Hello, and thank you for joining us to discuss Belite Bio's third quarter 2023 financial results. Joining the call is Dr. Tom Lin, Chairman and CEO, Dr. Nathan Mata, Chief Scientific Officer, and Hao-Yuan Chuang, Chief Financial Officer of Belite Bio. Before we begin, let me point out that we will be making forward-looking statements that are based on current expectations and beliefs. These statements are subject to certain risks and uncertainties, and actual results may differ materially. We encourage you to consult the risk factors discussed in our SEC filings for additional detail. Now, I'll turn the call over to Dr. Lin. Thank you. Thank you for joining our reporting for the third quarter. I'm Tom Lin, CEO of Belite Bio. Joining me is our CSO, Nathan, and CFO, Hao. I'd like to start off by giving an overview. So, Tinlarebant is a novel once-a-day oral tablet designed to bind to serum retinol binding protein, or known as RBP4, as a means to specifically reduce retinol delivery to the eye. This approach is intended to slow or stop the formation of the toxic retinol derived byproducts, which are generated in the visual cycle and are implicated in the progression of Stargardt disease and geographic atrophy secondary to dry AMD. We believe that early intervention directed at emerging retinal pathology, which is not mediated by inflammation, will be the best approach to potentially slow disease progression in Stargardt disease and geographic atrophy. There's still significant unmet need for both indications, as currently there is no approved treatments for Stargardt disease, and there are currently no approved oral treatments for GA, and we are already in global phase III trials for both indications. So far, we have been granted Fast Track Designation, Rare Pediatric Disease Designation, and Orphan Drug Designation. We have several patent families and with composition of matter patents lasting until 2040, and with patent term extension and new patents to be filed, which, we will have patent protection way past the 2040s. So we still have a very long patent life on this drug, and we are already in late-stage development. For Stargardt indication, the phase III is already fully enrolled, with estimated interim readouts by second half of 2024. We've also just recently presented positive 24-month treatment results from our phase II, which Nathan will be presenting the results later on. For GA in dry AMD indication, the phase III is already enrolling subjects. And with this, I would like to pass this on to our CSO to give an update on our clinical trials. Nathan? Thank you. Hello, and thank you for joining us to discuss Belite Bio's fourth quarter and full year 2023 financial results. Joining the call today are Dr. Tom Lin, Chairman and CEO of Belite Bio; Dr. Nathan Mata, Chief Scientific Officer; and Hao-Yuan Chuang, Chief Financial Officer. Before we begin, let me point out that we will be making forward-looking statements that are ba- Our CSO to give an update on the clinical trials. Nathan? Thank you, Tom. So I'll go right into the clinical trial designs. When we first, I should say in the previous financial updates, we've shown you the overview of our open-label phase II, as well as the well-controlled phase III study design, which is our pivotal phase III study. And we emphasized that the big differences between these two studies was that in the patients in the open-label phase II, they came in with a very early stage of disease, which is characterized by the presence of autofluorescence, but not atrophy of retinal lesions, whereas in the phase III, all the subjects have retinal atrophy. Well, it turns out that in our phase II study, when we look retrospectively back at those baseline images, we find, in fact, that a number of these subjects actually do have atrophic lesions. They were just not measurable by the routine imaging algorithm that most clinical researchers use. So our imaging center has developed a new algorithm, much more sensitive, in terms of identifying atrophic retinal lesions. So we do, in fact, know that in the phase II open label study, many of these subjects did start with very, very small atrophic lesions that grew over time. And of course, we showed you the data about the lesion growth, which I'll jump to right now. Next slide. So as I mentioned, before, these kids came in with early lesion types. Some of them did have atrophy, but we wanted to compare to natural history growth to determine whether or not we're having any real treatment effect. We showed this data previously in a comparison to ProgStar, a cohort of subjects that have similar baseline characteristics as our phase II subjects. As you can see here on the left-hand side, we see a really dramatic slowing of lesion growth in Tinlarebant treatment group, which is the red lines, versus the natural history group in ProgStar, which is the blue lines. As I said before, we know now that these patients did come in with atrophy, so there's a lot of similarities now between the phase II patients and the phase