Good afternoon, everyone, and welcome to the session with Altimmune. We are fortunate to have Vipin Garg and Scott Harris here from the team. Maybe first, we could just start with an overview of the company and with a particular focus on what you view as key value drivers over the next, let's call it 12-24 months. Okay. Yeah, perfect. Thank you for having us. At Altimmune, we are developing peptide-based therapeutics for obesity and for liver diseases. Our most advanced asset is pemvidutide, which is a GLP-1 glucagon dual receptor agonist that we're developing for obesity and for NASH. Of course, we talk more about that. We also have a immunotherapeutics, another peptide-based therapeutics that we're developing for hepatitis B. For both of these programs, we're making significant progress. Pemvidutide, we are in the process of conducting a 48-week Phase II obesity trial. Recently, we announced the 24-week data from that, very compelling weight loss, very significant improvement in lipids. We think the profile of pemvidutide is very different from your standard GLP-1 and GIP type of agents. By bringing glucagon into the picture, we are having direct effect on the liver, having a very profound effect on serum lipids, which we think is important because as the obesity market matures and grows, it's going to segment into different patient populations. Right now, we're focused on diabetic patients with obesity, but as time progresses, there is need to treat patients. There's actually a larger patient population that has dyslipidemia or liver fat that needs to be corrected, in addition to losing weight, and that's where, you know, an agent like pemvidutide would be very, very, very important going forward. 48-week data, that trial, we have completed enrollment, and expect to announce that data in the fourth quarter of this year. The hepatitis B program, we're expecting data in the first quarter of next year. We are also in the process of starting a Phase IIb biopsy study, in NASH, with pemvidutide in the middle of this year, and that data we expect in the first quarter of 2025. On both of these programs, we expect to make significant progress and have significant milestones for all of these indications. Great. Maybe just spend a minute on the structure of pemvidutide and how it compares to other assets. Like you said, a number of peptides targeting things like GLP, GIP, GCGR. Help us understand the profile and where it sits versus the rest of the landscape. Scott? pemvidutide is a GLP-1/glucagon dual receptor agonist. It's a peptide-based molecule, 29 amino acids, and it has a side chain that extends its life in serum to allow weekly dosing. Another important aspect of the side chain is that it slows the entry of the molecule into the bloodstream, which we think is also associated with this tolerability in the absence of heart rate changes that we're seeing with many other molecules in the class. An important attribute of the molecule is that it's designed to be 1-to-1. That is the biological ratio of GLP-1 to glucagon, which studies that came out of Merck about 10 years ago, showed was optimal for maximizing efficacy while also maximizing safety. Wonderful. All right, let's turn to obesity first. You recently reported an interim readout from the phase II study. Maybe let's just go with an overview of the results to start. Sure. The study is designed to have 320 subjects. This interim analysis was on one half of the subjects, 160, and not at the 48-week time point, as Vipin mentioned. The whole trial was planned or read out at 48 weeks, but we did one half of the subjects at the 24-week time point. We observed in the leading dose, an absolute 10.7% reduction in body weight and adjusted for placebo, was just shy of 10%. To put that into perspective, tirzepatide placebo adjusted, is 12%. At that same time, point of 24 weeks, semaglutide at 8%. We were right in the middle between the two, and we were very happy with that because it led us to believe that we would hit our target of the mid-teen sometime at the 48-week time point. We also saw very nice reduction in serum lipids. As Vipin mentioned, this is an attribute of glucagon, and also the 1-to-1 ratio that we have, and the 15% or so reduction we saw in total and LDL cholesterol was several fold higher than reductions that you see with the GLP-1 or GIP-based agents alone, which generally run in the range of 3%-5%. We also saw these reductions in patients who were taking existing statin therapy, meaning there was a possibility of dropping their lipid levels lower, even after stable doses of statins. We saw nice reductions of blood pressure that should be cardioprotective, and we saw them in the absence of heart rate changes. You know, it's a readout that we were just very pleased with. Understood. One of the things that did come up in this study was the tolerability profile and the discontinuation rate. Maybe just help us understand what we saw, put it into context, and we can then go from there. All right, great. We only saw it at the highest dose of 2.4 milligrams. The adverse event rates at the other two doses, including the 1.8 milligram dose, they gave almost the same weight loss as the 2.4, was considerably less and much more in range of what we'd seen before. This adverse event discontinuation that we saw at the 2.4 milligram dose was not consistent with what we had seen in three prior trials. In our NAFLD trial, the adverse event discontinuation rate of that 2.4 milligram dose was only 4%. We also did a diabetes study