Dimitry Nuyten: I’ll give you minimal. I mean, what I’ll say is it was done with metadata. It was done in an extremely rigorous way, very much to get matched patients. And quite frankly, when you start to think about, particularly in trials that aren’t like 1,000 patients or 800 patients, the reality is you actually, from a control standpoint, get a better patient population that’s more matched to your data set, assuming that they have a large enough, well-annotated data set, which they do. And that was even, that took a couple months to just even do that part of the analysis to make sure that they could do it. So I think everyone’s going to be very pleasantly surprised by the quality of that data set. I think it’s going to bring a lot of confidence. It’s the type of data set that you can certainly even take to regulatory agencies in discussing your plans going forward. So we think that’s going to be a big deal in part of our total package for that program.
Operator: Our next question comes from Mara Goldstein from Mizzou. Please go ahead.
Mara Goldstein: Great, thanks so much. During the plenary today, there was a comment along the lines of the presentation of this data. There’s a hope that this would also help facilitate STAR-221 enrollment. So can you talk a little bit about where that trial is from an enrollment characteristics perspective and what the timing looks like from here?
Terry Rosen: Yeah, so I love the question. Even though we can’t give you a bottom line answer, the trial is enrolling gangbusters. So when we talk about help, it isn’t so much like, oh, it’s in need of help. It’s that it’s enrolling incredibly well. In fact, I would go and say that more likely than not, if you ask us to bet, I think that’s probably going to be our first trial to read out. Our guidance has been that our trials will be, let’s say 2025 plus. We’re not changing our guidance, but it’s enrolling well ahead of schedule. A couple comments on the reasons. I think there’s been a lot of enthusiasm that’s data-driven what’s going on just in the TIGIT field. In this particular setting, as you can tell from the discussions, there’s also a lot of clinical trial need.
There’s simply not a whole lot happening in an innovative sense. And we believe this data set unquestionably, so all of the investigators we’ve spoken to are really excited about the data and we think it’s just going to accelerate things further. So I keep an eye on this. I think what’s interesting about this, when you think holistically about the field, for us, this trial is going to help us close the distance on who and what ends up being the first doublet that comes to market in the field.
Operator: The next question comes from Donna Grabas from Lerink Partners. Please go ahead.
Unidentified Analyst: Jeff, hi, this is Dana. Do you think you could share your thoughts on the potential difference in characteristics of DOM relative to the various TIGIT antibodies beyond Fc function to these points? I mean, what else do you think could explain the arguably disappointing phase two data that we saw from osaprilumab, the competing function antibody that was recently presented to ESMO? Thank you.
Terry Rosen: Yeah, so I mean, I think primarily, we’re going to come to that FC as being a key differentiator. So, you know, it’s absolutely clear that FC enabled anti-TIGITs, and you wouldn’t know this until you get the empirical data, but they do deplete Tregs. And so by definition, that’s not going to be a good thing. If you deplete Tregs in the periphery, you’re going to see enhanced immune AEs. But secondarily, dose is different. And in fact, I think it’s telling. Bay gene is actually on the higher end of the spectrum for the FC enabled anti-TIGITs. And what you have to realize, it’s sort of surprising when you think about, because one of the fundamental, it’s not a shock that anti-TIGIT is turning out to have the safe mechanism that we see because it’s a tumor specific mechanism where you have that high CD155 is just being way over expressed as a survival advantage by the tumor.
So people keep asking questions about TIGIT expression. The key thing is CD155 expression. If you want to draw an analogy, you know how everybody focuses on PD-L1? PD-L1 is the correlate of CD155. So it’s not the PD-1 that’s the driver, it’s not TIGIT that’s the driver. But that component of then the higher dose, particularly with an FC enabled anti-TIGIT, you’re simply getting, don’t forget that that depletion of T cells, that’s an on target mechanism. So by going a higher dose, you would expect to see more. And in fact, Beijing is on the higher end of the spectrum. What’s telling? Okay, so this is where we sort of look at these data and point people to the forest in addition to the trees. And so far it’s not just this setting, but as you know, Merck is using co-formulation.
And not surprisingly, that co-formulation is a lot about Pembrol. It’s protecting Pembrol. And Merck explored 200 milligram dose of VBO. They explored a 700 milligram dose of VBO. And in the co-form, they’re using 200 milligrams. And that just speaks to this point we were talking about that going up in dose is more likely to give you more on target AEs and so we think that’s, it’s as simple as that.
Jennifer Jarrett: Thank you. I think what I’ll point out is, you know, OC Prelimab, particularly the data that was just printed at CENTIS, it as though was in very different settings than anything that we’re doing. You know, and they tended to be going after the second line setting. So their data was presented second line cervical, second line esophageal squamous cell carcinoma. So a different histology that we’re pursuing with gastric esophageal. But like I said, going after the second line setting without chemo and tumors that are progressing very rapidly where you have a PFS of sort of two to four months. So not only is their antibody different when you look at a superior amount, but their development plan and the tumor types that they’ve been pursuing and settings have been very different than ours.
Operator: Our next question comes from Lee Watzak from Cantor Fitzgerald. Please go ahead.
Rosemary Li: Hi, this is Rosemary on for Lee. Thanks for taking our question. So for STAR-221, hypothetically, if you were to hit the survival endpoint for the PD-L1 high patients, but not for all comers, do you think you still have a chance to get approved in that patient subset given that the PD-L1 status is a stratification factor?
