All right, I think we'll get started with our next fireside discussion. My name is Derek Archila. I'm one of the analysts here at Wells Fargo. Very pleased to have our next discussion with Altimmune. From the company, we have Vipin Garg, the CEO, as well as Scott Harris, the Chief Medical Officer. Gentlemen, thanks so much for joining us today. Pleasure. Maybe just to start off, you know, provide a little bit of background about the company, what you guys are focused on and, you know, kind of the ongoing programs before we dig into the questions here. Absolutely. Well, thank you for having us. So at Altimmune, we are developing peptide-based therapeutics for liver diseases. We're actually focused on liver diseases as well as obesity, and we'll talk more about that. So our most advanced product is a GLP-1 glucagon dual agonist that we're developing both for obesity as well as for NASH. For obesity, the drug is in a phase II. Right now, it's in a 48-week phase II trial. We had an interim readout from that study at 24 weeks back in the first quarter of this year, and we're expecting to have 48-week readout in the fourth quarter, coming up, basically next quarter, at the end of the year. For NASH, we've just started a phase II enrollment in a phase II biopsy study, and we expect that to read out in the first quarter of 2025. In addition, we have another peptide-based therapeutics that we are developing for Hepatitis B, and that, we expect to have a readout on that, also a phase II readout, in the first quarter of next year, of twenty twenty-four. So lots of data coming out. We have very exciting data already from our dual GLP-1 glucagon agonist program that's called pemvidutide. The name of the molecule is pemvidutide. We'll refer to that as Pemvi, and we'll talk more about that data. Very excited about what some of the milestones that are coming up. Awesome. Well, I mean, obviously, the obesity, you know, drugs in that area has been all the rage- Absolutely - as of recently. So, yeah, maybe you can just kind of talk or provide a little bit more background about Pemvi in terms of the molecule and how it might be differentiated versus, you know, some of the other, you know, therapies out there, and then we can kind of dig into the trial design. Scott? Well, if you look at the space, it emerged from the diabetes space, and the GLP-1 monoagonist, like semaglutide and dulaglutide, came about first at the end of the first decade of this century, around 2008. Semaglutide itself came out about 2017, 2018. And again, they were developed for diabetes. So when these drugs started moving to obesity, and they got there by going to higher doses, it was a very diabetes-biased orientation, oriented around blood sugar, even though diabetics only comprise about 20% of the diabetic space. But as semaglutide progressed, we got weight loss of about 15%-16%, and the question was: How do you get higher? With bariatric surgery, you have weight loss in the range of 25%-30%. Can we achieve that with medicinal therapy alone? Well, what companies did is they started adding other agents to it. And because this was a peptide-based molecule, and because it was hormonally based, it was an incretin, they started looking for other GI hormones to add to it, either as separate molecules, but specifically with regards to the newer molecules, dual agonists, where you have within the same peptide, you actually have activity towards GLP-1 and another agonist in the same molecule, and that's what's called dual agonist. So you hear about tirzepatide, which is also a dual agonist. It has GLP-1 on one end and GIP on the other, and with that, they're able to push weight loss to about 22%. So that was achieving that goal of reaching higher weight loss with another potency or activity. Our molecule combines GLP-1 with glucagon, and the rationale for that is that GLP-1 and GIP only work to stymie appetite, whereas glucagon increases energy expenditure. So it's a synergistic effect. It's like diet on one hand and exercise on the other and combines them. But the other important point is that there are no GLP-1 and GIP receptors in the liver, whereas the liver is rich with glucagon, and consequently, you see something with our molecule and other molecules that contain glucagon that you don't see with the other molecules I mentioned- Mm-hmm ... which is potent defatting of the liver and also potent reduction in serum lipids. Why is that important? Because the reimbursement for these drugs is gonna be based on cardiovascular outcomes. You probably saw the recent SELECT trial, which was really based only on the weight loss properties of semaglutide. But if you combine it with LDL reduction, with LDL being the most potent surrogate for cardiovascular risk, and also liver fat, which correlates directly to cardiovascular risk, you can see that you can drive even better cardiovascular outcomes with a glucagon-containing molecule. And flipping it around now to the NASH space, since we'll