Morning. I'm Adam Jolly. I'm an associate on Tim Anderson's U.S. Biopharma team. This morning, I have the pleasure of introducing Dr. Tien Lee of Aardvark Therapeutics. He's the founder, chairman, and Chief Executive Officer. Without further ado, I'll turn it over. Thank you, Adam. Appreciate it. All right. Can you all hear me? All right. Great. Great to be here today and have the opportunity to talk about Aardvark. Let me advance the slides. It's not working to advance. Can you—sorry. Can you advance the slide for me, if you don't mind? Yeah. Aardvark, ticker symbol is AARD, a publicly traded company based in San Diego, California. We have a drug that is an oral small molecule drug that targets bitter taste receptors or attached to ours. By virtue of that, we can invoke gut-brain signaling pathways to abrogate hunger as opposed to appetite, and more on that later. I just want to go all the way to the beginning. Thank you. Okay. Great. We have several clinical programs. Our most advanced program is in Prader-Willi syndrome, which is a potentially pivotal phase III program that's currently ongoing with expectation of readout top of 2026. We also intend to initiate a phase II program for hypothalamic obesity and other rare conditions, as well as advancing another formulation, ARD-201, for general obesity. In that case, we're looking to look at comparative benefit of muscle preservation versus GLP-1, additive effect on top of GLP-1, and also protection from weight regain when one is off of GLP-1. This is our executive team. We have a very well-seasoned team with experts in clinical regulatory and business development. The core to our story is the dichotomy of appetite and hunger. A lot of folks might not conceptualize that as anything more than two extremes of the same condition, but they're really two different drivers that regulate eating behavior in your brain. In general, appetite is a pleasure-seeking drive. Your brain's trying to chase something positive, whereas hunger is a pain-avoidance drive where your brain's trying to get away from something uncomfortable. The best way to really walk through this in terms of conceptually is that if you like ice cream, for instance, appetite is compelling you to eat that ice cream. If it were to turn to dog food, for instance, then your appetite would go to zero, and appetite would not drive you to eat that. If that was all you had to eat, given enough time, hunger would compel you to eat that dog food. We believe GLP-1 drugs are primarily anti-appetite pathway drugs. They diminish the appeal of food. They're concordant with nausea. Naturally, your body co-secretes GLP-1 and CCK to mediate satiety across these two axes. CCK is a target that is really not amenable for systemic targeting. Our drug, by virtue of its gut restriction and invocation of gut-brain CCK, is able to get at anti-hunger through this gut-brain pathway to mediate hunger through the brainstem. The downstream reflection of this is through the diminishment of ghrelin, which paradoxically increases with GLP-1 treatment. In our case, we're driving down ghrelin. It's complementary to GLP-1, works in a different pathway. We believe there are conditions where hunger is more represented than appetite, which represents the conditions that we are initially targeting, including Prader-Willi syndrome. To kind of differentiate our approaches, our single agent is for rare disease and mechanistically valid. We think CCK deficiency is also a driver for a lot of the manifestations of Prader-Willi syndrome. For general obesity, we also believe that we have other benefits conveyable through our drug's MOA, including normalization of a number of metabolic indicators of metabolic syndrome as well. To kind of summarize our clinical strategy, I mentioned that we are ongoing with our Hunger Elimination or Reduction Objective- HERO trial, which is in Prader-Willi syndrome. I will step through that in a later slide. Hypothalamic obesity is a phase II trial that we intend to initiate later this year, as well as that general obesity trial, which I mentioned all the desired endpoints for that study. Going through the Prader-Willi syndrome indication, there are anywhere upwards to 10,000-25,000 patients in the United States. It is a 1 in 15,000 occurrence rate for live births across the world fairly consistently, which is giving rise to an approximation of 350,000 or more patients worldwide. There is an approved drug currently on the market for Prader-Willi syndrome, but we believe there's still a lot of unmet medical need available for this indication. For our drug, we've completed phase one and several phase IIs in different populations, including in Prader-Willi syndrome. Overall, we've had over 70 patients that have been dosed ARD-101. We have not seen anything more than a grade 2 AE across our studies. We've seen very compelling signals of effect in our phase II, which really motivated us to conduct this phase III that is now ongoing. To step through the data we've had to date, we've had 18 patients in Prader-Willi complete dosing in a relatively short 28-day dosing period. At a time when the company conducted these studies, we were only permitted to dose for 28 days. Since that time, we've now completed our nine-month GLP-12 studies that theoretically should allow us to dose indefinitely. The chart on your left denotes the first 12 subjects that completed dosing at a lower dose of 200 milligrams b.i.d. You see that there's a withdrawal period too that's shaded, and that's the assessment of their HQ-CT or hyperphagia score, two weeks off of drug, which reflects concordance that the patients were deriving benefit during the dosing period. We had an average of - 9 reduction for the patients that were measured with the HQ-CT 9, which is the validated endpoint for Prader-Willi syndrome. I want to emphasize again, this was actually within the relatively short dosing period of 28 days that this was achieved. We also saw very encouraging anecdotes of patients leaving food in their plate, having a really strong resolution of their hunger. Other clinical features of Prader-Willi that we believe are driven by deficiency of endogenous CCK release, including anxiety, inflammation, and gut transit, we believe are also potentially addressed with ARD-101. On the right, you see the six patients that were dosed at the dose escalation cohort. This is six patients that were treated with 400 milligrams b.i.d. for one week, then 600 for one week, then 800 twice a day for the remaining two weeks. A rationale for this is that one of the observations was that patients that tended to dose their drug in between meals had a better effect. There is a