Thank you for standing by, welcome to the MyPEAK-1 Interim Data Call. All lines have been placed on mute to prevent any background noise. After the speaker's remarks, there will be a question and answer session. If you would like to ask a question during that time, simply press star followed by the number one on your telephone keypad. Thank you. I'd now like to turn the call over to Michelle Corral, Vice President of Corporate Communications and Investor Relations. You may begin. Thank you, Rob. Hey everyone, and thank you for joining us today. I'm Michelle Corral, as he said, Vice President of Corporate Communications and Investor Relations at Tenaya. Today, we are excited to share interim data from both cohorts of our MyPEAK-1 phase I-B/II clinical trial of TN-201 gene therapy for potential treatment of MYBPC3-associated hypertrophic cardiomyopathy, or HCM. While the data we are discussing today will be described in full verbally, please note that during the course of today's call, we will be making references to slides. A PDF file of the slides accompanying this webcast is available on the Tenaya website in the IR section under Events and Presentations. Before we dive in, let me remind you that the information discussed during this call will include forward-looking statements, which represent the company's views as of today, June 3, 2026. These statements involve certain assumptions. We caution investors not to place undue reliance on this information. Please refer to today's press release, as well as our filings with the SEC for information concerning risk factors that could cause actual results to differ materially from those expressed or implied by these statements. On the call with me are Faraz Ali, Tenaya's Chief Executive Officer, Dr. Kathy Ivey, our Senior Vice President of Research, and Dr. Whit Tingley, Tenaya's Chief Medical Officer. With that bit of business out of the way, let me turn the call over to Faraz Ali for opening remarks. Faraz? Thank you, Michelle. Good morning, everyone, thank you for joining us today. We're incredibly excited to share today's TN-201 update in MYBPC3-associated hypertrophic cardiomyopathy. As you know, a genetic heart disease driven by insufficient MyBP-C protein. On slide four, we remind you of the scale of MYBPC3 mutations within the broader context of HCM, as well as some of the defining characteristics and the toll of this disease on patients' lives. MYBPC3-associated HCM is a chronic progressive condition affecting an estimated 120,000 adults, teens, children, and even infants in the U.S. alone. For those with the mutation, we know disease progression is more rapid and that their risk of serious cardiac events is far greater than those with other forms of HCM. The prognosis for those diagnosed at younger ages is even more grim, as we will cover in more detail later. Turning to slide five. In MYBPC3-associated HCM, the mutated gene involves a deficit in a key sarcomeric protein needed to regulate the heart's contraction. Without that protein, the heart contracts with excess force, and over time, the walls of the left ventricle thicken or hypertrophy, reducing the ability for the heart to fill with sufficient oxygenated blood to meet the body's demands. The result of this progressive condition is heart failure and other comorbidities. We believe TN-201 has the potential to fundamentally change the trajectory for these patients by delivering a fully functional MYBPC3 gene to the heart muscle cells, increasing MyBP-C protein levels, and potentially halting or even reversing the course of genetic HCM with a single treatment. Importantly, TN-201 is targeting the underlying cause of the disease, and therefore, its impact is not dependent on phenotype. While great inroads have been made in the availability of myosin inhibitors for obstructive disease, 70% of the patients with the MYBPC3 mutation have the non-obstructive form of the disease. Today's update represents a significant milestone for our program, one that we believe highlights the growing strength and consistency of treatment data for TN-201. Since we last shared data at the American Heart Association meeting in November 2025, we have meaningfully extended follow-up across both those cohorts with some patients now reaching up to two years of observation at the 3E13 vector genome per kilogram dose, and up to one year for those who received TN-201 at the 6E13 vector genome per kilogram dose. On slide six, we summarize the key findings for the compelling data set we are sharing today, which show consistent improvements in cardiac structure, including reversals in multiple measures of hypertrophy, sustained over extended follow-up, reductions in symptom burden for all patients, and emerging improvements in functional capacity, particularly among those at the higher dose level. From biopsies, we continue to generate evidence that TN-201 is reaching the heart and robustly transducing and expressing in cardiomyocytes. We are also pleased with the continued tolerability profile across both dose levels as we expand enrollment and gain additional experience with the therapy. Together, these findings support our expectations that TN-201 can drive a meaningful and durable impact on disease burden, which is especially encouraging given the limitations of today's standard of care. With that, let me turn the call over to Whit Tingley, who will walk you through these compelling data in greater detail. Whit? Thank you, Faraz. We begin with a reminder