Q2 2023 Belite Bio Inc Earnings Call

I believe bio. Please go ahead sir.

Thank you Sarah and.

Thank you everyone for taking the time to join this meeting Tom Lacey almost be like bio.

I'll start off by giving the overview and the milestones we have achieved so far.

So for this debt for so for those that are <unk>.

<unk> story, the drug that we are developing narrowband.

<unk> is a novel once daily oral tablet designed to bind to serum retinal binding protein as a means to specifically reduced rate of our delivery to the eye.

This approach is intended to slow or halt the formation of toxic retinal Devry byproducts, which are generated in the visual cycle and are implicated in quick question I'll start with disease and geographic atrophy secondary to secondary to dry AMD.

<unk> believes that.

Earlier intervention directed at emerging retinal pathology.

He is not media filing information would be the best approach to potentially slow disease progression and Starbucks disease and Ges client indeed.

So there is still significant unmet need for both indications.

Currently there is still no approved treatment for <unk> disease, and there are currently no approved oral treatment for Ta.

Our treatments are expected to capture a much higher much wider market for advanced dry AMD.

We have so far received fast track designation rare pediatric disease designation and orphan drug designation, which allows us to frequently discussed with FDA of our progress and see how we can expedite expedite the approval of this drug if we show positive results from our phase III study.

I'd also like to mention that we still have a long patent life with the first composition of matter patent expiring in 2035.

And this is without patent extensions and with new patents being filed.

<unk>, which will extend the patent portfolio in 2015.

Now in terms of important milestones achieved this quarter.

Our phase III 80 months treatment data continues to show slow of lesion growth.

We are also expecting a phase 234 months final data readout in Q4 this year.

We've also recently completed enrolment of our global Phase III startup of Saba trial, and we are now expecting interim readouts around mid 2024.

We've also started enrollment for our global phase III trial in dry AMD.

And with this I'll pass over to Nathan to go through the.

Clinical trial results.

Yes, thanks, Tom So I'd like to first start by providing an overview of the trials we have going on in <unk>. We have two studies as Tom mentioned, we have an ongoing open label Phase II study and so the two year study, which is just about ready to end in October I'll give you some more information about that as we move forward, but we've got 18 months data to share with you and provide that number.

Moment, there's also the phase III data, which as Tom mentioned has recently stopped enrollments we've met our target in fact, we've exceeded our target by about 10 subjects. We've got 100 subjects in there. Both of these studies are two year studies, they're both looking at the primary endpoint, which is the growth of atrophic lesions that as PDF and I'll explain what that is at the moment, so theres a lot of.

Similarities between these designs the differences are as follows in the open label Phase two there's only 13 subjects. In this subject came in was only auto fluorescent lesions and I'll show you some of the biology on how the auto for resolutions turn into this atrophic lesion that we call <unk>. So thats one of the differences. The other difference of course, it's an open label study we're looking at the same efficacy.

Measures are the same assessments by imaging modalities, such as a funding source in our photography to look at the lesion growth and you can see here at the bottom with the key inclusion criteria, where the startup phase III study is also a two year study and design of course, its global there'll be a two one randomization favoring <unk> and you can see there the various inclusion criteria at the bottom of this slide.

Next slide please.

So I want to show you first as Tom mentioned this age or <unk> is a retinal binding protein for antagonist and so the first biomarker you will if you will that we will see is a reduction in the retinal binding protein for levels in serum and that's what's shown here from the phase III data out to 18 months you see the very first point, which is shown there at 100%.

For the patients got dose and you can see over the period of 18 months, we've achieved about 80% reduction from baseline of retinal binding protein for you see here this target threshold of greater than or equal to 70% reduction. This number has been determined in a clinical study in geographic atrophy with a different retro binary protein for <unk> I'll share that data with you.

Well, but this has become our market because we believe that you need to achieve at least this level of RBC for reduction to effect a change in lesion growth and by the way the daily oral dose. These kids are getting these searching on listen starter kits is five milligrams per day and no one's a study out to 18 months I will go over the safety data as well next slide.

