Corvus Pharmaceuticals, Inc. (NASDAQ:CRVS) Q4 2024 Earnings Call Transcript

Corvus Pharmaceuticals, Inc. (NASDAQ:CRVS) Q4 2024 Earnings Call Transcript March 25, 2025

Corvus Pharmaceuticals, Inc. misses on earnings expectations. Reported EPS is $-0.18 EPS, expectations were $-0.12.

Operator: Good afternoon, everyone. Thank you for standing by. And welcome to the Corvus Pharmaceuticals Fourth Quarter and Full Year 2024 business update and financial results conference call. At this time, all participants are in a listen-only mode. Later, we will conduct your question and answer session, and instructions will follow at that time. It is now my pleasure to turn the call over to Mr. Zack Kubow of PR Chemistry. Thank you. Please go ahead, sir.

Zack Kubow: Thank you, operator, and good afternoon, everyone. Thanks for joining us for the Corvus Pharmaceuticals fourth quarter and full year 2024 business update and financial results conference call. On the call to discuss the results and business updates are Richard Miller, Chief Executive Officer, Leiv Lea, Chief Financial Officer, Jeff Arcara, Chief Business Officer, and Ben Jones, Senior Vice President of Regulatory and Pharmaceutical Sciences. 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’s annual report on Form 10-K for the year ended December 31, 2024, that was filed today 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 Leiv Lea. Leiv?

Leiv Lea: Thank you, Zack. Excuse me. I will begin with a quick overview of our fourth quarter and full year 2024 financials and then turn the call over to Richard for a business update. Research and development expenses in the fourth quarter of 2024 were $5.2 million compared to $3.2 million for the same period in 2023. The $2 million increase was primarily due to an increase in socalitinib clinical trial expenses. R&D expenses for the full year 2024 totaled $19.4 million compared to $16.5 million for the full year 2023. For the full year 2024, the increase of approximately $2.9 million was primarily due to higher clinical trial costs associated with the development of socalitinib. The net loss for the fourth quarter of 2024 was $12.1 million, including a non-cash loss of $2.2 million related to Angel Pharmaceuticals, our partner in China.

In addition, we recorded a non-cash loss of $2.3 million from the change in fair value of Corvus’ warrant liability during the fourth quarter of 2024. This compares to a net loss of $6.7 million for the same period in 2023, which included a $1.4 million non-cash loss related to Angel Pharmaceuticals. The net loss for the full year 2024 was $63.3 million, including a $3.2 million non-cash loss related to Angel and a non-cash loss of $33.4 million from the change in fair value of Corvus’s warrant liability during the year. This compares to a net loss of $27.0 million, including a $5.3 million non-cash loss related to Angel for the full year 2023. Total stock compensation expense for the fourth quarter and full year 2024 was $0.8 million and $3 million, respectively, compared to $0.6 million and $2.1 million for the same periods in 2023.

As of December 31, 2024, Corvus had cash, cash equivalents, and marketable securities totaling $52 million as compared to $27.1 million at December 31, 2023. In May 2024, of note, associated with our financing, we also sold common stock warrants that have an exercise price of $3.50 and expire on June 30, 2025. Two investors early exercised their warrants during the fourth quarter of 2024, resulting in $18.6 million in cash to the company. If all the remaining warrants are exercised, we’ll receive approximately $41 million in additional cash. Based on our current plans, we anticipate our cash provides runway into the first quarter of 2026. I will now turn the call over to Richard, who will discuss our clinical progress and elaborate on our strategy and plans.

Thanks, Leiv, and good afternoon, everyone.

