Q2 2024 Belite Bio Inc Earnings Call

2024 financial results.

Operator: and Chairman and CEO of Belite Bio, Dr. Nathan Mata, Chief Scientific Officer, and how Juan 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.

Speaker Change: Joining the call today are Dr. Tom Lin, Chairman and CEO of BeLight Bio, Dr. Nathan Mata, Chief Scientific Officer, and Hao-Wan Zhang, Chief Financial Officer.

Speaker Change: 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.

Operator: 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 made different materially. We encourage you to consult the risk factors discussed in our SEC filings for additional details.

Operator: We encourage you to consult the risk factors discussed in our SEC filings for additional details. 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.

Speaker Change: We encourage you to consult the risk factors discussed in our SEC filings for additional detail.

Speaker Change: 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.

Operator: 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.

Tom Lin: Now I'll turn the call over to Dr. Lin. Thanks, Julie. Thank you, everyone, for joining our second quarter 2024 earnings call. We had another strong quarter advancing our televent trials, and I'm pleased with our progress in the year-to-date.

Operator: and Chairman and CEO of Belite Bio; Dr. Nathan Mata, Chief Scientific Officer, and Hao-Wan Zhang, Chief Financial Officer.

Dewey: Now I'll turn the call over to Dr. Lin. Thanks, Dewey.

Operator: 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. Thank you.

Speaker Change: Now I'll turn the call over to Dr. Lin.

Julie: Now I'll turn the call over to Dr. Lin. Thanks, Julie.

Dr. Lin: Thank you everyone for joining our second quarter 2024 earnings call. We had another strong quarter advancing after 11 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 giving an overview of our program. We had a productive quarter marked by several advancements in our program. We have initiated the Phase 1B and Phase 2, 3 trial of cannabinoids in adolescent Stargardt patients, also known as the Dragon 2 study, and we have already completed enrollment for the Phase 1B portion with six 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 since its initiation in 2015.

Tom Lin: Thank you everyone for joining our second quarter 2024 earnings call. We had another strong quarter, advancing after 11 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 giving an overview of our program. We had a productive quarter marked by several advancements in our program.

Dr. Lin: Thanks, Julie. Thank you, everyone, for joining our second quarter 2024 earnings call. We had another strong quarter advancing our 2011 trials, and I'm pleased with our progress in the year to date.

Tom Lin: Thank you, everyone, for joining our second quarter, 2024 earnings call. We had another strong quarter advancing our televent trials, and I'm pleased with our progress in the year-to-date. Let me start off with our accomplishments during the second quarter, for the overview of our programs. We had a productive quarter marked by several advancements in our programs. We have initiated Phase 1-B and Phase 2-3 trial of televent in analysis and style of patients.

Tom Lin: Let me start off with our accomplishments during the second quarter, for the overview of our programs. We had a productive quarter marked by several advancements in our programs. We have initiated Phase 1-B and Phase 2-3 trial of televent in analysis and style of patients. Also, now there's a training to study, and we have already completed enrollment for Phase 1-B for him with six subjects in Japan. We've also received Saagigake designation in Japan, which means Pioneer Drugs designation in English. Such designation has only been granted to 27 drugs since its initiation in 2015, and to now ban these the first of only drugs received Saagigake Designation, which is a testament to the groundbreaking potential of the drug, and the immediate sense to address the people living with stronger disease.

Dr. Lin: Let me start off with our accomplishments during the second quarter by the overview of our programs.

Dr. Lin: We had a productive quarter marked by several advancements in our programs.

Tom Lin: We have initiated the Phase 1B and Phase 2, 3 trial of cannabinoids in adolescent Stargardt patients, also known as the DRAGON2 study, and we have already completed enrollment for the Phase 1B portion with six 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 since its initiation in 2015.

Speaker Change: We have initiated the Phase I-B and Phase II-III trial of Tenerbene in adolescent STAGA patients, also known as the DRAGON2 study, and we have already completed enrollment for the Phase I-B portion with six subjects in Japan.

Tom Lin: Also, now there's a training to study, and we have already completed enrollment for Phase 1-B for him with six subjects in Japan. We've also received Saagigake Designation in Japan, which means Pioneer Drugs Designation in English. Such designation has only been granted to 27 drugs since its initiation in 2015, and to now ban these the first of only drugs received Saagigake Designation, which is a testament to the groundbreaking potential of the drug, and the immediate sense to address the people living with stronger disease.

Speaker Change: We've also received Sakigake designation in Japan, which means pioneer drugs designation in English.

Speaker Change: Such designation has only been granted to 27 drug-sensitive individuals in 2015.

Dr. Lin: And Tenerbent is the first of only drugs to receive Sakigake designation, which is a testament to the groundbreaking potential of this drug and the unmet need it stands to address for the people living with Saga disease. We've made progress in our pivotal global phase 3 trial of Tadarabin in geographic atrophy subjects as well, known as the Phoenix Study, and have already enrolled nearly 200 subjects up until now. In addition, we've also raised $25 million from the Registered Direct Offering in April this year to strengthen our balance sheet.

Tom Lin: And Tenerbent is the first of only drugs to receive Sakigake designation, which is a testament to the groundbreaking potential of this drug and the unmet need it stands to address for the people living with Saga disease. We've made progress in our pivotal global phase 3 trial of cadaver band in geographic atrophy subjects as well, known as the Phoenix Study, and have already enrolled nearly 200 subjects up until now. In addition, we've also raised $25 million from the registered direct offering in April of this year to strengthen our balance sheet.

Speaker Change: and Tenerife is the first of many tribes to receive a Sakigake designation.

Speaker Change: which is a testament to the groundbreaking potential of this drug and the unmet need it stands to address the people living with Stargardt disease.

Tom Lin: We've made progress in our pivotal goal, Phase 3-12, after they have been in telemetry therapy subject as well, known as the Phoenix Study, and have already enrolled nearly 200 subjects to up front up until now.

Speaker Change: We've made progress in our pivotal global phase 3 trial of Tadarabin in geographic atrophy subjects as well, known as the Phoenix Study, and have already enrolled nearly 200 subjects up until now.

Tom Lin: We've made progress in our pivotal goal, Phase 3-12, after they have been in telemetry therapy subject as well, known as the Phoenix Study, and have already enrolled nearly 200 subjects to up front up until now. In addition, we've also raised 25 million from the registered direct offering in April this year, for strengthening our balance sheet. The Phase 3-1 study is fully enrolled, worth estimated, in trouble readouts by 24-22-4 or early 23-5-8 days.

