Hello, everybody. My name is Jay Duker. I'm the President and CEO of EyePoint Pharmaceuticals. I'd like to thank the Goldman Sachs team for inviting us to speak here today. We are a publicly traded company, and as such, we will be making forward-looking statements today. You can go to our website for more details. EyePoint is a drug delivery company to the back of the eye. Our lead product is called DURAVYU. DURAVYU is a sustained-release intravitreal insert that contains a small molecule tyrosine kinase inhibitor called Vorolanib. Vorolanib has activity against all the VEGF receptors, and we're studying it in VEGF-mediated diseases. In particular, DURAVYU is currently in three phase two trials: a wet AMD trial, which is called the DAVIO 2 trial, which reported top-line data in December of last year. We're in an NPDR trial in phase 2 called the PAVIA trial, and we also started a diabetic macular edema trial called the VERONA trial. The PAVIA trial read out top-line data at nine months. Approximately a month ago, we should have the full 12-month data set this summer, and the VERONA trial is due to read out its top line in the first quarter of next year. We are on track to start our first pivotal trial in wet AMD in the second half of this year. That will be a primarily U.S. trial, and the second pivotal will start several months later. Our pipeline also consists of EYP-2301, which is the small molecule razuprotafib, which is a Tie-2 agonist. It downregulates Ang-2 while upregulating Ang-1. We have formulated it into our sustained-release Durasert E platform, and this represents a new potential mechanism of action for serious retinal disease. Durasert, in its previous iteration, has been in 4 FDA-approved products. Durasert E is bioerodible fully, and that is what we're studying in DURAVYU. EyePoint has a strong balance sheet. As of the end of last quarter, we had $299 million of cash and investments, which gives us a cash runway through top-line data of our 2 phase 3 pivotal trials in wet AMD. This is our pipeline. I've gone through this already. Again, we're in wet AMD, NPDR, and DME. EYP-2301 for serious retinal diseases is still preclinical, and we're also studying the potential of complement inhibition using sustained-release. It's a picture of one of our Durasert inserts compared to a pencil tip on the left. The 4 FDA-approved products are listed at the bottom right on this slide: YUTIQ, ILUVIEN, RETISERT, and VITRASERT. We no longer commercialize any of these. We do still continue to manufacture YUTIQ. The main difference between Durasert non-erodible and these products and Durasert E, as in DURAVYU, EYP-1901, is that there's no polyamide shell. That polyamide shell is non-erodible, inert, but we don't need it in the vorolanib-based products, so we took it away. These are delivered in the office via standard intravitreal injection, and they feature what's called zero-order kinetics. In all our products, once the steady state has been reached several weeks after insertion, we continue to really set that steady state until the insert is almost depleted. Vorolanib is a new mechanism of action. It blocks VEGF-mediated disease at the receptor level. It blocks all the receptors of VEGF, including PDGF. By blocking all receptors, we should block all isoforms of VEGF as well. By blocking PDGF, we should also have an antifibrotic effect. We've got excellent patent protection with composition of matter patents out to 2037, which may be extendable to 2042. In addition, vorolanib has shown the potential for neuroprotection in an animal model of retinal detachment. At doses we're using in humans, we do not block Tie-2. Again, blocking Tie-2 would cause vascular instability in the human eye. This is a picture of one of the inserts. They're solid. They're cylindrical. Again, injected in the office. Each is about 1/5,000th of the vitreous cavity, so they're quite tiny. They're also heavier than water, so after insertion, they drop to the bottom of the vitreous cavity, so they're out of the patient's line of sight and, in fact, are hard to view even by the doctor, even when the pupil's dilated. We do get immediate release of drug with bioactive levels within hours, at least in animals, and certainly we believe that in humans too. These inserts are designed to fully erode the vorolanib prior to the matrix going away. We want to control drug release to the very end. The matrix is bioerodible and should take several months to go away after the vorolanib is gone. One of the other big advantages we have over all of the sustained-release competitors in the market, or potentially in the market, is that we're shipped and stored at ambient temperature. This is a review of our phase 2 wet AMD data, the top-line DAVIO 2 data. This is a randomized trial of previously treated wet AMD patients. They were randomized to one of three groups: either 2 milligrams of our drug, 3 milligrams of our drug, or EYLEA on label. All patients got monthly