where the adverse event discontinuation rate was 0. To go up to what we saw, which was in the mid to high teens in this trial, was very surprising. In fact, the rates of adverse events and the severity of adverse events, particularly in the GI tract, was no different from the other trials. It led us to believe there was something about the patient characteristics that were different. Obesity patients, perhaps their commitment to the trial, the availability of other agents and the like. We saw people dropping out with mild adverse events. That being the case, this is something that we can easily address. One thing that we did not write into the study was an allowance for reducing the dose. It was a rigid escalation, and the patient had to stay there at that dose. In the trials of the other agents, they have allowed dose reduction. In fact, in the tirzepatide and semaglutide programs, 30% of subjects, approximately in each trial, dose reduced in order to stay in the trial and avoid an adverse event discontinuation. If they had not had that in their protocols, they would have seen adverse event rates that were much higher. What we can do is, going forward, we can put this in our protocols. In fact, we've already done this in our NASH study because we want to be consistent going forward, even though that NASH or NAFLD population in past trials did not need dose reduction. Even though it appears to be unique for this population, it's something we'll just incorporate and allow moving forward. The other thing I'd like to say about that is that an adverse event rate in the 20% is what's been seen in all the other obesity trials. In the tirzepatide and the semaglutide Phase II trials that were conducted, the adverse event discontinuation rates in the first Phase II trials they did were in the range of 25%-30%. They were able, with modifications that were made, to achieve the single-digit adverse event rates that are seen right now. The important thing is when you're comparing these trials, it's important to compare the safety and tolerability of Phase II versus Phase II and not Phase III. We're very optimistic about handling this with very simple measures going forward. Yeah, one thing I would emphasize is that this is not a safety issue. This is a tolerability issue, a patient behavior issue. Again, if you don't offer them an alternative, just offering dose reduction gives them an option to stay in the trial. You know, you're offering them something that they can negotiate essentially in, during the trial. But if you have a very rigid protocol, they have no place to go. I mean, either they stay in the trial or they drop out. Really, offering dose reduction would be a very simple and straightforward fix for this. Understood. You mentioned the 48 week data is expected later this year. How are you thinking about potential success scenarios for that study? You alluded to this earlier. Right. Yes. Yeah, go ahead. It's important to realize that the product is very differentiated. We think it's going to have very meaningful effects on outcomes, particularly cardiovascular outcomes, with the reductions that we're seeing in serum lipids and also hepatic lipids. You know, we think that to be competitive, and we think that we will hit in the mid-teens based on the data, and we think that would make the product very attractive with its other attributes. It's not simply a race for a number in weight loss. Beyond a certain point, that perhaps is just cosmetic. What insurance payers are going to look for with doctors is what really impacts the patient, and we think that to have a weight loss in the mid-teens, which we project will be up by the 48-week time point, plus the attributes, makes this a very attractive drug. Thanks. Yeah, I mean, the other thing to keep in mind is that we are comparing 48 weeks versus 68 or 72 weeks for other trials. There is still additional weight loss beyond 48 weeks. Again, as Scott said, if we hit that mid-teen number in 48 weeks, we think we have a very competitive profile, particularly with all the other attributes. When you talk to doctors, they're looking for options, they're looking for choices. It's not going to help to have 5 different GLP-1s out there or 10 different GLP-1s. What we are bringing to the table is a different mechanism that allows your doctors to treat different patients with different profiles, and that market segmentation can only happen if you have different mechanisms of action. Understood. Just to make sure we're clear here, the safety, the discontinuations, the tolerability, will you have been able to implement the dose modifications prior to the 48-week readout, or should we expect something similar to what we already saw? By the time we read out the study in March, on the first 160, the great majority of patients in the second half of the trial had already gone past that 12-week time point. In other words, those adverse event discontinuations, as you would expect, were mainly due to GI intolerability and occurred early. There's really no opportunity to further modify the ongoing current trial. Nonetheless, we're happy with what we've seen so far. These adverse event discontinuations have virtually stopped, as we've observed blindly in the trial, and there'll be opportunity to modify going forward for future trials. Understood. Pending results, like you described, what do you view as the appropriate next steps for this program within obesity in particular? Yeah. As we have said, before, our goal is to find a partner to move this program