Good afternoon, everyone. Thank you for standing by, and welcome to the Corvus Pharmaceuticals First Quarter 2025 Business Update and Financial Results Conference Call. At this time, all participants are in a 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 Zack Kubow of Real Chemistry. Please go ahead, sir. Thank you, Operator, and good afternoon, everyone. Thanks for joining us today on the call. This conference call is being webcast with presentation slides. We encourage participants to join the webcast in order to view the slides. You can find the link to join the webcast on the Investor Relations homepage of the Corvus website. Turning to slide two, 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 10Q for the quarter ended March 31st, 2025, 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. The agenda for the call is shown on slide three. We will begin with a short overview of the first quarter financial results, followed by a detailed review of the Soquelitinib atopic dermatitis phase I data announced today and being presented at the Society for Investigative Dermatology annual meeting this week. We will then provide a broader business update and then open the call for questions and answers. On the call from Corvus are Dr. Richard Miller, Chief Executive Officer, Leiv Lea, Chief Financial Officer, Jeff Arcara, Chief Business Officer, and Dr. Suresh Mahabhashyam, Vice President of Clinical Development. With that, I'd like to turn the call over to Leiv Lea. Leiv. Thank you, Zack. I will provide an overview of the key financial highlights from our first quarter. Research and development expenses in the first quarter of 2025 total $7.5 million, compared to $4.1 million for the same period in 2024. The $3.4 million increase was primarily due to higher clinical trial and manufacturing costs associated with the development of Soquelitinib, as well as an increase in personnel-related costs. Net income for the first quarter of 2025 was $15.2 million, including a non-cash loss of $0.5 million related to Angel Pharmaceuticals, our partner in China. In addition, we recorded a non-cash gain of $25.1 million from the change in fair value of Corvus' warrant liability during the first quarter of 2025. This compares to a net loss of $5.7 million for the same period in 2024, which included a $0.2 million non-cash gain related to Angel Pharmaceuticals. Total stock compensation expense for the first quarter of 2025 was $1.3 million, compared to $0.7 million for the same period in 2024. As of March 31st, 2025, Corvus had cash, cash equivalents, and marketable securities totaling $44.2 million, as compared to $52 million at December 31st, 2024. In May 2025, holders of 8,945,000 common stock warrants exercised all of their warrants in advance of the June 30th, 2025, expiration date, which resulted in cash proceeds to Corvus of approximately $31.3 million. Richard Miller also exercised all of his 559,000 warrants. All of the warrants were exercised at $3.50 per share. Based on our current plans, we expect our current cash, including the warrant proceeds, to fund operations into the fourth quarter of 2026. I will now turn the call over to Richard, who will review the Soquelitinib phase I data reported today and discuss other company progress and updates. Thank you, Leiv, and good afternoon, everyone. Thank you for joining us today for our update call. I am excited to be joining you from San Diego, site of the Society for Investigative Dermatology annual meeting, or SID. Data from our phase I trial with soquelitinib in patients with atopic dermatitis will be presented in a poster later today and on Saturday in an oral session given by Dr. Albert Chu from the Department of Dermatology at Stanford University Medical Center. We view the data as very encouraging, with all treatment cohorts demonstrating a favorable safety and efficacy profile compared to placebo. Cohort three data is especially interesting, demonstrating earlier and deeper responses compared to cohorts one and two. In addition, the latest biomarker data from the trial continues to support the ITK inhibition mechanism of action, including the potential induction of anti-inflammatory T regulatory cells. I will review the details of the data being presented at SID, along with an overview of the ongoing trial and our future plans for the phase I trial and the planned phase II trial in atopic dermatitis. Slide six shows the design of the phase I clinical trial. Eligible patients have met the Hanifin and Rajka criteria and have moderate to severe atopic dermatitis who have failed at least one prior systemic or topical therapy regimen. There are four cohorts that are sequentially enrolled, and we have completed enrollment in the first three cohorts of the trial. 