Good morning, and welcome to Ocugen's webcast to discuss the top-line 12-month results from phase II ArMaDa clinical trial evaluating OCU410 for geographic atrophy, or GA, secondary to dry age-related macular degeneration. Please note that this call is being recorded. All participants are in current listen mode only. Following the speakers' prepared remarks, we will open the line for questions. I would now like to turn the call to Tiffany Hamilton, Ocugen's Head of Corporate Communications. Please go ahead. Hello, everyone. Joining us today are Dr. Shankar Musunuri, Chairman, Chief Executive Officer, and Co-founder of Ocugen, Dr. Huma Qamar, Chief Medical Officer of Ocugen, and our distinguished clinical investigators, Dr. Lejla Vajzovic, MD, FASRS, Professor of Ophthalmology, CME Program Director, Duke Department of Ophthalmology, Duke University School of Medicine, and Chair, Ocugen Scientific Advisory Board. Dr. Jay Chhablani, MD, Professor, University of Pittsburgh and UPMC Vision Institute, and President of NetraMind. We are also pleased to be joined for the Q&A by clinical investigators and the Ocugen management team. Clinical investigators include Dr. Victor Gonzalez, MD, Retinal Surgeon, Valley Retina Institute, McAllen, Texas, faculty at University of Texas Rio Grande Valley. Dr. Syed Shah, MD, Vice Chair for Research and Digital Medicine, Director of Retina Service, Department of Ophthalmology at Gundersen Health System La Crosse, Wisconsin. Ibn Al-Haytham Professor, Department of Ophthalmology, Aga Khan University. Finally, Dr. Arun Upadhyay, PhD, Chief Scientific Officer, Ocugen. A replay of this webcast, along with the accompanying slide presentation, will be available on the Ocugen website after the event. I'll now turn the call over to Dr. Shankar Musunuri. Thank you, and good morning, everyone. Today, we are pleased to share top-line 12-month data from the phase II ArMaDa trial of OCU410 in GA, an advanced form of dry age-related macular degeneration. These results mark an important milestone for Ocugen as we advance a potential first-in-class modifier gene therapy designed as a one-time treatment for patients with GA. Here are our forward-looking statements. We have organized today's webcast to provide a comprehensive view of the program. I will begin with a brief overview of Ocugen's mission and the unmet medical need in GA. Dr. Huma Qamar will review the clinical design, safety, and tolerability profiles. Dr. Lejla Vajzovic and Dr. Jay Chhablani will then review the phase II ArMaDa trial top-line 12-month efficacy results. We will then move into the Q&A with clinical investigators, Dr. Victor Gonzalez and Dr. Syed Shah, and Ocugen scientific officer, Dr. Arun Upadhyay, followed by closing remarks on OCU410's upcoming milestones. Ocugen is focused on transforming the treatment of serious eye diseases through innovative gene therapies. Leading ophthalmic gene therapy treatments, our goal is to address major causes of blindness with potential one-time modifier gene therapies that target the underlying biology rather than simply slowing a single pathway. In GA specifically, patients today face a lifelong burden of frequent intravitreal injections with therapies that act only on the complement system. Our vision with OCU410 is different. A single subretinal administration designed to modulate multiple disease-relevant pathways and provide durable protection of retinal structure and function. To set the stage for the phase II data, let me briefly review the GA patient clinical representation and OCU410's mechanism. OCU410 is built on a novel mechanism of action that we believe has the potential to disrupt the current treatment paradigm in GA. Today, patients with GA face a progressive, irreversible loss of retinal tissue that ultimately affects central vision, and this can translate into difficulties with reading, recognizing faces, and performing everyday tasks. Once GA develops, the disease continues to progress, and the vision loss cannot be recovered. There are an estimated 2-3 million patients with GA in the United States and Europe. Importantly, this number is expected to increase significantly as populations age. Currently, approved treatments target only the complement pathway and require six-12 injections per year indefinitely, leading to substantial burden and significant dropout rates in real-world practice. There remains a clear need for a differentiated therapy that addresses all key disease pathways, including complement, inflammation, oxidative stress, and lipid dysregulation, while reducing treatment burden. OCU410, through RORA modulation, was specifically designed to address that need. It is a modifier gene therapy that potentially delivers the RORA gene using an AAV5 vector that targets retinal pigment epithelium and photoreceptor cells using a single subretinal injection. This multi-pathway profile distinguishes OCU410 from complement-only inhibitors that are on the market today and provides a strong biologic rationale for the clinical effects we are seeing. The phase II ArMaDa data demonstrates that OCU410 may offer meaningful advantages over currently approved therapies for GA. First, OCU410 is designed as a potential one and done subretinal gene therapy. In contrast to the six-12 intravitreal injections per year required with the current standard of care complement inhibitors. Real-world data already shows up to 40% dropout rates with the current intravitreal therapies, highlighting the impact of injection burden and treatment fatigue on long-term adherence. In the ArMaDa trial, we observed promising data in both phase I and phase II, including suggested structural preservation at the level of the GA lesion and preservation of the ellipsoid zone, which correlates with visual function. Importantly, the safety and tolerability profile has been favorable to date, with no serious adverse events or adverse events of special interest deemed