Xencor at Cantor Conference: Strategic Advances in Immunology

On Thursday, 04 September 2025, Xencor Inc. (NASDAQ:XNCR) took the stage at the Cantor Global Healthcare Conference 2025, outlining its strategic progression in the field of immunology. The company emphasized its advancements in bispecific T cell engagers and TL1A assets, while also acknowledging the challenges in clinical data generation and drug modeling.

Key Takeaways

• Xencor is advancing its XmAb819 program targeting ENPP3 in renal cell carcinoma, with upcoming data presentation in October.
• The company is leveraging its XmAb Protein Engineering Platform to develop innovative molecules for severe diseases.
• Xencor’s TL1A program includes XmAb942 for ulcerative colitis, with a bispecific antibody entering trials in 2026.
• Quantitative systems pharmacology models are being used to optimize drug design and predict tissue exposure.
• The company is exploring B cell depletion strategies to potentially reset the immune system in autoimmune diseases.

ENPP3 T-cell Engager (XmAb819) Program Update

• ENPP3 Target: Highly expressed in renal cell carcinoma, even after prior PD-1 and VEGF TKI treatments.
• Molecule Design: Utilizes a 2+1 bispecific design to differentiate between tumor and healthy cells.
• Clinical Data: Initial dose escalation data will be presented at the AACR NCI EORTC meeting in October.
• Market Potential: Successful drugs in this area have the potential to become billion-dollar products.

TL1A Program Update

• XmAb942: A potent antibody in a Phase 2b study for ulcerative colitis.
• Bispecific TL1A: Targets both TL1A and IL-23, with Phase 1 trials planned for 2026.
• Exposure-Response: Aims for improved outcomes by enhancing drug exposure in the gut.

B Cell Depletion Strategy

• Reset Hypothesis: Potential for deep B cell depletion to reset the immune system in autoimmune diseases.
• Development: Creating agents for deeper tissue depletion compared to existing treatments like Rituxan.

Strategic Outlook

• Continued Innovation: Focused on leveraging protein engineering for novel therapeutic modalities.
• Clinical Focus: Prioritizing the advancement of clinical programs and data generation.

Q&A Highlights

• ENPP3 Expression: Remains high in tumor samples post multiple therapies.
• TL1A Indications: Exploring beyond ulcerative colitis to include Crohn’s disease and fibrotic diseases.
• Dosing Strategy: High blood exposure from XmAb942 aims for effective gut inhibition.

For more detailed insights, please refer to the full transcript below.

Full transcript - Cantor Global Healthcare Conference 2025:

Steve Seedhouse, Biotech Analyst, Canthar: Good morning. Welcome everyone to day two of the Cantor Global Healthcare Conference. It’s a privilege to, welcome next, participating company, Zencore, and I’m joined by CEO, Basil Dahiat and EVP and CSO, Dane Leone. Thanks everyone in the room and on the webcast, for joining us. I’m Steve Seedhouse, biotech analyst with Canthar.

Maybe to start, we’d love to invite perhaps you, Basil, just to give an introduction to current state of affairs at Zegvoir. Busy time at the company, obviously, really interesting strategic evolution as well, advancing into some immunology indications. How has that been going? How has that message been resonating? And I would love to get an update to start and we’ll dive into Q and A.

Basil Dahiat, CEO, Zencore: Yeah, I’ll take a step back. We’ve always been a company that strives to or clinical stage company that strives to build drugs that we can advance in severe diseases using the platform we created, our XmAb Protein Engineering Platform over the couple of decades to create differentiated molecules that can address real unmet needs for patients. We’ve used that across different therapeutic areas with partners for many years and we have more recently added specific indications against targets we thought our tool kit could really make a difference for in autoimmune disease to build off of the the long standing core we’ve had in oncology. You know, our specialty is creating molecules where the structure is going to make something new happen, whether it’s our bispecific antibody t cell engagers for cancer or tuned for autoimmune disease use to deplete pathogenic b cells or whether it’s optimized monoclonal antibodies with extremely long half life and high potency for autoimmune diseases or novel structures that use bispecific tools to make, to create multiple inhibition of of targets in autoimmune disease. So you could see the threat is always build molecules we can advance to the clinic and get to key inflection points using this protein engineering.

So it’s all kind of a unified theme. It’s just where we lean in at any given time. And I think the message has been resonating quite well because people really want to hear about something where the drug can position itself in its own competitive landscape with unique differentiators.

