Good afternoon, everyone. Thank you for standing by, and welcome to the Corvus Pharmaceuticals' Third Quarter 2024 Business Update and Financial Results Conference Call. At this time, all participants are in the listen-only mode. Later, we will conduct a question-and-answer session, and instructions will follow at that time. It is now my pleasure to turn the call over to Mr. Zack Kubow of Real Chemistry. Please go ahead, sir. Thank you, Operator, and good afternoon, everyone. Thanks for joining us for the Corvus Pharmaceuticals' Third 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, Leiv Lea, 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' quarterly report on Form 10-Q for the quarter ended September 30, 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. Leiv? Thank you, Zack. I will begin with a quick overview of our Third Quarter 2024 financials and then turn the call over to Richard for a business update. Research and development expenses in the Third Quarter 2024 total $5.2 million compared to $4 million in the same period in 2023. The $1.2 million increase was primarily due to an increase in soquelitinib clinical trial expenses. The net loss for the Third Quarter of 2024 was $40.2 million, including a non-cash loss of $0.7 million related to Angel Pharmaceuticals, our partner in China. In addition, we recorded a non-cash loss of $32.8 million from the change in fair value of Corvus' warrant liability during the Third Quarter 2024. This compares to a net loss of $6 million for the same period in 2023, which included a $0.9 million non-cash loss from Angel Pharmaceuticals. Total stock compensation expense for the third quarter 2024 was $0.7 million compared to $0.5 million for the same period in 2023. As of September 30, 2024, Corvus had cash, cash equivalents, and marketable securities totaling $41.7 million as compared to $27.1 million at December 31, 2023. Of note, associated with our financing in May 2024, we also sold common stock warrants that have an exercise price of $3.50 per share and expire on June 30, 2025. One investor early exercised their warrants in October, resulting in $5.9 million in cash to the company. If all the remaining warrants are exercised, we will receive approximately $54 million in additional cash. Based on our current plans, we anticipate our cash, including the recent early exercise of common stock warrants, provides runway into 2026. 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, and good afternoon, everyone. Thank you for joining us today for our business update call. We are advancing our lead programs with soquelitinib on multiple fronts. A registration phase III trial for peripheral T-cell lymphoma, PTCL, is now enrolling patients, and a phase I trial for atopic dermatitis is moving along according to plan. Soquelitinib is a first-in-class oral therapy that selectively inhibits ITK to modulate and control parallel signaling pathways in the immune system. There is growing evidence, both from our own clinical efforts and preclinical research conducted by us and others, that this mechanism of action may provide a powerful new approach for the treatment of a broad range of immune diseases and cancers. Our ability to move quickly and efficiently into autoimmune diseases such as atopic dermatitis was facilitated by our T-cell lymphoma clinical trials, which provided valuable information regarding dosing, safety, pharmacokinetics, and most importantly, effects on immune cells. Now I will provide more detail on our progress, starting with soquelitinib phase I clinical trial in patients with atopic dermatitis. The trial is designed to enroll 64 patients with moderate to severe atopic dermatitis that have progressed on at least one prior topical or systemic therapy. The study is randomized, placebo-controlled, and patients and the treating physicians are blinded to the treatment assignment. The company is not blinded, and therefore we can evaluate the data as the trial progresses. There are four dosing cohorts that are sequentially enrolled: 100 milligrams twice per day, 200 milligrams once per day, 200 milligrams twice per day, and 400 milligrams once per day. The rationale for the dosing regimens is based on pharmacokinetic and pharmacodynamic data obtained from our lymphoma trial. Patients are randomized within each cohort at a 3:1 ratio to receive either active drug or placebo for a total of 16 patients per cohort, 12 active, four placebo. The treatment duration is 28 days, followed by an additional 30 days off therapy for a total of 58 days of participation in the trial and monitoring of endpoints. We have completed enrollment, including the entire follow-up in the initial 16-patient cohort, and the Data Safety and Monitoring Review Committee has completed its review with no safety signals observed. The second cohort is now enrolling with the same design as the first cohort, except the soquelitinib dose is 200 milligrams once daily, the same total daily dose as the first cohort, which was 100 milligrams twice daily. Cohorts 3 and 4 will examine higher daily doses using the same design: 200 milligrams twice daily and 400 milligrams once daily, respectively. For reference, the dose in our phase III lymphoma trial is 200 milligrams twice daily, which provides continuous full receptor occupancy. The primary endpoint is safety and