Good morning, everyone. My name is Michel Detheux. I'm the founder and CEO of iTeos Therapeutics. I would like to thank JP Morgan for this invitation this morning and to really focus on an introduction where I started iTeos over a decade ago to develop an expertise in tumor biology to build differential therapeutics. Today, iTeos has reached a unique vantage point with both near and long-term potential, long-term growth, making 2025 an exciting year, as I'm going to show you. As usual, we'll make forward-looking statements in this presentation. 2025 is a pivotal year for iTeos, where we'll be generating the most clinical data in the history of the company. We have two key objectives. First, with our TIGIT program, belrestotug, we will be generating over 400 patients' data this year in first-line lung and head and neck cancers. At ESMO last year, we and our partner, GSK, presented one of the strongest clinical data sets ever in the first-line lung. In 2025, we want to see that impressive tumor reduction translate to progression-free survival. Second, we want to advance two emerging programs in our pipeline, which could be the next breakthrough in immuno-oncology due to the large combination opportunities spanning numerous indications. These are first and best-in-class therapies addressing key immunosuppressive mechanisms, and our goal is to generate early signals from each phase I program to reveal their potential. With our cash runway through 2027, we can continue to build a high-value pipeline with runway through multiple inflection points. Let me show you where we stand for each of the programs. For TIGIT, illustrated here in blue, let me start with the top line. We and GSK are continuing the global expansion of our phase III GALAXIES Lung-301 in first-line high PD-L1 non-small cell lung cancer. Below, you see three additional lines. These are the key trials that will generate the bulk of our clinical data through 2025. For GALAXIES Lung-201, we anticipate top-line data in the second quarter, which will include more than 240 patients in high PD-L1 non-small cell lung cancer. Later, in the second half of 2025, we will present this data in detail at a scientific conference. Then, for our head and neck studies, GALAXIES H&N-202 and TIG-006, we will have initial data on over 200 patients in 2025. For us, we are excited because this data set will answer critical questions on the potential of TIGIT. I will touch on this more in a moment. Our next program in yellow, EOS-984, is a small molecule inhibiting ENT1, a major nucleoside transporter expressed on immune cells. To us, this program represents the potential cornerstone for the revival of T-cell activating therapies. We plan to present the first data set of the monotherapy and PD-1 combination data in the second half of 2025. On the bottom, in orange, we are excited to announce our newest program, EOS-215, an antibody which inhibits TREM2, a receptor expressed on macrophages. This mechanism holds the power to potentially overcome PD-1 resistance by reprogramming the hostile tumor microenvironment. We look forward to providing updates on this program shortly as we expect an IND submission this quarter and plan to present preclinical data early in the second quarter of 2025 at a conference. Let me provide more detail on our flagship TIGIT program, which we are advancing in collaboration with our partner, GSK. When it comes to TIGIT, the landscape has evolved a lot over 2024, and I'm proud to say that the most important highlight last year was our presentation of the GALAXIES Lung-201 data at ESMO, which put us into a unique position for 2025. Why is this initial data from this trial so promising? When I was in front of you last year, I stated that quality of component, indication selection, and optimizing the trial design would be critical for a successful study for TIGIT. Not only did we see that play out over the course of 2024, but we believe those three points are also leading to our success. Each of these points matters. When it comes to designing therapies for patients, we are rigorous. Our decisions are always driven by data. This is why belrestotug is unique in the field, and 2025 holds the potential to be a fruitful year where our strategy will pay off. Now, let's take a step back to understand exactly where the field is today and why our belrestotug combination stands out. For us, belrestotug and dostarlimab represent a highly unique combination because together they have three distinct characteristics. One, an optimal anti-TIGIT antibody needs to show strong target engagement with both TIGIT and Fc gamma receptor, a key regulator of the immune response to evoke a multifaceted mechanism that can enhance the anti-tumor response. Two, you want to see clinical activity. To date, belrestotug has generated very promising clinical activity both in monotherapy and in combination with dostarlimab. Three, your PD-1 must be as good