Good afternoon. Thank you for standing by, and welcome to Xencor's second quarter 2022 conference call. At this time, all participants are in the listening mode. After the speaker's presentation, there will be a question and answer session. Please be advised that this call is being recorded at the company's request. Now, I would like to turn the call over to your speaker today, Charles Liles, Head of Corporate Communications and Investor Relations. Thank you and good afternoon. Earlier today, we issued a press release which outlines the topics we plan to discuss today. The press release is available at www.xencor.com. With me on the call are Bassil Dahiyat, President and Chief Executive Officer, Allen Yang, Chief Medical Officer, John Kuch, Chief Financial Officer, and John Desjarlais, Chief Scientific Officer. We will open up the call for your questions after prepared remarks. 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, the plans and objectives of management, future operations, the company's partnering efforts, capital requirements, future product offerings, and research and development programs. These forward-looking statements are not historical facts, but rather are based on our current expectations and beliefs and are based on information currently available to us. The 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. Thanks, Charles. We've used our array of modular protein engineering tools to create a broad internal development portfolio in oncology and autoimmune disease, which allows us to take multiple simultaneous shots on goal in the clinic. Our intent remains using proof of concept data from our early-stage studies to guide which programs we advance, which we terminate, and which we partner, so we use our resources on those programs with the greatest potential for success and make room in our portfolio for the next wave of XmAb bispecifics and engineered cytokines. The plug-and-play nature of our XmAb technologies and our ability to generate biologic drug candidates rapidly and efficiently provides us with many opportunities to generate revenue from strategic licensing and collaboration agreements, which has allowed us to avoid accessing public markets for capital for over four years. Supporting our development work are three royalty-producing marketed products, including Ultomiris, which incorporates our XmAb Fc domain to enhance antibody half-life and allow for longer duration of action, less frequent dosing, and reduced patient burden of therapy compared with parental antibody. Ultomiris recently received a positive opinion from CHMP in Europe for generalized myasthenia gravis. AstraZeneca has guided to gMG regulatory decisions in the E.U. and Japan as well as regulatory submissions for neuromyelitis optica spectrum disorder in the U.S., E.U., and Japan, all this year. Now we're looking externally for tools and assets that can expand our technology for creating new drug molecules and complement our pipeline candidates. Yesterday, we and our new partner, Caris Life Sciences, announced a target discovery collaboration and license agreement to create XmAb bispecific or multi-specific antibodies directed against up to three novel targets discovered with Caris' unique human tissue bank and bioinformatics approach for finding addressable tumor markers. Our goal is to use our protein engineering tools to create molecules that tackle hard-to-address biologies and that we can potentially advance to approval and to market if the data and environment support it. Our two newest programs, our first XmAb plus one CD3 bispecific and our first CD28 bispecific T-cell engagers, are now advancing to first-in-human studies. I'll now turn the call over to Allen Yang, our Chief Medical Officer, to update on our clinical portfolio and cover upcoming plans. Thanks, Bassil. Last quarter, we went through our whole clinical portfolio, but today we will briefly review upcoming plans for our data presentations, our clinical data presentation at ASCO, and some recent and near-term study starts. We plan to present data from three studies through the end of the year. First, we expect to present data from the single ascending dose healthy volunteer study XmAb564, our wholly-owned IL-2 Fc cytokine fusion, which targets regulatory T-cells that we are developing in patients with autoimmune disease. We also plan to initiate in the coming months a multiple ascending dose study in patients. Next, for the CD20 x CD3 bispecific antibody, plamotamab, we will present data from the expansion cohort in the ongoing phase I IV monotherapy study in patients with advanced non-Hodgkin's lymphoma. Our plans to introduce subcutaneous dosing into this study are underway, and additionally, our phase II study of the triple combination with Monjuvi and Revlimid is ongoing. For our PD-1 CTLA-4 bispecific, vudalimab, we'll also present some early data from the first of our two phase II studies, the chemotherapy combination in patients with metastatic castrate-resistant prostate cancer. Our second phase II study in patients with clinically defined high-risk metastatic castrate-resistant prostate