Corvus Pharmaceuticals at H.C. Wainwright Conference: Socolitinib’s Promising Trials

On Thursday, 27 March 2025, Corvus Pharmaceuticals (NASDAQ: CRVS) presented at the H.C. Wainwright 3rd Annual Autoimmune & Inflammatory Disease Virtual Conference. The company provided an update on its lead drug candidate, socolitinib, highlighting both advancements and challenges in its development. Corvus is actively progressing with clinical trials for relapsed peripheral T cell lymphoma (PTCL) and atopic dermatitis (AD), showcasing promising early results but also facing the complexities of clinical trial enrollments and regulatory pathways.

Key Takeaways

• Corvus’s socolitinib is in a Phase 3 registration trial for relapsed PTCL and a Phase 1 trial for moderate-to-severe AD.
• A Phase 2 trial for Autoimmune Lymphoproliferative Syndrome (ALPS) has been initiated.
• Socolitinib has shown a 39% objective response rate in PTCL and a 55.9% reduction in EASI score for AD.
• The drug is noted for its oral administration, novel mechanism, and favorable safety profile.
• Future plans include a Phase 2 AD trial and exploration of socolitinib in solid tumors.

Financial Results

• ADCETRIS, an antibody drug conjugate, generated $1.6 billion in sales last year.
• Sales were equally split between Hodgkin’s disease and a subset of T cell lymphoma, each contributing $800 million.

Operational Updates

• Phase 3 Registration Trial (PTCL):

- Enrolling in the US, Canada, and Australia with a target of 150 patients.

- Randomized 1:1 to socolitinib or belinostat/pralatrexate, focusing on progression-free survival.

- Allows crossover from the control arm to socolitinib upon progression.

• Phase 1 Atopic Dermatitis Trial:

- Randomized, placebo-controlled, with four cohorts of 16 subjects each.

- Promising results with a 55.9% reduction in EASI score in the active group.

- Data from cohorts 1-3 to be presented at the Society of Investigative Dermatology meeting in May.

• Phase 2 ALPS Trial:

- Conducted by the National Institutes of Allergy and Infectious Diseases.

- Enrolling patients aged 16 and older.

• Solid Tumor Studies:

- Planned to start in the third quarter of the year.

Future Outlook

• Atopic Dermatitis:

- Full data set expected in the third quarter.

- Phase 2 trial expected to start later this year.

• Milestones:

- Presentation of AD data at the Society of Investigative Dermatology meeting in May.

- Initiation of solid tumor studies in the third quarter.

- Start of a Phase 2 AD trial later this year.

Conclusion

Readers interested in further details are encouraged to refer to the full transcript below.

Full transcript - H.C. Wainwright 3rd Annual Autoimmune & Inflammatory Disease Virtual Conference:

Arabella, Analyst, H. C. Wainwright: Annual autoimmune and inflammatory disease conference. My name’s Arabella, and I’m an analyst on the corporate access team at H. C. Wainwright. H.

C. Wainwright is a full service investment bank dedicated to providing corporate finance, strategic advisory, and related services to public and private companies across multiple sectors and regions. We have a total of 24 publishing senior analysts and over six fifty companies covered across all sectors. If you would like more information, please go to our website, hcwco.com. From a logistics standpoint, please make sure you reference the virtual conference online portal that provides your individual links to join meetings and all presentations.

With that said, have a great day, and I’d like to introduce Richard Miller, the CEO of Corvus Pharmaceuticals.

Richard Miller, CEO, Corvus Pharmaceuticals: Thank you, Arabella. And good morning, everyone. And thank you for joining us on this presentation. I have a lot to cover, so I’ll jump right in. My name is Richard Miller.

I’m the CEO of Corvus. So, let me just jump in. What I’d like to spend most time today is on our first in class immune modulatory drug, which is a very specific ITK inhibitor. This drug is now in in a phase three registration trial for relapsed peripheral T cell lymphoma that’s enrolling in The US as well as Canada and Australia. This drug is also, because of its biologic properties in a phase one randomized placebo controlled trial in moderate to severe atopic dermatitis.

