vTv Therapeutics Inc. Class A Common Stock KOL event

Please go ahead, Paul. Good afternoon, everyone, and welcome.

I'm Paul Sekhri, Chairman, President, and CEO of vTv Therapeutics, and on behalf of the entire team, thank you for joining us today for our KOL event on hypoglycemia in type 1 diabetes and the cadisegliatin phase III program. Next slide, please. Before we begin, I'd like to remind you that today's presentation and accompanying remarks may include forward-looking statements about vTv's plans, products, operations, and other matters as reflected in this slide. Also, today's guest speakers are independent clinicians and advocates who have generously agreed to share their time and expertise. The views they express are their own opinions and do not necessarily reflect the views of vTv Therapeutics. Next slide, please. Today's agenda focuses on the burden of hypoglycemia in type 1 diabetes.

Despite advances in diabetes management technology, hypoglycemia remains a persistent burden, one that extends beyond individual episodes to daily vigilance and fear of going low. We'll bring together clinical expertise, lived experience, and market research to better understand that burden. We'll begin with the clinical picture of hypoglycemia and then hear directly from someone living with type 1 diabetes. That perspective will bring that clinical picture to life. Next, we'll share findings from our recently completed market research, building on the clinical and personal perspectives you'll hear today. We'll then turn to cadisegliatin, our lead investigational program in its phase III CATT1 clinical trial, followed by a brief corporate summary. We'll then conclude with a question and answer session. Now let me introduce our guest speakers on the next slide.

Our first featured speaker today is Dr. Schaefer Boeder, a board-certified endocrinologist, medical director at Paradigm Clinical Research, and associate professor of medicine at the University of California, San Diego. He'll explain why hypoglycemia remains an inherent challenge of insulin therapy, even with today's most advanced technologies. He'll also discuss how its burden extends beyond severe events to frequent lows, impaired awareness, and fear of hypoglycemia, shaping daily life and decisions about glucose management. I'll then be joined by internationally acclaimed cellist Alisa Weilerstein. Alisa has lived with type 1 diabetes since age 9. She will take us inside a day in the life of someone living with type 1 diabetes. We'll talk about quality of life, the anxiety and fear that come with the risk of a low, and where today's technology still falls short.

Our third guest speaker is Dr. Klara Klein, Assistant Professor in the Division of Endocrinology and Metabolism at the University of North Carolina at Chapel Hill and Director of the Endocrinology, Diabetes, and Obesity Clinical Research Unit. Dr. Klein will review the expected mechanism of action of cadisegliatin, review the phase II data, and walk through the design of our phase III CATT1 clinical trial. You will also hear from Martin Lafontaine, vTv's Chief Commercial Officer, who also lives with type 1 diabetes, and he will present findings from our recently completed market research. With that, I will turn it over to Dr. Schaefer Boeder to discuss hypoglycemia in type 1 diabetes.

Thank you, Paul. It is a pleasure to be here today. I am looking forward to this discussion, and my goals today are pretty straightforward. I want to spend some time introducing type 1 diabetes, talking a bit about how we approach therapies for type 1, and then ultimately pointing out why despite our current therapies and advances in technologies that we use for type 1, hypoglycemia remains a major problem. These are my disclosures. I will begin with type 1 diabetes. Type 1 diabetes is characterized by autoimmune attack on the beta cells of the pancreas. These are the cells that actually produce insulin, and this is a process that has nothing to do with diet or lifestyle, but clinically diagnose it. We see antibodies sometimes happening years or decades before there is any sort of clinical evidence of disease.

Over time, this autoimmune attack kills off the beta cells and will ultimately lead to absolute or near absolute insulin deficiency. By the time type 1 diabetes is diagnosed in an individual, that individual usually needs insulin, usually needed it yesterday, and will therefore need insulin for a lifelong, from thereafter, not just to maintain blood glucose control, but actually to survive. This is a disease that affects roughly 2.1 million individuals in America. Global estimates are close to 9.5 million. Interestingly, this is a disease that we have traditionally thought of as sort of a childhood disease or a pediatric disease. It is not. It certainly is an important disease in children, but the vast majority of people living with type 1 diabetes are adults, and you can be diagnosed at any age. Importantly, too, these numbers are increasing.

We have seen not just in the U.S., but globally, that the number of people living with type 1 diabetes is increasing rapidly. The standard of care now for the treatment of type 1 diabetes, of course, we use insulin, but how do we deliver it? Diabetes technologies are really the cornerstone of our therapies for people living with type 1 diabetes. These include continuous glucose monitors. These are sensors that are worn on the skin with a small filament that goes under the skin and continuously senses the blood glucose values and reports those out. We also use insulin pumps.

These are external devices with small cannula that sit under the skin and deliver that insulin, both continuously providing sort of an ongoing insulin amount that's circulating in the body, but also used for boluses or for more insulin amounts that go along with meals or to correct for high blood sugars. More recently, our standard of care has become automated insulin delivery, and this is when we have a CGM combined with an insulin pump and an algorithm to tie that all together so that the insulin pump is able to automatically adjust the amount of insulin that's being given in response to the blood glucose being measured by the CGM. We know these technologies are useful. They certainly improve our diabetes care.

When we look at CGM alone in comparison against the old traditional finger stick glucose values, they improve A1C values by about a quarter of a percent. This is a clinically meaningful amount. They increase time in range, and I'll talk a little bit about our time in range targets, but time in range that we want people to have blood glucoses that are generally between 70 and 180. That's our target range, and the higher the time in range, the more time that's spent in that range. So an increase in time in range of about 5.6% by CGM, that's equivalent to about 80 minutes per day spent in target range. CGM can also reduce hypoglycemia, so the amount of time spent below range, that's with a blood glucose less than 70 by 2.4%.

That in and of itself is a reduction in time below range of about 30 minutes per day. So these are really important numbers. However, even amongst individuals who are using the most advanced AID system, these second generation AID systems that are currently commercially available, 42% of them reported that their A1C was not at target. So these systems are good, but they have not completely solved our problems. Here we see some of our target ranges that we use in our CGM metrics. Our target range is there in the middle in blue, right between a blood glucose of 70 and 180. That's where we want our folks living with type 1 diabetes to spend most of their time. Above that, we consider hyperglycemia. That's time above range, a blood glucose of 180 or higher.

Hypoglycemia, we begin to define as a blood glucose at 70 or less. So below 70 is hypoglycemia. Above 180 is hyperglycemia. We know hyperglycemia, high blood glucose over time can increase the risk for chronic complications, so damage to eyes, kidney, nerves, as well as the heart and other vital organs. So over time, we know that it's really important to minimize time in hyperglycemia. However, when we use insulin to do that, we unfortunately increase the risk of hypoglycemia, low blood glucose. Hypoglycemia can be acutely dangerous, causing things like seizure, loss of consciousness, increased risk for falls and accidents. As providers and certainly people who are actually living with the disease day to day, we are constantly fighting against these two opposing forces. We know from good data and good studies that decreasing hyperglycemia is important for reductions in long-term complications.

However, more intensive insulin therapy directly increases the risk of hypoglycemia, and in particular, severe hypoglycemic events. Why is this happening? it is really just the nature of external insulin therapy. When we give insulin through the wrong route, normally insulin is secreted from the pancreas. When we give insulin through an injection under the skin, it acts very differently. Normally, insulin is secreted from the pancreas in an individual who does not have T1D, gets secreted into the portal circulation. It enters the liver, where it has its first effect. In fact, 50%-70% of the insulin that is released from the pancreas actually is used or pulled out by the liver, and the rest of it gets circulated into the rest of the body. That process is relatively quick.