Corvus Pharmaceuticals, Inc. (CRVS) Q2 2026 Earnings Call Transcript

Good afternoon, everyone, and thank you for standing by. Welcome to the Corvus Pharmaceuticals Second Quarter 2026 Business Update and Financial Results Conference Call. At this time, all participants are in listen-only mode. Later, we will conduct a question-and-answer session, and instructions will follow at that time. It is now my pleasure to turn the call over to Zach Cabo of Real Chemistry. Please go ahead, sir.

Thank you, Operator, and good afternoon, everyone. Thanks for joining us for the Corvus Pharmaceuticals Second Quarter 2026 Business Update and Financial Results Conference Call. On the call to discuss the results and business updates are Richard Miller, Chief Executive Officer, Lace Leeds, Chief Financial Officer, Jeff Arcarra, Chief Business Officer, and Ben Jones, Senior Vice President of Pharmaceutical Development. The executive team will open the call with some prepared remarks followed by a question and answer period. I would like to remind everyone that comments made by management today and answers to questions will include forward-looking statements. Forward-looking statements are based on estimates and assumptions as of today and are subject to risks and uncertainties that may cause actual results to differ materially from those expressed or implied by those statements, including the risks and uncertainties described in Corvus' annual report, a quarterly report on Form 10-Q for the quarter ended June 30, 2026, and other filings the company makes with the SEC from time to time. The company undertakes no obligation to publicly update or revise any forward-looking statements except as required by law. With that, I'd like to turn the call over to Leif Lee. Leif?

Thank you, Zach. I will begin with a brief overview of our second quarter 2026 financials and then turned the call over to Richard for a business update. Research and development expenses in the second quarter of 2026 totaled $16 million compared to $7.9 million for the same period in 2025. The increase in R&D expenses was primarily due to higher clinical trial costs associated with the development of socolitinib, as well as an increase in personnel costs. Net loss for the second quarter of 2026 was $18 million compared to a net loss of $8 million for the same period in 2025. Included in the net loss for the second quarter of 2026 and 2025 were non-cash losses of $0.7 million and $0.4 million, respectively, from Corvus' equity method investment in Angel Pharmaceuticals and a non-cash gain of $2 million in the second quarter of 2025 associated with a change in fair value of the company's warrant liability. Total stock compensation expense for the three months ended June 30, 2026, was $2.6 million compared to $1.3 million for the same period in 2025. As of June 30th, 2026, Corvus had cash, cash equivalents, and marketable securities totaling $215.2 million as compared to $56.8 million at December 31st, 2025. Cash, as of June 30th, 2026, included approximately $189.4 million in net proceeds received in a follow-on offering completed in Q1. Also, as announced on June 9th, 2026, Corvus invested $5 million in a $13.5 million financing completed by Angel Pharmaceuticals in the second quarter of 2026. Based on our cash position at June 30th, 2026 and our current plans, we expect our cash to fund operations into the second quarter of 2028. I will now turn the call over to Richard, who will discuss our clinical progress and elaborate on our strategy and plans.