of the trial design on slide eight. MyPEAK-1 is intended to characterize the safety of two different doses, 3E13 and 6E13 vector genomes per kilogram of body weight. In addition to dose finding, the trial collects heart biopsy data to give us a sense of pharmacodynamics and includes several exploratory endpoints measuring changes in key parameters. The ultimate goal of treatment is to see multiple parameters of disease, biomarkers, echo measures, symptom burden, all improving with directional consistency within each patient and across all patients. We have completed enrollment of both initial dose cohorts, and we are currently enrolling patients in our 6E13 vector genome per kilogram expansion cohort. The data presented today includes safety, biopsy, and clinical results from six of the seven patients enrolled. Slide nine shows the baseline characteristics for the patients in MyPEAK-1 who have more severe disease than the average HCM patient, consistent with their genetic mutations. All patients enrolled to date have non-obstructive hypertrophic cardiomyopathy. Four of the seven have previously undergone myectomy. Their ages at the time of enrollment ranged from 27 to 63. They all have marked hypertrophy with LV mass well above typical HCM patients. They all have symptoms of heart failure that impact the activities of daily living, as measured by the New York Heart Association classification. The majority of MyPEAK-1 patients entered the study with elevated cardiac biomarkers. On slide 10, we show cardiac troponin I levels at baseline and most recent visits. Troponin is a marker of injury to the heart cells. We follow it closely in HCM as it is a known prognosticator for increased risk of adverse cardiac events. In the chart, you can see troponin levels declined or remained essentially stable in all but one patient. Patient seven in the high-dose cohort had a large and rapid drop. NT-proBNP is a circulating biomarker that indicates strain of the heart muscle and is known to be sensitive to diverse factors, including immunosuppression. NT-proBNP has declined from baseline in three patients. On slide 11, we turn to a critical assessment in hypertrophic cardiomyopathy, cardiac hypertrophy. All patients treated with TN-201 show improvements in hypertrophy. That means the defining characteristic of this condition, LV mass and thickened walls, have been reduced. On the graph, we show the decrease in left ventricular mass index, a measure of the proportion of the LV size normalized to the total body surface area. Elevated LVMI is a strong independent predictor of cardiovascular events like heart failure and sudden cardiac death. All patients entered MyPEAK-1 with severe hypertrophy, making these reductions in LVMI all the more important. For the first two patients dosed, improvements have been maintained through year two. Four of six patients have 10% or larger reductions in LVMI. We're not just seeing a decrease in a single measure. We see corresponding improvements in wall thickness as well. For example, the thickness of the intraventricular septum, or IVS, decreased in five of the six patients. Other echocardiographic measures of cardiac structure and function remained stable. Taken together, these positive changes in hypertrophy suggest that favorable cardiac remodeling is taking place consistently and persistently over time. For context, on slide 12, we have mapped the average reductions in LVMI, posterior wall thickness, LVPWT, and IVS thickness for our MyPEAK-1 patients in comparison to reported average changes for the cardiac myosin inhibitors pulled from available published data. With the caveat that cross-trial comparisons are always limited by differences between the trials, and therefore can risk over-interpretation, we do see that the decreases in hypertrophy after TN-201 compare favorably to the results reported for the cardiac myosin inhibitors. We are certainly excited by these data, particularly the durability of changes in Cohort 1 and the pace and depth of changes emerging in Cohort 2. We certainly also want to know that patients feel better, and we are encouraged by the early changes in symptom burden. On slide 13, we're measuring how patients are feeling using two measures. New York Heart Association Class, a physician assessment of how disease affects daily living, and the Kansas City Cardiomyopathy Questionnaire, a well-validated measure used to assess health status, symptom burden, and quality of life among cardiomyopathy patients, including HCM. Most importantly, I'm happy to share that all patients in MyPEAK-1 are feeling better and experiencing fewer symptoms by at least one of these measures. Starting on the left, all but one patient is now New York Heart Association Class 1, meaning that although they started the trial with heart failure symptoms affecting daily activities, they now have no limitations on daily activity. On the right hand of this slide, we're sharing more encouraging new data. Two-thirds, or four out of six MyPEAK-1 patients report meaningful improvements in their clinical summary score. KCCQ clinical summary score uses a 100-point scale from very poor to poor, fair, good, and excellent, with approximately 25 points between categories. A five-point difference is considered the minimum change in score that is clinically meaningful. Patients in MyPEAK-1 started the study with scores as low as 22 points, or in the very poor category at baseline. Four have had meaningful improvements, and their