tolerability, and efficacy is measured using the clinically validated measurements of improvement in eczema area and severity index, also known as EASI score, and the Investigator Global Assessment, or IGA Score. We are also measuring levels of TH2 and TH17 cytokines in the serum, such as IL-4, 5, 13, 17, and many others. We believe we may be able to determine effects on cellular cytokines with these serum measurements, and possibly this could guide future monitoring or disease assessment. One other property of selective ITK inhibition should be noted. Published work from scientists at Cornell University this past summer in 2024 and Janssen Research in 2019 have shown that the ITK protein controls a switch between inflammatory TH17 cells and anti-inflammatory T regulatory or suppressor cells. When ITK protein is active, TH17 differentiation dominates. ITK inhibition results in a shift to T regs and away from TH17. The Cornell group utilized soquelitinib for their studies. The Janssen group used siRNA to knock down ITK protein expression because at that time, selective ITK inhibitor was not available. These studies and others suggest that due to the induction of T regs, the anti-inflammatory effects of soquelitinib could be very durable. There is strong interest in an oral safe drug for atopic dermatitis, and we are receiving positive feedback on soquelitinib's anticipated profile from our investigators and collaborators. Overall, we are very excited with the progress of the atopic dermatitis trial. In December, we plan to present the complete data set for the safety and efficacy from Cohort I and available data from Cohort II. We plan to compare our data with analogous published data from approved agents currently used to treat atopic dermatitis. In summary, we believe that soquelitinib has several potential advantages for the treatment of immune diseases: an oral medication, attractive safety and tolerability profile, novel mechanism of action, durable response, and ability to address a broad spectrum of autoimmune and allergic indications, for example, comorbidities such as asthma in patients with atopic dermatitis. The broad potential of soquelitinib and our next-generation ITK inhibitors is supported by new preclinical data showing that soquelitinib is active in systemic sclerosis, a chronic autoimmune disease that causes fibrosis and inflammation in many organs, including the skin. That data will be presented later this week at the annual meeting of the American College of Rheumatology. We continue to advance a range of second and third-generation ITK inhibitor product candidates, which are designed to deliver precise T-cell modulation that is optimized for specific immunology indications. We are focusing our preclinical development on asthma, psoriasis, scleroderma, inflammatory bowel disease, and fibrotic diseases, with a host of additional indications identified for future work. Now for an update on soquelitinib in oncology. In September, we initiated our registrational phase III clinical trial for relapsed PTCL. There are currently no FDA fully approved agents for the treatment of relapsed PTCL, and the FDA has granted orphan drug designation and fast-track designation for soquelitinib for the treatment of relapsed T-cell lymphoma. The study is designed to enroll 150 patients randomized to soquelitinib or standard-of-care chemotherapy, which is either pralatrexate or belinostat. The primary endpoint for the study is progression-free survival. We are now enrolling patients at multiple clinical sites, and we are on track with our plan. Our team is working to open additional sites with a goal of about 40 to 50 centers in the United States, Australia, Canada, and South Korea participating in the trial. The vast majority will be in the United States, including centers such as MD Anderson, Memorial Sloan Kettering, City of Hope, Washington University, and other high-profile institutions. We are delighted to have the participation of leading centers with extensive experience and expertise in conducting clinical trials in T-cell lymphomas. While we are no longer enrolling new patients in our phase I trial, we continue to monitor patients on therapy as they complete their scheduled follow-up assessments. There are four patients who remain on therapy, including three with the previously reported complete responses, which are sustained, and one patient who achieved a partial response. The patient with the partial response continues to demonstrate tumor regression over time but has not yet reached a complete response. Therapy in one additional patient who achieved a complete response was discontinued while in CR after 24 months on treatment, per the study protocol. The objective response rate for the phase III patients remains at 39%, or nine out of 23 patients. This includes six complete responses and three partial responses. The median PFS remains 6.2 months. Published median PFS for vorinostat and pralatrexate are 1.6 months and 3.5 months, respectively. We are also planning a single-agent soquelitinib solid tumor trial in relapsed renal cell cancer, or RCC, representing a new approach to immunotherapy of this disease. The biochemistry, mechanism of action, and preclinical data in solid tumors for soquelitinib tumor immunotherapy is now in press in the peer-reviewed journal Drug Discovery, a