Thank you, Leif, and good afternoon, everyone. Thank you for joining us today for our update call. We are highly focused on Soqualitinib, our first-in-class selective ITK inhibitor. Our efforts are primarily directed to driving patient enrollment and executing on our clinical trials to reach the next milestones for Soqualitinib's two lead opportunities, our Phase 3 Peripheral T-Cell Lymphoma Program, or PTCL, and our Phase 2 Atopic Dermatitis Program. In parallel, we continue to advance socolitinib's development across broad areas of medicine, including near-term plans to initiate trials in adhidradenitis superotiva, and asthma, as well as the ongoing trial at the NIAID in ALPS. The growing body of clinical and preclinical evidence supports the broad potential of socolitinib based on its novel mechanism of action and ability to reset or rebalance immunity. Our ongoing development efforts with Socolitinib position Corvus to deliver key data readouts and milestones associated with our pipeline over the next year. I will start with a brief update on our Phase III trial in relapsed refractory PTCL, which is planned to enroll 150 patients, randomized one-to-one between Socolitinib and standard of care chemotherapy with bilinostat or pralatrexate. The primary endpoint is progression-free survival, or PFS, which with current treatment options has a median of about three months. Enrollment is on track with our expectations, with the next milestone being a futility analysis that will be conducted after a predefined number of PFS events have occurred. Based on current trends, we believe this interim futility analysis will occur in the first quarter of 2027. The futility analysis will be conducted by an independent data monitoring committee that will determine whether the study should be continued or terminated for futility based on available safety and efficacy data at the time. No safety or efficacy data will be publicly released at that time. We remain excited about the potential of Sokal and Nib to provide a new treatment option for patients with relapsed refractory PTCL, particularly given the challenges with current therapies, none of which are fully approved for this indication. I should also mention that the results of our Phase I trial are now in press in BLOOD, the peer-reviewed medical journal of the American Society of Hematology. We expect the results will be published later this year, providing an important overview of so-called NIPs' mechanism of action, rationale, and data obtained from the Phase I trial. Some of this data was presented at the ASH meeting last year. Turning to our other high-priority indications for socolitinib atopic dermatitis, we remain very excited about the data to date and our path forward in this indication. During the second quarter, we presented the final data from the randomized, blinded, placebo-controlled phase 1 trial evaluating socolitinib in patients with moderate to severe atopic dermatitis at the Society for Investigative Dermatology or SID annual meeting. The data demonstrated safety and positive efficacy results, including 75% of so-called indiv patients achieving EZ75 in cohort 4 compared to 20% of placebo patients. Cohort 4 studied is the highest dose and longest dosing period tested in the trial, covering 24 patients randomized in a one-to-one ratio to receive 56-day, 8-weeks, 200-milligram, twice-day daily regimen of socolitinib or equivalent placebo. In addition to the compelling EZ75 result, 25% of socolitinib patients in cohort 4 achieved EZ90 90, and 33% achieved an IgA 0 or 1. No patients receiving placebo achieved EZ90 or IgA 01. Importantly, soculitinib's efficacy results were observed in patients who received prior systemic therapy, some of whom were confirmed to be treatment-resistant to these systemic therapies. The data also showed a dose-dependent efficacy trend and and additional clinical benefit with longer treatment of significant interest was the observation of prolonged treatment benefit extending beyond the period of dosing without evidence of disease rebound disease rebound has been observed with other agents including dupilumab jack inhibitors and stacks stat 6 degraders and inhibitors the finding of socolitinib durable activity was not surprising given research done by Corvus and others demonstrating that ITK blockade results in enhancement of T regulatory function. In the SID presentations, we presented compelling data correlating the induction of Tregs with prolonged clinical responses. If confirmed in future studies, these findings may usher in a new treatment paradigm for autoimmunity, resetting or rebalancing of immunity. On the safety front, no significant safety issues were observed, no severe or serious adverse events were reported, and no significant lab abnormalities were seen. There was no conjunctivitis and, of course, no injection site problems since it is an oral drug. There was no difference in adverse events seen comparing placebo to the active groups. All of this is in line with our experience with socolitinib in lymphoma patients, some of whom are on continuous drug for over two years. Based on its novel mechanism of action, oral dosing, and the safety and efficacy data to date, we believe Socolitnib could become a leading therapy for atopic dermatitis that may find a valuable role in frontline therapy or treatment of relapsed refractory disease. Our strategy is to progress SOCALINIP as quickly as possible through the typical development pathway, similar to the other approved systemic therapies for atopic dermatitis. This includes our Phase 2 trial, the Sierra 1 trial, which is currently enrolling patients, followed by the usual Phase 3 trials. These trials will have a primary endpoint based on EASY score, an IGA score at 12 or 16 weeks of therapy compared to placebo. Our goal is to make Soqualitinib available as soon as possible for patients and then expand the clinical evidence and label with post-marketing studies exploring some of its more unique attributes. The Phase II Sierra trial is planned to enroll approximately 200 patients with moderate to severe atopic dermatitis that have failed at least one prior topical or systemic therapy. It is double-blind, randomized, that includes four cohorts of 50 patients each with socolitinib doses of 200 milligrams once per day, 200 milligrams twice per day, and 400 milligrams once per day, along with a placebo group. The treatment period is 12 weeks with a 90-day follow-up period with no treatment. Again, the primary endpoint is reduction in mean EASY score at 12 weeks compared to the placebo. There is no OLE or open label extension because we believe there will be durability of remissions that we do not want to obscure with additional treatment. Our OLE is no treatment. Enrollment and site activations are on track with our plans. with anticipated enrollment completion in early 2027 and top-line data in the third quarter 2027. In parallel, we are working in close collaboration with our partner in China, ANGEL Pharmaceuticals, on their Phase 1B2 clinical trial of socolitinib in moderate to severe atopic dermatitis. The ANGEL trial has similar design to our Phase 2 trial. It is blinded, placebo-controlled, and is evaluating a 12-week treatment regimen and 90-day follow-up period across a