Belite Bio, Inc (BLTE) Q2 2024 Earnings Name Transcript

Belite Bio, Inc (NASDAQ:BLTE) Q2 2024 Earnings Conference Call August 12, 2024 4:30 PM ET

Company Participants

Tom Lin – Chairman and Chief Executive Officer
Nathan Mata – Chief Scientific Officer
Hao-Yuan Chuang – Chief Financial Officer

Conference Call Participants

Basma Radwan – Leerink Partners
Jennifer Kim – Cantor
Yi Chen – H.C. Wainwright
Bruce Jackson – Benchmark

Operator

Hello, and thank you for joining us to discuss Belite Bio’s Second Quarter 2024 Financial Results. Joining the call today are Dr. Tom Lin, Chairman and CEO of Belite Bio; Dr. Nathan Mata, Chief Scientific Officer; and Hao-Yuan Chuang, Chief Financial Officer.

Before we begin, let me point out that we will be making forward-looking statements that are based on our current expectations and beliefs. These statements are subject to certain risks and uncertainties, and actual results may differ materially. We encourage you to consult the risk factors discussed in our SEC filings for additional detail. Please note that you can submit questions throughout the call by clicking on the Q&A box at the bottom of your screen, and we will respond to questions following our prepared remarks.

Now I’ll turn the call over to Dr. Lin.

Tom Lin

Thanks, Julie. Thank you, everyone, for joining our second quarter 2024 earnings call. We had another strong quarter advancing our Tinlarebant trials, and I’m pleased with our progress in the year-to-date.

Let me start off with our accomplishments during the second quarter by the overview of our programs. We had a productive quarter marked by several advancements in our programs. We have initiated the Phase Ib and Phase 2/3 trial of Tinlarebant in adolescent stargardt patients, also known as a DRAGON II study. And we have already completed enrollment for Phase Ib portion with 6 subjects in Japan.

We’ve also received Sakigake designation in Japan, which means Pioneer Drug Designation in English. Such designation has only been granted to 27 drugs in its initiation in 2015, and Tinlarebant is the first ophthalmic drug to receive Sakigake designation, which is a testament to the groundbreaking potential of this drug and the unmet need it tends to address the people living with stargardt disease.

We’ve made progress in our pivotal global Phase 3 trial of Tinlarebant in geographic atrophy subject as well, now as the Phoenix study and have already enrolled nearly 200 subjects to upfront — until now.

In addition, we’ve also raised $25 million from the registered direct offering in April here for strengthening our balance sheet. The Phase III DRAGON I study is fully enrolled with estimated interim readouts by Q4 2024 or early 2025 at the latest. As we enter the second half of the year, we are well positioned to execute on key milestones, and we look forward to sharing interim analysis from – initial interim analysis from our pivotal Phase III DRAGON study in the fourth quarter.

Next slide, please. Okay. So for those of you, they were new to the story, that’s the story. Tinlarebant is a novel once a day oral tablet designed to bind to serum retinol binding protein 4 as a means to specifically and reduce retinol delivery to the eye. This approach is intended to slow or stop the formation of toxic retinol-derived by-products which are generated in the visual cycle and are implicated in progression of stargardt disease and geographic atrophy. We believe that early intervention directed at emerging retinal pathology, which is not mediated by inflammation, is the best approach to potentially slow the disease progression in stargardt disease and also in geographic atrophy.

Importantly, there is still a significant unmet need for both indications as currently, there is no approved treatment for stargardt disease and no approved oral treatments for geographic atrophy, and we are already in global Phase III trials for both indications.

To give you an indication of the importance and potential for our oral therapy. So far, we have been granted fast track designation, rare pediatric disease designation and orphan drug designation in the U.S., EU and Japan and Pioneer Drug designation in Japan, as I just mentioned.

