Welcome everyone to the 39th Annual J.P. Morgan Healthcare Conference. My name is Anupam Rama. I'm one of the senior biotech analysts here at J.P. Morgan. I'm joined by Matt Bannon and Tessa Romero from the team. Our next presenting company is iTeos. Before I turn it over to Michel, I just wanted to remind everybody, for everybody on the webcast, if you want to ask a question, please submit it through the portal via the Ask a Question feature, and I'm happy to ask a question on your behalf. With that, I will turn it over to Michel. Michel? Thank you very much for the introduction, Anupam. I'm very pleased to present iTeos at this 2021 J.P. Morgan conference. iTeos has built an expertise in immuno-oncology by developing novel therapies focused on well-established mechanisms of immunosuppression with differentiated strategies. I'm going to describe today our pipeline, the progress made in 2020, and the multiple opportunities and inflection points in the near future. On slide two, the presentation contains forward-looking statements that could impact our risk factor. This risk factor can be found in our public filings to SEC and in our most recent 10-Q. Moving to slide three, 2020, despite all its challenges, has been a tremendous year for iTeos. First, we have continued to expand our deep expertise in the biology of the tumor microenvironment. This has allowed iTeos to build its differentiated pipeline. Second, we have progressed with our clinical programs. Inupadenant, previously called EOS850, a unique A2A receptor antagonist currently in phase IIa, and EOS448, our anti-TIGIT antibody, which has just completed its enrollment in the phase I dose escalation. Third, we completed a crossover followed by an IPO that allow iTeos to be well-capitalized. Finally, we have been very proud how our team reacted and adapted in 2020. We have continued to invest in our capabilities to accelerate and expand our clinical development plans, we have been able to move forward in our clinical execution despite the limitations triggered by the pandemic. The slide four summarize our pipeline and the data disclosure in near future. In blue, adenosine pathway has been well-known as an important mechanism for the control of immune response. Inupadenant is moving in several phase I/IIa in monotherapy and in combination with pembrolizumab or chemotherapy. We will present additional data related to this program in 2021. In green, EOS448, our anti-TIGIT antibody, has just completed the enrollment in phase I. We will report this data in second quarter, then we'll start a series of phase I-B/II-A in multiple indication with several combination. We are also developing a preclinical pipeline. In dark blue, this pipeline currently includes a first-in-class program in the adenosine pathway targeting a novel mechanism of immunosuppression. We are planning to add a second program in 2021. Now, let's go into detail for each of our clinical program. Stopping on slide five, there are several possible targets in the adenosine pathway. We decided to focus on adenosine receptor as the endpoint of this pathway, which allow to target a larger panel of cancer indication, whatever the mechanisms responsible for adenosine production. I'm going to explain how we have developed a potentially best-in-class adenosine receptor antagonist currently in phase I-B/II-A. On slide six, iTeos scientist designed inupadenant to overcome immunosuppression in the tumor microenvironment. In tumors, there are very specific conditions like hypoxia and cell necrosis that induce an increase of adenosine concentration. First, we design an antagonist that maintains potency at any concentration of adenosine found in human tumors. It has been possible by optimizing the resident time of inupadenant. This is a major difference compared to other competitive antagonists in clinics. Second, this potency profile triggers a prolonged pharmacodynamic effect that will improve the target coverage compared to classical competitive antagonists. Finally, we have purposely designed a very selective antagonist of A2A to improve its safety profile. Some other antagonists currently in clinical development are actually pan-adenosine receptor antagonizing A2A, A2B, and also A1. Slide seven is an update of the dose escalation data presented at AACR in April 2020. On the left, the swimmer plot describes the data of the dose escalation. We have tested 21 late-stage patients with different tumor types at five dose levels and have observed two partial responses, the green stars, and five stable diseases, the orange circles. We have observed in these 21 patients a good safety profile with no DLT, and several patients have been treated for more than one year with inupadenant. On the right, the data obtained with two different pharmacodynamic assays show that all the BID doses, 40 mg, 80 mg, and 160 mg, medium blue, dark blue, and gray respectively, gave a full inhibition of A2A receptor signaling at 24-hour post-doses. Let's focus on this partial response in slide eight. On the left, this is an inflamed tumor responsive to immunotherapies. It's a metastatic melanoma patient with a disease on the right arm who was refractory to two courses of pembrolizumab and one courses of ipilimumab. Seven weeks after starting dosing of inupadenant, the patient showed stable disease with a 26% tumor reduction and reported clinical benefit with a decreased pain and improved mobility of the arm. In the following tumor assessment, a partial response with a 44% tumor reduction was observed, then confirmed later on. On the right, this is a non-inflamed tumor type, which has been rather