A little bit about the biology, so early in the disease course, or only auto fluorescent lesions and thats shown on the left hand side here. The image. These lesions are called the Kressley decreased auto fluorescence by ophthalmologists basically what they do is they represent sales lead and with auto fluorescence entities. These auto source of entities are best retinoids.

These are the agents that were trying to reduce because these best retinoids are formed from vitamin E. We've reason that by reducing the amount of retinal going into the <unk>. We can have effect on reducing the accumulation of these certain words and slow the growth of these auto fluorescent lesions. So these auto fluorescent lesions are amendable to rescue, but if left alone which of course they have to be because there's.

No treatment they will transition into a terrific retinal lesions, which is shown on the right hand side, you see that black demarcated image that basically is irreversible photoreceptor sell lost those sales are never coming back that a trophic areas were ophthalmologist referred to as definitely decreased auto fluorescence and stopping the growth of that leasing type.

Is the primary endpoint, but of course ophthalmologist look at the combined lesion grocery because both of these lesions are pathologic and so in one study conducted in 2020 by Georgia, One co workers, they found and 53 analysts and starter kits the growth rate of the combined lesion was roughly about seven millimeter square per year.

Here when we look at that same anatomical feature in our 18 month data and annualize it up to a year, we see a growth of only about two eight millimeter square per year. So that represents about a 60% reduction in the combined lesion growth rate based upon comparison to this very well conducted natural history study, which by the way at that time was the largest natural history study conduct.

In adolescent patients, but we are very concerned about comparing the atrophic lesion growth because that is after all the endpoint and for that comparison, we had to go to the largest natural history study of startups conducted today called Prague Star. This study enrolled hundreds of patients with startups disease. Many of them are adult patients, but among these <unk>.

Since there was a small group of 20 subjects that had the exact same baseline characteristics as our subjects in the open label Phase II that is there were 18 years or younger and they had no atrophic lesions at baseline only auto fluorescence. So we were able to compare the combined leasing growth rate and that trucks are group to ours as well as the atrial technician growth.

Combined lesion growth as shown on the left hand side. This is called D E F or decreased auto fluorescence. So it represents the <unk> area plus the DTF area and you can see here out to 18 months, we're getting about a 50% reduction in the combined lesion growth rates and you'll remember this slide previously showed you at 60% reduction so it's a pretty pretty good comparison between these two.

Separate and independent natural history studies, when we look at the a terrific lesion growth is the DDA F. We see at 18 months about 50%, sorry, 60% reduction in that atrophic lesion growth rate and noticeably not many subjects are converting in fact, there seems to be a slowing of the conversion and our treatment group transitioning from the auto for the rest of it.

Two the atrophic retina lesion types and that is all very consistent with our hypothesis that we would first effect a change on the auto fluorescence and then subsequently a change in the atrophic lesion growth and we believe that's what these data are showing us.

I Should've mentioned, but the investigators from the previous study by Georgia, and this study products start which was Hendrick shoal commented that we are seeing a definite a bonafide treatment effect in these natural history study comparisons. So that's very promising for us to see next slide.

This is showing you the visual acuity data, we're showing you. Both is the study of <unk> of course, both eyes are going to get the same treatment. Because this is an oral systemically applied drug we're showing you. This because in clinical studies you do have to designate a pillow.

That study and then the other I just becomes it felt like we just want to show you that across 18 months, we're having a stabilization of visual acuity in the subject and this is a very promising trend because typically these subjects, losing where from four to six liters per year. So the fact that we stabilized over 18 months is a very promising trend that combined with the slow lesion growth tells us we're affecting exactly what.

We wanted to stop the lesion growth and eventually have an effect on preserving or improving vision and you can see there the letters losses roughly.

Within the noise of the variability of the visual acuity assessment next slide please.

So now we want to get into the safety data I should start by saying there have been no systemic toxicity is noted to date. So knows currently snippet findings in relation of vital signs physical exams cardiac health, Oregon functions, but we are seeing our two expected features.