related to OCU410. On this slide, you will see a comparison of mean change in GA area from baseline relative to natural history reported for lesion growth in published data from OAKS and DERBY and GATHER2 studies. OCU410 shows a 31% reduction in lesion growth versus natural history compared with 15% and 19% reductions reported for currently approved therapies, respectively, and a 31% reduction in our treated group versus control with the ArMaDa study. These findings underscore the potential of OCU410 to deliver robust lesion control with a single administration and redefine the landscape of GA treatment globally. I'll now hand it over to Dr. Huma Qamar to discuss the phase II study, clinical design, and study results. Huma. Thank you, Shankar. The phase II ArMaDa trial was designed to evaluate the safety and efficacy of OCU410 in patients with GA secondary to dry AMD. We enrolled subjects 50 years and older with GA lesions within the foveal or non-foveal region, a total GA area between 2 mm² and 20.5 mm², corresponding to approximately 1-8 disc areas, and a baseline BCVA of at least 21 ETDRS letters. Patients were randomized 1:1:1 to receive a single subretinal administration of OCU410 at a medium dose of 1 × 10^10 vector genomes per eye, a high dose of 3 × 10^10 vector genomes per eye, or no treatment in the control group. Each injection volume was 200 µL. Of note, choroidal neovascularization in the fellow eye was not exclusionary, and patients with prior exposure to pegcetacoplan or avacincaptad pegol were eligible following a three-month washout. The primary endpoint was change in GA lesion size at 12 months, measured in square millimeters by fundus autofluorescence, an FDA-accepted structural endpoint used in recent GA registration trials. Exploratory endpoints included ellipsoid zone or EZ preservation on OCT, a key biomarker for photoreceptor integrity, which correlates with visual function. Let me now show you who we enrolled and how well the groups were balanced at baseline. Starting with the table on the left, this slide summarizes baseline characteristics for the medium dose, high dose, and control groups. All participants were older adults with mean ages of about 75 years of age in the medium dose arm, 78 years of age in the high dose arm, and 77 years of age in the control arm. Patients ranging from 60-88 years of age were enrolled in this trial. Mean baseline GA lesion size was roughly 8 mm² -9 mm², and the corresponding square root transformed lesion size was about 2.8 mm -2.9 mm, consistent with lesion sizes enrolled in pivotal trials for currently approved therapies. Foveal and non-foveal lesion involvement was broadly similar between arms, and most patients were pseudophakic, reflecting typical real-world GA demographics. Baseline BCVA averaged around 57 ETDRS letters in both OCU410 dose groups and approximately 47 letters in the control group, with a mix of unifocal and multifocal lesions. Overall, these well-balanced baseline characteristics support the interpretation that subsequent differences between arms are more likely related to treatment effects than to initial imbalances. Turning to the clinical trial flow on the right, 51 subjects were dosed and allocated approximately equally to control, medium dose, and high dose groups. In the control arm, 17 subjects were enrolled, with four later categorized as lost to follow-up. In the medium dose arm, 17 were enrolled with 1 lost to follow-up. In the high dose arm, 17 subjects were enrolled, one experienced a serious adverse event assessed as unrelated to OCU410, and two additional subjects were excluded from the efficacy population, one for not meeting lesion criteria and one due to an inevaluable GA lesion. After these exclusions, 45 subjects contributed to the overall safety population. Of these, 42 met the primary overall efficacy criteria based on pre-specified lesion size thresholds, forming the main efficacy analysis set. A modified intent-to-treat population of 39 subjects used slightly narrower lesion size boundaries for more robust analysis, and the same lesion size criteria were used for approved clinical trials. Finally, 31 subjects met the potential phase III intent-to-treat criteria defined by higher baseline lesion sizes, providing an early look at how the therapy may perform in a population aligned with anticipated phase III eligibility. For context, phase I was a dose ranging, dose escalation portion of the OCU410 clinical trial designed to identify a safe and biologically active dose range. We established the maximum tolerated dose in phase I. Phase II builds on the clean profile observed in phase I. Across 45 subjects, there were no serious adverse events and no adverse events of special interest deemed related to OCU410. We closely monitored adverse events, serious adverse events, and adverse events of special interest including endophthalmitis, retinal detachment, retinal vasculitis, and vascular occlusion, choroidal neovascularization, intraocular inflammation, ischemic optic neuropathy, and treatment emergent serious or serious adverse events. In both the medium dose and high dose OCU410 groups, there were no treatment-related serious adverse events or no treatment-related adverse events of special interest reported today. One case of mild intraocular inflammation was reported in the high dose cohort and was deemed related to the surgical procedure and resolved with standard management of care. CNV events reported as adverse events were assessed by the independent data and safety monitoring board and related to natural history of the disease and study procedure. Overall, these findings support a favorable safety and tolerability profile for a one-time subretinal gene therapy in this older GA population. I'll now turn it back to Dr. Lejla Vajzovic and Dr. Jay Chhablani to review the efficacy data. Thank you, Huma. This slide summarizes the magnitude of treatment benefit we see with