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spk04: Good afternoon, ladies and gentlemen, and welcome to the Corvus Pharmaceuticals Business Update and Reports First Quarter 2024 Financial Results Conference Call. At this time, all lines are in a listen-only mode. Following the presentation, we will conduct a question-and-answer session. If at any time during this call you require immediate assistance, please press star zero for the operator. This call is being recorded on Monday, May 6, 2024. I would now like to turn the conference over to Zach Cobo, your real chemistry. Please go ahead.
spk01: Thank you, operator, and good afternoon, everyone. Thanks for joining us for the Corvus Pharmaceuticals first quarter 2024 business update and financial results conference call. On the call to discuss the results and business updates are Richard Miller, Chief Executive Officer, Leif Lee, Chief Financial Officer, Jeff Arcara, Chief Business Officer, Jim Rosenbaum, Senior Vice President of Research, 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' annual report on Form 10-K 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 Lace Lee. Lace?
spk08: Thank you, Zach. I'll begin with a quick overview of our first quarter 2024 financials and then turn the call over to Richard for a business update. Research and development expenses in the first quarter of 2024 totaled $4.1 million compared to $4.6 million for the same period in 2023. The net loss for the first quarter 2024 was $5.7 million, including non-cash income of 0.2 million related to Angel Pharmaceuticals, our partner in China. This compares to a net loss of $7.9 million for the same period in 2023, which included a $1.7 million non-cash loss related to Angel Pharmaceuticals. Total stock compensation expense for the first quarter of 2024 was $0.7 million compared to $0.5 million for the same period in 2023. As of March 31st, 2024, Corvus had cash, cash equivalents, and marketable securities totaling $22.1 million as compared to $27.1 million at December 31st, 2023. Today, we closed a $30.6 million financing that included a premier group of biotech investors, as well as some members of the Corvus leadership team. Including the proceeds from this financing, pro forma cash at March 31st, 2024 was approximately $52.7 million, extending our cash runway into Q4 of 2025. I will now turn the call over to Richard, who will discuss our clinical progress and elaborate on our strategy and plans.
spk06: Thank you, Leif, and good afternoon, everyone. Thank you for joining us today for our business update call. Since our Q4 update in mid-March, we have continued to make progress against two key value drivers that we are focused on for 2024. First, for our planned registrational phase three trial of soqualitinib for patients with relapsed peripheral T-cell lymphoma, we remain on track to begin enrollment in the third quarter. And our confidence in this trial continues to grow as two additional patients in our Phase 1 1B trial recently achieved objective responses at first follow-up. Second, our placebo-controlled Phase 1 trial of soqualitinib for patients with moderate to severe atopic dermatitis. We began patient enrollment in April, which keeps us on track to report early data from the trial before the end of the year. In addition to these two priorities with soqualitinib, today we are reporting encouraging initial data from our phase 1B2 trial of cifrodenant, our adenosine A2A receptor antagonist, in frontline metastatic renal cell cancer, or RCC. Based on the significant deep response rate seen in the initial set of patients, the protocol pre-specified statistical criteria for expanding the study has been met, and the Kidney Cancer Research Consortium, or KCRC, is enrolling additional patients. Combined with our ongoing business development efforts aimed at further unlocking the potential of ITK inhibition in a broad range of oncology and autoimmune indications, we believe Corvus is positioned to continue building value and advancing our unique pipeline to help improve clinical outcomes for patients. Now I will provide more detail on our progress, starting with socolitinib for PTCL. While we are no longer enrolling new patients in our Phase I trial, the data continues to evolve as patients on therapy complete their scheduled follow-up assessments. In the most recent data cutoff from May 3, 2024, we had two additional patients that achieved an objective response at their first follow-up visit. The first was a complete response confirmed by PET CT scan, and the second was a partial response with over 80% tumor volume reduction. These patients both had multiple sites of disease and had failed two prior therapies. Both of these patients are continuing on therapy. With these additional valuable patients, The objective response rate, or ORR, for the phase 3 eligible patients is now 9 out of 23, or 39%, including 5 complete responses and 4 partial responses. Although not studied head-to-head, the complete response rate for soqualitinib at 22% is approximately double that seen with belinostat or pralatrexate, the standard chemotherapies for PTCL that we will be comparing to in our Phase III trial. Similarly, the ORR, disease control rate, progression-free survival, and overall survival for this group compares favorably to the results seen with belinostat or pralatrexate. The median PFS for our patients, which is the primary endpoint for the Phase III trial, is 6.2 months. This is substantially better than reported results for the standard agents which is 1.6 and 3.5 months for Belinostat and Pralotrexate, respectively. The durability of our responses is impressive, with some of the earlier enrolled patients maintaining their responses for more than 24 months. We plan to begin patient enrollment in our so-called registrational phase three clinical trial in relapsed PTCO in the third quarter of 2024. We are working with or are in advanced discussions with a number of leading centers in the United States and Canada. We anticipate about 40 centers will participate in the trial. The vast majority will be in the United States. Now