Thank you, Mike, and good morning, everyone. It is my distinct pleasure to welcome you all to the Edgewise Therapeutics conference call to discuss our positive top-line data from the phase II CANYON trial of Sevesantan in individuals with Becker muscular dystrophy. This morning, we issued a press release that outlines these results. You can access the press release, along with the slides we will be presenting today, by visiting the Investors and News section of our website at www.edgewisetx.com. A replay of the conference call will also be available as a webcast on our website. Joining me today are Dr. Kevin Koch, Chief Executive Officer, Dr. Joanne Donovan, Chief Medical Officer, and Dr. Alan Russell, Chief Scientific Officer. As a special guest, we have joining us Dr. Craig McDonald, Distinguished Professor and Chair of the UC Davis Health Department of Physical Medicine and Rehabilitation and a Principal Investigator in the CANYON and Grand CANYON trials. Before we begin, I would like to remind you all that some of the statements, sorry, some of the statements made during the call today are forward-looking statements that are subject to a number of risks and uncertainties. These may cause our actual results to differ materially, including those described in our reports filed with the SEC. You are cautioned not to place any undue reliance on these forward-looking statements, and Edgewise disclaims any obligation to update these statements. I will now turn the call over to Kevin. Thanks, Brian. Thanks to all of you for joining us today. I think we've got some really exciting news and really compelling data to provide to you. Edgewise Therapeutics is a leading muscle disease biopharmaceutical company developing novel therapeutics for the treatment of muscular dystrophies and serious cardiac conditions. The company's deep expertise in muscle physiology is driving a new generation of novel therapeutics. Sevesantan, the subject of today's disclosure, is our orally administered type 2 skeletal myosin inhibitor in late-stage clinical trials in Becker and Duchenne muscular dystrophies. Edgewise 7500, our novel cardiac sarcomere modulator for the treatment of hypertrophic cardiomyopathy and other diseases of diastolic dysfunction, is currently in phase II clinical development. The entire team at Edgewise is dedicated to our mission of changing the lives of patients and families affected with serious muscle disease. By way of introduction, let me tell you a little bit about how we discovered Edgewise 5506, now called Sevesantan. This was the first program we chose to target at Edgewise. Alan Russell, our Chief Scientific Officer and Founder, developed a novel therapeutic hypothesis for the treatment of muscular dystrophy. In the literature from the 1980s, he noticed that certain types of skeletal muscle, called fast skeletal muscle, were selectively degraded in Duchenne patients. He postulated that if you could selectively prevent fast skeletal muscle damage, one might attenuate the loss of muscle and subsequently the loss of function in patients. Later, other papers supported this hypothesis, where small tool molecules that selectively modulate type 2 myosin and ATPase prevented the progression of disease in preclinical models of muscular dystrophy. We initiated our program by running a high-throughput screen using a functional myofibril assay with skeletal muscle as an assay constituent. We evaluated over a million molecules to identify lead molecules that provided starting points for drug optimization and ultimately led to Sevesantan. From our preclinical studies, Sevesantan showed potent selective activity toward modulation of type 2 myosin in vitro. In vivo studies in models of muscular dystrophy, Sevesantan showed decreases in edema and muscle damage, both histologically and via plasma muscle damage biomarkers. It also showed increases in grip strength or general activity in advanced models of muscular dystrophy. We subsequently moved Sevesantan into human clinical trials, where we observed a well-tolerated safety profile with pharmacokinetics amenable for daily oral dosing and pharmacodynamic measures of target engagement. After our initial studies in Becker patients, over 14 days showed potent inhibition of plasma-associated muscle damage biomarkers. We then initiated the open-label ARCH study, where 12 patients were treated with Sevesantan with increasing doses from 10 milligrams to 20 milligrams over a 12-month period. In parallel, we initiated a placebo-controlled phase II dose ranging study called CANYON. This study, as you can see on the left side of the slide, was originally designed as a dose-finding study to evaluate Sevesantan on safety, pharmacokinetics, biomarkers, and functions in individuals with Becker's. The 12-month interim data from ARCH study supported the hypothesis that reduction in contraction-induced muscle damage has potential to preserve and improve muscle function while preventing disease progression, as measured by the North Star Functional Assessment Tool. With this result in mind, after consultation with regulatory authorities, we converted CANYON