Hello. Welcome to Vir Biotechnology Second Quarter 2023 Financial Results and Business Update Call. As a reminder, this conference call is being recorded. At this time, all participants are in a listen-only mode. After the speakers' presentation, there will be a question-and-answer session. I will now turn the call over to Sasha Damouni Ellis, Executive Vice President, Chief Corporate Affairs Officer. You may begin Ms. Damouni Ellis.

Thank you and good afternoon. With me today are Marianne De Backer, Chief Executive Officer; Dr. Phil Pang, Chief Medical Officer; and Sung Lee, Chief Financial Officer. Before we begin, I would like to remind everyone that some of the statements we are making today are forward-looking statements under the securities laws. These forward-looking statements involve substantial risks and uncertainties that could cause our clinical development programs, future results, performance, or achievements to differ significantly from those expressed or implied by such forward-looking statements. These risks and uncertainties and risks associated with our business are described in the company's reports filed with the Securities and Exchange Commission, including Forms 10-K, 10-Q, and 8-K. I will now turn the call over to our CEO, Marianne De Backer.

Thank you, Sasha. Good afternoon and welcome to Vir Biotechnology's first earnings call. I'm Marianne De Backer, CEO of Vir, and I'm pleased to welcome you all here today. I joined Vir four months ago, and every day since I'm reminded of how well Vir aligns with my commitment over the past 30 plus years to bring new medicines to patients. Vir is one of those unique companies that uses ingenuity in the discovery of neutralizing antibody in the fight against COVID-19 and this during the very worst times of the pandemic. This was achieved in just 15 months and brought to nearly 2 million people around the world. Before that, the Vir discovery engine had already yielded an antibody to treat Ebola. Now recognized by the World Health Organization for its impact. After four months of learning about Vir's differentiating capabilities, platforms, pipelines, and strong partnerships, I could not be more enthusiastic to lead this team of passionate driven professionals who always have the end goal in mind, serving patients. Today, and over the next few quarters, I will share more about our focused efforts to drive our pipeline and our science forward. We hope you take away an understanding of our strategy, our development programs, and the ability to execute. Infectious diseases continue to pose a major threat to global health, economic security, and to society as a whole. Just last month, in talking to a patient living with chronic hepatitis B, I was reminded of the deep personal impact such a disease has on not just the individual, but also on their families and their communities. We aim here at Vir to address these needs with a broad range of drug candidates and additional data to come this year. First, I want to touch on our recently…

Thank you, Marianne. Before speaking to our future research and ongoing development efforts, I want to address the topline data from our influenza Phase 2 clinical trial. This trial failed to demonstrate a statistically significant difference between those who received VIR-2482 and placebo. Specifically, at 1200 milligrams, which was the highest dose of VER-2482 tufted, there was a non-statistically significant reduction in influenza illness of approximately 16%. Interestingly, in this same group, an approximate 57% reduction in influenza A illness was observed when illness was defined according to CDC criteria. More analysis is going to be needed to address why this study was unsuccessful. We are looking at the data from the perspective of how different symptoms, their duration, and severity might influence outcomes, and understanding drug concentrations, time to infection, and the sequence of the actual viruses the participants were exposed to will also be important. As far as next steps, any other significant development of VIR-2482 will be guided by these analogies. To be clear, however, we will not be initiating Phase 3 trial. In the influenza space, as Marianne noted, we are continuing our efforts on VIR-2981, an investigational [Indiscernible] targeting monoclonal antibody. That covers not just flu A, but also flu B. In some animal models, it has shown markedly greater potency. The characteristics of VER-2981 parent antibody was recently published in nature. Because VER-2981 has a different mechanism of action, targeting the enzymatic activity of the neuraminidase, not the stem of a hemagglutinin, we believe in its potential to prevent influenza illness. As we learn more from the PENINSULA trial, we will certainly apply relevant findings the ongoing development of VIR-2981. More broadly, as Marianne noted earlier, the antibody platform in beer has already resulted in a medicine for COVID-19 in just fifteen months, and…

