Good afternoon, ladies and gentlemen. Thank you for standing by, and welcome to the Corvus Pharmaceuticals Investor Conference Call. At this time, all participants are in a listen-only mode. Later, we will conduct a question-and-answer session, and instructions will follow at that time. It is now my pleasure to turn the call over to Zack Kubow of Real Chemistry. Please go ahead, sir. Thank you, operator. Good afternoon, everyone. Thank you for joining us for the Corvus Pharmaceuticals conference call to provide an overview of the CPI-818 data presented today at the ASH meeting and an update on the company's development programs. This conference call is being webcast with presentation slides. We encourage participants to join the webcast in order to view the slides. You can find the link to join the webcast on the investor relations homepage of the Corvus website. Joining me on the call from the company are Dr. Richard Miller, Chief Executive Officer, Dr. James Rosenbaum, Senior Vice President of Research, and Leiv Lea, Chief Financial Officer. The executive team will open the call with some prepared remarks, followed by a question-and-answer period. Turning to slide two, I would like to remind everyone that comments made by management today and answers to questions will include forward-looking statements. Forward-looking statements are based on estimates and assumptions as of today and are subject to risks and uncertainties that may cause actual results to differ materially from those expressed or implied by the statements, including the risks and uncertainties described in Corvus's most recent quarterly report on Form 10-Q and other filings the company makes with the SEC from time to time. The company undertakes no obligation to publicly update or revise any forward-looking statements except as required by law. With that, I'd like to turn the call over to Richard Miller. Richard? Thank you, Zack. Good afternoon, everyone. I am Richard Miller, the President and CEO of Corvus. Thank you for joining us today to discuss an update on our ITK INHIBITOR, CPI-818. I am here with Jim Rosenbaum, our Senior Vice President of Research, at the ASH Meeting in New Orleans, where our poster presentation on CPI-818 is being presented today. As outlined on slide three, we will begin with a quick introduction of the agenda and of Corvus Pharmaceuticals. Next, we will provide an overview of the prognosis and management of T-cell lymphomas, which is the lead indication for CPI-818. This will be followed by a review of the CPI-818 data presented at ASH, and based on this data, our development plan for CPI-818 in T-cell lymphoma and immune diseases. Jim is leading our efforts with 818 in immune diseases and will cover this portion. We will conclude with a brief update on our broader clinical pipeline and near-term milestones. After which, we will open the call for Q&A. Let's move to slide four. This graphic provides a high-level overview of our clinical pipeline and how each program plays an important role in precisely targeting and controlling key steps of the tumor immunity axis. I'll describe each briefly. On the right is CPI-818, our ITK INHIBITOR,. Blocking ITK plays a critical role in T-cell differentiation in the lymph nodes and tumor, which has potential therapeutic applications in oncology, autoimmune, and allergic diseases. On the left is SIFROLIMOD, our adenosine A2A receptor antagonist.SIFROLIMOD blocks immunosuppressive adenosine from binding to the A2A receptor, research has shown it may synergize with checkpoint inhibitors. Last, in the middle is MUPADOLIMA B our anti-CD73 antibody. We believe MUPADOLIMAB'S primary mode of action is stimulating B cells in the lymph nodes and tumor. B cells play an important role in tumor immunity. Its mechanism also impacts the adenosine axis by blocking the production of adenosine. With that as an overview of the company, let's focus now on 818, our lead indication for which we're reporting to the data today at ASH T-cell lymphoma. Slide five highlights the significant need for new treatment options for T-cell lymphoma, which is a very bad disease with a poor prognosis. In the left panel, we provide data demonstrating that patients with T-cell lymphomas have inferior outcomes compared to patients with B-cell lymphomas. This is based on the widely used International Prognostic Index, or IPI. Patients with PTCL-NOS, also known as peripheral T-cell lymphoma not otherwise specified, which is the most common type of T-cell lymphoma that also have high IPI factors, have a five-year overall survival rate of only 11% compared to 58% overall survival rate for diffuse large B-cell lymphoma or DLBCL patients with similar high-risk factors. In the middle panel, we focus on some key challenges with treatment options for T-cell lymphomas. There is no standard treatment option. The common treatments employed by physicians are various chemotherapy regimens such as CHOEP or BV-CHIP, which have reasonable response rates in the front-line setting but lead to remissions of short duration. In addition, these treatment regimens are toxic and poorly tolerated, particularly because many patients have significant problems with immunosuppression and other comorbidities that limit treatment options. The other option is autologous bone marrow transplant, which has similar challenges and is mostly limited to younger patients with more favorable disease. There is no landmark study or clear clinical evidence supporting the use of these therapies. In the right panel, we look at the prognosis for relapsed refractory patients. These are the patients we are