I'm with iTeos. Please take it away. Okay. Thank you, Nick, good morning, everyone. I would like to thank Cowen for the opportunity to present iTeos today, and I'm very pleased to be here. While it's a small venue, then we can really enjoy interacting or interactive discussion. I founded iTeos 10 years ago with the willingness to develop better drugs. My mission then and now has been to build a company that would master tumor immunology to select the most relevant targets and develop differentiated drugs. I'm very proud of what we have done over the 10 last years. During the presentation, I will make forward-looking statements. I would like to start this presentation with a summary of why we believe we can develop better drugs. You can see here that we have everything we need for success. A deep and growing pipeline. Nearly a dozen of ongoing and planned clinical trials in major indication. I want to draw your attention on the yellow box on the top right. We have $ 750 billion and a cash runway to pursue our plan into 2026. A partner in GSK who shares our commitment. Finally, our expertise in tumor immunology. Now moving to the detail of the pipeline. You can see our focus on two major mechanisms of immunosuppression. On the left, EOS-448 targets TIGIT, one of the most promising new mechanisms to generate an antitumor immune response. We selected an antibody optimized to activate multiple types of immune cells, and our collaboration with GSK enables an expansive and unique development plan to leverage the TIGIT/CD226 axis. On the right, inupadenant and EOS-984 are small molecules targeting the immunosuppressive adenosine pathway. At iTeos, our scientists have built a unique understanding of this pathway, which has been frustrating for others. We are exploiting this knowledge to fully unlock its potential and moving forward with a focused development plan. Let's go to the clinical plan. You can see here the ongoing and upcoming studies to develop our pipeline. Starting with EOS-448 in blue, we have a very rich and deep effort with six ongoing studies and a first phase III plan with several major indication and novel combination. Turning to the adenosine pathway, we have three trials for inupadenant in orange with our main study is in post-IO non-small cell lung cancer in combination with chemotherapy. We are also very excited about the potential to identify the patient most likely to benefit from inupadenant using a new biomarker. In addition, we've identified a new target in the pathway and expect to bring EOS-984, a novel first-in-class molecule, to the clinic this year, as we announced in early January. Let's go into the detail of our anti-TIGIT program and our ambitious collaboration with GSK. Before I go to specifics, we view 2023 as the definitive years for TIGIT. There will be a great deal of data coming this year, both internal and external, that will provide further proof of the potential for this target. We feel we are into an excellent position with the differentiated plan we are developing with GSK. As we entering this definitive year, we have a great deal of confidence not only in the target we have chosen to pursue, but in the way we are approaching it. TIGIT has a potential to be the next major advance in cancer treatment. A potential that grew from early preclinical and clinical data, which has now been validated in two randomized trials. With EOS-448, we feel that we have the ideal molecule to explore this target. We spend a great deal of time in antibody selection and optimization. Finally, the best way to maximize the potential of our high-quality TIGIT is with high-quality combination and a partner as committed as we are. We have this with GSK. The data emerging from dostarlimab, the GSK PD-1, has exceeded our high expectations. We reject the notions that all antibodies are created equal. We are convinced that optimized antibodies will have better outcome. On top of this, iTeos and GSK have combined portfolio that can increase the antitumor benefit of TIGIT with additional combinations. We are fortunate to have a partner who is as committed as we are to be. for a differentiated and expansive development strategy. The TIGIT CD226 pathway has attracted a lot of interest due to a very unique mechanism of action and expression profile. EOS-448 can activate multiple immune cells to enhance antitumor response, both by binding to TIGIT, as shown on the left, but also by binding to Fc gamma receptor, as shown on the right. The design of EOS-448 matter is the first example of how we are mastering tumor immunology to develop better drugs. To maximize the immune response to the tumor, we've optimized both ends of EOS-448, selecting the best antibody to bring forward. This is a key differentiator for EOS-448. Here are the data validating our approach, which has been presented at AACR last year. In the middle panel, we've identified an antibody with strong potency to get the maximum impact of the TIGIT CD226 axis. In the right panel, we have obtained clinical validation that EOS-448 is doing what it should. With the depletion of immunosuppressive cells in the tumor of patient treated with EOS-448. This is the first time that such data has been generated for an anti-TIGIT antibody. Of course, a great dog deserves a great combination partner, and you will see on the next slide exciting data with GSK dostarlimab. Several data readouts in multiple cancer support the use of dostarlimab as treatment backbone for use in combination with standard of care and of future novel cancer therapies. Here you see the parallel study data by GSK presented in the oral presentation at ESMO IO in last December. The key readout is that dostarlimab plus as good as if not better than pembrolizumab. PERLA is a head-to-head comparison of dostarlimab and pembrolizumab in first-line non-small cell lung cancer. dostarlimab plus chemotherapy in pink achieve very promising results for progression-free survival when compared to pembrolizumab chemotherapy in blue with a similar safety profile. We believe we have the best TIGIT antibody, and it enhance the value of the clinical plan to pair it with a high-quality PD-1 combo partner. We feel incredibly optimistic about where we are and where we are going with this program. Wrapping up on TIGIT, let's revisit our initial development plan on the top left. With the ability to combine two high-quality combination partner, EOS-448 and dostarlimab, in doublet to drive differentiation and generate near-term value. We are pursuing