Good morning, ladies and gentlemen, and thank you for standing by. Welcome to the Corvus Pharmaceuticals phase III Initiation conference call. At this time, all participants are in a listen only mode. A question and answer session will follow the formal presentation. Should you require operator assistance during the conference, please press star zero to signal an operator. Please note this conference is being recorded. I will now turn the conference over to your host, Matt Clawson from W2O Group. Thank you. You may begin. Thank you, David. Good morning, everyone. Thank you for joining us for the Corvus Pharmaceuticals conference call to discuss the initiation of a COVID-19 phase III clinical trial. This call is also being webcast with presentation slides. We encourage participants to join the webcast in order to review the slides while we speak. 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 this morning are Dr. Richard Miller, Chief Executive Officer, Leiv Lea, Chief Financial Officer, and Dr. Mehrdad Mobasher, Chief Medical Officer. The executive team will open the call with some prepared remarks, followed by a question and answer period. Turning to slide two, I'd 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' 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. Good morning, Richard. Thank you, Matt, and good morning, everyone. Thank you for joining us today to discuss the exciting news that we have initiated a registration phase III clinical study of CPI-006 for the treatment of hospitalized patients with COVID-19. This is a major milestone for Corvus, marking the company's first phase III program. I want to thank our entire team and our collaborators for their tireless efforts during the pandemic to move this program forward. Thanks to you, we moved from inception to phase III in less than eight months. The agenda for today's call is shown on slide three. We will begin by providing an overview of the priorities for our pipeline in 2021, highlighted by our phase III program for 006 in COVID-19. We will walk through the details of this program, including an overview of the ongoing need and context for novel COVID-19 treatment options, the current therapeutic landscape and challenges, CPI-006's mechanism of B-cell activation, and the key results from our recently completed phase I study. We will discuss our phase III study that has been designed with input from FDA and review our anticipated milestones. After this, we will provide an update and plans for our ITK inhibitor, CPI-818, and ciforadenant. We will close with a summary of Corvus' anticipated key milestones. Following the prepared remarks, Leiv and Mehrdad will join me for a Q&A session. In 2021, on slide four, we see several potential transformational opportunities in our pipeline. Our main priority this year is the execution of the global phase III study of 006 in COVID-19. We believe 006's novel immunotherapy approach provides unique advantages that could be beneficial in the ongoing fight against COVID-19 and potentially other infectious diseases. Our second priority in 2021 is working with Angel Pharmaceuticals to initiate clinical trials with CPI-818 in peripheral T-cell lymphomas, or PTCL. We will be working with Angel to file an IND in China and begin clinical trials. Together with Corvus, these trials will form the foundation for a global phase II trial, and we expect that these efforts will accelerate enrollment and development timelines. Given our focus on 006, we have refined our strategy with ciforadenant and plan to study it in a phase II trial as a triplet combination with pembrolizumab and a tyrosine kinase inhibitor in frontline renal cell cancer. Let's go to slide five and put the challenges facing COVID-19 vaccines and therapeutics into perspective. Despite the encouraging news that we have started to roll out COVID-19 vaccines to prevent the disease, we continue to believe that there will be a need for effective therapies, as summarized in this slide. It has been extensively reported that new COVID-19 cases increased dramatically in the fourth quarter and into 2021. While our discussion and immediate opportunity is in the United States, we are taking a global approach to our study in recognition that COVID-19 continues to be a global problem. We look forward to reaching a point when the majority of the population has been vaccinated against COVID-19. However, that is a significant task that will still take many months or even years to accomplish. Along the way, there are several unknowns that are becoming evident, including the level of acceptance of the vaccine, its durability of protection, and the efficacy in select subgroups. All of these factors lead us to believe that vaccines are a major advance, but COVID-19 will remain a significant health problem for years, likely associated with endemic and epidemic outbreaks. Most concerning is the recently described problem of mutation and emergence of variants or new strains of the virus that may escape therapies, including vaccinations. To date, the variants are occurring at a faster rate than was predicted, and it is occurring without any selective pressure of vaccines or therapies. One would expect to see more threatening immune evasion as effective therapies and vaccines