Belite Bio, Inc (NASDAQ:BLTE) Q2 2022 Earnings Conference Call August 11, 2022 4:30 PM ET
Tom Lin – Chief Executive Officer
Nathan Mata – Chief Scientific Officer
Hao-Yuan Chuang – Chief Financial Officer
Conference Call Participants
Bruce Jackson – The Benchmark Company
Unidentified Company Representative
[Call Starts Abruptly] First Half 2022 Financial Results Conference Call. After today’s presentation, there will be an opportunity to ask questions. [Operator Instructions] Please note, this event is being recorded. Yesterday, Belite Bio issued a news release announcing the company’s financial results for the first half of fiscal 2022. And it’s available within the new section of the company’s IR website at www.investorsbelitebio.com.
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I’d like to remind you that the statements we are about to make today may include statements relating to Belite Bio’s business plans and future prospects that are forward-looking statement in the meaning 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 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 ethical law.
Representing Belite Bio today, are Dr. Tom Lin, CEO; Dr. Nathan Mata, CSO; and Mr. Hao-Yuan Chuang, CFO. I’d now like to turn the call over to Tom. Tom?
Thanks, Chris. And thanks everyone for joining this call. I’m Tom Lin, CEO of like Belite Bio, and just like to give a quick background on myself. I’ve trained in Medicine of Surgery and 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 developments in multiple therapeutic areas. And prior to founding Belite Bio and Lin Bioscience, I have led to startup companies to IPO.
On this call with me today is our CSO, Nathan Mata; and our CFO, Hao-Yuan Chuang. Nathan, would you like to introduce yourself?
Sure. Thanks, Tom. Hello everyone I’m Nathan Mata. I am the Chief Scientific Officer for Belite 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 dry AMD and first visual cycle modulator in both advanced dry AMD and Stargardt’s disease. And I look forward to discussing more with you and showing you some of our data. Thank you.
Hi, everyone. Thank you for joining the call today? My name’s Hao-Yuan. 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 conglomerate on there, oversee listing and acquisitions. Also got an MBA from Columbia University. Thank you. Back to you, Tom.
Thanks. Thanks, Hao-Yuan. So the business highlights. Our goal is to deliver treatment for dry AMD and Stargardt disease, these which is leading cause of vision loss where AMD affects around about 200 million patients worldwide and as for Stargardt’s disease being 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 LBS-008 is in late-stage clinical development, which we have already started enrolling patients in our global Phase 3 study for Stargardt disease. We also have been granted a fast track designation, a rare pediatric – and a rare pediatric disease designation in the U.S. and often drug disease designation in both the U.S. and EU for Stargardt disease.
Now upon a successful Phase 3, LBS-008 is also eligible for a priority review voucher, which vouchers have been sold for $80 to $150 million. So the milestones to date is that we’ve completed Phase 1 trial in 11 – sorry, in 111 healthy adults in both the U.S. and Australia. Now currently a two-year open-label Phase 2 trial is ongoing. We’ve presented very promising six-month treatment data in May this year. And with the 12-month treatment data is expected to readout around October this year.
At the same time, a two-year double-blind Phase 3 trial has already commenced in the U.S., UK, 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 Stargardt patients globally. For Phase 2/3 trial in dry AMDs also plan for end of the year.
So, we have a clear clinical development pathway. That’s to – so we have clear clinical development pathway towards approval since the currently 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 point – another important point to mention is that we have a good idea of the level of RBP4 reduction that’ll be required to achieve a treatment effect against lesion growth. The data that I’m referring to comes from Phase 2 proof-of-concept study led by our CSO about 10 years ago in dry – in advanced dry AMD patient that’s treated with retinoid, Fenretinide which is an anti-cancer drug with some are before antagonist activity.
Now in that study, patients will achieve at least a 70% reduction on RBP4 had a statistical it can slowing of lesion growth compared to placebo. So from our – both of our Phase 1 study in healthy adults and our ongoing Phase 2 study in adolescent Stargardt subjects, we have identified the optimal dose to be a low dose of five milligrams that could achieve RBP4 reduction of more than 70%. We’re also seeing very promising data from this Phase 2 study in adolescent Stargardt patients that’s treated with five milligrams of LBS-008, which Nathan will be presenting later on.
Finally we also have a very strong patent portfolio with 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 Stargardt 1 and advanced dry AMD. Nathan?
Very good. Yes. 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 in 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 five milligram dose per day was effective to get to at least the 70% reduction that Tom referred too, 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 retinol binding 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 referred to as definitely decreased autofluorescence, you want to remember that, because I’ll talk about that in another side or two, that’s basically dead retina. The precursor to DDAF 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 coherence tomography, and then looking at type like sensitivity of the retina with a microperimetry device.