into phase III. Obviously, we've got everything ready. We'll have the 48-week data. We will also have an End-of-Phase II meeting with the FDA. We are preparing for, you know, CMC to be ready for phase III, and we're also in parallel, pursuing partnership discussions. We're very encouraged with that. Obviously, the 48-week data is going to be an important driver of that, so our goal is to have that in place. Obesity will only move forward in phase III once we have that partnership in place. Understood. Maybe before we move on to NASH, obesity, it probably goes without saying, is a relatively large addressable market. How do you think about where this profile would fit within that space? Absolutely. Scott? The market's going to be quite segmented. It's not mature right now. All we really know is we're following a number, which is weight loss. The market's going to be very differentiated. We see that if you wish to treat obese patients and get diabetic glucose control, you probably want to go with a GLP-1 or a GIP or a combination of both. We've never professed to develop in that space. It's well known that there's a balance between GLP-1 and glucagon. Here, we're going to have neutral glucose effects, and that's the way the molecule is designed. There's clearly a marketplace which needs the glucagon mechanism. Only about 20% of the obesity marketplace is diabetic. About 70% has high liver fat or dyslipidemia. We think that that part of the marketplace is ideal for glucagon-based compounds like pemvidutide. We really see ourselves fitting into that space. Great. maybe shifting gears here to NASH. You mentioned this, but you plan to initiate a phase II study later this year. first, let's talk about what you've seen to date in NASH. Right. We've conducted a non-invasive study, not in patients with NASH, but in NAFLD, Nonalcoholic Fatty Liver Disease or fatty liver. With that, at 24 weeks, we saw approximately 75% relative reduction in liver fat and over 50% of subjects actually normalizing their liver fat. We believe that this is industry-leading. We think that we have the best effects or among the best effects in the reduction of liver fat. With that, we not only saw a reduction of liver fat, we also saw a very prominent reduction of liver inflammation, both a reduction of serum ALT level, as well as an MR technique known as cT1, which has been highly correlated with liver outcomes as well as NASH inflammation. There's also been analyses that have been done that have shown that the degree of liver fat reduction correlates with the degree of NASH resolution and fibrosis improvement. In fact, if you look at the compounds that are read out to date, the ones with the greatest fibrosis improvement have also had the greatest liver fat reduction. Based on that, we're very optimistic about having a positive readout when the trial is completed. Great. As you think about the phase II design, could you just walk us through some of the key aspects of that trial? Sure. The trial will be comprised of 190 subjects. We've decided to take two doses forward, the 1.2 milligram dose and the 1.8 milligram dose, and we're not pursuing the 2.4 milligram dose. The reason being is that the dose response curve on liver fat plateaued at the 1.8 milligram dose. There was no reason to go ahead and study or spend patients on the 2.4 milligram dose. It also happened to be the only dose that showed the discontinuation, intolerability. Consequently, we really feel not only good about the efficacy, but the safety of the doses we picked. The randomization scheme between placebo, the 1.2 and the 1.8 mg doses, will be 2 to 1 to 2, meaning between the placebo, the 1.2, and the 1.8 mg doses, 76 patients, 38, and 76 patients. We'll dose people for a full year or 48 weeks, but we'll read out the biopsies at 24 weeks, that will be consistent with what many of the sponsors are doing. The primary endpoint of the study will be both NASH resolution and fibrosis improvement. With the power of the study, which is quite good, we feel that we're highly powered to see statistical significance on both. I'd also point out that we're doing a larger study when we compare 76 versus 76, the primary comparison of placebo to the 1.8. That's a large study when you look at the other sponsors. We're doing that to really give the trial the best chances of success, but also give us a better understanding of the correlation of the biopsies with the non-invasive markers to have a more robust discussion with the agency at the end of the trial, about the possibility of using non-invasive endpoints, non-invasive markers as primary endpoints in the Phase III trial. Understood. What should we know about the inclusion criteria for this study? Were there any specific choices you made there? Right. Patients will be required to come into the study with an 8% liver fat content. We're allowing both diabetics and non-diabetics, requiring the patients have F2 and F3 fibrosis. The reason is that really strengthens the possibility of having a positive readout on the fibrosis endpoints. Great. In terms of the number of clinical trial sites and the cadence you could anticipate with respect to enrollment, what should we think about? Right now, the trial is designed to be conducted in the United States. We're looking at 50-plus sites. We may decide to increase the number in order to implement faster rates of enrollment. All of these sites are highly qualified and have done NASH studies in the past. In terms of the biopsy procedure, we're going to be using