Hi everyone, good afternoon, and thanks again for joining us at the annual TD Cowen Healthcare Conference. It's my pleasure to introduce the management team of iTeos. I'm going to pass it on now to Michel Detheux for opening remarks and the presentation. Thank you. Good afternoon everyone, and thank you for the invitation, Mike Owen. I'm really pleased to be here today, just after releasing our fourth quarter 2023 earnings this morning, and I would like to explain what we are doing at iTeos. Over the last decade, we have spent a lot of time to master tumor immunology in order to select relevant targets and develop differentiated assets, and this is what I'm going to show you today. As always, I will do forward-looking statements in this presentation. 2024 will be a defining year for iTeos. We are going to show you progress and data across the clinical pipeline. We are going to show you two TIGIT readouts in 2024. Both of these readouts will set the stage for how our TIGIT PD-1 doublet is differentiated and could be a potential best-in-class in the field. We have 2 adenosine readouts with a differentiated strategy compared to all of our competitors for programs which have been developed into this adenosine pathway. Finally, with $623 million in cash and a runway through 2026, we are very well positioned to meet a series of inflection points in our clinical pipeline. Let's start with the pipeline where we are today. We are going to launch our first registrational study, which is in preparation, in the frontline squamous non-small cell lung cancer. In parallel, we are going to release 2 phase 2 readouts. The first one will be our GALAXIES Lung-201, which is the largest TIGIT trial phase 2 ever done in frontline non-small cell lung cancer. We'll also be able to release data on TIG-006, which is a study in head and neck cancer. Both of these readouts will set up how our doublet is positioned compared to the other ones in terms of the quality of the clinical benefit. We have also four ongoing clinical trials that you can see in blue, on the bottom, which are evaluating novel triplets. For adenosine pathway, in orange and in green, we have a phase two data from our best-in-class A2A receptor antagonist inupadenant in second-line non-small cell lung cancer. And we have an ongoing phase one dose escalation with 984, a first-in-class program with potential to be a paradigm shifting therapy for oncology due to this ability to restore T-cell proliferation. Moving to specifically our TIGIT program, belrestotug, I'm going to show you why we believe that we have the potential to have the best-in-class TIGIT PD-1 doublet. 2023 could not have been better for the TIGIT landscape, where we learn a lot from the different results which have been published in multiple studies, but also our own data. First, TIGIT provides significant efficacy on top of a PD-1 or a PD-L1. Second, it's super important, and I'm going to show you in more details, to have the highest quality anti-TIGIT antibody. And we are also very confident that with dostarlimab, we have a potential best-in-class PD-1, and I will show you some exciting data. It's also super important to select the right indication. There are more than 15 phase 3 ongoing now in the TIGIT field, but some of the indications are not supported by the biology. And we are going to show you this is important also to stick to the biology and the manufacturing. Finally, the right study design and the high-quality doublet compared to the standard of care will allow to reach conclusive data in phase 2 and phase 3. Our TIGIT program is set up for success with a distinct advantage, and I'm going to show you how it's pan out. Here you have all the competitors today in the TIGIT landscape at the clinical stage. Last year, I was stating here that not all antibodies are created equal. This is the opportunity today to show you that you are going to see that play out why antibodies are different. We believe that there's ample room for improvement. For anti-TIGIT PD-1 doublet to succeed, there are three elements. You need to see some TIGIT monotherapy activity, and this is what we have seen with our TIGIT antibody. You have to get also a PD-1 which is as good as pembrolizumab, the standard of care. I'm going to show you this is a case with standard with dostarlimab. Finally, you need to get an active isotype, which is going not only to engage TIGIT on one side, but also Fc gamma receptor on the other side in order to get a multifaceted mechanism to trigger the best possible antitumor responses. Today, there are only two companies which have provided data convincing for TIGIT antibody: iTeos and Roche. iTeos has been the only one to show in the dose escalation phase 1 monotherapy activity. And Roche has shown some convincing data in different indication and combination, but every time in combination. For the other companies, either we have not