Greetings, and welcome to this morning's conference call hosted by Altimmune. All participants are in a listen-only mode. A brief question and answer session will follow the prepared remarks. To ask a question during the session, you will need to press star one one on your telephone. As a reminder, this conference is being recorded. I would now like to introduce your host for today's conference call, Rich Eisenstadt, Chief Financial Officer of Altimmune. Rich, you may begin. Thank you, Michelle, and good morning, everyone. Thank you for joining us. Members of the Altimmune team joining me on the call today are Vipin Garg, Chief Executive Officer, Scott Harris, Chief Medical Officer, Scot Roberts, Chief Scientific Officer, and Dr. Stephen Harrison, Medical Director of Pinnacle Clinical Research and Principal Investigator on our trial. Please note that we issued a press release and posted an accompanying slide deck this morning, which is the subject of our discussion today. You may find copies of these items on the IR section of our website, www.altimmune.com. Before we begin, I would like to remind everyone that remarks about future expectations, plans, and prospects constitute forward-looking statements for purposes of safe harbor provisions under the Private Securities Litigation Reform Act of 1995. Altimmune cautions that these forward-looking statements are subject to risks and uncertainties that could cause actual results to differ materially from those indicated, including those related to the ongoing conflict in Ukraine, COVID-19, and the impact on our business operations, clinical trials, and results of operations. For a discussion of some of the risks and factors that could affect the company's future results, please see the risk factors and other cautionary statements contained in the company's filings with the SEC. I would also direct you to read the forward-looking statement disclaimer in our press release issued this morning and now available on our website. Any statements made on this conference call speak only as of today's date, Wednesday, September 14th, 2022, and the company does not undertake any obligation to update any of these forward-looking statements to reflect events or circumstances that occur on or after today's date. As a reminder, this conference call is being recorded and will be available for audio replay on Altimmune's website. With that, I will now turn the call over to Dr. Vipin Garg, Chief Executive Officer of Altimmune. Thank you, Rich. Good morning, everyone, and thank you for joining us today as we review the positive data from our phase I-B 12-week NAFLD clinical trial for pemvidutide. Pemvidutide is our investigational GLP-1/glucagon dual receptor agonist under development for obesity and NASH. The results of this trial were announced in a press release this morning, as well as accompanying slide deck posted this morning on our website. As you will see, we believe the phase I-B clinical data we have collected is compelling, including significant reduction in liver fat, serum ALT, and body weight. Pemvidutide was well-tolerated, and there were no clinically significant ALT elevations defined as threefold or greater the upper limit of normal. In fact, serum ALT was observed to decline significantly in all but the lowest dose cohort. These results strengthen our enthusiasm for the potential impact pemvidutide could have on the multibillion-dollar NASH and obesity market. I will now turn the call over to Dr. Scott Harris, our Chief Medical Officer. Scott? Thank you, Vipin, and good morning, everyone. I'd like to start off setting the stage for today's discussion. The clinical trial results we are reporting are from a clinical trial in obese and overweight participants with significant liver fat content. For inclusion in the study, the participant was required to have at least 10% liver fat fraction, and in the end, the mean liver fat fraction across the study participants was 22%. These subjects represent a unique subset of the general obese and overweight population. I would like to add that we are fortunate to have Dr. Stephen Harrison, Medical Director of Pinnacle Clinical Research, serve as a clinical investigator on this trial. Dr. Harrison is a renowned hepatologist who has conducted numerous NAFLD and NASH studies. With that, it is a pleasure to introduce Dr. Harrison, so he can walk you through the top-line trial data, and he'll follow the sequence on the slides that have been loaded on the website. Following his presentation, the entire management team and Dr. Harrison will be available for Q&A. I'm gonna turn the presentation over to Dr. Harrison, starting with slide four of the slide deck. Stephen? Yeah. Thank you, Scott. It's an honor and a pleasure to be here today to discuss the results of this exciting phase I-B NAFLD trial. I just want to take a few minutes to walk you through what we have. Here on slide four is the trial design. It's a 12-week randomized placebo-controlled study of pemvidutide in subjects that are overweight or obese and that have non-alcoholic fatty liver disease. 94 subjects were randomized to 1:1: 1:1 and dosed across 13 sites to one of the four treatment arms you see listed here. Treatment was for 12 weeks, and they were stratified by the presence or absence of type 2 diabetes. If you look at the high-dose arm, there was a four-week titration period, and then a stable 2.4 milligram weekly dosing for eight weeks. The remainder of the dosing arms were not titrated. I think it's important to also note, unlike a standard obesity trial, there were no calorie restrictions, no lifestyle intervention recommended here. All right. Let's go to the next slide five. It's important to recognize the key eligibility criteria. Again, this is a couple points I wanna make that maybe are a little different from a classic fatty liver study. The age is typical 18 to 65, the BMI greater than or equal to 28 kilograms per meter squared. Here, you also had to have liver fat content as defined by MRI of at least 10% liver fat fraction. Now, when you do that drives up the mean value of liver fat, as Scott mentioned, of around 22%, which is quite high. In addition, we wanted to have some metric where we could exclude significant fibrosis in this early phase I-B study, and we set that as a non-invasive FibroScan liver stiffness measurement of less than 10 kPa. In addition, when we looked at eligibility criteria for our non-diabetic or diabetic population, you know, they had to be on a stable dose of metformin or SGLT2 therapy. They could not use insulin, sulfonylureas, DPP-4s, or be on current GLP-1 treatment. They had to be reasonably controlled in their diabetes. This is again a standard value through all NAFLD/NASH trials, at least the ones I've been involved with. A hemoglobin A1c needed to be less than 9.5%. Maybe a critical component here is the note that ALT and AST, the two liver chemistry tests we follow routinely in liver disease, had to be 75 IU/mL or less. Typically, we're looking for a minimum threshold of ALT and AST to enroll patients, and typically, we exclude them if they're greater than 3-5 times the upper limit of normal, usually around 200. In this particular trial, we had two criteria that were quite different. We had to have a liver stiffness measurement less than 10 and ALT less than or equal to 75. We'll talk about that more as we go through the deck. I'm gonna move to slide six, which is study endpoints. The overall primary endpoint was reduction in liver fat content by MRI PDFF. We looked at both absolute and relative fat reductions. Key secondary endpoint was percent body weight loss. Of course, in this early phase trial, we're very keen to look at safety and tolerability, particularly serious and severe adverse events, and in particular, those adverse events that could lead to discontinuation. As consistent with this mechanism of action, we wanted to assess, in particular, the GI tolerability. In addition, we know that ALT is a safety lab. We wanted to look to see if there were