Steve Seedhouse, Biotech Analyst, Canthar: Okay. And just on, I mean, the bispecific T cell engager side, obviously, I think this is one of the more near term upcoming catalysts for the company, which is eight nineteen, the ENPP3 T cell engager and clear cell renal cell carcinoma. I think you’ve guided for an update before the end of the year, perhaps at a medical meeting. Maybe you can just recap that program timeline and expectations for that initial data.

Basil Dahiat, CEO, Zencore: Sure. Maybe I’ll introduce the design of the molecule, where we’ve gotten so far clinically and then, you know, I know Dane always has some good comments on how that positions in the in the landscape. So the program is XmAb819. It targets a molecule called ENPP3, which is very, very surface protein that’s expressed very, very brightly on renal cell carcinoma. It’s expressed in a smaller proportion of patients, but also very strongly in other forms of not just clear cell carcinoma but papillary as well as a variety of other solid tumors.

We built a bispecific molecule that engages that side, the tumor target side with high avidity. So that is the actual binding affinity if you measure it, it’s modest. Right? But we built the structure using our XmAb tools to create two binding domains molecule, to the eMPP3 side, so that the low binding affinity of any one of those domains won’t really stick when there’s not a lot of target around, like when you’re on a healthy cell and there’s not a lot of handholds for that domain to grab, not a lot of eMPP3s to grab. When there’s a high density on a tumor cell, you’ve got both domains that are able to engage multiple copies of that target and that high expression of the tumor cell drives binding.

And then when you’ve got that happening, that then triggers the other side of the molecule, the T cell engager side, the CD3, to bind on a T cell in a way that agonizes it and turns on its cytotoxic function. It jumps perforins and granzymes, blows apart the target cell and it just creates a general immune uplift to keep going. And so that’s the design of the molecule. That came out of an effort to look for targets that had that property of high on tumor, low on healthy tissue because we believed we built a tool, our XmAb2 plus one design with those two domains against the tumor and one against the T cell. That two plus one design lets us exploit that difference in target density.

So when you have new tools like these XmAb2 plus one bispecifics, you can go after biologies that have been left behind. And we were the first ENPP three t cell engager in the clinic. I I believe there’s only one other program we’re aware of actively in the clinic, at our both competitor and partner Janssen or J and J biology now, I guess they call themselves. And we’ve we guided data for the program from our dose escalation cohorts this this fourth quarter. And in fact, we’ll say today that we’re gonna be presenting a poster at the triple meeting, the AACR NCI EORTC triple meeting in Boston in October.

So we’ll have that poster, we’ll be able to present data on the dose escalation to date and in particular the initial part of the dose escalation that we’ve gotten to in the target range of doses for the molecule. So I know the positioning of it and people always ask us, So tell us about why RCC and what matters there? You know, maybe you can jump in on that, Dane.

Dane Leone, EVP and CSO, Zencore: Sure. Happy to. Yeah. No. Very excited to get some preliminary data from the dose escalation phase and and, you know, kind of demonstrate why we believe in the program and and the advancement of 08/19 as monotherapy and and kind of the development pathway going forward.

So, advanced clear cell renal cell carcinoma is complicated from a clinical perspective. You ask a treating oncologist what they use for first line and second line therapy and invariably you get different answers. What kind of remains true though is in the frontline setting, generally you’re going to get a PD-one either pembrolizumab or nivolumab and that’s usually either plus or minus a VEGF TKI of kind of the clinician’s choice and comfort and maybe less so in contemporary times, still but we do see ipilimumab as a combination therapy. What’s different about this is you’re not seeing frontline chemo. Chemo is not effective in clear cell renal cell carcinoma, so you’re immediately going to kind of advanced targeted therapy.

Thereafter, the first line becomes a complicated question because there’s really a lack of modalities or differentiated modalities available to the clinicians and their patients. Usually, you’re re challenging with a VEGF TKI increasingly cabozantinib. And you do not re challenge with a PD-one as over multiple studies, it’s just been proven that there’s no efficacy and it’s not beneficial to the patient. And, you know, unfortunately, invariably, patients progress past the second line and then you’re thinking about the third line and what the salvage line is. The good news for the clinical community patients is belzutafan does have a differentiated mechanism of action, has been approved as experiencing rapid uptake as a different type of targeted therapy targeting HIF two alpha.