for an update on soqualitinib for atopic dermatitis, the first immune disease indication we are evaluating. In April, we initiated patient enrollment in the first patient cohort of the trial. There is high interest in our trial from physicians due to several attractive features of soqualitinib. First, this is a first-in-class drug with a novel mechanism of action. Soqualitinib acts upstream by blocking Th2 and Th17 cells and thereby results in inhibition of many different cytokines involved in disease. Second, it is an oral therapy and in our cancer studies has been shown to have very good safety profile. And third, it may have broad utility across many different autoimmune and inflammatory diseases, and this trial may provide proof of concept for the treatment of other immune diseases. The trial was designed to enroll 64 patients with moderate to severe atopic dermatitis that have progressed on at least one prior therapy. The study is randomized, placebo-controlled, and blinded to patients and treating physicians. There will be four sequentially enrolled cohorts of 16 patients, with patients in each cohort being randomized three to one to different dosing regimens of soqualitinib or placebo given for 28 days. The primary endpoint is safety and tolerability, and efficacy is measured using investigator global assessment and the clinically validated measurement of improvement in eczema area and severity index score, also known as EZ. It should be noted that while the trial is double-blind, the company is not blinded. We plan to evaluate the data in an ongoing manner as successive cohorts complete enrollment. We also will be measuring the levels of various serum cytokines at baseline and on treatment. These measurements may provide useful biomarkers. Based on current enrollment trends, anticipated site activations, and follow-up timelines, we believe data from the initial cohorts will be available before the end of 2024 with study completion in early 2025. Outside of our PTCL and atopic dermatitis trials, we are still planning a so-called solid tumor trial as a single agent and in combination with nivolumab in relapsed RCC. and we remain active with our corporate partnering discussions. Our business development strategy is to find partners with development and commercialization expertise in immune diseases, as well as seek regional partnerships in oncology that would be complementary to our focus and expertise in cancer. I'm excited to update you on the progress with cifroadenin, our adenosine A2A receptor antagonist. We have been one of the leaders in the development of adenosine A2A receptor antagonism for the treatment of cancer. Over the past few years, published preclinical and clinical studies have demonstrated the anti-tumor activity of ciforadenate as a monotherapy and when given in combination with checkpoint inhibitors. In particular, in our preclinical studies published in 2018, we found that anti-CTLA-4 antibody combination with CIF or adenine produces striking anti-tumor efficacy in several animal models. Further research has revealed the probable mechanism for this synergy, which involves modulation of the tumor microenvironment, specifically the blocking of myeloid-derived suppressor cells. In other words, we believe that anti-CTLA-4 antibodies are a much better combination partner for A2A antagonists than anti-PD1s. These findings led to our collaboration with the Kidney Cancer Research Consortium. This group of institutions brings the leading physicians and researchers in kidney cancer, whose goal it is to discover improved therapies for patients with renal cancer. Our Phase 1b2 clinical trial, which is led by Dr. Katie Beckerman from Vanderbilt University Medical Center, is evaluating ciforadenate as a potential first-line therapy for metastatic renal cell cancer in combination with ipilimumab and nivolumab. The study is now open at MD Anderson, Vanderbilt, Duke, and the University of Pennsylvania. The clinical trial is currently in the Phase II portion and overall is designed to enroll up to 60 patients. There are currently over 27 patients enrolled. The trial employs a stringent efficacy endpoint, deep response rate. Deep response rate is the CR rate plus the PR rate, only counting PRs that achieve greater than 50% tumor volume reduction. Note, the usual criteria for PRs is 30% tumor reduction. Data from the KCRC has shown that deep response rate correlates with long-term progression-free survival and overall survival, and in their previous studies is 32%, with ipilimumab and nivolumab. In an interim analysis, our protocol-defined, pre-specified statistical threshold for efficacy is the demonstration of at least a 50% increase above the 32% deep response rate seen with previous ipinivo combination trials in renal cell cancer conducted by the Kidney Cancer Research Consortium. This means we need to exceed a deep response rate of 48%. As of May 2nd, 2024, the interim analysis that was conducted indicates that we have met the statistical threshold for efficacy so the trial continues to enroll patients. We are excited about these results given the positive clinical implications for patients. In addition, they are consistent with our laboratory and preclinical findings and we believe may represent a novel immunotherapy approach. Summarizing the outlook for the remainder of 2024 with our recent financing, our current cash gives us runway into late 2025, allowing us to achieve several near-term milestones, including starting our registrational Phase III clinical trial of soqualitinib and PTCL in the third quarter, generating interim results from our soqualitinib phase 1 atopic dermatitis trial before year-end, followed by final data in early 2025, reporting additional data from the sephoradenin phase 1B2 clinical trial later this year, and initiating a phase 2 clinical trial with soqualitinib in solid tumors in the fourth quarter, with initial data anticipated in the second half of 2025. We look forward to providing updates on our programs in the coming quarters. I will now turn the call over to the operator for a questions and answer period. Operator?
