Hello, and welcome to the H.C. Wainwright at Home event. I'm very pleased this morning to have with us Arbutus Biopharmaceuticals, and joining us, representing the company, is the interim president and CEO, Mike McElhaugh. Mike, welcome. Thanks very much. I appreciate you having me today. Great to have you with us. So why don't we start with just a brief overview of your pipeline and how those assets might fit in achieving your strategy of achieving a functional cure in treating HBV patients? Sure. And so, as you know, Arbutus Biopharma is a company that's exclusively focused on developing a functional cure for hepatitis B virus, a virus that affects 250 million patients globally. And it's a chronic infection. We have two products in our pipeline. Our lead product is called imdusiran. It's an RNAi therapeutic that targets all HBV transcripts and leads to knockdown of, importantly, hepatitis B surface antigen, which is responsible for the exhaustion of the immune system that leads to chronicity of HBV. We also have in our pipeline, and that's currently in phase 2, and we can talk about the data that we've generated in the phase 2a studies to date. We also have a program called AB-101 in our pipeline. It's a small molecule PD-L1 inhibitor. This is a way that we've developed to eliminate some of the issues that exist with the potential checkpoint antibody use in hepatitis B. Obviously, the checkpoint antibodies were developed for oncology applications, and there is a different risk-benefit ratio for oncology patients than there are for hepatitis B patients. We think the small molecule approach targeting the liver could really be an important way to utilize this asset for hepatitis B patients. There is significant evidence that the checkpoint blockade plays an important role in HBV maintenance. All right, so obviously, AASLD's Liver Meeting just wrapped up two weeks ago today, and you presented some pretty impressive data from your IMPROVE-1 study. First, before we get into the data, first remind us of the details around the trial design for that study. Sure. So IMPROVE-1 is a study that looked at imdusiran, our RNAi therapeutic, in combination with pegylated interferon. And what we did was we dosed imdusiran for 24 weeks to really lower surface antigen for those patients. These patients were already suppressed on the nucleoside analog, so their HBV DNA was undetectable. And then once we lowered the hepatitis B surface antigen, we re-randomized those patients into one of four groups, either 24 weeks of interferon or 12 weeks of interferon. And that duration of interferon is an important component of the regimen overall because interferon generally is given for 48 weeks. It's tough to tolerate for 48 weeks. But if you can shorten, and it leads to very few functional cures as a monotherapy. But if you can shorten that duration and increase functional cure rates, people are much more willing, physicians are much more willing to tolerate the interferon component of the regimen. So after we reduced surface antigen with imdusiran for 24 weeks, we re-randomized into one of four groups, either 24 weeks of interferon in two groups, either with or without continued imdusiran dosing, or interferon for 12 weeks, either with or without continued imdusiran dosing. And then we, of course, followed those patients off of therapy for an additional 24 weeks while they took their nucleoside, and then we stopped all therapy going forward and assessed for functional cure. That functional cure data is the data that you just referenced at the AASLD conference that we presented just a few weeks ago. It feels like a lot longer, but it was just a few weeks ago when we were together at AASLD, and we are extremely impressed and happy with the data that we received. We achieved a 25% functional cure overall in the best-performing cohort, which was Arm A1, which looked at 24 weeks of imdusiran with 24 weeks of interferon and continued imdusiran dosing during that 24-week interferon period, and importantly, we saw a 50% functional cure rate in patients who had baseline surface antigen less than 1,000, and that's just a tremendous number, Ed. We're very excited for what that could mean for patients. Great. And then talk about, in addition to this functional cure rate, some of the other data for cohort A1 in terms of seroconversions and what you saw in terms of safety and tolerability. Sure. So as far as safety is concerned, imdusiran, knock on wood, was very safe and well tolerated. No major issues with regards to safety. The safety profile looked really good. With regards to seroconversion, we did see seroconversion in patients who achieved functional cure, at least those patients in the A1 cohort that achieved functional cure. You do see this nice increase in hepatitis B surface antigen antibody as the surface antigen is coming down. As you know, the definition of functional cure is actually with or without antibody development. So the importance of that on a