Good morning and welcome to the Lexeo Therapeutics Webcast Presentation on LX2006 for the treatment of Friedreich ataxia cardiomyopathy. As a reminder, this call is being recorded today, October 7th, 2025. I would now like to turn the conference over to Louis Tamayo, Chief Financial Officer of Lexeo Therapeutics. Louis, please go ahead. Earlier today, we released the regulatory update on our discussions to date with the FDA regarding a potential accelerated approval pathway for LX2006 for the treatment of Friedreich ataxia cardiomyopathy, alongside new interim clinical data from two ongoing phase I/II clinical studies. The press release outlining these updates is available on our website, lexeotx.com, and an 8K was filed with the SEC this morning. Joining us on today's call will be Nolan Townsend, Chief Executive Officer, and Dr. Sandi See Tai, Chief Development Officer of Lexeo Therapeutics. Dr. Eric Adler, Chief Medical Officer and Head of Research, and Dr. Manuel Otero, Chief Technical Officer, will also be available for Q&A following the call. Before we begin, I would like to remind you that this call will contain forward-looking statements regarding Lexeo's future expectations, plans, and prospects, which constitute forward-looking statements for the purposes of the Safe Harbor provision under the Private Securities Litigation Reform Act of 1995. Actual results may differ materially from those indicated by these forward-looking statements as a result of various important factors, including those discussed in our filings with the SEC. With that, I would like to turn the call over to our CEO, Nolan. Thanks, Lou, and thank you all for joining us. Today, we are pleased to share regulatory feedback on LX2006, as well as the latest safety and efficacy data from ongoing studies in FA cardiomyopathy. As we shared this morning, the FDA is open to a BLA submission that pools clinical data from the ongoing phase I/I I studies of LX2006, with data generated in the upcoming pivotal study, and we are planning to submit enhanced comparability data to support this approach. The FDA has also agreed to evaluate the coprimary endpoint of LVMI at a time point earlier than 12 months, which we believe has the potential to shorten the length of the pivotal study. We will share more details on our progress with the FDA on this call, and we expect to continue discussions with the agency into 2026 on the pivotal trial protocol and comparability requirements. Looking at the interim clinical data since our last update, we are pleased to see sustained or deepening improvements over time in both cardiac and neurologic measures of FA. All participants with abnormal LVMI at baseline have now reached at least 12 months of follow-up, and we've observed a 23% mean improvement in LVMI at this time point. We've also seen 18% mean improvement at six months after dosing, well above the FDA line threshold for the pivotal study of 10%. We have also observed what we believe is clinically meaningful improvement in the modified Friedreich Ataxia Rating Scale, or mFARS, which we will detail this morning. From a safety perspective, LX2006 remains generally well tolerated across all dose cohorts, utilizing relatively low doses for a systemic gene therapy program. These data collectively give us great confidence in the therapeutic potential of LX2006. Lexeo is proud to collaborate closely with the FA community, and we've highlighted three stories this morning from Allie, David, and Anne-Marie, and Ron and Rachel. We deeply appreciate them sharing their experiences with FA, and I know these stories are highly motivating to myself and all Lexeo colleagues as we continue our work to progress the development of LX2006. Friedreich ataxia is a devastating condition, and cardiac complications are the most common cause of death in FA, leading to an average life expectancy of just 35 to 40 years. Treatment options are urgently needed for those impacted by FA cardiomyopathy, and we are hopeful that our research can bring this one step closer. I will now share a brief background about this condition and ongoing LX2006 research before jumping into more details of the regulatory update. Friedreich ataxia is a rare, progressive, devastating multi-system disorder that impacts approximately 5,000 people in the United States and 15,000 globally. Almost all people with FA will develop some cardiac complications during their lifetime, and up to 40% have left ventricular hypertrophy as defined by abnormal LVMI, which is a key inclusion criteria for the LX2006 pivotal study. Importantly, as I previously noted, cardiac complications are the leading cause of death in FA, and currently there are no approved treatments for FA cardiomyopathy. Individuals with FA have very little frataxin protein expression, which leads to impaired mitochondrial function in the heart and throughout the body. LX2006 is designed to treat the root cause of this disease by restoring frataxin. We packaged the full-length frataxin gene in an AAVrh10 vector, which has an increased affinity for the cardiomyocyte cells in the heart, allowing us to use relatively low doses in this program, which we believe could support a more favorable