as pembrolizumab. And no one has successfully performed this comparison except GSK. Then, out of the entire field, our partnership is the only one with all three characteristics. So why does our TIGIT stand out so clearly from the field? Simply put, better molecule design drives better clinical data. belrestotug is unlike any other TIGIT as it has a very unique profile for its affinity and potency. Because of this profile, we were the only company to observe monotherapy activity. And as illustrated on the graph on the right, we are the first and only TIGIT which proven Treg depletion at all doses in the periphery and in tumor sample of patients. So why is it important? It's important because Treg depletion reflects how effectively you're activating Fc gamma receptor, a critical measurement of a multifaceted anti-tumor response. We saw significant Treg depletion at every dose, and even at our lowest dose, 20 mgs, we observed 80% Treg depletion, something that no one else has come close to, and now we began to see that these characteristics translate to patient outcomes in our ongoing phase II trial, so let me walk you through the design of GALAXIES Lung-201. This is a robust and highly informative phase II evaluating pembrolizumab and dostarlimab monotherapies, again, three distinct doses of belrestotug combined to dostarlimab, as well as a triplet evaluating dostarlimab, belrestotug, and nelistotug, an additional immune checkpoint in the TIGIT pathway only developed by GSK. In last September, we presented data on the first 120 patients from the different arms shown in blue here. We saw exactly what we wanted to see. We saw clear clinically meaningful separation by our dostarlimab-belrestotug doublet from dostarlimab monotherapy, and we have surpassed every historical pembrolizumab benchmark at each dose. This data confirms our choice of 400 mg as the recommended phase III dose. On top of that, the ctDNA data further confirms a clearly enhanced anti-tumor response for the doublet compared to dostarlimab alone. Most importantly, the safety profile observed at the recommended phase III dose was manageable, something that was confirmed to us by dozens of clinicians involved in the study. Based on the new safety protocol we are implementing, we believe we can further improve the discontinuation rates, which would allow patients to remain on treatment longer and potentially derive greater benefit from our TIGIT doublet. On the right, let me orient you in the waterfall plots for dostarlimab monotherapy on top and the 400 mg combo on the bottom. Progressive disease is illustrated in gray, stable disease in yellow, and the partial response in green. We have observed 12 partial responses out of 28 patients in the dostarlimab monotherapy on the top. On the bottom, we have seen 21 partial responses out of 28 patients for the doublet with deeper and faster responses illustrating the benefit of the combination. After seeing this exciting preliminary data from GALAXIES Lung-201, we and GSK launched GALAXIES Lung-301, a thousand-patient study going head-to-head with pembrolizumab in high PD-L1 non-small cell lung cancer patients. Notably, in the last quarter of 2024, we activated sites in the U.S., Europe, and China, and we are pleased to announce enrollment is continuing as planned. To us, GALAXIES Lung-301 represents the right study with the right control arm and the right statistical power to give us the best shot at success. I think this is something that we do incredibly well in our collaboration with GSK. I also want to touch upon GALAXIES H&N-202, our next most advanced randomized phase II evaluating our TIGIT PD-1 doublet in first-line head and neck cancer. We believe this indication could be highly relevant due to the similar biology to non-small cell lung cancer and the high proportion of immunosuppressive Tregs. This is a large randomized control phase II platform study evaluating dostarlimab monotherapy, our dostarlimab belrestotug doublet, and novel combination with nelistotug and PVRIG, two additional immune checkpoints in the TIGIT pathway developed by GSK. We've also completed a smaller study, TIG-006, head and neck which evaluated belrestotug and dostarlimab combination in first-line head and neck cancer in low and high PD-L1 cohorts. I really want you to keep this slide in mind today because it clearly captures why 2025 is so pivotal for us. We plan to present more than 400 patient data starting in the second quarter. And this data set will be able to address many of the remaining questions we and the field have on TIGIT. Starting on the left-hand side for GALAXIES Lung-201, we'll be announcing top-line interim data from the initial 124 patients and response rate, safety, and ctDNA data for a total of 244 patients, including 30 patients treated with pembrolizumab monotherapy and 30 patients with the triplet. We then plan to present the full interim data set at a scientific