a consensus read that'll be based on two readers who have to come to an agreement. If they don't come to an agreement, there will be a third reader that will adjudicate the read. Great. as you mentioned, it's a 24-week histology-based endpoint. just based on the mechanism of action and that duration of therapy, how are you thinking about the potential to hit on fibrosis, NASH resolution, and the magnitude? We're very excited about that possibility, and that's based on the analyses that I quoted before, that have shown the more liver fat reduction that you have, based on the MRI-PDFF, the higher the likelihood of hitting both NASH resolution and fibrosis improvement. Based on that, our confidence in being to hit those, both of those endpoints is really quite high. Yeah, one thing I would add is it's not just the magnitude of liver fat reduction, it's also the speed, how fast you're reducing that. What we've seen in our, in our trials is that just within six weeks, we're having very profound change in liver fat. It's that period that you're providing, you know, fat-free environment for the liver to heal, that's going to make the difference in fibrosis. That's very important. We're getting some of the fastest liver fat reduction out there. Great. As you think about the landscape in NASH, I guess, what are you monitoring with respect to recent updates, and, you know, that competitive landscape moving forward? Right. We think that probably the best compounds in the space are gonna be the FGF21s and the GLP-1/glucagon combinations. Regarding first, the FGF21s, we've seen liver fat reduction, which are good, perhaps as good or close to being as good as pemvidutide. We're optimistic that they could also hit those endpoints. We saw recently with 89bio and Akero Therapeutics, they've had FGF21 compounds that have hit their primary endpoints, both in NASH resolution and fibrosis improvement. That gives us confidence that we can hit those endpoints as well, because our liver fat reduction and speed is as good, if not better. When you look at the GLP-1 based compounds or even the GLP-1 GIP compounds, like semaglutide and tirzepatide, these compounds are not potent in reducing liver fat. The reason is that there are not GLP-1 or GIP receptors in the liver, and they drive liver fat reduction only indirectly by weight loss. Consequently, we're seeing about 1/2 of the liver fat reduction at a slower rate than with these other compounds. That's why we're seeing companies combine FGF21s with the GLP-1s. With the GLP-1s, you get very good weight loss, but you don't get liver fat reduction. Flipping it around with the FGF21s, you get the good liver fat reduction, but you don't get good weight loss. Consequently, wouldn't it be ideal to have one compound that could do both? We see that with GLP and glu containing compounds. There was a recent readout, or at least a publication of an abstract at the EASL Meeting of a compound, a similar compound by, now being developed by Merck, previously been developed by Hanmi. We think that compound is one-to-one. They got a very robust reduction in liver fat. It's further confirmation of the potential of GLP glu compounds to have this robust reduction in liver fat. One of the things that people are talking about increasingly, and you alluded to it a bit, is the potential for combination strategies in NASH. How are you thinking about the role of combinations here? we believe pemvidutide is a combination therapy in itself, because again, we're bringing two very different mechanism. When you have GLP GIP, you're really doubling up on the same mechanism. By having glucagon, we're going directly after the liver fat here, because as Scott said, there are no GLP-1 or GIP receptors in the liver, but it's loaded with glucagon receptors. That's sort of the starting point. Beyond that, it is quite possible that as time progresses, there'll be a lot of people on background GLP-1 therapies. The question is, can our compound be layered on top of that, and can there be additional benefit? We believe so, because it can further drive weight loss, but it'll also drive liver fat and overall lipid profile will improve. The combination will work there as well. I mean, basically, we think we already have the combination therapy, and as the landscape changes, we'll be able to layer it on top of other therapies. Yeah. Great. You mentioned you're also evaluating the non-histology endpoints or non-invasive tests, at the 48-week readout. Remind us which of these you're looking at, and how do you think about the slew of options there? Sure. MRI-PDFF, is which is probably the gold standard for measuring liver fat, cT1, which may be the gold standard or soon to become the gold standard for measuring inflammation, but also ALT. On the fibrosis side, we'll be looking at FibroScan and some other liquid markers like ELF, in order to see if we can get that strong correlation with the biopsy. That would be convincing for the agency in a discussion about using these markers as phase III endpoints. Okay, great. That's a good segue to my next question, which is just like, as you think about the role for non-invasives, how do you see that fitting into the regulatory and clinical and regulatory landscape for now. Right. It's a bit easier to go first to the clinical landscape because I can tell you as a hepatologist, and in speaking to my hepatology friends, no one's using liver biopsies anymore. The reality is that people are being staged for these diseases and NASH based on non-invasive