are introduced into the population and resistant strains win out or are advantaged. The current suite of targeted monoclonal antibody therapies and/or vaccines could be rendered less effective or ineffective. This may occur gradually over time. For example, perhaps vaccine efficacy goes from 95%- 70%- 50%, along with corresponding increase in infections. While we have come a long way in understanding this disease and treating patients, the current therapy options are limited for several reasons as shown on slide six. On the left, monoclonal antibody therapy requires a prolonged IV infusion, has toxicity limitations, and does not provide long-term immunity to prevent future reinfection. Large quantities of antibody are required, several grams. Currently, these are approved for certain outpatient situations, and uptake has been slow due to the various logistical considerations, including finding a clinic or doctor's office willing to administer the agent to a contagious patient. As discussed above, the problem of mutation, immune evasion, and escape makes this approach challenging. These agents may become less effective over time as the virus changes. Moving to the center column, repurposed antivirals and convalescent plasma have toxicity limitations and may not provide long-term immunity and have shown limited efficacy thus far. Finally, we have anti-inflammatories and steroids to help address the most severe symptoms. Again, these have limited efficacy and toxicity issues, and so far have only been found effective in the most severe ICU cases. Of course, the goal would be to keep patients out of the ICU. The topic of viral escape via mutation is something that we have been highlighting since we announced our phase I study initiation back in July. This problem has now become apparent. Note these reports on slide seven from the European CDC on the new U.K. variant, recent report on the Brazilian variant, and articles in Science and the lay press such as The Wall Street Journal. In a relatively short time, without being affected by mass vaccinations or selective pressure, the virus has already mutated with variants that have proven to be more transmissible and/or have mutations on the spike protein that cause resistance to monoclonal antibody therapy and vaccines. The recent variants were first identified in the United Kingdom, South Africa, and Brazil, but are already here in the United States. On the vaccine side, initial research indicates that sera from vaccinated subjects binds less avidly to the U.K. variant. Whether protection is compromised remains a question. Of great concern is the recent E484K mutant in the South African and Brazilian variants. A recent article in bioRxiv showed that sera from many convalescent patients had greater than 10-fold reduced binding to this variant. A recent paper on the Moderna vaccine showed reduced binding to this strain from sera from vaccinated subjects. How these findings translate into protection from infection remains to be seen. Recent reports with the Novavax and J&J vaccine trials indicate that protection is reduced. It is likely that additional variants will continue to emerge and become more complex as additional mutations are acquired. This also implies that if the virus mutates enough, prior infection may not provide immunity to the new variant, as happens with influenza. The result of this is reinfection. This appears to be happening in Brazil and South Africa. We believe CPI-006 provides an elegant and practical solution to many of the potential issues with current therapies. Vaccines and the problem of viral mutation as highlighted on slide eight. The potential advantages of CPI-006 are it is designed to enhance the generation of anti-SARS-CoV-2 antibodies to any viral variant, potentially improve long-term immunity and protection from reinfection, could accelerate viral clearance and reduce the risk of spreading, could increase cross-protection to mutants of SARS-CoV-2 and other coronaviruses. It has the potential to be a foundational therapy for treatment or prevention of other infectious diseases. From a practical standpoint, a single, relatively low dose of one or two mg per kg are being evaluated in our phase III study. This allows for a relatively short 10-minute infusion time, less pressure on supply, and the longer-term potential to transition to a more convenient subcutaneous administration. CPI-006's mechanism of action is to activate the immune system against the invading virus, auto-vaccination. In this case, any one of the known or unknown variants of the SARS-CoV-2 virus to produce a polyclonal humoral immune response. Our phase I data showed that these responses occurred quickly, were polyclonal, and that it also generated memory B cells that are responsible for long-term immunity. We believe this response could help patients to accelerate viral clearance and reduce the risk of further spreading. In our phase I study, this translated to all patients being discharged from the hospital in a median of 3.5 days, and no patients progressed to requiring mechanical ventilation. The polyclonal antibody response and mechanism of action could reduce the potential for immune evasion. The immunotherapy approach or mechanism of action with CPI-006 is highlighted