talk about that in a minute, you don't get much liver defatting with GLP-1 or GIP, whereas you see potent, potent reductions in liver fat, and we can discuss that in greater detail, by adding glucagon. So when you're looking for the value proposition in the obesity space, it's just weight loss. You've heard the argument that insurance companies don't want to pay for that. They want to pay for the outcomes, which is why that SELECT trial was so important, because it meant that you can get cardiovascular outcome changes simply by treating obesity. But add to that, the effects on lipids and liver fat, and you can drive even better outcomes and greater possibilities for reimbursement. Got it. Great. I mean, in terms of, like, the MOMENTUM trial that you guys are running, and obviously, maybe you can set the stage in terms of the trial design, and the interim results. Obviously, I guess, what's kind of the bar for efficacy of that trial that you're looking at at 48 weeks? I know it's kind of a loaded question, but, yeah, maybe, again, just start with the background of the, the trial a little bit first. Well, let's go all the way out to the end and then come back to the beginning, and then talk about what we've read out so far, which is an interim analysis in the middle. So it's important to recognize with the molecules that are read out, which have been the target, we're looking at 68-72 weeks after a year and a half of therapy, right? So, when you look at our trial, we're reading it at 48 weeks. So you have to read it comparable time points across trials and then project what we would have at the end of 68-72 weeks. But what we did do is we read out at 24 weeks, and with that, we saw weight loss that was in between the weight loss of semaglutide and tirzepatide. So to give actual numbers at 24 weeks, when we talk about placebo-adjusted, the weight loss of semaglutide was about 8%. The weight loss with tirzepatide was 12%, we were about 10%. So we met our goal of hitting that mid-range, but now also supplemented with the other attributes that we just talked about. So let's now go to 48 weeks. When you look at semaglutide, you're at about placebo-adjusted 12.5%. With tirzepatide, you're at about 18%. So we feel very good about being in the middle teens in terms of our weight loss, supplemented by the other properties. At 24 weeks, we got, in addition to that weight loss that I described, very potent reductions in serum lipids. And we haven't even talked about safety, but the safety profile of this compound has been excellent. But I'll stop at that point. Got it. That's perfect. So I guess, and maybe we can just kind of expand on, like, again, that differentiation on the properties. Like, how much do you think that's gonna, I guess, matter, you know, from a payer perspective? Obviously, you know, outcomes or well, could even be improved, but, you know, large outcome trials are very expensive. So like, I guess, how do you kind of figure that out in terms of how you get that data longer term and prove, you know, basically, the glucagon component of the, the dual agonist is actually going to lead to better benefit there? Right. So ultimately, an outcomes trial will have to be done. But we started on a nice basis because the outcomes we saw with semaglutide in that recent SELECT trial was totally weight loss-based, and we're getting at least as good, if not better, weight loss. And with semaglutide, reduction of LDL cholesterol is only about 3%. The reduction of liver fat is not very great. Mm-hmm. If we take a weight loss readout, it's very favorable to us, and we add in our other properties. Probably the strongest predictor of cardiovascular risk is LDL cholesterol, and we're coming in with that reduction, so we're optimistic, but we're gonna have to wait for an outcomes trial. Yeah, but just having that data on LDL cholesterol is going to be fairly important here. You're showing significant weight loss combined with very profound decrease in LDL cholesterol. As Scott said, that's an accepted surrogate- Sure - for cardiovascular outcomes. So we think that's sufficient to really differentiate the molecule. That's just the beginning of the differentiation. You're gonna be looking at, you know, serum lipids - sorry, liver fat reductions as well, because most patients with obesity have, dyslipidemia- Sure ... both, liver fat as well as serum lipids. So if you can show an impact on both of them, that really makes for a very strong package. Yeah, I was gonna ask, like, I mean, is there a way to, like, figure out a specific population within the more general obese population that would be- Absolutely. I mean, maybe you can talk to that, 'cause obviously, like you said, a lot of these patients have dyslipidemia, like, all these other, like, you know, NASH, liver fat, like, all these sorts of things, so- Right ... how do you narrow it down, to get the best benefit for the profile of your drug? Yeah. So, so one thing that, most people don't