管理層發言
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. We will conduct a question-and-answer session later in the call, and instructions will follow at that time. It is now my pleasure to turn the call over to Zack Kubow 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 A. Miller, Chief Executive Officer; Leiv Lea, Chief Financial Officer; Jeffrey Arcara, 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 and quarterly report on Form 10-Q for the quarter ended 06/30/2026 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 would like to turn the call over to Leiv Lea. Leiv?
Thank you, Zack. I will begin with a brief overview of our second quarter 2026 financials and then turn the call over to Richard for a business update. Research and development expenses in the second quarter of 2026 totaled $16.0 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 Soquelitinib as well as an increase in personnel costs. Net loss for the second quarter 2026 was $18.0 million compared to a net loss of $8.0 million for the same period in 2025. Included in the net loss for the second quarter of 2026 and 2025 were noncash losses of $700 thousand and $400 thousand, respectively, from Corvus' equity method investment in Angel Pharmaceuticals, and a noncash gain of $2.0 million in the second quarter of 2025 associated with a change in fair value of the company's warrant liability. Total stock-based 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 06/30/2026, Corvus had cash, cash equivalents, and marketable securities totaling $215.0 million as compared to $56.8 million at 12/31/2025. Cash as of 06/30/2026 included approximately $189.0 million in net proceeds received in a follow-on offering completed in the first quarter. Also announced on 06/09/2026, Corvus invested $5.0 million in a $13.5 million financing completed by Angel Pharmaceuticals in the second quarter of 2026. Based on our cash position at June 30, 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, Leiv Lea, and good afternoon, everyone. Thank you for joining us today for our update call. We are highly focused on Soquelitinib, 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 Soquelitinib's two lead opportunities: our Phase III peripheral T cell lymphoma program, or PTCL, and our Phase II atopic dermatitis program. In parallel, we continue to advance Soquelitinib's development across broad areas of medicine, including near-term plans to initiate trials in hidradenitis suppurativa and asthma, as well as the ongoing trial at NIAID in ALPS. The growing body of clinical and preclinical evidence supports the broad potential of Soquelitinib based on its novel mechanism of action and ability to reset or rebalance immunity. Our ongoing development efforts with Soquelitinib 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 1-to-1 between Soquelitinib and standard-of-care chemotherapy with belinostat 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 Soquelitinib 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 1 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 Soquelitinib's mechanism-of-action rationale and data obtained from the Phase 1 trial. Some of this data was presented at the ASH meeting last year. Turning to our other high-priority indication for Soquelitinib, 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 Soquelitinib in patients with moderate-to-severe atopic dermatitis at the Society for Investigative Dermatology Annual Meeting. The data demonstrated safety and positive efficacy results, including 75% of Soquelitinib patients achieving EASI-75 in cohort 4 compared to 20% of placebo patients. Cohort 4 was the highest dose and longest dosing period tested in the trial, covering 24 patients randomized in a 1-to-1 ratio to receive a 56-day (8 weeks) 200 mg twice-daily regimen of Soquelitinib or equivalent placebo. In addition to the compelling EASI-75 result, 25% of Soquelitinib patients in cohort 4 achieved EASI-90 and 33% achieved an IGA 0 or 1. No patients receiving placebo achieved EASI-90 or IGA 0 or 1. Importantly, Soquelitinib's efficacy results were observed in patients who received prior systemic therapy, some of whom were confirmed to be treatment-resistant to those systemic therapies. The data also showed a dose-dependent efficacy trend 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, JAK inhibitors, and STAT6 degraders and inhibitors. The finding of Soquelitinib's 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 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 laboratory abnormalities were seen. There was no conjunctivitis and, of course, no 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 Soquelitinib 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 Soquelitinib 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 Soquelitinib as quickly as possible through the typical development pathway similar to the other approved systemic therapies for atopic dermatitis. This includes our Phase II trial, the SEERA-1 trial, which is currently enrolling patients followed by the usual Phase III trials. These trials will have primary endpoints based on EASI score and IGA score at 12 or 16 weeks of therapy compared to placebo. Our goal is to make Soquelitinib 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 SEERA-1 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 a double-blind, randomized trial that includes four cohorts of 50 patients each with Soquelitinib doses of 200 mg once per day, 200 mg twice per day, and 400 mg once per day, along with a placebo group. The