Hello, welcome to the Xencor DDW 2026 webcast. We ask that you please hold all questions until the completion of the formal remarks, at which time you will be given instructions for the question and answer session. Reminder, this conference is being recorded today. If you have any objections, please disconnect at this time. I will now turn the call over to Charles Liles. Thank you and good morning. Yesterday, we issued a press release introducing the topics we plan to discuss on this webcast, including results from the Phase I study of XmAb942 and the preclinical characterization of XmAb412. The press release is available at www.xencor.com. Providing comments on the call from Xencor are Bassil Dahiyat, President and Chief Executive Officer, John Desjarlais, Executive Vice President and Chief Scientific Officer, Dane Leone, Executive Vice President and Chief Strategy Officer, and Mark Osterman, Senior Vice President and Head of Clinical Development for Xencor's Autoimmune Programs. We are also joined by Dr. Vipul Jairath, Professor of Medicine in the Division of Gastroenterology at Western University and Chief Medical Officer at Alimentiv, who will join Mark for a discussion about the Phase IIb XENITH-UC study. After the prepared remarks and presentation, we will open up the call for management to answer your questions. Slides that we are using today should be visible here on the webcast and will be made available for download on the Events and Presentations page of our website around the time our remarks are concluded. 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 plans and objectives of management, future product offerings and research and development programs, as well as future financial and operating results, future market conditions, future operations, the company's partnering efforts and capital requirements. These forward-looking statements are not historical facts, but rather are based on 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 or most recently filed annual report on Form 10-K. With that, I'll pass the call over to Bassil. Thanks, Charles, and welcome everyone. Xencor is a clinical-stage biotech company dedicated to making better medicines based on our world-class XmAb protein engineering platform. Our purpose is solving the hardest science engineering problems to create new drugs and then developing them to advance the standard of care for patients and their caregivers. Our protein design tools and novel antibodies have been validated many, many times over through our commitment to using strategic partnerships when the best development strategy for a program involves another company. That approach has produced real advances in the standard of care for patients and caregivers. There are many ongoing programs across oncology, autoimmune, and infectious disease poised to continue that into the future. Xencor's wholly owned clinical-stage development pipeline is centered on six programs with differentiated molecules, all built with our protein engineering tools to enable better clinical outcomes and utility. Today, we'll discuss our TL1A portfolio consisting of XmAb942, our potential best-in-class monoclonal antibody that targets TL1A, an emerging biologic target implicated across a growing number of autoimmune and inflammatory diseases, and XmAb412, a novel bispecific antibody targeting TL1A and IL-23p19. XmAb942 is currently enrolled in XENITH-UC, a global Phase IIb study of patients with moderately to severely active ulcerative colitis, and XmAb412 is starting Phase I in Q3 of this year. During the ongoing Digestive Disease Week conference, we're presenting posters updating our progress on these programs. Our poster for XmAb942 provides PK/PD analysis based on our phase I data that shows how our XENITH-UC study is testing our best-in-class drug exposure and target inhibition to 10 to deliver better clinical results versus those observed from studies of first gen TL1A-targeted biologics. We plan to provide a progress update on XENITH-UC around year-end and expect the results of the 12-week induction period during 2027. We're also presenting the preclinical characterization of our XmAb412 bispecific program. Our poster for XmAb412 details the novel design of our bispecific targeting TL1A and IL-23p19 to deliver dual inhibition of these two key inflammatory pathways in autoimmune disease. Our first human study is on track to start during the third quarter of this year and is expected to support moving into phase II development during 2027. You can see here the large and growing landscape of inflammatory bowel disease therapies, and we're particularly drawn by the opportunity to address the high remaining unmet need by targeting the new and compelling biology of TL1A. We believe our XmAb tools can bring next generation, highly potent and long-acting molecules to these patients to improve quality of life through lower injection burden and better target inhibition over the course of maintenance therapy. Our design philosophy for both XmAb942 and XmAb412 was to address the key clinical pain points with our well-validated XmAb antibody modules and tools. For 942, we built a highly stable antibody with class-leading potency and applied our Xtend Fc domain to get a 74-day half-life in humans, a high concentration formulation, and Q12-week dosing. For XmAb412, we built a novel bispecific 1+1 format that John will tell you about to minimize immune complex formation and simplify formulation. Of course, we used our Xtend Fc domain for long half-life. We dialed in ultra-high potency, including sub-picomolar binding, so this bispecific can match or beat existing traditional antibodies. We consistently challenge ourselves to push the boundaries of protein engineering to deliver better medicines to patients. We believe XmAb942 is positioned to be the best-in-class anti-TL1A antibody, which we think creates a significant market opportunity within the emerging TL1A class for the treatment of inflammatory bowel disease. Also longer-term positions XmAb942 can be developed for a broad range of autoimmune inflammatory diseases, like the many currently being studied within the class. XmAb412 is poised to deliver on the promise of dual-targeted therapy for inflammatory bowel disease, which you can see exemplified by the most recent DUET-UC data, where 412 can deliver potentially class-leading combination potency in a single molecule format that can follow the efficient clinical and commercial pathway of monoclonal antibodies or oral medications and avoid the highly costly and complex development of combinations and co-formulations, like the nearly 3x size of the DUET Phase IIb studies over standard programs. John Desjarlais, our Chief Scientific Officer, will walk us through the preclinical characterization of XmAb412 and introduce our Zenlock Fab platform. Go ahead, John. Thanks, Bassil. To address this need for bispecifics optimized for autoimmune disease, we aim to make a very high potency and long-acting bispecifics with low immunogenicity potential and stability needed for high concentration formulation. To do this, we expanded our modular XmAb platform with our new XenLock Fab format that lets us readily combine full Fab domains into highly stable multispecifics in a native-like IgG format. This allows us to generate binding domains from full variable domain diversity and highly optimize their affinity and stability without the limitations of common light chain or VHH approaches. XenLock lets us assemble these Fabs with our XmAb Fc domains and readily produce molecules with ultra-high affinity into whatever format we like. The result is XmAb412, our TL1A by IL-23p19 bispecific, with femtomolar affinity, or sub-picomolar for IL-23, and single-digit picomolar affinity for TL1A. We can see how the stringent engineering that we did to make XmAb412 into a very potent molecule. Cell-based assays for both TL1A activity on the left and IL-23 on the right show the same or better potency for suppressing these pathways from this bispecific compared to leading clinical TL1A and marketed IL-23 antibodies, with XmAb412 shown in the dark blue. The XenLock approach lets us get this very high potency from only half the number of binding domains per target in the monospecific antibodies. This smaller single binding domain construct means less mass to put into the