safety profile while still offering efficacy in treating cardiac disease. LX2006 also includes a CAG promoter, a strong, clinically validated, ubiquitously expressed promoter that could enable expression in other tissues with frataxin deficiency beyond the heart, such as in skeletal muscle. As a reminder, LX2006 is being evaluated in two parallel trials: one multicenter study sponsored by Lexeo, and another investigator-initiated study run by Dr. Ron Crystal at Weill Cornell. These two trials are very similar, both enrolling adult patients with FA cardiomyopathy, although cardiac biopsies were only performed in Lexeo 's SUNRISE-FA trial, so frataxin expression has only been evaluated in participants in this study. The SUNRISE-FA trial completed enrollment at the end of last year. Based on FDA feedback to date, we believe we now have the potential to reduce the size and length of the LX2006 pivotal study, possibly accelerating our overall timeline for BLA submission. First, the FDA is open to a BLA submission in which we pool the phase I/II LVMI data with data from the upcoming pivotal study, as long as enhanced comparability data are provided. The phase I/II studies both use an adherent HEC-293 process that is not commercially scalable, and Lexeo has since migrated to an optimized SF9 baculovirus manufacturing platform, which produces high-yield, high-quality vector with a low empty capsid ratio. We intend to use this process for future clinical and commercial supply, and we will be submitting enhanced comparability data to the FDA to support this change, including analytical comparability and data from a non-clinical murine bridging study using pre- and post-change drug products. By pooling this data, we believe that we have a potential pathway to a smaller pivotal study, with sample size determined primarily by the LVMI treatment effect. The FDA has also agreed to assess LVMI at an earlier time point, which could reduce the length of the pivotal study, as we previously guided to assessing LVMI at 12 months. We continue to discuss the final pivotal protocol design with the FDA, including the precise time point for this assessment, and we expect to provide further regulatory guidance in early 2026. I should note that in discussions to date, there have been no changes to the previously disclosed alignment with the FDA on key parameters related to the LX2006 planned registrational study, including the aligned coprimary endpoints for this pivotal study, which remain LVMI and frataxin expression, and the thresholds for clinical benefit, which remain 10% reduction in any change from baseline expression, respectively. Finally, the other coprimary endpoint, frataxin expression, will need to be assessed with a validated assay in the pivotal study. The biopsies in the SUNRISE-FA study were analyzed with a frataxin LCMF assay appropriate for a phase I/II study, but not a validated assay intended for BLA submission, so this data will be supportive evidence for BLA. We remain highly encouraged by the phase I/II data, and we appreciate the FDA's willingness to collaborate on an expedited development strategy for LX2006, especially given the urgent unmet need for treatments in FA cardiomyopathy. We plan to initiate the pivotal study as quickly as possible in the first half of 2026, pending finalization of the pivotal protocol. I will now turn the call over to our Chief Development Officer, Dr. Sandi See Tai, to review the latest interim data for LX2006. Thanks, Nolan. I will now review interim clinical data as of July 2025, which were also shared with the FDA as part of our most recent interaction. On this slide, we are sharing baseline characteristics of the 17 participants treated to date across the SUNRISE-FA and Weill Cornell Medicine trial. The dark pink shading represents an abnormal cardiac measure, or a value that is at least two standard deviations above the mean from healthy volunteers. The lighter pink shading represents a measure within the normal range with greater than one standard deviation above the mean, which we are labeling high normal. At baseline, all participants had some evidence of cardiac abnormalities, and six participants had abnormal LVMI, which is often seen in this population as the heart thickened. We will focus much of our discussion today on this subset of six participants with abnormal LVMI, given they closely match the population we intend to enroll in the pivotal study, representative of those in most urgent need, as higher LVMI is associated with increased risk of death. At the bottom of the table, we are sharing for the first time baseline data relevant to m FARS, the neurological functional scale specifically developed to measure FA disease severity and progression. You can see each participant's m FARS score at baseline, with a score of zero representing no impairment and a score of 93 representing maximum impairment on the scale. The mean baseline score across the two studies is 63, which reflects a meaningful level of neurologic impairment at baseline, and is consistent with our adult study population, most of whom were also non-ambulatory. You can also see which study participants used Skyclaris or Omeprazole at