Corvus Pharmaceuticals, Inc. (NASDAQ:CRVS) Q1 2025 Earnings Call Transcript

Corvus Pharmaceuticals, Inc. (NASDAQ:CRVS) Q1 2025 Earnings Call Transcript May 8, 2025

Corvus Pharmaceuticals, Inc. reports earnings inline with expectations. Reported EPS is $-0.13 EPS, expectations were $-0.13.

Operator: Good afternoon, everyone. Thank you for standing by, and welcome to the Corvus Pharmaceuticals First Quarter 2025 Business Update and Financial Results Conference Call [Operator Instructions] It is now my pleasure to turn the call over to Zack Kubow of Real Chemistry. Please go ahead, sir.

Zack Kubow: 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 2. 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 March 31, 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 3. We will begin with a short overview of the first quarter financial results, followed by a detailed review of the soquelitinib atopic dermatitis Phase 1 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?

Leiv Lea: Thank you, Zach. I will provide an overview of the key financial highlights from our first quarter. Research and development expenses in the first quarter of 2025 totaled $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 noncash loss of $0.5 million related to Angel Pharmaceuticals, our partner in China. In addition, we recorded a noncash gain of $25.1 million from the change in fair value of Corvus’ warrant liability during the first quarter 2025.

This compares to a net loss of $5.7 million for the same period in 2024, which included a $0.2 million noncash gain related to Angel Pharmaceuticals. Total stock compensation expense for the first quarter 2025 was $1.3 million compared to $0.7 million for the same period in 2024. As of March 31, 2025, Corvus had cash, cash equivalents and marketable securities totaling $44.2 million as compared to $52 million at December 31, 2024. In May 2025, holders of 8,945,000 common stock warrants exercised all of their warrants in advance of the June 30, 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 1 data reported today and discuss other company progress and updates.

Richard Miller: 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 1 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 Chiou 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 3 data is especially interesting, demonstrating earlier and deeper responses compared to Cohorts 1 and 2.

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 1 trial and the planned Phase 2 trial in atopic dermatitis. Slide 6 shows the design of the Phase 1 clinical trial. Eligible patients have met the Hanifin & 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 3 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 know 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 received 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 Global Assessment. Each of the cohorts examines a different dosing regimen. The four cohorts are: first, 100 milligrams oral twice a day for a total dose of 200 milligrams per day; second, 200 milligrams oral once a day, a different schedule, but also a total dose of 200 milligrams per day; the third cohort, 200 milligrams oral twice a day for a total dose of 400 milligrams per day; fourth cohort, 400 milligrams 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 milligrams twice a day is the dose we are evaluating in our ongoing Phase 3 registration lymphoma trial.

The next slide shows the characteristics of the 48 patients enrolled and treated in Cohorts 1, 2 and 3. 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 3 for both the soquelitinib and placebo groups was about 27 to 28, significantly higher than Cohorts 1 and 2, which were in the range of 17 to 20. This indicates that Cohort 3 patients had worse disease at baseline. Consistent with this is that Cohort 3 patients also had a higher percentage 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 cohort 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 3 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 8. This table shows the results at day 28 for patients in the soquelitinib and placebo groups. Cohorts 1 and 2 are combined since the characteristics and results were very similar. The left side shows results for the combined Cohorts 1 and 2 and the right side shows the results for patients in Cohort 3 that have completed 28-day follow-up, eight active and four placebos. Four additional patients in Cohort 3 receiving active drug have completed day 15 follow-up but have not yet completed the 28-day follow-up.

For Cohorts 1 and 2, 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 3, the mean percent reduction of EASI score in the placebo group is 42.1% and a 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 achieved EASI 50. The situation is much different for EASI 75, EASI 90 and IGA 0 or 1, which are the endpoints considered to be clinically meaningful. No placebo patients reached EASI 75, EASI 90 or IGA 0 or 1. In the soquelitinib group for Cohorts 1 and 2, 29% achieved EASI 75 and 4% achieved EASI 90, while in Cohort 3, 63% achieved EASI 75 and 13% achieved EASI 90.