Richard Miller: Thank you for joining us today for our business update call. As we look into 2025, we remain optimistic on the potential for socalitinib to provide a powerful new approach for the treatment of a broad range of immune diseases and cancer. Socalitinib is well positioned as a first-in-class oral therapy that selectively inhibits ITK to modulate and control parallel signaling pathways in the immune system. Our confidence is backed by a strong and growing body of evidence both from our clinical efforts and preclinical research conducted by us and others. First, we have reported a 39% objective response rate from our Phase 1 trial of socalitinib in patients with relapsed T-cell lymphoma. This included a 26% complete response rate, which is more than double the rate seen with standard chemotherapies.

Based on this data, we are enrolling a registrational Phase 3 trial of socalitinib in patients with relapsed peripheral T-cell lymphoma, and we have gained a significant amount of experience that we are applying to our other socalitinib programs. Second, we observed a favorable safety and efficacy profile from interim data from our Phase 1 trial of socalitinib in patients with moderate to severe atopic dermatitis. This includes significant responses in the socalitinib treatment groups compared to placebo for the clinically significant endpoints of Investigator Global Assessment (IGA) zero or one and Eczema Area and Severity Index (EASI) 75. Third, preclinical data supports the potential of ITK inhibition in a broad range of indications, including solid tumors, immune conditions such as autoimmune lymphoproliferative syndrome (ALPS), systemic sclerosis, pulmonary fibrosis, and graft-versus-host disease, and inflammatory conditions such as asthma, psoriasis, and inflammatory bowel disease.

The data also highlights its mechanism of action, skewing differentiation to TH1 cells, reducing TH2 and TH17 cells, and their downstream cytokines, and promoting a switch to T regulatory cells that suppress inflammation. Given the broad applicability of its mechanism of action, we view the potential of ITK inhibition as analogous to BTK inhibition, a category that members of the Corvus team, including myself, helped to develop. BTK inhibitors were first approved for B-cell malignancies and then expanded into autoimmune conditions. Today, I will recap our previously reported data in atopic dermatitis and next steps for the trial, share some detail on the recently initiated NIH trial in ALPS, and highlight the upcoming milestones for socalitinib.

In January, we reported interim data from the Phase 1 trial with socalitinib in patients with moderate to severe atopic dermatitis. The trial includes four cohorts that are enrolling sixteen subjects each at a three-to-one ratio of active to placebo. Twelve active, four placebo. The trial is double-blind, meaning the patient and the doctor do not know what they’re taking, and the active medicine and placebo are indistinguishable tablets. The company and the data review committee are not blinded. The treatment period is twenty-eight days, and then we follow patients off therapy for another thirty days. The twenty-eight-day treatment period is relatively short compared to later-stage atopic dermatitis studies with other agents, which typically treat up to sixteen weeks or longer.

The primary endpoint is safety and tolerability; secondary endpoints measure based on IGA and EASI scores along with patient-reported measures of itch and biomarkers. The first two cohorts received socalitinib doses of one hundred milligrams twice a day and two hundred milligrams once per day. The same total dose of drug was used in the first two cohorts. Based on our lymphoma studies, we know that one hundred milligrams will provide fifty percent of occupancy of the target, and two hundred milligrams will provide about eighty to a hundred percent occupancy. In January, we reported data from sixteen patients in cohort one and ten patients in cohort two for which twenty-eight days of treatment had been completed. In total, from the combined cohort one and two, this included nineteen patients treated with socalitinib and seven patients treated with placebo.

In the socalitinib group, twenty-six percent achieved IGA zero or one, and thirty-seven percent achieved EASI 75. Recall, these have been accepted as measures of clinical benefit and have been used as the basis for regulatory approval for several approved treatments for atopic dermatitis. In the placebo group, no patients achieved IGA zero or one or EASI 75. No significant safety issues were observed, and no clinically significant laboratory abnormalities were seen. Cohort three of the trial, which administers a dose of two hundred milligrams twice a day, that is twice the total daily dose we used in the earlier cohorts, is nearing completion of enrollment, and some patients have already reached the twenty-eight-day follow-up period. The efficacy results so far in the trial, including full cohort one and two, and the initial experience in cohort three, have been positive and consistent with what we have reported to date.

