Q1 2024 Corvus Pharmaceuticals Inc Earnings Call

Participants

Zack Kubow; IR; Real Chemistry

Leiv Lea; Chief Financial Officer; Corvus Pharmaceuticals Inc

Richard Miller; Chairman of the Board, President, Chief Executive Officer; Corvus Pharmaceuticals Inc

Eden Husnob; Analyst; Ladenburg

Jeff Jones; Analyst; Oppenheimer & Co Inc.

Greg Servanovich

Roger Song; Analyst; Jefferies

Presentation

Operator

Good afternoon, ladies and gentlemen, and welcome to the Corbus Pharmaceuticals business update and reports Quarter 2024 financial results conference call. At this time, all lines are in a listen only mode. Following the presentation, we will conduct a question and answer session. And with time during this call, you require any sorry, zero for the operator. This call is being recorded on Monday, May sixth, 2024. I would now like to turn the conference over Zack Kubow, your real chemist.

Zack Kubow

Thank you, operator, and good afternoon, everyone. Thanks for joining us for the Corbus Pharmaceuticals First Quarter 2024 Business Update and Financial Results Conference Call. On the call to discuss the results and business updates are Richard Miller, Chief Executive Officer; Leiv Lea, Chief Financial Officer; Jeff Arcara, Chief Business Officer; and Ben Jones, Senior Vice President of Regulatory and Pharmaceutical Sciences.
The executive team will open the call with some prepared remarks, followed by a question and answer period. I would like to remind everyone that comments made by management today and answers to questions will include forward looking statements. Forward looking statements are based on estimates and assumptions as of today and are subject to risks and uncertainties that may cause actual results differ materially from those expressed or implied by those statements, including the risks and uncertainties described in Cobasys annual report on Form 10 K and other filings the company makes with the SEC from time to time. The Company undertakes no obligation to publicly update or revise any forward-looking statements except as required by law. With that, I'd like to turn the call over to Leslie Yes.

Leiv Lea

Thank you, Zach. l begin with a quick overview of our first quarter 2024 financials and then turn the call over to Richard for a business update. Research and development expenses in the first quarter of 2024 totaled $4.1 million compared to $4.6 million for the same period in 2023. Net loss for the first quarter of 2024 was $5.7 million, including noncash income of $0.2 million related to Angel Pharmaceuticals, our partner in China. This compares to a net loss of $7.9 million for the same period in 2023, which included a $1.7 million noncash loss related to Angel pharmaceuticals.
Total stock compensation expense for the first quarter of 2024 was $0.7 million compared to $0.5 million for the same period in 2023. As of March 31, 2024, corporates had cash, cash equivalents and marketable securities totaling $22.1 million as compared to $27.1 million at December 31, 2023. Today, we closed a $30.6 million financing that included a premier group of biotech investors as well as some members of the corporate leadership leadership team.
Including the proceeds from this financing, pro forma cash at March 31st, 2024, was approximately $52.7 million, extending our cash runway into Q4 of 2025. I will now turn the call over to Richard, who will discuss our clinical progress and elaborate on our strategy and plans.