Thank you, Phil. We're pleased to share our financial results for the second quarter of 2023. Total revenues were $3.8 million compared to negative $40.6 million for the same period a year ago. Recall that in 2022, the company recorded a revenue constraint related to sotrovimab in the amount of $397.4 million, which caused the total revenues and collaboration revenue in the second quarter of 2022 to be negative. Specific to sotrovimab in the second quarter of 2023, collaboration revenue was negative $13.8 million, mainly due to sotrovimab sales being more than offset by manufacturing costs and expenses to support activities in countries where sotrovimab continues to have a marketing authorization. Going forward and barring a reauthorization of sotrovimab in the US, we believe collaboration revenues will be at minimal levels and potentially make a negative contribution to our topline due to the ongoing required investments to support the marketing authorization, which our partner GSK leads in the upper 10%. Turning to operating expenses. R&D expenses in the second quarter of 2023 were $171.9 million compared to $115.1 million in the same period in 2022. Included in the 2023 amount is a non-cash charge of $10.7 million related to the impairment of legacy in process R&D and consolidation of our labs. The year-over-year growth in R&D expenses was primarily driven by investments in the Phase 2 study PENINSULA for VIR-2482 and manufacturing activities in anticipation of initiating a Phase 3 study. While the costs associated with the PENINSULA study will ramp down in the next few quarters, we are currently evaluating the impact of the day three manufacturing capacity and supply for VIR-2482. We expect to communicate more on this with our third quarter result. SG&A expenses in the second quarter of 2023 were $47.1 million compared to $41.6 million…

Thank you, Sung. We will now start the Q&A section. Please limit questions to two per person so that we are able to get to all of our covering analysts. Operator, please open up the lines.

Okay. Our first question comes from Gena Wang from Barclays. Your line is open.

Thank you. I have two questions regarding the flu 2482 program. So, first, regarding the PENINSULA study, so why the design didn't have a lower band of a 30% like Pfizer and Moderna studies, if we use 30% lower bound, the study would look like underpowered. Could that be the reason leading to the failure? And the second question is, was the negative topline, are you -- and also the work in flu and also any week through to the other via programs or antibody platform?

Thank you, Gina. Really appreciate that chance to answer your questions and let me begin with your first question with regard to the design of the potential of the trial. So, the first thing I want to say is that, the real -- the short answer is that it was a well powered study, and we need to think of it in the context of the fact that our desire was to show an efficacy beyond that traditional vaccines. So when you think about how to power study, it's not just about demonstrating statistical significance, but it's about demonstrating clinical significance in the context of that. And so, for example, we could have powered a study demonstrate that a 10% effect size was statistically significant. However, of course, as you know, Gena, that wouldn't have been clinically meaningful given the vaccines that are currently out there. This is in contrast to vaccine flu trials, which do have a desire to that that basically power their study for clinical significance and statistical significance to a lower bound confidence interval of 30%. But I would like to remind you that with regard to monoclonal antibodies, both RSV and COVID, neither of them used such a flu vaccine specific endpoint. So, I think that we were definitely well powered to ask the question and answer the question, could we achieve transformative efficacy and, unfortunately, we did not. With regard to the other aspects of 2482, I really want to point to the fact that we are undergoing more analysis right now as to why this study was unsuccessful. And we're looking at it from many different angles, including different symptoms, the PK, time to infection, and a number of the other things I talked about earlier on this call. And really, we need to be guided by those results and that analysis and that data to really decide what next to do. But clearly, as I said earlier, also, we're not going to be embarking on a Phase 3. Then finally, with regard to your question about read-through, I would say that as I think that Marianne said it best when she said that we've already had two successes with our anti-body platform; the Ebola antibody, the only single antibody to treat and cure Ebola, as well as the [Indiscernible], which was, brought to market in less than 15 months. So, I don't think there's any read-through on our ability to really, design and identify successful medicines using this antibody platform.