appreciate that, we think of obesity in the context of diabetes today, because that's how, you know, all the first-generation drugs that have been developed- that are being developed for obesity are really diabetes drug, and then they're being repurposed for that. But if you look at the numbers, only about 20%-25% of obese patients have diabetes, whereas about 70% have dyslipidemia, the much larger- Mm-hmm ... patient population. They don't have diabetes, so not necessarily— So basically, you have much larger patient population that you need to treat, who will benefit from losing weight, but also significantly benefit by improving their serum lipids. So I think that's where a glucagon-based agent is gonna be more focused. It's not really designed to treat for a, for acute control of glycemia, but it's designed to improve lipid profile fairly quickly, and I think that's gonna have very important downstream effect on, in cardiometabolic outcomes. Yeah, and moving ahead, very quickly to the marketplace, Derek. Obesity is still very primitive as a marketplace. I trained in era of ineffective antihypertensive drugs. Now we have 120, and we have about five mechanisms since that time. An average primary care physician knows exactly what drugs he's gonna use for a specific patient phenotype. With obesity, we're gonna move in that direction. There are gonna be multiple types of patients and the need for multiple drugs in a market that's very segmenting and saying it's all gonna be driven by weight loss number is foolish. Got it. And then, just in terms of the endpoints that you're running in this trial, kind of beyond kind of the weight loss, like, what are the other things that, like, you think you're gonna be monitoring? Obviously, you're probably looking at, like, again, lipids and things like that, but like, you know, what will also kind of drive home that differentiation for, for this approach versus the others? Right. Well, lipids are gonna be important. As we mentioned, we had a very nice readout- Yeah ... at 24 weeks. We expect to maintain it. Let's see if we can improve upon it as we increase time. We're also gonna be looking at some important other points that help predict cardiovascular risk. We're seeing a very nice reduction in systolic and diastolic blood pressure, which is also gonna be cardioprotective. We're taking people and bringing, making them normotensive, who are not normotensive on antihypertensive therapy before. We're doing that, by the way, without getting an increase in heart rate that's been seen with many other compounds, which may be associated with arrhythmias. And we'll also look at blood sugar control, but we've never contended to be an anti-diabetic drug. The patients who are enrolled in the MOMENTUM trial have normal hemoglobin A1cs, right, about 5.5. So there might be a slight change. We'll see if we can pick it up in small patient numbers. But, you know, if we do see a change in hemoglobin A1c, it will be a benefit, but the trial is not designed that way. Longer term, we'll also look at body composition. We'll have that data also available. Right. We won't have that in the initial readout- Okay in the fourth quarter. That'll be top-line data, but we do expect to have that as a follow-on soon after that top-line readout. Got you. Are you looking at... I mean, well, I guess first, in terms of the lipids, like, how fast, you know, do those kind of normalize or at least, you know, reduce? So I just wanna understand that effect. But then also, are you having any impacts on, like, CRP and like, kind of the inflammation component, you know, to kind of, you know, cardiovascular disease and things like that? Have you measured that in the trial? Yeah. So the effects on lipids are relatively quickly, but there's still room to go. Yeah. You see an initial improvement. We're looking to see whether that improvement will grow over the course of time. We don't have data on CRP at this point. We hope to read out at that at the end of the trial. I know we'll talk about NASH in a second, but are you doing any, like, you know, MRI-PDFF on these patients as well, or optional scans just to kind of inform, you know, even more so on kind of liver fat reduction? Yeah. As part of the body composition readout- Okay ... that I mentioned, that'll be a follow-on. We'll have liver fat as part of that as well. Gotcha. So then just thinking, so trial reads out, it kinda comes in line with your expectations of kind of mid-teens at 48 weeks in terms of, you know, weight loss, placebo-adjusted, I believe. And then, so what's kind of the development plan after? Is this gonna be an asset that you look to partner, obviously, 'cause of the cost associated with some of these larger trials? So what's kind of the overall strategy for, for Pemvi there? Yes, our strategy has always been to look for a partner after completion of phase II. So our goal is to be phase III ready, sometime towards the middle of next year. You know, obviously, have an end