vial when we make high concentration subcutaneous formulations, a big help for it. The other big advantage of this one plus one ultra-high potency format is the much lower propensity to cause immune complex formation and much smaller size of these complexes. In particular, for trimeric targets like TL1A, antibodies with 2 TL1A binding domains can create large immune complexes, as you can see in this schematic. Large immune complex formation is an important driver of antibody drug immunogenicity. Our 1 plus 1 format does not have that potential for a large complex formation, as there's only 1 domain per drug molecule to stick to TL1A. We experimentally showed this with size exclusion chromatography. You can see just a single peak for XmAb412 in the presence of TL1A compared to the messy mixture of very high molecular weight complexes formed with a 2 plus 2 bispecific antibody using 2 TL1A binding domains, a common format used to make bispecifics quickly, but they potentially suffer from this liability. Turning to the in vivo data for XmAb412, we show on the left the long half-life observed in non-human primates of greater than 20 days, which extrapolates to an expected 60-70 days in humans, possibly enabling every 12-week dosing. XmAb412 uses our Xtend Fc domain for long half-life. This PK gives a very durable pharmacodynamic profile, and you can see that the complete suppression of free TL1A below detection limit has outpaced two months from a single dose. In summary, XmAb412 is poised to deliver potentially best-in-class innovation of both TL1A and IL-23. In addition to potency and extended half-life, we have a high concentration formulation for simple sub-Q administration ready to go into our phase I study starting in Q3 of this year. We expect this trial to validate our XenLock approach to making bispecifics tuned for the needs of autoimmune disease and have a second program in preclinical development behind XmAb412. Mark? Thanks, John. Our first-in-human healthy participant study of XmAb942 was a randomized, double-blind, placebo-controlled phase I study with a primary endpoint of safety, a secondary endpoint of pharmacokinetics, and exploratory endpoints of immunogenicity and pharmacodynamics. We studied 4 different dose levels across single ascending dose and multiple ascending dose cohorts. The single ascending dose cohorts tested 3 different dose levels given both subcutaneously and intravenously in 48 healthy volunteers. The multiple ascending dose cohorts tested 2 different dose levels, each given 3 times every 4 weeks intravenously in 16 healthy volunteers. As expected, XmAb942 was found to be safe and well-tolerated in healthy participants, with a similar rate of treatment-emergent adverse events between the XmAb942 arms and placebo. Specifically, all treatment-emergent adverse events were mild or moderate. The rates of overall treatment-emergent adverse events were similar in XmAb942 and placebo. There are no serious or severe treatment-emergent adverse events and no adverse events that led to discontinuation of either the drug or the study. Headache was the most common adverse event, occurring in 33% of participants administered XmAb942 compared to a slightly higher 38% of participants administered placebo. There are only two definite treatment-related adverse events, both of which were mild. One mild injection site reaction and one mild administration site bruise, both occurring in the highest dose subcutaneously. XmAb942 was found to have high and extended exposure after 20 weeks of follow-up in both single ascending dose and multiple ascending dose cohorts. The estimated terminal half-life of 74 days supports adequate drug levels at the 12-week dosing interval being used in the ongoing XENITH-UC Phase IIb study. We see here dose-dependent and durable target engagement with complex soluble TL1A after 20 weeks of follow-up, which again supports effective target inhibition for the 12-week maintenance dosing interval being used in the ongoing XENITH-UC Phase IIb trial. Reduction in free soluble TL1A was dramatic, rapid, and durable and was very consistent with the pharmacodynamic effect on total TL1A, with levels remaining below the lower limit of quantification through 20 weeks. XmAb942 has demonstrated best-in-class immunogenicity on rates of anti-drug antibody positivity and observed neutralizing antibodies compared to reported rates across healthy participant studies with first generation anti-TL1A drugs. Importantly, for the target dose induction and maintenance regimens we are using in the ongoing XENITH-UC Phase IIb study, there were no healthy volunteers with neutralizing antibodies, and only 25% had positivity for anti-drug antibodies at any time point. In summary, we remain confident that the innovative design of XmAb942 can deliver a best-in-class clinical profile and supports our optimism for success of the ongoing global Phase IIb XENITH-UC study in moderate to severely active ulcerative colitis. It is my distinct pleasure to welcome Vipul Jairath, who I've known for years from our academic work and mutual interest in endoscopic and histological assessment of disease activity in inflammatory bowel disease. As I was an inflammatory bowel disease academic on faculty at the University of Pennsylvania for almost 16 years, I had the good fortune to get to know Vip quite well over the years as we thought through a number of clinical and scientific questions together on many occasions. Vip is a Professor of Medicine in the John and Susan McDonald Endowed Chair in Inflammatory Bowel Disease at Western University in London, Ontario, Canada, and also the Chief Medical Officer of Alimentiv. He has former training in the U.K. in London and Oxford. Of note, Vip has contributed so much to our field so far in his career in terms of clinical trial understanding and endpoints. Vip, thank you so much for joining us. Great. Thanks very much, Mark. Pleasure to be with you here, and the rest of the team. Thank you for having me. Clinical remission rates from large randomized controlled trials show that more than half of ulcerative colitis patients do not adequately respond to their advanced therapy irrespective of mechanism of action. Although the data appear to be potentially more promising with the TL1A inhibitor class. We've seen this trend now for 2 decades. Vip, what is your feeling regarding the unmet need with respect to efficacy in UC at the present day? Mark, I entirely agree with you. We've seen this disappointing trend in the last 2 decades in ulcerative colitis. We have several approved drugs with different mechanisms of actions in ulcerative colitis, but we haven't yet broken this efficacy ceiling. Therefore, we still need new mechanisms for patients because there's still a substantial proportion that do not respond to their initial therapy or sometimes subsequent therapies that they lose response to. I agree with you. There's a chance that these data results could be more promising for our patients with the TL1A class, particularly given its more pleiotropic nature in terms of mechanisms of action. Thank you, Vip. As has been well described through a number of studies across multiple drugs and mechanisms of action, including vedolizumab and guselkumab most recently, there is often a strong drug exposure response relationship in inflammatory bowel disease, both in Crohn's disease and also in ulcerative colitis, with higher drug concentrations being associated with higher rates of clinical remission. The vedolizumab analysis shown in this slide I did with Takeda while I was in academia, we see the largest delta between highest and lowest concentration strata of the 3 drugs portrayed here as we used individual patient-level data from the GEMINI I randomized control trial and actually adjusted for the 5 variables that are known to most prominently affect vedolizumab clearance. Oflimabart also, not surprisingly, has been reported to exhibit an exposure re-response relationship with higher drug concentration tertiles associated with higher rates of clinical remission in its phase IIb UC trial. What is your opinion about the importance of drug exposure optimization in IBD and with the TL1A inhibitor class? Mark, as key observation, I think it's really likely that we'll see a dose or exposure response relationship with all of the TL1A class because