similar range of socolitinib doses. Cohort 1 includes 24 patients randomized evenly to socolitinib doses of 100 mg twice per day, 200 mg once per day, or placebo. Cohort 2 will include 24 patients randomized evenly to so-called doses of 200 milligrams twice per day, 400 milligrams once per day, or placebo. Depending on the results from these 48 patients in cohorts 1 and 2, an additional 60 to 90 patients are anticipated to be enrolled in the phase 2 portion of the study. The trial is open at several leading dermatology centers in China who have been involved in many global registration trials. We anticipate that ANGEL will complete patient enrollment from the first cohort in September, and data from the first cohort of the trial will be available before year-end 2026. The soqualitinib doses studied in this cohort are the same as the lower dose level studied in our Phase I trial, 200 mg total per day, taken as either 100 mg tablet twice per day or 200 mg once per day. The treatment period, however, is significantly longer at 12 weeks compared to the four-week period studied for these doses in our Phase I trial. Recall, we found evidence of efficacy at these lower doses in our Phase I trial with four weeks of therapy. ANGEL is evaluating these doses in a 12-week dosing regimen. We anticipate that data from the Cohort 2 will be available in the second quarter of 2027. So, just to reiterate the timelines for ANGEL, we expect they'll complete enrollment of the first cohort in September, data from this cohort by the end of this year, data from the second cohort in Q2-27. With the ANGEL data, together with our own data that will be generated during the year of 2027, we could be in a position to start a Phase III trial by the end of the year in 2027. In addition to providing clinical data supporting the value of socolitinib and atopic dermatitis, there is another important strategic feature to the ANGEL trial. It is widely reported in the literature that Asian patients with atopic dermatitis have a greater component of TH17 disease and don't respond as well to IL-4 and IL-13 targeted treatments like dupilumab, which is designed to treat TH2 disease and does not respond to TH7 and does not affect TH17. Based on mechanism of action with ITK inhibition, which decreases both Th2 and Th17 cell function and their downstream cytokines, we think this positions socolitinib well for this population. Finding results in these types of patients may serve to broaden and confirm the potential utility in Th17 diseases. An example of the importance of ANGEL to Corvus is our participation in ANGEL's recent $13.5 million financing. Corvus is a founder of ANGEL and continues to be its largest shareholder with $5 million invested in this new financing. The funding is anticipated to support ANGEL's ongoing phase 1b2 trial of socolitinib for atopic dermatitis and a new phase 2 trial of socolitinib for asthma that is expected to start in early 2027. We believe Corvus is positioned to benefit from both of these trials, which will contribute to the overall dataset for socolitinib in these indications and enhance the opportunity for ITK inhibition in the large Chinese inflammation and immunology market. I am the CEO and chairman of ANGEL, and I must add that it has been a privilege and delight to work with the very talented team in China. In the U.S., Corvus remains on track to initiate our own Phase II asthma trial later this year, along with a Phase I-B proof-of-concept trial in patients with HS-hydradenitis superotiva. Our plan to expand the sopolitinib pipeline into these indications is aligned with the biology of ITK inhibition. We started with Th2 cells in T-cell lymphoma. and then move to atopic dermatitis, which is primarily driven by Th2 cells. Next, we are moving to hydrionitis superotiva, which is primarily driven by Th17 cells, and then into asthma, which is primarily driven by Th2 cells, but in certain types, dominated by Th17 cells. There is an important strategy to our clinical programs, With each program designed to not only address an important clinical indication, but also to provide data supporting so-called Nib's mechanism of action and potential utility across a spectrum of underlying drivers of disease. For the Phase 1B hydradenitis superativa trial, we currently anticipate the trial will enroll up to 25 patients with moderate to severe disease. There will be no placebo group. All patients will receive the same dose of socolitinib for 12 weeks, 200 milligrams BID. In addition to measuring safety and the standard hidradenitis superotiva clinical response score, we're also planning to include intensive monitoring of skin and blood biomarkers looking for Th17 effects. We plan to start this study in September. The potential broad utility of socolitinib is an important factor in the design of our planned asthma study. We intend to enroll both the allergic or eosinophilic and non-allergic types of asthma. You may also hear these referred to as T2 and non-T2. Most asthma drugs and most clinical trials address only the allergic T2 patients. We intend to enroll both types based on our mechanism of action, which we believe will address both T2 and non-T2 disease. Approximately 40 to 50 percent of asthma patients have the non-T2 type. It is a very substantial proportion of asthma patients. This doubles the potential population of patients. The trial design will include an interim analysis, which will allow us to discontinue a disease type, such as T2 or non-T2, if there is futility. We remain excited about socolidinib's potential to modulate several key cellular functions that are not currently targeted by approved and in-development stage biologic therapies with an oral tablet. At the SID meeting, Stanford professors Chu and Saren presented new immunologic and biomarker data that showed the potential of ITK inhibition with socolitinib to increase persistent Treg cells and influence multiple inflammatory pathways. These data support the potential for soqualitinib to reset or rebalance the immune system and treat a range of autoimmune and inflammatory diseases. Longer term, it also raises the very intriguing potential to produce drug-free remissions, a long-sought goal. In closing, our confidence in socolitinib continues to grow, and we are making good progress with our key priorities to unlock the opportunity to help a broad range of patients with the ITK inhibition. Over the remainder of the year, we are focused on, first, driving enrollment in our socolitinib Phase III registration PTCL trial and our Phase II atopic dermatitis trial. Second, coordinating closely with our partner in China, China Angel Pharmaceuticals, on their Phase 1B2 atopic dermatitis trial with data from the first cohort before year end and data from the second cohort in the second quarter of 27. Third, advancing the broader soqualitinib opportunity with the planned initiation of trials for asthma and hydradenitis superativa before year end. As we achieve these milestones, we believe there will be increased appreciation for the potential of ITK inhibition and immunomodulation, which could lead to new and better therapies for inflammatory autoimmune fibrotic diseases and cancers. I will now turn the call over to the operator for questions and answer period. Operator?