of phase II meeting with the FDA, and in parallel, we're pursuing partnership discussions. So again, we will move into phase III, in conjunction with the partner. That's, that's, that's our strategy. And clearly, we're not gonna be commercializing a drug in this space. Yeah. There is so many commercial infrastructure, so much out there- Right that people are better than us who can commercialize it. So we believe it's better to bring the partner on board sooner rather than later, to sort of integrate that commercial strategy into the phase III trial design. I guess, what's that interest look like? I guess, among, you know, people that you talk to, again, the strategics or whatever, but I guess, do they view it similarly to how you guys are viewing it, in terms of, like, there are gonna be these different subsegments of patients within obesity? 'Cause right now, it's just kinda like, you know, we have a bunch of drugs out there. We see them on the news, there's shortages, but, I mean, again, the market's doing very, very well. Like, is this-- 'cause you guys are in a little bit more of a nuanced area and having a more nuanced understanding, is that coming across to some of the folks that you talk to, that, you know, could be potential partners, or is that something that still needs to kinda be fleshed out, and they're gonna kinda leave it to you to do that? No, absolutely, people understand that. I mean, if you are the third or fourth pharma going into the obesity space, you don't want to be launching another GLP-1 without any differentiation. Yeah. What's the point? What's... You know, how are you gonna detail it against the existing drugs that are already there? So in fact, they are looking for that differentiation. They're looking for that market segmentation. Where does this drug fit, and how are they going to detail it against the existing therapies that are already on the market or would be on the market by that time? So that part of our story is very appealing. You know, weight loss, there is no argument that if you can reach mid-teen- Sure ... that's competitive weight loss. So we, you know— So the question is: What do you bring to the table that goes beyond that competitive weight loss? And that's where the differentiation comes in. There are many different things that, you know, our drug brings to the table. We haven't talked about the lack of dose titration, for instance. We've got at least one effective dose that can be administered without dose titration. Ultimately, this is going to be a $100 billion market. It's really gonna be a primary care drug, just like blood pressure and statins and so on and so forth. So all of these, the primary care docs don't want to go into—have to deal with the dose titration. We have at least one effective dose that we can provide the option with that can be administered without dose titration. So there are a lot of different levels. Ease of administration is going to be very important. Obviously, we talked about the lipid profile. We think that's gonna be very important, and competitive weight loss, and that's how the partners are looking at it as well. Is the MOMENTUM trial only looking at a single dose, or is that the one dose, or is it multiple doses? MOMENTUM trial is looking at three different doses. Okay. 1.2, 1.8, and 2.4. 1.2 and 1.8 have no dose titration. 2.4 has a very short dose titration. So we're trying to maintain that flexibility, that if a physician and a patient desire to have dose titration, that option is there- Sure ... but also there's option for no dose titration. Got it. But you're not seeing any sort of safety-related issues that would warrant, like, a titration, really? No. It's very clean and- No, this is all, you know, this is all standard, tolerability- Yeah ... that you see with these types of drugs, nausea and vomiting, is trying to mitigate that. Yeah. But there is no safety issue there. Scott? Yeah, I think one of the most important safety issues that's emerged in the field is this heart rate increases that we're seeing with multiple other compounds in the range of 10-15 beats per minute, even as high as 30 beats per minute with initial dosing. In one study, there's been an imbalance of arrhythmia that's been concerning. No one quite understands the mechanism of that. But it's tempting to think it's related to the stimulation of the heart and the heart workload. And, you know, this concern as you go to populations that are at risk, you know, when you do a cardiovascular outcomes trial, you're enrolling at-risk patients. So what's gonna pop there? We don't know. I would say that we've consistently not seen that heart rate increase, and we've not seen any imbalance of arrhythmias. Gotcha. So maybe, yeah, maybe we'll shift gears to NASH and just maybe give a little bit of background on that program, and obviously, talk a little bit about defatting the liver. So maybe you kind of expand on that in terms of the mechanism of action there. Sure. So what