iTeos Therapeutics, Inc.

condition, 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 annual report on Form 10-K. The year ended December 31, 2020. in our quarterly report on Form 10-Q for the quarter ended March 31, 2021, that will be filed with the SEC today and 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, for the introduction, and thank you for joining us for our first quarter of 2021. For today's call, I will provide a brief recap of our corporate strategy and overview of progress within our pipeline programs, as well as the multiple opportunities and readouts for our clinical programs. And we'll turn the call over to Dr. Joe Leger, our chief medical officer, to provide the status update and review of our most recent results from our ongoing clinical trials. Finally, Our chief financial officer, Matthew Gold, will summarize our financial status, after which I'll return for closing remarks. We will be all available for the Q&A sessions. I would first like to highlight the key strengths that set ITOS apart as a cancer immunotherapy company. We are developing therapies focused on well-established mechanisms of immunosuppression. involves targeting pathway that relieves cancer-induced suppression of the immune system, and our goal is to develop therapies with the potential to fully restore the immune response against cancer. Through the first quarter of 2021, we continue to advance our differentiated clinical programs, US448, our potent high-affinity antitiget antibody, and inopadenant, a potent and highly selective A2A receptor antagonist with a robust clinical strategy to strengthen our position in the cancer immunotherapy space. We have released encouraging initial data and are pleased with the activity and safety profiles we have observed with single-agent monotherapy in both our clinical programs. We think that the monotherapy responses that we have seen with our programs are seniors of differentiations. We are looking forward to continuing the development of these drugs in combination where we see the most potential to benefit patients. We have combination studies well underway with Inopadenone, and we'll be initiating combination with EOS44AID mid-year. With our headquarters in Cambridge, Massachusetts, and our R&D center in Belgium, IT has a global presence, allowing us to attract talent worldwide and remain at the forefront of innovation in the field of immunology. Lastly, we are well capitalized with a runway well into 2023. This allows us flexibility to follow the data and competitive landscape in the design of our clinical plan with significant financial constraints. Having summarized this status, this is an exciting time for ITOS as we continue to make progress advancing our two clinical programs and our ongoing discovery efforts with the goal of improving the life of people with cancer. Our recent data presentation for our anti-digit antibody, US448, at ACR, showcased a favorable safety and tolerability profile, encouraging signs of clinical efficacy including disease stabilization and one partial response, and significant depletion of immunosuppressive T-rex and exhausted T-cells in periphery in patients with advanced cancer. While Joe will provide a more detailed review of the data and our clinical development plan later in the call, I would like to highlight that our complete data are in line with, if not better than, others in the TGX pair. We are initiating phase 1b2 combination trials in both checkpoint-naive and resistant patients. We expect that our work over the next 12 to 18 months will confirm the position of our TIGIT program within the immunology treatment landscape. We are also advancing our second clinical program, the highly selective adenosine A2 receptor antagonist in upadenone. At ASCO in June, we will report updated results from our monotherapy dose escalation study. In our view, the unique potential of inupiatin-N is based on its high potency and selectivity for the A2A receptor, the resistance to attenuation by the high adenosine concentration found in the tumor microenvironment, the favorable efficacy and safety profile as demonstrated by the Phase I data presented last year at ACR, and identification of a potential predicated biomarker based on the expression of the A2A receptor in the tumor microenvironment. We are evaluating inopanin in combination with pembrolizumab, with chemotherapy, and with EOS448 in disease-specific cohorts. In tandem with the progress of our clinical programs, we are also advancing research programs focused on targets that complement the mechanism for action of A2A receptor and TGIT programs and address additional mechanisms of immunosuppression. We are building our pipeline and expect to nominate an additional product candidate for IND enabling studies before the end of 2021. For our strategy, TGIT is an exciting new immuno-oncology target with external validation. And we have demonstrated that EOS44-AIDs potentially engage the target and the F-sigma receptor. We are exploring opportunities to accelerate and expand our development plans, potentially through a strategic partnership. Adenosine plays an important role in the suppression of the tumor microenvironment. And there have been some encouraging signals of activity with drugs that inhibit adenosine receptor and other pathway targets. Our inipadenone program was designed with properties to overcome the limitation of other drugs in this class, and we look forward to achieving a clinical proof of concept in the ongoing and planned trials in the near future. I will now pass the call over to our chief medical officer, Joe Lager, to discuss the progress in clinical development of both of inipadenone and EOS-448 in more detail. Joe, please.

