Okay, here we go. Thanks for joining us, everybody. Our next session is with Belite Bio. I have Nathan Mata, who is the CSO of the organization. Thanks for joining us. Obviously, a very exciting time for the company. Truly is. What's going on with tinlarebant? Maybe just give us a little step back for a second and just explain to people about the drug and what is it and what Stargardt disease, just kind of the frame everything, the opportunity for us here. Yeah, let's start with the indications that we're going after first. Stargardt disease is an inherited juvenile macular dystrophy. It affects children as well as adults, but in children, the disease is much more severe because the genotypes are much more pathogenic versus adults. That's one indication. The other indication is geographic atrophy in AMD, which is the advanced form of dry AMD. Interesting in both these diseases, the accumulation of toxins, vitamin A-based toxins, is implicated in disease progression. What we've reasoned is that since these toxins are derived from circulating vitamin A, by reducing the amount of vitamin A going into the eye, we have an effect on slowing the accumulation of these toxins and slowing the disease progression. We do this by targeting a protein called retinal binding protein 4, which is the sole carrier protein for delivery of vitamin A from the liver to the eye. That's what our drug, Tinlarebant, does. Tinlarebant is an oral, once-a-day, small molecule drug that is an antagonist of retinal binding protein 4. It competes with vitamin A for binding to RBP4, and it slows the amount of vitamin A going into the eye. By doing this, we slow the accumulation of these toxins and slow disease progression. That's the idea. This mechanism works in Stargardt because why? It's interesting. In Stargardt disease, the reason these children and adults go blind is because there's a broken pump in the back of the eye. This pump is responsible for circulating vitamin A throughout the eye. When this pump is broken, the vitamin A gets backed up. When this vitamin A gets backed up, it actually starts turning into these toxins. This broken pump creates these toxins, which then destroy retinal tissue. These toxins are derived from circulating vitamin A. In Stargardt disease, we are confident that the only reason there's disease pathology and eventual blindness is because of the accumulation of these toxins. We can slow them by reducing the amount of vitamin A going into the eye. It sounds counterintuitive because we all learn that vitamin A is important for your eye, but too much vitamin A in a diseased eye is actually very, very bad. Interesting. Help us size the Stargardt opportunity. Yeah. Stargardt disease, there's never been a true epidemiological study. It's estimated to be approximately one in eight to ten thousand patients or people. That's roughly about 30,000 people in the U.S. Of course, you have much larger numbers in countries like China, where even though the prevalence isn't higher, there's a larger population. In fact, China was one of our major enrollers in our phase III study. Okay, good. Let's talk about the data that you have so far, the phase two data before we get into the phase III. Talk about the outcomes functionally, anatomically, just what you saw. This is where we started. Once we had tinlarebant ready to go, we enrolled an open-label phase II study with 13 adolescent Stargardt patients, age 12 to 18 years of age. All of these kids had biallelic pathogenic mutations, and of course, they had the clinical presentation of Stargardt disease. We gave these patients an amount of tinlarebant that reduced their circulating vitamin A by about 80%. They are dealing with about 20% of the normal amount of vitamin A. What I should mention is that when we start talking about systemic vitamin A reduction, people start thinking, you are going to create vitamin A deficiency across the body. That is not true because retinal binding protein 4 is only required for delivery of vitamin A to the eye. It is not required for delivery to extrahepatic target tissues, such as, for instance, spleen, muscle, fat, et cetera. Those tissues can uptake vitamin A from other carriers and other sources. Our approach is really specific to the eye. Having said that, this 80% reduction resulted in a slowing of lesion growth over two years in these subjects. In fact, it was about a 50% reduction in the growth rate compared to natural history. There was, in fact, a subgroup of subjects that never even spawned atrophic lesions throughout the study. Roughly 42% of the cohort never grew a lesion. In those subjects that did, the growth rate was significantly lower than predicted by natural history. We were very, very excited by that. That is why we went forward with the phase IIIstudy. Just back up one second. Let's make sure everybody understands what are the outcome measures. Yeah. Yeah. The endpoint for drug approval in both of these indications, Stargardt disease and GA, is to slow the growth of the atrophic lesions because the growth of the atrophic lesions will eventually impact vision. While that's the most clinically meaningful outcome for a patient, that is vision loss, the vision loss in patients with Stargardt disease and GA is exceedingly slow, whereas the lesion growth is very rapid. It makes sense that if you really want to preserve vision, you slow the lesion growth first because that eventually will read out into stabilized or improved visual outcomes