Thank you, Phil. I would just, Gina, obviously, we want to be very strategic about how we allocate our capital and Phil pointed out, we are not going to rush into any next steps. We really want to do a thorough analysis of the data and then really be guided by that outcome as to what we will be doing there.

Thank you.

All right. Our next question is from Paul Choi from Goldman Sachs. Your line is open.

Hi, thank you. Good afternoon everyone. My first question is, if we think about stripping out the one-time true-up for the excess sotrovimab supply and manufacturing to GSK. And I know there's a couple of moving parts there still. If we strip that out -- if we look at the maybe the year ago OpEx, is that sort of the normalized rate that you would think, think would be normal here going forward? And what does that imply for your cash runway? If you're you can prepare and just say how long your cash balance will go through. And then secondly, on hep B for the, 2218 3434, plus or minus, peg data set that will be coming up in the, later this year. Can you maybe level set patients on how we should think about potential efficacy there? Is there potential for synergy, or should we potential think about it largely as additive And also, what can you say on potential tolerability of the regimen given, head interference, historical challenges? Thank you.

Okay. Thank you very much, Paul. Maybe the first question on cash runway, Sung you can give some more information there.

Yes, Paul. thanks for your question. So, I think you had a couple of questions there on basically operating expense normal levels, is last year comparable and the implications for our cash runway going forward. So, when you think about our operating expense and specifically R&D expense for the last several quarters -- the last three or four quarters, it's been heavily driven by the investment in the flu Phase 2 study, the PENINSULA study. In addition to that, we also invested in manufacturing activities for an anticipated Phase 3 study in flu. So, these have been the primary drivers of our R&D operating expense for the last several quarters. Now, going forward, obviously, as I go back to the prepared comments I made on the ramping down of the PENINSULA study in the next, few quarters, there are some variables here where we have an ongoing Phase 2 study in hepatitis B and hepatitis Delta and we're going to get to some important data readouts in quarter four this year. So, depending the readouts of those data, that could be a big swing factor for where our OpEx trajectory will be in the future. And certainly, has implications for our cash utilization as well. But I just want to make a clarification here. The cash utilization when you go from Q1 to Q2 is not indicative of a run rate. As I mentioned in my prepared comments, was a $273.6 million payment, to GSK related to a liability booked last year. So, I think you have to really, cancel that noise out and then you'll kind of understand what our true cash utilization has been and it's been averaging somewhere close to $120 million per quarter, in each of the quarters of this year so far. And then going forward, just coming back to something I said before, the cash utilization will largely depend on the data readouts for hepatitis Delta and Hepatitis B. But just to finish answering your question, with $1.9 billion of cash and investments, we're really in a good position here to fund not only to the end of phase two for those programs, but also through Phase 3.

Thank you, Sung. And then, Paul, related to your question on our chronic hepatitis B functional cure program, as you rightly pointed out, in fourth quarter of this year, we will be reporting data on combining 2218, our siRNA, with 3434, our antibody plus minus interferon alpha, 24 weeks end of treatment. So, and we have actually some really promising data that we have seen and have announced at E-Zone earlier this year. So, I would invite Phil to talk a little bit more about what we have seen as to signals of efficacy and also additivity.

Thank you, Marianne. So, Paul, great to talk to you again. And before we get going here, as Marianne mentioned, I think it's important to say before we can talk about what's going to be new, I just wanted to reiterate what we've seen most recently at the last two liver congresses. So, as Marianne noted, at AFLB last year, we saw that a short course of the siRNA-2218 and 3434 was additive, but that duration was only four and 13 weeks. And so what we're looking for that's going to be new at ASLB in the fourth quarter of this year is the 24 week data of combining the two of these drugs together. We're also going to be looking at these two drugs together with the addition of interferon alpha. And I think all of that together is what will be new, along with of course, new data from hepatitis delta.