injections of EYLEA at the beginning of the trial, and at month 2, they either got, after their EYLEA shot, an injection of their dose of EYP-1901, or they got a sham. They were then looked at monthly, and if they met rescue criteria, they got a supplement injection, and there were, in fact, supplements in the EYLEA control group in this study because the investigators are masked, which group the patients were in. The DURAVYU was not re-injected, but the EYLEA was given every 2 months. This is the baseline demographics, and as you read across the slide, you can see they were well-balanced in the 3 arms. The red circle highlights the fact that this was a relatively heavily pretreated group. What that means is, on average, these patients got between 9 injections in the year leading up to the trial. So their doctors had determined that they needed a lot of shots. So the reduction in treatment burden, when we talk about that as an endpoint, was against the previous treatment. We've calculated it. We've also calculated the reduction in treatment burden prospectively compared to the EYLEA control. This is a relatively well-controlled group of patients because all of them had to receive an anti-VEGF injection 2 weeks to 5 weeks prior to their screening. Here's a summary of the top line. The primary endpoint for this trial was non-inferiority change in visual acuity against the EYLEA control, and we hit that. The change in visual acuity in the 2 milligram and 3 milligram arm are listed in their less than half a letter. This was statistically non-inferior to a 97.5% probability, even in a relatively small trial. Again, the end of this trial was about 160. We've not seen any DURAVYU-related SAEs, either ocular or systemic, and you can see the reduction in treatment burden hovered around 80%, depending on which arm and how you calculated it. About two-thirds of the eyes were able to go up to six months without supplement, and the anatomic control refers to the measurements on OCT, optical coherence tomography, of the macular thickness. Normal macular thickness is about 280 microns. A standard deviation is about 10 microns. So while there was a slight change in the thickness compared to EYLEA, it was less than a standard deviation. This is the graphic of the visual acuity result, and you can see it hovers right around no change. Here is a summary of the safety profile. There were four ocular SAEs in a study eye, but none of them were deemed secondary to DURAVYU. We had no insert migration at the anterior chamber, no retinal oclusive vasculitis, no cases of IOI that were associated with DURAVYU, and there's a very low patient discontinuation rate up to week 32. You expect about 10% in a wet AMD trial. We were at 4%, and none of them were due to the DURAVYU treatment. So to summarize safety, we've got data from 3 trials that are listed here: the phase 1, phase 2 wet AMD trial, and the phase 2 non-proliferative diabetic retinopathy trial. We've dosed about 170 patients with our drug. We have a minimum of 10 months follow-up, and we've had no ocular or systemic SAEs. Reduction in treatment burden, this is just the calculation for this prospective reduction. The thing to note here is, on average, the DURAVYU eyes got about a half of a supplement over 6 months. The aflibercept eyes got three injections that were mandated, but notice the number isn't 3.0. It's 3.32 because 6% of the EYLEA eyes needed a supplement, despite the fact that they were getting EYLEA every two months. This is a graphic representation of the supplement-free percentages at each visit, and you can see up to month 6 after DURAVYU went in, which is month 8 of the study, two-thirds of the patients remained supplement-free. Swimlane chart. Everything on the left is what they got leading into the study. Everything on the right is what they got afterwards, again, illustrating the reduction in treatment burden. Most of the patients who did get supplemented only got one. This is the 2 milligram arm. This is the 3 milligram arm, and you can see very similar for both arms. This is the anatomic outcome. The green line is the EYLEA control. One of the things to note about the Eylea control is, after month four, you notice it goes into a sawtooth pattern. Every other month, the OCT shows more fluid. This is the same sawtooth pattern that Eylea showed in the VIEW 1, VIEW 2 studies, which were the pivotal trials that got Eylea approved. It's the same change from visit to visit of about 12 microns. That tells us that this was a group of patients that needed treatment because if they didn't need treatment, their OCT would have stayed the same with every other month Eylea. It also shows us that the patient population that we enrolled in this trial was very similar to the VIEW 1, VIEW 2 patient population. Now look at the two EYP-1901 arms. They are basically flat, showing pretty good anatomic control over that length of the study. We did a subgroup analysis then to look at