Tom Lin: In addition, we've also raised 25 million from the registered direct offering in April this year for strengthening our balance sheet. The Phase 3-1 study is fully enrolled, worth estimated, in trouble readouts by 24-22-4 or early 23-5-8 days.

Speaker Change: In addition, we've also raised $25 million from the registered direct offering in April this year for strengthening our balance sheet.

Dr. Lin: The Phase 3, DRAGON1 study is fully enrolled with estimated interim readouts by 2024 or early 2025. 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 our pivotal phase 3 DRAGON study in the fourth quarter. Next slide, please. Okay, so for those of you that are new to this story, That's the story.

Tom Lin: The Phase 3, DRAGON1 study is fully enrolled with estimated interim readouts by 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 our pivotal phase 3 DRAGON study in the fourth quarter. Next slide, please. Okay, so for those of you that are new to the story, that's the story

Speaker Change: The Phase III-Dragon 1 study is fully enrolled with estimated interim readouts by 2024 or early 2025 at the latest.

Tom Lin: As we enter the second half of the year, we are well positioned to execute on key milestones, and we look forward to sharing in-term analysis from, initiated in-term analysis from our pivotal Phase 3-3-3 study in the fourth quarter.

Speaker Change: 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 our pivotal Phase III DRAGON study in the fourth quarter.

Tom Lin: As we enter the second half of the year, we are well positioned to execute on key milestones and we look forward to sharing in-term analysis from, initiated in-term analysis from our pivotal Phase 3-3-3 study in the fourth quarter. Next slide please. For those of you, they were new to the story. The story, Tenebren is a novel once a day on a tablet designed to bind to serum retinal binding protein as it means to specifically reduce retinal delivery to the eye.

Operator: Next slide, please.

Tom Lin: For those of you, they were new to the story. The story, Tenebren, is a novel once a day on a tablet designed to bind to serum retinal binding protein, as it means to specifically reduce retinal delivery to the eye. This approach is intended to slow or stop the formation of toxic retinal-derived by-products, which are generated in the visual cycle and are implicated in the progression of star Therapy. We believe that early intervention directed at emerging racial pathology, which is not media by information, is the best approach to potentially slow the disease progression in star disease and also in geographic atrophy.

Speaker Change: Next slide, please.

Speaker Change: Okay, so for those of you that are new to the story, Geneva is a novel once-a-day oral tablet designed to bind to serum retinal binding protein as a means to specifically reduce retinal delivery to the eye.

Dr. Lin: Janelban is a novel once-a-day oral tablet designed to bind to serum retinal binding protein as a means to specifically reduce retinal delivery to the eye. This approach is intended to slow or stop the formation of toxic retinol-derived byproducts which are generated in the visual cycle and are implicated in the progression of Starlet disease and geographic atrophy. We believe that early intervention directed at emerging retinal pathology, which is non-medially caused by inflammation, is the best approach to potentially slow the disease progression in heart disease and also in geographic atrophy.

Tom Lin: Tenerbren is a novel once-a-day oral tablet designed to bind to serum retinol binding protein as a means to specifically reduce retinol delivery to the eye. This approach is intended to slow or stop the formation of toxic retinol-derived byproducts, which are generated in the visual cycle and are implicated in the progression of Starlet disease and geographic atrophy. We believe that early intervention directed at emerging retinal pathology, which is non-medially caused by inflammation, is the best approach to potentially slow the disease progression in heart disease and also in geographic atrophy.

Speaker Change: This approach is intended to slow or stop the formation of toxic retinol-derived byproducts, which are generated in the visual cycle and are implicated in the progression of Starlet disease and geographic atrophy.

Tom Lin: This approach is intended to slow or stop the formation of toxic retinal derived by products, which are generated in the visual cycle and are implicated in the progression of star Therapy. We believe that early intervention directed at emerging racial pathology, which is not media by information, is the best approach to potentially slow the disease progression in star disease and also in geographic atrophy. Importantly, there is still a significant amenity for both indications as currently there is no improvement for star disease and no approved oral treatments for geographic atrophy and we are already in global phase three trials for both indications.

Speaker Change: We believe that early intervention directed at emerging retinal pathology, which is non-media by inflammation, is the best approach to potentially slow the disease progression in heart disease and also in geographic atrophy.

Dr. Lin: Importantly, there is still a significant unmet need for both indications, as currently, there is no approved treatment for SARS disease, and there are no approved oral treatments for geographic atrophy, and we're already in global phase 3 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 open drug designation in the US, EU, and Japan, as I just mentioned.

Tom Lin: Importantly, there is still a significant unmet need for both indications, as currently, there is no approved treatment for SARS disease, and there are no approved oral treatments for geographic atrophy, and we're already in global phase 3 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 open drug designation in the US, EU, and Japan, as I just mentioned.

Tom Lin: Importantly, there is still a significant amenity for both indications, as currently there is no improvement for star disease and no approved oral treatments for geographic atrophy, and we are already in global phase three trials for both indications.

Speaker Change: Importantly, there is still a significant unmet need for both indications, as currently there is no approved treatment for SARS disease and no approved oral treatments for geographic atrophy. We are already in global phase 3 trials for both indications.

Tom Lin: To give you any 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 US, EU, and Japan, and pioneer drug designation in Japan and such as mentioned. Finally, we have strong patent protection for 14 patent families, and most of these are compositional matter patterns. And the latest compositional matter pattern is expected to last up to 2040, with additional patent term extension potential with new patterns to be filed. We will have patent protection passed the 2040s.

Speaker Change: 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.

Tom Lin: To give you any 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 US, EU, and Japan, and pioneer drug designation in Japan and such as mentioned. Finally, we have strong patent protection for 14 patent families and most of these are compositional matter patterns. And the latest compositional matter pattern is expected to last up to 2040 with additional patent term extension potential with new patterns to be filed. We will have patent protection passed the 2040s. All of this highlights the potential of the relevant people who are living with this debilitating needs and capitalized on the large market opportunities.

Dr. Lin: Finally, we have strong pattern protection for 14 pattern families, and most of these are compositional meta-palettes. The latest composition of matter pattern is expected to last up to 2040, with additional pattern term extension potential with new patterns to be found.

Tom Lin: Finally, we have strong pattern protection for 14-pattern families, and most of these are compositional metapatterns. And the latest composition of matter pattern is expected to last until 2040, with additional pattern term extension potential. With new patterns to be found, we will have pattern protection past 2040.

