Colleen Kusy: Hi. Good morning. Thanks for taking our questions. Can you remind us how you’re dealing with the B7-H4 biomarker in the Phase I/II dose escalation? Are you measuring it at baseline, but not preselecting patients? And then would we expect any of the biomarker data in the midyear update?
Martin Huber: This is Marty. At this point in time, we are gathering data pretreatment on B7-H4 expression. However, we are not using that to select for patients. Patients are enrolled regardless of the outcome of the test. With regards to data display, as Jason noted, we are in a highly competitive environment. Of note, neither Pfizer nor Hansoh shared their biomarker data, and so we will have to make a judgment call at the midyear data presentation will we or will we not share that data.
Colleen Hanley: Great. That’s helpful. Thank you. And then on 2056, how involved is GSK at this point and kind of restarting the study?
Brian DeSchuytner: Well, maybe I’ll take that. So the product is – has an option with GSK, as you will recall. And they have not exercised that option. And so we retain decision-making control over what we do in that product. But that said, GSK has been very engaged in the process. And we’re very pleased with the partnership.
Colleen Hanley: Great. Thanks for taking the questions.
Operator: Thank you. The next question comes from Kaveri Pohlman with BTIG. Please go ahead.
Christian Cubides: This is Christian. I’m on for Kaveri today. So actually, the previous question answered parts of what I was wondering. But for the Phase 1 trial for 1660, how much overlap do you expect to see between B7-H4 and some of the other ADC targets such as TRP-2, folate receptor alpha and CDH6. And my second question is for the STING ADC. Could you tell us how you’re thinking about 2056 potentially fitting into the current treatment landscape? Is it mostly going to be a combination drug?
Martin Huber: It’s Marty. With regards to 1660, while we don’t have detailed data on that yet, one thing we do know is there’s a trend for B7-H4 and PD-L1 on the tumor to not be overlapping. The Venn diagram of those two population tends to be fairly separate. With regards to folate receptor alpha, do not have any specific data available at this point in time. And I wouldn’t want to speculate on that. But there is no – we’re not aware of any overlap in biology between the two targets, but as far as specific data that says whether the populations overlap or not, I can’t give you that answer today.
Christian Cubides: Okay.
Martin Huber: And with regards to the STING, we are certainly thinking in terms of combinations for 2056. We think one of the advantages of having a locally tumor-directed STING agonist is that, that would allow you to do combinations with other systemic treatments. For example, you could give potentially an anti-PD-1 in a setting where you normally would not be able to systemic STING activation, combined with the PD-1, would just be really too toxic for patients. So that is one of our long-term strategies is surely want to show activity monotherapy, but ultimately, we think it will be a combination agent. And one last point on that, the actual epitope for HER2 is different than the HER2. So you could, in theory, actually do a HER2 combo.
Christian Cubides: Okay. Got it. Thank you. And if I can just throw one last one in there. Sorry if I missed this, but how many patients will be in the upcoming data for 1592 next week?
Jason Fredette: For 1592, I think now the ESGO abstract is available. And so in that data set, there were 31 patients.
Christian Cubides: Okay. Thank you.
Operator: Thank you. [Operator Instructions] We have the next question from Michael Schmidt with Guggenheim. Please go ahead.
Michael Schmidt: Hi, guys. Good morning. Thanks for taking my questions. Just a couple more on 1660. In the Phase 1 study, could you comment on how the tumor histologies in the study compare perhaps to what Seagen, Pfizer have shown in their Phase 1? And I think they had a pretty decent signal in breast cancer. Is that – is the overlap in sort of patient types in your study and theirs? And then just as we think high level, you mentioned your planning to initiate the expansion cohort soon. Any views on just general positioning longer term relative to the Seagen ADC in terms of differentiation, perhaps? Is it mainly lower tox on your end or increased efficacy, or both perhaps? And then how do you think about differential development opportunities versus what they have been doing? Thanks so much.
Martin Huber: Good morning, Michael. I’m going to take the first part of your question, and then I’m going to turn it over to Brian to kind of talk to you about how we’re thinking about the molecule longer term. With regards to the current data, we are enrolling patients with triple-negative breast cancer, hormone receptor-positive breast cancer, endometrial cancer and ovarian cancer. So as part of the dose escalation, any one of those four histologies is eligible for the study. Once we get into backfill, we can be a little more specific. And while we have not given detailed information on who we are enrolling, I think a couple of points can be made is, clearly, triple-negative breast cancer is an area of high unmet medical need, in which, after patients progress on TRODELVY and/or in HER2, there’s essentially nothing for those patients.
So you will – I mean, while we’re not giving the details of how many of each, that is a patient population that we will have in our data set.
Brian DeSchuytner: And if I can just expand on your question about differentiation and positioning, as Marty remarked earlier, one of the things that we’re looking for in the ESMO data with any indication of a B7-H4 on-target types, you didn’t see that, which is a nice validation both the safety and the efficacy from those abstracts. As a reminder, we’ve compared Dolasynthen ADCs versus vcMMAE ADCs extensively preclinically. And we show that our platform preclinically can deliver payload to the tumor much more efficiently and effectively. In addition, we’ve shown in our past clinical presentations for other product candidates that our payload appears to avoid the severe neutropenia or peripheral neuropathy that tend to be dose-limiting with MMAE.
And so when you think about what that means, it’s about expanding what an ADC can do in the clinic and whether that’s combinations or earlier lines to create very strong regimens. I think if you contrast with the Hansoh, GSK and sort of the TOPOs in general, keep in mind that our payload is very much orthogonal to that class. And many patients in this setting are receiving prior TOPO ADCs. And so we believe this could be consideration in the future landscape, and you see echos of that in sort of commentary around the Hansoh data. And the Hansoh program also seems to have relatively profound myelosuppression that raises similar considerations about combinations and moves into earlier lines. So we think that the landscape that’s been established by that ESMO data disclosure leaves opportunity.
Michael Schmidt: Great. Thanks so much.
Operator: Thank you. The next question comes from Asthika Goonewardene with Truist. Please go ahead.