Thank you, Michelle. I'd like to begin by providing a summary of the progress with our adenosine receptor antagonist in the pattern, for which we'll be presenting an update at ASCO next month. The adenosine pathway is a critical mechanism which suppresses the immune response against tumors and inhibits responses to current cancer therapies. Though there are multiple potential therapeutic targets in the adenosine pathway, The adenosine receptor A2AR is a key receptor responsible for mediating adenosine's immunosuppressive effects on immune cells. A2AR is highly expressed on effector immune cells, and potent inhibition of A2AR has the potential to block immunosuppressive signaling and restore an antitumor immune response. We selected this critical target based on our characterization of unique conditions of the tumor microenvironment. We sought to design a therapeutic that could selectively and potently inhibit A2AR, despite the high concentrations of adenosine present in the tumor microenvironment. Imifadmin is a next-generation A2AR antagonist with differentiated pharmacologic properties. Unlike prior generations of adenosine receptor antagonists, inopatinib was designed to inhibit A2AR even at high concentrations of adenosine. Inopatinib is also highly selective for A2AR and has a minimal blood-brain barrier penetration, properties which are expected to reduce off-target safety effects and improve the therapeutic index. We're currently evaluating inopatinib in several Phase 1b-2a studies, both as a monotherapy and in combination with pembrolizumab or chemotherapy. The results from the dose escalation portion of the Phase 1 study in patients with advanced stage cancer were presented at AACR last year and showed that inopatinib is well tolerated with no dose-limiting toxicities. In addition, Inopatinib demonstrated clinical benefit as monotherapy across multiple heavily pretreated advanced cancers, with durable partial responses seen in the patient with checkpoint inhibitor-resistant melanoma and in the patient with heavily pretreated castrate-resistant metastatic prostate cancer. We've also shown that when given twice daily, all of the tested doses resulted in a full inhibition of A2AR signaling at 24 hours after dosing. These results have generated much excitement for the program, and we look forward to presenting an update on our monotherapy cohort at ASCO next month, which will be focused on the tumor biomarkers evaluated in this study, and a finding that the expression of the A2A receptor in the tumor may be associated with clinical outcomes. We're currently executing a multi-arm phase 1-2A clinical trial in adult patients with advanced solid tumors where there's a strong rationale for treatment with an A2AR antagonist. We're enrolling patients in four distinct cohorts as both a single agent and in combination approaches. We have two cohorts evaluating independent in patients with castrate-resistant metastatic prostate cancer. One is monotherapy and the second cohort in combination with pembrolizumab. The third cohort is evaluating inopatinib in combination with pembrolizumab in patients with checkpoint inhibitor resistant melanoma. The fourth cohort is evaluating inopatinib in combination with chemotherapy in patients with triple negative breast cancer. We will continue to integrate a biomarker driven approach into our A2AR clinical program to choose optimal therapeutic combinations and identify the patients most likely to benefit from treatment. I'll now provide an overview of our progress with EOS-448, our high affinity potent anti-tigit antibody with a functional FC domain designed to enhance the anti-tumor response through a multifaceted immune modulatory mechanism. Yes, porphyrate has the potential to achieve significant immune-stimulatory effects through three mechanisms. One, blocking the binding of tigets with ligands, resulting in immune-mediated killing of tumor cells. Two, engaging the FC-gamma receptor-expressing effector cells that further promote anti-tumor immune responses, including through the release of pro-inflammatory cytokines and chemokines, and the activation of antigen-presenting cells. And three, depleting cells that are known to dampen the immune response, immunosuppressive Tregs and exhausted T cells. Last month at AACR, Dr. Van de Meuter presented first-in-human data from the open-label dose escalation phase one portion of the clinical trial in patients with advanced solid tumors. We were very pleased to report encouraging signs of clinical benefit with EOS-448 as a monotherapy in patients with advanced cancers. Of note, we observed a confirmed partial response with single-agent treatment with EOS-448 in one pembrolizumab refractory BRAF mutant melanoma patient. We also observed a manageable safety profile consistent with other drugs within this class and all of the tested doses were generally well tolerated. Our peripheral biomarker data demonstrated TIGIT-positive Treg depletion and a reduction in exhausted TIGIT-positive CD8 T cells, reinforcing our initial hypothesis about the FD gamma receptor engagement activity of ELS448. These robust biomarker data, coupled with the preliminary signs of efficacy as a monotherapy, indicate that ES448 is highly active with strong on-target immune responses and may potentially drive even stronger responses in combination studies. Based on these early positive results, we're pursuing a robust clinical development plan for ES448 with new combination approaches and three checkpoint-naive and checkpoint-resistant settings. We will assess the combination of ES448 with PD-1 inhibition in patients where pembrolizumab is indicated as a monotherapy, but where the addition of ES448 may improve clinical benefit to patients. We will first assess the safety of the combination of ES448 with pembrolizumab in solid tumors. And then we'll move into disease-specific trials in first-line non-small-cell lung cancer and head and neck squamous cell cancer, where we'll assess both the PD-L1 high and PD-L1 low populations. We are also planning to evaluate the combination of inopatent and EOS-448 in patients with checkpoint inhibitor-resistant melanoma and EOS-448 in combination with an image in relapsed or refractory multiple myeloma. We're planning to start these studies in mid-2021 and are continuing to evaluate our clinical development plans for ES4-4A and other solid tumors, including triple-negative breast cancer, gastric cancer, and pancreatic cancer. I now hand the call over to Matthew Gall, our Chief Financial Officer.