studying in our current phase I, 1B trial and our planned phase two trial. This data is based on a published study of 153 patients with relapsed refractory PTCL-NOS, AITL, or anaplastic large cell lymphoma. This is a very poor survival curve with a 6.5-month median overall survival rate after first relapse. As you can see from the sharp drop in the curve, many of these patients are dying in a few months, and they are desperately in need of an effective therapy. Now let's look more specifically at the treatment landscape for relapsed refractory T-cell lymphoma. Slide six provides an overview, and starting on the left slide, we show a section from the National Comprehensive Cancer Network's treatment guidelines for patients with Peripheral T-cell lymphomas. Specifically here focused on first relapse. It is striking to note that once a patient has relapsed from initial therapy, the preferred option for second-line therapy is enrollment in a clinical trial of an experimental therapy, even though there are three approved agents for this setting. The reason why is summarized on the right-hand side. The table in the top right lists the available single-agent therapeutics for T-cell lymphoma that have been FDA-approved. PRALATREXATE is an anti-metabolite similar to METHOTREXATE. ROMIDEPSIN and VORINOSTAT are HDAC inhibitors. Unfortunately, the overall response rates are only 25%-30% with a very short duration. In addition, these agents are inconvenient to administer, toxic, and are difficult to combine with other therapies due to their toxicity. In fact, one of these agents has been removed from the market. Bone marrow transplant may be considered for some younger, more favorable patients, but its role is very limited, including the need for patients to have chemotherapy-responsive disease. These data indicate that patients are in need of an effective therapy. We believe that CPI-818 has the potential to address this need and are excited to share the latest data from our study and research that supports this thesis. As shown on slide seven, today, Dr. Ryan Wilcox, who is the Lymphoma and Myeloma section head at the University of Michigan, is presenting our CPI-818 poster at the ASH meeting. This study involves centers in the United States, China, South Korea, and Australia. I would like to thank Dr. Wilcox and all our investigators for their efforts and participation in this trial. I will add that Dr. Wilcox has a recent article published in Blood Cancer Journal on the molecular biology of T-cell lymphomas, including the expression of ITK and the vulnerability of malignant T-cells to ITK blockade, specifically using CPI-818. Let's look at the function of ITK, as shown on the next two slides. ITK, which is short for IL-2-inducible T-cell kinase, is expressed in T-cells and has at least two functions. First, it is involved in the activation of T-cells following exposure of the T-cell receptor to antigen. Second, it plays a vital role in control of T-cell maturation or differentiation into various subsets with differing functions. CPI-818 is a novel agent with exquisite selectivity for ITK. This is highlighted in the table on the bottom right of this slide, which shows that 818 is a 100-fold more selective for ITK over very closely related RLK or resting lymphocyte kinase and other structurally similar kinases. In our design and synthesis of an ITK inhibitor, we set out to produce a molecule that would be selective for ITK. While this was a challenge, the reason is apparent when we examine ITK's role in T-cell differentiation, as shown on slide 9. ITK is required for the generation of TH2 and TH17 helper T-cells, which are involved in inflammatory processes. Both ITK and RLK are involved in the generation of TH1 helper T-cells, which are needed to produce CD8 positive T-cells, which kill viruses and cancer cells. RLK plays a redundant function to ITK in these cells. By precisely blocking ITK and not RLK, CPI-818 is able to block the inflammatory-causing cells while allowing TH1 cells to function normally. This is called TH1 skewing, resulting in a biasing of T-cell differentiation toward the generation of T effector cells that kill cancer cells. If CPI-818 did not selectively inhibit ITK and also inhibited RLK, the result would be general T-cell suppression or blocking everything on the right-hand side of the slide. We built CPI-818 to have ideal features that biologically result in more killer T-cells, which is good for treating cancer, and blocking TH2, which is good for treating certain immune-mediated diseases. One other point to make here is that the concentrations or dose of CPI-818 needed to block T-cell activation is different than the dose or concentration needed to modulate T-cell differentiation. Not surprising, this means that dosing in patients will be important, and we will share later in this presentation the data identifying the optimal dose of CPI-818 for achieving TH1 skewing. I would like to describe some key preclinical animal findings shown in slide 10. In this study, mice with established EL4 tumors, which is an aggressive murine T-cell lymphoma, were treated for seven days with 10 or 30 milligrams per kilogram dose of 818 or a placebo control. Three days after the last dose of CPI-818, tumors were measured and analyzed by immunohistochemistry, or IHC. In the left panel, you can see that mice treated with 818 had smaller tumors compared to the control group, indicating that a brief course of 818 inhibited tumor growth. In the middle and right panels, we show IHC stains from control and 818-treated mice, showing a dramatic infiltration of tumors with