Hello, everyone. I'm Jay Olson, one of the biotech analysts at Oppenheimer, and it's a pleasure to welcome you to Oppenheimer's 35th Annual Healthcare Conference and our discussion with Coya Therapeutics. It's my pleasure to introduce Arun Swaminathan, CEO of Coya Therapeutics. With that, I'll turn it over to you, Arun. Thank you so much for joining us today. Thank you, Jay, and thank you for inviting Coya to join the conference. We appreciate it. Good morning, everyone. The next slide is our forward-looking statement and disclaimers. Coya Therapeutics, we are a biotechnology company focused on advancing innovative therapies to address complex neurodegenerative diseases. We do this by targeting the regulatory T cell. Increasing the number and suppressive function of these T regs can result in reduced neuroinflammation. We believe that neuroinflammation is fundamentally the driver of most of these neurodegenerative diseases, and that by addressing neuroinflammation, we can address multiple of these complex diseases. Our pipeline consists of multiple products. COYA 301 is our proprietary recombinant interleukin-2. COYA 302 is our proprietary combination of the low-dose interleukin-2 with CTLA4. More recently, we announced that we have COYA 303, which is a proprietary combination of low-dose interleukin-2 with GLP-1 agonist. Through multiple investigator-initiated trials, we have been able to demonstrate some remarkable proof-of-concept clinical data. With the combination of the low-dose interleukin-2 plus CTLA4 in an IIT study, we were able to demonstrate stopping progression of ALS at six months in a small sample of patients. In addition to that, additional investigator-initiated trials with low-dose interleukin-2 alone, including a double-blind study in mild to moderate Alzheimer's disease patients, showed the ability for low-dose interleukin-2 to stop the cognitive decline, as measured by ADAS-Cog and a few other measures, at five months. The combination of all of these clinical data gives us a lot of confidence in our ability to move forward with our programs. We are advancing COYA 302 in ALS, which is a disease with very limited options, and in frontotemporal dementia, a disease with zero approved drugs from the FDA. In addition to that, we do look at COYA 301, our low-dose interleukin-2, as potentially set up well for combinations with other modalities in treatment of Alzheimer's disease, as well as outside the neuroimmune space in autoimmune diseases. We will be pursuing these in terms of business development opportunities. We also will be looking at pursuing COYA 302, which is our combination with CTLA4 in Alzheimer's and Parkinson's disease as well. For COYA 302 in ALS, we are partnered with Dr. Reddy's Laboratories, who are our strategic partner and will help us commercialize ALS in several key markets. It essentially includes all global markets with the exception of Japan, South America, and Mexico. This strategic partnership with Dr. Reddy's gives us line of sight to up to $700 million in non-dilutive milestone payments upon, obviously, hitting these milestones for Coya through our life cycle. As of October 31st, we reported about $40 million of cash in hand, and we have previously guided that this supports our operations into 2026. Before I get into our pipeline and walk you through our products, I wanted to share with you what you can expect from Coya in 2025. We have a lot of exciting milestones and what we believe are value-creating milestones in 2025. Coya has two pathways to value creation in 2025. One is through the generation of critical data, and I will walk you through some of the key ones that are coming ahead in 2025 that we believe will be value-creating to Coya. In addition to that, we also believe that our COYA 301 programs and our COYA 303 program are well set up for strategic partnerships, and we are hoping that we can advance some of those partnership conversations in 2025, adding another element of value creation to the Coya story. Briefly, we recently announced from our investigator-initiated Alzheimer's disease data, not only in late October we announced the positive results from the trial, but recently also announced positive impact from inflammatory markers and cytokines in this study. We will continue to be reporting additional data from this trial that should further validate our mechanism and hopefully support our hypothesis of why this combination and this product can work in Alzheimer's disease and other neurodegenerative diseases. Later in this quarter, we also anticipate publishing the data that shows synergy between GLP-1 agonists and our COYA 301, which can be pretty value-creating, and we expect to publish that data later this half. In addition to that, later this year, we plan to initiate a phase 2B potentially registrational trial in patients with ALS and plan to submit the supporting IND documentation to the FDA in the second quarter of 2025. There is an ongoing investigator-initiated trial in frontotemporal dementia, an open-label trial, and we anticipate reporting top-line results from that study in the early part of the second half of 2025. This study will help us refine the planned phase 2B study in frontotemporal dementia, for which we plan to submit an IND to the FDA by the end of 2025. In summary, a lot of exciting things happening this year that will continue to advance our programs. From a scientific perspective, as I briefly mentioned before, our core focus is in addressing inflammation. We