Richard Miller

Thank you. Leiv, and good afternoon, everyone. Thank you for joining us today for our business update call. Since our Q4 update in mid-March, we have continued to make progress against two key value drivers that we are focused on for 2024. First for our planned registrational Phase three trial of so-called maintenance for patients with relapsed peripheral T-cell lymphoma, we remain on track to begin enrollment in the third quarter, and our confidence in this trial continues to grow as two additional patients in our Phase 1b trial recently achieved objective responses at first follow-up.
Second, our placebo-controlled Phase 1 trial of so-called fitness for patients with moderate to severe atopic dermatitis. We began patient enrollment in April, which keeps us on track to report early data from the trial before the end of the year.
In addition to these two priorities with Soquelitinib today, we are reporting encouraging initial data from our Phase Ib two trial of C4 of ciforadenant, our adenosine A2A receptor antagonist in frontline metastatic renal cell cancer or RCC. Based on the significant deep response rate seen in the initial set of patients the protocol. Prespecified statistical criteria for expanding the study has been met in the kidney cancer research consortium or KCRC is enrolling additional patients.
Combined with our ongoing business development efforts aimed at further unlocking the potential of ITK. inhibition in a broad range of oncology and autoimmune indications, we believe Corvus is positioned to continue building value and advancing our unique pipeline to help improve clinical outcomes for patients.
Now I will provide more detail on our progress, starting with so-called ID for PTCL. While we are no longer enrolling new patients in our Phase 1 trial. The data continues to evolve as patients on therapy complete their scheduled follow-up assessments. In the most recent data cut off from May 3, 2024, we had two additional patients that achieved an objective response at their first follow-up visits.
First was a complete response confirmed by PET CT scan. And the second was a partial response with over 80% tumor volume reduction. These patients both had multiple sites of disease and had failed two prior therapies. Both of these patients are continuing on therapy with these additional evaluable patients. The objective response rate or ORR for the Phase 3 eligible patients is now 9 out of 23 or 39%, including five complete responses and four partial responses. Although not studied head-to-head, the complete response rate for so-called Litton at that 22% is approximately double that seen with Belinda stat for pralatrexate standard chemotherapies for PTCL that we will be comparing to in our Phase 3 trials.
Similarly, the ORR disease control rate, progression-free survival and overall survival for this group compares favorably to the results seen with Belinostat or pralatrexate. The median PFS for our patients, which is the primary endpoint for the Phase 3 trial, is 6.2 months. This is substantially better than reported results for the standard agents, which is 1.6 and 3.5 months for Belinostat and pralatrexate, respectively.
The durability of our responses is impressive with some of the earlier enrolled patients maintaining their responses for more than 24 months, we plan to begin patient enrollment in our so-called witness registrational Phase 3 clinical trial in relapse PTCO. in the third quarter of 2024. We are working with our we are working with are in advanced discussions with a number of leading centers in the United States and Canada we anticipate about 40 centers will participate in the trial. The vast majority will be in the United States.
Now for an update on so-called Litton for atopic dermatitis. The first immune disease indication we are evaluating in April, we initiated patient enrollment in the first patient cohort of the trial. There is high interest in our trial from physicians due to several attractive features of so-called fitness. First, this is a first-in-class drug with a novel mechanism of action. Soquelitinib index upstream by blocking Th 2 and Th 17 cells and thereby results in inhibition of many different cytokine involved in disease. Second, it is an oral therapy and in our cancer studies has been shown to have very good safety profile. And third, it may have broad utility across many different autoimmune and inflammatory diseases, and this trial may provide proof of concept for the treatment of other immune diseases.
The trial was designed to enroll 64 patients with moderate to severe atopic dermatitis that have progressed on at least one prior therapy study is randomized, placebo controlled and blinded to patients and treating physicians. There will be four sequentially enrolled cohorts of 16 patients with patients in each cohort being randomized 3 to one two different dosing regimens of soquelitinib or placebo for 28 days. The primary endpoint is safety and tolerability and efficacy is measured using Investigator Global Assessment and a clinically validated measurement of improvement in Eczema Area and Severity Index score, also known as easy.
It should be noted that while the trial is double-blind, the company is not blinded, we plan to evaluate the data in an ongoing manner as successive cohorts complete enrollment. We also will be measuring the levels of various serum cytokine at baseline and on treatment. These measurements may provide useful biomarkers based on current enrollment trends, anticipated site activations and follow-up time lines we believe data from the initial cohorts will be available before the end of 2024.
We'll study completion in early 2025 outside of our PTCO. and atopic dermatitis trials. We are still planning a so-called witness solid tumor trial as a single agent and in combination with nivolumab in relapsed RCC. And we remain active with our corporate partnering discussions. Our business development strategy is to find partners with development and commercialization expertise in immune diseases as well as seek regional partnerships in oncology that would be complementary to our focus and expertise in cancer.
I'm excited to update you on the progress with ciforadenant, our adenosine A2A receptor antagonist. We have been one of the leaders in the development of adenosine A2A receptor antagonism for the treatment of cancer. Over the past few years, published preclinical and clinical studies have demonstrated the enter anti-tumor activity of ciforadenant as a monotherapy and when given in combination with checkpoint inhibitors. In particular, in our preclinical studies published in 2018, we found that anti-CTLA-4 antibody combination with ciforadenant produces striking antitumor efficacy in several animal models.
Further research has revealed the probable mechanism for this synergy, which involves modulation of the tumor microenvironment, specifically the blocking of myeloid-derived suppressor cells. In other words, we believe that anti-CTLA-4 antibodies are a much better combination partner for A2A antagonist than anti PD ones. These findings led to led to our collaboration with the Kidney Cancer Research Consortium. This group of institutions brings the leading physicians and researchers in kidney cancer whose goal it is to discover improved therapies for patients with renal cancer.
Our Phase Ib two clinical trial, which is led by Dr. Kati Beckermann from Vanderbilt University Medical Center is evaluating ciforadenant as a potential first-line therapy for metastatic renal cell cancer in combination with ipilimumab and nivolumab study is now open at MD Anderson Vanderbilt, Duke and the University of Pennsylvania clinical trial is currently in the Phase two portion and overall is designed to enroll up to 60 patients. There are currently over 27 patients enrolled.
The trial employs a stringent efficacy endpoint, deep response rate. Deep response rate is the CR rate plus the PR rate only counting PRs that achieve greater than 50% tumor volume reduction. Note, the usual criteria for PRs is 30% tumor reduction. Data from the KCRC has shown that deep response rate correlates with long-term progression-free survival and overall survival and in their previous studies is 32% with ipilimumab and nivolumab.
In an interim analysis, our protocol defined prespecified statistical threshold for efficacy is the demonstration of at least a 50% increase above the 32% deep response rate seen with previous ipi-nivo combination trials in renal cell cancer conducted by the Kidney Cancer Research Consortium. This means we need to exceed a deep response rate of 48%.
As of May 2, 2024, the interim analysis that was conducted indicates that we have met the statistical threshold for efficacy. So the trial continues to enroll patients. We are excited about these results given the positive clinical implications for patients. In addition, they are consistent with our laboratory and preclinical findings, and we believe may represent a novel immunotherapy approach summarizing the outlook for the remainder of 2024 with our recent financing, our current cash gives us runway into late 2025, allowing us to achieve several near-term milestones, including starting our registrational Phase 3 clinical trial of soquelitinib mid and PTCL. in the third quarter, generating interim results from our soquelitinib and phase one atopic dermatitis trial before year end, followed by final data in early 2025, reporting additional data from the ciforadenant Phase Ib two clinical trial later this year and initiating a Phase two clinical trial with soquelitinib and solid tumors in the fourth quarter, with initial data anticipated in the second half of 2025. We look forward to providing updates on our programs in the coming quarters.
I will now turn the call over to the operator for questions and answer period. Operator?