Of this therapy and their expected because we are reducing the amount of vitamin E going into the <unk>. So we expect effects on rod and cone photoreceptors, which are the two photos separate cell types in the retina. The first AE. We're finding is a form of chromatopsia called Xanthopsia. This is mediated by cone photoreceptors and it typically happens when patients transitioning.

Suddenly from a very dark light to a very bright light for instance from leaking after sleeping and being exposed to very high room night, where sunlight and so basically comfort receptors are activated they will demand chromophore under our treatment regimen that promo for the us and kept up quite as quickly. So there'll be a delay in the timing for these comfort receptors to fill up with chromophore and during that time they will miss.

<unk> produced these artificial electrical mediated Hughes of color in the visual field. In this case xanthopsia is yellow, but you can see here. The majority of subjects are experiencing xanthopsia, but no one's leaping study because of that and in fact, we are seeing some recovery over time and we're not taking subjects of drugs. They are recovering while still getting dose the second <unk>.

AE has known as delayed documentation. This is mediated by <unk> receptors and again when rod photoreceptor when you transition some of them from a very bright light to a very dim light rodford receptors activate they require chromophore there'll be a delay in the timing of that from a port to fill up the rod photoreceptors and during that time. These rod photoreceptors will not have maximum.

In light sensitivity. So there was a delay in the accommodation to them like this is not night blindness I'd want to make that very clear. This is simply a delay sometimes eight to 12 minutes in cases, where it's very severe out to 20 minutes and there was one subject it's called night vision impairment, but overall, we're very satisfied with these findings we basically lost one subject to follow up at 12.

Months out of 13 subjects. We are now at 12 subjects at 18 months, but this is still very very promising safety profile on.

Next slide please.

So now I want to talk about that proof of concept study I told you about the 70, 70% marker how did we get there well. This was a study I conducted approximately 12 to 13 years ago. When I was with another company I also have this idea that reducing retinal delivery to the eye might have an effect on slowing lesion growth I didn't have a drug to do that with but I did find an anticancer drug <unk>.

Fin Retinite, which had a side effect of reducing retinal binding protein in the blood as I said before it was developed as an anticancer drug but in all the cancer studies, what the investigators noted was a dose dependent reduction of RFP for so I repurposed spend retinite into a two year phase II proof of concept study enrolling 246 patients to see if this drug will have any effect.

On slowing lesion growth there were two treatment arms and placebo 100 milligram 200 milligram and of course placebo I want to show you. The lesion growth data just from the high dose arm and placebo because the middle dose the 100 milligram and absolutely no effect on lesion growth what you're seeing here on this histogram as shown on the left hand side. The button. The black bars is the lesion growth in the placebo.

Group expressed as a percent increase from baseline. So we're getting about a 50% increase over 24 months in the placebo subjects in the 300 milligram group. There was something very interesting. There was a group of subjects had a very profound reduction of retinal binding protein sort of at least 70% or more in those subjects. There was about a 25% slowing of Lee.

Asian growth over two years in the subjects that did not have this reduction of retinal binding protein important 70% or more there was absolutely no effect on the lesion growth rate. So we're pretty convinced especially MGA that this is this is the level of production that would be required to effect a change in lesion and of course. This is the same sort of approach that we're applying to start.

<unk> disease and interesting thing about this lesion cost reduction you'll notice it started right at about the 12 month time point and it's stabilized between 18 and 24 months, but when we look at the visual acuity loss in these subjects. We also noticed at least such as that had a preservation of lesion, but there is a reduction of lesion growth. There was also a stabilization of visual acuity loss.

Right about the same time 12 months. It was the six letter loss and there was no further loss after 24 months. Meanwhile, the placebo group and the patients or subjects that did not get that profound reduction of our before continue to lose vision article about 11 or 13 letters over the two years. So we have a very significant visual acuity gain and a very significant <unk>.

<unk> reduction that has never been observed before energy a study the problem with this phase II study was the only one in three subjects actually achieved this profound reduction of RBC in the 300 milligram group and the reasons for that are twofold one.