OCU410 at 12 months. On the left, you can see the overall analysis for all evaluated eyes with baseline lesion area between 2 mm² and 20.5 mm². The red bar represents the control group, and the orange bar shows all OCU410-treated eyes, combining the medium and high doses. At 12 months, treated eyes have smaller increase in geographic atrophy lesion area compared to the control, and corresponding to the overall 80% reduction in lesion growth versus control. The middle panel narrows in on lesions between 2.5 mm² and 17.5 mm², which as mentioned earlier, is the criteria that captures the majority of patients in both ArMaDa and the prior pivotal GA trials that supported approval of currently available therapies. Here we separate out medium dose in green and high dose in blue with natural history and control bars for the context. In this range, the medium dose group shows about 31% reduction in lesion growth versus control, and the high dose group shows about 16% reduction at 12 months using mean change in the GA lesion area from baseline. For context, the gray box highlights that currently approved products typically demonstrate roughly 15%-22% lesion growth reduction. OCU410 is delivering approximately 2x greater anatomic benefit in half the time after a single treatment. On the right, we focus on subgroup with a baseline lesion 5 mm² -17.5 mm² an interval that includes most evaluated subjects in ArMaDa and in other contemporary geographic atrophy programs. This is where the treatment effect becomes even more pronounced. In this subset, OCU410 at the medium dose achieves 33% reduction in lesion growth versus control at 12 months, and the high dose shows 31% reduction against the mean change in the GA lesion area mm² from the baseline to month 12. Now, taken together across overall population and establishing within this 5 mm² -17.5 mm² window, a single subretinal administration of OCU410 consistently slows GA progression versus control. Most patients in current GA trials fall within this range, which provides a strong evidence base for our planned phase III inclusion criteria. In summary, this data demonstrated efficacy of OCU410 across multiple dosage levels. However, medium dose was observed to be optimal dose for GA patients across wider demographics. This dose will be selected for further clinical development in pivotal phase III confirmatory trial. I will now hand it over to Dr. Jay Chhablani. Thank you, Lejla. Here you can see the efficacy results from phase II demonstrate a consistent treatment benefit on both structure and a structure parameter that correlates with visual function. On the left side of this slide, you see the primary endpoint that is change from baseline in GA lesion area at month 12. In the medium dose OCU410 group, we observed a statistically significant reduction that is P less than 0.05 in lesion growth that is 31% compared to control using mean change in the GA lesion area from baseline to month 12. On the right, you see the exploratory endpoint of ellipsoid zone area loss, which correlates with the photoreceptor integrity and visual function. The EZ represents the inner segment-outer segment junction of photoreceptors as visualized on spectral domain OCT imaging. This is a critical anatomical marker of photoreceptor health and integrity. Loss of ellipsoid zone indicates photoreceptor degeneration and death. Preservation of the ellipsoid zone indicates maintained photoreceptor structure and by extension, likely maintained or improved photoreceptor function. Here, treated eyes showed a 27% slower rate of EZ loss compared to control, indicating preservation at the level of the outer retina, which correlates to visual function. These findings are consistent with OCU410's mechanism of action and our preclinical findings regarding RORA's neuroprotective and antioxidative mechanisms, providing clinical evidence that OCU410 can preserve photoreceptor structure in GA patients. The ability to protect both photoreceptors and RPE with a single therapeutic intervention underscores the advantage of our multi-path pathway targeting approach. We are not just addressing one aspect of GA pathogenesis. We are supporting the health and survival of the entire photoreceptor RPE unit. In conclusion, medium dose not only showed effect on GA lesion growth reduction, but also demonstrated preservation of EZ layer, which correlates with visual function. Based on this data, medium dose will be chosen as an optimal dose for phase III confirmatory trial. I will now hand it over to Lejla. Thank you, Jay. Another way to look at treatment benefit is through responder analysis based on different reduction thresholds in GA lesion growth. On this slide, we show the proportion of treated patients who achieved at least 10%-50% reduction in lesion growth compared to controls and natural history. More than half of the subjects treated, specifically 55%, achieved a reduction of at least 30%. The median reduction across treated subjects was approximately 33%. Responder rates at these thresholds were statistically superior to natural history. These responder data underscores the robustness of treatment effect at the individual patient level and support the potential for OCU410 to deliver meaningful, clinically relevant slowing of GA progression. I will now ask Shankar to walk you through the next slide. Thank you, Lejla. As you have seen, we believe OCU410 has the potential to create a new standard of care for patients with GA. It is a first-in-class RORA-based gene therapy designed to support central retina and photoreceptor integrity through a multi-pathway mechanism, targeting drusen, inflammation, oxidative stress, and complement activation. The phase II ArMaDa results demonstrate a compelling efficacy profile, including a 31% reduction in GA lesion growth and a 27% slowing of ellipsoid zone loss, alongside a favorable safety and tolerability profile. By offering a one-time treatment, OCU410 