Corvus Pharmaceuticals at Jefferies Conference: Advancing Socolitinib Trials

On Thursday, 05 June 2025, Corvus Pharmaceuticals (NASDAQ:CRVS) presented at the Jefferies Global Healthcare Conference 2025, offering insights into its strategic focus on drug development. The highlight was the progress of socolitinib, an ITK inhibitor, showing potential in multiple therapeutic areas. While the company is optimistic about its market opportunities, the absence of financial data left some questions unanswered.

Key Takeaways

• Corvus is advancing socolitinib, targeting a $30 billion market in atopic dermatitis.
• The drug is in Phase 3 trials for peripheral T-cell lymphoma and Phase 1 trials for atopic dermatitis.
• Socolitinib’s selective ITK targeting is expected to provide safer, more effective treatments.
• Results from an extended cohort in atopic dermatitis are anticipated by November 2025.
• Patents for socolitinib extend beyond 2040, providing long-term protection.

Operational Updates

• Phase 3 Trial (Peripheral T-cell Lymphoma):

- Open in four countries with a 1:1 randomization of 75 patients per arm (socolitinib vs. standard of care).

- The primary endpoint is progression-free survival, with crossover permitted.

• Phase 1 Trial (Atopic Dermatitis):

- 48 patients enrolled across three cohorts, with Cohort 3 showing the most promise.

- Cohort 3 extended with an additional 24 patients at 200mg BID for two months.

- Conducted at 17 centers in the United States.

• Phase 2 Trial (Atopic Dermatitis):

- Planning is underway, focusing on socolitinib’s efficacy and safety profile.

• Patents:

- Composition of matter patents in the United States extend until November 2037, with pharmaceutical extensions expected to provide protection beyond 2040.

Future Outlook

• Socolitinib as a Platform:

- Corvus views ITK selective blockade as a platform opportunity with applications in oncology, immune diseases, neurology, and dermatology.

• Extension Cohort Results:

- Results from the extension cohort (Cohort 3) are expected in the fourth quarter of this year, around November.

• Market Opportunity:

- Corvus is targeting a potentially $30 billion market in atopic dermatitis with a safe and durable oral treatment.

For a complete understanding of the presentation, readers are encouraged to refer to the full transcript below.

Full transcript - Jefferies Global Healthcare Conference 2025:

Roger Song, Senior Analyst, Jefferies: Alright. Welcome, everyone, to Jefferies twenty twenty five, global health care conference. My name is Roger Song, one of the senior analysts covering semi cap biotech in The US. It’s my pleasure to introduce our next printing company covers. We have the CEO, Rich Miller.

Rich Miller, CEO, Corvus: Thank you Roger and good morning everyone. I want to thank Jeffries for the invitation to the healthcare conference and thank you all for attending. What I would like to do today is update you on our drug development for socolitinib and ITK inhibitor, especially with our clinical results in patients with atopic dermatitis, as well as set the foundation for what we believe is becoming really a drug development franchise. So we’ll go through some of the data for that. So just to sort of start with an overview, we now look at ITK, selective blockade of ITK as a platform opportunity.

As a new drug target because of the selectivity that has been really discovered by some of the chemistry going on at Corvus. Our lead product, socolitinib, has a novel mechanism of action with broad opportunities in oncology, immune diseases, neurology, dermatology, other things. The lead drug, socolitinib, is in a registration phase three trial in peripheral t cell lymphoma and also in a phase one trial in patients with moderate to severe atopic dermatitis. This drug is oral and has an established safety profile now in over a hundred different patients with lymphoma. Some of those patients treated for up to two years, over two years, with doses three times higher than what we’re using in our atopic dermatitis trial.

Obviously the markets for this agent are quite large. Cancer, lymphoma, immune diseases. The drug invented by Corvus has issued composition of matter patents in The United States that run until November 2037. The patent has been issued in major countries already. With pharmaceutical extensions, you can expect protection beyond twenty forty easily.

Now, Corbus has a management team that’s done this before. This idea of blending lymphoma and immune diseases together has been done before by several of the members of my team. Think about drugs like Rituxan. Think about drugs like Ibrutinib. And we’ll touch on some of those in a moment.

