Back to H.C. Wainwright & Co.'s 27th Annual Global Investor Conference held on September 8th to 10th, 2025. My name is Patrick Trucchio. I'm a senior healthcare analyst at H.C. Wainwright & Co. That said, it's my pleasure to introduce our next company, Altimmune, a late-stage biopharmaceutical company focused on developing novel peptide-based therapeutics for liver and cardiometabolic diseases. The company's lead program is pemvidutide, a GLP-1 glucagon dual receptor agonist for treatment of metabolic dysfunction associated with steatohepatitis, or MASH, obesity, alcohol use disorder, AUD, and alcohol-associated liver disease, or ALD. From the company, it's a pleasure to introduce Vipin Garg, CEO, and Scott Harris, CMO. Welcome to the conference. Thank you. Thank you for having us. So maybe just to set the stage, if you could introduce us to pemvidutide, you know, dual GLP-1 glucagon mechanism, you know, rationale in metabolic liver disease, and just the status of the program. Yeah, absolutely. Well, again, thank you for having us. As you mentioned, pemvidutide is a dual agonist. It's a glucagon-GLP-1 dual agonist. So the idea is to, it's really ideally suited for treating conditions where you need both weight loss and a direct effect in the liver. So MASH, for instance, is a disease that's caused by obesity. So the ideal way to treat MASH would be to have both direct- acting agent in the liver and weight loss. That's exactly what pemvidutide does. So really, to be successful in the liver space, in treating serious liver diseases, you need the drug that has dual effect, direct effect in the liver, weight loss, good tolerability, and lack of dose titration. Pembi brings together all of these. As we'll go through the data, you'll see that we have very compelling 24-week data from our MASH trial. That's still continuing. We're expecting 48-week data in the fourth quarter. We're preparing for our end of phase II meeting at the end of the quarter, end of the fourth quarter. So really well positioned to start phase III trial next year. What's the sort of key headline takeaway from the 24-week impact data, particularly on MASH resolution, and what should we be looking for at 48 weeks? Yeah, Scott, you want to take that? Let me describe the trial in general. It's a 48-week trial. We're reading out the primary endpoint, which is based on the biopsy. That's the FDA definition of approval at week 24. Yet we're following non-invasive tests, and you're aware they've gotten a lot of attention in the last couple of weeks as the FDA has reviewed a letter of intent for the approval of what's known transient elastography, nicknamed FibroScan, for the treatment of MASH, so we have the biopsy at 24 weeks, but we follow weight loss in these non-invasive tests all the way through week 48. In addition to the traditional biopsy read by pathologists, which is manual, which is felt to be outdated, error-prone, poor reproducibility, et cetera, et cetera, we also had computer-based reading in the readout, so we had two doses of pemvidutide, 1.2 and 1.8 mg. We did not employ our 2.4 mg dose, which is our best dose for weight loss, although we're looking to implement that in phase III. But the 1.2 and the 1.8 milligram doses, importantly, were given without dose titration. That's very important to hepatologists. If you talk to the guys out in the field right now and they look at the concomitant use of semaglutide, for example, yeah, it was approved at the dose of 2.4 mgs weekly for the treatment of MASH. Well, what they're telling you is that very few of their patients get up to or are taking the 2.4 mg dose. And even worse than that, in their practices, these are not obesity practices, but they're hepatology practices. They don't have the patients or the staff to monitor the titration. And if you do titrate, we know in practice that although in a clinical trial, it was titrated over 16 weeks, in real-world practice, we know from the obesity field that it takes months to get up to that 2.4 mg dose. So this is a very delayed, slow onset of effect. It mimics weight loss. Because weight loss does impact MASH. We know that from the bariatric surgery literature, but it takes three to five years. You need something that's going to work faster than that. And as mentioned, you take pemvidutide, which is GLP-1- based. It gives you the weight loss. But in addition to that glucagon effects, which is a direct effect on the liver, robbing the liver of its fat, and really having tremendous effects in fat-induced inflammation and then fibrosis, this is really the perfect mechanism. So what do we get? At week 24, now on the biopsy, we saw class-leading effects in MASH resolution. This was comparable or better than all other drugs, even reading out to week 72. This is what we had hypothesized. pemvidutide has class-leading reduction of liver fat. That's a direct effect on the liver. Remember, there are no GLP-1 receptors in the liver. There's plenty of glucagon. So we saw that very rapid fat reduction, that very rapid reduction of inflammation, and very rapid MASH resolution. Probably the most that's been seen since. We did not hit the fibrosis improvement endpoint. That was based on stages of MASH using a criterion that will soon be outdated. But we reread the biopsies using the computer. We're all aware it's much more accurate, has much greater reproducibility and accuracy, and the pathologist got outstanding readouts. That computer-based readout has been accepted by EMA for MASH approval. We've already met the endpoint in Europe for MASH, and we know that FDA is reviewing that same application this year, so it's quite frankly possible that by the end of this year, we will have met the FDA-approvable endpoints for both MASH resolution and fibrosis improvement. Now, you're also aware of the NITs and the recent discussion from the last weeks, and our NITs at 24 weeks are excellent. They're comparable to what others are seeing at weeks 48- 72. They're more representative of the process of fibrosis improvement than the actual stage, so what it means is that the NITs are a bit out in front of the pathologist-staged improvements, but they're showing tremendous effects. When you combine it with the computer read, you got a very potent readout in fibrosis improvement. Now, we're following patients out to week 48. We'll have that readout in the fourth quarter of this year. What will we get from that? Continued weight loss. That's going to be very important to see. The growth of the non-invasive test responses over time. I think we'll see at week 48, those responses are going to be as good, if not better, than all their compounds at week 48. Why? It's the glucagon effect, and it's the MASH resolution driving the fibrosis improvement. We also have no dose titration. Very attractive to hepatologists in our market research. Very convenient. This trial enrolled faster than any other MASH trial. What it means is that patients and their docs like the drug. That's valuable market research right there in a real-world setting. So we're really excited about. So, you brought it up a few times, and I think, you know, I've asked over the years many times about FDA's openness to non-invasive tests in terms of evaluating MASH. And so I'm wondering, what's your take on this latest update from the FDA? How is it going to impact this program going forward? The FDA wants to approve NITs. I think it really does. The FDA, however, is a law-based institution. You know, they can only approve drugs based on certain standards. They can only choose endpoints for approval based on certain standards, and I think there's tension within the organization as the ones who want the NITs, who think they're valuable, who see the science, and really the legal definition of an approval endpoint, and that's public policy. You're all familiar with that. It goes slowly. You got to be careful, and you got to appreciate it. I think the FDA is very motivated to do it. It's accepting applications, letters of intent for the.