on slide nine. CPI-006 has demonstrated activation of B cells, the generation of plasmablasts that produce durable high-titer polyclonal IgG, IgM, and IgA neutralizing antibodies, as well as memory B cells that could provide long-term immunity and protection from reinfection. Our scientific team at Corvus has a long track record of targeting B cells to treat diseases. Targeting B cells has been a successful approach. For example, RITUXAN and ibrutinib. CPI-006 targets B cells to stimulate or activate them. Once primed, antigen drives them through a process known as clonal selection to produce antigen-specific antibodies and memory B cells. This mechanism is not restricted to COVID-19. CPI-006 is not like passive monoclonal antibodies that directly bind to and neutralize the virus. CPI-006 activates or primes the B cells that are then driven by antigen or the infectious agent to proliferate and expand to produce a multitude of specific antibodies. Our approach of activating B cells to enhance immunity, active immunization, represents a therapy with broad applicability. If approved for COVID-19, it could potentially be immediately deployable for the treatment or prevention of the next viral pandemic, for other infectious diseases, or an adjuvant to enhance the efficacy of vaccines. We now have data from 28 patients treated in our phase I study of CPI-006 for COVID-19. The high-level results from the phase I study are summarized on slide 10. There were no treatment-related adverse events or dose-limiting toxicities. The treatment was delivered as a short five to 10-minute infusion at doses from 0.3 mg per kg to 5.0 mg per kg. We believe these single low doses will position CPI-006 to be conveniently delivered in the real-world setting, both in terms of supply and infusion times. We are very encouraged by the data from the phase I study. 95% of the 28 enrolled patients had comorbidities and other high-risk factors for adverse outcomes. As mentioned earlier, none of the 28 patients progressed to needing mechanical ventilation, and all were released from the hospital with a median time to discharge of 3.5 days. 79% were discharged from the hospital by day seven. For a point of reference, recent literature shows that about 20% of patients with moderate disease will progress to requiring invasive mechanical ventilation. Slide 11 shows the anti-SARS-CoV-2 response generated in patients treated with CPI-006 in the phase I study. The level and duration of antibody protection has been shown in other studies to be a good predictor of clinical outcome. In the two upper panels on the left side of the slide, you see the serum titers over time from the pretreatment to day 28, day 56, and day 84 for IgG antibodies to the trimeric spike protein and its receptor binding domain or RBD. Cohorts are color-coded, and with convalescent plasma control on the far right in gray. Antibody responses increase out to day 28 post CPI-006 treatment to very high titers, and these titers are sustained for more than 84 days. Titers well above 100,000 were observed. For example, at 1 mg per kg, day 56 IgG spike was to about one to 200,000. Although not shown here, similar results were observed for IgM. We see a dose-response effect, with 0.3 mg being least effective and a plateau being reached at one to three mg per kg. For comparison, on the bottom of slide 11, we compare the antibody responses in our patients to similar patients recently described in the literature. CPI-006-treated patients appear to generate higher titers, and they are more sustained. Sustained titers have been recently shown in the literature by Chen et al. to be associated with shorter disease duration. Slide 12 shows the polyclonal nature of the antibody response demonstrated in the CPI-006-treated patients. Patients in the study generated a diverse set of antibodies, recognizing binding sites along the entire length of the spike protein. The recognition of multiple sites or epitopes reduces the risk of the virus escaping the immune response due to mutation. Not shown here, antibodies were generated to not only the spike protein, but to other protein components of the virus, such as the nuclear protein. High titers of antibodies with reactivity to multiple sites on the virus would be expected to provide protection against the emergence of variants. Slide 13 shows an example of reactivity against the wild type and U.K. variant virus from two patients treated on our phase I trial. These patients were enrolled in July 2020, prior to the emergence of the U.K. variant. That's the N501Y mutant. They were not infected with that strain of the virus. In a neutralization assay measured by serum blocking of RBD to the ACE2 receptor using day 28 serum samples, we find high titers to the wild type. This was the virus responsible for infection. The titers are also high for neutralization of the U.K. variant. This indicates significant cross-reactivity. Indeed, the titers for these two patients are 4.5 and 1.7-fold higher against the variant compared to the wild type, and they are higher than convalescent serum. This results from the generation of high titers of antibodies to a broad range of epitopes on the virus. Slide 14 shows the design of our phase III trial. We plan to enroll approximately 