Operator, can you go to the next question?

Okay, our next question comes from Roanna Ruiz from Leerink Partners.

Great, thanks. Hello, everyone. So maybe first question on Delta virus, what specific measures could you disclose in the Phase 2 SOLSTICE trial and what's the efficacy bar that you're looking for?

Thank you for that question, Roanna. I will ask Phil to give you some more details on that.

Thank you, Marianne, and thank you Roanna. So with regard to our Delta trial solstice, remember at Eazl this last year, this last June, actually, sorry, this past June, we just showed that in preclinical models 3434, our FC enhanced monoclonal antibody was able to knock down the hepatitis delta virus or the RNA from the virus. And we also showed that 2218, our siRNA could do the same and that when combined in an animal, they were additive in their behavior. So now we're looking at solstice, which also began in the early part of the spring. And we're asking ourselves the question, can 3434 alone, 2218 alone, and what's going to happen if you add the two of these drugs together in terms of their ability to knock down hepatitis delta RNA virus? So that's what we're looking forward to seeing at in the fourth quarter of this year. As you know, the efficacy bar is, rather the bar for getting approval is a two-long reduction in hepatitis delta RNA and normalization of ALT, which is only seen 45% of the time with the only currently available drug, and that drug requires daily subcutaneous injections. What we're hoping for is transformative efficacy along with maybe having only an injection once or twice a month. So I think that that can be very differentiating for us. Now in terms of what we're going to actually see in terms of data, as I mentioned, it'll be the monotherapy and the combination, but this is early data from a small cohort. So we want to be able to see are they actual antivirals in patients? And that's what we look forward to seeing.

Yes, a few more days are coming forward to us next year.

Okay, great. And I have a quick follow-up. Yes, maybe bigger picture. Could you give us a sense of what your strategic priorities for the company will be in 2024? And I guess thinking about flu, Delta virus, HPV, and all the programs you have going on, are some of them going to shift to like higher focus next year? And like, what should we be following more closely along those lines?

Yes, thank you for that question. As mentioned before, as it relates to our flu program, what next steps are going to be are really going to be determined by further analysis of the data. But our, near and intermediate focus is really on our clinical programs. So, chronic hepatitis B and chronic hepatitis delta, those are really our top priorities. We will also be bringing HIV program into the clinic in the next, this quarter. So our focus, our capital allocation will really be all around making sure that as fast and as efficiently as possible we can progress those programs towards data.

Got it. Thanks.

Our next question comes from Eric Joseph from JPMorgan.

Hi. Good afternoon. Thanks for taking the questions. Just one or two on HBV, just trying to get a better sense of the update we might see from March Part B in the fourth quarter, whether we should expect – well, well really the types of patient numbers, I guess we should anticipate, and whether we should expect readouts across the four different treatment regimens. And then I'm also curious to get a sense from you guys of what level of S-antigen clearance would support the addition of 3434 being additive to what you've reported so far from the Yuan trial of 2218 plus PEG, the doublet alone. Thanks.

All right. So, Eric, thanks for the question. I would like to begin by stating let's level set to what was shown at easel. At easel what we showed was that 48 weeks of 2218 with interferon alpha was able to result in an off treatment response in about 16% of patients six months after the end of treatment. That was preceded by an on treatment seroclearance, as you referred to earlier, of around 30%. So, basically 30% of patients had an on treatment response and then 16% had a continued off treatment response with 48 weeks of 2218 plus interferon alpha. What we're going to be seeing in the fourth quarter of this year is of course the 24 week on treatment data from the triplet and the doublet. And so what we should be looking for is that 2218 plus 3434 gets us to patients who have a seroclearance. And remember when you give 2218, 1, 8, and 34, 34 for only four or 13 weeks, we did not see any patient with seroclearance. So therefore, the goal will obviously be to see more patients or a number of patients with seroclearance, and whether or not we can match or exceed the 30% we saw with 48 weeks of the prior double. The other thing that's important to look forward to is, of course, adding interferon onto that combination of 2, 2, 1, 8, and 34, 34, and seeing how much better we can do with that. Now, going back to, Paul's earlier question about tolerability, clearly interferon alpha has some tolerability issues, if given for a long period of time, but that's in the context of low efficacy. If we can achieve functional cure rates greater than 30% or 40%, we think that this is something that patients will really be keen to understand better and appreciate given the fact that living with a chronic disease is, as Marianne alluded to in the prepared remarks, something we've heard a lot about patients, as something that they want.