normal CD8-positive T effector cells, findings consistent with our proposed mechanism of action. These are normal T cells because the tumor only expresses CD4 and not CD8. The takeaway from this data is that CPI-818 induced a robust CD8-positive antitumor T cell response, leading to tumor growth inhibition. In the data on slide 11, we further confirmed 818's TH1 skewing activity in an in vitro study using peripheral blood mononuclear cells, or PBMCs, from 12 human healthy subjects. PBMCs include T cells, B cells, NK cells, and monocytes. In this study, the donor T cells were stimulated in vitro with anti-CD3 and CD28 to activate the T cells in the presence of varying concentrations of CPI-818. Recall earlier I highlighted that concentration or dose is an important factor in terms of controlling effects on activation and differentiation with 818. On the left side, you can see in the green band that at CPI-818 concentrations between 0.01 and 1 micromolar, there is evidence of TH1 skewing based on a conventional assay that looks at interferon gamma and IL-4 expression. At higher concentrations, we see loss of skewing. Correspondingly, on the right side, you can see in the green band that at the higher concentrations there is a reduction of T cell proliferation. In other words, higher concentrations block T-cell activation and proliferation. No skewing or drive to TH1 is possible. What about the effects on TH2? In slide 12, we explore CPI-818's effects on cytokine production. In this study, human CD4 positive cells from normal subjects and malignant Sézary cells from patients were incubated in vitro with varying concentrations of CPI-818. We would expect that CPI-818 would block the secretion of TH2 cytokines such as IL-4, IL-5, and IL-13, which are associated with diseases such as atopic dermatitis, asthma, and many others. You can see in the plots underlined by the blue bars for both normal CD4 positive and malignant Sézary cells, which are known to be TH2 cells, there is a concentration or dose-dependent inhibition of these cytokines. We would also expect that interferon gamma would be unaffected at lower concentrations of 818 because it is a TH1 cytokine. You can see in the plots underlined by the green bars, we saw just that. Last, on the far right, TARC or CCL17 is a cytokine that attracts T cells to the skin. It is considered a useful biomarker for many skin diseases. As you can see in the plot underlined by the orange bar, it is inhibited by 818, a point that highlights the potential value of 818 for inflammatory skin diseases. Overall, these preclinical data show that ITK inhibition with a highly selective agent such as CPI-818 can induce TH1 skewing, block TH2 function, and be a potentially important new therapy for cancer, autoimmune, and allergic diseases. Let's look at the clinical data from our phase I trial. Slide 13 shows the patient characteristics. As of September 2022, we had enrolled 43 patients with relapsed or refractory T-cell lymphoma in a single agent dose escalation trial with CPI-818. The median number of prior therapies for these patients was three, ranging from 1 to 15. Based on the information I shared with you earlier, these are, as you would expect, very sick patients. Most of the patients had PTCL-NOS. We explored 818 doses of 100, 200, 400, and 600 milligrams oral twice daily. In the box at the bottom of the slide, we have listed the most common adverse events. There was no dose-limiting toxicity. Nearly full target occupancy was achieved with doses at or above 200 milligrams twice daily. The swimmer plot for all patients in the 200 milligram cohort is shown on slide 14. Histologies are indicated. During the trial, dose escalation was performed in sequential cohorts. Over time, it became clear that the best tumor responses and duration of disease control were in the cohort receiving 200 milligrams twice daily. In this cohort of 11 evaluable patients, there has been one complete response of 25 months duration in a PTCL-NOS patient that has failed both CHOP and high-dose myeloablative therapy and an autologous bone marrow transplant. one nodal complete response of 20 months in a refractory cutaneous T-cell lymphoma patient. two partial responses ongoing at over eight and six months. Note, PR in this study is used as the by the Lugano criteria, which is at least a 50% reduction in tumor volume. One additional partial response was seen in the 600 mg cohort. This patient went on to receive a bone marrow transplant. Why is the optimum dose 200 mg? As predicted based on the studies noted earlier, high doses or concentrations of CPI-818 will lead to inhibition of activation and proliferation. Basically, a carpet bomb instead of a guided missile. There is a range of concentrations that affect T-cell differentiation without blocking T-cell activation. These types of effects are not uncommon in immunology. To summarize, this phase I trial has identified 200 mg twice daily as an optimum dose. This dose leads to plasma concentrations of drug that have been shown to induce TH1 skewing and blockade of TH2 functions without affecting general T-cell activation. In this cohort, there has been an overall response rate of 36% or a response in four of 11 evaluable patients. The responses have been remarkably durable at 25 months, 20 months, and two ongoing at six-plus and eight-plus months. Based on this data, the 200 mg cohort is now being expanded and will be the dose we use in our upcoming phase II trial, which will also enroll relapse refractory patients, but with a more restrictive number of prior therapies and othe inclusion criteria that