any elevations in ALT. We wanted to look at vital signs and glycemic control as well. Now I'll move to slide seven, which is the baseline characteristics of the study participants. It is a relatively busy slide, but I think it speaks to the population, and I wanna pull out a couple salient features of our patient population. As you can see, the overall treatment numbers were roughly 23-24 in each group. They were relatively evenly split between male and female, and age was roughly close to 50. Importantly, disparate from other trials in NAFLD and NASH, there is a predominance of Hispanics. In fact, you can see in the treatment arms, 75%-87% of our population were white Hispanic. That I think is important to note. When we look at BMI, they're in the obesity range here, 35-37, depending on which group you're in, and about a third of the patients are diabetic. We've already alluded to the liver fat content being quite high, around 22%, looking at the ranges here from 20-23.8. That is a function of the requirement to have at least 10% liver fat content on MRI. Some studies are looking at 8% liver fat content for inclusion. When you do that, you tend to have mean values in the high teens, something like 17, 18%. When you push it to a requirement of 10%, you actually push those mean numbers over to the 20 point, and that's what we're seeing here. It is important to note that ALT is relatively low here across the group, 32.4-39.5, and that again is a function of the requirement to have a low ALT or less than 75 at baseline when we included these patients. That'll come up as we move through the deck. The remainder of the data is representative of a NAFLD/NASH population. You see the cholesterol here, generally being in the normal range, high normal range. The triglycerides do tend to be a little bit elevated as you see. But at the end of the day, I think very representative of a NAFLD population. Let's move on to slide eight. That's the study disposition slide. As I alluded to in the study trial design slide, 94 patients were randomized and dosed. You see the breakdown here between the four different treatment arms. In this consort diagram, you can see those lost to follow-up. In the pemvidutide 1.2 mg, there were one withdrew consent, one lost to follow-up, and ultimately 21 patients completed treatment. In the 1.8 mg pemvidutide arm, there was one adverse event, three withdrew consent, one lost to follow-up, and 18 completers. In the pemvidutide 2.4 mg, there was one adverse event, two protocol deviations, one non-compliance, which led to 20 completers. If you look at the adverse event dropouts, the one in the 1.8 mg and the one in the 2.4 mg, those were due to GI intolerability. Let's move on to the next slide. This is slide nine, and it's the primary endpoint, which is exciting to show reduction in liver fat content, both absolute and relative, were highly significant relative to the change in placebo. You see it peaked at the 1.8 milligram dose on both absolute and relative at 14.7 and 68.5. In general, very, very good reductions. I think it's important to note also that this was at an early time point at week 12. Next slide. This is slide ten. Here we wanted to break down the liver fat content reduction at week 12 in what we call a responder analysis. The field of NAFLD is very used to this. We're looking at 30% liver fat content reduction, and you might say, "Why did we pick that number?" Well, that is the magnitude of effect threshold at which we begin to see histopathologic improvement, both in the NAFLD Activity Score as well as in NASH resolution. Here, you can see, 94.4% was the peak at the 1.8 milligram dose and achieved this 30% liver fat content reduction versus 4.2 for placebo. Low dose, 1.2 milligrams, 65%, which was also very good. At the high dose, 2.4, it was 85%. When we look at a more stringent or a higher degree of liver fat content reduction, still very, very good. None of the placebo hit this 40% low dose, 72 for the mid dose, and 2.4 hit 70%, achieving this 50% liver fat content reduction. Then, probably the most stringent, the hardest criteria to hit is complete normalization of liver fat content. That is defined as a liver fat content less than or equal to 5%. Remember, we're starting at a very high level of around 22% mean value on liver fat content. These patients have to fall a long way to get to less than five, and you're doing that in about half of the patients in the mid and high dose group, again, compared to none for placebo. Again, these are highly significant findings relative to placebo. If you look at the N's at the bottom, 83 patients in this cohort completed 12 weeks of dosing and had MRIs at both baseline and week 12 and were included in this analysis. This is again a responder analysis. Moving to slide 11, we're gonna shift a little bit and look at the other non-invasive test that also helps us with safety, but it also is an important predictor of response. As hepatologists, we always want to try to improve ALT and even normalize ALT. When we look at all subjects, again, you can see the different dosing arms. Just to orient you to the graph, the vertical axis is mean change from baseline, and the horizontal axis is the different doses. Placebo would be the first bar on the left at -6.2, the 1.2 milligram -11.2, and in the green bar -13.8, which is significantly different from baseline placebo or from placebo. Then the high dose 2.4 milligram -13.6, again significant relative to placebo. That's all subjects. Remember, we're starting at a mean baseline in the 30s range. Seeing reductions on an absolute scale of this magnitude are very, I think, very, very encouraging. When we look at those that actually had what we considered arbitrarily elevated ALT, and we picked 30 as that number for elevation, we can see even more striking changes because the patients actually have room to fall on their ALT. Here, a very nice dose-response relationship relative to placebo. You see significance here for the high dose group where the mean change was 27 units per liter. Now, I think it's also important to note, because I mentioned this for the PDFF response, I said 30% relative drop in liver fat correlated with improvement in underlying histopathology, and we see that ALT can do that as well. The data that we have from the FLINT trial with the obeticholic acid, it has been shown that 17 units per liter drop in ALT has been correlated with improvement in underlying histopathology, particularly the NAFLD Activity Score, and we see that being achieved at all dosing groups, 1.2, 1.8, and 2.4. Let's go to the next slide 12, and look at weight loss. Now here, we broke this down into non-diabetics, diabetics, and then all subjects. On the vertical axis is weight loss, and then on the horizontal axis, as we've shown on other slides, we have the different dosing arms. You see for placebo, very little weight loss, in fact, 0.2 in non-diabetics, 0.5 in diabetics, and overall, all subjects, 0.2. For low dose, you're seeing about a 3.4-3.3% body weight loss in the low dose, 4.9% in non-diabetics with the mid-dose, and 3.5% in non-diabetics for the 2.4-milligram dose. When we look at diabetics, it's more of a dose-response relationship. Although the numbers are smaller here, we're talking 6-7 patients in each arm. It is also important to note that whether it's non-diabetics or diabetics, there is significant differences in weight loss, particularly in the mid and high-dose groups. When we look at all subjects, comparing everybody together, there's significant differences in all the groups, and you see the change between 3.4 and 4.3. I think it's important to note here that the weight loss is what we would typically see, I think, for a NAFLD population that at least is exposed where there's a significant amount of liver fat content. In addition, it's also important to note that this population was largely Hispanic, you know, relative to other trials, and there was no lifestyle intervention brought to bear in this particular study. It is a new