any point during the LX2006 study period. Concomitant use is permitted in the protocol, as long as participants were either stable on Omeprazole prior to dosing or they can begin treatment later following dosing. Omeprazole was approved based on its impact on m FARS, and those with green check marks took Omeprazole for some period of time during the ongoing study, though not every participant is continuing on therapy today. These baseline characteristics will be important when we review neurologic functional measures later in the presentation. I will start by sharing the safety data. LX2006 continues to be generally well tolerated to date. We have not observed any clinically significant complement activation or instances of TMA. We have observed minimal elevations in liver function tests or LFTs, with no participant exceeding three times the upper limit of normal. Notably, even the highest dose of LX2006 at 1E12 vector genomes per kg is significantly below the doses used in other programs in which LFT elevations or liver injury have been observed. This dose is 100X lower than the recommended dose of Zolgensma, for example, and 133X lower than the recommended commercial dose of Alavitus, and we believe the low dose is an important consideration for safety. As we previously shared, there was one participant who was diagnosed with myocarditis one year after dosing. This individual had multiple comorbidities at enrollment, and their early treatment course was complicated by multiple pneumonias with required modification to their immunosuppression. At their 12-month visit, this individual presented with elevated troponins, and cardiac MRI suggested a focal myocarditis, although the participant was otherwise asymptomatic, and a biopsy performed at that time could not definitively confirm myocarditis. This individual has since been treated with corticosteroids and other immunosuppressants to manage the myocarditis, and their biomarkers are improving but remain elevated. Expert opinion on this case has suggested this may be intermittent episodes of myocarditis on top of disease progression for the underlying FA cardiomyopathy. Additional biopsy samples have been collected, which will be assessed to better understand the underlying frataxin expression and potential disease progression. Of course, we continue to monitor this participant closely, and we are pleased to see their recent cardiac measures begin to come down. Looking now at the efficacy data, here you can see cardiac biomarker data for the six participants with abnormal LVMI at baseline, which, as noted, matches the inclusion criteria for the planned pivotal study. This group represents a segment of the FA population with more severe later-stage cardiac disease, as evidenced by the baseline LVMI measurements that are significantly elevated, at least two standard deviations or more above the mean in healthy volunteers. This slide shows the change observed in clinical biomarkers between baseline and latest visit, and the dark green shading shows where treatment with LX2006 led to meaningful improvement from baseline. All of these participants have now reached at least 12 months of follow-up, and on average, they achieved an 18% reduction in LVMI at six months and a 23% reduction in LVMI at 12 months. Looking at patients in cohorts two and three, the mid and high-dose cohorts, the mean reduction in LVMI was 28% at six months and 33% at 12 months, so we are seeing evidence of a dose-dependent treatment response. These reductions well exceed the target mean improvement of 10% in LVMI, previously aligned with the FDA for the planned pivotal study. We're also very encouraged to see the directional consistency between LVMI improvement and improvements in other biomarkers, including lateral wall thickness and troponin, and in subsequent slides, you can see the durability of the improvement over time, now that participants have reached at least 12 months. This chart visually demonstrates the sustained and deepening treatment effect over time. All of these six participants have reached the normal range for LVMI at latest follow-up, which is a highly encouraging signal for the potential of LX2006 to stabilize or even reverse cardiac disease due to FA. We are pleased to see durable improvements over two years in cohort one, suggesting persistent transgene expression with an underlying disease-modifying impact, and we are beginning to see similar trends in cohorts two and three, now that these participants have reached 12 months of follow-up. Looking at the other cardiac measures for those with abnormal baseline LVMI, we have continued to observe a pattern of sustained or deepening improvement over time with a potential dose response. Lateral wall thickness is on the left, and high-sensitivity troponin I is on the right. We're particularly encouraged by the troponin result, as elevated troponins are a marker of myocardial injury, and this is a simple blood-based biomarker that is easy to evaluate in clinical practice. You can see that participants achieve reductions in troponin from 25% to over 85% from baseline. Lateral wall thickness is also a relevant measure in FA cardiomyopathy, but it's important to