Hello, everyone. Thank you for joining me today. My name is Mike McElhaugh. I'm the Interim President and CEO at Arbutus Biopharma. Our strategy at Arbutus is to create a functional cure for hepatitis B. The way we'd like to do that is via combination therapy that includes antivirals and immunologics to help improve the functional cure rate over what you currently see with standard of care, which is less than 5%, to something greater than 20%. This is our current pipeline. Our lead product in our pipeline is Imdusiran. Imdusiran is an RNAi therapeutic, currently in phase 2A trials, and we'll get into the details of those trials as we move forward here. We also have an oral PD-L1 inhibitor called AB-101. It's currently in phase 1.
Our goal, obviously, is to get these two products into combination as quickly as possible, but given that they're not at the same stage of development, we have some work to do before we get to that point. We'll do that as quickly as we possibly can. Thinking about HBV, generally, HBV is a life-threatening viral infection caused by the hepatitis B virus. Long-term issues related to hepatitis B include cirrhosis and liver cancer. And these are increased when a patient has hepatitis B. There are currently two treatments that are available. Both are suboptimal. One is pegylated interferon. That's currently given for 48 weeks and yields a functional cure rate that's less than 5%.
We also have nucleoside analogues, which are given lifelong, and the functional cure rate is less than 5% for those as well, not across any given time, but over the course of a, you know, of a lifetime of taking these medications. Hepatitis B is a very large market. There are almost 300 million patients globally, currently chronically infected with hepatitis B. About 2 million in the United States, 15 million in Europe, 90 million in China, and about 820,000 people die every year due to complications related to the hepatitis B virus. The market is currently very underserved. Only about 10.5% are diagnosed, and a pittance of those are actually treated, a little over 2%.
So tremendous opportunity to improve what's currently available for patients with hepatitis B. This is our overall strategy for how we anticipate delivering a functional cure for hepatitis B. It's a three-pronged approach. We believe we need to suppress HBV DNA, reduce HBV viral antigens, and importantly, boost the host immune system. And we believe if we can accomplish these three things: suppress, reduce, and boost, that we can deliver a functional cure in the range where we'd like to be. I'd like to talk to you now about our RNAi therapeutic. So imdusiran, also known as AB-729, is our RNAi therapeutic. It's a single trigger RNAi targeting all viral transcripts, which inhibits HBV replication and lowers all HBV antigens.
It is delivered via proprietary GalNAc conjugate delivery technology, and it actively targets the liver. What you most see impact on is hepatitis B surface antigen, which is responsible for tolerizing the host immune system to hepatitis B virus. I'm going to run through some data now. This is the data from our first trial with AB-729. This was a trial, the Phase 1a/1b trial, where we looked at lots of different things. We looked at both e antigen positive and e antigen negative patients. We looked at patients who were both DNA suppressed on a nucleoside and also naive to treatment. We looked at 60 milligrams and 90 milligrams, dosed anywhere between 4 and 12 weeks.
What we saw at the end of the day, and you can see this on the left-hand side of the slide here, we saw a very consistent reduction in hepatitis B surface antigen, regardless of the parameters that I just mentioned, leading to a reduction in surface antigen of about 1.8 logs, across all those cohorts. AB-729 was well tolerated at all dose levels, intervals, and based on this trial, we decided to move forward into our phase 2A program with a 60 milligram dose, dosed every 8 weeks. We'll get into the phase 2A data in a second. I mentioned earlier that one of the key components to curing chronic hepatitis B is reactivation of the host immune response.
This is some data from the phase 1A/1B study that shows that imdusiran does increase HBV-specific T-cell activation and also decreases exhausted T cells. So this is the phenotype that you want to see when you're thinking about curing chronic hepatitis B. We moved from the phase 1 trial into some phase 2A clinical trials. We currently have two ongoing, and I'll give you some background on some of the data that we have from those 2A trials now. The first trial here is our phase 2A clinical trial, combining imdusiran with interferon. So in this trial, we dosed 24 weeks of imdusiran plus a nucleoside analog to lower hepatitis B surface antigen.