disappointing for cancer immunotherapies treatment. This patient with metastatic prostate cancer has been treated with five previous rounds of therapies, including enzalutamide, before to start the monotherapy with inupadenant. Measurement of target lesions show a stable disease at eight weeks with a small increase in the lesions, a partial response at 16 weeks that was confirmed thereafter with a 49% tumor reduction. The patient also reported decreased pain linked to bone metastasis and stopped taking the painkiller. We have been very excited to see this confirmed partial response in patient who were not expected to respond to a new immunotherapy. The slide nine summarize our clinical development plan to rapidly expand inupadenant in three indication with different combination. We are currently in the safety and PK/PD expansion cohort, as shown in the middle of the slide, with monotherapy, combination with pembrolizumab or with chemotherapy. The initial results of this expansion cohort will be reported later in 2021. We will also complete the analysis of the matched biopsies of the dose escalation. We are currently analyzing pharmacodynamics and predictive biomarkers by immunohistochemistry and gene profiling with NanoString. The expansion, we'll report the data in 2021. For the signal-seeking expansion, we have currently selected three indication. prostate cancer is attractive based on data obtained so far. It is a large market potential, but has been so far disappointing for immunotherapies. It contains a non-canonical source of adenosine production that could explain why iTeos and others have seen a clinical benefit with A2A receptor antagonist. We are moving with a first cohort in monotherapy on the top right to analyze the mechanism of action and the specific prostate cancer population of interest for inupadenant. We will test in parallel prostate cancer patient with a combination of inupadenant and pembrolizumab. melanoma is the second indication that we selected to combine inupadenant with pembrolizumab. This is a path for a proof of concept of clinical benefit of inupadenant in PD-1 resistant patient. We selected triple negative breast cancer in combination with chemotherapy known to lead to adenosine production through immunogenic cell death. In this indication, CD73, one important enzyme to produce adenosine, has been associated to a poor prognosis and with a reduced antitumor activity. Let's move now to our second clinical program, EOS448, on slide 10. TIGIT has been one of the most exciting targets in cancer immunotherapies in 2020 after a positive phase II readout and the launch of several pivotal studies by Genentech. iTeos has started the clinical phase of EOS448 in February 2020 and just completed enrollment of this phase I. Slide 11 recapitulates the mechanism of action triggered by the different isotypes currently in clinical development for TIGIT. There are two main type of antibodies, IgG1 antibodies, able to engage Fc gamma receptor and silent isotypes. iTeos has decided to develop an IgG1 antibody, which engages Fc gamma receptor based on this preclinical data package. Why is it so important? The left panel shows the initial rationale to target TIGIT as a co-inhibitory immune checkpoint. TIGIT is expressed by T cells, NK cells, and immunosuppressive Tregs. Activation of TIGIT by main ligands, CD155 and CD112, triggers an immunosuppression. When this activation is blocked by an antibody, the ligands will be able to bind to other immune checkpoints, including CD226, which is a costimulatory immune checkpoint expressed by T cells and NK cells. This will trigger an antitumor response. Both anti-TIGIT isotypes, the IgG1 and the silent isotype, will activate these mechanisms. Only an IgG1 isotype will be able to engage Fc gamma receptor, which will increase antitumor response by additional mechanisms. In the middle panel, when the high affinity anti-TIGIT antibody like EOS448 binds to cell expressing high level of TIGIT, there is a Fc gamma receptor engagement by the IgG1 isotype on NK cells and macrophage that will trigger depletion of cells with this high level of expression of TIGIT like immunosuppressive Tregs and exhausted T cells. This will have a positive effect on the immunosuppression in the tumor microenvironment. In the right panel, engagement of Fc gamma receptor by an anti-TIGIT IgG1 will also activate myeloid cells, like dendritic cells and macrophage, and will increase antitumor response by secreting pro-inflammatory cytokines. These additional mechanisms, specific for an IgG1, should contribute to a better clinical efficacy for a TIGIT antibody without any downside compared to a silent isotype. Initial concerns of using IgG1 isotype were related to the safety profile. Several programs have demonstrated that IgG1 antibodies are well-tolerated at effective doses. Moving now on the specific characteristics and differentiation of EOS448 on slide 12. On the left, the competition assay show that EOS448, in blue, is very efficient to block binding of CD155 and to TIGIT. EOS448 compares favorably to the other antibodies tested in this assay. On the right, the functional assay indicates that EOS448, in blue, has a differentiated potency compared to the other antibodies. For example, it's being 50% more potent than Genentech and Merck for this assay. Considering the added value to use IgG1 on slide 13, and another difference of EOS448 compared to the Genentech antibody. Here on the left, we have tested EOS448 with a sample from a lung cancer patient. We have observed a preferential depletion of Tregs when compared to the CD4 and CD8 T cells. Such