scores now range from 78 to 100 points, meaning their symptoms and quality of life are now in the good to excellent category. I'd like to underscore the consistency among Cohort 2, whose average change from baseline was an impressive increase of 36 points. This exceeds the typical change seen in the placebo arms of blinded HCM studies. Let's turn to slide 14, where we share results from two tests used to evaluate exercise capacity, six-minute walk distance and cardiopulmonary exercise testing for Cohort 2. A majority of patients receiving the high dose of TN-201 showed improvement in at least one measure of exercise capacity. As to Cohort 1, not shown, there are several factors that may be confounding their functional performance, given that we're seeing improvements in other parameters for patients in that cohort. Confounders include comorbidities and unrelated medical events during the study. Of note, Cohort 1 patients received more immunosuppression for a longer duration than Cohort 2, which can impact exercise capacity. We are actively enrolling new patients at the 6E13 dose level to further understand the positive observations we have seen so far, and we plan another data readout later this year. Now I'd like to ask Kathy Ivey to speak about TN-201's pharmacodynamics. Kathy? Thank you, Whit. I'm glad to share details of the data we have obtained from heart biopsies. Turning to slide 16, in MyPEAK-1, cardiac biopsies were collected from Patients 1 and 2 at 8 weeks post-dose and again at 52 weeks. All other patients were biopsied prior to dosing and are intended to be biopsied two additional times, with the latest being at 52 weeks. The biopsy collection and analysis process was described in more detail in our RIDGE-1 data release webinar on May 15th. In brief, during each biopsy procedure, six to eight small snips of tissue, about one millimeter in size, are collected from the septum using a catheter. Each of these valuable tissue samples is preserved and allocated to a specific quantitative analysis of DNA, RNA, or protein. The graph at the top of slide 16 shows the number of TN-201 transcripts per microgram of RNA from the six patients at their earliest and most recent biopsies. Importantly, the RT-qPCR assay used is designed to specifically detect TN-201 and not detect mRNA from the endogenous MYBPC3 gene. These results provide clear evidence that TN-201 gene therapy is reaching the heart, entering the cardiomyocytes, and producing messenger RNA, which ultimately provides instructions needed for the heart muscle to produce MyBP-C protein. Notably, the average TN-201 mRNA levels in Cohort 2 at the most recent visit were about 2x higher than that of Cohort 1, reaching up to 3.2 E6 in Patient 7. Those higher mRNA levels in Cohort 2 were achieved at an earlier time point. DNA transduction levels, not shown here, were also higher in the second cohort, confirming the expected dose response. The lower graph shows the ratio of MyBP-C to myosin heavy chain peptides, as determined by liquid chromatography and mass spectrometry. Normalization to myosin heavy chain, which is a protein restricted to cardiac muscle cells, helps to account for differences in the cellular composition among biopsy samples. We also analyzed multiple samples per protein where possible and consider the average value to help account for variability. As intended, TN-201-derived MyBP-C protein is indistinguishable from endogenous MyBP-C protein. Acknowledging that the variance between and among samples, patients, and clinical sites complicates interpretation, we nevertheless detect an average overall increase in total MyBP-C protein in both cohorts over time. Consistent with the mRNA results, the protein increase in Cohort 2 is comparable to Cohort 1, even at an earlier post-dose time point. Together with the latest clinical data, the totality of the DNA, RNA and protein data from biopsy samples support that TN-201 is reaching and having effects in the heart. I'll now invite Whit back to review results of safety and tolerability. Thank you, Kathy, for that clear explanation of our biopsy results. Before handing the call back to Faraz for closing remarks and then Q&A, I'd like to cover two slides on TN-201's safety, starting on slide 18. Safety is our primary objective, and I'm very pleased to report that there are no new safety events since our last data presentation in November 2025. TN-201 has been generally well-tolerated at both doses, and the few adverse events related to treatment have primarily been mild, manageable, or reversible. The most common AEs associated with treatment have involved safety laboratory values such as elevated liver enzymes, low platelet counts, or elevation in complement factors. Platelet and complement changes all self-resolved without need for treatment. As for the elevated liver enzymes, these were asymptomatic and responded well to steroid treatment. Patients in MyPEAK-1 received sirolimus and prednisone prophylactically before TN-201. As shown in slide 19, we refined our dosing and monitoring regimen during Cohort 1 to reduce the overall need for immunosuppression. As a result, we've been able to taper immunosuppression faster in Cohort 2 than Cohort 1, despite the higher dose of TN-201. This limits side effects and is clearly better for patients. Faraz? Thank you, Whit. Turning to slide 21, as we continue to build the data set, what stands out to us is the consistency of effect we're seeing across multiple measures of disease, from