21% of the patients in the Cohort 1 and 2 soquelitinib groups achieved IGA 0 or 1, while in Cohort 3, 25% in the soquelitinib group achieved IGA 0 or 1. The next slide shows the kinetics of response for the patients treated with soquelitinib in each of the Cohorts 1, 2 and 3 and the combined placebo patients from all three cohorts. The orange line represents placebo. You can see that Cohorts 1 and 2 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 1 and 2 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 3, shows earlier and deeper separation from placebo at day eight with EASI score improvement continuing through day 15 and 28. Cohort 3 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 1, 2 and 3 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 0 or 1. Significant differences are seen for the treatment groups compared to placebo with Cohort 3 appearing to be better than the other cohorts. Data from the combined soquelitinib cohort 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 1 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 1 trial protocol as outlined on Slide 13. At the bottom of the slide in purple, we show that the previously planned Cohort 4 is being replaced with an extension cohort that will evaluate an additional 24 patients at the 200-milligram 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 4 would not likely provide more useful information. And by replacing the cohort with a new cohort, we don’t expect to lose any time. The 24 patients will be randomized in a blinded fashion 1:1 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 2 trial, which we are working on in parallel and remain on track to initiate before the end of this year. Phase 2 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 3 with 200-milligram twice per day dose showed earlier and deeper responses than Cohort 1 and 2, data that is consistent with our pharmacokinetic analysis. Cohort 1 and 2 results evaluating 200-milligram once per day versus 100-milligram 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 Treg cells.

No rebound events such as seen with JAK inhibitors was observed. The safety profile across all three cohorts show 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 8-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 3 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 2 trial of soquelitinib in patients with ALS or autoimmune lymphoproliferative syndrome.

Depending on enrollment trends, it is possible we could see initial data from the Phase 2 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?

Q&A Session

Operator: [Operator Instructions] Your first question comes from the line of Aydin Huseynov from Ladenburg. Please go ahead.

Aydin Huseynov: Hi, good afternoon everyone. Congratulations, Rich, with the great data. A couple of questions on my end. So it seems like your Cohort 3 EASI 75 data at week four beats the DUPIXENT data at week 16. And it also seems that your data is actually getting closer to JAK inhibitors than DUPIXENT. So do you think eventually soquelitinib would be used ahead of Dupixent and competing with JAK inhibitors? Just curious of your opinion.

Richard Miller: Thank you for the question, Aydin. Well, first of all, the Cohort 3 is a small sample size. So we have to put that in a little bit of perspective. But yes, 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.

Aydin Huseynov: Thank you. I appreciate that. Another question I have is in terms of the efficacy curves and again, looking at JAK inhibitors, I mean, for JAKs, I think it’s plateaus at week 8. And based on soquelitinib mechanism of action, where do you think can this potentially plateau? Is it — is it going to be week 8, 12, 16? Any thoughts on this?

Richard Miller: Well, yes. So 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. So the question — I mean, it begs the question, if you were to continue therapy, would you get deeper, better responses. And so 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. They were — by day 28, we had to stop the drug by protocol. So 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.

Aydin Huseynov: Thank you. Very helpful. And the last question is, there’s a significant jump in EASI efficacy between Cohort 2 and Cohort 3. And obviously, as you mentioned, Cohort 3 had even more severe patients. So how do you explain such a sharp jump in efficacy? And again, it’s small numbers, et cetera, but just curious on your thoughts on this.

Richard Miller: Well, we have more drug. It’s twice the drug. Cohort 3 is double the dose, total daily dose compared to Cohorts 1 and 2. So the dose of drug has been doubled. And 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. And that could be important. So 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. So this all makes perfect sense. And 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, and it is. Now I think it’s still an open question whether 200 BID versus maybe 400 once a day would be equal. So we need to ultimately test that. And that’s something we’re thinking about in our Phase 2 trial design.