cancer and certain gynecological malignancies is now dosing patients. This June at ASCO, we reported initial data from the monotherapy escalation portion of the phase I study of our PD-1 ICOS bispecific antibody, XmAb104, in patients with advanced solid tumors. XmAb104 was well-tolerated and exhibited a distinct safety profile compared to other clinical-stage ICOS programs. We observed antitumor activity and biomarker activity consistent with T-cell engagement. We are currently enrolling the expansion portion of our phase I study in combination with ipilimumab in parallel cohorts of several different advanced solid tumors. Now on to our clinical trial starts. First, we recently initiated and dosed the first patient in a phase I study of XmAb819, our ENPP3 x CD3 bispecific antibody in patients with advanced renal cell carcinoma. XmAb819 uses our XmAb 2+1 multivalent format for enhanced tumor target selectivity. Pre-clinically, antibodies built with our 2+1 format, including 819, have shown preferential killing of tumors with high target antigen expression relative to normal cells, which is particularly exciting tool for developing drug candidates targeted to solid tumors. XmAb819 is our first 2+1 bispecific to enter the clinic. However, Amgen's similarly engineered STEAP1 targeting bispecific is already advancing through phase I and has shown encouraging early PSA response data. We look forward to following its progress as well. Next, we now have an open IND and are now initiating a phase I study of XmAb808, our B7-H3 x CD28 bispecific antibody, our first CD28 targeting molecule in combination with Pembrolizumab. CD28s are a new class of bispecific engineered to provide conditional co-stimulation of T cells through the CD28 receptor when the molecule is bound to tumor cells with the goal of enhancing activity of CD3 bispecifics and checkpoint inhibitors. We'll have more to say about this study in the coming months. Now with that said, I'll hand the call over to John Kuch, our CFO, to review our financial highlights. John? Thank you, Allen. Total revenue for the second quarter and the first six months of 2022 was $31 million and $115.6 million, respectively. Revenue for the second quarter and the first half of 2022 was primarily royalty revenue from our Vir and Alexion partnerships related to the sales of Sotrovimab and Ultomiris, respectively. Revenue from these royalty streams and income from other partnerships and collaborations help offset our spending on operations and clinical programs. For the first six months of 2022, the total revenue that we received fully funded our operations and further strengthened our balance sheet. Total cash equivalents, receivables, and marketable debt securities at June 30 totaled $679.7 million, which is approximately $50 million more than the $664.1 million balance reported at the beginning of the year. We are updating our year-end guidance and now estimate that we will end 2022 with between $550 million and $575 million in cash equivalents, receivables, and marketable debt securities. We continue to guide that we will have sufficient cash to fund our R&D programs and operations through the end of 2025. I refer you to our press release this afternoon and to our SEC filings for further details about our financial results. With that, we'd now like to open up the call for questions. Operator? Thank you. To ask a question, you will need to press star one one on your telephone. Please stand by while we compile the Q&A roster. Our first question comes from Mara Goldstein with Mizuho. Your line is now open. Oh, great. Thanks for taking two things for me or three rather. The first is on XmAb808. Can you maybe just talk a little bit about the target there, the B7H3 target, just given what we've seen in the competitive landscape on the AE profile perspective. On vudalimab, can you maybe give a little bit of color on which of the groups you do anticipate having data on and how many patients we should start thinking about for the data disclosure there? Just lastly, on the Caris arrangement, you do have some financial obligations, milestones and whatnot. When should we anticipate that something would be required to be paid from that program? Hi, Mara Goldstein. Thanks. I guess I'll start maybe with the Caris one. There was an upfront payment that, you know, is a relatively small percentage of the total disclosed basket of payments. I think the subsequent ones are gonna be driven a little bit later into the collaboration. We're at the start taking these initial information on these targets and starting to validate them through antibody discovery efforts and lead creation. Those are gonna be subsequent events. I think it'll be a little while, I think, before we start hitting those obligations. Okay. Okay, Okay, great. Maybe John, do you wanna touch on, I guess you're referring for 808 to both CD28 and B7H3, both targets, Mara? Yeah. Most specifically B7H3 target, just what, you know, we've seen over the last few months with competitor setbacks. Yeah. Yeah, thanks. You know, first of all, we like B7H3 as a target. You know, we selected it because it's very