III. The other new update that we didn't have last time is a genetic analysis, because we did note, in terms of the lesion growth, there were five of 12 subjects that never converted to atrophy over the two-year study. We now know that those five subjects have severe biallelic mutations, which predict retinal pathology. So the absence of the transition from the early lesion type to the atrophic lesion type in these five subjects could not be attributed to benign or mild mutations. They, in fact, had very severe mutations. So all these data really point to a profound treatment effect of our drug. Next slide. This is an overview of the phase III trial design and geographic atrophy. As I mentioned before, the trial designs between the Stargardt disease phase III study and the GA phase III study are very, very similar. It's the same drug, it's the same dose, it's the same endpoint, same randomization, same trial duration of two years. The only real difference in these two studies is, well, there's two. First, being the indication, GA rather than Stargardt, and of course, in the GA study, we have more patients to reflect the higher prevalence of the disease in the population. So with that, now I'll throw it over to Hao-Yuan, so we can talk about financial year. Thank you. Thank you, Nathan. In 2023, we had R&D expenses of $24.8 million, compared to $8.9 million in 2022. The increase was primarily due to increase in expenses related to conducting the DRAGON and the PHOENIX trials. On G&A expenses, in 2023, we had G&A expenses $6.8 million, compared to $4 million in 2022. The increase was primarily due to increase in share-based compensation granted in 2023, and an increase in professional service fee. We had a lower professional service fee in 2022 as we complete the IPO by end of April 2022. Thus, we only had eight months of professional service fee related to being a public company in 2022. But for the year 2023, we had 12 months of professional service fee. On net loss, we had a net loss of $31.6 million in 2023, compared to $12.8 million in 2022. In terms of cash, we had $88.2 million in cash by end of 2023, as compared with $42.1 million by end of 2022. The increase was primarily due to a total of $52 million raised from the follow-on offering and exercise of the warrants issued in the follow-on offering, an additional $29 million from ATM offering, with stacked cash runway to end of 2026. Thank you. Back to you, Tom. Thank you, Hao-Yuan. I would like to conclude with the key milestones to expect for this year. We are currently making good progress in the phase III study in GA, as there are now many sites activated and enrolling subjects. We'll be presenting- All right. I see we have a question from, from Marc Goodman with Leerink. I'm gonna give you permission to talk now. You have permission to talk now. Hi, good afternoon. First, I have a question about the timeline of the Stargardt disease trial. You mentioned we expected now either toward the end of the year or early 2025. If the trial was already fully enrolled on time, why the trial is delayed by this whatever, this little delay to early 2025? And also, what we should be expecting at this interim readout in terms of the efficacy and safety that you're gonna disclose to us, and what are the scenarios? If the data looks good, are you gonna keep the study ongoing, or what are the different scenarios for this interim readout? Thank you. Sure. Thank you. So the first question is to clarify, there's no, there's no delay. Actually, this, as you mentioned, the trial is fully enrolled already. The timing for the meeting, the interim data analysis, falls within the second or half or this time, to be more exact, Q4. So this basically ends up with in the hands of DSMB. They will be reviewing that data, and I guess they'll, they'll determine when they will meet the enough data points for for that interim analysis. So so roughly or for between Q4 and and Q1 next year. This is because this depends on the CRO cleaning the data and how much data, or the timing of the CRO getting all the data in, and cleaning all the data, and then arranging for all the DSMB's time. So that is all in the hands of the CRO and in the DSMB on how fast they could get everything prepared for the interim analysis. Sorry, for the second question, the question that you asked. If the safety, something around the safety? Just really what we should be expecting, and also, what are the different scenarios for this particular readout? Like, let's say if the data is good, what are you gonna do? So the DSMB will observe if we should, if the study will be moved on and there's no changes, then there's no expected changes, or they will recommend that we would increase the sample size. And this means that the positive trend is observed and possibly that they will recommend adding another 30 subjects to increase the statistical power and then the probability of getting statistical significance at the 24-month readout. If they suggest to move on and not move on as is, it means