And I’ll spend most of my time this morning going through over that data and what we’re anticipating over the next few months. Recently, we also announced that socolitinib, our ITK inhibitor, has begun a phase two trial of being conducted by the national institutes of allergy and infectious disease in a rare genetic disease called, ALPS or autoimmune lymphoproliferative syndrome. The pipeline slide, just to, just to review again, this is a drug that’s in a phase three registration trial. I’ll give you an update on that quickly. We’ll talk about atopic dermatitis and what we expect for the remainder of the year.

And then, talk about a little bit at the end about the ALPS study. Now we’ve always been interested in the intersection of lymphoma, which are cancers of the immune system and autoimmune or inflammatory diseases. And my team and I have, ran this playbook before it was called rituximab. Rituxan is an antibody, of course, reacts with CD 20 was developed in B cell lymphoma and then, extended into various autoimmune diseases. Same thing with ibrutinib.

Ibrutinib is a BTK inhibitor, small molecule, members of my team, including myself, invented and developed ibrutinib, started in B cell lymphomas and now, extended into autoimmune diseases as well. So, returning to this, which in the past successful playbook, socolitinib, interacts or blocks an enzyme called ITK. And we’ll go over the details of that in a moment. Because ITK is expressed in T cells, we start with T cell lymphomas with the intention to extend beyond T cell lymphoma into other cancers, solid cancers, as an immune modulator and into inflammatory or autoimmune diseases. So very quickly, I’ve shown this many times before, but ITK stands for interleukin two inducible T cell kinase.

It is a kinase that’s involved in multiple functions in a T cell. Its tissue distribution is very restricted. It’s only expressed in T cells and NK cells. And that, is one of the factors that I think leads to the safety that we’re seeing in both our lymphoma and our, or immune studies. So it was shown twenty five years ago by some basic scientists that if you genetically knock out ITK, you, you block the differentiation of normal naive helper T cells into Th two and Th 17 cells.

You prevent that those cells from forming. Now those are the cells that make cytokines that you’ve heard about like IL four, IL five, IL 13, IL 17 and others. Those cytokines are involved in a range of autoimmune diseases like psoriasis, atopic dermatitis and many other asthma and many other, immune diseases. Now blocking ITK selectively allows the differentiation of the TH1 lymphocyte, which leads to the killer T cells that are important for rejecting cancer cells and also for rejecting certain infections, especially viral infections. Now this happens because the TH one lymphocyte has a redundant enzyme called resting lymphocyte kinase RLK.

So based on my team’s experience with ibrutinib and with kinase inhibitors, we were able to develop a drug that does or recapitulates what the genetic studies showed many years ago in these genetic knockout mice. That is, we were able to make a drug that very selectively blocks ITK, but spares RLK. This was published, in December. The chemical structure of this compound is shown on this slide. The specificity of binding is shown on this slide and I won’t spend too much time on this.

The details of the enzymology, the chemistry and the immunologic properties can be reviewed in this paper. Now more recently, one other one other aspect of this mechanism that is turning out to be very important, was published by a few different laboratories. And we’ve been able to confirm this on our own lab. And very briefly, ITK is involved in the generation of, T regulatory or immunosuppressive cells, cells that can suppress an autoimmune reaction. That, that occurs when you block ITK.

ITK is responsible for a switch from Th17, a pro inflammatory cell to a suppressor cell. And, some of our coworkers, Avery August at Cornell University showed that either by genetic knockout or by using Sokolitinib, you induce these T regulatory cells, which I believe are going to be turning out to be the most important aspect of this therapeutic modality. Now, as I mentioned earlier, our playbook start in lymphoma, T cell lymphoma in this case, and I’ll be, I’ll go through this very quickly, but T cell lymphoma is a very bad disease, especially when it is not as common as B cell lymphoma, but it also has no approved drugs in the relapse setting. Really no competition, no good approved agents, except for an antibody drug conjugate called ADCETRIS or brentuximab vedotin, which only addresses a very small part of the T cell lymphoma market. Yet ADCETRIS did $1,600,000,000 last year.

Now half of that was Hodgkin’s disease. The other half was, was for T was for this subset of T cell lymphoma. So as you can see on the right here, relapsed T cell lymphoma has a very, very bad prognosis with a median survival of around six and a half months. So I’ll skip some of the phase one data that we’ve done. We did your typical dose escalation single agent study in very refractory T cell lymphoma patients.