into two placebo-controlled studies that you can see on the right, where we selected a 10 milligram dose for the smaller CANYON cohort of 40 patients using the biomarker creatine kinase as the primary endpoint, and a larger 120-patient trial, potentially a pivotal cohort called Grand CANYON, using the North Star as the primary endpoint. As you know, Becker muscular dystrophy is a devastating neuromuscular disease with no approved therapies. Today, I'm pleased that Edgewise was able to report on the top-line results of the first successful placebo-controlled study in Becker. I'll hand it over to Joanne. Thank you, Kevin. Good morning, everyone. Here at Edgewise, our goal has been to positively impact the course of Becker muscular dystrophy. As you know, Becker is a rare, genetic, life-threatening, debilitating, and degenerative neuromuscular disease. It predominantly affects males, and it imposes significant physical, emotional, financial, and social impacts on these individuals and their caregivers, which we have been privileged to hear from the community. Individuals with Becker lose mobility, function, and independence in the prime of their lives. And importantly, there is currently no pharmacological treatment for Becker. Sevesantan is a first-in-class fast myofibril myosin inhibitor, which is designed to protect against contraction-induced muscle injury, the root cause of injury in Becker and Duchenne muscular dystrophy. In the absence of fully functional dystrophin, excessive contraction-induced muscle damage leads to progressive disease pathology in the sarcomere. Inflammation leads to replacement of muscle with fat and fibrosis, which ultimately leads to loss of muscle and consequently loss of function, all because of the contraction-induced muscle injury. By binding to myosin in the sarcomere, Sevesantan modulates contraction and prevents contraction-induced injury. When muscle is damaged, the sarcomeric membrane becomes permeable, producing elevated circulating levels of muscle injury biomarkers, including creatine kinase and fast skeletal muscle troponin, TNNI2. Elevated levels of these both indicate ongoing muscle damage in muscular dystrophies, and because these are circulating levels, we can measure these to determine ongoing muscle damage in muscular dystrophies. Our commitment to Becker is shown here with a number of both completed and ongoing clinical trials. We're going to focus today on CANYON, the phase II trial in Becker. As Kevin told you, this rests on previous information from the ARCH and DUNE studies, and it ultimately led to the pivotal cohort, which is ongoing, the Grand CANYON study. Patients in all of these studies can enroll in the MESA study, the open-label extension study for patients with Becker. I'm going to focus on the top-line results here. The CANYON study was designed as a phase II multi-center study to assess Sevesantan's safety and effect on biomarkers in adults with Becker. The primary efficacy endpoint is change from baseline in CK averaged over six, nine, and 12 months, basically looking at sustained effects on muscle damage biomarkers. Importantly, the study is not powered for functional endpoints. The key inclusion criteria was including ambulatory males, age 12 to 50, with a dystrophy mutation and a Becker phenotype, not on corticosteroids, and a focused group for adults with a North Star between five and 32. That is the group that is known from natural history studies to be in the decline phase of the disease. We enrolled 40 adults and 29 adolescents. As you can see here, the adults are considered to be one cohort. The adolescents were at two different doses. The study was conducted over 12 months, and there were a number of key additional endpoints, safety, and functional endpoints that we've been collecting. The study was conducted in three countries at 16 sites, and CANYON is the largest interventional Becker study to date. We screened a total of 80 patients with 69 patients enrolled. There was a low discontinuation rate, 4% overall, one of the 40 adults enrolled. To date, 99% of the eligible participants have continued to be enrolled in, gone on to the MESA open-label study. Currently, there's about 85 patients in the MESA study. Now, the restriction on the North Star score between 5 and 32 led to enrolling a group of patients with mutations that were associated with progression of the disease. These are the 45,X mutation as well as other mutations. The very slow progressing mutations, the X51, Del48, and 45-55, were not evident in the trial. There was only one adult in the trial. So the screening criteria was successful in recruiting a group of patients that were predicted to have progression. Baseline function is shown here. As you can see, we wanted to compare it first to the ARCH population, where we had seen two years of stability in the open-label study in patients with Becker. In general, the patients in the CANYON study were slightly better functioning, but generally characteristic of the ARCH population. However, as shown on the next slide, the functional measures were not well matched at baseline despite