Good afternoon. Thank you for standing by. Welcome to Xencor's second quarter 2023 conference call. After the speaker's presentation, there will be a question and answer session. To ask a question during the session, you will need to press star one one on your telephone. You will hear an automated message advising that your hand is raised. To withdraw your question, please press star one one again. Please be advised that this call is going to be recorded at the company's request. I would now like to turn the call over to your speaker today, Charles Lyles, Head of Corporate Communications and Investor Relations. Go ahead, Charles. Thank you and good afternoon. Earlier today, we issued a press release which outlines the topics we plan to discuss today. It's available at www.xencor.com. Providing comments on the call is Bassil Dahiyat, President and Chief Executive Officer, and Nancy Valente, Chief Development Officer. Afterwards, we will open up the call for your questions, we'll be joined by John Desjarlais, Chief Scientific Officer, and John Kush, Chief Financial Officer. Before we begin, I would like to remind you that during the course of this conference call, Xencor management may make forward-looking statements, including statements regarding the company's future financial and operating results, future market conditions, plans and objectives of management, future operations, company's partnering efforts, capital requirements, future product offerings, and research and development programs. These forward-looking statements are not historical facts, but are rather based on our current expectations and beliefs and are based on information currently available to us. Outcome of the events described in these forward-looking statements are subject to known and unknown risks, uncertainties and other factors that could cause actual results to differ materially from the results anticipated by these forward-looking statements, including but not limited to, those factors contained in the Risk Factors section of our most recently filed annual report on Form 10-K and quarterly report on Form 10-Q. With that, I'll pass the call over to Bassil. Thanks, Charles, good afternoon. We'll have brief comments and then get to the Q&A because we've received positive feedback on having abbreviated comments on our calls the past two quarters, I think we'll keep to that. At Xencor, we're advancing a broad internal development portfolio of antibodies and engineered cytokines in oncology and autoimmune disease that we've built with our array of modular, continually advancing protein engineering tools. By taking multiple simultaneous shots on goal in the clinic, we can let clinical data guide which programs we advance, which we terminate, which we partner, that we focus our resources on programs with the greatest potential for success and make room in our portfolio for the next wave of innovative biologics. Before heading into our pipeline, we'll cover some updates on partnerships which provide validation across our suite of XmAb technologies and revenues, which offset our development costs. First, the label on Ultomiris continues to expand in the EU and Japan, where it is now also approved to include neuromyelitis optica spectrum disorder. We earned $11.2 million in royalties in the second quarter. If Ultomiris sales keep up, we would anticipate earning our remaining sales-based milestone payments of $20 million this year. Notably, we're enhancing our Xtend patent coverage and term in multiple global geographies. We've begun to see country-by-country progress in Europe. Our CD28 bispecific collaborations with Janssen Biotech are also progressing well for both the prostate and B-cell-targeted CD28 bispecific programs. We anticipate both of them to advance into clinical testing. Finally, as noted in the abstract titles for the European Society for Medical Oncology, we anticipate data from Amgen's study of AMG 509 in prostate cancer at ESMO. AMG 509, or now xaluritamig, that's with an X as in XmAb or Xencor, utilizes our XmAb 2+1 bispecific antibody format that allows for multivalency of targeting domains. Amgen previously presented very encouraging PSA response data in early 2022. In the case of xaluritamig, the 2+1 format allows for higher avidity and tighter binding to a receptor that is barely exposed extracellularly. We also use this highly versatile format to dial into high expressing tumor cells much more selectively over lower expressing normal cells, like we do with our XmAb819 and XmAb808 programs, or to distinguish between nearly identical receptors in the same family, like we do with our XmAb541 program. Now for updates this quarter on our wholly owned clinical portfolio, I'll turn it over to Nancy Valente, our Chief Development