I'm Michael Tung, Chief Financial Officer of vTv Therapeutics, and I'm joined today with Dr. Thomas Strack, our Chief Medical Officer. vTv is a late-stage biopharmaceutical company focused on metabolic diseases. Our lead program, cadisegliatin, or KADI, is a potential first-in-class oral adjunctive therapy to insulin for people living with type 1 diabetes. Today, we'll walk you through the opportunity. Before we begin, please note that today's discussion contains forward-looking statements. A full description of the associated risks can be found in our SEC filings. All right. Let me quickly frame the vTv investment thesis. Our lead asset, cadisegliatin, is in phase III development as a potential first oral adjunctive therapy for type 1 diabetes. Top-line data from our CATT1 trial is targeted later this year, a near-term value-creating catalyst. The unmet need is substantial. 75% of people with T1D in the U.S. fail to achieve the ADA or American Diabetes Association recommended blood sugar target of hemoglobin A1C less than seven. Hypoglycemia is the major limiting factor in achieving optimal blood sugar management. Our management team has a strong track record of advancing novel therapies for metabolic disease and diabetes. We are well-capitalized to execute. We ended third quarter 2025 with approximately $99 million in cash and raised an additional $20 million this past February, providing runway well past the CATT1 readout. Beyond KADI, we have a pipeline of clinical stage programs in inflammation, metabolism, and oncology, which represent sources of potential non-dilutive funding. In short, we have a late-stage asset, a near-term catalyst, and the capital and team to deliver. This slide illustrates what it's like to manage type 1 diabetes every day. We use the metaphor of driving a fast car on a narrow, dangerous mountain road. If your blood sugar runs too high or hyperglycemia, you're scraping the car against the cliff wall on the left. The damage is gradual but cumulative, and over time, you can get the long-term consequences of hyperglycemia, such as neuropathy that can lead to amputations, retinopathy that can lead to blindness, and cardiovascular disease, just to name a few. Drive too far on the other direction on the right, and you risk hypoglycemia or potentially crashing the car. You basically encounter potential immediate neurologic damage. When your blood sugar gets low, you can get confusion, potentially fall into a coma, and it can actually, if low enough, it could actually be life-threatening if severe. Every person with T1D is navigating this trade-off every single day. What they need is a therapy that acts as a guardrail on both sides of the road, one on the right to prevent hypoglycemia and one on the left that could prevent hyperglycemia, and that's what we're working towards with cadisegliatin. The challenge, lowering blood glucose to target while preventing hypoglycemia. What you can see here is a representative seven-day continuous glucose monitoring tracing. What you can see is there are a lot of highs and lows. This is representative of insulin's narrow therapeutic window. Too little insulin, the glucose climbs. Too much, and it drops. Even with the most advanced technologies, such as CGM, calculating the right dose of insulin to stay in the proper range is extraordinarily difficult. One other thing to note, CGM sensors actually sample the interstitial fluid. After a meal or at other times of rapid blood glucose change, there can be a five to 15-minute lag versus a blood glucose measurement. Insulin is a life-saving medicine, but given its narrow therapeutic index or window, it was not designed to solve this program on its own. We believe cadisegliatin is a large opportunity in a long-underserved market. First, scale. There are approximately 1.5 million Americans living with type 1 diabetes, and that number's growing. There are 10 million people globally, and that number is expected to grow to 15 million by 2040. The burden is real and immediate. 75% of T1D patients fail to achieve American Diabetes Association glycemic targets of hemoglobin A1C of seven or below. Hypoglycemia is common. Most patients experience several mild to moderate episodes per week, and severe events can be fatal. In the 100 years since the discovery of insulin, there has been no oral adjunctive therapy for type 1 diabetics ever approved in the U.S. The only advances you have are new forms of insulin and new ways to deliver it. Pens, pumps, fast-acting insulin, short-acting insulin, it's all still insulin with its inherent narrow therapeutic index. Cadisegliatin has the potential to address a critical gap in a long-overlooked market. Our solution is cadisegliatin, a novel glucokinase activator with the potential to become the first oral adjunctive therapy to insulin for type 1 diabetes. KADI has been studied in multiple phase I and phase II trials in over 500 patients, and it's demonstrated a strong safety profile with clinically meaningful reductions in both hypoglycemia and hemoglobin A1C when added to optimized insulin therapy. Importantly, KADI has received FDA breakthrough therapy designation. This designation is reserved for therapies targeting serious conditions with a meaningful clinical advantage over existing treatments. This underscores the unmet need and supports an expedited development pathway. Our