self-depletion is driven by the level of expression of TIGIT, therefore TIGIT high T cell will be more depleted than TIGIT low T cells. Interestingly, the top right panel shows that the TIGIT high CD4 and CD8 T cells are exhausted, with a decreased production of pro-inflammatory cytokines like interferon gamma, IL-2, and TNF alpha, compared to the TIGIT low CD4, CD8 T cells, as shown on the bottom right. This indicates that in addition of the Tregs depletion by EOS448, the depletion of CD4 and CD8 T cells will preferably target exhausted T cells, not anymore able to trigger an immune response against tumor cells. Moving now to our clinical strategy on slide 14. There are currently several randomized studies ongoing in different indications, all of them in combination with PD-1 or PD-L1. iTeos has completed their enrollment of the phase I dose escalation and will report the data in the second quarter of this year. This is a biomarker-rich study in which we also analyze sample by immunohistochemistry and NanoString, and we will quantify immune cell population in periphery and ultimately in the tumor microenvironment. In mid 2021, we are going to start the combination of EOS448 with an IMiD molecule in multiple myeloma. Through a collaboration with Jeff Hill, we have shown that there's a strong biological rationale to target multiple myeloma. TIGIT is much more important than PD-1 as an immunosuppressive immune checkpoint. It's upregulated during the disease progression, and preclinical models indicate that this upregulation is correlated to exhausted T cells. In these preclinical models, the combination of an IgG1 anti-TIGIT antibody combined with Revlimid gave a strong antitumor effect. We will also combine EOS448 with pembrolizumab in indication with a high expression for TIGIT. Even if we are behind some competitors, our differentiated antibody and a biologically driven approach should help iTeos to build a competitive position. Finally, we have obtained promising data in preclinical models when combining EOS448 with inupadenant, and we are going to test this intra-portfolio combination synergy in one solid tumor. Slide 15 is going to conclude the presentation. As I told you, 2020 has been very successful for iTeos and it has allowed to build the foundation to support transformative acceleration in 2021. The company is well capitalized with a cash runway until the second half of 2023 to support sustained growth in clinical and preclinical operations. Significant data update on both inupadenant and EOS448 will be presented later in the year. We continue to progress inupadenant monotherapy and combination studies in multiple solid tumor types, and we will also advance EOS448 in combination studies in both solid and liquid tumor types. We continue to build our pipeline with original approaches for new cancer immunotherapies, and we will add one additional program in addition to moving the new adenosine pathway inhibitor program to our clinical development. I thank you for your attention, and I wish you the best for 2021. Anupam, if we can come back to the Q&A. Yeah. I just wanted to remind all those on the webcast that you can submit a question to me via the Ask a Question feature in the portal. Do you want to introduce, Michel, the broader management team that you have here on the line? Yes. I invited my team for the Q&A. I have Matthew Gall, our CFO, Matthew Call, our COO, Yvonne McGrath, our CSO, and Joanne Lager, our CMO. Good. Maybe we'll start out with inupadenant here for the A2A program. You've talked about some single agent data as well as some combination safety data expected in 2Q from the phase I-II trial in advanced solid tumors. Maybe just going into a little bit more detail about the size and scope of the data that we're going to be getting, and then what's a win scenario, in your view, given the competitive landscape? Jo, do you want to start with this one? Yeah. We last presented data on this program at AACR in 2020. For us, it was already a win to see partial responses in patients who would be resistant to PD-1 therapy, so the melanoma patient and the prostate cancer that Michel presented. This year, we will be presenting an update of our data. We have done quite a bit of translational work in our study, so we're looking at pre- and post-biopsies, looking at both protein expression, markers of a pathway, immune cell infiltrates, as well as gene profiling and RNA-Seq data. We've enrolled an additional 24 patients in selected tumor types. We are in the process of evaluating the safety of combinations. We are more advanced with the combination with pembrolizumab, and so expect to have some data on that. Okay. I think Matthew Bannon from the team actually had a more specific question on EOS850. Matt? Yeah. Just on the melanoma patient, was just wondering if there was any details on metastases to other organs and how those sites responded to therapy? That patient actually mainly had disease in the right arm. He didn't have visceral lesions or really measurable disease by CT scan. The response was in the skin lesions. Got it. Okay. What about the prostate cancer patient? Were there any notable metastases there? Yeah. That patient had really two enlarged lymph nodes and an adrenal gland metastasis that were the target lesions. Those are what we showed on the screen. The lymph nodes have essentially reduced down to normal size, and he's had a substantial reduction in the size of the lesion in the adrenal gland. He didn't have other measurable lesions. He did report significant improvement in bone pain and was able to come off narcotics. Michel, if it's okay