for patients. This is on an OCT. We're basically looking. Actually, it's FAF photography. FAF? It's retinal imaging. We're actually looking at the back of the retina and watching these lesions grow. Okay, so we're watching the lesions grow. You had 13 patients that you watched for how long? Two years. Two-year study. They take five mg of our drug daily, which reduces their vitamin A level about 80% relative to the baseline status. Okay, that was after two years. What was baseline status? Talk about the natural history work that you've done. Yeah, that's interesting. The natural history work was led by Dr. Hendrik Scholl, who is now our CMO. Prior to becoming our CMO, he led the largest natural history study of Stargardt ever conducted. He's, in fact, responsible for many of the key findings that we have now in terms of the natural history and really helped us design—his data helped us design the trial because we knew from natural history how to select patients and what their growth rate would be over time based upon that work. That was very critical. Those were called the ProgStar studies, a huge collection of reports over many years, both prospective and retrospective studies looking at the natural history of Stargardt disease. Do you think 13 patients is enough to give you a sense of what's really going on? You know, we wanted to get more, but the fact is that for the sites that we had, they were ready to go, and we just wanted to get an answer. It was enough of a sample size for us to get a response to see, are we, in fact, changing their trajectory of lesion growth? I think we got our answer. Yeah, yeah. Yeah, it's interesting. And it's also a new outcome for people. Right. Just having an oral therapeutic by itself is amazing that you would get that sort of efficacy in the eye. A lot of people think that it wouldn't work that way. Again, because we are targeting that receptor in the eye, it works very, very nicely. What about speed? Because you mentioned you looked at two years. How is it working after three months, six months? Yeah. There is a sort of a latency in terms of how the drug kicks in because you have to give some time for the systemic vitamin A level to equilibrate with the ocular level. That's typically three to six months. Once that happens, you're starting to see a change in lesion growth. Six months after that, you start seeing changes. I see. Are we, I guess I'm just thinking about Stargardt patients, if they have this problem, right? Obviously, they're starting to see these lesions. How much time after the lesion starts to become a problem do we have vision problems? Is it correlated completely, or is it a lag effect? No, that's a good question because, in fact, in children, which again, have much more severe genotypes, they have a much more severe disease, they lose their vision much more rapidly. A kid who's diagnosed at six years of age will be legally blind by the time they're 20. That's a pretty rapid loss of vision. In adults, it's much more slowly progressive because they have more mild mutations. In kids, that's why it's so critical, that's why we designed our study in adolescents, because these kids have a rapid disease progression. The other differentiator about our approach that is very important is early intervention. We went after children that have very small lesions, but they're very close to the fovea. They're very close to where the visual acuity center is. These lesions will grow into the fovea. If we can stop those lesions growth into the fovea, we'll preserve vision. Yeah, yeah, yeah. Let's talk about the phase III DRAGON study. I know that you have some slides. It might be easier to kind of. Yeah, let me just skip to that real quick. This is just an overview, just to provide the audience some idea of the clinical studies we have going. We've already spoken about that phase two 24-month study, that open-label study in the 13 Stargardt kids where we showed a slowing of lesion growth. The phase III study is one we recently got an interim readout from. This is called DRAGON. This study completed enrollment at 104 subjects. Again, it was a two-year study. They're getting the same dose that the kids in the phase two study got: five mg per day. Again, they're having this 80% reduction in vitamin A. That reduction actually starts right away, but it does take some time for that to have an effect in the eye. As I said, we have some interim data that's very exciting. We're really, really thrilled about what the DSMB gave us over the past couple of weeks. Of course, we're also having another Stargardt study called DRAGON 2. This is to take advantage of a designation that we received from the Japanese Regulatory Authority, PMDA, called Sakigake designation. We're the first ophthalmology company to ever receive it, so we're very honored. Basically, what this designation allows us to do is get an approval in Japan based upon just one study. Basically, all they wanted to see in this DRAGON 2 study was 10 Japanese subjects going through two years of treatment and having promising safety and efficacy outcomes, and then we get approval in Japan. It also serves as a backup in case the FDA or some other regulatory agencies ask for a confirmatory study of our DRAGON study. DRAGON 1 and DRAGON 2 are our Stargardt studies, phase III, that we're very optimistic about. Of course, we have a study in geographic atrophy going, a phase IIIstudy. We're enrolling, targeting about 429 subjects. We're at