yet seen any data, or the data have not been convincing. The second point is it's super important to get an excellent PD-1. There's only one company which has performed a head-to-head comparison with their PD-1 and pembrolizumab. This is GSK. I'm going to show you that, indeed, they have obtained very good data confirming that their PD-1 could be one of the best in the field today. We are very confident that combining this PD-1 with our TIGIT will bring very different dataset. If I want to go into more detail why we believe that we have a best-in-class TIGIT, I want really to focus on this data. First, we have spent a lot of time to this to select a very specific antibody, and we believe that we have the best molecule that we can give to patients with a unique epitope that is shown that is a very high affinity, but also unique potency compared to all the other TIGIT antibody in clinics. We have also the first and only TIGIT antibody which has shown a Treg depletion at all the doses that has been tested in humans. Why it's important? It's important because this Treg depletion is showing that you engage effectively Fc gamma receptor, and they're going to trigger activities not only for the macrophage, but also dendritic cells and NK cells. Here on the right, as you can see in this data, we have shown that 20 milligrams in blue for our antibodies that we have a Tregs depletion in the blood of people treated with our antibody of 80%. BeiGene, on their side, have shown a depletion between 20%-30% at 18 milligrams. 1,800 milligrams. Roche, initially did not provide any data. Two weeks ago, they published a paper showing that they also observed some Tregs depletion in the blood, but this Tregs depletion is still limited at 600 milligrams. We don't know for Merck, and we know that Arcus cannot see any Fc gamma receptor engagement because they have developed an inactive isotype. This data are really the foundation why we believe that we have a differentiated antibody. By the way, this data are the reason why GSK paid $625 million to enter into collaboration with iTeos for our TIGIT program. The other component which is super important will be the dostarlimab. Here you can see the PERLA which has been published last year. This trial is important because this is the largest clinical trial ever comparing two PD-1 inhibitors. You can see here that there is a similar efficacy profile to pembrolizumab, but also a median overall survival of 19.4 months exceeding pembrolizumab four months. We believe that with this PD-1, with a quality PD-1 backbone, which is going to be super important for our combination and our strategy. Now, if we go back to the most important data released in 2023 in the TIGIT field, we believe that this second interim analysis, which has been published, which has been leaked, I apologize, following Roche data has given a lot of information to refine our phase 3 clinical strategy. We have obtained a number of key insights in this study. First, we are convinced that TIGIT is a validated target. I know that it has been a roller coaster. There have been a lot of questions about TIGIT, but here, it cannot be longer disputed. By adding TIGIT to their PD-L1, Roche has been able to show an additional six months in overall survival. They show that this combination is safe also, which is important because it's an active isotype like iTeos. We also believe that this is a baseline that you can obtain with a doublet between a PD-1 or PD-L1 and TIGIT, and we believe there's room for improvement. We believe that a better trial can be designed by using the standard of care as a control arm. Here, they have used atezolizumab in blue. We believe that if we use pembrolizumab, we'll be able to make a direct comparison to the standard of care in this patient population. And we also believe that we can adapt the statistical design in order to get a power study that will be convincing not only in terms of clinical data, but also for commercial applications. All of these learnings from SKYSCRAPER-01 have been incorporated in our phase 3 design. This data or this trial, the GALAXIES Lung-201 phase 2, is the largest TIGIT phase 2 ever in frontline non-small cell lung cancer. It's going to be a very important readout for us in 2024. We are going to show a direct comparison to pembrolizumab. It has been missing in other trials. Because this study is so robust, it's allowing us and GSK to make near-term data-driven investment decisions. We are also going to be able to justify the dose that we are going to use in the phase 3 and fulfill Project Optimus obligation. We'll also show the contribution of components. With CD96 on the bottom in a triplet combination, we are going to explore another immune checkpoints in the TIGIT pathway. Finally, we have a significant effort in the biomarker analysis. What we are going to release in the near future is an interim analysis