that's been demonstrated through robust data across multiple different mechanisms of actions in IBD already, including some of these data that you've shown here. What we see here is that higher drug concentration levels have been associated with higher rates of response. What we also know is that immunogenicity to IBD drugs is often seen in the setting of low drug concentrations. Optimization of drug exposure is essential to protect against the formation of anti-drug antibodies, because if you develop these, we know it can impact both the rates of response and durability of response to our drugs. I suspect that the same phenomena will hold true for the TYK2 inhibitors, and therefore it's really critical that optimization of drug exposure is likely to be important both to maximize the rates of clinical endpoints, such as clinical remission, but also importantly, those sustained long-term durable clinical remission rates that are so important. Thanks a lot, Vip. We developed a unified quantitative systems pharmacology, QSP, model integrating clinical and published data on XmAb942, tulisokibart, and efimcobart, and extended it to support virtual population simulations and comparative population-level PK/PD predictions across compounds using the expected pivotal dose regimens for tulisokibart and efimcobart compared to our target Phase IIB dose re-regimen of XmAb942. In the induction phase, our QSP model-based projections indicate that XmAb942 provides markedly enhanced TYK2 inhibition, with predicted greater than 99% inhibition in 86% of patients, compared to only 30%-40% of first-generation anti-TL1A antibodies. Regarding maintenance, it was also shown that higher exposure with efimcobart was associated with higher response rates in the Phase II UC trial. XmAb942 is designed to deliver maximal TYK2 inhibition and is projected to achieve greater than 90% inhibition in 90% of patients versus 60%-70% for first-generation antibodies during maintenance therapy, despite being dosed much less frequency. These higher drug exposures for XmAb942 during both induction and maintenance position our molecule very well to test whether increased exposure improves efficacy. Vip, what is your impression of our QSP modeling data and the potential efficacy profile of XmAb942? Yeah, thanks, Mark. You know, I'm frankly impressed with these modeling data for XmAb942. You know, my reading of this is that Xencor have really optimized the molecule's potential for getting high drug exposures, which are essential, as we just said, both during induction and maintenance. Ultimately, the importance of that is it could translate into high rates of clinical response and remission during the induction period, sustained during the maintenance period. You know, perhaps, this will give lasting durable response for our patients. You know, as I mentioned earlier, I do think there'll be an exposure-response relationship for the TYK2 class of drugs. These model differences in TYK2 inhibition between XmAb942 and these leading first-generation TYK2 competitors, is substantial and is compelling. You know, my reading here is that XmAb942 appears to be well-positioned, and it potentially could be a best-in-class molecule in terms of efficacy. You know, really I'm excited and the community's excited to see the results of XENITH-UC. Thanks a lot, Vip. XmAb942 has a terminal half-life, as we mentioned, of 74 days, which not only is approximately 4 times as long as first-generation anti-TL1A antibodies, but also enables at minimum every 3-month dosing, which is what we are studying in our Phase IIb UC trial. Compared to the first-generation anti-TYK2 antibody competitors, the number of subcutaneous injections administered during maintenance therapy with XmAb942 is significantly less. Vip, how do you feel that this difference in injection burden will be received by patients and their physicians? What impact do you think that XmAb942 could have on overall patient experience and satisfaction? Yeah. This is a key point. We know from many patient preference studies, and I know from my clinical practice of treating many patients with IBD, that injection burden is important, and it matters to patients. It also matters to the treating physicians. The key thing here that stands out, there's a markedly reduced injection burden with XmAb942 compared to first-generation anti-TYK2 antibody competitors, and this has to be an attractive feature of this next-generation drug. I think ultimately, what I see is this has been enabled by the technology of your protein engineers, and they've been able to manufacture this XmAb942 to lengthen its half-life so much. The infrequent dosing requirement is not only very convenient for patients, but it's also a really nice addition in terms of the potential unpleasantness that patients sometimes report having to inject themselves with a needle. I'm sure patients will almost certainly welcome this improvement compared to first-generation anti-TL1A antibodies. Really taken together with the optimization of drug exposure to help maximize efficacy, you know, I believe that XmAb942 is really uniquely poised to be a best-in-class drug. Thanks so much, Vip. Appreciate that. We have designed a proper and rigorous dose-ranging, double-blind, placebo-controlled, randomized phase IIb trial in ulcerative colitis that can inform a single induction dose selection for phase III. There are 3 active drug arms, each separated by a half logarithm in dose compared to placebo. There's asymmetric randomization such that the highest dose arm will include the most patients. In fact, overall, 77% of patients during induction will receive active drug, and only 23% will receive placebo. Even the lowest dose arm is designed to achieve greater than 90% target inhibition over the dosing interval, such that we expect some efficacy even at this lowest dose. The doses have also been selected to have the highest dose maximize drug exposure to potentially achieve greater induction efficacy than has been observed in competitor trials. In addition to the convenient and patient-friendly every 12-week maintenance dosing, all patients will receive active drug at week 12 for up to 2 years, as there will be an open label extension for at least an additional year. Vipul, what are your thoughts regarding this phase IIb UC trial design? Thanks, Mark. Well, as you know, I spend a lot of my time thinking about these things, I think you've really designed an excellent trial, a state-of-the-art trial. It's been very well thought out. A number of reasons I say this. First, it's well-crafted to do a full exploration of induction dose ranging, that will give you confidence in the results to inform a single induction dose to be selected for phase III. There's a number of other aspects that bring rigor to this phase IIb. Secondly, your trial is attractive to patients, I think, for a number of reasons. First thing, obviously, there's a high probability of getting the active drug. I think the second thing is the drug doses have been well selected to potentially lead to efficacy with the highest dose potentially maximizing efficacy due to optimized drug exposure. Third thing, there's only a 12-week placebo period with attractive to the sites in terms of recruitment. The fourth thing is there's very convenient and patient-centric Q12 maintenance dosing. In addition, there's an open label extension that enables up to two years of free drug for patients. The final and sixth thing here is I think it's a relatively de-risk MOA, given that we've seen three positive phase II trials already of the first-generation anti-TL1A antibodies in UC. Given all of these features, I really expect this to be an impactful trial, and XmAb942 will be an impactful drug. Thanks a lot, Vip. As a glimpse into the future, at this DDW, we showcase a poster of our preclinical data of our TL1A by IL-23p19 bispecific molecule, as John has already talked to us about XmAb412. Our protein engineers have built a fantastic molecule in a 1 plus 1 format that enables sub-picomolar affinity. We purposely chose to target P19 rather than P40 for IL-23, given the superior efficacy of P19 blockade over P40 blockade in IBD and also in psoriatic conditions. XmAb412 was found to robustly suppress both TL1A and IL-23 inflammatory pathways. In cellular assays, XmAb412 demonstrated IC50 values