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spk02: First half, 2022 financial results conference call. After today's presentation, there'll be an opportunity to ask questions. If the participant calling in would like to ask a question, please press star one one on your telephone keypad. If a participant joining via webcasting would like to ask a question, please submit questions by clicking on ask a question at the top right of your screen. Please note, this event is being recorded. Yesterday, Be Light Bio issued a news release announcing the company's financial results for the first half of fiscal 2022, and it's available within the news section of the company's IR website at www.investors.belightbio.com. Additionally, the presentation has been uploaded to the event section of the company's IR website. If participants joining via webcasting find that the slide presentation is not synchronizing, please refresh the webpage and make sure to click on the play icon at the bottom left corner. Alternatively, please visit the events section of our IR website to view the presentation. I'd like to remind you that the statements we are about to make today may include statements relating to Be Like Bio's business plans and future prospects that are forward-looking to the ending of the Private Securities Litigation Reform Act of 1995. These statements cover many events and matters that are subject to various risks that could cause actual results to differ materially from those expressed or implied in any forward-looking statement we make. I encourage you to review the forward-looking statement section included in our Form 6-K, furnished on August 10th, for a detailed description of the risk factors affecting our business that could cause those differences. In addition, any forward-looking statement mentioned above represents our views only as of today, and we do not undertake any obligation to update any forward-looking statement except as required under applicable law. Representing Be Like Bio today are Dr. Tom Lin, CEO, Dr. Nathan Mata, CSO, and Mr. Haoyuan Cheng, CFO. I'd now like to turn the call over to Tom. Tom?
spk05: Thanks, Chris, and thanks, everyone, for joining this call. I'm Tom Lin, CEO of Be Like Bio. And I'd just like to give a quick background on myself. I'm trained in medicine and surgery, and I also did my PhD in neurology, where my research focus was on developing treatments for neurodegenerative disease. For most of my career, I've led several novel drug governments in multiple therapeutic areas. And prior to founding Be Like Bio and Limbao Science, I've led two startup companies to IPO. On this call with me today is our CSO, Dr. Nathan Mata, and our CFO, Hao-Yuan Zhuang. Nathan, would you like to introduce yourself?
spk01: Sure. Thanks, Tom. Hello, everyone. I'm Nathan Mata. I am the Chief Scientific Officer for Be Light Bio. My PhD is in neurobiology. I have a master's degree in biochemistry as well. I've been in the biotech space for about 18 years. The majority of that 15 plus has been in ophthalmic drug development. specifically looking at advancing therapies, developing therapies for neurodegenerative diseases such as AMD and Stargardt's disease. I'm credited with leading the development of the first RBP4 antagonist in advanced RIMD and the first visual cycle modulator in both advanced RIMD and Stargardt's disease. And I look forward to discussing more with you and showing you some of our data.
spk05: Thank you.
spk09: Hi, everyone. Thank you for joining the call today. My name is Haoyuan. I have more than 10 years of capital market experience, including being an investment banker in Hong Kong for several years and also worked for several Chinese conglomerates on their overseas listing and acquisitions. I also got an MBA from Columbia University.
spk07: Thank you. Back to you, Tom. Thanks. Thanks, Haoyuan.