we will incorporate it that should lead to a more immunocompetent population. We have highlighted a patient case study on slide 15. This patient with PTCL-NOS had failed four prior therapies and had bulky disease involving bone marrow, blood, spleen, lymph nodes, and subcutaneous tissue. The latter is a large abdominal wall mass that you can see in the slide. That's about as big as a football, that mass. Within two weeks of starting on CPI-818 single agent treatment, she had significant regression of tumor in all sites of disease, including the large subcutaneous mass on the abdominal wall. She is now doing well with an ongoing partial response at eight-plus months. Slide 16 shows some of the immunologic studies that have been performed in this patient and illustrate how much we can learn from studies on the effects of 818 on normal lymphocytes. Here are the results of immunophenotyping of peripheral blood and tumor samples from this patient at various time points. The top left chart shows an increase in blood TH1 and a decrease in blood TH17. The top right chart shows a reduction of the eosinophil count in IL-5. These results are consistent with TH1 skewing and both TH2 and TH17 blockade. The reduction in eosinophils is related to blocking IL-5, IL-13, and others, and supports potential applications in allergic diseases such as asthma. In the bottom two charts, we show levels of TH1 and terminally differentiated T effector memory cells, otherwise known as TEMRA cells, at baseline and on treatment in tumor biopsies and blood. TEMRA cells are T cells that have experienced antigen exposure and are able to mediate effector functions such as destruction of tumor cells. As you can see, there is an increase in both, particularly localized in the tumor. The key takeaway from this data is that 818 is behaving in the patient as we would predict. ITK inhibition at an optimized dose is blocking TH2, TH17, and skewing to TH1. More importantly, the tumor is responding. Slide 17 shows an example of another patient that had tumors in multiple nodes in the neck, mediastinum, abdomen, pelvis, and groin. She had a partial response on CHOP chemotherapy lasting a few months and then received an autologous bone marrow transplant, which led to a relapse in less than one year. Following treatment with single agent 818, she had a complete response lasting 25 months, documented by PET scan, a very durable response, especially given her prior history. On the right-hand side of the slide, you can see the baseline and post-treatment PET scan. Note the disappearance of cervical adenopathy shown in the red circle. Additional information pertinent to our mechanism of and potential use of biomarkers is shown on slide 18. We were able to carefully measure TH1 and TEMRA cells in a few patients repeatedly over time. On this slide, you can see the results for TH1 cells in the top row and TEMRA cells in the bottom row. The colors in the chart represent the single patient. Red is the first patient case study we discussed with an eight-plus month partial response. Orange is the patient with a six-plus month partial response. Green is the patient with stable disease for three-plus months. Blue is a patient with progressive disease. It appears that increases in TH1 were associated with tumor response. We also found that patients who were lymphopenic were unlikely to respond, which is not surprising given the mechanism of action. It is likely that we cannot induce an immune response in patients who are profoundly immunosuppressed. Overall, we believe the CPI-818 data in our ASH presentation provides strong rationale to advance it into phase II trial and to expand into autoimmune and allergic diseases. We have outlined the key highlights from the ASH presentation on slide 19, which include, in our phase I study, 818 was well-tolerated, and other studies have shown that it's highly selective for ITK. At the optimal dose of 200 milligrams, CPI-818 has shown antitumor activity in very sick, difficult to treat relapsed refractory T-cell lymphoma patients with objective responses in 4 of 11 evaluable patients. These responses are very durable. In vitro and in vivo evidence demonstrate that the optimal dose of 818 induces TH1 skewing and TH2 and TH17 blockade, which is important for antitumor effects and in the treatment of TH2 and TH17-mediated diseases. Looking forward, we will continue to enroll patients in the 200 mg cohort of this phase I study, and we plan to initiate a phase II clinical trial in relapsed PTCL by mid-2023, and we plan to initiate our first trial in autoimmune disease in early 2023. Before we transition into the broader opportunity for CPI-818, we want to take a moment to thank our participating centers and investigators, which are shown on slide 20. Importantly, we thank all the patients and their families for participating in this trial. I want to take a moment to put our scientific and development strategy into perspective, as illustrated on slide 21. We have a strategy and development path that several of us have at Corvus have been on before with Rituxan and ibrutinib. Both of these agents affect immune cells, B cells, and were studied initially in lymphoma, where safety, activity, and immunologic effects could be determined. Lymphoma provided a rapid route to approvals. From there, these agents expanded into other immune diseases. We are taking the same approach with CPI-818. We are starting with lymphoma, T cells this time, as our pathway for initial approval, while also exploring in parallel CPI-818's potential in other non-malignant diseases. Now I would like to turn the