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Hello, and thank you for joining us to discuss Belite Bio’s Fourth Quarter and Full-Year 2023 Financial Results. Joining the call 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 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. [Operator Instructions] Now I'll turn the call over to Dr. Lin.

Thank you. Thank you, everyone, for joining our reporting for 2023 and for this quarter. I'm Tom Lin, CEO of Belite Bio. Joining me is our CFO, Dr. Nathan Mata and CFO, Hao-Yuan. 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 retinal binding protein or 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 by products, which are generated in the visual cycle and are implicated in progression of Stargardt disease and Geographic Atrophy. Belite Bio believes that early intervention directed and emerging retinol pathology, which is not mediated by information, will be the best approach to potentially slow disease progression in Stargardt disease and in GA. There's still a significant unmet need for both indications as currently, there is no approved treatment for Stargardt disease, and there are currently no approved oral treatments for GA, and we're already in global Phase 3 trials for both indications. So far, we have been granted fast track designation, rare pediatric disease designation and open drug designation in U.S., EU and now Japan. We have several patent families and with composition of meta-patents lasting until 2040, and with patent term extension and new patents to be filed, which will have patent protection way past the 2040s. For Stargardt indication, the Phase 3 is already fully enrolled with estimated interim results by end of 2024 or early 2025. We will also be presenting further positive findings and treatment results from our annual Phase 2 results, which we'll be presenting at ARVO in May this year. For GA in Dry ND indication, we currently have more than 50 subjects enrolled in our global Phase 3 trial. With this, I would like to pass this on to our CSO to give an update on the clinical troughs. Nathan?

Thank you, Tom. So I'll go right into the clinical trial designs. When we first -- I should say in previous financial updates, we've shown you the overview of our open-label Phase 2 as well as the well-controlled Phase 3 study design, which is our pivotal Phase 3 study. And we emphasize that the big differences between these two studies was that in the patients in the open-label Phase 2, they came in with a very early stage of disease, which is characterized by the presence of autofluorescence, but not atrophy of retinol lesions, whereas in the Phase 3, all the subjects have retinal atrophy. Well, it turns out that in our Phase 2 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, but 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 2 open-label study, many of these subjects did start with very, very small atrophic lesions that grew over time. And of course, we've shown 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. And we showed this data previously in a comparison to ProgStar, a cohort of subjects that have similar baseline characteristics as our Phase 2 subjects. And as you can see here on the left hand side, we see a really dramatic slowing of lesion growth, intraband treatment group, which is the red lines versus the natural history group in ProgStar, which is the blue lines. And 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 2 patients and the Phase 3. The other new update that we didn't have last time as 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 [Indiscernible] 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 3 trial design and geographic atrophy. And as I mentioned before, the trial designs between the Stargardt disease Phase 3 study and the GA Phase 3 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 granting in 2023 and an increase in professional service fee. We had 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 $52 million raise from the following offering and exercise of the warrants issue in the following offering, an additional $29 million from ATM offering. We expect hash 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 3 study in PA as there are now many sites activated and enrolling subjects. We'll be presenting further findings and more positive data from our Phase 2 in Stargates disease at major conferences this year. We're also expecting the interim data for Phase 3 in Stargates disease later this year or early next year. We have a short presentation today, as most of you would be familiar with the MOA right now. So we are focusing this presentation on the key updates and hopefully have more time for Q&A. We are pleased with the progress we've made in 2023 and we ended 2024 energized and optimistic as we look forward to our progress for the year. I would like to now to turn this back to the operator to start the Q&A. Thank you.

First, I have a question about the time line of the Stargardt disease trial. You mentioned, we expect now either toward the end of the year or early 2025. If the data -- if the trial was already fully enrolled on time, why the trial is delayed by this whatever, this little delay of the early 2025, and also what we should be expecting at this interim readout in terms of the efficacy and safety that you're going to disclose to us. And what are the scenarios, if the data looks good, are you going to keep this study ongoing or what the different scenarios for this interim readout? Thank you.

