Nasdaq under the symbol MTVA, and their presentation is moderated by David Boutz. He's a senior analyst with Zacks Small Cap Research. Welcome back, HH and David. Let's dive right in, and let's start with DA- 1726. Of course, this is your obesity therapy that you're developing. The company recently announced what I would consider pretty promising data from their four-week multiple ascending dose phase I trial. Why don't you give us a little bit of an overview of that data, and then, in your opinion, what differentiates DA- 1726 from the other obesity therapies that are out there right now? Yeah, I think that's a very good starting point. 1726, GLP-1 glucagon dual agonist. We did release an interim data readout. We said it was top line, so interim top line data readout of our phase I. It was a four-week study over in a single site in Florida. We started with a 4 mg dose level. We went up to a 32 mg dose, and we believe 32 is a starting dose because the safety tolerability was completely different than any other GLP-1 glucagons out there. The weight loss, it came out to be the max weight loss was 6.3% weight reduction in four weeks, with mean weight loss reduction of minus 4.3%. The most important part of what we have done with 1726 is that we didn't do any titration. Non-titration, we went straight with 32 mg, and it showed a great safety profile and very compelling weight loss. Now, the differentiation point that we have is coming from the ratio. Our drug is 3:1. Other drugs like pemvidutide, 1:1. Survodutide, which is Germinaline acid, 8:1. Mazdutide, in Lilly's drug, is 6:1. Everyone's ratio is different. Why is it important? It's because the ratio shows different aspects coming from in-human or in-animal trials. What we did with our 3:1, starting with the safety profile, very safe. Everything was mild in GI, no treatment-related discontinuations, which is quite amazing for dual agonists because GLP-1 and glucagon, both of them do have GI adverse events. Having both of them in one drug do tend to show a lot of AEs, but our drug did not because we believe it is the unique ratio of 3:1. With that, weight loss, as I mentioned, very competitive weight loss coming out with just four weeks of non-titration. Let's look at GLP-1 and glucagon, right? GLP-1, what does it do? It reduces glucose levels, and it controls it. What does glucagon do? It actually increases the glucose level. When you add these two together, the balance is the key to it. For example, when you have pemvidutide, which is 1:1 complete balance, it offsets everything so that they cannot use the drug in type 2 diabetes patients. Now, for us, 3:1 balance, it almost showed very close to DPP-4 inhibitor, which is quite amazing in just four weeks. That highlighted by our GLP-1 side of the drug. Then glucagon, what does it do? Energy expenditure, plus it breaks down the white adipose tissues. What did it show with the waist circumferences? The max of 3.9 inches reduction with four weeks of treatment, mean of minus 1.4 inches reduction in just four weeks of treatment. That's like the mean reduction is about a buckle and a half reduction after just four weeks of treatment. We believe that's coming from our glucagon, breaks down the white adipose tissues, and it was very efficient. On that side, the most important part of it is that day 47, this is a month after the last dosing. These subjects, they went discharged, completely discharged off the drug for a month. They went back home. They've been eating. They've been doing normal life, living their normal life. They came back in day 47, and they're still at minus 3.7 centimeters, which is just amazing. They didn't increase their waist. Why is that possible? Because breaking down the white adipose tissues, once it's broken, it takes time to rebuild it up. That's how effective the glucagon aspect of our drug was. I believe that kind of it was a short, yes, the study was short, four weeks. The number of subjects, six active, three placebo in the cohort. It's small, but it showed just amazing results. Yeah, absolutely. All right, thanks for that. You mentioned the 32 mg dose you're viewing as kind of a starting dose. What are you going to do to follow up on those results? We are thinking of running additional cohorts in the phase I. We are planning to run a 48 mg cohort first, and then we'll look at the data and see what comes to be. I really personally then I really hope we don't go above 48, but if the safety tolerability shows similar and there's more weight loss coming out, then we'll have to run higher dose levels. We'll start with the 48, and we'll be able to report that result within this year. Okay. The company has mentioned part three, if you will, this phase I trial. We're going to be looking at early dropouts from Wegovy treatment. Why did you decide to focus on that patient population? What percentage of Wegovy patients, if you know, would you estimate are "early dropouts"? The reason for that is how different this drug has shown with this phase I study. The Blue Cross reports and other reports do show it's not just Wegovy, but GLP-1 therapies in general with obesity. When the patients start, about 20-30% of those patients drop out within the first two months. That is purely because of the tolerability and side effects. When you go longer, about 70% of the patients drop out within the year. That has other impacts, right? It could be the economical issues, the drug's too expensive, or it could be just people already hit their minimum weight loss requirement and don't want to continue on. That's the current landscape right now. The reason we are focusing on the 20-30% is that when our research center developed this, the ultimate goal for us was never to reach the magic number of 30% weight loss. That wasn't the goal. That's never been the goal. We have never been interested in fighting over who loses the most weight and which time point because our goal was purely on control of side effects while highlighting both agonists. That was receptor agonists. That was what we were focused on. Because of that, that 20-30% of the people who can't tolerate the current obesity drugs is logically our target because there are patients who want the drug, really wish to have it, who are committed in spending money and just had to drop out because they couldn't tolerate it. That's a