comparable or superior to clinical-stage TL1A inhibitors and approved IL-23 inhibitors. Allometric scaling predicts that XmAb412 will have a half-life between 60-70 days in humans. As in non-human primates, it achieved a half-life exceeding 20 days, with similar target engagement to monospecific antibodies. XmAb412 also supports a high concentration, low viscosity, citrate-free formulation suitable for subcutaneous dosing. Evaluation of XmAb412 in healthy volunteers is expected to begin in the third quarter of this year. Given the exciting results of J&J's DUET phase IIb trials being presented here at DDW today, in fact, especially in multi-MOA refractory patients, where the combination of guselkumab and golimumab was found to be meaningfully superior to either monotherapy, we present here the DUET-CD data in this slide. What are your views, Vip, on the potential transformational efficacy that could be achieved with a combination of TL1A with IL-23, the safety profile of such a combination, and the streamlined regulatory and clinical development path offered by a bispecific in this context? Thanks, Mark. Look, I think combination of TL1A and IL-23 inhibition is probably the most exciting prospect I see in our field, potentially even more so than anti-TNF and IL-23. That's given the possibly even more pleiotropic, anti-inflammatory, and even potentially anti-fibrotic potential that we see with TL1A inhibition. You know, I expect this combination could be truly transformational, and it has the potential to yield efficacies that we've not yet seen in IBD and possibly even other immune-mediated inflammatory diseases. Equally in this situation, safety, you know, such a combination has to have a favorable safety profile, and I think that that's potential here, unlike JAK inhibitors, where we've seen differential efficacy in some indications but with some safety concerns that make their long-term use far from ideal. You know, given the VEGA data here showing superiority of combination of TNF, IL-23 inhibition versus either monotherapy in predominantly a bio-naive UC population, and now the DUET data showing superiority of this combination in the more refractory patients, you know, I do feel that this combination of TL1A and IL-23 could be a very strong first-line and later-line option for patients to deliver transformational efficacy but in a safe form. Your new bispecific XmAb412 seems to be, you know, expertly constructive with very impressive affinities for both TL1A and IL-23. You know, I'm glad that you actually chose P19 as your target rather than P40 for the IL-23 blockade, given we've seen superior efficacy in IBD and psoriatic conditions that you mentioned by targeting P19. You know, on top of this, the very long expected half-life and promise of subcutaneous delivery are really the, you know, icing on the cake here to make this an ideal drug in many ways. That doesn't even take into account the fact that there are large and distinct advantages from regulatory and clinical development standpoints of testing a bispecific compared to a combination or co-formulation, as comparisons to each monotherapy are not a requirement for a bispecific entity, which not only improves the probability of technical and regulatory success for clinical trials with bispecifics, but it also saves an enormous amount of time and money and expediency in the development programs. I'm really looking forward to the commencement of your Phase I program for XmAb412 later this year. I'm very much looking forward to a phase II program in 2027. You know, I can say that many of my academic and community IBD colleagues around the world, who are really eagerly awaiting a phase II trial of XmAb412 in IBD, and really hope to be included as investigators in this program also. Vip, we really appreciate your time and thoughtful comments. Thank you so much for joining us. Thank you. Real pleasure. It's always great to see you, my friend. You too. Next, Dane Leone, our Chief Strategy Officer, will speak to TL1A strategy and development roadmap. Dane? Thank you, Mark and Vip. Great conversation, and really appreciate all the insights. Today we've discussed the key points to why our TL1A pipeline is primed to deliver the next generation of advanced therapies for patients living with moderately to severely active inflammatory bowel disease. Our focus on novel best-in-class therapies targeting TL1A aims to deliver both an improvement in clinical outcomes over today's drugs, while also providing the convenience of less frequent injectable dosing for a best-in-market biologic class. We view the future landscape of innovative medicines in IBD to be defined by branded TL1A monotherapy, the emergence of bispecifics, and oral inhibitors of traditional biologic targets. Biosimilar versions of today's branded medicines will also continue to play an important role, as more affordable monotherapy drugs targeting IL-23 and integrin inhibitors will add to the armamentarium of cost-effective options for patients, as the TNF class does today. Looking ahead at a roadmap, we are hard at work executing on our timeline to enable exciting data-driven decisions during 2027 for the next phase of development for our TL1A pipeline. As you can see, we expect to report the primary analysis set of XENITH-UC 12-week induction period during 2027 and use that data in tandem with the first-in-human XmAb412 study data to optimize our investment across our TL1A pipeline for the next phase of development. Longer term, we expect the full data of XENITH-UC, along with early looks at phase II patient data for the XmAb412 program, to provide us with rational decision-making around planning registration-enabling studies. Of course, data will allow us to evaluate opportunities to optimize the development of our TL1A pipeline through strategic relationships. Going back now to our overarching business strategy, as Bassil provided in his intro, we view our commitment to delivering innovative medicines as part of a life cycle that we also assess through the lens of business development opportunities. We think there is good precedent that programs delivering on the potential of better medicines in IBD to have optionality when it comes to strategic relationships. We plan to make these decisions driven by our data as our programs progress. Our XmAb412 first-in-human study is on track to start during the third quarter of 2026. For XmAb942, we expect to report an update on enrollment progress around year-end, along with a recommendation of the Data Monitoring Committee on the pre-specified blinded interim analysis for XENITH-UC. 2027 will be another exciting year for both programs, with the interim results of the first-in-human study of 412 expected during the first half of 2027, which will help validate the pharmacokinetics and pharmacodynamics of the novel bispecific platform that we now call XmAb. The second half of 2027 will provide a clear answer to the pharmacological thesis of XENITH-UC, whether best-in-class drug exposure can support best-in-class clinical results with XmAb942. In conclusion, the hard work and dedication of the Xencor team to delivering better medicines to patients living with inflammatory bowel disease is at a clinical inflection point, we are committed to continuing to rapidly advance our TL1A pipeline in the coming years. With that, we're ready to take questions. Operator? Thank you. At this time, if you would like to ask a question, please click on the Raise Hand button, which can be found on the black bar at the bottom of your screen. When it is your turn, you will receive a message on your screen from the host allowing you to talk, and then you will hear your name called. Please accept, unmute your audio, and ask your question. If you are dialing via phone please use Star 6 to unmute. Our first question comes from Jonathan Chang with Leerink Partners. You may now unmute your audio and ask your question. Good morning. This is Albert Agustinus on for Jonathan Chang. Thank you for taking my questions, and congratulations on the data. How do you see this XmAb942 data fit into your plan to expand the program into Crohn's disease and indications beyond IBD? What do you need to see from the program for you to make the decision? Thank you. Thanks, Jonathan. I'll take that question for the team. It's a great part of the roadmap