Belite Bio, Inc

Hello, and thank you for joining us to discuss Be Light Bio's fourth quarter and full year 2023 financial results. Joining the call today are Dr. Tom Lin, Chairman and CEO of Be Light Bio, Dr. Nathan Matta, Chief Scientific Officer, and Hao-Wang Zhang, 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'll respond to questions following our prepared remarks. Now I'll turn the call over to Dr. Lin.

Thank you. Thank you, everyone, for joining our reporting for 2023 and for this quarter. I'm Tom Lin, CEO of Be Like Bio. Joining me is our CSO, Dr. Nathan Maher, and our CFO, Hao Yuan. I'd like to start off with an overview. So Teneroband is a novel once-a-day oral tablet designed to bind to serum retinal binding protein, or RBP4, as a means to specifically reduce retinal delivery to the eye. This approach is intended to slow or stop the formation of the toxic retinal derived byproducts, which are generated in the visual cycle and are implicated in progression of Stargardt's disease and geographic atrophy. ReliveBio believes that early intervention directed at emerging retinal pathology, which is not mediated by inflammation, would be the best approach to potentially slow disease progression in Starr's disease and in GA. There's still a significant unmet need for both indications, as currently there is no approved treatments for Starr's disease, and there are currently no approved oral treatments for GA. And we're already in global phase three trials for both indications. So far, we have been granted fast-track designation, rare pediatric disease designation, and open drug designation in U.S., EU, and now Japan. We have several patent families and with composition of meta-patents lasting until 2040, and with patent term extension and new patents to be filed, which will have patent protection way past the 2040s. For Starless indication, the Phase III is already fully enrolled with estimated interim readouts by end of 2024 or early 2025. We will also be presenting further positive findings and treatment results from our end-of-Phase II results, which we'll be presenting at Arvo in May this year. For GA in Dry MD indication, we currently have more than 50 subjects enrolled in our Global Phase III trial. With this, I would like to pass this on to our CSO to give an update on the clinical trials. Nathan? Thank you, Tom.

So I'll go right into the clinical trial designs. When we first, I should say, in previous financial updates, we've shown you the overview of our open label phase two, as well as the well-controlled phase three study design, which is our pivotal phase three study. And we emphasize that the big differences between these two studies was that in the patients in the open label phase two, they came in with a very early stage of disease, which is characterized by the presence of autofluorescence, but not atrophy of retinal lesions, whereas in the Phase III, all the subjects have retinal atrophy. Well, it turns out that in our Phase II study, when we look retrospectively back at those baseline images, we find, in fact, that a number of these subjects actually do have atrophic lesions. They were just not measurable by the routine imaging algorithm that most clinical researchers use. So our imaging center has developed a new algorithm, much more sensitive in terms of identifying atrophic retinal lesions. So we do in fact know that in the phase two open label study, many of these subjects did start with very, very small atrophic lesions that grew over time. And of course, we showed you the data about the lesion growth, which I'll jump to right now. Next slide. So as I mentioned before, Kids came in with early lesion types. Some of them did have atrophy. But we wanted to compare to natural history growth to determine whether or not we're having any real treatment effect. And we showed this data previously in a comparison to ProgStar, a cohort of subjects that have similar baseline characteristics as our Phase II subjects. And as you can see here on the left-hand side, we see a really dramatic slowing of lesion growth in Tenlarabat treatment group, which is the red lines, versus the natural history group in ProgStar, which is the blue lines. And as I said before, We know now that these patients did come in with atrophy, so there's a lot of similarities now between the Phase 2 patients and the Phase 3. The other new update that we didn't have last time is a genetic analysis because we did note in terms of the lesion growth, there were five of 12 subjects that never converted to atrophy over the two-year study. We now know that those five subjects have severe biallelic mutations which predict retinal pathology. So the absence of the transition from the early lesion type to the atrophic lesion type in these five subjects could not be attributed to benign or mild mutations. They, in fact, had very severe mutations. So all these data really point to a profound treatment effect of our drug. Next slide. This is an overview of the phase three trial design and geographic atrophy. And as I mentioned before, the trial designs between the Stargardt disease phase three study and the GA phase three study are very, very similar. It's the same drug, it's the same dose, it's the same endpoint, same randomization, same trial duration of two years. The only real difference in these two studies is, well, there's two, first being the indication, GA rather than Stargardt's. And of course, in the GA study, we have more patients to reflect the higher prevalence of the disease in the population. So with that, now I'll throw it over to Hao Yan so we can talk about financial data. Thank you.