Good morning, ladies and gentlemen. Thank you for standing by, and welcome to the Corvus Pharmaceuticals SITC 2021 Data and Company Update 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, and good morning, everyone. Thank you for joining us for the Corvus Pharmaceuticals conference call to review preclinical and phase I/I-B clinical data presented today at SITC. Joining me on the call from the company are Dr. Richard Miller, Chief Executive Officer, and Leiv Lea, Chief Financial Officer. The executive team will open the call with some prepared remarks, followed by a question-and-answer period. 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 those 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, and good morning, everyone. Thank you for joining us today to discuss an update on mupadolimab and our program investigating the potential clinical applications of immunomodulation through B-cell biology. At the SITC meeting today, we will be presenting a very comprehensive set of data on the biology, immunology, and clinical activity of mupadolimab, a humanized anti-CD73 antibody with unique properties. As outlined on slide three, we will begin the call with a review of mupadolimab's properties, including details on its mechanism of action. This will include a comparison to other anti-CD73 monoclonal antibodies in development. Next, we will review data from the mupadolimab phase I/I-B clinical trial, which has demonstrated preliminary efficacy signals in patients with very advanced refractory non-small cell lung cancer and head and neck cancer. We will discuss our ongoing development plans for mupadolimab and provide brief update on our other clinical programs. Leiv will then provide an update on our financials. Following the prepared remarks, we will open up the call for a Q&A session. Let's move to slide four. Why the focus on B cells? Basic immunology teaches us that B cells have at least two very critical functions in the immune system. Number one, they encounter antigens and generate antibodies to these antigens, which then trigger elimination or destruction by other immune cells. Two, B cells present antigens, and they do this powerfully well. They communicate with T cells and other immune cells in specialized regions of lymph nodes and other tissues. I don't have to tell you that antibodies are valuable treatments for cancer and other diseases, and modulating B-cell function has been highly successful. Think Rituxan, which depletes B cells, and ibrutinib, which blocks B cells. Think COVID vaccination, which stimulates B cells. In 2020, a series of papers in Nature, which are shown on the left of slide four, demonstrated the important role of B cells in therapeutic response to immuno-oncology agents such as anti-PD-1s. In these papers, B cells infiltrating the tumor were more predictive of a response to immunotherapy than T cells. For decades, pathologists have noted that infiltration of tumors with B cells forming miniature germinal centers and known as tertiary lymphoid structures, or TLS, are a favorable prognostic sign. More pertinent to our discussion, recent papers by others have shown that lung cancers and head and neck cancers are the tumors most often infiltrated with large numbers of B cells. The accumulating evidence is mounting that B cells play a vital role in the tumor microenvironment. Data demonstrating mupadolimab's mechanism of action is shown on slide five. On the top of slide five, we show in vivo preclinical data that demonstrates that mupadolimab blocks adenosine production. This has been the generally understood mechanism of most anti-CD73 antibodies. They block adenosine production, which is thought to be immunosuppressive in the tumor microenvironment. In this experiment, mupadolimab or control antibody was given to nude mice, immunodeficient mice with a CD73-positive human tumor growing in the flank. The panels show that both mupadolimab and another anti-CD73 antibody both bind to CD73. However, mupadolimab binding does not result in the internalization of CD73. It does result in complete inhibition of adenosine production. Mupa reacts with an epitope or region on the CD73 target that does not cause loss of the antigen but does block production of adenosine. We will say more about that later. CD73 has many other important functions other than making adenosine. It is involved in lymphocyte activation and in lymphocyte trafficking. On the bottom of this slide, we show something more dramatic. mupadolimab activates B cells, resulting in differentiation into plasmablasts, the cells that secrete antibodies specific to particular antigens. The graph on the bottom left shows that mupadolimab greatly increases the expression of CD69, a marker of B-cell activation, compared to oleclumab, AstraZeneca's anti-CD73 antibody, which is in development. Interestingly, oleclumab