ground with respect to populations being studied, and at 12 weeks of treatment to see this degree of weight loss I think is very, very encouraging. Let's go to the next slide. This is the changes in serum lipids at week 12, and we see total cholesterol changes of 9%-12% in the treated groups compared to roughly 6% in placebo. No real change in LDL cholesterol. HDL dropped slightly. You see about 5% in placebo and 1%-9.7% in the treated groups, consistent with acute weight loss. When we look at triglycerides, there was a bigger reduction here relative to placebo, but none of these reached statistical significance. Let's move to safety in slide 14. I think it's important when we look at this graph to note that there are no serious adverse events. There were no SAEs, and AEs leading to treatment discontinuation were small. In fact, two patients or 4.2% and 4.3% in the two highest doses of pemvidutide. When we break down the GI tolerability, the GI side effects that you see listed here, nausea, vomiting, diarrhea, and constipation, there was more nausea, but it was generally mild in nature and again only led to treatment discontinuation in two cases. For vomiting, again generally mild, and you see that it was three cases in the low dose, two in the mid dose, and two in the high dose. When we look at diarrhea, not a lot of differences between placebo and treated on a percent-wise, 16.7% for placebo and between 4% and 21.7% for the dosing arms. When we look at constipation, a few more cases of constipation here, again, mild in nature. It's also important to note that there was no clinically significant increases in ALT in this study. Let's move to the next slide. This is blood pressure and heart rate. For blood pressure, if you look on the left-hand slide, and we're looking at on the vertical axis, again, blood pressure in millimeters of mercury. We have systolic on the top, diastolic on bottom. Each line represents a different cohort. Gray is in placebo, and the color scheme stays the same here, whether it's a bar graph or a line graph. It's important to note that the mean systolic blood pressure decreases were around 6-10 millimeters of mercury for the dosing arms compared to placebo, and a little less than that in the diastolic of 3-7 millimeters of mercury. When we look at heart rate, the mean heart rate increases, you see that on the right, were 1-3 beats per minute compared to placebo. In slide 16, we look at glycemic variables, and we break this table into non-diabetics and diabetics. On the top are non-diabetics. Across the top, you see the treatment cohorts, placebo, low dose, mid dose, and high dose. The take-home point here is there really are no changes in HbA1c or fasting glucose, compared to placebo in this relatively short time period of 12 weeks of dosing. If we move to slide 17, just to summarize, I think it's important to note that the primary endpoint of this trial was met, which was a liver fat content reduction at 12 weeks that was robust at 68%, better than or equal to the effects of other leading NASH candidates. There was a concomitant significant reduction in serum ALT despite a mean value that was relatively low compared to other trials. I believe this also points to a potential histopathological benefit, if and when we go to a liver biopsy trial. Overall with weight loss, the placebo-adjusted weight loss in non-diabetics was 4.7% at week 12, and for diabetics it was 3.9%. We look at safety and tolerability, no serious or severe adverse events and a low rate of adverse events, leading to only a couple treatment discontinuations. Overall, well-tolerated, without a need for dose titration and consistent with our prior experience. Importantly, there were no three-fold or greater ALT elevations and glycemic control was maintained. At this point, I'd like to thank you for your attention, and I'll turn this back over to the CEO, Vipin Garg. Thank you, doctor. Thank you, Dr. Harrison. Dr. Harrison will join us for the Q&A session today. Operator, can you open the line for questions and answers, please? As a reminder, to ask a question, you will need to press star one one on your telephone. Please stand by while we compile the Q&A roster. The first question comes from Seamus Fernandez with Guggenheim. Your line is now open. Oh, thanks for the questions, everybody. Maybe just a few questions for Dr. Harrison. You know, Dr. Harrison, I think what we're all trying to get a better understanding of is, you know, how you see pemvidutide lining up to other potential products, you know, as it relates to NAFLD. But also, I think you've seen a number of obviously NAFLD obese patients. Just wondering how you're thinking about these data from an obesity patient population. The second question, there is, you know, as you look at the safety and tolerability of this product, how is it lining up to some other products when we look at the data that was presented by Akero yesterday. Actually, it does look like this product is better tolerated, but obviously different patient populations. Maybe if you can just weigh in a little bit on the pace of the liver fat reductions that we're seeing here, that would be helpful. I just have a couple of follow-up questions for the team. Yeah, sure. I mean, I think. Look, in the field of NASH, we have come a long way in the past decade, for sure in the past couple of years. It's been exponential in the way we've been able to understand the disease and develop targets to hit the disease. In addition to that, we've also learned that some of our non-invasive tests can be insightful as to what we're potentially likely to see on underlying histopathology. Despite any of that, I think it's important to note that in the setting of fatty liver, just like it is with any liver disease, what we wanna do is get rid of the inciting insult. Whatever is causing the liver to be irritated, that's what usually drives the activation of stellate cells, which begin to lay down the collagen that can get the patient in trouble over time as it progresses through to cirrhosis. In, just parenthetically and maybe pragmatically, what we wanna do in liver disease is get rid of whatever the insult is that's causing it. You know, treat the C, suppress the B, treat the autoimmune hepatitis, quit drinking alcohol if that's what's causing your problem. In the setting of non-alcoholic fatty liver, it's intuitive to me that what we wanna do is get rid of the fat in the liver or reduce it as much as we possibly can. One of the ways we can measure that is the gold standard PDFF. We've seen through work done with Madrigal and resmetirom, work done with aldafermin and NGM and efruxifermin, with Akero and a few others, that if you're able to reduce liver fat content, that does link or is correlated to improvement in histopathology. The more you're able to lose, the better that effect can be. In fact, we started with 30% relative, and this was work generated from Rohit Loomba and myself with the Madrigal trial. Then we've accentuated that with other mechanisms showing that 50% is. It gives you a better shot on goal, 70% complete resolution of liver fat content. It just makes sense. The more fat you lose, the better you know the healthier the liver is gonna tend to be. That's despite knowing that liver fat content is really a neutral triglyceride, which by itself should not injure the liver, but it just so happens that, at least in my mind, when you're improving liver fat content by measuring PDFF, you're probably also reducing toxic lipid species, whether that's ceramides, diacylglycerols or whatnot. Even though we don't measure that directly. I think at the end of the day, what we've been able to show in the literature is when you do see a PDFF response, that tends to correlate with histology when histology is available. However, it doesn't mean that you can't have a histologic response if you do not move liver fat content. It's not agnostic to mechanism, but when you do see it move, we can feel good that we're likely to have histopathology change. Now, having