Good afternoon, everyone. My name is Eva Fortea- Verdejo. I'm a biotech analyst here at Wells Fargo, and we're thrilled today to have the iTeos team with us. So we have Matthew Gall, Chief Financial Officer, and Carl Mauch, Head of IR. So perhaps for those that are not familiar with the story, could you guys provide, you know, a quick overview of the company, and then we can dive into some questions? Sure. So the company was founded a dozen years ago in Belgium, you know, with the goal to develop a profound understanding of immunology and the role of immunology and immuno-oncology in cancer. The founder, Michel Detheux, remains the CEO. He's been with the company through its life. The main source of initial capital was an out-licensing deal in IDO1 to Pfizer. With that capital, Michel built a full internal discovery infrastructure, early clinical infrastructure, and all of our pipeline comes out of those laboratories. Our lead asset is EOS-448, now belrestotug, an anti-TIGIT partnered with GSK three years ago for $625 million upfront. We've announced we have phase II data presented in a couple weeks at ESMO. We're currently in phase III with that asset in first-line stage IV non-small cell lung cancer. We have two earlier assets, one in phase II and one in phase I in the adenosine pathway. And again, all of these come from internal discovery, and more preclinical work continues to move, you know, advancing towards the clinic. Awesome. So perhaps we can start talking a little bit about the TIGIT space and latest developments there. And just, like, what are the key learnings from the trials, you know, run by the other companies that you're implementing in your development strategy? Okay. So I joined iTeos about four years ago when TIGIT was pretty hot. There were 15 phase III launched around that time, largely off of the CITYSCAPE trial, which is really 29 patients of PD-L1 high had a very robust response, as compared to 29 on atezolizumab. So a pretty small data set to launch billions of dollars of investment. And what we've learned over time is, you know, some of those studies were, you know, designed, you know, based on that, you know, significantly robust signal. There was a thought that TIGIT could be used broadly, you know, everywhere there's a hot tumor. And so what we've seen from that is choppy data coming out. There have been studies and indications like small cell lung cancer that really lacked biologic rationale. SKY-01 showed a really compelling proof of concept with a six-month survival benefit, but, you know, largely has suffered due to, you know, stats deficiencies, again, chasing that really strong CITYSCAPE signal. So what we have is, you know, we think a best-in-class TIGIT that has shown best-in-class data preclinically in monotherapy, in translational medicine, you know, biomarkers and surrogates like T-reg depletion. And we're really excited about the phase II data that we're gonna be presenting. And what we've learned is you need to pursue the right indication. Right now, we're in stage four PD-L1 high non-small cell lung cancer, the same indication where Roche demonstrated, again, a six-month survival benefit in SKY -01. And we've designed a study that incorporated the learnings of the data disclosure that Roche made. Primarily, one, the separation of the curves didn't occur there until six months, so any early signals, really early looks at PFS and OS are likely to just be burning of alpha and that you need a larger study so Roche went in with about 600 patients. We've designed our phase III with 1,000 patients, and that study kicked off about four months ago. Great. So perhaps going a little bit deeper into, you know, your main drug candidate the belrestotug. How is it? What are the key points of differentiation from, like, other TIGITs, and what have you seen so far that suggests, you know, that this TIGIT could be successful? Yeah. So, you know, from the early days, and this goes back long before I joined the company, you know, we've had a belief that really understanding the biology and really driving to best-in-class molecules, spending time to design the best molecule, is gonna be the key to success. So even preclinically, you know, our assays demonstrate that we have a differentiated binding, that leads to more potency and more affinity to the target than the other TIGITs in this class. And where we've seen that play out in the clinic is, again, the best monotherapy data. So even in late stage, you know, monotherapy, we had a 50% disease control rate. We're the only company to have a response in monotherapy in late-stage patients. And the other surrogate is the T-reg depletion I mentioned earlier. We see profound T-reg depletion even at the lowest dose we took into monotherapy at 20 milligrams. As a comparison, BeiGene saw 30% T-reg depletion at a dose nearly 20 times ours, where we saw 80% T-reg depletion. Genentech has indicated they didn't see