also activates B cells a little bit, but much less than mupadolimab. AZ reported this property at the 2021 AACR meeting. Most other anti-CD73 antibodies do not do this. CD69 is of importance because it is a cell surface protein involved in the trafficking of lymphocytes to lymph nodes, where further differentiation and maturation occur, eventually culminating in immunologic memory. Time does not allow us to present the data here, but the SITC poster shows data indicating that the effects on B-cell activation are not dependent on adenosine. Activation is another property of CD73 that is separate from its enzymatic activity. These properties make mupadolimab a unique anti-CD73 antibody. Slide six shows that mupadolimab completely inhibits CD73 enzymatic activity with no hook effect observed, as shown by the blue line in the chart on the left. This compares to oleclumab, which also inhibits CD73 activity, but at higher concentrations demonstrates a reversal of this inhibition, otherwise known as a hook effect, and as. Shown in the green line on the chart. Hook effects are well known in immunology and are caused by extremes of the ratio of antigen to antibody. A reduction in binding is seen with either excess antibody or excess antigen. The reasons for this have to do with the nature of the macromolecular complexes formed. No hook effect is seen with mupadolimab. It reacts with a different epitope than avelumab. The clinical relationships to hook effects are not established, but the presence of a hook effect suggests that you need an optimum ratio of antigen to antibody. This is difficult to predict or obtain reliably in vivo. Slide seven provides a high-level overview of the anti-CD73 landscape. Corvus, along with AZ, have been the leaders in the CD73 area based on publications and presentations at scientific meetings. The recent ESMO presentation of positive results from a randomized prospective phase II study in first-line therapy of stage III non-small cell lung cancer with a combination of oleclumab and durvalumab has focused a great deal of attention on the CD73 target. We believe mupadolimab is well-positioned compared to other anti-CD73 antibodies because it provides a full adenosine blockade and strong B-cell activation. It is also one of the most studied antibodies and, as we will discuss later, is positioned to enter late-stage clinical development in 2022. Slide eight provides a more detailed comparison between mupadolimab and oleclumab. As noted previously, they bind to different epitopes or regions on the CD73. Mupadolimab binds to a region that allows it to competitively block CD73's substrate adenosine monophosphate or AMP, whereas oleclumab binds to a region that changes the conformation of CD73. It is an allosteric inhibitor. As we discussed already, there's no hook effect or internalization of CD73 with mupa, but there is with oleclumab. As I just highlighted, mupa exhibits robust B-cell activation. We believe the unique properties of mupadolimab compared to other anti-CD73 antibodies make it an attractive partner for combination with anti-PD-1 therapy. On slide nine, we have illustrated the rationale for combining mupa with anti-PD-1s. On the top, we depict activation of B cells and stimulation of the immune system by producing anti-tumor antibodies and by presenting antigen to T cells. On the bottom, you can see how anti-PD-1 therapy releases the brake on the checkpoint that prevents T cell activation. Together, by stepping on the gas for the immune system and simultaneously releasing the brake, we believe we can enhance anti-tumor immune responses. We are exploring this combination in the ongoing expansion portion of our phase I/IB study in patients with lung cancer and head and neck cancers. On slide 10, we have summarized the clinical trial design for our ongoing phase I/IB trial. This study was conducted in patients with very advanced, multiply recurrent disease and included patients with colorectal, pancreatic, renal, breast, prostate, lung, head and neck tumors, and other tumors. All of the patients had failed multiple prior therapies and many failed immuno-oncology agents. This is a large, comprehensive trial designed to address several questions, such as immunologic effects, pharmacokinetics, pharmacodynamics, lymphocyte trafficking, safety, and potential early signs of efficacy, and to establish optimum dosing. Cohorts of patients received one of four treatments, mupadolimab alone, mupa in combination with ciforadenant, our A2A receptor antagonist, mupa in combination with pembrolizumab, and a triplet. We have determined that a dose of 12 mg/kg intravenously or greater is well-tolerated and leads to complete CD73 target occupancy both in blood lymphocytes and in the tumor. In the SITC poster, we focus on patients receiving an optimum dose, and we report the experience in