We randomized patients to either imdusiran, plus a nucleoside analog, plus pegylated interferon, or a nucleoside analog and pegylated interferon for either 24 or 12 weeks, total additional duration, and then followed those patients up from there. We expect end-of-treatment data from this particular trial in the first half of 2024. We've already presented some data on this trial, which you can see here on this very busy slide. The data that's in the tables and also in graphical form on the right, same data, just viewed in different ways. And what we saw from this trial in the limited data set that we presented last year was that we see a consistent reduction in hepatitis B surface antigen during those first 24 weeks of treatment with imdusiran plus a nucleoside analog alone.
Then it appears as though interferon may contribute to additional declines during the interferon treatment period. Obviously, that interferon treatment completed was not a complete data set. That's what we'll be seeing in the first half of this year when we present some additional data. We did have 4 patients reach surface antigen level less than the lower limit of quantitation during the interferon treatment, so we're excited to see what happens with these particular patients. The second phase 2A trial that we have ongoing is a combination study with our partners, Barinthus Biotherapeutics. In this study, what we wanted to explore was the combination of an RNAi, followed by an immunotherapeutic, in this case, a therapeutic vaccine called VTP-300.
It's a chimp adeno platform, so chimp adeno prime and MVA boost. And what we did in this study was, for the first 24 weeks, we gave imdusiran plus nucleoside analog, again, to reduce hepatitis B surface antigen to low levels, and then we randomized patients to either receive VTP-300 plus nucleoside analog or nucleoside analog plus placebo, from there on forward. We added a second arm to this study, that's what you see in the bottom half of the slide. Adding in low dose nivolumab to that VTP-300 plus nucleoside analog piece. And this was based on some data that the Barinthus team had with their own internal VTP-300 program. It showed that nivolumab, when given with the boost, actually improved outcomes, so we wanted to explore that as well.
We will have some data from the first arm of this study, and the treatment data, in the first half of the year. The second arm will come later, later in the year. We have already presented some preliminary data with this first, in this first arm. So, we presented this last year as well. And what you see here is that surface antigen levels were reduced and sustained with imdusiran and VTP-300 p- treatment. So I'll draw your attention to the graph on the right. You see the blue line, which is the active arm, including VTP-300 plus imdusiran, and the red arm, which includes just imdusiran plus the nucleoside analog. And you can see after the 24 weeks of treatment, that red line actually starts heading back up to baseline levels.
That's the imdusiran plus placebo arm. The blue line, which includes VTP-300, actually stays low. These, I will say that these are a very small subset of patients, so only 7 patients in the placebo arm, 5 in the VTP-300 arm. So obviously, we'll need to see some more data from that, which we'll be presenting in the first half of this year. Interestingly enough, if you look at the bottom part of the table, if you compare the placebo versus VTP-300 at weeks 34 and 48, you can see a larger percentage of patients in the VTP-300-containing arm, reaching levels of surface antigen less than 100 or less than 60 relative to placebo. So important as we continue to move forward.
This is some data that shows HBV-specific T-cell responses. On the left-hand side, the cohort that includes imdusiran plus VTP-300. On the right side, imdusiran plus placebo. And what you can see via ELISpot analysis, looking at interferon gamma release, you can see higher levels of, HBV-specific T-cells in the VTP-300 plus imdusiran containing arm relative to placebo. So also encouraging, knowing that we need to, boost the host immune response in order to functionally cure hepatitis B. Before I get to our oral PD-L1 inhibitor, I also want to mention another study that we're going to, initiate in the first half of this year. We're going to evaluate imdusiran in combination with durvalumab, a, PD-L1 monoclonal antibody.
Looking at the combination of those two at different durations, let's put it that way. With the goal of really understanding what the PD-L1 can do in combination with imdusiran, to help inform the ultimate combination of imdusiran plus AB-101, our oral PD-L1 inhibitor. So you may be wondering why we would think about an oral PD-L1 inhibitor instead of just using an antibody. Well, the antibodies are a bit challenging because once you give them and they block the receptors, they are there, they are hard to turn off. There's issues with immune-related adverse events that we hope to reduce with our oral small molecule approach. So thinking about the rationale here, HBV immune tolerance is critical, as I mentioned, to HBV infection and tolerance. Okay?