As we refined the dose and the eligibility criteria, we did it an extended extension of the study into what we call our phase three eligible patients. We’ve reported this just last week at the T cell lymphoma forum, a meeting in San Diego with, T cell lymphoma experts, and the data that was presented there in 23 evaluate evaluable patients, you can see the waterfall on the right there. We had nine objective responses, six complete responses, three partial, nine out of twenty three, thirty nine percent, twenty six percent CRs. CRs are very hard to get in T cell lymphomas. Our CR rate is probably double, is double what you would see with conventional or standard chemotherapy.

These responses can be long lived as was shown on that swirmer plot. We’ve had patients on this treatment out to over two years in remission. So with this data, we have now initiated or several months ago initiated a phase three registration trial, which is shown here. The design of this trial is to, is is patients with greater than one, but less than or equal to three prior therapies. And the types of T cell lymphoma histologies are shown on the left there.

The eligibility PTCL NOS means peripheral T cell lymphoma not otherwise specified. That’s the most common. The other, types there, collectively, this is about eighty five, ninety percent of the T cell lymphomas. So a one hundred and fifty patients will be randomized 75 into each arm to receive socolitinib two hundred milligrams orally twice a day or either belinostat or pralatrexate, which are two drugs that receives accelerated approval about fifteen years ago. There is no fully approved drug for T cell lymphoma.

Belinostat and pralatrexate are basically chemotherapy drugs are given intravenously and have the usual side effects associated with chemotherapy. The endpoint of this trial is, PFS, progression free survival, and the secondary endpoints are shown there, duration of response, overall survival, etcetera. The study does allow crossover. So if you’re on the control arm and you progress, so you’re an event, then you can crossover to get, soqualitinib. The data we presented last week at the T cell lymphoma forum showed a meet that we had a median PFS of six point two months.

For perspective, the control agents are usually a one to three month published, median PFSs. Balinostatin and Pralotrexate are one to three months. CR rates around ten, twelve percent. As I mentioned, we have about twenty six percent CRs, thirty nine percent overall response, and, PFS of six and, PFS of six point two months with, a 30% PFS at eighteen months and, average duration of therapy, over seventeen months. So our durability looks very good.

Oral agent safety looks very good. And, efficacy appears to be superior to the standard of care agents. Just a few quick examples. I’ve shown this many times. We can see dramatic responses in large tumors.

These tumors, by the way, and this is relevant when I talk about atopic dermatitis, they often involve the skin, T cells that like to go to the skin. Here’s a big mass about the size of a football. This patient had a PR in fifteen days, went on to a CR lasting for two years. In these cancer patients, we can also monitor the effects on normal lymphocytes and cytokines. And as predicted or anticipated by the mechanism of action, we see in the blood and in the tumor changes in normal T cells and cytokines that you would be expected on the mechanism of action.

And I won’t go through these details. These slides are on our website and you can study them more carefully. We are interested in some of these T cell lymphomas that involve the skin like shown here, a patient with what’s called cutaneous T cell lymphoma. This is transformed cutaneous T cell lymphoma. That’s a very poor prognostic factor.

This patient had failed the usual standard therapies, and has been on, socolitinib now for over two years, and has had continued slow regression of cutaneous tumors, cutaneous plaque disease and circulating, leukemic cells. And why I like to show this slide is that this disease under the microscope is very, very very similar histologically to atopic dermatitis, which is also a disease that involves TH2 lymphocytes. So as we were enrolling the, as we are enrolling this trial and getting more data, we recognize that there might be applications of selective ITK inhibitor to autoimmune diseases. And this led us to begin to investigate various animal models and leading to a human clinical trial. So unlike other agents or most of the other agents that you’ve heard about where, where for example, you give an antibody or a drug that blocks a particular cytokine or maybe a couple of cytokines or the receptors like a Dupixent, for example, blocks IL thirteen and four receptor.

Socolitinib’s mechanism is, upstream, blocking the cellular functions or the cellular differentiation that is responsible for the production of potentially many of these cytokines as well as other activities like the regulatory suppression I mentioned earlier. So the potential opportunity here is quite large. TH2 driven diseases blocking, ITK prevents the formation or limits the formation of TH2 cells. So the opportunity opportunities here are asthma and atopic dermatitis, IL seventeen driven diseases like psoriasis, IL five diseases like allergies and even the fibrotic diseases. We’ve presented papers at the ACR meeting last year.