So it all starts with the target. I’ve changed my pipeline slide because as I think about this really the target is the key as you all know. And ITK which has been known for fifty years or so as a critical target in T cells. But what hasn’t been known that if you’re going to attack ITK, you have to do it very selectively. So what I would like to talk, cover with you today is although there are opportunities in all these areas, pulmonology and fibrosis, gastroenterology, rheumatology, we are currently in the clinic in three main areas.

Oncology, immune diseases, like autoimmune lymphoproliferative disease, and dermatology. And what I’ll report on today and update you on is the results from our phase one trial with additional patients from cohort three, as well as tell you something about the effects that we’re seeing on pruritus and our plans for extending the trial and initiating a phase two trial. So let’s get back to this strategy of Corvus. This game plan. So early on in my career, we viewed an anti b cell antibody as potentially having a role in lymphoma and immune diseases.

And of course b cell depletion has become a foundation of treatment for lymphoma and also for immune diseases. The same playbook was used for a drug called ibrutinib which became as you well know, a top selling cancer drug and of course now there are several BTK products on the market to treat lymphoma and now beginning in neuro immune diseases. So with socolitinib, a drug that hits ITK, a target in T cells, the game plan was start with T cell lymphomas and then move that into immune diseases where T cells play a role. Of course that’s a lot of immune diseases. So let’s review some of the biology or mechanism of what we know about ITK.

Let’s focus in on the right side of this slide. So ITK stands for interleukin two inducible T cell kinase. So first of all, it is very limited tissue distribution. It’s only in T cells and K cells and another cell called an ILC two. It’s a very rare cell, very important in asthma, atopic dermatitis and inflammatory bowel disease.

So very selective target. It’s not widely expressed in the body. Why do I emphasize that? Because that speaks to eventual safety. So it’s been known for some time based on studies that were done in late nineteen ninety’s, that ITK controls the differentiation of different T cells.

It controls the differentiation of T cells to what are called Th one, Th two, and Th 17. And other t cells now which I don’t have time to go into. Genetic knockout studies done in the early two thousand from several different laboratories show that if you selectively block ITK, nothing else, you inhibit the production of Th two and Th 17 cells and the resulting cytokines that come from those cells. You hear about those cytokines every night. IL four, IL 13, IL five, IL 17, IL 31, 30 three, etcetera.

I can’t name them all. Now you still get the differentiation of what’s called the Th one cell. And that occurs because the Th one cell has a redundant enzyme called resting lymphocyte kinase. And as we were thinking about our strategy, we said, wow, this is the perfect target. We can inhibit inflammatory cytokines.

We can still permit the development of Th one cell, which of course is important in fighting cancer and fighting infection. So it should not be immunosuppressive and our experience tells us it’s not. So the strategy was make a drug that’s specific for ITK. Now the story gets a bit more interesting. In the last few years, workers at Janssen Research Labs, workers at Cornell University, Doctor.

Avery August’s lab at Cornell have shown that Th 17 cell has plasticity. It can take different forms depending on the micro, the tumor, the microenvironment, the tissue microenvironment. And that is under the control of ITK. And what Doctor. August showed and what we’ve shown in our laboratory now is if you block ITK with our drug or genetically, you skew towards this T regulatory cell, a suppressor cell, FOXP3 suppressor cell.

That could be really important. That’s the holy grail of autoimmune disease because that could give you lasting or durable effects. So we published this in December. I won’t go through the details. The chemistry, enzymology, etcetera is in this paper.

The drug is shown on the upper left there. You’ll notice it’s a covalent drug. It has an acrylamide group or a Michael acceptor. Same substituents that’s on ibrutinib. So we learned a lot.

My team learned a lot from ibrutinib and this family of molecules. So if you look on the right, this is called the dendrogram of the kinases, the kinome. There’s over 300 kinases in the body and a drug like ibrutinib, which is a pretty good drug, well established drug, that hits BTK, of course that’s what it was made for. And it hits ITK and it hits a bunch of other things including RLK which you don’t want for autoimmune disease. So look at soquelitinib.