has the potential to eliminate the chronic treatment burden associated with monthly or every other month intravitreal injections and to reduce treatment attrition driven by patient fatigue. We are incorporating these learnings into an optimized phase III trial design, including targeted GA lesion size window for vision preservation, and an adaptive design powered at over 95% with approximately 300 patients globally. We're targeting initiation of the global phase III program in the third quarter of 2026, subject to regulatory alignment, and we look forward to working with the investigators and broader retina community as we move OCU410 into late-stage development. You have now heard the key elements of phase II ArMaDa trial data, a favorable safety profile, robust structural and mechanistic signals, and clear rationale for dose selection and phase III design. To round out the discussion, we have asked our investigators to share their perspectives on what these results mean in the context of current clinical practice. Now we will open the line for Q&A. Thank you. We are now opening the floor for question and answer session. If you'd like to ask a question, please press star followed by one on your telephone keypad. That's star followed by one on your telephone keypad. Your first question comes from the line of Robert LeBoyer of Noble Capital. Your line is now open. Thanks for taking my question and congratulations on this data. Arun's magnificent data, the ArMaDa trial. I knew it all along. My question has to do with the patient population and the patients that would be candidates for the treatment. The patient population is very large, and I was wondering which patients would be selected and if there was a target or would it be all GA patients? Would you wait until the AMD progresses to the point where you have GA or would you treat earlier? Just, I was wondering if you could give some perspective on how this would be used in practice after approval. This is Huma Qamar. Thank you for your question. In terms of phase III, this will be first of all global trial, and we will be having geographic atrophy. That's the clinical presentation of geographic atrophy secondary to dry age-related macular degeneration. Of course, the most important criteria is around the diagnosis of 50 years of age and older, and it also depends on the clinical signs and symptoms. That would be all comers who are presenting with the geographic atrophy with the foveal and non-foveal lesions. At that time, we will have a pre-specified criteria on the lesion size, and that would be something that would be unique to this phase III trial that we are looking into in future. Okay. Thank you. Can you give the expected enrollment criteria or, well, more the enrollment size of the phase III? Yes. As we have stated, there will be approximately 300 patients globally, and we will have a unique adaptive design, which will be powered. The trial will be powered at 95%. Great. Thank you very much. Your next question comes from the line of Michael Okunewitch of Maxim Group. Your line is now open. Hey, guys. Thank you so much for taking my questions today. Congrats on the really great-looking data here. Thank you. Um. Thank you, Michael. Go ahead. Just to start things off, there seems to be quite a difference in performance, in particular for the high-dose group when you exclude those patients with less than the 5 mm² lesion size. Could you provide a bit of color on why this might be, what might be more challenging about those patients with the smaller lesions? Yes. I think it has more to do with the few outlier in the high-dose group, I would say. If you look at, you know, cut-off criteria, we are talking about with more than 5 mm² and less than 17.5 mm². Few outlier present in the high-dose group at the extreme were basically impacting the data readout. But on top of it, there are also, like, confounding factors, you know, related to some of the patients', you know, medical history. As well as, you know, if you look at our preclinical published data, I think purpose of this whole phase II study was to understand and find the optimal dose. In preclinical study, we also noted that medium dose was kind of optimal dose, and this molecule does demonstrate a bell-shaped curve for dose response. If you take everything together, it appears that medium dose is optimal dose for the GA patients. High dose may be slight towards tapering end, and the few outlier and confounding factor taken together may have led to the lower, slightly lower efficacy in high-dose group compared to the medium dose group. That's our analysis. Thank you. I appreciate the additional color. Just one more for me, and I'll hop back into the queue. Yeah. I think it's pretty obvious what the patient benefit here is for a one-time therapeutic. But have you had any feedback from KOLs that you might need to clear a higher bar for efficacy or long-term safety to make them comfortable given just how novel the modifier gene therapy modality is? I'll take this question, and thank you for the question. In terms of safety, I will say that the safety and tolerability profile of these patients was very favorable. We have, if you look at it, the lower limit was in the 60s for this patient, and the higher limit was 88 years with comorbidity. We have not seen any adverse events or, you know, serious adverse events, or adverse events of special interest. Also, in terms of, I'm not concerned about the safety and tolerability profile at all, because the phase I was the dose ranging, dose escalation portion of the study where we established a maximum tolerable dose. Also from efficacy, if you look at it, we have foveal and non-foveal lesions, and majority of the efficacy was coming from, like, the aggressive lesions as well. This is a not only from safety perspective and tolerability perspective, but also from efficacy, we address those concerns. I don't think so we have