cardiac biomarkers to cardiac structure, to how patients feel and function in their daily lives. This is especially true for patients who received the higher dose of 6E13 vector genomes per kilogram. We believe this growing body of evidence reinforces the core promise of TN-201, namely that our one-time gene therapy has the potential to modify the underlying biology of disease rather than simply manage symptoms. As we look ahead, we have every reason to believe that TN-201 could have a positive impact on any patient with a MYBPC3 mutation causing HCM. Today, we are treating adults with either phenotype. MyPEAK-1 has thus far enrolled only non-obstructive patients, as we would expect, given that this phenotype is much more common among the MYBPC3 variants and the lack of available non-obstructive treatment options. Turning to slide 22, we also have long maintained that the significant unmet need in severe and rapidly progressive pediatric patients demands an answer and presents an important opportunity to fast track our late-stage development. It is with this sense of urgency that we initiated the MyClimb natural history study even before we started dosing adults with TN-201 in the MyPEAK-1 interventional study. MyClimb has thus far enrolled more than 220 patients at 29 sites in four countries. That includes retrospective patients who have already unfortunately passed due to their disease, as well as prospective patients who could be eligible for future pediatric studies. Now that we are generating increasingly positive efficacy and safety data with TN-201 in adults, we're excited to engage on next steps in that direction and to explore multiple possible pathways ahead to pivotal studies in adults or severe pediatrics. On the topic of pivotal paths, one of our key goals as a company this year is to engage with regulatory agencies on our growing body of evidence and to pursue alignment on a path forward. We are indeed engaged in such discussions and which are, by their very nature, iterative, and we expect to provide an update by year-end. In the meantime, we have two encouraging new items related to this to share on slide 23. The European Medicines Agency, or EMA, has granted TN-201 PRIME Designation. PRIME designation is intended to offer early and proactive support to sponsors in order to accelerate the review and progress of promising new medicines. We have long considered the EU as a near-at-hand extension of our U.S. development program and utilize the MyClimb study as a means of establishing relationship with KOLs and leading cardiomyopathy treatment centers, which given the nature of medicine there, tend to be more consolidated versus a mix of centers of excellence and community docs we have in the U.S. Exciting. TN-201 has also been accepted into the FDA's new RDEP process for the indication of severe MYBPC3-associated pediatric patients. RDEP stands for Rare Disease Evidence Principles and is part of the agency's effort to provide sponsors with additional guidance on the development of genetic medicines for ultra-rare and severe genetic diseases, typically affecting fewer than 1,000 patients in the U.S. The process enables early and ongoing collaboration with the agency to align on regulatory strategy, trial design, and approaches to generating convincing approvable evidence from multiple sources. Turning to slide 24, as a reminder of the opportunity in severe pediatric patients, we offer a snapshot of how we're thinking about the treatment of children with MYBPC3 mutations. We estimate that there are approximately 3,000 diagnosed patients under the age of 18 in the U.S.A. alone at any given time. We know that younger age of diagnosis leads to worse outcomes, a faster pace of disease progression, and higher risk of heart failure, arrhythmias, symptom burden, and hospitalizations, transplant, or death. What we've learned from MyClimb is that there is an opportunity for further refinement within that population. Outcomes differ even within this severe population based on genotypes. For example, 85% of severe pediatric patients who are homozygous die or require transplant before the age of 1, and 64% of compound heterozygous children experience heart failure-related hospitalizations before age 10, and 27% require transplant or die. These data from the MyClimb Natural History Study offer the tantalizing possibility of being able to show movement on hard clinical endpoints sooner versus the natural history and then expand to additional populations among additional patients under the age of 18. As a reminder, there are no approved condition-specific treatments for these very severe pediatric patients, leaving a clear and urgent need. That sense of urgency among families was illustrated by the results of a survey of patients of young children with severe cardiomyopathy that confirmed high interest in gene therapy. The survey was conducted in collaboration with the Children's Cardiomyopathy Foundation and the DDC Clinic, a center of excellence taking care of such patients. We shared these results via poster at the recent ASGCT conference. It is available on our website. As a reminder, in addition to being admitted into the RDEP process for biallelic patients, we have received rare pediatric disease designation, which offers another incentive for pursuing this subgroup as a potential first path to approval in the form of a priority review voucher. In addition to continuing to enroll adults in the 6E13 vector genomes per kilogram