Speaker Change: Finally, we have strong pattern protection for 14-pattern families, and most of these are compositional meta-patterns.

Speaker Change: And the latest composition of Mata pattern is expected to last up to 2040 with additional pattern term extension potential with new patterns to be found. We will have pattern protection past the 2040s.

Dr. Lin: We will have pattern protection past 2040. All of this highlights the potential of developing to create people who are living with these debilitating needs and capitalise on the large market opportunity. We are very excited about the path ahead, and our team is focused on our mission to leverage Sundarban to address the unmet needs of patients suffering from blindness. I would like to pass this to Nathan, our CSO, and give you a clinical and scientific update. Nathan?

Tom Lin: All of this highlights the potential of the relevant people who are living with this debilitating needs and capitalized on the large market opportunities. We are very excited with the path ahead, and our team is focused on our mission to leverage the lab and to address the amenities of patients suffering from blindness.

Tom Lin: All of this highlights the potential of developing people who are living with these debilitating needs and capitalizing on the large market opportunity. We are very excited about the path ahead, and our team is focused on our mission to leverage Sundarban to address the unmet needs of patients suffering from blindness. I would like to pass this to Nathan, our CSO, and give you a clinical and scientific update. Yeah, thank you very much, Tom.

Speaker Change: All of this highlights the potential of developing people who are living with these debilitating needs and capitalise on the large market opportunities.

Speaker Change: We are very excited with the path ahead, and our team is focused on our mission to leverage Sundarban to address the unmet needs of patients suffering from blindness.

Tom Lin: We are very excited with the path ahead and our team is focused on our mission to leverage the lab and to address the amenities of patients suffering from blindness.

Nathan Mata: I would like to pass this to Dr. Pazestor to Nathan, our CSO, and give you a clinical and scientific update. Nathan? Yeah, thank you very much, Tom. So what I'd like to share with you is the data from our two-year open label phase two study in adolescent Stargardt subjects. This study was, as I mentioned, a two-year study, 13-year-old subjects from Taiwan and Australia. When a lot of people don't understand about Stargardt disease, 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 or benign.

Nathan: I would like to pass this to Nathan, our CSO, and give you a clinical and scientific update. Nathan? Yeah. Thank you very much, Tom. So, what I'd like to share with you is the data from our two-year open-label Phase 2 study in adolescent Stargardt subjects.

Nathan Mata: I would like to pass this to Dr. Pazestor to Nathan, our CSO, and give you a clinical and scientific update. Nathan? Yeah, thank you very much, Tom.

Nathan Mata: Yeah, thank you very much, Tom. So what I'd like to share with you is the data from our two-year Open Label Phase 2 study in adolescent Stargardt subjects. This study was, as I mentioned, a two-year study with 13 enrolled subjects from Taiwan and Australia. What a lot of people don't understand about Stargardt's disease is that 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 or benign.

Nathan: Yeah, thank you very much, Tom. So what I'd like to share with you is the data from our two-year Open Label Phase 2 study in adolescent Stargardt subjects. This study was, as I mentioned, a two-year study of 13-year-old subjects from Taiwan and Australia. What a lot of people don't understand about Stargardt's disease is that 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 or benign.

Nathan Mata: So what I'd like to share with you is the data from our two-year open label phase two study in Adolescent Stargart Subjects. This study was, as I mentioned, a two-year study, 13-year-old subjects from Taiwan and Australia. When a lot of people don't understand about Stargart diseases, there are over 1,500 known mutations that are associated with the disease. Not all of them are known to be a pathogenic, in fact many are mild or benign.

Nathan: This study was, as I mentioned, a two-year study, 13-year-old subjects from Taiwan and Australia. What a lot of people don't understand about Stargardt's 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 or 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, a preeminent geneticist in Stargardt's disease in the world, Dr. Randall Alkemitz at Columbia University. He evaluated our genetic data and determined that 11 of 13 subjects in our cohort had severe bioallelic mutations which would predict pathogenicity. And in those two where there was a moderate allele in these two subjects,

Nathan: So, one of the analyses we did initially was to determine the genetic composition of our cohort, and we actually gave the genetic data to one of the premier, preeminent geneticists in Stargardt's disease in the world, Dr. Randall Alkemitz at Columbia University. He evaluated our genetic data and determined that 11 of 13 subjects in our cohort had severe bioallelic mutations which would predict pathogenicity. And in those two cases where there was a moderate allele in these two subjects, in vitro testing actually showed that these were pathogenic alleles.

Nathan Mata: 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, a preeminent geneticist in Stargardt disease in the world, Dr. Rando Alchemist at Columbia University. He evaluated our genetic data and determined that a level of 13 subjects in our cohort had severe biolil mutations, which would predict pathogenicity. And in those two where there was a moderate allele in these two subjects, in visual tests he 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.

Nathan Mata: 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, a preeminent geneticist in Stargart disease in the world, Dr. Rando Alchemist at Columbia University. He evaluated our genetic data and determined that a level of 13 subjects in our cohort had severe biolil mutations which would predict pathogenicity. And in those two where there was a moderate allele in these two subjects, in visual tests he actually showed that these were pathogenic allele.

Nathan Mata: So one of the analyses we did initially was to determine the genetic composition of our cohort. And we actually gave the genetic data to one of the premier, preeminent geneticists in Stargardt's disease in the world, Dr. Randall Alkemitz at Columbia University. He evaluated our genetic data and determined that 11 of 13 subjects in our cohort had severe bioallelic mutations, which would predict pathogenicity. And in those two where there was a moderate allele in these two subjects, in vitro testing actually showed that these were pathogenic alleles.

Nathan: 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 a CAD score, which stands for Combined Annotation Dependent Depletion Score.

Nathan Mata: 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 a CAD score. That stands 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.

Speaker Change: 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 a CAD score. That stands 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 in the section of subjects 3 and 5 had these CAD scores above 20. So we have two independent confirmations of the severity of the genotypes of these kids. Despite the severity of these genotypes, we had five subjects, which represents four

Nathan Mata: 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 a CAD score that sounds for combined annotation dependent depletion score. It tells you that the degree of severity of a particular genetic variant or genetic mutation scores above 20 are predicted to be among the one percent most illiterious. And every single one of our subjects, these sections of subjects three and five had these CAD scores above 20.