first-line non-small cell lung cancer where there's an existing proof of concept, and we are also targeting another major indication with head and neck cancer. With our partner at GSK, we are also pursuing other doublets and triplets with a strong biological rationale. These triplets are uniquely enabled by our partnership with GSK. This plan is an opportunity to improve the life of tens of thousands of patients diagnosed each year in the targeted indication, as you can see on the top right. We anticipate more to come as we and GSK continue to explore the best regimen for various indication. In summary, we really believe we have a differentiated clinical strategy that will enable us to win with the quality of our therapies, major indication, and unique combinations. Moving to the adenosine pathway, we have leveraged our deep understanding of the pathway to better overcome adenosine-mediated immunosuppression. It's worth taking some time to discuss why adenosine pathway remains of interest, why we believe in our molecule, and why we feel we are best positioned to maximize the tremendous potential of this pathway. Let's start with the pathway. There's no dispute about the major immunosuppressive role of adenosine in cancer after the validation into a randomized trial. Leveraging our unique understanding of the pathway, we continue to lead the adenosine field. Inupadenant is uniquely positioned for application in oncology, as I'm going to show you. With the deliver response we have seen, we are optimistic that we are on the right path. We are the first and only company to identify biomarkers that appear to be associated with the clinical benefit of Inupadenant. We are incorporating the biomarker in our current and future efforts to maximize the potential. In the tumor microenvironment, there is a very important production of pro-inflammatory ATP, which is transforming immunosuppressive adenosine by several mechanisms. Adenosine inhibit the activity of multiple immune cells by binding to several targets expressed on these immune cells. iTeos has developed two unique program to address the adenosine-mediated immunosuppression. Let's focus on the most advanced program to unlock adenosine-mediated immunosuppression. Inupadenant is a new strategy to target the A2A receptor, an important endpoint of the adenosine pathway. We are not the first company to target this receptor, but we believe that we have been the first to design an adenosine A2A receptor antagonist for application in oncology. You can see on the left that the adenosine concentration in tumor is much higher than it was previously thought. We have been the first ones to confirm that the concentration of adenosine in multiple human tumors is above 100 micromolar, as you can see with the dotted line. Based on our adenosine data, we designed the first insurmountable antagonist for A2A receptor. In other words, an antagonist tailored to keep its activity at the high concentration of adenosine found in human cancer. In the right panel, you can see that inupadenant in blue maintains nanomolar potency in a range of adenosine concentration going from 1 to 1,000 micromolar. Other compounds in clinical development suffer major losses of potency when confronted with high levels of adenosine, rendering them effectively useless in most tumors. As a result of this unique profile, we have observed durable partial responses in several late-stage patients, both in monotherapy and in combination with standard of care. Moving to the biomarker data. We're excited by our differentiated biomarker data. On the left panel, using what we believe to be the only validated biomarker assay for the A2A receptor, we have demonstrated a clear trend between A2A receptor levels and a change in tumor size on inupadenant monotherapy. As you can see, the patient in blue with high A2A receptor level has a better clinical outcome. These data have been presented at ASCO last year. On the right, in addition to the A2A receptor, we've identified a second biomarker. I'm excited to show you data of a study where we recruited patients with higher level of biomarker and treated with inupadenant in monotherapy. Here, we have observed what is now a complete partial response into a patient with the highest observed level of the biomarker, with target lesions in lymph node coming close to normal size. This is another example of our commitment to master tumor immunology and understand what's happening in the tumor microenvironment to make better drugs. We are incorporating these biomarkers into all ongoing studies and plan to evaluate it going forward. If this trend holds, it will be a powerful tool to identify indication of interest and select patients in a targeted development plan. Wrapping up on the adenosine pathway, you can see in orange the three ongoing studies for inupadenant, with the main focus on a randomized trial testing inupadenant plus chemotherapy into patients with non-small cell lung cancer after IO treatment. Another important milestone for 2023 will be the start of our first-in-human study of EOS-984. In summary, we believe that our scientific investigation of the adenosine pathway, the continued understanding of the mechanism for action, a potential predictive biomarker, and the identification of a new target with a first-in-class program entering the clinic this year, uniquely position iTeos to unlock the potential of this pathway. In conclusion, 2023 is shaping up to be a consequential year for iTeos. We are poised to capitalize on the opportunities we have created. We look forward to keeping you all updated on our progress through the year. In particular, our phase III plan with GSK and novel advances in the adenosine pathway as we continue to advance our mission at iTeos to create better immunotherapies and to improve the life of people living with cancer. Thank you very much. Great. Thank you very much. If anyone from the audience has questions, you can feel free to speak up. I'll start out with a question. Can you walk us through the deal that you have with GSK and maybe give us why there's a positive benefit for iTeos with that deal and some of the details around it? Yes, for sure. We enter into this deal in June 2021 with an upfront of $625 million for our phase I asset. I would like to let Matt explain in more detail where we are and where we go. What attracted us to GSK is a few things. Of course, their global reach, the upfront payment that Michel already mentioned, as well as having an approved PD-1 in dostarlimab, and