call over to Dr. Rosenbaum to discuss our development strategy for CPI-818 in the context to autoimmune and allergic diseases, as well as our plans for moving forward. Jim? Thank you, Richard. Good afternoon, everyone. Moving to slide 22. Richard showed this diagram earlier in the presentation. I want to highlight it again here because it provides important context on why CPI-818 has broad potential beyond T-cell lymphoma and cancer in an array of immune diseases. ITK has a major role in the signaling through the T-cell receptor that occurs after the T-cell encounters an antigen recognized by a specific T-cell receptor. T-cells are divided into subsets based on the cytokines they produce. ITK is critical in T-cell differentiation into so-called TH2 cells or TH17 cells. TH2 cells are responsible for allergic disease, which is also called atopic disease. These diseases include atopic dermatitis, asthma, eosinophilic esophagitis, allergic conjunctivitis, nasal rhinitis with polyps, and many other diseases. Turning to slide 23, we provide some detail on how allergic diseases are caused by TH2 cells. The slide shows a cartoon of an antigen-presenting cell, also called a dendritic cell, activating a T-cell to produce inflammatory mediators. Many of the commercially successful approaches to treating allergic diseases are shown here in the list on the right-hand side of the slide. The right column shows the cytokines they are targeting, and you can see most of these approaches involve the inhibition of one or two cytokines produced by TH2 cells. CPI-818 has the potential to influence many more by targeting the TH2 cell itself, the upstream mechanism. Let's look at cytokine production more closely on slide 24. Richard also presented this slide earlier, but it has added relevance in the context of the information I just shared. It shows how well CPI-818 blocks the production of IL-4, IL-5, and IL-13, which are the prototypic TH2 cytokines. The effect is seen in healthy T cells or T cells from a patient with Sézary syndrome, in which T cells are malignant TH2 cells. interferon gamma is produced by TH1 cells, and its synthesis is blocked minimally by CPI-818 or only at the highest concentrations of 818. TARC is a chemokine which is used as a biomarker to track the activity of atopic dermatitis. Its level is also reduced by CPI-818. Moving to slide 25, CPI-818 has been studied in several mouse models of T-cell-mediated disease. These three panels show results in models of lupus, psoriasis, and pulmonary fibrosis. In the left panel, we highlight a mouse model in which the animals get lymphadenopathy, nephritis, skin inflammation, and autoantibodies to red cells and white cells. If you treat these animals with CPI-818, they're cured, as shown in the blue lines. The result is similar to treatment with cyclophosphamide labeled as CTX. These data were presented in 2020 at ASH. In the middle panel, we show results from an imiquimod psoriasis model. Imiquimod is a chemical that causes inflammation by activating the immune system. In the bottom two samples, you can see that the results of treatment with CPI-818 on the left is as good as the steroid dexamethasone, labeled as Dex on the right. In the right panel, we show a model of pulmonary fibrosis induced by bleomycin, an agent known to cause pulmonary fibrosis. Fibrosis, a form of tissue repair, is also controlled by TH2 cells. You can see in the green and purple clusters that treatment with CPI-818 results in a lower Ashcroft score, which is a measure of the severity of fibrosis. The benefit from CPI-818 is comparable to that achieved with Nintedanib, an FDA-approved drug to treat pulmonary fibrosis. Turning to slide 26, while atopic dermatitis is our first immune disease target, other TH2 diseases could also be treated, including other atopic diseases, fibrotic diseases, TH17-mediated diseases, and mast cell disease. I will now focus on our first disease target, atopic dermatitis. The right side of slide 27 shows a quote from a review that appeared one year ago in the New England Journal of Medicine. The author concluded that the most promising approach to treat atopic dermatitis is to inhibit TH2 cells and their products. The left side of the slide outlines the high-level rationale for advancing CPI-818 for atopic dermatitis. In short, the science supports it, there is patient need, and CPI-818 has already generated data in humans that suggests it will have an effect. Turning to slide 28, companion dogs often develop atopic dermatitis, and the pathology, clinical symptoms, and treatments are very similar to human disease. Many clinical trials evaluating new treatments for dogs have been performed using validated clinical assessment methods, including the PDAS, Pruritus Visual Analog Scale, and CADLI, Canine Atopic Dermatitis Lesion Index. These indices quantitate itching and signs such as skin redness, excoriation, and scaling. We are conducting a pilot trial of CPI-818 in dogs with refractory atopic dermatitis. They are treated with twice-daily CPI-818 for 28 days. The charts on the slide show improvements in both assessments within 14 days in five of the five dogs in our ongoing study. All dogs had clinically significant reduction in itch based on the owner's assessment. Most dogs had improvement in the CADLI, a scoring by the veterinarian of dermatitis severity. Slide 29 shows that not only did the itch improve in all dogs, in all cases, improvement could be shown within 24 to 48 hours of starting CPI-818. These last two slides demonstrate proof of concept. The ongoing study will provide important information for our