Sure. Thank you. So the first question is to clarify, there's still -- there's no delay. Actually as you mentioned, the trial is fully enrolled already. The timing for the meeting, the interim data nurses falls within the second 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 we have to -- they'll determine when we meet the enough data points for that interim analysis. So roughly or for between Q4 and Q1 next year. And 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 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 that could get everything prepared for the interim analysis. Sorry, for the second question. The question that you asked, if the safety, something along the safety?

It's really what we should be expecting. And also, what are the different scenarios for this particular readout? Like, let's say if the data's good, what are you going to do?

So the DSMB will observe, if we should -- if the study will be moved on and there's no changes, that 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 a 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 though, 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. [indiscernible] answers the questions.

Well, if I may, I can explain a little bit about why you guys feel like that timing was early 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's so many patients signed up and we have to let the NIM before we are fully enrolled. That's why we ended with 104. And the last patient, he was not able to get the drug in August, that's 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 instead of it has to be in Q4. That's why we made the adjustment on when the interim is expected. We just want to give you -- give the market the latest update that we know.

Yes. So CIO 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 that time line, but the exact date we wouldn't know until the exact date, when the DSMB will convene for -- the for DSM -- for all members to be available to review the data, and of course, the procedure wise from the CIO.

That's great. And we have a question from Jennifer Kim with Cantor.

I have a couple here. Maybe to start off, a follow-up on the last question. When you're talking about the potential outcomes in the interim analysis later this year, you laid out the 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?

Sure. So and then I’ll refer to this to Nathan to give more details on explaining that. And then the second question, Hao, could you comment on the cash run rate?

Yes. Thanks, Tom. So I'll take the first one. So Jennifer, when we talked about this effect size range, that range was really for determining exactly the design of the study. So 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. And so we used treatment range that was observed to have approvals with the FDA. So this 22% to 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 or GA. That aside, what the DSMB is actually looking for is a statistical significant difference regardless of the effect size. So we're looking for a clinically meaningful effect between the trajectory of lesion size grows in 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. 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 overenrolled 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 120. So basically, it would be 26 patients additionally, if we had -- if we didn't have the statistical significance that was meaningful at the interim. So I want to make 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 in placebo and the trajectory of lesion size growth in the Tinlarebant treatment arms. Is that clear, Jennifer?

Yes, yes. That's very helpful. And then maybe on the second question on PHOENIX enrollment and thoughts on cash runway?

Yes. So we have enrolled 56 subject so far. And with the new cash coming from the warrants and ATM so far, we're having -- sorry, 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 pay the milestones that we need to pay to Colombia for these milestones. Yes, I do think that we do have enough cash for that.

All right. And we have a question from Yi Chen with H.C. Wainwright.

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 to -- for this method to be widely adopted?

Yes. You're talking about the new imaging algorithm that's been developed by our reading center. Is that what you are referring to?

Yes.

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 2 study, which was recently completed, but also the Phase 3 in Stargardt to use not only the traditional algorithm, the Heidelberg region finding 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 is. It's not widespread because, in fact, this methodology, this algorithm was just recently developed, and they used our Phase 2 data to develop. And the reason this is very important, the reason they were able to do this is because in our Phase 2 study, we enrolled subjects that only had the early lesion type to sort of predecessor lesions 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 Region Finding 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 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 lesion finding software doesn't do that. So we'll use this data to validate that algorithm and probably going forward, I think 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 -- we mentioned 42% of subjects never transitioned to an atrophic lesion growth despite having very severe genotypes that would predict pathology. They never converted, which is astounding, and it can 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 and what we're finding is and 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 are seeing is we didn't see the first atrophic lesions until 12 months. But it turns out there, 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 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 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 the validity of the technique.

Got it. I mean, do you think when the drug reaches the market, the patients need to be at least have some preliminary 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 3, all 104 subjects in the Stargardt Phase 3 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 will be for 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 autofluorescelations, which persist for years sometimes, they will eventually convert to atrophic lesions which, of course, will cause vision loss. So PIs, physicians or patients are not going to wait until the autofluorescent lesion converts and say, "Oh, 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, the onset of lesion -- atrophic lesions and spreading in the fovea. But why not be preventative and give those patients is an oral once-a-day therapeutic, very safe drug, 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,2 I'm not going to wait until I see atrophic lesions. If they have diagnosed with Stargardt disease, and they have autofluorescent lesions in their retina, I'm going to give it to them as early as possible. I expect that once the drug is approved, and I'm optimistic, that's why I saying 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 will be prescribed this drug.

