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spk04: Hello, and thank you for joining us to discuss Be Light Bio's fourth quarter and full year 2023 financial results. Joining the call today are Dr. Tom Lin, Chairman and CEO of Be Light Bio, Dr. Nathan Matta, Chief Scientific Officer, and Hao-Wang Zhang, Chief Financial Officer. Before we begin, let me point out that we will be making forward-looking statements that are based on our 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. Please note that you can submit questions throughout the call by clicking on the Q&A box at the bottom of your screen, and we'll respond to questions following our prepared remarks. Now I'll turn the call over to Dr. Lin.
spk08: Thank you. Thank you, everyone, for joining our reporting for 2023 and for this quarter. I'm Tom Lin, CEO of Be Like Bio. Joining me is our CSO, Dr. Nathan Maher, and our CFO, Hao Yuan. I'd like to start off with an overview. So Teneroband is a novel once-a-day oral tablet designed to bind to serum retinal binding protein, or RBP4, as a means to specifically reduce retinal delivery to the eye. This approach is intended to slow or stop the formation of the toxic retinal derived byproducts, which are generated in the visual cycle and are implicated in progression of Stargardt's disease and geographic atrophy. ReliveBio believes that early intervention directed at emerging retinal pathology, which is not mediated by inflammation, would be the best approach to potentially slow disease progression in Starr's disease and in GA. There's still a significant unmet need for both indications, as currently there is no approved treatments for Starr's disease, and there are currently no approved oral treatments for GA. And we're already in global phase three 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 Starless indication, the Phase III is already fully enrolled with estimated interim readouts by end of 2024 or early 2025. We will also be presenting further positive findings and treatment results from our end-of-Phase II results, which we'll be presenting at Arvo in May this year. For GA in Dry MD indication, we currently have more than 50 subjects enrolled in our Global Phase III trial. With this, I would like to pass this on to our CSO to give an update on the clinical trials. Nathan? Thank you, Tom.
spk00: 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 two, as well as the well-controlled phase three study design, which is our pivotal phase three study. And we emphasize that the big differences between these two studies was that in the patients in the open label phase two, 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 two 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, 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 II subjects. And as you can see here on the left-hand side, we see a really dramatic slowing of lesion growth in Tenlarabat 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 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 three trial design and geographic atrophy. And as I mentioned before, the trial designs between the Stargardt disease phase three study and the GA phase three 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's. 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 Yan so we can talk about financial data. Thank you.
spk06: 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 a month 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. Our 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 ATN offering. We expect cash runway to end of 2026. Thank you. Back to you, Tom.
spk08: Thank you, Haoyan. I would like to conclude with the key milestones to expect for this year. We are currently making good progress in the phase three 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 Stargardt's disease at major conferences this year. We're also expecting the interim data for Phase 3 in Stargardt's disease later this year or early next year. We have a short presentation today, as most of you would be familiar with the MOA by 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 now to turn this back to the operator to start the Q&A. Thank you.
spk01: 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 time? 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 the study ongoing, or what are the different scenarios for this interim readout? Thank you.
spk08: Sure. Thank you. So the first question is to clarify this, 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 that will be reviewing that data. And I guess we have to, they'll determine when that we meet the enough data points for that interim analysis. So roughly or four 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 CO getting all the data in and cleaning all the data and then arranging for all the DSMBs time. So that is all in the hands of the CO 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 around the safety.
spk01: 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 is good, what are you going to do? Okay, let me, yeah.
spk08: So, yeah. So the DSMB will observe if we should, if the study will be moved on and there's no changes, 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 end point 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 and there's no way by adding sample size would change the study and then they wouldn't, they would probably say move on as well. So those are the three scenarios.
spk03: All right. Yeah.
spk06: Well, Basma, if I may, I can explain a little bit about why you guys feel like that timing was earlier 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 them in before we fully enroll. 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. He said he has to be in Q4. That's why we make the adjustment on when the interim is expected. We just want to give the market the latest update that we know.
spk08: Yeah, so the COO 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 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.
spk03: That's great. And I see we have a question from Jennifer Kim with Kantor. Sure. Jennifer, you have permission to talk now.
spk05: 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 DSMV 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.
spk08: Sure. So I'll refer to this to Nathan to give more details on explaining that. And then the second question, how could you comment on the cash round? Thank you.
spk00: Yeah, 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 a treatment range that was observed to have approvals with the FDA. 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 statistical significant difference regardless of the effect size. So we're looking for a clinically meaningful effect between the trajectory of lesion size growth 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. 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. As Haoyan mentioned, we over-enrolled the study based upon actually demand from PIs and investigators to 104. The maximum number of patients would actually be enrolled would be the difference, so up to 120. Basically, it would be 26 patients additionally, 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%, 20%. 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 tenlariband treatment arms. Is that clear, Jennifer?
spk05: Yeah. Yeah. That's very helpful. And then maybe on the second question on Phoenix enrollment and thoughts on cash runway.
spk06: Yeah. So we have enrolled 56 subjects so far. And with the new cash coming from the warrants and the ATM so far, we are, we having, you know, end to end, sorry, to 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'll need to pay to Columbia for these milestones. Yes, I do think that we do have enough cash for that.
