Hello, and thank you for joining us to discuss Belite Bio's Q3 2024 Financial Results. Joining the call today are Dr. Tom Lin, Chairman and CEO of Belite Bio, Dr. Hendrik Scholl, Chief Medical Officer, 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 vary 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. We'll respond to your questions following our prepared remarks. Now I'll turn the call over to Dr. Lin. Thank you for joining our Q3 conference call. Before diving into the details of this quarter's performance and status of our pipeline, I would like to introduce an exciting addition to our leadership team. It is my pleasure to welcome Dr. Hendrik Scholl, our new Chief Medical Officer, to the call. Professor Scholl is the world's foremost expert in Stargardt disease and age-related macular degeneration. He has pioneered some of the most significant ophthalmology and retinal disease advancements of our time, including the world's largest ever natural history study of Stargardt disease. We are thrilled to have him lead our clinical program at such a pivotal time of Belite, and I'm certain his expertise and dedication will be instrumental in advancing our efforts to bring much-needed treatments to patients living with Stargardt disease and dry AMD. Dr. Scholl, welcome. Thank you, Tom. I'm honored to be joining Belite Bio at a time when the company's clinical programs are showing such promise. Having served as the Chair of the Data and Safety Monitoring Board for Belite's phase II and phase III Stargardt disease trials, I feel immensely confident in Tinlarebant's potential. I have dedicated my career by improving the lives of people suffering from serious retinal, and specifically macular diseases, which are almost always debilitating and have a profound negative impact on people's quality of life. I'm deeply impressed by Belite Bio's pioneering approach to Stargardt disease and late dry AMD, which have historically lacked effective treatment options. Having seen firsthand the toll these diseases can have, I look forward to working with our talented team to drive our clinical programs forward and hopefully bring transformative therapies to patients in need. Thanks, Hendrik. Now moving on to our Q1 update, we continue to make strong progress towards advancing Tinlarebant in patients living with Stargardt disease and geographic atrophy. For those who are new to our story, Tinlarebant was developed from our retinal binding protein intellectual property portfolio. Tinlarebant is a novel oral therapy intended to reduce the accumulation of toxic vitamin A byproducts in the retina, an approach that is intended to slow or stop the formation of toxic retinal-derived byproducts, which are generated in the visual cycle and implicated in the 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 slowing the progression of these diseases. And to give you some perspective on the importance of this potential therapy, Tinlarebant has been granted Rare Pediatric Disease and Fast Track designation in the US and Sakigake designation, which translates to Pioneer Drug designation in Japan. Tinlarebant has also been granted Orphan Drug designation in the US, EU, and Japan. We believe this speaks to the significant unmet need for both indications, as currently there is no approved treatment for Stargardt disease and no approved oral treatment for geographic atrophy. And we are uniquely positioned, as we are already in global phase III trials for both indications. So with that, allow me to provide a high-level overview of the progress we have made in Q3. We have two studies underway with Tinlarebant in people living with Stargardt disease. These are phase III DRAGON trial and the phase 2/3 DRAGON II trial. The DRAGON II trial is fully enrolled with 104 patients with an estimated interim analysis by end of 2024 or early 2025. The DRAGON trial is expected to enroll 60 subjects across the U.S., U.K., and Japan. For GA, we have the phase III PHOENIX trial, which is expected to enroll 429 subjects. So in summary, for this quarter, the DRAGON II trial continues to progress rapidly. We have successfully dosed the first patient in the phase 2/3 portion and have completed the phase 1b study in Japanese subjects at the Tokyo Medical Center. Enrollment is now also underway at sites in the U.S. and U.K. In GA, we also continue to progress in our pivotal global phase III PHOENIX trial, which has already enrolled more than 280 subjects to date. That concludes my part of the update, and we'll now turn over the presentation to Hendrik. Hendrik, please. Thank you, Tom. So I'll be happy to go over aspects of the phase II trial. And the first is actually looking into lesion growth of patients with Stargardt disease. And the data that was obtained in the phase II study with Tinlarebant can be compared with natural history data that was collected in the ProgStar study. And as Dr. Lin mentioned earlier, I led a multicenter worldwide natural history study called ProgStar, where patients have been investigated over two years every six months. And they entered the study already with lesions that were defined as so-called decreased autofluorescence, definitely decreased autofluorescence, DDAF. And these lesion growth was measured over time and was put together as a growth curve that you can see in that slide as the blue curve. So there's inevitable loss of tissue that is measured as the growth of DDAF lesions over time. In the study, the subjects that developed such lesions, and it was only a minority of five of 