Morning, welcome back. Thank you for joining us for our 38th annual ROTH Conference. I'm Adam Walsh, Managing Director and Senior Biotechnology Analyst with Roth. Our next presenter is Mike Tung, CFO of vTv Therapeutics. Welcome, Mike. Thanks for coming to the conference. Great, Adam. Thanks so much for the invitation. Really excited to be here. Why don't you start, Mike, by giving us a quick background and overview on vTv for a few minutes, then we'll dive into some questions. Excellent. Welcome, everyone. Before we get started, just forward-looking slide here. A full description of our associated risks can be found in our SEC filings. Let me quickly frame the vTv investment thesis. Our lead asset, cadisegliatin, or CADI for short, is in phase II development as a potential first oral adjunctive therapy for Type 1 diabetes, we expect to complete enrollment in the third quarter of this year. The unmet need is substantial. 75% of people with T1D in the U.S. fail to achieve the ADA, 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're well-capitalized to execute. We ended 2025 with approximately $89 million in cash and then raised an additional $20 million this past February. This provides runway well past the CATT 1 readout. Beyond cadisegliatin, 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. I'm not sure how many of you know somebody with Type 1 diabetes, but this slide illustrates what it feels like to manage Type 1 diabetes every single day. We use the metaphor of driving a fast car on a narrow, dangerous mountain road. This is the daily reality of insulin therapy's narrow therapeutic window. 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. Over time, you can get the long-term consequences of hyperglycemia, such as neuropathy, leading to amputation, retinopathy, leading to blindness, and cardiovascular disease, to just name a few. Drive too far in the other direction on the right, and you risk hypoglycemia or potentially crashing the car off the side of the cliff. Hypoglycemic episodes involve immediate neurologic issues and range from life disruptive, things such as confusion or coma, to even life-threatening if severe enough. 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, and that is precisely what we are working towards with CADI. If approved, we believe CADI represents a significant commercial opportunity. First, there are approximately 1.5 million Americans living with Type 1 diabetes, and this number is growing. There are 10 million people globally with T1D, and this is expected to grow to 15 million approximately by 2040. The burden is real and immediate. 75% of T1D patients in the U.S. fail to achieve ADA glycemic targets. Hypoglycemia is common, with most patients experiencing several mild to moderate episodes per week, and severe events, as noted before, can be fatal. Finally, despite the discovery of insulin over a century ago, there's no oral adjunctive therapy for Type 1 diabetes that's ever been approved in the United States. The only advances have been new forms of insulin, new ways to deliver it. You have short-acting insulin, long-acting insulin, fast-acting insulin delivered by a syringe, a pen, or a pump, but it's all still insulin with its narrow therapeutic window. CADI has the potential to address a critical gap in a long-overlooked market. CADI's been studied in over 500 patients to date in multiple phase I and phase II trials and has demonstrated a strong safety profile with clinically meaningful reductions in both hypoglycemia and hemoglobin A1c. Importantly, CADI has also received FDA Breakthrough Therapy designation, a designation reserved for therapies targeting serious conditions with a meaningful clinical advantage over existing treatments. This underscores the unmet need and supports an expedited development path. Our global IP portfolio is robust, with multiple patent families covering formulations, combinations, and methods of use, providing protection through 2041 and potentially through 2042, 2046 with extensions. To summarize, this is a first-in-class asset with phase III data on the horizon, Breakthrough Therapy designation in hand, and strong IP. Really quickly, let's just walk through how CADI works. In people without Type 1 diabetes, the pancreas delivers insulin directly to the liver, where one of its key actions is maintaining adequate levels of glucokinase. Glucokinase is the key enzyme that allows the liver to metabolize glucose when blood sugar is high and storing this extra glucose as glycogen. When blood sugar is low, the liver breaks down the stored glycogen and releases glucose back into the bloodstream. Thus, the liver serves as a buffer, and this helps regulate blood glucose homeostasis. In people with Type 1 diabetes, the pancreas cannot deliver insulin directly to the liver. Instead, insulin is administered exogenously and must circulate through the body before reaching the liver. In this case, the levels of insulin in the liver are only about one-eighth the levels that are normally found in a person without T1D. The lower levels of insulin lead to reduced glucokinase, and this creates two problems. When blood sugar is high, as you can see in the bottom left, the liver has a limited ability to take that extra sugar and store it as glycogen. Later on, when the blood sugar falls, the liver doesn't have enough glycogen stores to break down, and therefore, you continue to have hypoglycemia. This is a fundamental limitation of exogenous insulin delivery, and it sets the stage for how CADI can help address this issue. CADI is a glucokinase activator, meaning it makes glucokinase more effective or efficient at metabolizing glucose, essentially turbocharging it. It works directly in the liver, increasing glucokinase activity when glucose levels are high. This boosts glucose uptake and metabolism, helping reduce the hyperglycemia and restoring