16 subjects are enrolled in each cohort, four placebo and 12 actives. The study is double-blind. Neither the patient nor the doctor nor the treatment assignment, the placebo and active tablets, are indistinguishable. The company is not blinded, and we are able to evaluate the data as the study progresses. We wanted to maintain the ability to adjust or amend the trial based on available data as the study progressed, since this is a novel agent with a mechanism of action not studied previously in this indication. Patients receive study drug or placebo for 28 days, and then they are followed for an additional 30 days off of therapy for a total of 58 days on study. We designed the study in this way to evaluate safety and efficacy while on the drug and to identify the possibility of persistent effects after the drug is discontinued. The endpoints of the trial are safety and efficacy measured by EASI, Eczema Area and Severity Index scores, and IGA, Investigator's Global Assessment. Each of the cohorts examines a different dosing regimen. The four cohorts are first, 100 mg oral twice a day for a total dose of 200 mg per day. Second, 200 mg oral once a day, a different schedule, but also a total dose of 200 mg per day. The third cohort, 200 mg oral twice a day for a total dose of 400 mg per day. Fourth cohort, 400 mg oral once a day. These doses were selected based on our experience in T-cell lymphoma patients. We have shown that these doses result in significant or complete ITK target occupancy. 200 mg twice a day is the dose we are evaluating in our ongoing phase III registration lymphoma trial. The next slide shows the characteristics of the 48 patients enrolled and treated in cohorts one, two, and three. The placebo and Soquelitinib groups are shown, as well as the combined cohorts. There are a few characteristics to point out. The mean baseline EASI scores in cohort three for both the Soquelitinib and placebo groups was about 27-28, significantly higher than cohorts one and two, which were in the range of 17-20. This indicates that cohort three patients had worse disease at baseline. Consistent with this is that cohort three patients also had a higher% of patients who failed prior systemic therapies. In fact, two treated patients had disease that was refractory or resistant to DUPIXENT. There is a high percentage of African Americans in all groups. Such patients are reported to have worse prognosis. Generally, the Soquelitinib and placebo patients are very well balanced with regard to patient characteristics. The cohort three placebo patients are younger, but age is not a prognostic variable. Now let's move on to the efficacy results, which are shown in the table on slide eight. This table shows the results at day 28 for patients in the Soquelitinib and placebo groups. Cohorts one and two are combined since the characteristics and results were very similar. The left side shows results for the combined cohorts one and two, and the right side shows the results for patients in cohort three that have completed 28-day follow-up, eight active and four placebos. Four additional patients in cohort three receiving active drug have completed day 15 follow-up but have not yet completed the 28-day follow-up. For cohorts one and two, the mean reduction of EASI score in the placebo group is 30.6% and is 54.6% for the Soquelitinib group, an absolute difference of 24.0%. For cohort three, the mean percent reduction of EASI score in the placebo group is 42.1% and is 71.1% for the Soquelitinib group, an absolute difference of 29.0%. Looking at EASI 50, we see that both placebo and Soquelitinib treated patients often achieve EASI 50. The situation is much different for EASI 75, EASI 90, and IGA zero or one, which are the endpoints considered to be clinically meaningful. No placebo patients reached EASI 75, EASI 90, or IGA zero or one. In the Soquelitinib group for cohorts one and two, 29% achieved EASI 75 and 4% achieved EASI 90, while in cohort three, 63% achieved EASI 75 and 13% achieved EASI 90. 21% of the patients in the cohort one and two Soquelitinib groups achieved IGA zero or one, while in cohort three, 25% in the Soquelitinib group achieved IGA zero or one. The next slide shows the kinetics of response for the patients treated with Soquelitinib in each of the cohorts one, two, and three, and the combined placebo patients from all three cohorts. The orange line represents placebo. You can see that cohorts one and two, represented by the blue and red lines respectively, begin to separate from placebo at day 15 and show continued separation at day 28. This separation is maintained during the 30-day post-treatment period. The curves for cohort one and two are nearly overlapping, indicating that there are no differences in the twice per day compared to the once per day dosing regimen. It appears that QD dosing is possible for this drug. The green line, which represents cohort three, shows earlier and deeper separation from placebo at day eight, with EASI score improvement continuing through day 15 and 28. Cohort three data includes all 12 Soquelitinib treated patients in the cohort through day 15 and then for eight patients at day 28, as there are four patients that have not yet reached their 28-day follow-up. Of note, those four patients in the Soquelitinib group are demonstrating results at day 15 that are consistent with the other patients, so we should expect that trend to continue to day 28. All placebo patients have reached the day 28 follow-up. I would like to point out that the downward slope of the curves in all treatment cohorts at day 15 to 28 suggests that longer treatment duration could potentially deepen responses further. On slide 10, we show the same analysis as the prior slide, but with the data for cohorts one, two, and three combined, shown in the blue line. This is the data from all patients. Separation from placebo begins by day 15, and by