Nature partner journal. Given our focus on our atopic dermatitis and PTCL trials, we now plan to initiate our solid tumor clinical trial sometime in early 2025. We also continue to advance our other clinical stage development programs. We have been one of the leaders in the development of the adenosine A2A receptor antagonism 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 is evaluating ciforadenant as a potential first-line therapy for metastatic renal cell cancer in combination with ipilimumab and nivolumab. The study is enrolling at MD Anderson, Vanderbilt, Duke, and the University of Pennsylvania. As of the most recent data analysis on September 30th, 46 patients were enrolled, and the trial continues to meet our pre-specified statistical hurdle for continuation, which is the achievement of at least a 50% improvement in the deep response rate of 32% associated with Ipi and Nivo combination alone. Deep response rate is the CR rate plus the PR rate, only counting PRs that achieve greater than 50% tumor volume reduction. Along with our partners at the Kidney Cancer Research Consortium, we have decided to continue our follow-up of patients on the trial before presenting the data. Therefore, we will not be presenting this data at the GU Malignancy Conference taking place in late November and will instead target a presentation sometime in early 2025. Outside of RCC, new data highlighting the potential of ciforadenant to treat prostate cancer was presented this past weekend in an oral session at the Society for Immunotherapy of Cancer, or SITC, annual meeting, where it was selected as one of the top 100 abstracts. This research was led by Dr. Larry Fong from the Fred Hutch Cancer Center and UCSF. The data demonstrate the potential of ciforadenant to overcome immunotherapy resistance in metastatic castration-resistant prostate cancer. This includes elucidating the role of the adenosine pathway on the immunobiology of the disease, including the importance of immunosuppressive myeloid cells and the adenosine gene signature, a biomarker discovered and published by Corvus and academic collaborators. The preclinical results build upon the data from a previously completed phase 1b/2 clinical trial of ciforadenant in patients with metastatic castration-resistant prostate cancer, in which PSA partial responses were observed in patients receiving ciforadenant alone and together with atezolizumab. Overall, we believe these data highlight that ciforadenant could be an important advancement for patients with tumors that are resistant to checkpoint inhibitors and is supportive of our ongoing clinical trial in combination with Ipi and Nivo in frontline renal cell cancer. The data also underscore the importance of the adenosine gene signature as a biomarker for future studies. Summarizing the outlook for the remainder of 2024 and into 2025, we have important clinical milestones for soquelitinib. Upcoming milestones include: Number one, preclinical data presentation at the American College of Rheumatology meeting later this week. Number two, initial data from Cohort I and Cohort II from our phase I atopic dermatitis trial in December. Number three, final data from all four cohorts of the phase I atopic dermatitis trial in the first half of 2025. Number four, initiating a phase II clinical trial with soquelitinib in solid tumors in early 2025, with initial data anticipated in late 2025. Number five, continuing to activate sites and drive enrollment in the registration phase III clinical trial of soquelitinib in PTCL. Our current cash, plus the exercise of outstanding warrants, gives us runway into 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 in the coming quarters. I will now turn the call over to the operator for a Q&A period. Operator? Thank you. Ladies and gentlemen, we will now begin the question and answer session. Should you have a question, please press * or follow up by the one on your telephone keypad. You will hear a prompt that your hand has been raised, and should you wish to cancel a request, please press * or follow up by the two. If you are using a speakerphone, please lift the handset before pressing any keys. One moment, please, for your first question. Your first question comes from the line of Li Watsek from Cantor. Please go ahead. Hey, great. Thanks for taking my questions. Rich, I wonder if you can just comment on the kinetics of ITK inhibition on the clinical scores in AD. And then, do you sort of expect the EASI score to further improve after the 28-day mark? And also, can you maybe just tell us a little bit about how you're thinking about the bar for success, given it's an oral drug? Thank you. Okay. Thank you for the question, Lea. The kinetics of the response are very quick. We see improvement in about the first week. I'll elaborate more of this in our call in December. We expect the criteria for success to be similar to what you've observed for other approved agents, for example, Dupixent. We'll be looking at 28-day data and comparing it to 28-day data for similar compounds or for Dupixent and other approved agents. We do expect that there would be a very durable effect from soquelitinib based on its mechanism of action and potential for further improvement. Okay. Thank you. Thank you. And your next question comes from the line of Roger Song from Jefferies. Please