Finally, we have strong a patent (ph) protection for about 14 patent families, and most of these are composition of matter patents. And the latest composition of matter patents is expected to last until 2040 with additional patent term extension potential with new patents to be filed, we will have patent protection past to 2040. All of this highlights the potential of Tinlarebant to treat people who are living with this debilitating needs and capitalize on the large market opportunities. We are very excited with the path ahead and our team is focused on our mission to leverage Tinlarebant to address the unmet needs of patients suffering from blindness.

I would like to pass this down to Nathan, our CSO, and to give you a clinical and scientific update. Nathan?

Nathan Mata

Yes. Thank you very much, Tom. So what I’d like to share with you is the data from our 2-year open-label Phase II study in adolescent Stargardt subjects. This study was, as I mentioned, a 2-year study, 13- enrolled subjects from Taiwan and Australia. What a lot of people don’t understand about Stargardt disease is there are over 1,500 known mutations that are associated with the disease. Not all of them are known to be pathogenic. In fact, many are mild to benign. So one of the analyses we did initially was to determine the genetic composition in our cohort.

And we actually gave the genetic data to one of the premier preeminent genetics in Stargardt’s disease in the world, Dr. Rando Allikmets at Columbia University. He evaluated our genetic data and determined that 11 of 13 subjects in our cohort had severe biallelic mutations, which we predict pathogenicity. And in those two, where there was a moderate allele (ph) in these 2 subjects, in vitro testing actually showed that these were pathogenic alleles. So our entire cohort really has severe pathogenic mutations that were predicted to progress very rapidly through the disease course.

An independent assessment of the genetic severity is provided by something called the CAD score. That sounds for combined annotation dependent depletion score. It tells you the degree of severity of a particular genetic variant or genetic mutation. Scores above 20 are predicted to be among the 1% most deleterious. And every single one of our subjects with the section of 3 and 5 had these CAD scores above 20. So we have two independent confirmations on the severity of the genotypes of these kids.

And despite the severity of these genotypes, we had five subjects, which represents 42% of the cohort that never developed atrophic lesions. So I should have mentioned that in this study, these adolescent subjects came in with an early form of disease, where they only have a type of lesion, which is autofluorescent. This is known as a questionably decreased autofluorescent lesion. Over time, these autofluorescent lesions convert to atrophic lesions and that’s one of the parameters we’re looking at. And we see here in 42% of subjects, that conversion never occurred.

Another interesting outcome from the genetic data was we found two pairs of siblings that had the exact same identical mutations. This is important because there are companies — competing companies of ours that are using as a premise for their therapeutic approach that identical mutations predict an identical disease course. So this gives us an opportunity to evaluate that premise and determine whether or not there’s any validity to it.

Because this is an open label study, one of the metrics we want to look at to see if we’re having an effect to improve patients, that essentially well-being is visual acuity. So we looked at visual acuity in subjects prior to enrollment. And we look specifically for subjects who are losing letters in both eyes, that’s called bilateral BCVA loss. And we found a subgroup of six subjects within our larger cohort that was losing a mean of 10 letters per year prior to enrollment.

The natural history in our study, basically over 2 years predicts that there would be clinically significant vision loss in these subjects during the duration of the study. So we want to keep an eye on that to see how these subjects fare.

Another important thing about these data, these sort of pre-enrollment data is the fact that they’re losing vision, all these kids are losing vision and some of them significantly, and they don’t have atrophic lesions suggests that non-atrophic lesions, these QDF lesions can actually compromise visual acuity. That’s very important because all of these kids have foveal-involved lesions, which means they are compromised, their vision will be compromised over time.

But the current thinking in the scientific and clinical community is that you have to have atrophic lesions before there starts being some effect on actual visual function, and that seems not to be the case.

And finally, regarding the sibling comparisons, we did find that sibling subjects with identical mutations do, in fact, have different levels of BCVA loss, and this data can be found in the appendix of this presentation.