glycogen stores. When blood sugar drops, the liver now has enough glycogen to release, thus helping prevent hypoglycemia. In short, CADI elegantly restores the liver's natural buffering capacity, smoothing out both highs and lows, and addressing the limitations created by subcutaneous insulin delivery. Now let's turn to the cadisegliatin CATT1 phase III study. Based on FDA guidance via our Breakthrough Therapy designation, the primary endpoint is a reduction of level 2 and level 3 hypoglycemic events. All patients will wear CGM devices throughout the trial and receive either CADI once daily, CADI twice daily, or insulin alone. The study is 90% powered to detect a 30% difference or reduction in hypoglycemia in either the once daily or twice daily arm versus the insulin-only arm. A difference above 20% is considered clinically significant by the FDA. On the secondary endpoint of hemoglobin A1c, the study is 90% powered to detect non-inferiority and 70% power to detect superiority. As a reminder, the FDA wants to see a reduction in hypoglycemia, but not at the expense of hemoglobin A1c. Finally, in summary, CADI is a late-stage phase III asset expected to complete enrollment in the third quarter. It's clinically de-risked. Over 500 subjects have been studied in the phase II data demonstrate a favorable profile on both reduction of hypoglycemia and hemoglobin A1c. CADI has FDA Breakthrough Therapy designation, which speaks to the seriousness of the condition and the potential of the therapy to address a critical unmet need. The market opportunity, 75% of the 1.5 million Americans with T1D are not meeting glycemic targets. Hypoglycemia is the primary barrier. There's no FDA-approved oral adjunctive therapy for T1D. We are not creating a market, but rather we're addressing a gap that clinicians and patients have been waiting more than a century to fill. Finally, the balance sheet. We ended 2025 with approximately $89 million in cash, then added another $20 million in the first quarter, providing runway well past the CADI readout. First in class asset, Breakthrough designation, proven mechanism, massive unmet need, the capital to deliver. That's the opportunity. Now I'll turn it back to Adam to answer some questions. Awesome, Mike. Thanks for the great overview. Let's start with the CADI trial execution. You recently expanded trial sites from roughly 25 to 51 and described a meaningful acceleration in enrollment momentum. Can you walk us through what drove the initial kind of decision to expand and perhaps marginally slower than expected pace of enrollment, and what specifically changed operationally to improve it? Absolutely. As with most phase III trials in Type 1 diabetes, the primary challenge early on was identifying patients who met all our eligibility criteria and were willing to commit to a structured protocol. CADI is a treat to target trial, which includes a 10- to 12-week run-in period comprising of screening, device training with the CGMs, and insulin optimization to reach ADA glycemic goals. This includes a four-week baseline period to establish the patient's hypoglycemia event rate before randomization. This level of upfront commitment creates a higher screening bar than many trials. From the outset, we built flexibility into our operational plan to expand sites if doing so would accelerate recruitment, and this is exactly what we did. As enrollment trends became clear in the early months, we made the decision to activate additional sites, and as you mentioned, we're up to 51 sites across the U.S. The result of this has been a steady and improving enrollment pace. Again, just to reiterate, we're guiding to completing enrollment in the third quarter of this year. Okay. Thanks. That's helpful. In the phase II, hypoglycemia was captured through patient journaling. CATT1 uses CGM, as you mentioned. How do you expect the methodological difference to affect the number and reliability of level 2 events that you capture? Great question. This is an important difference that actually works in our favor. In parts of SimpliciT-1, symptomatic hypoglycemia was collected as a patient-reported adverse event. Self-reported data, as you know, inherently suffers from recall bias, and asymptomatic events are particularly likely to go unreported. In CATT1, all patients will utilize CGM continuous glucose monitoring devices throughout the entire trial. CGM captures glucose readings in real time, including asymptomatic and nocturnal or nighttime level 2 events that patients would never self-report. The net effect is that CGM should capture more events per patient, improve the completeness of the data, and reduce recall bias. It should also aid in patient retention because participants no longer have to do the fingerstick blood measurements that other trials potentially have. This design should give CATT1 greater statistical power and data quality. Hey, that's helpful. The CATT1 includes both a once daily and a twice daily dosing arm. What's the scientific rationale for adding the BID arm, and how should investors think about the different data readouts from each dose? That's a great question again. Let me begin with cadisegliatin, or CADI, has been extremely well-tolerated with very few side effects across the 500 patients that have been studied to date. The 800 milligram twice-a-day arm was included to test whether twice daily dosing could provide an incremental efficacy benefit, specifically for overnight hypoglycemic episodes. We have data from a type 2 diabetes study that suggested that maintaining CADI exposure around the clock rather than with a single daily dose might better support hepatic glycogen buffering through the overnight fasting period. From an investor standpoint, the BID arm provides additional optionality. If 800 milligrams once a day delivers strong efficacy on the primary endpoint, that represents the simplest