drives NASH, which is an inflammatory disease of the liver that goes on to fibrosis and cirrhosis, and complications of that, is the liver fat. There are many studies that show that if you reduce the liver fat, you take care of the disease. It's a lipotoxic species, the toxic liver fat, that actually drives the inflammation. So if you bring down the fat in the liver, multiple studies have shown that you reduce NASH inflammatory activity as well as fibrosis. The more potent you defat the liver, the greater you drive down both the liver inflammatory activity and the fibrosis. In that regards, because of the glucagon effect, we're seeing class-leading effects in liver fat reduction, approximately 75%. We're also seeing accompany that some very strong markers of reduction in inflammatory activity, and those have included, a MRI-based test called cT1 and also ALT levels. We're also, at least in preclinical studies, seeing very potent reduction of fibrosis. We've seen that in animal models. We've seen this in gene expression studies as well, and we have about as good of activity or, evidence in that area as any company for anti-fibrotic effects. We're very excited about having a good readout. We're planning that readout in the first quarter of 2025. We have two primary endpoints of that study. We have a NASH resolution and also improvement of fibrosis, which are the FDA endpoints. Gotcha. Yeah, I mean, I guess, you know, having covered the NASH space, you know, for a little while back in the day, like, the fibrosis endpoint's been very challenging, and obviously, now we've seen some more data in terms of, you know, like FGF 21, FGF 19. Some of them have shown some, some have not. So I guess, what, I guess, in your preclinical data maybe is different, or at least again, mechanistically, you think is different that will ultimately, you know, lead to fibrosis benefit? Well, we'd say that FGF21s have potent effects on liver fat, and you would expect, as they've demonstrated, potent effects of fibrosis. So we support that. Our liver defatting effects are greater. Mm-hmm. They have some preclinical models of fibrosis, and we do as well. So we think that we have very comparable data in terms of, fibrosis reduction as well. Yeah, I mean, you can actually look at all of the data, and if you compare different drugs and different mechanisms of action and compare the liver fat reduction with ultimate benefit in terms of fibrosis improvement, they stack very nicely. Okay. Faster and higher the liver fat reduction, greater the fibrosis improvement. So that's just consistent across the board, and we, you know... So therefore, we are showing both, profound liver fat reduction, class-leading, but also very fast. Within six weeks, we are seeing 75%, in the order of 75% reduction in liver fat. And, and the other thing is, that's equally important, is normalization of liver fat. Mm-hmm. So reduction is one thing, but what percentage of patients are you normalizing? And we are also seeing very significant, greater than 50% of the patients are actually normalizing their liver, liver fat. So both the speed of improvement and the magnitude, that's, that's important here. But Brian, after drawing similarities, I want to draw a contrast to FGF 21. The biggest contrast is that we get potent weight reduction. Yeah. You don't see that with FGF 21s. It's weight neutral. So consequently, you take a NASH population, which dies predominantly not of the liver disease, but of the cardiovascular disease, and what moves that is the reduction in body weight, which is something that you won't see with the FGF 21s. They may be predominantly a drugs for late NASH, in that sense. So we think that for the entirety of NASH, not just the late effects of NASH, but early NASH, we think that we offer the widest possibilities for treatment. In terms of the NASH population you're recruiting, what does that look like relative to the obesity population for MOMENTUM? Like, again, I would presume that these patients have diabetes and, you know- Right ... maybe, maybe a little bit worse off. But, I guess, what would you expect in terms of weight loss, you know, in that population of the NASH trial? Yeah. So it's gonna be about 60% diabetics. That's typically what NASH studies have run, and diabetics lose less body weight. But interestingly, we did a diabetes trial where we saw more weight loss in diabetics at 12 weeks than had been accomplished by tirzepatide. So it is possible that we'll see those effects in diabetics as well. That's still preliminary data, but we do expect to see potent weight loss in this population. It's a population of individuals with F2 and F3 fibrosis. We picked that, as other companies have, because of the patients most likely to so far show a fibrosis benefit, which we feel is the most important endpoint in the trial. There'll be 190 subjects. We've only picked two doses of pemvidutide to move into that trial, 1.2 and 1.8 milligrams, and the reason is, is that we