that we have and the flexibility to make these decisions that are data-driven. Has been part of the plan since the initiation of the 942 program. We've looked at UC as the first proof of concept on drug exposure, given there's clear benchmarks of what we can deliver with a best-in-class and best-in-market biologic. As we think about moving towards the primary analysis set of XENITH-UC in 2027, that can trigger or catalyze additional investment and obviously parallel development pathways into Crohn's disease, as has been very traditional with many other IBD programs from our peers. We feel very confident about the profile here. That said, to be rational about our data-driven decisions, we do wanna see that data in the back half of 2027 as a trigger point. Thank you. Our next question comes from Tara Bancroft with TD Cowen. Please go ahead with your question. Thank you, guys. Congrats on the data. This is Ikenna on for Tara. Across the TL1A class, you know, we've seen clinical remission rates pretty high. You guys showed it on the chart there. Given your modeling suggests deeper and more durable TL1A inhibition for 942, how do you think about the extent to which that could translate to higher remission rates in the phase IIb? Like, where is the ceiling? That's a great question. Before I turn it over to Mark and Vip to comment, I don't think anybody knows where the ceiling is. There are some glimmers of data implying there's some directionality from existing studies like TUSCANY-2. Maybe I'll let you guys opine on that. Yeah, there's an element of uncertainty inherent, which is why we're so excited about the XENITH-UC experiment. You wanna talk more? Yeah, I'll start, turn it over to my friend. Since I'm no longer the KOL. We see for many of our drugs in IBD, both in UC and in Crohn's disease, that there's efficacy left on the table. We see it both in clinical trials, we see it clinically with patients every day. You know, we are confident with the design of this molecule that we will capture additional efficacy, given that we can maximize exposure to this drug. As far as where that ceiling is for this MOA in a completely optimized manner, it's unclear. There are some patients who will never respond to a TL1A drug because their pathobiology is different. At the current time, we don't have a great way to individually pathotype patients to find out what's driving each of their diseases and which pathways are most important for them. I think it's unclear what the actual ceiling will be, but I'm confident that there's efficacy left on the table that could potentially be recaptured with this drug. I agree, I agree with that, Mark. I mean, I think we've seen with some of the other assets that we've seen consistent data which have been, you know, 20%-25% deltas over placebo, which is really better than anything that we have today. Obviously, JAKs are up there with that kind of efficacy, but there's some trade-off with safety. I think really that's the sort of margin of delta that we've seen in the existing programs. As you've outlined, there are some potential additional attributes of this that could move that needle a little bit more, and that's incremental and important for our field to get to those benchmarks. Yeah. Thanks, Vipul Jairath. Thanks, guys. Thanks. Our next question comes from Etzer Darout with Barclays. You may now unmute your line and ask your question. Great, thanks for taking the question. Just one for me. Curious about the relative positioning of 412 relative to 942. Really is just 412 meant as a follow-on or next gen path? Or maybe aiming at a different patient population, refractory disease or TL1A responders versus non-responders? Just how you're thinking about the two molecules coexisting in IBD. Thank you. Yeah, thanks, Etzer. I think the TL1A class is still revealing itself where it can have an impact. I mean, if you recall from our earlier slide, there's more than half a dozen additional autoimmune and inflammatory indications where TL1A is being tested with really very good underlying preclinical and genetic rationale for why it oughta be a good target in those diseases. I think when we look at XmAb412 and XmAb942, this TL1A mono and TL1A plus P19, you know, mechanisms, we see sort of first an ability to address all of these other indications where P19 might not be a target of use. That's a great additional benefit of XmAb942 as a monotherapy. Of course, there are some other non-IBD indications where IL-23, like in derm, can be very useful. First, there's sort of just the ability to be positioned for the long-term future of a broad potential pipeline in a product. Maybe within IBD, you know, Dane, if you can comment on more of the subtleties about how we're using our experimental data coming out of our clinical trials. No, absolutely. I think there's a kind of a short-term window of the answer here, then maybe a longer term window of the answer. The short-term window of the answer is with 942, obviously we wanted to provide a best-in-class monotherapy biologic that can be optimized for clinical convenience as well as drug exposure. I think that's what we're delivering with the 942 program, which gives us a really clear pathway into what we think the next great branded drug class will be for IBD specifically. As Bassil mentioned, the opportunity for the TL1A class is rapidly expanding with over an $80 billion potential TAM outside of IBD as it currently stands today in a number of our peer proof of concept studies. We'll be watching those studies to see how they read out, and feel confident that the clear and thorough dose characterization that we're doing in the XENITH-UC study ongoing today with a readout in 2027 will allow us to actually move into other indications much more rapidly through that knowledge of our PK/PD and dose characterization as it relates to inpatient study with clear disease in a controlled study. With XmAb412, as Bassil said, that's a very clear, almost rifle shot at certain indications that are implicated in TL1A and IL-23, which are very large indications even outside of IBD. For 412, it's also validating our next generation bispecific platform that we call XenLock. There's a duality there of the importance of the validation of our first-in-human studies for 412 that will have first data in the first half of 2027, allowing us to really invest in that program and platform. As we said in the survey and market research we've done with gastroenterologists, 412 represents a real position in the market to help clinicians provide better care for their patients that are not only looking for a best-in-class, next-in-class biologic to use as a first-line agent, as we said, many clinicians in our surveys and market research would also use a bispecific approach or multispecific approach when the patients are inadequately responding or non-responding to a frontline IL-23. There's a lot of different opportunities within our portfolio. Yes, you're absolutely right in your question that 412 and 942 will continue to differentiate from each other as our clinical portfolio advances. Can I piggyback another. Absolutely thought. Based on sort of a looking at this thing as a clinician, as an epidemiologist, you know, even within the IBD space, there is a home for both of these drugs. Now remember that even though you might have more differentiated efficacy with the combination therapy on a population level, on an individual base level, individual pathotyping, many patients do not require combination therapy in clinical practice or in clinical trials. There is a home even within IBD space itself for both drugs that they can both live in the same space and serve different patient populations. I don't know, Vip. Yeah, no, I fully agree. You know, where bispecifics or other combination assets fit into the treatment paradigm is evolving. I mean, obviously we're seeing direct results today, which is in a refractory population for a co-formulation. I think from a bispecific population, there will be patients where you might want to use this first line and patients where you might want to use it downstream for those specific reasons. Absolutely I see a space for both of these, and where, you know, where they land in the treatment paradigm will evolve, but it's a combination of both first line and in refractory patients. Thanks for that. Thank