Officer. Thanks, Bassil. We'll be starting with Vudalimab, our PD-1 CTLA-4 T-cells selective checkpoint inhibitor. In light of encouraging competitor data that we saw last fall for PD-1 CTLA-4 bispecific and our own phase I experience, we are moving Vudalimab into frontline treatment for patients with locally advanced or metastatic non-squamous, non-small cell lung cancer. First part of this study will randomize patients one to one at two different doses of Vudalimab plus chemotherapy. The second part will take the recommended dose and randomize two to one against pembrolizumab, with both arms in combination with chemotherapy, with the primary endpoint of PFS. Preparations for initiating sites are ongoing and we plan to get this study started by the end of the year. We anticipate having data from our other ongoing phase II studies in metastatic castration-resistant prostate cancer in early 2024. Recall, one study is testing Vudalimab monotherapy in clinically defined high risk prostate cancer in advanced gynecologic malignancies. The other study is taking prostate cancer all comers, and we're evaluating Vudalimab in combination depending on subtype. Moving along to other earlier stage bispecifics, XmAb819, our ENPP3, targeted CD3 bispecific, and XmAb808, our B7H3, targeted CD28 bispecific. Both have strong enrollment and dose escalation, with more interest from investigators than available slots per cohort. These are just two examples of novel XmAb 2+1 bispecifics, with unique designs enabling us to potentially fill a gap in treatment approaches. We also anticipate submitting our IND for our third internal two plus one bispecific, XmAb541, a claudin-6 targeted CD3, to be developed in ovarian cancer and other solid tumor types later this year, and plan to submit an IND for our second internal CD28 bispecific in 2024. In regard to our cytokines, we've initiated a phase I study this quarter for XmAb662, our engineered post-potency reduced IL-12 Fc fusion protein in oncology. Now, with that, please refer to our press release for financial results, and we'll open the call to your questions. Operator? Thank you. We will now conduct our question and answer session. As a reminder, to ask a question, please press star one one on your telephone and wait for your name to be announced. To withdraw your question, please press star one one again. Please stand by while we compile our Q&A roster. Our first question comes from Mara Goldstein of Mizuho. Your line is open. Great. Thank you. This is Mara Goldstein. Hey, I wanted to ask just on the xaluritamig. I, I understand there's probably limited information that you can share, but given now that the compound has a name and we're gonna see more data, I guess the question is: Is it fair to assume that this will advance, you know, we're looking at advancement here? Then the second question I just had is on Vudalimab, and when you will provide results for the prostate cancer part of the study, can you talk a little bit about, you know, what should the expectations there be around the patient numbers and whatnot? Sure. I'll take the first one, Mara. We do know that Amgen has, and they publicly disclosed this, expanded their phase I study quite substantially to include many different cohorts, both in combination with androgen deprivation therapy, as well as a subcutaneous dosing format, as well as continuing to advance this monotherapy IV. You know, I think that's a, that's a pretty good sign that that's a good commitment to advancement. I think that we should also keep in mind that in today's day and age in oncology, you know, people stay in phase I and keep adding patients for quite a long time, so I can't speak to their specific tactical approach. We are very encouraged, and we're, we're, you know, we're watching closely as they keep moving forward. You know, for the results for the prostate cancer that we mentioned we would have in early 2024 from both our monotherapy and combo study, you know, roughly maybe, maybe Nancy could give a little bit of rough guidance on that. Yeah, I mean, we're excited. Yeah. We're excited about Vudalimab in prostate cancer. We previously presented data in phase I, where there were a few responses, two responses with long duration of six and 10 months. Then in combination with chemotherapy at last year's SITC, again, with some responses and duration of about eight months. These studies are enrolling well. It's hard to say right now, more than that. We'll, we'll have data in early 2024, from the monotherapy cohort and some of the, the chemo combination cohort. Remember, the combination cohort includes combination both with chemotherapy and a PARP inhibitor. We hope to have some early data from that, as well as longer-term data or, or more data from the monotherapy