looked at the dose response. We saw it plateauing at 1.8 milligrams, and we didn't see a reason to have to go higher to 2.4 milligrams in this trial. So we have a 2:1:2 randomization, placebo:1.2:1.8 milligrams. So 76 patients, 38, 76. We'll treat patients for a total of 48 weeks, but the endpoint will be read on biopsy at 24 weeks. Then we'll continue to follow patients another 24 weeks for safety, but also to look at their biomarkers. And we have a very nice power calculation. That's 76 in the primary comparative arms, the 1.8 versus placebo. That's relatively high. If you look at the other trials, they're more in the range of 40-60, and we've done this because we want to really increase our chances of success and have a potent readout, and also give better results in biomarkers. Because we have an opportunity here to do good correlations between the biopsy results and the biomarkers and take this to an end-of-phase II meeting and have a discussion with FDA about using those biomarkers in phase III, rather than to having to do biopsies. Very helpful. Odd question. Always wanted to know this. So even with the FGF21s and some of these other therapies, when you defat the liver, where does the fat go? It gets... There are two things that happen. Recognize it's a balance between synthesis and degradation. Yeah. So when we have this data, and we published on this before, you reduce the amount of de novo synthesis coming from fatty acids and periphery, and you increase the burn, the beta-oxidation. So we see a rise in ketone bodies. Mm-hmm. Which is the beta-oxidation. We see a drop in serum triacylglycerol, which is the de novo lipogenesis. So it's both. So the lack of synthesis, the increase in degradation, we get 75% of our liver fat reduction, and as Vipin mentioned, we see it quickly. That's a key thing. We see it very quickly. Weight loss is a slow mechanism for reducing liver fat. If you look at semaglutide, you know, it-- weight loss is, is-- they, they get 34% liver fat reduction, about one half or less of what we get at 24 weeks with tirzepatide. Mm-hmm. You know, the weight loss involved in that, only 39% at the end of a year. And we're basically seeing these effects at six weeks. So if you're going to do a 24-week trial, you want to get that effect as early as possible in order to have success in the endpoint at 24 weeks. Got it. So what do you think... Like, what are the bars now? Again, I'm a little bit removed from NASH, but, like, in terms of NASH resolution endpoint and also for, on fibrosis, like, what, what's kind of the, you know, kind of responder rate you need to see nowadays to kind of be competitive in those markets in NASH? Yeah, we saw with, Madrigal. We saw 25% approximately in both NASH resolution and fibrosis improvement, kind of the low to mid-teens in the placebos. They had about a 12% treatment response. Now, that's a phase III study. In phase II studies, we've seen higher numbers. Mm-hmm. I think we saw approximately the 40% from the FGF21s, but also higher placebo response rates in Akero, but lower in the FGF in the 89bio program. I think the important point is that we offer patients a higher response rate. 25% may be the basis for Madrigal's approval, but it leaves 75% of people who aren't getting benefit. So you obviously want to have statistical significance, and you want to do that with the best response. Got you. And then just going back to, you know, typical, like, you know, GLP-1s. I mean, we've seen that data for sema in NASH, and it didn't have really any impact on fibrosis, right? They had kind of high rates of NASH resolution, but, you know—Right... even after, I forget, it was, like, a year and a half or two years, like, nothing on fibrosis. So maybe you can just walk us through in terms of, like, why this is going to be potentially different. Right. And also, I should mention a negative trial in cirrhosis, where it looked like placebo was a lot better than the drug in terms of fibrosis improvement in that population. The answer is very simple: There are no GLP-1 receptors in the liver. The defatting effect on the liver is entirely mediated by weight loss, period. So, as I mentioned before, at 24 weeks, you only see about 30% reduction in liver fat. That compares to 75%, one half. If you don't defat the liver quickly, you're not going to see the fibrotic effect, and that probably explains that observation. Got it. Maybe the last five minutes, spend some time on your Hepatitis B program. Maybe just, I don't know, Vipin or, you guys want to just provide some background on that program? Sure. Scott? This is a program that we acquired in 2015 from a company called ITS. HepTcell is a series of nine peptides. These express epitopes of the highly conserved regions of the Hepatitis B proteome. And what these epitopes do is they stimulate T cell activity, which has been desensitized in Hepatitis B patients. So it's an immunotherapeutic that arouses the HepTcell to attack the Hepatitis B target