Coya Therapeutics, Inc. (COYA) Earnings Call Transcript & Summary

Good day, and welcome to the iAccess Alpha Virtual Best Ideas Summer Investment Conference 2025. The next presenting company is Coya Therapeutics Inc. [Operator Instructions] I'd now like to turn the floor over to today's host, Arun Swaminathan, Chief Executive Officer at Coya Therapeutics Inc. Sir, the floor is yours.

Thank you, and appreciate it. I appreciate the opportunity to present the exciting work we are doing at Coya Therapeutics. Thank you all, and good morning. Here are some forward-looking statements that we cover. Eric Dane, the TV actor; Stephen Hawkins, a brilliant physicist, Bruce Willis, actor famous for his Die Hard movies; and President Ronald Reagan, who, among many things, famously brought down the wall. Now you may be wondering what do these people have to do with Coya Therapeutics. What they all have is they all either live or lived with the diagnosis of a devastating neurodegenerative disease. Our vision at Coya is to make the lives of people like this, not just the celebrities, but all patients suffering from neurodegenerative diseases to be a normal life where their life stories about their successes, their families or whatever, but not about their disease. That is the vision at Coya, is to make these devastating neurodegenerative diseases like ALS, also known as Lou Gehrig's disease because it's named after the famous Yankees Lou Gehrig, who was known as the Iron Horse because he did not miss a single game of 2,000-plus games. And in fact, his record was held for a long time until Cal Ripken Jr. surpassed it. But ALS, which was not called ALS then, cut short Lou Gehrig's not only career in baseball, but also his life. So that is our vision at Coya to address these types of diseases. What we do is unique and differentiated. Not only do we target these diseases with high unmet need, ALS has very few options in the market and patients with ALS typically die between 3 to 4 years of diagnosis with a rapid decline in quality of life. Frontotemporal dementia is another disease we focus on, a disease with 0 approved therapies from the FDA and equally devastating in the cognitive decline these patients face and with shortened lifespans as well. And finally, of course, everybody is very familiar with the huge impact Alzheimer's disease and Parkinson's disease have on our society as a whole, not only on the patient, but the toll it takes on the caregivers and our economic system as well. So our approach to this is an elegant scientific approach, and I'll talk a little bit more about it as we proceed in our -- in this presentation is to address something called neuroinflammation at its core by addressing regulatory T cell dysfunction. By doing this, we believe that we can stop -- potentially stop the progression of these diseases. We also take a derisked approach to our programs by taking targets that have been well established in other diseases and taking a unique approach through a combination strategy in addressing diseases. In addition, diseases like ALS and frontotemporal dementia are orphan diseases, thereby also providing a faster potential path to the market and higher regulatory flexibility. While these are tough diseases, they do have high commercial potential as well. So while our focus and core and central belief is doing what is right for the patient, we also recognize that doing what is right for the patient comes with high commercial potential as well. And I will talk a little bit more about what our pipeline is and what we're doing. In addition to that, I think what makes us strong is our strong cash runway. We have a very clean cap table with a good investor base, including people like Greenlight Capital, David Einhorn, who is our lead investor; AIGH, a biotech-focused fund and many other strong investors who have been part of our story from inception. On top of that, as a small private company, we are fortunate to be in a strategic partnership with a multinational company, a $13 billion-plus market cap company, Dr. Reddy's. What this partnership allows us to do is a strategic deal worth over $700 million in deal value, allows us line of sight to a steady stream of non-dilutive cash coming our way in a steady basis, which really strengthens not only our financial position, but also we are able to leverage the expertise and overlaps and synergies that the 2 companies have to advance our programs in the most efficient, not just cost but also time-efficient manner. And finally, we have a very accomplished management team that has a proven track record of creating value in every company they've been at. We have a lot of exciting milestones coming ahead in the very near future as well as through this year and into next year. You will see through the course of this presentation that I will share with you some data that is remarkable. Across 4 small investigator-initiated trials across 3 different indications: ALS, FTD and Alzheimer's, we have seen something very promising. What we have seen is that a consistent ability to stop the progression of these neurodegenerative diseases. That gives us a lot of confidence that moving forward to the bigger trials, we have a good potential of showing a meaningful difference and making a meaningful difference for these patients. On that end, one of our key immediate milestones is going to be the submission of the data required to support the initiation of a Phase IIb study in patients with ALS. We plan to submit that to the Food and Drug Administration imminently and then upon green light, initiate this potentially registrational trial in the fall of this year. That also triggers a milestone payment of $4.2 million and $4.2 million for a total of $8.4 million in a non-dilutive manner from our strategic partner, Dr. Reddy's. In addition to that, we have multiple other milestones in the other diseases I talked about. We will have additional data from a small investigator-initiated trial in patients with frontotemporal dementia. We anticipate filing an IND to support a Phase II