Yeah, there we go. Good morning, everybody. My name is Cory Kasimov, one of the senior biotech analysts here at Evercore ISI. It's my pleasure to host our next discussion with Coya Therapeutics and the company's CEO, Arun Swaminathan. I hope I got that right. Arun, thanks very much for being here today. Really appreciate it. I guess to start, I mean, it's hard to believe we're already in December. Given the timing, I'd love to begin the discussion by asking you to reflect back on 2025 and kind of talk about what you think were the company's biggest accomplishments this year.
Thank you. Thank you, Cory, for having me here. Really appreciate it. 2025, reflecting back, has been a really great year for Coya because we have really made progress in our lead asset entering the clinic. We're now in a phase to be potentially registration trial.
Let's bring your USB at some point.
That's a big milestone.
Got lost in the chat. I don't know when it is, but they'll show.
Many other milestones.
Can I say they'll show up with it.
The FDA is doing all of our trial design and moving forward. We had interim data from an investigator-initiated trial in frontotemporal dementia, which looks very promising. We had great preclinical data on the combination and synergistic potential of GLP-1s with our COYA 301, our proprietary low-dose interleukin-2. This is just to name a few of the accomplishments we have had this year. We've had some good publications. Not to take credit for itself, but we were honored that our scientific advisory board member, Dr. Shimon Sakaguchi, won the Nobel Prize in Medicine and Physiology for his work around Tregs. We feel pretty proud that in 2025, a lot of these things happened, including some external validation of the science that we are building the company around.
Got it. Got it. Your double mic now, that's pretty impressive too.
Wow. Yeah.
All right. Before we get into specific products, can you talk a little bit more about the platform you're building at Coya with the Treg biology and the various targets that you've selected?
Yeah. I mean, at Coya, we're focused on neurodegenerative diseases. How we believe we can address these diseases and stop their progression is by restoring the numbers and functions of Tregs. By doing this, we essentially stop inflammation. We believe that if you can address inflammation, you stop the progression of these diseases. We have three pillars that I think give us a lot of confidence in our approach forward and confidence that we will potentially have good outcomes in our ongoing clinical trials. One is the science. I briefly touched on it. The science is about Tregs. We really believe that if you can address and make Tregs stay functional, then you can really address inflammation. As I mentioned, work done by Dr. Stanley Appel, by Nobel Prize-winning people have shown that if you do this, you can stop the progression of neurodegenerative diseases.
Second pillar is how we do this, I think, is our secret sauce. We do this through a combination biologic approach because we believe that combinations are the future in neurodegenerative diseases. We do this through an approach where we combine a proprietary low-dose interleukin-2 with a CTLA-4. In short, what it does is it allows the Treg numbers to go up, and it keeps these Tregs functional for a sustained period of time. The third pillar that excites us is that across four small investigator-initiated trials across three diseases, ALS, FTD, and Alzheimer's disease, we see something remarkably consistent, which is that when we keep the Treg functions up and sustained, we are stopping the progression of diseases. That is kind of what is the basis of what Coya is doing. Everything we're doing is focused on bringing down neuroinflammation.
Okay. It's super interesting. I want to follow up on this with your lead program, COYA 302. You just mentioned kind of the wide spectrum of indications you're going after. You have the big ones like Alzheimer's, Parkinson's, and then there's also diseases like ALS and FTD. Did you select these via the investigator-sponsored trials, or is there something else that went into the selection of these indications?
The investigator-initiated trials were critical in informing our decision on which diseases to go forward with. Ahead of those trials even being initiated, there was a lot of fundamental science done in the Houston Methodist labs that told us that these are the types of diseases. ALS and FTD, I like to use the analogy, they're like raging forest fires, highly inflammatory. We chose those as our primary indications for those reasons. One is we believe we can make the most impact there because of the inflammatory nature of those diseases. The pathway to registration, the pathway to the market, is a little bit better for a small company like Coya.
There's a path where we can get their beach—I call them our beachhead indications that then open the door for Alzheimer's and Parkinson's, which are equally inflammatory diseases, but I compare them to burning embers of coal. They're going to be equally destructive, but they do it over a longer, prolonged period of time. That's why we're going after both. As you know, Alzheimer's and Parkinson's are long programs. With a company like us, we also like to have programs where the unmet need is really high and the path to market is reasonably fast. That's why ALS and FTD.
Makes sense. Makes sense. Okay. Your phase two is now underway in ALS. Can you kind of walk through the key elements of that study and what the ultimate objectives are there?