said that as a backdrop, when we look at this particular trial, this is what I'm excited about because the liver fat content reductions are significant, but maybe more so in a short period of time. At 12 weeks, we're seeing the changes you know that I mentioned and even 50% normalization of liver fat content. We can't throw aside the fact that we're starting with a very high level of liver fat content. You know, I think you asked me, how do I put this in comparison to the Akero data? Well, I think the Akero data was very exciting. You know, when you look at the liver fat content reduction and what we saw histopathologically. That was at 24 weeks. Remember, the mean value of liver fat content was lower than it was in this particular dataset. We're starting with a higher liver fat content, and we're treating for a shorter period of time, but seeing very similar changes in liver fat content reduction. Now, what does that mean on a read-through to histology? Not sure, but it is encouraging based on the data we saw yesterday from Akero. If you also look at PDFF, if you look at ALT reduction, and I alluded to this earlier, work done again by Rohit Loomba from the FLINT trial showing 17 unit per liter reduction correlating with histopathologic improvement. We are seeing that even if we started at a lower baseline value of ALT, we see in those people that had abnormal ALTs, as defined by greater than 30, a very nice dose-response relationship in ALT response, all of them hitting that 17 unit per liter threshold as a collective group. There was a more recent paper that just came out, it's in press now, looking at the combination of PDFF and ALT reduction enhancing the probability of histopathologic response. Now, we haven't done those post hoc analyses in this trial yet, but it would be interesting to see if our patients hit both PDFF response and that ALT threshold response, you know, what percentage hit that, and would that actually continue to increase our enthusiasm for what might happen on histopathologic response. I think the tolerability question is also important because when we think about therapeutic index of drugs, it's not just the efficacy, but it's also, you know, can the patients take it? Will they take it? Is it going to be well-tolerated? Is it going to be safe? It's important to know that with all these injectables that involve FGF21 or FGF19 or GLP in any form, there tends to be some GI tolerability issues. Again, it's small numbers of patients treated for a relatively small time, but I do think that I stand behind the fact that this is well-tolerated, and to have only two discontinuations for adverse events, I think, is very, very encouraging. Long-winded answer, but you asked me a lot of questions. I was trying to wrap it up as quickly as I could. Thank you. Great. Just for the team, you know, and for Dr. Harrison, as you guys look at the prospects for the 24-week OLE, just wanted to get a sense of, you know, we have two different opportunities to see longer term weight loss data. You know, just wondering, you know, how heavily should we rely on the OLE, and the prospects for incremental weight loss in this patient population, versus really focusing in on MOMENTUM. That's the first question. Then just the second question, Dr. Harrison, you know, you sort of alluded to this with the Hispanic patient population, but in datasets, have you seen other, you know, limitations to, you know, whether it be weight loss or other characteristics when evaluating the results of, you know, drugs in this category in a Hispanic patient population? Would just be helpful to understand that a little bit better if you think that that's a point of influence. Thanks, and I'll drop it with you. Let me just answer that directly. This is Dr. Harrison again. Generally speaking, when we look at trials in general, not just NASH trials, you know, the FDA and the regulators in general have made a point that we're not really enrolling patients across the broad spectrum of ethnic diversity that we see. That's true. We tend to enroll Caucasian patients in the majority of our trials. In this particular trial, it's flipped the other way. The vast majority of these patients are White Hispanic. Just to give you an example of that, if you look at the semaglutide NAFLD trial that I was part of, and we published at New England Journal, only around 11% of those patients were Hispanic. If you look at the weight loss, for instance, in that NASH population, at the 12-week time point, you're hitting around 4.5%-5% body weight loss, very similar to what we're hitting here. The point being, we don't know a lot about if you have an ethnic diversity that's divergent from other trials, are there genetic influences that could be playing a role such as PNPLA3 or other single nucleotide polymorphisms that may impact the rate of weight loss or may impact the rate of liver fat content reduction? It's just hard to know that. The point in bringing that up is that when we look at baseline demographics, this study is different from others, and that is, it is enriched for that Hispanic population. I didn't mention this before, but I do think it's important to note here that the weight loss that was seen in our trial was linear. You know, I think that's an important point to make. The other one is, what we're seeing weight loss-wise in this NAFLD obese population is consistent with the other trial that looked at a weight loss medication in a NAFLD population at the 12-week time point. Hey, Seamus. Thanks for your question. Let me follow up on the other parts of your question. You were talking about the two 24-week readouts. The extension of the current study is not open label. It's being conducted in a blinded fashion. To be clear, it's an extension, but it's not an open label extension. It's blinded. I think the important thing to point out is to distinguish critically between the study populations. The fact that the read-through of this trial at 12 or 24 weeks is distinctly different from the read-through in the MOMENTUM trial. The patients are entirely different. There's a substantially lower proportion of Hispanics in this population. In addition, if you look at the obesity population in general, studies have shown that the average MRI-PDFF in a comparable population as in this trial is probably in the range of 7% or less. Very, very different than the 22% mean that we saw on this trial. Methodologically, it's important to understand that this was conducted as a NAFLD trial, meaning there was no diet or exercise intervention. I think it's important to realize that to understand the impact of that on the overall results is not simply a question of arithmetically subtracting the placebo response. There are synergistic effects of diet and exercise in an obesity trial that cannot be predicted by a simple arithmetic correction. The whole nature of the way the trial is conducted makes a very, very different response. We're very, very bullish about the prospects. We're seeing much better weight loss when we go to a committed obesity trial, such as the MOMENTUM trial, and read that out at 24 weeks in the first quarter of next year. Thanks, guys. I'll drop back in the queue. Please stand by for our next question. The next question comes from Yasmeen Rahimi with Piper. Your line is now open. Hi, team. Dr. Harrison, a couple questions for you. Maybe I'll go one by one. The first question to you is what is different between a NAFLD population to a NASH population to an obese population and weight loss? As you can imagine, despite really compelling data, you know, investors are a little confused why in the obese population study that Altimmune team conducted saw, you know, an 8.7 placebo-adjusted weight loss, and here we have 4.9%. Can you just really clearly outline to us? We talked about the Hispanic population and contribution to weight loss, but what else is mechanistically different in these patients that could have led to a different weight loss? I have a couple more follow-ups. Yeah. Good