If we look at the overview of visual acuity in all subjects that’s shown on the left-hand side, over the 2-year study, we see a mean loss of about 2.5 letters per year. That is significant because that essentially shows stabilization. This vision is not really changing in all subjects. But significantly, if we look at those subjects with prior vision loss, that is those subjects that were losing 10 letters per year before coming into the study that’s shown on the right-hand side, now they’re only losing about 1.9 letters per year. So we’ve significantly altered the visual acuity progression in these kids, and we’ve stabilized it. That’s very significant. And really, the only reason you could do that is if you’re having some effect on lesion growth. So I want to go to that right now.

As I mentioned, 5 of 12 subjects never grew in atrophic lesion, but I want to show you sort of anatomically what that looks like. The images you see here on the upper right-hand side are representations of what basically all these subjects look like. This is subject 10 at baseline. But all these projects have these types of autofluorescent lesions that are encroaching the fovea. They’re just of different sizes. And we’re measuring over time how this autoforestent lesion converts to an atrophic lesion. And as I said before, there are 7 out of the 12 that actually grew these atrophic lesions.

And what we found was something very interesting. In every case, except one, the increase of the atrophic area was matched by a decrease in the autofluorescent area in every single subject. So wherever you see an orange bar, that’s an increase of atrophy and where you see a blue bar, that’s a decrease of the autofluorescent lesion size.

The reason that’s significant is because the boundary, the perimeter of the lesion is not actually growing, only the atrophic lesion is growing within the autofluorescence. So it suggests that this lesion could potentially burn itself out over time because there’s no place else for the lesion to grow.

So sort of what these data are telling us is that there are cells that are predestined to die perhaps we cannot save them with our treatment, but we’re certainly preserving the margin of cells on the outside that would lead to further lesion growth. They’re not growing anymore. So this is a pretty important finding. There was only one subject where we found a lesion that was outside of initially area of QDAF lesion, so just this one subject.

And finally, getting back to the genetic mutations, it was subjects 9 and 10 and subject 12 and 13 that had the identical mutations. But if you look at 9 and 10, yes, they have both, lesion goes (ph) somewhat, somewhat different in subject 10 versus 9. But then if you look at 12 and 13, there’s absolutely no lesion growth. Yet all these kids have essentially the same — they have the identical genotypes and very similar disease duration. So these data, again, suggest on a lesion growth metric, identical mutations do not predict an identical disease course.

We have one other very important piece of information to pass along, and that is an assessment of how these lesions are actually graded. So currently, we’re using the routine methodology that everyone is using. It’s basically a autofluorescent camera that takes a picture of the lesion. And then a reader, a physical reader goes in and draws the boundary around the perimeter of that lesion so that the computer can then tell you the area.

So two readers have to grade every single image because there has to be an agreement in terms of the lesion size before it can move on into basically being validated. And if those two readers don’t agree with a certain variance, a third reader has to come in and sort of be a tiebreaker.

So this particular method is subjective to enter an intra-reader bias. It doesn’t look at any one specific area and the red is looking all over, and it’s very time consuming. So in order to address the shortcomings in this currently used methodology, our reading center has developed a new AI-based method for assessing the size of these lesions. This is a mathematical classification of lesions that uses basically the gray level density in area of healthy tissue, let’s say, out here to the area of disease tissue, which would be sort of represented by the density of the optic nerve disc.

So it’s doing a scan of the gradation in gray levels, and it’s just looking at the macula for different areas of gray that would predict either autofluorescence or atrophic lesions. In this case, we’re looking at atrophic lesions. So this is important because it removes the reader and the potential subjective bias out of the equation.

When our reading center used that methodology to rescan our images at baseline, they found 12 eyes of 8 subjects that had atrophic lesions within the macula at baseline. And this is something the traditional methodology did not pick up.

So we asked our reading center to go back and reread all these images to see what’s happening with macular lesion growth in these subjects that it was identified in. This is the data that they developed.

On the left hand side shows you the growth of the lesions into the macular area over time. It’s pretty linear until about month 16, at which time it completely stops and there’s no further lesion encroachment into the macula during the subsequent 18 months.