cohort. Okay, thanks. I appreciate it. Okay. Thank, thanks, Mara. Thank you. One moment for our next question. Our next question comes from the line of Etzer Darout of BMO Capital Markets. Your line is open. Great, thanks for taking my question. I guess the first one, just wanted to know if you could comment a little bit more on some of the interest that you're seeing from investigators on XmAb819. Is it just really more around sort of the pace of enrollment that you're seeing? Secondly, just wondered if you'd made constructs of some of the other PD-1 CTLA-4s that are in the clinic, and then maybe specifically, you know, about, you know, lung cancer, if you see anything differentiating about your molecule and how that may do in non-small cell lung cancer versus what we've seen from some of these other PD-1 CTLA-4s. Thank you. Sure. Thanks, Etzer. You know, I'll just say on XmAb819, I think, yes, just to be clear, the interest is from really strong enrollment and strong engagement, and maybe the rationale for that and why investigators think this agent has a place. Maybe, Nancy, you want to comment on that? Yeah. I mean, we've heard comments that they are really thrilled that someone is developing a product specific for kidney cancer. Typically, kidney cancer is included with other solid tumors, studied along with them. We are really studying the ENPP3 in only kidney cancer because it's highly expressed there. It makes scientific sense to go there. No one... I guess no one's ever done that. Yeah. I think that given the mechanistic rationale and the very strong and specific expression of ENPP3 in renal tumors, I mean, it's a really good fit. A targeted agent against a tumor-specific or a tumor-associated antigen in RCC, I think it's really is very, very timely. You know, to your question on sort of competitor CTLA-4 PD-1s and lung cancer, I'll just comment maybe on the structural piece, and maybe Nancy can comment on the, you know, some of the more clinical rationale for why there's a big unmet need. Our PD-1 CTLA-4, Vudalimab, was designed to really only engage well with target T- cells that express both antigens. We really dialed down the affinity on each side, in particular, on the CTLA-4 binding side. You have to have both targets there to engage, or you really don't get much binding and derepression of the T-cellss response. I think that's important, really, when we think about how we're looking at competitor data, in particular, the molecule formerly known as MEDI5752 at AstraZeneca, which was designed with a very similar rationale, and that's the only one that we're aware of in the clinic with the same kind of highly selective rationale for the cells that have both PD-1 and CTLA-4. Essentially, your CTLA-4 engagement is conditional on PD-1 being there. The hope is to reduce the scope of cells, the T-cellss that you're activating, that you don't want. Maybe you want to comment on why frontline lung? Yeah. I'd love to. You know, when we looked at the MEDI5752 data and really compared the patient populations, what we had previously observed in our phase I dose escalation and expansion, we thought it would make sense to go into frontline lung. Our patients, in particular, are really heavily pretreated, so they have a median of three prior lines of therapy. All but one received prior checkpoint inhibitors, and 40% actually received two checkpoint inhibitors. A much different population than the competitor, where those patients are checkpoint naive and not as heavily pretreated. We thought, you know, this would be a great place to go. They provided a proof of concept, and maybe we'll see something really interesting there. Great. Thank you. Thank you. One moment for our next question. Our next question comes from the line of Edward Tenthoff from Piper Sandler. Please go ahead. Great. Thank you very much. Excited about the various updates. This is really cool. When it comes to lung cancer, again, appreciating that initially it'll be sort of a, you know, reasonable-sized study, longer term, you know, is this an area where you think you might seek to partner, or how are you guys thinking about that right now? Thanks. Yeah. I think right now we want to focus on building value in the program by generating data in this, you know, really large population of frontline lung in combo with chemo and, and, and demonstrate that we can have the kind of activity that would get us excited. You know, we certainly see AstraZeneca was excited by their initial activity, as well as the hopefully differentiated safety profile that we have, have seen so far from PD-1 CTLA-4 combination therapy. I think beyond that initial engagement, sorry, beyond that initial data that we want to see, I think it does make us think about partnering in a different way than when