spk05: So the business highlights, our goal is to develop a treatment for dry AMD and Stargaz disease, which is leading cause of vision loss, where AMD affects around about 200 million patients worldwide. And as for Stargaz disease, being a rare disease, it is the most common form of inherited retinal disease, which affects one in 10,000 children and adults. There is a significant unmet need and a large market opportunity where there is currently no approved treatment for both these diseases. Our lead asset, LBSO8, is in late-stage clinical development, which we have already started enrolling patients in our Global Phase III study for Stargardt's disease. We also have been granted a fast-track designation and a red pediatric disease designation in the U.S. and orphan drug disease designation in both the U.S. and EU for Stargardt disease. Now, upon a successful phase three, LBSO-8 is also eligible for a priority review voucher, which vouchers have been sold for $8,250 million. So the milestones to date is that we've completed phase one trial in 111 healthy adults in both the U.S. and Australia. Now, currently, a two-year open-level phase two trial is ongoing. We presented very promising six-month treatment data in May this year, and with the 12-month treatment data is expected to read out around October this year. At the same time, a two-year double-blind phase three trial has already commenced in the U.S., U.K., Germany, Belgium, Switzerland, Hong Kong, Taiwan, and Australia. And several patients have already been enrolled. And then we also expect to apply for enrollment in more jurisdictions and enroll a total of 60 adolescent STAGA patients globally. The phase two, three trial in dry antibodies is also planned for end of the year. So we have a clear clinical development pathway. So we have a clear clinical development pathway towards approval since the county accepted primary efficacy endpoint for both Stargardt and dry AMD is well known. Both the FDA and EMA have expressed a willingness to accept the slowing of lesion growth as the primary endpoint for approval. Now, another important point to mention is that we have a good idea of the level of RBB4 reduction that will be required to achieve a treatment effect against lesion growth. The data that I'm referring to comes from a Phase II proof-of-concept study led by our CSO about 10 years ago in advanced dry AMD patients that's treated with fenretinide. Fenretinide, which is an anti-cancer drug, with some RB4 antagonist activity. Now, in that study, patients who achieved at least a 70% reduction of RB4 had a statistical significant slowing of lesion growth compared to placebo. So from both of our Phase I studies in healthy adults and our ongoing Phase II study in adolescent stutter subjects, we have identified the optimal dose to be a low dose of 5 milligrams that could achieve LB4 reduction of more than 70%. We also see very promising data from this phase two study in LS and Saga patients that's treated with 5 mg of LBSO8, which Nathan will be presenting later on. Finally, we also have a very strong patent portfolio with nine distinct patent families and IP protection until at least 2034 without patent term extension. and we are still filing new patents. With this, I'll now hand off to our CSO, Dr. Nathan Mata, so he can discuss the pathophysiology of Stargardt1 and advice of DryMD. Nathan? Great.
spk01: Yeah, thanks, Tom. So first, I'd like to sort of outline the clinical trial design for our Stargardt studies. As Tom mentioned, we did the single sending dose and multiple sending dose and healthy volunteers. We then moved to our target patient population, which are adolescent Stargardt patients. We had 11 of those patients involved in a phase 1B where we determined and confirmed that the 5 milligram dose per day was effective to get to at least the 70% reduction that Tom referred to. I call that the therapeutic threshold. We then added additional two patients. We have 13 participants in an ongoing two-year open-label phase 2 study. Of course, there's no placebo because there's an open label. We're looking primarily at safety, tolerability, and, of course, matching the dose with the reduction of retinobinding protein 4, and then looking at the ophthalmic assessments, such as the most important, the primary measure, lesion size growth. This is done by a parameter that ophthalmologists refer to as definitely decreased autofluorescence. You'll want to remember that because I'll talk about that in another slide or two. That's basically dead retina. The precursor to DDF is questionably decreased autofluorescence, or QDAF. So this is what leads to the lesion. I'll show you some clinical data in a moment. We'll also be looking at best corrected visual acuity. We'll be looking at anatomical features by spectral domain optical tomography, and then looking at light sensitivity of the retina with a microperimetry device. In the phase three study, the design will be very, very similar. It is the same patient population, but because there's a pivotal study, there'll be more participants. We'll have at least 50 participants in this global study. As Tom mentioned, we have already enrolled patients in the UK and Europe. This is a double-blind, well-controlled study with a two-to-one randomization wherein every two patients will get LBS zeros or eight, and every one will get placebo. It's a two-year study. We'll be looking, again, at safety and tolerability, but more importantly, we'll be looking at efficacy this time because we're already establishing safety and tolerability in our ongoing phase two. So we'll be looking very closely at efficacy measures, the same exact efficacy measures and the same exact measurement modalities will be used. Now what I'd like to do is really... justify why we believe this treatment effect would be effective for both Stargardt's disease and dry AMD. Next slide, please. So what you have here are two case studies. In the upper panel, you have retinal observations from a patient with late-onset Stargardt's disease. On the bottom panel, you have the same data from a patient with dry AMD. And what you're looking at are images taken by what's called fundus autofluorescent photography, FAF. And the FAF photography actually lights up the cytotoxic-based retinoids which have been implicated in the progression of both of these diseases. So that's the commonality in terms of the pathophysiology. Both of these diseases have, as a hallmark feature, the accumulation of vitamin