expansion cohort, and engage with the regulators on the data being generated from MyPEAK-1, we are actively exploring the advancement of TN-201 in a severe pediatric population as a key component of our pivotal trial planning and strategy for achieving a potential approval for TN-201. While these are still early data from a small number of patients, we believe the breadth, depth, and consistency of the signals we are seeing provide increasing confidence in the potential of TN-201 and support our ongoing development strategy. Turning to slide 25, as we look ahead, we remain focused on continuing enrollment in the higher dose expansion cohort, generating additional follow-up to further characterize durability and dose response, and engaging with regulators on the path forward for this very promising program. Finally, on behalf of the entire Tenaya team, I'd like to express our gratitude to the MyPEAK-1 and MyClimb investigators and their clinical site teams. As always, a special note of gratitude to the patients and their families and caregivers. These individuals are at the heart of Tenaya's purpose, and without their willingness to believe in our mission and join us in our efforts, these data would not be possible. With that, we have concluded our prepared comments. Operator, let's now open the lines for Q&A. Thank you. We will now begin the question and answer session. If you would like to ask a question, please press star one on your telephone keypad. If you would like to withdraw your question, press star one again. Your first question today comes from the line of Mike Ulz from Morgan Stanley. Your line is open. Good morning, thanks for taking the question. Maybe just one on protein expression, just for the two patients in Cohort 2 that didn't experience an increase. Just curious if there's anything unique about those patients or any interpretation as to why that might be. Thanks. Hi, Mike. Thanks for the question. For that, I'll first turn it over to Kathy Ivey. I don't think anything about the baseline protein expression was particularly remarkable, although it's perhaps notable that Patient 4 had the highest baseline protein that we detected in any of our patients at baseline. I think the evidence that we see from clinical improvement suggests that our detection of protein may just be a limiting factor here, and we think there really are underlying increases in protein over time. Yeah, I agree. Thanks for the question. I mean, overall, the RNA data and the totality of the data, including the transduction data that we haven't shown here, just support that overall, we're getting higher transduction and RNA expression at the higher dose. We do believe that obviously we're adding protein to these patients' hearts, and the clinical results seem to bear that out. Yep. Makes sense. Thank you very much. Your next question comes from the line of Thibaut Pardo from LifeSci Capital. Your line is open. Hi. Thank you for taking my question. When you look patient by patient, how should we reconcile improvements in hypertrophy measures with some mixed changes in feeling function measures beyond the immunosuppression in Cohort 1, how that could affect, for example, the six-minute walk? Particularly Patient 6, and how we saw a decrease in hypertrophy, but the six-minute walk test did not improve. Yeah, it's a great question, Thibaut. Good to hear from you. For that, I'll turn it over to Whit. Yeah. As we noted, the changes in exercise capacity depend on multiple factors and can be confounded by underlying comorbidities or adverse events unrelated to the trial that can occur during the course of the trial or even right before an exercise assessment. Overall, though, we are very pleased, as you know, to see improvements in multiple parameters and consistent improvements within patients and across groups. Yeah. Great. Thank you, Whit. Just to add to that, Thibaut, I think our results in some ways are, you can also make a comparison with what has been demonstrated with myosin inhibitors. They've shown clear functional improvements. That's why they've been approved. The level of hypertrophies are not quite as profound on average as what we're being able to demonstrate early on. It's an imperfect relationship. It's an important overall relationship, but an imperfect relationship at any individual patient level between the level of hypertrophy reduction you might see and the level of improvement in some functional measure like six-minute walk test or pVO2. That's been seen in other studies, and we're seeing it here too. Ultimately, the totality of the evidence does suggest that we are getting patients or moving them in the right direction by modifying the underlying disease. Got it. Thank you. Your next question comes from the line of Whitney Ijem from Canaccord Genuity. Your line is open. Hey, guys. Congrats on the update. Thanks for taking the question. In particular, congrats, I guess, on the progress on the pediatric side. Just wondering if we can get any more color there in terms of the discussions with regulators and maybe what feels like pushback or you kind of talked about the iteration. What needs to be iterated? It feels, in particular on the back of some of the natural history data you presented, that there should be a faster, more straightforward path. Are we thinking about that correctly, or what's been the pushback? Why haven't you treated any pediatric patients as yet, and what do you need to do to get there going forward? Thanks. Oh, Whitney, thanks