It only hits, it only binds ITK. To my knowledge, and I’ve been working in this family of proteins for twenty years, there is no drug I’m aware of that has the specificity for ITK and acceptable pharmaceutical properties. Now, over in the middle there is the binding constants, the Kd’s, association constants. And you can see that soclinip’s clean, doesn’t hit any of the others. But I think what’s really interesting about these family of targets, cause again we’re into targets, is that think about this group of proteins that are involved in this ITK, BTK, etcetera list of targets.

These are about 11 different proteins that comprise the so called tech family. And there’s some proteins that you’ve heard of. You’ve heard of BTK, that’s a successful therapeutic target. You’ve heard of EGFR, HER2, JAKs. These are all very successful targets.

So you can now, I believe, add ITK to that list. So this has really turned out to be valuable real estate. And that’s been proven over the last twenty five years. Just think about the magnitude and the utility of the drugs for those targets. Okay, so using our playbook, our strategy, let’s start in lymphoma.

Bad lymphoma. We’re now conducting a phase three registration trial based on phase one data that gave us a forty percent response rate in similar patients with mostly CRs of durations up to two years. Now this is a disease with a median survival of six months. There’s been really no new treatments for this disease in twenty years. There’s no fully approved drug for these diseases.

The relapse peripheral t cell lymphomas. And I won’t go through the details of the trial but this trial is now open in four countries and is enrolling. And it will enroll one hundred and fifty patients randomized equally one to one, seventy five in each arm to monotherapy with socolitinib versus the standard of care which is either pralotrexate or balinostat Which are intravenous, inconvenient, very toxic drugs. The endpoint of our trial is progression free survival, very standard endpoint. And we will allow crossover in patients who progress on the control arm of course.

Now this is really a pretty interesting phase three trial. Think about this. The median time to progression in the control arm is about three months. It’s pretty short. Also, it only takes a 50 patients to have a power of 90% to show about a one and a half month improvement which would give you a hazard ratio of about point six.

So this is a very manageable phase three trial for this really is an unmet need. There is no treatment for this disease, fatal disease. Now along the way, we’re validating, again back to our strategy, patients with T cell lymphoma have normal immunity, normal immune cells too. And we can look at their T cells and their lymph nodes and their skin and all this other stuff. Now one disease where we’ve seen a lot of activity is so called cutaneous T cell lymphoma.

So T cell lymphomas in general, not just the cutaneous T cell lymphomas, have a high propensity to involve the skin. We’ve known that as oncologists for decades. They like to go to skin. Now cutaneous T cell lymphoma is a Th2 lymphocyte. Often makes the Th2 cytokines.

So it becomes a really interesting model for immune diseases. You can see this patient who failed chemotherapy who has what’s called transformation of CTCL, a bad disease. That’s a fatal All the CTCLs are basically one hundred percent fatal. This is your worst nightmare of atopic dermatitis. It’s not atopic dermatitis but it’s the malignant counterpart.

So here’s an example of a patient who failed a bunch of stuff, took our drug, had slow regression of skin disease, complete clearance of bone marrow and circulating tumor cells, and reduction of lymphadenopathy. This patient’s been on treatment with two hundred milligrams BID of our drug for over two years now. Our study actually doesn’t allow you to go more than two years and we had to get an exception for her because her doctor and the patient don’t want to stop this. Okay, so with the escalating data that we get from our patients, animal studies, in vitro laboratory studies, we begin to see a picture that wow, we can block a lot of the cytokines and a lot of the functions that are important in immune diseases. So we have a drug, oral drug with a potentially really interesting mechanism of action.

Unlike something that blocks just IL four or 13 or IL five or this or that other thing, Inflammatory disease is really complicated. There are probably hundreds of cytokines. And if you really want to have a big impact in the disease, and we want to have a big impact in the disease, then you really want to hit a more fundamental or a more upstream mechanism. And so that’s the thinking that went into using our drug in autoimmune inflammatory disease. So what’s the opportunity for us?