any concerns regarding moving forward in terms of the safety and tolerability database for these GA patients. One more thing I would like to add, and I would like to acknowledge our surgeon, Dr. Lejla Vajzovic, and all the other investigators as well. We have a very standardized surgical manual and procedures. We have a standardized volume. We have a standardized dose, so what we were giving in the medium and high dose. In fact, when we did look at that, there were no adverse events or serious adverse events as well. We have also added very standardized surgical procedures. We will be following the same across. This has been across all our gene therapy programs, and we are very confident that there will be no safety or tolerability issues moving forward. Michael, just to, in addition to Huma's comments, very nicely put it together, I'd like to add there is a significant unmet medical need across the globe for this disease. Remember that. When we're showing a treatment benefit within a year, I mean, obviously agencies will work with us. That's anticipation, and they're not going to extend. In the safety perspective, all our clinical trials for gene therapies, FDA mandates, even it's a one-year needed for, let's say, total trial for registration trial, we have to monitor the patients for five years. That means just like we did with the OCU400 other programs, by the time we file for our potential approval BLA in 2028, if everything goes according to plan, we will have at least three years of data from phase I and data from phase II, and that will be supporting the safety of the molecule. Michael, if I may add. Yeah, go ahead. Please. Sorry. Go ahead, Lejla. Thank you. This is Lejla Vajzovic. Thank you for that question. I'm excited to see overall positive results as early as one year in overall what I would say a small group of patients. Yes, this is a very robust trial for gene therapy in phase II. Geographic atrophy is a heterogeneous disease with really, you know, various progression rates that we see among patients. I think that's the biggest challenge we have currently with geographic atrophy in general. To see in this diverse patient population that were included in this trial to see actually positive results in both doses is encouraging to me. Yet it's exciting to see the medium dose did well better than higher. Overall, I'm encouraged to see early positive results at one year. Thank you. You know, this is, Victor Gonzalez. May I make a comment also? Yeah. That's a great question. Yeah, go ahead. I think, you know, as someone in the trenches taking care of these patients, you know, the excitement, aside from all the great results that you had presented here is the fact that it meets one of the biggest concerns and issues that I have, and that's the treatment burden on these patients. I cannot give the treatment benefit to these patients if the patients don't show up for the current application of medications. The fact that I can take care of these patients, give them a treatment once and have the benefit over that year is going to address, you know, the biggest concern that's happening out there. There's a 40%+ dropout on these patients because they get burned out from having to require all these recurrent treatments. The ability to do this with a one-and-done treatment like this one, is going to address that big unmet need, and that is getting the treatment effect, getting the medication to these patients. Thank you for your question. Thank you. I appreciate all the additional commentary. I'm looking forward to seeing more data come out from this program and the others. Thank you. Thank you. Your next question comes from the line of Leland Gershell of Oppenheimer. Your line is now open. Good morning, and great to see these data and thanks for taking our questions. A couple from us. First, just a question that's really directed at the specialists who've joined the call. The data clearly supports OCU410's potential in GA and could have considerable market opportunity given the number of patients with this disorder. Wanted to ask, given the subretinal injection versus the intravitreal which is how the currently approved treatments are delivered. I want to ask kind of how you see the pace of adoption given the need for maybe training for subretinal injections. Do you think that patients would be referred to specialists and centers who have expertise in that? Do you think that the ability to give those injections will expand as this drug becomes available again, given the much larger size of this population versus the other two opportunities that the company is going after? Also want to ask the company what's your plan for continuing to follow these patients beyond 12 months and when might we see a incremental follow-up? Thank you. I would first of all direct the question to either Lejla, Dr. Shah or Victor. Any of you guys can answer that. That's first. The second part I will answer later on. Yeah. Thank you. I'm happy to take on the question regarding surgical approach versus intravitreal injection and benefits and related to that. Now, you know, yes, intravitreal approach is something we're routinely doing and quite, you know, commonly a retina specialist is doing quite a few injections throughout the week for patients. So we are very comfortable and obviously it's in-office procedure approach. Now, it has been mentioned that with current therapies, repeating injections once a month to every other month definitely presents its challenges with follow-up rates. Just keeping up with that treatment burden is definitely troublesome. When it comes to developing a one-time approach surgically, yes, any surgery comes always with the risks. I think in this day and age, there has been across Ocugen and other programs, quite a few investigations and potentially approved products in the near future that will very much give us this option of gene therapy delivery in common retinal