No patients in the active treatment groups received concomitant topical steroids or required rescue medications. One patient in the placebo group did receive concomitant topical corticosteroids. In cohorts one and two, two placebos experienced flares in their disease during the twenty-eight-day treatment period, whereas no disease flares were seen in the patients receiving active drug during the twenty-eight-day treatment period as well as the follow-up period off treatment. Socalitinib has been very safe to date as well, with no patients requiring interruption of therapy. We now have experience in over one hundred patients with lymphoma and atopic dermatitis, representing more than nine thousand patient days of treatment, including patients with lymphoma on therapy for up to two years.

We continue to believe that socalitinib is an active medicine with several advantages: oral route of administration, attractive safety profile, a novel mechanism of action with an opportunity for unique positioning, including the potential to bridge between topical therapies and systemic injectables. We plan to report data covering the first three cohorts at the Society of Investigative Dermatology meeting taking place May 7 to 10 in San Diego. Our abstract has already been accepted for an oral and poster presentation at this meeting. Outside of atopic dermatitis, we continue to enroll patients in our registrational Phase 3 trial of socalitinib in patients with relapsed PTCL. Recently, we presented updated data from our Phase 1 trial at the T-cell Lymphoma Forum with longer follow-up showing that the median progression-free survival is 6.2 months and the eighteen-month progression-free survival is 30%.

The median duration of response was 17.2 months. DFS or progression-free survival is the primary endpoint of our Phase 3 trial, which is comparing socalitinib to either belinostat or pralatrexate, the standard of care agents with reported median PFSs of about three months and eighteen-month PFSs of under 20%. We also have recently announced the initiation of enrollment in a Phase 2 trial of socalitinib in patients with ALPS, autoimmune lymphoproliferative syndrome. This study not only addresses a disease with unmet need but will also provide additional information on the activity of selective ITK inhibition in a serious autoimmune disease. ALPS patients are born with a genetic mutation in FAST signaling that results in lymphoproliferation and a myriad of autoimmune problems such as anemia, neutropenia, thrombocytopenia, and others.

Some of these patients go on to also develop malignant lymphomas. The ALPS trial is being conducted under a clinical research and development agreement with the National Institutes of Allergy and Infectious Diseases at NIH. It will enroll up to thirty patients aged sixteen years or older with confirmed ALPS based on genetic testing. There will be two dosing cohorts, two hundred milligrams or four hundred milligrams of socalitinib twice per day for a period of up to 360 days. The primary endpoint of the trial is efficacy determined by reductions in spleen and lymph node volumes as measured by CT scans. In addition, improvements in cytopenias or lowered blood cell levels will be assessed by complete blood counts. Improvements in cytopenias can improve quality of life and overall health and serve as a biomarker associated with ALPS disease activity, including autoantibody levels that are reactive with red cells, white cells, and/or platelets.

Secondary endpoints include safety and tolerability. We are also planning a single-agent socalitinib solid tumor trial in relapsed renal cell cancer or RCC, representing a new approach to immunotherapy of this disease. We plan to initiate this trial during the third quarter of 2025. Outside of socalitinib, we also continue to advance our other clinical stage development programs. We have been one of the leaders in the development of adenosine A2A receptor antagonists for the treatment of cancer with ciforadenant. This includes our Phase 1b/2 clinical trial that is being conducted in collaboration with the Kidney Cancer Research Consortium. The trial was evaluating ciforadenant as a potential first-line therapy for metastatic renal cell cancer in combination with ipilimumab and nivolumab.