12 subjects in the study, the lesion growth of these subjects was significantly smaller than when compared with a subset out of the ProgStar study, namely 51 patients that were age-matched, that matched the age of the patients in the phase II study. And when you look at the growth rates of the red curve, it's significantly lower than that of the blue curve. And that means that lesion growth could be slowed under the treatment with Tinlarebant. And this treatment effect was significant because the lesion growth rate could essentially be halved from one square millimeter per year to only half a square millimeter per year. And this difference was highly statistically significant. And from a clinical point of view, it's also highly clinically significant. Next slide, please. There is inevitable loss of visual acuity, and clinically, we measure visual acuity on visual acuity charts, and the so-called ETDRS visual acuity chart has 100 letters. Patients that have macular diseases, such as Stargardt disease, are affected in their central visual acuity and would and will lose vision over time. So they lose letters that they can discriminate on a visual acuity chart. In Stargardt disease, when patients develop lesions that affect the macula, they inevitably lose vision over time and eventually lose many letters. A significant vision loss defined by the FDA would be three lines of vision loss that corresponds to 15 letters. Patients can, over time, lose much more because typically they are eventually at a letter loss of, let's say, 40 or 50 letters over a couple of years. So in the phase II study, it was shown that under the treatment, it was an open-label study. Visual acuity loss could be stabilized in subjects that were treated with Tinlarebant. And this is shown for all subjects on the left slide. We can see that there was some loss, but the loss was about five letters in two years that corresponds to an average letter loss of only two and a half letters per year. It was a specific observation in the phase II trial of in patients that before entering the trial had significant loss of visual acuity, about 10 letters a year, which is very significant. And those patients also underwent treatment with Tinlarebant. And their visual acuity could also be stabilized. And this is shown on the right slide. And they now, under treatment, only lost about three letters per year. We can conclude that their visual acuity loss was also stabilized under the treatment with Tinlarebant. The next slide, please. This slide shows the safety results of the 24-month phase II clinical trial. It shows that Tinlarebant, with a daily dose of five milligrams, continues to be safe and well tolerated in these adolescent Stargardt patients. The treatment produced a mean of an 80% reduction of retinal binding protein four from baseline throughout the study. Some of the adverse events, namely delayed dark adaptation and xanthopsia, which is a form of chromatopsia, are the most common drug-related ophthalmic adverse events and are anticipated events because they relate to the mechanism of action of Tinlarebant, namely reducing the amount of retinal entering photoreceptors. That can, and in some instances, lead to yellowish appearance of a scene, typically going from dark to light. This typically would be experienced by patients in the morning when they wake up and then enter a well-lit room, and that leads to this appearance of yellowish color that is transient and would typically not bother these patients. The other one is even more typical: delayed dark adaptation. Keep in mind that 95% of the photoreceptors are the rod photoreceptors that allow us to see in the dark, and these photoreceptors now have less access to vitamin A. Eventually, they will get fully sensitive and reach a final threshold, but it takes more time to get all the vitamin A into these photoreceptors, and that leads to, we call it delayed dark adaptation, that it needs more time to fully adapt to a not-so-well-lit environment. Again, this adverse event can be well tolerated and was experienced by about two-thirds of the patients in the trial. All instances of delayed dark adaptation, night vision impairment, xanthopsia were mild and transient. There were no severe and moderate drug-related AEs reported and no AEs that required discontinuation of the treatment. There were no clinically significant findings in relation to vital signs, physical exams, cardiac health, or organ functions. Next slide, please. So I pass it over to Dr. Nathan Mata, the Chief Scientific Officer. Thank you, Dr. Scholl. I'd like to move forward with describing the clinical trial designs in our two Stargardt studies, the DRAGON study and the DRAGON II study. It's important to know that in both Stargardt studies and our GA study, we are looking at the growth rate of atrophic lesions, as Dr. Scholl expressed, the definitely decreased autofluorescence lesions. These are the atrophic lesions that the FDA considers as a surrogate marker for eventual visual acuity loss. And so we're looking at the growth of these lesions as an endpoint for approval in all of our trials. The other thing I want to mention is that in all of our studies, we are implementing a five milligram dose. This dose produces the same pharmacodynamic reduction of retinal binding protein 4 of about 80%. This is very important because in a prior clinical study, we determined in GA subjects, reductions of retinal binding protein for a 70% or more were found to lead to a slowing of lesion growth. So we want to