planned phase I human trial. I want to emphasize that this is a spontaneous natural disease and not a model. Natural canine disease was also used for proof of concept for ibrutinib in B-cell lymphoma, a JAK inhibitor for atopic dermatitis, and CPI-818 in dogs with T-cell lymphoma. A summary of our excitement about CPI-818 for atopic dermatitis is discussed in slide 30. First, as I mentioned, there is strong scientific rationale for ITK inhibition in this disease, and it represents a mechanism of action that distinguishes it from its competition. Importantly, the results from our studies with CPI-818 in atopic dermatitis should extrapolate to other TH2-mediated diseases like asthma. Second, we can and are leveraging the work we've done in oncology. Third, we believe we have several advantages over competitive approaches. Eight-one-eight is oral, reduces all TH2 cytokines, and is highly targeted. Fourth, a clinical trial in this disease has relatively short endpoints, so there is the potential for near-term data. We believe that initial data will be in hand before the end of 2023. To summarize on slide 31, we highlight the key data and opportunities for CPI-818 in cancer and immune diseases. We have shown that CPI-818 has an attractive profile. It has already demonstrated in patients anti-tumor activity and the ability to modulate T-cell function. We have several clinical activities planned and ongoing to continue its development. I will now turn the call back to Richard. Thank you, Jim, for sharing those very exciting results. Jim, in 2023, we plan to move 818 into a phase II trial for T-cell lymphoma and a phase I trial for atopic dermatitis and potentially other autoimmune and allergic indications. Looking at our broader pipeline on slide 32, we are efficiently advancing our other clinical programs,SIFROLIMOD and MUPADOLIMAB. This gives us the potential for important catalysts across all three programs in 2023. For SIFROLIMOD, our lead opportunity is frontline renal cell cancer in combination with nivolumab and ipilimumab. For MUPADOLIMAB, we are phase II-ready in the U.S. for a randomized trial in frontline stage 4 lung cancer. In China, our partner, Angel Pharmaceuticals, is close to initiating a phase I trial in patients with lung cancer and head and neck cancer. On slide 33, we provide an overview of the phase I/2 clinical trial design for ciforadenant as a potential first-line therapy for metastatic renal cell cancer in a triplet combination with ipilimumab and nivolumab. This trial was initiated in October by the Kidney Cancer Research Consortium and is being led by The University of Texas MD Anderson Cancer Center, which is one of the seven partner institutions that make up the consortium. The trial is planned to enroll up to 60 patients with newly diagnosed or recurrent stage four renal cancer that have not received any prior systemic therapy. The primary endpoint of this trial is the% of patients who achieve deep responses. This is defined as complete responses and partial responses that have, that have greater than 50% reduction in tumor volume, reflecting our goal to raise the plateau on progression-free survival and overall survival by adding SIFROLIMOD. Recent historical data has shown that deep responses correlate with prolonged progression-free survival and is seen in approximately 32% of patients receiving nivo and ipi. This is an open label, single-arm trial, so we anticipate that we will get a good feel for efficacy early in the trial. In summary, here are the key takeaways from our ASH presentation and company outlook on slide 33. First, we are focused on the development of CPI-818, which is the most advanced ITK inhibitor program that we are aware of. Based on the data presented at ASH, we are positioned to initiate a phase II trial in T-cell lymphoma and have strong rationale, including from human data, to expand into autoimmune and allergic diseases. The development strategy is analogous to what members of the Corvus team did in the past, developing the first BTK inhibitor. Second, we believe Corvus is well-positioned with several potential catalysts for our programs in the next 12 months. For 818, we expect additional T-cell lymphoma data from our phase I trial in the second quarter of 2023, followed by the initiation of a phase II trial around mid-year. We also expect to initiate a phase I trial in atopic dermatitis in early 2023, which gives us the potential for initial data in late 2023. For SIFROLIMOD, we expect to have interim phase II data in the frontline renal cancer cell setting around middle of 2023. For MUPADOLIMAB, our partner in China may have data from their phase I trial in 2023. Third, we have an efficient development approach, partnering with the Kidney Cancer Research Consortium and Angel Pharmaceuticals, which contributes to our strong foundation with three clinical-stage program, combined with a cash runway into early 2024. With that, we will now open the call for questions. Operator? Thank you. We will now begin the question and answer session. To ask a question, you may press star then one on your touchtone phone. If you are using a speakerphone, please pick up your handset before pressing the keys. If at any time your question has been addressed and you would like to withdraw your question, please press star then two. At this time, we will pause momentarily to assemble our roster. Our first question will come from Aydin Huseynov with Ladenburg Thalmann. Inc. Please go ahead. Good afternoon, everyone. Thank you very much for the interesting presentation. I wanted to ask a little bit more detail on the phase II