note that it represents a two-dimensional measurement compared to LVMI, which is a three-dimensional assessment of the heart's entire mass. Compared to LVMI, lateral wall thickness measurements may have greater variability. Even with some measurement variability, the directionally consistent improvements observed across cardiac measures, from LVMI to lateral wall thickness and troponin, give us great confidence in the treatment effect and therapeutic potential of LX2006. We've reviewed the results for participants with abnormal baseline LVMI. Now, I would like to share data for the other 10 participants who began the study with baseline LVMI measures within the normal range. Those with a baseline more than one standard deviation above the mean for healthy volunteers are noted in pink, which we are labeling high normal. In this group, we are still seeing signs of clinical improvement and disease stabilization across biomarkers. Almost all participants remained within the normal range for LVMI at their latest visit, excluding participant 10, who, as I noted before, was diagnosed with myocarditis and myocardial edema 12 months after dosing and is a potential non-responder. Participants seven, eight, and 15 with higher baseline LVMI values showed greater improvements in LVMI, and almost all participants demonstrated stabilization of lateral wall thickness and meaningful reductions in high-sensitivity troponin I. Taken holistically, we believe these data demonstrate the potential of LX2006 to positively impact cardiac status at earlier stages of disease, even before severe hypertrophy has emerged. Now looking at the complete picture for LVMI, on this slide, you can see the absolute change in LVMI across all 16 participants with six months or more of follow-up. The normal LVMI ranges for men and women differ, so we are showing men on the left and women on the right. As you can see, 15 of the 16 participants reached or remained within the normal range for LVMI at their latest visit, with evidence of sustained or deepening response over time, again, powerful evidence for the therapeutic potential of LX2006. Looking at the supportive endpoints again, now for all 16 participants, we continue to see consistent trends of improvement or stabilization of cardiac disease across most of the group. As noted previously, the lateral wall thickness measurements are small in millimeters, so there is some measurement variation, but overall, the pattern of improvement is consistent with the LVMI data. On the right, almost all participants experienced large reductions in troponin, anywhere from 25% to almost 100% from baseline. Participant 14 in green appears to be an outlier, but I will note their absolute change in troponin was relatively small here, from 11 at baseline to 16 at latest follow-up, and both values are within the normal range. Finally, I'd like to share the exciting evidence of functional improvement observed to date. We have assessed functional status using the modified Friedreich Ataxia Rating Scale or m FARS, where reduction is favorable and reflects less physical or neurologic impairment. This scale matches function in people with FA across four subscales: bulbar function, upper limb coordination, lower limb coordination, and upright stability. A change of one to two points is generally considered clinically meaningful, and without treatment, individuals generally progress by approximately one to two points per year on average. Here was the evidence that LX2006 improved functional outcomes specific to FA. While some of this improvement may be due to the observed cardiac changes, for example, making some physical movements easier by reducing heart failure burden, we hypothesized the improvements may also be explained by extracardiac changes. In preclinical murine and non-human primate studies of LX2006, we did observe some transduction of LX2006 beyond the heart, for example, in the dorsal root ganglia and in skeletal muscle. While the AVRH10 capsid is cardiotropic, the systemic delivery of LX2006, combined with the ubiquitous promoter, means that there could be beneficial off-target effects of this therapy impacting neurologic disease. Skeletal muscle biopsies are being performed in a subset of participants from the SUNRISE-FA study as part of an investigator-initiated study, and we look forward to further evaluating this hypothesis and sharing those data in early 2026. Looking now at the chart, you can see the mean improvement over time relative to natural history on the left. Since this is an interim update, we have participants at different stages of follow-up, and we've noted the sample size for each time point. We are seeing clinically meaningful improvement of one to two points on average, with a sustained response over time. To give you some perspective on this improvement, it represents greater ease with daily activities, such as brushing teeth, handling food and utensils, or dressing. Although study participants had very different baselines, 11 of the 16 participants showed improvement or stabilization relative to baseline at their latest visit. Also included on the chart is natural history data from the FACOMS database. This graph is based