Nathan Mata: An independent assessment of the genetic severity is provided by something called a CAD score that stands for combined annotation dependent depletion score. It tells you that the degree of severity of a particular genetic variant or genetic mutation scores above 20 are predicted to be among the one percent most illitrious. And every single one of our subjects, these sections of subjects three and five had these CAD scores above 20. So we have two independent confirmations of 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 atrial thick lesions.

Nathan Mata: And every single one of our subjects in the section of subjects 3 and 5 had these CAD scores above 20. So we have two independent confirmations of the severity of the genotypes of these kids. 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 had a type of lesion that is autoclorescent.

Nathan: 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 in the section on subjects 3 and 5 had these CAD scores above 20. So, we have two independent confirmations of the severity of the genotypes of these kids. However, despite the severity of these genotypes, we had five subjects, which represents 42% of the cohort, that never developed atrophic lesions.

Nathan Mata: So we have two independent confirmations of severity of the genotypes of these of these kids. And despite the severity of these genotypes, we had five subjects which represents 42% of the cohort that never developed atrial thick lesions. So I should have mentioned that in this study, these adolescents such as came in with an early form of disease where they only have a type of lesion which is autoflorescent. This is known as a quest to be decreased autoflorescent lesion.

Nathan Mata: Over time these autoflorescent 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 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.

Nathan: So, I should have mentioned that in this study, these adolescent subjects came in with an early form of disease where they only had 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 that we found two pairs of siblings that had the exact same identical mutations.

Nathan Mata: So I should have mentioned that in this study, these adolescents such as came in with an early form of disease where they only have a type of lesion which is autoflorescent. This is known as a quest to be decreased autoflorescent lesion. Over time, these autoflorescent 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 competing companies of ours that are using as a premise for their therapeutic approach that identical mutations predict an identical disease course.

Speaker Change: 42% of the cohort that never developed atrophic lesions.

Speaker Change: So, I should have mentioned that in this study, these adolescent subjects came in with an early-formed disease where they only have a type of lesion which is autoclorescent. This is known as a questionably decreased autoclorescent lesion. Over time, these autoclorescent 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.

Nathan Mata: This is known as a questionably decreased autoclorescent lesion. Over time, these autoclorescent 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.

Nathan Mata: Another interesting outcome from the genetic data was that 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.

Speaker Change: from the genetic data was we found two pairs of siblings

Nathan: This is important because there are competing companies of ours that use 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.

Speaker Change: 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.

Nathan Mata: 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 we're having an effect to improve patients' essentially, well-being, is visual acuity. So we looked at visual acuity and subjects prior to enrollment, and we looked specifically for subjects who are losing letters in both eyes; that's called bilateral BCVA law, 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.

Nathan: 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' well-being is visual acuity. So we looked at visual acuity in subjects prior to enrollment, and we looked specifically for subjects who were losing letters in both eyes. That's called bilateral BCVA loss.

Nathan Mata: 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' well-being is visual acuity. So we looked at visual acuity in subjects prior to enrollment, and we looked specifically for subjects who were 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.

Speaker Change: 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' essentially well-being is visual acuity.

Nathan Mata: Because this is an open-label study, one of the metrics we want to look at to see we're having an effect to improve patients, essentially, well-being, is visual acuity. So we looked at visual acuity and subjects prior to enrollment, and we looked specifically for subjects who are losing letters in both eyes, that's called bilateral BCVA law, 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.

Speaker Change: So we looked at visual acuity in subjects prior to enrollment.

Nathan: 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. Thus, the natural history in our study, basically over two 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, some of them significantly, and they don't have atrophic lesions. That suggests that non-atrophic lesions, these QDF lesions, can actually compromise visual acuity.

Speaker Change: and we look specifically for subjects who are losing letters in both eyes. That's called bilateral BCDA loss.

Speaker Change: And we found a subgroup of six subjects within our larger cohort that was losing a mean of 10 letters per year.

Nathan Mata: The natural history in our study basically over two 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, suggest that non-atrophic lesions, these QDF lesions, can actually compromise visual acuity. That's very important, because all of these kids have full-wheel involved lesions, which means they are compromised; their vision will be compromised over time.

Nathan Mata: The natural history in our study, basically, over two years predicts that there will 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, some of them significantly, and they don't have atrophic lesions. This suggests that non-atrophic lesions, these QDF lesions, can actually compromise visual acuity.

Speaker Change: prior to enrollment.

Speaker Change: The natural history in our study, basically over two 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.

Nathan Mata: The natural history in our study basically over two 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, suggest that non atrophic lesions, these QDF lesions, can actually compromise visual acuity.

Speaker Change: 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.

Nathan: That's very important because all of these kids have foveal-involved lesions, which means they are compromised, and 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 BCGA loss, and this data can be found in the appendix of this presentation.

Nathan Mata: That's very important because all of these kids have foveal-involved lesions, which means they are compromised, and 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 BCDA loss, and this data can be found in the appendix of this presentation.

Nathan Mata: That's very important, because all of these kids have full-wheel 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 a trolleysic lesions before this 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.

Nathan Mata: But the current thinking in the scientific and clinical community is that you have to have a trolleysic lesions before this 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 show on the left-hand side over the two-year study, we see a mean loss of about 2.5 letters per year.

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

Nathan Mata: If we look at the overview of visual acuity in all subjects, which is shown on the left-hand side over the two-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.

Nathan: If we look at the overview of visual acuity in all subjects, which is shown on the left-hand side over the two-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.

Speaker Change: If we look at the overview of visual acuity in all subjects that's shown on the left-hand side over the two-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.

Nathan Mata: If we look at the overview of visual acuity in all subjects that show on the left hand side over the two-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 we're losing 10 letters per year before coming into study that show 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.

Nathan Mata: 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 we're losing 10 letters per year before coming into study, that show 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.

Nathan Mata: 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.

Nathan: 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.

Speaker Change: 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 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. Thank you.

Nathan Mata: As I mentioned, 5 of 12 subjects never grew in atrial fieg 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 subjects have these types of autofluorescent lesions that are encroaching the phobia. There are just some different sizes. And we're measuring over time how this autofluorescent lesion converts to an atrophic lesion. And as I said before, there are 7 out of the 12; there actually grew these atrophic lesions.

Nathan: As I mentioned, 5 of 12 subjects never grew an 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 subjects have these types of autofluorescent lesions that are encroaching on the fovea. They're just of different sizes. And we're measuring over time how this autofluorescent lesion converts to an atrophic lesion. And as I said before, there are 7 out of 12 that actually grow these atrophic lesions. And what we found was something very interesting.