Yes, and I would just add that as it relates to enrollment and timing, I mean, we're right on track as to our expectations.

Okay. Would it be premature in the fourth quarter to see any post-treatment follow-up or off-treatment follow-up for patients that only received the 20 or 24-week regimen?

So, Eric, at this time, all we've guided to is the on-treatment data from the 24-week ONs. And we are definitely looking forward to that information along with, as I alluded to earlier with marijuana, the chronic hepatitis D delta. So I think those are going to be the two exciting data sets that we hope to be able to share in the fourth wave.

Excellent, thanks very much. Looking forward to it.

Our next question comes from Eva Privitera from TD Cowen.

Hi. Good afternoon, and thanks for taking our questions. To just follow up on the prior question, for the triple combination with data in the second half, what rate of on-treatment seroclearance would get you excited or be indicative of the off-treatment clearance?

Yes, so to answer that question, I think, again, context is important. For 2218 plus interferon alone, for only 24 weeks, we saw only a 5% rate of seroclearance on treatment. So I think anything beyond that is biological proof of principle that 3434 when added to 2218 interferon is moving the needle. And of course, if you can get there without interferon and 2218 plus 3434, I think that would also be quite impressive. So I think both of those things are important steps forward. And then of course the higher the on-treatment response rate, the more excited we'll be in terms of whether or not this is going to be able to make a meaningful difference to patients.

But what delta between, what delta would you anticipate between the on-treatment and the off-treatment? Is there any way to know?

Well, I think one of the exciting things that we saw at Eazl was one of the first times that there was a predictor of off treatment response. Now, granted, it was a small cohort of patients, but we demonstrated in that small cohort of patients that patients who seroconverted, not just serocleared, but seroconverted to anti-S antibodies at high levels, greater than 100 or 200, that they were the ones most likely to have an off-treatment response. So certainly we're going to be looking at that metric in our studies to see what the off-treatment response will be. Clearly in our studies it went from 30% down to 16%, but really I think it's going to be guided by which patients mount an anti-S response and what level of anti-S response that they mount, and we'll look forward to seeing what that data looks like.

Great, thank you very much.

Our next question comes from Mike Ulz with Morgan Stanley.

Hey guys, thanks for taking the question. Maybe just another follow up on the March Part B data expected later this year. Just based on what you've seen so far, in terms of some of the other studies from Part A, et cetera, do you think 24 weeks will be enough? Or do you think you may have to go to 48 weeks? And is this a situation where longer term tends to be better? Or could there be a reason why longer would not be better for some reason? And then maybe your thoughts on the need for PEG interferon or not. Thanks.

