Good morning, everyone. I'm Amy Reilly, Senior Vice President, Head of Corporate Communications and Investor Relations at Dyne. Thank you for joining us for Dyne's virtual event to review compelling new clinical data from our phase 1 DELIVER trial of DYNE-251 in people with Duchenne muscular dystrophy who are amenable to exon 51 skipping. Before we get started, I'd like to remind everyone that we will be making forward-looking statements today that are subject to the safe harbor protections provided under the Private Securities Litigation Reform Act of 1995. Actual results may differ materially from these forward-looking statements as a result of various important factors, including those discussed in the Risk Factors section of our most recent Form 10-Q. These statements represent Dyne's views as of today's date, and we disclaim any obligation to update these statements except as required by law. For today's program, John Cox, Dyne's President and CEO, will offer some brief remarks on the DELIVER trial and the leadership appointments that were outlined in the press releases issued earlier this morning. Dr. Wildon Farwell, our Chief Medical Officer, will review new data from our DELIVER clinical trial, and we will open for questions. Our Chief Scientific Officer, Dr. Oxana Beskrovnaya, will join us for the Q&A, as will Doug, Dr. Doug Kerr, our incoming CMO. You can submit questions at any time using the Q&A box at the bottom of the video player. A couple of notes, you can access the presentation for today's program in the tab underneath the video player. If you experience any technical issues during the broadcast, we suggest you refresh your browser, and if that does not resolve the issue, please message via the technical support chat on the bottom right corner of the screen. With that, I'll hand it over to John for opening remarks. Thank you, Amy, and thanks to everyone for joining us today. This Saturday marks World Duchenne Awareness Day, a day dedicated to raising awareness for this devastating disease. Despite important progress over the last decade, too many families face a life-changing diagnosis and then wonder what the future will hold for their child as they deal with the progression of the disease. Despite recent approvals, people living with Duchenne still need new therapeutic options. They clearly demonstrate meaningful, functional benefit, and there are still parts of the world, such as Europe, where there are no disease-modifying treatments available. At Dyne, we strive to transform the treatment of this disease by developing medicines that generate functional benefit for patients. Our update on our DELIVER trial of DYNE-251 is another important step in our ultimate goal. We have new data from our dose optimization cohorts, including the 20 mg per kg cohort, which illustrate the potential for DYNE-251 to be best-in-class therapy for Duchenne, achieving unprecedented dystrophin expression and meaningful improvement in multiple functional endpoints across multiple cohorts and a favorable safety profile. The FORCE platform was designed to drive broad distribution into tissues that matter in muscle diseases. Preclinically, we observed significant delivery to skeletal muscles, including the heart, as well as to the diaphragm, meaning that our platform delivers to the muscles that are critical to disease progression. We are excited by the dystrophin expression that we will present today, as dystrophin is an established path to expedited approval. But we know that what patients care about is functional benefit. For the first time, we are seeing meaningful functional improvement in just six months in two different cohorts. This suggests we may be able to move from just slowing progression to actually improving the course of this disease. We wanted to share these data today because we now have an additional cohort of data demonstrating unprecedented functional improvement. We've completed our dose optimization cohorts and are working to initiate registrational cohorts, all while pursuing expedited approval pathways to move quickly to advance DYNE-251. In addition, we're building the leadership team to execute on Dyne's next chapter, including preparing for potential registration and commercialization, and now I'll turn things over to Wildon to review our latest data from Deliver. Thanks, John. Many of you are familiar with Duchenne muscular dystrophy. It is a devastating progressive disease that is 100% fatal. People with Duchenne lack the ability to make dystrophin, which leads to progressive muscle weakness, loss of lower and upper limb function, and eventually cardiac and respiratory failure that ultimately results in death, typically around thirty years of age. We are focused on the opportunity to build a best-in-class exon skipping franchise of therapies for DMD, starting with DYNE-251, and are excited today to share additional data from the DELIVER trial in patients