morning, Yasmeen. Thanks. You know, that's a great question. I think we don't have a lot of data on weight loss in a NAFLD population, at least well-defined in well-defined clinical trials. Again, I alluded to the semaglutide trial because that really is the comparison that I think makes the most sense. Again, it's early days. 12 weeks of treatment, and you're seeing the changes in body weight that we showed, which is in line with what Novo was showing in the same time period. Now, what could be the reason for that? It could be the power of the study, relatively small numbers, you know, 24 patients or so in each group. It could be the ethnic diversity, although there I can't give you a solid reason as to why ethnic diversity would play a role in, you know, weight loss percentage. I think it's all we can do is point out the differences and then continue to explore what's going on here. I do think it's also important to note as I pointed out, that the weight loss is linear at this point. Very similar again to what was shown in the semaglutide paper. I don't wanna speculate. I don't know the answer to your question completely. I just wanna point out that there are differences here that I think are potentially important. Thank you, Dr. Harrison. Just to clarify, when you say the shape of the curve is linear, are you referring to the changes when you compare week six to week 12? Given that there was not a scatter plot of weight loss, could this data be maybe impacted by some outliers? If you could comment on both of these questions for us. Yeah. Yasmeen, perhaps I should have Scott chime in on that particular question. Yeah, Yasmeen. So I wanted to point out, you know, first regarding the comparison to the earlier trial. Yes, it was a small study, but there are no Hispanics, and the average liver fat content was well below 5%. In other words, as a mean, these patients did not have high liver fat content, so a very distinct difference from the current trial. In terms of the outliers, yes, there were outliers in at least the 2.4 mg group that created some scatter in the data, and we're still looking at that. Okay, team. Thank you. Then one last question for you. I know publicly you guys have said that you have accessibility to blinded data, and this is across, you know, the MOMENTUM study as well as the NAFLD study. Looking at the placebo ranges, which end up being very, very small, are you still very confident based on what we saw this morning, that you're gonna achieve greater than 20% weight loss at week 48? Like, what does the shape of the curve look like when we go beyond, you know, 12 weeks? I appreciate any commentary you could provide us on this question. Thank you. Stephen, let me address this question. When we have done blinded looks at the data across the studies, and I wanna emphasize the limitations of blinded data, and we looked at the MOMENTUM trial, the overall weight loss that we're seeing in a blinded fashion is much more similar to the original study than in this study. Again, it's blinded data, but just to be direct to our investors, we think that what we're achieving based on that blinded look in MOMENTUM is similar to the first study and not the study that we're discussing today. Okay. Given that, we think that, the prospect of achieving 20% weight loss at the end of the year in the MOMENTUM trial is very, very good. Okay. Thank you, team. I'll jump back into the queue. Please stand by for our next question. Our next question comes from Roger Song with Jefferies. Your line is now open. Great. Thank you for taking the question. A lot of questions already being answered. Maybe just to clarify a few things here. First, just curious about the weight loss kinetics here. Maybe just to clarify how this kind of before the trial week, the weight loss starting looking at. Also I think, Scott, you mentioned earlier, maybe just to clarify how this data changed your expectation for the weight loss at the later time point, 24 and the 48 week. Granted, you have slightly different populations here. Yeah. Thanks, Roger. As Stephen mentioned, the kinetics were linear in the dose groups. This is the pattern or the trajectory that we saw in the data from the first study. We suspect that it will remain linear for some time. It could remain linear all the way out for many, many weeks. Without having that data at this point, I can't comment on where we're gonna land. In terms of the expectation for 24 and 48 weeks, for the MOMENTUM trial, we remain very bullish. As I mentioned before, this population, this was conducted as a NAFLD trial in a NAFLD population that not only had high liver fat content, but had a close to 80% mainly Hispanic population. We don't know what the impact of that is. Very, very important, the absence of diet and exercise may also have had a very, very important effect. Again, as we look at the blinded data across the three studies, the MOMENTUM study, which is the 48-week obesity study, looking at the blinded data looks much more similar to the data from the first study than this study. It suggests that this study is an outlier because of the differences in populations that have been described. Consequently, we remain bullish about hitting those targets in the MOMENTUM trial. Scott, this is Dr. Harrison again. Let me just add. You know, at the end of the day, I'm speaking from a NASH perspective. You know, this is a NAFLD study, right? It's not an obesity study. It's a study looking at obese NAFLD patients. I don't think we should lose sight of the fact that what we were measuring here, the result was very positive. I mean, the liver fat content reduction that we're seeing is highly significant and relative and is associated with significant changes in serum liver chemistry tests like ALT. You know, for a short trial duration of 12 weeks, to be able to achieve this degree of liver fat content, this degree of drop in ALT when our mean values are relatively low to begin with, is very, very positive. You know, the weight loss that was seen here is also important. I think it's important to note that this population of patients, as you alluded to, is different from a standard obese population. Really, what we were trying to look at in this trial was change in liver fat content, which was significantly improved. I just don't wanna lose sight of that, 'cause to me, that's the intent of this study and that's what we showed. Got it. Yeah. No, that's clear now. Thanks for all the comments. Another point I wanna ask is the serum lipid reduction. As we remember for the phase I-A in overweight study, you see 30%-40% kind of serum lipid reduction across different LDL and triglycerides and the total cholesterol. This trial seems kind of a lesser degree. Maybe just contextualize this, is that also due to the baseline kind of the NAFLD patient population? Sure, Roger. This is Scot Roberts. You know, I think there's a couple of aspects that we're thinking about when we look at the lipid response here. I mean, overall, I would say it's very good, right? We have significant reductions in triglycerides, 40%, you know, approximately. Total cholesterol is also down, you know, 10%-12%. You know, the LDLs seem to be a bit less than what we saw in the 101 study. When we think about what might be behind that, I think there's two things. One is this idea that this patient population is really very differentiated from the 101 for the reasons we've already talked about, primarily high liver fat content, possibly also a demographic effect there. That certainly has to be, you know, contemplated. I think the other issue is that there's a kinetic thing here, that we've reduced the fat in the liver significantly over this period of time, and maybe some of these lipids are lagging a bit. I think that the 24-week data will be very interesting to take a look at the, you know, the lipids and see what they're doing at that point. Got it. Okay. That's great. Maybe just the last one for the team from the company is since we're getting this very significant liver fat reduction, understanding