on published data, which is not propensity matched to the LX2006 study population, but it gives a directional sense of disease progression without treatment in an FA population of similar age. Finally, we'd like to share individual patient data to demonstrate the improvements in m FARS scores relative to natural history in red. There is some measurement variability both inter and intrapatient with this type of assessment, but in general, we are seeing functional improvement with 11 of 16 participants improving or stabilizing relative to baseline. On the left, you can see evidence of the potential dose-dependent impact, with each participant highlighted by their dose cohort. On the right, we are addressing the concomitant use of Omeprazole. Participants were not excluded from taking this in the phase I/II studies. Ultimately, we did have eight participants who received this drug for some amount of time during the study period, including three who were on therapy at the time of dosing and five who began therapy at least seven months or more after dosing. It's natural to ask how much of the m FARS benefit observed in these studies may be due to underlying Omeprazole treatment. To help answer this question, we have isolated data for the eight participants that have never tried Omeprazole in yellow, and as you can see, we're still observing positive trends in the subset of participants, which suggests that LX2006 alone can improve neurologic functional measures of FA. In light purple, you can also see those participants that did not begin Omeprazole treatment until later in their follow-up, and many of these participants still saw neurological improvement in early time points. Finally, these data have been previously reported, but I'd like to remind everyone that all participants in the SUNRISE-FA study did show an increase in frataxin expression at three months post-treatment, with evidence of dose-dependent increases across cohorts. Cardiac frataxin expression remains a coprimary endpoint in the pivotal study, along with LVMI, and the FDA aligns thresholds as any increase in frataxin expression over baseline using a validated assay for assessment. I've covered a lot of data this morning. To summarize, FA is caused by a deficiency of frataxin, and following dosing with LX2006, we have shown an increase of frataxin in the target organ of interest, the heart, and coupled with this increased expression, we have observed improvement in cardiac structure and in biomarkers of cardiac cellular injury, as well as directionally favorable changes in neurologic functional scores. Taken together, these data illustrate the therapeutic potential of LX2006 and its potential to treat the underlying cause of FA. I will now turn the call back over to Nolan to close the call. Thank you, Sandi. I believe these interim data continue to demonstrate the potential of LX2006 to be a first and best-in-class treatment for FA cardiomyopathy. We've observed improvements in cardiac and neurologic measures of FA across a majority of participants, alongside a generally favorable safety profile, and we are meeting or exceeding the FDA-aligned thresholds for target improvement. We are collaborating with the FDA to fully understand the necessary conditions to leverage the phase I/II data for BLA for accelerated approval, and we are working to design a pivotal study that is potentially more efficient while advancing the necessary work on manufacturing comparability. I want to thank the study participants, caregivers, and investigators who have helped us reach this exciting milestone, and we will now take questions. Thank you. To ask a question, please press star 11 on your phone and wait for your name to be announced. To withdraw your question, please press star 11 again. Our first question will come from Paul Mattis with Stifel. Your line is now open. Hi, this is Matthew on for Paul. Thanks for taking our question and congrats on all the progress. My question is on the pooling, and I understand that the SAS plan hasn't been finalized yet, but in terms of the threshold for LVMI of 10, what sort of scenarios do you envision that that might apply to the pool data? Do you think it's the overall pool data that needs to meet that threshold, or does the phase I/II and the pivotal study need to hit that threshold separately? As a quick follow-up, on the natural history study, how do you envision that playing a role in the analysis for the pivotal analysis? Thanks. Thank you for the question. If I can repeat the first question, you're asking if the data from the phase I/II study and the effect size required on LVMI would be measured separately from the data for the upcoming pivotal study and the effect size required there. Is that correct? Is it just one, you know, just the pooled LVMI between both the phase I/II and the pivotal that will be compared against the threshold? Yeah, I'll pass it to our Chief Development Officer, Sandi, to say a few words about that. Yes. When we talk about pooling data, we envision it being a combined single endpoint that would meet that threshold that we've discussed in terms of LVMI, not as two separate analyses. This will be finalized, as you noted, when