Because we hit a lot of different of these cytokines. Well, TH2 driven diseases for sure. I just showed you an example of that. Asthma, atopic dermatitis, etcetera. IL-seventeen, okay, driven diseases.

Psoriasis, psoriatic arthritis, ankylosing spondylitis, etcetera. IL-five driven diseases, allergy, fibrotic diseases. We have a paper next week at EULAR meeting in a mouse model of scleroderma for example. Very active in that model. So the markets of course are very large for atopic dermatitis.

There is interest in an oral agent that’s safe. And I won’t go through the details here. The people in this room are quite familiar with this, but this is a potentially $30,000,000,000 market and only a small percentage of patients now with moderate to severe disease are being addressed. What physicians want, and I’ve been talking with these physicians now, oral compound safe, durable activity. Nobody likes to take a drug forever.

Okay? Cancer, different. Benign diseases, you don’t want to take a drug forever. Okay, so we’ve been conducting a phase one trial as outlined in this slide. I’ll go through the design quickly because I’ve presented this before.

But patient eligibility is moderate to severe atopic dermatitis. You have to have failed either one prior systemic therapy or a topical corticosteroid. Patients are sequentially enrolled into four different cohorts. One, two, three, four. 16 subjects in each cohort, then you go to cohort two, then you go to cohort three, etcetera.

The randomization, it’s randomized. Patients are randomized three to one. 12 get the active drug. Four get placebo. Sixteen in each arm.

The treatment period is twenty eight days. That’s short. Twenty eight days. Then we follow them for another thirty days. Fifty eight days total.

The study is blinded. The patient and the doctor don’t know what pill they’re taking. There’s a dummy pill, placebo pill. The company’s not been blinded. It’s a phase one study.

No requirement for that. We wanted to be able to analyze the data and make modifications as if they were necessary. So these cohorts are evaluating different doses and schedules. Very quickly, a hundred milligrams BID. That’s half the dose we use in lymphoma.

Then we went to two hundred once a day. We were interested in Cmax because it’s a covalent drug and our work with ibrutinib and our experience with covalent modification told us that Cmax might even be more important than AUC. So that’s why we were evaluating that. The third cohort, which I’ll update you on today, is two hundred BID. Same dose as the lymphoma study.

That is a doubling of the doses that we studied in cohort one and two. Now what are we monitoring these patients? Safety, EASI scores, IGA, PPNRS, the itch, other biomarkers as well. Okay, here are the patient baseline characteristics of forty eight patients. Patients with atopic dermatitis.

Forty eight subjects have been enrolled now and followed. Cohort one, two, and three are shown on the slide. And then the combined groups are shown on the far right. This is pretty much standard demographics I would say for an adult population with atopic dermatitis. There are a few things to point out.

Number one, we have a high proportion of African Americans, forty to fifty percent or so in each of the cohorts. That just has to do with the sites where the clinical testing was done. All the centers, 15 centers, now we have 17 centers, all The United States. A couple of academic centers and other dermatology practices. So 50% African Americans.

African Americans are thought to have worse prognosis, worse disease, more difficult to treat. Second thing to point out, you’ll notice in cohort three. Cohort three is sicker. Sicker patients. The mean baseline EASI score, 27, 20 eight.

And the other cohorts was around 18 to 20. Remember 16 and above is moderate disease. 21 and above is severe disease for easy score. Okay and then one final point that goes along or is consistent with the sicker patients is that the patients in cohort three, there were a higher proportion, forty percent or more, that failed a systemic biologic like a doopy. And I hope we have time at the end to give you some vignettes on doopy failures and doopy refractory.

Okay, here’s the efficacy at twenty eight days, four weeks. The mean change in EASI score, and I’ll show you the curves in a bit, for the cohort one and two, the one hundred or two hundred milligram total dose per day. I combined those because really the results are very similar as you’ll see from the curves. 54.6, the mean reduction for cohort three, sixty four point eight. Placebo 34.4.

That’s combined placebo from each of the cohorts. That’s a 20 to 30% difference. Pretty darn good for a phase one study at four weeks. Doopy like four week. Okay.