for the question. Let me first, I'll turn it over to Whit again, then I'll add some comments on top of that. Whit? Yeah, we're having productive discussions. I wouldn't say pushback. I would say we are aligning on a path forward for pediatric development that will be tailor-made for TN-201 therapy. That process can take a little while. Yeah, I agree. It's not pushback at all, Whitney. In fact, I would say quite the opposite. The inclusion of TN-201 in this new program, RDEP, that was introduced by this FDA is actually, we take it as a positive sign that they understand the severity of this rare disease population and very severe population and want to work with us, actually. As we pointed out, there's heterogeneity within this group. As we show in the MyClimb data, some patients, you could have a hard endpoint like survival. Others who are on VADs might have different endpoints, and yet other patients present on a spectrum that's more consistent with the adults. I think there's nuances here in this population, and we're very pleased with the engagement that we're having. The devil is always in the details, and so it's iterative, not because of pushback, but because actually, in many ways, this is the first time that, to our knowledge, somebody is trying to align on something with this kind of rapidly progressive early severity, including kids who are dying in some cases as early as the first few days, weeks and months of life. We haven't dosed any patients in a pediatric study yet because we haven't initiated one. We would initiate a pediatric study only under the site of full alignment on the design of pivotal studies to support that population. We would only either amend the current study or launch a new study with that under our belt. Just please rest assured, the iteration is a good thing. Understood. Thanks very much. Your next question comes from the line of Mani Foroohar from Leerink Partners. Your line is open. Hey, guys. Thanks for taking the questions. I know it's been touched on a little bit, wanted to circle back first on the data. With three patients, Cohort 1 saw an increase in protein, quite robust results, bouncing around by time point as you expect, versus Cohort 2, though, again, obviously not a perfect metric. The Cohort 2 patients, to my eye, did better on some functional endpoints. Can you sort of a little bit cast light on how to interpret this? Then I have kind of a follow-up on broader strategy. Yeah, sure. Thank you, Mani. Good to hear from you, and thanks for the question. Let me turn it over to Whit to sort of share his impressions of the differences between Cohort 2 and Cohort 1. Yeah, we are seeing early signs that patients may be responding more strongly and more quickly to the higher dose. We can see that in how they're reporting their symptoms. We can see that in hypertrophy measures. As you're noting, we're seeing encouraging signs for functional assessment. As you see, it's still early. There's still more functional assessments we need to get from the high dose. We need longer follow-up, and we are dosing additional patients in that high dose cohort to fully understand it. The overall trend appears to be better efficacy at the higher dose, and as we mentioned, is very well tolerated. Very encouraging overall. The RNA results are also encouraging for that cohort. The protein, clearly more data will help. Yeah, the only thing I'd add to that is that while on the functional side, we didn't yet quite see those same improvements for Cohort 1. The reductions in hypertrophy in a patient population that has some of the most hypertrophied hearts studied when we compare to other peer programs, that is meaningful as in many cases as we've shared in the past, reductions in hypertrophy below certain levels are predictive of better long-term outcomes for these patients, including survival benefits. We are very pleased with the improvements we're seeing in Cohort 1 and even more pleased with what we're seeing in Cohort 2. It sounded like you had a follow-up question, Mani. I do. Well, I guess I have a separate question. Obviously, there's meaningful differences between nHCM and oHCM, obstructive and non-obstructive. As we think about your continuing engagement with the FDA, what are the range of sort of strategies you could pursue in terms of separate studies, multiple cohorts, or a stratified approach with a single study? These are clearly very different patient populations in terms of tempo of response and underlying clinical course. Just walk us through what the possible outcomes and development strategies might be to serve patients with different needs and underlying clinical courses. Yeah, great question. Again, I'll first turn to Whit to see if he'd like to comment on that. On slide 22, we lay out the different populations that I think you're referring to. Many non-obstructive and obstructive adults, and then the adolescents, peds, and infants. Whit, anything you'd like to add about our development strategies in the different groups and different studies or one study with different subtypes or subgroups? Yeah. There are different possibilities. As you know, we are necessarily going to have to follow the path that CMI followed. We have, as you're suggesting, we have deliberated discussions ongoing with regulators but still in the discussion phase. It would be premature to hint to any potential direction. Needless to say, Whit would agree, and I think these are different populations, as you