go ahead. Great. Congrats for the progress. And then, so a couple of questions also related to the atopic dermatitis, the data release. Given you will have the initial data readout in December and then the final data early 2025, how should we think about the follow-up time period for those cohorts? And then, in terms of the efficacy endpoint, do you see those endpoints will have different kinetics with different follow-up? Thank you. We will report in December, 28-day data. We'll report on the kinetics of, as I mentioned to the last question. We are seeing responses rapidly, like within a week. We'll report the 28-day data. I would expect, of course, we'll have complete follow-up on cohort number one. Cohort number two, we won't have the entire 58-day follow-up. As we get into cohort three and four, we'll start to evaluate the kinetics and durability of the responses over the two-month period. Got it. Thank you. Maybe to follow up on the dose, based on the PK/PD and then maybe preclinical modeling, do you expect to see the dose dependence for the four arms you're testing in phase I? Thank you. Well, the purpose of this study was to determine the optimum dose, and we've looked at four different doses, dosing regimens, and doses. I would expect the efficacy to improve as we go higher in the dose, just based on what we've seen in lymphoma studies and getting more saturation of the target. However, atopic dermatitis is a different disease than lymphoma, so I'm not sure that that would turn out to be the case. But the purpose of our study was to determine what would be the optimal dose, and we benefit from the lymphoma studies, which gave us sort of a lower end and a higher end to examine. Got it. Thank you, Rich. That's it from us. So, Roger, just to maybe elaborate a little bit on that, we know that 100-milligram dose, the first cohort, and we know this from our lymphoma studies, gives you reasonable saturation of the target, but not complete, reasonable. And we're able to. We have measurements from our lymphoma patients where we've been able to measure that immediately after taking a dose and then at the nadir, at the low point. And we know that 100-milligram dose gives you reasonable coverage, but not total coverage. We know at a higher dose, for example, at 200, you get better coverage, etc. Now, the question is, what kind of coverage do you need for atopic dermatitis? That's not lymphoma. Do you really need 100% occupancy all of the time? Nobody knows the answer to that question. We're going to figure that out. Thank you. That makes sense? Thank you. And your next question comes from the line of Aydin Huseynov from Ladenburg. Please go ahead. Hi, everyone. Hi, Richard. Congratulations on the progress this quarter. Got a couple of questions. So first, a question again on atopic dermatitis. So you got 64 patients enrolled in the trial. Could you share what is the most typical prior therapy that these patients have? Is it a local regimen like ruxolitinib? Is it systemic like dupilumab? And is there any physician feedback in terms of the enthusiasm of the patients and etc.? If you could share any details. Okay. So first, Eden, we don't have all 64 patients enrolled yet. The intent is to have 64 patients enrolled. We're enrolling cohort number two now. The eligibility for entry is you have to have failed a systemic or topical therapy for your AD. You have to have moderate or severe disease. So far, the patients enrolled (and we'll present more of the details on this in December) have not failed a systemic therapy but have failed topical therapies. Just about all of the patients that we've treated so far have discontinued their topical therapy while they're on our drug. Okay. So mostly, this is sort of topical failure. It's pre-Dupixent, essentially, patient population. So far. So far. Now, we're in the middle of the study. Okay. Makes sense. Yeah, so I also want to go back to PTCL indication, and maybe it's a sort of outdated question, but do you have any updates on phase 1B patients? Any CRs turned into PRs or any PRs? Any sort of PRs turned into CRs or any updates on the duration of response for phase 1B? I mentioned in my remarks that there are four patients still on therapy. The three of those are CRs that are, oh God, months. I don't remember. 6-12 months out there, at least. One of the PRs has continued tumor regression. That patient has been on treatment about 18 months now and just has slow improvement, slow continued improvement in his disease. It is not yet a CR, but it's looking pretty promising for that. Now, one of the CRs, we stopped therapy while in CR per protocol. We can't treat beyond 24 months by our protocol. So that patient discontinued therapy while in CR. Okay. So one PR may potentially turn into CR. And how do you explain overall such a broad availability of CRs versus PRs? You have more CRs than PRs, which is unusual. So how do you explain? What does it tell us about the mechanism of action here? Well, I think it tells us that it's effective at eradicating microscopic disease, and it's effective at eradicating, remember, these tumors are very heterogeneous, so they have a lot of different mutations and a lot of different clones, etc. And I think what this tells us is the mechanism of action is able to handle a broad spectrum of tumors and the associated