All right, hello everyone, and welcome to the H.C. Wainwright 27th Annual Global Investment Conference. My name is Maya, and I'm a research associate here. I'm here with Arun Swaminathan, CEO of Coya Therapeutics. Welcome, and I yield you the floor now to introduce yourself and the company. Thank you, Maya. Appreciate it. Good morning, everyone, and thank you for the opportunity to share the innovative work we're doing at Coya to bring transformative therapies for patients suffering from neurodegenerative diseases. These are diseases like ALS, Lou Gehrig's disease, frontotemporal dementia, Alzheimer's, Parkinson's. ALS and FTD have been in the news a lot lately through celebrities like, I forget his name, but one that has been openly talking about ALS, Eric Dane, and Bruce Willis' wife has been openly talking about the struggles of caregiving with frontotemporal dementia. These are difficult diseases that today have almost no options. Our vision at Coya is to make these diseases livable diseases, where the stories of these patients, not just the celebrities, but the stories of these patients are not about the disease, it's about whatever else they're doing in their lives. So that is our vision. That is our mission. Today, this is not an option for these patients, so how are we going about achieving this vision? Do you know how I can advance the slides? Oh, there we go, so how are we going about achieving this vision? It is based on fundamental and solid science. What we fundamentally believe is that neurodegenerative diseases are highly neuroinflammatory diseases, and if you can address neuroinflammation at the core, you can stop potentially the progression of these diseases, and that is what I'm going to talk to you about today, and what we know is we are encouraged by what we have seen, not only from the scientific literature, but also from investigator-initiated clinical trials we ourselves have done across multiple neurodegenerative diseases. What we see is a consistent pattern where when you can address neuroinflammation by addressing dysfunctional regulatory T cells. Regulatory T cells are the brakes of the immune system. When these brakes don't work well, the immune system goes out of whack and causes nerve cells and neurons to die. So our fundamental scientific premise is that by increasing the numbers and function of Tregs and keeping them sustainedly functional, we can stop the progression of these diseases. And I mentioned as neuroinflammation increases, neurons or nerve cells start miscommunicating or die. These are our internal spark plugs. When they're not firing well, that leads to these different neurodegenerative diseases. So fundamentally, we are focused on restoring the function and numbers of Tregs, keeping them functional, thereby addressing neuroinflammation, which in turn should translate to stopping progression of disease. So where are we with this? Our lead program that is focused on this is Coya 302. It is an innovative combination of a proprietary low-dose interleukin-2 with a CTLA-4. So why are we excited about this program? Number one, we are now embarking, and we're pretty pleased that we're going to be entering a potentially pivotal phase IIB study in about 120 patients with ALS very soon. We received the FDA green light a couple of weeks ago, and we're going full speed ahead towards the first patient being dosed, and we'll keep you updated as that milestone is achieved. We fully anticipate dosing the first patient in the fourth quarter. In addition to that, we are honored that the NEALS Foundation, the NEALS, we are now a NEALS-affiliated study, and NEALS is the world's largest ALS consortium, so we have their backing and Dr. James Berry, and therefore should be able to recruit faster in this trial, hopefully. And then we will also be presenting our PI, Dr. James Berry, who will be presenting details of this clinical protocol on September 29th at the NEALS meeting. So what is Coya 302? And why do we feel a high degree of confidence that this double-blind multicenter controlled trial is likely to show positive outcomes? It is backed by science and the data to date. From a mechanistic perspective, low-dose interleukin-2 increases T reg numbers and increases T reg functions as well. But in diseases like ALS, FTD, and a lot of the neurodegenerative diseases, the microenvironment remains highly inflammatory. And when that remains inflammatory, although we have made the T regs functional, they tend to revert back to becoming dysfunctional in a short period of time. And that is where our approach is differentiated. We leverage the positive effects of low-dose interleukin-2 and combine it with CTLA-4, which acts on CD80/86, a different aspect of the immune system. So we are simultaneously addressing both the adaptive and innate immune systems, and through this combination approach, are able to keep the macrophages anti-inflammatory and the activated myeloid cells. What this does in effect is prevents the T regs from being converted back to becoming dysfunctional. Our data shows that we keep T reg numbers up, the combination increases the T reg function or the individual IL-2, and also keeps the T regs functional for a sustained period of time. So that is the key differentiator of how we approach T reg therapies. ALS, I'm sure many of you are familiar, is a devastating disease. The average patient diagnosed with ALS dies in three to five years from diagnosis. Not only is their lifespan shortened. Their quality of life during that period rapidly deteriorates. ALS is measured by a score called ALS-FRS, which is the FDA-accepted endpoint for ALS, and that is the primary