The study has reached full enrollment of sixty patients at sites including MD Anderson, Vanderbilt, Duke, and the University of Pennsylvania. The patients are being followed, and we anticipate our partners at the Kidney Cancer Research Consortium will present data from the trial sometime later in 2025. Finally, I should mention that we are advancing several second and third-generation ITK selective inhibitors designed to preferentially affect particular ITK signaling pathways. Summarizing the outlook for the remainder of 2025, we remain focused on advancing the broad opportunity for socalitinib, which has several potential upcoming catalysts. This includes, number one, additional data from the Phase 1 trial in atopic dermatitis in May at the Society for Investigative Dermatology meeting; number two, full data from the Phase 1 trial in atopic dermatitis in the third quarter; number three, initiating a Phase 2 clinical trial with socalitinib in solid tumors in the third quarter of 2025 with initial data anticipated in the first half of 2026; number four, initiating a Phase 2 atopic dermatitis trial in late 2025; number five, continuing to activate sites and drive enrollment in the registration of socalitinib and PTCL, driving towards interim data in late 2026.

And depending on enrollment trends, it’s possible we could see initial data from the Phase 2 ALPS study in late 2025 or early 2026. Our current cash gives us runway into the first quarter of 2026, allowing us to execute on these important milestones and further demonstrate the value of our programs and, in particular, the significant opportunity for ITK inhibition in immunology and cancer. We look forward to providing updates on our programs. I will now turn the call over to the operator for a question and answer period.

Q&A Session

Operator: Thank you. Ladies and gentlemen, we will now begin the question and answer session. Should you wish to cancel your request, please press star followed by the pound key. If you’re using a speakerphone, please lift the handset before pressing any keys. One moment, please, for your first question. Thank you. And your first question comes from the line of Jeff Jones from Oppenheimer. Please go ahead.

Jeff Jones: Good afternoon, guys, and thanks for taking the question. Lots of data updates to come, so really exciting time for you guys. I guess starting out on the AD front and the update in May, will the what would should we expect full data on cohorts three as well as additional patients on cohort two? And then as you think about the efficacy hurdle there, what do you guys have in your head to move this ahead in the Phase 2a that you just mentioned? Or, you know, in just competitiveness in the field.

Richard Miller: Okay. So Jeff, the meeting in May, the Society of Investigative Dermatology, we intend to report the full dataset on cohort one, the full dataset on cohort two. We’ve already completed enrollment and follow-up in those two cohorts. Cohort three is almost completed enrollment, twenty-eight-day follow-up is coming in on patients now. We’re also gonna have additional one-month follow-up beyond that. So we’ll have the full data for cohort one, two, and three, I also expect to have biomarker data for those first three cohorts as well.

Jeff Jones: Okay. Great. And then just in terms of the success hurdles and efficacy bar that you guys are looking at?

Richard Miller: Well, first of all, we’re pretty pleased with the efficacy we saw in cohort one and two. Let me remind you of you know, that’s twenty-eight days of treatment. We see, what, a thirty percent difference in some of these twenty-five, thirty-five percent difference between placebo, which was zero in cohort one and two, and our actives, that’s a pretty good number. And, you know, that number sustained or improved would be, you know, would be very good. In our opinion. Now, of course, many people are asking about what would happen if we increase the duration of therapy, and that’s something that we’re thinking about and will come in time. So we’re pretty pleased with the efficacy results we have to date in terms of a competitive landscape.

Of course, we’re oral. We have a different mechanism of action. Safety looks really good so far. Convenience, the study, the design of our study was really intended to determine whether or not selective inhibition of ITK had some role in immune diseases. Is there some signal, some indication of efficacy in an autoimmune disease? And I think we’ve got that. Now, of course, as we think about Phase 2 trials and beyond, we’ll begin to think about, you know, what it what’s required for registration, etcetera. But I think from a competitive standpoint, to my knowledge, we’re the only selective ITK inhibitor. I know there are some other companies that have ITK inhibitors and are talking about it now, but they’re not selective, and we view that as critical in the biology.

And so I think we’re, you know, in pretty good shape on this.

Jeff Jones: Great. Richard. I’ll hop back in queue.

Operator: Thank you. And your next question comes from the line of Aydin Huseynov from Ladenburg Thalmann. Please go ahead.