diseases. Through all of these programs across all the companies, we now have more than, you know, hundreds of clinical surgeons involved in U.S. and globally that have been delivering these therapies through trials for patients. Patients overall, from all the reports we're, you know, getting, are doing quite well. To answer your question, the challenge was this gonna be a specialty referral to, you know, a surgeon who's just gonna be doing that? I think I believe the answer to that will be no. I think any retina specialist will feel comfortable doing this procedure. I think more the logistics would be whether, you know, that therapy would be, you know, available at that hospital they're performing the surgery at. The surgical steps are very, I would say at this stage, routine for all of us, and then adding the gene therapy product is not that uncomplicated of a process. Yeah. This is Dr. Shah. I would like to add as well, given I have a large catchment area of rural America or Wisconsin for that matter, I cannot tell you how many patients when they come in with GA, and you offer them the standard of care, and they just back out because traveling for them from half an hour, one hour, two hours away, having somebody drive them because they cannot drive themselves is a big challenge. If you have something like this, which is one and done treatment, I think there'll be so many patients just in this rural catchment area I treat would be very amenable to treatment, even if it's subretinal injection. This is across the board to all injections. You know, people do not like monthly, every other month injections because not just the patient who has to come in. Remember, these patients cannot see very well, so they have to have someone in their family take off and bring them in, and that's a whole day gone for them. If you offer them something and they actually ask that, "Is there anything else you can give me which is one or twice a year or something like that?" How many patients? There are plenty of patients like this. I think, enrollment and adoption of treatment, which is less burdensome than what we have right now, would be a great thing for our patients. You know, this is Victor Gonzalez. Just to make a comment to you. I'll tell you, I'm gonna date myself, but this was exactly the same question that we had when we first started doing intravitreal injections. Everybody first was horrified to think that we would be doing that and would the patients really come back. I think the retina community, noticing the benefits that were created, you know, was able to adapt this. As Lejla and everyone has mentioned, there is a learning curve, but I think the environment is such that there's so many of these subretinal options coming that it'll become similar to an intravitreal injection. People will adapt it and there'll be, you know, the training that's necessary to be able to deliver these new therapies. Your next question comes from the line of Swayampakula Ramakanth of H.C. Wainwright. Your line is now open. Good morning. This is RK from H.C. Wainwright. Thank you very much for doing this call. It's obviously, you know, great data. A couple of quick questions from me, one on the data and one just on a high level thought. On the data itself, regarding the EZ, the method by which the EZ was measured, EZ preservation was measured. You know, you have a competitor who says in the central 1.5 millimeters, they have a 59% preservation of the EZ region, and when we compare that against your 27%. How do we think about that? Is that because you're looking at the entire macula or you're looking at a certain subfield? I will direct that question to Jay. Jay, would you like to take that question? Yeah. Thank you. Thank you so much. Very interesting question. I think that I would say the jury is still out that, you know, which area on the GA pretty much defines the vision. I would rather be more interested to understand that, you know, which area of the GA in the macular region pretty much defines the functional vision. I think that the central one millimeter definitely plays an important role, but so far we haven't done the zonal analysis for this data. Because I was primarily involved in the EZ analysis of this data. What we learned, which we could not share in this dataset now, is that, because of time limitation, the patients who did not have foveal involvement, they actually had a significant benefit of both EZ preservation and hopefully corresponding to their functional vision, as we believe that EZ could relate with the functional vision. We will be able to share more information on the central and the paracentral area. EZ is certainly something becoming a very important anatomical biomarker which corresponds with the functional benefit. Thank you for that. The next question is just trying to understand the benefits of this therapy and timeline. What am I saying? You know, if you consider the sizes of the lesions, it looks like the smaller lesion sizes did not get as much benefit as the medium to large size lesions, plus considering the heterogeneity of the disease, and you are only taking a 12-month time point here. If we get to see additional time points, you know, would this treatment track to better benefit either depending on the size of the lesion or the time spent on the disease or the time point that you are looking at? I'm just trying to understand how, as the disease progresses, does the benefit get better? RK, I'll take that, and if anyone has additional comments, they can chime in. In terms of your question about the lesions, first of all, we had all foveal and non-foveal. Our criteria was around 2.5 mm² -20.5 mm². We have demonstrated different graphs, and the reason for that was if you look at it as a bifurcation between 5 mm² -17.5 mm², as well as because the mean lesion size in all the approved pivotal trials was between 7.02 mm² -8.03 mm². We also looked at the smaller lesions as