All right, great, thanks. Good afternoon, everybody. I'm Eric Joseph, Senior Biotech Analyst with JPMorgan, and our next presenting company is Vir Biotechnology. Presenting on behalf of the company is CEO Marianne De Backer. There'll be a Q&A session after the presentation. Just raise your hand if you have a question. We'll bring the mic around to you. And for folks tuning in via webcast, feel free to submit a question via the portal. So with that, Marianne, thanks for joining us. Yeah. Thank you. Good afternoon, everyone, and thank you, Eric, and thank you, JPMorgan, for the opportunity to present Vir Biotechnology and the fast progress that we are making across our pipeline in infectious diseases and cancer. I will be making forward-looking statements. Is this moving? Yeah. I will be making forward-looking statements. For more details, you can find our notice about legal disclaimers and regulatory filings on our website, so at Vir, our vision is to harness the power of the immune system to transform patients' lives, and we intend to do that both in infectious diseases and in cancer, so I'm looking forward to sharing with you how we are translating this vision really into action, and I believe we are at a pivotal moment. We have several programs with compelling data. We have a clear path forward. And so I will be sharing with you how we are hopefully going to create a lot of new hope and better outcomes for patients. So at the core of what we do is the intersection between two different but really related threats to human health: cancer and viruses. And in normal circumstances, the human immune system is remarkably well equipped to deal with these threats. If a cancer cell is developing in your body or a virus is attacking you, the immune system typically very quickly identifies and can eradicate both of these threats. However, both cancer and viruses have evolved quite sophisticated systems to evade your immune system. And when that happens, as you can see there in the middle, either a tumor can develop, and we are having a focus on targeting metastatic solid tumors, as you will see later on, or in the case of a viral threat, a viral debilitating disease can develop, such as Hepatitis Delta, which I will talk about a little later. And that's where our approach at Vir Biotechnology comes in. So we develop therapeutics that really help you fight, help the immune system fight these evaders. And we do that in different ways. In the case of cancer, we are using masked T-cell engagers, and we are really activating the T-cells in the human body to fight cancer cells. In the case of viral threats, we are developing really engineered therapeutic antibodies that can help clear the virus and viral infected cells. This strategy has resulted in a robust clinical pipeline, as you can see here, across oncology and infectious disease. Our focus in oncology is on metastatic solid tumors. And there we're really leveraging our dual-masked ProXTEN platform. In infectious diseases, we're really focused on hepatitis, specifically Hepatitis Delta and Hepatitis B. And there we're leveraging our antibody therapeutics platform. In oncology, we have three programs. One is a HER2 CD3 dual-masked T-cell engager, which is in phase one. And we are exploring that for a number of potential indications: metastatic breast cancer, metastatic colorectal cancer, and other HER2-defined tumors. We have a second program, which is a PSMA CD3 dual-masked T-cell engager, also in phase one, still in dose escalation, that we are exploring for metastatic castration-resistant prostate cancer. We're also really excited about initiating phase one for our dual EGFR CD3 dual-masked T-cell engager in the first half of this year. That is, of course, a target that has the application to a number of different tumor types. Metastatic non-small cell lung cancer, metastatic colorectal cancer, head and neck, and so on are potential indications there. On the infectious disease side, our focus is on hepatitis Delta, which is a very severe viral disease. We are initiating phase three registrational trials in the first half of this year. What we are really aiming to achieve there is a chronic suppressive treatment that is very different from our target in chronic hepatitis B. In chronic hepatitis B, we have a phase two program. There, our target is really a functional cure. This is a program that is going to read out in the second quarter of this year. Our goal there is to find a partner for the global development and commercialization of that program. Underpinning all of this is a very focused capital deployment. At the beginning of this year, our cash and investments are approximately $1.1 billion. We have guided cash runway into mid-2027. Now, let me take you into our oncology programs. We're really leveraging there the ProXTEN masking platform. You all know T-cell engagers have a formidable potential and even curative potential. However, the fields of using T-cell engagers in solid tumors have been held back by debilitating toxicity. That toxicity is caused by off-tumor activation and cytokine release syndrome. What we are trying to do here, our solution at Vir Biotechnology, is masking the T-cell engagers. So you see here in this visual the dual T-cell engager depicted in blue. In light blue, you have the tumor-associated binding domain. In darker blue, you have the CD3 T-cell binding domain. And what we have done is we have designed protease cleavable linker on each side of these molecules that are connected to an XTEN mask. And that XTEN mask is a hydrophilic mask. And it really forms a sort of capsule around the T-cell engager. So what happens is that if you get this dual-masked T-cell