In the Phase 3 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 we’ll get LBS-008 in every one we’ll get placebo. So two-year study, we’ll be looking again at safety intolerability, but more importantly, we’ll be looking at efficacy this time, because we’re already establishing safety intolerability in our ongoing Phase 2. 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 justified 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 autofluorescence photography, FAF. And FAF photography actually lights up the cytotoxicity with 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 essentially in the baseline image, there’s these two areas of blackened lesion that’s dead retina. That’s what the ophthalmologist referred 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 best retinoid.
And if you look serially out every year, you will notice the autofluorescence expands centrifugally and the lesion expands into its weight. So, you can look at the autofluorescence as sort of feeding the territory for new retinal cell death. And that’s what we’re trying to do is stop the bisretinoids, 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 truncate 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 auto autofluorescent areas are bisretinoids and because the bisretinoids are derived from circulating vitamin A, it makes sense that by slowing the admittance or the delivery of vitamin A into the eye will be able to slow the accumulation of these compounds and therefore slow the amount of DDAF that is a dead retina of 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 2 study our ongoing Phase 2, we’ll start first with some adverse event data, some safety data, excuse me. These are the Phase 2 results from the six months 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-008 every day. And we’re seeing the expected features that we want to see. They are adverse events, but there’s restricted to the eye as we’d expect.
Xanthopsia is 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 it’s not an aggregation of cone photoreceptor function. It’s simply a reflection of the slowing of the vitamin A getting into cone photoreceptor. So there will be a mild in transient hue color that that patients see upon wake or when they go from a dark light into bright lights that’s expected. So is delayed dark adaptation. Delayed dark adaptation 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 photoreceptor.
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 DDAF 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 QDAF, this autofluorescence is questionably decreased autofluorescence leads to DDAF. So the first thing we want to do is look at the distribution of change in the QDAF in our subject at six months. And what we found was that eight of 13 subjects showed a reduction or no change in QDAF. 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 autofluorescence, which is the primary thing we’re going after, because remember these are the best 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 autofluorescent lesion at baseline to a retinal atrophy lesion at six months. And that growth was about 0.3 millimeter 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 mechanism 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 is not the end point. And that is vision. Best corrected visual acuity. And remarkably, we found eight 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, eight or 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 six of eight. So the six of eight 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 in retinol binding protein 4 which I told you is at least 70%. The reduction in QDAF, 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 and 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-Yuan, so we can discuss the financial results for the first half of 2022. Thank you.
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 3 clinical trial.
Regarding the G&A expenses, the first half 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 proceed, which was about $36.1 million.
This is the end of our presentation. Thank you for listening. We will now take questions if any back to you, Chris.
Unidentified Company Representative
Great. Operator, if you will, could you open up the call for questions from the phone dial-in.
Well, Chris, I have some question on the webcast here. I think we can start with those?
Unidentified Company Representative
Yep. And 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?
Yes, of course. So, we have patients in the Phase 2 studies, 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 2. So by October, we should have majority of those 12-month data. So expecting about October this year.
Thank you, Tom. The next question I have is, what is your commercialization plan, Tom?
Well, so at this moment we still have about – three years until the drug is approved roughly around three years. So assuming that in the three years we still have a lot to think about commercialization plan. But at this moment we are open to partnerships and licensing with pharmaceutical partners.
Unidentified Company Representative
Thank you. Operator, I think you can open up the line for the hand raise, on the phone dial-in.
Certainly. Our first question comes from the line of Chaitanya Gollakota [ph] with H. C. Wainwright.
Hey everyone. Congratulations. This is Chait on behalf of the Lee Chen [ph] from H.C. Wainwright. I just have a few quick questions. Based on what you’ve seen so far from your Phase 2 study, what are your expectations for the I know, it’s a long way off, but what are your expectations for the pivotal Phase 3 study in STGD1 patients?
And also I know you spoke about 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 quick follow up to that is, do you also need two pivotal studies for an approval or just one is fine? And I’ve a few other follow up after this. Thank you.
Nathan. This is your expertise.
Yes. 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 3, right? But let’s talk about Phase 2 first, right? So at one year, if we’re seeing the same trends where we’re seeing a reduction in the auto fluorescence, a reduction in number of patients converting to [indiscernible] atrophy and preservation or improvement vision, if we see that at one year, so we have two data points, six months in 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, very shocked if we get, we come out of this Phase 2 with fellow results and going to the Phase 3 with exactly the same patient population and I’ll get the same result.
So that’s the first thing. So, I expect to see what we’re seeing now, what I’ve presented today. In terms of the treatment effect versus RBP4 reduction. What I can tell you in that bisretinoid study, which I led by the way, in that 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% of 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 with 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% reduction, you got the same level of treatment effect. Again, that’s in GA where the bisretinoid are not the primary player in Stargardt disease they are, and Stargardt disease, bisretinoid are the primary players. 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 that – remind me of that one please. The third component I remember.
Yes. So, I think some regulatory standpoint, do you need to pivotal studies? Or just this – just, this is fine, right?
Good point. So everything is under advised, 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 disease, where the prevalence is one in 10,000. So you have 30,000 patients with Stargardt disease in the U.S. alone. 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 2, again they will only accept a well controlled study.