Nathan Mata: As I mentioned, 5 of 12 subjects never grew an 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 subjects have these types of autofluorescent lesions that are encroaching on the fovea, they're just of different sizes.

Nathan Mata: So, I want to go to that right now. As I mentioned, 5 of 12 subjects never grew in atrial fieg 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 subjects have these types of autofluorescent lesions that are encroaching the phobia.

Speaker Change: As I mentioned, 5 of 12 subjects never grew an atrophic lesion, but I want to show you sort of anatomically what that looks like.

Nathan: In every case except one, the increase in 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 in atrophy, and where you see a blue bar, that's a decrease in 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.

Speaker Change: 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 subjects have these types of autofluorescent lesions that are encroaching the fovea. They're just of different sizes.

Nathan: 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

Nathan Mata: And we're measuring over time how this autofluorescent lesion converts to an atrophic lesion. And as I said before, there are 7 out of 12 that actually grow these atrophic lesions. And what we found was something very interesting. In every case except one, the increase in 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 in atrophy, and where you see a blue bar, that's a decrease in 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.

Nathan Mata: There are just some different sizes. And we're measuring over time how this autofluorescent lesion converts to an atrophic lesion. And as I said before there are 7 out of the 12, there actually grew these atrophic lesions. And what we found was something very interesting. In every case, except 1, 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 the increase of atrophy.

Speaker Change: And we're measuring over time how this autofluorescent lesion converts to an atrophic lesion.

Nathan Mata: 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

Speaker Change: 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.

Nathan Mata: And what we found was something very interesting. In every case, except 1, 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 the increase of atrophy. And when 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.

Speaker Change: by a decrease in the autofluorescent area in every single subject. So wherever you see an orange bar, that's the 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 the initial...

Nathan Mata: And when 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.

Nathan Mata: 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 an area of 2D af lesion, such as this one subject. And finally, getting back to the genetic mutations, it was subjects 9 and 10, and subjects 12 and 13, that had the identical mutations.

Nathan Mata: 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 an area of 2D af lesion, such as this one subject. And finally, getting back to the genetic mutations, it was subjects 9 and 10, and subjects 12 and 13, that had the identical mutations.

Nathan: So this is a pretty important finding. There was only one subject where we found a lesion that was outside of initially an area of QDAF lesions, so just this one subject. And finally, getting back to the genetic mutations, it was subjects 9 and 10 and subjects 12 and 13 that had the identical mutations. But if you look at 9 and 10, yeah, they both have lesion growth somewhat different in subjects 10 versus 9.

Nathan Mata: So this is a pretty important finding. There was only one subject where we found a lesion that was outside of initially an area of QDAF lesions, so just this one subject. And finally, getting back to the genetic mutations, it was subjects 9 and 10 and subjects 12 and 13 that had the identical mutations. But if you look at 9 and 10, yeah, they both have lesion growth, 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 are essentially the same; they have the identical genotypes and very similar disease duration.

Nathan Mata: But if you look at 9 and 10, yeah, they have both somewhat different in subject 10 versus 9. But then if you look at 12 and 13, there's actually no lesion growth. Yet, all these kids have essentially the same, they have the identical genotypes and very similar disease duration.

Speaker Change: area of QDA athlesia and so just this one subject.

Speaker Change: And finally, getting back to the genetic mutations, it was subjects 9 and 10 and subjects 12 and 13 that had the identical mutations. But if you look at 9 and 10, yeah, they both have lesion growth 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,

Nathan Mata: But if you look at 9 and 10, yeah, they have both somewhat different in subject 10 versus 9. But then, if you look at 12 and 13, there's actually 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, so just 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.

Nathan: 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 that on a lesion growth metric, identical mutations do not predict identical disease progression. 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.

Nathan Mata: So these data, again, suggest that on a lesion growth metric, identical mutations do not predict identical disease. 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.

Nathan Mata: So, these data again, so just on a lesion growth metric, identical mutations do not predict an identical disease, course.

Speaker Change: Identical mutations do not predict an identical disease course.

Speaker Change: We have one other very important piece of information to pass along, and that is an assessment of how these lesions are actually graded.

Nathan Mata: 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 an auto fluorescent camera that takes a picture of the lesion and then a reader of physical reader goes in and draws the boundary around the perimeter of that lesion so that the computer can then tell you the area.

Nathan Mata: It's basically an auto fluorescent camera that takes a picture of the lesion, and then a reader of 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 lesions and 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 intro reader bias.

Nathan: It's basically an 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 agreement in terms of the lesion size before it can move on to 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 subject to inter- and intra-reader bias. It doesn't look at any one specific area in the red. It's looking all over, and it's very time-consuming.

Nathan Mata: It's basically an 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 agreement in terms of the lesion size before it can move on to 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.

Speaker Change: So, currently we're using the routine methodology that everyone is using. It's basically an 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.

Speaker Change: 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 inter- and intra-reader bias.

Nathan Mata: So two readers have to grade every single image because there has to be an agreement in terms of the lesions and 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 intro reader bias. It doesn't look at any one specific area in the red is looking all over and it's very time consuming.

Nathan Mata: So this particular method is subjective to inter- and intra-reader bias. It doesn't look at any one specific area in the red. It's looking all over, and it's very time-consuming.

Nathan Mata: It doesn't look at any one specific area in the red; it 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.

Speaker Change: It doesn't look at any one specific area in the red, it's looking all over, and it's very time-consuming.

Nathan: 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 the area of healthy tissue, let's say out here, to the area of diseased 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.

Nathan Mata: 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 the area of healthy tissue, let's say out here, to the area of diseased 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.

Speaker Change: 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 diseased tissue, which would be sort of represented by the density of the optic nerve disk. 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 atropic lesions. In this case, we're looking at atropic lesions.

Nathan Mata: 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.

Nathan Mata: 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 eight subjects that had atrophic lesions within the macula at baseline. And this is something that 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 matular lesion growth in these subjects that it was identified in.

Nathan Mata: And it's just looking at the macula for different areas of gray that would predict either autophorescence or atrophobic lesions. In this case, we're looking at 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 eight subjects that had atrophic lesions within the macula at baseline.

Speaker Change: So this is important because it removes the reader and the potential subjective bias out of the equation.

Nathan: When our reading center used that methodology to rescan our images at baseline, they found 12 eyes of eight 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.

Nathan Mata: When our reading center used that methodology to rescan our images at baseline, they found 12 eyes of eight 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.