you. Our next question comes from Timur Ivannikov with Cantor Fitzgerald. You may now unmute your audio and ask your question. Yes, hi. Thank you. This is Timur on for Steve Seedhouse with Cantor. Can you just talk a little bit more about how you will use 942 monotherapy data and 412 phase I data to make a follow on development decision, just in terms of immunogenicity or inhibition data that you're looking at? Since it's not, you know, the mechanism not completely apples to apples, you're inhibiting 2 different pathways with the bispecific. If 412 looks similar in terms of inhibition of TL1A pathway, how would you position it, I mean, in terms of 942? Thank you. Yeah. It's our data where we're gonna be looking for 412 to see what kind of half-life and target coverage it gives us in terms of durability and depth. That will obviously have an important role. With 942, you know, verifying our thesis of better drug exposure leads to better efficacy is a part of that thinking package. Remember, there's all of the work going on around the industry validating or potentially not validating TL1A in a range of other indications. Those pieces are all gonna come together in that 2027 timeframe and help us make decisions how to maximize the value of both assets. That's sort of the big picture. I don't know if there's anything to add to that? I mean, the technical point, Timur is in 2027 we'll have a coinciding of both the first in human healthy volunteer data for 412, as Bassil said, will give us PK/PD immunogenicity check on a novel bispecific platform and the drug properties of 412, which we're very excited about. Also we'll have that 12-week primary analysis set and induction data and ulcerative colitis from the XENITH-UC phase IIB study of 942. That will help us understand how to optimize both of those development pathways potentially in IBD or other areas. You look ahead, we're looking to rapidly move 412 if all goes well in the first human study into proof of concept Phase II studies in patients, and that data we hope will also coincide with the maintenance period readout of the XENITH-UC study, which will occur a little later after the primary analysis set. Those two data packages together will be really powerful in informing us on how to optimize both of these programs for a longer term success and registration enabling studies. Thank you very much. Our next question comes from Sean McCutcheon with Raymond James & Associates. You may now unmute your audio and ask your question. Hey, guys. Thanks for the question. On 412, can you maybe speak a bit more to the stoichiometric considerations for the bispecific versus combination of monospecifics and your conclusions from the preclinical data that drive confidence in translating this into humans? Maybe to be a bit coy, do you expect the dosing to be driven by the TL1A component? Thanks. Yeah. That's a good framing of the question. The beauty of bispecifics is that you don't have to address all the different ways you might dose a combination together. Now, some might flip that around and say, "Oh, I can't optimize the dose of the two different arms." A part of the reason why when you really look zoom out and look at why did Xencor pick this pair of targets as its first real autoimmune bispecific, you know, something that wasn't a T-cell engager, it's because the stoichiometry has been driven by the biology here. We have seen a very, very large amount of data in humans across a decade of the excellent safety record of IL-23p19 inhibition. In fact, better drug exposure, higher doses, you see this in post-marketing studies, higher doses give you potentially better efficacy as you get more exposure, but also the safety, the excellent safety track record seems to be maintained. Just this past weekend at DDW, I've seen a number of talks about that. You've got 1 drug class that's incredibly well-validated to be very safe where more drug seems to maintain that safety. With TL1A, certainly less data is out there. We've seen across the class now 3 different programs, different drug molecules, different antibodies with different designs also have just an outstanding track record of safety in all the reported data. We have an opportunity here to take 2 targets where we can just turn both knobs to 11, right? Maximize drug inhibition in the molecule and really truly take the best advantage of a bispecific approach and avoid having to do unnecessary dose ranging and combination, you know, sort of dose matrices. That was the basis of our design. Just push the limit on the affinity, which pushes the potency because these targets are validated to be very safe and more inhibition is believed to be better. I think that's a pretty universal belief. You know, I mean, I don't know, Vip and Mark, if you would agree with that thought. I see them nodding. Good. Yeah. When we look at the preclinical data, aside from the affinity, you know, sub-picomolar on the P19 side, about 1 picomolar on the TL1A side, you know, John and his team did just a remarkable job of design. The XenLock piece enabling that, as John said, when now you look into non-human primates for the other half of it, exposure is also about half-life. We see a 20-day half-life that essentially matches the half-life in non-human primates we saw for 942, which translated into an over 74-day human half-life. We're really optimistic that we're gonna get that kind of durability and coverage, hopefully the patient convenience. You know, the last piece of the puzzle when you think about actually making a practical drug, you've gotta actually make it. You've gotta make kilograms of it, put it in vials, ship it all around the world, and then have it be easily injected into patients in a sub-Q format. The XenLock format, you know, put on top of our long track record of X. Fc domains, bispecific Fc domains, we've been able to produce this, you know, in standard antibody manufacturing processes at scale. And we're delivering drug now to clinical sites in the next couple of months in a very high concentration formulation with yields that we're quite proud of. You know, all the pieces of a biophysical optimized molecule with the right underlying biological thesis that more is better for these 2 targets, I think really came together beautifully. It's the perfect first case for an autoimmune bispecific on the biology side. Our next question comes from Gregory Renza with Truist Securities. Please go ahead with your question. Great. Thanks for taking my question. In your preclinical benchmarking studies, you've shown that XmAb might be superior to first-generation TL1A. Just curious if you've done similar experiments with second generations, you know, like SpIs, Asians, or other assets, you know, out of China. How does it look compared to those? If I may tag along one more question, how do you view the potential commercial trade-off between your 12-week, you know, once every 12 weeks, versus maybe a more aggressive or less frequent dosing like Q12-week to Q24-week? You know, that your second-generation PS marketing. Thanks so much. Sipawat, the first maybe third of your question was inaudible. I'm sorry. Could you possibly repeat your whole question? I just wanna make sure we address it properly. We really couldn't hear about the first one third. Sorry about that. Okay. Basically I'm just curious if you've done any preclinical benchmarking for XmAb942 to the second generation TL1A. I mean, it looks better than first generation, just curious how it compares to, you know, the second generations TL1A agents. Yep. I see. A benchmark XmAb942 versus other second-gen agents. Well, I mean, we're aware of some data from peer program on initial half-life disclosures that look promising based on using long half-life Fc domains. I don't know that we've seen from any second generation TL1As any immunogenicity disclosure from human data. I do believe that from published preclinical data, XmAb942 has the highest affinity, and that should translate quite directly to higher potency, again, based on preclinical data of inhibition of the target TL1A on human cells. You know, I don't know that we've seen any other details of early clinical characterization of other second-gen TL1As in any kind of thorough way. Obviously, we await further data. We know it's a very active class. We feel very confident about our positioning