engager, as if a patient gets it, it basically gets into the circulation, gets into the blood, but it stays protected. It's only when it reaches the tumor microenvironment, where you have a high protease activity, that the protease cleavable linkers will be cleaved. The XTEN mask will fall off. And then the T-cell engager will get activated. And the T-cell engager will then bind with its tumor-associated binding domain to the tumor cell, with its CD3 binding domain to the T-cell. And by bringing the cancer cell and T-cell in close proximity, of course, the T-cells will get activated and will exert killing of the cancer cell. So what we're really trying to achieve here is that you don't get that off-target toxicity anymore, but you really only get that incredible potential and incredible potency at the right site at the right site within the body, really within the tumor microenvironment. So we expect the differentiation from this platform in a number of different ways. One is maximizing the therapeutic index. You can imagine that if you don't see that off-target toxicity, that you're going to potentially be able to dose higher. The safety is going to be better. This allows you to potentially achieve a much different therapeutic index. Secondly, as mentioned, less toxicity. By avoiding these off-tumor side effects in healthy tissues, you can really achieve a better safety profile. And you will see when we walk through the clinical data how that is achieved. Thirdly, and importantly, by putting these XTEN masks on the T-cell engagers, you are creating molecules with a longer half-life. And because of that, it allows you the potential for every three-week dosing. You will see later on, while we talk about our clinical programs, we currently have a weekly dosing. But obviously, it's much more convenient for patients to have an every three-week dosing. And it also would allow us to move into earlier lines of therapy if we would be able to achieve that. Fourth, these masks, the XTEN masks, have been clinically validated. There is a drug that is already available to patients in the hemophilia space. And also, you will see from our own clinical data with both our VIR-5818 asset and our VIR-5500 asset that we have clinical validation now of the masking platform. And then finally, and that is really important for sort of the exploitation of the ProXTEN platform, this is a universal masking platform. So it's exactly the same mask that we put on each molecule. We don't have to, for every new oncology target, design a new mask and do a lot of optimization. So for the HER2 program, for the PSMA program, for the EGFR program, we're using the same mask. And we can also, of course, deploy that to new novel oncology targets down the road. So let's switch now to looking at our clinical data. I want to start with one really compelling case of a patient in her 50s with breast cancer, HER2-associated breast cancer. This was a patient that had already received nine prior lines of therapy, including in HER2, was highly resistant. Nothing had really worked. As you can see in the top left corner, the patient presented with very extensive ulcerated chest wall lesions, very extensive involved tumor. When the patient was given VIR-5818, our HER2 CD3 dual-masked T-cell engager, you can already see in the visual, the top panel in the middle, that very quickly after having received the first dose of VIR-5818, there was a reaction. You can sort of visually see that the immune system is kicking into gear and fighting the tumor. And as the patient progressed over different cycles of therapy up to 1,000 micrograms per kilogram, you can see in the bottom right up to cycle four that the majority of the lesions had really disappeared. Now, what is really important is that this result was achieved with really minimal cytotoxicity, so no CRS, no elevated IL-6, no elevated cytokines, so a really well-tolerated profile, so this is the type, of course, it's one patient example, but it sort of shows you the type of transformational response that we are looking to see across our TCE programs going forward. Further data on VIR-5818, and again, this is a HER2 CD3 dual-masked T-cell engager. We saw some really remarkable responses in metastatic colorectal cancer patients, and you might know that metastatic colorectal cancer patients are an especially challenging patient population. They have very few treatment options. They have typically very poor outcomes. Responses are typically in the low single-digit range, so what we did here, and it was a basket trial, we had patients that had been heavily pretreated. You can see there at the bottom of the graph the number of prior lines of therapy, so these are patients that typically have exhausted all standard of care, have seen a lot of different therapies, have been unresponsive, and in that patient population, as you can see in the white box to your right, we saw 33% confirmed partial response rate. We saw 100% biomarker response, CEA, and the, sorry, disease control rate was over 80%, so a very remarkable response in a very difficult patient population. I want to point out one patient here, the one in dark blue on the right-hand side of the graph. This is a patient that had colorectal cancer, obviously HER2 defined, had been receiving multiple lines of chemotherapy, also darolutamide, was unresponsive, had very extensive evolution of his cancer, was given VIR-5818, actually initially at 60 micrograms per kilogram, and started showing a response. And this patient was dosed up to 600 micrograms per kilogram and has now shown a durable response for over 18 months. So a very remarkable case study of an otherwise very tough