day 28, it is statistically significantly better than the placebo with a p equal to 0.03. The next slide summarizes the efficacy for each treatment cohort and for the combined placebos. No placebo achieved EASI 75 or IGA zero or one. Significant differences are seen for the treatment groups compared to placebo, with cohort three appearing to be better than the other cohorts. Data from the combined Soquelitinib cohorts is statistically significantly better than placebo. Now let's review the safety. As shown on this slide, there were no significant safety issues observed with Soquelitinib, with no differences between treatment and placebo groups. Only one treatment-related adverse event was seen in a patient receiving Soquelitinib, a grade one nausea. No clinically significant laboratory abnormalities were seen. The total treatment experience with Soquelitinib now involves over 100 patients with T-cell lymphoma or atopic dermatitis, representing approximately 9,000 patient treatment days. In our lymphoma trial, some patients have been on continuous daily therapy for up to two years. Based on these results, we have amended the phase I trial protocol as outlined on slide 13. At the bottom of the slide in purple, we show that the previously planned cohort four is being replaced with an extension cohort that will evaluate an additional 24 patients at the 200 mg twice per day dose given for eight weeks with an additional 30-day follow-up without therapy. Based on our studies of occupancy and pharmacokinetics, we determined that cohort four would not likely provide more useful information. By replacing the cohort with a new cohort, we do not expect to lose any time. The 24 patients will be randomized in a blinded fashion, one to one with placebo, 12 active and 12 placebo. We believe this amendment gives us the opportunity to evaluate the potential for greater efficacy with longer treatment duration. We anticipate data from the extension cohort will be available in the fourth quarter of this year. This additional experience should help optimize the design of our phase ii trial, which we are working on in parallel and remain on track to initiate before the end of this year. Phase II will likely evaluate different doses and durations of therapy, including once per day administration of the drug. In conclusion, we continue to be encouraged by the results from the trial, which show a favorable safety and efficacy profile with a convenient oral tablet. Key highlights from the data include all three cohorts showed a significant reduction in EASI score at 28 days of treatment, with clear separation from placebo. Cohort three with 200 mg twice per day dose showed earlier and deeper responses than cohort one and two. Data that is consistent with our pharmacokinetic analysis. Cohort one and two results evaluating 200 mg once per day versus 100 mg twice per day dosing showed no differences in activity, suggesting that QD dosing is possible. Post-treatment, all three cohorts showed a sustained benefit for 30 days, potentially due to increased T reg cells. No rebound events such as seen with JAK inhibitors were observed. The safety profile across all three cohorts shows Soquelitinib is very well tolerated. Based on the results to date, we are adding a new extension cohort that will evaluate longer 56-day or eight-week treatment duration. More broadly, the safety, mechanism of action, and other properties suggest that Soquelitinib could be an important new treatment for a broad range of immune diseases. Now for a brief business update for the quarter. We continue to enroll patients in our registrational phase III trial of soquelitinib in patients with relapsed peripheral T-cell lymphoma, driving towards interim data in late 2026. The first patient has been treated in our phase II trial of Soquelitinib in patients with ALPS or autoimmune lymphoproliferative syndrome. Depending on enrollment trends, it is possible we could see initial data from the phase two ALPS study in late 2025 or early 2026. In closing, the Soquelitinib results in atopic dermatitis further underscore its broad potential for a range of oncology and immune disease indications. This includes our clinical programs for PTCL, atopic dermatitis and ALPS, our planned study for solid tumors, and a long list of immune diseases that we have the potential to address with Soquelitinib or our next generation ITK programs. We are delighted with the early exercise of warrants announced today, which results in an additional $31 million and enables us to advance Soquelitinib on multiple fronts, including key data from the next 24 patients in the atopic dermatitis trial, which we expect to have in the fourth quarter of 2025. Current cash takes us to late 2026. 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 question and answer period. Operator. 