and the, you know, very thorough job we did maximizing and making best in class potency and half-life for the program, as well as a very robust phase II design. I think there's a philosophy component here. Xencor sat down to make something that could solve a clear clinical problem and unmet need in inflammatory bowel disease. We really like the TL1A target from emergent data three years ago. As world-class protein engineers with a protein engineering platform that's been validated many times over, we had our heart and our passion to make these molecules as good as they possibly could be. I think it's hard for third-parties or third-party protein engineering platforms to have that same commitment and dedication when they're making molecules for other people to develop that they'll never have a part in the clinical development. Our research team walks hand in hand with our clinical development team on a daily basis to design the best molecules and solve the clinical problems. We feel confident that the molecules we make across the entire spectrum of our portfolio are best-in-class designed and delivered medicines at the end of the day. The other component of this is of the second-gen class, we're ahead of everyone else by a long shot in the development pathway to market. That's why we engaged a phase IIb study right out of the gate from a first-in-human healthy volunteer study and have executed that relentlessly. We started in clinic first-in-human in November 2024 with XmAb942. Less than a year later, we were in a global phase IIb study. We're on track 2 years from that point to deliver a phase IIb study results that will be registration enabling in the traditional efficient pathway of biologic drug development. We feel very good in our market position of delivering the best in class and best in market biologic targeting TL1A. Thank you so much. Our next question comes from Madeline Stone with William Blair. Please go ahead with your question. Great. This is Madeline on for Matthew Phipps. Thanks for taking our question. One on XmAb942 or on XmAb412, actually, could you maybe discuss a bit more on how confident you are that XmAb412 will not lead to an immune complex formation that could drive autoantibody response? Thank you. Yeah. What we're very confident of is that the very well sort of, you know, understood and accepted possibility of a trimeric ligand like TL1A or other members of the TNF superfamily, like how a trimeric ligand when you bind it with a bivalent antibody like your standard Y-shaped antibody, that's gonna create this ability to easily form these clusters, right? Where you have TL1A trimer one binding on the left side of the antibody, TL1A trimer two binding on the right side. Meanwhile, TL1A trimer one has another antibody in its other side. Trimer two has yet another antibody in its other side, and you get these big clusters like we had that picture of. It's simply not possible for these multimolecular clusters to form when you only have one TL1A binding equivalent on your antibody drug. Obviously, you have to make sure your antibody drug is stable and soluble, in itself is not prone to aggregation, right? If it is aggregating itself, then you can have these artifacts emerge. We always strive to make the most stable and soluble antibodies. It's just like the bedrock biophysical underpinning of all of our design work, which I think we've amply demonstrated over the decades. You will never completely eliminate the ability of the immune system to surveil anything you put into the human body. That's just a predicate, right? You put a drug into the human body, it will notice. We believe we've done is greatly, significantly reduced the ease of that recognition by the immune system relative to what happens when you have bivalent molecules against a trimeric ligand. That's the essence of that one design choice that we hope skews the probabilities in the favor of X. Our next question comes from Eva Fortea-Verdejo with Wells Fargo Securities. Please go ahead with your question. Hi, good morning. Thanks for taking our question. A quick one from us. Are you considering other potential mechanisms to combine with 942 beyond your TL1A IL-23 bispecific strategy? Thanks. You know, that's a great question about how the future might unfold. There are certainly a lot of other mechanisms that we can imagine combining XmAb942 with as the development of the molecule advances, as we establish our dose, our dose efficacy relationship as we hope to do in XENITH-UC and push the program forward. There are certainly other bispecifics we have in our preclinical development and as well as on the design table for a variety of targets using this new XenLock format that lets us get these really high affinities into simple, simply engineered and produced molecules. You know, I think our current focus is establishing the efficacy response relationships, hopefully pushing that ceiling of efficacy higher, and then establishing how XmAb412 fits against XmAb942. I think there's just so much uncertainty about how that future's gonna unfold, we're just gonna wait and see. I don't know if there's anything more concrete we can add on that. I think from a market research perspective, it goes back to the point we made in the presentation. We believe TL1A is going to be the branded anchor of biologic monotherapy and combination therapy in the future, which is a good thing for our portfolio and retains a lot of utility for the monospecific in development, even though we're also taking this very targeted shot with X. We believe we've done is greatly, significantly reduced the ease of that recognition by the immune system relative to what happens when you have bivalent molecules against a trimeric ligand. That's the essence of that one design choice that we hope skews the probabilities in the favor of XmAb412. We believe we've done is greatly, significantly reduced the ease of that recognition by the immune system relative to what happens when you have bivalent molecules against a trimeric ligand. That's the essence of that one design choice that we hope skews the probabilities in the favor of XmAb412. Our next question comes from Eva Fortea-Verdejo with Wells Fargo Securities. Please go ahead with your question. Our next question comes from Eva Fortea-Verdejo with Wells Fargo Securities. Please go ahead with your question. Hi, good morning. Thanks for taking our question. A quick one from us. Are you considering other potential mechanisms to combine with XmAb942 beyond your TL1A IL-23 bispecific strategy? Thanks. morning. Thanks for taking our question. A quick one from us. Are you considering other potential mechanisms to combine with XmAb942 beyond your TL1A IL-23 bispecific strategy? Thanks. morning. Thanks for taking our question. A quick one from us. Are you considering other potential mechanisms to combine with XmAb942 beyond your TL1A IL-23 bispecific strategy? Thanks. morning. Thanks for taking our question. A quick one from us. Are you considering other potential mechanisms to combine with XmAb942 beyond your TL1A IL-23 bispecific strategy? Thanks. morning. Thanks for taking our question. A quick one from us. Are you considering other potential mechanisms to combine with XmAb942 beyond your TL1A IL-23 bispecific strategy? Thanks. You know, that's a great question about how the future might unfold. There are certainly a lot of other mechanisms that we can imagine combining XmAb942 with as the development of the molecule advances, as we establish our dose, our dose efficacy relationship as we hope to do in XENITH-UC, and push the program forward. There are certainly other bispecifics we have in our preclinical development and as well as on the design table for a variety of targets using this new XenLock format that lets us get these really high affinities into simple, simply engineered and produced molecules. You know, I think our current focus is establishing the efficacy response relationships, hopefully pushing that ceiling of efficacy higher, and then establishing how XmAb412 fits against XmAb942. You know, that's a great question about how the future might unfold. There are certainly a lot of other mechanisms that we can imagine combining XmAb942 with as the development of the molecule advances, as we establish our dose, our dose efficacy relationship as we hope to do in