much, if any, T-reg depletion, and anecdotally, you know, we've heard from Merck that they didn't see it until they had a dose beyond what they've taken into the clinic. We don't claim T-reg depletion is what's driving the response rate that we're seeing, but what we claim is you will get profound levels of T-reg depletion if you're binding effectively to your target, the Fc gamma receptor. Again, the extra time that was spent, the extra work in the lab coming up with it, we think it's a superior molecule. We're seeing play out clinically now, and we think that gives us a huge advantage as we move forward. So you mentioned, you know, binding to Fc gamma receptor. So, you know, there's some TIGIT candidates that are not binding to the Fc gamma receptor. What do you think, you know... Is there gonna be, like, a safety benefit to this? Is there an efficacy benefit to actually binding? Yeah, we believe the evidence is on the side of binding to the Fc gamma receptor. If you go back several years, there was a split of companies who was pursuing Fc- silent and who was pursuing Fc- active. Arcus is now the last one standing on the Fc- silent side. BMS dropped their candidate, Astellas dropped their candidate. BMS then brought in an Fc- active, because they believed in that profile. Roche initially started with an inactive and moved to the active isotype. You know, and when they made that decision, they said they were willing to trade efficacy, for what could be potential safety, that binding to that target was important. We view it as important. But, you know, I think the right answer at this point is, you know, we're a data-driven company, and there isn't enough data in the field right now to draw a conclusion. We're happy with the position we took. We believe the evidence is pointing that it's the right decision, but, you know, we haven't seen enough data across, you know, the TIGIT readouts that would let us say, y ou know, the data's on our side. I think the data's early, and we'll see how it evolves over the coming years, but we think we're on the right side of this one. Can you provide a little bit more color? You said a few companies kind of, like, dropped their Fc- silent TIGITs. Are there hypotheses on specific safety issues with, like, Fc gamma receptor engagement, or is this all, you know, kind of like theoretical and not specific, you know, AEs that we should be looking at? I think it's more efficacy-driven than it is safety, specifically when you're looking at the difference between an Fc- active or an Fc- silent, and it comes down to that secondary mechanism that you get with an Fc- active, which is ADCC or antibody-dependent cellular cytotoxicity. And so I think that's why you see a lot of companies drifting towards that Fc- active domain to get that potential extra boost of efficacy you could potentially see in solid tumors. I think when it comes to Fc- silent, I think there is some efficacy that you can still get there from that type of domain. But the way that we view it is, do you really want to be leaving any additional efficacy on the table with manageable adverse events that you could be handling? So could this be also tumor-specific? Like, could there be some tumors that, like, could benefit from efficacy for, like, engaging with the receptor and other tumors that, like, it doesn't really matter? I think, you know, we had a program, you know, that we terminated a couple of years ago in multiple myeloma, due to the shifting in the competitive landscape. I think there are some of those liquid tumors where you have to have an Fc- active isotype. You know, I think for others, you know, the jury is still out in terms of would work or wouldn't work. I think we're talking about increments here, not would or wouldn't work. As Carl said, you know, we think having the extra activity is to our advantage. If there's a safety difference, look, you know, we've dosed. You know, the field has dosed thousands of patients with Fc- active isotypes. We're not seeing major safety signals with the active isotype. Certainly in our data, we're very confident in the safety and tolerability profile we're seeing. So it's increments rather than will and won't. I think is the better way to phrase it. And one of our board members says all the time, I don't have the stats to back it up, but I'll take his word for it: "Far more assets in oncology fail due to lack of efficacy than due to tolerability issues." And if we're gonna make a choice, and we don't think we had to make a choice, we don't think there was a major safety sacrifice. The data supports that we didn't make any major safety sacrifices, but we'll choose extra efficacy every time. Just real quick. I mean, when it comes to tumor indication selection, I think one of the things that Matt was talking about earlier is, you know, we kind of view it as a quality of components issue. We view it as an indication selection issue. We also view