Aydin Huseynov: Hi. Good afternoon, everyone. Richard, congratulations with the progress this quarter. I got a couple of questions here. So regarding the potential cohort four, so could you clarify your plans for cohort four, whether you still would like to enroll in four hundred milligrams? And just if you could give us, like, a general idea what is the difference in terms of the doses. I mean, why would you why would you like four hundred milligram dose? As compared to the oncology trial where your optimal dose was just two hundred milligram.

Richard Miller: Thank you, Aydin. Good question. So just for the benefit of everyone else, cohort one was a hundred milligrams, BID, cohort two was the same total dose, two hundred milligrams once a day. Cohort three, two hundred milligrams twice a day. And cohort four, as you indicate, would be four hundred milligrams at the same total dose, one time. So before deciding whether we’re gonna do cohort four, that is the plan, but, you know, we wanna look at the full dataset from cohort three. We already have cohort one and two. We’ll look at the data from cohort three, and then we’ll decide whether we would do that or not. Right now, the plan is to do that, although we are thinking about other possibilities, like extending the duration of treatment.

You know, each of the doses, one hundred, two hundred, four hundred, is very good occupancy of the receptor. And of course, as I’ve indicated in previous calls, we don’t really know what it takes to get a clinical effect or a biologic effect in atopic dermatitis, whether you really need a hundred percent occupancy. But even at our starting dose of one hundred, there’s pretty good occupancy. So right now, the plan is to do cohort four. But before we decide, you know, definitively on that, we want to look at our data.

Aydin Huseynov: That makes sense. And regarding the prior therapies, I know that many of those patients previously failed DUPIXENT. First two cohorts. How about the cohort three? Did you see the patients Sorry. Sorry. They’re DUPIXENT naive, sorry, the first cohort. So is the cohort three also sort of mostly DUPIXENT naive patients?

Richard Miller: We have deliberately searched for sicker patients in cohort three. So we do have more DUPIXENT and systemic treatment failures in cohort three. We also have so far, I mean, we’re not done with the cohort, we do appear to have higher baseline EASI scores. So we’ll have to look at that, and we’ll see how, you know, how that turns out. Whether there’s an, you know, whether there’s a particularly good or effect in the DUPIXENT failures, we don’t know yet. We don’t really know how that variable fits in yet.

Aydin Huseynov: Okay. Understood. And the last one, is the biomarker question. I think you mentioned that you will be talking about biomarkers in May. So could you elaborate a little bit on that? What kind of biomarkers are out there for atopic dermatitis?

Richard Miller: Well, I would say that some of the work that we presented back in January on biomarkers or in December is being confirmed in our ongoing studies. In addition, we’ve picked up a couple of other things that I think are quite interesting. You know, I’ve been talking about we’ve been talking and studying these T regulatory suppressor cells and other cells, and I think those are turning out to be extremely interesting. We continue to see a very durable effect of our treatment in patients who receive the drug. And I mean, it’s a small dataset. It’s very early. But it’s also very provocative at this point.

Aydin Huseynov: Okay. Understood. Thanks so much.

Operator: Thank you. And your next question comes from the line of Graig Suvannavejh from Mizuho Securities. Please go ahead.

Graig Suvannavejh: Hi. This is Sam on for Graig. Thanks for taking our questions. Maybe one on ALPS, just given that it’s a new indication. Can you just tell us in terms of, like, the addressable patient population that you guys are kind of a due diligence and also, you know, what if there’s a subset of patients that would be ideal candidates for socalitinib among people with ALPS? Thank you.