global IP portfolio is robust. We have multiple patent families covering formulations, combinations, and methods of use, providing protection through 2041 and potentially to 2046 with extensions. To summarize, this is a first-in-class asset with phase III data on the horizon, Breakthrough Designation in hand, and strong IP protection. Let me hand it over to Thomas, who will walk you through the mechanism of action. Thank you, Michael. Is my mic on? Okay. What is the problem? I'll start with just some basics on anatomy and physiology. It's really about two organs that are like the dynamic duo of glucose management in our bodies. Pancreas, of course, everyone is familiar with its function in regards to diabetes. It senses glucose, and glucokinase actually is a glucose sensor for these organs too. It adjusts insulin secretion from beta cells as well as glucagon secretion from alpha cells. As you may remember, insulin is sort of the agent that lowers glucose. Glucagon, most times, does the opposite. It raises glucose. That is a very important step informing other organs how to manage glucose, and the liver is indeed the main manager of glucose. The liver helps to stabilize glucose levels in an appropriate physiological range that doesn't expose you to hypo or hyperglycemia. When glucose is high, the liver actually absorbs a lot of glucose, especially after meals, and it stores it away as glycogen. Glycogen is an important reserve for glucose when glucose levels drop. It's the immediate response, if you like, that helps to prevent hypoglycemia, even in people without diabetes. I think what you also may notice is the close physical proximity of the two organs, and that has a particular reason, because this way the pancreas can very quickly and at very distinct high hormone levels trigger responses from the liver. I think that's important to keep in mind when I'm talking a bit about why we think cadisegliatin is such an important improvement in the management of type 1 diabetes. As I said earlier, in those who do not have diabetes, the portal vein, which is really the big blood vessel that comes not only from the pancreas but also from the gut, transports important information for the liver to be aware of. One is, of course, nutrients. Glucose arrives in high amounts with other nutrients from the gut after ingesting a meal and triggers, if you like, the response from the liver. Insulin also arrives at high concentrations from the pancreas. It's something that is critical to understand here. Insulin is not directly impacting the activity of glucokinase, but it maintains healthy levels of glucokinase in the organ. It basically helps to transcribe from genome to proteome, glucokinase as a protein, and maintains those healthy levels each time that you have a meal. It stimulates the liver to replenish glucokinase. When glucose arrives in the liver, glucokinase will phosphorylate glucose. It will basically bind a phosphate group to glucose and lock it in the liver. That's basically the one function that it takes care of, and thus pushes phosphorylated glucose down into synthesis of glycogen. When glucose levels are high after meals, a lot of glucose, about 30% of glucose is being absorbed by the liver, and when glucose levels drop, exercise during night times, glucagon and glycogen's going to be released to maintain glucose levels in a normal green range. In people with type 1 diabetes, the situation is dramatically different. There is no pancreas secreting insulin, and the exogenous insulin, the insulin that you subcutaneously administer, cannot deliver the kinds of insulin levels you normally see in the liver. It's about eight times less insulin that the liver can see, and there's just no way to correct for this. The result is that glucokinase levels in the liver drop, and thus the ability of liver to take up glucose after meals and synthesize glycogen to prevent hypoglycemia drops as well. Result is that you have more hyperglycemia and you have more hypoglycemia. What tirzepatide does is not replacing insulin. It cannot do this. What it can do is enhancing activity of whatever glucokinase levels are in the liver present, and thus compensates for that deficiency that exists without intervening at that step. It will help to mitigate hyperglycemia after meals, and it will also make sure that more glycogen is produced to mitigate hypoglycemia when patients exercise, when they don't eat, basically overnight periods. With that, I want to switch to some of the evidence to support the theory of how tirzepatide works. These are three studies that I just want to introduce you to. As Michael mentioned, we have exposed more than 500 subjects to date to tirzepatide, about 120 or so are type 1 diabetes patients. I'm starting on the left-hand side with the AGATA phase II study, which was the longest study we've been undertaking up to this point in time. Initially, tirzepatide was designed to be used for type 2 diabetes. In the future, it may still be. It was the first study that was six months long, and it showed that in patients who were only using metformin to control their glycemia, we had a sustained reduction of A1C by 0.9%, which is very significant, and there was no, if you like, tapering off of this effect up to the end of the trial. I think equally important, and in distinction from other glucokinase activators in the past, there