May I add. So it is well known that the pathogenesis of the disease, Stargardt disease is the base ABCFO mutation leading to development 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 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 that the treatment effect of Tinlarebant 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 that vitamin A.

Got it. And could you comment on when do you expect the PHOENIX trial to complete enrollment? Could that happen before the end of 2024?

Nathan?

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 GE 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 for 129 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. 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.

All right. And before we get on to our next analyst, if anyone is watching the webcast, if you have a question, you can ask a question in the box below the webcast. Bruce Jackson from Benchmark.

So there's been a fair amount of buzz around the complement therapies, the C3 and the C5 therapies in particular. And I think it would be helpful to compare and contrast the mechanism of action between Tinlarebant and 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?

Nathan, I guess this is a perfect question for you.

Yes, I'm happy to address this because it is a very relevant question. 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 developed these nascent or early lesions, these geographic atrophy lesions, there is 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'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 up the fire at the border, but it's still raging within. What we're doing is go early on with the pharmacotherapy that addresses these earliest incipient molecules, these toxic BIM 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 [indiscernible] 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 retinal binding protein for reduction, but also because their lesions were actually smaller than the mean. So we're talking about lesions less than 5-millimeter in size. And when you look at the study is where complement inhibitors were effective, those lesions are much larger, 8 to 10 or even 12 millimeters at baseline. And 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, and it could be due to the fact that there's pegylation of these molecules, both the Ivera 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 as very should be very likely in the patients treated with the Ivera as a 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 -- that a clinically meaningful mean to the patient until after two years. So there will be a tremendous treatment burden for those patients to endure these injections over a period of two to three years, perhaps before they 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 retinal degeneration that goes on for years and years. So if you get in the early, you can prevent the loss of vision late stage. So I hope that was clear enough, Bruce, but I just want to make this differentiation because it is very important.

So Bruce, I may also add that -- so if you look at both the Apellis and the Ivera 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 during the first year, when the drug, the anti compliments are suppressing the inflammation. Once the inflammation is gone, there is still a trend of the disease still growing and at a similar rate. I'm talking about a treatment arm growing at a similar rate as a placebo. That may be that there's still the underlying pathology that's still not being taken care of. So once you got 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 corners that's still not been taken care of. We believe that there may be OA2E that we're going after, but of course, there is evidence that even if the C3, C2 take care of the information, there is still -- in the second year, there's still medium growth at a rapid rate.

Yes. I want to 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 disease GA and you have this rampant 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. So 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 extremely helpful. Then 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.

Yes. I would say conservatively at this point, I think AAO is roughly in October.

Early November, I think.

Early November. Possible, but I won't be too aggressive on the time line depending on sites that enrolling those last patients that the CRO are able to get in there to those sites, arrange site business to clean up all the data and then having the DSMB convened at the most, I would say, as soon as possible. So it may be possible, but I think to be conserved that I would say later Q4.

Sorry. Yes. 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 2 study because we find that's very, very interesting data hasn't been communicated before. And as I mentioned before, what we're finding is that the majority of patients at 87% of patients in the Phase 2 have very severe [indiscernible] mutations that predict 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.

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 the sponsor to not to know a blind study because they really worry that we have additional one more year to go, and that information will bias some of the PIs on the patients. So that's why it has been kind of adjusted to, that going to be the DSMB who have in a blind study data and they're just going to inform us to increase the sample size or not. So we probably would not be able to disclose the blind study even out to AAO as well.

All right. I believe we finished all the questions from the analysts. I'm going to hand it off to Hao-Yuan just to see if there's any on the webcast.

I don’t have any questions here.

All right. Do you have any final thoughts you want to say before we wrap up?