Great. Well, welcome back everyone to Citi's Immuno-Oncology Summit for 2022. As you know, I'm Yigal Nochomovitz, one of the biotech analysts here at Citi. Most of you know me. I'm very interested in your questions, so if you'd like to email me questions, yigal.naquem-abetz@citi.com, and I will relay them to the company. For this session, it's my pleasure to introduce Michel Detheux. He is the President and CEO of iTeos, ticker iTeos. Great to have you here. I know you wanted to start with just a bit of an introduction on the company, and you have some slides as well. If you could perhaps just give us the general overview of the pipeline, the general corporate strategy, and maybe some of the key milestones for 2022. With pleasure, Yigal, and thank you very much for this invitation. Good afternoon, everyone. I'm very excited to be here at the current stage of development for iTeos. Going to one slide to summarize where we are today, we believe that we are at a very unique time to lead the next wave of new cancer immunotherapies. Today, iTeos is a company with two potential best-in-class therapies. We have EOS448, an anti-TIGIT antibody, and inupadenant, A2A receptor antagonist, against the adenosine target with clinical proof of concept. We are planning to run this year 11 clinical trials, including 3 registration-directed studies that will allow us to move forward toward clinical proof of concept and registration. We have also a unique cash position. At the end of the third quarter of last year, we got $900 million that gives us 4 years plus of cash on hand, which will allow us to deliver the clinical development plan and strategy. You were mentioning the corporate strategy. Well, today we have 5 strategic collaborations with obviously the landmark collaboration with GSK that we signed last year to co-develop, co-commercialize our TIGIT antibody. We received $625 million upfront for a total value of $2 billion. This is one of the largest deals ever for a phase I asset in oncology and more importantly, a collaboration with a partner that will help us to accelerate, expand, and differentiate our TIGIT antibody. We have additional collaboration with a clinical supply agreement with Merck and BMS, and we have also academic collaboration that help us to continue to develop our pipeline in addition to the 80 scientists that we have based in Belgium and in Boston in order to develop best-in-class cancer immunotherapies. This year will be a year of execution. We are not expecting any major readout from our side, but both for TIGIT, especially for TIGIT and also A2A, there will have additional readout from other companies, including the four readout from Genentech with their TIGIT program. We believe this will be a very exciting year. We are going to execute on our clinical trial and be ready to deliver the first data during 2023. I will stop here for the introduction. Okay, sure. No, that was a good introduction. Well, let's start with a more detailed discussion. Perhaps we can start with EOS-448, which is the anti-TIGIT antibody that's Fc-enabled. So obviously it's a very competitive space, the TIGIT space. There's several antibodies in development. So it'd be great if you could give us a little more detail on EOS-448 and how you believe it is differentiated in terms of its profile as well as the clinical development strategy. Indeed, this is a very competitive landscape, and this is why we believe that the strategic collaboration with GSK will help us to differentiate. Well, we have an antibody with a different profile. When we started this program a few years ago, we directly decided to focus on an IgG1, and we spent a lot of time to optimize the affinity and the potency of our antibody. We believe it's the first difference. When we consider the two extremities of the antibody, we rapidly realized that the affinity was not correlated to the potency, and we spent time to identify EOS-448, which is differentiated from the other antibodies in clinic, and we believe this is due to a different epitope. On the other side, we have identified, and we have selected an IgG1 that allowed to engage, Fc gamma receptor because we believe that TIGIT is really unique amongst all the immune checkpoints due to the multifaceted mechanism of this antibody, both in the capacity to block the binding of TIGIT with its ligand, but also activate Fc gamma receptor and activate additional immune response against the tumor. The data that we presented at AACR last year are the best data presented so far for a monotherapy dose-escalation phase I. In addition, we have been the first one to demonstrate engagement of the Fc gamma receptor at all the concentration tested in the dose escalation. Amongst the 20 patients that we have evaluated for response, we observed 9 stable disease and one confirmed partial response into a PD-1 resistant melanoma. We believe that this compare favorably to the initial monotherapy dose escalation of Merck vibostolimab, where they saw a decrease in tumor size in 20% of patient and one unconfirmed partial response in the patient with non-small cell lung cancer. Also the data with the domvanalimab, where they observed a decrease in tumor size in only 70% of their patient and no partial response. In addition, at AACR, we also share data that demonstrate this depletion of Tregs in the peripheral blood that illustrate this very efficient engagement of the Fc gamma receptor that could trigger this multifaceted mechanism. Okay, great. Now as I understand with with EOS-448, you're in several different combination cohorts and in a variety of of cancer types. Could you just give us a little bit of