potential food dilution effect. An 800-milligram dose allows a buffer for accommodating those types of issues. You will see another line here with patients that were included that were off protocol. There were two subjects that had different raters for HQ-CT, which is something that's generally not permitted for consistency. We left that data in there so you can cross-reference. We see a consistency of signal across both of these studies, as well as a rebound effect off of drug, which is something that you'd expect if the drug were conveying an effect during the dosing period. Also wanted to zero in on what the effect size is. Again, only 28 days. We saw an average of -30% reduction on the HQ-CT, which we think not just the absolute value, but the relative reduction. It was very dramatic in a competitive space. If you actually look at the patients with similar features as what we anticipate in terms of the inclusion and exclusion criteria for phase III, those subjects had a -48% reduction in their HQ-CT during the dosing period, which encourages us that we have a high probability of success going into our phase III. Our phase III trial is a traditional design. We'll have a screening period and a reassessment of screening to accommodate for any variation in their baseline. Then we'll have a treatment arm with ARD-101 and matching with placebo. It'll be randomized. The assessment of HQ-CT at week 12 will be compared to the baseline for our primary endpoint. We're also looking at secondary endpoints of clinical global impression, DEXA scan for body composition, inflammatory biomarkers, ghrelin, and a number of other parameters where we hope to delineate and show the drug's effect in this population. These patients will be offered open-label extension with optionality in the future, perhaps to run a randomized withdrawal study. This is something that we're not necessarily counting on because we're looking at the prospect of design to be the potentially pivotal endpoint for us. I just want to walk quickly about the hypothalamic obesity program. Hypothalamic obesity is an acquired condition, often a result of interventions for craniopharyngioma. Results in treatment of that leave many patients with an overactive hunger. Mechanistically and neurophysiologically, there are a lot of similarities with Prader-Willi syndrome. Prader-Willi syndrome is, in fact, sometimes referred to as congenital hypothalamic obesity. There is a lot of clinical features that overlap. Also, in Prader-Willi syndrome, there is also a smaller hypothalamus size anatomically versus normal individuals at the time they first manifest their hyperphagia. In addition to this, we're encouraged by the logic of using our drug in this space because there's previous clinical data from others showing the benefit of serum CCK to abrogate overeating in hypothalamic obesity. As far as our 201 program for obesity, this is our fixed dose combination with the DPP-4 inhibitor. The combination potentiates the activity of ARD-101 alone. We believe it's a much more potent formulation. However, the inclusion of the DPP-4 inhibitor makes it incompatible for use in Prader-Willi because that introduces risk of gastroparesis, but mostly for that population. That shouldn't be a problem for the majority of other patients that we intend to deploy ARD-201. This is just data denoting the benefit of adding that DPP-4 component on top of ARD-101. This is preclinical data. On the left, you see more preclinical data that suggests that we can lower LDL cholesterol and hemoglobin A1c. This is also reflected in their clinical experience. We had a randomized placebo-controlled phase II study in general obesity patients, and we saw signals of reduced LDL as well as reduced hemoglobin A1c in the patients with elevated parameters. Looking also at that obesity phase II study that we had conducted in the past, again, to underscore the relevance of anti-hunger, self-reported hunger scores from patients versus placebo, we saw a statistically significant reduction in self-reported hunger. This is also reflected in lower serum ghrelin. We measured it two different ways. In the middle chart, you see patients were fasted overnight, skipping breakfast. The placebo group had increasing ghrelin, but it was flat in the 101 group. Again, comparing day 28 to baseline, there was a lower ghrelin level relative to baseline. This is something that is not generally seen with GLP-1. In fact, GLP-1 is associated with an increase in ghrelin, and our drug is decreasing ghrelin as a downstream effect of this gut-brain CCK engagement. The schema for our EMPOWER study is a general obesity study. We'll have multiple arms in part one. The purpose of this trial is to, number one, show additive benefit on top of GLP-1 because we think that these approaches are orthogonal in nature and not mutually exclusive. I want to underscore that our drug is 99% gut-restricted, which is normally not a feature that is a favorable one for most drugs. The target of our drug is in the lumen of the gut. It works because it's gut-restricted. By virtue of its gut restriction, it elevates the safety assurance of the drug because it's anatomically restricted. It's potentially additive to lots of different therapies. We want to show additive effect on top of WIP1. We want to show a better quality of weight loss with better lean body mass preservation versus WIP1, which we have confidence that it'll be reflecting our preclinical data that suggests this is part of the MOA of our drug. In part two, there'll be patients that are bridged off of WIP1 with expectation of rapid weight rebound. We think based on the mechanism of our drug, it will protect from that weight regain because patients that do not have hunger as their primary driver for overeating generally start having elevated hunger as they are on WIP1 for a while. That basically feeds into the MOA of our drug. The second part of our trial, we are very optimistic that we can show protection from that weight regain that is typically seen. In summary, Aardvark is targeting an orthogonal approach to GLP-1, targeting hunger pathways. Our lead asset is strategically deployed. We are in a potentially pivotal phase III trial now. We have historic data that gives us confidence of our probability of success moving forward. There will be multiple readouts in 2026, including the phase III HERO trial and then top-line readouts of those two phase II programs in hypothalamic obesity and obesity that I mentioned earlier. I think I'm exactly out of time. I figure I made it into the wire. All right. Any questions? I can always have a sidebar with anybody that wants to speak after the presentation. Thank you.