spk04: Thank you. Ladies and gentlemen, we will now begin the question and answer session. Should you have a question, please press the star followed by the number one on your touchtone phone. You will hear a prompt that your hand has been raised. Should you wish to decline from the polling process, please press the star followed by the number 2. If you are using a speakerphone, please lift the handset before pressing the key. One moment please for your first question. Your first question comes from the line of Aiden Hosnope from Leidenberg. Your line is now open.
spk02: Good afternoon, everyone. Congratulations with the progress, and most importantly, with two additional responses on PR and CR. Quite unexpected from phase 1b. So regarding sucralipnib in PTCL, so you got 23 patients, DCR 61%, five CRs, four PRs. So could you remind us, what is the standard of case CRs in other PTCL trials, Belinostat, the prolatrexate, or any other agents?
spk06: Thank you, Aidan, for the question. So the approval studies for both belinostat and pralatrexate were single-arm studies. Those drugs received accelerated approval about 15 years ago. They each had CR rates of about 10% and overall response rates of about 25% to 30%. They had PFSs, progression-free survivals, of about one and a half to three and a half months.
spk02: Okay, that's helpful. And with the new responses, how much this is going to increase your sort of preliminary PFS and OAS? I know you reported previously 6.2 months in PFS, 28 months in OAS. So is it going to increase significantly?
spk06: So the current ORR now, overall response rate, is 39%, just to remind you of that. And by the way, in lymphoma, we use the Lugano criteria, which is 50% for a PRR. And I should add that the PR that I just mentioned has about 87% reduction of tumor. One tumor was totally gone. I suspect he could be on his way to a CR very soon. The PFS, we expect the PFS to improve as these last few patients move through the median.
spk02: Okay. Understood. And regarding the data from... from the phase three trial. When do you think we will have a first glimpse on the readout? I know this is a randomized trial, blinded trial, but when do you think we'll have the first look at it?
spk06: Well, it is a randomized trial. It is not a blinded trial. I mean, we know who gets chemotherapy and who gets our drug. It's hard to disguise that in an oncology trial since the chemotherapy drugs have side effects. The median PFSs, as I mentioned, for Pralutrexate and Belinostat are short, only a few months. Therefore, the study is not that long. It's 150 patients. We think we could probably enroll that thing fully in about 18 months, and then you'd need some follow-up after that to get to the final data. There is an interim. There is a point that we conduct an interim analysis which is when half of the events occur, the events being the PFS events. But that occurs so late in the study that we would probably wait for the end of the study to make a final determination. Now, having said that, we do have an outside data monitoring committee, and I guess if the results were so persuasive or compelling, you would possibly have an ethical reason to discontinue the study. Okay, makes sense. And the last one, if I may. So, let me just say, so I think you have data from this trial in 24 months.
spk02: Okay, so like 26, 26. Okay, so I'm trying to understand, you know, these drugs seem to be working, but there is 40% who don't respond, essentially, right, 39%, you know, based on DCR. So is there any way to come up with some other potential biomarkers to screen patients who would be more likely to respond or somehow choose patients?