believe that addressing neuroinflammation is the key to addressing these diseases. Inflammation in the neurons leads to the selective loss of neurons that then lead to neurodegenerative diseases. We address this by, and they're primarily driven, this inflammation is primarily driven by dysfunctional regulatory T cells, also known as Tregs. Our approach at Coya is to restore this balance. We convert dysfunctional Tregs to functional Tregs by increasing both the number and function of these Tregs and by trying to keep the function, suppressive function of Tregs durable for long so we can have sustained efficacy. Now, let me switch to our lead product, COYA 302, which is a combination of IL-2 low-dose interleukin-2 with CTLA4. It's a combination. The low-dose interleukin-2 increases the number of T regs and also increases the suppressive function of Tregs. However, with only low-dose interleukin-2, we have observed that the environment can become pro-inflammatory again and leading to the T regs becoming dysfunctional once again. We have found that adding CTLA4, which acts through a different mechanism on the immune system and converts the pro-inflammatory macrophages to anti-inflammatory macrophages, adding that in combination with low-dose interleukin-2 allows for the T regs to stay functional much longer. We are increasing the durability. Also, what we have seen is it increases the suppressive function of the T regs. This combination provides synergistic neuroprotection and we believe has a great potential in multiple neurodegenerative diseases. With COYA 302, we believe it is a pipeline within a product because we believe it has applications across multiple neurodegenerative diseases. Our primary disease that is the most advanced is ALS that we plan to begin a phase 2B trial later this year. ALS is a disease with a high unmet need. There are about 30,000 patients in the U.S. alone affected by ALS, with 6,000 new patients diagnosed every year. ALS has a commercial potential upwards of $2 billion globally. The second indication that we pursue with COYA 302 is frontotemporal dementia, a disease that has no approved therapies today. Again, there are about 100,000 patients in the U.S. with different forms of FTD, and it is a pretty high unmet need, and the market is quite open for a product that can find a solution for these patients. In addition to that, with COYA 302, we are also exploring and evaluating the potential in Alzheimer's disease, which has over 6 million patients in the United States, with huge impact not only on the patients, but also on the caregivers and our economic system, as well as in Parkinson's disease. A little bit of background about amyotrophic lateral sclerosis, ALS, also known as Lou Gehrig's disease, named after the famous New York Yankee, Lou Gehrig, who was known as the Iron Horse because if I'm right, he played over 3,000 games without missing a game until he was diagnosed with ALS that not only cut short his career at the peak, but also cut short his life. ALS is a disease where the average patient unfortunately passes away within three to four years on average after diagnosis and are rapidly declining in their quality of life in this time period as well. There is a database known as the PRO-ACT Database, which is the largest ALS database. What the database shows is that the average ALS patient declines on the score known as ALSFRS. This is an FDA-accepted score that measures how poorly or how well an ALS patient is doing. Simply put, the lower the score, the worse the patient is doing in terms of their progression of ALS. It is a zero to 48-point score with the lower scores being worse. What this database has historically shown is that ALS patients progress at about one point a month. They decline at about one point a month with the current interventions, with the current standard of care. What that means is about a six- to seven-point decline in six months and a 12- 14 point decline in about one year. Now, what does this mean clinically? As an example, a six-point decline can be the difference between a patient being able to walk on their own versus being on a wheelchair. A 12- 14 point decline can be the difference between a patient being able to walk on their own and needing complete care from a caregiver or even being on a ventilator. A one-point shift in the ALSFRS score is very clinically meaningful. Today, there is really no therapy that provides a good solution for these patients who continue to decline and progress. In an investigator-initiated trial, we looked at the combination of low-dose interleukin-2 with CTLA4 in a small group of patients with mild to moderate ALS. The study trial was for 48 weeks, almost one year, with a six-month readout and a 48-week readout. The patients in this trial, their characteristics were similar to what you would expect in the average ALS patients as per the PRO-ACT Database. We had a mix of patients, including familial type ALS, that is, C9orf72 gene positive patients who are at very high risk of developing either ALS or frontotemporal dementia, as well as the sporadic ALS patients, which is the most common type of ALS where the cause is not driven by a known genetic factor and is mostly unknown. More importantly, the patients in our trial were declining at approximately the average rate you would expect ALS patients to be declining. What was observed in this investigator-initiated trial was remarkable. While it's a small number of patients, what was seen in this study was that