we work to finalize the SAP with the alignments of the FDA. Could you repeat the second question? Yes. For the natural history study, how do you anticipate the data from that supporting your pivotal analysis, for which endpoints? We would anticipate that study being supportive in terms of utilizing LVMI data from the natural history study. In addition, we are collecting other biomarkers that include troponin as well as m FARS data, so we envision that this can be supportive data. How exactly it would be analyzed remains to be further discussed and finalized. The natural history study has already begun earlier this year, so we're in a place where we've begun to identify patients that match the inclusion criteria of the registrational study. To the extent we are getting to the place where we have a smaller, shorter study, I think this just helps us to de-risk the enrollment even further from where we are today with respect to the enrollment of that natural history study. Thanks. That's very helpful. The next question will come from Tessa Romero with JP Morgan. Your line is open. Hi, Nolan and team. Thank you so much for the questions here. What are the bookends for when you think you will be able to submit the BLA to the FDA? What is the additional non-clinical requirement exactly, and how long roughly will it take for you to complete? Final question is, what is the nature of the dialogue that you have had specifically around comparability? Thank you. Okay. A few here, which we'll take. The first on BLA timing. We won't be able to guide today to updated BLA timing. I think we'll be able to provide clarity in this guidance once we have finalized the protocol and the SAP with the FDA. I would say that's an early 2026 update for BLA timing, but I would just note that given some of the parameters we're working with here in terms of study size and length, it's likely to be timing that's pulled in from our prior guidance. Your next question was about the non-clinical requirements. We need to complete a murine study with head-to-head of the pre-change product and adherent HEC-293 relative to the post-change SF9 suspension baculovirus material. We have a lot of experience with this SF9 suspension process. It's the same process we're using for our PKP2 program, so we have multiple GMP batches we've produced for that program. As well, we've done quite a bit of comparability work. We're confident in our ability to achieve the comparability requirements that the FDA has outlined. I'd say if we weren't confident in it, we would not be pursuing the strategy that we've outlined today. I think we have a lot of familiarity both with the process and also with the murine model for which we'll be introducing this comparability. We have confidence in our ability to get there. Lastly, on comparability, the detail we described around the FDA interactions came from a meeting with the FDA. This included both CMC and clinical discussion as part of it. The comparability discussion came up in the context of that meeting, and there's minutes that have come out of it. That's the structure and scope of the discussion that's occurred around the clinical path and the CMC requirements. Thank you. Our next question will come from Brian Skorney with Baird. Your line is open. Hey, good morning, everyone, and thanks for taking the question and congrats on the regulatory update and the continued good clinical data. I guess my question is, for the pivotal design, are you planning on using the Kyle Baum criteria for enrollment criteria as what the threshold for normal is on LVMI? I ask because it does seem like there's a pretty consistent effect of higher baseline LVMI resulting in a larger numerical and% improvement, and I'm just wondering if you would consider an easier target to enroll a patient with like 100 or 110 gram per meter squared versus an 86, because I think the 10% improvement may be easier to achieve, and the clinical relevance of getting like 110 to an 84, would you consider that more obvious than getting an 86 to a 74? Yeah, just would love to hear your thoughts on maybe raising the criteria threshold for baseline LVMI. Yeah, thanks, Brian, for the question. Just if I can read it back, you're asking if we would further enrich for elevated LVMI even beyond the two standard deviations that we have assumed in the inclusion criteria? Exactly, right? Like I'm questioning, like there's an 86 to an 84, like participant six. You know, if you got all patients like that, would that have less meaning than, like, you know, patient 13 where you're taking 110 to a 54, and therefore, like, raising that criteria would benefit the study to some extent. Yeah, I'm following. I think one, this abnormal LVMI, so the patients with two standard deviations above normal represents, you know, 40% of the FA population as per our adult population, as per our natural history, the natural history data that we have access to, and actually represents roughly the same percentage in our phase I/II studies. I think that that's a very appropriate pool from which to draw patients for enrollment. I think we'll continue to focus there and keep the inclusion criteria identical to what we described. I mean, even