1,000 patients with COVID-19 who are hospitalized with mild to moderate symptoms. These patients require oxygen in order to have a blood oxygen saturation of at least 93%. Patients will be randomized one to one to one into one of three treatment arms of a single dose of 2 mg per kg or 1 mg per kg of CPI-006 or placebo, and all patients receive standard of care for COVID-19. The study is double blind. The primary endpoint of this study will be the proportion of patients who progress to respiratory failure or death during the 28 days after dosing. Respiratory failure is defined as requiring invasive or non-invasive mechanical ventilation. Key secondary endpoints include time to recovery, time to symptom resolution, antibody responses, viral clearance, and others. These endpoints, as well as the study design, have been reviewed by FDA. This will be a global study, including about 80 sites across North America, Europe, Latin America, and South Africa. There will be an interim futility and efficacy analysis conducted by an independent data monitoring committee after 60% of patients are enrolled and followed for at least 28 days. We anticipate we will complete full enrollment near the end of this year. To summarize, this pivotal registration trial with CPI-006, if positive, provides a novel therapeutic approach to COVID-19, which may address many of the therapeutic challenges we now face with this pandemic, such as immune escape, duration of immunity, and reinfection. 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. The importance of blocking T-cell function is shown in the two illustrations on slide 15. On the left, CPI-818 has demonstrated inhibition of proliferation of malignant T-cells by blocking ITK signaling. On the right, 818 inhibits the activation of autoreactive T-cells that drive autoimmune dysfunction. In December 2020, we presented updated data from the 818 phase I/1b clinical trial at the ASH meeting. The data shown on slide 16 continue to show encouraging antitumor activity in very advanced refractory, difficult to treat T-cell malignancies. We are now focused on studying an expansion cohort in patients with PTCL. In seven evaluable PTCL patients, there have been two objective tumor responses. This includes one patient who previously failed chemotherapy and then high dose chemotherapy and autologous bone marrow transplantation, who achieved a complete remission at eight months while on CPI-818. The 818 was discontinued after 12 months per protocol, and this complete response has now persisted beyond discontinuation of therapy now at more than 15 months. The other PTCL patient had failed multiple prior therapies and achieved a partial response now at five months and ongoing. Based on these phase I results, Angel Pharmaceuticals, together with Corvus, plans to initiate a global phase II study of 818 in T-cell lymphoma. PTCL is more common in China than in the U.S., representing about 26% of non-Hodgkin's lymphomas. This puts it on a par with some of the more common B-cell lymphomas in the U.S.. This is one of the reasons we launched Angel, and we are optimistic about its prospects and our corresponding ownership position, which is currently a 46% equity ownership stake. Angel will file the IND for the study in China, and they will be executing the study, including responsibility for all expenses in their territory. On slide 18, we have outlined our go-forward strategy for ciforadenant, our small molecule inhibitor of the adenosine A2A receptor. Ciforadenant is one of the most advanced agents in this class, having been tested both as a monotherapy and in combination with atezolizumab. In addition, we have identified an adenosine gene signature biomarker, which is present in around 50% of renal cell cancer patients. This biomarker appears to identify patients that do poorly with anti-PD-1 agents and are more likely to respond to adenosine blockade. In our phase I study in renal cell cancer presented at ASCO 2020, we saw antitumor activity in the adenosine signature-positive patients with advanced refractory renal cell cancer with both ciforadenant monotherapy and in combination with atezolizumab. Refractory late-line RCC has become a crowded space, with several recently approved drugs resulting in extensive patient heterogeneity and complexities, making development of combinations with new agents in this setting difficult. Given these considerations, our prioritization of CPI-006 in COVID-19, and the mechanism of action and safety of ciforadenant, we have decided to pursue a strategy in frontline renal cell cancer. In frontline RCC, the field is most interested in strategies that increase response rate, especially complete response rate or deep responses. We are now planning a phase II study of ciforadenant in a triplet combination with pembrolizumab and a TKI. We plan to do this study in collaboration with the Kidney Cancer Consortium. We will be discussing more details on the design of this trial at a later date. Our key near-term milestones are shown on slide 19. It is worth emphasizing that our agents target critical cellular elements of the immune system, B cells and T cells. We are excited to be enrolling patients in the company's first phase III study, and we believe we have a significant