That is terrible bioavailability. So we asked subjects to take this drug with a high fat meal dinner to increase exposure into the blood many patients complied out to about one year, but after one year, we had a lot of patients falling off of that compliance and we knew that because the RVP levels. In these patients would inflect upward, indicating in fact that they're no longer having suppression of RVP.

For the second problem was the low potency of fin Retinite FINRA.

So in retinitis, a terribly turbo drug for desktop with different titles because that's the same affinity for the target as does the native ligand vitamin a with 10 layer that we have designed a drug that specifically overcomes those deficits.

So it has greater bioavailability and a 100 fold greater potency than does spend retinoid. So were convinced with this better purpose designed RVP four antagonist, we can achieve at least this benefit and probably even greater because again, we'll have better compliance and will have greater potency of the drug on target.

Next slide please.

So now a little bit about a little bit of our phase III study in geographic atrophy.

It is important to note. So we were concerned that with the higher age and higher BMI of patients <unk> versus startups disease, we would have to do a dose higher than five milligram. So we did a PK PD study with both five milligram and 10 milligram and what we found was a five milligram dose produces the same pharmacokinetic profile as it did in younger subjects. So when these healthy.

Adults were seeing about 80% reduction of RP before across the dosing period with this five milligram dose and it's also important to note and we see this in the analyst and such as well once you withdraw the treatment. The RVP four level start bouncing back upward showing nice reversibility of the Pharmacodynamic effect, which of course is a nice safety feature in the event of any untoward.

Or you want to return the patient back to baseline status.

Sorry about that.

Now a little bit about the clinical trial design overview for our phase III study, we called Phoenix. This study design is going to be nearly identical to the phase III trial design for Star Guards that is it's two years in duration and has the same randomization frequency two to one favoring to learn about it is the same endpoint measures. So we're still looking at the same DTF measure.

As a primary measure for efficacy and of course, we're looking at other measures such as <unk> and looking at the auto fluorescence. There are two major differences. One of course is the indication geographic atrophy not star Guards and the second one is that we will be enrolling up to 430 subjects. Instead of the 90 that we targeted for these startups as you study. This of course reflects the higher prevalence of <unk>.

In the population.

But otherwise these studies are essentially identical and I think Tom mentioned that we've actually kicked off the start we've enrolled our first patient I believe it was last week and we continue to get more interest in more patients rolling into this phase III study as we move forward.

With that I believe I can turn it back to <unk>. So he can discuss the 2020 Q2 financial results. Thank you.

Thank you Nathan.

So as of June 33, we had $57 4 million in cash and the <unk>.

R&D expenses on a three month.

And at June 30, we had research and development expenses balance about $5 5 million compared to $1 6 million for the same period last year.

The increase was mainly due to an expense on the Phoenix trial and also the increase on the wage and salary due to our R&D team and expansion.

The G&A expenses again in Q2.

We had G&A expenses, $1 4 million compared to <unk> 9 million for the same period last year and the increase is due to increased professional service fee and also the wage and salaries.

The net loss.

With $6 8 million this quarter compared to $2 4 million last year.

Same quarter.

And about the key milestone one as Tom mentioned earlier, so we initiate the study in Q1 and we just got the first patient in.

This quarter and we also fully.

Complete enrollment of a Dragon study in Congress, Okay. So parks and we expect to have a 24 month data.

Q4, this year NSO.

You got to have the interim readout from the phase III Dragon studying starting a disease at mid next year.

With that I'll turn it back to Sara.

Thank you at this time, we will begin conducting our Q&A session.

For those analysts that are in the zoom with US. Please raise your hand to indicate you would like to ask the question and for those on the webcast. As a reminder, if you are in full screen mode, you may need to exit in order to.

See the Q&A portal.

So with that I'm going to open it up for questions from our first analyst weekend.

<unk> mine from Leerink partners, you May go ahead and any airline.

Hi, Good afternoon. This is <unk> on for Mike Goodman.

We have two question on the upcoming final readout by between two times type IPD.

First question is really why should we expect in terms of the efficacy at 24 months.