Great. So that sounded, I think, like a three-part question, Mike. So let me make sure I get all three parts. So the reason for longer being better biologically is, of course, based on historical precedent that when you give PEG interferon alpha for 24 versus 48 versus even 72 weeks, you do get a better response even if it's still low single digits. So that's why longer has been historically better. Of course, that's balanced by what I think Paul was alluding to earlier when he talked about tolerability, which is the issue is that the longer you give PEG-related interferon alpha, the more side effects accumulate for the patient. So you're trying to find a balance between those two things, because in the end, it's really going to come down to efficacy. And as I was once jokingly told, efficacy is always, along with safety, really where the balance gets, where the rubber hits the road. So I would say that if we can demonstrate a 24 week cure that is similar to the 48 week cure, we will of course go with the 24 weeks because I think that that would allow patients to have a shorter course of interferon therapy. But really if it's a delta, a meaningful efficacy delta, then we'll have to decide as we look forward to talking to patients and talking to providers, what exactly would be most desirable in that group. So that's really the balance between longer is better from an efficacy perspective, and longer being less ideal from a safe, not a safety, but a tolerability perspective. Did that answer your question, Mike?

Yep, that'll make sense. And then your thoughts on the need for PEG, I guess. Shorter with PEG might work, but longer maybe doesn't make sense.

So I would say that the -- let me answer that in two ways. Let me answer that from a biological perspective, and then from a patient perspective. From a patient perspective, I think that it is really going to depend on what the efficacy is. So imagine you're a patient right now, and someone says, I'm going to give you a year-long course of therapy, it's going to have some side effects, but you only have a one in 20 chance of it actually benefiting you at all. Most people say, I'm not willing to roll the die in that circumstance. However, if you were to come back to that same patient and say, I'm going to give you a year of therapy, but if I do it in combination with these other drugs, I could increase your chance of cure to, one in three or one in two, I think that's a very different story. So I don't think it's just about absolute duration. I think it's about efficacy in the context of that duration. As far as the biological need for interferon, I think there are things in favor of suggesting why it might be necessary. I think the fact that, it is the only known way to cure hepatitis B right now that has been approved is one interesting point. But I think it points more broadly to the need for an immune modulator to really achieve a functional cure, which is really an immunologically-induced remission. So, one of the aspects about VIR-3434 that we're really excited about is the fact that it's not just a neutralizing antibody. It has a modified Fc domain, which allows it to act as a potential therapeutic vaccine. And if that aspect of the VIR-3434, which we believe may allow it to act as a substitute or an alternative to interferon alpha. So of course the jury's still out on that. We're going to see what 24 weeks looks like on treatment this coming Q4. And then we'll of course have what 48 weeks of that treatment look like next year.

That's helpful. Thank you.

All right. Our next question comes from Joseph Stringer from Needham & Company.

Hi. Thanks for taking our questions. Two from us. First on the HIV program, you were previously evaluating your 1111 and Phase 1 trials. What's different about 1388 and what gives you confidence that this T cell vaccine is the right approach and what are timelines around initial data? And then secondly, given current cash balance, what are your thoughts on external BD? What's your appetite for bringing in external assets, whether they be early or late stage? Thanks.

Thank you, Joe. So maybe I'll start with the last question first. And obviously, we are in a very unique position where we have a strong balance sheet that will allow us to really fund our critical Phase 2 and phase one assets for the next stages of inflection. It also offers us the opportunity to remain opportunistic. And if we see assets or opportunities out there that can really strengthen our pipeline and our capabilities within field biotechnology, then of course we will take advantage of that. For your first question related to the differentiation of VIR-1111 versus VIR-1388. Maybe Phil you can take that one.

Thanks, Marianne. So, Joseph, we are on track to dose our first patient this quarter in Q3 with VIR-1388, which as you noted is a prophylactic HIV vaccine. In terms of what's different about it compared to VIR-1111, I think that, obviously, we need to wait for the results in humans, but at least we can say in tissue culture, the biggest difference is that VIR-1111 was deliberately attenuated, which means we made it less able to replicate in tissue culture, because we wanted to really get some basic understanding of how this vector, which is based on human CMV, behaves in people. We now have the opportunity with 1388, based on that safety information from VIR-1111, to take what we call the less attenuated virus into the clinic. So this virus, at least in tissue culture, is able to replicate a little bit better, and therefore, we believe can be more immunogenic in humans. So I think that that's really the big difference. And there is of course some other minor differences in terms of some other deletions or insertions we have made, but that's the key difference between VIR-1111 and 1388.