we were focusing on smaller populations in later line patients. Certainly, the opportunity is huge to try to do better than standard of care therapy, because again, the majority of patients do relapse, you know, within or don't respond at all within the first two years. There's a lot of opportunity, but it does make us think about how a partnership with the added scope and scale could accelerate things. We'll, we'll consider that when it would accelerate things, which we don't think is now at this, you know, critical stage of establishing that we have the right efficacy safety profile. Right. That makes sense. Awesome. Great. Thank you for the update. Thank you very much. Thanks. Please stand by for our next question. Our next question comes from the line of Brian Cheng from JP Morgan. Your line is open. Hey, guys. Thanks for taking my question this afternoon. Maybe just one on Vudalimab, in your new indication in non-small cell lung. Can you give us some color on, you know, how you're thinking about the bar for non-small cell, given the, the, the targets that you're shooting for? You know, I'm interested to see if you have a sense of, you know, especially in the second part, where you're trying to compete against pembro plus chemo, how much delta are you looking for in terms of PFS that you, you, that you would need to push this program for? And I have a follow-up. Thank you. Sure. I think without... we don't quite want to comment yet on specific deltas we're targeting for or how we powered the study, but, you know, we do note that it's extension of PFS that, that we saw with the competitive PD-1 CTLA-4 that really seemed potentially differentiated, and that's why we made that the primary endpoint. I don't think we're quite ready to comment quantitatively on the bar of success. We, we will absolutely address that a little bit later. Okay. maybe just one more on just, you know, as a recap on data flow for the near term. Can you remind us, you know, aside from the Vudalimab and also the XmAb564, data updates more towards the early part of 2024, what other data callous or potential callous that investors should look out for? Yeah. As we've sort of been doing this year, we're not guiding on specific timing of data until we get, you know, closer to the events. We want to, you know, make sure we can offer certainty and not distraction. But we do expect in next year, we would have updates on our XmAb-104 PD-1×ICOS program, which has been enrolling really well in microsatellite-stable colorectal cancer. We are also. That's expansion cohorts. We would also expect to have next year, data from our XmAb-819 program, which is our, our ENPP3 targeting CD3. You know, we, we are hopeful also we'll have some things to say about our XmAb-808 program, which is our first CD28 bispecific in the clinic, by then as well. That's the setup. There's a, there's a lot of flow from these earlier stage programs for next year. We're not going to comment on our partners, which obviously will have their own, their own news flow. Beyond the Vudalimab and 564, those are the things to watch for, and we'll give specific guidance as we get a little closer to the dates. Great. That was helpful. Thank you. Thank you. One moment for our next question. Our next question comes from the line of Alec Stranahan from Bank of America. Your line is open. Great. Hey, thanks, guys. Thanks for taking our questions. Just a couple from us. The first is on the lung cancer study for Vudalimab. Any additional thoughts around not including a Vudalimab monotherapy cohort in the study? Is this driven more by the standard of care in non-small cell lung, or is there something from the prostate study that you're seeing that's driving this? Second question is just on expectations around partnership revenues, specifically, any color around what you expect from daratumumab from Vir this year, given that it was a pretty big contributor last year? Thank you. I'll take the daratumumab question. We expect none. We reported almost none in the second quarter. Yeah. We, we expect daratumumab to be none. Maybe on the, on the lung cancer and, and why not monotherapy, you know, Nancy can go through the rationale there. Yeah. You know, most of lung cancer, non-squamous, non-small cell, is treated with chemotherapy, even patients, it turns out, that should be eligible for just checkpoint inhibitor alone. We decided we'd go there. We're going to look at PDL-1 expression or TPS 50, less than 50%, 49% and lower. That's also sure- you know, specifically the chemotherapy, you know, part of the non-small cell lung cancer world. Like, that's definitely where it's used. Those are the reasons. Great. Thank you. Thank you. Please stand by for our next question. Our next question comes from Kaveri Pohlman of