the eyes that were unsupplemented. So all the eyes that went through the eight-month trial that didn't receive a supplement, to see if the supplementation was what was driving the good visual acuity result. And the answer is just the opposite. When you take out the DURAVYU eyes that got supplemented, you end up with a visual acuity result that was even better than EYLEA. The 2 milligram arm was 0.6 letters better, and the 3 milligram arm was just slightly 0.1 letters better. So clearly, these eyes, after month two, received nothing else besides DURAVYU at month two, and we were controlling the visual acuity quite well with our drug alone. And here's the anatomic results for that same subgroup. Remember, the blue and the purple are being held in check with our drug alone, but you see that sawtooth pattern that's apparent in the EYLEA arm, showing that this was a group of patients that needed treatment. So on to the phase 3 pivotal design. This pivotal design has really been a couple of years in the making because a couple of years ago, we were considering going directly to pivotal after our phase 1, and we had a type C meeting with the FDA to talk about the pivotal program, and we reached agreement back then with the pivotal program. Subsequently, we decided to do a phase 2. That's the DAVIO 2 study that I just reviewed, and we had positive data out of that, and now we've had an end of phase 2 meeting with the FDA back in April, and what we have agreement on with the FDA is listed here. We are going to do non-inferior trials. They're versus aflibercept control. All the patients will get loaded with aflibercept at the beginning of the trial. The primary efficacy endpoint will be approximately 12 months. It's a blended visual acuity. We will be redosing DURAVYU every 6 months for a total of 4 doses. Now, the primary efficacy endpoint is 1 year, and we're able to submit for NDA after 1 year of the second trial has been completed. We will run the trials out 2 years, though, for safety and to get label for redosing. This is another important difference between our program and all the other sustained-release programs that are out there, is we're the only one testing redosing and presumably, therefore, if successful, the only one that will get a label for redosing. We are doing sham injections for masking. In the retina community, there was some discussion as to whether the FDA will permit that. They never told us that they wouldn't, and they reconfirmed in the end of phase 2 meeting that sham is fine. So we remain on track to initiate the first trial in wet AMD phase 3 called the LUGANO trial, which will be a primarily U.S. trial, with the LUCIA trial, which is the second trial several months afterwards, and that'll be approximately half the sites will be in the U.S. and half OUS, including Europe, South America, and sites in Asia. So the PAVIA trial was the name of the non-proliferative diabetic retinopathy trial, or NPDR. NPDR is a disease for which there are two approved drugs, Lucentis and EYLEA, but retina specialists really aren't using them. And the reason they're not using them is that it's an asymptomatic disease, relatively younger patients, and there's a very high treatment burden to achieve the results. In the first year, most patients needed to get 7-8 injections, and that is something that doesn't really coincide with their treatment frequency or visit frequency going to their eye doctor. So only about 2%-3% of the potential population was being treated, and we believe that if you had a sustained release that was every 6 months or 9 months, you could capture much more of the potentially treatable patients. This study design is very simple. These are patients with moderately severe to severe non-proliferative diabetic retinopathy. That degree of retinopathy is determined by a reading center on a fundus photograph, so it's determined independently. Day 1, the patients either got 2 milligrams of our drug, 3 milligrams of our drug, or they got a sham. No treatment. And then they're just watched. No other treatment is then given in the trial. Anti-VEGF treatment could be given if they reached a milestone like diabetic macular edema or proliferative diabetic retinopathy that required it, but it wasn't necessary in this trial. Now, the top line, when we created this study, the top line was an improvement of two steps in this DRSS, diabetic retinopathy severity score, and we did not achieve that. You can see that on the right, that there was really no difference in the number of eyes in the control versus treated who got a two-step improvement. However, what we appear to show on the left is that we do have what appears to be a dose-dependent prevention of worsening. Subsequent to the start of this trial, the FDA has agreed that that is an approvable endpoint, prevention of worsening. And so we're anticipating, hopefully, the 12-month data will see further separation in the curves, and that may be a potential pathway