it as the way that you competently design your trial. So when it comes to indication selection, I think people saw the CITYSCAPE data from Roche with 29 patients in their TIGIT PD-1 doublet, and they saw it compared to their atezolizumab PD-L1. And to them, it seemed like this is, you know, a foregone conclusion, this is gonna work. This is adding a good amount of efficacy on top of that PD-1, and people rushed into indications. We didn't take that approach. We were held back by FDA's Project Optimus, so we really had to be thoughtful about the dose optimization and the strategy in that exercise, and so we're really excited to present that data later at ESMO next Saturday, but I think one of the bigger things is when it comes to the indication selection, I mean, you have to be very methodical about it. For instance, small cell lung cancer was an indication that both Roche and Merck went into. It's a very difficult to treat cancer. On top of it, you have low immunogenicity, which makes it very difficult to elicit a robust immune cell response, especially one that you could potentially enhance with a TIGIT, and so for those reasons, we were kind of never really attracted to that indication and to really pursue it in the first place. Most recently, you've seen Merck's KeyVibe-008 play out that way as well. Roche had a readout, I believe, back in March 2023, that had the same fate. So it's something that you just have to be very smart about. Our emphasis right now is on lung, just because we've seen other TIGITs work there. We have a differentiated TIGIT PD-1 profile. We think we can make an impact there, but we once again want to be methodical. We're looking at head and neck, very similar biological rationale to lung. We also have a biomarker that we're currently working on, where we think that we could potentially look at subgroups within different indications that would actually be, amenable to, an IO doublet, so hypothetically, PD-L1 low in the lung. We think that could be something that would be very interesting to pursue. Okay, so you know, kind of like following up on this, you're using the dostarlimab as the combination partner. Do you think it makes a difference, the combination partner here? Do you think this could, you know, help your strategy? And what have we seen so far from this molecule that would suggest this? Yeah. So there's a ton of momentum behind dostarlimab right now, just a series of approvals and readouts. The adoption is increasing quarter- over- quarter for that molecule. You know, what's the unknown? One, let me take a step back. We think it's important in any study, and we have this in our phase II, and we have it in our phase III, to compare to whatever the market leader is. In Stage IV, PD-L1 high lung, it's pembrolizumab. So in both of those studies, we're comparing to pembrolizumab and, you know, TIGIT is additive to PD-1. What we have in dostarlimab is an asset that's gone head-to-head against pembrolizumab, and it's the only PD-1 or PD-L1 to do this and come out on top. And that was in the PERLA study, a large randomized study. So we go into that knowing at a baseline we're at or above where pembro is, and then we're building on top of that. You know, and it's an unknown for others. You know, the recent phase III readout from Roche showed, you know, their doublet or their triplet with chemo underperforming pembro chemo. There's no reason to believe the TIGIT was deteriorative or somehow TIGIT and chemo counteracted each other, so you must have had a sign. The only explanation we come up with is there was a significant underperformance from atezo versus pembro, that led to even the doublet or the triplet in this case, still underperforming pembro chemo. Okay, yeah, makes sense, and moving on to your Lung-201 readout, which is happening, you know, very soon. So you reported in a PR that, and I'm gonna read this: "Exceeded predefined efficacy criteria for clinically relevant activity." What does this mean? I believe the PR also mentioned it did so at all doses. So have you shared any information on this? Was there a dose-dependent effect? Are you expecting a dose-dependent effect? Okay. So yes, Carl already alluded to Project Optimus. There are four arms they're gonna report on next Saturday. There's dostarlimab monotherapy, and there are the doublet with three different doses of belrestotug. To answer your last question, we were not expecting to see a dose response in this study. I mentioned earlier about the T-reg depletion, where we saw profound levels at the lowest dose we took into phase I, and it was very moderate, insignificant, immaterial, you know, relation to dose beyond that. So we think every dose that went into this phase II is gonna have high levels of activity. So what did we see? First of all, the data is going to be. The primary endpoint of the study is unconfirmed response rate. We're also gonna have confirmed response rate, we're gonna