Liang Cheng: Yes, yes. okay. Thank you. That’s all from us.
Richard Miller: Thank you for the question.
Operator: Our next question comes from Li Watsek with Cantor Fitzgerald. Please state your question.
Rosemary Li: Hi there. This is Rosemary on for Li. Thanks so much for taking our questions. Maybe firstly, could you reiterate the benchmarks for the relapsed/refractory PTCL, what you’re hoping to see? There was some interference on the call earlier, so I didn’t catch that. And then I do have a follow-up question.
Richard Miller: So, pralatrexate and belinostat are currently the standard agents for relapsed peripheral T cell lymphoma. Those agents received accelerated approval approximately 15 years ago, and the companies never did the confirmatory trials. So, there is no currently fully FDA-approved drug for relapsed PTCL. Pralatrexate and belinostat are basically chemotherapy drugs. Belinostat is an HDAC inhibitor, pralatrexate is a folate antagonist. Both of those drugs suffer from the usual chemotherapy toxicities, which are neutropenia, thrombocytopenia, anemia. Pralatrexate suffers from an additional toxicity, mucositis. The response — those patients — the approval of those drugs was based on single-arm Phase 2 studies that enrolled somewhere between 100 and 120 patients.
The response rate was about 25%. The PFS, progression-free survival, was, in the case of belinostat, I believe it was 1.6 months and in the case of pralatrexate, it was around three months, if my memory is correct. We have a slide about this up on slide presentation on our website. So, we see a 33% response — 33.3% response rate with more than half being CRs. CR rate in ours is about double of the 25% or so response rate with pralatrexate and belinostat about 10% with CRs. In our responders, most of the responders are CRs, albeit a small number. So, CRs are very important in hematology and especially in the lymphoma world. The progression-free survival in our hands is 6.2 months, which is substantially better than the 1.6 and 3.0 months I mentioned earlier.
So, we — our study of — just to go on because I think I know where we are headed, the — our study design, the statistical design is to enroll 150 patients, 75 in each arm, standard-of-care versus soquelitinib, 75 in each arm, as I mentioned. We — the power, we have about 89%, 90% power to see an improvement from about three and a half months to five and a half months, which is our target, okay?
Rosemary Li: Thank you so much. Yes. Thanks for the really thorough answer. And then I just have a quick question on atopic dermatitis. So, for the data that we may get later this year, do you have any anticipation around like the nature of that data, like how many patients, how many doses? Or is it just too early to tell? Thanks.
Richard Miller: No, no, we have very good estimation of that. Okay, so, first of all, we know a lot about the dosing of this drug already since we’ve been evaluating it in patients with lymphoma. We know a lot about the pharmacokinetics, the occupancy of the target, the safety, et cetera. So, we’re going to be studying four cohorts of patients that are enrolled sequentially. So, we start with, let’s say, the low dose cohort, which, in our case, is 100 milligrams BID. 200 milligrams BID is our dose in the lymphoma studies and in the proposed Phase 3. So, 100 milligrams BID, we’ll enroll 16 patients in a 3:1 randomization where 12 will get soquelitinib and the other four get placebo. Then we go to the next dose regimen, which is 200 milligrams once-a-day, because we think that once-a-day dosing will be effective, and we think it’s more convenient, of course.
So, same thing, 16 patients go in there. Again, 3:1 randomization, 12 get the soquelitinib, four get the placebo. And then we go to the third cohort, where that — which is 200 milligrams twice-a-day, the same regimen that we’re using in lymphoma. Same idea, 12 patients get the drug, four get the placebo, again, randomized. And then the final cohort would be 400 milligrams once-a-day. Now, the reason that we’re studying those cohorts is that we know that at 200 milligrams, you get complete occupancy of the receptor. 100 gives you pretty good occupancy, but not — it’s not complete, but probably good enough to cause some biologic effect. So, I would not be surprised if we see some effect at the — even at the lowest dose regimen. So, as I mentioned earlier, the doctor and the patient are blinded.
The company is not. So, we can look at the data and we have a data monitoring board that can look at the data after each cohort is enrolled. And we’re able to report that data or not. I mean I don’t anticipate we’re going to be reporting it every week. But at our discretion, we can be reporting that data. Now, there’s also a very rich amount of biomarker data that’s going to be accumulating during the study. We’re measuring a number of different cytokines and lymphocyte subsets, et cetera, et cetera. And we know already from our lymphoma studies and our other animal studies that we’ve done and published, we know what biomarkers, what cytokines are affected like IL-4 and IL-5 and others. So, what we would be looking for at each cohort, of course, is safety.
We would be looking at changes in biomarkers in our treatment group relative to baseline. We would expect to see changes in IL-4 and 5 and all these things as comparing each patient to his or her baseline. And of course, we’ll be — doctors will be assessing the efficacy based on the grading criteria I mentioned earlier, the EASI score and the global — investigator global assessment. So, we’re going to learn a lot from each of these. Now, in terms of the dosing, we — as I mentioned, we know a lot about the dosing already. So, we’re able to start at 100 milligrams BID. I would expect to see something very early in this study. And I think we’ll get an idea very early, not only about the efficacy, but also about the biologic activity because remember, the reason that we’re picking atopic dermatitis first is that it is very much what’s called a Th2, T helper cell 2 disease, a disease mediated by IL-4 and 5 and 13, and we know that our drug blocks the Th2 function very well.