disease, obviously, with typically very, very bad outcomes. And this patient, we now learned, is back to work, even got married. So this is a real inspiration for our people that are working so hard on these trials. Again, very important is that the safety profile was exceptional. So no CRS, very well tolerated. The good news here is that we feel we have still given that very nice safety profile significant room to dose escalate. And also, because of the half-life of the drug, given the XTEN masking, the half-life of VIR-5818 when masked is around five to six days. So again, here, it allows us the potential for every three-week dosing, which again is going to be important potentially down the road. Our second program is VIR-5500. As I mentioned, this is our dual-masked PSMA T-cell engager. And here, we saw also remarkable responses, as you can see in the graph and also in the white box to the right. In 12 patients that received doses above 120 micrograms per kilogram, we saw everyone responding. So everyone showed a PSA decline. 58% of the patients saw a PSA 50 decline. One patient, even at this early dosing, showed a PSA 90% decline. Again, no association with significant cytokine release syndrome, no IL-6 elevations. As you can see, sort of, at the bottom of the graph here, there were only three patients that showed some very limited CRS. Again, a very, very tolerable safety profile. Also here, we feel we have significant room to dose escalate. The half-life of this drug when masked is between eight and 10 days. Again, the potential here for every three-week dosing. Really compelling early data in this patient population. Again, this was a patient population that was heavily, heavily pretreated. I want to just draw your attention to the PSA 90% patient. So this is a patient in his 70s that had very extensive bone metastasis, more than 20 lesions across his body, very high starting PSA profile, around 1,000, was dosed with VIR- 5500. And over several months, have shown very remarkable response. The PI that is responsible for this patient has done a full-body MRI on the patient and could show actually liquefaction of the tumor. So you could really see on the MRI how the tumor lesions were disappearing. So also, again, one patient case, PSA 90, but with very remarkable outcomes. So in summary, we are moving forward for both of these assets in dose escalation. They are both in phase one. Dose escalation is ongoing. We are evaluating weekly dosing, every three-week dosing. And for VIR- 5818, we're also exploring a combination with pembro. We are really looking forward to VIR-5 525, bringing that to the clinic. This is our EGFR dual-masked T-cell engager that can potentially unlock value across a number of different indications. And because of the universal nature of our mask, we also have the potential here to really exploit the platform and to explore novel targets in research and preclinical development. So a lot more to come here. So I'm now switching gear to our infectious diseases portfolio. As mentioned, in infectious diseases, our focus is really on hepatitis, more specifically Hepatitis Delta, Hepatitis B. And there we're really leveraging our therapeutic antibody platform. So just to talk very briefly about the unmet need in Hepatitis Delta. Hepatitis Delta is the most severe form of viral hepatitis. People that are diagnosed with the disease, typically more than 50% of them, unfortunately, die within 10 years of liver-related complications. The progression of the disease is incredibly fast. Patients often get diagnosed in their 40s. But diagnosis to cirrhosis and liver failure is typically only about five years. And you can only get hepatitis Delta infection if you are also infected with hepatitis B. And so what you see is that when you have that dual infection, you actually progress to liver cancer three times faster. So it's a very debilitating disease. The estimation is that there are about 100,000 patients here in the United States. In the U.S., there is no treatment available for hepatitis Delta. So there's really no options for patients. In Europe, the estimation is that there are about double as many, 200,000 patients. And there, there's one standard of care that is a daily subQ for a chronic treatment with efficacy that is far below, as you will see, from what we are showing. I think these figures sort of underscore the high unmet need and really the need for a new treatment to be made available for patients. Now, let's look at our regimen. We have a regimen here of a combination of an antibody, Tobevibart, and Elebsiran, which is an siRNA. And what is special about Tobevibart, again, our vision is really harnessing the power of the immune system to fight disease. And we do that here as well. Tobevibart was isolated out of an HBV-infected patient. So B cells were isolated, clonal cells were isolated. And eventually, a candidate antibody was generated. That was further protein engineered for half-life extension, but also for immune engagement so that the Fc domain of the antibody can dock to immune cells and really help with the clearance of the viral infected cells. Tobevibart, in combination with elebsiran, the combination has really shown transformative virological response in hepatitis Delta. And the hallmark for any viral disease is obviously to get rid of the virus. What you see here in the graph on the left-hand side is how many patients are getting rid of the virus entirely. We look at the blood of patients, and we look at target not detected being 0 IUs per mL. The virus is no longer detectable, no longer PCR amplifiable. And what we saw with our monthly treatment only after 24 weeks is that already more than 40% of the