Good morning, and welcome to the iTeos Therapeutics second quarter 2021 financial results conference call. My name is Emily, and I will be your moderator today. At this time, all participants are in a listen-only mode. However, following the formal remarks, we will open the call up for your questions. Please be advised that this call is being recorded at the company's request. I would now like to turn the call over to Ryan Baker, head of investor relations at iTeos. Please proceed. Thank you for joining us today. Joining me from iTeos with prepared remarks are Michel Detheux, president and CEO, and Matthew Gall, chief financial officer. Dr. Joanne Lager, chief medical officer, will be available for Q&A. Before we begin, I would like to remind you all that the team will be making forward-looking statements in the prepared remarks and during the Q&A session. Any statements made during this call that are not statements of historical or current facts are intended to be forward-looking statements pursuant to the safe harbor provisions of the Private Securities Litigation Reform Act of 1995. We want to emphasize that such forward-looking statements reflect our current expectations and assumptions regarding timing, progress, and success of our current ongoing clinical trials, therapeutic potential thereof, expected milestones, our financial condition, including cash runway, our business operation, development efforts, and relationships with third parties and collaborators, and are neither predictions nor guarantees of future events or performance. Actual results could differ materially from those stated or implied by these forward-looking statements due to risks and uncertainties associated with our business, including those under the heading entitled Risk Factors in our quarterly report on Form 10-Q for the quarter ended June 30, 2021, which was filed yesterday with the SEC, as well as in subsequent reports, including our current reports on Form 8-K. The company disclaims any obligation to update or revise any forward-looking statements except as required by law. Michel? Thank you very much, Ryan. Good morning, good afternoon, everyone. I would like to begin today's call by reflecting on the substantial progress we have made at iTeos and the recent announcement of our strategic partnership with GlaxoSmithKline for our potent high-affinity anti-TIGIT antibody, EOS-448. This partnership brings enormous value to iTeos, not only giving this program best-in-class resources for clinical development now and as we look forward for broad commercialization, but also validating our scientific approach and rigor. It also provides a catalyst for our talented team to continue to grow our pipeline of highly differentiated immuno-oncology therapeutics. Our team is deeply committed to developing therapies that focus on mechanisms of immunosuppression. Our approach involves targeting the pathway to reduce immunosuppression and restore the immune response against cancer, meeting the high unmet need that remains for cancer patients. In the last four years, we have put three distinct and highly differentiated programs into clinical trials. With these classical of significant value creation, we have shown that we can leverage our expertise in tumor immunology and continue to build a robust pipeline going forward. Before I go into more detail on EOS-448 in particular and on our plan to further grow our pipeline, let me just take a moment to summarize our partnership with GlaxoSmithKline. We selected GSK as our partner for EOS-448, as there is a strategic focus on the TIGIT CD226 axis. They share our belief that combination of TIGIT, CD96, and CD112 receptor inhibitor can transform cancer care for the many patients who lack effective treatment options. The deal recently closed, and as a result, we received a $625 million upfront payment. We will be eligible to receive up to an additional $1.45 billion in milestone payments should the EOS-448 program achieve certain development and commercial milestones. GSK and iTeos will share responsibility and costs with a 60/40 ratio, respectively, for the global development of EOS-448 and will jointly commercialize and equally split profits in the U.S. Outside of the U.S., GSK will receive an exclusive license for commercialization, and iTeos will receive tier royalty payments. These attributes, both in the partner and in structure, will allow us to expand and accelerate the development of EOS-448 and meaningfully participate in the development process, commercialization, and in the value created. We could not be more happier to be working with a partner with the capabilities and portfolio of GSK, and we leverage this collaboration to generate significant value for all our stakeholders. EOS-448 has the potential to achieve significant immune stimulatory effects through three mechanisms. one, blocking the binding of TIGIT to its ligand, resulting in immune-mediated killing of tumor cells by T cells and NK cells. Two, engaging the Fc-gamma receptor to further promote antitumor immune response in dendritic cells and macrophage through the release of pro-inflammatory cytokines and chemokines, and the activation of antigen-presenting cells. Three, activating NK cells and macrophages to deplete PD-positive cells that are known to dampen the immune response, like immunosuppressive Tregs and exhausted T cells. We have highly encouraging initial first-in-human data for EOS-448 and are pleased therapy in advanced solid tumor during our phase I. Data presented at AACR in April show that out of 20 patients treated with single agent EOS-448, half of the patients had stable disease or better, and there was a confirmed partial response in a patient with pembrolizumab-resistant melanoma. Peripheral biomarker data confirmed depletion of PD-positive Tregs cells and reduction in exhausted PD-positive CD8 T cells, whereas the other effector T cells remain unchanged, demonstrating a multifaceted mechanism based on potent engagement of both PD and the Fc-gamma receptor by EOS-448. Based on the robust biomarker data, preliminary signs of