pretty big chunk of the market. If we could go into that market and effectively have them go through like a 12-week study or even beyond that and have very competitive weight loss, then as a small biotech, isn't that a potential for a winner? Yeah, absolutely. Quick follow-up. Is it only patients who are from Wegovy, or would you take other patients that were on other meds? You mentioned 12 weeks. Is that what you're looking to do, a 12-week trial with those patients? We're currently just looking at for our trial, it would be Wegovy. Okay. What we learned from we talked to a lot of different obesity clinics, and the real-time practice for these clinics is that obesity patients come in and consult. They start with Wegovy first. Then they'll move into Zepbound. Wegovy is the first line of drug that they use. Logically, we would rather focus on those patients rather than Zepbound because it gets way too complicated in recruitment. Got it. Yeah, makes sense. As far as timelines go, when would the Wegovy dropout trial get underway? Kind of looking a little bit into the future, when we start talking about phase II trials, when do you see those being able to get underway? If you really want to expand into the future, ultimately, when would we potentially see DA- 1726, phase III, and then potentially to market? Our goal to market, let's work from there. Our goal to market is 2030. That's always been our target. For the near-term milestones, we are focused on finishing up the phase I on the SADMAT. We were thinking about starting the part three, the early Wegovy dropout patients, but for us, maybe we need to find that max tolerated dose first is going to be the near-term goal. To give you a little more light to it, when we released this, I believe, a very strong, compelling data in April. That day of data release, our stock went up like 25% pre-market. Then suddenly, I get an email from one of our shareholders. The legal team told me not to mention the name, sent me an email saying they're exercising all of their pre-funded ones. That's right around when the market was opening. That gave me a very bad feeling of what's going to happen that day, but it actually did come to life. When you have about more than 10% dumping into the market, I don't know they did, but if they did, or when the market opened, there was algorithm trading going on pre-market, and it just completely switched on the other way. It was quite devastating. It was freaking hard to see the stock going down, just selling all day long. There was nothing I could do. It just never, the stock price just does not reflect on what cash we have in hand and what the data really means. Back then, our focus was to maybe be able to just run this 32 mg, the starting dose, and look at part three and try to get more data out as faster. Right now, we're more focused on why don't we get this dosing regimen on, be done with starting 32, maybe the optimum dose could be 48, could be higher. Nobody knows at the moment, but let's run a little more of these cohorts. Then we can look into what we can do with a potential part three or maybe just go straight into phase II. Okay. That makes sense. And this next cohort, just to clarify, you think you'll have data for that this year? Yes. Excellent. All right. So kind of a general question about how obesity trials are run, if I could, but I'm curious how the patients are monitored in these trials and specifically, I guess, their diets as well. When you're trying to do comparisons between trials, it gets tricky, but how is that accounted for in these obesity trials? Everyone's different. It's quite interesting. I think earlier this year, was it, or later last year, late part, there was a company, I don't want to name, who came up with a pretty good, compelling weight loss data in four weeks. I was like, wow. I noticed that it was all inpatient four-week study. Now, what does the inpatient period do? We're talking about obese, otherwise healthy, right? People tend to like snacking all day and all those things. When you go into an inpatient period, what happens is that you're under a controlled environment. It's not your home, so you're stressed. There has to be a little bit of those environmental weight loss coming into play. It's very hard to have an early-stage clinical trial apples to apples. It's hard, especially if you want to measure everything in the right way. It's hard to control everything, especially on the eating side. For us, when we're running this phase I up to now, because it was short in four weeks, we didn't do DEXA scan, and we didn't really put any measure on HbA1c as well. We didn't monitor dietary changes. Now, with what we have seen with the current design, we believe that we have way too great of a data set that we need to dig into it more. The new cohorts in phase I will have different aspects to it. We're going to look at DEXA scan because the waist circumference has changed. The waist reduction is just amazing. We want to see it in the whole body. We'll be running that. We'll be running energy expenditures, and we'll be looking at dietary changes as well. Although it's going to be a very short trial compared to others, four-week, still we've shown in the 32 very compelling data, and we'll be digging into more within that four-week time frame with a higher dose. Okay. Great. That sounds good. Maybe quickly, but a lot of companies have started focusing on oral therapies, and I'm kind of curious what your thoughts are with the subcutaneous versus oral administration and if you think that the oral therapies are going to get much market share. I think the orals are a little different, right? I totally understand people. There are people who just cannot tolerate injectables. Orals are much easier to keep, much easier to administer, and I completely agree with that. It's just all these GLP-1 injectables are peptides other than Amgen's. Now, peptide turned into oral, is that going to work? There are a lot of companies working on it. It's just that daily pills are like 100 mg, 150 mg of peptide in GLP-1 going in. I'm not even sure is that even healthy for the patients. For one, two, it's similar to injectable or even more drug going in. Because it's going into the body with your stomach and everything, it just does not fully work as an injectable. I'm not even sure long-term how it's going