So, if we come out of the Phase 2, 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 3, that is, we see the same thing, the same efficacy trends in Phase 3, and bring that to the agency, particularly if we’re saving vision. So, if you look at the competitive landscape, there’s no treatment effects out there in dry AMD or Stargardt that are actually having an improvement in vision this early in the disease course in the treatment course. So, if we have that trend at, in Phase 3, 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.
Excellent. Thank you. And last, so…
Nat, may I just add onto the first question that you ask? So regarding what do we expect from a Phase 3 trial? So, we know that Stargardt disease, especially in childhood onset Stargardt, which we are targeting this group of patients they are – they have the worst or the most progressive type of disease based on natural history. Then their leisure growth rate is about more than eight millimeter square, millimeter per square per year. And they lose about, about 10 meters a year. So based on that and comparing to what we are seeing in our Phase 2 data if we are seeing a maintenance or seeing that slowing, or even halting that vision growth at one year, I think that gives us a very good idea of what to expect from our Phase 3. I hope that answers your question?
It does. It does. Thank you so much for the 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.
Nathan, you want to?
Yes, I can take the first one, in terms of competitive landscape, I mean, what you see are basically two therapeutic approaches out there. You see the very late-stage approaches with the compliment inhibitors, right? And that’s both for geographic atrophy and for Stargardt 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 right now, what we see the here and now is, the people going after compliment inhibitors, because at the end of these diseases, both Stargardt disease and AMD, it’s basically just an inflammatory cascade. And so, agents that will inhibit the complement activation will be effective to stop that end stage disease.
The second camp is where we are the early stage, the early intervention, which is we’re not, 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 lesion. So it’s a very different clinical presentation than, 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 saying that all 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 compliment inhibitor. So that’s my thinking about it, but I’ve always been a very strong advocate of early intervention.
Thank you. Makes sense, Tom. I can answer the question about cash. So, we expect the cash is enough for our operation until early 2025, which we will have our Phase 2 completed already and obtain Phase 3 intern result, at least. We may also even have completed Stargardt Phase 3 and obtain the dry AMD Phase 3 interim result depending on the clinical trial approval. And of course the enrollment progress. But of course, if we conduct a second Phase 3 in dry AMD, we will seek further fundraising or, licensing partnership. Thank you.
Unidentified Company Representative
So operator, I think you can open up the next question.
Certainly. And our next question comes from the line of Bruce Jackson with The Benchmark Company.
Hi, good afternoon. Thank you for taking my questions. Most of which have been answered. So with the dry AMD trial that’s set at the beginning, Q1, are you still on target to do that?
Yes, so right now we’ll probably, we probably have about 80% or 90% of the study protocol designed. So we are 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 3. So, we expect probably about end of the year or beginning of next year to initiate that study.
Okay, great. That’s it for me. Sorry, I don’t have any more questions, but you guys doing a great job. Thank you very much.
Thank you, Bruce.
Yeah, I have another question here on the webcast Q&A. And so what kind of criteria are you thinking of to select for earlier dry AMD patients for your Phase 2/3 trial? Nathan, do you want to answer that?
Yes. There’s two anatomical features. I mean, one is called reticular pseudodrusen. So the presence of these reticular pseudodrusen 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 want, after these larger lesions, we’ve learned our lessons. 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, the lesion size.
We do not want a very large lesion size. It’s been shown very clearly from data with RBP4 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 the dry MD patient population that will be our best responders.
Thank you. And also have another question here is asking about, can you explain the MOA of the drug again. Nathan?
Right? Yeah. So LBS-008 is an RBP4 antagonist. What it does is it competes with Vitamin A, for binding to retinal binding protein for, and by doing this, it actually reduces the delivery of vitamin A [ph]. Oh, thank you for this 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, that expresses RBP4 receptor. So that, 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 LBS-008 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 Allda [ph] eyes because these Allda eyes are the precursors for the bisretinoids. So by reducing the retinoid content, retinoid just means all vitamin A content in the eye. We will reduce the level of these cytotoxin the primary one being A2E so-called because it’s formed from two Alda eyes and [indiscernible], I mean, and this thing kills tissue through myriad mechanisms. And in fact has been identified in post-mortem tissues with patients that have Stargardt disease and patients with advanced Dry AMD. So, I hope that answers the question on MOA.
Unidentified Company Representative
Thank you, Nathan. I don’t have any question received here. Is there any other questions, if no, then we will conclude the earnings call today. Okay. I’ll now send Mike back to Tom for closing remarks.
So thank you everyone. For listening to the call we are excited to be listed on the NASDAQ and very pleased with LBS-008s progress in the clinic. We look forward to our upcoming data release in October, and we’ll be discussing our one year treatment results from the Phase 2 Stargardt 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.
Unidentified Company Representative
Before we end today’s conference call, I’d like to remind everyone that this call will be available for replay via week webcast, about two hours after 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.