pointed out, Mani. The endpoints that might be most relevant are going to be different. For example, you can't measure a pVO2 and six-minute walk test in a homozygous infant. That's obvious, right? What we're going to study in these different populations may be different, and then there's a little bit of logistics of what's the best way to incorporate these different groups. Can some groups be addressed by amending MyPEAK-1 or other groups require just an entirely separate study because the sites and the endpoints are just completely different. I think more to come on this front, Mani, as the year progresses and as we provide updates on where we have aligned with the FDA on endpoints and design of pivotal studies and with specific populations. We continue to see that severity of the end and the unmet need in the pediatrics as something we've been talking about, frankly, consistently for probably the last five years since we first launched the MyClimb natural history study. More to come on that front. Thanks, guys. That's really helpful. Your next question comes from the line of Yasmeen Rahimi from Piper Sandler. Your line is open. Good morning, team. Thank you so much to these great data. Really profound changes in feel and function of the patients. Putting that slide you have, 13, into perspective, right? You're getting normalization of patients feeling and functioning good. Question for you, just one minor is you see Patient number 6 really changing KCCQ Class I normalization. The six-minute walk test regresses. What is the disconnect in that patient where everything is tracking well, but then the six-minute walk test for some reason goes down instead of going up, even though everything else is really astonishing? The second question is, given the KCCQ data in the NYHA class responses, is it fair to think about in the future when you think about a pivotal study, and we have seen pivotal studies in non-obstructive with the CMIs that sponsors have picked KCCQ as a key regulatory endpoint. Would love to get your thoughts on the data that you just reported on slide number 13, if that's the way we should be thinking about primary endpoint selections for the pivotal programs, and the robustness of the effectiveness that you're seeing? Sorry for these long-winded questions. No, yeah. It's always good to hear from you. Thank you for the question. Again, I'll turn it over to Whit to take a first response. Yeah, very good questions. Certainly, to your second question, Kansas City Cardiomyopathy Questionnaire is established as a potential pivotal endpoint. New York Heart Association class as well. These are certainly on the table as options for pivotal studies. In terms of parsing out patient 6 that is improving in multiple domains, the six-minute walk test is encouraging at that particular day. I would encourage you to think about integrating the preponderance of the data. Again, as a patient is reporting their symptoms, it's not limited to one activity or one particular day. When they say they're feeling better and their physician has interviewed them and found they're less limited on daily activities, that carries a lot of weight. Individual exercise capacity measurements can be confounded. We've seen from the CMI data, some published data will show the individual changes in pVO2, for example, and there's a huge range up and down amongst each individual patient. That's not a drug effect or lack thereof. That's the variability of where people are at on that particular day of the test. Whit, thank you. I agree. As we said earlier, I think there's any given patient will have some variability. We know some of these patients or our team does intimately know, aware of other comorbidities they may have that may impact individual results. We look at the totality of data and are pleased with what we're seeing, Yasmeen. Again, yes, KCCQ is an endpoint, six-minute walk test, pVO2. I will go back to in the pediatric population, those might not be as relevant, particularly as we're talking about very severe young patients. When we set out to do MyPEAK-1, we always said it was going to be a data-rich study, and that we were looking at a lot of things. I think you're seeing the fruit of that bear out, being able to now describe improvements in circulating biomarkers and multiple, in many cases, multiple forms of hypertrophy, and now multiple ways of capturing both feel and function. This is exactly what it's set out to do, and this will help us inform both dose selection as well as design of future pivotal studies in different subpopulations. We're exactly where we wanted to be with the data set that are maturing. Still early days. We look forward to providing more updates in the second half of the year. Thank you. That concludes our question and answer session. I will now turn the call back over to Faraz for closing remarks. Thank you, Rob. Thank you all for joining us on the call today. Exciting results on top of the exciting results we delivered for TN-401 just a few weeks ago. A great first half of the year for Tenaya and an even more exciting second half of the year to come. We look forward to meeting some of you over the coming days, weeks, and months and diving deeper into the data and answering your questions, and to providing additional important clinical and regulatory updates on the TN-201 program and the TN-401 program in the second half of the year. With that, have a good day. This concludes today's conference call. You may now disconnect.