three of the four patients either improved in their ALSFRS score or stayed stable at six months. Recall that I said that the historic data shows that the ALS patients at six months would have declined by about six to seven points. This was a pretty remarkable observation. There was one patient that declined pretty rapidly in the first month of treatment, but later on stabilized. If you look at our mean data, the patients came in at an ALSFRS score of 33.5, which is considered to be mild to moderate ALS. What is remarkable is that at six months, there was no decline in the ALSFRS score when you would have normally expected a decline where the score would have been about 27. At 48 weeks, one would have expected this score to be at around the 20s, which means the patient has progressed pretty severely, but we saw a 1.5-point reduction in this trial. Again, a small trial, but remarkable results. More importantly, when this therapy was stopped, the patients started declining at the one-point-a-month average that you would anticipate them doing. The results from this study gave us a lot of confidence in moving forward and advancing our proprietary COYA 302 in ALS. What was also important to observe is that these clinical outcomes were strongly supported by biomarkers and mechanistic data. The dosing of low-dose interleukin-2 plus CTLA4 showed increase in Treg numbers as well as the Treg suppressive function, which is what we would expect from a mechanistic perspective. More importantly, upon stopping dosing, these effects get reversed. We also saw that biomarkers of oxidative stress, including oxidative LDL, 4-hydroxynonenal, and neurofilament light all moved in the right direction, giving us a lot of confidence that we are hitting the target, the biomarkers are moving in the right direction, and we are seeing supportive clinical outcome. Armed with this data, we have had discussions with the FDA. We plan to submit the full IND package in the second quarter of 2025 and, with the blessing of the FDA, initiate a randomized double-blind phase 2B study that we have had discussions and aligned with the regulatory authorities on. Very briefly, this is going to be we are proposing a 120-patient trial with two-dose arms of COYA 302, including one-dose arm that was the dose of the low-dose interleukin-2 and CTLA4 used in the small proof of concept study, a placebo-controlled trial with a six-month ALSFRS endpoint, which is an FDA-accepted endpoint. After six months, the patients on placebo will be crossed over into one of the treatment arms. We also have inclusion and exclusion criteria that I will not go too deep into that ensure that we have the average ALS patients and do not include outliers that includes patients that for some reason do not advance that much in their ALS or patients that are advancing too rapidly. We will also have appropriate cutoffs for ALSFRS at 35, which means that we're bringing in patients before they're too far advanced in their disease state. Now, switching our focus to the next disease that we are focusing on, COYA 302 is frontotemporal dementia. There's an investigator-initiated trial being conducted by Dr. Alireza Faridar at Houston Methodist that is currently ongoing. We anticipate getting top-line results by the early second half of 2025. Those results will help us further refine our planned phase 2B study in these patients. The science was found interesting enough that the Alzheimer's Drug Discovery Foundation, one of the preeminent organizations with expertise in this space of dementia, has supported us with a $5 million investment to support the progress of this trial. We will be submitting an IND to the Food and Drug Administration towards the end of this year and will initiate this phase 2B trial soon after green light from the regulatory authorities. Now, I'm going to transition to our other pipeline assets. As I briefly mentioned in the introduction, COYA 301 is our low-dose interleukin-2 proprietary as a standalone. We really see advancing COYA 301 more as a combination with other modalities in Alzheimer's disease as well as in other diseases, including autoimmune diseases, where there is a lot of potential in combination. However, we plan to do this only in partnership with a larger strategic partner or through significant grant funding and do not plan to advance these on our own at Coya. We feel pretty good that there are opportunities here for strategic partnerships. COYA 303 is a combination of a proprietary low-dose interleukin-2 with GLP-1 agonist. We have filed intellectual property on this combination with strong IP life, and we have early preclinical data that demonstrates synergy where addition of GLP-1 agonist with our COYA 301 shows synergistic effects on several neurodegenerative and other markers, and we will be publishing details of this data in the upcoming months. In addition to that, at a very early preclinical stage, we have a couple of exosome programs that we will share more updates at an appropriate time with the market. Briefly, with low-dose interleukin-2 alone, in an open-label investigator trial, what was observed in an eight-patient trial is that the cognitive function, as measured by Mini-Mental State Exam, was improved in patients with Alzheimer's disease, and the biomarkers followed. This study was encouraging enough that the Alzheimer's Association and the Gates Foundation funded a full double-blind study, placebo-controlled studies in mild to moderate patients with Alzheimer's disease. Very