spk05: Thanks again.
spk03: All right, and we have a question from Yi Chen with HC Wainwright, Yi Chen, you have permission to talk.
spk07: 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 to use? for this method to be widely adopted.
spk00: Yeah, you're talking about the new imaging algorithm that's been developed by our reading center? Is that what you are referring to? 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 two study, which was recently completed, but also the phase three in Stargardt's to use not just not only the traditional algorithm the heidelberg region finding software that everyone is using but this new imaging algorithm which actually defines uh the the atrophic lesions more clearly more discreetly 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 2 data to develop. 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, the predecessor lesion type, this QDA of the autofluorescent lesions that will transition to atrophic lesions. 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 discreetly 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 region-finding software doesn't do that. So we'll use 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 transitioned 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 earlier 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, as I said before, there are patients with lesions at baseline, but they grew so slowly they couldn't be detected. 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 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.
spk07: Got it. 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?
spk00: 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 three. All 104 subjects in the Stargardt phase three 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 and 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 slowing of lesion growth in subjects with autosomal recessive Stardart's 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, you know, PIs, physicians, and 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, you know, the onset of lesion, atrophic lesions and spreading in the fovea. But why not be preventative and give those patients, it's 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, 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.
spk08: Got it. So, E, may I add a So it is well known that the pathogenesis of the disease, Stiles disease, is the ABCF4 mutation leading to the vitamin A toxic bipolar depositing and causing the retinal cells to die. And this is exactly the mechanism of action that Tenebrin is going after. 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. of tenarabine and with placebo. But once the drug is approved, basically it's for all because the drugs mechanism is basically going after that pathology of that vitamin A. Got it, thank you.
spk07: And could you comment on when do you expect the PHOENIX trial to complete enrollment? Could that happen before the end of 2024? Nathan?
spk00: Yeah, so it's a good question. That is our overarching goal. 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 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.
spk07: Got it. Thank you. And lastly, just to clarify, When you say the cash runaway supports operation to 2026, that's into 2026 or possibly throughout the 2026? Throughout 2026. Okay. Got it. Got it. That's very helpful. Thank you. Thank you.
spk03: 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. You now have permission to talk.
spk02: Thank you. Can you hear me okay? Okay, super. 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'd be helpful to compare and contrast the mechanism of action between telenerbent 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. Thank you.
spk08: Nathan, I guess this is a perfect question for you.
spk00: Yeah, 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 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'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 bis retinoids 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 the pharmacotherapy that addresses these earliest incipient molecules, these toxic byproducts, which have been implicated in early stage disease in GA and certainly in all of disease in Stargardt's. We believe, and again, the finretinide data 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. We're talking about lesions less than five millimeter in size. When you look at the studies 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 is 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 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 iverizate 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. 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. Clinically meaningful meaning to the patient, until after two years so there will be a tremendous treatment burden for those patients to endure um you know these injections over 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 it early, it's just like anything with cancer, with respiratory disease, anything like that, early intervention is the key to long-term curative outcomes. a 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 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.
spk08: So, Bruce, may I also add that, so if you look at both the PALIS and the Ayurvedic 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-complement are suppressing the inflammation, once the inflammation gone, there is still a trend of that disease still growing and at the similar rate, I'm talking about treatment, it's growing at a similar rate as the placebo. That may be that there's still the underlying pathology that's still not being taken care of. So once you call the inflammation, there is still pathology that is causing that lesion growth at a rapid rate, same as the placebo. So it may be a disease that there's there's underlying causes that still not been 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, C2 take care of the inflammation, there is still, in the second year, there's still lesion growth at a rapid rate. Nathan, do you have any comment on that?
spk00: Yeah, 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.
spk02: 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?
spk00: Well, as Tom mentioned, go ahead, Tom.
spk08: Yeah. I would say, conservatively, at this point, I think AAO is roughly... October, end of October?
spk00: Early November, I think.
spk08: Early November. Possible, but I won't be too aggressive on the timeline depending on sites that those last patients that the CO 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 but I think to be conserved that I would say later Q4.
spk02: Okay.
spk06: The AAO looks like it is on October 18th.
spk00: Sorry. Okay. It's even earlier. Okay. Sorry. Yeah. 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 two study, because we find that that's very, very interesting data. Has it been communicated before. And as I mentioned before, what we're finding is that, you know, the majority of patients, 87% of patients in the phase two 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 times.
spk06: 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 Freeman effect with the interim data. And they actually want a sponsor not to know the blind study because they really worried 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 kind of adjusted to that. It's going to be the DSMB who have in-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 in-blind study even after AAO as well.
spk02: Okay, got it. Thank you for taking my questions. Thank you.
spk03: All right, I believe we've finished all the questions from the analysts. I'm going to hand it off to Haoyun just to see if there's any in the webcast. No, I don't have any questions here. All right, then. Do you have any final thoughts you want to say before we wrap up?
spk08: No, I guess I'd like to thank everyone for taking 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'll make in the Phoenix studies.
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