These are very histologies, very different histologies under the microscope. They have different patterns of spread in the body and they have different 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 antitumor 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 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. Did I answer your question, Jeff?
Jeff Jones: Yes, you did. That was really helpful. I appreciate it. I’ve always wondered a little about those cutaneous responses, which are obviously, generally good responses.
Richard Miller: Jeff, hold on. The responses that we see in these cutaneous patients, it’s 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 cutaneous, it’s throughout the body.
Jeff Jones: Okay, fair. Sorry, that was poor language choice on my part. In the atopic dermatitis study you mentioned, I believe patients had been on two prior lines of therapy. Are there going to be, are you including patients who have previously had dupilumab and failed, or 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, 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 got a recent patient who failed the JAK inhibitor, for example. So really, we have to put this, this trial was really intended to show, of course, that the drug is well tolerated in a patient population like this, and we’re looking for activity. You know, obviously, subsequently, we’ll be trying to figure out how does it stack up against some of these other agents. But right now we’re confirming mechanisms, safety, and yes, we are measuring efficacy against the placebo.
Jeff Jones: Got it. No, I appreciate the clarity. And then last question on cifo, I know that you had said 27 patients were enrolled, but you didn’t specify how many were included in that interim efficacy analysis?
Richard Miller: I think there are 18 patients in that. You’re right, because some of them haven’t come back for their first visit yet. So this protocol, by the way, was prepared by the KCRC, and they have, there are sort of blocks of, I forget how many patients each, eight or nine patients each. And there’s a criteria, efficacy threshold that you have to pass to continue. The results so far are really pretty good. And in fact, we’re organizing a meeting at ASCO to think about discussing things like adding a control arm or where do we go from here?
sunitinib:
Jeff Jones: Got it. Just one clarification. You had mentioned in your remarks, I think 27 enrolled. And then going over this threshold of deep responses to expand that trial, did you mean just up to the 60 expand further up to the 60 planned or is there a potential expansion beyond those 60 patients?
Richard Miller: No, there’s no expansion beyond the 60. 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 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 3?
Jeff Jones: Yes, understood. All right, thank you very much, guys. That’s it from me.
Richard Miller: Thanks.
Operator: Your next question comes from the line of Graig Suvannavejh [Mizuho Securities]. Your line is now open.
Graig Suvannavejh: Good afternoon. Thanks for taking my questions. I have two in particular. One, maybe I’ll start with your second asset. I know you mentioned that you were able to pass, like the bar for success, for moving forward. 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 valuable 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 you through the Phase 3 for soquelitinib? Thanks.
Richard Miller: Okay, Graig, let me take the first one first. So the statistical threshold was a 50% increase. So the statisticians, 50% increase above the 32%, which is obviously 48%. If you meet that, you have a difference with a P value of 0.1 on only 18 patients. That’s a pretty stiff hurdle. 50% increase is a big 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 in a small study, but we’re better than 48% deep response rate. Okay? And again, I want to emphasize 50% improvement in deep response rate, that’s a stiff hurdle. And the reason we wanted that is we didn’t want to waste time on something that didn’t have a significant probability of working. So we made it, nor did they. So we’ve deliberately made these hurdles pretty strict. Now, your second question. I’ll let Leiv answer.
Leiv Lea: So, Graig, associated with our financing, we also sold warrants. Now, these warrants, first of all, have an exercise price of $3.50, but more importantly, maybe they expire June 30 of 2025, so a little over a year from now. So if all those warrants were exercised, we’d raise about $60 million. So the $30 million plus the $60 million, should those warrants be exercised, would get us through the Phase 3 trial.
Graig Suvannavejh: Okay. Thank you for that clarification. Thanks again.
Operator: Your next question comes from the line of Roger Song from Jefferies. Your line is now open.
Liang Cheng: Good afternoon. This is Liang Cheng on for Roger Song. So, thank you for taking our questions. I guess a few questions from us. First one is the soquelitinib, the modified inclusion criteria, so about the absolute lymphocyte count about 900. So if I remember it correctly, there a big overlap between this 900 plus ALC count, between the patient population. So could you clarify what, in general, this population looks like?
Richard Miller: So the 900 absolute lymphocyte count we determined based on the early part of the trial where we were taking anybody who failed any number of prior therapies. And we recognized that those patients above 900 did better, much better. And then we recognized 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. 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. I don’t recall, I’m sorry. Go ahead.