conference in the second half of 2025. In addition, on the right side for our two GALAXIES H&N-202 studies for GALAXIES H&N-202, we intend to present response rate and safety for more than 150 patients across four arms, including dostarlimab monotherapy, our belrestotug and dostarlimab doublet, dostarlimab and nelistotug doublet, and the triplet of belrestotug, dostarlimab, and nelistotug. For TIG-006, we plan to announce response rate, PFS, and safety data on 42 patients in the same release. A detailed breakdown for each trial can be found on our corporate deck online. This data set represents years of hard work, and we are excited for what 2025 will bring for our TIGIT program and our collaboration with GSK. Moving to our other innovative programs, let me first update our strategy to address adenosine-mediated immunosuppression. Adenosine is a major immunosuppressor produced in high concentration in the tumor microenvironment, which impacts the benefit of standard of care. For over a decade, the focus of multiple players, including iTeos, has been on trying to stop the impact of extracellular adenosine on immune response. Let me point you to the picture on the right. We initially targeted this adenosine-mediated suppression with inupadenant, the first A2A receptor antagonist being able to compete with the very high concentration of adenosine found in the tumor microenvironment. We saw some encouraging data for inupadenant in combination with chemo, but unfortunately, even if this best-in-class asset was not sufficient to justify further development. What's exciting is the work completed by our discovery team, who was able to show that intracellular adenosine appears more important to trigger the adenosine-mediated immune response. And we have discovered ENT1, which essentially acts as a channel allowing for adenosine to flow into immune cells, playing a critical role to shut down their ability to proliferate and fight cancer. In preclinical studies, we demonstrated that inhibition of ENT1 restores T-cell activity and proliferation despite this high level of adenosine in the tumor microenvironment. I am very proud to state that we are not only the first company to identify this mechanism and the first to develop EOS-984, a potent ENT1 inhibitor to target cancer, and you can see on the right. In the second half of 2025, we'll get our first look into how EOS-984 is behaving in monotherapy and in combination with pembrolizumab in our phase I trial in advanced malignancies. Now, let me introduce our newest program. At iTeos, we focus on developing first or best-in-class therapies that can truly make a difference for patients. And our latest program does just that by targeting a receptor called TREM2. Our new program, EOS-215, is a selective and highly potent best-in-class anti-TREM2 antagonist, and it has the opportunity to not only reprogram the immunosuppressive tumor microenvironment but overcome PD-1 resistance. As illustrated on the right, TREM2's uniqueness comes from being a multifaceted mechanism with macrophage, which regulates tissue homeostasis and repair. Compared to the previous strategies based on macrophage, TREM2 aims to reprogram the protumoral macrophage into antitumoral ones. When co-opted by cancer, it's one of the key reasons for the creation of the immunosuppressive tumor microenvironment and the growth, progression, and survival of cancer cells. From our efforts to understand this complex mechanism, select the right antibody, and run the right preclinical studies, we are thrilled to announce that EOS-215 represents the most potent TREM2 antagonist in the field of oncology right now. By reprogramming the hostile tumor microenvironment at primary tumor and in metastatic lesions, we think we can address one of the key immunosuppressive mechanisms, making the combination opportunities incredibly broad and exciting. We look forward to providing an update on trial progression with the IND submission this quarter and the presentation of preclinical data next quarter. And to conclude here this presentation, the past decade has been an incredible journey, which has led us to the most pivotal year ever for iTeos. This year, you are going to see over 400 patient data for TIGIT. And if any TIGIT is capable of succeeding, belrestotug is the best investigational therapy to potentially prove that. For our emerging pipeline, we look forward to sharing phase I and preclinical data from what we believe to be the next wave in immuno-oncology. We look forward to disclosing this data to you. iTeos is well positioned to build a sustainable leading oncology company, improving patient outcomes on the basis of our expertise to build differentiated therapeutics, candidate, our diligent approaches, our operational excellence, and our strong capital position. Thank you very much. Thanks, everyone, for joining the following Q&A session. I'm Brian Cheng. I'm a senior biotech analyst here at