A byproducts, which are called bisretinoids, and they're highly cytotoxic, but they also fluoresce. So now if you look at the images, looking at baseline and then serially out from left to right, these are one-year images, 12 months, 24 months, and 36 months. We'll look first at Stargardt's disease. You'll see centrally in the baseline image, there's these two areas of blackened lesion. That's dead retina. That's what the ophthalmologists refer to as definitely decreased autofluorescence. But all around that lesion tissue, which is never coming back, that's irreversibly lost, there's autofluorescence. That autofluorescence is the bisretinoid. And if you look serially out every year, you will notice the autofluorescence expands centrifugally and the lesion expands into its wake. So you can look at the autofluorescence as sort of seeding the territory for new retinal cell death. And that's what we're trying to do is stop the bis-retinal, the autofluorescent accumulation. Look now at the dry AMD patient at the baseline. You see a smaller lesion that's very unifocal lesion, but you'll notice all around the lesion, these areas, the little punctate areas of autofluorescence. And if you follow those little areas of autofluorescence out, 12 months, 24 months, 36 months, you will see those autofluorescent areas then become lesion. So just like in the Stargardt's patient, These autofluorescent areas lead to lesion tissue, and because those autofluorescent areas are dysretinoids, and because the dysretinoids are derived from circulating vitamin A, it makes sense that by slowing the admittance or the delivery of vitamin A into the eye, we'll be able to slow the accumulation of these compounds and therefore slow the amount of DDF that is the dead retina that is spreading and ultimately preserve vision. Next slide, please. So now what I'd like to do is go into some clinical data from our phase two study, our ongoing phase two. We'll start first with some adverse event data, some safety data. Excuse me. These are the phase two results from the six-month interim analysis. Again, it's a two-year study. We're looking at six months of treatment. These patients, these subjects have been getting five milligram of LBS zeros or eight every day, and we're seeing the expected features that we want to see. They are adverse events, but they're restricted to the eye as we'd expect. Vanisopsia is a a manifestation of cone photoreceptors. We're having a little bit of a signal here that we're seeing that we're getting cone photoreceptor slowing. We want to see that. This is not an abrogation of cone photoreceptor function. It's simply a reflection of the slowing of the vitamin getting into cone photoreceptors. So there will be a mild and transient hue color that patients see upon wake or when they go from a dark light into bright light. That's expected. So is delayed dark adaptation. Delayed dark adaptation is is a delay in the ability to accommodate to dim light environments. It is not night blindness, so there's probably a three to four to five minute delay in the ability to go from a very bright light environment to a dim light environment, and that's rod photoreceptors. So we're having the intended and anticipated effect on both cone and rod photoreceptors, but it's very important to note that in most cases, the DDA especially was asymptomatic, and that's because it's part of the disease, and perhaps even more importantly than that, no severe AEs or SAEs reported, no AEs requiring discontinuation from treatment, and also no clinically significant findings in relation to vital signs, physical exams, or cardiac health. Now let's go to some efficacy data. Next slide, please. So I mentioned before that the QDF, this autofluorescence, this questionally decreased autofluorescence leads to DDF. So the first thing we want to do is look at the distribution of change in the QDF in our subject at six months. And what we found was that eight of 13 subjects showed a reduction or no change in QDF. And that's quite remarkable when you consider that this disease is slowly progressive. It never abates and certainly never regresses. So the fact that we're seeing a reduction or no change in QDF autofluorescence, which is the primary thing we're going after, because remember, these are the bis-retinoids that we're targeting by reducing vitamin A delivery to the eye. So we're seeing that intended effect. This is what we want to see, a reduction in the autofluorescence. Next slide, please. From that, what we want to look at is the actual lesion that definitely decreased autofluorescence, or what I call dead retina. And remarkably, only one of 13 subjects converted from an autophorescent lesion at baseline to a retinal atrophy lesion at six months. And that growth was about 0.3 millimeters square. When you do that average across the entire cohort, the mean lesion growth in these subjects is far below the mean lesion growth rate that has been documented for this patient population. But because we don't have a placebo comparator, we can't say what the exact comparison is. We can only say we're seeing a trend here that's leaning towards establishing our methods of action. and, in fact, establishing an efficacy trend in these subjects. Next slide, please. We then want to focus on perhaps the most critical thing, but it is not the endpoint, and that is vision, best corrected visual acuity. And remarkably, we found 8 of 13 subjects, 62%, actually had either no change or improvement, so no loss of letters or improvement in 62% of subjects. And you remember that it was also 62% of subjects, 8 of 13, that had the reduction in autofluorescence. And we don't have the correlation in front of you right now, but I can tell you that 75% of subjects, or 6 of 8, so the 6 of 8 subjects who had a reduction in the autofluorescence also had a stasis or improvement in visual acuity. So that's 75% correlation there. That's pretty strong. So all of these outcome measures, the reduction of retinobionic protein 4, which I told you is at least 1%, 70%. The reduction in QDF, which is the thing we want to see. The reduction in the lesion growth, and now a preservation, or at least a stasis, and in some cases, improvement in visual acuity. So at six months, all signs are sort of signaling an efficacy trend, and we look very, very optimistically towards our next interim analysis at one year. With that, I'll turn it over to Hao-Yen so we can discuss the financial results for the first half of 2022. Thank you.