forward for approvability of prevention of two-step worsening. This next slide versus one-step worsening, and again, you can see the same trend. DURAVYU patients in a dose response had fewer eyes worsening one step, and they actually had more eyes improving one step. So we do think this shows a biological effect with a potentially approvable endpoint of prevention of worsening. So to summarize PAVIA, we did not hit the primary endpoint, but we did show a biological activity. We hope to see improved biological activity even more so at 12 months. And this result appears to be disease-specific in that the TKIs, all the studies of the TKIs recently have shown that they're beneficial in wet AMD, but there's now two trials run independently by two different companies with TKIs, which showed minimal benefit for two-step improvement. So it appears to be a disease-specific finding. On the other hand, we think there's no read-through to wet AMD, different diseases, different patient population, and we have very robust wet AMD data, and we think we've got the most robust data set across all of the TKI programs at present. The VERONA trial is the name of the trial we're doing phase 2 for diabetic macular edema, and that started rolling earlier this year. These are all patients who previously treated DME, but they have to have active disease, meaning they had to have fluid. Unlike the wet AMD trial, which we enrolled patients who were relatively dry, these patients have fluid. They all got a single shot of EYLEA on day one, and they would ramp up to doses of DURAVYU. Notice that the dosing is a little bit different. We have multiple payloads that we can put vorolanib into the inserts. We've tested 440 micrograms. We've tested 1 milligram, and now we've tested 1.3 milligrams in this trial. Going forward, we believe we're going to be using the 1.3 milligram dose in the pivotal trials. But we tested both 1.3 and 2.7 in this trial against aflibercept control, and the primary endpoint here is time to first rescue. It isn't visual acuity. So we're trying to show that, again, our drug works as a maintenance therapy to apply longevity and stabilization to these exudative eyes. We should have the top line of this, again, Q1 of next year. This is the supplemental criteria, the rescue criteria, which is the primary endpoint. Looks very similar to what we did in wet AMD with one exception. The last bullet point, we needed to show a 10% reduction in CST compared to baseline, or the eyes would get rescued. So not only do we want to try to show maintenance of these eyes, but there had to be some improvement or a rescue injection would be given at month 3. So finally, covering razuprotafib in our pipeline. Again, this was a small molecule studied subcutaneously for non-proliferative diabetic retinopathy and DME. It actually showed really good anatomic results, but the visual results were a little bit mixed and never went forward. We obtained all of the assets from the company that was studying it and able to reformulate it so it should work in Durasert E for a minimum of six months. Tie-2 activation is important. It works hand in hand with VEGF in the sense that if you activate Tie-2, you downregulate Ang-2. Ang-2 results in vascular instability. Ang-1, you upregulate by agonizing Tie-2, and that's a good thing. This is a very potent drug that's able to do that. We hope and expect to study it in combination initially with anti-VEGFs to try to get visual acuity superiority over VEGFs alone. To summarize again the cash, we have a strong balance sheet with $200 million-$300 million as of the last quarter. This gives us a cash runway sometime into 2026, which coincides with what we expect to be the top line readout from the phase 3 wet AMD trials. Currently, we have no debt. To summarize our execution, one of the things that I think has really been the hallmark of this company in the last few years is really good execution. We say what we're going to do, and then we go out and do it. The first patient ever to receive DURAVYU EYP-1901 received it in January of 2001, and we reported robust top line data from a phase 2 study in December 2023. So while the program has been very deliberate, we've gone very rapidly. So the checkboxes are all things that we've done most recently. What's upcoming is the open boxes. We actually have an R&D day scheduled for New York in about two weeks. If you make it, great. Otherwise, you can actually log on online, but we do expect to have some of the top line 12-month DAVIO 2 data released at that R&D day. The PAVIA 12-month data for NPDR should be later this summer, and wet AMD initiation, as I said, second half of this year with VERONA top line first quarter of next year. And just recently, we've expanded our SAB. We've got a new Chief Medical Officer who's highly experienced in running phase 3 trials internationally, and the R&D day coming up in about two weeks. So happy to entertain any questions that you have.