mutations. Whereas if you treat with, let's say, a chemotherapy agent, you're going to eventually select out resistant clones, we seem to be less susceptible to the emergence of resistance, and I think that's because we're inducing an immune response, and an immune response, as you know, can respond to different antigens and different diversity of antigens. Makes sense? Yep. Absolutely. Absolutely. And the last question I have on systemic sclerosis, the preclinical data that they will present, so another hard-to-treat indication, autoimmune indication, so historically, it's been two endpoints that they were looking for systemic sclerosis. One is lung, FVC, and the other one is Rodnan skin score, so what do you think soquelitinib may focus? I know this is too early, but this is an active drug, one indication in oncology, one indication in autoimmune, so it wouldn't be totally unexpected if you start directly from phase II at some point, so just wanted to hear your thoughts on systemic sclerosis. Well, I mean, people die from the lung disease, the interstitial pneumonitis and fibrotic lung disease, interstitial lung disease, so that would be the thing to focus on, and that's what we have focused on, so the model that's going to be, and the abstract is already out on this, I think the paper's on Sunday at ACR, is a very interesting model, a very good model, probably the best animal model for systemic sclerosis. These animals get, they have what's a FRA2 mutation, it's very much a TH2 disorder, and they have fibrosis, fibrotic lung disease. They get right heart failure, and all of that responds to treatment with soquelitinib. In addition, we've also tested soquelitinib in your typical idiopathic fibrotic interstitial lung disease, and it's very active in that model as well. I think down the line, systemic sclerosis. I mean, the thing that we would focus on would be lung disease because that's what kills people, and that's the biggest, the most serious part of the problem. As you know, lung disease and right heart disease go together and arterial hypertension and so forth. That would be. That's an interesting disease for us. It also gives us a window in fibrotic diseases. Fibrosis is very much TH2. We block TH2 very well. This opens up a whole new set of diseases that have to do with fibrosis, everything from scleroderma to cirrhosis to other fibrotic diseases. Right. Yeah. Makes sense. I'm sorry, just the last question I want to ask. How do you differentiate dosing between oncology and autoimmune diseases? These are two big sort of indications. Just wanted to hear your thoughts on this. Well, I think it's a little early to speculate on that. I mean, we're in the middle of a trial now where we're going to learn a lot about dosing and regimen. But I think I'll go out on a limb here and say I don't think we're going to need to treat atopic dermatitis continuously. I think cancer, you will. Got it. Got it. Got it. Yeah. Makes sense. Makes sense. Okay. Thanks so much, Richard. Congrats with the progress this quarter. Thank you, Eden. Thank you. Your next question comes from the line of Graig Suvannavejh. Please go ahead. Hi. Thanks so much for taking my questions here. Congratulations on all the progress that you've been making. If I could just revisit the readout, the interim readout in atopic dermatitis that you're expecting in December? As it relates to EASI, just if you could clarify, will you be specifically reporting on both EASI- 50 and EASI- 75? And then a follow-up is just going back to comments, Richard, you made in response to, I think, one of the first questions on the Q&A, which was expectations around what the bar for success would be. I think you had mentioned you would expect something similar to approved agents such as Dupi, but I'm wondering if, since you're on oral therapy, if you feel the need to be as effective as perhaps some of the injectables like a Dupi. And then I have a follow-up. Thank you. Okay. So thank you for the question. So we expect to report for cohort one and cohort two. Now, we'll have more follow-up on cohort one, of course, because it was enrolled first. We expect to report on the mean% EASI score reduction for placebo and for active. We expect to report on EASI- 50, EASI- 75, EASI- 90. We expect to report on IGA 0 and 1. Those are very typical things. So we will be reporting on that. Obviously, we report on safety as well. Now, your question about, "Oh, what will we compare to?" Well, our regimen, again, this is the first dose we've tested. It's 28-day dosing. We can compare and will compare to, let's say, Dupixent phase I trial where they had already optimized their dose and treated for 4 weeks and 12 weeks. So we can compare to things like that. And that's what we plan to do. Now, your question about, "Do we have to be as good because we're oral and safe and more convenient?" We're pretty excited about the mechanism of action of our drug. So I want to be better. I plan to be better. Okay. Appreciate that and appreciate the confidence that you have in the potential readout there, so, and then a follow-up is almost a segue from the topic of an oral agent. Could you just remind me, given obviously the promise of having an oral-based agent for atopic dermatitis versus an injectable, what the competitive landscape looks like in terms of orals that are in the