Now easy fifty’s of course, there’s a lot of placebos that reach easy 50. Everybody has seen that. So we don’t pay much attention to that. Although it should be pointed out that almost all of our patients who get so called in, achieve an easy 50. Now crucial endpoints are easy 70 five’s, ninety’s, IGA zero one.

And you can see in our study, zero placebos achieve those levels of activity. Zero Versus 29, 50 percent or so in the soclolitinib group. So here are the curves. This is the change in easy scores over time. Let’s go over this a little bit carefully.

This is placebo cohort one, cohort two, cohort three separately. First of all, I’d like to point out that we did something I think was really crucial and speaks to the quality of the data. We get your easy score at screening and then we get it again at baseline. When I say we, I mean the physicians who are doing this blinded. So you’ll notice that for all the patients, forty eight patients, the EASI score at screening and baseline is really pretty flat and pretty identical.

That’s really amazing given that there is some subjectivity to the EASI scores. Then patients go on treatment for twenty eight days. And you can see there is a reduction in EASI score for placebo. Everybody’s been seeing that there is a placebo effect to an oral medication. More placebo effects actually with oral medications.

And then you start to, let’s look at cohort one and two. Cohort one and two are on top of each other. It’s the same total dose per day. One conclusion from that is QD BID doesn’t doesn’t matter. Because those curves are on top of each other.

So and that’s probably due to the covalent nature of the drug. So you’ll notice that the cohort one and two, you start to see separation at day twenty, at day fifteen rather. More separation at day twenty eight. And then it’s flat. It even goes down a little.

And I’ll come back to that point later. Look at cohort three. The higher dose. The doubling of the dose. Separation now at day eight, more separation at 15, more at day 28, flat, even down a little bit again for the thirty day follow-up out to day 58.

Interesting. So again, day twenty eight to 58, you’re not taking any therapy but the study’s still blinded. Okay, now a couple of other things to point out here which speak to our strategy. First of all, you’ll notice that the curves are still going down. If you look at the curves at fifteen and twenty eight, they’re still going down.

Begs the question, if I continued people on therapy, would it go down further? We had patients, now that the study’s over and unblinded, where the docs are saying, gee, I wish I could have given my patient more drug because he was improving continuously and Doctor. Miller, you made me stop the drug. Of course we had to stop the drug. That’s the protocol.

Okay, here’s the combined treatment groups. Cohort one, two, three together versus the placebo. Again, you see separation beginning at day eight. You see good separation at fifteen and twenty eight. And again a little bit more separation over time.

Now the p value, we never powered the study for this. I’m surprised and encouraged by the fact that we see a p value of point zero three six at day twenty eight. Which is obviously the logical efficacy endpoint that you would use for this study. Now, so we find these results to be quite interesting in that a study with a novel agent, although it had much safety and biologic data from our lymphoma study, we find in forty eight patients to come up with a statistically significant number at only twenty eight days to be quite remarkable actually. Okay, now this is the EZ 75s and IJ zero ones for placebo.

Again, just summarizing it. Again, placebo zero, zero. Now most studies in the literature will show you ten to twenty percent. We have zero. Perhaps it’s due to the shorter follow-up, I’m not sure.

But then of course you see a little bit better results with cohort two versus one and better with cohort three. Now at the SID meeting a few weeks ago, we only had eight patients out to day 28 and I reported five of eight easy 70 five’s. That’s sixty three percent or whatever. The next four patients who got out to day twenty eight, one out of four had an easy seventy five. That was an easy eighty nine, by the way.

So the number went from 60 something to 50 and people are hysterical now even though the p value on my curves went from o three three to o three six, really the same. Now, here’s another interesting thing. That curve, that 50% at day fifty eight is now seventy five percent. Now that’s interesting. Okay.

Whoops. Okay, regarding safety, this could be very quick. We saw in the entire study, we really don’t see any difference between the cohorts with dosing. There was only one treatment, thought to be treatment related AE that was a grade one nausea and one patient did not interfere. Nobody interrupted their therapy during the course of the study.