treatment period is 12 weeks with a 90-day follow-up period with no treatment, and the primary endpoint is reduction in mean EASI score at 12 weeks compared to placebo. There is no open-label extension because we believe there will be durability of remissions that we do not want to obscure with additional treatment. Enrollment and site activations are on track with our plans, with anticipated enrollment completion in early 2027 and topline data in the third quarter of 2027. In parallel, we are working in close collaboration with our partner in China, Angel Pharmaceuticals, on their Phase 1b/2 clinical trial of Soquelitinib in moderate-to-severe atopic dermatitis. The ANGEL trial has a similar design to our Phase II 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 Soquelitinib doses. Cohort 1 includes 24 patients randomized evenly to Soquelitinib doses of 100 mg twice per day, 200 mg once per day, or placebo. Cohort 2 will include 24 patients randomized evenly to Soquelitinib doses of 200 mg twice per day, 400 mg 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 that have been involved in many global registration trials. We anticipate that ANGEL will complete patient enrollment for the first cohort in September and data from the first cohort of the trial will be available before year-end 2026. The Soquelitinib doses studied in this cohort are the same as the lower dose levels studied in our Phase 1 trial—200 mg total per day, taken as either a 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 1 trial. Recall we found evidence of efficacy at these lower doses in our Phase 1 trial with four weeks of therapy. Angel is evaluating these doses in a 12-week dosing regimen. We anticipate that data from Cohort 2 will be available in the second quarter of 2027. So, just to reiterate the timelines for Angel: we expect they will complete enrollment of the first cohort in September, data from this cohort by the end of this year, and data from the second cohort in Q2 2027. With the ANGEL data, together with our own data that will be generated during 2027, we could be in a position to start a Phase III trial by the end of 2027. In addition to providing clinical data supporting the value of Soquelitinib in 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 do not respond as well to IL4 and IL13-targeted treatments like dupilumab, which is designed to treat Th2 disease and does not affect Th17. Based on the mechanism of action with ITK inhibition, which decreases both Th2 and Th17 cell function and their downstream cytokines, we think this positions Soquelitinib well for this population. Finding results in these types of patients may serve to broaden and confirm the potential utility in Th17-driven 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 $5.0 million invested in this new financing. The funding is anticipated to support Angel's ongoing Phase 1b/2 trial of Soquelitinib for atopic dermatitis and a new Phase 2 trial of Soquelitinib 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 data set for Soquelitinib 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 1b proof-of-concept trial in patients with hidradenitis suppurativa (HS). Our plan to expand the Soquelitinib pipeline into these indications is aligned with the biology of ITK inhibition. We started with T cells in T-cell lymphoma and then moved to atopic dermatitis, which is primarily driven by Th2 cells. Next, we are moving to hidradenitis suppurativa, which is primarily driven by Th17 cells, and then into asthma, which is primarily driven by Th2 cells but in certain types is 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 Soquelitinib's mechanism of action and potential utility across a spectrum of underlying drivers of disease. For the Phase 1b hidradenitis suppurativa 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 Soquelitinib for 12 weeks, 200 mg twice daily. In addition to measuring safety and the standard hidradenitis suppurativa clinical response score, we are 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 Soquelitinib 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, which you may also hear 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% of asthma patients have the non-T2 type. It is a very substantial proportion of asthma patients, which 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 Soquelitinib's potential to modulate several key cellular functions that are not currently targeted by approved and in-development biologic therapies, and to do so with an oral tablet. At the SID meeting, Stanford Professors Chiou and Sarin presented new immunologic and biomarker data that showed the potential of ITK inhibition with Soquelitinib to increase persistent Treg cells and influence multiple inflammatory pathways. These data support the potential for Soquelitinib 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 Soquelitinib 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 ITK inhibition. Over the remainder of the year, we are focused on, first, driving enrollment in our Soquelitinib Phase III registration PTCL trial and our Phase II atopic dermatitis trial; second, coordinating closely with our partner in China, Angel Pharmaceuticals, on their Phase 1b/2 atopic dermatitis trial with data from the first cohort before year-end and data from the second cohort in the second quarter of 2027; and third, advancing the broader Soquelitinib opportunity with the planned initiation of trials for asthma and hidradenitis suppurativa 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.