bright and very broadly expressed across a lot of different solid tumor histologies. I assume you're referring to some of the AEs that were seen, disclosed by MacroGenics in the head and neck cancer patients. You know, we don't know how to interpret that. I mean, the drug conjugates haven't seen those same kinds of events, you know, either the Daiichi Sankyo or the MacroGenics program. Allen, you wanna add anything to that? Yeah. I mean, we don't have any details around where the bleeding events were or whether they were related to the product. I mean, they seem to say that head and neck cancer has a lot of bleeding events, and in their phase I, they didn't have that many bleeding events, so we're not concerned about it at this time. Right. Great. Just on the vudalimab and the different cohorts, what you anticipate you might share? Right. It's going to be data from the patients that came in, right? It's all the cohorts recruited at the same time. Note that the great majority of patients are receiving the same therapy combination of a platinum plus cabazitaxel with vudalimab, except for the small portion that received based on their genotyping of PARP inhibitor or where there's no chemo and it's just a monotherapy. The great bulk are gonna be the chemo combo. The real point of this data is that initial look at can we combine a dual checkpoint blockade PD-1, CTLA-4 with potent chemo. How do we look? What kind of results are we seeing, and what's the path forward for trying to get chemo combos into dual checkpoint blockade? It'll be a few handfuls of patients, and that's the disclosure we plan. It'll be spread across the cohorts, but again, almost all patients are getting the chemo combo. Okay, thanks. I appreciate it. I'll hop back on. Thank you. Thank you. Our next question comes from David Dai with SMBC. Your line is now open. Hi. Sorry. David? Thanks. Yeah, sorry. Can you hear me okay? Yes. Great. Thanks for taking my questions. I have a couple questions. This question is around the IL-15, IL-15Rα-Fc program, you have 306 program. We saw that FDA has accepted a BLA from a competitive program in bladder cancer. How should we think about potential read-through to your 306 program? Could you maybe share with us some of your differentiation of your IL-15 asset compared to theirs? I have a follow-up after. Sure. I guess I'll address that question. What we understand the BLA in question is for a super agonist IL-15 receptor alpha fusion in non-muscle invasive bladder cancer. That is not a systemic therapy. It's a therapy given in combination with BCG, you know, through cystoscopy, right, into the bladder. It's not a systemic therapy. I think that maybe relates to the fundamental difference in design of the molecules. Ours was engineered XmAb306, our IL-15, as well as our whole family of cytokine therapies, was engineered with dramatically reduced affinity to the signaling receptors and reduced potency to smooth out that activity time curve. You don't have the big spikes of activity early on that can drive toxicity, and you don't have the big sink of receptor-mediated clearance lowering the duration of action. That's a fundamental difference to a super agonist design, which is trying to amplify things. I think we're committed to the systemic route and to being able to be used broadly and widely across many different tumor types. We're not just enrolling in solid tumors with Genentech in the phase I dose escalation in combo with atezolizumab, a PD-L1 inhibitor. Now Genentech has started the combo with daratumumab and myeloma. We're gonna be starting a study of our own. We'll disclose the details of that and the indication in the coming months. We know Genentech is working on further studies. I think systemic versus a local delivery is a pretty fundamental difference. I'm not sure how much read-through there is, IL-15 to IL-15. Got it. That's really helpful. Second question is for the IL-2 Fc program, 564 program. We know that it's currently a healthy volunteer trial. Any updated thoughts on which autoimmune indications are you planning to move the program into? You know, there's a lot of potential indications for a T-reg amplifier. Not a lot of deep clinical data, though, from anybody really, about what indications a T-reg therapy is going to be able to treat, just glimmers of information. There was recent information released by a competitor program that seemed to show, from a very small cohort of patients, promising data, randomized against placebo in atopic dermatitis. We're certainly exploring derm indications and looking across the spectrum as information starts to come out from competitors at what to add to the mix. We've done a lot of work. We are gonna be disclosing the initial indications we're doing in our multiple ascending dose study in patients that we do expect to start within the next few months, so shortly. We'll be able to guide a lot more when we have our first data readout this half of the year from the single ascending dose in healthies. We'll also guide on the specific indications shortly. All right. That's really helpful. Thank you so much for the color. Thank