detail as far as how you've selected the combinations as well as how you've chosen which tumors to explore? Yes. Well, this is indeed a very important component. Just to be clear, we don't consider that TIGIT is just an add-on on PD-1. We believe there are multiple combination to perform. The initial combination will be with dostarlimab, the PD-1 antibody of GSK, which has been approved in traditional indication. There's a clear proof of concept of an active IgG1 TIGIT isotype with PD-1 based on the Genentech data. The benefit of this collaboration with GSK is that the next wave of development could pull a third component from either of our diverse portfolio. We'll be evaluating the safety of two triplets, TIGIT and PD-1 with inupadenant, our selective A2A antagonist, and GSK CD96 program, which is the first CD96 program in clinic. We could also leverage additional program such as the GSK TIGIT Ig program. We have announced an intent with GSK to initiate two registrational trials with the doublet of TIGIT and PD-1. Non-small cell lung cancer, where there is a clinical proof of concept data, giving us the highest probability of success and an opportunity to confirm in the clinic the differentiation we have observed with EOS-448 compared to other TIGITs. The second indication is head and neck cancer. What we like about this indication is that these tumors are highly immunogenic, giving a strong scientific rationale. There is a high unmet need. Also, by moving rapidly towards registration, we can be competitive on time to market as well. There's a third indication that we have not yet disclosed. That will be an indication which is an immune sensitive tumor type, where today there is no other clinical trial in development. With this mix of very competitive indication where we can differentiate both on the basis of the characteristics of our antibody and the triplet, plus head and neck, where there's a low level of competition, and the third indication where there is no competition, we believe that we have multiple shots on goals. On top of this PD-1 combination, we are also combining EOS-448 with inupadenant. We believe there is an opportunity for PD-1 resistant melanoma patient based on our phase I data monotherapy for each of the program. We have also started a clinical supply agreement collaboration with BMS to combine EOS-448 with iberdomide, which is a next-generation CELMoD molecule of BMS in multiple myeloma because we have generated and presented at ASH last December very exciting data showing that the combination of Fc gamma receptor active TIGIT with an IMiD was giving a very strong antitumor effect in multiple myeloma models. Okay, good. You've touched on a lot of the topics that I wanted to cover. So maybe starting with the combo of EOS-448 and durvalumab, the anti-PD-1, you said you're doing the studies in first-line PD-L1 high lung cancer, head and neck, and then a third undisclosed indication. Could you just give us a sense as to when these studies are getting started, when we might see data, and if you could provide any more details on the design of these trials? In agreement with GSK, we'll give more information at the time we are ready to start. We are working very hard to be ready to start this different registration-directed studies. We are currently evaluating the safety of the combination durvalumab with EOS-448, and we are planning to start in the near future these different registration-directed studies. We will release the first set of data somewhere in 2023. Okay. Is the scientific hypothesis that you expect to see synergy between EOS-448 and the anti-PD-1? What do you think for each of these indications for lung cancer, head and neck, and then the undisclosed one? Well, the undisclosed one, I guess we'll have to wait. What's the bar for clinical success in non-small cell lung and head and neck? Well, for the non-small cell lung cancer, there is obviously the data of Genentech with their SKYSCRAPER-02 that will come later this year. SKYSCRAPER-01 and SKYSCRAPER-02, that will be very important to define, I would say, a new reference. Today, the reference in our trial and the comparative arm will be with pembro. The response rate of pembro in the high PD-L1 will be our standard. For head and neck, we are rather at a response rate, which is typically lower for pembro. That will be also the competitor. We'll use this reference in order to evaluate the benefit of TIGIT. It's difficult at the current stage to evaluate if it could be additive or synergistic. As you know, that require a lot of data. For the moment, we are targeting at least an additive effect of the two programs. Okay. When could we expect to find out what this undisclosed indication is? When we are ready to start. As you said, it's a very competitive landscape, and we have identified a new responsive tumor type, which is very interesting based on our science and the data that we have generated on each side, GSK and iTeos. We want to be sure that we discuss the information at the time we are ready to start. Okay. You have the registrational directed study with EOS-448 and dostarlimab. I'm curious why you're also planning to start a phase I with pembro in solid tumors. Why that study? Yes, indeed. Just to clarify where we are for that. With regard to the combination with pembrolizumab, at the time we entered into the collaboration with GSK, the initiation of this study was well underway. Both parties were interested in keeping the study on track as an efficient way to generate data to support the safety and the dose selection for the TIGIT PD-1 combination. We are building a data set that will be