Liang Cheng: Do we know, in general, how many patients meet this criteria?
Richard Miller: Oh, in our trial, the percentage of patients that will meet this criteria are very high. Again, in a Phase 3 trial, we’re already hearing from doctors. We’re going to get patients right after they failed their first line therapy, maybe a second line therapy. I would expect the number of eligible patients to be nearly 100%.
Liang Cheng: Got it. Thank you. So our second question is about AD studies. So it mentioned there we could expect some early data read out in by year end. So how, 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. And as you recall were, our first dose is 100 mg b.i.d., which is a pretty good dose. It’s a dose that we know occupies the target, maybe 50% or so, give or take. It’s not the best dose, but it’s a pretty good dose. The second cohort gets 200 mg, and then we have 200 b.i.d. So I think that we very well may see some signs of efficacy in the first cohort. I would expect in the second cohort we would see it. Obviously, I think it would be better in subsequent cohorts than the first cohort. But we’re also looking at these biomarkers, the serum cytokines that we know we affect and how they’ll change. So I’m hoping that sometime by the end of the summer, we’ll start to get a feel for the clinical activity of the drug and also its effect on circulating cytokines.
Liang Cheng: Got it. So, since you talked about dosing regimens, just in general, how should we think about this circulating dosing regimens in AD, considering if there’s a different indication compared to the dosing in T cell lymphoma?
Richard Miller: Okay, so we know, and we’ve tested this not only in T cell lymphoma patients, but in other normal people in vitro. We know what it takes to saturate the T cell ITK in the T cells. So, as you recall, it’s a covalent drug, similar to the way ibrutinib 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 at least occupying the T cells. Now, we don’t know for sure that the same pharmacodynamics will apply in AD as in lymphoma. I mean, the occupancy will be the same, but what it takes to affect your immune response, that we don’t know. And that’s why we’re looking at different doses in this study.
The reason to look at different doses is what does it take to affect the immunology in these patients? And also, of course, looking for or as low as possible, the lower the dose, one would think, the safer it would be. So that’s why this is a Phase 1 study. But, I mean, this is basic chemistry. Soquelitinib reacts with the ATP binding pocket of ITK, and that’s the fact. That’s what happens. And once that’s occupied, that enzyme isn’t going to work, unless until a new one is made. So of course, as you know, the rationale is that atopic dermatitis patients have an intense Th2 helper T cell component in their disease. And we think if the drug gets there and it binds covalently to ITK, we know that we block Th2 cells. We know we block Th2 cytokines.
We think that will have an impact on the disease. But the purpose of the trial is to show that.
Liang Cheng: Sure. Maybe I can squeeze another question here. So, regarding the ITK inhibitors, I know you have a couple more coming up in the pipeline. So, what are some key differences between this one, the soquelitinib, and the other candidates?
Richard Miller: So, first of all, we have over a dozen other ITK inhibitors that we’ve been evaluating. Some are completely different chemical structures. Some are covalent, some are non-covalent. But the interesting biological feature is some seem to affect some T cell subsets more than others. And we find that to be quite interesting, quite novel, and provides for I think, some very strong intellectual property.
Liang Cheng: Got it. Thank you. That’s all from us. Thanks again.
Operator: Your next question comes from the line of Li Watsek from Cantor Fitzgerald. Your line is now open.
Rosemary Li: Hi, this is Rosemary on for Li. Thank you so much for taking our questions and congrats. So, just two quick ones from us. For atopic dermatitis, do you have a benchmark in terms of improvement in eczema area and severity index?
Richard Miller: No, we don’t have a benchmark.
Rosemary Li: Okay. Okay, thank you. And then for a second question for your next and ITK inhibitors, do you plan to generate any human data for BD discussions or just, like the clinical?
Richard Miller: I’m sorry. I can’t understand the question. Can you repeat it?
Rosemary Li: Oh, sorry. So, for your next gen ITK inhibitors, do you plan on generating any human data before going for BD discussions?
Richard Miller: Well, we’re doing both in parallel. We’re now selecting some of these backup or second generation ITK inhibitors. They’re in their IND enabling studies. We’re scaling them up. We’re moving down parallel tracks.
