Great. First, welcome to Jay Duker and George Elston from EyePoint Pharmaceuticals here at the 47th Annual Goldman Sachs Healthcare Conference. Welcome, gentlemen. Thank you very much. For those in the audience and listening who may be newer to the story, can you start at a high-level overview of EyePoint today, core clinical programs that are advancing, and key milestones that you've got investors' radars? Sure. Happy to answer that question. Again, we really appreciate the invitation. EyePoint is a drug delivery company for the back of the eye. We hope to improve patients' lives who have serious retinal diseases. Our lead product is called DURAVYU or EYP-1901. It's a combination of a small molecule tyrosine kinase inhibitor called vorolanib, in our proprietary bioerodible delivery system. Vorolanib is a bit unique because it has activity against all the VEGF receptors. Again, it is a receptor-based treatment as well as PDGF, and we also block the JAK1 receptor, which means we have an anti-inflammatory effect, which does appear to be important in retinal diseases. We are currently in phase III in the two largest retinal indications: wet age-related macular degeneration and diabetic macular edema. The wet AMD trials are called LUGANO and LUCIA. They are traditional non-inferiority trial endpoints. The first trial, LUGANO, is on target to read out sometime in August of this year. The LUCIA trial is about two months behind and therefore will read out approximately two months after that. The diabetic macular edema trials are still currently enrolling, and as of last week, they were two-thirds enrolled. They are simultaneous, identical non-inferiority trials called COMO and CAPRI, and they should be fully enrolled in the third quarter of this year. Given that their endpoint is 56 weeks, the top-line data should be out in the fourth quarter of 2027. We have some really exciting milestones coming up in the next year and a half. Great. Maybe dig in a little bit deeper in terms of your view of the differentiation. At a high level, where do you see the key differentiation versus standard of care from both standard of care as well as other emerging clinical agents? Sure. At a high level, what we can provide is sustained-release anti-VEGF effect for six months or longer with a single injection. We have some excellent biologics that are direct ligand blockers that are approved. We have multiple biologics, and while some of them have extended duration, they really don't have sustained release. My opinion, the only true sustained release that's approved is the port delivery system. The differentiator there is port delivery requires surgery for placement. Our medications are injected in the office with a standard intravitreal injection procedure. I might add, we do come in a prefilled sterile syringe injector, shipped and stored at room temperature, which is not a major differentiator. We believe commercially, the fact that we don't need to be refrigerated or frozen will prove to be an advantage should we be approved. I think the durability obviously is the big high-level differentiator. The next issue around durability, of course, people talk about reduction in treatment burden. How many fewer injections or visits will that provide? While that's important, what we believe, and I think the retina community is coming to believe, that durability with sustained release means in the long term, patients will get better vision. That's really what we're trying to accomplish. The reduction in treatment burden, let's call it a beneficial side effect of that. That's not our true value. We believe the true potential value here is better vision in the long term. That's the high level. I think also I mentioned that we do appear to have activity against the JAK1 receptor, which means we should reduce the downstream effects of IL-6, which is an inflammatory pathway that's been implicated in both DME and in wet AMD. That, again, can prove to be a differentiator for us. If we're approved with an every six-month label and we provide both anti-VEGF activity and anti-inflammation activity, I think that has the potential to set us apart from the current therapies and frankly, from the other therapies that are currently in study. Yeah. Let's dig a little bit deeper there. When you talk about, especially some of your recent ARVO work around IL-6, JAK1, et cetera. Can you talk a little bit more detail on why you see the anti-inflammatory potential benefit as differentiated? Specifically, how is that going to translate to meaningful clinical benefit or eventually commercial? Sure. Great question. Let me start at the beginning in what prompted this discovery that we were not only anti-VEGF, but we were anti-inflammatory. I'd like to go back and review a little bit of our phase II DME trial, which is called the VERONA trial. In the VERONA trial, we recruited patients who had active DME. It meant that they