go-forward basis is unknown at this point, but there was antibody generation in those patients. All right. And then this data really haven't been seen at all, in particular with other RNAi in development. Can you talk about what makes imdusiran different than some of your competitors in the same class? What aspects of the profile make it different than other RNAi? Sure. So So you're right, Ed. We have not seen, particularly in combination with interferon, we have not seen these results to date. This is a phase 2a trial. It's relatively small, but all phase 2a trials that we've seen in the field to date are relatively small as well. There has been a historic tendency to sort of group the RNAi together into one bucket and say, "Okay, if you have an RNAi, it should perform exactly as another RNAi across the class." We're pretty convinced at this point that we have some differentiation with imdusiran. That could be due to a couple of different things. One, the sequences of the nucleotides are obviously different across the various siRNAs, right? The modifications that are made to the various nucleotides can be different and are different across all the various siRNAs. The place where they cut, so some spare X antigen, for example, some don't, and also the GalNAc delivery that's used to deliver the siRNA component to hepatocytes is actually different across the various siRNAs as well, so any individual piece there or the totality of those differences could be manifesting in differences in functional cure rates. There's actually been very few interferon and siRNA-containing regimens that have shown functional cure to date. The important thing is that the duration of interferon differs and the functional cure rate changes, so, for example, Roche, who presented some data at AASLD as well, showed a 20% functional cure rate overall in patients with surface antigen at baseline less than 1,000, but remember, that was for 48 weeks of interferon with 48 weeks of their siRNA. So that's very different from the 50% that we saw with only 24 weeks of interferon. Right. Okay. And then you mentioned Roche. There are other competitors in this space. Perhaps discuss the difference with imdusiran to others in terms of the lower dose and also the dosing frequency. Yeah, great point. So actually, all of the siRNAs in the field outside of imdusiran are dosed monthly, right? Imdusiran is dosed every other month, so every eight weeks. And we're seeing very consistent responses with that every eight-week dose. The amount of drug that's given is also different. So our dose is lower. We use 60 mg every eight weeks. Some of the competitors are into the hundreds of mg every month. So there are definitely differences in dose and duration across the siRNAs as well, again, leading to some differentiation with regards to imdusiran. And then with regard to this early interim data from cohort A1, this, of course, is from an open-label trial design, and the sample size is quite small. I'm wondering if you could help us understand your thoughts around the level of confidence that you have going forward with this data, in particular how you think that could translate, especially in those low baseline patients that saw the 50% level. Sure. So I actually think the data is quite translatable to a larger study, Ed. You're right. It is a small cohort of patients. But as I said, it was meant to be a phase 2a proof of concept study. And like all other phase 2a proof of concept studies in the field, it was appropriately sized for what we were trying to accomplish. We believe that, especially in the low surface antigen patient population, at baseline, which I think is what we're going to explore in a follow-on study, we think that data is definitely repeatable and will be repeated. Of course, we have to run the study in order to definitively say that. But historically, patients with lower baseline surface antigen tend to respond better, and that's exactly what we're seeing. So I would suspect that trend's going to continue as we move the program forward. Looking again towards some of the competitive data, I know you just briefly mentioned Roche. I know in our discussions, we've talked about some of these. Of course, there's always caveats when looking across trial data sets. But importantly, there are some aspects to the design and some of the endpoint definitions that make it difficult comparing sort of apples to oranges. Maybe talk around some of that as some of the investors try to look at the space and compare imdusiran to others. Sure. So you're right, Ed. It's very difficult to compare these trials apples to apples because of the way that they're designed. So I would highly suggest that as people take a look at the data sets, they look at things like, as you said, what the endpoints are, what data is presented. It may be that we get to the same place at the end of the day as far as what actually gets presented. But in context of what's been presented to date, things that are