about 400 now, so we don't have too much further to go. That's basically the overview of the study. Before you go on, we have 104 patients. How many sites? And how many of those sites are the same? Like the 10 patients that you had in the phase II, how many sites were those? A couple of sites? There were only three sites. Three sites. Each of those sites were involved in the DRAGON. All three are here. Okay. How many additional sites did you have to do? An additional 22. So about 25 sites. Is it fair to say that that's where all the Stargardt patients are in the United States, pretty much? I would say so. I mean, we went to every KLO, every ophthalmologist of these Stargardt kids that we could think of that had a sufficient number of patients. That is all across the globe. I think we've captured as many as you could potentially get in terms of adolescent Stargardt patients. In fact, this is the largest study of adolescent Stargardt disease ever conducted. Interesting. Okay. It is a two-year study. Are we going to get to the interim? Yeah. You'll talk about it. Okay. And then just so people understand the geographic atrophy, it's the same exact product. Same exact product, same exact dose, because it's the same endpoint, same trial design. Everything in all of our studies is identical except for the patient population. Right, exactly. They have to have GA already? Absolutely. They have early GA? Is it late GA? That's another important point because, again, we're after early intervention because we believe if you stop these lesions when they're small, you have a better chance of slowing overall and eventually preserving vision. I should mention in terms of the competition, because most people who are interested in ophthalmology, if you're here today, you must be interested in ophthalmology, you're aware of the two approvals in geographic atrophy: Syfovre and Izervay. These are complement inhibitors that are injected into the eye that essentially quell an inflammatory response that occurs in late-stage disease. You do not have inflammation in early-stage disease. Those products would not be expected to be effective in the patients that we're selecting for our GA study or our Stargardt study because, again, the lesions are too small. That's another differentiator in addition to an oral therapeutic. I just wanted to provide that contrast. Talk about the endpoints. I guess the endpoints are the same at both studies. Just give us, so make sure we understand the, because I want to talk about the key secondaries in the anatomical vision that you're looking at. Right. For all the studies, the approvals for SYFOVRE and I ZERVAY and for what we're doing, it's all the same. Slowing the trajectory of lesion growth relative to placebo in a statistically meaningful way. Over two years, you want to see a divergence of growth: placebo here, your treatment here. Hopefully at the end, you've got a delta that gives you stat-sig. What have the FDA given you as far as guidance to? The FDA has actually been very workable with us because they've allowed us to build a protocol that was quite novel, to use a drug that is also quite novel. They weren't concerned about the systemic vitamin A deficiency for the reasons I spoke about earlier. They gave us a lot of leniencies, again, because these are children going blind. Of course, they want to see a product approved. At the same time, they're the most conservative regulatory agency that we've confronted. We're working with eight regulatory agencies right now across the globe to get approvals. Many of them have said they will grant an approval based upon one well-controlled phase III study. The FDA has not said that. They said it will be a review issue. They're the only ones that are being a little bit tough in terms of the approval requirement. I don't understand. How can they even, I mean, given all of the different diseases that we've seen get approved with one trial, I mean. It's the division of ophthalmology. There's nothing for Stargardt. Yeah. You wouldn't see this in oncology, for instance. The division has changed leadership. Has Boyd any nicer than Chambers? It's interesting you ask that because we've seen a pretty good consistency between what Dr. Chambers has told us and what Dr. Boyd is telling us now. Maybe that philosophy will change. He's new. Maybe he's still adopting some of his own principles. Right now, he seems to be very Wiley-esque, Wiley Chambers. Wiley-esque. I'm going to use that one if you're okay with that. Talk about the secondary endpoints. Yeah. Our secondary endpoints is also another lesion growth endpoint. I should mention that I talked about the growth of atrophic lesions. There's also something called an autofluorescent lesion. The autofluorescence actually precedes the atrophy. When you combine the autofluorescence and the atrophy, that's our secondary endpoint, is to stop the overall growth of all lesions, whereas the primary is just the atrophic lesion. What we found is the autofluorescent lesion actually does cause visual acuity damage, visual acuity loss. In our phase II study, all of the 13 kids had foveally involved autofluorescence at baseline, and they were all losing vision. They didn't have any atrophy, but they had autofluorescence. Because our drug would primarily first reduce the autofluorescence and then the atrophy, we wanted to include that as our key secondary endpoint to slow the growth of the overall lesion. It's called decreased autofluorescence, but