分析師問答
I will now turn the call over to the operator for the question-and-answer period. Ladies and gentlemen, we will now begin the question-and-answer session. Press star followed by 1 on your touch-tone phone to ask a question. One moment, please, for your first question. Your first question comes from the line of Jeffrey Jones of Oppenheimer. Your line is now open.
Hi, Richard, and congrats on all the continued progress for this program. 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 that study design could look like?
Jeffrey, everything we are doing now is straightforward—comparing Soquelitinib to placebo on EASI scores, EASI-75, and IGA at 12 or 16 weeks. That is what is required and what is in our protocols. Regarding remission periods or drug-free periods, studies like dupilumab and JAK inhibitors continued to treat some patients while others were allocated to placebo to determine whether there was disease rebound, and there almost always is; therefore maintenance therapies were found to be required for many patients. Those maintenance or rebound assessments were not part of the original approvals. So they are not necessary for initial approval. Now, we think it is very important that if we observe sustained remissions that do not require drug, that represents an exceptional and unique advantage for Soquelitinib. But that is not part of the initial regulatory strategy. Later, if we wanted to generate a specific claim around retreatment or drug-free remission, we would conduct additional trials to confirm that. Does that make sense?
Yes, makes perfect sense. And then just one follow-up: obviously top dose appears to be 200 mg BID right now. Are you doing any work to look at extended-release formulations?
We do have work going on in the company looking at other formulations. We also have work on other ITK inhibitors and other chemical structures, etc. I think we will likely end up with a once-daily dosing regimen because, as we treat patients longer than four weeks, there will probably be suitable efficacy with once-daily dosing. We are examining various regimens. In our cancer study, we went up to 600 mg BID, but we know that a single dose of 200 mg will completely saturate the ITK target. Thank you very much, and congrats again.
Thank you. Your next question comes from the line of Graig Suvannavejh of Mizuho. Please go ahead.
Hi. This is Sam on for Greg. Thanks for taking our question, and congrats on the progress. Maybe just on the PTCL: it seems that the potential interim readout was delayed by a quarter. I am curious about the considerations there and whether you still anticipate the Phase III final data by the end of next year, or is that now more of a 2028 story?
We anticipate the final data late 2027, as originally stated. The interim analysis timing is projected based on events, so it's hard to say exactly when it will occur. It is based on the number of events according to our statistical plan and agreement with the FDA. Based on event rates, we are now projecting the interim futility analysis in early 2027. That could change a bit depending on the number of events that occur.
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. Are you able to use the Angel partner data as part of the safety database for further FDA filing? And are you assuming incrementally better efficacy in the Chinese population for atopic dermatitis? Can you provide color on how you expect efficacy to differ 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 is one of the reasons we initiated the collaboration several years ago: to accelerate and leverage the Chinese population, regulatory authorities, and clinical trial infrastructure. As for efficacy expectations, I expect comparable data from Angel, but it is a different study at different centers and a different point in time, so direct comparisons are difficult. Theoretically, because Soquelitinib affects both Th17 and Th2 pathways, one might expect favorable effects in populations with a larger Th17 component, such as some Asian patients. But cross-trial comparisons are challenging. The Angel trial sites are reputable academic hospitals and dermatology clinics commonly used in global registration trials, so we feel good about the quality of the data we will receive.
