 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, we 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 have -- 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?

Like alpha yes, no alpha penalty.

No alpha penalty. Okay. You referenced currently available treatment options and including belinostat. And can you maybe just refresh us on what have 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 soquelitinib might do in terms of improving on efficacy here?

Yes, yes. So unfortunately, they don't work very well. These drugs were approved a long time ago. 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 see anywhere from, unfortunately, like 1.5 to 3 months 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 belinostat or palatrexate, they can cross over to soquelitinib. So unfortunately, just still a high unmet 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?

Yes. So the primary endpoint is PFS. And I think we're looking at just under 5 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 we're almost 28 months. So very different. So we are seeing an effective -- an effect on these patients. And again, to keep it, it's a novel oral drug, which is also a big advantage for the [indiscernible]

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 a regular approval? Or are you thinking about more of an accelerated approval with a final approval post your data or full approval downstream?

Okay. Yes. So we have fast track status today for soquelitinib. There's a high unmet need that we just talked about. So assuming the data is supportive, we will and can talk to the FDA about regulatory path, so potentially an accelerated approval or breakthrough therapy designation.

Great. 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 PTCL is and how you think about the commercial opportunity there?

Sure. 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. So -- 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.

Okay. Can you remind us, you have fast track status for soquelitinib 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 possibility of extensions there, but just maybe sort of what are the exclusivity implications from getting it maybe the first new drug approved for PT cell in a long time.

ure. Yes, absolutely. And so we also have orphan designation. So obviously, assuming a successful approval in the U.S., it gets you 7 years of exclusivity and in Europe, it gets 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.

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're investigating soquelitinib currently beyond those 2 lead indications and where you think ITK biology might be applicable?

Yes. Yes. So as I mentioned, we'll -- in the second half of the year, we'll start a Phase II trial in 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 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 don't respond to current 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. BIMZELX 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 soquelitinib. 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 of $500 million. So I think it's going to grow. So I think both opportunities are significant for soquelitinib.

Maybe just sticking with the asthma advancing soquelitinib. Can you talk about which in terms of -- you talked about moderate and severe patients. But is there a particular group within that, whether it's EoE-driven disease, other areas that make most sense for you to investigate first?

Yes. Obviously, EoE makes sense. In addition to blocking IL-4 and 13, we block IL-5, right? And so obviously, you've got Fasenra, you've got Nical, are very successful drugs. They're a couple of billion dollars each, and they're effective in asthma. 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, the drugs like TEZSPIRE that are approved there. So we're still designing the Phase II 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, typically, patients go through HUMIRA, which is approved for that. But clinical development in HS has been a bit of a land -- mind field, excuse me, for clinical stage drugs. Can you maybe talk to what your learnings are from competitor programs that have had some stumbles recently as you think about developing a clinical program in HS?

Yes. 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 HS versus saying a Phase II trial in asthma. So I think we want to be -- 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 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 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?

Yes. I think in our slide deck, we have a slide that kind of talks about the diseases by biology. So Th2, Th17, fibrotic diseases, IL-5. So I think it's interesting is 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 soquelitinib that's in the clinic. So we may do a number of these proof-of-concept studies with soquelitinib. But then the question might be, would it make sense maybe to switch to a next-generation ITK inhibitor just to maximize the opportunity, right, 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 does -- takes you to in terms of prosecuting your current programs in the clinic and just how you think about the needs for your pivotal trial program, pivotal stage programs?

Sure. So in January, we raised $200 million. Our balance sheet as of March 31 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 SIERRA1 as well as the asthma and the HS study. And that gives us a runway into mid-2028.

Okay. Great. There are no questions from the audience. I think we'll end it there. My thanks to Jeff and Corvus for joining us today.