get to that threshold. And with our subjects, as Hendrik just noted, we're getting to about an 80% reduction with the five milligram dose. That said, you can see in both our Dragon study and our Dragon II study, there are a lot of similarities. There are only three differences in the trial designs. The first is the number of subjects. So we have 104 subjects recruited in our Dragon study, and we have 60 subjects that we're aiming for enrollment in our Dragon II study. The second difference is the geography. The DRAGON phase III study is a global study, while the phase 2/3 study, DRAGON II, is recruiting subjects from Japan, U.S., and the U.K. And finally, the third difference is the randomization. Because we have a larger number of subjects in the DRAGON study, we can afford a two-to-one randomization, which favors Tinlarebant. Whereas in the DRAGON II study, we have a smaller number of subjects. So we're using a one-to-one randomization of Tinlarebant to placebo. And as you can see, all of the other elements of the trial design, the masking, the treatment duration, the primary measures, other secondary measures, and an interim analysis, as well as the key inclusion criteria, are all the same. Next slide, please. So we'll move to the geographic atrophy study that we call PHOENIX and show you that trial design as well. As I mentioned, it is very, very similar to the phase III trial designs in Stargardt. There's only two real differences here. The first, of course, is the indication, geographic atrophy versus Stargardt. And the second is the larger number of patients we'll be enrolling to reflect the higher prevalence of GA in the patient population. That said, all other elements of the trial design are similar. This is very important because we believe with the similarity in the trial designs, the dosing, the endpoint, what we see in our Stargardt studies, which is preceding ahead of our GA studies, could be predictive of what we expect to see in our GA studies. And as Hendrik noted, in our phase II open-label study, we're seeing very, very promising safety and efficacy studies. So with that, I'll end, and I'll turn it over to Hao-Yuan to discuss the financials. Thank you. Thank you, Nathan. In Q3 2024, we had R&D expenses of $6.8 million compared to $8.7 million for the same period in 2023. The decrease was mainly attributable to the fewer CRO milestone payments related to the DRAGON trial, which was partially offset by the increase in the DRAGON II trial expenses. On G&A expenses in Q3 2024, we had G&A expenses of $2.9 million compared to $2.2 million for the same period in 2023. The increase was primarily due to an increase in the share-based compensation granted in the Q3 of 2024. On net loss, we had a net loss of $8.7 million in Q3 2024 compared to $10.9 million for the same period in 2023. Regarding cash, we continue to maintain a strong balance sheet and have a total of $109 million in cash in money market fund, time deposit, and U.S. Treasury bills. With the funds raised here today and our recent warrant exercise, we expect about four years of cash runway to execute all our key milestones. Thank you. Back to you, Tom. Thanks, Hao. We have had an exciting year so far, and we continue to make meaningful strides in advancing Tinlarebant in clinical trials for Stargardt disease and geographic atrophy across several countries. And now we'll open the call for questions. Hi, operator. I think you're on mute. Thank you. We will now begin the question and answer session. If you would like to ask a question, please raise your hand, and the moderator will unmute you. Our first question comes from Mark Goodman with Leerink. Please proceed. This is Basma Radwan for Mark Goodman. Thank you for taking our question. We would like to ask if you have done any market research to assess the tolerance of the GA patients to the ocular AEs? Would you expect those AEs to actually impact the uptake in this patient population, or do you think they're going to be resilient to these particular AEs? Thank you. Thanks. So, Nathan, you want to take this one? And maybe you can answer. Yeah, Basma, thank you for the question. I assume you're referring to ocular AEs in the GA study? Yeah, which is basically the same ocular AEs in the Stargardt. Right. I just want to make sure. Yeah. So in GA, we would expect probably a little bit higher incidence and severity of these AEs because primarily the GA retina is much more disease-ridden, right? These patients have had their disease for decades versus the Stargardt adolescent subjects who have had it for years. So there's going to be much more macular involvement. So yes, we would expect perhaps a higher incidence of low luminance visual acuity. There should be no effect on best-corrected visual acuity. That is visual acuity in ambient light. But in low-level light, GA patients, first of all, have a problem with low-level visual acuity. The reduction of vitamin A locally within the macula would make that a little bit worse for patients that have more extensive macular involvement. So yes, the short answer is we would expect a higher incidence of low luminance visual deficits in the GA patient population under Tinlarebant treatment. Would you expect that to be tolerated by the patients? Oh, yes. So we can say, yeah, I mean, we're recruiting that study now. I think we're up to about 288 subjects. We certainly have seen instances of low luminance visual acuity, but it's a minority of subjects, not the majority. So clearly, patients are dealing with it. The