Thank you. Ladies and gentlemen, we will now begin the question and answer session. If you have a question, please press star followed by the number one on your touchtone phone and you will hear a prompt that your hand has been raised. If you wish to decline from the polling process, please press the star followed by the number two. One moment please for your first question. And your first question comes from the line of Jeff Jones of Oppenheimer. Your line is now open.

Hi, guys. Can you hear me?

Yes, you're fine.

Great. Hi, Richard. And congrats on all the progress and continued progress for this program. You know, on the topic of drug-free remissions, have you had any discussions with the agency about the potential for drug-free remissions and how you would generate a claim on the label and what study design could look like?

So, Jeff, everything we're doing now, the design is straightforward. We compare so-called itinib to placebo, easy scores, easy 75s, IGAs at 12 or 16 weeks, same as everybody else. That's what's required. Those are our protocols. Now, what we do in the remission periods or drug-free periods, just like everybody else, dupilumab, JAK inhibitors, they continue to treat some patients or some they were allocated to placebos to determine whether or not there was disease rebound, and there almost always is, and therefore they determined that the maintenance therapies were required for those diseases. But those were not part of the original approvals. So that is not necessary to do that. Now, we think it's very important if we have sustained remissions that don't require a drug, that represents, I think, an amazing opportunity and unique advantage for soqualitinib. But that is not part of the regulatory strategy. Now, later, should you want to be able to retreat patients, then, of course, additional trials, you would do additional trials to confirm that. Does that make sense?

Yep, makes perfect sense. And then just one follow-up. Obviously, top dose appears to be 200 MIG BID right now. Are you guys doing any work to look at extended release formulations?