well. However, we had two doses that we're looking into it, and the optimal dose is the one that performed regardless of the lesion size across all groups. Of course, the purpose of those double graphs, triple graphs was to show various scenarios and pictures in terms of lesion size and also the dose response to that. We have addressed that. The purpose of this trial was also to find the optimal dose, which we did it, and that's what we anticipated, that we will have one optimal dose, and that's what we picked up. In terms of the 12 months, that's the standard, you know, duration of the trial, and that's what we have done here. In addition, RK, I mean, we'll always monitor patients. We have obligation, you know, with FDA and agencies, and also ethically, we would like to continue to monitor patients. Typically, all gene therapy trials for five years, as I mentioned before. That means the phase II data, we got one-year data now. We'll continue to monitor by 2028, three years. As we monitor them for two years, second year, third year follow-ups, the data will be available at the time of submission. You will have some durability data from early-stage clinical trials with the BLA. Thank you. Thanks for taking my question. Your next question comes from the line of Elemer Piros of Lucid Capital Markets. Your line is now open. Yes. Thank you. Good morning. Shankar, just to reiterate your last comment. You would have efficacy measures taken at 24 months, 36 months, et cetera. Is that correct? As a part of the safety, we'll be monitoring patients. Key measures. Okay. I'd just like to verify that your phase III enrollment criteria would it be narrowed down to the 2.5 mm² -17.5 mm² baseline size? Yes. Yes. Okay. Yes. The efficacy measures will also be included in the follow-up. That is correct. The patients will be coming not only for safety, but of course their examination will include the efficacy parameters. Yes. Thank you very much, Huma. That's all what I had. Your next question comes. Go ahead. Yeah. I would like to add one thing. Even though you run the trial, like, you know, even for currently approved therapy between 2.5 mm² -17.5 mm², however, like in a clinical practice, you know, every GA patient get the treatment. Yeah. It doesn't put any restrictions on the label. Label doesn't, you know, yeah, going to carry different size. Yeah. Yeah, that's right. Next question. Your next question comes from the line of Daniil Gataulin of Chardan Capital. Your line is now open. Hey. Hey, good morning, guys, and thank you for taking my question and congrats on those data. A few questions from me. First on the dose response. Do you think it was driven primarily by a couple of outliers, or is there another hypothesis why medium dose performed better than the high dose? Daniil, this is Arun. There are two aspects. Definitely outliers did contribute to it. But in addition to that, we also believe that the pharmacological response, what I just mentioned briefly, that bell-shaped dose-response curve. In our preclinical study also, we noted that, you know, certain doses were optimal doses where we saw the maximum benefit. And if you go across both lower or higher end of that dose, then you see some drop in the overall efficacy. Maybe in this clinical setting, whatever lower response we are seeing for high-dose group, it is not just attributed solely to outliers. Yeah, they are major drivers, but on top of it, the pharmacological dose-response curve has also contributed to that lower efficacy. Okay. Gotcha. Okay. My other question is with respect to vision. Did you collect BCVA data, and do you anticipate sharing those results? Daniil, this is Huma. Yes, we did collect the visual acuity, and as you know, with this population, and with the LLVA. With the LLVA it's gonna be like it takes 18 to 24 to 36 months to show the maximum benefit. The BCVA was within, you know, in any single subretinal injection, is kind of like 15-20 days and also up to three-four months, can be fluctuating. However, LLVA, as we have seen and consistently demonstrated in our previous gene therapy trials as well, the durability happens around 24 months and more. That is why we have ellipsoid zone analysis, which is structural and anatomical factor or biomarker, which is correlating, as Jay has rightly said, with visual function. Got it. Makes sense. My last question is, you mentioned that, you, the inclusion criteria are open to patients who have previously taken complement inhibitors. What fractions- Mm-hmm. Of those patients were in your trial, and did they perform any different? Yes. We did have a three-month washout period with, you know, the approved therapies. Approximately 10%-12% of the population was that. Okay. Did they have any different results versus those who are naive? Their safety was outstanding, and those are also part of the analysis here, the efficacy analysis. They contributed. CNV was also not exclusionary in the fellow eye. That's good that, you know, even naive or patients who have taken complement or any other approved therapies have contributed to the efficacy profile here. Got it. Okay. Excellent. Thank you very much, and again, congrats on the data. Thank you. Our final question comes from the line of Whitney Ijem of Canaccord. Your line is now open. Hey, guys. Thank you for taking our question. This is Angela Qian on for Whitney. We realize it's currently relatively small numbers here, but is there anything in terms of baseline characteristics that you've been seeing in the better responders, that might help enable you to enrich a pivotal population? Yeah, it is a small population, but actually, if you look at the inclusion/exclusion criteria of this trial, this was approved, consistent with the approved therapies as well. In terms of the baseline characteristics, we do not see any differences, and this is what we have represented here. Whitney, I think just to clarify, I mean, again, we