On the left hand side is shown basically the same exact data, except here we’re looking at the percent change of lesion into the macula over time, where 100% would mean the entire six millimeter zone of the macula is occupied with lesion. And you can see in our subjects, they never get to more than about single digit involvement into the macula.

So this is significant and it renders our visual acuity data sensible, because now we understand why we’re getting a stabilization of vision, because we’re halting lesion growth into the macula. Again, a very significant observation.

Finally, the safety data. This is the two year safety data. I want to start by saying that over this two years of observation, there hasn’t been one drug related systemic AE (ph) whatsoever in these kids. And this is a testament to the specificity of this drug, the way it was designed by the scientists at Columbia University.

Basically, this drug targets just the residues that are in the binding pocket of retinal binding protein 4. And these residues exist nowhere else in biology in terms of their three dimensional orientation. So this drug was supposed to be very specific. And the AE data systemically tell us that basically it is very clean.

What we’re seeing in terms of jugulated AE’s are anticipated ocular events that we want to see because they’re telling us we’re having the intended biological effect in the retina. And the other important thing about these AE’s is they’re completely manageable by accommodating to differences in light, because these AE’s are driven by light.

The first is a form of xanthopsia or chromatopsia, called xantopsia. This is mediated by a cone photoreceptor in your eye, which confers bright light and color vision. So when patients transition suddenly from a dark light to a bright environment, these cone photoreceptors wake up. They want vitamin A immediately. But under our treatment regimen, we’re only supplying it, supplying it sort of slowly. So there’ll be a period of time in which these cone photoreceptors don’t have maximal amount of vitamin A. They will electrically misfire and produce transient hues of color in the visual field. In this case, yellow, that xanthopsia. But all the kids are reporting it as mild. And of course, no one’s left study because of this AE.

Finally, the other one is delayed dark adaptation. This is the opposite manifestation. So this is mediated when you transition from a bright environment to a very darkened environment. There’ll be a delay in the ability to accommodate to dim light.

This particular AE is actually a manifestation of the disease process. So patients with Stargardt’s disease already have delayed dark adaptation, so they’re used to accommodating it. And that’s probably why most of them are reporting this pharmacological immediate DD (ph) as mild or transient. And again, no one’s left study because of this. And importantly, as I said, these AE’s can be mitigated by moderating transitions from bright to dark and vice versa. And this has been very, very helpful for our kids. I can say that in over one year of dosing, in our Phase 3 study, the dropout rate from these AE’s is less than 4%. So that is significant.

Night vision impairment is a more severe manifestation of the delayed doc adaptation, which the delay is 20 minutes or more. The increasing error score on the FM 100 is a more severe exacerbation of the chromatopsia. You see that in one subject. And the intermittent headaches we think can occur when subjects strain to use their visual acuity while they are experiencing these AE’s.

So with that now I’ll move over to the overview of the trials that Tom discussed. The DRAGON I and DRAGON II Stargardt trials. We’re showing you here the overview of those studies. These studies are essentially identical. There’s differences in the geography. As Tom mentioned, we have Japan involved vis-à-vis the Sakigake designation.

Essentially, the demographics are similar, except for that both studies are done double blind. There is a difference in the randomization. We’re doing a 2:1randomization in the DRAGON study and a 1:1 randomization in the DRAGON II. Again, principally because the DRAGON II study has fewer patients.

But other than that, every other assessment, safety, efficacy, et cetera, is the same, as is the key inclusion criteria for these subjects. So because of the similarity in these two studies and how they match the Phase 2 study, and because the Phase 2 study is trending quite well, we believe, or we have optimism that we’ll have very promising safety and efficacy data in both DRAGON I and DRAGON II studies.

Moving forward to geographic atrophy, to show you the trial design in GA, it as well is very, very similar to the Stargardt disease Phase 3 trials. The only difference in the trial design in GA is the indication, of course, geographic atrophy and the higher number of subjects to reflect the higher prevalence of the disease in the population. Otherwise, these studies are essentially identical.