focused on the four blue arms that you see in the center of the slide. Later on, we'll disclose additional data to reach a total amount of 300 patients as indicated here on the bottom of the slide. We have also another important trial that we anticipate a data readout for this year. This is TIG-006. This is a smaller study, single arm, in head and neck cancer in both PD-L1 high, CPS above 20%, and PD-L1 low, CPS between 1%-19%. What makes this indication so exciting is that we have the potential to be the first or second to market. For us, the interest in targeting head and neck cancer started because of the biological similarities to lung cancer, but also because there is a very high proportion of Tregs in this patient. We believe that with the specific properties of our antibody, we could get a significant clinical benefit. Now, in comparison to GALAXIES Lung-201, this trial design is much simpler. It's composed of two arms, and we'll see the first interim analysis of this one. I want to stress also that we are currently running another randomized phase 2 in head and neck, where we compare dostarlimab to dostarlimab with TIGIT or dostarlimab with CD96 and a triplet with dostarlimab, belrestotug, and the CD96 antibody. We are going to get a complete footprint on head and neck to define what will be the best condition to move into phase three. Moving to the second pathway that we are exploring with a very different strategy compared to other companies. We believe that iTeos stands in its own as a company that not only knows how to tackle adenosine-mediated immunosuppression, but also how to design best-in-class molecule to oppose it. I want to start with a general principle on this pathway. It could be a complicated slide, but what I want to stress is that adenosine is produced at very high concentration in the tumor microenvironment. There are multiple mechanisms to produce adenosine. It's very difficult to shut down this production of adenosine. In fact, in the tumor microenvironment, you're going to get a very high level of ATP, which is released following hypoxia, tumor necrosis, and apoptosis. ATP is pro-inflammatory. Rapidly, the tumor microenvironment degrades ATP into adenosine, which is immunosuppressive. We have always claimed that it will be important to target the endpoint of this pathway, which is the A2A receptor, expressed on multiple immune cells like T cells, plasma cells, and other cells. What is also important is that most of the companies historically have targeted, either A2A or the enzyme producing adenosine. What we have been able to do is that recently, we have identified an additional mechanism, which is an adenosine transporter called ENT1. And we have developed a first-in-class compound, 984, targeting this transporter. We believe that this transporter is super important for proliferation of immune cells in the tumor microenvironment and will be able to make differences. Starting with the A2A receptor. In fact, other companies have targeted this mechanism or this receptor and designed their molecule as classical, competitive antagonists. These compounds have lost efficacy in the high tumor adenosine concentration, which is found in the tumor microenvironment. In fact, we have been the first one to show that concentration, as you can see on this diagram in the bottom, can reach level concentration above 100 micromolar. This is human data. And we have been the first one also to show that using what we call an insurmountable antagonist, as you can see on the bottom right, with a compound that will keep the same potency on the Y-axis at any concentration of adenosine used in the assay, as you can see on the X-axis. Then we believe that we have a very unique compound that will show a differentiated profile compared to the other compounds which have been tested so far in clinical trials to modulate the A2A receptor-mediated immunosuppression. What we are currently doing in clinical trials in this, ongoing phase two, in second-line lung, it's post-IO chemo-naive patients where we combine, inupadenant, our A2A receptor antagonist, with chemotherapy. We are currently completing the dose escalation portion of that trial on the left side, in blue. After confirming clinical benefit, we'll move in the second portion, which is the randomized part. We believe there's a high rationale to combine inupadenant with chemotherapy because chemotherapy will trigger a release of adenosine that will impact the immune response. And by doing this combination, we believe that we are going not only to increase the response to chemotherapy, but also expand their progression-free survival. We also believe this is an important indication. As I told you, chemotherapy is triggering an immunogenic cell death, which is impacting the immune response. With inupadenant, we'll increase the response. And we believe this is a large indication. And this program