you're focusing on obesity, for the phase II, so what is the plan for the NASH moving forward? Yes, Roger, this is Vipin. Just, look, we continue to look at both of these indications. We're very bullish on the obesity indication. Based on this data, you know, we have to look at the 24-week interim analysis in the first quarter, and that would really guide us which way to take this program. We've always said that the purpose of this NAFLD study was to create the foundation for NASH discussion, and I think we have that now. I think it's gonna help us in our strategic evaluation of the program overall as to where we take it from here. This combined with the 24-week interim results would really guide us whether to pursue both indications or continue pursuing obesity over NASH. We'll figure that out once we have all of that information. Excellent. Thank you. That's it from us. Congrats on the data. Please stand by for our next question. The next question comes from Liisa Bayko with Evercore. Your line is now open. Hi there. Thanks for taking the question. Dr. Harrison, could you maybe comment on the magnitude of impact of diet and exercise that you would expect in a study of this duration? I mean, if diet and exercise had been kind of overlaid here, you know, I guess what kind of additional benefit do you think we would see just based on your historical understanding? Yeah. Hey, that's a good question. You know, I think probably around 2% or so additional, if you look at historical studies that have, you know, kind of overlaid lifestyle modification on top of therapy. That'd be, you know, that roughly something around that range. In the first 12 weeks, is it that 2% or is that more over a year or? No. I mean, when we look at least in my experience, when we look at weight loss, there's what I call a smile curve in clinic. That is, you tell people to modify their lifestyle, you know, cut the carbs, exercise more, decrease their total calorie intake, cut out the sweetened beverages. People are highly motivated at first, and generally maximum weight loss is achieved by around 12 weeks, and then they tend to gain it back over the next 12 weeks. When we see weight loss changes in clinic, it tends to be relatively early. Uh. My guess is that would be in the first 12 weeks or so. Liisa. Liisa, this is Scott. I'd like to add to Stephen's response. We think that diet and exercise is particularly important in the first 12-week periods. If you look at the placebo curves in studies with diet and exercise, the effects always occurs in the first 12 weeks. Also, you know, let's get back to the concept of the speed of the weight loss and the momentum, not a pun on words, maybe because our trial is named MOMENTUM, but the momentum that's gained by having that rapid weight loss early is a positive feedback to the patient to get more exercise, to put down that second serving or the like. We think that of all things, that diet and exercise intervention is extremely important. It accelerates the weight loss, it gives better effects, better patient participation, buy-in, and encouragement. You know, as I said before, it's difficult to say that you can just simply subtract the placebo, and get a number called placebo-adjusted. We think it has a big impact. We think that methodologically, to really understand the effect in an obesity population in a trial conducted the way obesity trials are conducted, you need to have that diet and exercise intervention to actually understand what's happening over the course of time in the population and the response to the drug. Okay. I noticed in the study, and I don't know if this is just a function of small numbers, but you know, the diabetic patient population didn't really have the typical like, you know, we kind of described it as about a 30% discount in weight loss, and it seemed a little bit less than that. In fact, on the higher dose is actually higher. I don't know if this is just a function of small numbers or do you think there's something mechanistically that would make sense to explain that differential? Yeah. Liisa, let me take that one as well. I think it's really a question of the small numbers. Okay. You know, you can look at the data different ways. You could say it's comparable. You could say it's less. You have to look at different dose groups. You have to subtract the placebo. Is it the right placebo to subtract from each dose group? We can say in general that it's probably less. We don't know how much. It may be comparable. It's tough with small numbers. I think if you just take a general average across the groups and placebo-adjusted, it's about 30% less. You know, again, there's a lot of wobble in those numbers. Okay. Dr. Harrison, can you maybe comment on the tolerability? How does the tolerability here look relative to some of the, you know, the other drugs either in development or already approved? Sure. I mean, I think from a tolerability perspective, it is, if you look at it relative to other injectables for this disease indication, I'm focused on fatty liver and NASH. It's well-tolerated. I mean, you see, majority of these adverse events are mild and very few discontinuations as a result of that. You know, comparatively speaking, I think it's well-tolerated. Relative to obesity drugs? You know, I'm not as certain, you know, that's not an area that I focus on routinely. For NASH, yes, for sure. Yes. Liisa, let me fill in on the obesity. You're generally seeing with obesity drugs adverse event discontinuation rates approaching about 10%, and this is lower than that. You know, we and by the way, they're achieving that with dose titration. We're not using dose titration, and if anything, we think that these results are strong confirmation that dose titration is not needed with pemvidutide. That's a big improvement over other drugs that are titrating out to you know, four or five months. We think the adverse event profile, even if comparable, though we actually think it could even be better, is strong confirmation that the absence of dose titration is a real possibility with these drugs, especially as we move to obesity. Even with the 2.4 mg? I know you dose titrated in this study. Yeah. That's a little harder to say for that reason. Okay. Absolutely. You know, you kind of try to find the sweet spot here. You know, the 1.8 milligram dose appears to be the best in this trial, also like the 101 study. If you kinda focus on you know, we're not seeing a better response to 2.4. It's not convincing and maybe not. If you focus on the 1.8 milligram dose, you look at the tolerability there, you know, it's very acceptable based on the adverse event discontinuations. We stand behind the second confirmation, the second trial confirming that GLP-1 based agents with the proper agent, with the proper kinetics, with the proper medicinal chemistry do not have to be dose titrated, and that's in stark contrast to other drugs in the class. Okay. Just final question, and then I'll let you move on. I guess I'm just wondering about like, the effect of higher BMI and higher baseline weight. It seems like that's a major factor we've seen in other studies that this can be a variable that leads to you know, lower weight loss. Do you think that was an impact here? You know, we are seeing lower weight loss in the, obviously, than in the first study, and there is a considerable difference in baseline BMI and baseline weight, which is probably more comparable to the other. Now to the other, weight loss drugs in the mid, you know, for BMI in the mid-thirties. Do you think that's, you know, another big factor here? Thanks. Yeah, thanks, Liisa. Great question. The short answer is no, we don't think it's a factor. For several reasons. Number one, if weight were a factor when you got to the higher dose, we should have seen a better effect. The reduction in weight loss with drugs when you get to the super obese and the heavier people is that their serum concentrations drop, and that leads to less body weight. That's been in the public domain for