patients showed a target not detected. Delta virus had disappeared. After 36 weeks, we saw 64% target not detected. And I haven't shown the data here, but we have a small rollover cohort that we have now followed over 60 weeks, and we see 80% of target not detected. So we see really deep virological responses to our regimen. It is certainly not perfect, but just to put into context here, I've put here on the right-hand side of the graph the Bulevirtide standard of care that is being used in Europe. This is a daily subQ. And you see here that after 48 weeks of treatment, 20% of target not detected was achieved. So clearly, we have a potential very best-in-class profile. Looking at this combination, there's a number of differentiators that I want to point out. First, as I mentioned, very deep, immediate, and consistent antiviral responses. Second, a continued deepening of that response over time from 41% to 64% to 80%. So, really, what you would want to see. We also could significantly three-log drop the S-antigen levels. And the Delta virus needs S-antigen for its life cycle, for its replication. The level of S-antigen drop, so the three-log drop that we saw with the combination, was really far superior to what you can achieve with a monotherapy. Monotherapy, an antibody, you typically achieve around one, one-and-a-half log drop. So this is really significant. And then also important because, as I mentioned, patients progress to cirrhosis really, really rapidly. So we saw similar efficacy in both cirrhotic patients and non-cirrhotic patients. So I'm really looking forward to informing you when we are starting our registrational trials in the first half of this year. And this is a look at what that will look like. The good news is that the regulators have really recognized the potential impact of our regimen. We have achieved FDA breakthrough designation. We have achieved FDA fast-track designation, EMA PRIME designation, and EMA orphan drug designation, and we have designed our ECLIPSE trial to really be very encompassing. Our ECLIPSE 1 trial is targeted to, for example, the U.S. market, where Bulevirtide is not available. ECLIPSE 2 is there to really pick up patients that have not responded well to Bulevirtide. It's a switch trial, and the combination of ECLIPSE 1 and ECLIPSE 2 together are really providing the pivotal studies that will support our marketing applications in the U.S. and Europe, and then ECLIPSE 3 is really there to provide further evidence for value creation ex-U.S. Predominantly, it's a head-to-head with Bulevirtide to ensure that we can get good pricing and reimbursement in that region. So again, very much looking forward to updating you all as we are starting those trials in the first half of this year. So all these clinical development programs, both in oncology and in infectious disease, are underpinned by a strong balance sheet. We have been really conducting very strict financial discipline. We have reduced our fixed cost over the past year with 30%. So we have a cash runway that we guided to into mid-2027. And at the beginning of this year, we had a cash and investments balance of about $1.1 billion. Our focus programs, the programs that we really want to accelerate and invest in, are hepatitis Delta, where we want to start a phase three registrational trial, our masked T-cell engagers, where I have shown you really compelling early data for both VIR-5818 and VIR-5500. And of course, we want to start first inpatient dosing for 5525. We are going to look for a partner for Hepatitis B. Hepatitis B, we're going to have functional cure data in the second quarter of this year. With pending positive data, that's going to require really big trials, very expensive as well. And so we think that we can create the most value there by securing a worldwide development and commercialization partner. This is a look at our comprehensive pipeline. I really want to just point out here that beyond the programs where we want to accelerate and invest, and Hepatitis B, where we are seeking to find a partner, we also have an HIV cure program preclinically with actually a very compelling antibody cocktail, again, an engineered antibody cocktail, for which we are potentially going to look for a partner. Because we have the ProXTEN platform exclusively licensed for the entire field of oncology, we can explore novel targets with this platform. That is going to be another area where we could potentially look for partners. 2025 is going to be a very event-filled year for us. Last week, we actually shared comprehensive data across our HER2 program and our PSMA program. In case you have not seen that, I really invite you to look at our TCE Investor Deck from January 8th that is available on our website. We will be starting our ECLIPSE registrational study in the first half of this year. We are going to start our EGFR first inpatient dosing first half of this year. We're going to get our functional cure data for hepatitis B in the second quarter of this year. And then, of course, we are continuing to progress our HER2 and our PSMA programs. They are going to further evolve into dose escalation. We're going to explore weekly dosing, every three-week dosing, and also the combination of 5818 with pembro. So the next data sharing on that is to be announced. Of course, we have a lot of room to dose escalate. So it's a little bit unclear at what time we're going to be ready to share data with you. But we will do that, of course, as quickly as we have confidence. In summary, so we have been delivering on the promise of universal dual-masked T-cell engagers in cancer treatment. And we have shown you clinical proof of concept for the ProXTEN