Bassil Dahiyat: We’re not — we don’t have enough information to comment in more detail than we’re hopeful, and we’re making good progress with the subcu, but we haven’t got data to share this moment.
Kaveri Pohlman: Got. Thanks for taking my questions.
Operator: Thank you. One moment for our next question. Our next question comes from the line of Charles Zhu of Guggenheim Securities. Charles?
Charles Zhu: Hey, guys. Thanks for taking the question and for providing progress across your pipeline. I’ll start off with a quick clarifying one on vudalimab. So obviously, an intriguing choice to pursue frontline non-small cell lung cancer. One quick one regarding the chemotherapy backbone. Could you remind us or maybe provide color, is this the standard schedule of 4 cycles in maintenance or maybe or what have you? Or is this something that’s more like a CheckMate 9LA where they stopped at two cycles? Thank you.
Nancy Valente: This is a standard schedule for non-squamous. It’s Pemetrexed and a taxane. I think it’s given four cycles. And yeah, and there is a maintenance component as well.
Charles Zhu: Great. And then maybe another more side —
Nancy Valente: With vudalimab. Sorry, with vudalimab, of course.
Charles Zhu: Great. Thank you. And maybe I just want a bit more. And my second one, maybe a bit more scientific mechanistic one for XmAb564. What’s your view on the potential for a differential expression profile of CD25 as you move from healthy volunteers over to atopic dermatitis and psoriasis patients? And could this potentially impact the clinical profile of your drug? Thank you.
Bassil Dahiyat: I don’t know that there’s any real strong information on CD25 expression levels in those 2 patient populations. Maybe John, do you want to comment on what is known about CD25 expression levels in other populations and how that might change things. I don’t know that we would expect it to have a profound impact but John would know more.
John Desjarlais: Yeah. I mean there is some — when you go into autoimmune diseases, there is some literature suggesting that the Tregs might have slightly lower CD25 expression. And you can also have a deficit of Tregs compared to T effector cells, but of course, that’s exactly why we developed the therapy to expand that deficit of Tregs to catch up to the effector cell population and have a better suppressive capacity. But I don’t think there’s going to be anything prohibitive in terms of CD25 expression for our 564 to actually mobilize those Tregs.
Charles Zhu: Great, thank you.
Operator: Thank you. One moment for our next question. The next question comes from Charles Zhu of Leerink Partners. Johnathan, I apologize.
Matt Kemper: Hey, guys. This is Matt Kemper on for Jonathan Chang. Just one quick one for me. For the 662 study, are there any tumor types that you are — any investigators are particularly keen to evaluate the compound in? Thank you.
Bassil Dahiyat: For 662, the IL12 program, I think we’re just really at this point, exploring a range, making sure we can get a dose where we get the right kind of pharmacodynamics and tolerability data. I don’t know that there’s a particular ones that we’re even most excited about. But I mean, John, do you want to correct me on that?
John Desjarlais: Well, yeah, I mean, we’re sort of going across the board, right, because we’re looking at immune responsive tumors, of course. But on the flip side, we’re also very intrigued to look at 662 in histologists like colorectal cancer, where PD-1s by themselves are known not to do much. And since we’re doing a pembro combination, if we see something, the signal will be more clear. Likewise, for prostate cancer and a few other histologies. So we really want to cast a wide net on this one and see what the signals are.
Matt Kemper: That’s really helpful. Thanks for taking my question guys.
Operator: Thank you. One moment for our next question. Our next question comes from the line of Boris Peaker of TD Cowen. Go ahead.
Boris Peaker: Great, thanks for taking my questions. I have two questions. On vudalimab in lung cancer. Just curious how do you anticipate safety to compare to the competitor by specific, obviously, and also to the combo of KEYTRUDA plus chemo? And on 564, maybe a kind of a broad question, how do you see this drug distinguish in psoriasis and atopic derm given kind of the pretty hot competitive landscape in those indications?
Bassil Dahiyat: Yeah, maybe I’ll touch on the 564 rationale for those indications before I hand it off to Nancy to talk about the vudalimab. Our thinking on safety there, which is pretty early. So for 564, we selected atopic derm and psoriasis as our Phase 1b population because it is a multiple ascending dose study where our key goal is to understand what kind of dosing interval can we treat patients with where we get a long enough duration of T-cell — Treg expansion to cover them throughout the dosing interval and of course, that would be tolerable. We saw dramatically improved duration of T-cell — Treg expansion for 564 relative to what we saw from competitors for single-dose studies. So we’re hoping to exploit that to see if we can exceed the every other week dosing that the competing Treg IL2 programs seem to be at.