patients with uniform histologies, non-small cell lung cancer and head and neck squamous cell cancer. Details on PK, target occupancy, and other biologic parameters are shown in the poster. Patient characteristics for the study population are shown in slide 11. Patients had a median of three prior lines of therapy, with all but one having failed anti-PD-1 or PD-L1 therapy. I want to emphasize a point here. I suspect that some of you will be comparing this data to the COAST trial data. COAST was conducted in front-line stage 3 lung cancer. COAST patients have locally advanced, not metastatic disease and receive initial chemotherapy and radiotherapy prior to going on to treatment with durvalumab and avelumab. Patients who grew through the chemoradiotherapy were also excluded. Bottom line, this is a very different group of patients we're presenting here at SITC than was presented by AZ in their COAST trial. In terms of safety, the adverse events were in line with expectations and demonstrate that 12 mg/kg IV every three weeks or greater doses was well-tolerated. The waterfall plot on slide 12 illustrates the results from the 16 evaluable patients that received 12 mg/kg or higher doses of mupadolimab. There are 12 patients with non-small cell lung cancer and four with head and neck cancer. Since these patients had failed multiple prior therapies, it is relevant to compare the tumor responses to the best tumor response to the most recent prior therapy before mupadolimab, as outlined in the bottom two rows of the chart. This provides additional perspective on the biology and potential clinical utility. The first point is that tumor control was observed in most patients. On the right side of the plot, boxed in red, you can see that tumor regression was seen in five patients who had progressive disease PD as the best response to the most recent therapy, which included an anti-PD-1 or PD-L1 therapy. This means that these patients had tumors that grew right through an anti-PD-1. No response, no stable disease. The disease progressed immediately. Although we show data for mupadolimab alone and in combinations, I think it is safe to conclude that the driver of response here is mupadolimab. Three of the five patients received mupadolimab alone as a monotherapy. Looking forward, we are enrolling two expansion cohorts focused on non-small cell lung cancer and head and neck cancer. Each cohort will enroll up to 15 patients that have failed treatment with an anti-PD-1 and chemotherapy. These patients will be treated with mupadolimab in combination with pembrolizumab. The endpoint for both studies will be response rate. Results are expected in 2022. We believe that the data presented at SITC today, combined with data obtained from these ongoing expansion cohorts, provide the rationale for a randomized control study of mupadolimab, as outlined in slide 13. Our current plan would be to focus on first-line therapy of patients with stage 4 PD-L1-positive non-small cell lung cancer randomized to treatment with a combination of mupadolimab and pembrolizumab versus the control pembrolizumab only. Other anti-PD-1s are also under consideration. The primary endpoint would be progression-free survival, with secondary endpoints consisting of response rate, overall survival, and of course, safety and tolerability. To summarize on slide 14, first, mupadolimab is a differentiated anti-CD73 antibody with the potential to provide a novel immunotherapy of cancer based on dual properties of B-cell activation and adenosine blockade. Second, the data presented at SITC suggests mupadolimab may overcome resistance to and/or complement anti-PD-1 therapies, an opportunity we are exploring with two expansion cohorts in our ongoing study. Third, we are now positioned to initiate a prospective randomized phase II/III study of mupadolimab combined with pembrolizumab or other anti-PD-1 in frontline therapy of stage 4 non-small cell lung cancer. Now let's briefly discuss our ITK inhibitor, CPI-818, an oral covalent inhibitor of ITK targeting T-cell mediated diseases, including lymphomas and autoimmune diseases. Corvus is evaluating CPI-818 in an ongoing phase I/IB trial in T-cell lymphoma. In China, where certain types of T-cell lymphomas are more common, we are partnering with Angel Pharmaceuticals for the development of CPI-818. Angel received Center for Drug Evaluation or CDE approval for their IND in October and plans to initiate a phase I/IB clinical trial of CPI-818 in China in early 2022. They will focus on the treatment of refractory T-cell lymphomas with the potential to expand into autoimmune diseases over time. Angel Pharmaceuticals will be responsible for all expenses related to executing the trial in China. We continue to be optimistic about Angel's prospects and our corresponding ownership position, which is currently a 49% equity ownership