Question and Answer Session

Operator

(Operator Instructions) [Eden Husnob], Ladenburg.

Eden Husnob

Your line is now open and good afternoon, everyone, and congratulations with the progress and most importantly, with two additional responses from PR and CR that quite unexpected from Phase Ib.
So regarding a soquelitinib and in PTCL. So you've got 23 patients, the CR, 61%, five CRs, one PR. So could you remind us what is the standard of care CRC and other PTCL trials, of projects, eight or nine other agents?

Richard Miller

Thank you, Eden, for the for the question. So the the approval studies for both Belinda stat and pralatrexate were single-arm studies those drugs received accelerated approval about 15 years ago. They each had CR rates of about 10% and overall response rates of about 25% to 30%. They had PFS is progression-free survivals about 1.5 to 3.5 months.

Eden Husnob

Okay. That's helpful. And with the new responses on how much this is going to increase your sort of preliminary PFS and OS. I know you reported previously, so in two months in PFS, 28 months away or is it going to increase significantly?

Richard Miller

So the current ORR now, overall response rate is 39%. Just to remind you that and by the way, in lymphoma, we used the Lugano criteria, which is 50% for a PR. And I should add that the PR that I just mentioned has about 87% reduction of tumor.
One tumor was totally gone. I suspect he could be on his way to a CR very soon from the TSS., we expect that PFS to improve as these last few patients move through the mediums.

Eden Husnob

Okay. And regarding the data from the Phase three trial on what do you think will have a first glimpse on the on the readout? Any on I know this is a randomized trial blinded trial, but when you think we'll have a first look at it.

Richard Miller

And while it is a randomized trial, it is not a blinded trial. And I mean we know who gets chemotherapy and who gets our drug. It's hard to disguise that in an oncology trial since these drugs at the chemotherapy drugs have side effects from the the median PFS is, as I mentioned, for Pralatrexate and balloons that are short only a few months. And therefore, the study is not that long. It's 150 patients.
We think we could probably enroll that thing fully in about 18 months and then you'd need some follow-up after that to get to the final data. There is an interim there is a point that we conduct an interim analysis, which is one half of the events occur, the events being the PFS events. And but that occurs so late in the study that we would probably wait for the end of this study to have and to make a final determination.
Now having said that, we do have an outside data monitoring committee. And I guess if the results were so persuasive or compelling, you would do have possibly have an ethical reason to discontinue the study.

Eden Husnob

Okay, makes sense. And the last one, if I may --

Richard Miller

let me just say so I think you have data from this trial in 24 months.