majority of patients are dealing with it quite well. Got it. Thank you. You're welcome. Our second question will come from Jennifer Kim with Cantor. Please proceed. Hi. Thanks for taking my questions. Maybe to start off, similar to the last question, for the patients in PHOENIX who have been enrolled to date, do you have any comments on the discontinuation rates you've seen? Nathan, do you want to comment? I believe we're right at around 15% right now, but that's all in. That's not just ocular AEs. That's the total number. We're somewhere around 15%. I believe that was the last number. Okay. And then going to Dragon, can you walk through what's left to get the interim analysis? And then what is your latest thinking around how you'll provide that update? Nathan, do you want to take it? Yeah, yeah. Do you want to take it? Yeah. When you say what's left, I mean, really, all the patient data are in. The trigger for the interim analysis is when all subjects have completed their month 12 visit. That is, we have month 12 images for all subjects. Of course, we're going to have some at 18 months and some that have already completed study, so really, what has to be done is that data has to be cleaned. It has to be provided to the DSMB, and the DSMB has to schedule a meeting to review that data in an unmasked analysis. We predict that timeline is going to be somewhere around December. At the very latest, it'll be early January. But there really is nothing more to be done other than data cleaning and then providing the data to the DSMB, followed by the DSMB internally scheduling a meeting with all members. And then in terms of disclosure on your end, would that come in the form of a press release, a call, or something else? Yep. So Jennifer, what will happen is that we will be told by the DSMB about whether we need to increase the sample size or not. We will announce that to the market as soon as we know. And then we'll host a press release to talk about what we have been told and what does that mean to us. At the same time, I would like to add that another moving factor on the interim analysis will be the new DSMB chair. As you guys probably are aware, Dr. Scholl was our DSMB chair. So we have to find a replacement for that. We have some progress, but as you can imagine, we have to go through all these hospitals' process. So it takes a while. So once the new DSMB chair is on board, then we will schedule the committee's time for that DSMB meeting. And given the Christmas vacation, that's why we don't have a clear timeline about the timing of it. Okay. If I could fit one more question. On DRAGON II, I know you've announced the first patient dosed in the phase 2/3 portion. Can you say anything about how many patients have been enrolled in total so far? Do you have sort of an insight to when that enrollment could complete? I think first, I don't have a specific number at the top of my mind now, but I think most of the Japanese subjects who passed the phase 1b should be enrolled into the phase II. We start to enroll some patients in the U.S. and U.K. as well. I think we're getting there. It should be maybe Q2 next year if we fully enroll for DRAGON II. Okay. Thanks. Our next question comes from Yi Chen with H.C. Wainwright. Please proceed. Thank you for taking my questions. My first question is for the Phoenix trial. So this trial has enrolled more than 280 subjects. Could you tell us whether these subjects have similar baseline characteristics compared to subjects enrolled for the approved GA therapy, which are the complement inhibitors? Thanks. Okay. I'll refer this to Hendrik and if Nathan can add in on the baseline characteristics. Hendrik, you want to take this? Essentially, this is about geographic atrophy to typical GA, which means patients would have drusen. To elaborate what Dr. Mata pointed out earlier, that these patients have a thickened Bruch's membrane and therefore are used to have difficulty seeing in the dark. When it comes to specific inclusion-exclusion criteria, when we compare Phoenix to the trials that have been run with injectables, the main difference that comes to mind is that the lesion size that we target is somewhat smaller than that was targeted with the injectables. That's, to me, the only obvious main difference between the two larger trials with injectables targeting C3 or C5 in the complement system and the Phoenix trial where we target bisretinoid decomposition, the RPE. Dr. Scholl, in your experience, patients with smaller lesion size, should they be? I mean, is it easier for them to observe efficacy in terms of slowing of lesion growth compared to patients with larger lesion at baseline? That's not so easy to say, so when smaller lesions are being targeted, there will be a subpopulation where eventually the fovea has not been reached by atrophy. I think this, especially when the drug becomes available on the market, will be the patients that will benefit the most because for those patients, vision can actually be saved, and they may even maintain 20/20 vision for a while. If and when atrophy encompasses the foveal center, vision is being lost to a significant degree, typically goes to a level of 20/100 or lower. For patients, it's not so easy to experience progression of disease or a possible slowing down of that progression. For physicians, it's much easier because they can measure the atrophy area quite precisely and can compare what the natural history progression is and what the progression will be under therapy. And they will see the difference. For