stake. Turning to soquelitinib, we are working in collaboration with the Kidney Cancer Research Consortium to launch a phase II study of soquelitinib in a triplet combination with pembrolizumab and another IO agent in front line renal cell cancer. Altogether, we have significant near-term opportunities for each of our clinical programs, setting 2022 up to be in a very important year for Corvus. With that, I will turn the call over to Leiv for a brief update on our financial outlook. Thank you, Richard, and good morning, everyone. We ended the third quarter with cash equivalents and marketable securities totaling approximately $76 million. Consistent with our prior guidance, we anticipate full year 2021 net cash used in operating activities to be approximately $36 million. This implies a year-end 2021 cash balance of approximately $70 million, which will allow us to continue advancing mupadolimab into a randomized trial. With that, we'll now open the call for questions. Operator? Thank you. At this time, we will be conducting a question and answer session. If you would like to ask a question, please press star one on your telephone keypad. A confirmation tone will indicate your line is in the question queue. You may press star two if you would like to remove your question from the queue. For participants using speaker equipment, it may be necessary to pick up your handset before pressing the star keys. One moment, please, while we poll for questions. As a reminder, if you would like to ask a question, please press star one on your telephone keypad. A confirmation tone will indicate your line is in the question queue. For participants using speaker equipment, it may be necessary to pick up your handset before pressing the star keys. Our first question is from Swayampakula Ramakanth of H.C. Wainwright. Please proceed with your question. Good morning, Richard. Thanks for this presentation. It's certainly interesting to see how mupadolimab has generated the PR responses in patients who have been exposed to Pembro. My question is, if the patients have already been exposed to Pembro in your phase II/III, I know it is first line, but you know, should you try? You know, you are also saying that you could be looking at other anti-PD-1 or anti-PD-L1 inhibitors. You know, what's the rationale to go back to the same drug and give it as a combination? Why not combine it with a different anti-PD-1 or PD-L1? The randomized control trial that we're contemplating, the phase II/III trial, would be first-line therapy of lung cancer in PD-L1-positive patients. Pembrolizumab, for example, is already approved for 1% positive or more as a monotherapy, often given with chemo, but often in many other countries given alone. Some of the other anti-PD-1s will also get approval pretty soon for frontline PD-L1-positive lung cancer. The patients that we're contemplating treating in our randomized trial have never received an anti-PD-1. We'll take newly diagnosed stage IV metastatic lung cancer, and patients would be randomized to, let's say, Pembro alone, which is approved for that indication, versus Pembro plus mupadolimab. Now, we also are considering other anti-PD-1s because other ones are coming online for approval in that indication. We believe that we might offer an opportunity for some of these PD-1s to leapfrog or advance their programs very quickly by combining with mupadolimab. In any event, the patients that we're contemplating treatment are going to be previously untreated, newly diagnosed, untreated patients. Now, regarding the mechanism, lung cancer is a very bad disease once you've relapsed. You can look at, I don't remember exactly, but I'll bet you the progression-free survival for second, third line lung cancer treatments on the order of a couple of months. It's a very bad disease. We have been treating a very, very sick population. The rationale to move it up front is partly we need better patients with more intact immune systems. The rationale for combining two agents is we have two immunotherapies now that are working by completely independent mechanisms. This is very exciting. Mupadolimab stimulates B cells. Anti-PD-1 stimulate T cells by releasing the brakes. We think that coming at these better patients with more intact immune systems by stimulating B cells and by stimulating T cells, we're gonna have a much more effective therapy and a great opportunity. This is a very, very unique approach to immunotherapy. You know, not only is Mupa a novel drug, but I think this is a very new concept in immunotherapy of cancer. Anyway, is that clear, RK? Yeah, it was good. Thank you. Thank you for taking the question. As a reminder, if you would like to ask a question, please press star one on your telephone keypad. A confirmation tone will indicate your line is in the question queue. For participants using speaker