with this two standard deviations cutoff, we're achieving an over 20% improvement in LVMI at 12 months. We're achieving an 18% improvement at six months. If you look only at the higher doses, we're achieving even greater improvements. I think with the inclusion criteria matching that of the elevated LVMI that we have in the phase I, we should be pretty easily clearing the threshold that the FDA has set for us. You know, I'd note even for the patients that start at lower baselines and look at the high-dose patient that starts at a lower baseline amount, we're still getting to, I believe, about 12% improvement. We're clearing the bar even for patients that are just above that two standard deviations change in respect to hypertrophy. I think we're pretty comfortable with the inclusion criteria because it's supported this result we're seeing in the phase I, and we think it should support a similar result in the registrational study. Okay, thank you. The next question will come from Mani Foroohar with Leerink. Your line is open. Hi, good morning. This is Lili Nsongo on for Mani. Just a quick question regarding the m FARS data, acknowledging that this is relatively exploratory at this point. It appears that most of the benefit is seen at the earlier time point with some potential challenges at 18- 24 months. Based on your understanding of the underlying mechanism of action for this result, do you have any incentive as to whether this should be expected to be a transient benefit, or is this just, you know, something that we will have to weigh against natural progression? Good question. Maybe I'll ask our Chief Development Officer, Sandi, to say a few words, and maybe also Eric after this to also comment as well. Yeah, the changes that we see early on may be impacted by the fact that patients are aware they have received treatment, but once you move beyond that early time point, we are seeing that sustained reduction in terms of the score on m FARS. FARS. There seems to be an improvement even relative to baseline that is sustained well beyond a period where you might expect to see a placebo effect for these patients. We are seeing it as a durable improvement relative to baseline and even more so relative to natural history data, and we're seeing that at the 12 and 18-month time points. There is definitely persistence that we're seeing in the scores, so that it's very pronounced in terms of looking at these changes, in terms of what it means for functional benefits for these patients, whether it is improving activities such as brushing their teeth, being able to get dressed, that it really may be meaningful from the standpoint of, you know, from the patient perspective. Eric, is there anything you'd like to add to that? I agree that you would expect a placebo effect to be strongest in the beginning and decline over time, and here you see the sustained and deepening effect. I think that's very suggestive of an impact. I’d also note, if you were to take a look at other studies that have looked at the similar endpoint, you would see a similar trend of some deepening effect at six months that could be placebo, but once you look at the longer time points, I think you see the true, you know, treatment effect, and I think that's likely what we're observing here. I would think the time points at, you know, 12 months and beyond are, you know, very relevant for the treatment effect of this particular therapy. Thank you. Our next question comes from Leland Gershell with Oppenheimer. Your line is open. Good morning. Thank you for this positive update and taking our questions. Just two from us. First, I just wanted to ask, with the FDA indicating a shorter time frame for the LVMI than 12 months, just wondering if you have any thoughts in mind in terms of what you may propose, you know, six months, nine months, if you could share thoughts there, and then also want to ask if you continue to look forward to the update from the PKP2-ACM study later this year. Thank you. Okay, on proposal of time points, I think it's early for us to comment on that, but I think we've shown data here that is showing a meaningful treatment effect as early as six months. I think it's early for us to guide to what time point we may land at, but you can see that the treatment effect is meaningful and relatively rapid, in particular at the higher doses. More to come on that as we get through this conversation to finalize the protocol with the FDA. We today are not focused on PKP2-ACM. That's a discussion to come a bit later in the year, so I would defer questions to that later time point in respect to PKP2-ACM. Great, thank you. Our next question will come from Luca Issi with RBC Capital Markets. Your line's open. Thank you. Good morning, team. This is Cassie on for Luca Issi, and congrats on getting potentially closer to a product here for FA. This question is a follow-up on your comparability study/cell line. How should we think about the 4:2 empty capsule ratio here between the HEC cells and SF9? Assuming here that SF9 has actually a higher ratio, does that mean that you could potentially use an incrementally lower dose for the pivotal versus your phase I/II? Any color there much