So, we do have work going on in the company looking at other formulations. We also have work at the company looking at a lot of work going on in terms of other ITK inhibitors, other chemical structures, et cetera. But I think that we're going to end up here probably with a regimen that's once a day dosing, because I think as we treat patients longer than four weeks, there will be very suitable efficacy with a once a day dosing regimen. Now, we're looking at various regimens. As you know, in our cancer study, we went up to 600 milligrams BID. But we know that a single dose of 200 milligrams will completely saturate the ITK target.

Great. Thank you very much, Richard. And congrats again on all the progress.

Thank you. And your next question comes from the line of Greg Suvanave of Missouri. Please go ahead.

Hi, this is Sam on for Greg. Thanks for taking that question. Congrats on the progress team. Maybe just on the PTCL, it seems that there was a delay in the potential interim readout by a quarter. I'm just curious what the considerations were there, and do you guys still anticipate the phase three data by the end of next year, or is that more of a 20-28 story now?

We anticipate the final data, late 27, as originally stated. The interim analysis, of course, is projected based on events. So it's hard to say exactly when they occur, plus it's based on number of events, according to our statistical plan and agreement with FDA. Based on event rates, we're now projecting early in 2027. that could change a little bit depending on the number of events that occur.

And your next question comes from the line of Paul Choi of Goldman Sachs. Please go ahead.

Hi, this is Eric on for Paul. Thanks for taking the question. I have a quick question. Can you – are you able to use the ANGEL partner, you know, data as part of the safety database for further FDA filings? And are you assuming incrementally better efficacy in the Chinese population for AD, or what are your thoughts? Can you provide us some color on what your thoughts are on, you know, how you expect efficacy to change in the Chinese population?

Yes, we can use the Chinese safety and efficacy data in our regulatory filings and vice versa. They can use our data in their filings. That's one of the reasons we initiated this collaboration several years ago. The idea behind it was accelerated and extend our capabilities and leverage the Chinese population and regulatory authorities and clinical trial infrastructure, all that. So, yes, the data can be shared. The second part of your question is, you know, do I expect it to be? I expect comparable data from ANGEL. It, you know, it is a different study. It's an entirely different clinical trial done at a different point in time at different institutions. Hard to predict exactly, theoretically, I think that we'll be, we could beat the placebo by more because we have this combined effect on the TH17, TH2. So one might expect, let's say, compared to other treatments, a better effect. But, you know, it's going to be hard to compare across clinical trials and across the Pacific Ocean. But the Chinese trials are being done at, I think there's around 10 centers now. They're very good, well-known, academic, large hospital and dermatology clinics. They're commonly sites for large pharma and many other agents in dermatology and atopic dermatitis in particular. So we feel very good about the quality and, you know, the information we're going to get out of there.

Really helpful. Thanks.

Your next question comes from the line of Chacha Young of Jeffries. Please go ahead.

Hi, this is Chacha on for Roger. Thanks for taking my question here. I have two. So one is, can you just tell us more about the thought process behind doing a 12-week versus the 16-week trial for AD for your phase two? And then my second question is, you may have touched on this. I may have missed it. But can you just tell us more about the trial design and some of the baseline characteristics for your HS and asthma trials?

So, we have looked at four weeks on the length of time, we looked initially at four weeks of dosing, then went to eight, and now we're doing 12 weeks of dosing. We saw very good efficacy at four weeks with 200 milligrams BID. We saw very good efficacy at eight weeks with curves continuing to go down. So we'll look at the 12-week data that we get both from ANGEL and from what we're, you know, what we're doing in our phase two, and we'll make a decision beyond that. I know that there's a lot of questions like 16 weeks is magic. It isn't. In our view, if you can get excellent efficacy with a shorter dosing regimen, why wouldn't you do that? So now eventually, if we see the curves continuing to go down, we will go to 16 weeks. But I don't see any reason to do that now. We've had some of our dermatology experts tell us that, gee, your results at four weeks are as good as what you're seeing at 16 weeks. And by the way, I would go back and look at the publications on dupilimab and JAK inhibitors, and you'll see 12 and 16 weeks of treatment. And guess what? those curves plateau at around six or eight weeks. So, most of the efficacy in these 12 and 16-week regimens, go back and look at the easy curves, most of the efficacy is seen in the first couple of months. And after that, the changes are really pretty small. Okay, was there another part of your question? Can you repeat?

Yeah, just about trial design and baseline characteristics for your HS and asthma trial.