BTIG. Your line is open. Good afternoon. Thanks for taking my questions. For XmAb819, I just want to know what makes a kidney cancer attractive for this molecule? I know you mentioned ENPP3 has a strong expression, but do you expect T-cellss to work fairly well after first line checkpoint inhibitors? Are there any other tumor types where you see opportunities? You know, I, I think I'll let John, John Desjarlais, our, our CSO, take that question. He's expert in all things ENPP3. Yeah, yeah. Thanks for the question. I guess the maybe the better way to think about it is we like ENPP3 because we're, we're basically first in class for a CD3 bispecific. It is very strongly and essentially uniformly expressed in clear cell renal cell carcinoma. You know, there, there's a few other histologies where there could be high ENPP3 expression, but we wanted to prioritize for renal cell mostly just to develop a signal. Once we establish that, sure, with perhaps a companion diagnostic, we could expand it to a few other tumor types. Yeah, oh, John, maybe the question- I think the other aspect. T-cellss. ... of your questions, yeah, was T-cellss. Yeah, it's, it's interesting you asked that. It turns out that kidney cancer, if you look at RNA expression levels for, for T-cellss markers, it's actually one of the highest histologies for, for having a T-cellss presence, kind of consistent with, you know, with the immune checkpoint inhibitors, being very active in renal cell carcinoma. We, we don't, we don't think there's any scientific reason why, you know, progression on a checkpoint inhibitor would, would have much impact on a CD3 bispecific. Got it. That's very helpful. Thank you. Maybe one on Plamotamab. You know, you, you selected a step of dosing to manage CRS, but can you tell us about the safety profile? Do you think with this step up schedule, you can avoid hospitalization requirement that other bispecifics have? We'll address that in the context of the formulation moving forward, our subQ in, in collaboration with Janssen, which does limit somewhat how much detail we can give. I mean, I don't know, Nancy, do you want to take that, or? That's a goal. I don't know that we have enough data to- Right. ... say yet. Certainly that'd be a goal. I think there's some bispecifics that require a lot of hospitalization, some that are minimal. Our goal would be to go for the minimal amount that's appropriate for, as we look at the safety. And then it's really about optimizing, you know, the step doses to make sure that you have CRS, that the patient's primed, and not having too much CRS such that, you know, it's dangerous and requires hospitalization or... Definitely that's our goal, and I think a product like Plamotamab, given subQ, could probably reach that, like, having less hospitalizations. What, 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 subQ, but we haven't got enough data to share this moment. Got it. Thanks for taking my question. Thank you. One moment for our next question. Our next question comes from the line of Charles Zhu of Guggenheim Securities. Charles? Hey, guys. Thanks for taking the question and for providing progress across your pipeline. I'll start out with a quick clarifying one on the Vudalimab. 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 four cycles and maintenance, or maybe I got, or what, what have you? Or is this something that's more like a CheckMate 9LA, where they stopped after two cycles? Thank you. This is a standard schedule for non-squamous. It's pemetrexed and a taxane, pemetrexed and a taxane. I think it's given four cycles, and yeah, and there is a maintenance component as well. Great. maybe am I, another more- With Vudalimab. Sorry, with Vudalimab, of course. Great, thank you. Go ahead, Charles. Maybe my second one a bit more. Yep. Yeah, 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? Could this potentially impact the clinical profile of your drug? Thank you. Gosh, I don't know that there's any real strong information on CD25 expression levels on those, in those two patient populations. Maybe, John, do you want to comment on what is known about CD25 expression levels in other populations and, and how that might change things? I, I don't know that, that, we would expect it to have a profound impact, but John would know more. Yeah, I mean, it, you know, there, there is some. You know, when you go into autoimmune diseases, there, there is some literature suggesting that the Tregs might have, you know, slightly lower CD25 expression. You could also have a deficit of Tregs compared to T- effector cells. Of course, that's exactly why we developed the therapy, to, to, you know, expand that deficit of, of Tregs, to, to catch up to the effector cell population and, and, have a better suppressive