Eden Husnob

Okay. So like the 26. So I'm trying to understand on genome, these trucks are still seems to be working and and but there is 40% who don't respond to Central, right, 39% based on DCR. So is there any way to come up with some other potential biomarkers to screen patients who would be more likely to respond or longer choose patients yet.

Richard Miller

But we are working on that. We're looking all the time for mutations in baseline immune status et cetera. But you'll remember that several months ago we implemented and on conference calls, I talked about the immune status at baseline, the absolute lymphocyte count and then using a number of prior therapies. And I'm happy to report that since we've implemented those eligibility criteria, we have seen, I would say not only more responses, but I would say the kinetics of the responses also has been faster. And so I think that those moves that we made several months ago or maybe now are really have made a difference. And those moves were based on our better understanding of the mechanism of action.
So I expect that in the Phase 3 trial, we already know this a Phase three trial. We're going to get better patients, they're going to have better immune status to start with Phase one trials, usually get sicker patients just by the nature of the fact that they've exhausted the other prior or any other therapies that are available. So I would expect that of our results could get better and we are continuing to look at it different markers. But so far, I don't know, other than the baseline immune status. I don't have no if we have a specific molecular marker.

Eden Husnob

Understood. Thank you. Thank you so much and congratulations with the progress.

Operator

Jeff Jones, Oppenheimer.

Jeff Jones

Thank you, operator, and congrats on the news, guys. That's great and congrats on the financing as well. On one question on soquelitinib. There are a number of responders in the Phase one that were cutaneous T-cell lymphoma patients. And can you remind me if cutaneous T-cell lymphoma patients are point to be included in the Phase 3 and what impact that might have on the PFS.

Richard Miller

There are a couple of patients who are included in our 23 that had cutaneous T-cell lymphoma. Both of those patients had transformed cutaneous T-cell lymphoma that portends a very bad prognosis when you get what's called large cell transformation. That's not your typical CTCL is my point CTCL patients are not going to be enrolled in our Phase three trial because it really is a different disease. It's treated with different drugs and it can be a chronic disease early in paper. People who have just skin disease can have disease for many years. That's not the patients we're talking about in this trial.
But Jeff, I think you raise a good point, which I forgot to mention. We see responses in cutaneous lymphomas, anaplastic lymphoma, peripheral T cell lymphomas with something called NGO. M&o blastic are now known as T follicular helper cell lymphoma. These are very histologies, very different histologies under the microscope. They have different patterns of spread in the body and they have different mutations, genetic mutations the fact that we see activity in this very diverse group of lymphomas of T cell lymphomas is really again consistent with our mechanism, which is to induce a host anti-tumor response and one of the motivating factors that we think we can extend this into solid tumors. That was the reason we started doing preclinical work with the solid tumors that data has been presented and confirmed by others. And this is the reason why we're also excited about looking at this drug in solid cancers that I answer a must-have.

Jeff Jones

Yes, you did on those really helpful. I appreciate it. I've always wondered about a little about this cutaneous responses, which are obviously generally good responses on quality.

Richard Miller

Yeah, hold on. The responses that we see in these cutaneous patients were not fair to call them that they have cutaneous disease. They have circulating tumor cells. They have lymphadenopathy. Sometimes they have visceral disease. The responses that we've seen in the responding patients is not just continuous. It's a throughout the body.
Okay.

Jeff Jones

Fair. Sorry. There was poor language choice on my part arm in the atopic dermatitis study on you mentioned, I believe the patients had been on two prior lines of therapy. Are there going to be do you including patients who have previously had dupilumab and failed or is that are you not being that specific?

Richard Miller

We're not being that specific and they have to have failed at least one prior therapy of one prior either systemic or topical therapy, some of the patients, we assume that some of the patients that come in our trial will have failed dupi, but it's not required. They will have also failed others. I think we've got a recent patient who failed a Jack inhibitor, for example. So really, we have put this this trial was really intended to show, of course, that there is well tolerated in a patient population like this, and we're looking for activity. Obviously, subsequently, we'll be trying to figure out is it how does it stack up against some of these other agents. But right now, we're confirming mechanism safety. And yes, we are measuring efficacy against the placebo.

Jeff Jones

Got it. Now I appreciate the clarity on. And then last question on CFO. I know and that you had said 27 patients were rolled on, but you didn't specify how many were included in that interim efficacy analysis.