study in patients with frontotemporal dementia. This study is partly funded by a strategic investment from the Alzheimer's Drug Discovery Foundation into the company. ADDF is a highly scientifically rigorous organization, and we feel honored that they believe in our approach and our combination strategy as a way forward to address these diseases. Between the Dr. Reddy's partnership and the ADDF investment, we have significant external validation on our technology and our approach, and we are proud of this. And we have multiple other milestones and data points on our combinations with GLP-1 and Alzheimer's disease as well that will be coming through the next second half of this year. But what do we do different? And what is it that differentiates us? The Coya solution is focused on addressing what fundamentally we believe drives the progression of these diseases, and that is neuroinflammation. We believe that addressing neuroinflammation at the source can stop or slow down the progression of these diseases and the early investigator-initiated data that we have seen supports this hypothesis. We are continuing to build evidence that what our mechanism, our approach does truly have the potential to transform the future of how these patients are treated. And as I mentioned before, not only are they high unmet need indications, even orphan diseases like ALS and FTD have great commercial potential because of the lack of any other options for these patients, upwards of billions of dollars in sales potential across the major markets. Scientifically, how do we address this neuroinflammation? What we do is there are these cells called the regulatory T cells. As the name implies, they regulate or modulate the immune system. They keep things in check. T cells are -- and helper T cells together usually tend to attack what they think is foreign. What happens in neurodegenerative diseases as well as in autoimmune diseases, but I will use neurodegenerative as my example, is that these T cells can sometimes get out of control when Tregs are dysfunctional. When the regulatory T cells are not doing their job, the T cells can hurt or affect the communication between nerve cells, cause damage of neurons, which eventually leads to the various neurodegenerative diseases. So what we want to do is to keep these Treg numbers high and keep these regulatory T cells functional for as long as possible. That is a fundamental scientific premise of our approach and what differentiates us from many other approaches because we are working upstream on the disease process and not focusing on just one downstream marker that may or may not address the complexity of these diseases. In addition to that, these diseases are complex, and we believe that one pathway is not enough. You have to use combination strategies to address these diseases across multiple pathways. And that is exactly what we do with our lead candidate, Coya-302. Coya-302 is a proprietary combination of a low-dose interleukin-2 with a CTLA-4. And we have strong intellectual property around this combination as well as the individual assets. What in summary, it does is that the low-dose interleukin-2 increases both Treg numbers and function, which is a good thing, and that is what we wanted to do. But we also know through extensive studies and data we have generated that low-dose IL-2 alone, while it will do the job of increasing Treg numbers and function, because the macro environment remains inflammatory in these diseases, the Tregs tend to revert back to becoming dysfunctional. And we want to stop this from happening and keep the Tregs functional. And through a series of experiments and a lot of work that happened at Dr. Stanley Appel's lab at Houston Methodist, we were able to figure out that adding CTLA-4, which acts on a different aspect of the immune system keeps the myeloid cells, keeps the macrophages anti-inflammatory, thus preventing the Treg function from reverting. Therefore, we get durable efficacy. In addition to that, we have seen data that the combination actually increases the Treg function as well. So together, we have seen good and positive effects on this combination. Now as I mentioned before, we are in partnership with Dr. Reddy's to advance Coya-302 in patients with ALS. Dr. Reddy's will be responsible for the commercialization of Coya-302 in most major markets. Coya retains the rights for Japan, North -- South America and Mexico. What this also does for a small company like us is for our first indication, for our launch indication, Coya is not responsible for the commercial expenses associated with this launch. And we obviously also closely partner with Houston Methodus to generate all the scientific evidence required to advance our programs. The Reddy's partnership is a $700 million partnership with milestone payments, mid-teen royalties and sales milestones up to $650 million, which sets us up well for a steady stream of nondilutive funding, as I mentioned before. Now I'll transition and talk to you a little bit about our lead asset in ALS. ALS, for those of you who know, is a devastating disease, and it is typically measured by the score called ALSFRS, which is the endpoint that the FDA accepts and as a primary endpoint. Based on this database known as PRO-ACT database, which is a database of thousands and thousands of patients coming out of Mass General and Harvard University, we know that the average ALS patient declines about 1 point a month on the score, so approximately 6 points in 6 months, 12 points in 12 months. So what does 6 points mean? As an example, 6-point difference can be the difference between a patient's ability to walk with a cane versus being on a wheelchair. So every point of change in the score is a dramatic impact on the quality life -- quality of life for these patients. A 12-point difference could be the difference between walking with a cane and being on a ventilator. So this is very impactful. Currently, there are really very few therapies available that can address this disease. And on the right of the screen, you see in