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 one on your touch-tone 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 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 Aydin Huseynov from Ladenburg. Please go ahead. Hi, good afternoon, everyone. Congratulations, Richard, for the great data. A couple of questions on my end. It seems like your cohort three EASI 75 data at week four beats the DUPIXENT data at week 16. It also seems that your data is actually getting closer to JAK inhibitors than DUPIXENT. Do you think eventually Soquelitinib would be used ahead of DUPIXENT and competing with JAK inhibitors? Just curious of your opinion. Thank you for the question, Ayden. First of all, the cohort three is a small sample size, so we have to put that in a little bit of perspective. Yeah, I think that our data at four weeks is competitive with other agents that are approved for atopic dermatitis. I do see with the safety and convenience that we have with an oral tablet that this could become an early line of systemic therapy. We have a lot more work to see exactly where that fits in, but I think that the work we've done here shows a novel mechanism which has the potential to be used early on in the therapy of atopic dermatitis. Thank you. Appreciate that. Another question I have is in terms of the efficacy curves, and again, looking at JAK inhibitors, for JAKs, I think it plateaus at week eight. Based on soquelitinib mechanism of action, where do you think can this potentially plateau? Is it going to be week eight, 12, 16? Any thoughts on this? Yeah. Look, we're struck by the fact that the curves are still decreasing from 15 to 28 days in a pretty steep slope, and then it flattens out as soon as you stop the drug. The question, I mean, it begs the question, if you were to continue therapy, would you get deeper, better responses? We want to test that in our amended protocol. We also have examples in our study of patients who were responding, were continuing to get better at day 28, including some of the very sick ones. They were getting better by day 28 when we had to stop the drug by protocol. It really does raise the question, and even raised by their physicians, "Gee, why can't we continue this since they were improving on the therapy?" Thank you. Thank you. Very helpful. The last question is, there's a significant jump in EASI efficacy between cohort two and cohort three. Obviously, as you mentioned, cohort three had even more severe patients. How do you explain such a sharp jump in efficacy? Again, it's small numbers, et cetera, but just curious on your thoughts on this. We have more drug. It's twice the drug. Cohort three is double the dose, total daily dose compared to cohorts one and two. The dose of drug has been doubled. Very careful analysis we did from our lymphoma patients shows that when you raise the dose to that level, you pretty much have occupancy 24 hours a day. That could be important. It makes a lot of sense. We ended up at 200 BID in our lymphoma study after carefully looking at a lot of different dose levels. This all makes perfect sense. Listen, even early on, I think back in December, January, when we were talking about this, we always said we expected the third cohort would be better. It is. I think it's still an open question whether 200 BID versus maybe 400 once a day would be equal. We need to ultimately test that. That's something we're thinking about in our phase II trial design. Got it. Thanks so much, Richard. Congratulations again with this great data. Thank you. Your next question comes from the line of Graig Suvannavejh from Mizuho Securities. Please go ahead. Great. Thanks for taking my questions. We'll extend our congrats on the data in atopic dermatitis as well. I was wanting to ask about the modification to the phase I study and the extended duration cohort. I think I completely understand the logic of wanting to treat longer. I think I heard, and I might have misunderstood, but I think I heard that you might consider adding a QD dose in that. If that is indeed true, and given the comments that the 400 QD dose may not be all that differentiated, I'm just wondering what that potential QD dose would be if you were to test that in the extended duration cohort. Thanks. The extended duration is 24 patients, 12 active, 12 placebo. One dose, I mean, a single dosing regimen will be studied, 200 mg BID. Okay. Thank you. Thank you. What I mentioned is in. Yeah. Yeah. Okay. It does seem like optimally, at least as of today, 200 mg BID seems to be the optimal dose across both your oncology and at least atopic dermatitis indications. That's correct. Okay. Thank you for that. If I could ask, just going back to the data that you shared today, if we look at the data in cohort two, there was a difference in what was seen on at least EASI 75 with numbers coming down. I'm going to assume that's because of the extra patients that you included. You didn't really see them achieve EASI 75. As I'm thinking now about the remaining four patients that have not been reported out yet because I don't think they've finished follow-up, any thoughts on what their potential contribution could be to the efficacy scores that you're seeing as of today? Thanks. I'm not totally sure what you're saying. The numbers for the 200 QD are a little bit lower than we showed in January, you're saying. The additional patients. Yeah. Okay. First of all, again, small numbers, but a couple of those patients were EASI 72 and EASI 68. I mean, some of this is really very close. I think it was really there was really no substantive difference. If you look at our cohort three, if you look at the EASI scores in the eight patients at day 15 and the four that are also at day 15, they're darn close. You can see that actually, if you look at the standard error bars on the green, are very