informative and supportive as we move quickly into the randomized studies with dostarlimab, particularly around the justification of the dose for PD-1 combination. As you know, this is a more and more important consideration for the discussion with the regulatory authorities. Okay. Understood. That makes sense. You also mentioned the combo of EOS-448 and iberdomide, the IMiD in myeloma. Maybe go into a little more detail there about what you showed in the preclinical data that supports the combination and the potential synergy of those two molecules. Yes. We have had a collaboration with Geoffrey Hill at the Fred Hutch in Seattle, where we have demonstrated that there does seem to be a significant benefit of the combination of EOS-448 and an IMiD molecule. We have also shown that during the progression disease, there's an increase of TIGIT expression on the multiple myeloma cells, and we believe that there is an opportunity here which is so far unexplored. We decided to work with iberdomide, which is a novel potent oral cereblon E3 ligase modulator, a CELMoD compound with enhanced tumoricidal and immune stimulatory effect compared with the IMiDs, which has demonstrated activity in the relapse refractory multiple myeloma patient previously treated with IMiDs. We believe there is a very interesting opportunity to explore there with an original combination on top of what we do with PD-1 or with inupadenant. Okay, makes sense. You also mentioned that you're going to have triplet studies with four-four-eight, dostarlimab and either the CD96 or inupadenant. Could you just tell us a little bit more about the rationale for the triplet combination? Yes, indeed. This is very specific for, I would say, the most competitive indication like the non-small cell lung cancer PD-L1 high. As I told you, we are starting a phase III there because we believe that we have a potential best in class, and we could already see a benefit with the combination of dostarlimab and EOS-448. We also believe that we can go one step further and move in evaluation of triplet combination, even if they are more complex to set up. With the fact that GSK is invested into the TIGIT CD226 pathway with multiple combination to explore. We have PD-1, the dostarlimab, EOS-448, and CD96. GSK is also moving with this PVRIG program they've licensed from Surface Oncology, which is the second one. Obviously inupadenant will be an important part. We will initially evaluate the safety of this combination. I expect to evaluate this combination in a randomized trial once safety has been demonstrated. The recent guidance that Arcus has provided is highly encouraging and consistent with our assessment of the rationale of triplet of therapeutics targeting TIGIT, A2A, and PD-1. We feel that the Fc-enabled TIGIT antibody and our insurmountable A2A antagonist position us to be differentiated in this combination if Arcus release positive data from their ARC7 study in the second half of the year. For CD96, GSK has generated very exciting data in preclinical model in their current phase I showing that CD96 could be a very interesting add-on to the combination of dostarlimab and TIGIT. I want to specify that TIGIT remain the main component of the strategy for GSK and ITOS, and that additional combination in triplet could be specific for given indication. Okay. Maybe tell us a little bit more about CD96. I think most people are not familiar with that target. Is that one in the adenosine pathway or is it different? Yes. Thanks for asking the question. This is one of the component of the TIGIT pathway. In fact, there are three different immune checkpoints that bind similar set of ligands, CD155, CD112, and CD113, plus some accessory ligands. TIGIT is the most important one. It's a negative costimulatory immune checkpoint. You also have PVRIG or CD112 receptor, which is also one of the program developed by GSK, and you have CD96. These three receptors are negative costimulatory immune checkpoint. The first receptor in this pathway is CD226, which is a positive costimulatory immune checkpoint in the pathway binding to the same ligand. CD96 is an original approach that could be an add-on on the TIGIT inhibition. Understood. Thank you. Now, if we could just move over to talk a little bit more detail about inupadenant, the A2A receptor antagonist. Obviously, that's, you know, a fairly crowded landscape in terms of drug development. Help us understand how inupadenant is differentiated. Then also, you know, give us a little bit of an understanding of why you picked A2A, for example, as opposed to CD39 or CD73. Indeed. If you take, I would say the basic mechanism in this adenosine pathway, ATP is released at very high concentration, up to 500 micromolar in the tumor microenvironment following necrosis, and hypoxia. ATP is pro-inflammatory. You have enzymes that are able to transform ATP into AMP, CD39. AMP is transformed into adenosine by CD73. Adenosine binds to receptors expressed by immune cells in order to trigger an immunosuppression. This mechanism has been known for decades to be very important to controlling inflammation. It's only a few years ago that several companies started in parallel to target this pathway, either with antagonists of the adenosine receptor or inhibitor of CD39 and CD73. First, we believe, and it has been shown that A2A is the high affinity adenosine receptor playing the key role in immunosuppression. A2A is the receptor with the highest expression in all immune cells from the tumor microenvironment, and the affinity for A2A is 100-fold better than the affinity for A2B. A2A is a key component. I don't discard the fact that A2B could