opportunity to bring a new medicine to patients with COVID-19. Based on the results to date, we believe 006 has the potential to be a novel immunotherapy for the treatment of COVID-19 and other infectious diseases. Its mechanism of action is unlike any other therapies approved or being studied for COVID-19 that we are aware of, as it is designed to stimulate the body's adaptive immune response to increase levels of anti-SARS-CoV-2 antibodies and memory B cells. This could benefit patients by reducing the severity and duration of their infection and potentially enhance their long-term immunity to repeat infection. Executing on the phase III study is the main focus for Corvus in 2021. We currently expect to have results in the fourth quarter. We are also working with Angel Pharmaceuticals to initiate a trial of 818 in T cell lymphoma, which we expect to start before the end of the year. We continue to be very enthusiastic about our ownership stake in Angel and the potential to accelerate our pipeline globally through that partnership. For ciforadenant, as I just covered, we expect to initiate a phase II study in frontline renal cell cancer. With that, we will 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. If at any time you wish to remove your question from the queue, please press star two. For participants using speaker equipment, it may be necessary to pick up your handset before pressing the star keys. One moment while we poll for questions. Our first question is from Tony Butler with ROTH Capital. Yes. Good morning, Richard. Thank you very much for the presentation. Three brief questions, if I may. Two on the phase III trial in COVID patients. The assumption here that you've mentioned is that the enrollment of these patients, all patients would be hypoxic when they enter the hospital. Is that correct? I just want to define how the protocol is defining hypoxia for those patients. That's question one. Number two is, 80 sites, that's great and certainly global. ClinicalTrials.gov, as you know, has three sites currently. How long do you think it will take you to get to that max number of sites? My final question really is on the program in RCC. Correct me if I'm wrong, previous studies were with atezolizumab as the checkpoint. You're moving to pembrolizumab. Any particular reason why? I think that you would then, therefore, need to also pay sort of the wholesale price of Pembro, if I'm correct, in patients that you enroll and treat with triple. Just would love to confirm that. Thanks for your time. Okay. Tony, those three questions, if I remember them. Yes, the patients are hypoxic to come on the trial because the eligibility is that they cannot maintain a PO2 or oxygen saturation of 93% on room air. 93% is pretty low. You would be short of breath at 93% O2 saturation. These are patients who are hypoxic. That's a definition of hypoxia. Okay? They're requiring oxygen when they're admitted. Okay? In terms of a global study yes, it's going to take some time to get 80 sites open across the world. Regulatory agencies differ in their requirements. I think within the next two, three months, we'll have those sites open. Why moving to Pembro? Well, Pembro is approved for frontline renal cell cancer and atezolizumab is not. We don't expect any difference in the efficacy or safety of atezo, which is an anti-PD-L1. Pembro, of course, is an anti-PD-1. It's just that from a regulatory standpoint, the fact that Pembro is approved for frontline makes it better for us, easier. In terms of paying for the Pembro, this is a study that's going to be done by an academic consortium, and we're not going to have to pay for that. Appreciate it. Thanks a lot, Richard. Our next question is from Mara Goldstein with Mizuho Securities. Hi there, Richard. This is Gabriel on behalf of Mara Goldstein. Thanks for taking the question. The first question here is that you mentioned that CPI-006 could be used in combination with vaccines. When do you see a trial that could possibly be assessing this to be initiated? Another question here on the SEHO in the later lines in RCC, is the company no longer pursuing at all the pivotal study or any other studies in this setting as well? Just wanted to confirm that. Thank you. Okay. In terms of the first question was combining 006 with vaccines. We think that's a really good idea. We have some discussions going on now with both academic and other industry associations or organizations to think about that. We have animal data in the laboratory where we're looking at that. There's no immediate plans to do that. I mean, we're focused now on the hospitalized patient. With regard to the RCC, we do not plan to pursue pivotal phase III trial in late-line renal cell cancer for the reasons I mentioned. There are several agents approved, designing a trial where you can dissect out the activity of each of these agents is pretty difficult. There's more interest now in renal cell cancer in frontline, much more interest in frontline, not only because patients are more homogeneous, but because even though we have more treatments for renal cell cancer, and we've improved the progression-free survival, and we've improved the overall response rate, the CR rate, complete response rate and cure rate is not changing very much. People