Richard Miller: Okay. So in the United States, ALPS or ALTS, autoimmune lymphoproliferative syndrome, is a genetic disease. You’re born with it. I’ll give you a little background on the disease. Babies are born with it. They at around age two, they start to develop anemia and dysplains and lymphadenopathy. Infections, and they get a diagnosis made, of course. And then they’re on lifelong, immunosuppressive therapies, chemo cyclophosphamide, steroids, mTOR inhibitors, things like that, and they can be on that a long time. The disease is not curable, and they’ll have waxing and waning, adenopathy, and cytopenias, anemia, neutropenia, thrombocytopenia. Can live thirty, forty, fifty years old now. But they’re, you know, they suffer a lot of the complications.

They have massive splenomegaly. That’s another problem they have, which sometimes can rupture. A subset of these patients, maybe ten, twenty percent go on to develop malignant lymphomas. Usually, they’re B-cell lymphomas. But the abnormal cell in ALPS is a T-cell. It’s an abnormal T-cell. Called the double negative T-cell. That does not have CD8 or CD4. I won’t go into the biology of it, but it has a lot of ITK expression. And in our work looking at the effect of socalitinib in various murine autoimmune models, we found that the same there’s a strain of mouse called the MRLLPR negative negative mouse that has the very same mutation that you see in these patients. Same disease, basically, genetically. And when we treated animals with our drug, it was dramatically effective.

Really dramatically effective. Cytopenias go reverse and become normal, splenomegaly, lymphopenia, all that thing. Basically, these animals become normal. And so that prompted us to say hey. Let’s go treat the human genetic, you know, identical genetic disease in humans. And that led us to the NIAID that has a very big collection of these patients. Now most pediatric hospitals have patients like this, and you asked about the market. There are about two thousand five hundred patients with this disease in the United States. Currently. They live a long time. They live to be age forty fifty, as I said, some die sooner. But that in general is their lifespan. I don’t think there’s any particular subset that would be not to our knowledge now that would be more or less amenable to this therapy.

So I just, you know, we just don’t know. Sometimes there are slightly different mutations in patients. But the main problem in the mouse and in the human beings is that their cells, their lymphocytes do not undergo apoptosis. Now there’s a very strong connection between T-cell receptor signaling and apoptosis. Think about it. When there’s antigen or you have an infection, you want your T-cells to proliferate, kill off the infection, but then you want those T-cells to go away. When the infection is eliminated. That requires apoptosis. That is regulated by ITK. ITK has many roles in various signaling pathways. And when you block ITK, you restore apoptosis to these cells. And so that’s the rationale for this. So, basically, this is a treatment that I think you would take for a long time.

And, you know, given the safety we’ve seen so far, I think this could be very important. Now, also from a regulatory standpoint, this is not a disease, I don’t think, where you’re gonna be asked to do big randomized clinical trials. So that’s something else to think about. We’re very excited and interested in this disease. You can tell by my long-winded answer. And then finally, what this does is I mean, this is really an opportunity to look at the effect of our drug on all sorts of autoimmune manifestations. Anti-red cell antibodies, anti-platelet antibodies, all that sort of stuff. Which we think will have important relevance to other autoimmune diseases. Does that answer your question? Probably.

Graig Suvannavejh: Definitely. Very insightful. Thanks so much, Richard, for taking our question.

Operator: Thank you. And your next question comes from the line of Roger Song from Jefferies. Please go ahead.

Roger Song: Hi. This is Cha Cha Yang on for Roger. I’m looking towards your phase two for AD, and I’m wondering if you can give some color on what subpopulations within the disease you’re hoping to target. More specifically, if you could talk about aspects like prior medication use, baseline EASI scores, and then any demographic insights, that would be great.

Richard Miller: Well, that’s a pretty tough question considering we haven’t finished Phase one yet, but moderate to severe atopic dermatitis failed topical corticosteroids, or systemic therapy. Very similar to the criteria we’re using now. Don’t know if I would require I mean, baseline EASI scores to be moderate are sixteen or greater. So I don’t think we would have any requirements beyond that. You know, I think a typical study would be look at two different dose levels plus a placebo. So probably a three-arm study maybe around two hundred patients total. But, you know, that’s an s you know, kind of an approximate answer at this point. But that’s all pretty standard. Okay. Sounds good. And the endpoint would be either EASI 75 those who achieve EASI-seventy-five. Or IGA zero one. That’s pretty standard endpoint now.