be interesting in some specific tumor types, especially when A2B is expressed on tumor cells. However, most of the compounds in current development which are both targeting A2A and A2B also target A1, and A1 could be red flag in terms of safety. We believe that with our program, which is highly specific for A2A, we target the most important receptor responsible for inflammation, and we also have the best possible safety profile. Coming back to the two other enzyme involved in the pathway, CD39 and CD73 are mainly targeted to decrease the production of adenosine in the tumor microenvironment that impact the activity of adenosine on immune cells through A2A receptor. We believe that there are other mechanism which are able to produce adenosine. When you inhibit CD39 and CD73, you could have, in some patient or some indication, a significant decrease of adenosine. But in other indication it could not be sufficient because other compensatory mechanism will be able to produce adenosine. Therefore, we believe that targeting the endpoint will be important. The recent data obtained with CD73, the randomized study in lung cancer, is very encouraging for the clinical proof of concept of adenosine-mediated immunosuppression. We remain convinced that targeting the endpoint of the pathway will give the most important clinical benefit in the largest set of indications. Okay. That's very helpful. I think you answered my question about A2B, so thanks. But you also mentioned A1, which you said is a red flag for safety. What exactly is the problem there? In our characterization of the different adenosine receptor antagonists in clinics, we have found that the receptors which are dual antagonists are also in fact pan-adenosine receptor antagonists. They are also inhibiting A1. A1 in the past has been developed. A1 antagonist has been developed by several pharma for application in cardiovascular therapeutic area. At least one program by Merck, rolofylline, showed that in phase III there was a significant increase in stroke and seizure in patients treated with rolofylline compared to the control arm. We believe that it could be a limitation because this increase in the toxicity of rolofylline was only observed in pivotal trials and has not been observed in previous clinical trials in phase I or phase II. We believe that having a compound which is highly specific for A2A will give the best possible safety profile, in addition to the fact that A2A, as I told you, is the most important receptor to target. What you're saying is, if you want to design an A2A/A2B dual blocker, the problem is if you want to design it, you're also gonna end up being a pan-adenosine receptor blocker because of the chemistry of the receptors. Is that? This is what has been obtained so far. Yeah. by company developing such kind of antagonist. Got it. Interesting. Now you also have a predictive biomarker strategy for this drug, for inupadenant. Tell us more about that. Which biomarkers are you assessing, and how does that help- Yes. How does that help you choose indications? Indeed, if we consider our position in the adenosine pathway, there are three component that make us unique. Well, first, for this A2A receptor targeting, we have developed a highly selective antagonist, but which is also insurmountable. In other words, whatever the adenosine concentration that we find in the tumor microenvironment, our compound will be always active. Whereas the other adenosine receptor antagonists are classical competitive antagonists that will be competed by adenosine. Second, we have identified another target in the adenosine pathway, that will bring an additional benefit on top of targeting A2A. This is a first-in-class program that we will progress through IND-enabling studies this year to start a phase I early next year. We believe that it will be an additional value on top of inupadenant. Finally, at ASCO last year, we presented results from our initial study in monotherapy, where we found that the number of cells expressing the adenosine receptor A2As, the adenosine A2A receptor in the tumor was correlated with clinical benefit in the patient based on immunohistochemistry assay. We have also looked at other marker by immunohistochemistry and by NanoString, looking at mRNA, and we have identified other markers that are also potentially allowing us to identify patients that could benefit from the treatment with inupadenant. Okay, got it. And then you're also doing a study with inupadenant in PD-1-resistant melanoma. What's the thinking there as far as how an A2A receptor antagonist would overcome PD-1-resistant melanoma? Well, as we previously disclosed, we saw a very promising response to inupadenant monotherapy in a patient with melanoma that was resistant to both pembrolizumab and ipilimumab. In fact, this patient continues to be in a durable response more than two years after starting therapy with inupadenant. We have also seen a response to TIGIT monotherapy in a patient with melanoma resistant to pembrolizumab. Effective treatment in the post PD-1 setting remains an unmet medical need in melanoma and in many other solid tumor, and we believe that inupadenant combination could have value in the post PD-1 melanoma and in other solid tumor. This is the reason why we are currently dosing this patient population. That could be a key proof of concept for a new mechanism of resistance in PD-1 resistant patients. Okay. Did you wanna add anything else on inupadenant? I wanted to also ask you about your preclinical pipeline. Yes. With inupadenant, we are going to announce by mid of this year or to disclose a randomized phase II in combination