Aydin Huseynov: Got it. Thanks so much. Congratulations again with this great data.

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

Graig Suvannavejh: Oh, 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 1 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. And so 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.

Richard Miller: The extended duration is 24 patients, 12 active, 12 placebo. One dose, I mean, a single dosing regimen will be studied, 200 milligrams BID. What I mentioned is in — yes, yes.

Graig Suvannavejh: Okay. So it does seem like optimally, at least as of today, 200-milligram BID seems to be the optimal dose across both your oncology and at least atopic dermatitis indications.

Richard Miller: That’s correct.

Graig Suvannavejh: Okay. Thank you for that. And then if I could ask just going back to the data that you shared today, if we look at the data in Cohort 2, the difference — there was a difference in what was seen on at least EASI 75 with numbers coming down. And I’m going to assume that’s because of the extra patients that you included, you didn’t really see them achieve EASI 75. And so 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?

Richard Miller: So 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 —

Graig Suvannavejh: Yes, believe so.

Richard Miller: — the additional patients — yes. Okay. First of all, again, small numbers, but a couple of those patients were EASI 72 and a EASI 68. I mean, some of this is really very close. So I think it was really — there was really no substantive difference. And if you look at our Cohort 3, 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. And you can see that actually, if you look at the standard error bars on the green are very tight.

Graig Suvannavejh: 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 3 data from all 12 patients?

Richard Miller: I think we could share that in a press release probably in a month or 2.

Graig Suvannavejh: Congratulations again on the data.

Operator: Thank you. Your next question comes from the line of Li Watsek from Cantor. Please go ahead.

Li Watsek: Hi. 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 didn’t really rebound. So 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?

Richard Miller: So there were placebos that rebound and get worse. In fact, you can — if you look at the standard error bars on the placebo, you’ll see that they’re quite broad. And so there were a couple of patients that, in fact, did get worse. And yes, 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 track the EASI scores. If you look at the graphs on Slides 9 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.

And so EASI scores are done at the beginning of that and of course, before they go on treatment and note how stable they are for all the groups. So this is a tribute to the physicians and our staff and the training in terms of EASI scores and how stable they were. But the minute you start taking a pill, there is a placebo effect, clearly, and some of those placebos improve. So no, there’s nothing strange about our placebos here. I think that one thing, our placebo is 0% of EASI 75s and 90s, that’s much lower than you’ll see on the Dupixent or JAK inhibitor studies where you’ll see 10%, 15%, 20% reach EASI 75 or IGA 0 and 1. But keep in mind, those studies are done longer. So there you’re on study for three months or six months or longer. So the longer you’re on study, the more there is a chance that a placebo could have an improvement and reach that.

That make sense?

Li Watsek: Yes. And then just curious if you see any differential response in patients with or without prior systemic treatment?

Richard Miller: Too early to talk about that, but we had in Cohort 3, 2 patients, one was completely refractory to DUPIXENT, had a baseline EASI in the mid-40s. Another — 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 n equals 2. So I don’t know if responder versus non — or refractory or 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. But I would suggest that given our mechanism of action is not 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. So I think all of this is falling into line, very consistent based on what we’ve learned in the lab, what we’ve learned in animal models and frankly, what we’ve learned from our lymphoma studies.

Li Watsek: Congrats again.

Operator: Thank you. Your next question comes from the line of Jeff Jones from Oppenheimer. Please go ahead.

Jeff Jones: Good afternoon, guys. 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 3 of 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?

Richard Miller: 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. And we know what that level is, by the way, it’s 300 nanograms per ml of drug.

Jeff Jones: And looking at this data, obviously, the EASI 75 numbers came down somewhat from what you initially reported from a subset of the Cohort 2 patients. And I believe that was around a 57% EASI 75. And that number is somewhat similar to the 63% you’re reporting now for Cohort 3 and n equals eight out of the total 12 treated patients at this point. Clearly, the drug is highly active. And I guess it’s just a question, what is — what particular is giving you confidence in the dose effect you’re seeing between Cohort 2 and 3, given the small numbers at this point?