that we could be positive and that we are on track to meet that endpoint by end of 24 months. So, that's a positive thing as well. And then the other scenario is that, if they could detect no difference at all, and there's no way by adding sample size would change the study, and then they wouldn't, they will probably say move on as well. So those are the three scenarios. All right, and- Answer the questions. Yeah. Well, last one, if I may, I can explain a little bit about, why you guys, you know, feel like that, the timing was early as second half, now it's Q4. It's because, as you guys probably remember, in the very beginning, we only want to enroll 90 subjects. But in the end, we were over-enrolled because there are so many patients signed up, and we have to let them in before we are fully enrolled. That's why we ended with 104. And, the last patient, he was not able to, you know, get the drug in August, as what we wanted. So therefore, he only get the drug by mid-September last year, and therefore, that's why we are now confirmed that, the interim couldn't be in Q3. He said it has to be in Q4. That's why we made the, you know, adjustment on when the interim is expected. We just wanna, you know, give you, give the market the latest update that we, we know. Yeah. So of course, the CRO would need to get that data as well, clean up the data of the last few patients that came in. So it's all within the timeline, but the exact date we wouldn't know until the exact date when the DSMB will convene for all members to be available to review the data. And of course, the procedure-wise from the CRO. That's great. I see we have a question from Jennifer Kim with Cantor. Sure. Jennifer, you have permission to talk now. Hi, thanks for taking my questions. I have a couple here. Maybe to start off, I'll follow up on the last question. When you're talking about the potential outcomes in the interim analysis later this year, you laid out three scenarios, and I just want to make sure. The scenario where the treatment effect that the DSMB is seeing falls below the sort of treatment effect range that you've set, you said that they will recommend expanding the patient number to or by 30 patients. In that scenario, how or what kind of conclusions do you think investors should draw from that? And then my second question: Could you give us your latest thoughts on your cash runway, and are there levers that you expect to pull to drive enrollment in PHOENIX? Thanks. Sure. So, I think I'll refer to this to Nathan to give you more details on explaining, that. And then the second question, how could you, comment on the cash runway? Take it. Yeah, thanks, Tom. So I'll take the first one. Jennifer, when we talked about this effect size range, that range was really for determining exactly the design of the study. You need to, let's say, anticipate or hypothesize a treatment effect that you would get in order to properly power your study and get the right number of patients. We used a treatment range that was observed to have approvals with the FDA. So this 22%-28% that you're aware of now and that everyone now is aware of really comes from the precedent approvals and clinical breakthrough therapies in either Stargardt's or GA. That aside, what the DSMB is actually looking for is a statistically significant difference, regardless of the effect size. So we're looking for a clinically meaningful effect between the trajectory of lesion size growth and placebo, and the trajectory of lesion size growth in the treatment arm. So if that difference is statistically significant, it's regardless of whatever the effect size actually is, whether it's 22% or 20%, or even 30%, it has to be the difference between the two treatment arms. So that's what the DSMB is looking at. So they'll be making their decisions on whether or not we've achieved that statistical significance in terms of whether or not to move forward or to add additional patients. And I want to make one clarification. You mentioned the addition of 30 additional subjects. That's back when we had the sample size estimated at 90, and as Hao-Yuan mentioned, we over-enrolled the study based upon actually demand from PIs and investigators to 104. So the maximum number of patients would actually be enrolled would be the difference, right? So up to, up to 120. So basically, it would be 26 patients additionally, if we had to, if we didn't have the statistical significance that was meaningful at the interim. So that's, those are... I want to make those, those clarifications. So it's not so much that the DSMB is looking for an effect size, right? Whether it's 22, 26, 28%. They're actually looking for a statistically meaningful difference between the trajectory of lesion growth and placebo and the trajectory of lesion size growth in the Tinlarebant treatment arms. Is, is that clear, Jennifer? Yeah, yeah, that's very helpful. And then maybe on the second question on, PHOENIX enrollment and bottom line cash runway. Yeah. So we have enrolled 56 subjects so far. And with the, you