PD-L1, the PD-1, PD-L1 checkpoint is known to play a key role in immunity, in HBV. And there's been some data from competitors that show that, an antibody, a PD-1 antibody, can actually lead to a reduction in HBV surface antigen. So interesting data presented to date, not in combination with an siRNA, which is something that we, intend to do and will do, but quite interesting nonetheless. So small molecule approach, allows controlled checkpoint blockade and enables oral dosing, as I mentioned. It really allows us to sort of dial in the effects, right? Because, AB-101 works via a different mechanism than the antibodies. It actually binds to PD-L1 on the surface, causes it to dimerize, internalize, and get marked for degradation. Okay?
But the interesting thing is you can, if you wash it out, you actually get reconstitution on the cell surface... relatively quickly. So it, we can monitor closely, and if we see issues with immune-related adverse events, hopefully we can avoid those by washing out the drug. We can also. This is also targeted to the liver, so hopefully we can keep it in the liver microenvironment, which is where we want it for this particular drug. This is some of the data that we have for AB-101. This is preclinical data. On the left-hand side, you can see that AB-101 reinvigorates HBV-specific chronic hepatitis B patient T cells as well as a commercially available PD-L1. Again, this is ELISpot analysis, interferon gamma as the readout.
And you can see, you know, inactive versus active, quite a bit of difference there. And then on the right-hand side, we have an MC38 tumor mouse model comparing AB-101 to atezolizumab, versus a vehicle control. And you can see that AB-101 reduces tumor volume to the level of atezolizumab, which means it's working as it should. AB-101 is currently in a phase 1A, 1B clinical trial. It's currently, we're beginning part 2 now. The data that we're going to present at the end of the year is going to come from part 1, the single ascending dose data.
But interestingly enough, with this particular molecule, even though these are healthy subjects, we can get at least a surrogate for potential efficacy in terms of the receptor occupancy and engagement. Okay? So we should have that data as well when we present this. Obviously, we'll move it into Part 3, which is chronic hepatitis B patients, as quickly as possible. And as I mentioned, our goal here is to get it into combination with AB-729 as quickly as possible. I'd be remiss if I didn't mention our LNP litigation and give a brief update on this. I can't say too much because obviously this litigation is ongoing, but what I can say is here on the slide.
So if you look down on the, in the bottom at the schematic here, this is the way any royalties and or litigation-related damages get distributed. So, 20% to Arbutus, 80% to our partners, Genevant. It's important to also note that Arbutus owns 16% of Genevant. With regards to the Moderna trial, we now have a trial date, and it's currently set for April 21, 2025. This is, of course, subject to, the court's scheduling and availability. Fact discovery is ongoing. A Markman hearing did occur on February 8, 2024, and that's when arguments were heard regarding claim construction. You'd expect that the issue is ordered within 60 days of the hearing date, and then next steps will be expert testimony and deposition. With regard to Pfizer, that's a little bit further behind. The lawsuit's ongoing.
Date for the claim construction hearing has not been set so far. Before I summarize with 2024 key milestones, I'll mention our cash balance and runway. Cash balance as of the end of 2023 was $132 million in cash, with runway out into the first quarter of 2026. Our 2024 net cash burn is expected to be in the mid-60s, somewhere between $63-$67 million, significantly less than what we spent in 2023. Just to review the milestones, in the first half of the year, we expect to have data from both the interferon plus imdusiran-containing phase 2A trial that we have ongoing.
We'll have end of treatment data from that trial, and also the imdusiran plus VTP-300 phase 2A trial that we have ongoing with our colleagues at Barinthus, and the treatment data will be available from that as well in the first half. We have our imdusiran plus nivolumab trial that I mentioned. We anticipate initiating that in the first half of the year as well. We should have phase 1A data from part one of the AB-101 trial in the first half of this year as well, in healthy subjects. And then, in the second half of the year, we have our imdusiran plus VTP-300 plus dur-- excuse me, plus nivolumab data coming. We should have some preliminary data from that study that we'll present in the second half of the year.
With that, I will close. Happy to take any questions if you have any. Thank you. Okay, thank you very much.