with you, I'm just going to keep referring it to it as inupadenant until I learn how to say inupadenant. We are going to get there. Maybe switching gears to EOS448, the TIGIT antibody. I think you said the dose escalation has been completed here, and then we're going to get an update in 2Q. Similar question. There's a competitive landscape here. What within the data in 2Q would get you excited, and what would you point us to a win scenario? I'll take that one again if you want, Michel. We have done the dose escalation. It went quickly. We have monotherapy data with this drug. I think one of the things we're looking at around the mechanism of action is we did see preclinically significant Treg depletion and an increase in the ratio of T effector cells to Tregs. That's something that we're looking at in clinic to see if we can confirm that and anticipate giving an update on that. Of course, we'd like to see a safety profile that's consistent with what others have seen, because in general, the anti-TIGIT antibodies have been very safe and well-tolerated to date. We would be thrilled to see some single-agent efficacy in this study. There haven't been very many responses to monotherapy. If we could show that, we think that would be significant. We continue to build our biological rationale. We are convinced that we can combine TIGIT with other standard of care, and we are also very exciting to move TIGIT with inupadenant in order to be able to explore other opportunities based on the biological rationale using TIGIT as a reference immune checkpoint. We have got a question in the portal, which is, I guess, what is your partnering strategy? It's one of my questions as well for EOS850, EOS448. These are both unencumbered assets. How are you thinking about strategically partnerships, business development, either regionally or globally, keeping U.S. rights, that type of a thing? Yes. I'm going to start and let Matt continue. We want to find a partner that will allow us to accelerate and expand our clinical development plan. This is our top priority. Matt, if you want to give some flavor of what would be the best fit for us. Sure. Michel's exactly right. We view partnering as a means to be able to expand and accelerate beyond what we could do on our own. We are in the enviable position of being very well capitalized and having a very strong development team in-house. We are in that position where we can push these assets forward through the development stages that we're currently at. Should we choose to partner-either of these assets, we will certainly retain significant rights in key commercial markets, Anupam, as you referred, and preserve that upside downstream for the company. Okay. Then for EOS850 and EOS448, with the updates in 2Q, should we be thinking about scientific or medical congresses for the data, or is it more of a top-line press release when you get the data in-house conference call type of situation? No, we are targeting key conferences, both scientific and medical conferences. Okay. I guess one of the things, and I can't remember if you addressed this, but the 80 mg BID dose for EOS850, can you walk us through why you chose that as a recommended phase II dose, given it looks like you got some stable disease at lower doses, and I think one of the responses was at a higher dose as well? Mm-hmm. Jo? I think we have a drug that has a pretty large therapeutic index, so we aren't limited by toxicity with this drug. What we did see was that, in terms of pharmacokinetics, we had a plateau in exposure. The 160 mg BID dose, we did not see a higher exposure than we did with 80 mg BID dose. The 80 mg BID dose is actually where we saw our highest exposure. We didn't see a significant difference in toxicity or tolerability at different doses. When we looked at the pharmacodynamics, the BID doses 40 mg BID and above, we really got full inhibition by both of our assays, and with a quick onset of effect within the first day of dosing. Ultimately, we chose 80 mg BID for our recommended phase II dose for monotherapy because it was the dose at which we saw the highest exposure, and we thought it was worth choosing that dose just in case there are some differences between the pharmacodynamic effect in the periphery and in the tumor. Got it. We've got another portal question here, which is, I think it specifically relates to EOS448, which is obviously the TIGIT antibody space is crowded and competitive. Do you think that it is a modality that can basically support multiple therapies in the same class? I guess you can address how you're thinking about differentiated development here. This is one of our, I would say, challenges and a very interesting one. So far, the most advanced players have positioned their TIGIT mainly to reinforce their PD-1 or PD-L1 franchise. In terms of biology, there is multiple indication that could support the combination of TIGIT with other standard of care. We have obtained preclinical data going in that direction. We believe that TIGIT is going to be the next generation IO drug for solid tumor at least, but there's also potential in hematological cancer. We are still working both at the level of biomarker, but also biological rationale to identify additional combinations. I agree with you that what will be important, on top of having an excellent antibody like EOS448, will be the clinical strategy to build a path for approval. Jo, Yvonne, do you want to add something? Any more email questions, I want to thank Michel and the iTeos team here for a really productive session. Thank you so much. I hope you guys have a great rest of the day. Thank you very much.