know, new cash coming from the warrants and the ATM so far, we are, we're having, you know, over into, to the end of 2026 cash runway. So yes, that will be enough for us to complete the DRAGON study, interim and final. And we think we should be able to also get to the interim from PHOENIX as well, and also, you know, pay the milestones that we need to pay to Columbia for these milestones. Yes, I do think that we do have enough cash for that. Thanks again. All right, and we have a question from Yi Chen with H.C. Wainwright. Yi Chen, you have permission to talk. Thank you for taking my question. My first question is for Dr. Mata. You mentioned that this new method to discover patients with initial lesion development. Is that method currently widespread in terms of usage? And if not, how easy for this method to be widely adopted? Yeah. You're talking about the new imaging algorithm that's been developed by our reading center? Is that what you are referring to, Yi? Yes. Yeah. So obviously, this has to go through a clinical trial, right? And this is the clinical trial that that data will be analyzed by. So this would be sort of the validation study. We would be using the data from not only our phase II study, which was recently completed, but also the phase III in Stargardt's to use, not just, not only the traditional algorithm, the Heidelberg RegionFinder software that everyone is using, but this new imaging algorithm, which actually defines the atrophic lesions more clearly, more discretely. And so we'll be looking at both methods. Regarding how widespread it is, it's not widespread because, in fact, this methodology, this algorithm was just recently developed, and they used our phase II data to develop. And the reason- this is very important, Yi. The reason they were able to do this is because in our phase II study, we enrolled subjects that only had the early lesion type, this sort of predecessor lesion type, this QDA of the autofluorescent lesions that will transition to atrophic lesions. So when we looked at the traditional imaging modalities, none of our patients had atrophic lesions at baseline. But when we applied the new algorithm, this newly developed imaging algorithm, we found that in fact, many patients at baseline did in fact have atrophic lesions, but they just couldn't be identified by the Heidelberg RegionFinder software. So this is really the difference, and I don't want to get into the technical detail, but the fact is that this algorithm is much more discretely looking at, it's basically looking at a central lesion and then looking out in concentric rings, out into the outlying areas until it gets to healthy retina, and then it's comparing the intensity from healthy retina to what we call a lesion, whether it's autofluorescent or atrophic. And so it's just much better at using a reference value of healthy tissue to determine what is atrophic. And the Heidelberg imaging re-reading, region finding software doesn't do that. So we'll use this, this data to validate that algorithm, and probably going forward, I think, and we'll present this obviously to the FDA, but I think it will catch on because it allows a more definitive and discrete determination of what really is atrophic retina. But with this new algorithm, what's very, very important is when we go back and we analyze this data, we find that these patients, you know, we mentioned 42% of subjects never transition to an atrophic lesion growth despite having very severe genotypes that would predict pathology. They never converted, which is astounding, and it could only speak to a treatment effect. But the most important fact about that is that other patients, those patients that actually converted, we actually have atrophic lesions before we could actually measure them by using the new algorithm. What this means is that we can go back to that data and actually look for the growth rates in those lesions. What we're finding is an actually further suppression of growth rates because we're actually seeing atrophic lesions further, earlier, I should say, in the development program. Typically, what we were seeing is we didn't see the first atrophic lesion until 12 months. But it turns out there are actually, as I said before, there are patients with lesions at baseline, but they grew so slowly they couldn't be detected. So this is very important because it tells us that we're actually having a more robust treatment effect than we earlier thought. So we know we're getting a slowing of the conversion from the autofluorescent to the atrophic lesion, and once the atrophic lesions, we're seeing a slowing of that. But now with the new algorithm, what we're seeing is that overall, all subjects have, in fact, this reduced lesion growth rate. And so this is why we're very optimistic going forward. And again, this will require validation in a, you know, clinical trial like we're doing, and it will probably be another year or two before other investigators really start using it. And of course, that will require the publication of the