Thank you, Phil. And then maybe, Sung, if you could comment a little bit more about our cash position.

Yes, happy to do that, Joe. This is Sung. So I mentioned earlier I think there was a question about our cash runway. So with $1.9 billion on the balance sheet it gives us a lot of financial flexibility and as Marianne said earlier, certainly to fund our current development programs which are broadly in Phase 2, and HIV obviously is in Phase 1, but we can get to the next inflection points for all of those programs should the data support it. So it's a real fortunate position to be in. Just to reiterate again, and I really want to make this clarification because I do think some information might have been misunderstood. We did have a large payment to GSK during the second quarter and that certainly is, we don't consider that to be part of our run rate.

Great. Thank you for taking our question.

All right. Our next question comes from Patrick Trucchio from H.C. Wainwright.

Thanks, and good afternoon. I have a couple of follow-up questions on the HPV program. So, first, I'm just wondering if you can talk about the bar for regulatory success in HPV, specifically if you need to demonstrate a 30% sustained clearance of the HB surface antigen six months after treatment is halted to achieve approval, or if a rate below this can be sufficient for approval in the setting of HPV. And then, can you talk about the potential for demonstrating a partial cure in HPV? What's the latest around how this is being defined and if it could at some point become part of maybe a regulatory bar for approval in the setting of HPV treatments? And then separately with the preclinical pipeline candidates unveiled today, how should we think about the remaining preclinical work that remains in potential timing for filing of INDs?

Excellent. Thank you so much, Patrick. So perhaps, Phil, you can start me talking a bit about our preclinical pipeline.

Definitely, Marianne. So, Patrick, in terms of your third question, I think that, it really is an exciting time for Vir. I already mentioned to you with the last question, 1388, which is the HIV prophylactic vaccine that is going to be entering the clinic this quarter. I did want to actually add a note to that, which is to say that it is based on human cytomegalovirus, as I noted earlier, and human cytomegalovirus is one of the most immunogenic vectors that has ever been described. Sometimes up to 20% of your T cells can be mounted against that vector, and importantly, it generates a type of T cell known as an effector memory mucosal T cell, which is quite important, we believe, in the prevention of diseases like HIV, but also allows us to use it in other diseases such as human papillomavirus. And that is another thing that is going to be entering the clinic in the next 24 months, basically a therapeutic T cell vaccine called VIR-1949, which is for the control of precancerous lesions caused by human papillomavirus. So both of those things are quite unique and exciting for Vir. In terms of the respiratory franchise and the antibody platform, we've already talked about VIR-2981, our neuraminidase-targeting monoclonal antibody that has activity not just against influenza A, but influenza B. We also have VIR-8190, which I touched on earlier, which is uniquely able to neutralize not just RSV but human metapneumovirus, and also VIR-7229, a next generation COVID-19 monoclonal antibody that has really shown quite broad activity and quite potent activity against historical and current strains. So we really have a broad set of things that we believe will, that can make a huge patient impact in the future that will be entering in the…

Thank you, Phil. And Patrick, just to reiterate what we have focused here today is on discussing those preclinical candidates for which we could potentially expect an IND within the next 24 months. Thank you.

Thank you so much.

All right, if there are no other questions, I will now turn the call back over to Dr. Marianne De Backer.

Thank you, operator, and thank you all again for your attention today. Vir Biotechnology is a truly vibrant and dynamic company that I believe is poised for significant growth and most importantly for patient impact. I am thrilled to lead Vir into what I believe will be the next transformational trajectory, as we build on the progress that we have achieved so far. I feel confident that we have the internal scientific expertise and the passion to power our mission forward. So thank you all for joining us here today. We really appreciate your time and your interest in Vir Biotechnology. Thank you. Operator, you may end the call.

This concludes the meeting. You may now disconnect.