efficacy as monotherapy, and data showing EOS-448 was well tolerated with no dose-limiting toxicities, the clinical development plan with GSK is geared towards advancing rapidly to registration-directed trials in indication and combination where we see the most potential to benefit patients. Having a partner with an approved PD-1 and a portfolio of potentially complementary programs gives us the ability to move rapidly towards approval and to work with GSK on novel regimens. We plan to start combination studies of EOS-448 with GSK's recently approved anti-PD-1 drug, JEMPERLI or dostarlimab, later this year, and plan to initiate trials in non-small cell lung cancer and additional indications in 2022. We are currently initiating a trial of EOS-448 in combination with pembrolizumab and with our novel A2A receptor antagonist, inupadenant, in patients with solid tumor. We are also moving forward with a trial to evaluate EOS-448 as a monotherapy and in combination with an IMiD molecule in patients with multiple myeloma. Turning to inupadenant, adenosine suppresses the immune response against tumor and inhibits responses to current cancer therapies. The adenosine receptor, A2A receptor, is a receptor responsible for mediating adenosine immunosuppressive effect on immune cells within the tumor. Based on our understanding of the unique condition within the tumor microenvironment, we thoughtfully designed inupadenant, a drug that could selectively and potently inhibit A2A receptor, even in high concentration of adenosine in the tumor microenvironment. Inupadenant is a next-generation A2A receptor antagonist with differentiated pharmacologic properties. Unlike prior generations of adenosine receptor antagonists, inupadenant was designed to inhibit A2A receptor even at high concentrations of adenosine. Inupadenant is highly selective for A2A receptor and has no brain penetration properties, which are expected to reduce off-target safety effects and improve the therapeutic index. At ASCO in June, we reported updated results from our monotherapy dose escalation phase I trial study. In 43 patients with advanced solid tumor treated with single agent inupadenant, we saw durable responses of stable disease greater than six months in five patients with advanced solid tumor, including the previously reported confirmed partial response in patients with checkpoint inhibitor-resistant melanoma and heavily pretreated castrate-resistant prostate cancer. Both of these responses have lasted greater than 12 months. We also newly reported a patient with heavily pretreated non-small cell lung cancer with stable disease lasting for more than 10 months. We are pleased with the depth and durability of anti-tumor responses we have observed to date and with the tolerability of inupadenant. Preliminary analysis of tumor biopsies indicated that the expression of A2A receptor in pre-treatment tumor samples is associated with clinical outcome in patients with solid tumor treated with single agent inupadenant. We will continue to integrate a biomarker-driven approach into our A2A receptor clinical programs to choose optimal therapeutic combination and identify the patients most likely to benefit from treatments. We are currently evaluating inupadenant in combination with pembrolizumab and with chemotherapy, and we are planning expansion in selected solid tumor, including PD-1 resistant melanoma and another large indication, and we will continue to evaluate potential biomarkers. More information about our complete development plan will be shared in the near future. We will also be initiating evaluation of a triple combination of inupadenant, EOS-448, and PD-1. Turning to our discovery engine, we have a robust discovery effort ongoing, and we continue to progress research programs focused on additional targets that address pathway of immunosuppression. As we build our pipeline, we expect to nominate an additional product candidate for IND-enabling studies before the end of 2021. The team is very excited about this candidate, which targets an internally discovered mechanism of immunosuppression in the pathway, and which we believe will be a best-in-class agent. We believe that we have assembled significant expertise in target identification, modality selection, and tumor immunology that we can leverage to build upon our demonstrated track record of success to build a differentiated IO pipeline. With our headquarters in Cambridge, Massachusetts, and our R&D center in Belgium, iTeos' global presence allow us to attract talent worldwide and remain at the forefront of innovation in the field of immuno-oncology. I will now hand the call over to Matthew Gall, our Chief Financial Officer. Thanks, Michel. I'd like to provide a brief update on our financial results for the second quarter of 2021. The company's cash and cash equivalent position was $302.9 million as of June 30th, 2021, as compared to $136.9 million as of June 30th, 2020. Following receipt of the upfront payment from GSK pursuant to our collaboration and license agreement earlier in August 2021, we believe that our existing cash and cash equivalents would enable us to fund our operating expenses and capital expenditure requirements into 2026. Research and development expenses were $14.2 million for the quarter ended June 30th, 2021, as compared to $6.1 million for the second quarter of 2020. This increase was primarily due to an increase in activities related to clinical trials for EOS-448 and inupadenant, and increased headcount. General and administrative expenses were $15.1 million for the quarter ended June 30th, 2021, as compared to $2.4 million for the second quarter of 2020. This increase was primarily due to increased headcount, professional fees, and other costs associated with becoming a public company, along with advisory fees incurred by the company for the collaboration and license agreement with GSK. The net loss attributable to common shareholders was $26.5 million, or a net loss of $0.75 per basic and diluted share for the quarter ended June 30th, 2021, as compared to $10.3 million, or a net loss of $29.49 per basic and diluted share for the second quarter of 2020. I'll now turn the call back over to Michel for closing remarks. Thank you, Matt. As we move into this period of running our proof of concept trials in several immuno-oncology combinations, we have also begun to prepare for pivotal trials, which we plan to initiate in the next 12 to 18 months. We will be focused on execution of our clinical programs and on continuing to elucidate the mechanism of action of our drugs to inform our development programs. We expect to generate data across multiple indications in different combination with both of our clinical stage assets, including the initiation of several clinical trials with our partners at GSK over the coming months. Thank you very much for your attention on today's call and your ongoing interest. I'd like to now turn the call back over to the operator for questions. Thank you very much. If you would like to ask a question, please do so by pressing star followed by one on your telephone keypad. If you change your mind please press star followed by two. When asking your question please make sure your line is unmuted locally. first question today comes from Chris Raymond from Piper Sandler. Chris, please proceed. Hey, thanks, and congrats on the progress this quarter. Just a couple. Maybe first, a strategic question. I guess it's pretty remarkable that you guys have funded now out about 5 years or so. I'd say that kind of runway is kind of at the high end of what we've seen for an earlier stage company like you guys. Just as you think about maybe your, I guess, intertemporal, maybe investment choices, can you talk about the assumptions that went into this cash runway guidance? I guess, long and short of it, is there any sort of business development embedded in this? Is there any other activities? Thanks. Hi, Chris. Michel speaking. Yes, indeed, this is something which is remarkable and that will allow to create multiple short on goals. The plan that we have designed with GSK incorporates us moving as quickly as possible. This includes initiating several phase II studies. That said, with GSK paying 60% of development expenses, this program still only consumes about one-third of the cash balance. We believe that the data for inupadenant will support the advancement into the phase III studies. We have indicated that in our cash runway. The company has put three existing programs in clinical trials over the past four years, as we said. There's a track record of clinical value creation that we feel is sustainable for generate future programs. We are in discussion with integrating several programs that we developed in-house, and we believe we'll be able to address different mechanisms involved in modulating immunoresponse against tumor cells. We have also integrated a few academic partnerships that will expand our expertise in tumor immunology and drug discovery, and we are also integrating, I would say, opportunities in external innovation. I want to stress that we'll be really opportunistic and cash efficient there. We know what we are looking for, and we take the time to find the best opportunity to expand our pipeline within this cash runway. Okay. Just a follow-up, maybe more detailed. Do you have an update on the A2A biomarker for inupadenant? Just any progress there and any sort of guidance as to when we'll see additional data? Yes. I'm going to turn the question to Jo to give the most recent update. Jo, please. Thank you, Michel, and thanks, Chris. We have reported some initial data on our biomarker at ASCO this year, showing that the expression of A2A receptor itself is associated with clinical outcome for the patients treated with monotherapy. We are continuing to investigate those biomarkers, and using that data to understand what types of cells are expressing A2AR within the tumor, and are developing a, I think, a more profound understanding of the mechanism of action of the drug, which is informing our indication selection, and which we will be incorporating in our clinical development plan as we move forward. We anticipate reporting that data out sometime next year, as we kind of put all the pieces of the story together. Okay. Thank you. Our next question comes from Daina Graybosch from SVB Leerink. Please go ahead. Hi. Good morning. Thank you for the question. I'd like to get into now that we're a little bit past the GSK deal, your guys' perspective on the broader TIGIT CD226 axis. There's four members now that the collaboration has together. You mentioned the CD96, and of course, there's also PVRIG, and with the potential to count PD-1 as well. I wonder of all those, three questions. What gives you confidence to double or triple down on the CD226 axis? Which of the various combinations are you guys most enthusiastic about? With CD96, I find it perhaps the most complex and controversial, with some literature suggesting you should inhibit it, and other literature suggesting you should stimulate it for antitumor immunity. I believe even from the GSK approach is inhibition, and what gives you confidence that's the right approach? Thanks, Daina. I want to mention that the primary goal of the collaboration is to move forward with the combination of dostarlimab, the PD-1 from GSK, and our TIGIT antibody, IRX-444. In some specific indication, we could look for TIGIT combination that will include different options. CD96 or CD112 receptor could be appropriate in some specific indication where you have high level of one of these two partners on top of TIGIT. We are also evaluating the triple combination of PD-1 plus our TIGIT antibody and our A2A receptor antagonist, inupadenant. We believe there's a strong rationale there with good clinical data. Coming to the specific question of CD96, GSK built a strong dataset showing that inhibiting CD96 will provide a significant antitumor effect, and that the combination of CD96 plus TIGIT plus PD-1 in some setup could create an additional synergy that will allow to be differentiated from the double combination of PD-1 plus TIGIT. Got it. No near-term plans for the PVRIG in