to turn out to be. The pills are going to be huge, and it's going to be very expensive. Peptide or oral peptide, GLP-1 oral peptides, I don't think it's going to be a market changer or a game changer. Now, GLP-1 oral small molecule, that's another class. That's the Eli Lilly's drug. I think it's quite promising. Is it going to be as effective as injectable peptide? Probably not. Looking at the weight loss, impressive, but can it be overtaken? I don't see how it will. To me, it feels like maybe it's going to be one of the great maintenance drugs that people can take. Could work really well on that side. I'm not sure how Eli Lilly is going to position it, but it does not look like it can. I don't know if people want to take an oral pill for a year and lose like 10% of their weight. I'm not sure if that's going to be the goal. Rather, just go with the injectables and be over with. I think looking at the real-time data, 70% of people don't even last up to a year anyway. Faster, greater weight loss. To me, it's a little off the oral part of it, but the titration part is really important. I think whether it's oral, injectable, when you have that titration period, the patients are paying money, right? They're paying money to get to their optimum dose level. Right now, semaglutide towards Zepbound, it takes about six months. With the current insurance landscape moving and administration views changing, non-titration is going to be the key. Plus, how tolerable is it? I think those are going to be the keys moving forward. Yeah. Definitely some good points. It segues nicely into the next question. When talking to potential partners, what is it that they're looking for? What's the most important thing to them? Is it the efficacy? Is it tolerability? Kind of like to sweet spot operate with both. What are you hearing from other companies that you're talking to? Novo Nordisk and Eli Lilly did just one amazing, one heck of a job in creating this obesity market. I have to applaud them. They're doing an amazing job. Nobody imagined this. Now, the followers, what do they need to do? Novo Nordisk, Eli Lilly, they're way ahead of the competition. In order to have a dip in the market, they need something different. Is a GLP-1, GIP going to work? Probably not since Zepbound is so strong. They need to have something very different. I think they are quite interested in non-titration and interested in a difference maker. I think our drug is a difference maker because glucagon showing up a true dual agonist. Both of sides blossoming with data, although it's a short period. These are the things that I believe people are looking for. All right. Sounds good. Switching gears a little bit, let's talk about DA-1241 for a little bit. Of course, this is the drug you're developing for MASH. If you can give a brief overview of that compound and then the results that the company released not too long ago about that in MASH. Just briefly on it, it's a GPR119 agonist. It's a small molecule, once daily, oral. We ran a phase II-A 16-week study on presumed MASH patients. We hit the primary endpoint, which is change from baseline on the ALT levels. We have other FAST scores, CAP scores that show direct hepatic effect. It showed great safety profile, actually one of the best safety profiles in MASH assets. Now, the mechanism of action is it promotes production of natural GLP-1s in the gut. That is the main activation, the mechanism of action. It helps fighting inflammation as what the GLP-1 drugs do as well. Now, the best part of this is that because of its safety profile, we'll be able to use as a very good combination target. Plus that, other MASH drugs like resmetirom, FGF21s, they're very focused on hepatic effects, but this drug actually controls glucose as well. Very similar to it, probably better than DPP-4 after the 16-week study. Added benefits come in. We're just trying to figure out where to position this drug within the MASH space. Everyone is focused on GLP-1s because everyone's running a MASH trial. FGF21 is the talk of the day right now because they showed amazing effects in F3 and F4, early F4 patients. With that, we are looking into different aspects of a combo. Last year, at EASL, we did a poster presentation for DA-1241 and semaglutide combination therapy. It did show great effects, better than semaglutide standalone. I'm really excited to do another poster this year at the ADA this month and show another great combination opportunity. Okay. What are the next steps for that drug? I know you mentioned that it's probably going to be part of a combination therapy. Do you foresee forming a partnership to then advance it further in clinical trials? That's the goal. That's the goal. Now, FDA requires for all of the MASH agents to run a biopsy-proven trial during the phase II. It's a requirement to go into phase II. Our phase II-A did not include a biopsy because our drug is very strong on the anti-inflammation side and, of course, on direct hepatic effects, but we wanted to do a phase II-A without a biopsy. Now, in order to go into a phase II-B, phase II, we will have to run a biopsy test next time. I'd rather do that while we have a solid partner to go with us so that we can expand our coverage, not just on F1, 2, and early stage 3. If we can expand more into the early stage of F4 and more solidified in earlier stages, I think it will justify our investment for the next clinical trial. All right. That sounds good. I would say lastly, why do not you give us an overview of why you think or why should investors view MetaVia as a good opportunity right now? When you look at, for everyone, when you look at any other biotech companies in the obesity space, and although it's a short study, but showed this much data, the price is not where we are. I can tell you that. We have a very near-term, very near-term catalyst coming up. I think people should pay attention to us. All right. If investors have any more questions, what's the best way to reach out? We're open to a one-on-one conversation. I think, as described in the first, on the right upper corner, you can see the one-on-one meeting requests. I'll be more than happy to meet everyone there and try to have very good discussions on these assets and our company. All right. Sounds good. HH, thanks for joining today. Thank you, David. Thank you everyone for joining.