and most patient-friendly label. If the twice-a-day arm shows meaningful superior reduction in overnight level 2 events, it could potentially support a differentiated dosing recommendation for higher risk patients. Both arms are compared against the placebo arm. Again, the CATT1 trial is 90% powered to detect a 30% reduction in level 2 and level 3 hypoglycemia in each active arm versus the control. Okay, great. Thanks. Mike, in the phase II, 40% of CADI-treated patients achieved simultaneous reductions in both A1C and total daily insulin dose. Can you explain the clinical significance of that correlation and why it matters for adoption? Yeah. This is actually one of the most compelling findings from the SimpliciT-1 trial and speaks directly to CADI's differentiated mechanism of action. In type 1 diabetes, the conventional trade-off is well understood. Intensifying insulin to improve A1C increases the risk of hypoglycemia, and backing off insulin to reduce hypoglycemia risk tends to worsen glycemic control. Patients and their physicians navigate this tension every day. The fact that 40% of CADI-treated patients achieved simultaneous A1C reduction and insulin dose reduction suggests that cadisegliatin is addressing the underlying physiology rather than simply moving one metric at the expense of the other. The mechanism of action is consistent with this. By restoring hepatic or liver glucokinase activity, CADI helps the liver resume its role as the body's natural glucose buffer, reducing the burden placed on exogenous insulin to manage postprandial glucose excursions while also reducing hypoglycemia risk. For physician adoption, this profile is extremely attractive. Endocrinologists are not looking for a drug that simply shifts the glucose curves, but rather they want something that can improve the overall quality of blood glucose management. Reducing insulin dose while improving A1C means fewer hypoglycemic events, less fear of lows, and potentially greater flexibility in daily management. Fear of hypoglycemia is consistently cited by the FDA, by the ADA, as the primary barrier to achieving target glycemic control, and a drug that addresses this barrier while also improving A1C would be a differentiated clinical proposition. DKA risk derailed prior adjunctive therapy programs in type 1 diabetes, such as SGLT2 inhibitors. How is CATT1 designed to monitor for DKA, and what have you seen across the 500-plus patient exposures to date? Again, the FDA's always made it clear that clinical programs must demonstrate an acceptable risk-benefit ratio. It's always safety and efficacy. DKA risk is a legitimate and important question in any type 1 diabetes program, and it was central to the FDA's rejection of sotagliflozin, which received a second CRL citing concerns that the risk of DKA did not outweigh the potential benefits. CADI's mechanism is fundamentally different than that from SGLT2 inhibitors and does not share the same DKA pathway. SGLT2 inhibitors increase urinary glucose excretion, which can suppress insulin secretion and promote ketogenesis, particularly in the setting of carbohydrate restriction in people with T1D. CADI does not affect renal glucose handling at all. Its activity is confined to the liver, where it works in a glucose-dependent manner, meaning it only activates glucokinase when blood glucose is elevated. It does not force glucose-independent insulin secretion and does not disrupt the glucokinase regulatory protein interaction. Again, the clinical data to date support this, and across more than 500 patients, including patients with type 1 diabetes and type 2 diabetes, CADI has shown no increase in DKA incidence versus placebo, and in fact demonstrated a reduction in abnormal keto events in the phase II trial. In a type 1 diabetes insulin withdrawal study, data suggested that CADI may actually reduce the risk of DKA, though this was a small study and will need to be confirmed with a larger phase III program. In CATT1 specifically, the protocol includes exclusion of patients with DKA in the prior three months, monitoring of ketone levels as a safety endpoint, and an adjudicated review of any DKA events. DKA incidence is also a key secondary endpoint, ensuring that we'll have a well-characterized safety data set on this exact question. Excellent. In our KOL discussions, as we were initiating on the company, we spoke to a diabetologist who participated in SimpliciT-1, she described the dual benefit of improving A1c while reducing hypoglycemia is extremely valuable clinically because fear of lows is the main barrier to keeping patients on target for their A1c. How do you see that clinical message translating to physician adoption if CATT1 is successful or the drug is ultimately approved? Yeah. That KOL's framing aligns precisely with how we think about the commercial opportunity. It reflects a clinical reality that is well documented but often underappreciated by investors. The ADA explicitly identifies fear of hypoglycemia as the primary barrier to achieving glycemic targets in T1D. 75% of the T1D patients in the U.S., roughly 1.1 million people, do not achieve the ADA-recommended A1c target of less than 7%, despite using modern insulin therapy, CGM, and in some cases, AID systems. The primary reason is that patients and physicians deliberately maintain glucose targets higher than optimal to create a buffer against hypoglycemia. This is rational behavior given the consequences. Untreated severe hypoglycemia can lead to severe neurological consequences and even death. If CATT 1 confirms the phase II findings, the physician adoption story is straightforward. An oral once or twice daily adjunctive treatment to insulin that simultaneously reduces level 2 and level 3 hypoglycemia events and improves A1c means that trade-off disappears. Physicians can now titrate more aggressively toward target without exposing