trial of CPI-818 in T-cell lymphoma. You mentioned that you're gonna start this in 2023, but how big the trial will be, and would you select only second-line PTCL patients, not necessarily third and fourth line? What kind of patients are you planning to recruit? Thank you for the question, Aydin Huseynov. Our current thinking on the trial is it would be about 150 patients with a futility analysis after 40 or 50. The goal of the futility analysis would be to see about a 30% response rate or better. The eligibility for the trial will be a little bit different than our current phase I, where we took really very sick, late-stage patients. We're gonna limit it to three prior therapies, no more than three prior therapies. We feel that enables us to catch, you know, most of the patients who are gonna be around at these hospitals. We're also adding some other things that we learned from our phase I. For example, I mentioned it in my presentation, it turns out that lymphocyte count is a very good prognosticator for us, a very dramatic prognosticator. We'll have criteria based on having a certain level of lymphocytes to be eligible. Basically, 150 patients, single arm study, monotherapy, I should point that out, response rate as the primary endpoint. That futility analysis will be in by the end of 2023, given how early you can get these responses? That might be pushing it maybe early 2024. I think that it's an open label study, so we will, you know, be looking at the data as it's collected. However, unlike a lot of companies, I don't like to be looking at it every day because I think that can influence the study. We'll have some rules about when to look at it. I think data late 2023 is possible, but certainly by early 2024. Okay. Okay? Given the precedent approvals in PTCL and T-cell lymphoma, do you think this trial can become a pivotal one? I do think it can become a pivotal trial. There continues to be. We're at the ASH meeting, and I just reviewed all the papers on T-cell lymphoma here. Really, there is nothing coming down the pipe that I think is competitive. Some of the agents have response rates, are very toxic, difficult to give. I, you know, given the prognosis that I outlined earlier in the talk, given the safety we're seeing, given the novel mechanism of action, ability to combine with other therapies, I think there's gonna be a high level of interest in this drug for T-cell lymphomas. Okay. All right. Thank you. One question I have regarding the atopic dermatitis trial, I think you mentioned in the first half of 2023, the phase I. What would be the patients? Are the patients will be those who failed on Dupixent or, you know, the nova patients? Could you give me a little bit more details on this one if possible? Sure. Can you handle that one? Sure. Thanks, Aiden. All the patients will have moderate to severe atopic dermatitis. All of them will have failed at least one therapy. In some cases, that will be only topical therapy, but we also hope to enroll over 50% who will have failed a systemic therapy such as Dupixent. It's randomized placebo. Yes, it's randomized, and it's placebo-controlled and will evaluate three different doses of 818. what would be the endpoints of that trial? The endpoints for atopic dermatitis studies are fairly standardized. The primary endpoint will be the% improvement in the EASI, the Eczema Area and Severity Index, but also the investigator global score, the pruritus, the sleep index. These are the standardized quantitative endpoints in atopic dermatitis trials. At 28 days. Yes. We expect to see improvement within 28 days based on our response in dogs and based on the responses of other trials that have been conducted, such as with Dupixent or with JAK inhibitors. Aiden, thank you for that question. We think we can have data, even though it's a randomized placebo-controlled study, looking at three doses in a placebo. The primary endpoint's day 28, the EASI score, as Dr. Rosenbaum mentioned. That's pretty short. Prior studies have shown that most of the effects of these agents occur in 28 days. Our experience in our animal models and in the dogs with naturally occurring atopic dermatitis, we are seeing improvement in those dogs in days, hours. We think we'll have a good feel for this by the end of 2023. Interesting. yeah, that's pretty fast. And given the upstream mechanism, do you think people would be eventually it would be possible to use it before Dupixent, before systemic therapy? I personally think that an oral drug will be preferable to an injectable drug. Yes, I envision this as potentially being the first-line systemic therapy. Got it. Okay. Thanks so much- Aydin, we expect that in our phase I trial, it is a phase I trial, that will get mostly patients who failed the systemic therapy, which is good, because that's a, that's an opportunity right there, and that's what, 50%, 60% of the patients. This is, I mean, this represents, I mean, just to step back a second. To my knowledge, knocking out ITK was shown in late nineties, early two thousands using genetically altered mice to cause Th1 skewing and to block Th2 and Th17 function. That's been well shown in mice 20 years ago, 25 years ago. To my knowledge, we are the first, and this is the first agent that I'm aware of that has shown solid evidence for Th1 biasing and blockade of Th2 and Th17 in humans. This the first agent that I'm aware of to show that, certainly the first, even the first human data to show that. I hope that that point gets across. Richard, if I could add, in theory, 818 should be more effective than Dupixent. For example, interleukin 31 is a major TH2 cytokine. It's primarily responsible for itch, which is the major symptom from atopic dermatitis. 