Michel already touched on the data they've generated that just looks better and better. Dostarlimab is a late entry, and they have a commitment to the TIGIT axis that's going to be their pathway to success there. They have a CD96, they have a PVRIG that allows us to do things that others can't in the space. We're about a year and a half into the deal and happy to see we're through phase I. We have two phase II's up and running, and we've already started our work with the triplets in the clinic. Great progress there. Going forward, the deal terms, GSK pays 60% of all development expenses. iTeos pays 40%. We have $550 million of development milestones, which we'll start realizing this year with the start of phase III. $900 million of commercial milestones. Outside the U.S., GSK pays a royalty up to 20%, teens up to 20%. Within the U.S., it's a full U.S. co-commercialization. Not just iTeos gets a couple sales reps, but an equal seat at the table and everything related to commercialization and a 50/50 profit split on all U.S. activities. That's great. I know that you mentioned the phase III trial, it may still be early, but could you provide a potential design on that trial if you have one? Well, we are still working with GSK. We agreed that we will disclose more detail when we are ready to launch. What is important to consider and what could have been a limitation so far in the different trials made on the TIGIT targets is that we want to compare our combination of dostarlimab with EOS-448 with the standard of care. That will help us to make that a A 2 A comparison to show the benefit of our workloads. Great. You mentioned that there's a lot of information and new companies coming out with TIGIT data, specifically you guys as well as others. Can you provide some detail on what other TIGIT data may be coming out rather than iTeos's? Yes. Indeed, on top of our ongoing phase II, in lung and head and neck, both in doublets and soon in triplets, we are obviously interested also in the outcome of Roche with being the first one to move forward in late-stage trials and this long-waited readout in non-small cell lung cancer with SKY-01 study. This study will have a final readout during the summer. That will be an important one. I want to stress the fact that Roche will have at least two other readout, a phase III in esophageal cancer and a phase II in cervical cancer, plus a phase II in head and neck. There are also three randomized phase II that will come from BeiGene and additional data from Merck. We want to, I would say, insist on the fact that even if Roche data will be important, there are so many activities today that is super important to keep a global view on what's happening today in the TIGIT field that will also enable us to differentiate with our approach and the combination of our EOS-448 with pembrolizumab. Thank you. Now moving on to the adenosine pathway and the preclinical asset that you're moving into the clinic this year, can you explain or give us a little bit more detail on why you believe that iTeos' candidate will succeed on any adenosine pathway? Yes, certainly. As I explained, we have, I would say, three assets that we are leveraging today. I know that adenosine pathway has been frustrating for many companies. There are several readout which has been negative in phase I, phase II. There is a positive readout in phase II by AstraZeneca with a CD73 antibody. CD73 being one of the mechanisms to produce adenosine. We believe that we have a unique understanding of the pathway. We have been the first one to design A2A receptor antagonist, which is suitable for application in oncology. We've been the first one to show that in human tumors, there's a very high concentration of adenosine. We have designed an insurmountable antagonist that can compete with this concentration of adenosine at any concentration. This is a first unique added value. We are also targeting the endpoint of the pathway, meaning that whatever the way that adenosine is produced by CD73 or the enzyme, we'll be able to modulate the adenosine-mediated immunosuppression. The second dimension is the biomarker. We have not only one, but two biomarkers, and we'll show more data at AACR in a couple of weeks, where we have the opportunity to select indication, but also the patient that will have the best chance to respond to inupadenant. Finally, following the work done by our scientists, we've identified a totally new target in the pathway, which is also at the end of the pathway, which is complementary to A2A receptor, and we are moving EOS-984 in clinics later this year. Great. If there's any questions again from anyone in the audience, just feel free to speak up. I know that you guys have the deal with GSK, which will have some revenue coming in. Other than that, and with potential, what is your cash runway? Where do you guys see your cash taking you to? What potential milestones will that take you through? Cash is into 2026, and that includes the full plan that Michel presented, including the advancement of programs that are in earlier stages of development into the clinic. It's a full utilization of cash against our entire plan, and that's not counting anticipated milestones from GSK over that horizon. What it takes us through everything you saw, multiple phase II readouts, phase III readouts, getting prepared for launch. Everything is going to come in that horizon. A full definitive year for TIGIT, as Michel mentioned. You know, we feel well-positioned to execute across the pipeline. We don't have to get concerned about cash. We don't have to run a study to generate a catalyst to finance on the back of. Everything we do is path to registration. That's great. Then in the adenosine pathway, just again, what biomarkers should we be looking for in the clinical trials that could show somewhat proof of concept that could lead to later stage clinical trials, things like that? Ben, as I show, we have been the first one to validate an assay for the A2A receptor, and we have showed the correlation with clinical benefit. We've also identified a second biomarker that will be more amenable to late-stage trials. Again, we'll show some data at AACR in the coming conference in April. We really believe that this biomarker, if validated, will be directly incorporated in our late-stage trial strategy. Sure. If there are no more questions at this time, I just want to thank iTeos very much for meeting with us and for this presentation, and thank you everyone for coming out. Thank you.