spk09: Thank you, Nathan. So on the income statement for the first half of 2022, we had R&D expenses of $2.5 million, comparing to $3.6 million for the same period last year. The $1.1 million decrease on the R&D expenses is mainly due to the fact that we had higher drug manufacturing and tox study costs last year for the preparation of our Phase III clinical trial. Regarding the G&A expenses, the first half of 2022 was $1.1 million, which was about the same as the $1.2 million of the same period last year. The net loss of first half of 2022 was $3.5 million, comparing to the $4.7 million last year. The difference mainly comes from the decrease on the R&D expenses. On the balance sheet, the majority of our total assets is cash, which is $48.7 million. The increase of the cash mainly comes from the IPO net proceeds, which was about $36.1 million. This is the end of our presentation. Thank you for listening. We will now take questions, if any.
spk07: Back to you, Chris. Great.
spk02: Operator, if you will, could you open up the call for questions from the phone dial-in?
spk09: I have some questions on the webcast here. I think we can start with those.
spk02: Sure.
spk09: Yep. So I think the first question I have here is, when do you expect to release the first year data from the Phase 1B2 study? Tom, do you want to answer that? Yeah, yeah, of course.
spk05: So we have patients in the Phase 2 study that has already reached 12-month treatment. And some of those data are coming in already. So between August and October, we have majority of patients reaching their 12-month treatment mark for the phase two. So by October, we should have majority of those 12-month data. So expecting about October this year.
spk09: Thank you, Tom. The next question I have is, what is your commercialization plan, Tom?
spk05: Well, so at this moment, we still have about three years until the drug is approved, roughly about three years. So assuming that in that three years, we still have a lot to think about commercialization plans. But at this moment, we are open to partnerships and licensing with pharmaceutical partners.
spk09: Thank you. Operator, I think you can open up the line for the hand raised on the phone.
spk08: Certainly. Our first question comes from the line of Chaitanya Galakadha with HC Wainwright.
spk04: Hey, everyone. Congratulations. This is Chase on behalf of Yi Chen from HC Wainwright. I just have a few quick questions. Based on what you've seen so far from your Phase II study, what are your expectations for the – I know it's a long way off, but what are your expectations for the pivotal Phase III study in STGD1 patients? And also, I know you spoke about the 70% RBP for reduction. Is that the minimum that you need? to see for any kind of lesion reduction, or is that the amount that you're expected to reduce to see the target reduction that is essentially required for an eventual approval? And also, a quick follow-up to that is, do you also need two pivotal studies for an approval, or just one is fine? And I have a few other follow-ups after this. Thank you.
spk05: Nathan, this is your expertise. Okay.
spk01: Yeah. So in terms of expectations, I mean, it's very straightforward, right? We expect to see what we're seeing now. We expect to see, you mentioned phase three, right? But let's talk about phase two first, right? So at one year, if we're seeing the same trends, where we're seeing a reduction in the autofluorescence, a reduction in the number of patients converting to tranquil atrophy and preservation or improvement in vision, if we see that at one year, so we have two data points, six months and one year where we're seeing the positive trends, I expect that will continue I mean, all sorts of things happen between Phase 2 and Phase 3, but we have the same patient, same drug, same design, same efficacy endpoints. I would be very shocked if we come out of this Phase 2 with stellar results and go into the Phase 3 with exactly the same patient population and don't get the same results. So, that's the first thing. So, I expect to see what we're seeing now, what I presented today. In terms of the treatment effect versus RBP4 reduction, What I can tell you in that finretinide study, which I led, by the way, in 246 patients with geographic atrophy, if you were at 69% reduction, you didn't have a slowing of lesion growth. That means over two years, if you didn't break the 70% threshold, you did not have a slowing of lesion growth. So it's very binary. I can't explain exactly why, but it was very clear from the data set that when we cut those patients who had below a 70% reduction, that means zero to 69%, there was no efficacy on lesion whatsoever, but those patients that had 70 or more percent reduction did have an efficacy trend. And what's interesting is it didn't matter if you were at 75, 80, or 85 percent reduction, you got the same level of treatment effect. Again, that's in GA, where the bisretinoids are not the primary player. In Stargardt's disease, they are. In Stargardt's disease, bisretinoids are the primary player, so I would expect to see a more stellar outcome in our Stargardt patient population. than in, for instance, intermediate or sort of advanced dry AMD. But again, that's about picking the patients right. And because I've been through many, many studies in AMD, I think we have an ability to do that better than most. The third question, I'm sorry, remind me of that one, please. The third component.