equipment, it may be necessary to pick up your handset before pressing the star keys. Our next question is from Mara Goldstein of Mizuho. Please proceed with your question. Hey, great. Thanks so much for taking the question. Just a couple, if you wouldn't mind. The first has to do with the clinical program. In the phase II program, understanding that it's a different trial than COAST, obviously, would you expect your program to just be similar in size and scope to COAST, just so we can kinda think about how that might look. I wanted to ask a question about overcoming resistance to the anti-PD-1 and the concept of treating to true progression and sort of what the biology is around adding potentially mupadolimab as patients are progressing as opposed to, you know, doing it concurrently. The last question I just had, just on the responses from the phase I trial. The plot indicates that these are patients who were treated with greater than or equal to 12 mg/kg, but you did go up to 24. Yeah. Can you talk about sort of these responses and who had responses at 12 mg/kg and why those other doses were not selected? 'Cause there was some activity, if I recall, in the higher doses. Yes. Well, let me take your third question first, Mara, 'cause I've already forgotten the first two. The third question. I haven't had enough coffee yet. Sorry. The third question is yes, we went up to 24 mg/kg, you know, 'cause the purpose was obviously to find a dose-limiting toxicity, which we did not find. There were patients treated at higher doses, 18 and 24, and this shows patients at 12 or greater. Now, not very many patients were treated at 18 and 24. Mm-hmm. A number of lung cancer patients was very small numbers. There was no indication that there was any better signal, efficacy signal at the higher dose. The 12 milligrams gives us complete occupancy, gives us nice PK. Actually, what we're probably gonna do in our phase III trial is use a flat dose, and it's gonna be somewhere in the neighborhood of 12 mg/kg. Now I think, going backwards to your second question. Anyway, the 18 and 24 is safe. No indication there's any better immunobiology there. By the way, the lymphocyte activation and trafficking that occurs at a very, very low dose. In the blood. Okay. We see that at a mg/kg. This is a very potent antibody. The effects on lymphocytes here are really potent. In vitro, Mara, you can see changes in lymphocyte markers and activation in minutes, in minutes. Mm-hmm. It reminds me a lot of what we used to see with Rituxan, where you would see stuff happen, like, right away. Okay. Okay, now backing up to your. Let me add something. Obviously, this is different than Rituxan was, an antibody that depleted B cells. This stimulates them. Mupadolimab has an Fc region that's been incapacitated, as you know. It's been designed so that it doesn't fix complement or ADCC. This is a purely agonistic effect in terms of its activity on B cells. Now, I think your second question, I think there's some confusion here. Let's back up a little bit. I can tell by RK's question and yours. COAST, let's just talk about COAST first. COAST was stage three lung cancer. Stage three lung cancer briefly means you got locally advanced lung cancer. It's not metastatic. It's a big tumor growing into your mediastinum, basically, your chest. Mm-hmm. Middle of your chest. Those patients are not resectable. You can't cut the tumor out 'cause it's too big. By the way, that's only about 15% of lung cancer. It's not that common. Those patients get chemotherapy and radiation therapy first. Some platinum-containing regimen and very high dose radiation therapy to the mediastinum and to the lung, frankly, the whole lung. Then they went on to get durvalumab or, in the PACIFIC trial, the initial trial that AZ did, they went on to get their anti-PD-L1, and that worked. They had a better PFS by far. In the COAST trial, they obviously compared durva alone to addition of oleclumab, and there was an improvement both of response rate, but more importantly, a very prolonged prolongation of PFS with a hazard ratio of 0.44, which is quite good, very impressive result. The patients that are getting treated then have really pretty minimal disease. That's a, you know, Okay. Stage III after chemoradiation. I mean, they still got tumor. They do poorly. If you don't do anything after that, they'll recur very rapidly. There's still cancer there for sure, but it's at a. Those are kinda like really good patients. Now the patients that we've described here in our SITC, that's like the other end of the spectrum. You know, three failures. Yeah. Tumors growing in every location you can think of, and lots of prior therapies. I think all but one had a prior PD-1. The phase III trial we're talking about doing is gonna be a newly diagnosed stage four lung cancer. That means people have metastatic