Richard Miller

I think there's 18 patients in that. You're right, because I'm going to have some of them haven't come back for their first visit yet. So so this protocol, by the way, was prepared by the KCRC um, and um, they have there are sort of blocks of I forget how many patients each at eight or nine patients each and there is a criteria efficacy threshold that you have to pass to continue on the results so far and really are really pretty good. And in fact, we're organizing the meeting at Asco to think about, oh, discussing things like adding a control arm or where do we go from here? Obviously, at some point you want to have a control arm.
I'm sure, by the way the deep response rate of 32% ipi nivo. I know people always critical of historical controls as they should be, but that's based on a 900 patient Checkmate two wells. The Checkmate study with ipi nivo versus seat count was over 900 patients. And then there was a nivo cabo versus of intent that was 700 patients. So this is this this is based on a pretty good foundation of data.

Jeff Jones

I just one clarification, and you had mentioned in your remarks, I think 27 enrolled and then going over this threshold of deep responses to expand that trial. What did you mean just up to the 60 length expand further up to the 60 planned doors there, a potential expansion beyond those 60 patients?

Richard Miller

No. There's no expansion beyond the 60 from what I talked that were nice when I mentioned expanding, I think at some point, it would be nice to add a control arm, maybe ipi nivo alone, ipi nivo placebo. But I probably cannot leverage that raises the whole question of do you want to do a randomized Phase 2?
Or do you want to go right to a Phase three get Understood.

Jeff Jones

All right.
Thank you very much.

Operator

[Greg Servanovich].

Greg Servanovich

Good afternoon. Thanks for taking my questions. I have two in particular one, Tom, maybe I'll start with that. Your second asset, I know you mentioned that you were able to pass like fee the bar for success for moving forward on. I don't know if you I might have missed this, if you quantified how much better beyond that bar that you had seen from, I guess, your 18 evaluable patients. So I'm wondering if you can perhaps shed more color on that. And then secondly, just on your current cash and congrats on the recent raise. But if you could clarify whether that cash gets chewed through the Phase three and for Soquelitinib, you see upside.

Richard Miller

Okay, Greg, let me take the first first. So the statistical threshold was a 50% increase. So the statisticians, a 50% increase above the 32%, which is obviously 48%. If you meet that you have you have a difference of with a p-value of 0.1 and only 18 patients, that's a pretty stiff hurdle, 50% increases that they've hurdle. And so we exceeded that. I can't give you the exact number because the KCRC doesn't really want to disclose that yet.
And I understand why, because these numbers jump around a lot in a small study, but we're better then 48% deep response rate.
Okay. And again, I want to emphasize 50% improvement in deep response rate is a that's a deferral. And the reason we wanted that is we didn't want to waste time on something that was that didn't have a significant probability of working. So we made it nor today. So we've deliberately made these hurdles pretty strict.
Now your second question, I'll let Lisa answer.

Leiv Lea

And so Craig, associated with our financing, we also sold warrants. These warrants first of all, have an exercise price of $3.50. But but more importantly, maybe stakes. They expire June 30 of 2025, so a little over a year from now. So if all those warrants are exercised, we raised about $60 million.
So the $30 million plus the $60 million should those warrants be exercised would get us through the Phase three trial.

Greg Servanovich

Yes. Thank you for that clarification. Thanks again.

Operator

Roger Song, Jefferies.

Roger Song

Good afternoon. This is the downtown for Roger so on. So thank you for taking our questions. I guess a few questions from us. First one's about the quality of the modified inclusion criteria and so about the absolute lymphocyte count at about 900. So if I'm remembering correctly, there's a big overlap between the nine 99 hundred plus ALC. count between the patient population so could you clarify what's going on in general, this population looks like.

Richard Miller

So the 900 absolute lymphocyte count, we we determined based on the early part of the trial where we were taking anybody who failed in our any number of prior therapies, and we recognize that those patients above 900 did better, much better. And then we recognize that those were the patients who had no more than three prior therapies less than or equal to three prior therapies. And so that's the criteria that we're using because they're less immunocompromised and those are the those are what's been used on the patients that have been reported in today's press release. It's the number of prior therapies greater than or equal to one less than or equal to three?
Yes.
Now I know I don't I don't all that.
I'm sorry.

Roger Song

Do we know a general or a home now? How many patients or have they not meet these criteria.

Richard Miller

If we in our trial, the percentage of patients that will meet this criteria of very high, again, in a Phase three trial, we're already hearing from doctors we're going to get we're going to get patients right after they fail. Their first-line therapy may be a second-line therapy. I would expect the number of eligible patients be nearly 100%.