important to consider. One, things like duration of the interferon dosing, right? The duration of the siRNA and the interferon dosing. That differs across companies. Too, oftentimes people will keep their patients on nucleosides and never stop the nucleosides and only talk about surface antigen loss, which is a nice improvement over what we've seen historically, but it is not functional cure, right? So the definition of functional cure is very specific. It's HBV surface antigen loss and HBV DNA less than lower limit of quantification, 24 weeks off of all therapy. And that includes the nucleoside, right? So you really need to take a look at what specifically is presented and how. And oftentimes it's not easy to do because you have to look at different presentations in order to figure out exactly sort of how that all plays together. So there are lots of differences that one might look at if they were trying to compare best they could apples to apples, which is hard to do. Right. So just taking a high-level look at this data set and the 50% functional cure rate that you've got, talk to us about how relevant you feel that is in terms of some of the recent data, especially given that it's in the lower baseline patients. And then why did you choose 20% as your original functional cure rate goal or threshold? Sure. Yeah, good question. So the original functional cure threshold goes back many, many years, Ed. So the current issue, of course, with hepatitis B treatments is they don't deliver functional cures, right? It's very low numbers, low single digits. Whether you're talking about a nucleoside that's given for the rest of someone's life or interferon, which is given for 48 weeks, you're talking about low single-digit functional cure rates, right? When we originally set out to increase that functional cure rate, deliver a cure for patients in hepatitis B, kind of like we did in hepatitis C, we talked to physicians, we talked to patients, and we said, "What might be, excuse me, what might be a meaningful increase in the functional cure rate that would get patients, physicians excited?" And what they typically said at the time was, "I don't know. If we could get somewhere around 15 or 20% as an initial regimen, that would be pretty exciting for us, okay, so we sort of had to put our stake in the ground somewhere, so we went a little bit higher than that and said, 'We'll say 25% as sort of a beacon to sort of get to.' Now, as far as the low, and this was before quantitative surface antigen was being used and before the value of increases in response rate to patients with low baseline surface antigen was even in consideration, right, so as the field has continued to evolve, that's the way that things have moved. I think that the baseline surface antigen less than 1,000 is very relevant patient population going forward because, as we've talked about in the past, it's going to be an iterative process, similar to how it's been in HCV, how it was in HIV, we're going to iterate as we continue to move things forward, but if you think about a situation where we can give potentially a patient a one-in-two chance of getting a functional cure at that 50% rate, that patient population will be interested in taking therapy, and that patient population is quite a bit larger than one might think originally, so remember, there's 250 million patients globally chronically infected with hepatitis B, so even a smaller piece of that pie is a really big number, and based on the research that we've done to date, about 40% or so of patients fit into that bucket. So it can potentially bring a regimen that is extremely meaningful to a large swath of patients who are currently suffering with chronic hepatitis B. Right, and so if we translate that into, say, patient numbers in the U.S., and just for purposes of conservatism, we assume initially only that low baseline patient group, what would that look like? Yeah. So there's about two million or so patients with chronic hepatitis B in the U.S., okay? And about half of those are probably 70% of those are e-antigen negative. And 40% of those could be surface antigen less than 1,000. So you can see it's still a really significant number of patients, even in the United States. And then the rest of the world, even in parts that are accessible for medicines, for a company like Arbutus, meaningful patient numbers globally. You've already defined functional cure. But perhaps for those who may not be as familiar with the space, maybe discuss why that's the goal here and why is it important versus other goals, in particular, as you think about hard outcomes like HCC? Yeah. So what the data has shown, Ed, is that a patient who achieves functional cure actually can significantly lower their risk of HCC on a go-forward basis, right? Nucleosides lower it to a certain level. Functional cure lowers it even further, okay? So that's really important to the patients to lower their risk of HCC on a go-forward basis to get to this functional