have safety tolerability, and we're gonna have exploratory measures like ctDNA. We'll also have visuals, waterfalls, spider plots. So while we won't be reporting on depth and duration of response, it'll be very visually apparent, you know, to the audience around what we're seeing there in these early days. So there were two benchmarks we had going into that study. One, we had to beat, and meaningfully beat any pembro benchmark. We had to give investigators into phase III, we had ourselves confidence that we would beat pembro. There's uncertainty around, you know, what numbers pembro would deliver today. Would they still reach a 40% response rate, or was that a bit of an artifact of, you know, 10 or 12 years ago when those studies were conducted? But irregardless of that, we had to meaningfully beat that benchmark. And then talking about the quality of dostarlimab, we had to make sure it wasn't just dostarlimab leading to a beat, and we weren't adding very much on top of dostarlimab. So we need to see, you know, a meaningfully beat of the dostarlimab monotherapy as well. And we saw both of those things as we announced back in May. So when can we expect the PFS data? Are you gonna do any more readouts before the end of the year, or is this a 2025 event? 2025. Okay, makes sense. And perhaps moving on to the phase III, right? Like, you've already started the phase III. Yep. Can you provide any update on, you know, how's enrollment going? It's early days. Not opening. Yeah, look, it's a thousand-patient study that we launched a few months ago. It's pretty early days. I can say we've met all of our internal benchmarks as early as that is, but it's on track to our plans. But, we don't have any updates beyond that right now. How long do you expect a study this big will take to enroll? I mean, we're not guiding on that. It's important. You know, one of the reasons, you know, some people could question: "We saw the data back in May, why didn't you, you know, announce it then?" With all of the headwinds in the TIGIT space, we felt it was important to go to a major medical meeting, have investigators, clinicians, you know, kind of butts in the seat and sit down in front of them and explain the data and why we're so encouraged and excited about it, primarily to ensure that enrollment is robust. You know, beyond that, we're not guiding as to, you know, what we expect enrollment to be. I would say, if you think about some of the earlier messages, it's a bigger study. We're gonna wait a little longer to take cuts of the data. You know, this is not gonna be a five-year study, but it's not gonna be on the absolute fast track. We think to get it right, we wanna make sure we're conservative in the cuts of data that we take. In terms of the phase II, we're still waiting on data from other arms that were part of the study, which you're not gonna be presenting at ESMO. Is there potential to modify this phase III trial if, you know, efficacy from these other arms is better than expected? Or how are these arms going to inform at all your phase III strategy? One thing that attracted us to GSK as a partner is their commitment to the broader, what we call the TIGIT axis, they call the CD226 axis, and they had programs in PVRIG and CD96. And those programs, you really need a TIGIT. I mean, it was one of the reasons, you know, they were a good partner for us, and we were a good partner for them with the quality TIGIT we have. You're not going to see much if you just put a PVRIG, you know, with a PD-1, you need the TIGIT component to activate the axis. So their commitment to the pathway was unquestioned,. We're intrigued to see, you know, what that CD96 arm, which is the only other arm, you know, in that study of interest. Right now, we're really excited by what we've seen in the doublet. I would not expect this phase III to become a triplet. We think, particularly in lung, there's other indications where the triplet could make sense. We can apply learnings more broadly. We're going to have, at the end of the day, basically 200 patients, the doublet, and we're going to have 60 of CD96. I think we'll have to be careful about what type of conclusions we draw about modifying, you know, a large phase III that's up and running based on 60 patients. But the CD96 triplet with nelistotug, which is GSK CD96, so that's contemplated in the GALAXIES Lung-201 trial, like Matthew was pointing out. We also have it included in the GALAXIES Head and Neck-202 trial. So we have the ability to understand it a little bit there. There's contribution of component there, so we have dostarlimab by itself, belrestotug with dostarlimab, then you have dostarlimab with nelistotug, and then you have the triplet version as well. So that's something that we're also evaluating in a different indication. Okay, makes sense. And in terms of the phase III, can you just remind us what's the active arm that you're comparing to? Is it going to be