markers, non-invasive tests. This is the landscape. When one goes to regulatory, it could be a different story. We'll find out with the resmetirom review. We do think that drug will go to approval, what the FDA states about that. We believe that at least in the near future, the biopsy will still be the standard in clinical trials, but we're doubting that the FDA would impose a biopsy standard in order to treat a patient, and certainly an insurance company wouldn't foresee that. Yeah. There was a recent advisory committee meeting, which is kind of the first look we've gotten at how regulators are thinking about NASH. I guess, were there any takeaways that you had coming out of that meeting? Right. We think, and talked to a number of people about this, it was probably a one-off. You know, when Intercept got its complete response letter, no one really knew what to make of it. Was this a shadow over the whole field of NASH? Well, when you listen to the meeting, and when you read the briefing package, there were real safety concerns. I, as a hepatologist and physician, think there were safety concerns. The biggest being drug-induced liver injury, which was real. The LDL elevations were of great concern. The pruritus is not well tolerated in these people. What I've spoken to people about, physicians, who have their, let's say, primary biliary cholangitis patients on this therapy. They also mentioned glucose controls being a problem, we think that came much lower in the order of concern compared to the others. We really see this as being a one-off. I think we have to look towards the histological evaluation to really see what the intent of the agency is. We're optimistic that this drug is going to have a good safety profile. And it met its primary endpoint in efficacy, let's point out the fact that only 25% of people responded to the drug. That's good and bad. It was statistically significant, it'll get approved. The good thing for Altimmune and the other drug developers in this area, is that there's so much room for improvement. The liver fat reduction was only about 50% at 24 weeks. Ours is 75%, 76%. We really think that we can beat that 25% mark. Great. I guess last question on NASH, then we can move on. As you look at the competitive landscape, and particularly the commercial market opportunity, I think there's a lot of questions that still remain in terms of how that will play out. What are you looking to see, kind of, if we do get a first drug approved, and how do you expect kind of the commercial landscape to play out over the coming years as more drugs enter late stage and come to market? Yeah, I mean, the big question there is that how the reimbursement will take place. What would be required to give a drug to a patient, do you have to do biopsy? I mean, that's number one question. We don't think so because, you know, you're going to have to change the entire practice. Then pricing is going to be the other issue. I mean, there is this thought that NASH can be premium priced because it's, you know, significantly greater burden than obesity, if you're comparing the two indications, for instance. If you want to have a large market in the liver space, in the NAFLD NASH space, then you're going to have to treat a lot more patients, and you'll have to treat them without biopsy. You know, with suspicion of NAFLD NASH, that's what's going to drive the penetration. I think that play, it'll be interesting to see how that develops over time, because that's important for pemvidutide, because we're going to be treating both obesity and NASH. We want to see that, how those play with each other in terms of acceptance in the marketplace and pricing, and how the payers ultimately will see these indications. I lied. I want to stay on NASH for a little bit. As you look at... Like, when we talked about obesity, we talked about expecting a stratification of the market based on some of the other comorbidities. Do you expect that to play out similarly in NASH? If so, where do you see pemvidutide as fitting most appropriately? One of the things that, and we've already mentioned that we see as a big advantage of pemvidutide, not only are we getting very, very good liver fat reduction, both in terms of speed and magnitude, but we're also combining it with weight loss, which most of these patients have, you know, they need to lose weight as well, because that would be another treatment for NASH, if you think about it. We're the only drug that combines these two features, very profound, very robust, liver fat improvement and weight loss at the same time. We think that's very motivating for these patients, because, again, to keep them on therapy, NASH is a silent disease. They don't even know what's going on until it's too late in many cases, whereas losing weight is something everybody can relate to. We think that's, you know, that's going to be a unique opportunity for pemvidutide. Mm-hmm. will really differentiate, if you think about it, differentiates us from everybody in the NASH space. As you think about pending positive results from this Phase II study, how would you think about next steps for the program here? For NASH? In NASH. Obviously, this data is very important. Hitting that fibrosis endpoint is very important, which, you know, we feel very good about. Beyond that, you know, NASH is an indication we can even develop on our own. Again, if you're looking for a partnership for obesity, we'll combine that with NASH at some point, because it's the same molecule. It's very hard to separate these