the firm. I'm joined by my associate, Marion Wager, who is also in the audience. If you have any questions from the audience who are live here, please feel free to put your hands up. We have one on the floor. And you can also submit questions on the conference portal. Thanks, everyone. Thanks to the team for joining us for the Q&A. I guess, Michel, can you give us a better sense of just how we should think about your GALAXIES Lung-301's enrollment progression in terms of enrollment? Any color that you can give on enrollment pace or just trial opening, sites opening, that would be super helpful? OK, good morning, Brian. Well, please let me introduce David Feltquate, our CMO, and Matthew Gall, our CFO. This was really the power of presenting our phase II data at ESMO last year as one of the keynote presentations for this major conference. The clinicians who participated in GALAXIES Lung-201 were so excited with the data that they wanted to jump into the phase III study. David, you want to add more color on that? Yeah. So just to set the tone of where we're at, so in June, we began the phase III study. We initiated that. First, patients came on in July, and currently, we're on track in terms of what our goals are for enrollment. Part of that was also to ensure that we got the FDA buy-in for the choice of dose. This was the first program that had to go through the full Project Optimus to verify an acceptable dose. That process went very well, and now we're initiating U.S. sites and likewise throughout the world, opening up in Europe, China, South America. OK. And just as we think about the next set of catalysts from your TIGIT collaboration, which one is most important? Or just can you talk about just the importance of the different catalysts that are upcoming throughout 2025? And just what are the roles? And how do you think that this will have implications for the next step forward? Yes. And this is why I showed this morning how we are excited with 25. Matthew. Yeah. Michel spent a good amount of time talking about the big data set release from GALAXIES Lung-201. That is, by far, it's the most mature data set. It's the largest data set. It's a data set where there's comparisons that other TIGITs have generated data. So that's going to be the most informative to us, and I think the most informative to those watching the story, both on the investment side as well as investigators. The head and neck data, 150 patients, rounds it out nicely. It's a little less mature. But again, it's a strong, large data set. And another indication, some bolstered by the TIG-006 data, that's a little smaller, same indication, but we're going to get that maturity. So when you put all that together, 400 patients, super powerful, interpretable, and we think it's going to define the future of our program, again, both internally and the external view and perception. Any questions from the audience? And maybe just looking at particularly the interim Lung-201, I think there are a couple of components that we haven't seen yet, right? One of them is the active comparator arm's performance. And maybe just setting that aside, how should we think about what the key focus is for Lung-201, the next interim readout, especially? We We already have seen the first data cut not too long ago. Yes, David. Sure. So what are we going to see at this next data cut, right? So what we saw and what we showed in the fall was outstanding changes in response rate relative to the internal control of dostarlimab. And as Michel pointed out, the dostarlimab is an excellent PD-1 as a reference to understand this effect. Now what we need to see is, with greater follow-up, is that improvement in response rate is that translating in an improvement in progression-free survival. And so that's what we're going to get insight on with this next set of data. Maybe just turning to 984, can you just kind of frame what we could expect there from the 008 study later this year? And just what would be a good thing to see in terms of efficacy? I mean, of course, safety is the foremost important milestone here. But what would be a good bar to hit from a mono and also combo perspective? Yes, Brian. Well, let me start with, as I mentioned during the presentation, we are super excited with ENT1 because it's a very different, a new approach to address the adenosine-mediated immunosuppression. And we believe that it will be really the cornerstone to unlock this immunosuppression. David, on 008? Yeah. I'm definitely very excited about this. One thing is to point out, when we think about targets in oncology and whether they're important, we always like to have some form of validation. So sometimes that form of validation comes from genetic experiments, accidents of genes, abnormalities. So there's a condition called severe combined immunodeficiency syndrome, the boy in the bubble disease. And this is caused by a rare genetic abnormality that leads to an abundant