Speaker Change: When our reading center used that methodology to re-scan 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 re-read all these images to see what's happening with macular lesion growth in these subjects that it was identified in.

Nathan Mata: And this is something that 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 matular 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 macula area over time. It's pretty linear until about month 16, at which time it completely stops.

Nathan Mata: This is the data that they developed. On the left hand side, it shows you the growth of the lesions into the macula 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 you'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 on our subjects, they never get to more than about single digit involvement into the macula.

Nathan: The left-hand side shows you the growth of the lesions into the macula 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 6-millimeter zone of the macula is occupied with lesions. And you can see in our subjects, they never get to more than about single-digit involvement in the macula.

Nathan Mata: The left-hand side shows you the growth of the lesions into the macula 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 lesions. And you can see in our subjects, they never get to more than about single-digit involvement in the macula.

Speaker Change: This is the data that they developed.

Speaker Change: On the left-hand side shows you the growth of the lesions into the macula 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.

Nathan Mata: 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 you'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 on 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.

Speaker Change: 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 percent would mean the entire 6-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.

Nathan: 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.

Nathan Mata: 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.

Nathan Mata: 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 eat 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 for.

Nathan: This is the two-year safety data. I want to start by saying that, over these two years of observation, there hasn't been one drug-related systemic AE 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 retinol-binding protein 4, and these residues exist nowhere else in biology in terms of their three-dimensional orientation.

Nathan Mata: I want to start by saying that over these two years of observation, there hasn't been one drug-related systemic adverse event 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.

Speaker Change: Finally, the safety data.

Nathan Mata: 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 eat 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 for.

Speaker Change: This is the two-year safety data. I want to start by saying that over this

Speaker Change: two years of observation, there hasn't been one drug-related systemic AE 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.

Nathan Mata: 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 aid data systemically tell us that basically it is very clean. What we're seeing in terms of drug related AEs are anticipated ocular events that we want to see because they're telling us we're having the intended biological effect in the retinal. And the other important thing about these AEs is they're completely manageable by accommodating to differences in light because these AEs are driven by light.

Nathan Mata: 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 aid data systemically tell us that basically it is very clean. What we're seeing in terms of drug-related AEs are anticipated ocular events that we want to see because they're telling us we're having the intended biological effect in the retinal. And the other important thing about these AEs is they're completely manageable by accommodating to differences in light because these AEs are driven by light. The first is a form of dantopsia or chromatopsia called dantopsia.

Nathan Mata: 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 drug-related AEs 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 AEs is that they're completely manageable by accommodating to differences in light because these AEs are driven by light.

Nathan: 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 drug-related AEs 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 AEs is that they're completely manageable by accommodating to differences in light because these AEs are driven by light.

Speaker Change: What we're seeing in terms of juggler AEs 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 AEs is they're completely manageable by accommodating to differences in light because these AEs are driven by light. The first is a form of xanthopsia or chromatopsia called xanthopsia. 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 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 transit-using light.

Nathan Mata: The first is a form of xanthopsia or chromatopsia called xanthopsia. 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 sort of slowly. So there'll be a period of time in which these cone photoreceptors don't have the maximal amount of vitamin A. They will electrically misfire and produce transient hues of color in the visual field, in this case, yellow; that's xanthopsia.

Nathan: The first is a form of xanthopsia or chromatopsia called xanthopsia. 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 sort of slowly. So there'll be a period of time in which these cone photoreceptors don't have the maximal amount of vitamin A. They will electrically misfire and produce transient hues of color in the visual field, in this case, yellow; that's xanthopsia.

Nathan Mata: 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 her 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 a maximal amount of vitamin A. They will allegedly misfire and produce transit use of color in the visual field. In this case yellow, that's Dantopsia. But all the kids are reporting this mild, and of course no one's left study because of this AEs.

Nathan Mata: The first is a form of dantopsia or chromatopsia called dantopsia. 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 her 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.

Nathan Mata: They will allegedly misfire and produce transit use of color in the visual field. In this case yellow, that's dantopsia. But all the kids are reporting this mild and of course no one's left study because of this AEs. Finally, the other one is delayed documentation. This is the opposite manifestation, so this is mediated when you transition from a bright environment to a very darkened environment. There will be a delay in the ability to accommodate to dim light.

Speaker Change: of color in the visual field, in this case yellow, that's xanthopsia. But all the kids are reporting it as mild, and of course no one's left to study because of this AE.

Nathan Mata: Finally, the other one is delayed documentation. This is the opposite manifestation, so this is mediated when you transition from a bright environment to a very darkened environment. There will be a delay in the ability to accommodate to dim light. This particular A.E. is actually a manifestation of the disease process. So patients with Stargardt's disease already have delayed documentation, so they're used to accommodating it. And that's probably why most of them are reporting this pharmacological mediated as mild or transient. And again, no one's left study because of this. And importantly, as I said, these A.E.s can be mitigated by moderate transitions from bright to darkened, vice versa.

Nathan: All the kids are reporting it as mild, and of course, no one's left to 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 will be a delay in the ability to accommodate to dim light.

Nathan Mata: But all the kids are reporting it as mild, and of course, no one's left school 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.

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

Nathan: 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 ADD as mild or transient. And again, no one's left unstudied because of this. And importantly, as I said, these AEs can be mitigated by moderating transitions from bright to dark and vice versa. And this has been very, very helpful for our kids.

Nathan Mata: 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 ADD as mild or transient. And again, no one's left unstudied because of this. And importantly, as I said, these AEs can be mitigated by moderating transitions from bright to dark and vice versa. And this has been very, very helpful for the report of kids.

Speaker Change: This particular A.E. is actually a manifestation of the disease process. So patients with stargases already have delayed dr. Tations, so they're used to accommodating it. And that's probably why most of them are reporting this pharmacological meeting at D.D. as mild or transient and again, no one's left studied because of this. And importantly, as I said, E.E.E.E.E.E.E.E.E.E.E.E.E.E.E.E.E by monitoring transitions from bright to dark and vice versa. And this has been very, very helpful for your four kids. I can say that in over one year of dosing in our phase three study.

Nathan Mata: This particular A.E, is actually a manifestation of the disease process. So patients with stargars disease already have delayed documentation, so they're used to accommodating it. And that's probably why most of them are reporting this pharmacological mediated as mild or transient. And again, no one's left study because of this. And importantly, as I said, these A.E.s can be mitigated by moderate transitions from bright to darkened vice versa. And this has been very, very helpful for the poor kids.