Most specifically I'm talking about the reduction of the DTF.

Leasing roughly.

Should we expect a similar level of reduction Indonesia roughly.

Level demonstrated at month, 18, which is a 50% reduction.

When you compare it to the match funded.

<unk>.

The second question.

It's about the comparison.

Due to the <unk>.

So at month 18.

12 patients cannot advance GBS seasons.

Versus nine of 20 patients.

Kenny.

What changes the proportion should be expect at months 24 months.

And the final question is about any updates you have about.

You can study can we still expect to have patience.

At that point then.

I would point at March 24.

I have a question for the phase III.

In our mind.

Sure Nathan.

You want to take this yes.

I'd be happy to Italian can go exactly exactly go here. So the first question related to what we expect to see at 24 months. If you follow these trajectories are particularly for the D. P F.

Basically you're going to see the same thing basically add another particular lines will continue to sort of track the same way. So we'll get at least a 50% reduction we already noticed a 24 month data look like.

In Prague Star, So it's going to go a little bit higher than where it is where it is now and of course, our DD effluent inflect upwards, a little bit as well, but this study is going to end in October so basically two and a half months from now I don't expect that there's going to be any significant change from these trajectories over the next two to three months. So I think.

What youre seeing here is a very good snapshot of what you can expect to see at 24 months and in terms of the numbers that numbers of subjects I don't expect we'll lose.

Any additional subjects again, we lost one out of 13, when we first started due to.

Last follow up at 12 months no one has slipped because of any safety or AE concerns. So don't have any real concern about that your other question was related to the conversion from auto fluorescent lesion to the atrophic retinal lesion and so I expect that probably by 18 months, which I'll start by FY 'twenty four months, we should see at lease.

Two more subjects convert again thats based upon the sort of run rate that we're going but there will be a significant percentage difference numerical difference in the percentage of subjects in Prague star that converted versus the number of subjects in the RSA. This converted our study will show a lower number which again is consistent with our hypothesis in our MAA that reducing.

Auto fluorescence will then slow the transitioning of the auto Fortunately isn't too the atrophic retinal lesion. So I think I addressed all three points puzzle, but please let me know if I missed anything. Thank you that was very helpful.

One question, we know about the phase III study about the inclusion criteria.

Hi, Neil and the inclusion criteria lithium side.

Within three areas could you provide more color on the rationale behind this inclusion criterion.

Yeah. So this goes to our approach for early into the intervention. So I've done number a number of studies in Starbucks disease in geographic atrophy. One thing are consistently seen and by the way all of the studies I've done in these diseases have been with oral therapeutics in either visual cycle modulators or RVP four antagonist to sort of mitigate the effect and so.

I've seen consistently in these studies is that lesions that are smaller at baseline tend to respond better to these types of therapeutic approaches and thats, even been shown in natural history studies, where you look at growth rate of lesions that are small versus large you do tend to see faster lesion growth rates and lesions that are smaller than they tend to sort of slowdown.

They get large and this term I'm using large and small of course is ambiguous, but when I say small lesions I'm talking about lesions that are less than for instance, five millimeter square and certainly nothing bigger than 10 millimeters versus anything bigger than 10 millimeter square is what I consider to large and in fact, that's where inflammation starts kicking in so it's important to know.

Sort of the chronology of the pathology early in disease course, theres very little inflammation. So when these early lesions.

And could you go to the lesion comparison, the QD F in DDA.

Yes sure. So so these are QTS lesions that youre seeing here are really the first lesions are actually going to convert right in and turn into.

The atrophic retinal lesion, but once the lease if you look at.

The left hand, right hand side right now once that atrophic lesion gets too large there is nothing you can do to slow it down. So the reason that we're specifying less than a three disc areas again based upon all the prior clinical studies that I've done and natural history studies in both G&A and startups that showed that smaller lesions respond better.