spk06: Well, we are working on that. We're looking all the time for mutations in baseline immune status, et cetera. But you'll remember that several months ago we implemented, and on conference calls I talked about, the immune status at baseline, the absolute lymphocyte count, then using a number of prior therapies. I'm happy to report that since we've implemented those eligibility criteria, we have seen, I would say, not only more responses, but I would say the kinetics of the responses also have been faster. So I think that those moves that we made several months ago or maybe a year ago now really have made a difference. And those moves were based on our better understanding of the mechanism of action. So I expect that in a phase three trial, we already know this, phase three trial, we're going to get better patients. They're going to have better immune status to start with. Phase one trials usually get sicker patients just by nature of the fact that they've exhausted any other therapies that are available. So I would expect that you know, our results could get better. And we are continuing to look at different markers. But so far, I don't know, other than the baseline immune status, I don't know if we have a specific molecular marker.
spk02: Understood. Thank you. Thank you so much, and congratulations with the progress.
spk04: Your next question comes from the line of Jeff Jones from Oppenheimer. Your line is now open.
spk11: Thank you, operator. And congrats on the news, guys. That's great. And congrats on the financing as well. One question on so-called lit nib. There are a number of responders in the phase one that were cutaneous T cell lymphoma patients. Can you remind me if cutaneous T cell lymphoma patients are going to be included in the phase three and what impact that might have on the PFF?
spk06: There are a couple of patients who are included in R23 that had cutaneous T cell lymphoma. Both of those patients had transformed cutaneous T cell lymphoma. That portends a very bad prognosis when you get what's called large cell transformation. That's not your typical CTCL is my point. CTCL patients are not going to be enrolled in our phase three trial because it really is a different disease. It's treated with different drugs. And it can be a chronic disease early. People who have just skin disease can have disease for many years. That's not the patients we're talking about in this trial. But Jeff, I think you raise a good point which I forgot to mention. We see responses in cutaneous lymphomas, anaplastic lymphoma, peripheral T cell lymphomas, something called angioimmunoblastic or now known as T follicular helper cell lymphoma. These are very histologies, very different histologies under the microscope. They have different patterns of spread in the body. And they have different mutations, genetic mutations. The fact that we see activity in this very diverse group of lymphomas, of T-cell lymphomas, is really, again, consistent with our mechanism, which is to induce a host antitumor response. And one of the motivating factors that we think we can extend this into solid tumors, that was the reason we started doing preclinical work with solid tumors. That data has been presented and confirmed by others. And this is the reason why we're also excited about looking at this drug in solid cancers. Did I answer your question, Jeff?
spk11: Yeah, you did. That was really helpful. Appreciate it. I've always wondered a little about those cutaneous responses, which are obviously generally good responses.
spk06: Jeff, hold on. The responses that we see in these cutaneous patients, it's not fair to call them that. They have cutaneous disease. They have circulating tumor cells. They have lymphadenopathy. Sometimes they have visceral disease. The responses that we've seen in the responding patients It's not just cutaneous. It's, you know, throughout the body. Okay?
spk11: Fair. Sorry, that was poor language choice on my part. In the atopic dermatitis study, you mentioned, I believe, patients had been on two prior lines of therapy. Okay. are there going to be, are you including patients who have previously had dupilumab and failed, or is that, are you not being that specific?
spk06: We're not being that specific. And they have to have failed at least one prior therapy, one prior either systemic or topical therapy. Some of the patients, we assume that some of the patients that come in our trial will have failed dupy, but it's not required. they will have also failed others. I think we got a recent patient who failed the JAK inhibitor, for example. So really, we have to put this, this trial is really intended to show, of course, that the drug's well-tolerated in a patient population like this. And we're looking for activity. You know, obviously, subsequently, we'll be trying to figure out is it, how does it stack up against some of these other agents? But right now we're confirming mechanisms, safety, and yes, we are measuring efficacy against the placebo.
spk11: Got it. No, I appreciate the clarity. And then last question on CFO. I know that you had said 27 patients were enrolled, but you didn't specify how many were included in that interim efficacy analysis.