appreciated, and congrats again, team. Thanks. Thank you for the question. I'll pass it to our CTO, Manuel, to say a few words about this. Thank you for that question. As we noted in the presentation, the SF9 material to date has been showing a lower empty capsid ratio. I'll point to you that, and it's included in the press release, we presented manufacturing CMC data at ASGCT this year. There are two posters on that, and those posters also describe in detail our quality attributes around the product, including the empty low capsid ratio. I'll also highlight that we have been manufacturing using SF9 as a platform across our clinical stage programs, and we've been manufacturing at a relevant commercial scale that includes for FA. We believe that we've got data that's highly representative of our go-to commercial process moving forward. The next question will come from Mitchell Kapoor with H.C. Wainwright. Your line is open. Hey, team. Thanks for taking the questions. I wanted to ask if the FDA mentioned anything about post-approval commitments. For example, are they looking for some type of m FARS follow-up, or could you just comment on what they might expect if you do receive some type of accelerated approval? Separately, on the comparability package, is this something the FDA requested, or was it a proactive step by Lexeo to de-risk the manufacturing? Does the FDA need to sign off on that comparability package before pivotal dosing? Thanks. Yeah. I'll take the first question on post-approval commitments. We've not reached any final agreement on post-approval commitments. Obviously, as with any accelerated approval, we need to reach alignment on that post-approval confirmatory study before we file the BLA. I think we still have some time for that one, but our working assumption from the data that we've observed to date is that m FARS would likely be the confirmatory endpoint. The size, structure, and length of that m FARS study to confirm that as a confirmatory endpoint is, as I mentioned, yet to be discussed. In terms of the comparability, I think this was a back-and-forth dialogue with the FDA. We asked the question of finding ways to accelerate or expedite the pathway to a BLA from our base case plans. This resulted in a conversation where they showed an openness to that expedited pathway in respect to the clinical benefit we're observing and the use of the phase I/II data, but they wanted to ensure that the product was as close to identical as they deemed for the purposes of pooling. That was our focus in that conversation, and we've already filed some analytical comparability data with the FDA, so they have a sense of the comparability profile here. It's a matter of checking a few boxes on these requirements in order to reach the point of pooling, which we believe will ultimately result in this expedited pathway that we've been discussing with the FDA. I think in general, this was certainly a positive step, the openness to this type of approach. I think the requirements we've been asked for here are relatively modest in exchange for the acceleration that this could likely produce, so we're happy with the outcome here, and it matched what we were looking for. Is comparability a gating factor to starting the pivotal dosing? We have certain requirements that are certain that are not. I think we will have to work through that, but I think we're in a place where we've begun to submit this data already, so we can guide to the start of the study in the first half of 2026, and we think we can confidently get there with the data we've already begun to submit to the FDA to support that. Awesome. Thank you, guys. I am showing no further questions in the queue at this time. I would now like to turn the call back over to Nolan Townsend for closing remarks. Thank you for joining today. We appreciate the interest in the program. I think we're excited about this update. I think in one sense, it shows a continued interest and engagement with the FDA in getting rare disease gene therapy treatments to patients faster, in particular with diseases that have high unmet need and no existing therapies out there. At the same time, I think we're showing increasingly promising clinical data. I think the improvements in that particular mass are sustained, and they're significant, and we're seeing these improvements as early as six months, all that meet the pre-aligned thresholds with the FDA. The m FARS benefit is something that we think is very important both for patients, but also ultimately for the confirmatory path for this therapy, and ultimately being able to show benefit for all FA patients, those that are earlier in the disease that are struggling with the neurologic disease, but also patients that are later in the disease that have both cardiac and neurologic manifestations of FA. We think this update and the product profile that's developing here has the potential to be a step change in the standard of care for FA treatment, and we're excited to see this continued progress both on the regulatory and clinical front, and thank you for taking the time to speak today. This does conclude today's conference call. Thank you for participating. You may now disconnect.