randomization based on North Star scores. The patients in the Sevesantan group had a consistently lower functional status. They had lower baseline North Stars. They had lower velocities in the timed functional tests, 4-stair climb, rise from floor, and 10-meter walk-run, as well as the 100-meter timed test. All of these were sometimes statistically significantly lower than the placebo, and that baseline imbalance is really a direct consequence of small study size, very limited placebo population. We anticipate that that will not be the case in the much larger Grand CANYON cohort of 120 patients. First, safety. Sevesantan was well tolerated. This is an overview of the treatment emergent adverse events. There was one discontinuation overall. Sevesantan was well tolerated. Individual AEs are shown on the next slide for you to peruse at your leisure. The bottom line was that it was well tolerated. There were no additional safety signals that were observed compared to our previous experience with Sevesantan. Now, the primary endpoint. We saw a statistically significant decrease in CK averaged over 6-12 months. The decrease was 28% versus placebo, with a p-value of 0.02. As you can see on the left, the change from baseline over time, we saw a rapid and sustained decrease in CK in the Sevesantan group. The placebo group of 12 was much more variable. On the right is shown the overall between-group differences at the average of 6 months -12 months. We also saw fast skeletal muscle troponin specific for the target of Sevesantan. TNNI2 decreased 77% from baseline in the Sevesantan treatment group versus placebo, with a p-value of 0.001. We see rapid and sustained decreases in these biomarkers of muscle damage with Sevesantan treatment. The key secondary endpoint was North Star. To remind you, not powered for North Star. However, as we saw in ARCH, the Sevesantan group, the North Star remained stable over the one-year period here. Placebo declined, consistent with previous observations in multiple natural history studies. The between-group difference was a least-squares mean of 1.12 points, favoring Sevesantan compared to placebo decreasing consistent with natural history. Now, what's important to patients? They want to remain stable or even improved. We saw that 63% of patients that were treated with Sevesantan showed stable or improved function after 12 months. The placebo group, 33%, had stability or improvement. That corresponds to an odds ratio of 3.4 for improvement or stability versus decline. This forest plot shows the trends across functional measures. The North Star least square mean difference of 1.12. There were small advantages for 10-meter walk-run, 100-meter timed test, and 4-stair climb velocity. On the right are the least square mean differences. Those are not p-values. These are all not significant, as you can see by the bars extending over the zero point. And rise from floor was close to the same for both of those. So to summarize, Sevesantan was well tolerated at all doses, both in adults and adolescents. There were no safety concerns identified in this trial compared with previous trials. In terms of biomarkers, the primary endpoint was achieved with a 28% average decrease in CK versus placebo, and plasma TNNI2 decreased 77% from baseline versus placebo. Again, significant with a p-value of 0.01, less than 0.01. In terms of function, Sevesantan treated patients towards stabilization of their North Star, with trends towards improvement compared to the placebo group, who declined in line with natural history. I will say that the imbalance between groups does confound the interpretation of some endpoints, including MRI, and evaluation of the full set data set is ongoing. Now, where do we go from here? Grand CANYON is ongoing. This is a global multi-center placebo-controlled pivotal cohort, so within the CANYON protocol, it assesses efficacy and safety of Sevesantan in Becker. The primary endpoint is North Star at 18 months. The key inclusion criteria are similar to, if not the same, actually, as in CANYON, with Becker patients having a North Star between 5 and 32, not taking corticosteroids. We planned an enrollment of 120, and we anticipate completing enrollment with over-enrollment in the first quarter of next year. The study was originally powered at 90% over 90% for observing a difference corresponding to the natural history decline of 1.2 points per year, 2:1 randomization at the dose of 10 milligrams. Now, where are we with that in terms of the power, and we can reassess in light of our results in CANYON, and the assumptions are shown on the left. We have a 2:1 randomization, the treatment difference, and standard deviation, as we saw in CANYON, assuming a 10% dropout rate and assuming that the treatment effect would linearly increase between month 12 and month 18. That leaves us with a 96% power based on an anticipated 1.68-point North Star difference at 18 months. The study is well powered based on the results of CANYON. We're pleased to say. In summary, we think these results support our continued engagement with FDA and EMA regarding marketing authorization filing