spk04: Yeah, yeah. So I think from a regulatory standpoint, do you need to pivotal studies or is this Oh, yeah, right.
spk01: Good point. So everything is under advisement, right? So when it comes to AMD, no question, you will have to have two Phase 3s. That's just because the disease is so prevalent. You have to show this effect in hundreds of patients. In Stargardt's disease, where the prevalence is 1 in 10,000, so you have 30,000 patients with Stargardt's disease in the U.S. alone, you know, there is a little bit of a leniency and some hesitance on the agency to require you to do two years. So if you come out of this phase two, again, they will only accept a well-controlled study. So if we come out of the phase two, which is this open-label study with just stellar results, it won't mean anything to the agency. But if we bring that data into the phase three, that is, we see the same thing, the same efficacy trends in phase three, and bring that to the agency, particularly if we're saving vision. So, you know, if you look at the competitive landscape, there's no treatment effects out there in dry MD or stargazers that are actually having an improvement in vision in this early in the treatment course. So if we have that trend in phase three, preserving vision, slowing lesion growth, stopping the autofluorescence, I think it will be a very strong case for a single pivotal study for registration with a post-marketing commitment to do the follow-on study, as I say, a post-marketing commitment.
spk04: Excellent. Thank you.
spk05: So may I just add on to the first question that you asked? So regarding what we expect from a phase three trial. So we know that Stargardt disease, especially in childhood onset Stargardt, which we are targeting this group of patients, they have the worst or the most progressive type of disease. Based on natural history, their lesion growth rate is about more than 8 mm square per year. And they lose about, you know, about 10 letters a year. So based on that and comparing to what we're seeing in our Phase II data, if we are seeing a maintenance or seeing that slowing or even halting that lesion growth at one year, I think that gives us a very good idea of what to expect from our phase three. I hope that answers your question.
spk04: It does, it does. Thank you so much for that clarity. And lastly, from me, any comments on the competitive landscape? I know that a few competitors have tried, but some of them have not been successful. So any comments on the evolving competitive landscape in this space? And lastly... any color on the cash runway. Thank you.
spk05: Nathan, you want to?
spk01: Yeah, I can take the first one. In terms of competitive landscape, what you see are basically two therapeutic approaches out there. You see the very late stage approaches with the complement inhibitors, right? And that's both for geographic atrophy and for Stargardt's disease. Of course, you have gene therapy going on as well. I'm not even going to sort of credit that because I sort of see that way in the future, but But right now, what we see the here and now is, you know, the people going after compliment inhibitors, because at the end of these diseases, both starters disease and it's basically just an inflammatory cascade. And so agents that will inhibit the compliment activation will be effective to stop that end stage disease. The 2nd, camp is where we are the early stage, the early intervention. which is we don't even want to see lesions. If we could, we'd start with autofluorescence, patients who just present with autofluorescence, and treat them forever so they never convert to a lesion. That is our objective. That's what we're trying to do. And there's probably one other company, maybe two, that also have the same sort of mindset that we have, is that we want to treat early. But again, they're not going after the same patients we're going after. The adolescent Stargardt patient is the most aggressive, as Tom mentioned, in terms of their disease course. Most of the Stargardt trials out there have started with adult onset, which is a slower progressing disease. And these patients, most of them already have retinal lesions. So it's a very different clinical presentation of what we're looking for. We want to start early and prevent any retinal cell death and certainly preserve vision at all costs. That's basically our approach. So I think we have an advantage in that respect because I think people will end up seeing that oral once a day Early intervention, especially for children, is going to be preferred to waiting until the disease captures most of your vision and your eye is diseased, and now we're going to give you a complement inhibitor. So that's my thinking about it, but I've always been a very strong advocate of early intervention.
spk09: Thank you, Nathan. I can answer the question about the cash. So we expect the cash is enough for our operation until early 2025. which we will have our Phase II completed already and obtain Phase III interim results at least. We may also even have completed STAGA Phase III and obtain the DryMD Phase III interim results, depending on the clinical trial approval and, of course, the enrollment progress. But, of course, if we conduct a second Phase III in DryMD, we will seek further fundraising or licensing partnership. Thank you. So, operator, I think you can open up the next question.