cure rate. There's been lots of considerations about different endpoints, things like partial cure, which is lowering surface antigen, but not undetectable. But we really tried to focus on that functional cure goal because there is some data that suggests that that is beneficial for patients. And right now, as I said, therapy with nucleosides, which is standard of care, is lifelong. Patients do not want to be on therapy for the rest of their lives. There's significant stigma associated with this disease. They just want to be cleared of the virus and not thinking about it on a daily basis and not have to worry about taking their drugs daily, which historically, people have a hard time doing, right? If you tell someone they need to take their drug for the rest of their lives, they don't typically always do it, right? So there's a compliance issue in the field generally that we can also address through functional cure. That goes back to your infrequent dosing schedule, which could help alleviate that. It does. So that's important too, the infrequency of the dosing, but also the fact that this is finite, right? So in order to get to functional cure, as I mentioned, you have to be off all therapy, which means you're not taking any more drugs, right? So it's a finite duration. Once they get through that regimen, assuming they reach functional cure and stay undetectable, they are off drug. Yeah. All right. So given this strong data initially that you've seen, what are your next steps? I know you've talked about moving into perhaps a larger well-controlled phase 2b, maybe perhaps have an arm. Obviously, you'd want to focus at least in one arm on those lower baseline patients. But just maybe talk through what your thoughts are now. Yeah. It's a great question, Ed. And we're still having debate internally about what the optimal study design is. Obviously, we have to have discussion with regulators as well. But at least directionally, you're right. We're leaning towards focusing on those patients with baseline surface antigen less than 1,000. The goal here really is to maximize functional cure, right? And then get a regimen into patients as quickly as we can. So yes, I think that's the way to think about it. A nicely controlled phase 2b trial. It doesn't have to be extremely large to meet the endpoints that we're thinking about going forward. But we really would like to make sure that things continue to trend as they are and position imdusiran best to get it to market as quickly as we can. So that's our plan there. We'll be back with additional details as we continue to work through those, hopefully early in 2025. Yeah. That was going to be my next question. I know that as you confer with the regulators, these timelines are somewhat out of your control. But just thinking about timelines, as you mentioned, maybe any sort of steps along the way that you can mention. And also, I know maybe it's a bit early, but maybe thinking about what the cost might be as you think about this larger study. Yeah. All good questions, Ed. Not many that I can answer at this point. So I'd say stay tuned for those as far as the cost and the actual size. As far as time is concerned, we want to get this kicked off just as quickly as we can. So that's our goal, to get through the internal and external hurdles that we need to do in order to kick this off. But our goal is to get this through as quickly as we can. And we'll be back with some more details, like I said. And I think this is something you'll likely ask me is, "When will we have some more details?" We typically have some more guidance around the J.P. Morgan conference. We anticipate that we'll probably be providing some more updates about this around that time. We'll see how things progress here. But that's typically what we've done in the past. And I'd like to try to hold to that sort of timeline to give a little bit more detail so that there's not uncertainty as far as where we're headed. Right, and then I just want to take a step back and take a look at the perspective and impressions from both big pharma and investors going back a number of years now in the HBV space. There's been some fits and starts in terms of data readouts and programs and so forth. And I'm wondering if in two weeks or so since you announced this data, you feel like this could be sort of the seed that starts to help to re-energize the space, re-engage both investors as well as strategic partners. Yeah, well, what I can say is I sure hope so, right? I can tell you definitively that the response at AASLD with the physician base was fantastic. The data were extremely well received. We were highlighted in all the relevant summary sessions that are not Arbutus-sponsored, but they're society-sponsored. There was quite a bit of buzz about the Arbutus data at the AASLD conference. With regards to strategic partners, we've had this conversation in the past. We have conversations with all relevant partners. We'll continue to do so. If it makes