So again, we expect, because the GA studies are lagging behind the Stargardt studies, whatever we see in Stargardt, it could be highly predictive of what we see in GA. And a principle reason for that is that we’re using the same dose and there’s a very high pathological similarity between Stargardt’s disease and geographic atrophy in the particular patients we’ve enrolled.

So with that, I’ll turn it back over to Hao-Yuan or turn it over to Hao-Yuan for the financial results.

Hao-Yuan Chuang

Thank you, Nathan. So in Q2 2024, we had R&D expenses of $9.1 million compared to $5.5 million for the same period in 2023. The increase was primarily due to increase in expenses related to the milestone payment to Colombia for the completion of the Phase II study and share-based compensation.

On G&A expenses, in Q2 2024, G&A expenses were $1.4 million, basically the same as Q2 2023. On net loss, we had a net loss of $9.5 million in Q2 2024 compared to $6.8 million for the same period in 2023.

Regarding cash, we have cash deposit in U.S. treasury bills of total $112 million. We still expect around 3 years of cash runway. Thank you. Back to you, Tom.

Tom Lin

Thanks, Hao-Yuan. To summarize, we had a strong start to the first half of the year and continue to make meaningful strides in advancing Tinlarebant clinical trials for Stargardt disease and geographic atrophy across several countries.

We’re also proud that we have received Sakigake designation in Japan, which we believe is a testament to the groundbreaking potential of this drug and the unmet – unmet need as there is no currently – no treatment for Stargardt disease. We’re also in a strong financial position with $110 million in cash and cash equivalents.

As we enter in the second half of the year, we are well positioned to execute on key milestones and look forward to conducting period of Phase 3 interim analysis from our DRAGON study in the fourth quarter.

Finally, we look forward to seeing some of you next week at the H.C. Wainwright 4th Annual Ophthalmology Conference and hope you join our presentation on August 15. Please also note that in September, we will also be attending conferences with H.C. Wainwright, Cantor, Deutsche Bank and hope to see some of you there. Thanks again for joining this call, and now we open the call for questions.

Question-and-Answer Session

Operator

Our first question comes from Marc Goodman with Leerink Partners. Marc, your line is now open.

Basma Radwan

Hi, good afternoon. This is Basma on for Marc. Our question is on DRAGON II. Could you provide color about this trial and what’s the goal of this trial exactly does? Statistical significance needs to be achieved with this trial yes or no? And do you think the powering is enough?

And do you also need to run another safety, long-term safety trial in these global sites as well for the submission OUS or only the DRAGON II will be enough and safety database in the US will be sufficient? Thank you. That’s it.

Tom Lin

Nathan, do you want to take this?

Nathan Mata

Yes, I’m happy to take that, Basma. So thank you for the question. Regarding statistical significance, yes, of course, we’ll have to — we’re powering for statistical significance at the 2-year time point, that will have to be achieved in order to essentially meet that requirement for showing efficacy.

Conditional power will not be a problem because in this particular study, we’re actually randomizing 1:1 versus 2:1 in our original DRAGON study. So in the original DRAGON study drag in the study, there’s roughly about 35 placebo subjects and the remainder of the 104 are the Tinlarebant-treated subjects, whereas in the DRAGON II study, there’s an equal distribution in the randomization. So that helps the conditional power.

And no, I don’t believe we’ll have to do — I believe that you asked about an open-label extension study to evaluate safety based upon what the PDMA has told us in Japan is that they would only require the 2-year safety data from the required Japanese subjects that will be enrolled in Dragon II, which is a minimum of 9 Japanese subjects, which is exactly what we’re complying with. So I hope that addresses all the questions, Basma?

Basma Radwan

Yes. Thank you. Very helpful.

Nathan Mata

Sure.

Operator

Our next question comes from Jennifer Kim with Cantor. Jennifer, in is now open.

Tom Lin

Jennifer, I think, you are mute.

Jennifer Kim

Oh, hi. Can you hear me now?

Tom Lin

Yes.