818 should block the synthesis of IL-31, whereas Dupixent doesn't affect it at all. Right. Good point. It's blocking all the cytokines instead of just one or two. Anyway, let's. Maybe, Aydin, thank you for those questions. Maybe we can take questions from someone else. Our next question will come from Mara Goldstein with Mizuho. Please go ahead. Great. Thanks so much for taking the question. I'm wondering if you could just go through, you know, there were a handful of adverse events, hematologically driven, grade 3s, and I'm just wondering if you can kinda go through the profile and also maybe in the same context that you talked about, looking at lymphocyte parameters as potentially, you know, prognostic, you know, just what we're seeing in terms of adverse events and how that relates to either on treatment or disease. Mara, I can give you a very short answer. Really, there aren't any hematologic side effects. These patients, again, we're talking about lymphoma patients who've had multiple rounds of prior therapy. Anemia is part of the disease. Some patients progress. Not every patient responded to our treatment, so they progress, they get anemia, they get other, you know, they get other problems. A lot of that was due to their disease progression. Really, I don't think that I'm able to give you a specific side effect. Now we've, you know, we've gone to doses of 600 BID, and we're planning to use 200 BID. It's one-third of our maximum dose. We get great occupancy at 200 mg BID. I don't really think there's gonna be any problem combining this drug. I mean, eventually, what are you gonna do with this drug? I mean, we'll hopefully get it approved as a monotherapy for refractory disease. Ultimately, already, people are asking us, "Well, can we combine it with chemotherapy? Can we combine it with this?" I think this is gonna be very readily combinable with chemotherapy. It has a different mechanism of action. It has a non-overlapping toxicity profile. The problem with some of these other agents, duvelisib, for example, is you do have significant PI3K inhibitor. You do have significant myelosuppression, liver dysfunction. It's very hard to give a drug like that together with combination chemotherapy. I think the safety is a big deal here, even in the oncology setting. It's of course a big deal when we talk about the non-malignant diseases. I think you had another question also. Maybe I didn't answer it. Okay. Yeah, can you hear me? Sorry. Yeah, I hear you. If I could just also ask, cause I don't know if I missed it or not, but the dose for autoimmune, is that also the 200 mg, or are you looking to dose differently there? The phase I atopic dermatitis trial will have a dose escalation. We'll start at 100 mg BID for the first 16 individuals, and then we'll do 200 BID and then 400 BID. Okay. We won't go to six. Most likely it'll be 200 or maybe even lower. Okay, great. I see no reason- Thank you. -for it to be higher. We'll have to look at that because we haven't done it in people yet. In the dogs with... Again, to remind you, the dogs have naturally occurring just disease. Dogs get... Atopic dermatitis, as Jim mentioned, is very common in dogs. We've been working with a veterinary dermatologist, and we're using the dose in the dogs that's giving us levels very comparable, and we did this deliberately, of course, very comparable to the 200 mg dose we're using in the lymphoma study. Okay? All right. I appreciate it. Thank you. Any other questions? Again, if you have a question, please press Star then One. Our next question will come from Li Watsek with Cantor Fitzgerald. Please go ahead. Hi there. This is Rosemary. Okay. Let me see if I can remember all three of those. The gating items, the gating items are finishing our protocol, signing up sites, you know, filing the protocol with our with the FDA, getting IRB approvals. I think we're probably looking at another four months, five months or so to get it open. There really is no technical challenge. It's merely now the contracts and IRBs and all that stuff. In terms of the bar, as you know, I'm a medical oncologist who has focused his whole life on treating lymphomas. Based on what's out there, I would say if you have a 30% response rate with a safe agent that... It's durable meaning six months or more in this patient population, I think that would be a very good result. I think that would be a very good result. The final question was more data. We're continuing to enroll the phase one. We're getting a lot of good biology data that's helping our autoimmune program and a lot of other things going on in the company in terms of immunology. We're continuing to enroll. We do have a abstract we submitted to AACR. That's in April. Okay. Hopefully we'll have some more data there. You know, obviously we wanna transition into the phase two. Got it. Thank you. I think I answered your three questions. Thanks. Yeah. Any other questions? As there are no further questions, this concludes our question and answer session. I would like to turn the conference back over to Richard Miller for any closing remarks. First of all, I'd like to thank everyone for joining our call today. We're really excited about 818 and our other programs as well. If you have any additional questions or you would like to arrange a meeting to discuss these things further, please reach out to Leiv Lea or to me to coordinate. Thank you very much and have a nice day. The conference is now concluded. Thank you for attending today's presentation. You may now disconnect.