you. Next question comes from Kaveri Pohlman with BTIG. Your line is open. Yeah, good afternoon. Thanks for the updates and for taking my question. Maybe just one for me. In terms of format for CD3 T-cell engagers, you recently discontinued development of tidutamab. Does that mean two plus one formats are the way to go for solid tumors? How would you compare it to two plus two formats in the clinic? I think it's gonna be tumor antigen by tumor antigen. I think when you've got one where you wanna separate binding from healthy normal tissue with low expression and high expression on tumor, two plus one is almost certainly gonna be the way to go. Again, you need to do the experiments and look at the details. I think there's gonna be cases where that won't be such a clean or simple situation. You know, we're still learning a lot from it. I think we think there's a lot of promise in two plus ones, and so we're certainly pursuing them because in many cases, you do have that high, low expression on tumor versus healthy. As for two plus two formats, John, I'm not familiar with too many. There have been a few historically tried. I don't know of that much clinical data I've seen from those. Yeah. Most people avoid having two binders to CD3 because you're worried about non-selected T-cell activation. It's definitely not a direction that we're pursuing internally at Xencor. Got it. Thank you. Thank you. Our next question comes from Charles Zhu with Guggenheim Partners. Your line is now open. Hello, can you hear me? Yes. Okay, great. Yeah, thanks, guys, for taking the questions, and congrats on the progress. My first one on XmAb819. Given that it's a CD3 T-cell engager as well as the ongoing buzz around FDA Project Optimus, how should we think about progression of dose escalation and exploration, particularly when you compare how you might progress with XmAb819 relative to how historical CD3 T-cell engager dose escalation has been conducted previously? Thanks. Well, I think it's way more informed by the data and the science now that there's data and science to go from. I mean, John, you've maybe dug into this more than any of us about Project. Yeah. I mean, I think the Project Optimus just puts a little bit more pressure on having enough biomarkers in your study, to you know, that you can really defend that you pick the optimal dose. But of course, we're still gonna, you know, go by old-fashioned standards as well. What's the maximum tolerated dose? You know, how much CRS is happening at different dose levels? I think the biggest learning is the knowledge about priming doses and step-up doses, the magnitude of priming dose you need and what biomarkers you look at to set that dose. I think relative to what we thought maybe five years ago, priming doses are lower than you might have thought, and they can be quite a lot lower than your ultimate dose, and you can still get there fast. I think we all expect to be able to move faster because there's a lot more confidence in these serum biomarkers like IL-6 levels and how you can step up this to mitigate CRS. Like, I think we've been pretty successful with plamotamab and certainly numerous other programs that our competitors or collaborators have done. Yeah. Bassil, maybe I can add something here. You know, in my experience, what I've observed, and it's still early days on this Project Optimus, is that usually for CD3, the agency is requiring you to explore two different doses in terms of your efficacy or expansion. You know, I don't know if they'll keep that going, but it seems to be like the MTD and maybe a dose lower that seems to be efficacious with maybe lower toxicity. I'd just say for the XmAb819 study, we have a lot of learnings from our previous studies, so there's a lot of flexibility. The biomarkers are pretty novel, the design is pretty novel, so it'll give us a lot of flexibility in terms of understanding our dose when we go into that expansion step. Got it. Great. That's really helpful. Thanks for all that color. Yeah. Maybe just one follow-up question regarding vudalimab. I guess with respect to your upcoming data readout, how much will we be able to glean from that data set? You know, given the wide spread of different patient populations characterized by molecular subtype you're enrolling, you know, will we be able to kind of determine or I guess I should say, would you be able to determine, you know, particularly interesting subsets of patients, either from a clinical or strategic perspective for longer-term development? Thanks. At this data readout, it's gonna be too early with too few patients to make any kind of conclusions about the different subtypes. Remember, these are all still metastatic CRPC patients, right? They've all gone through essentially the same therapies prior. There's no need to consider them differently outside of their medical, rather outside of the therapy we're giving them. Again, the bulk of them, chemo plus vudalimab, you can think of those as a group. As we accrue greater numbers, we'll see if any patterns emerge, right? This initial look will be, I think, too early to make any conclusions about