endpoint in our planned phase IIB trial. For those of you not familiar with the score, from a simple perspective, the lower the score, the worse the patient is doing. On average, ALS patients today, with the currently existing therapies which barely work, and one of them has been withdrawn from the market, patients decline at about one point a month. You would expect an average decline of about six points in six months, which is what you see on the left side here from the PRO-ACT Database, which is a database of a large ALS patient repository from the Massachusetts General and Harvard University. Six points in six months, what does that really mean for a patient? As an example, six points can be the difference between walking with a cane versus being on a wheelchair. In one year, the expected progression is 12 points. That can be the difference between walking with a cane and being on a ventilator. Every point is clinically meaningful, and being able to stop the progression is very clinically meaningful, and today's therapies really don't do much towards that front. We had conducted a small investigator-initiated study with this combination. For the brevity of time, I will not go into the details of the study, but it was a 48-week study, almost one-year study with a follow-up period. We looked at it at six months, but also at 48 weeks. Now, what we saw, and this included patients of all ALS types, both with genetic mutations as well as sporadic ALS. Genetic mutations contribute to about 15%-20% of ALS patients. The majority of ALS patients are sporadic, which really means that we don't know what drives their ALS. But what we found in the small study is that remarkably, almost all patients either improved in their score or stabilized. As you'll notice, there was one patient that declined in the first month, but then stabilized pretty rapidly. So this is remarkable because to our knowledge, no one has demonstrated the ability to stop the progression of ALS in this tough-to-treat patient population, even in small clinical studies. This is the main data that basically shows that at six months, we had no change in ALS-FRS in this study. As you recall from my previous slides, you would expect a six-point decline in six months with the currently existing therapies. So the 33.5 would have been somewhere around 27.5 in a normal study. We saw that we had no change. This is pretty remarkable. And at one year or approximately one year, 48 weeks, we saw the same thing. We saw a one-point mean decline in ALS-FRS when you would have expected a 12-point decline in the same period. And I previously told you what each point means from a clinical outcome for these patients and the survival as well. And more importantly, when we stopped the therapy, the patients started declining at that one point a month again, showing that as long as the combination of low-dose IL-2 and CTLA-4 is on board, we are able to potentially stop the progression of this devastating disease. So this, along with the biomarker data, which shows that we're doing what we said we will do. We increase the Treg numbers, we increase the Treg functions, we keep the Treg function sustained, and when we take patients off this combination, all of that starts reverting back. And we also see markers of oxidative stress, like 4-Hydroxynonenal, ox-LDL, NfL, all of that move in the right direction. So this is why we feel pretty good about our probability of success in the upcoming phase IIB study, because the science lines up and the early clinical data is showing remarkable promise in the potential of stopping progression of ALS. We are seeing the mechanism work, we are seeing the biomarkers move the right way, and we have seen in a small group of patients that we're stopping the progression of ALS. And what is exciting, and I'll talk to you about our next indication, we are seeing the same trend in diseases like FTD, which then gives us increased confidence that our approach, our scientific approach, has potential to truly make a difference for these patients. Now, I briefly already mentioned we're about to kick off the phase IIB study. We have certain inclusion and exclusion criteria. I'll just highlight a couple. We will bring in patients that have an ALS-FRS of 35 or higher. So these will be mild to moderate ALS patients. They also need to be declining within a certain range, close to that one point a month as they come into the study. Their placebo is not a true placebo. Placebo means they're on standard of care. So whatever standard of care they're on, they stay on. Obviously, they have to be on a steady dose of that coming into the study and through the study. Our primary endpoint is six months, and after six months, we will randomize the placebo patients to go into one of the treatment arms, and the people on treatment arms will continue on the treatment arms for one year, so we will have long-term data as well, but six months is the FDA endpoint for registration, so we will, assuming our discussions with the FDA and the data supports it, we'll approach the FDA about potentially filing for a BLA at the end of the six-month study. In addition to that, for ALS, the first indication, we have partnered with Dr. Reddy's Laboratories, a $13 billion public multinational company who will commercialize Coya 302 when it is approved in major global markets. We have written rights in a few markets like Japan, South America, and Mexico. What this also does for a company like Coya is we now know we have a path to a commercial partner who is going to pick up the expenses of commercialization for this product. So when we get approved on our first indication, we're