data and for people to really analyze it, vet it, and use it in their own practices to determine the accuracy and validity of the technique. Got it. I mean, if... Do you think when the drug reaches the market, the patients need to be at least have some atrophic lesion development to be eligible to be treated by this drug? And if so, then this new imaging algorithm could be a crucial component for market adoption, right? Absolutely. I want to answer the first part of the question because it's really important. So for the FDA and for other regulatory agencies, because the endpoint is slowing the growth of the atrophic lesion, all patients will have to have some measure of atrophic lesion at baseline, and that's what we've done in our phase III. All 104 subjects in the Stargardt phase III study have atrophic lesions at baseline, and certainly we'll be looking at that growth rate versus placebo. But the point is that if the drug does get approved with this patient population, investigators are not going to wait for patients to spawn atrophic lesions before they prescribe the drug. In fact, I doubt the label will restrict doctors from prescribing. It'll be for you know slowing of lesion growth in subjects with autosomal recessive Stargardt disease. That's what it will be. And because these patients, some of them develop early autofluorescent lesions, which persist for years, sometimes they will eventually convert to atrophic lesions, which of course will cause vision loss. So it you know PIs, physicians and patients are not going to wait until the autofluorescent lesion converts and say, "Oh, well, let's give them the drug now, because we know now it's going to slow atrophic lesions." They understand the pathophysiology. They know that those autofluorescent lesions will eventually lead to blindness, vis-a-vis the atrophic you know the onset of lesion on atrophic lesions and spreading into the in the fovea. But why not be preventative and give those patients. It's an oral once a day therapeutic, very safe, drug, with minimal side effects. We know there's anticipated ocular ease, but the fact is that if I'm a physician with Stargardt patients who are in great need of a drug that's going to prevent them from going blind, I'm not going to wait until I see atrophic lesions. If they have diagnosed with Stargardt's disease and they have autofluorescent lesions in their retina, I'm going to give it to them as early as possible. So I expect that once the drug is approved, and I'm optimistic, that's why I say once, that you'll see a widespread adoption of it across the spectrum of Stargardt's early autofluorescent lesions, as well as late atrophic lesions. I think all subjects, you know, will be prescribed this drug. Got it. So, Yi, may I add, so it is well known that the pathogenesis of the disease, Stargardt's disease, is the base ABCA4 mutation leading to the vitamin A toxic byproduct depositing and causing the retinal cells to die. And this is exactly the mechanism of action that Tinlarebant is going after. So, basically, with lesions or without lesions, the drug is to prevent or slow the pathology of this disease. So, I would expect that the drug will be labeled as for all Stargardt patients. The fact that we're enrolling patients with atrophic lesions is strictly for the study purposes of getting measurable disease to compare the treatment effect of Tinlarebant and with placebo. But once the drug is approved, basically, it's for all, because the drug's mechanism is basically going after that pathology of the vitamin A. Got it. Thank you. And, could you comment on, when do you expect the PHOENIX trial to complete enrollment? Could that happen before the end of 2024? Um, Nathan? Yeah, so it's a good question. That is our overarching goal, Yi. It has been ever since we started recruitment just a few months ago. We slowed down a little bit, and quite frankly, it's because there are quite a lot of GA studies going on right now. So we're running into sites that have limited resources because of competing trials. That's just something you have to deal with. But certainly, we're ramping up those efforts. In fact, over this past week, we've gotten very fortunate and identified some sites with huge numbers of patients, both in the U.S. and abroad. And so I still think that this overarching goal of end of the year is still possible, but we're putting a little buffer in there, up to Q1 of 2025. So again, optimistically, end of the year, but I think we may need another quarter to get to this number. It is a huge number, 429 GA subjects. I think we're currently approaching 60, maybe 55, something like that. So we're expecting to ramp that up significantly over the coming months. And obviously, that is our goal, is to get to complete study enrollment, 429 subjects, by the end of the year. But we realize there could be some impasses in the way, and so we've given a buffer of another quarter into 2025. Got it. Thank you. And lastly, just to clarify, when you say the cash runway supports operation to 2026, that's