Yeah. I mean, the study is a randomized double-blind placebo-controlled trial. It's about 120 patients randomized either to treatment or placebo arm. When I say placebo, it is background therapy. If the patients are on Riluzole or Radicava, they'll stay on those background therapies. It's a six-month blinded period. Six months is the endpoint. ALSFRS is the FDA-accepted endpoint at six months. That is our primary endpoint. We have other secondary endpoints, including neurofilament light, which you probably are aware, is a biomarker that is highly accepted in ALS. We have other endpoints, of course, safety and other endpoints. Some of the unique features of the trial is that we are ensuring that patients come in with an ALSFRS score that is not too far advanced. We have a cutoff of 35 for ALSFRS. We're also stratifying patients by neurofilament light.
This way, the groups are evenly distributed in the range of inflammation or the range of damage as well, which is something we have learned from the previous ALS trials. We did not do this in a vacuum at Coya. This is working with key opinion leaders. Our PI is Dr. James Berry at Massachusetts General Hospital. That is kind of some of the key elements. At the end of six months, we plan to submit to the FDA the blinded portion of the data, which on its own should be sufficient data supporting for an approval pathway with the FDA. We will continue the trial past six months. We re-randomize the placebo groups to the treatment arms and continue that for one year as well.
Now, that'll give us some additional insights, including we anticipate that the placebo arm of patients would have declined in ALSFRS pretty substantially because the average patient declines about one point a month, which means they'll be below the criteria of our inclusion. It will be interesting to see how the drug does in an open label with patients who have kind of advanced more as well. It is a very smart design, if I may say so myself, that's going to get us a lot of good data.
Yeah. No, I agree for sure. You sort of addressed my next question, but regarding some of the biomarkers that you're using, you mentioned neurofilament light, oxidative stress. Just how receptive is the FDA to these as endpoints? Should we be thinking about them more as supportive evidence for future trial design, or are these approvable biomarkers given the obvious unmet need that you have with ALS?
No, it is a question that I can't with certainty say what the FDA is going to do. Obviously, they're going to look at the data and determine. They have approved products just based on NfL. Of course, that was QALSODY, which is for a much more limited ALS population, the SOD1 mutation population, were approved just based on NfL. We do know that the FDA puts a lot of faith in NfL. I think they look at the data holistically. They're going to look at ALSFRS. They're going to look at NfL. They're going to look at the oxidative stress markers like 4-Hydroxynonenal and oxLDL and probably make a holistic kind of decision whether they all tell a story together. I do think those biomarkers will be very impactful as we have discussions with the FDA when we have the data.
Of course, the primary endpoint is always going to be the most important.
Right. Right. Right. All right. Staying on this topic, but taking a step back a little bit within the context of ALS again, I'm curious your perspective on the current regulatory environment, especially saying, I mean, we've had what looked like progress with analytics and then products removed from the market. Where do the regulators stand on ALS more broadly right now?
Our impression is that based on things they've said publicly as well, is that they do want to prioritize diseases like ALS and frontotemporal dementia, diseases where there are so few options. I think rare and orphan diseases are something that the FDA administration has publicly stated that they want to prioritize and see them approved in a more efficient manner. Having said that, obviously, the FDA's job is to make sure that the data supports an approval. Short answer is they're not going to give us a clear answer until they actually see the data, which I think they use the word review decision, which seems appropriate to me. They really can't say that without seeing the data.
We feel based on the evidence we have, both the scientific preclinical as well as those investigator-initiated trials, we feel pretty good that our probability of technical and regulatory success is going to be good and that we are likely to see a positive outcome in the trial, hopefully enough to convince the FDA that they should get us in the market for these patients that have high unmet need.
Right. Now, if you are fortunate enough to have compelling data that leads to approval, can you talk a little bit about how you see the opportunity in ALS? Is this the type of product and the approach that you're taking, kind of going after inflammation and everything, where it would technically be amenable to any ALS patient?
Yes. That is actually one of the key differentiators of our approach with COYA 302. It is agnostic to genetic mutations. So C9orf72, SOD1, non-sporadic ALS, which is basically a fancy way of saying we don't know what causes the ALS. It works across because we are addressing inflammation and Treg function, which is a driver of progression regardless of the genetic mutations. We are agnostic to it, which means that technically all ALS patients should be eligible for treatment. Of course, our label will be driven by our protocol, but yeah.
Okay. When you go beyond ALS and you go back to the other indications we've talked about, how do you prioritize those going forward?
Yeah. Our next priority is frontotemporal dementia. We are anticipating getting full results from our IIT study towards the very end of this year, early next year. We also plan to submit an IND to the FDA to support a phase II- A study in FTD. This will be a double-blind randomized study. That is our next big trial or significant trial that we anticipate initiating in the first half of 2026.
