Anish Suri: Yes, Mark, we’ve actually, in previous meetings, and there’s an upcoming Treg meeting in May, where we’re talking. But in a meeting in Paris last year, we presented on this where we compare this to CD25-biL-2-mutein where we show clear induction by CUE-401 where the IL-2 mutein as expected, did not convert. And that’s not surprising. It is the anticipated immunological outcome. We’re continuing to build on that data and in vivo models as well, and we’ll be discussing that in the future. But so far, the biology strongly supports the induction and generation of new populations of Tregs which 401 can do but obviously a CD25 biased IL mutein cannot.
Mark Breidenbach: Okay. Thanks for taking the question.
Anish Suri: Thanks Mark.
Operator: Thank you. And our next question comes from the line of Stephen Willey with Stifel. Please proceed.
Stephen Willey: Yes, good afternoon. Thanks for taking the questions. Congrats on progress. So on CUE-102, I know you’re talking about monotherapy dose escalation initiating dose expansion monotherapy. But are there plans to initiate dose escalation with CUE-102 in combination with the checkpoint inhibitor? And I guess, is that something that you would expect to start in parallel with monotherapy dose escalation?
Dan Passeri: Very good question. And the answer is yes. I mean, obviously, it’s very similar to 101. We expect same general pattern. We are — just to remind everyone, our first trial is with pembrolizumab, but we expect that our drugs in platform will work with any checkpoint. So we’re looking at various options and alternatives presently, but that is our intent to also survey in combination it’s first to show the monotherapy tolerability profile, which we expect to, in essence, mirror what we’ve seen with 101. But obviously, having that data will be important. And then as you have stated, that’s the natural next step.
Stephen Willey: Okay. And would you be prespecifying tumors to be WT1 positive with the combination as well? And then I guess, does the monotherapy dose expansion then maybe inform select tumor types for expansion with combo?
Dan Passeri: So the answer is yes to both of those questions. Yes, we will be stratifying patients based on WT1 expression and then also in terms of the type of cancers. And the 101 — I’m sorry, the 102 monotherapy will certainly guide our thinking of tumors that are more responsive. So that’s absolutely spot on both questions.
Stephen Willey: Okay. And I guess, there appears to be a bit more discussion just around the pursuit of partnering opportunities. And I guess just philosophically, curious if you think that the more proximal opportunities for you are also autoimmune focus, maybe with the CUE-300 series? Or do you think that there’s an opportunity here with either the two CUE-100 programs we know about, maybe some more that we don’t know about that could be kind of put out to bid?
Dan Passeri: Yes. So Steve, it’s a really important question, complicated question because there are a lot of different perspectives on that and variables we have to consider. I think what we’re trying to emphasize is this partnership we just announced with Ono. It’s not a — it’s sort of classic license for some money. We’re actively involved. They’re a collaborator. They’re supporting the preclinical development work. We have an option to codevelop. They pay milestones along the way. Those milestone payments go a long way to subsidizing our portion if we decide to co-develop and that allows us to basically retain a significant upside. And what we’re trying to basically state here is we have no intention of partnering assets where we’re doing preclinical work and then licensing the upside so that we’re just monetizing assets.