semaglutide and the FDA comments and their review of the drug. We're seeing levels of exposure here that are comparable to our initial trial. Very, very importantly, if you take the exposures and you line them up in this study versus the first study, at the same exposures, we're seeing less weight loss. It's not a question of exposure. We wanna make that clear. There's something different about the populations, such that given the same exposures between this study and the first study, we're seeing different weight loss, and that's probably related to the study population. I mean, that's the only explanation that we can come up with, really, at this point in time. We wanna point out, to follow that, Liisa, that the MOMENTUM study population will be different from this population. It'll look like the population in the first human study. Therefore, we expect the exposures that we will achieve, which we're hitting both in this study and in the first study, but also in the MOMENTUM study, will lead to the weight loss that we saw in the first study because of the similarity in the study populations, which is causing a disconnect in the exposure response. Okay. Thank you. Please stand by for our next question. Our next question comes from Mayank Mamtani with B. Riley. Your line is now open. Good morning, team. Thanks for taking our question. Maybe first hearing Dr. Harrison's perspective on the, you know, drug's mechanistic contribution on diet intake versus energy expenditure, given, you know, the dual mechanism here. I'm just curious, Dr. Harrison, are there markers that delineate sort of the non-clinical measures of, you know, just relative impact of those two phenomena on kinetics, et cetera? 'Cause to your point, you know, sema weight loss, semaglutide weight loss in phase III across NAFLD and obesity, you know, can't really be compared 'cause of, you know, the dose differences and treatment duration, but it does look kind of comparable. Then kind of a second part question, do we know of other glucagon-mediated programs or glucagon targeting drugs where we kind of know of the kinetics for glucagon, you know, beyond 12-24 weeks? Hey, Mayank. This is, Scot Roberts. You know, I think, you know, we're looking at this continually, you know, and obviously, you know, thoughts include the ones that you're alluding to. You know, I think that the rapid defatting of the liver, which I think everybody associates, you know, with glucagon because you just don't see that with the indirect effects of, like, for example, semaglutide. You know, we're seeing that, right? We're seeing that in spades. You know, with 70%, nearly 70% reduction in just 12 weeks. You know, that's not where we're at right now. We think that there's a, you know, a metabolic insensitivity that characterizes this patient population. It's related, we believe, to the, you know, high amount of liver fat and possibly also demographics. You know, we're looking at it a little bit more holistically when we look at markers. I think that the liver fat, the rapid liver fat reduction is the sort of biomarker that you're talking about, for example, and that looks like it's working extremely well. You know, we're gonna continue to think about this and to try to understand how this population differs from 101 from our first in human and the Momentum study that's coming up. We're convinced for the reasons we've talked about already, that it is quite distinct and that gives us confidence in moving forward with the obesity. Mechanistically, and I understand that's where you're trying to go with this, you know, I go to the liver fat reduction and say things are looking good there. Okay. Maybe just staying on that point of liver fat reduction and also ALT and you know putting also in context what we saw with the Akero data yesterday. Like, just can you comment on, like, if there is a hypothetical phase II-B NASH study, you know, what size and duration would look like? You know, just your updated thoughts there. Then, maybe also if you're able to, just process questions, when will we be able to see the patient level disclosure from this NAFLD study, like kind of how you guys did for the earlier phase I study in a very transparent way? Then, on the hyperglycemia kinetics, you know, could you just comment on specifically that cohort, you know, diabetic cohort where you did have some fasting glucose and HbA1c data. Just, do you have those sort of kinetics between 0-12 weeks data and kind of when can we see that? Scott, do you wanna take the hypoglycemia or sorry, the diabetic question? Yeah. Mayank, you know, we have that data. It just kinda looks flat. You know, we just thought that the summary data at week 12 was a lot easier to understand. No, we're not seeing excursions of glucose. Hemoglobin A1c is only measured at week 12. I think the important thing to recognize as our base case was that we would not see a change in hemoglobin A1c or any glucose homeostasis at week 12. Similar to the 101 study, that's pretty much what we saw on this study. We wanna emphasize that as further weight loss will occur, we think we're gonna see the 24 weeks. We'll probably end up seeing that, we could see it in both studies, but certainly in the MOMENTUM study, although the MOMENTUM study doesn't have diabetics. We think we're gonna see general improvement of hemoglobin A1c over time. Yeah. Mayank, with regards to your other question, I mean, look, we will continue to focus on our strategy as we have laid out so far. You know, we are proceeding with our Momentum study. We wanna see that data. We're not speculating right now what we're gonna do on a NASH study. We'll have plenty of time to evaluate that. We'll look at all of the data and wait for the 24-week interim data from the obesity study. We'll stay tuned. We'll talk more about it as time progresses, but right now our focus is our strategy is the same as it's always been. Drive the obesity program. We don't, you know, we see that there's significant value in that, and then we'll evaluate our strategic options with regards to NASH, or further NASH studies. On the patient level data disclosure, will we get that sort of after your 24 week data, I guess? Will that be within this year by any chance? That's right. I mean, the 24-week data, as we have said, we'll have it in the fourth quarter, and that's when we'll have the full study readout. Obviously there'll be a number of conferences coming up that we'll be participating at. I would also. Thanks for the. I would also note, Mayank, that we're planning to submit a late-breaking abstract to the AASLD meeting, so it'll be a better opportunity to see all of this data in that meeting in November in Washington, D.C. Okay. Looking forward to that. Thanks for taking your questions. Please stand by for our next question. Our next question comes from Patrick Trucchio with HCW. Your line is now open. Thanks. Good morning. Just a few follow-up questions from me. You know, it's the understanding that the NAFLD study and MOMENTUM study are in different population and have different endpoints. I'm wondering if there's any predictors of either response or, you know, GI intolerability that have emerged from the NAFLD study that would perhaps impact involvement of patients in the MOMENTUM study or if, you know, the baseline characteristics of those patients that have already been involved would be consistent going forward in the MOMENTUM study. Right. So Patrick, the MOMENTUM study population looks like the cross-section that we've seen, and we haven't finished the randomization. We will very shortly. You know, it will occur this month, as we promised before. We anticipate that population will look like the classic obesity population in terms of BMI, body weight, and also low liver fat. As I said, if you do MRI-PDFFs in the general obesity population, you see average MRI-PDFFs of 7% or less. You know, we think that the tolerability profile between the first study and the NAFLD study are remarkably similar. I would anticipate that that would also