are interested now in drugs with novel mechanisms of action that can be conveniently and safely administered upfront to the existing agents, where we can deepen the responses or increase complete responses. That's sort of the goal that most experts in this field have now. Great. Just one more, if I may add. The data so far for CPI-006 has been very interesting and, of course, encouraging for the COVID-19 patients. Has that had any impact on the enrollment on the oncology programs as well? No. I don't know. No, I wouldn't say that. They're different programs. Okay, great. Thank you. Our next question is from Swayampakula Ramakanth with H.C. Wainwright. Thank you. Good morning, Richard. Thanks for holding this call. Looking at some of the slides on the presentation, I noticed that with the 5-mg dose of CPI-006, it seemed like it was producing a less of an antibody response compared to the other doses. What do you think is the reasoning for the five-milligram dose producing a less of a response? I wouldn't make that conclusion if I were you. First of all, there's a small number of patients in each group, and there's a lot of variability in the patients, age and underlying diseases and severity of disease. When we look at antibody concentration versus activation of B cells in vitro, we have a very, very nice dose response, where when you get levels of about a microgram per mL or higher of the antibody, of the 006 antibody, you get maximal activation. When you're at 0.3 mg dose, you don't get that, and when you're at one or higher, you get that. I think anything at one or higher milligram per kilogram is going to be a good dose. We're studying one and two milligrams in the phase III trial. 2 mg is more than we need. We know it's safe, but we also want to make sure that we get enough antibody into solid tissues like lymph nodes. CD73 is also expressed in lymph nodes, and it plays a really interesting and important role there. One of the problems with COVID patients that's now been well described is, especially the severely ill ones, is they lose their germinal centers in the lymph nodes. Germinal centers are the structure in lymph nodes where antibodies are made. Anyway, 1 mg and higher is a good dose. Looking at the neutralization assays that which you had showed from two patients with the U.K. variant, do you feel comfortable with that sort of data as to make the statement that you can extrapolate it to be able to neutralize other variants as well? I think we have to do more patients and test the other variants, and we plan to do that. I feel comfortable that a polyclonal response is going to reduce the risk of immune evasion. I feel confident that 006 not only increases the level of antibodies but broadens the diversity of antibodies. We've seen that in our cancer studies. These are all good features that we think should enable us to cover variants. There's variants that haven't been described yet, so it's going to take more testing to determine if that's the case. Don't forget that your question almost doesn't matter because the response is going to be to the patient's virus, to the virus that's inside the patient. We don't have to cross-react with somebody else's variant. We're trying to eradicate the virus that's in the patient. If a patient's infected with the South African variant, the 006 is stimulating the antibody response to that variant. It's possible, I guess, if the virus changes enough in the future, the issue of reinfection could be an issue. Again, the more antibody you make and the more diverse, the better off you're going to be. The last question from me is there going to be any interim readout on this study? Yes. Since it's short-term, you may not have. Yeah, I mentioned that there's going to be an independent data monitoring committee, and there's an interim futility and efficacy analysis when 60% of the patients are enrolled and followed for 28 days. Does that have an early stoppage rule in the interim look? It could be stopped for futility, yes. Okay. Mehrdad, do you want to comment? Mehrdad. Yes. Maybe Mehrdad Mobasher can comment on it. Sure, yeah. Like Richard said, it does have futility boundaries if we find out the study is futile. If we make the pre-specified statistical boundary, the IDMC can actually recommend to unblind the data and specifically claim efficacy with the regulators. Okay, perfect. Thank you, folks. Sure. Ladies and gentlemen, we have reached the end of the question and answer session. I would like to turn the call back to Richard Miller for closing comments. All right. Thank you, operator. Let me just again summarize our opportunity. Our phase III trial on COVID is examining a novel therapeutic approach that could address many of the worrisome challenges we face with this pandemic, such as mutation and variants, duration of immunity, and reinfection. This could be a foundation for potential therapies of other diseases, infectious diseases, and cancer. We plan to have the data from this trial later this year. We look forward to completing the trial and reporting on our progress with 006, 818, and ciforadenant throughout the year. Thank you all for your attention. This concludes today's conference. Thank you for your participation. You may disconnect your lines at this time.