sense for us as a company, we will consider partnering when the time is right. But it has to make the most sense for imdusiran and Arbutus. So we'll continue to have all those relevant conversations, and we'll see where it goes. But I'm hopeful that our data and the competitor data that we saw at the AASLD conference, and we'll continue to see as we move here to the AASLD conference early in the next year, we'll continue to help reinvigorate the space and the focus on hepatitis B. Then just thinking about sort of the breadth and optionality embedded in your pipeline, you also announced additional data at AASLD from the other study, another phase 2a called IMPROVE-2. And that's combining imdusiran with Barinthus Biotherapeutics VTP-300 and low-dose nivolumab. What data did you see in that particular cohort? Yeah. So you're right. IMPROVE-2 is a study that looked at imdusiran. Remember, our goal with imdusiran when we originally set up these phase 2a studies was to enact our strategy, our global strategy, which is to reduce hepatitis B DNA, suppress hepatitis B surface antigen, and boost the immune system. So those two studies, IMPROVE-1 and IMPROVE-2, were put in place to test that strategy, right? So we use a nucleoside to address HBV DNA. We use imdusiran to address surface antigen. And we were playing around with the immune-boosting component. So we used interferon in IMPROVE-1, which we've talked about. And in IMPROVE-2, we decided to use Barinthus Biotherapeutics' therapeutic vaccine, VTP-300, with or without nivolumab, which is an antibody for PD-1, okay? We added that third arm, which looked at the nivolumab addition based on some data that Barinthus had in their own internal programs that suggested that there was a contribution with adding nivolumab to the mix. What we presented at AASLD was that Arm C, the combination of 24 weeks of imdusiran to lower surface antigen, VTP-300 prime and boost, and in conjunction with the boost component of VTP-300, a low dose of nivolumab, okay? What we saw was that there was a better response in Arm C relative to the two other arms, Arms A and B. Arm A was a placebo arm that looked at just 24 weeks of imdusiran, and then placebo during the follow-on. Arm B, which included imdusiran for 24 weeks and then the prime and boost of VTP-300. Arm C performed better. We actually got 23% of patients undetectable for, excuse me, who had surface antigen loss at the time point that we presented at the conference, and we're excited to follow those patients going forward. It certainly looks like nivolumab is contributing, which speaks to AB-101, our small molecule program as well, which I'm sure we'll get to. Right. Right. Well, so sticking with this study for a moment, I know you have another data readout coming forward. In particular, I'm curious if at some point you would read out data on the potential for functional cure from this study as well? Yes. So that would likely be the next readout, Ed, which would be functional cure. Now we're following these patients after they're done their treatment. Those that are off all treatment will continue to follow and deliver functional cure. So we're excited about that. We'll see where that goes. Right now, obviously, we're focused on the results that we saw in IMPROVE-1, which is imdusiran plus interferon. But we'll see how that data continues to evolve. Do you have in mind a timeline for that next data readout? Off the top of my head, no. We haven't actually provided any guidance with relation to that, Ed. But you can probably roll those patients forward and get a good sense for when that data might be available. And then at that point, you would decide whether to move forward with that one as well or maybe just develop the combo with interferon. Yeah. You know, Ed, at this point, what we're leaning towards, subject to change, of course, as the data continues to evolve. Our goal has always been to maximize functional cure, right? The fact of the matter is we now have functional cure data in hand with the interferon-containing regimen, right? We want to move that forward as quickly as we can. That's what we're focused on currently. Then we'll see how the data continue to evolve, and we'll figure out what any potential next steps might be with Barinthus Biotherapeutics as we continue to move forward here. We are happily focused on the interferon data given the positive data that we saw at AASLD. All right. And then so turning to your other lead asset, AB-101, as you mentioned, this is a PD-L1 program. But importantly, it's an oral small molecule. And so maybe perhaps discuss some of the differentiating aspects between that and say, for example, some of the antibody PD-L1s. Yeah. Sure. So as I mentioned earlier, the issue with antibodies in hepatitis B is that they were originally designed for oncology patients, right? And they're antibodies. So the problem is when you give an antibody, it binds as it should, but you can't turn it off, right? So in many cases, you