And that is, you know, definitely an advancement and probably starts, you know, what we would say is a contemporary benchmark for monotherapy development in this space. So, in the phase one dose escalation of belzutafan and clear cell renal cell carcinoma that was, you know, a largely heavily appreciated patient population where they had seen a prior PD one and a prior VEGF TKI. They had about a twenty five percent response rate, which is great for the indication but obviously still a little low. And that was fairly stable and and translated into the pivotal study where it was about a twenty two percent overall response rate. Good m d o r, but on PFS, obviously, did not really move the needle a lot.

So we’re about a five point six month median PFS in their pivotal light SPARC O5 study, which was the same point estimate for Avril Lemus, which is, you know, the the de facto standard of care still salvage line therapy that I think the clinical community is trying to move beyond for a number of reasons. But, yeah, it’s it’s it’s been a very tricky setting. Response rates are generally low for these patients that are heavily pretreated, and the PFS range for these salvage line patients haven’t hasn’t really moved out of that five to six month range. So, you know, with all that said, I caveat, obviously, we’re doing preliminary look at dose escalation while dose escalation remains ongoing, and we look forward to moving towards expansion phase and thereafter. So we’ll be focused on initial anti tumor activity, as Basil said, to those first couple cohorts that are target dose range and be looking at, obviously, things like MDOR for those patients that had clinical response.

So I think it’ll be good to get out there. We’ll present obviously a full characterization of the data to date, which will include the safety and and how we’re thinking about the algorithm, which I guess we haven’t touched on yet, but is a unique feature of the t cell engagers where you’re managing through CRS and and kind of those first several weeks to get that patient to target dose while trying to do everything you can to maximize the drug exposure because, obviously, these patients are rapidly progressing and you need as much drug exposure on board to attenuate that disease progression. So, really looking forward to having that first data in October and, yeah, the outlook for, 08/19 is, I think, very exciting, in clear cell renal cell carcinoma and we’ve seen, you know, the drugs that make it become billion dollar drugs and I think that substantiates the reason that we’re going put so much time and effort into the development.

Steve Seedhouse, Biotech Analyst, Canthar: Great preview. Just a follow-up on that programming. ENPP3, do we know you talked about the different lines of therapy in clear cell renal cell, do we know about the expression of that antigen and if that differs with refractory status or exposure to any of the PD-1s or VEGFs, etcetera?

Basil Dahiat, CEO, Zencore: Doctor. So we’re treating patients in a later line. These are phase one multiple they’ve all had VEGF TK. They’ve all had PD-one, sometimes multiple times. And we see uniformly high expression of ENPP3 in the tumor samples we’ve taken from our patients.

So we feel pretty good that the initial characterization of ENPP3 and where it’s expressed in disease carries through all the modern lines of therapy. Maybe

Steve Seedhouse, Biotech Analyst, Canthar: we can put a pin in that and discuss some of the other programs. Obviously, a lot going on in TENCORE. I want to make sure we cover as much ground as possible. I mean, the introduction of the TL1A assets into the portfolio, obviously, that’s a very intriguing target. There’s some very promising data and there’s been a lot of strategic activity in that space also.

Maybe you could just talk about that opportunity set you see for TL1A and where you anticipate over the next three to five years ultimately honing your focus for that asset because it can be IBD, but it can be a lot more also.

Basil Dahiat, CEO, Zencore: We saw in TL1A a target that was sort of the perfect kind of one for us to go after to try to make a best in class molecule with our protein engineering tools. Just seen exciting phase two data from a couple of programs showing in in really hard to treat IBD, potential best in disease efficacy, But they’re just exiting phase two. And they’re molecules with clear liabilities, whether modest potency, need for multiple dosing frequencies, unclear dose response relationship or potential for immunogenicity. And yet, we still had years to go before any drug was launched. So now is the time to jump It’s hard to make a bio better against something that’s already been on the market five years.

So was a great timing for us. So we took an incredibly well validated toolkit of ours, our ability to make high potency antibodies and our ability to make long half life antibodies with our Fc engineering to get, extended half life, you know, multiple marketed products that that have used that technology from us in many, many, clinical programs that had partners or academic collaborators. And so we built XmAb nine four two. And then we do see a potential broad indication space there. We’re focused on the highly validated ulcerative colitis.

We’re starting this quarter our phase 2b dose, multiple dose, randomized study, in ulcerative colitis, which we’ve talked about. It’s called Zenith UC. And we’ll be hoping hopefully following up in other indications that we’ll announce as we we go forward. Crohn’s disease is an obvious one, but we’re looking at a at a at a of them because this could be your your sort of classic product in a pipeline. You know, and how that plays out and and and how we think about the next agent.