was no hypoglycemia and there was no disturbance of lipid metabolism. Encouraged by these results in the center panel, we undertook the first study in type 1 diabetes patients, and the study was designed primarily to look at reductions of A1C. The study was designed as a treat-to-target study, meaning that all patients, before they even were randomized, were pushed to achieving close to ADA goals in terms of A1C and daily glucose excursions. On that backdrop, we still achieved a reduction of A1C by 0.36% compared to the insulin control arm. We had 50% fewer symptomatic hypoglycemic events at the same time. We had no events of ketoacidosis, which is an important safety concern for the FDA. I think an interesting aspect of the study results was also that about 40% of patients treated with tirzepatide were able not only to reduce the A1C, but also the insulin dose. Normally, you wouldn't be able to do both. In order to reduce A1C with insulin, you have to give more insulin, not less. It shows really that tirzepatide, independent from insulin, can help to reduce hypoglycemia. We also did, on the right-hand panel, a small study, proof of concept study, if you like, in patients who were using pumps. One of the frequent reasons for diabetic ketoacidosis is that the pump insulin delivery is disconnected. The lines may be clogged, displaced. It's a good model in a way to see, is there a liability with regards to diabetic ketoacidosis for tirzepatide? Lo and behold, we had no events of DKA once we disconnected insulin in the tirzepatide group, whereas about 40% of patients in the control group developed DKA. At the same time, even though it was only a 10-day short-term study, we saw improving fasting glucose as well as no hypoglycemic events. I want to switch back to the Simplici-T1, the phase II study in type 1 diabetes, because that's really at the center of our argument. The study was impressive not just because it lowered A1C. On the left-hand panel, you see the curves for both the placebo insulin only treated people and those in blue of those who are using tirzepatide on top of the insulin. We're also able to reduce hypoglycemia on the right-hand panel over the course of the study. In HbA1c, you see something that is always described as the hockey stick. People improve a little bit, then they pull back in terms of insulin because they're incurring too many hypoglycemic episodes. On the right-hand panel, you clearly see that this is in fact what happens. People, as they continue to try to be true to target, are incurring more hypoglycemic events and ultimately discouraged, pull insulin back to mitigate some of these hypos. In contrast, with tirzepatide, you see a continuous decline in A1C, and again, on the right-hand panel, the reason is obvious. There's much fewer hypoglycemia occurring in this patient group, they don't have to pull back insulin. They can actually more confidently dose and maintain good control. I think this was basically the result that motivated FDA to grant us breakthrough status, because it's something that we have never seen before, really, in attempts to improve management of type 1 diabetes. Often the question is asked, why are the curves separating late for hypoglycemia? I think there are two possible reasons. One is, because it was the first study in type 1 diabetes, we instructed all patients to reduce their bolus insulin dose by about 20% before being randomized. They took some time for people to basically catch up, if you like, with insulin doses that would expose them to hypoglycemia risk. The second reason might be that, yes, glucagon is formed fairly quickly, it may take a little bit before it actually becomes an effective way of reducing hypoglycemia. An important aspect, of course, of any of these studies is safety, this is just a snapshot of the safety database from Simplici-T1. As you can see on the panel here, there is no difference in terms of adverse events, whether serious or non-serious. We had no liver signal, as I mentioned before, we had no DKA events and no difference in the formation of ketosis. Equally important, that's based on past experience of other glucokinase activators, is observing the lipids. These are the fasting lipids, triglyceride, fasting LDL, HDL, and non-HDL cholesterol. Again, you can appreciate there is no difference between the two groups when it comes to lipid levels. With that, I want to turn to the present. This is the ongoing phase III study, CATT1. It's a double-blind randomized trial, it has been very significantly involved and influenced by our discussions with FDA. I mentioned breakthrough status that allows us very frequent communication. The agency actually often reaches out to us and sort of gives advice. The study is also fully aligned with the current guidelines from FDA in regards to efficacy endpoints. This time, this is a study that has hypoglycemia as the primary endpoint, this is the level 2 and level 3 hypoglycemic numbers. The important part here is that all patients are using continuous glucose monitors, we're going to extract the hypoglycemia level 2 data actually from the CGM devices, which actually improves also very much our ability to collect events rather than just relying on patient-reported data. The key secondary endpoint is HbA1c. The goal here is to improve hypoglycemia incidence of tirzepatide without at least making HbA1c worse. The study is 90% powered to show a 30% difference in hypoglycemic incidence. 