with chemotherapy. We have generated data showing that it would make sense to go in this specific combination to mesothelioma indication, which is an important step for us starting this randomized phase II. We are also planning to start additional studies. Obviously, the readout this year of ARC-7 will be also a catalyst to move forward with our inupadenant program. The first step will be this randomized phase II by mid of the year that we'll start with in combination with chemotherapy. Okay. You have in the preclinical pipeline EOS-984 monotherapy. Well, can you tell us what the target there is and what tumors would be likely choices? Well, I cannot tell you the target due to the competitive intelligence. In fact, this is really first-in-class. Nobody has ever characterized this target in the adenosine pathway. We identified this target as we continue our in-depth mechanism of action studies on inupadenant. We believe that this new mechanism will bring a significant added value, not only in combination with inupadenant, but also with different standard of care due to a specific impact on T-cell proliferation. We believe that we have discovered something fundamental about how adenosine works to generate immune suppression and how we can better tackle that immunosuppression in a targeted way. Well, we are completing the CMC and we are preparing the GLP tox. We plan on dosing our first patient in the first half of 2023, and we are going to work also and continue to accumulate data to determine what could be the best indication to target and what could be the different, combination to consider. It's still too early to define exactly what could be the most relevant indication to target. As I told you in the introduction, we have 80 scientists working with their expertise in tumor immunology to identify additional target. We will continue to develop our pipeline in order to be able to bring a new breakthrough immunotherapies, to our patient. Okay. The EOS-984, am I correct that it's in the adenosine pathway or it's different? Yes. This is in the adenosine pathway. Okay. Okay, got it. Now we have a question coming in from one of our investors who's listening. They wanted to know a little more detail about CD96. Could you tell us when we might see data from the phase I trial? And they're also wondering, you're doing the combo with TIGIT, why not do a combo with CD96 plus PD-1? Well, first the data will be disclosed by GSK. This is their program, and they will decide when they disclose the data. Second, as I told you, we consider that CD96 will be an add-on on our mainstay with EOS-448. As I said, we are planning to get the evaluation of the triplet of TIGIT plus dostarlimab plus CD96. Can you repeat the question if I did not answer that to it? Because you just asked me, are we going to combine CD96 with TIGIT and PD-1, correct? Well, yeah. Yeah. We are planning to do that. In parallel- You are. Yes. In parallel, in the collaboration, GSK is also moving forward with the PVRIG program they've licensed from Surface Oncology. This program will start very soon, its phase I and will be another opportunity to evaluate this triple combination. I believe, as I said, that this triple combination will be really tailored for specific indication. Based on the expression profile in this indication, the main target will be TIGIT, and for some specific cases we will consider the triplet combination. You are doing that. Then the question, the other question is. One second, I just have to go back to my screen with the email. They're also asking why not do a broader program? I mean, a really broad program looking at a whole bunch of different solid tumors as opposed to just in certain tumors. I want to be clear that what we are discussing today is a starting point. We want to go stepwise. We want to remain amongst the frontrunners. I know that there are other companies having 6, 7 different clinical trials. This is obviously a consideration for us. We want to continue to generate the data, and we are just at the starting point of what we are going to develop. We believe that TIGIT is one of the most exciting immunotherapies of the new generation. There are 3 or 4 readouts this year by Genentech that will be a potential catalyst to expand our clinical development in collaboration with GSK. This is something that we are going to do in a diligent way. Again, what I've presented today is a starting point which is based on our scientific and clinical evaluation of what could be the first opportunities for us to develop TIGIT and validate a potential best-in-class. Understood. Okay, thanks. Just to finish up the session, just some housekeeping. You mentioned the cash of $900 million. Just remind us what's the runway, again? This cash of $900 million, that was the cash at the end of September 2021, including the receipt of the full upfront payment of $620 million from GSK. In a full success scenario, where we are funding an aggressive plan across both clinical programs and if success bring additional programs from discovery to the clinic, we still have more than four years of cash runway sorry, during which they will have readouts from multiple phase III for both EOS-448, where GSK support 60% of the cost and significant progress and data on inupadenant. This guidance of four years runway includes all the expenses to run this plan while also expanding our pipeline and building toward a potential commercial launch. Got it. Okay. If you could just maybe summarize, you know. I know you said you weren't gonna have data this year, but any other milestones that you could point to either this year or next year? Well, we