had fluid, and they had decreased vision. Randomized either to receive a single EYLEA injection or an EYLEA injection 30 minutes later with EYP-1901. If you look at the week four result, the earliest time point, the eyes that received our drug were already four to five letters better than the eyes that received a single dose of EYLEA. They're about 40 to 50 microns drier on OCT. We believe we have a very good anti-VEGF drug. When we looked at that data, I said to the R&D team, "I don't think we're that much better than EYLEA. There must be something else active here. That's when we went back and did a further kind of analysis and discovered that the IC50 for vorolanib in the JAK1 receptor is about 80 nM, which means at the doses we're using in humans, we should be active against the receptor. Subsequently, we did some cell-based studies, including a study where IL-6 was applied into cells, and vorolanib was able, at doses that were equivalent to what we're using in humans, reduce the downstream activity of the IL-6 by about 50%. At ARVO, just recently, we reported another trial, cell-based, which essentially looked at leakage from cells. If you add VEGF and IL-6 to cells, they will leak. If you then add an anti-VEGF, they'll leak less. If you add an anti-IL-6, they'll leak less. If you add both, you get minimal leakage. We added vorolanib at approximately the dose we can get into humans, and we were essentially the same in leakage reduction as the IL-6 blocker and the anti-VEGF. It's additional data to suggest that the anti-VEGF. I do want to mention a couple other things from the VERONA trial. I mentioned the rapidity of onset and also the rapidity of the dryness. If you look at the eyes in VERONA, and it was over 70% in the high dose that did not get rescued, they just received our drug for six months. Those eyes improved over 10 letters. Now, again, cross-trial comparison is difficult. If you look at the improvement in a previously treated population in patients receiving EYLEA, it was less than that. In the phase III, we've designed the trial to show this difference at week four. We're dosing our drug at day one. At week four, we can replicate the findings that we had in the phase II. I think that even in the end, if we're non-inferior to EYLEA, but we can get the patients to see better, faster, and get them drier faster, that means, I think, potentially a huge commercial success. Great. Back to VERONA. One other data point here. A leakage in eyes can be measured quantitatively by fluorescein angiography, and a reading center that's independent can rate the leakage, and that's a sign of inflammation. In a dose-dependent fashion, EYP-1901 reduced the leakage more than EYLEA did. Another data point that suggests that this anti-inflammatory effect is real. Great. We'll get into wet AMD and DME in a little bit more detail shortly. Before doing so, can you talk about the delivery platform and kind of how that is part of the story in addition to active drug itself? Sure. Again, a great question. Just to remind people, EyePoint has been in the sustained drug delivery to the back of the eye space for almost 30 years. We've had four FDA-approved products with sustained delivery. All of them, however, prior, were not bioerodible. The way they were designed is you had the drug admixed with a matrix, then the drug disk or cylinder was then surrounded by an impermeable plastic that was inert. The plastic was open. There was essentially pores at either end, and that allowed the drug to diffuse out. The reason you needed that is if you had a very soluble drug, like a corticosteroid or ganciclovir, for example. Without that reduction in the surface area, the inserts wouldn't last very long. That matrix, though, is very similar to the matrix that we're using in the current version of EYP-1901, and it's been in tens of thousands of patients safely. The difference here is we removed that impermeable plastic. We want the whole surface area of the inserts to be able to release the drug because we want it to get higher levels, number one, and number two, we didn't want any residual long-term plastic to be remaining in the eye, given that on average, wet AMD patients can live over a decade requiring treatment. We really didn't think there was any reason to keep that design. In effect, the current inserts have less excipients than the four that were FDA approved. In addition, what our scientists were able to do with the latest version is increase the payload of the drug. Our inserts are now 94% vorolanib, only about 6% matrix. That gives each insert a payload of about 1.34 milligrams of drug, which means we're able to achieve high tissue levels with two inserts in a single injection. Our injector actually can hold up to three inserts. Which again, down the road, one could then potentially see the possibility of using multiple drugs in a single injection, which is something that we