green, RADICAVA, which is one of the few approved products available does not really completely stop the progression of this disease, neither does Riluzole, which is the other drug that is approved and the previous drug that was approved has subsequently been withdrawn from the market. So there's almost no choices for these patients and nobody has really demonstrated the ability to stop progression of this disease to date. What we saw in a small investigator-initiated trial that combined the low-dose interleukin-2 and CTLA-4 was something remarkable. At 6 months, we saw that there was no change in the mean ALSFRS score of these patients. As you recall from my previous slide, you would expect a 6-point decline in 6 months. So a baseline of 33.5%, approximately, we would expect that those patients would be at a score of 27. But what we saw is they stayed stable at the same 33.5. And further, talking to the durability of response, which is what I was talking about why the combination keeps the Tregs functional longer, we saw that even at 48 weeks, almost 1 year, very little decline in the ALSFRS score in these patients when you would have normally expected a 12-point drop in the same period. So this is a very encouraging data. It also is backed up with a lot of good biomarker data that I'm not sharing here today that shows that the biomarkers, the oxidative stress markers, all of them move in the right direction and lines up well. So this has given us confidence in moving forward with a potentially pivotal Phase II study in patients with ALS. This will be a double-blind randomized controlled study that we anticipate submitting the package to the FDA by the end of this quarter and upon green light subsequently initiating this trial later this year. So we're pretty excited about the potential of this study. Now in addition to ALS, what we have seen is that the same combination in an IIT study in frontotemporal dementia, the low-dose IL-2 and CTLA-4 showed that we did increase the function of the Treg. So again, consistently showing that we are hitting the target we are planning to hit. And then it's translating into the biomarkers moving the right way. And that in turn has translated into the cognitive function as measured by FTLD scores as well as by Montreal assessment scores in these patients saying stable. So again, we're seeing a consistent pattern, although in small studies that's giving us confidence that our approach is likely to work. And then finally, we studied just one of the components, the low-dose IL-2 in Alzheimer's disease. And this was a fully funded study from the Gates Foundation and the Alzheimer's Association, double-blind randomized study in Alzheimer's disease patients and again, a consistent pattern. What we saw was the ability to stop cognitive decline in this case, as measured by ADAS-Cog, changes in things like beta -- amyloid betas that show that, that is being removed from the brain, change in Treg function, Treg numbers. So again, what we see is a consistent pattern that is starting to give us confidence that our approach of combining a low-dose interleukin-2 with other modalities with our lead product that is CTLA-4 makes a lot of scientific sense and has a good probability of technical and regulatory success. The data we generated with the low-dose interleukin 2 alone in Alzheimer's disease has given us immense confidence in 2 ways. One, it again confirmed our hypothesis that low-dose IL-2 alone is not always the right thing. We need something else that keeps the Tregs functional. In the case of ALS and in the case of 302, we have used CTLA-4. But we also have a new asset Coya-303, which is a combination with GLP-1 agonist, the popular weight loss drugs like Wegovy, Ozempic, Mounjaros, et cetera. GLP-1s alone have shown potential in slowing down or preventing onset of dementia. There was a retrospective study published in Lancet early this year that showed that across approximately 1.5 million patients, patients taking GLP-1 agonist had lower incidence of onset of dementia and progressive dementia compared to patients who are taking other therapies to manage their diabetes. And then, of course, Novo Nordisk is doing a big Phase III trial, 2 of them, EVOKE and EVOQUE+ in mild Alzheimer's disease using their semaglutide alone. We believe, and we have shown preclinically that combining Coya-301, our proprietary low-dose interleukin-2 with these GLP-1 agonist are synergistic, meaning that our effect on the neuroinflammatory markers was better than 1 plus 1 is 2. It was better than 2. This gives us a lot of confidence that this combination has the potential to be transformative in Alzheimer's disease and also unlock tremendous potential for Coya in the upcoming months and year. And we look forward to continuing strategic discussions around this asset because we do strongly believe there's a lot of potential for partnership opportunities here that would also be value creating for Coya. So in short, what you've seen hopefully through this presentation is a consistency of our data -- of the data generated to date that really holds strong promise in our ability to deliver transformative therapies for these patients that could potentially allow these patients to live with these diseases as normal life as they can, which would be the -- a vision that Coya wants to be part of. And finally, I had previously walked you through the milestones, but I just want to remind you again that we have multiple key milestones coming imminently as in starting soon through the next month, through 3 months, through 6 months, through 1 year and so on. So we have a steady value-creating milestones that are coming this year as well as into next year. And we are very excited about the potential of Coya in the future. I really appreciate all of your time, and thank you for giving me the opportunity to tell you what the exciting potential we have here at Coya Therapeutics. Thank you.

Thank you. That concludes Coya Therapeutics Inc. presentation. You may now disconnect. Please consult the conference agenda for the next.