capacity. I don't, I don't think there's gonna be anything prohibitive in terms of CD25 expression for our, 564 to actually mobilize those Tregs. Great. Thank you. Thank you. One moment for our next question. The next question comes from Charles Zhu of Leerink Partners. Go ahead. Jonathan Chang, I apologize. Hey, guys. This is Matt Cowper, on for Jonathan Chang. Just one quick one for me. For the 662 study, are there any tumor types that you or any investigators are particularly keen to evaluate the compound in? Thanks. Oh, gosh, for XmAb662, the IL-12 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 and tolerability data. I, I don't know that there's particular ones that we're even most excited about. I mean, John, do you wanna correct me on that? Well, I mean, we're sort of going across the board, right? We're looking at immune-responsive tumors, of course. On the flip side, we're also very intrigued to look at XmAb662 and histologies like colorectal cancer, where, you know, PD-1s by themselves are known not to do much. 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. You know, we really wanna, you know, cast a wide net on this one and see what those signals are. That's really helpful. Thanks for taking my question, guys. Thank you. One moment for our next question. Our next question comes from the line of Boris Peaker of TD Cowen. Go ahead. Great. Thanks for taking my questions. I have two questions. On Vudalimab and lung cancer, just curious, how do you anticipate safety to compare to the competitor, bispecific, obviously, and also to the combo of Keytruda plus chemo? on 564, maybe a kind of a broad question: How do you see this drug distinguishing in psoriasis and atopic derm, given kind of the pretty hot competitive landscape in those indications? Maybe I'll, I'll touch on the XmAb564 rationale for those indications before I hand it off to Nancy to talk about the Vudalimab, you know, our thinking on, on safety there, which is pretty early. For XmAb564, we selected atopic derm and psoriasis as our phase IB 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, of T-cells-- of Treg expansion to cover them throughout the dosing interval, and of course, have it be tolerable. We saw, you know, dramatically improved duration of T-cells, of Treg expansion for XmAb564, relative to what we saw from competitors for single dose studies. We're hoping to exploit that to see if we can exceed the every other week dosing that the competing Treg IL-2 programs seem to be at. That could be a very important differentiator across the board. We selected psoriasis and atopic derm because those are populations where there's a large number of patients, and we felt we could enroll them well, and you can, you can look at the clinical response easily, with well-understood endpoints and even get biopsy samples if you want, because it's in the skin, and the tissue is easily accessible. That was the rationale. I think in particular for psoriasis, that was really the, the mostly the entire rationale. For atopic dermatitis, we were really, really excited by the initial data we had seen out of one of our competitor programs in atopic derm showing strong efficacy, albeit small population in their phase IB, but durability beyond the end of treatment that, that was perhaps surprising a bit, but maybe even consistent with the mechanism of enhancing Treg function and perhaps tolerance. We wanted to chase that down because that could be an exciting area to differentiate in atopic derm, that sort of long durability post-treatment that we know current agent, agents in AD are every other week or might be getting to monthly soon. I'll let Nancy. Can you restate your question on Vudalimab, Boris? I was pretty long-winded there. Sorry. Yeah, no, that was just asking in terms of safety, in lung cancer, how do you anticipate it to compare to obviously competitor bispecifics as well as just the Keytruda plus chemo combo? Yeah, that's, that's a bit hard to answer without any data, in lung, of the combination, and that's why we're doing that's why there's a part 1 and a part 2. The part 1 allows us to look at 2 different doses of Vudalimab in combination with the standard chemotherapy of pemetrexed and carboplatin. And then we'll see what happens. Like, you know, what, what does that safety look like, when you add, you know, a bispecific to that chemo versus just a monoclonal, you know, PD-1 antibody? Just to clarify, so prior question, it is 4 cycles of Vudalimab, Vudalimab, I'm sorry, we call it Vudalimab, Vudalimab plus carbo and pemetrexed, and then maintenance with Vudalimab and pemetrexed. It's not a limited dosing, as mentioned by somebody else, so it's, it's full force, 4 cycles. Great. Thanks for taking my question. Thank you. One moment for our next