Right. Target t l one a and use our tools. You know, that’s when you go to the bispecific approach in autoimmune disease, which is nascent, but is it gonna be be be a very, very important class. And, you know, Dane, why don’t you you touch on some of the the drivers for what brought us to wanting to make a bispecific with t l one a binding as an anchor and, you know, some of the interesting studies that are coming up soon from big pharma.

Dane Leone, EVP and CSO, Zencore: Yeah. No. Happy to. Yeah. It’s it’s the the t l one a pipeline that that we are developing has, you know, breadth of opportunity to your point, Steve, on the t l n a monospecific.

And, obviously, the the big question for the class is, is there really an anti fibrotic component to to targeting t l one a? And I I think there’s good supportive science to that theory, and now we’re just starting to, I I think, test that out in the clinic in in early stage in in some of our peer studies. We’re obviously very interested in in that angle as well and are evaluating different opportunity sets to explore that while we push ahead in in ulcerative colitis. And I I think in in ulcerative colitis, for a quick moment, provides a unique opportunity, as Basil mentioned, to get fast to market after maybe a first in class that has some liabilities and test our thesis where better drug exposure will lead to better clinical outcomes for patients. We’ve had good validation of that with recent clinical publications, especially from the Pfizer Tuscany two b study supporting that thesis.

And I think our phase two b is designed well to explore that that possibility. I think later this year, we’ll provide more timelines around the phase two b study as we’re going through the global rollout right now and are very excited to to, you know, figure out how to bring that data forward and and share it as fast as possible as that study is going on. But with regards to the bispecific, which will be first in human in 2026, this is kind of the killer app in certain indications where IL twenty three has has been validated as a bona fide, you know, best in disease, as Basil said, target. And that goes, you know, not just in IBD but in some other disease areas as well. And the biology of t l one a seems to match that as potentially synergistic or potentially orthogonal to some degree in those different disease areas.

And what we liked about putting both those targets in in a bispecific is they both have very individually safe profiles in the clinic, meaning you have a lot of play with the dose intensity and exposure that you can give to patients, which is a lot different than some of the other biologic targets in including the TNF glass, for example. So we felt our engineers felt that we could fix the stoichiometry, dial in the monovalent potency to be equipotent to the parental bis monospecifics that we were looking at for each of the targets and that could be something that could be developed like a monospecific drug very effectively through regulatory development and CMC into commercial, that would just be truly differentiated. And, you know, Basil brought up some of the kind of peer studies that that will likely read out this year. So, obviously, everyone’s waited with beta breath on the J and J DUET study, which is a combination of a TNF and an IL 23 in IBD. And, you know, I think there’s there’s probably read through more to the companies that are doing kind of one one, you know, mono specific combinations or co formulation approaches.

But I think nonetheless, seeing if there is true synergy or kind of a one plus one equals two or a one plus one equals three type outcome for patients with a TNF in IL 23 is still a good experiment. We just view TL one a as a superior target and obviously, you know, maybe differentiate from the bispecific that’s in the clinic targeting IL 23. We’re going after p 19 versus p 40 and p 19 as a subunit of IL 23 in head to head studies has outperformed p 40. So we’re really happy with our construct and I’ll, you know, all focus on getting this first in human study up and started next year.

Steve Seedhouse, Biotech Analyst, Canthar: And we’ve certainly seen mentioned not only orthogonal, but maybe there’s there’s actually synergy to these mechanisms. I mean, we’ve seen some of that literature too. So that’s gonna be, I think, at the level of IL 17 signal, which is going be fascinating to see how that plays out. This is bispecific, just to talk for a moment. Does that everyone’s okay here?

Basil Dahiat, CEO, Zencore: Dropped my mic. Sorry.

Steve Seedhouse, Biotech Analyst, Canthar: Does the bispecific have a role outside of IBD in psoriasis or psoriatic arthritis or RA? Or does anything stand out as maybe interesting to pursue that?

Basil Dahiat, CEO, Zencore: For the bispecific?

Steve Seedhouse, Biotech Analyst, Canthar: For the bispecific, yes.

Basil Dahiat, CEO, Zencore: I think we’ve seen good validation for IL twenty three in in various skin diseases. Right? And so that’s a potential direction to take. I think, rheumatology, you know, has some opportunities. I think I think right now we’ve got a bunch of data sets coming from big pharma that we’re gonna look at across a different range of TL1A indications.

We’ve got the the IL-twenty three. I think for starters, there’s a lot of wood to chop in IBD, though.