pembro? H ow is this relevant? Are you hearing from KOLs that pembro monotherapy is more relevant or pembro plus chemo is more relevant? So in this setting, all of the data, both ours and GSK have generated suggests 70% of patients in that setting are pembro monotherapy. We think that's the right comparison. TIGIT is unproven in the triplet setting. I talked about SKY -06 earlier. We think there's a good proof of concept from SKY -01 and from our own emerging data with the doublet. So we think the doublet against pembrolizumab is the best comparison to attract the majority of patients. And we think with a strong doublet response, we could see those chemo levels in frontline go down and have chemo saved for second line, which is what you see, you know, in other settings. And then the other interesting data set at ESMO 2023 last year, they had a real-world data set that was essentially looking at first-line lung PD-L1 high, where they were doing a comparison between pembro and chemo versus just pembro. And what they were able to find was that there was no difference in overall survival or median PFS. And so, the one thing that we've been talking about with the recent results of SKY - 06 is that there's really been no proof of concept for using a chemo triplet with a TIGIT and a PD-1 in this setting or other settings. I think that's something that we're definitely interested in. Obviously, we were running the phase Ib to evaluate whether or not this was a safe combo with our TIGIT and PD-1, but it's something that we're still looking at and assessing. Okay. Okay, great. Perhaps moving on to head and neck. Can you kind of like, just give us an overview of, like, the program there, and, like, how are you planning to develop your TIGIT in this tumor type? So we think, you know, head and neck. Carl mentioned, you know, GALAXIES Head and Neck-202, head and neck up and running already. We think it's important in head and neck to establish proof of concept there before we move to a phase III. We think the 201 data could be extrapolated to other settings in lung and perhaps other tumor types, but it's important in head and neck for us to generate a robust, independent proof of concept before moving to phase III. We had hoped that proof of concept would come from SKY -09, from Roche. They were talking that up a few years ago, and now it's completely disappeared. We still like head and neck as an indication, but we think strong proof of concept is required for phase III. Unfortunately, we were hoping to leverage Roche's balance sheet to get that and then move forward, but it looks like we're going to have to do it on our own, and that's well underway now. The reason being also for targeting it, the rationale, it's very similar from a biological standpoint to non-small cell lung cancer. So we see a high density of TIGIT-positive T-regs that are highly immunosuppressive. So our belrestotug, our TIGIT, we've shown in preclinical and in phase I data as well, that it has a keen ability to preferentially deplete TIGIT-positive T-regs. The other thing is you're seeing a lot of infiltration by T cells into the tumor. And then the third thing is we have seen activity by PD-1s here, so we think we can potentially enhance that with the TIGIT. So that's something that we're definitely contemplating. Have you or are you planning to share any data from the TIG-006 study, on head and neck this year? I believe you have, like, a small readout prepared. Have you shared where is this going to happen or, like, what's the plan there? We haven't shared when or where, but we have said that we anticipate the presentation of the data before year-end. One thing we announced back in Q1 of 2024 earnings was that we had passed the futility analysis here. And so, just as a reminder, the trial is set up where it's just two arms, and we're evaluating CPS high and CPS low in the first-line head and neck setting. So the first portion of that was just 20 patients in each arm. So after passing the futility analysis for both safety and efficacy, we decided we didn't want to pursue that trial any further beyond that, and that we really just wanted to focus our energy on GALAXIES Head and Neck-202, because it's a randomized controlled data set. From there, we really feel like that is the trial that is going to give us a clear answer because it's randomized and controlled, but yeah, so we do plan on showing something from TIG-006 head and neck before the end of the year, but it will be more minimal, so 40 patients total. What sets the bar here? Are you expecting similar numbers for, you know, CPS high versus low? Yeah, what are your thoughts there? So CPS high and CPS low, so Keynote-048 is setting the bar here. And so what you wound up seeing there with pembro monotherapy, you were seeing about a 19% ORR rate in CPS low, and then a 23% ORR rate for CPS high. So you're not seeing much there. The thing that we talk about