it's basically the autofluorescence and the atrophic lesion. Of course, we have visual acuity as another. Did we look at all those endpoints with the 13 patients in the phase II? We did. We saw promising results. Yeah, that's what I was going to ask you. Just help quantify. What did you see? It's tough to quantify because, again, it was an open-label study. If you look at, again, compared to natural history, we're getting about a 50% reduction in the growth of both the atrophic lesion as well as the overall lesion. The overall. Okay. Yeah, yeah. Interesting. Yeah. Very, very promising data. Yeah. Side effects. Talk about side effects. What we've seen in the phase II? What do we expect to see? What's on target? What's off target? Great question because people envision that because we're reducing vitamin A delivery to the eye, we're going to trigger all of these ocular AEs that are going to be intolerable, and patients are going to drop out of study. What I can tell you is that in the two-year phase II study with those 13 kids, we didn't lose one subject to an ocular AE. In fact, there were no withdrawals due to any AEs, and there were no drug-related systemic AEs. So we were happy to see that. Now, going forward into our phase III study, where we now have 104 subjects, we're seeing exactly the same thing. We are seeing the overall dropout by time of interim. By the way, the interim analysis was conducted two weeks ago. By that time, more than half of the kids had already finished two years of dosing. The total withdrawal rate was 9.8%. Ten out of 104 subjects. That due to ocular AEs was only 3.8%. Four out of 104 subjects. As I said, 50% of them had already gone through the whole two-year. This whole idea that these children would not be able to tolerate these ocular adverse events, it's just not true. They're tolerating it quite well. It gives us very, very high hopes for the future dosing going forward. Let's talk about what are the AEs? Yeah. When I say ocular AEs, there's two. The first is called delayed dark adaptation. Many people may have heard of this. Sometimes it's called night blindness. That's a misnomer. Basically what this is, is a delay in your ability to accommodate to dim light settings. Again, that's due to reduced vitamin A delivery to the eye. Typically, for instance, here's an example. If you're out on a bright sunny day and you walk into a movie theater, it takes you about maybe four or five minutes to find your seat because you're accommodating to that dim light. A patient receiving our drug will take perhaps two to three times longer because their vitamin A delivery is slower. They'll need more time for those photoreceptors to fill up with vitamin A. That is called delayed dark adaptation. The other ocular adverse event is called chromatopsia. It's the opposite effect. It happens when you're exposed to bright light suddenly from a dark state. Almost all the kids, we have diaries from our studies. When you read these diaries, what you see is all these kids are reporting it. The ones that have it say that when they wake up from sleep, they get this hue of yellow in their visual field, which lasts seconds to minutes. That hue of yellow is caused by cone photoreceptors electrically misfiring because they don't have enough vitamin A. Again, that lasts seconds to minutes. The vitamin A fills up and it goes away. These are transient, mild ocular adverse events, which, as I said, are being tolerated quite well. Yeah, yeah. Is there some type of bar that the FDA has talked about for what's necessary for efficacy, for approval? You know, they have not. That's an important question because until the approvals of the GA drug, Syfovre and Izervay, we had no idea of what the agency was looking for. Now we look at it, it's 20%. If you look at the overall studies, I mean, you have 14%, you have 20-22%. If you do the mean, it's roughly about 20%. What that tells us, the fact that they approved those drugs with a 20% slowing of lesion growth says that's the bar. If you can get to 20% or more, you've got an approved drug with a good safety profile. By the way, the safety profile on those drugs is not that great. It's not nearly as good. No, no, no. Absolutely not. It is a needle in the eye. We are a pill in the mouth. Right, right, right, right. Interesting. As far as that's concerned, I mean, what are you thinking about for the endpoint? What's the number for you? Where do I predict? Yeah. I powered the study. I'm involved in designing the studies. A lot of people don't know this, but I've been doing this for about 20-some years. We never found the right drug. I believe tinlarebant was the right drug. I powered the study for a 40% treatment effect at two years. Okay. Fingers crossed. 