patients to greater low glucose risk. For the approximately 8,000 endocrinologists and diabetes specialists in the U.S. who manage the majority of the T1D patients, this is a compelling clinical proposition. Mike, that exactly echoes what our KOL was saying to us, that the trade-off there is meaningful, and to be able to do both simultaneously is really at the core of what they're trying to achieve with their patients. In terms of the commercial strategy, vTv owns U.S. and major market rights, while G42 has the Middle East and Africa. You've indicated ex-U.S. partnership discussions might resume post-data. Can you frame for investors how you're thinking about the optimal structure and timing for those discussions? To review really quickly, our current partnership structure on cadisegliatin with G42 covers the Middle East, Africa, and Central Asia. They are actually in the midst of conducting a phase II trial in type 2 diabetic patients who are on insulin in their territories, and we expect the first patient to be dosed in 2026. Under the agreement, vTv will receive single-digit royalties on net sales in their territories. We actually retain the rights to the remaining major ex-U.S. markets, which represents a significant component of the total value opportunity. As you can imagine, partnership discussions for these territories will be most productive following a positive CATT 1 readout, when the risk profile of the asset is hopefully materially reduced and the regulatory pathway is better defined. In terms of structure, we're open to all options, including full regional licensing, co-development, co-commercialization, and even milestone-based collaborations. The optimal structure will depend on the strength of the data and the market conditions at the time. I will add that maximizing the value of the ex-U.S. rights while minimizing dilution to our shareholders is a core strategic priority. That's helpful. Now turning to the financial position with the $20 million Nusura payment received in February that you mentioned earlier and your existing cash, can you walk us through how you're thinking about runway relative both to CAT T1 top-line data and then also subsequent development activities? Just again, to remind everybody, we ended 2025 with approximately a cash balance of approximately $89 million. In the first quarter, we brought in an additional $20 million of non-dilutive capital from the expansion of a new license with Nusura. This provides a strong cash balance, and we've said that we're financed well through the CATT 1 top-line data. We expect to reach this readout, our primary value-creating catalyst, without requiring any additional dilutive financing. That's an important message for investors. We will be very disciplined in how we deploy capital. That's helpful. I want to circle back just to the first question that we talked about, the expansion of the sites and the enrollment completion guidance now for the third quarter. Can you just do the math for investors on when they should expect the CATT 1 top-line data set? Yeah. We will announce when we've completed enrollment. From the time that we complete enrollment, the math is the trial is six months, and then I would think that another one to two months in order to kind of clean up and present the data. Anywhere from, let's say, roughly seven to eight months from the time that we've completed enrollment would be the proper way to think about it. Okay, that's helpful. We're coming up almost on time, just off the top of your head, you do have some interesting assets still in the pipeline. Are there any that you'd like to highlight for us that could be potential partnership opportunities or potential for development down the line? Well, I think that it's almost like, we'd say all your children. You try not to pick favorites, I will highlight, we actually had the very first oral GLP-1 ever. That one could be interesting as well. We have a PPAR agonist that could potentially have some interesting indications as well. NRF2/Bach1 modulator. Again, we have the Nusura was an oral PDE4. They had China rights. We expanded that to a global license very recently in the first quarter. Yeah, stay tuned. Again, just to reiterate, the focus of the company is really cadisegliatin. We're using our pipeline as sources of non-dilutive capital predominantly. Yeah, no, there's some interesting little assets in there. I think what was interesting in my own research on the GLP-1 product was the tolerability profile was really different on the efficacy side. I think it was not comparing as well to some of the more strong results that we've seen with other products, but on the safety side and tolerability side, and just in our own thinking, we thought that could possibly fit as a maintenance therapy because a lot of the patients that come off these drugs have rebound effects, and they come off largely because of tolerability issues. If you could have a drug that could kind of blunt that rebound effect because of tolerability, that might be appealing to some partners. Maybe just some thoughts on that. Yeah. I think you hit it right on the head. Stay tuned, but there is some rationale for why we believe our oral GLP-1 could have potentially a differentiated GI side effect profile. Imagine potentially less nausea, less vomiting, less diarrhea. Again, I say potentially because it remains to be seen, but there could be some value there, right? Again, imagine an option where maybe you don't get as much weight loss, but it's much more tolerable. Or to your point, potentially after a patient's done with injectable GLP-1 and they want to just maintain, right? Stay tuned. Excellent. That's it. That's a wrap. Mike, I'd like to thank you so much for coming. Great presentation and look forward to following this story with interest. Great. Thanks again. Thank you. Thanks so much for the invitation.