two indications. Ultimately, for both NASH and obesity, we would want a partner to help us develop this through phase three and ultimately commercialize it. Yeah, that's a great segue to my next question, which is: How do you think about the profile of a partner, particularly if you're looking for one that can do obesity and NASH, and what's the right timing in terms of making sure you get the right kind of value for that program? I mean, that's a great question. Again, in order to get into phase 3 development for obesity, which is ahead of NASH by 18 months or so, we need a partner for that now. That's what we're focusing on, is to find a partner for obesity. Some of those partners may also want NASH in addition to obesity. We'll just have to make sure we're getting the value for NASH, you know, when we do that. Otherwise, we may have to hold on to NASH for a little bit longer. There are different ways to structure these, where, you know, you don't give away everything upfront, but, you know, you can, you can have gated, structured deal, where you can ultimately, the partner can acquire the whole asset. We'll look at various structures. In terms of timing, obesity is right now, NASH can be later, or it can be right now as well, depending upon who the partner is. The good news is most players are interested in both of these indications. It's, you know, basically cardiometabolic disease area, which is where many of these large pharmas have been, and they know this space quite well. We think it's a good thing to have both of these indications because they drive the valuation and the discussion. Okay, great. so we don't leave it out, the HepTcell study is reading out first quarter of next year. How should we think about what a successful outcome looks like for that trial? Let me just say something about the trial and the molecule itself or the compound itself. It's an immunotherapeutic that's specifically directed against the epitopes of the hepatitis B virus without cross-reactivity to human proteins. Consequently, unlike some of the general immunostimulants, this is specific for the virus and safe. It doesn't have the side effects. The tolerability is excellent. It's meant to stimulate T cell responses against hepatitis B and drive down viral responses, in particular, the hepatitis B surface antigen, which is the functional marker of the disease. The primary endpoints of this study are the reduction, a 1-log reduction in the hepatitis B surface antigen and also clearance of the virus. Right now, we're doing a study in patients with naturally low levels of the antigen, because these are the patients who are most responsive to immunotherapeutic interventions. That is a population known as inactive chronic hepatitis B. It actually comprises two-thirds of the hepatitis B population worldwide. We don't currently treat these people because the therapy, which is pegylated interferon, is too toxic. In addition, there's the potential to combine the immunotherapeutic with some of the newer direct-acting agents, like the small interfering RNA that are treating people with active disease, high viral levels, bring the levels down, and then we combine it with the immunotherapeutic in order to wipe out the virus. This dual mechanism or combination has been postulated by a number of experts to be necessary to wipe out the virus. You know, we really see that potential in the endpoint for this and a huge population, and we'll read that study out in the first quarter of next year. Pending positive results from that study, what are the next steps for the HepTcell program? Go ahead. Well, you know, we're having discussions with companies right now. There's a great deal of interest in combination therapy, mainly with companies that have these novel direct-acting agents, like small interfering RNA and oligonucleotides, who do not have an immunotherapeutic and want to combine it. We're in active discussions about with companies that want to combine. Obviously, it's going to be data dependent, and probably wouldn't announce anything until we actually read out the study. There's that pathway and also the pathway to actually treat this huge population of individuals with chronic inactive hepatitis B, who are infectious and have still the potential for liver flares and hepatocellular carcinoma. Yeah, I mean, there's general agreement in the field that it'll be important to combine an immunotherapeutic with these direct-acting antivirals. The challenge has been nobody has been able to come up with a really powerful, active immunotherapeutic. If you have that, there'll be multiple players who would want to combine it with, and we'll have to decide what makes more sense, because they're also generating data on their direct-acting agent. Mm-hmm. We really want to combine two powerful forces together, in order to really eradicate the virus in the end. Maybe with our last couple seconds here, we can wrap up on cash runway. What's the current cash position, and what does that take you through? At the end of March, with approximately $165 million, that's sufficient cash to complete all of these milestones that we are talking about, 48-week data in obesity, HepTcell data, as well as completion of the, as well as 24-week data from the NASH study. Mm-hmm. You know, over the next 18 to 24 months, we're in a good shape, and we'll have multiple other obviously news coming during this period. There will be potential financing opportunities. Wonderful. Great. Thanks so much for the time today. Thank you. Thank you.