are going to continue to deliver additional data to validate our potential best-in-class. For example, with a groundbreaking new abstract, which has been accepted at AACR for the presentation of the impact of EOS-448 in the tumor microenvironment in patients treated with the antibody. Indeed, 2022 will be a year of execution for us as we work to initiate all the studies that we have discussed today. In addition, this year will be very important with the results of Genentech in small cell lung cancer, non-small cell lung cancer and esophageal cancer, and from Arcus also with the ARC-7 trial in non-small cell lung cancer that is comparing PD-1 with the doublet of TIGIT and PD-1 and the triplet of TIGIT, PD-1 and adenosine antagonist. The first data readout for our clinical trial will come later in 2023. Understood. Okay. Since we have a little bit more time, if you could answer this. If not, that's okay. Just the patent landscape. Like how much IP protection do you have on the different assets? We have been very diligent and very professional for our different patents. This program has been initiated recently. Our patent coverage is going to the end of the piece. We continue to work on the patent life cycle management. We continue to work on that. We have a very strong patent position for our two programs, and we will continue to develop and protect this patent position. Okay. Obviously, you have a great partner with GSK. Are you continuing to look for other partners, or are you happy with the GSK partnership? This is a very important point. As I explained, we believe that having identified GSK as our partner for TIGIT was the best move for us. We have a partner which is totally dedicated to the CD226 TIGIT pathway with significant investment in order to develop this program. We have kept 50% of the U.S. market in this landmark deal. We have checked all the boxes of what we are planning to do to remain amongst the frontrunners in this very competitive TIGIT pathway. For adenosine, this is a very different situation. We believe that we have all the resources to move forward with our best-in-class adenosine receptor toward registration. We have the collaborations, we have the clinical supply agreement, we have a clear path toward registration. We are currently validating this biomarker. We have this additional program, and we don't feel that we need today a partner to move forward with inupadenant and be the first, if not amongst the frontrunner for that program. We are very confident that we'll be able to deliver the strategy that will allow us to go toward registration as efficiently as possible. Okay. I'm just curious also about your scientific advisory board. How much of a role do they play in helping you drive the clinical strategy and in designing the clinical studies? Well, I would say that we really focus our SAB on our new program and the review of our data. For example, we discussed a lot with the SAB, the biomarker that we've generated and what could be the use of this biomarker beyond the clinical development to have a better understanding of the adenosine pathway and the TIGIT pathway and identify new possible combination. Example of this collaboration with Fred Hutch for the iberdomide combination is an excellent outcome, I would say, of our scientific approach, which is supported by our SAB. For our clinical strategy, we have a different approach. We have ad hoc meeting with clinical expert in each different indication, and we are discussing our clinical strategy for each indication with these different panels. We have almost 10 different panels that we use as a sounding board in order to refine our strategy with the evolving landscape in each of the different indication. We will continue to integrate in our SAB additional expert, and you will see some new names coming soon in order to be sure that we address also other mechanism of immunosuppression that could be interesting to start new programs. Okay. You have the one preclinical we talked about, EOS-984. I know you can't tell us the target yet, but I'm just wondering how much more effort is there in the research, the early discovery stage at the company? I mean, should we expect that there are going to be other preclinical assets that you're going to disclose, in the next, you know, one to two years? Yes. We have a second program, which is targeting macrophage, which is currently into the hit-to-lead stage. We are also planning to validate several new targets. I mean, iTeos, in its 10 years of existence, has been able to put in clinic 3 major targets in cancer immunotherapy, IDO1 in 2018, then A2A in 2019 and TIGIT in 2020. That has been a significant journey for us. We continue to leverage our expertise in tumor immunology. We are currently working on several targets for validation. One of the main differentiations of iTeos is that we have learned to, I would say, master tumor immunology in order to select target. What is also important and well illustrated with inupadenant and A2A, we've also learned to develop differentiating modalities. Today, iTeos is a company which is able to develop both small molecules and antibodies, and we want to be sure that once we have identified a relevant target, we are able also to bring a differentiating modality that will allow us to develop a best-in-class compound and not just a me-too. All right. Well, thank you very much, Michel. This was a very interesting discussion. Appreciate the time. Of course, best of luck as you progress with the GSK partnership and your own proprietary pipeline. Thank you. Thank you very much for the support, Anthony. Have a good afternoon. Bye. Bye.