question, please. Our next question comes from Gregory Renza of RBC Capital Markets. Your line is open. Yeah. Hi, guys. It's Anish on for Greg. Congrats on the quarter, and thanks for taking my question. Just wanted to ask a couple on sort of your, your views on positioning of, of two of your pipeline assets here. Just kind of wanted to see with Plamotamab, with multiple CD20, CD3 bispecifics approved, how do you believe Plamotamab's combinations will position among competitors? Then just on XmAb564, just kind of building on a previous question, you know, not necessarily in terms of differentiation with approved drugs right now, but in terms of, you know, lines of care, for example, would, would you guys see XmAb564 being slotted in for patients with poorly controlled atopic derm or psoriasis that might be being treated with, you know, drugs like Sotyktu, Otezla, Skyrizi, et cetera? Thanks so much for, for the questions, and congrats again. Yeah, with plamo positioning, we think the crux of this is the same logic that attracted Janssen as a partner for plamo, and they are the ones leading the program now, taking on the great majority of its cost, 80% of the cost. I think that the key there is the combination with our CD28 could provide that, that differentiation, and I will say that our competitors in combining with their CD28 bispecifics are really just at the very earliest stages. You know, with plamo, I think showed competitive efficacy, safety profile, IV. We're moving rapidly on the subQ. That the positioning is really in combo to try to leapfrog with better efficacy, the just initially established monotherapy and probably soon to be established chemo combos with the other CD20, CD3s. That's why, you know, we, we were excited to get a partner like Janssen, which has a outstanding, you know, capabilities and scale in heme malignancy to help drive this strategy, because that's a strategy that is tough to do alone as a small company. I think, you know, hopefully, that addresses the positioning for Plamo. For 564, I just want to emphasize that we haven't, we don't have a final indication strategy. This is phase IB, where we wanna demonstrate durability of, of action of Treg enhancement and hopefully tie that to efficacy where it's easily seen. Certainly, depending on what we see, atopic derm could be a, a go forward. We are considering other indications and would expect to announce if we propose to advance in any. There's a wide range of autoimmune indications where Tregs very likely play a role. We would expect to announce those later as we've nailed down our, our regimen. This is not a commitment in phase one to an indication strategy. I will say that this idea of sequencing in AD is gonna come up more and more, not just for Treg enhancers, but all the therapies. You know, that's certainly been a place where, where new additions have had a huge impact in other autoimmune indications, and we do expect that to happen more and more in skin, like it has, say, for example, in, in, arthritis. Great. Thanks so much. Really appreciate the color there. Thank you very much. One moment for our last question. Our last question comes from Peter Lawson of Barclays. Your line's open. Hey. Hey, good afternoon. Thanks. This is Alex on for Peter. Thanks for taking our questions. Just one on the ENPP3 program. If... I was wondering if you could remind us, you know, some of the shortcomings of the Astellas ADC going after the same target and, you know, what might be the benefits of a bispecific approach. Thank you. Yeah, John, do you wanna tackle that one? Yeah, sure. Yeah, in fact, it was... You know, when we, we kind of discovered ENPP3 ourselves, using a bioinformatic approach, looking for selectively expressed tumor-associated antigens. Then we became aware of the Astellas programs once we, we dug into the literature. I have to say, they had half-decent data. I mean, they, they saw responses in phase I. Of course, because they had an auristatin payload, they had dose-limiting ocular toxicity. I think that was an interesting time because, because that was an Agenus program that Astellas, and Astellas had acquired Agenus. From, from what we know from, from folks that, that have worked there, it was more of a strategic decision to discontinue that program. We, we saw it as actually excellent validation for the, the selectivity of the target and the safety of going after the target. Thank you very much. At this time, I would now like to turn the conference back over to Bassil Dahiyat for closing remarks. Hey, thanks very much, everybody, for joining us this afternoon. Have a great evening, and we look forward to updating you again in the near future. This concludes today's conference call. Thank you for participating. You may now disconnect.