Nathan Mata: And this has been very, very helpful for the poor kids. I can say that in over one year of dosing in our phase three study, the dropout rate from these A.E.s is less than 4%. So that is that a significant night vision impairment is a more severe manifestation of the delayed documentation, 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're experiencing these A.E.s.

Nathan: I can say that in over one year of dosing in our phase three study, the dropout rate from these AEs was less than 4%, so that is very significant. Night vision impairment is a more severe manifestation of the delayed dark adaptation, where the delay is 20 minutes or more. The increasing error score on the FM100 is a more severe exacerbation of chromatopsia, and you see that in one subject.

Nathan Mata: I can say that in over one year of dosing in our phase three study, the dropout rate from these AEs was less than 4%, so that is very significant. Night vision impairment is a more severe manifestation of the delayed dark adaptation, where the delay is 20 minutes or more. The increasing error score on the FM100 is a more severe exacerbation of chromatopsia, and you see that in one subject.

Nathan Mata: I can say that in over one year of dosing in our phase three study, the dropout rate from these A.E.s is less than 4%. So that is that a significant night vision impairment is a more severe manifestation of the delayed documentation, 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're experiencing these A.E.s.

Speaker Change: the dropout rate from these AEs is less than 4 percent. So that is significant. Night vision impairment is a more severe manifestation of the delayed documentation, which the delay is 20 minutes or more. The increasing error score on the FM100 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're experiencing these AEs.

Nathan Mata: So with that now, I'll move over to the overview of the trial that Tom discussed, the Dragon 1 and the Dragon 2 Stargars 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. These are the Saki Gaki 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 2-1 randomization in the Dragon study and a 1-1 randomization in the Dragon 2. Again, principally because the Dragon 2 study has fewer patients.

Nathan: And the intermittent headaches we think can occur when subjects strain to use their visual acuity while they're experiencing these AEs. So with that, now I'll move over to the overview of the trial that Tom discussed, the DRAGON-1 and the DRAGON-2 Stargardt trials. We're showing you here an overview of those studies. These studies are essentially identical. There are differences in geography, as Tom mentioned. We have Japan involved, vis-à-vis the Sakigaki designation. Essentially, the demographics are similar except for that.

Nathan Mata: And the intermittent headaches we think can occur when subjects strain to use their visual acuity while they're experiencing these AEs. So with that, now, I'll move over to the overview of the trials that Tom discussed, the DRAGON1 and the DRAGON2 Stargardt trials. We're showing you here an overview of those studies. These studies are essentially identical. There are differences in geography, as Tom mentioned. We have Japan involved, vis-à-vis the Sakigaki designation.

Speaker Change: So with that, now, I'll move over to the overview of the trials that Tom discussed, the DRAGON1 and the DRAGON2 Stargardt trials.

Nathan Mata: So with that now, I'll move over to the overview of the trial that Tom discussed, the Dragon 1 and the Dragon 2 stargars 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. These are the Saki Gaki designation. Essentially, the demographics are similar except for that. Both studies are done double blind. There is a difference in the randomization.

Speaker Change: 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-a-vis the Sakigaki 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 two-to-one randomization in the DRAGON study and a one-to-one randomization in the DRAGON2, again, principally because the DRAGON2 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.

Nathan Mata: 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 two-to-one randomization in the DRAGON study and a one-to-one randomization in the DRAGON2, again principally because the DRAGON2 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 between 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 DRAGON1 and DRAGON

Nathan: Both studies are done double-blind, but there is a difference in randomization. We're doing a two-to-one randomization in the DRAGON study and a one-to-one randomization in the DRAGON2, again principally because the DRAGON2 study has fewer patients. But other than that, every other assessment, safety, efficacy, et cetera, is the same as the key inclusion criteria for these subjects.

Nathan Mata: We're doing a 2-1 randomization in the Dragon study and a 1-1 randomization in the Dragon 2. Again, principally because the Dragon 2 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.

Nathan Mata: 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 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 1 and Dragon 2 studies.

Nathan: So because of the similarity between these two studies and how they match the PHASE II study, and because the PHASE II study is trending quite well, we believe, or we have optimism that we'll have very promising safety and efficacy data in both DRAGON1 and DRAGON2 studies. Moving forward to geographic atrophy, to show you the trial design in GA, it is, as well, very similar to the Stargardt disease 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.

Speaker Change: So because of the similarity in these two studies and how they match the Phase II study, and because the Phase II study is trending quite well, we believe, or we have optimism, that we'll have very promising safety and efficacy data in both DRAGON1 and DRAGON2 studies.

Nathan Mata: So because of 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 1 and Dragon 2 studies. Moving forward to geographic entropy to show you the trial design in GA, it as well is very, very similar to the start our disease of phase 3 trials.

Nathan Mata: Moving forward to geographic entropy to show you the trial design in GA, it as well is very, very similar to the start our disease of phase 3 trials. The only difference in the trial design in GA is the indication, of course, to your basketrophy, 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 starter studies. Whatever we see in the starter, it could be highly predictive of what we see in GA.

Nathan: 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 could be highly predictive of what we see in GA. And a principal reason for that is that we're using the same dose, and there's a very high pathological similarity between Stargardt disease and geographic atrophy in the particular patients we've enrolled.

Nathan Mata: Moving forward to geographic atrophy, to show you the trial design in GA, it is, as well, 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 could be highly predictive of what we see in GA, and a principal reason for that is that we're using the same dose, and there's a very high pathological similarity between Stargardt disease and geographic atrophy in the particular patients we've enrolled. So with that, I'll turn it back over to Haoyan or turn it over to Haoyan for the financial results.

Speaker Change: 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 principal reason for that is that we're using the same dose.

Nathan Mata: The only difference in the trial design in GA is the indication, of course, to your basketrophy, 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 starter studies. Whatever we see in the starter, it could be highly predictive of what we see in GA. And the principal reason for that is that we're using the same dose. And there's a very high pathological similarity between starter disease and geographic hatchery in the particular patients we've enrolled.

Nathan Mata: And the principal reason for that is that we're using the same dose. And there's a very high pathological similarity between starter disease and geographic hatchery in the particular patients we've enrolled. So with that, I'll turn it back over to Halian or try it over to Halian for the financial results.

Haoyan: And there's a very high pathological similarity between Starvius disease and geographic atrophy in the particular patients we've enrolled. So with that, I'll turn it back over to Haoyan, or turn it over to Haoyan for the financial results.