look forward to studying in the future. Great. Very helpful. Moving on to, I guess, digging in a little bit deeper on wet AMD. Talked a little bit about VERONA and some of the prior data there. Can you talk about DAVIO 2 and how that underpins plans within wet AMD? Sure. DAVIO 2 was our phase II study in wet AMD. It enrolled approximately 160 patients, and they were randomized to either receive three milligrams of our drug versus two milligrams versus on-label EYLEA control, two milligram EYLEA. The patients all were previously treated, and in order to enter the study, we only wanted to enroll patients that had responsive to an anti-VEGF. They had to receive an anti-VEGF two weeks to five weeks prior to screening, and they had to show a response. They were enrolled. The primary endpoint was at month eight, and eyes were not re-injected with our drug. They only received a single injection. At month eight, we were statistically non-inferior to EYLEA, and the actual numerical difference in the vision was only 0.3 in the two milligram arm and 0.4 in the three milligram arm. That's 0.3 letters. Now, those of you who've been to the eye doctor, you know. You read a line, that's five letters on a line. It's less than half a letter difference. Which is, again, statistically equivalent. Equally important is we found that the safety was quite good, and we really had no safety signals that were identified in that trial. There were no ocular systemic SAEs that are attributed to our drug or our inserts. We're quite pleased with the safety, and we've reported safety on over 190 patients from the phase II and phase I trials. Again, the safety has been quite good. From the perspective of, for example, the anatomic results, we measure anatomy using the device called the OCT. Normal anatomy on an OCT is up to 325 microns in thickness. Anatomic control is important because in wet AMD, what's been shown is if you allow patients to gain fluid and have more leakage, even if you get it back under control, if that cycle continues, you can lose vision and get fibrosis as a result. Our maintenance of the anatomy was quite good in DAVIO 2. In the higher dose, the three-milligram dose, there was about a five-micron difference in the end between us and EYLEA, which is really, really small. More importantly to the doctors, having the fluid go up and down in a sawtooth pattern is something that they really don't like to see. Our fluid control was quite good through the whole study. That's, again, important. If you look at the eyes in DAVIO 2 that were unrescued, meaning they only got our drug, there was straight anatomic control all the way through. What that tells you is that the drug was working till the end, because you would expect if the drug started to run out at month seven or eight or nine, you would start to see an increase in fluid, and we didn't see that. It gives us confidence that we truly have a six-month or longer drug. Reduction in treatment burden was about 80%, and about two-thirds of the eyes were free of a rescue up to month six. Even though we didn't re-inject the drug, at one year, about 50% of the eyes in the DAVIO 2 arms were unrescued. We had quite good durability, even with a single injection. That gives us quite a lot of confidence going into the phase III about the results, and we've obviously used what we learned in the phase II to model the phase III. Great. Good transition to phase III. Can you remind investors of study design and, in particular, why you chose non-inferiority versus, there's certainly other approaches out there. Additionally, kind of the current status. You mentioned it earlier. Sure. Non-inferiority, the way the last five approvals have been in wet AMD have been using a non-inferior approach. It's a de-risked approach. There's a lot of risk in this business. Our belief is that any time you can reduce the risk without harm to patients or harm to your label, you should. Obviously, we're taking a de-risked approach. Non-inferiority, again, the doctors understand it. They've seen it before. Our control arm, two milligram EYLEA, is still the treatment of choice of a lot of doctors out there. When the data comes in, if we're non-inferior to that two milligram on-label, I think the doctors are going to understand very well where we fit into their paradigm. Non-inferiority, again, to us is a de-risking, and it's the way to get to FDA approval, we believe, the fastest. The study design is very similar to DAVIO 2, except in a few ways. First of all, we enrolled the majority of patients who were actually treatment-naïve. About 75% treatment-naïve, about 25% previously treated. We believe the addition of the treatment-naïve patients, if approved, will not only help us on the label, but also de-risk the trial. What I mean by that is, in W02, we had a very tough to treat population. On average in the United States, patients get about six injections a year. In