strategies for Sevesantan in Becker. I mentioned Grand CANYON is nearing full enrollment. It is ongoing in 51 sites across the United States, Europe, New Zealand, Australia, and Israel. We are thrilled with the enrollment to date, anticipating over-enrollment the next quarter. To date, 99% of our participants that are eligible to participate have enrolled in MESA, which speaks to the well-tolerated nature of the drug. We are increasingly confident in the Grand CANYON study. And this is now based on the Sevesantan clinical experience in ARCH and now in CANYON, as well as natural history data and modeling. So with that, I thank you. And I would like to turn it over to Dr. Craig McDonald to provide some perspective on the clinical implications of these data for Sevesantan and its role in Becker. Great. Thank you very much, Joanne. And if we could go to the next slide, I just want to comment on this emerging natural history data that is being developed in Becker muscular dystrophy, specifically the NSAA natural history data. The NSAA has been now utilized in multiple Becker muscular dystrophy natural history studies to longitudinally assess function. And here's the data from three studies shown on the right. You can see this linear decline that occurs in the NSAA, specifically on the range of about 1.2 to 1.8 points annually when the baseline NSAA shows at least a 2-point decrement, so in the range of 5 to 32 points, with the peak value on the North Star being 34 points. And so there's really this emerging natural history data set, even before CANYON, that has been used to provide support that the NSAA decline is consistent in Becker muscular dystrophy patients who are already progressing and have that baseline deficit in NSAA of at least two points. If we could go to the next slide, I just want to provide some context with regard to the observations here from CANYON, and specifically providing a clinician's perspective in terms of interpretation of a one-point change in the NSAA. And what does a one-point change mean to a patient? So for instance, a one-point change in patients living with Becker, this decline could look like going from using stairs or steps independently to requiring assistance from another person or a mobility device to go up or down stairs. It could translate to using a toilet independently, going from sit to stand independently, to then requiring assistance for help to get up from the toilet. Or it could translate to a patient who perhaps has a fall or is on the floor, perhaps playing with their children, for instance, so really being able to get up from the floor independently to all of a sudden requiring someone else's assistance to transition from the floor. I think, again, we would expect a linear based on the natural history data and the data that we've seen now from ARCH and from CANYON, we would expect a linear decline to continue from 12 to 18 months, and so I'm actually really quite excited about this data. I think this is really, from my perspective, I think really a seminal time for the Becker muscular dystrophy community in terms of clinical translational research and clinical trial development, and for years, we've really grappled with the challenge of how do we design a clinical trial for Becker muscular dystrophy, and I think the CANYON study really demonstrates that the NSAA appears to be working well as a clinically meaningful endpoint. We see much less variability with the NSAA in terms of test-retest reliability and inter-rater reliability than we see in young Duchenne patients, and I think this probably adds to the statistical power of this use as an endpoint in clinical trials, and also, I think we're fairly confident now. We've been thinking for a long time about the duration of clinical trials needed to demonstrate treatment effects in Becker muscular dystrophy. I think that we're pretty confident that that trial duration needs to be approximately 18 months in length. I think really I'm excited about the data. The CANYON and Grand CANYON studies are really the first studies of their kind in Becker muscular dystrophy. I've treated a number of patients with the open-label Sevesantan as part of the MESA study, the open-label extension from CANYON. I've really been quite impressed with the stability of these patients that we're seeing in clinic. Based on this data, I really have great enthusiasm for the prospect of Sevesantan for our Becker patients. Also, I think this provides added confidence that Grand CANYON is a well-designed trial with good prospects of succeeding. Thank you, Craig. I also want to extend thanks to you, to all of the investigators and site personnel, and most importantly, the patients and their families. They have lives. This is an imposition to ask them to come in for all of these visits. And so we are enormously grateful for their participation in the study. Yes. Thank you, Craig, as well. You've been great and provided a lot of guidance for our studies and a great consultant for us. As you've heard from Dr. McDonald, Becker muscular dystrophy is a devastating disease where patients are typically diagnosed in