get these instances of immune-related adverse events that you can't well control. And as I mentioned, hepatitis B patients have a different risk-benefit profile than oncology patients typically have, right? So what we don't want to do is trade one issue for another. So hepatitis B for, for example, a thyroid issue, right? Which is an immune-related adverse event that you sometimes see with antibodies. So what we did was we decided to take a small molecule approach, as you mentioned, liver-targeted small molecule approach. Because with a small molecule, you can actually fine-tune using PK/PD relationships the effect that you might ultimately see. So if you start to see issues related to immune-related adverse events, you can turn it off, right? Which you can't always do with an antibody. At least that's the intent. And we're currently in the clinic, and we're in a phase 1a, 1b study that looked at single doses, now multiple doses, and we're currently in HBV patients. So the program is moving, and we are hopeful to have some data from the HBV cohorts in the first half of 2025. Right. Okay. So that was going to be my next question. Maybe just discuss for those who may not be familiar, the current status. And then if you've got this next readout, is that the only one, or are there other readouts coming from that study later on? Yeah. So what we're looking for in the phase 1A, 1B study is, of course, safety, right? First and foremost, but we can also look at something called receptor occupancy, which is a good surrogate for potential efficacy, right? So receptor occupancy just means how much of the binding do you see? How much of the receptor is occupied that you can see on the hepatocytes, right? Or in the periphery in this case, which is where we're measuring it, right? We use that as a surrogate for what's happening in the liver because we're not actually doing biopsy in the study, right? So we're looking at peripheral cells. We look at receptor occupancy. And what we're seeing is a nice dose response with regards to receptor occupancy as we've made our way through single doses in healthy volunteers, multiple ascending doses for seven days in volunteers. Now we're moving into patients. Now, I don't have any patient data that we can talk about yet, but we're seeing in the single and multi-dose healthy subjects, we're seeing good receptor occupancy at the doses that we actually tested in the study, suggestive of potential efficacy down the line. We're excited about that. We haven't yet said specifically what we're going to present with regards to hepatitis B data in the first half, but we will do that. Then, of course, as the study continues to evolve, we will continue to present data as it moves forward. The goal with 101 is always to get it into combination with imdusiran as quickly as we can and see where we go from there. We just have to wait because they're not at the same stage of development. So it's dependent upon AB-101 continuing to perform as it should. So as you mentioned, your three-prong strategy has long been this sort of suppress, reduce, and then boost. And you're now at a time, I think, is really interesting because you're thinking about a larger well-designed study with your lead asset, imdusiran, but you've also got now VTP-300 as well as your own AB-101. And I'm wondering if perhaps you might consider a future study that would have arms, for example, that would include AB-101 or VTP-300 and that combination and sort of look at all potential triple combinations. So given unlimited capital, I would love to do all of those things, Ed, for sure, right? But we do recognize that capital is limited in biotech in general. So we want to make sure we're choosing the best regimen that makes the most sense for patients going forward. So right now, that's the interferon combination, and we want to make sure that we move that forward as quickly as we can because we want to get it into patient hands so that they can actually get functionally cured and get off drug and feel good about themselves and eliminating their hepatitis B. With regards to 101, we'll see how that continues to evolve, right? As I mentioned, it's a little bit further behind. We can speculate about where we might take it as things continue to evolve. But until we're ready to put it in combination, there's really not a whole lot to talk about other than to say we'd like to get it into combination with imdusiran as quickly as we can. And that's always been our goal. And we'll see where we go from there. Right. Right. Understood. So obviously, take forward, bird in the hand, and then maybe to potentially sequential improvements along the way. Correct. And that's the way we've always thought about it, Ed. There's always sort of this in virology historically for chronic diseases. There's always been this sort of iterative approach, right, where you deliver an initial regimen, and then you have the potential to build on that initial regimen to increase the