W02, if you looked at the prior year and normalized the number of injections, it was about 10. That makes sense because those are the patients we'd call frequent flyers who need a lot of treatment. We got very few easy to treat patients in W02. Our hypothesis is if you have a patient who can go three or four months on any of the anti-VEGFs between injections, they should do really well with our drug. We think the addition of the naive patients allows us to get a proportion of those easy to treat patients. We think that's going to actually improve the end result. The second difference I mentioned already is we're re-injecting every six months over two years because we'd like an every six-month label. We didn't re-inject in W02 at all. The third difference is we altered the supplement criteria. We studied the supplement criteria in W02 and found out that three of the criteria that we used did not result in an improvement in vision after supplementation, therefore you could call it a wasted supplement. We didn't include those in the pivotal trial. Ultimately, we think with positive data, doctors will know exactly how to use this, and our label should be very straightforward. When you think about what does good look like, how should investors frame BCVA in the context of non-inferiority? Sure. That's a really good question, one that's very pertinent given that our data is coming soon. I think the way to look at our data from the top line from the phase III is really quite simple. The first is we need to hit non-inferiority. We need to be statistically non-inferior. That's obvious. That's the primary endpoint. I'd also argue that the exact numerical difference probably doesn't matter. This is, again, a piece of data to share, but if you look at the wet AMD study of high-dose EYLEA that got it approved, the high-dose EYLEA arm was 1.4 letters worse than the two milligram arm. It doesn't stop us retina specialists from using it all. It's a great drug. That amount of vision we believe is inconsequential to the patient. Frankly, the agency believes that too. That's why the non-inferior margin letter or two or even three is impersonal. Most of us physicians don't really care. I would argue that the exact numerical difference probably doesn't matter. We need to hit the primary endpoint. I'm going to reverse myself though and say there's a chance we could be superior. We're able to test for that without penalty if we hit the non-inferiority margin. Obviously not guiding to this, we could be statistically superior, even numerically superior, I think obviously either of those, if we hit it, would be very beneficial to us commercially. The second piece of data you should look for at the top line is safety. Those of you who follow retina companies, you know safety is of paramount importance. The good news for us is I've already mentioned the safety in the prior studies, we've talked about this publicly. A few weeks ago, we had the DSMC meet, they see not only the masked safety from the trials, they see the unmasked safety, they didn't recommend any changes in the protocol or the trials, which is of a relief. We see a masked safety. As we've reported publicly, the masked safety looks very similar to what we have seen in the prior 190+ patients that we've already reported on. While the studies are not over, anything can happen. I'd also like to remind everybody that most of the safety events occur at or just after the time of injection. In this last look at the safety, all the patients in LUGANO and LUCIA had received their second dose of our drug, about a third of them had received the third dose. The third thing to look for at the top line is reduction in treatment burden. We believe this may be the easiest bar for us to hit, the reason is that it's a statistical superiority test for the FDA. We only need to be 8% less than the control arm to be statistically superior. The way treatment burden is going to be measured in this trial was a little different than prior, and I do want to go into a little detail about it so investors and analysts can understand. Because both arms of the trial get the three injection EYLEA load at the beginning, those injections don't count for treatment burden. In the DURAVYU arms, all eyes will receive two DURAVYUs, mandated. In the EYLEA arms, all patients will receive five EYLEAs. If there were no supplements and everybody follows protocol, the most reduction in treatment burden you could possibly see would be 60%. We know there's going to be some supplements probably in both arms. If you then look at W02 and you say what if you had the same supplement rate in W02 as you do in the phase III, it'd be about a 35% reduction in treatment burden, which we believe would be excellent. If you talk to the KOLs, and we've talked to a lot of them, and you ask them, "What's your floor for using a TKI?" They'd like to see at least a 20% reduction. Which again, remember