40%. Remember the number. Let's see what happens. I'm not promising anything. You just asked what I think. Yeah, yeah, yeah. Okay. Let's move to the interim. What did we learn? What did you talk about the other day? Right. The trial designs, just to break out DRAGON 1 and DRAGON 2, just so you can see. If you look at the top three lines, that's where these studies differ. That's the only place, right? Basically, the number of subjects, the geographical location, and the randomization two to one versus one to one. Everything else in these studies is identical. The dosing and, of course, the endpoint is the same. I just want to give you an overview for the similarity of these two trial designs. The DRAGON study is the one where we have the interim analysis. That interim analysis was triggered once all subjects had reached their 12-month imaging visit. By that time, a number of subjects had also completed month 16. The DSMB, this independent DSMB, was looking at data all the way up until month 16. They're looking at efficacy. That means the lesion growth. They're looking at safety, both systemic and ocular safety. This is a little bit about the demographics. You can see these kids are very young. These are school-age kids. Typical height and weight for kids that age. Roughly 60% male to 40% female. You can see the race distribution. The reason why you see such a high representation by the Asian population is because we did enroll in China. China was our biggest enroller for Stargardt disease. We got about roughly 55% of our subjects coming out of Asia. The rest of Caucasian, European, and North American subjects round out the rest of that at about 40%. That's the overview of the demographics. Here is what the DSMB provided for our interim analysis. Before I go through the data, I do want to say that this was a sample size re-estimation exercise. That is the reason we did the interim. The idea here was to take a look at the data to see if we see a trend in efficacy. If we did, that would allow us to add up to 30, three-zero additional patients. The reason you want to do that is because if you see a trend in the middle of your study, you want to preserve that trend. You add more subjects to give you a greater chance for statistical power by the end of year two. The DSMB had one thing to do, to tell us whether or not we are going to add subjects or not. If we add subjects, they are telling us there is a trend for efficacy. We want to preserve it. We're going to add 30 subjects. If they said don't add subjects, you're either on the positive side of that window, which we call the promising zone. That means we're doing much better than we thought. There's more than just a trend. There's a clear signal. Or it's futile. If it's futile, you don't want to add patients. If you're doing way too good, you don't want to add patients. They told us not to add any more subjects. I'll go right there to the bottom where it says additional DSMB comments, it is recommended to submit the data for further regulatory review for approval. Now, the DSMB would not add this note if we were on the futility side. Clearly, without saying so, I believe we're on the positive side of that promising zone, which tells me we have a pretty good treatment effect. We're all a little surprised to get that, I suppose. Is there even. As were we. Is there even precedent for DSMBs to kind of do that? I hadn't really heard that. I've done three trials in Stargardt disease. I've done two in geographic atrophy. I've never seen this kind of recommendation ever. It really took us by surprise. Your takeaway is something good is going on here. What now? What does the FDA need? Anything different from because this is not the FDA talking. This is just the DSMB talking about the quality of the study. We're going to do exactly what the DSMB has asked us to do, which is to reach out to these regulatory authorities, and there are eight of them that we're going after, and show them the data. The way it's going to happen is everyone on the sponsor side is masked except for two individuals, our Head of Regulatory and our Chief Medical Officer, Dr. Hendrik Scholl. They will have access to all of the data that the DSMB saw so that they can engage in conversations and discussions with the regulatory authorities regarding either breakthrough therapy designation, expedited approval, conditional approval, these types of things. Within the next three to six months, we'll have some hopefully harmonization amongst these eight regulatory authorities so we can understand what they are all looking for in common and then pursue that path. We won't go to the FDA until we've had this harmonization across regulatory authorities. We'll need to meet with all of them to understand what they want. In fact, EMA has told us very clearly right after we got our approved pediatric investigational plan, which paves the way for an MAA, by the way. They told us with a completed phase IIIstudy and a PIP that that would be enough for approval by their perspective. That's EMA. Japan has said the same thing with the Sakigake designation, as I mentioned earlier. China has indicated the same thing. One study's enough. One study. It's FDA that's sort of holding back. They'll come around. I honestly cannot imagine that they're going to make you do two. I mean, there's nothing approved for Stargardt. It doesn't make any sense. That's the reason for going out to the other agencies to see what their opinion is. Maybe that'll shake up the FDA a little bit and help them shape their opinion. Right, right. This is to do. You haven't gone to the FDA. We're doing it. All this is happening. The FDA is pretty fast. We can get in there pretty fast. They give you an answer within 30 days. The other agencies are three months, roughly. We want to do those first because they're a longer timeline. Then we'll circle back to the FDA. Just to understand, even if the FDA says, "Okay, that's wonderful, finish the study. Yeah. When will the study be finished? The study will end at the end of this year. The data after QC and cleaning all that, probably available by Q1 of 2026. Right. Everyone will know exactly how this study read out by Q1 of 2026. If everything