into 2026 or possibly throughout 2026? Throughout 2026. Okay, got it. Got it. That's very helpful. Thank you. Thank you. All right, and before we get on to our next analyst, if anyone is watching the webcast, if you can ask a question in the box below the webcast. But, Bruce Jackson from Benchmark, you now have permission to talk. Thank you. Can you hear me okay? Yeah. Okay, super. So, there's been a fair amount of buzz around the, the complement therapies, the C3 and the C5 therapies in particular. And, I think it'd be helpful to compare and contrast the, the mechanism of action between, Tinlarebant and, these, these complement therapies. And in particular, if you could touch on the, intraocular inflammation and the, occlusive retinal vasculitis that they've seen in some of the complement drugs. Thank you. Nathan, I guess this is a perfect question for you. Yeah, I'd be happy to address this because it is a very relevant question, and thank you for asking it, Bruce. The fact is that we're looking at two different spectrums of the same disease, right? So when you're looking at the efficacy of complement inhibitors, which are essentially quelling an inflammatory response, you're talking about the treatment of an inflammatory-based disease, which is a late-stage phenomenon in GA. So when patients early on develop these nascent or early lesions, these geographic atrophy lesions, there's very little inflammation going on, and that's the patient population that we're aiming to target prior to the inflammation. So by the time you get to the inflammatory disease, your retina is on fire, and, you know, you're just basically trying to put out the fire with these complement inhibitors and quell this inflammatory response. But in fact, you still have this underlying pathology, whether it's bisretinoids, like we believe, or it's oxidation or mitochondrial stress. Whatever it is, you still have this underlying pathology, and so all you're doing really is putting out the fire at the border, but it's still raging within. What we're doing is go early on with a pharmacotherapy that addresses these earliest incipient molecules, these toxic bisretinoid byproducts, which have been implicated in early stage disease in GA, and certainly in all of disease in Stargardt's. So we believe, and again, the fenretinide data sort of speaks to that, because our greatest treatment effect in that study was not just because of the patients who achieved a certain level of retinol binding protein 4 reduction, but also because their lesions were actually smaller than the mean. So we're talking about lesions less than 5 mm in size. When you look at the studies where complement inhibitors were effective, those lesions are much larger, 8-10 or even 12 millimeters at baseline. Again, those larger lesions are characterized by inflammation. So this is the biggest difference between our pharmacotherapy and the complement inhibitors, is that they're addressing very late-stage disease, and we're addressing very early-stage disease. With regard to the occlusive vasculitis, which is a blinding phenomenon, and it's certainly terrible for these patients, I think it's still unknown exactly what's causing that. They first thought it was the gauge of the needle, and then they thought it was maybe some immune response because it's very isolated and rare. Only certain patients get it. It could be due to the fact that there's pegylation of these molecules. Both the Iveric compound and the Apellis compound both have pegylation. So even though we've only seen these, side effects in the Apellis, treated patients, if in fact pegylation is the reason for it, then we should also see it, it should be very likely in the patients treated with the Iveric drug, the Iveric drug. So that's really all I can say about it, because, again, the jury is still out. We know that it is a safety risk, a significant safety risk for patients, and we know that, in fact, this is a very important point, that those patients getting treated with these intravitreal complement inhibitors will not have a clinically meaningful treatment effect, and clinically meaningful, meaning to the patient, until after two years. So there will be a tremendous treatment burden for those patients to endure, you know, these injections over a period of two to three years, perhaps, before they're actually getting a benefit in visual acuity and visual function. The same could be said for an oral therapy like ours, but the fact is, there's a much lower treatment burden. So there's a lot of differentiation between the complement inhibitors and what we're doing, both from a safety perspective as well as an efficacy perspective, because we believe by getting in early, it's just like anything, with cancer, with respiratory disease, anything like that, early intervention is the key to long-term curative case in a disease where there's, you know, retinal degeneration that goes on for years and years. So if you get in there early, you can prevent, prevent the loss of vision late stage. So