tight. Okay. Maybe one last one, if I'll sneak in. It should be a short, easy question to answer. When would you expect to share the complete cohort three data from all 12 patients? I think we could share that in a press release, probably in a month or two. Okay. Thank you so much, and congratulations again on the data. Thank you. Your next question comes from the line of Lee Watzek from Cantor. Please go ahead. Hey, congrats on the data as well. Maybe a couple of questions from us. The first, just on the placebo group, when I look at the EASI change from baseline, it looks like this group also went down and did not really rebound. I guess the question is, is this placebo effect typical compared to other AD trials and was this placebo effect driven by a handful of patients? There were placebos that rebound and get worse. In fact, if you look at the standard error bars on the placebo, you will see that they are quite broad. There were a couple of patients that, in fact, did get worse. Is this standard? Actually, I think our placebos behaved pretty much like others. I mean, some recent studies have had even more, I guess, more improvement in placebo groups, but we really haven't seen that. One of the things we did, and I didn't really have time to go into this in the presentation, is we tracked the EASI scores. If you look at the graphs on slides nine and 10, screening to baseline, that's a period of about two weeks. That's the time the patient comes in and goes through the necessary testing to make sure they're eligible. EASI scores are done at the beginning of that and, of course, before they go on treatment. Note how stable they are for all the groups. This is a tribute to the physicians and our staff and the training in terms of EASI scores and how stable they were. The minute you start taking a pill, there is a placebo effect, clearly, and some of those placebos improve. No, there is nothing strange about our placebos here. I think that one thing, our placebos, 0% of EASI 75s and 90s, that is much lower than you will see on the DUPIXENT or JAK inhibitor studies where you will see 10%, 15%, 20% reach EASI 75 or IGA zero one. Keep in mind, those studies are done longer. There you are on study for three months or six months or longer. The longer you are on study, the more there is a chance that a placebo could have an improvement and reach that. Okay. Understood. That makes sense? Yes. Thanks for clarifying that. Just curious if you see any differential response in patients with or without prior systemic treatment. Too early to talk about that, but we had in cohort three, two patients, one was completely refractory to DUPIXENT, had a baseline EASI in the mid-40s. Okay, let me just talk about that patient first. That patient had failed DUPIXENT, didn't respond at all. JAK inhibitor and methotrexate didn't respond to any of that, went on our drug and improved significantly, was improving throughout the study, but again, we had to stop at day 28. Physician wanted us to continue, of course, but we couldn't. The second patient was a patient with EASI in the high 30s, was on DUPIXENT for a while, responded to that, then progressed again, was put on DUPIXENT again, did not respond, did not respond at all, went on our drug, had an EASI 90, achieved an EASI 90 on our drug. So that's N equals two. I don't know if responder versus non or refractory versus resistant versus no prior systemic therapy. I don't know what the prognostic significance of that is because we only have a couple of those patients. I would suggest that given our mechanism of action is non-overlapping with those agents, I would see no reason why there would be any difference between someone who had a JAK or a DUPIXENT or not. I think all of this is falling into line very consistent based on what we've learned in lab, what we've learned in animal models, and frankly, what we've learned from our lymphoma studies. Great. Congrats again. Thank you. Your next question comes from the line of Jeff Jones from Oppenheimer. Please go ahead. Good afternoon, guys, and congrats again on the really outstanding data here. Richard, you've talked a little bit about receptor occupancy. Have you looked in these patients through cohort three at receptor occupancy at all to see if there might be differences in what you've seen with the T-cell lymphoma patients versus AD patients? We have not looked in these patients because we've done so many lymphoma patients, and this is just chemistry, Jeff. If you have a concentration of a certain level, you're going to bind that receptor. It's a covalent drug. We know what that level is, by the way. It's 300 ng per ml of drug. Okay. Looking at this data, obviously, the EASI 75 numbers came down somewhat from what you initially reported from a subset of the cohort two patients. I believe that was around a 57% EASI 75. That number is somewhat similar to the 63% you're reporting now for cohort three in n equals 8 out of the total 12 treated patients at this point. Clearly, the drug's highly active, and I guess it's just a question, what particular is giving you confidence in the dose effect you're seeing between cohort two and three given the small numbers at this point? First of all, again, look at the kinetic curve on nine. Look at slide nine and the kinetics of response. I mean, not only is there a