continue in the MOMENTUM obesity trial with good evidence of tolerability sufficient not to have to rely on dose titration. Got it. Then, maybe just a follow-up. You know, this was, you know, addressed earlier, I think. Just if you could elaborate a bit more on why, you know, some measures like ALT reduction and weight loss in diabetic patients, there did appear to be more of a dose response on some of these other measures. There wasn't. I'm just wondering, and I know, you know, you alluded to this earlier, but if you could just kind of maybe talk to those specific measures specifically. Yeah. You know, Patrick, with low numbers, it's a bit difficult to, you know, make strong statements about dose titration. We think there's variability between the groups. Remember that there are only about seven subjects in each of the diabetes groups. So consequently, one outlier changes the means very greatly. So I would encourage you not to look at the dose response in the diabetic population. You know, all in all, it looked like 1.8 was doing at least as well as 2.4. Remember that 2.4, however, was titrated for the first four weeks, although two of those weeks were at 1.8 milligrams. So the question is, did we lose some effect from the first two weeks at lower doses, and we'll see that better in the 24-week data? We really don't know. At this point in time, the way we interpret the data is that the 1.8 milligram dose appears to be the best at this point in time. That's remarkably similar to the first study, but we'll continue to explore 2.4 to see if there's any additional benefit, especially in patients who are heavier who might need higher exposures. Got it. Thank you. Please stand by for our next question. The next question comes from Yasmeen Rahimi with Piper. Your line is now open. Hi, team. Thanks again for the follow-up question. Dr. Harrison, did you measure any type of fibrotic NITs in the study? Do you feel now, based on the data we saw yesterday from Akero, that really the greater the fat reductions and defatting of the liver occurs, the greater is the propensity to show both NASH resolution benefit, but also fibrosis benefit? If you could just clarify both of these for me, that would be great. Thank you. Yeah, sure. Yes. You know, in reference to your second question first, I do think the totality of the data that we're generating on these specific non-invasive tests do point to the fact that the higher the liver fat content reduction, the greater the probability that you'll impact underlying liver disease, not just the components of NASH or NASH resolution, but ultimately on fibrosis as well. You know, you and I have talked a lot about this before. It's important to realize that. Again, this is just my opinion. The components of histology that we focus on in NASH, steatosis, inflammation, ballooning, and fibrosis, in my opinion, are all very dynamic and can move relatively quickly. Whether you look at the aldafermin data, the efruxifermin data, or any other data set where we've done early liver biopsies, we've been able to show changes in fibrosis, not just changes in steatosis inflammation or ballooning. Interestingly, if you look at some of the post-hoc work done off of the Madrigal trial data, when you achieve significant liver fat content reduction, that's, you know, in the super responder range, we are beginning to see, you're beginning to see changes in fibrosis. You know, we haven't done post-hoc correlations with liver fat content in the efruxifermin data, to my knowledge. It would make sense that, you know, given the robust changes in fibrosis there, that's likely correlated with keeping that fat reduction. I think at the end of the day, the more fat you lose, the better off your liver is gonna be, and I think those changes can occur relatively quickly. In response to your first question, we do not have that data relative to things like PRO-C3 or ELF in this small data set, to my knowledge. Let me comment on that. We do have markers of fibrosis. We haven't presented them in this presentation simply to concentrate on the metrics that we have. We are planning to present that data at the AASLD when we submit the late-breaking abstract. Okay, great. Thank you, team. Please stand by for our next question. Our next question comes from Jonathan Wolleben with JMP. Your line is now open. Hey, thanks for taking the question. Just hoping you could comment on your overall thoughts on the profile for the 2.4 milligram dose and the effects of the titration. Do you think that's necessary, or do you think the 1.8 is giving you everything you need so far? Yeah. Hey, Jonathan, good morning, and thanks for the question. Yeah, that's a tough one at this point. I think based on just the data from this study, the 1.8, again, looks like the sweet spot. I'm not sure we're seeing any additional benefit of 2.4, although we take a little bit of you know, we lose a couple of weeks early on 'cause doses that are probably less effective. We don't know. Let's take a look at later time points. I think certainly that 24-week readout and the MOMENTUM interim analysis is gonna be really important. I think the preliminary answer is that we've hit it with 1.8. You know, getting back to the idea of higher body weight and BMI affecting this, we're not seeing this, because if we are, we'd have a better response at 2.4 milligrams, we think. We think we're hitting the exposures that we saw in the 101 study, and that the difference is not the exposures. It's not the body weight. It's actually the biological response to the drug for some reason, probably for the factors that we've talked about before. The short answer is that we don't think the 2.4 is necessary, but let's just see the rest of the data. Yeah, I would just add that even if we take it forward, there is a real chance that we don't need to do titration on 2.4 either. We just did a short titration. Going forward, if we continue to include 2.4, we'll definitely include an arm that does not have titration. We think, you know, 2.4 also has a real chance of being a successful dose without the need for titration. Got it. Maybe one for Dr. Harrison. We hear a lot about the associations between liver fat and histologic response, but how well do we understand the kinetics or the lag time between, you know, reducing liver fat and when something could show up on a biopsy in terms of NASH resolution or fibrosis improvement? Just wondering, given how quickly we're seeing the liver fat improve here versus, you know, standard time points for the longer NASH trials. Yeah, that's a. You know, we don't really know the answer to that yet. One of the things that we're focusing on now in the NASH field is the kinetics of response. In other words, if you have week four PDFF or week six and week 12 and week 24, you know, if you hit a magnitude of effect, let's say you hit the 30% relative change at week four, does that give you a better shot on goal of histology improvement compared to somebody that, say, hits that at week 24? What we do know, from at least the aldafermin data, where I did liver biopsies at week 12, and I have PDFFs, as well, is that, you know, there is significant liver fat content reduction. There was significant improvement in the NAFLD Activity Score, and there was fibrosis improvement that was seen at that early time point. That kinda gets me back to my original comment that said, you know, I don't think that's sampling variability because the NITs all moved in a very positive direction. I do think that all the components of NASH to include fibrosis are dynamic and can change relatively quickly. Whether or not we could use PDFF to predict the time of that change, I think is still unknown. That's helpful. Thanks for taking the questions. At this time, there are no more questions in the queue. I would now like to turn the conference back to Vipin Garg for closing remarks. Thank you, everyone, for participating today. Have a nice day. This concludes today's conference call. Thank you for participating. You may now disconnect.