in a good place from a financial perspective at Coya because we already have a partner lined up. We have, however, retained the rights to all other indications. Coya still retains them. So we retain the value of all the other indications. We also have a strong partnership with Houston Methodist that allows us to do a lot of the basic science work through the laboratories of Dr. Stanley Appel, who is a legend in the field of ALS. So we're very proud of this. Dr. Reddy's partnership, in addition to that, it's a $700 million partnership. What it does in simple words for us is it provides us a steady line of sight to non-dilutive cash flow. Just when the IND was approved, we received $4.2 million from our strategic partner in a non-dilutive manner. We will receive another $4.2 million from them when we dose the first patient, which is going to occur in the upcoming months. So we are well positioned that way with their partnership, allows us the flexibility to take our cash a lot further than most companies can at our stage, and that really strengthens us. But beyond all that, the partnership brings a lot of value on the regulatory front, the manufacturing front, the CMC front, on top of the commercial front, obviously. So it is a partnership of synergy that drives value and allows us to hopefully bring this therapy to patients faster. So that's about ALS. I want to spend a couple of minutes on the few other indications we're pursuing. Frontotemporal dementia, the same combination, Coya 302, in a small investigator-initiated trial, saw the same thing we saw in ALS. This is interim data. We stopped the cognitive decline as measured by CDAS, FTD, and Montreal assessment scales, which are the cognitive scales that are standard for FTD. So we see the same thing. Biomarkers move the right way. The product seems to do the right things in terms of hitting Treg function and numbers. So this gives us confidence in moving forward with a smaller randomized study in FTD in 2026. We fully intend to file an IND for frontotemporal dementia this year with the FDA. Subject to the approval, we will initiate this trial in 2026. This trial, we have the support from the Alzheimer's Drug Discovery Foundation, who invested $5 million in us in support of this study because they believe in our approach that we're taking, especially with the combination approach for FTD. The likely patient target for this study will be non-fluent primary progressive aphasia subtypes. There are different subtypes of FTD, but we are pretty excited to move this program forward as well. So while ALS is our lead, we remain laser-focused on advancing Coya 302 and our other programs in other diseases in parallel, and we're all systems go. I want to spend the last few minutes I have talking about a very value-creating, or I believe it's an extremely value-creating potential combination. That is our product, Coya 303, which is a proprietary combination of Coya 301 with the popular weight loss drugs, the semaglutides, the Ozempics, the Wegovys, the Mounjaros of this world. Why is this exciting? What we have shown preclinically is that the combination of Coya 301 with semaglutide is synergistic. When we combine the two, we are seeing better suppression of neuroinflammatory markers, giving us a lot of potential in diseases like Alzheimer's disease. Now, when you pair this up with the retrospective data of GLP-1s alone, millions and millions of patients' data has been published in the Lancet and other journals showing that patients taking GLP-1 to manage their diabetes have lower onsets of dementia and lower progression of dementia when compared to patients taking other diabetic agents. Their blood sugars are controlled similarly, but the patients taking GLP-1 have lower onset of dementia. This is exciting. And what we're showing is by combining, we can make one plus one better than two. And of course, most of you are probably aware, Novo Nordisk is conducting two well-characterized phase III studies, EVOKE and EVOKE+, in studying semaglutide in patients with mild Alzheimer's disease. That data is expected imminently, anytime in the next month or three months, I believe. And that, we believe, will actually strengthen our position even further in the potential of this combination in Alzheimer's disease and opening up potentially good value-creating business development opportunities. So in closing, I want to close by saying we are moving forward in addressing diseases that are hard to, but with data that is showing us compelling confidence that we can deliver in these tough-to-treat diseases. We've already delivered on many of the value-creating milestones we have guided to in 2025, and there's more coming in 2025 alone. Just as a reminder, we will be dosing the first patient this year in the ALS phase II study. That triggers a $4.2 million payment from our partner, Dr. Reddy's, to us. We will be filing for an FTD IND with the objective of starting that trial in 2026. We will have additional data from the investigator-initiated FTD trial towards the end of this year. We will have preclinical data on Coya 303, the combination with GLP-1s that's coming, and the timing of that will be perfect. It's coincidental. We'll likely be around when Novo Nordisk is announcing their EVOKE and EVOKE+ data as well. A lot going on. We're very excited. And I just want to close by saying we have a tremendous team at Coya, a group of people that are personally affected, a lot of them, by these diseases and are hugely committed to making a difference. And I want to thank them all for everything they've been doing as we advance Coya. Thank you, and I'm happy to take questions.