that. We'll just give us an early look at is there an efficacy tolerability match up for this initial regimen we've come up with, which is simultaneous maximal chemo and vudalimab. Great. That makes sense. Thanks for taking all my questions, and look forward to your upcoming readouts. Thank you. Thank you. Our next question comes from Edward Tenthoff with Piper Sandler. Your line is open. Great. Thank you very much. Thanks for taking my question. It's gonna be an exciting 2025. I wanted to get a sense just with respect to the cytokine work that you're doing. Obviously this has become a big focus for the company, the partnership with Roche for IL-15 and then the work with IL-2. Maybe you can tell us sort of at a high level how you think XmAb's really differentiate in this space, because there's a lot of competitors who are looking at masking and other technologies. I just want to understand sort of how you see that differentiating and ultimately what you expect to do with maybe some of the other known cytokines. Yeah, I mean, I'll start maybe, you know, John, you can jump in, but the insight that our team had, that John's team had was that cytokines toxicity and overly fast clearance relative to what you want in a drug, that is caused by their naturally very high potency, and that you can dial that potency down and create a completely different pharmacodynamic and pharmacokinetic profile. How we use that for making the drugs and the future of the platform, there's a lot of ways to go, but I think that's the key insight and differentiation. Yeah. I mean, that's the unifying theme. What excites me about it is these long-acting lower potency cytokines are so much better tolerated in our experience so far that it gives us tremendous combination potential as well. You know, you could think about combining these with our CD3 engagers, combining them with checkpoint inhibitors, combining with NK engagers. There's just a ton of potential there. I think there's a simplicity there where the challenge of really complex protein engineering efforts like you see with masking approaches, conditional activation approaches, is there's a lot of biochemical pieces within the drug molecule that have to work exactly. It's based on assumptions about the biology going on in the body that are just that assumption. I think this simple sort of universal approach we think is really attractive and, you know, we've already applied it to two cytokines that are in the clinic. Our third one is coming on behind that, XmAb-IL-12. We have an IL-18 program that's in preclinical, and we're also doing targeting of these with, you know, antibody domains fused. We think that this general low potency platform with its tolerability and half-life lets you start thinking about cytokines as real drug development widgets and no longer these esoteric molecules. Yeah. Cool. Appreciate that. Helpful. Thank you. Our next question comes from the line of Gregory Renza with RBC. Your line is now open. Hi, this is Ning Long for Greg. Thanks for taking our questions. Maybe two from us. First on 808, just curious on your thoughts on the data from a CD28 bispecific in the space today, and how that referred to the clinical potential and safety considerations of 808, you know, as well as their combination strategy with Pembrol. Then secondly, maybe just on 564, you know, for the initial data in healthy volunteers, what are the level of change in T-regs and T effectors you'd expect to see to give you confidence in its clinical potential? Thanks. You know, I'll let John take XmAb808 since our CD28 platform is really something that grew out of the work that he led in his team. Let me answer on XmAb564 really quick. I think we've seen what our competitors have have delivered in their initial data disclosures from their single ascending dose studies and a little bit of multiple dose study. You see sort of a little bit north of fivefold increase in T-regs. You see it often decaying after a couple of weeks. You know, reasonable tolerability of the programs, you know, vary a bit in that. I think the bar we've set for ourselves is to be at least as good as the best in class. I think north of that kind of amplification of T-regs, it's got to be selective, no T effectors, and good tolerability, and we're hoping that our design gives us a longer half-life. Yeah. On the PSMA CD28 data that was disclosed today, I mean, it's obviously early days, right? Small number of patients, but we're actually pretty excited to see what they're saying about it. I mean, that puts some wind in our sails on eight oh eight. You know, a lot of potential in that class, and it's kind of the first clinical validation that you could really move the needle there. Yeah. We view that as clear proof of concept that you can improve PD-1 therapy, checkpoint inhibitor therapy with CD28 co-stimulation that's been seen in humans. I think that's a great step for the field, and we're excited to have an agent that's got an open IND, XmAb808, and it's going to be in the clinic in the coming months. It's a great first start. Great. Thank you very much. Thank you. Our next question