clinic and kind of where are you relative in terms of clinical development timelines to perhaps some other oral higher-profile oral programs that you're following closely? Thank you, well, that's a very hard question. So as you know, there are many drugs in development for atopic dermatitis. Most of those are injectables, biologics. There are some oral compounds in the clinic. I don't know if I'm in a position to comment on those. I think they're pretty early. I don't really know what their data is. I know there's some data readouts also before the end of the year. So I'm not sure I'm able to comment on our product relative to those. Okay. Thank you very much. Thank you. And your next question comes from the line of Jeff Jones from Oppenheimer. Please go ahead. Good afternoon, guys, and thanks for taking the question. I guess I'll switch over from AD and go back to PTCL. In terms of the phase III trial and the primary endpoint of PFS, how do you deal in the trial with patients who are complete responders and go on to transplant? And then interested in your view on the bar for success here given some of the data we're seeing on the PI3K inhibitors at ASH right now. And then I've got a follow-up. Okay. So first of all, Jeff, it is a randomized trial, and there's an equal number of patients in the standard of care, belinostat and pralatrexate, and the soquelitinib arms. So if you go on to a bone marrow transplant, you are censored at that point. We continue to follow you, but you're censored at that point. The number of patients that's anticipated to go to transplant in a study like this is maybe 10%, maybe not even that high. So that's not going to be a huge factor. But the answer to your question is they would be censored. You count their response and their PFS to the point in time that they go on for a transplant. Now, the second part of your question was criteria for success, I think. It was. Yeah. Well, that's built into the protocol, as is the censoring. That's all defined in the protocol. That's all been reviewed by FDA. So the statistical plan gives us about a 90% power, actually. I think it's an 89% power to see a one-and-a-half-month improvement over the control arm. So that would give you a hazard ratio of about 0.56. So that's what we need to do to win. Now, just getting back to the transplant question, just so people understand, I mean, most patients, most patients are too old for a transplant. This disease is mostly a disease of older people. Most patients are too old, and patients have to get into a good remission to get a transplant. That's why it's been such a small subset of patients who gets the transplant and why it's so hard to interpret the transplant data because you're selecting out a very favorable patient population to begin with. But in any event, in our study, we deal with that by censoring that data. Makes sense? I appreciate that. Yeah, it does. And I guess, so I mean, the data that's out at ASH right now on the PI3 kinase inhibitors, that's really, it's ORR data at this point. But I guess just your thoughts on what you're seeing there with some of those, I guess, between 40%-60% ORRs in a couple of those studies. Yeah. So the PI3Ks have been around for a long time now in PTCL. They give you reasonable responses. They're usually very short-lived. Those drugs are highly toxic with liver abnormalities and hematologic abnormalities as well. I don't really think that that is a significant competitor to soquelitinib should our trial be positive. Okay. Appreciate that. And one other thing to point out there, really, the soquelitinib trial is setting one up for the next trial, which would be frontline. I mean, this is a registration-approvable trial. But the next study, which people already want to do, is to combine soquelitinib with chemotherapy frontline and perhaps use it as maintenance therapy because of its safety and convenience. You're not going to do that with a PI3K. You can't just slam that together with a bunch of chemotherapy drugs. It would be too difficult to do that from a safety standpoint. And using it as a maintenance would be also problematic. Got it. Okay. Appreciate that. One quick follow-up on the renal cell study with soquelitinib. In terms of selecting patients for enrollment there, are you looking, going back to looking at absolute lymphocyte counts or using prior lines of therapy? How are you sort of looking at sort of T-cell health there? Yeah. So well, we're not using that as an eligibility criteria, although we're going to be collecting that data. The renal patients are not as beat up immunologically as these lymphoma patients. So I think we'll be in better shape there because, I mean, lymphoma patients are inherently pretty immunosuppressed from the disease as well as the types of therapy they've had. That's less of a problem in renal. Okay. So you're just collecting the data and sort of look at how it pans out for these endpoints or biomarkers post? Yes. Okay. Great. Thank you very much. I'll jump back into the queue. All right. I think that is all the questions we have this afternoon. I want to thank everyone for participating, and we look forward to giving an update in December to everyone on our atopic dermatitis trial. Thank you very much. Thank you. And this concludes today's call. Thank you for participating. You may all disconnect.