cannot compare the population in genetic medicine trials with other therapies, other modalities. There are many products which got approvals with 35 patients. Typically, when you see something in gene therapies, you go, you can go back and look at the data, the trends continue. Even the small population gives robust responses. That'll continue, and you'll see it in the larger population too. Got it. Thank you. To clarify, are we correct to think that you're using the high dose in the Stargardt trial? If so, what was the rationale there? No, we are not using high dose in Stargardt. No. We have, for pivotal study, chosen the dose between medium and high dose, and it is a different indication. If you look at our phase I Stargardt trial, the dose levels are different in that study compared to the dose levels in the GA because they are two different diseases. Okay? No, they're not similar. They're slightly different approach. I can add that as well because we have a pediatric population in the phase II/III, and Stargardt is primarily the disease of the pediatric population as well. We have chosen between the medium and the high dose with a standardized volume. Got it. Okay. Maybe last one on the Stargardt. Looking ahead to the interim this year, can you just remind us what you expect to share externally? Yes. This will be the masked interim analysis for 24 subjects, 16 in the treatment arm and the control, but it will be all blinded data. As we have been consistently showing our lesion size reduction data, we have recently shared ellipsoid zone and visual acuity. It would be somewhat around those parameters that will be available in the mid-year. Whitney, I think just to clarify, it's the outcome of the results. Again, how much we can share with the market, as she said, it's still a blinded study. The goal is to look at the DMC, the Data Monitoring Committee output will be discussed with FDA. The outcome is important for the trial. Outcome means adaptive design allows us to de-risk any risk to the clinical program because you have a true control group we'll be able to compare. What are the potential outcomes? You know, if the predictive analytics show you're going to hit it at 12 months, no change for the trial. That means top-line results are going to come out in the second quarter of next year, and following that, we'll file the BLA. Second option is, yeah, you need to adjust N up. That's an option. FDA also gave us third option, instead of adjusting N, sometimes, when you have these retinal degenerative diseases, especially orphan diseases, and based on the natural history, you can also extend the last time point instead of 12 months to 16 months. All those options are available to us, and we'll be closely working with FDA before we give any information to the market. Got it. That is helpful. Thank you guys so much. Now we can. Thank you. Open it for our KOLs, for any final comments. Victor, Shah, Lejla, or Jay, any final comments, you're welcome to say so. I just wanna make one comment. Hi. Victor, go ahead. No worries. No, I was just gonna say, you know, just wanna congratulate you and, you know, really excited about, you know, having the prospect of this drug. You know, again, as I mentioned, this addresses one of my biggest unmet needs right now, and that's the undertreatment of patients because of the dropout, you know. With the ability to have a safe one-time application of this treatment, I think I can really benefit my patients a lot more than I have currently. Thank you all. Thanks. Thank you. Yeah. Hi. This is Jay. I just wanted to make a comment and just to congratulate you all for an excellent study and, you know, excellent results so far. I would just say and kudos to Ocugen team that they are taking the right step to really bring the outcome measures. I'm very excited about the EZ preservation. We are really hoping that, you know, this will lead to a very useful functional outcome for our patients. Again, this is a single subretinal therapy which will really take away the burden of monthly injections from our patients, and we look forward to get started with phase III and eventually the approvals. Congratulations. Yeah. Yeah. This is Lejla Vajzovic. Right there. I'll add as well. Thank you to Ocugen team for leading really exciting program. Similarly from physician perspective, I am excited to see these early safety and efficacy results which are quite promising. We definitely need better solutions for our patients and having an option where we can provide a one-time delivery approach looks very promising. I'm excited about these early results, and thank you for leading such exciting program. Yeah. This is Dr. Shah. I would also like to add thank you, everybody for such a wonderful program, and I can't tell you enough that in the rural areas where there's a huge amount of geographic atrophy population, how beneficial this would be both on the burden as well. I wanna address one more thing which pertains to delivery of this, vector. We in a small town, Wisconsin, are able to do it because not just a surgeon, you have to have the ancillary support for the viral vectors and everything, and it's doable in a small town. I think it's doable everywhere in the U.S., especially in small towns where there's a large encompassed area living around that which will really benefit from it and looking forward to more results. Thank you so much, everybody. Thank you. Thank you. Thank you all, our speakers and panelists and everyone who joined us today. We have confirmed robust treatment effect from a well-controlled phase II trial for the genetic medicine for GA. Now we can move on to phase III with a high degree of confidence. This moves us one step closer to bringing transformative one-time treatments to GA patients globally who are desperately seeking rescue from vision loss. Thank you again. Have a great day. Thank you for attending today's call. You may now disconnect. Goodbye