Roger Song

Got it. Thank you, Tom. So our second question is about the AAT study. So it mentions there. We could expect some early data readouts in by year end. So how and some just just in general, how much data should we expect from there?

Richard Miller

I think you can expect data from the first couple of cohorts for and as you recall, we're our first doses, 100 milligrams BID., which is a pretty good dose, is a dose that we know occupies the target may be 50% or so give or take. It's not the best dose, but it's a pretty good dose.
The second cohort gets 200 milligrams and then we have 200 b. i. d. So I think that and we very well may see some signs of efficacy in the first cohort. I would expect in the second cohort, we would see it obviously, I think it would be better in subsequent cohorts than the first cohort. But we're also looking at these biomarkers, the serum cytokine that we know we effect and how and how they'll change.
So I'm hoping that sometime by the end of the summer, we'll start to get a feel for the clinical activity of the drug and also its effect on circulating cytokine.

Roger Song

Got it. So I think you talked about the dosing regimens of just in general. How should we think about this circulating dosing regimens in 80 of covering the different indication compared to the dosing in on T-cell lymphoma, okay.

Richard Miller

So so we know and we've tested this not only in lymphoma patients, T-cell lymphoma patients, but in in in other in normal people in vitro, we know what it takes to saturate the T cell ITK. and the T cells. So as you recall, it's a covalent drug similar to the way ibrutinib work. But except this is to a different target so that once the drug binds to the target, it doesn't come off.
So we know what it takes. We have a really good pharmacodynamic marker to know that we're blocking the T cells or if we're at least occupying the T cells. Now we don't know for sure that the same of credit, the same pharmacodynamics will apply in ADA.s and in lymphoma, I mean the occupancy will be the same, but what it takes to affect your immune response that we don't know. And that's why we're looking at different doses in this study. The reason to look at different doses is what does it take to affect the immunology in these patients? And also, of course, looking for as low as possible, the lower the dose that one would think the safer, it would be.
Yes. So that's why that's why this is that's why there's a Phase one study but I mean, this is basic chemistry, a so-called nib reacts with the ATP binding pocket of ITK. And that's that's the fact that's what happens. And once that's occupied that that Ensign isn't going to work less until the new one has made them. So and of course, as you know, the rationale is that atopic dermatitis patients have an intense Th two helper T cell component in their disease.
And we think as the drug gets there and it binds covalently to ITK., we know that we block Th two cells.
We know we bought Th two cytokine. We think that will have an impact on the disease. But the purpose of the trial is to is to and to show that Sure.

Roger Song

Maybe I can squeeze another question here. So regarding the ITK inhibitor, as you I know you have a couple more coming up in the pipeline. So what are some key differences between this one collecting and bind at the the other candidate.

Richard Miller

So first of all, we have over a dozen other ITK. inhibitors that we've been evaluating summer a completely different chemical structure, summer Covalence, summer non-covalent, some, but the interesting biological features is some seem to affect a T cell, some T cell subsets more than others. And we find that to be quite interesting, quite novel and provides for, I think, some very strong intellectual property.

Roger Song

David, thank you. That's all from me. Thanks again.

Operator

Lee Watson, Cantor Fitzgerald

Yes, I assume those were ancillary. Thank you so much for taking the questions and congrats on Zone two quick ones. From us for atopic dermatitis.
Do you have a benchmark in terms of improvement in Eczema Area and that's in and.

Richard Miller

No, we don't have a benchmark.

Okay. Okay. Thank you.
And then for a second question for your next-gen ITK inhibitors, do you plan to generate any human data will be the discussion there?

Richard Miller

Just like preclinical on HR can understand the question can you repeat it?

Sorry. And so for your next-gen ITK. inhibitors, do you plan on generating any human data before going through the discussion?

Richard Miller

Well, we're doing both in parallel. We're now selecting some of these backup for a second generation ITK inhibitors there, and they're in their IND-enabling studies. We're scaling them up. We're moving down parallel tracks.

Okay. Thank you.

Richard Miller

Okay. Operator, I think that exhausts our questions here for now, and I want to think.
Hello, any other questions that I missed?

Operator

And there are no further questions at this time. I will hand hand the call over to Richard Miller, CEO. Please continue.

Richard Miller

Thank you, operator. I want to thank everyone for participating in today's conference call.
We look forward to updating you on subsequent calls and appreciate your interest.
Take care.

Operator

Ladies and gentlemen, this concludes today's conference call. Thank you for your participation. You may now disconnect.