internally, though, is that PFS is the marker that you really want to be looking at and seeing what you can actually provide a benefit for patients with in that setting. They saw a median PFS of 2.3 months, so you're not really seeing much there. We do think that with the TIGIT, you could potentially enhance that. As of this point, there's no TIGIT benchmark, SKY-09, which is Roche's in head and neck, still has not been put out to the public for review, so that's really where our mindset's at. Is there going to be a difference from an ORR perspective? Potentially, you know, we would expect that the higher PD-1 response, PD-L1 level, you might be able to see more of a response, but I think that's something that we're gonna have to see. From a regulatory standpoint, is head and neck more streamlined, you know, going towards approval versus, like, non-small cell lung cancer, where you need, like, a larger trial? I don't know. I'm not sure about size of study. Certainly, you know, building on what Carl just said, it'll be a faster study. You know, your survival metrics come in a lot quicker than they do in lung, so that would be slightly different. We don't have enough data at this point to talk about what a phase III would look like, setting. So in terms of deciding what's next for this program, tumor types, indication selection, starting phase II, phase III studies, what's your strategy behind this? You know, I mentioned the term data-driven earlier, and we remain data-driven. Again, when it came to starting the phase III in the stage IV PD-L1 high, it was a combination of SKY-01 and our own internal data that got us confident to move forward there. Studies like head and neck, we think it's important to generate indications, you know, tumor-specific proof of concept. There are other indications where we think we can leverage our learnings from 201 and go straight to a phase III. We don't need to repeat Optimus in every single indication. It has broad applicability in solid tumors. You know, as data continues to emerge, as we generate PFS data from that study, we have a number of ideas lined up that could be launched pretty quickly. Again, head and neck data will come out next year, and that would be another natural place to build on a positive phase II and go into phase III. Is it fair to say you're waiting for this head and neck data before making decisions on other tumor types, or could this be something that you share before? No. Head and neck is driven by head and neck right now. There are definitely other tumor types we're in active discussion on, where leveraging likely more mature 201 data would give us the confidence we need to go direct to a Phase III. And again, the biomarker is always something that we could potentially leverage if we start to see that there are signals and different indications that we could really go after. That's something that we would definitely want to pursue. Are you gonna provide data on the biomarker and kind of, like, disclose what's the biomarker this year or? So, this year, not likely. Next year likely. Okay. M akes sense. So, moving forward to your adenosine pathway molecules, can you perhaps just educate us on the importance of, you know, adenosine synthesis and transport for, you know, solid tumors? Yeah. So, the adenosine pathway was really hot for some time just because of its role in immune modulation, right? So, cancer cells are always very tricky in their ability to evade the immune system. Extracellular adenosine is one of those mechanisms that they utilize. And so when you look at the adenosine pathway, the most important part of it is that adenosine is produced a myriad of ways. So, there are attempts to specifically go after certain proteins or like CD73 or CD39, which produce a significant amount of adenosine. But the issue is that if you just stop one of them, it's gonna be produced somewhere else. When it comes to our approach with the adenosine pathway, we really wanted to go after the final endpoint, which is the A2AR receptor or A2A receptor. The reason being is if you're continuing to have a high level or super physiological level of adenosine being produced, the best way to stop that is by stopping the endpoint, so that way, the immune cells can continue to function and not be inhibited or immunosuppressed. Really, that's how we came up with inupadenant, which is our lead asset in the adenosine pathway. Are there other programs that have the risk, you know, inupadenant already that we've seen phase I data perhaps, or phase II, which makes you confident that your strategy targeting the A2A receptor makes sense? We've seen data from Arcus, that was targeting A2A/B, and, they had, decent data, but the, the difficult part is that, when you look at drugs that were targeting the adenosine pathway. You had, companies like Corvus, AstraZeneca, Arcus is another one of them. And really the issue, though, is that they were taking these, classical