could release very interesting data for major unmet medical needs when this patient progresses on PD-1 or their immunotherapy. Now, turning to the second adenosine program, which is a discovery which has been performed by iTeos scientists. We have been very excited to enter into clinic in the second half of last year. EOS-984 is a first-in-class molecule targeting ENT1. This transporter is really unique because it's involved in all T cell function. We are the first company which has understood this mechanism. It's never been described before. This is the first ENT1 inhibitor in clinics for application in oncology. In fact, ENT1 inhibitor has been used decades ago for stroke and other cardiovascular diseases, showing that inhibiting this target was safe in humans. We have developed a better compound that will be relevant for application in oncology. EOS-984 has been designed to restore T cell proliferation in the tumor microenvironment. This mechanism will have a very important effect in different combinations with standard of care. We truly believe that this is a program, if it is behaving in the way that we expect, could have profound effects on the tumor microenvironment. I want to show you for the first time a slide, showing some preclinical data and why we are excited about this mechanism. If we look on the graph on the left, this is a patient-derived tumor fragment. And this is a piece of a solid tumor from a patient that we process very rapidly after sampling in order to be able to measure some activity. And what you can see here is that on the first column, this is the basal activity that you have with this patient tumor, patient fragment. The second one is when you activate the T cells by using a cocktail of different cytokines. Then the third one in blue is what happens when you add ATP as a source of adenosine. Adenosine being highly unstable, we use ATP as a source of adenosine. And you see that we shut down completely the T cell activity. Now, on the fourth column, we have added a PD-1 inhibitor. And you see that we don't restore at all the T cell activity. On the following column, we have used 984. And you see that we restore significant T cell activity. And finally, the last column is a combination between 984 and PD-1 where we completely restore the T cell activity. And we believe that this new mechanism will play a very important role to magnify the PD-1 activity when we are into very high adenosine concentration. On the right, this is a classical animal models. With EOS-984 being very specific for human ENT1, we have used a mouse model with a human tumor types. You see on the right that we have shown a very high concentration of adenosine in these specific tumor models. And what you can see here is that you have in the dark, the vehicle, in orange, EOS-984 alone, showing a very small antitumor activity. In blue, the anti-PD-1. And when you combine the both in red, you have a very strong antitumor activity. This data and a series of additional data that we will show at AACR in a few weeks are the reason why we believe that we have discovered a very fundamental mechanism to explain why adenosine is immunosuppressive in the tumor microenvironment. If we quickly take a look at the design, it's a classical phase 1 trial. We are currently in the third dose with a nice therapeutic window. We are evaluating up to five doses. We could stop before because we have already observed a very high receptor occupancy. We continue to move smoothly into this dose escalation. We are collecting a lot of information in terms of biomarker. After we identified the recommended phase two dose, we plan to run a small dose escalation in combination with pembrolizumab in order to further understand the potential of 984 to combine with PD-1 and its unique mechanism for actions. Now, as a conclusion, I want to stress that with nearly $623 million in cash at the end of the last quarter, we are funded through key inflection points. As I told you for TIGIT, you will see two phase two readouts. An interim analysis in the largest lung study ever performed so far with a TIGIT antibody in combination with dostarlimab and a readout in front-line head and neck cancer. The former study of which will provide a good setting to compare our TIGIT PD-1 doublet to the TIGIT field. And as for our adenosine pathway programs, as I said earlier, you will see phase 2 readouts for inupadenant in 2024. And in EOS-984, the phase 1 dose escalation in addition to some preclinical data that we release at AACR. I thank you for your attention. To conclude, 2024 will be a defining year for iTeos. And we continue to make great progress in the first quarter. We believe that we are very well positioned to show that we are able to deliver differentiated assets and differentiated strategy and with GSK with the best possible combination to be successful in the TIGIT pathway. Thank you very much.