adolescence, and with a slow, unyielding progression leads to patients ultimately losing their ability to function in society, often in the prime of their lives. Even though there are over 12,000 patients in the three major markets of the U.S., EU, and Japan diagnosed with Becker, and there are significant challenges of the disease, there are currently no therapeutic options for these patients. Edgewise is striving to become the first company to help address this huge unmet medical need. I'd like to provide an overview of our results over the past year and on some of potential future milestones. In September, we reported positive results from the first human data for Edgewise 7500, our cardiovascular asset for the treatment of hypertrophic cardiomyopathy and other diseases of diastolic dysfunction. Additionally, we reported that we had initiated 28-day studies in obstructive hypertrophic cardiomyopathy and non-obstructive hypertrophic cardiomyopathy, and we'll report these results by the end of the first quarter of 2025. In the muscular dystrophy space, we today reported positive results on our CANYON study, and then we have our potentially pivotal Grand CANYON study fully enrolled by the end of the first quarter of 2025. We will also file an IND for our cardiovascular asset for the treatment of heart failure in the second quarter of this year. With regards to our dose-ranging LYNX and FOX studies in Duchenne muscular dystrophy, we're encouraged by the observations from CANYON and believe that we've identified doses in LYNX and FOX that we believe could demonstrate the same level of functional benefit to boys with Duchenne. Specifically, we studied dose ranges from 2.5 milligrams- 30 milligrams daily and observed the 5 milligram and 10 milligram doses have been well tolerated, have shown biomarker changes suggestive of protection against contraction-induced muscle injury, and have shown preliminary evidence of functional stabilization. We are currently enrolling additional patients at these doses to provide additional support for these observations. We will discuss these results and the potential for phase III studies in future scientific forums. Next slide. Finally, we are well financed with $493 million in the bank, zero debt, and a cash runway through 2027. In conclusion, I'd like to personally thank everyone who has chosen to support our mission, including physicians, investors, and particularly our talented and dedicated employees and their families. Most importantly, I'd like to thank the patients and their families for their trust in us to deliver new therapies for their loved ones. With that, we go to Q&A. Thank you. If you'd like to ask a question, please click the raise hand button at the bottom of your screen at this time. We ask that each person ask only one question today. Our first question today comes from the line of Joe Schwartz from Leerink Partners. Please go ahead. Your line's now open, and please unmute. Thanks so much, and congrats on the strong results. I was wondering, it doesn't seem like any stratification was used to balance enrollment in CANYON. I was just wondering, is that the case also with Grand CANYON? Have you looked at baseline characteristics for Grand CANYON to see whether the trial is balanced? Yeah. So we did have a stratification in CANYON, but with the 3:1 randomization, it was not particularly effective, which led to the imbalance between the treated and untreated. Within the Grand CANYON, we have a similar stratification with above 22 or below 22, with an overall North Star range of 5 to 32. So with the greater number of Ns, we believe that we will have a more balanced study. But with the small Ns within CANYON and the stratification of 3:1, it just did not work out in the way we had predicted. I mean, Joanne, do you have any additional? It is the tyranny of small numbers in clinical trials with 12 placebo patients. Right. Yeah, that makes sense. Thanks. I'll get back in the queue. Fantastic. Thank you. And our next question today comes from the line of Yasmeen Rahimi from Piper Sandler. Your line is now open. Please unmute. Yep. Good morning. Tim, can you hear me? Yep. Okay. Thank you. Congrats on the data. I guess, Tim, one of the thoughts as you guys are going to be taking this data and engaging with the agency around the opportunity to file, could you talk about what have you been able to look at biomarker and their correlation to North Star? What is sort of the hierarchy of the data that you'll be presenting and the likelihood of the agency to sign off towards this data package to be able to be ready for approval while we're waiting for a Grand CANYON? Sorry for the long-winded one question. Yeah. Thanks, Yas. So I think we've said in the past, and I think this is still our position, that creatine kinase or biomarkers becoming a surrogate for function in muscular dystrophy will be challenging with the agency. And you've seen the variability, in particular with placebo, in those biomarkers, even though Sevesantan itself is quite reproducibly down versus these biomarkers and highly durable, and what we think is differentiated