Richard Miller: So first of all, again, look at the kinetic curve on 9. Look at Slide 9 and the kinetics of response. I mean, not only is there a deeper response with Cohort 3, but it’s earlier. We do know there’s more receptor occupancy, and we had sicker patients in Cohort 3. I mean, substantially sicker patients. And again, if we look at the Cohort 3, day 15 data, it’s all pretty tight. So that gives us confidence. And with regard to the Cohort 2 changing, again, very small number. And EASI 75 is it’s 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. And that’s just luck of the draw. The fact of the matter is that at 28 days, a substantial number are responding.

And in fact, I would even argue that in the Cohort 3, even if the next respond — even if the next set of patients didn’t respond, you still have what a 50% to EASI 75, which is a pretty good result.

Jeff Jones: No. I appreciate that, Richard. And I think the kinetics really help with that story and the fact that all of the patients are through day 15 here. And I guess one last question just on the runway guidance that you gave. Can you tell us what’s include — what trials are included in that because you guys have got a lot on your plate right now.

Richard Miller: So let me deflect that to Leiv. Leiv, can you?

Leiv Lea: Sure. So it includes the trials that Richard laid out, one, the extension cohort part of our Phase 1 AD trial, starting the Phase 2 AD trial, continuing with our Phase 3 lymphoma trial and at the end of the year, starting a solid tumor trial, a small Phase 1 trial. It includes all of those trials.

Jeff Jones: Great. Thank you guys very much, and congrats again.

Operator: We have one more question coming from the line of Roger Song from Jefferies. Please go ahead.

Roger Song: Okay. Great. Congrats to the data as well. Thank you for taking the question. Maybe just two quick ones. One is I just want to clarify, understanding your Phase 1 extension cohort will be BID 200-milligram eight weeks. But you mentioned something for Phase 2, you’re considering QD as one of the dose cohort. Would that be 4000-milligram or lower or higher? And then if it’s 400-milligram, so what’s the seeding on the dose and then in terms of the safety profile? And I have a quick follow-up.

Richard Miller: All right. So first of all, remember, in lymphoma, we went up to 600 milligrams BID and didn’t see any DLTs or maximally tolerated dose was not reached. So Roger, we have not finalized the Phase 2 trial yet. So I’m a little hesitant to give you exactly what the design of that is. What it will have is two — at least two active dose groups. And 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. So — and 200 milligrams BID will certainly be one of the active doses. So then 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. So we have not finalized that yet. And 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. Chiou will make on Saturday, there are changes that are emerging in the cytokines and in the Treg cells and Cohort 3 is superior. The changes — let me say it this way. The Cohort 3 changes are more dramatic.

Roger Song: That’s very helpful. Maybe just a quick last one. Understanding your cash runway is covering all the Phase 2 and then all the other indications, just curious about the thinking about the partnership. Do you — would you seeking discussion even before the Phase 2?

Richard Miller: 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. But in the meantime, we’re going to push forward. We — 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 2 and move forward. We’re not dependent on any partners.

Roger Song: Great. Thank you. Thank you, Rich.

Richard Miller: All right. I think that – is there one more question there? Okay. We’ll take another question.

Operator: We have one last question coming from the line of Sean Lee from H.C. Wainwright. Please go ahead.

Sean Lee: Hi. Good afternoon, guys. Congrats on the exciting results. 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?

Richard Miller: Lots of people are bringing up that question. Thank you for asking it. Because it has a nonoverlapping 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. And I mean, there’s a big list of agents. I mean, obviously, the IL-413 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. So I think that there’s a lot of opportunities there. But for now, we’re going to be plowing ahead with monotherapy.

Sean Lee: Okay. Thanks for that.

Richard Miller: 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.

Operator: Thank you, everyone, for participating.