Steve Seedhouse, Biotech Analyst, Canthar: Maybe back to the September then, this is the long acting TL1A. I mean, it’s if you think about sort of some of the analogs or what we can draw, you know, inspiration from or learning from precedence in immunology made, we’re still this month coming up on, like, you know, the third or fourth iteration of IL-seventeen data. Like, it just seems very clearly the first movers in any of these spaces, TL1A included, not going to be optimized to antibodies and you touched on that. And so we could stipulate to the fact that they could be improved on, I I think.

Basil Dahiat, CEO, Zencore: Absolutely. Absolutely. Not only that, that these are diseases where there’s cycling therapies. I think the earliest story I can think of is going from Remicade to Humira. Right?

Lower immunogenicity, easier to use, sub q format, you know, easy dosing, and yet we still had two or three TNF alpha, antibodies coming after that that were quite successful that found particular indications to focus on that had been left behind or offered a different, say, dosing schedule that would more convenient. From Zencor’s own technology portfolio, Ultomiris, the anti C5 antibody to go every two month dosing versus every two week dosing for Soliris, its parent anti C5 antibody that’s at AZ Alexion. There’s absolutely room to improve these things to give patients better options. We’re seeing in HAE now a trend towards, you know, longer acting agents. Instead of every two weeks, you’ve got whether it’s RNA or whether it’s long acting antibodies.

There’s loads of of analogs, I think, for making better ones where in particular where there’s large indications with waxing and waning diseases and multiple opportunities in different indications across the immune space. We think the opportunity is still enormous for these molecules.

Steve Seedhouse, Biotech Analyst, Canthar: Just on some of the specific data you’ve presented, mean, but the how should we think about bioavailability in the gut versus in circulation where clearly there’s pretty profound half life for nine forty two? I mean, there a way to model this accurately or is

Basil Dahiat, CEO, Zencore: Yeah. Well, we we we again, caveats always that that the data that you’re using for the models is always not as much as you would like. We’ve been very very aggressive at at adopting and using quantitative systems pharmacology models over the last decade to to actually understand better how to even design our molecules. The complexity of bispecific antibodies when you have different targets, and I’m talking about like on this on the t cell engager CD three side, different targets with different recycling times with different densities and different tissues really can be a challenge for understanding how do I make a molecule that’s gonna act and and be present in the right compartment long enough. And, you know, we’ve had success now, our partner Amgen with zaloritamab in phase three, there was a lot of thought on how we built that molecule, that’s the STEP-one CD3.

Same approach we took for the TL1A antibody design, we know we’re going to get long acting molecules in the blood with our XTend Fc domain for long half life. How does that transfer over into the gut where you’re have partial transfer? There is some data on that that you can model from animal models. Very high antigen load in the gut, very leaky, you’re losing your drug. And so we took the approach of you really have to get very high exposures in the blood.

And we did model it, we presented the data that our design metric was we want to have 99% inhibition of TL1A in the target compartment in the gut based on our QSP model for the dosing regimen we came up with. And so with such a long acting molecule, seventy one plus day half life was I believe the latest number that we’re, you know, as as the data continues to mature, we we we hope to to present, you know, you know, a more refined data. But that that long long half life gives us that 99% inhibition for an every three month dosing regimen in maintenance phase. And so we we we use those tools to really guide us and I think we’ve got something that should be really really attractive in XmAb942.

Dane Leone, EVP and CSO, Zencore: I’ll give you the counterpoint to the the the modeling, right? I I mean, obviously, peers that have developed an IBD are are rational in terms of how they dose and design their clinical algorithms. And yet over the past, you know, twelve to eighteen months, we’ve seen time and time again that for whatever reason you you have, you know, this this patient set that come out of induction period have not responded, you re induce them or do you give them an extended induction and roughly you’re getting a fifty percent response rate. That tells you that almost invariably the modeling is wrong in terms of the drug exposure that these patients need to have. And that goes all the way back to, I think, our first comments of our design thesis that we knew there was exposure response that did not align with dose response and that’s kind of the why of that is because modeling the soluble t l one a engagement and knockdown in the gut compartment is complicated.

It’s a complicated model. And so that’s our hope. I mean, in a nutshell, that’s our hope is that we can deliver outcomes in an induction period that look more like induction plus reinduction for, these first gens. And and we obviously even saw that with the t l one a class, I think, in the Artemis UC study where they did re induce patients that did not respond to that induction period and I think got somewhere around a fifty percent response rate. Saw it with the Lucent study as well with mirikizumab.