from placebo overall. I think ultimately what would win the day with the agency would be taking a different tack. This would be one where we point out the high unmet medical need of Becker patients, point out the safety of our drug, point out the change from baseline that we've observed between the placebo group and the treated group, and use the surrogate markers and other patient-reported outcomes as supporting evidence for the potential of this drug for accelerated approval. Now, you might have seen just in the last few weeks new draft guidance for accelerated approval, which might include essentially the functional endpoints as potential surrogates for approval. I think it's an interesting document and is thought-provoking of how we might, in rare disease, be able to move these drugs to patients in a more effective way. I think also there's at least some guidance to support that you can utilize propensity matching and other placebo subsets of historical data to support these small trials. All of these things will go into our strategy of discussing this with the agency. I think in our case that we will have completed enrollment of our Grand CANYON study. I think will go a long way into supporting the filing and also the enthusiasm for the patients going on to MESA and apparent interest in participating in the MESA study. I think all is good supportive data that the agency can consider for our filing. All right. Thank you. And the next question today comes from the line of Laura Chico from Wedbush. Laura, your line is now open. Please unmute. Good morning. Thanks very much for taking the questions and congrats on the data. Apologies if I missed any commentary here, but based on the CANYON data, what read-through should we be making to the LYNX and FOX study? I believe we still expect data in DMD before the end of the year. Thanks very much, guys. Yeah. I think what it says is that if you carefully control the studies and you look at both biomarkers and function simultaneously, I think that you can provide some guidance of what you would expect to see within the Duchenne population. I think it's more difficult in Duchenne because these patients are more heterogeneous, and the measures, particularly North Star, is not as effective in the younger Duchenne patients. But by looking at some of the other measures like time to rise and/or the SV95 driven by the stride device, which we are relying on heavily to interpret our potential of disease stabilization Duchenne, all of those considerations go into whether or not we think we can design an effective phase III trial in Duchenne. I think this is supportive of the drug, supportive of the mechanism, and we're now considering how we eliminate some of the heterogeneity within the Duchenne population to run a high-quality phase III trial. And Laura, as we've always said, right, the approach in Duchenne is a little bit different because we're working back through what will the competitive landscape look like at the time that we would be potentially launching, and then ultimately designing a clinical trial that selects the right patients with the right background medications and within the right age group to allow us to power a study to demonstrate efficacy that is going to be meaningful at the time of launch. So all of those considerations are really important as we continue to capture data from both the LYNX and the FOX trials. Thanks, guys. Looking forward to it. Thank you. And the next question today comes from Tessa Romero from J.P. Morgan. Please go ahead. Your line is open if you can unmute. Hi, Kevin and the team. Thanks for taking our questions here, and congratulations from us on the results. Based on these data, perhaps for Dr. McDonald and the Edgewise team, are there any anticipated changes to the design, any elements of the statistical protocol that you would recommend to increase the probability of success of Grand CANYON, and if anything at all? Are there any other analyses, Dr. McDonald, that you would like to see from the study to better understand the clinical benefit? Thanks so much. Yeah. Craig, maybe comment on the imbalance of this and what your thoughts on how to interpret the data from CANYON and how that might apply to modifications of Grand CANYON that would be more successful? Yeah. No, thanks. Thanks, Kevin, and thanks, Tess, for the question. I think, first of all, I think in terms of the imbalance, I think first and foremost in my mind is that imbalance likely to explain a difference in natural history of, say, the placebo patients, expected natural history in placebo patients versus the treated patients. And I think if anything, as you get to lower values on the North Star, actually what we tend to see is a little bit more robust and rapid decline, and it's the patients that are near the ceiling value on the NSAA that tend to have a bit more slow decline. So if anything, I think the fact that the imbalance was in the direction of the Sevesantan treated patients being a bit more impaired than the placebo patients, I think that gives us confidence that we are seeing a real effect. I think if the imbalance