deeper response with cohort three, but it's earlier. We do know there's more receptor occupancy, and we had sicker patients in cohort three. I mean, substantially sicker patients. Again, if we look at the cohort three day 15 data, it's all pretty tight. That gives us confidence. With regard to the cohort two changing, again, very small number. EASI 75 is important. It's somewhat arbitrary. As I mentioned earlier, a couple of the follow-up patients or subsequent patients had EASIs in the low 70s, didn't quite make it. That's just luck of the draw. The fact of the matter is that at 28 days, a substantial number are responding. In fact, I would even argue that in the cohort three, even if the next set of patients didn't respond, you still have, what, a 50% EASI 75, which is a pretty good result. No. Appreciate that, Richard. I think the kinetics really help with that story and the fact that all of the patients are through day 15 here. I guess one last question just on the runway guidance that you gave. Can you tell us what trials are included in that? Because you guys have got a lot on your plate right now. Let me deflect that to Leiv. Leiv, can you? Sure. It includes the trials that Richard laid out. One, the extension cohort part of our phase I AD trial, starting the phase II AD trial, continuing with our phase III lymphoma trial, and at the end of the year, starting a solid tumor trial, a small phase I trial. It includes all of those trials. Great. Thank you guys very much, and congrats again. Maybe we have time for one more question or operator? Yes, we have one more question coming from the line of Roger Song from Jefferies. Please go ahead. Great. Yeah. Congrats to the data as well. Thank you for taking the question. Maybe just two quick ones. One is just want to clarify understanding your phase one extension cohort will be BID 200 mg eight weeks. You mentioned something for phase two, you're considering QD as one of those cohorts. Would that be 400 mg or lower or higher? If it's 400 mg, what's the ceiling of the dose in terms of the safety profile? I have a quick follow-up. Thank you. All right. First of all, remember in lymphoma, we went up to 600 mg BID and did not see any DLTs or maximally tolerated dose was not reached. Roger, we have not finalized the phase two trial yet. I'm a little hesitant to give you exactly what the design of that is. What it'll have is at least two active dose groups. One you want to make lower. Hopefully, that has a lower response. One, you want your real dose. And then, of course, we'll have placebo. 200 mg BID will certainly be one of the active doses. I think that we would either look at 200 QD, maybe that's one dose level, or maybe the 400 once a day. All right. We have not finalized that yet. Part of the reason for doing more patients, I mean, part of what we're trying to do is confirm this 200 BID, get more measurements, look at more things. I should also mention, I didn't include this in the presentation, but if you look at our poster and the presentation Dr. Chu will make on Saturday, there are changes that are emerging in the cytokines and in the Treg cells, and cohort three is superior. The changes, let me say it this way, the cohort three changes are more dramatic. Got it. Yeah. Okay. That's very helpful. Maybe just a quick last one. Understanding your cash runway is covering all the phase II and then all the other indications. Just curious about the thinking about the partnership. Would you be seeking the discussion even before the phase II? Thank you. No. We're going to blast ahead on our own. We recognize, however, that developing drugs for a range of autoimmune diseases is difficult or complex. We are engaged in various discussions with companies. In the meantime, we're going to push forward. With the extra cash we got yesterday, we can move through our extension, which I think is going to be a very important milestone, get into phase II, and move forward. We're not dependent on any partners. Great. Thank you. Thank you, Rich. All right. Thank you. I think that is there one more question there? Okay. We'll take another question. Is everybody? We have one last question coming from the line of Sean Lee from H.C. Wainwright. Oh, yes. Please go ahead. Hey. Good afternoon, guys. Congrats on the exciting results, and thanks for taking my question. I just have one. Because we're looking at the almost nonexistent side effects of this drug, what are your thoughts on potential combinations either for AD or other indications? Thanks. Lots of people are bringing up that question. Thank you for asking it. Because it has a non-overlapping mechanism with other drugs, and because of its safety, and because it's oral and conveniently administered, there is an opportunity to combine with other agents. I mean, there's a big list of agents. I mean, obviously, the IL-13, like a DUPIXENT, JAK inhibitors wouldn't be a crazy idea, although I would worry about the toxicity of the JAK inhibitors, the anti-IL-13s. I think that there's a lot of opportunities there. For now, we're going to be plowing ahead with monotherapy. Okay. Thanks for that. All right. I think that concludes our conference call. Thank you all so much for participating. We look forward to providing updates on our programs as we move forward. Thank you. Thank you, everyone, for participating.