spk06: I think there's 18 patients in that. You're right, because some of them haven't come back for their first visit yet. So this protocol, by the way, was prepared by the KCRC. And they have, there are sort of blocks of, I forget how many patients each, eight or nine patients each, And there's a criteria, efficacy threshold, that you have to pass to continue. The results so far are really pretty good. And in fact, we're organizing a meeting at ASCO to think about discussing things like adding a control arm or where do we go from here. Obviously, at some point, you want to have a control arm in there. By the way, the deep response rate of 32%, ipinivo, I know people are always critical of historical controls, as they should be, but that's based on a 900-patient checkmate. What was it? The checkmate study with ipinivo versus SUTENT was over 900 patients, and then there was nivocabo versus SUTENT. That was 700 patients. So this is based on a pretty good foundation of data.
spk11: Got it. Just one clarification. You had mentioned in your remarks, I think, 27 enrolled and then going over this threshold of deep responses. to expand that trial. Did you mean just up to the 60, expand further up to the 60 planned, or is there a potential expansion beyond those 60 patients?
spk06: No, there's no expansion beyond the 60. When I mentioned expanding, I think at some point it would be nice to add a control arm, you know, maybe ipinevo alone, ipinevo placebo. But that probably, you know, that raises the whole question of do you want to do a randomized phase two or do you want to go right to a phase three?
spk11: Yeah, understood. All right. Thank you very much, guys. That's it for me. Thanks.
spk04: Your next question comes from the line of Greg Savanova. Your line is now open.
spk09: Good afternoon. Thanks for taking my questions. I have two in particular. One, maybe I'll start with your second asset. I know you mentioned that you were able to pass, like, the bar for success for moving forward. I don't know if you, I might have missed this, if you quantified how much better beyond that bar that you had seen from, I guess, your 18 available patients. So I'm wondering if you can perhaps shed more color on that. And then secondly, just on your current cash, and congrats on the recent raise, but if you could clarify whether that cash gets you through the phase three for soqualitinib in ETCL. Thanks.
spk06: Okay, Craig. Let me take the first one first. So the statistical threshold was a 50% increase, so the statisticians, 50% increase above the 32%, which is obviously 48%. If you meet that, you have, oh, you have a difference with a p-value of 0.1 on only 18 patients. That's a pretty stiff hurdle. 50% increase is a big hurdle. And so we exceeded that. I can't give you the exact number because The KCRC doesn't really want to disclose that yet, and I understand why, because these numbers jump around a lot in a small study. But we're better than 48% deep response rate, okay? And again, I want to emphasize, 50% improvement in deep response rate, that's a stiff hurdle. And the reason we wanted that is we didn't want to waste time on something that didn't have a, significant probability of working. So we made it, nor did they. So we deliberately made these hurdles pretty strict. Now your second question, I'll let Leif answer.
spk08: So Craig, associated with our financing, we also sold warrants. Now these warrants, first of all, have an exercise price of $3.50. but more importantly, maybe, they expire June 30th of 2025, so a little over a year from now. So if all those warrants were exercised, we'd raise about $60 million. So the $30 million plus the $60 million, should those warrants be exercised, would get us through the Phase III trial.
spk09: Okay, thank you for that clarification.
spk10: Thanks again.
spk04: Your next question comes from the line of Roger Song from Jefferies. Your line is now open.
spk07: Good afternoon. This is for Roger Song. So thank you for taking our questions. I guess a few questions from us. First one's about the modified inclusion criteria. So about the absolute lymphocyte count, about 900. If I remember it correctly, there is a big, you know, overlap between this 90%, you know, 900-plus ALC count between the patient population. So, could you clarify what, you know, in general this population looks like?
spk06: So, the 900 absolute lymphocyte count, we determined based on the early part of the trial where we were taking anybody who failed any number of prior therapies. And we recognized that those patients above 900 did better, much better. And then we recognized that those were the patients who had no more than three prior therapies, less than or equal to three prior therapies. And so that's the criteria that we're using because they're less immunocompromised. Those are what's been used on the patients that have been reported in today's press release. It's the number of prior therapies greater than or equal to one, less than or equal to three.
spk10: Now, I don't recall, I'm sorry?
spk07: Do we know in general how many patients meet this criteria?
spk06: Oh, in our trial, the percentage of patients that will meet this criteria is Very high. Again, in a Phase III trial, we're already hearing from doctors, we're going to get patients right after they fail their first-line therapy, maybe a second-line therapy. I would expect the number of eligible patients to be nearly 100%. Got it.
spk07: Thank you. So, our second question is about the AD study. So, it mentions that we could expect some early data readout by year-end. So, how... you know, in general, how much data should we expect from there?