had gone in the other direction, I think we'd be asking ourselves, well, is the difference in the one-year trajectory perhaps due to that imbalance? But I think fortuitously, I think that imbalance actually, if anything, favored the Sevesantan treated patients, probably showing more severe decline over time. I think in terms of modifications to the Grand CANYON, I think I'm really quite pleased going into this in terms of the statistical power that's being anticipated. And I think probably the decrease in variability that we see with the NSAA as an endpoint in Becker muscular dystrophy in comparison to, say, Duchenne muscular dystrophy patients who are ages four, five, and six, I think really drives that increased power that we're seeing with the NSAA as an endpoint. I think if anything, in order to get into this trial, I think there needed to be a two-point decrement in the baseline NSAA. I think it's entirely possible that perhaps looking at the data, we may anticipate perhaps more of a decline if there's perhaps a four-point decrement in the NSAA at baseline. So I think it's entirely possible that we may have a safety cohort that would be a larger, wider cohort with baseline values of, say, five to 32 on the NSAA. But the primary pre-specified statistical analysis for the NSAA, perhaps one could argue that perhaps that may be based on a population with NSAA values of 30 and below, for example. I'm sure we'll have to dig into that in terms of from a statistical point of view. But I mean, that's one of the potential modifications that I could see. I think we'll probably also, we've learned some aspects in terms of the hierarchy of the secondary endpoints based on the CANYON study results. So I think that will improve our determination of the key secondary endpoints and the hierarchy of those secondary endpoints in a pre-specified manner. But those are some of my initial thoughts in looking at the data. Thanks, Craig. Great comments. Thank you. Thank you. And the next question today comes from the line of Leonid Timashev from RBC Capital Markets. Your line is now open. Please go ahead and unmute. Hi, guys. Congrats on the data. I wanted to ask on the adverse events table, just curious in general what you're seeing there and then maybe more specifically look like earlier we had talked about perhaps some dizziness, headache that's associated with the drug. Is that still there? Can you talk about the course of that? And the fall imbalance, it looked like it was maybe a slight imbalance there. Was that related to the dizziness and the headache, or is that just small numbers? Thanks, but I'll hop back in the queue. Joy, I'll take that. Hi, there. Yeah. Dizziness and somnolence were seen as they had been in previous trials, typically at the initiation of dosing or in the first days or weeks and resolving spontaneously. We give the drug at night, and that has not been an issue for the patients that we have heard. With respect to the falls, that's something that's a good point, something we looked at carefully. None of the patients who had falls had dizziness associated with those falls. Only one of them even had dizziness at any time, and that was a couple of months prior to the fall. Falls are characteristic of this disease in terms of when you look at the amount of muscle mass in many of these men, that they have a considerable replacement of muscle with fat, and they really have very little reserve if they get off balance. And so falls are quite characteristic and imbalanced. And there's also the imbalance in the groups. So I think there was slightly more in the treated group, but that also reflects that they had lower North Star. And when you look at the folks with falls, you have the folks with the lower North Star scores. They're not the people with the 32. Yeah. So if you match the patients with the lower North Star scores from placebo to treated, there was no difference in falls. So it is really driven by the greater level of severity and the lower North Stars within the Sevesantan treated patient population. If I could just comment about the somnolence and dizziness, as Joanne pointed out, we really see this decrease in severity after the first month of treatment, and patients really begin to experience much less in the way of somnolence or dizziness. I will say there's really a wealth of published data indicating that Becker muscular dystrophy patients actually have fairly common reports of chronic musculoskeletal pain, and the pain is really a problem area in DMD, and I will say that it seems like the patients that have been treated long-term with this medication do seem to sleep better. Some of that may be some alleviation of pain. Some of it could be some somnolence that's experienced by taking the drug in the evening hours, which probably does help with sleep, so it really hasn't been a difficult adverse event to manage clinically. Thank you. The next question today comes from the line of Kripa Devarakonda from Truist Securities. Your line is now open. Please unmute. Hello? Hey, Kripa. Hey. Can you hear me? Sorry. Yes. Thank you. Congrats on the data, and thank you