patients, that is certainly a limitation of all these therapies. Vision will get worse, but not at the same pace. But for patients, it will not be easy to actually track the progression themselves. But they will understand that when their treating physicians tells them, "Look, this is the progression, but it would have been so far if you had not taken Tinlarebant," they will understand that. Okay. Thank you. May I just add to your question regarding the lesion size? Theoretically, the anti-complement inhibitors, they're more mechanistically, they are more targeting the inflammation process. Nathan, maybe you want to add on this and your experience with early stage and later stage lesions in GA. Yeah. Thank you, Tom. Yeah, I think Hendrik sort of hit on it peripherally in a way because obviously these larger lesions, the ones that you saw in the Apellis and Iveric studies, have more inflammation driving the lesion growth, right? That's why these complement inhibitors work because it essentially quells an inflammatory response. In our patient cohort, there's going to be less of that because, again, lesions are smaller, as Hendrik mentioned. They're probably not going to be as involved with the fovea as larger lesions, and there's going to be less inflammation. So there's a big difference in the sort of characteristics of the patients at baseline that we're looking at versus what was looked at in the Apellis studies and Iveric studies. And primarily, that is inflammation because these larger lesions are, again, triggering an inflammatory response that is really driving lesion progression. You don't see that in early stage disease, which is where we're having our focus with Tinlarebant. Got it. Thank you for the clarification. And for the interim analysis of the Phoenix trial, is it just a DSMB meeting, or there will actually be some efficacy readout? They will meet. Go ahead, Tom. So yeah, yeah. So it would be DSMB. I don't think the ethics would be involved. Okay. All right. Thank you. Our next question comes from Michael Okunewitch with Maxim Group. Please proceed. Hey, guys. Thank you so much for taking my questions today. First off, I guess I would like to see if you could just talk a little bit about DRAGON II and whether you expect that this would be something that would be required for an FDA filing or if you think you could go for Stargardt with DRAGON alone. So the DRAGON, I mean, we discussed with the FDA, which the FDA said would be a review issue. But the DRAGON II is more for a Japanese study because we got the Sakigake designation, which the Japanese authorities would want to be the first to approve this drug. But of course, that could also serve as a second study if we need that as a second well-controlled study. All right. Thank you. And then just to follow up on the prior question, given that there is a bit of a difference in terms of your target patients for the phase III Phoenix study in GA, would you expect something of a segmented strategy, or would you expect a broader label that allows you to go after the entire market and compete with the injectable complement inhibitors? I believe we have a broader label, and certainly, being an oral treatment, that would definitely be more convenient, in fact, for the broader label. Thank you. As you expect, not many people would want to have a needle in the eye. Yeah, certainly. And then one last one for me. I'll hop back in the queue. I'd just like to touch on Alkeus' miss in geographic atrophy earlier this year. You both have a similar underlying target, but could you talk a little bit about the differences and where Tinlarebant could be better positioned for success? I think Nathan is the perfect person to answer this question. Nathan? Was that in comparison to Alkeus, Michael? Yes, given the similar mechanisms. Yeah. There is a similar, but they're not identical, right? So the biggest difference between synthetic vitamin A and lowering vitamin A is by lowering vitamin A, we'll be reducing the accumulation of all-trans-retinal, which is the bleached photoproduct that is actually more toxic than the bisretinoids on a molar basis. So we will be reducing retinoids across the visual cycle, whereas with synthetic vitamin, they're actually increasing the amount of vitamin A in the visual cycle. And in fact, they'll be increasing the amount of all-trans-retinal. It'll be a deuterated all-trans-retinal, but it'll still be all-trans-retinal. So that really is the key difference. The toxicity associated with all-trans-retinal, as I say, is much more severe than the toxicity associated with bisretinoids like A2E. They're going to be primarily reducing A2E because they are reducing basically the conversion or the dimerization of the aldehyde to a bisretinoid, but they're still going to have high levels of all trans retinol. So I would say that's the biggest difference that I can say with respect to the MOA. And the fact that they saw a trend in their data, it's promising for our treatment approach. We believe we will see a better effect because, again, we'll be reducing the aldehyde as well as the bisretinoids. All right. Thank you very much for taking my questions today. Thank you. This concludes our Q&A portion of the call. I will turn it back to Tom Lin for closing remarks. Thanks. So thank you all for joining our call. We'll be in San Francisco during the J.P. Morgan Healthcare Conference Week in January. We hope to see some of you there and introduce you to Dr. Scholl, and have a great day. Thank you very much.