that has been dormant in these patients because of desensitization over the course of time. We have a trial that we finished enrolling in. We plan to read out probably in the first quarter of next year, and we've taken 80 patients, randomized 1 to 1, either to HepTcell or placebo. The primary endpoint of that study is either a 1-log reduction of the Hepatitis B surface antigen or clearance, and we're looking at a lot of other biological markers as well. It's important to point out in that population that we've taken patients who have low existing levels of the Hepatitis B surface antigen, which is probably what desensitizes the T cells... and results in lower T-cell activity over time. But in this population, you're seeing a reemergence of activity. So we thought for monotherapy, this was an ideal population. But in the population of need, we're taking patients with much higher levels Hepatitis B surface antigen. These are people currently being treated with nucleosides, but they're not getting very effective reduction of the Hepatitis B surface antigen, so they're still immunosuppressed. We now see novel agents, the small interfering RNAs and the oligonucleotides, and some antibodies, for example, that are getting pretty substantial reductions of the surface antigen, not enough to get functional cure, as we would say, or clearance, but low enough to match our population. What's the result of that? We see HepTcell's T cell as being ideal for combination therapy for these novel agents that are in development, to drive the surface antigen down to the levels in our current population, and then wipe out the virus with the immunotherapeutic. Got it. So is that kind of the plan to do combos? Like, is it kind of registrational, or is it like do monotherapy first? Well, we would do that with a partner. With a partner, okay. We could go forward in this population into phase III, and more likely, we would get a partner to do either that or a combination trial with one of their direct acting agents. Yeah, you can actually pursue both pathways here. Yeah. You can try to get it approved as a monotherapy, but as well as work with another antiviral to combine the two. Got it. Okay. Yeah, and maybe just taking a step back, again, the regulatory pathway for Pemvi in terms of NASH versus, you know, obesity, you know, does that kind of give flexibility to a potential partner in terms of where they might wanna pursue? And also, like, as it gives you some opportunity to maybe partner one or the other or both of the, you know, the indications. Yeah, I would say more than partnering, it's going to be hard to separate these two indications. Yeah. It's the same molecule, so we would want to get full value for the asset- Okay ... in any partnership. But it certainly gives that flexibility. You can actually get to obesity through the NASH door or vice versa. So depending upon the partner interest, you can go either way. We, you know, we're finding a lot of interest in both of these indications. Question is, does the partner pursue them in parallel? Do we pursue them in parallels? We'll have to make that decision, but ultimately, we think the drug is quite going to be quite effective in both of these indications. Because obesity, treating obesity is the cornerstone of treating NASH. I mean, for years and years, that's been the paradigm there. So clearly, if people are losing weight, that's going to benefit them. Similarly, in obesity, yes, people need to lose weight, but if they're also losing their liver fat as well as improving their overall serum lipids, that's going to be important as well. Got it. Sorry about the sidetrack. Maybe last question on Hepatitis B. So I guess, sounds like, again, potentially another partnering opportunity or collaboration. I guess, how do you think about that opportunity? Again, it's not a market that I'm too familiar with, but, like, can you frame that for us? Yeah, I'd say it's a very significant opportunity. I mean, obviously, there, you know, there's been a lot of attempts to come up with a cure for Hepatitis B. Hepatitis C, we've already seen the impact it has made. Right. It is a similar impact, both within the U.S., but also, you know, on a worldwide scale. It's a very significant opportunity, and there's a lot of pharma interest in that as well. Got it. Cool. You want to just recap, I guess, the upcoming catalyst and, and milestones- Yeah ... I guess, for the next 6-12 months? Yeah, absolutely. So starting with obesity, we're expecting our 48-week data in the fourth quarter of this year. And then, of course, we'll plan for our end of phase II meeting sometime in the first half of next year and, plan to be phase III ready by the middle of next year. On Hepatitis B, we are expecting data from our phase II trial in the first quarter of 2024, so next year. And then NASH trial, we're expecting data in the first quarter of 2025. Got it. All right, well, we'll leave it there. Gentlemen, thanks so much. Very good. Thank you.