so much for taking my question. I had a question about improvement seen in patients on placebo. There were about two patients with NSAA improvement of more than two points. There were four patients, I think, on treatment that showed similar improvement. So I was just wondering if there was a difference in the baseline characteristics of these patients. Anything you can comment on those patients? Thank you. Yeah. I think, Kripa, it's kind of small numbers. I don't think there was anything in particular that stood out at the moment, but I think we want to. We don't have, for instance, MRI data on every patient. So we're now looking at multiple different endpoints and trying to understand how individual patients might have responded to the drug with individual baseline characteristics, but I think it's small n's. And Joanne, one comment maybe. The other thing is, remember from the individual patient plots in the ARCH data, there was more variability at the higher North Star scores, probably because there you're looking at changes from can do the task without compensation versus needing to compensate, and that seems to go back and forth a little bit more than when you get down to the bottom of the scale where you can't do or can do, that is more concrete, so I think there may be more variability in the placebo patients at the upper end of the spectrum, but again, these are small numbers. Great. Thank you. Thank you. And the next question today comes from the line of Cory Kasimov from Evercore. Cory, your line's open. Go ahead and unmute. Great. Thanks, guys. Good morning. Appreciate you taking the question. Curious when we can expect to get an update on the adolescent cohort. Was that never supposed to be part of today's data release? And is there any kind of nuanced sort of interpretation when we look at the kids versus the adults? Thank you. Yeah. Historical data is pretty sparse on the adolescents, and we really included the adolescents as a safety cohort, and we had two different doses there in the safety cohort. So I think from a standpoint of function and for that matter, some of the biomarker studies, the adolescents is really there to understand the safety of the drug in a younger patient population. Ultimately, we will probably add additional patients in the adolescents cohorts to get a better understanding of which one is the appropriate dose for those patients. But fortunately, there was no change and no difference in the safety profile in the adolescents, and we'll be reporting that data at future forums in regards to what we actually saw there. Yeah. That's helpful. Thank you. Thank you. And it looks like we have another question from Kripa Devarakonda from Truist Securities. Krupa, your line is open. Hey, guys. Thank you for taking my question again. I just wanted to ask quickly. I know you've talked about it in your prepared remarks as well, but what you've seen here changes your strategy or thinking about the advanced trials in DMD and what is important and how you would design the trial in any way? Thank you. Yeah. I think we've already commented that. I think this validates the mechanism of the drug and the potential of this mechanism to provide benefit to muscular dystrophy patients broadly. I think inherently in the Duchenne population, you have higher levels of variability based on age and function as well as different background therapies. So from our standpoint, I think this encourages us to continue to study the Duchenne patients to identify the right way to design a phase III. So I think, and Behrad, you want to comment? Yeah. I think the other thing, Krupa, and up to this point, we've always said we're looking at a number of functional measures. I think even Dr. McDonald pointed this out. I think what you've seen here is a really nice and tight North Star response, which isn't always the case when you look at Duchenne trials because North Star, as you guys know, is really noisy in kids, so I think if anything, it's made us think more closely around using SV95, which appears to be a more sensitive measure, particularly in boys, and that's coming from work that's been done in Europe by Laurent Servais and others, and so I think maybe we're going to put a little bit more emphasis there and have a conversation with the FDA using SV95 as more of a sensitive measure for function. We've seen others do that in this space as well. Great. Thank you. All right. Thank you. It looks like that's all the time we have for questions today. So I'd like to pass the call back over to Kevin Koch for any closing remarks. Please go ahead. Thanks, all, so thank you all for joining the call today. In conclusion, I'd like to personally thank everyone who has chosen to support our mission, including the physicians and investors, in particular our talented and dedicated employees and their families. Most importantly, I'd like to thank the patients and their families for their trust in us to deliver new therapies for their loved ones. Thank you all for attending, and look forward to discussing this further. That concludes today's webinar. Thank you all for your participation. Good.