Haoyan: So with that, I'll turn it back over to Haoyan or turn it over to Haoyan for the financial results. 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 increased expenses related to the milestone payment to Columbia for the completion of the phase two study and share-based compensation. G&A expenses in Q2 2024 were $1.4 million, basically the same as Q2 2023.

Halian: So with that, I'll turn it back over to Halian or try it over to Halian for the financial results. 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 finally due to increasing expenses related to the milestone payment to Colombia for the completion of the phase 2 study and share-based compensation. On GNA expenses, in Q2-2024, the GNA expenses were 1.4 million, basically the same as Q2-2023.

Juan Zhang: 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 finally due to increasing expenses related to the milestone payment to Colombia for the completion of the phase 2 study and share-based compensation. On GNA expenses, in Q2-2024, the GNA expenses were 1.4 million, basically the same as Q2-2023. On their loss, we had a net loss of 9.5 million in Q2-2024 compared to 6.8 million for the same period, Secretary.

Haoyan: 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 2022. Regarding cash, we have cash on deposit in U.S. Treasury bills of a total of $112 million. We still expect around three years of cash runway. Thank you. Back to you, Tom. Thanks, Alvin. To summarize, we've had a strong start to the first half of the year and continue to make meaningful strides in advancing cannabinoid clinical trials for Starless disease and geographic atrophy across several countries.

Hao-Wan Zhang: 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 increased expenses related to the milestone payment to Columbia for the completion of the phase two study and share-based compensation. On G&A expenses in Q2 2024, the 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 on deposit in U.S. Treasury bills of a total of $112 million. We still expect around three years of cash runway.

Haoyan: Thank you, Nathan.

Haoyan: So in Q2 2024, we had R&D expenses of $9.1 million compared to $5.5 million for the same period in 2023.

Haoyan: The increase was primarily due to an increase in expenses related to the milestone payment to Columbia for the completion of the Phase II study and share-based compensation.

Haoyan: On GMA expenses in Q2 2024, GMA 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.

Halian: On their loss, we had a net loss of 9.5 million in Q2-2024 compared to 6.8 million for the same period Secretary. We've got in cash. We have cash on deposit and U.S. Treasury bills of total $112 million. We still expect about three years cash runway.

Juan Zhang: We've got in cash. We have cash on deposit and U.S. Treasury bills of total $112 million. We still expect about three years' cash runway.

Speaker Change: Regarding cash, we have cash-time deposits and U.S. Treasury bills of a total of $112 million. We still expect around three years of cash runway. Thank you. Back to you, Tom.

Hao-Wan Zhang: Thank you. Back to you, Tom. Thank y'all.

Juan Zhang: Thank you.

Tom Lin: Back to you, Tom. Thank you.

Tom Lin: To summarize, we've had a strong start to the first half of the year and continue to make meaningful strides in advancing cannabinoid clinical trials for Starless 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 need as there is currently no treatment for SARS disease. We're also in a strong financial position with $110 million in cash and cash equipment.

Haoyan: 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 need as there is currently no treatment for SARS. We are also in a strong financial position with $110 million in cash and cash equipment. As we enter the second half of the year, we are well-positioned to execute.

Tom Lin: To summarize, we have a strong start to the first half of the year and continue to make meaningful strides in advancing to never been clinging to a powerful dollar disease and geographic entropy across several countries. We're also proud that we have received such a targeted designation in Japan, which we believe is a testament to the groundbreaking potential of this drug and the amenity to as many as there is currently no treatment for starless disease. We're also in a strong financial position with 110 million in cash and cash equivalents.

Tom Lin: Thank you. Back to you, Tom. Thank you. To summarize, we have a strong start to the first half of the year and continue to make meaningful strides in advancing to never been clinging to a powerful dollar disease and geographic entropy across several countries. We're also proud that we have received such a targeted designation in Japan, which we believe is a testament to the groundbreaking potential of this drug and the amenity to as many as there is no currently no treatment for starless disease.

Tom: Thanks, Al. To summarize, we've had a strong start to the first half of the year and continue to make meaningful strides in advancing cannabinoid-linked clinical trials for Starless disease and geographic atrophy across several countries.

Speaker Change: We are also proud that we have received the Sakigake designation in Japan, which we believe is a testament to the groundbreaking potential of this drug and the unmet need as there is currently no treatment for SARS disease.

Speaker Change: We're also in a strong financial position with $110 million in cash and cash equivalents.

Tom Lin: 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 aggregate on key milestones and look forward to conducting third of phase three internal analysis from our Dragon Study in the fourth quarter. Finally, we look forward to seeing some of you next week at the HC, when right of annual after-market conference, and hope we join our presentation on August 15th. Please also note that in September, we will also be attending conferences with HC, when right, central, dodge bank, and hope to see some of you there.

Tom Lin: As we enter in the second half of the year, we are well positioned to aggregate on key milestones and look forward to conducting third of phase three internal analysis from our Dragon Study in the fourth quarter.

Tom Lin: As we enter the second half of the year, we are well positioned to execute on key milestones and look forward to conducting the third phase three interim analysis from our DRAGON study in the fourth quarter. Finally, we look forward to seeing some of you next week at the HCE Wainwright 4th Annual Ophthalmology Conference. And we hope you will join us for our presentation on August 15th. Please also note that in September, we will also be attending conferences with H.C. Wainwright, Kentor, and Deutsche Bank, and we hope to see some of you there. Thanks again for joining this call, and now we will open the call for questions.

Speaker Change: As we enter the second half of the year, we are well-positioned to execute on key biostars and look forward to conducting PIRTL phase 3 interim analysis from our DRAGON study in the fourth quarter.

Tom Lin: Finally, we look forward to seeing some of you next week at the HC, when right of annual after-market conference, and hope we join our presentation on August 15th. Please also note that in September, we will also be attending conferences with HC, when Right, Central, Dodge Bank, and hope to see some of you there.

Speaker Change: Finally, we look forward to seeing some of you next week at the HCE Wainwright 4th Annual Ophthalmology Conference, and hope you join our presentation on August 15.

Speaker Change: Please also note that in September, we will also be attending conferences with HCA Wainwright, Kentor, Deutsche Bank, and hope to see some of you there. Thanks again for joining this call, and now we will open the call for questions.

Operator: Thanks again for joining this call, and now we will open the call for questions.

Operator: Thanks again for joining this call, and now we will open the call for questions.

Speaker Change: Thank you for joining us today.