goes according to plan, we've got positive data, the DSMB is kind of leaning in that direction. First quarter, we get the data and we file soon after. Yes, sir. This is presumably on the market in 2027, no later than that, if that's the scenario. At least in ex-U.S. countries. Right. In the U.S., it's possible they make you do another, but. I think there will be so many patient advocacy groups that will bang their door down and yell at their congressmen to get the FDA to respond. They're not always responsive, but. Let's be even a little more aggressive here and think about any type of accelerated approval based on where we are now. It's like just file now. Yeah. Like with what you have. What's the likelihood? How are you thinking about that? I'm thinking it's 50/50. Because again, we don't know exactly what the DSMB saw. I certainly don't know. Yeah. I'm predicting, let's say it's something like a 25-30% treatment effect. That's astounding. Because if it's linear throughout, we're going to hit that 40% number. That's never been seen before in a degenerative retinal disease to have a 40% treatment effect. Something like that may change the opinion of the FDA, just that alone. Of course, the safety profile, which is amazingly clean, as shown here in the fourth bullet. It is kind of interesting how this has played out. Yeah, it really is. I guess you were talking about the adverse events. I just was thinking like adverse events, anything? Yeah, here we go. Those are the numbers. That's from the interim. This is new data. Right. So this is from the interim analysis looking at, again, data. Well, for safety, they looked at all available data. I mentioned what xanthopsia is. You can see that in about 26%, 27% of patients, delayed dark adaptation, same number. One interesting thing about delayed dark adaptation, I should have mentioned this, is that in both Stargardt disease and geographic atrophy, delayed dark adaptation is part of the disease process. Many patients are already accommodating that effect because they've been living with the disease for so long. It's on target. Right. The chromatopsia, which is part of the xanthopsia, those are related. Xanthopsia is just the color, yellow. That is sort of more rare. That is definitely a pharmacological effect. What I always tell people, you know, when they say, are these diseases concerning them? Absolutely not, as long as patients aren't dropping out. Because what this tells us is that we're having the intended biological effect on the retina. If you have these readouts, it's telling you that systemic treatment is reading out in the retina. That's exactly what we want to see. I mean, look, what's the alternative? I mean, right? The alternative is terrible. This is not the end of the world. Those are not horrible side effects. No, I think with approval with this profile, I think this is going to be a blockbuster drug. Yeah. The AEs, any reason to think that they would be different in the GA population? There is. I'm glad you brought it up. Because older damaged retinas are not going to tolerate reductions in vitamin A as well as these younger Stargardt retinas. I predict in patients with more macular involvement of the lesion, they will have a harder time with delayed dark adaptation. This could result in, for instance, deficits in low luminance vision over time in some subjects. Not in all, but I predict that because in patients who have extensive macular involvement of lesions, they could have a harder time with delayed dark adaptation than other patients. Good. Good. In our last minute, what have we not hit on? What else do we need to make sure we talk about? I think we got everything except this last slide, which is basically just showing you, again, from the interim data, stabilized vision. People say, "Okay, so stabilized vision. So what?" Actually, this is very profound. Because if you can stabilize vision while slowing lesions, it's telling you over time, you're preserving vision. You don't have to necessarily improve it relative to placebo. All you have to do is keep it the same. These kids over two years, if you look at the standard luminance vision, they didn't lose anything. Basically, the loss was roughly about less than three letters. If you look at low luminance vision, it's essentially the same. There's a little drop in the beginning, but then throughout time, and again, these are blended data, meaning that we don't know who's on treatment or who's on active. The fact is, according to the randomization, 66% of the subjects are on active. You can look at the data that way. Once you tease out 33%, it's not going to change these lines very much. I predict once you see the unmasking, you're going to see exactly these types of lines. Stabilization of visual acuity along with slowing lesion growth is a very, very positive outcome. If you put the curves for the natural history, then I think people would understand. Yeah, absolutely. Maybe you should do that right underneath. That is very important too. Because patients are not getting treated, they will be losing vision. They're getting worse and worse. Exactly. Exactly. Good. Thank you. Yeah. Thank you. That's great. Thanks for joining us. Thank you. Very exciting. I've not seen these DSMBs be that aggressive before. I think that's really, really good news. We're certainly the better for it. Okay. Yeah. Thank you all for attending. Appreciate it. Yeah. Thank you. Great to see you again. Thank you. All right.