Very nice data in a genetic animal model of scleroderma showing socolitinib very active in that model. That occurs because TH2 cells are critical in fibrotic responses. So the market in atopic dermatitis is quite large. I won’t spend time as I think everyone’s familiar that there’s still demand for effective agents, particularly agents that can be delivered orally. And that’s where, we see one of our key advantages.

So based on this, we have initiated and are well along now in a phase one randomized trial in atopic dermatitis where we take patients with moderate to severe atopic dermatitis that have failed at least one topical or systemic therapy. The schema of the study is shown on this slide. There are four cohorts that are sequentially enrolled. There are 16 subjects per cohort. So you fill up cohort one, then you go to cohort two, three, etcetera.

The 16 subjects are randomized three to one, active to placebo. So there’ll be 12 active and four placebo in each cohort. Now patients receive either placebo or active drug. They’re both tablets. And the tablets are indistinguishable.

So the trial is blinded. The patient and the doctor don’t know what they’re receiving. The company’s not blinded. We have an outside data monitoring board that’s also not blinded. So we can evaluate the data as it’s, as it’s being collected.

And that’s fine in a in a phase one trial. So the treatment duration is twenty eight days. That’s rather short. Most AD studies and trials involve months of therapy, three months, six months even, or beyond that. We elected to do a short, shorter trial for a variety of reasons, including the mechanism of action, which we thought, would result in meaningful activity in a shorter timeframe.

And that’s tending and that’s, turning out to be, a valid consideration. So the different cohorts examine different doses and schedules. And again, I won’t go through every detail here, one hundred milligrams BID, that, two hundred milligrams once a day, two hundred milligrams twice a day, four hundred milligrams once a day. We have completed enrollment and follow-up on cohort one and two. Some of that data was presented at the JPMorgan conference in January of this year.

Cohort three is almost done enrolling, and we’ll have the thirty day follow-up on everyone, by the time of our next presentation, which is going to be at the Society of Investigative Dermatology meeting on May 7, in, in San Diego. We will there report on, the data from cohort one, two and three. The, in addition to the, twenty eight days of treatment, we have been following patients thirty days beyond the treatment. And now in some cases, cohort one and two, even for one month beyond the thirty day drug free period. And the reason for that is, we are gaining confidence that there is a very durable effect and we want to see how long that effect can be maintained, how long the disease control can be maintained after discontinuing the therapy.

So cohorts one, two, and three are nearly done. We’ll look at that data, then we’ll decide about cohort four. We are considering considering, the need for cohort four. We don’t think it’s going to be necessary given that, we’re at doses that give pretty good saturation. We have a very good pharmacodynamic marker.

We can measure saturation of the ITK target. So very quickly, this is just a review of what I showed back in January. At that time, we had enrolled cohort one and two. We didn’t have all the follow-up on cohort two, but here’s the baseline characteristics in cohort one and two. Basically, a couple of just things to point out.

We have a high proportion of African Americans. They tend to do worse with atopic dermatitis and more refractory to disease. None of our patients were receiving, although they failed, none of them were on concomitant topical steroids. There was one placebo who was on, topical steroids. So we have 24 subjects with Sokolitinib and eight receiving placebo.

The cohort one data, we had a longer follow-up and there’s a couple of notable things here on this table. The mean percent reduction in EASI score. EASI score is the measurement of efficacy. It’s a commonly used measure of efficacy. Another commonly used measure of efficacy is called the IGA score, investigator global assessment.

That’s a four point score. Zero and one means you have zero means you have no disease. One, you have very minimal disease. Four, you have a lot of disease. EASI fifty, for example, is we have a 50% reduction in the score, high score being bad.

And if it’s reduced, that shows improvement. So basically the mean percent reduction in easy for placebo was 27. That’s pretty consistent with placebos and other studies. Although more recently that’s been creeping up in various published studies. Our active was 55.9.

That’s pretty good score. Pretty good improvement. Very interesting thing was that over the subsequent four weeks with no therapy, the placebo, a couple of the placebos got a little bit worse. So the score dropped to 19.1 because their disease is progressing. Whereas the patients receiving Sokolitinib had actually gotten some improvement and improved to about minus 60.