in a real world situation, using a supplement is not a failure for physicians. The idea of using two MOAs may be beneficial to patients, and therefore, just the idea of using a ligand blocker with a TKI may be an acceptable way to go. That's really the three things that I think are most important. I think we will likely talk about the anatomy and also talk about the percentage of patients that are rescue-free through the entire first year. While I'd argue also, given that the agency's interest seems to be more in reduction in treatment burden, that figure is probably not as important. I would hope that we could do at least as well as we did in DAVIO 2, where we were 50% rescue-free through the first year. Great. Switching gears a little bit to the commercial side. Obviously, a little premature, still need to get to the data, but to the extent data plays out as you expect, where do you see it fitting into the current treatment paradigm, especially vis-à-vis VEGF? I'm going to first of all say it's never too early to think about that. I think that companies need to start to think about it even when they're designing their phase I trial. This is a large continuum. We're focused on the clinical outcome because that's coming up, and it's easy to get focused on it. We haven't just been laser focused on that. We're focused on CMC because we know that that's where most of the CRL come from, and we're focused on commercial success. Ultimately what we're trying to do is improve patients' lives, which means we need to be able to get the drug to them. It's not just how it fits into the paradigm, is we need to be able to make enough inserts to satisfy what we hope to be a demand. How it fits in, I think our data will help dictate that. If you just look at us as a reduction in treatment burden, I think that we will be used in the majority of eyes. If we provide an additional benefit, a visual acuity benefit, or let's say we can show we're anti-fibrotic at the end of the trial, I think doctors will accept then that in the long term, if we can reduce fibrosis, we will reduce vision loss. They may choose to use us in the vast majority of their patients. This is backed up by what we've heard on the podium by KOLs recently, where they have said, "If approved, effective, tolerable, we use a TKI in 80% of our patients." I think at the beginning, it will be most likely used in the patients who require very frequent treatment. I think once doctors get comfortable with it, if our clinical profile is what we hope, I think it's going to be used in the majority of patients. Great. Switching gears to DME. Let's focus on COMO and CAPRI. Can you talk a little bit more detail or give a little bit more detail on study design, specifically learnings from VERONA? You already mentioned a few, but anything more specific there, as well as what investors should be looking for on balance of the year as you march towards full enrollment. I would say that the study design in the DME trials is very similar to the wet AMD trials. 75% naive, 25% previously treated. The N of the trials are less, only 240 patients in each trial. The reason we were able to use a lower N is that we will have the results of the wet AMD trials when we submit DME. The agency has allowed us to use the safety data, provided it's good. to inform the safety of the DME trial. We don't need to hit the safety numbers in DME that we would've otherwise. The two big differences in the DME trials versus the wet AMD trial is we are dosing our drug on day one, and there is a secondary endpoint of vision and anatomy at week four. We hope to replicate in the phase III what we showed in the phase II. If we do, we can show as early as week four that we're better than a single dose of EYLEA, even in the end, if we're non-inferior and we're the same as EYLEA, or even a half a letter, let's say, or a letter worse, but we're non-inferior, but we achieve the vision faster and we achieve dryness faster, I think the majority of retina specialists will choose to use us in almost all their DME patients. What patient wouldn't want to see better faster? I think they would. That's the first difference. The second difference is a little bit more subtle, which is the label for EYLEA 2 milligrams in DME is a five injection load, which is what we're doing. The agency really insists in a non-inferiority trial that you use on-label LUCENTIS or on-label 2-milligram EYLEA as your control. That's mandated. We're sticking to that. We don't believe the five injection load is necessary with DURAVYU, therefore we're only doing a three injection load. Very similar studies to wet AMD, but those small differences that I mentioned. Great. In terms of mechanistic rationale in DME, anything additional that you think the profile fits DME specifically? I think I mentioned this already, that we do have pre-clinical data with some supporting clinical data from VERONA that we have