comes from Etzer Darout with BMO. Your line is now open. Great. Thanks for taking the question. Just one quick one for me. You know, for vudalimab, data that you'll be disclosing in the second half, just trying to think about the right comparator for the combination with chemo. Is the right, you know, way to think about this is sort of, you know, chemo like Jevtana post docetaxel in patients with metastatic castrate-resistant prostate cancer, is that the right way to think about this upcoming data set from an efficacy standpoint? You know, I know you're asking about the chemo comparator, the right one. There's something that got garbled in the phone. Can you repeat what you stated was the right reference frame? Jevtana. Jevtana post docetaxel. Jevtana. You want to go, Allen? Yeah. I think you're asking, like, what to expect and how to benchmark the data that we'll be presenting. I think, comparison with a PD-1 in combination with docetaxel is a fair comparator, but not actually accurate 100%. In the sense that, remember from our phase I data, we found very good tolerability of our PD-1 CTLA-4. You know, we thought we could combine it with a very aggressive chemo regimen, the best chemo regimen for prostate cancer, which is a platinum plus cabazitaxel. You know, docetaxel, I think, is just a single agent chemo, and a lot of people use that. In terms of benchmarking it to other therapies, I mean, you may wanna compare it to the cabozantinib, atezo combo as well. You know, that response rate, I think, was 18% centrally reviewed. I wouldn't think about comparing it to those agents directly, but I think that gives you a ballpark of how to develop it in the future without giving out too much detail. Great. Yeah. Thank you. That's very helpful. Thank you. Sure. Thank you. Our next question comes from Jonathan Chang with SVB Securities. Your line is now open. Hi, this is. Hi. Hi, this is Matthew Kaplan on for Jonathan Chang. Congratulations on the recent progress, and thanks for taking my questions. Just a first question, in light of the KEYNOTE-921 data this morning, which is the pembro chemo and mCRPC, which missed on OS and radiographic PFS, do you have any updated thoughts on use of PD-1 targeting agents in this setting? I think it's clear that the limited activity that PD-1 agents have had in mCRPC has been now repeatedly confirmed. I think it shows you that they're not highly active, and I think that's why we feel convinced that our dual checkpoint inhibitor with PD-1 and CTLA-4 blockade simultaneously is a different hypothesis that really merits thorough testing. I think also it shows you the encouraging activity you see with the CD28 bispecific that we saw disclosed earlier today, and on top of a PD-1 agent showing, you know, a number of responses out of a very small patient cohort. Again, very early data, I think quite encouraging from concept standpoint. Note that we have not just our B7H3 CD28 coming to the clinic soon, and B7H3 is highly expressed in prostate cancer, and so that's obviously a place we're considering looking. That's in combo with pembro. Our partner, Janssen, has a CD28 against a prostate restricted antigen that is gonna be behind us in timeline. We'll be the first to the clinic with our platform, but that they're also excited about. I think we're gonna see a lot about how we can make checkpoint inhibitors work better, whether it's adding CTLA-4 blockade, adding CD28. I think there's a lot of promise, but with still a high unmet need. Yeah. I would just add, Bassil's correct. I think prostate cancer is. The landscape is shifting very quickly with the CD28 data. You know, specifically to the KEYNOTE-921 data, I don't think it impacts us, maybe gives us a little bit more breathing room. Remember, both Merck and BMS decided to move forward with their PD-1s, in combination with docetaxel to phase three, and we have the first readout. The interesting issue is that, you know, for PD-1, clearly Keytruda had a low response rate, and it appeared that the BMS data with Nivo/Ipi seemed to be higher, and that's why we were excited about using our PD-1 CTLA-4, vudalimab. Now, we are later to the game to them, and they've already started their phase threes with docetaxel. We tried to sort of do something that would be going to where the puck will be and not where the puck is. We tried to do a little bit more aggressive in terms of our chemo regimen. I think the fact that the docetaxel didn't work for them gives us some more opportunity if that option is there. I think Bassil hit the nail on the head. There's a lot of things changing in prostate cancer right now. Yeah. Thanks for the color and insight there. That's really helpful. Just another- Sure. A quick one from me if I may. Just how does the new partnership with Caris aid your target discovery beyond your own in-house capabilities? Do you have any specific targets in mind for the partnership? Yeah. I mean, the simple answer is we don't have a lot of in-house capabilities. I mean, that's a pretty specialized capability that Caris brought to the table, and it's something that we'd rather spend our resources, you