combination with your TIGIT that was licensed from Surface by GSK? Jo, do you want to comment on that question? That is another combination that we're interested in, Daina. The PVRIG CD112 receptor antibody at GSK has not yet entered into clinical trial, so it will be a later step. It is another combination that we're interested in. Thank you very much. Our next question comes from Swayampakula Ramakanth from H.C. Wainwright. Your line is now open. Thank you. This is RK from H.C. Wainwright & Co. Good morning, Michel. I apologize if this question has been asked. I've been jumping between calls. On the inupadenant, in your press release, you state that you're going to be looking at several indications and also will be using different biomarkers to select patients. Could you highlight a couple of indications that you would be going after? Also, what sort of biomarkers are you looking to work with? Good morning, RK. Well, we've been very excited by the data we published at ASCO two months ago about the relationship between expression of the receptor identified by immunohistochemistry and the antitumor effect in patients. We are currently expanding this biomarker validation in order to select a specific patient with different indication. Jo, can you give more detail on what you're planning to do for this biomarker strategy, please? Yes. Hello, RK. As Michel said, A2AR is correlated with clinical outcome. That's the data that we presented at ASCO. We are using this data to really explore the mechanism of action of the drug. We think that we're getting, from our translational data, from our clinical trials, new insight into how the drug is working to restore antitumor immunity. We are evaluating, based on that data, a number of indications. We are planning to proceed, as we've previously discussed, with a cohort in post-PD-1 melanoma, and we are evaluating other solid tumors based on the data that's coming in. We anticipate giving an update on the clinical development plan later this year. Thank you both. Then with the good war chest of cash now, thanks to GSK collaboration, Michel, if you had the chance to bring in molecules, or if you're looking for additional molecules to be brought into the pipeline, what sort of molecules would you be looking at? Would you be looking to add more to the A2AR franchise or to other tumor microenvironment molecules? Yes, indeed. With the 5+ years of cash runway, we have integrated our investment into the TIGIT clinical development plan, our inupadenant program also, and expanding the pipeline. As I said before, with our expertise in tumor immunology, we have shown that we have been able to select the right targets, the best possible modality, and that we have also an expertise in tumor immunology to select or to identify relevant patient population. We have a preclinical program, which is a new target into the application of our inupadenant program, and we are going to nominate a clinical candidate before the end of the year for this program, and we'll give more information about the specificities of that program and why we are excited to have discovered this first-in-class program. We are also considering other, I would say, axes in order to promote the antitumor response of the immune system. So far, we have worked with inupadenant on one mechanism which is targeting T cells, but also additional immune cells, and we will produce more data, as Jo mentioned, in the near future. With TIGIT, we are targeting T cells, NK cells, dendritic cells, and macrophage, and we believe there are other mechanisms that could be used either in pembro or in combination with standard of care or our pipeline to continue to boost the immune response against cancer cells in different tumor types. If we look for external innovation, it will be with mechanism targeting additional type of immune cells which are not covered by our current program at the clinical stage or in the preclinical pipeline. Thank you. Thank you very much, and good luck with everything. Thanks. You're welcome. Our next question today comes from Anupam Rama from JP Morgan. Please proceed. Hey, guys. Thanks for taking the question. Congrats on all of the progress. Maybe just a quick one on EOS-448 from me. Strategically, what's the rationale and value of studying in combination with pembro if the dostarlimab combination, I think, Jo, you said was supposed to start later this year or maybe early next year? Thanks so much. Hi, Anupam. Well, we agreed that our work on the combination with dostarlimab could help to inform our next steps and will work to getting started in order to generate data as quickly as possible on the safety of the combination and evaluate the efficacy in advanced lung cancer in PD-L1 high and low population. In parallel, we are also working to accelerate the evaluation of the combination of EOS-448 with dostarlimab, which will be evaluated in transform trials in non-small cell lung cancer to be initiated by GSK and will add additional indication that will be added to the clinical development plan. Jo, do you want to add something? I'll just emphasize what you said, Michel, that the intent of moving forward with this study is really to continue to accelerate the program and to generate data in this time as we're getting started with dostarlimab combination. Thanks for taking that question. As a reminder for everyone, if you would like to ask any further questions, please do so by pressing star, followed by one on your telephone keypad now. We currently have no further questions registered. I will now hand back to Michel for any closing comments. Well, I would like to thank everyone for taking time to review our progress. As we said, we are focused on the execution, both at the clinical stage and technical pipeline, and we will continue to move forward with our clinical strategy to deliver strong data for our clinical assets and to build our pipeline. Have a nice day. Bye. Thank you everyone for joining us today. This now concludes today's conference call, and you may now disconnect your lines. Please have a lovely rest of your day.