that... I hope that was clear enough, Bruce, but I just want to make this differentiation because it is very important. So, Bruce, may I also add that, so if you look at both, the Apellis and the Iveric studies, in the second year, the treatment effect is actually not much, there's not much difference between the placebo and the treatment. And that may be that, that during the first year, when the, the drug, the anticomplement, are suppressing the inflammation, once the inflammation is gone, you can, there is still, a trend of that disease still growing and, and at a similar rate. I'm talking about treatment, it's growing at a similar rate as the, as the placebo. That may be that, that, there's still the underlying pathology that's still not being taken care of. So once you quell the inflammation, there is still pathology there that's causing that lesion growth at a rapid rate, same as the placebo. So, it may be a disease that there's underlying causes that's still not being taken care of. We believe that there may be the A2E that we're going after, but of course, there is evidence that even if the C3, C5 take care of the inflammation, there is still, in the second year, there's still lesion growth at a rapid rate. Nathan, anything to add on that? Yeah, I wanna add that this is important because I don't necessarily see these therapies as being competitive, and I say this to many people. It's very likely these could be synergistic, because if in fact you have a late stage of disease, GA, and you have this rampant, you know, lesion growth and inflammation, and you take the intravitreal injections, you're able to quell that inflammatory response for a period of time, that's a good time to bring in an oral once a day as a maintenance therapy, to presumably keep the disease at bay while the patient's eyes recover. They won't have to be doing those intravitreal injections. I see a potential synergy here between complement inhibitors, which are acting late stage, and pharmacotherapies, such as ours, which are acting on early stage. Okay, that's great. That was, that was extremely helpful. Then the, the other question I had was about the interim data from the DRAGON trial. Do you think it will be out by AAO? Well, as Tom mentioned. Go ahead, Tom. Yeah. I would say conservatively at this point, I think AAO is roughly October, end of October. Early November, I think. Early November. Possible, but I won't be too aggressive on the timeline, depending on sites enrolling those last patients that the CL are able to get in there to those sites, arrange those site visits to clean out all the data, and then having the DSMB convene at the most, I'll say as soon as possible. So it may be possible, but I think to be conservative, I would say Q, later Q4. Okay. Yeah, it looks like it is on October 18th this year. Oh, sorry. Oh, October 18th. Okay, it's even earlier. Okay. Sorry. Yeah. I, yeah. So I did want to add, Bruce, that for AAO, for 2024, what we will be submitting for presentation is really the genotype, phenotype relationships in the phase II study, because we find that that's very, very interesting data. It hasn't been communicated before, and as I mentioned before, what we're finding is that, you know, the majority of patients, at 87% of patients in the phase II, have very severe biallelic mutations that predict, you know, retinal pathology in these patients, and yet that's not what we're seeing. So we'll be presenting that data along with the lesion growth data, not just the atrophic lesion, but also the autofluorescent lesion. And so that's what we'll be presenting. We're not anticipating presenting interim data at AAO. I suspect the DSMB will just be digging into that data around AAO time. Okay. And Bruce, I would like to add that, one of the things that FDA really want us to be able to do is just not to disclose too much information, especially on the treatment effect at with the interim data. And they actually want us, the sponsor, to not to, you know, know the unblind study, because they really worry that we have additional one more year to go, and that information will bias some of the PIs, some of the patients. So that's why, it is being, you know, kind of adjusted to that. It's gonna be the DSMB who have unblind study data, and they're just gonna inform us to increase the sample size or not. So we probably would not be able to, you know, disclose the unblind study even after AAO as well. Okay, got it. Thank you for taking my questions. Thank you. All right. I believe we have finished all the questions from the analysts. I'm gonna hand it off to Hao-Yuan just to see if there's any in the webcast. Nope, I don't have any questions here. All right, then, do you have any final thoughts you want to say, before we wrap up? Nope. I guess I'd like to thank everyone for attending this Q&A and asking very, very interesting questions. And we look forward to getting the data in Q4. And as we go along, we'd like to also update the progress that we're making in the PHOENIX studies. Thank you very much.