platform. We have shown you the transformative virological responses in Delta. We are starting our phase three in the first half of this year. We have a very healthy cash balance, again, with $1.1 billion in cash and investments and a cash runway into mid-2027. So by executing on these priorities, we believe we can create significant value for shareholders while transforming patient lives. Thank you so much for your attention. And I'm happy to take questions. Okay, great. Well, we have time for a couple of questions. And just as a reminder, if you have one, just raise your hand and wait for the microphone. But I thought maybe I can start off. And And just picking up on some of the recent data presented last week with your TCE platform, particularly with your HER2 agent across a number of histologies. I mean, one of the goals as you kind of do additional dose-finding work is to solidify a Q3, well, every third week dosing interval. Can you talk a little bit sort of the motivation behind that, the extent to which there may be trade-offs, the balance of just, I guess, trying to allow for less frequent administration, but also maintaining a certain amount of dose intensity to be active against tumors? Yes, there's a couple of reasons why we are exploring every three-week dosing. So first, obviously, convenience. If you think about if you are going to come up with a really potentially powerful regimen that is very safe, you can sort of start dreaming of not just going into these late-line patients, but progressing to earlier lines. For patients in earlier lines, the convenience of just having to go for your infusion every three weeks versus every week, I think, is really relevant. The other thing that it's a hypothesis is that by giving a weekly dose of a T-cell engager every time the T-cells get activated, there is a theory that it might actually be healthy to give the T-cells a little bit of a rest and that by dosing every three weeks, you might actually get equal efficacy and maybe even better efficacy. So that is something that we really want to explore a little further. We have just started our Q3 week dosing in the PSMA program, so we don't really have any insights there, but in our HER2 program, we have a number actually of Q3 week dosing patients already in our data set, and we have shown sort of similar efficacy, so if you can achieve this, obviously, with less frequent dosing, we think this can be a real benefit for a couple of reasons. Oh, any questions? And just on the point about evaluating combinations with pembrolizumab, just I guess there obviously is an immunological reason for wanting to explore that combination, pembrolizumab perhaps being enhancing to activity. As you sort of look to explore that, what both tolerability and probably additive activity profile would be worth kind of advancing that forward? Yeah, so the combination with pembro, we are exploring in our HER2 phase one trial. And remember, this is a basket trial. So we cannot really. There's 10 different tumor types. So we cannot really discern which ones are going to be in that combination cohort. However, the whole idea is that by continuously activating the T-cells, that obviously is something we want to solve potentially with Q3 week dosing. The other concern might be that there is T-cell exhaustion, right? And that you have the T-cells there, but you're just not going to be able to activate them. So that's obviously where pembro comes in and where it could help with making those T-cells, again, create a potential for these to be activated by our. So it's a very complementary mechanism of action between the T-cell engager, activating the T-cells, and then pembro making sure that exhausted T-cells can get activated again. And we'll see if that leads to an enhanced response. Again, we cannot really tailor at this moment in time what kind of cancer patients are going to be in the cohort. But it's certainly going to be interesting for us to see if that could lead to better efficacy. Can you talk a little about just perhaps additional innovation that might be forthcoming with the ProXTEN platform, whether you would look to pursue TCEs going against either new or novel targets or perhaps formulation and adaptations perhaps to kind of improve potency or the TI profile? Yes, so the good news is, as I said, it's a little bit of a plug and play situation. So you can really take this mask and put it on any protein, not just T-cell engagers, right? You can put it on cytokines. The T-cell engager platform actually has been proven in a product that is already available to patients, which is called Altuviiio. It's a product for factor VIII actually in hemophilia. It has three XTEN masks. The potential of the platform is quite significant. We have exclusive rights in the entire field of oncology and infectious diseases. What we are now doing, given the plug and play modality, is looking at what other novel cancer targets would this really be helpful for. Of course, we have a number of things that we are exploring ourselves. Also, Eric, given the news that we brought out last week, I think there's interest from external parties that have targets they think would benefit from this kind of masking. We're certainly going to explore that further. Maybe just also we have the original founder of the inventor of the platform works at Vir now. And he's sort of constantly thinking about how to make it better. But as you can see, it is actually working really well across two programs now. But he obviously continues to think about innovation in this space. Okay. Well, great. I think we might leave it there for time. So thanks, everybody, for tuning into the session. Thanks, Marianne.