spk06: I think you can expect data from the first couple of cohorts. And as you recall, our first dose is 100 milligrams BID, which is a pretty good dose. It's a dose that we know occupies the target maybe 50% or so, give or take. It's not the best dose, but it's a pretty good dose. The second cohort, gets 200 milligrams and then we do 200 BID. So I think that we very well may see some signs of efficacy in the first cohort. I would expect in the second cohort we would see it. Obviously, I think it would be better in subsequent cohorts than the first cohort. But we're also looking at these biomarkers, the serum cytokines that we know we affect and how they'll change. So I'm hoping that Sometime by the end of the summer, we'll start to get a feel for the clinical activity of the drug and also its effect on circulating cytokines.
spk07: Got it. So, you know, since you talked about the dosing regimens, just in general, you know, how should we think about this circulating dosing regimens in AD, you know, considering it is a different indication compared to the dosing in, you know, T cell lymphoma? Okay.
spk06: So we know, and we've tested this not only in lymphoma patients, T-cell lymphoma patients, but in normal people in vitro. We know what it takes to saturate the T-cell ITK in the T-cells. So as you recall, it's a covalent drug similar to the way ibrutinib worked, but except this is to a different target, so that once the drug binds to the target, it doesn't come off. So we know what it takes. We have a really good pharmacodynamic marker to know that we're blocking the T cells, or at least occupying the T cells. Now, we don't know for sure that the same pharmacodynamics will apply in AD as in lymphoma. I mean, the occupancy will be the same, but what it takes to affect your immune response, that we don't know. And that's why we're looking at different doses in this study. The reason to look at different doses is what does it take to affect the immunology in these patients? And also, of course, you know, looking for as low as possible. The lower the dose, one would think the safer it would be.
spk07: Yep.
spk06: So that's why this is a phase one study. But, I mean, this is basic chemistry. Socolitinib reacts with the ATP binding pocket of ITK, and that's That's the fact. That's what happens. And once that's occupied, that enzyme isn't going to work until a new one is made. And of course, as you know, the rationale is that atopic dermatitis patients have an intense Th2 helper T cell component in their disease. And we think if the drug gets there and it binds covalently to ITK. We know that we block TH2 cells. We know we block TH2 cytokines. We think that will have an impact on the disease. But the purpose of the trial is to show that.
spk07: Sure. Maybe I can squeeze another question here. So regarding the ITK inhibitors, I know you have a couple more coming up in the pipeline. So what are some key differences between this one and the the collitinib and the other chemidase?
spk06: So first of all, we have over a dozen other ITK inhibitors that we've been evaluating. Some are completely different chemical structures. Some are covalent. Some are non-covalent. But the interesting biological features is some seem to affect some T cell subsets more than others. And we find that to be quite interesting, quite novel. and provides for, I think, some very strong intellectual property.
spk07: Got it. Thank you. That's all from us. Thanks again.
spk04: Your next question comes from the line of Lee Watzik from Kantar Fitzgerald. Your line is now open.
spk00: Hi, this is Rose Mariano for Lee. Thank you so much for taking our questions and congrats. So just two quick ones from us. For atopic dermatitis, do you have a benchmark in terms of improvement in eczema area and severity index?
spk05: No, we don't have a benchmark. Okay.
spk00: Okay, thank you. And then for our second question, for your Nexen ITK inhibitors, do you plan to generate any human data for BD discussions or just like the clinical?
spk06: I'm sorry, I couldn't understand the question. Can you repeat it?
spk00: Oh, sorry. So for your next-gen ITK inhibitors, do you plan on generating any human data before going for BD discussions?
spk06: Well, we're doing both in parallel. We're now selecting some of these backup or second-generation ITK inhibitors. They're in their IND-enabling studies. We're scaling them up. You know, we're moving down parallel tracks.
spk10: Okay, thank you.
spk06: Okay, operator, I think that exhausts our questions here for now. I want to thank, hello, any other questions that I missed?
spk04: There are no further questions at this time. I will hand the call over to Richard Miller, CEO of Carvus. Please continue.
spk06: Thank you, operator. I want to thank everyone for participating in today's conference call. We look forward to updating you on subsequent calls and appreciate your interest. Take care.
spk04: Ladies and gentlemen, this concludes today's conference call. Thank you for your participation. You may now disconnect.
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