Operator: Great. Thank you for that. Thank you. And your next question comes from the line of Li Watsek from Cantor. Please go ahead.

Li Watsek: Hi, team. This is Daniel Bronder on for Li. I have a question about the prioritizing of opportunities for socalitinib in oncology versus inflammatory disease and how you look at it as you move into later stage trials.

Richard Miller: Okay. Well, right now, we have socalitinib in a phase three registration trial that could produce data in less than two years. And so we’re pushing on all fronts as aggressively as we can. So the idea, the strategy is to try to get an approval in lymphoma. Try to get an approval or in an immune disease. Now we are aware of some of the issues with having a similar same drug for autoimmune and cancer. We have a very aggressive program in second and third-generation compounds. We also think that the dosing and duration of are gonna be very different in oncology versus immunology. A very good example would be Rituxan, for example, which came out of my lab at IDAC. Rituxan is approved for lymphomas, as you know. It’s also approved for rheumatoid arthritis, pemphigus, ITP, and probably a few more autoimmune diseases.

And there is not really no issue with pricing because the treatment regimens are such that on a per milligram basis, it turns out to be pretty similar. So our strategy now is to push forward on all these fronts and, you know, get deeper and deeper into the pipeline and, you know, at some point, of course, we recognize that autoimmune diseases is a vast undertaking. There’s many different diseases and competitive areas, and of course, we would at the right time, consider some sort of a collaboration or partnership.

Daniel Bronder: Okay. Cool. Thank you so much for that detailed answer. And the other question we were wondering about is you alluded to earlier a little bit. The delay in the presentation of cohort four is that more driven by your waiting and seeing of cohort three results, or has there been a delay in enrollment more generally?

Richard Miller: No delay in enrollment. We’re waiting to see the data from cohort three. And we’ll make a decision about proceeding with cohort or maybe expand one of the other cohorts.

Daniel Bronder: Okay. Cool. Thank you so much.

Operator: Thank you. And your next question comes from the line of Jiale Song from H.C. Wainwright. Please go ahead.

Jiale Song: Hi. Good afternoon, and thanks for taking my question. I just have one on the upcoming solid tumor study that’s been planned. I was wondering whether there are specific indications that you feel are most suitable for socalitinib or will it be just a general basket study? And also, would you need to do a dose escalation again, or would you start with the PTCL dose? Thanks.

Richard Miller: So the first part of the question, which tumors? I would start with the we will start with the immune responses tumors. So what are those? Those are renal cell cancer. Lung cancer would be good. Those would be probably the top choices to start because you want tumors where you think there’s some evidence for immunotherapeutic effects. Melanoma might be another one, although that’s a much less common disease and is, you know, adequately somewhat adequately treated by other treatments. So I would say, you know, renal lung. I don’t think we need to do a dose escalation, but certainly, you would want to do different doses. You’d want to look at different doses. It wouldn’t be a dose escalation in the usual sense that you’re thinking of like a phase one oncology study.

But would probably want to look at different doses. But we have a pretty good handle now on, you know, the dose, and we have a very good pharmacodynamic marker, which is we know what it takes to saturate the ITK target. So, you know, one hundred, two hundred, three hundred, four hundred, we’re all in the same ballpark. They’re all gonna give you pretty much the same similar findings.

Jiale Song: Great. Thanks for that.

Richard Miller: Thank you.

Operator: There are no further questions at this time. I would now hand the call back to Mr. Richard Miller for any closing remarks.

Richard Miller: Okay. I want to thank everyone for participating in the call, and we look forward to additional updates in the future. Thank you very much.

Operator: Thank you. And this concludes today’s call. Thank you for participating. You may all disconnect.