Okay. For the larger indications like Alzheimer's and Parkinson's, is getting those up and running more a question of just because I completely agree to start here with your strategy of going after ALS and FTD first, but are the bigger indications a function of limited bandwidth, capital, all of those types of things that a smaller company has to deal with? Are there other signals that you would like to tease out first before having the confidence of putting the resources towards the larger indication?
No, it's more the former. It's really we have to be judicious as a small company in how we use our capital. Alzheimer's and Parkinson's are pretty capital-intensive indications. Ideally, we want to do one of two things: find the right partner to move forward in Alzheimer's or find grants and non-dilutive ways to move it forward in smaller studies. We're pursuing both actively. Our combination with GLP-1s, I know Novo Nordisk presented their Evoke data, or they've had the PR of it. They're going to present it tomorrow. We have seen some pretty remarkable synergies preclinically between GLP-1s and COYA 301.
Moving something like that forward with the right partner is something we're going to be looking at as well because we do still believe now we'll get more details from the Evoke trial that'll inform us that that combination has a lot of potential in Alzheimer's disease as well.
Okay. That was actually my next question was going to be the preclinical work that you did with GLP-1 and the combinations for neuroinflammation. Can you kind of just go a little bit more into the rationale there in terms of how that impacts Treg?
Yeah. Interestingly, GLP-1s express Treg receptors. What we've seen is the synergy in the inflammatory markers between GLP-1 and COYA 301. The proprietary IL-2 directly impacts Tregs, as you know. GLP-1s do not directly impact it, but have an indirect effect on inflammation. What we've seen is these two together in preclinical models, in LPS models in mice, as well as in in vitro models using human cells, shows that we are really tamping down a lot of the neuroinflammatory markers and in the animal model, making an impact in the brain level as well. We have seen all the markers move. We are characterizing it more to kind of being able to publish it soon. You will see some of the details of what the science is when we publish it next year.
We do feel excited about it because our assumption was that GLP-1s alone are not going to be sufficient to stop cognitive decline. That was always our hypothesis. That is why we have started combining with IL-2 because we do believe that these diseases have to be hit by combination approaches. You have to hit multiple pathways because neurodegenerative diseases are too complex that you just hit one target and it is going to work. We do believe in the power of combinations. We do believe it is going to kind of follow the oncology model in that you have to kind of combine a few things to get the final efficacy you want. Those individual components may not be sufficient to do it. Yeah, that is kind of our hypothesis. Some of it has been playing out.
As I mentioned, I think the Evoke data, we'll probably see some of it tomorrow. It sounds like we'll see the full depth of it at the AD/PD Conference in March. We're going to obviously pour through that data because a lot of the biomarker data from that trial, I think, will be very informative for us on how we kind of position the combination and also the designs of our future trials, etc.
Yeah. Okay. Can you describe the license agreement you have with Dr. Reddy's, just broad strokes, and then also the milestones and royalties, things like that?
Yeah. Very high level, it's approximately $700 million total deal value. We have received a portion of $16 million or so in milestone payments and upfronts already. We are due to receive another $4.2 million when we dose the first patient, which we expect this month. There are milestone payments prior to the approval of the product as well. Upon approval, it's a mid-teen royalty in their territories with up to $650 million addition to the royalties and sales milestones. What the deal really does for us is it has kind of given us a guardrail and a line of sight to non-dilutive money on a steady basis, which typically companies our size are not always fortunate to have.
It has also removed, I believe, one of the key overhangs for a small company like us, which is we get approval or we get great data and the market goes, how are they going to raise $100 million to commercialize this? We've kind of taken that first indication commercial pressure off ourselves. I mean, obviously, there will be pressure, but that's what this deal does for us. It's only for the one indication that Dr. Reddy's has rights, which is ALS.
Okay. I guess the follow-up to that is what is the status of the balance sheet now in your cash runway?
Yeah. On September 30, we reported approximately $28 million in cash. Subsequent to that, in late October, we raised $23 million. That was done in October towards the end of October. As I said, if everything goes well, which I fully anticipate upon dosing the first patient, we'll receive another $4.2 million from Dr. Reddy's.
Okay. You gave about 15 seconds to answer this when I'm done asking it. Given as we wrap up here, kind of a little sneak peek into 2026, kind of set the stage for your key catalysts and the kind of key objectives that you hope Coya can attain?
ALSTARS trial, full cylinders on. That's going to be priority number one. Initiating and getting the FTD approved and FTD trial, advancing the GLP-1 COYA 303 program. Those are the key priorities for 2026.
Terrific. We are out of time, Arun. Thank you very much. Really appreciate it.
Thank you. I appreciate it.