<unk> treatment and a sort of a real world evidence for that is data from the mix. You step study. This was a study conducted by Kubota pharmaceuticals, or maybe even talk about division, formerly Acura seller pharmaceuticals, as what it was and they were advancing a trial called the mixes that which is in RPE 65 inhibitor intended to do the same thing that we're doing which is reduce the threat.

And in fact, it worked very well in animal models, but it's a very aggressive approach because it hits us.

Zimmer the visual cycle, that's the rate limiting enzyme so anyway. They ran a phase III study with 194, Starbucks subjects and they didn't reach their end point at two years, but in a post hoc analysis. What they found was that patients who came in with smaller lesions at baseline and as much as a 40% slowing of lesion growth. So that's a very very important node for us, particularly in <unk>.

Startups disease, because that's exactly what we're doing is we're recruiting some subject with smaller lesions at baseline. We believe all of this clinical evidence and scientific evidence tells US we're doing the right thing for these for these kids. So again early intervention is the best way to stop these emerging retinal lesions that coupled eventually affect vision.

Great. Thank you that's very helpful. Yes.

Yes. Thank you.

Thank you for the question. The next question comes from Jennifer Kim at Cantor.

Hi, Thanks for taking my questions and congrats on the execution this quarter, maybe to start off with Dragon I believe the original announcement for enrollment completion highlighted 90 adolescent patients inherent says 100 subjects I was wondering maybe you could provide any color around that difference.

Yeah.

If I could just because.

I'm sure that was going to come up but it's important to note that when we when we stopped the enrollment at sites. There were a number of subjects in the screening Q. We can't just turn those subjects away. So basically we although we stopped accepting new patients the patients that were in the acute which amounted to roughly I think was about 20 patients in the queue went through screening and of those subjects approximately 10 quad.

Defied for study. So that's why we went from our target of 92, approximately 100 subjects to date.

Okay Wonderful and then a follow up for try again prior to the interim data next year.

Are you considering at all disclosing the baseline characteristics for these patients.

Pump.

Yeah. So.

It's right that we do want to.

But that data is a discussion with the PSM b and with FDA So right now.

So in discussing a bad thing this is a discussion when it comes closer to the date.

Okay, Great and then maybe.

Just as we're thinking about the October 24 month data.

Are you thinking of a venue for presentation.

Yes in fact.

We are looking forward to presenting this data at <unk> this year.

The 24 month data readout, which coincides with the <unk> conference.

Yes, I think thats in early November .

Okay, and then maybe one just in more of a broad question with safety, becoming even more of a focus given the concerns of a second I'm just wondering how does that play into your thinking around the opportunity for an oral once daily.

Yes, good question so.

We are talking about.

Quite elderly population in.

AMD with <unk>.

<unk>.

So I guess.

Again all.

<unk> treatment in a noninvasive treatments or.

<unk> is much more attractive and those that are.

So with safety and we're now keeping keeping.

The recent news of a palace.

I think in this elderly population I think.

Invasive intraocular injections are always going to be an issue for patients either.

Want to take the treatment and I would say.

Quite some majority of those elderly patients.

No.

With over one.

Hi.

You want to add more color to this.

No I think there's clearly a treatment burden for the patient with an injectable therapeutic.

And the fact is that theres not going to be a clinically meaningful benefit derived by the patient for at least two years, perhaps longer the same could be said with an oral therapeutic but theres less of a treatment treatment burden for the patient. So I think when offered the option between oral and injectable obviously the patient is going to choose the oral so it'll be a greater uptake for an oral therapeutic and with respect to.

Aes such as the <unk>.

<unk>.

Oscar Vasculitis.

Observe vasculitis as they call it in the eye.

This is even though our rare finding these are the risk factors associated with injections and there'll be others inflammation.

There's all types of things that can happen when you puncture and Idaho with the needle and you have to do it repeatedly every other month or every third months whatever it is this is a very aggressive invasive treatment therapy. So we believe once an oral therapeutic is approved I think patients will flock to it and that will certainly detract from the uptake of <unk>.

Sure.