know, making best-in-class modalities to address these kinds of targets. You know, we have other ways of trying to access other targets. I'll also remind you, we have our Atreca collaboration, which again gives us access to, you know, novel classes of targets. Yeah. I would just add, being a former clinician, I'm familiar with Caris from my clinical days. Remember, they have mountains and decades worth of tumor samples that they've collected from patients. I think that's a huge differentiating. We're good at making antibodies, but we do not have the sample database or the tumor databases that they have. Mm-hmm. Yeah. Great. Thanks for taking my questions. Thank you. Our next question comes from David Nierengarten with Wedbush. Your line is now open. Hey, thanks for taking the question. Most might have been asked, but maybe a follow-up on my B7H3 toxicity question. I heard, you know, MacroGenics also in that study combined it with, you know, various IO agents, and I was just wondering if that was a concern or potential cause of the added toxicity, you know, I don't know, bringing in immune cells to a vasculature that's targeted by B7H3 or something odd like that. I was just wondering if you know, had any insights or assay, you know, preclinical assays or anything that would show caution on different IO agents plus B7H3 targeted agents. No, I can't say we've had anything. We gave our B7H3 CD28, which of course is an immune target, CD28 at very high doses in our non-human primate tox studies with no effect, no ill effect. We don't have any more answers on that data than was offered earlier. I do note that is an antibody, a B7H3 antibody that is an immune Fc gamma receptor competent antibody. It would be expected to have some direct cytotoxicity on B7H3-bearing cells. Could that be playing a role? Possibly. Yeah. I mean, every modality is different. You know, it's really hard to predict. The other thing I'll add is that our XmAb808 molecule is a 2+1 that was specifically designed to be more selective for binding the tumor cells, which generally have a lot brighter B7-H3 expression. There could be other points of differentiation that'll help us on the safety side. Okay, great. Thanks. Thank you. Our next question comes from William Maughan with Canaccord Genuity. Your line is now open. Hi. Thanks for taking the question. So looking forward to this vudalimab readout. Are there any specific cohorts that you think are more or less key to the success of the program, whether that's due to, you know, read-through for vudalimab's mechanism of action being most appropriate for these patients or commercial, you know, unmet need for a specific cohort? We think that again, it's not really gonna be that different in terms of the potential or the insights on the readout from the different cohorts of chemo-receiving patients. Certainly, the PARP inhibitor-receiving patients, those that have, you know, DNA damage repair deficiencies are sort of a separate category. No, it really is again, all those cohorts together, the great majority of patients getting chemo, you know, platinum cabazitaxel combo are gonna help us read out sort of in aggregate on safety and on activity. Initially from very small patients. It gives us this first direction. I don't think there's gonna be that much insight gleaned on a narrowing of the program at this early of a stage. Okay. On the 104 data from ASCO, beyond just the efficacy and safety on the poster, were you able to glean anything on biomarkers, whether it be, you know, expression levels or, you know, T-cell proportions of different populations that might make a patient more or less likely to respond? Not really. It was a very cleanly well-tolerated molecule, and we saw activity in different tumor types and some, you know, long sustained, you know, stable disease for multiple years even, but no biomarkers that really popped up that correlated clearly with much of anything. We are trying a biomarker-driven hypothesis in our expansion cohorts, combining it with ipilimumab, which is known historically to upregulate ICOS. Okay. Last one, sorry if I missed this, I dropped briefly, but can you give detail on what drove the increase in guidance for your cash balance at the end of the year? John, do you wanna hop on and take that? Yeah, sure. We did update the guidance. You know, as you pointed out, it actually increased. We expect to have between $550 million and $575 million as of 12/31 based on current plans, with runway through the end of 2025. Okay. Is there anything explicitly that drove that update? Primarily I think the royalty revenue from Vir. We didn't have Okay. A lot of clarity into the actual timing and the dollar amounts of that. It's been a little bit higher than we expected. Okay. Thank you. Thank you. I'm currently showing no further questions at this time. I'd like to turn the call back over to Bassil Dahiyat for closing remarks. Have a wonderful evening. Everybody for joining us today, we look forward to updating you again soon, and have a wonderful evening. This concludes today's conference call. Thank you for participating. You may now disconnect.