Now importantly, what what the approvable endpoints and what are clinically meaningful endpoints are, almost every regulatory authority now is requiring this are the EZ75s and IgA zero and ones. And what you can see here, although the four placebos two, of course, reached an easy of 50, placebos can each reach 50 just based on the waxing and waning of their disease that can occur commonly. It’s not so common to achieve an easy 75 or better. And in fact, we had zero, whereas our, socolitinib group, twenty five percent or forty percent out at, eight weeks. So those are pretty good scores.

I’ll put that in perspective in a moment. So here’s a summary of the data we presented on January 5. We had about a 30% IGA or EASI 75, combine the groups together shown on the far right about a 30% difference from the placebos that were zero. None of the placebos achieved, the EZ seventy five or IG zero one. In most published studies, DUPIXENT and others, you’ll see maybe 15% placebos will achieve, EZ seventy five.

Now regarding safety, we have seen very good safety with, soclotenib not only in our lymphoma studies now, which have, which have been going on for a couple of years and patients have been taking our drug every day for up to two years. But in our AE, in the AD study so far, we see basically, no clinically significant laboratory abnormalities, no significant AEs, no interruption of therapy. Everyone has completed the planned treatment. Now, just comparing socolitinib to other agents. Socolitinib is an oral agent, novel mechanism of action.

To my knowledge, there has never been an ITK inhibitor tested in autoimmune disease, certainly not a selective one. We have the potential advantage, as I mentioned earlier, of blocking the production, the cellular production of multiple different cytokines, as well as exerting suppressive functions and other things, as opposed to a Dupixent or, some of the other, agents or INVOOC, which is JAK inhibitor, or some of the antibodies to IL 31 or, or IL 13. Okay. So, the results so far tell us that, socolotinib may represent a novel medication for autoimmune disease and in particular, atopic dermatitis. It’s oral, has novel mechanism of action, appear safe.

We’ve seen durable and deep responses in patients with moderate to severe disease. I’m not going through the details here, but we’ve seen cytokine changes in the serum that are consistent with the presumed mechanism of action. Responses appear to be very durable, and we think that this is going to be, have potential for a range of autoimmune diseases. We’re continuing, of course, to optimize the dose and schedule, in preparation for a phase two trial, which we believe can begin by the end of the year. Now, one other autoimmune disease just to mention really quickly that I wanna close on, which we’re excited about.

There is a very serious autoimmune disease called autoimmune lymphoproliferative syndrome. It’s a genetic disease. We showed in, a mouse model a couple of years ago that, sokolitinib was extremely effective in this mouse model. There is a human equivalent of the mouse genetic defect. It’s a disease that children are born with and they start to get sick when they’re about two years old.

Lymphadenopathy and a lot of autoimmune problems. There are no good treatments for ALPs. It’s unusual disease. There are about 2,500 patients or cases in The U. S.

They can live into their 30s, 40s and 50s, but have a lot of problems with infection, lymphadenopathy, anemia and cytopenias, etcetera. So we now have a trial going on at the NIH where we’re looking at patients who are age 16 and older because we can’t go right to children yet. And, this could be, really, the first, effective or useful drug. Currently these patients get cyclophosphamide and steroids and, and, sirolimus, other chemotherapy type agents to control their disease. So milestones coming up listed here really quickly.

Atopic dermatitis cohort two data, we’ve already completed the, ALPS Phase II trial initiation, atopic dermatitis data at the Society of Investigative Dermatology, meaning cohort one, two and three. Not sure we’re going to need to do four. Full data set with much longer follow-up later in the year, third quarter. Solid tumor studies starting. I didn’t really talk about that in the third quarter and a phase two trial starting later this year.

With that, I want to thank everyone for their attention. And again, these slides are up on our website. And, be happy to take any questions if we have time, Arabella or

Arabella, Analyst, H. C. Wainwright: other. Hi, Richard. Thank you so much for the great presentation. Unfortunately, I don’t think we have time for questions.

Richard Miller, CEO, Corvus Pharmaceuticals: Okay. That’s fine.

Arabella, Analyst, H. C. Wainwright: But we really appreciate the time and effort it takes. So thank you from the team.

Richard Miller, CEO, Corvus Pharmaceuticals: Alright. Thanks again. Bye, guys.

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