Moderate to severe HS, moderate to severe asthma. The only, the asthma trial in particular, that's worth talking about. So, as you know, most studies are allergic or T2, and they'll frequently use an eosinophil count of 300 or 150, above 300 or above 150. That's changing these days as an eligibility requirement. We're allowing both T2 and non-T2. That is, we'll take patients above 150 and below 150 eosinophils. Now, we have looked at our AD data with respect to eosinophil count. We have patients who are above 150 in patients who are below. And in terms of the efficacy, we see basically equal efficacy in both groups. Again, I think that, I think we're starting to now talk about what are the potential advantages of our novel mechanism of action? Well, the non-T2 asthma, if you look at their lungs, you don't see Th2 cells. You see a lot of neutrophils. You see other inflammatory cells that are induced by Th17 cells. Th17 cells make neutrophil attractant, things like GMCSF and things like that. And so we've seen in our animal models that we can affect that. And of course mechanistically we know we're we're blocking the differentiation of the Th17 cell. So that's the the major eligibility there is the eosinophil count. Now of course we look at pheno and other things but but that's the major thing.

All right? Thank you.

And your next question comes from the line of Lee Watsik of Cancer. Please go ahead.

Hi, this is Rubino, one colleague. One question about your asthma program. So you said that you're taking both the T2 and the non-T2 asthma. Can you explain mechanistically why you think superlastic nitinib would be able to work in both T2 and the non-T2 asthma?

Yes, well, the T2, the T2, of course, the reason it's called T2, because it's Th2-mediated. And, of course, as we've, you know, mentioned previously, we'll block the differentiation of Th2 cells in the resulting cytokines. So the Th2 is sort of obvious. The non-T2 is Th17. Mostly you see Th17 cells and other inflammatory cells. but the other inflammatory cells are induced by these Th17 cells. So since we block the differentiation of activated Th2 and Th17 cells, we would expect to see activity in both T2 and non-T2. Now, there's another important cell involved in both of these T2 and non-T, which is called the innate lymphoid cell type 2, highest expression of ITK of any lymphocyte, and we know we inhibit that very well also. So, there are many reasons to think that we would affect the non-T2, and this represents, you know, a great opportunity for us to test this in the clinic, and of course, provides a unique advantage over other asthma treatments. Thank you. It's helpful.

And your next question comes from the line of Kevin Peter of Leidenberg. Please go ahead.

Great. Thanks for taking our questions. I also have a question on the asthma program, specifically the Planned Agile Pharma Phase II program. Can you just comment a little bit more about potential study design there and how the learning from that study will be incorporated into the global program? Thank you.

Sorry, was that the…you're asking about the ANGEL-AD study or… Oh, correct.

Well, I'm not sure I'm… No, the ANGEL-AD study.

Okay. Yeah. The current plan is for the ANGEL trial to basically be identical to ours. Our current plan is to run two identical phase two trials. So it'll be essentially the same protocols in both places, but run independently.

Great.

And on those protocols, can you just help us better understand the decision tree with regard to the ability to drop either T2 or non-T2? Is there a certain number of patients that will kind of go into that assessment? And yeah, just a little bit more on that part of the study design. Thank you.

So, yes, we'll look at, actually, we're going to base it on the percentage of the trial patients treat it. And at that time, we'll look at the data. And we've written that part of it sort of with broad criteria because the success in non-T2 is different than T2. The bar for efficacy is lower. It's harder to treat. So we have general guidelines now after a certain number of patients are treated, if we don't meet a certain threshold in the T2 or the non-T2, we can drop either one of those, or we can drop them all. And the reason we're doing that is because let's just say it's not working in the non-T2. We wouldn't want to continue and dilute out the effect, let's say, positive effect on the T2.

Make sense? It does. Thank you very much.

And there are no further questions at this time? I would like to turn the call back to Zach for the closing remarks.

All right. Thank you, Operator. First of all, thank you, everyone, for joining us today. We're very busy here at Corvus. The team, which I might add, has a lot of experience in conducting randomized trials, is working very hard now meeting the goals I've outlined. We look forward to keeping you updated as we move through the rest of this year and next year. Thank you very much.

Ladies and gentlemen, this concludes today's conference call. Thank you everyone for participation. You may now disconnect.