disease. It's not stage three, it's stage four. It's an incurable tumor for the most part. They are treated now a little bit depending upon how much PD-L1 is expressed in the tumor. You know, some people have no PD-L1, and those patients get a chemotherapy. That's about a third of patients. Some patients have between 1% and 49% of positive or tumor cells positive for PD-L1, and pembrolizumab is approved for that. However, most physicians would probably give pembro plus some chemo, although that's debatable. That's about a third of patients that category, and then 50% positive or more, that's about the last third of patients. I think most doctors would just give an anti-PD-1 to the pembro alone, to them. Pembro is approved. As we sit here today, pembro is approved for first line stage four lung cancer, 1% positive or more. Okay? In many countries, that's what you would get. China, for example, if you're PD-1 positive, you get pembro alone, for the most part. Now, our trial would be comparing that's a standard of care, to addition of mupadolimab. Now, mechanistically, why would I expect it to work there? Because we think that we're overcoming resistance to PD-1. We're seeing tumors shrink in some patients who have failed, who were PD'd on that, you know, in our SITC trial. In a phase III trial in newly diagnosed patients, don't forget, most patients, the response rate with pembro is only 40%, so 60% don't respond, right? Mm-hmm. Yeah. By the way, go look at the curves on pembro alone or these other things. What you'll notice in the first 3 months, there's about 20%-30% that drop like a rock. There's a refractory subset of patients. They even do worse than chemotherapy in some studies, okay? There's a crossover in the lines in the Kaplan-Meier curves. By adding our additional mechanism to pembro, we think we're gonna add, pick up those patients who are inherently resistant, okay? In addition to the pembro. Don't forget the pembro patients who do respond, they eventually relapse. It's not that good. Unfortunately, our treatment is still not that good. The PFS even of PD-1 is only like 10 months median. That's not so great. We think we can improve upon those that are sensitive and pick up those that are refractory. That's the strategy, and it's a simple strategy. We have two complementary independent mechanisms of action. This was the rationale of adding, you know, drugs together. This has been the rationale of Mm-hmm. You know, cancer therapy over decades. Okay, now, that's sort of the strategy and the scheme there. The nice thing about this strategy is, you know, we have already in our phase, in our expansion cohorts, we know that we can give pembro and mupa together. There's no issue of toxicity. We know the doses. We've already learned a lot, and we're learning a lot as the ongoing study now. There should be no problem putting it together with pembro. Now, there are other anti-PD-1s. Regeneron antibody, I forget the name of it, cemiplimab or something, is approved now for 50% PD-L1 positive lung cancer. There are others coming along that will also be approved in frontline lung cancer. Now, some people ask me, "Well, why don't you go do COAST again?" Well, I mean, COAST, you know, is a pretty small subset of patients, and I think that we've now shown activity in highly refractory patients. You know, I think that we can make a bigger impact if we go into the main kind of lung cancer, which is stage four. Anyway, now your first question, I think I forgot. No, it was- I did three, two, one but I forgot. No, you know, I had asked about not a comparison to COAST per se, but around sort of size and scope. Yeah. What you might need. Oh. Um. I forgot that. Yes. I mean, listen, I mean a randomized trial in lung cancer. I mean, if you look at most, a lot of these studies being done now, you know, the strategy of adding, you know, pembro plus X, whatever your X is, you know, there are a lot of activity there now, a lot of studies going on. You know, those are usually 700 patient trials in that neighborhood. Okay. Right? I mean, COAST was a phase II trial, right? It was, you know, not a registration trial. So you're talking about, you know, a pretty good sized trial. All right. Now just one other thing. No, I think I can stop there. I think I've already addressed it. All right. Operator, if there are no other questions. Thank you, Mara, for the questions. Very good questions. I wanna thank everyone for joining us today. If you have any additional questions or you'd like to talk by phone or email, just reach out to me or to Leiv, and we'll be happy to coordinate that. Thank you for attending this call this early in the morning, and we look forward to providing updates very soon. Thank you. This concludes today's conference. You may disconnect your lines at this time. Thank you for your participation, and have a great day.