accumulation of adenosine in T cells. And we know the consequence of that is that those T cells cannot proliferate. They're not cytotoxic. And these infants are profoundly immunosuppressed. So we have validated, right? The The human genetics has validated that intracellular adenosine is very important. Whereas prior attempts at manipulating adenosine biology have focused on the extracellular adenosine and the consequences of that, we have now working on targeting what is happening with intracellular adenosine, and so this ENT1, this channel, which is always open, it's not a signaling molecule. It's an open channel. A high amount of adenosine in the tumor microenvironment will follow its gradient and go right into T cells, and so we think super physiologic amounts of this adenosine in T cells we know is toxic, and we think that's what's happening. This blocker we have prevents that from happening, and this is profound because it means that we have the ability now to restore or protect T cells from that toxic environment. That's important for any T- cell-directed therapy, checkpoint inhibitors, CAR- T therapies, T- cell engagers. We know, as an example, CAR T cells and T- cell engagers have worked very well in hematologic malignancies, but they're not working so well in solid tumors. And we know one of the differences is that tumor microenvironment adenosine. So it's possible that by controlling this, we can help those therapies work much better in those diseases across solid tumors, right? So the potential for this is off the charts. What we're going to see by the end of this year is the initial safety data, pharmacokinetic data, and preliminary anti-tumor data. Typical phase I, these are in resistant settings. So primarily what we're going to get insight on is the safety, the pharmacokinetics, and pharmacodynamics. And that's the most important information we're going to get. We certainly will look at efficacy. The likelihood that we will see meaningful effects with monotherapy is low by nature of what I just described. In combination with checkpoint, certainly we're hopeful to see something. But again, in the resistant setting, we need to be tempered by sometimes that's challenging. In looking towards 2026, obviously our efforts will be focused then on proof of concept and in, I would call them, naive settings where we can more substantially see impact. This is, I think, an advanced solid tumor, more resistant type of tumor setting. Can you talk about just the range of potential tumor type that we could potentially see? And maybe just to that end, is that as you think about the mechanism here, which indication do you think is probably sort of the low-hanging fruit here that will give you a good guidance on how it performs and has the most potential? Yeah. So what's interesting is, again, the breadth of potential. As I described, any tumor that has T- cells, but these T- cells are being held in check by abundant adenosine, is ripe for this kind of mechanism to bear fruit. So which specific tumor types we've not described what that's going to be, but we will definitely focus in with that biology I just described in mind, something where there's T- cells, something where we believe there's abundant adenosine. And you also started dosing the pembro combo arm. I'm just curious, does that have any implication on whether you saw any efficacy for mono? And just what was the bar that you need to hit or threshold that you need to hit before pushing the study into pembro combination study? Yeah. So typical phase I studies, we want to evaluate monotherapy for safety up through some maximum dose. And we want to understand the pharmacokinetics and pharmacodynamics. It's the pharmacokinetics and the safety, though, that we want to have adequate information before beginning the combination. And we were able to do that. And so last quarter, we began that initial combination escalation. And just going back to, again, I guess 215 is the new asset that you have talked about today. I'm just curious, how do you think about, first of all, 215, 984, how are you prioritizing your resources as you're also focusing on belrestotug on the side? Where does 215 fit into the big picture? There are different stages of development. Obviously, TIGIT is also empowered by our collaboration with GSK and their clinical operation power. For ENT1 and the 984, we are progressing, as we said, toward the end of the dose escalation. The next stage will be running a specific population study. For 215, we are at the end of the preclinical process with IND submission very in the near future and the start of phase 1, both in Belgium and in other countries. We are scaling the different program with different stages of development. Can you talk about how you got to TREM2 and also 215 as the next asset? Yes. Then, you know, that we have developed over more than 10 last years a very strong expertise in tumor immunology addressing