Again, we have experience in lymphoma with doses much higher than this given for weeks or months every day. So I think that we have a lot of data on safety. Again, speaking to safety, there’s two things to note here that I think are critical when you consider a target. It’s why CD20 and Rituxan was so successful, I think. Again, I mentioned you have a target that has very limited tissue distribution.

ITKT cells, NK cells, ILC2s. And you have a drug that’s very specific. So that confluence of selectivity and specificity is seldom reached in medicine, I would argue. There are not many drugs that do that. That’s why we think we have a potent and safe drug, oral drug.

Okay, now I want to report this is new data I haven’t shared before. So we did collect PPNRS data. That’s the peak pruritus numerical rating score which is patients have a diary. Zero is no itch. 10 is your worst nightmare itch.

This is a very subjective scale. Obviously different people have different thresholds for what the scoring is. Anyway, it’s a commonly used instrument. Look at cohort three. That is a dramatic effect.

You see us beginning and after one week, you see a drop in that green curve. Okay, in one week, a progressive drop. Cohort one and two, we’re not able to distinguish, dissect out. But here’s the interesting thing. Look at the lower right.

That’s IL 31 biomarkers. Serum IL thirty one levels. There is a difference in the patients who are treated and respond. Look at the dots, each dot is a patient, versus placebo and versus the non responders. There’s a big difference in non responders and everybody finds this in their studies.

I can show you the same thing for IL-thirty three. Thirty one and thirty three are itch. They speak to itch. So the data is very consistent and that’s a dramatic effect. If you look up at the top, fifty percent of the patients where we have the data have a four point or more change in their PPNRS.

That’s a dramatic effect. That is usually twenty to forty percent, let’s say with a JAK inhibitor, after months of therapy, not after one month. Okay, now what are we doing? I’ll go through this quickly. We’re extending cohort three.

We’re going to add another 24 patients randomized one to one, two hundred milligrams BID, same dose. The only difference, same eligibility, same centers. We expect the same patient selection, etcetera. Everything’s the same. The only thing that’s changed is we’re gonna treat for two months now rather than one month.

And we’re doing that primarily inspired or motivated by the fact that those curves are still going down. Even though, even where those curves are now at one month, many physicians would say, hey, why are you doing, why you extending it? That’s good enough for me right there. Nonetheless, we want to test that in preparation for phase two. Now let’s just review very quickly what we’re talking about here.

We have a really novel drug here. A very novel drug. I can’t help the fact that it’s such an important target. It works across different cancers and inflammatory disease. It just does.

Another drug like that was called Rituxan by the way. So look at the cytokines that we affect. And we have proof of this either in our patients with lymphoma, our patients with AD, animal models, in vitro. I can tell you with certainty that we block IL-four, five, 13, 30 one. We block the Th17 cytokine seventeen, twenty one, 20 two.

We block ILC2s like crazy. I haven’t had time to talk about that. ITK expression in ILC2s is the highest in any cell by far. Not surprising. And we have this incredible effect on T regs.

The other things, let’s take a Dupixent. Dupixent’s a great drug. It’s getting at part of the problem. You have to keep taking it or you fail. Oral versions will be cool to have.

That’s nice. But we’re trying to do something different. We want to be better if we can. So we have a new approach where we’re hitting multiple cytokines, perhaps more than we know of. If you ask me what I think is the most important effect, it’s probably ILC2s and Tregs.

Okay so just to summarize, we’ve shown now in patients with atopic dermatitis that we have a safe tolerable drug, Significant reduction in easy scores, dose dependency, two hundred milligrams bid looks good. Four hundred once a day will be great. We can do that. We’re just not going to do it right away. We have other trials going on in other diseases where we’ll explore that.

Sustained benefit for more than thirty days and our extension cohort is now enrolling. Okay, the key milestone is we expect to have the next slug of twenty four patients, one to one randomization In the fourth quarter of this year, probably around November of this year, we’ll update people on this extension cohort. While in parallel, we’re planning our phase two and that strategy and planning is already underway. Thank you very much for your attention. I think we’re out of time but unless Roger gives me a minute or so.

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