Steve Seedhouse, Biotech Analyst, Canthar: As you think about those precedent data sets in IBD as well for the TL1As, I mean, is there anything obviously, you have the molecular advantages, we think. Is there anything from a purely trial design standpoint? I mean, there were some patient selection, you know, sort of approaches that you can learn from those and that you can optimize or is it going to be pretty straightforward?

Basil Dahiat, CEO, Zencore: I think that there’s a sort of reality of how you’re gonna enroll these studies where you’re gonna have to go across many many different countries, many many different sites. You always want quality sites And you wanna have a patient mix that’s going to give you a a sort of representative mix. So prior advanced biologics, you know, you wanna have the right range. You don’t wanna skew one way or the other, it could throw off your powering assumptions. This is just about quality trial approach.

I think the place that we really did a lot of work was on the dose regimen to have, we believe we have a very well tolerated agent, a high intensity induction regimen, right, followed by that high exposure, long half life maintenance phase to give us the right mix.

Steve Seedhouse, Biotech Analyst, Canthar: Maybe in the last few minutes I wanted to get your perspective also on B cell depletion, B cell depleting antibody programs in autoimmune disease. I mean, in general, you know, there’s been some fascinating and inspiring data from CAR T in this space. But, you know, from a therapeutic index standpoint, who knows for some of these diseases. But from an efficacy standpoint, I mean, do you think you can get deep enough depletion to really achieve sort of like the immune system reset and a durable cure with a depleting antibody as you can seemingly get with a cell therapy?

Basil Dahiat, CEO, Zencore: Well, I think it’s not We we don’t have a good understanding of that even for the cell therapies. Are we truly getting immune resets? There’s anecdote there, right? There’s not large data sets. I think the promise is there which is why we’re chasing after it.

I I think beyond just the therapeutic index issues around cell therapies, just the simple logistical challenges of getting a a rheumatic disease patient or a a neurology patient to undergo the difficult preconditioning regimens, the hospitalization, the multiple sort of weeks of running around to get the therapy versus a relatively straightforward drug. What do they always call it? They call it therapy in a bottle, right? Which is like every therapy we’ve ever heard of for the last one hundred and fifty years of the therapy in a bottle. The world does not revolve around cell therapies.

But I think analog we have is from oncology where you have complete response rates for CD20, CD3 antibodies that rival the CAR Ts once you actually look at the CAR T therapies on a level playing field with true intent to treat, counting the denominator properly, looking at relevant lines of therapy. So I think we have precedent for these kinds of truly truly deep and durable effects from oncology. I I think the anecdote patients who are in long term remission is something that we do believe deserves real follow-up with agents that can deplete B cells, much more deeply in the tissues than the tried and true Rituxan. Though I will say there are anecdote, rare but anecdote of Rituxan, one induction regimen and a patient’s done forever. So clearly there’s something real about this B cell reset hypothesis.

We just need good drugs, once you get beyond the cell therapy hype cycle, drugs to actually address the need to have deep B cell depletion in tolerable and practical regimen.

Steve Seedhouse, Biotech Analyst, Canthar: Just to close in the last minute, I wanted to widen the aperture a little bit and we’ve talked about, obviously, the breadth of development that you have going on. And historically, you’ve been prolific developing novel antibodies. I mean, do you have, as you sit here today and you forecast the outlook for ZENCORE over the next, call it, three years, do you have enough on your hands currently with the bispecific program, the TL1As, the B cell depleting portfolio? Or are are you going to continue to, you know, develop novel assets, look for strategic partners for those? What’s the strategic focus?

Basil Dahiat, CEO, Zencore: We’re we’re always going to try to exploit our engineering tools to make the next generation of of great drugs. Right? We didn’t know we were gonna be making bispecific t cell engagers a decade ago. We started working on that because we thought that there was an area that there was a real unmet need that engineering could help. So absolutely, we’re gonna keep pushing forward into novel structures and novel modalities.

But the core focus of the company is getting our clinical data and getting the results that we need. The the research piece is about, you know, being creative and and and following your nose for what might be next. But but we got a lot of stuff to do, lot of wood to chop the next three years in the clinic.

Steve Seedhouse, Biotech Analyst, Canthar: We’re looking forward to following along. It’s gonna be an exciting time. Looking forward also to data the back end of this year at the triple meeting. So thanks so much, Dane and and Basil, for the time. Thanks to everyone in the room and and on the webcast for listening, and hope everyone has a great day at the conference today.

Thank you. Thank you, Steve.

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