Jennifer Kim

Okay. Great. Thanks for taking my questions. Maybe to start off with DRAGON 1. With the interim analysis later this year, can you just remind us what you’re thinking of in terms of the format of that update and what level of update we – of detail we should expect?

And then my second question is maybe following up on the last question on Dragon II. You’ve completed the Phase Ib portion. Any thoughts on when we could see initial data from this trial? Is it going to be the 2-year data? Or can we see an interim update? Thanks.

Tom Lin

Thanks, Jen. So the FDA guidance that we are not allowed to review any data. In fact, I mean, only the DSMB would have that knowledge, simply because the study — the treatment is ongoing and we don’t want to bias the data in any sorts. And the same question, Nathan, do you want to take it?

Nathan Mata

Regarding Dragon II?

Tom Lin

Yes.

Nathan Mata

Yes. Sorry, Jennifer, what was the portion on Dragon II?

Tom Lin

The interim data as well…

Nathan Mata

Yes. So the Phase Ib — so they’re sort of tied together, right? This is a PK/PD study originally just designed to make sure that the 5 milligram dose that we’re using in all of our other trials achieves the same pharmacokinetic and pharmacodynamic response in Japanese subjects, which we have every confidence that it will. We won’t be disclosing that data until we get to the end of the efficacy portion of the Phase II/III portion of the study, which, of course, is 2 years later. So we’ll allow all that data to be disseminated once we have all of the top line 2-year data, which would, of course, include the PK/PD which basically dose efficacy or dose finding study.

Jennifer Kim

Thanks. That’s helpful. If I could squeeze in one more question. Just on PHOENIX, could you confirm the timing of enrollment completion for PHOENIX? And what kind of 1-year interim look should we expect for that trial? Thank you.

Nathan Mata

Yes. So we’re targeting an enrollment size of 429 subjects. We’re about at the 200 mark right now. So roughly about halfway in. Based upon our run rate, we expect to close that enrollment by the end of Q1 of 2025. In terms of data coming out of that study, you said the interim data, we haven’t really decided what we’ll be doing in terms of the interim analysis. In fact, we haven’t quite developed or lease completely fleshed out the SAP, the statistical analysis plan for that study. So sort of put a tack on that one, you can get back to us later when we have a little bit more information for you.

Operator

Our third question comes from H.C. Wainwright, Yi Chen. Your line is now open

Yi Chen

Thank you for taking my questions. My first question is just to confirm that both data from DRAGON I and DRAGON II trial are needed to submit to PMDA under the Sakigake designation correct?

Tom Lin

Yes. That’s correct.

Yi Chen

And the same data set will be submitted to the US and European regulatory agencies as well. But under the Sakigake designation, do you think there’s a chance that Japan could approve the drug faster or first before FDA and EMA?

Tom Lin

Good question. So based on the information, Japan will want to be the first country to approve this drug. So a lot of discussion still needs to — we still need to discuss with the PMDA regarding when they want to see the data. So once the study for the DRAGON, we will still need to communicate with the PMDA regarding when would they want to see the DRAGON II database.

Nathan Mata

Well, Yi Chen, I want to clarify that. So the Japan FDA does not require us to complete the entire DRAGON II for Japan (ph) submission. I think the requirement is that we complete DRAGON I, and we complete those 9 patients from Japan in the DRAGON II, then we can submit. We don’t need to wait for the other U.S. and U.K. patients to complete their DRAGON II because the key point for them is that they just want to see how Japanese subjects are doing in this study. So they think DRAGON I is enough, and we just need to — and we decided to be able to carve out those Japanese data for submission for Japan.

Yi Chen

Thank you very much for clarification. And my follow-up question is regarding ABCA4 mutation, is that something being measured in the DRAGON I and DRAGON II trials? And how shall we interpret the Phase II observation regarding the mutation, those 5 patients into our potential projection of the DRAGON I and DRAGON 2 readout?

Tom Lin

Nathan?