20% is about what people consider to be clinically significant, including the FDA. Given that we have very good results from the Simplici-T1 study, we are actually confident that this is going to be met. The key secondary endpoint is A1C, of course, we have 90% power to show non-inferiority and 70% power to show superiority if that was the case. Patients are being randomized to three arms. We have two arms where cadisegliatin is dosed, 800 milligrams once daily, 800 milligrams twice daily. Both doses have been used in previous studies in patients with type 2 diabetes and of course 800 milligram in the type 1 diabetes study. This is shared with you. They both have very good safety profiles, we're hoping maybe with BID to see a little more efficacy. But again, the study results will ultimately show. The study has a run-in period, which is a bit lengthy, but that's for two reasons. One, this is again a treat-to-target study, we really want to bring our patients down as close as possible to ADA, meeting ADA targets in terms of A1C and glycemic control. Second, the FDA has asked us that we establish the baseline rate of hypoglycemic events within the study. The 4-week period is dedicated within the run-in period to collecting hypoglycemia rates. The study's currently enrolling at U.S. sites only, as Michael mentioned, we're hoping to potentially getting close to the data near the end of this year. With that, I'm handing it back to Michael. Let me bring this all together. First off, cadisegliatin is a late-stage phase III asset with a near-term catalyst top-line data target for later this year. Next, the program is clinically derisked. With over 500 patients who have been studied, the phase II data demonstrated a favorable profile on both hypoglycemia reduction and reduction of hemoglobin A1C. Regulatory, we have breakthrough therapy designation, which speaks to the seriousness of the condition and the potential of the therapy to address a critical unmet need. Fourth, the market. 75% of the 1.5 million Americans with T1D are not meeting glycemic targets. Hypoglycemia is the primary barrier. There is no FDA-approved oral adjunctive therapy for T1D. We're not creating a market, but rather addressing the gap that clinicians and patients have been waiting more than a century to fill. Finally, the balance sheet. We ended 3Q 2025 with approximately $99 million in cash, we added $20 million to our balance sheet in February of 2026 of non-dilutive capital. We have the runway well past CATT1 data readout, we're positioned to execute. First-in-class asset, breakthrough designation, proven mechanism, massive unmet need, capital to deliver. That's the opportunity. Let me turn it over for some questions. Ms. Brown? I think that's working. Yeah, it is. Thanks. Ritu Baral, TD Cowen covering analyst. Can you talk about how we should frame timing of data expectations for CATT1? Yeah. The guidance is second half of this year. What I would point you to is that includes all the way up to year-end this year, hopefully that helps you a little bit. How do you frame the value proposition that you're going to be presenting to payers? How do they understand this right now in the market research that you've done? Yeah. The value proposition is obviously based on both prevention of hypoglycemia, which can cause significant health costs. As well as at least a meaningful reduction in A1C. I think that's sort of the optimum of both worlds. I would also add to that, again, there's been nothing, no oral adjunctive treatment to insulin therapy, to insulin in over 100 years. Patients today only have insulin as a choice with a narrow therapeutic window. You can imagine, if approved, there would be nothing to set up against. If somebody wanted a prior authorization, you would say, "Okay, let me hit a button and download all my hypoglycemia data from my CGM." Again, I think it really speaks to the kind of unmet medical need out there. As we look through the phase II SimpliciT-1 data, what were some of the key learnings to set expectations for CATT1, either on enrollment, conduct, Certainly for framing expectations for the final data when it does come? Yeah. Obviously, the key outcomes for the data I shared, the hypoglycemia impact, the magnitude of hypoglycemia reduction, as well as to some extent the reduction in A1C. We learned a lot about how often actually do people experience hypoglycemia, particularly patients with CGM, without CGM. All that was in addition to obviously reviewing literature and FDA reviews. critical to, if you like, sizing up the CATT1 study. I think we made a lot of friends amongst the PIs. There was a lot of enthusiasm there, and I think that's something we could capitalize on when we start at CATT1. The PIs? PI. Principal investigator. Sorry. Oh, got it. Got it. Good question. Other questions? Great results. This could be an important drug. I know there have been at least two other glucokinase inhibitors in the clinic before, which did not succeed because of side effects. I would be curious about what are you doing differently? What's different about this molecule? Lastly, you're giving almost two grams in one part. I'd be interested in your dose selection. Yeah. What's different to all the other people or guys? I think something