Your next question comes from the line of Cha Yang of Jefferies. Please go ahead.
Hi. This is Cha on for Roger. I have two questions. First, can you explain the thought process behind doing a 12-week versus a 4- or 16-week trial for atopic dermatitis for your Phase II? Second, can you provide more details about trial design and baseline characteristics for your HS and asthma trials?
We initially studied four weeks of dosing, then went to eight weeks, and now are doing 12 weeks. We saw very good efficacy at four weeks with 200 mg BID and continued improvement at eight weeks. We will review the 12-week data from both Angel and our Phase II and then decide whether to evaluate longer durations beyond that. Many dermatology experts have noted that results at four weeks can be as good as at 16 weeks, and when you review published curves for dupilumab and JAK inhibitors, most of the efficacy is observed in the first 6 to 8 weeks; curves tend to plateau thereafter. So we do not see a reason to require 16 weeks now; we will consider it if the data support extending treatment. Regarding HS and asthma, the HS trial will enroll patients with moderate-to-severe disease and will be an open-label cohort of up to 25 patients receiving 200 mg BID for 12 weeks with biomarker sampling for Th17 effects. For asthma, the key eligibility is eosinophil count; unlike many trials that require elevated eosinophils for a T2 population, we plan to enroll both T2 and non-T2 patients. We have seen essentially equal efficacy in our AD data across patients above and below 150 eosinophils. Mechanistically, non-T2 asthma is associated with Th17-driven inflammation and neutrophilic infiltration, and we have seen in animal models that ITK inhibition can affect those pathways. So our asthma trial will include both patient types, with an interim analysis allowing us to discontinue one disease type for futility if necessary.
Your next question comes from the line of Li Watsek of Cantor. Please go ahead.
Hi. This is Rubina on for Watsek. One question about your asthma program: you said you are targeting both T2 and non-T2. Can you explain mechanically why you think Soquelitinib would be able to work in both T2 and non-T2?
Yes. T2 asthma is mediated by Th2 cells, and ITK inhibition blocks differentiation and function of those Th2 cells and their cytokines. Non-T2 asthma is often associated with Th17 inflammation, which leads to neutrophil recruitment via cytokines and chemokines such as GM-CSF. ITK inhibition blocks Th17 differentiation and function as well. Additionally, innate lymphoid cells type 2 (ILC2s), which also express ITK, are involved in both T2 and non-T2 pathways, and we inhibit those cells as well. For these reasons, we expect activity in both T2 and non-T2 asthma, which represents a unique opportunity versus other asthma treatments that primarily target T2 disease.
Your next question comes from the line of Aydin Huseynov of Ladenburg. Please go ahead.
Great. Thanks for taking our questions. I also have a question on the Angel Pharma planned Phase II asthma program. Can you comment on potential study design there and how the learnings from that study will be incorporated into the global program?
The Angel asthma study is planned to be essentially identical to our protocol. Our current plan is to run two identical Phase II trials—one led by Corvus and one by Angel—with the same design, run independently. That will allow us to generate complementary datasets and potentially accelerate development if both trials show supportive results.
On those protocols, can you 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 go into that assessment and any other specifics on that part of the study design?
Yes. We will base decisions on the percentage of trial patients treated. After a prespecified number of patients have been treated, we will look at interim data with broad criteria. The bar for efficacy differs between T2 and non-T2 populations; non-T2 is harder to treat and may have a lower threshold for declaring futility. If a cohort does not meet its threshold, we may drop that cohort to avoid diluting a positive signal in the other cohort. This approach helps preserve power to detect an effect in the subgroup that benefits.
There are no further questions at this time. I would like to turn the call back to management for closing remarks.
All right. Thank you, operator. First of all, thank you, everyone, for joining us today. We are 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 have 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 your participation. You may now disconnect.