Palaces drug or the Astellas Slashdot Barrick drug that just recent recently got approval. So we're not too concerned about the industrial predictable therapeutics I do want to emphasize as I said before those therapeutics address late stage disease, because actually what theyre doing is theyre, calling an inflammatory response, that's driving the disease process early in the disease course, Theres no inflammation.

Asian, either in <unk> or <unk> you just have these incipient bio molecules are factors that are causing sort of retinal pathology, but theres no inflammation yet.

Insulation really kicks in later so those therapeutics was injectables would not be effective in our patient population. Conversely, our therapeutic would be expected to be beneficial in that later stage sort of as a maintenance therapy for patients who are sort of getting treatment and they need to sort of keep the geographic atrophy that base. So we think that theres synergy rather than competition and we're certainly not concerned about any safety.

That they have because we don't think they're going to affect what we have in terms of an oral therapy, which to date has shown to be very safe and well tolerated in these adolescence startups subjects.

Got it that's helpful. Thanks, guys.

Yeah, I think server.

Thank you for the questions and.

The next question comes from <unk>, Chen H C Wainwright.

Thank you for taking my questions, you're just talking about the PAA is associated with <unk>. So just to clarify you believe that.

The retinal vasculitis is associated with injection, but not the drug itself.

In terms of the mechanism of action are a complement inhibitors.

It could be a combination of both U I was just saying that in other studies for instance, when they first started developing the first anti VEGF drugs and they had I believe at that time. It was maxygen. They had things like this as well and it wasn't necessarily attributed to the drug it was attributed to the procedure, but yes. It is possible that the drug itself could cause that but.

I think that's a rare.

Possibility because it didn't occur I don't think in their phase three studies. So again once you start getting real world evidence for how this drug is going to be applied youll start on <unk>. Some of these are potential risks.

These are not manageable risks. These are very serious concerns where patients are losing vision, even though it's a small number of patients. So yes, it could be BT by the drugs, but I believe a more about the actual intervention itself. That's just my personal belief.

So I.

I believe the one.

The causes of retinal vasculitis is infection and inflammation and visualization so all of that.

Can be associated with <unk> injections.

That causes that.

So it is reasonable to expect newly approved I certainly may have those as.

As well when its commercial lines right.

Very thoughtful.

I predict yes, yes.

Okay. Thank you.

Okay. Thank you for the question. The next question comes from Bruce Jackson of benchmark.

Hi, Thank you for taking my questions.

The increase in the study size for the Dragon trial. Originally you put it up to 90 patients in order to improve the probability of getting an efficacy signal now that you're at 100.

Has that increased your confidence that we're going to get an efficacy signal on the results.

Hey, guys.

Yes, yes, so it's not really about we always believed that we would be getting an efficacy signal since the six month data right. So and the start of our open label Phase II study, we have seen positive data at every six month interim analysis now out to 18 months. So it's not so much about changing the treatment effect size, it's about increasing the power that is.

The confidence in probability that that effect will be durable through two years. So yes that additional 10 subjects does give us an additional buffer for that power. It doesn't necessarily mean, we're going to get greater treatment effect or greater statistical significance at the end of study, but we will have greater power to say that that is a true bonafide robust.

Because again, there's more patients showing that treatment effect. So it's more about the power than it is rather the treatment effect size.

Okay. That's helpful solid gross add on that so we run the simulation and all of that so the sample size onto the study and now given that.

We've gone up to 100, and I think that gives us a better chance of getting a positive.

<unk>.

Statistical significance at insurance, so that gives us a better chance of reaching that.

Okay great.

And then.

One finance question I thought I'd throw O&M.

In terms of your cash balance and your burn rate, how many quarters of cash do you have right now.

Yes.

So we do expect that we have cash around to enter 2025 with the current rates.

Alright, perfect. Thank you very much thank.

Thank you.

Okay. This concludes that variable portion in the Q&A session.

Do we have any questions.

The webcast or should we hand, it back to Tom for concluding remarks.

No I don't that any questions here again coming back to Tom. Thank you.

Okay.

Well thanks, everyone for joining this call and we look forward to updating you on our end of phase II results shortly.

You very much.

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