different mechanisms of immunosuppression. And one of the most challenging mechanisms of immunosuppression has been with macrophage. And many programs have failed because they were targeting a mechanism called Don't Eat Me signal. CD47 is an example of such approach. And it took a lot of time for the field to understand how to address these polymorphic macrophage populations. And over the few last years, TREM2 has appeared as a cornerstone in this capacity of reprogramming macrophage from the pro-tumoral macrophage into anti-tumoral macrophage. And there are more and more publications showing that TREM2 is induced by a standard of care treatment, including PD-1, and could be a major mechanism to overcome immunosuppression trigger with these standard of care treatments. Maybe just to Matt, very strong balance sheets heading into the new year. Just how do you think about the burn rate heading into 2025? And any color on just how we should better model your expenses in the near term? Well, I mean, look. Big picture, runway through 2027, and that's conservative guidance, is intact. So we've given that guidance for over a year now. That contemplates at least one additional phase III. So I don't contemplate scenarios where we're meaningfully pulling that in. So I feel very comfortable with that guidance. When you think about 2025, there's a few gives and- takes. Net, I would expect burn to be slightly higher. We're going to have the full year impact of 301, even though GSK pays 60%. You talked about resource allocation. Inupadenant, despite this type of cash balance, we made the difficult decision to say it's good, not quite good enough to continue to invest. So you'll see that diminish. ENT1, 984, because there's still a small footprint, you're not going to see a tremendous amount of burn against those programs. Pretty light touch internally, light touch in terms of spend, so net-net, up a little bit, but you're not going to see a hockey stick-type expense ramp in 2025. While we're on inupadenant, your decision to discontinue program, maybe just going back to that point is that I think what did you see that drove that decision? And I guess I think the more important question is, do you think that there could be some potential read-through to 984? Just how confident are you in 984 after what you saw with inupadenant? Then, as I explained during the presentation, there are really two different mechanisms, even if they are triggered by adenosine, and we believe that it's really a new angle that could, as I said, unlock this adenosine-mediated immunosuppression. Coming back to inupadenant data, David. Yeah. So look, what do we know? We know from not only our work, but from work from others, whether they were going after the production of adenosine through targeting CD73 or CD39, or going after the receptors, the signaling. Basically, what the field has observed is that you get low single-digit response rates, whether it's with monotherapy or, let's say, a combination with a checkpoint inhibitor in a few tumor types. So that's telling us something that, that biology is important, but in a very, very narrow population. And until you actually have a marker that gives you the ability to enrich for or select those exact patients, doing an all-comer study is likely not to meet with success. And so again, we think we have best-in-class A2AR blocker, great safety profile. I think we saw some clinical activity in that study that we presented at ESMO IO last month. However, without that ability to do that enrichment and focus in MSI, we didn't think it was the prudent decision to carry that forward, and as Michel says, it's adenosine, but a completely different mechanism, and so there really is no association or read-through to its impact on 984. If anything, I think it underscores that 984, we should have more confidence because it's a completely different mechanism, right? We're not doing the same thing over and over again. I think one thing that ties back into investment and how we think about this program, the ongoing study, even though we're now combining with pembrolizumab, these are late-stage patients. They've almost certainly already failed one, maybe multiple IO regimens. So thinking about high levels of response, probably not going to see it. But what we looked at when we decided to invest in the randomized portion, or not randomized, the combination portion following monotherapy, was an impact on the TME. This company is incredibly successful at getting pre and post-treatment biopsies. We see an impact there. That unlocks future investment. We expect to see even more when we combine with pembrolizumab, a different type of impact that unlocks the investment into the next phase of development. So as you think about the 984 data later this year, that's the type of thing to focus on. Great. We will look forward to it. Thanks so much for your time today. Thank you. Thank you. Thank you.