highly, what we saw at a high level, what we saw was remarkable again and consistent with what we saw in ALS. After five months of once-a-month dosing, we saw the progression of cognitive decline stop or there was stabilization of cognitive decline. This was aligned with biomarkers such as A beta42 that went up in the cerebrospinal fluid, suggesting plaque removal in the brain. The study, the low-dose interleukin-2 administered subQ, was safe, well tolerated, and this gives us a lot of confidence in advancing the combinations of IL-2 with other modalities, but also gives us a lot of confidence in our mechanism and in advancing COYA 302 in ALS and frontotemporal dementia. Finally, very briefly, a lot of news about GLP-1s. are a lot of publications recently, both in Lancet last year and Nature Medicine this year, that show that GLP-1 agonists have the potential to slow the onset or advancement of dementia. As I mentioned before, we will be sharing additional data in the upcoming months that show the synergistic potential of our COYA 301 in combination with GLP-1s to address neurodegenerative as well as other diseases. Combined with our strong IP and science, we believe this provides us good optionality and value-creating potential for strategic partnerships. I will once again remind everyone of our key milestones in 2025. We have multiple readouts in additional data with the investigator-initiated trial in patients with Alzheimer's disease, additional publication on the combination potential of GLP-1 with COYA 301, initiation of our phase 2B ALS trial later this year, preceded by the submission of the IND to the FDA, top-line data from the investigator-initiated trial in frontotemporal dementia, and submission of the IND to initiate a larger FTD trial. Thank you for your time today. I appreciate it, and I'm happy to take any questions at this point. Excellent. Thank you so much, Arun. Really appreciate the update. I guess maybe one question we're getting is about your study in ALS. Do you plan to take all comers, or are there any particular genetic mutations that you'll be studying? Jay, no, we will be taking all comers. The nice thing about the way we approach neuroinflammation is that it is agnostic to the genetic mutation. We are not separating by SOD1 or C9orf72 mutations. We take them all. What we have seen with that small study is that it works across these patient populations. Okay, great. Have you found that in ALS patients, they have similar degrees of neuroinflammation, or are there some patients who have more profound neuroinflammation? Yeah, in general, we believe ALS is actually a highly inflammatory disease, a lot more than, for example, Alzheimer's, which is why I think our combination approach is critical to keep the dysfunctional Tregs functional and from converting back to becoming dysfunctional. Yes, it is a pretty inflammatory disease. We have seen positive data on FOXP3 and some of the markers that I am happy to go into detail later on. Yes, okay. All right. One of the biomarkers that a lot of investors are interested in is NfL. In your studies of 302 and ALS, have you seen any changes in NfL? Yes, we've seen positive changes in NfL, and NfL will be something we are measuring in this phase 2B study. It will be a key secondary endpoint that we measure. Okay, great. Do you think NfL could be a biomarker that could be used to pursue an accelerated approval pathway? I think that's something that we'll have to discuss, obviously, with the regulatory authorities at the right time. There's obvious precedence for it. That was done with a very small SOD1 population of ALS, which is less than 1% of the ALS population. Yes, NfL is definitely being recognized by the FDA and others as a good marker. We have other markers that we will discuss with the regulatory authorities as well, where we see great correlation. Yes, I think all that will depend on the data and our conversations with the FDA at the right time. Okay, great. Are you envisioning this new ALS study as being potentially registrational? There is precedence for it. I think it will come down to the data. I think if the data are compelling, which we expect it to be, there is obviously a path forward for an approval on one trial based on FDA's precedence with, for example, Relyvrio as an example. Okay, great. Do you think the 24-week treatment period is long enough to show a clinical benefit? Yes, we do because of the progression of ALS, as I mentioned before. Six-point decline is a very visible decline in ALS patients. We do believe that six months is sufficient to show a separation from placebo. Okay, great. I guess the last question is, when patients enroll in your study, will they be on any background ALS therapies? Yes. Short answer is they'll be on whatever standard of care. The usual criteria is that they've been on it for months before they come into the study and are not changing their therapies. Yes, they will be allowed to be on whatever standard of care they were in coming into the study. The study is designed to make sure that the placebo and treatment arms are balanced with that kind of treatments. Okay, great. All right. This has been super helpful. Thank you so much, Arun, for bringing us up to speed on all the impressive work that you're doing at Coya Therapeutics. It's a pleasure to catch up with you today. I appreciate your time. The pleasure, Jay. Thank you. Thank you for the opportunity to participate in the conference. Absolutely. Thanks, everyone, for joining us.