like this has to be carefully designed, and I think in the past, when people started, and I started actually when I was at Takeda working on TAK-329, which was one of the first generation glucokinase activator. These compounds were targeted at pancreas, and that was, of course, on the hindsight, it was basically type 2 diabetes. I think it's also neglected to really look at how the liver regulates glucokinase activity. I think the lessons learned where we have to look at what happens with genetic mutations of glucokinase. What are sort of the traps? How do they impact negatively, like the safety profile? I think the design, ultimately, of the molecule took into consideration, yeah, we want to be hepatoselective. We don't want anything to do with the pancreas, because the pharmacologic profile is just inappropriate to really meaningfully modulate islet cell activity. Number 2, we do not want to interfere with what the liver has established through evolution as a feedback loop. Also, liver is programmed not to have over hyperactivity of glucokinase. There's a particular protein in the liver that actually makes that happen. Interfering with that protein by binding to glucokinase creates havoc. I think that's where pretty much everyone failed to deliver. Because by interfering with that and creating kind of a hyperactive state in the liver, you create hypoglycemia, potentially, in contrast to what we show, and you create increased lipid levels. I think that was the reason even where some hepatoselective glucokinase activators ultimately failed to deliver a healthy risk-benefit. Again, we have not seen any impact on lipids, which is really critical. It's really essential here for inappropriate overactivity in the liver. We have never seen hypoglycemia in patients with type 2 diabetes. I think that makes me very optimistic about cadisegliatin and just having it hit the sweet spot, if you like, in terms of glucokinase activation. I think your second question was on the dosing, right? We are exploring 800 QD or 800 BID. You're right, I mean, 800 BID would be 1.6 grams, so it's not a small amount of material. Obviously, the data would have to be very compelling for us to go with a BID instead of a QD. We kind of put it on there because I think, as Thomas mentioned, the drug was very, very safe, so we wanted to see if we could get some additional coverage. The other thing you have to remember is there's nothing else. If you're a type 1 diabetic, all you have is insulin. There are lots of different forms of insulin, lots of different ways it's delivered, but there's been nothing in a century. Again, we'll have to wait for the data, but depending on how that looks, I think it is a very viable option and another tool for patients. By the way, the safety margin is huge for both doses. We know that this is low risk, and there's a little bit more efficacy in BID in type 2 diabetes. Our previous type 2 studies show that. There's a potential upside, even though it's BID and less convenient. Anticipatory regulatory pathway with FDA following CATT1. What other phase III trials do you think you need to do? What are the sort of data that you currently understand FDA would want in the evolving diabetes landscape to drive approval? Yeah. Certainly, we need more exposure. Ultimately, it'll also depend on how excellent the CATT1 data are. I think that's going to drive much of maybe if there's thinking about accelerated approval pathways and maybe abbreviated pathway to market. To be safe, I think we need at least one more study, not just for FDA purposes, but also to have really broad coverage. CATT1 covers patients who use CGM, pen, or open loop pump. As you all know, in the U.S., closed loop systems are gaining traction every year. Certainly we're going to dedicate one of the future studies to closed loop. There may be one or two studies, and maybe cumulatively five to 800 patients more in the program. Final question. Any other questions from the audience? You mentioned that 80% of type 1 patients experience hypoglycemic events. Do you know what portion are the level 2, level 3, moderate to severe? At our diabetes panel earlier this week, yesterday? Yesterday. Tomorrow. There's a suggestion within some of the data that we're going to discuss, that it might be a full 50ish% of the 50% of the 80%. Do you have any granularity on two and three? Yeah, I think that sounds about right. Unfortunately, the events are not as well captured, and now it is time below range. You know from the many studies that are based on CGM data that with closed loop, you have maybe 0.5% time below range. I'm talking about 54, I mean, where level 2 kicks in. Outside CGM, if you're not using CGMs, might be double. I think the guesstimate of 50% is probably correct, yeah. I think the event rates that we typically see in this population is probably two to four, depending on how aggressively they're using insulin to- Annually? No. Per month, per patient. Oh, per month. Yeah. Okay. It's pretty common to have at least level 2 events, sorry, level 1 events every day, but level 2, of course, is a bit more rare. We assumed about four events per patient per month when we were sizing up the trial, but it can be much higher. If you really go down to, let's say, 6.6%, 6.7% A1C, and without cadisegliatin, you have double that. Great. With that, we are at time. Thank you, guys