spk08: Certainly. And our next question comes from the line of Bruce Jackson with the Benchmark Company.
spk03: Hi, good afternoon. Thank you for taking my questions, most of which have been answered. So, with the dry AMD trial that's set to begin in Q1, are you still on target to do that?
spk05: Yeah, so right now we probably have about 80 or 90% of the study protocol designed. So we just need to further discuss the patient profile, the target population, and refine that. So basically with that, then we have a clinical protocol that we can initiate the phase three. So we expect probably about... end of the year or beginning of next year to initiate that study.
spk06: Okay, great. That's it for me. I'm sorry I don't have any more questions, but you guys are doing a great job. Thank you very much.
spk07: Thanks. Thank you, Bruce.
spk09: I have another question here on the webcast Q&A. So, what kind of criteria are you thinking of to select for earlier dry AMD patient for your phase 2, 3 trial? Nathan, do you want to answer that?
spk01: Yeah. There's two anatomical features. I mean, one is called reticular pseudodruzin. So, the presence of these reticular pseudodruzin in the eye is sort of an indicator for ensuing disease or impending disease progression. The other thing is we want to start with the smallest lesion possible. So in other GA studies I've done, we will always go after these larger lesions. We've learned our lesson. So we want to go after a very early advanced AMD, if you will. And some people call it intermediate AMD. But we certainly want to start with the smallest possible lesion with a presentation of a large degree of autofluorescence. So these are the sort of clinical phenotypes we're looking for. But the most important, the most relevant, really, is going to be the lesion size. We do not want a very large lesion size. It's been shown very clearly from data with RB4 antagonists that I've worked with, that large lesion size growth is not effective with this particular treatment. So anything over 10 millimeter square baseline is too far gone as far as I'm concerned, and I've seen the data. So for us, it's smaller lesions and, again, some anatomical features we're looking for for the dry MD patient population that will be our best responders.
spk09: Thank you. And I also have another question here is asking about, can you explain the MOA of the drug again, Nathan?
spk06: Right, yes.
spk01: So LBS008 is an RBP4 antagonist. What it does is it competes with vitamin A for binding to retinobinding protein 4. And by doing this, it actually reduces the delivery of vitamin A to that. Oh, thank you for the slide. Right. So in the back of the eye, there's a receptor for RBP4. which allows the admittance of retinol, and it's basically the only tissue in the body that expresses RBP4 receptors. So because of that, the eye has a unique preference for uptake of vitamin A-bound RBP4. So when we attack RBP4 with our drug LBF-0-Z and knock retinol off, the net effect is a reduction of RBP4 and retinol circulating. And because, as I said, the eye has unique preference for uptake of vitamin A-bound RBP4, it will be a reduction in the amount of vitamin A getting into the eye. Other tissues of the body won't be affected because they don't have that very unique preference for uptake of vitamin A bound to RBP4. Only the eye does. Therefore, our therapy is really site-directed. It will only have an effect in the eye. It will reduce the delivery of vitamin A to the eye and then reduce the level of all the retinoids and, most importantly, the aldehydes because these aldehydes are the precursors for the dysretinoids. So by reducing the retinoid content, retinoid just means all vitamin A content in the eye, we will reduce the level of these cytotoxins, the primary one being A2E, so-called because it's formed from two aldehydes and one ethanolamine. And this thing kills tissue through myriad mechanisms and, in fact, has been identified in post-mortem tissues with patients that have Stargardt's disease and patients with advanced dry AMD. So I hope that answers the question on MOA.
spk09: Thank you, Nathan. I don't have any questions received here. Is there any other questions? If no, then we will conclude the earnings call today. Okay, I'll now turn the mic back to Tom for closing remarks.
spk05: So thank you, everyone, for listening to the call. We are excited to be listed on the NASDAQ and very pleased with LBSOA's progress in their clinic. We look forward to our upcoming data release in October, and we'll be discussing our one-year treatment results from the Phase II Stargardt's disease trial. Have a great rest of your day, and thanks again, and we look forward to updating you more on our progress. Thank you.
spk02: Before we end today's conference call, I'd like to remind everyone that this call will be available for replay via Reek webcast. about two hours after the event for 30 days at the company's IR website. Thank you for joining the call today. This concludes today's conference call. You may now disconnect your lines.
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