XENITH-UC, and push the program forward. There are certainly other bispecifics we have in our preclinical development and as well as on the design table for a variety of targets using this new XenLock format that lets us get these really high affinities into simple, simply engineered and produced molecules. You know, I think our current focus is establishing the efficacy response relationships, hopefully pushing that ceiling of efficacy higher, and then establishing how XmAb412 fits against XmAb942. You know, that's a great question about how the future might unfold. There are certainly a lot of other mechanisms that we can imagine combining XmAb942 with as the development of the molecule advances, as we establish our dose, our dose efficacy relationship as we hope to do in XENITH-UC, and push the program forward. There are certainly other bispecifics we have in our preclinical development and as well as on the design table for a variety of targets using this new XenLock format that lets us get these really high affinities into simple, simply engineered and produced molecules. You know, I think our current focus is establishing the efficacy response relationships, hopefully pushing that ceiling of efficacy higher, and then establishing how XmAb412 fits against XmAb942. You know, that's a great question about how the future might unfold. There are certainly a lot of other mechanisms that we can imagine combining XmAb942 with as the development of the molecule advances, as we establish our dose, our dose efficacy relationship as we hope to do in XENITH-UC, and push the program forward. There are certainly other bispecifics we have in our preclinical development and as well as on the design table for a variety of targets using this new XenLock format that lets us get these really high affinities into simple, simply engineered and produced molecules. You know, I think our current focus is establishing the efficacy response relationships, hopefully pushing that ceiling of efficacy higher, and then establishing how XmAb412 fits against XmAb942. I think there's just so much uncertainty about how that future's gonna unfold, we're just gonna wait and see. I don't know if there's anything more concrete we can add on that. I think there's just so much uncertainty about how that future's gonna unfold, we're just gonna wait and see. I don't know if there's anything more concrete we can add on that. I think from a market research perspective, it goes back to the point we made in the presentation. We believe TL1A is going to be the branded anchor of biologic monotherapy and combination therapy in the future, which I think from a market research perspective, it goes back to the point we made in the presentation. We believe TL1A is going to be the branded anchor of biologic monotherapy and combination therapy in the future, which is a good thing for our portfolio and retains a lot of utility for the monospecific in development, even though we're also taking this very targeted shot with XmAb412 on TL1A and IL-23p19 biology. That said, we also don't really envision a future where combining two biosimilar targets together in a co-formulated approach is going to be necessarily viable as I think for the benefit of the payers, the system, the patients and their caregivers, as is today already used, you can take two biosimilar targets of different mechanisms off the shelf and provide them to your patients in the clinic. It would be kind of a hard argument to make why someone would pay a branded price that's more expensive than the individual components for their patients. We feel very good about TL1A being the right anchor to your question and fully agree that, you know, there will be different targets to engage with it as data continues to evolve in the clinical setting. Got it. Thanks. Our last question comes from Alec Stranahan with BofA Securities. Please go ahead with your question. Hey, guys. This is Matthew on for Alec. Appreciate you taking our question. On ADAs for XmAb942, the poster pointed to a 57% incidence. Can you maybe speak to the kinetics where you saw decreasing incidence and magnitude with increased drug exposure? Is this driven by, you know, small n baseline variability, or is there something, you know, different hypothesis going on? For XENITH-UC, you noted the target dose is at 25%, I guess. Is that just based on dose selection, or were there other changes to the trial design or patient characteristics? Thanks. I'll take the first one on ADAs. You know, this was a healthy volunteer study with an N of 6 per cohort. We did 8 different cohorts, so you can sort of, you know, IV, sub-Q, and we did MAD cohorts. At the 3 different dose levels tested, both SAD, IV, sub-Q, and MAD, it was a very consistent pattern of as you gave more drug, the magnitude of your ADA signal and the frequency of positivity went down. I think the consistency across IV, sub-Q, SAD, MAD makes it very clear that's a real signal, and it's frankly utterly unsurprising given that that is a very common, almost the dominant pattern seen in biologic drugs, particularly monoclonal antibody therapeutics in humans. The more drug you give, the more you sort of swamp out an immune response and tolerize. That we're very confident of. You know, we're very pleased that we saw a overall ADA rate, you know, I think it was 57%. That's lower than reported from two of the leading first generation TL1As, our NAB rate was as well significantly lower than the ones that have reported, so we're happy with that. Furthermore, when we look at our high dose, go-forward dose for XENITH-UC, so the highest induction dose and our selected maintenance dose, it had an even lower ADA rate of 25%. We think we're very well positioned with a very favorable profile relative to everything that's been reported by other people in their phase I. That speaks to the quality of the design of the molecule, because the underlying biophysical stability of your molecule is always the first thing that your body's immune surveillance has to, you know, first immune surveillance sees. So maybe on the second question, I know, Dane Leone, you were saying you wanted to touch on that? Sure, yeah. I'm obviously looking forward to seeing you guys at the BofA Securities Healthcare Conference next week, first and foremost. To your actual question, immunogenicity was one of the key things that we aimed to solve for from an engineering perspective when we were looking at the liabilities of the first generation TL1As. As Bassil said, you know, our focus on stability, epitope selection, and overall kind of design one would say of the molecule, I think has proven out to be best-in-class immunogenicity. The question from you and many others has been, can you make a molecular target of TL1A in a biologic have acceptable immunogenicity rates that we can feel confident are not gonna be deleterious to efficacy, as is the concern with some of the first gen TL1A molecules. We think we did it, right? To the point of an overall rate of 57%, which is lower than the 65% reported for tulisokibart and the 98% reported for afimkibart, you know, it we don't have that liability. Kinda driving to the point of the dose selection and dose regimen that we're actually using in the XENITH-UC Phase IIb study, we're using a obviously a high dose induction IV along with a single subcutaneous maintenance dose. That dosing regimen has 0% neutralizing antibodies and only a 25% ADA rate. We feel very confident of the drug exposure that we're going to get in XENITH-UC not being impacted by immunogenicity, and again, very clearly able for us to elucidate whether best-in-class drug exposure will drive best-in-class clinical efficacy. Helpful. Thank you. We have no further questions at this time. I will now turn the call back over to Bassil Dahiyat for closing remarks. Thanks very much. We'd really like to thank everybody who's joined us on this call. We're very excited by what's coming next for our TL1A programs. We're really looking forward to updating you as we advance XmAb412, our bispecific, into first in humans later this year, as we read out data from XmAb942 in 2027. We're also looking forward to initiating phase II studies with XmAb412 in 2027. A very busy year upcoming for us. Thank you again. Look forward to speaking soon. This concludes today's webcast. You may now disconnect.