functional cure rates even further. And that's kind of how we think about the pipeline beyond imdusiran as a way to sort of maybe increase that functional cure rate even further and continue to deliver functional cures for patients who need them. And then I know you mentioned this already. Typically, in the last few years around J.P. Morgan, early January, you talk about some of the milestones that you have in mind for that following year. Obviously, your interferon combination is going to be front and center. Is there any other aspects to that that maybe we haven't discussed or touched upon yet across those three assets? Yeah. Good question, Ed. I think it's a little premature to put that out. We're still working through exactly what that's going to look like. But historically, as you said, we are pretty good about giving some direction in the beginning of the year. So I don't anticipate that's going to change. That's still what we're working towards. Of course, we'll see what happens as the weeks and months here continue to evolve. But that's our current working hypothesis that we'll continue to think about what we can put out early in 2025 to give some direction to where we're headed. Yeah. All right. So then thinking about next steps, thinking about your cash balance position and also your runway, particularly what that runway would likely cover in terms of programs and perhaps value-enhancing catalysts. Yeah. Well, as you know, Ed, our key financial metric is cash, right? We currently have, as of the end of the third quarter, $131 million in cash. And that gives us runway out into the fourth quarter of 2026 currently. So about two years of runway, which is good for a biotech of our size. And we're always focused on cash conservation and thinking about the best ways to utilize the capital going forward. So we'll continue to provide updates as we continue to move forward. But right now, we're in pretty good shape. Right. All right. And then aside tangent away from sort of the daily operating focus, but something of interest to investors is sort of the ongoing status of this IP litigation. Where are we? Remind me on those two trials where we are and what's going on. Sure. Absolutely. So as you mentioned, we have two trials ongoing currently, one against Moderna, one against Pfizer. The Moderna one has been running ahead of the Pfizer one since the beginning. So let's start with Moderna. Moderna is on track right now to go to trial in September of 2025, okay? Of course, that's subject to the court's availability and timing, etc. We can never definitively say it's going to happen in September because we just don't know. It's not in our control. With regards to Pfizer, we've been quiet on the Pfizer front for quite a while, but it's starting to move. In fact, we have what's known as a Markman hearing or claim construction hearing upcoming here on December 18th. And once that is complete, we'll have a better sense for what the sort of court schedule looks like going forward. We'll have all the details about when things will evolve from that perspective. I would expect that it's going to take a couple of months before we get the judge's response on the Markman hearing. It did certainly in the Moderna trial. It's in a different jurisdiction. It's in Trenton versus Delaware. We'll see what happens as we move forward here. That's what I would expect going forward. We continue to pay close attention to that, obviously. We'll continue to update as we can. Okay. Maybe one final question. I look forward to 2025. Obviously, for years, you've been active at both EASL and AASLD. Just wondering, without any certain specific commitments, what other types of conferences would fit for data releases or any sort of participation? Oh, that's a good question, Ed. So there are several HBV-specific conferences that happen throughout the year. Seems like there's more and more as we continue forward, which I think is good for the field, right? There are meetings like the International HBV Meeting. There's an APASL. There's an HBV Cure meeting, which happens right before AASLD. Every other year, there's the Hep DART Conference, for example. I'm sure I'm missing a bunch, and it's not intentional. I just don't have a list in front of me. I'm just doing that off the top of my head. As far as specific data release at any of those, Ed, obviously, I can't comment on that. But they happen pretty regularly throughout the year, and we try to target medical conferences to release our data. So I think we'll probably continue to do that on a go-forward basis if we can, if the timing makes the most sense. But yeah, there's a lot of things going on in the hepatitis B space, for sure. Yep. Well, I think I'll wrap it up there. I thank you for your time, Mike. I know you have a lot of things going forward on your plate with that program and speaking to the regulators. And so I wish you the best of luck. Thanks again. Definitely. I appreciate your time, Ed. Thank you very much.