competitive antagonists that were going after the A2A or A2B receptor, but they were being outcompeted by supraphysiological adenosine. One of the things that we had actually worked on, and we were really proud of because we were one of the first companies to really demonstrate this, is that, a lot of companies, their A2A molecules were really only able to work at, one micromolar of adenosine. One of the things that we had shown that we had really thought about was that in these tumor microenvironments, you're not just getting one micromolar level of adenosine. What you're seeing is a hundredfold that. And so, the issue with being able to prove that is adenosine has a very short half-life. So when we were able to demonstrate that, we were seeing levels of 100 to 300 adenosine in micromolar in that tumor microenvironment. And so we realized that we had to build a very specific type of molecule that was going to be able to withstand that level of adenosine, and so that's how we came up with inupadenant. And so what we're really proud about there is that it has this insurmountable profile where it just has a really long time of being able to hold on to that receptor. And so one of the preclinical experiments that we actually show is that if you increase the level of adenosine over time, and you just go from one to 1000 micromolar of adenosine, we continue to maintain our activity at all levels. Everybody starts to drop off around one to three micromolar from the competitive landscape. And so that's one of the reasons why we really feel if there's any company that can show a difference when it comes to the adenosine pathway, which has had struggles in the past, it's iTeos. What's the rationale behind targeting second-line patients in non-small cell lung cancer? What can we expect from the upcoming readout? It's really interesting. Belrestotug, in combination with dostarlimab, is going after first-line non-small cell lung cancer, so it's going to be the first treatment that they receive. We're opting to not use chemotherapy in that setting because we're hoping to push chemotherapy towards, you know, later use or a later line, so that way, you can potentially use it as a last resort. Now, what we're doing with inupadenant in our phase II A2A-005 is, we're combining inupadenant with chemotherapy because of the synergistic mechanism that we think that could occur there. What's really interesting is that that setting that we're going after is second-line lung, specifically post IO chemo naive, so very simpatico with what we're seeing with belrestotug and dostarlimab going after just first-line lung. So if they don't necessarily see any benefit there, they could shift to second-line lung and to potentially see some type of synergistic benefit from both inupadenant and chemotherapy. That's really one of the reasons why we had carved out that indication for that setting. Chemo induces significant amounts of cell death. Cell death results in release of adenosine, and we have drugs set to counteract that adenosine release and help the immune system retain a level of activity again. And there's much data on efficacy out there in this patient population. What do you think would be, I guess, good enough to move the program forward? So, correct, you know, that you know this is essentially generic chemotherapy. There are not studies being run. The benchmark is not readily available. So what we're doing right now is conducting a meta-analysis to make sure we have a good understanding of what chemo is delivering in this setting. And we want to make sure, again, similar to what we're, our goal with belrestotug, we need to see in early data that we're significantly exceeding that benchmark to give us the confidence to continue to invest in this setting. Perhaps with the last minute, you can just give us a quick overview on your ENT1 program. Yeah. ENT1 is one of the more meaningful discoveries that we've come across in the adenosine pathway. And we were able to discover it, or at least discover its role in oncology, when we were trying to understand why inupadenant couldn't help T cell expansion or proliferation, in that setting. And what we were able to identify is that ENT1 was allowing for extracellular adenosine to get into T cells and essentially cause them to be immunosuppressed, so shutting down metabolism, expansion, survival, and effector function. And so, what we've been able to do with EOS-984, in our phase I study, is essentially design a molecule that can block this transporter from allowing the adenosine to get into the T cell, and potentially allow the restoration of T cell proliferation in the tumor microenvironment. When can we expect to see some data, some early data from this program? Before the end of the year, on the dose escalation portion of the phase I trial. Okay, great. I mean, we're done. So thank you so much for joining us today. Yeah. Thanks for having us. Thank you.