an anti-inflammatory effect. We expect to see that in the phase III trials. If we can show it, the combination of an anti-VEGF that's anti-inflammatory, that's given every six months d elivered in the office, shipped and stored at ambient temperature. I think that has the potential to have us stand heads above everybody else. Great. From a, I guess, mentioned earlier, commercial, and then I guess never too early to start thinking there. Can you talk a little bit about the commercial and medical affairs readiness as well as manufacturing readiness that you're doing in advance of hopefully good data? I'm going to let George answer that. Sure. Let's start with manufacturing. We have our own state-of-the-art facility, so we do drug development at EyePoint. This facility was started four years ago. We have registration batches already on stability, and we are scaling up and preparing not just for building commercial supply, but also being prepared for a pre-approval inspection. The team has really done a remarkable job there. We are just as prepared for that section of the NDA as we are for clinical data. That is well underway, and we will continue to push that, especially through 2027. Interestingly, on our medical affairs team, we have a robust MSL group that we actually retained. We had commercial products several years ago, which we transacted. We kept the MSL team, and they were really instrumental in helping us get our trials enrolled quickly, building relationships with the KOL community. We've continued to add to that. That group is already on the ground as part of a more robust medical affairs team, which we think is very important, not just for wet AMD and DME, but also for commercial readiness. On the commercial side, we have a new Chief Commercial Officer, Michael Campbell, who joined us probably two months ago now. We have people in place about patient access. That's really going to be key and part of our launch. While we have a small footprint right now on a commercial team, they're doing a lot of the legwork to be prepared on the other side of our data release starting this summer. Obviously, with positive data, we'll be looking to scale that team up. We are planning to launch this product in the United States ourselves, and we will be ready for that. From a payer perspective, we've had initial discussions and have gotten very good feedback from payers as we think about where does DURAVYU position versus the current standard of care. I think importantly, we're not another anti-VEGF. We're actually bringing a new MOA. We're really looking to position this program commercially in that same effect. I think the other interesting thing, Jay touched on this a little bit, our product's shipped and stored at room temperatures. In some of our interactions with the larger practice groups and the private equity groups, the message is, "Don't slow us down." I think what's really unique about this program is this is shipped and stored at room temperature. Because it's a prefilled syringe, there's really no change in practice. There's a lot of work between now and a potential commercial launch. We've got the right team and right infrastructure in place. There'll be more to follow. Great. Briefly on balance sheets, can you remind investors current cash runway, what does it fund, and what does that include? Sure. Our cash guidance has been unchanged for quite some time. It's into Q4 of 2027. That includes all four ongoing phase III trials and their readouts along with commercial scale-up for our facility and NDA filing. Obviously, I touched on this earlier, the commercial launch and scale-up would obviously come on the other side of data. As we look out over the horizon, we've got the two phase III's reading out this year in wet AMD. We'll have the DME trials reading out next year, NDA filing. We have a catalyst-rich upcoming 12 months that we're going to be in a position to transact and fund the company. We suspect it's going to be some combination of equity structure. There's been a lot of interest from all of those groups on the other side of our data. Great. In our final little bit of time, maybe just in closing, what do you think is the most underappreciated part of EyePoint that investors don't maybe appreciate as much as you think they should? I don't think there's a single thing other than the whole story. We are a de-risked asset with, we believe, very good phase II data going into the two largest anti-VEGF markets, total of almost $13 billion in the United States alone, with data readout coming very soon. We remain quite confident and quite optimistic in the results, and we think we can make a difference for patients. I think as people dig in and turn their attention to us, they're going to realize how underappreciated we are right now. Fair enough. Good place to leave it. Well, thank you so much for your time, and best of luck. Thanks so much for inviting us