Nathan Mata

I’ll take that. So of course, we do genetic analysis, genotyping on all subjects. They are required to have both a clinical and molecular confirmation of Stargardt disease. So that will be done regardless of which study we’re looking at, we’ll do that in all of our Stargardt trials.

In terms of the — sorry, sorry, Yi Chen, I lost track of the other part of your question.

Yi Chen

I mean the results you observed from the 5 subjects in the Phase II trial, how should we translate that into interpreting the Phase 3 data?

Nathan Mata

That’s really difficult because I think I mentioned before, there’s over 1500 known mutations in Stargardt’s disease. It’s very difficult to sort of gene match everyone to sort of evaluate, so for instance, in those 5 subjects that never evolved an instant atrophic lesion, they had severe genotypes. But there are other severe genotypes would probably behave similarly, but they would be different, right? Still severe, but none of the same genetic locus.

So it’s very difficult to sort of take those — the genotypes from those 5 subjects that didn’t basically span any disease and sort of infer what would happen in the larger patient population has different genetic mutations, because again, there’s such a varied genotype among these patients. You can see in our cohort just randomly our 13 subjects. They all had severe pathogenic mutation.

So our thinking is that if they have a genotype that has a mutation and they have the pathology, this is going to be a severe disease, very quickly progressing disease. And so we’re actually having that validation at screening. So we’ll know with some measure of confidence whether or not our patients have pathological gene mutations or not. So we’re not necessarily trying to match what we saw in those 5 subjects with what is happening in the other DRAGON studies. But it is important to note just generally speaking, those pathologic mutations that lead to disease have been sort of neutralized with our treatment. So we hope to see that, again, of course, with other severe genotypes. That’s our hope.

Yi Chen

Thank you.

Operator

Our next question comes from Bruce Jackson with Benchmark. Bruce, your line is now open.

Bruce Jackson

Hi. Can you hear me okay?

Tom Lin

Yes.

Bruce Jackson

Okay. Super. With the presentation of the interim analysis for DRAGON, is that going to coincide with the medical meeting?

Tom Lin

I don’t believe medical meeting, do you refer our AAO?

Bruce Jackson

Possibly AAO, yes.

Tom Lin

Yes. No, no, it’s not. So the interim analysis will be somewhere around, I think, end of the year. And — but that’s tricky time during Christmas, so we have to get the DSMB, the timing and them when they can review the data. So it may just run out into January 2025, but we are expecting end of the year to come back then interim analysis. And again, per FDA guidance, we are not allowed to review any data to the public, not to bias with data while the trip (ph) is going.

Bruce Jackson

Okay. Great. And then with the R&D expense, you had the milestone payment this quarter. Can you just remind me what the base rate of R&D is for the next couple of quarters? And how the milestone timing for the remainder of the year and 2025 might play out?

Hao-Yuan Chuang

So basically, well, this quarter, we have a higher expense because of that milestone payment. For the rest, I would expect to be probably the same between probably $7 million to $8 million a quarter. So for the entire 2024 is probably will be still around 30 to 35. Next year, 2025, it may be slightly higher, given that we expect some milestones to be achieved from the PHOENIX study. So I would say probably next year, it will be around 35 to 40. So I think for this year, next year until 2026, these three years will be pretty similar in terms of expense, around that 35 each expenses per year given we’re running the PHOENIX study for these three years.

Bruce Jackson

Okay, great. And congratulations on all the progress. Thank you.

Tom Lin

Thank you so much, Bruce.

Operator

Please let me know if there are any additional questions.

Tom Lin

No, I don’t have any on the written question here.

Operator

Great. This concludes our Q&A portion of the call. I will now turn it back to Tom Lin for closing remarks.

Tom Lin

Thanks. So thank you, everyone, for attending our earnings call for this quarter. We will certainly update the — once we have conferences at AAO, we’ll be presenting at AAO. And again, we will update all the events that’s coming up for the upcoming – as time comes. Thank you, everyone, and we’ll keep you updated.

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