with mutations amenable to exon 51 skipping. As a reminder, exon 51 skip amenable patients are the largest subsegment of the DMD population amenable to exon skipping, representing approximately 13% of patients. Additionally, this segment of patients has been shown to exhibit some of the most severe natural history in DMD, with low dystrophin levels and early loss of ambulation. Our goal is to effectively and broadly deliver Dyne two fifty-one to muscle to increase the production of dystrophin and drive functional benefit while offering a monthly or less frequent dosing regimen for these patients. The weekly standard of care for exon 51 has demonstrated limited dystrophin production, less than 1%, and requires weekly administration due to the challenge of delivering enough active drug to the muscle. Now to the trial design. DELIVER is a phase I/II global trial that we designed to be potentially registrational. It consists of a 24-week multiple ascending dose, or MAD, randomized placebo-controlled period, a 24-week open label extension, and a 96-week long-term extension. The trial is enrolling ambulant and non-ambulant males with DMD, who are aged four to sixteen years and have mutations amenable to exon fifty-one skipping. Patients who have been previously treated with exon skipping therapy can enroll in DELIVER after a twelve-week washout period. The primary endpoints are safety, tolerability, and change from baseline and dystrophin levels as measured by Western blot. Secondary endpoints include time function tests, as well as measures of muscle function like NSAA and SV95C. SV95C has been qualified as a primary endpoint by the EMA and is currently leveraged across multiple global Duchenne clinical trials. In the MAD placebo-controlled portion of DELIVER, participants are randomized to receive DYNE-251 or placebo every four or eight weeks. Open muscle biopsies are taken from the upper limb at baseline and six months, and following the MAD portion, participants are escalated to the highest tolerable dose in the OLE and then LTE. In January of this year, we shared dystrophin data from our 5 mg per kg Q four-week cohort. Then in May, we reported data from our 10 mg per kg cohort, and now today we are reporting FC data from our 10 mg per kg cohort at a longer time point, as well as our 20 mg per kg cohort. And with these robust data, we are positioned to turn our focus now to initiating registrational cohorts. We look forward to sharing details around these cohorts later in 2024, when we provide an update on the path to registration. We have seen tremendous enthusiasm to participate in the DELIVER trial, even with other therapies approved or in development, and we have progressed rapidly through enrollment. Turning to the baseline characteristics for the DELIVER trial. As we have noted previously, because DELIVER is potentially registrational, in order to maintain the blind, we have not broken these cohort characteristics out by placebo and DYNE-251 treatment groups. Overall, baseline characteristics are similar across cohorts and generally representative of a population of boys living with DMD, amenable to exon 51 skipping therapy. The study has enrolled a broad, diverse range of ages, BMI, baseline function, and ambulation status, which gives us a high level of confidence that all patients could potentially benefit from the treatment. However, there are some differences in age and baseline function across the cohorts that may impact our results. For example, participants in the 10 mg per kg Q four-week cohort were younger than participants in other cohorts, and participants in the 20 mg per kg Q four-week cohort had a lower NSAA than participants in other cohorts. Now, moving on to the safety profile, which overall has been favorable to date for DYNE-251, based upon 54 participants enrolled thus far in DELIVER, with approximately 675 doses administered to date, representing over 50 patient years of follow-up. The majority of treatment emergent adverse events were mild or moderate. There have been three serious treatment emergent adverse events potentially related to study drug that occurred in two participants in the same country in Europe, in the 40 mg per kg Q four-week cohort that we had initiated after having observed favorable safety profile in the 40 mg per kg Q eight-week cohort. These events had multiple confounding factors suggestive of infection or background risk that likely contributed to their presentation. One participant presented with fever, vomiting, and diarrhea. They were then found to have heme-positive stools and developed hemolysis and acute kidney injury. Together with our external consultants, we believe these events are consistent with hemolytic uremic syndrome, with a possible infectious etiology, and are continuing to further evaluate the underlying etiology of this event. The other participant presented with low-grade fever and tonsillitis. Symptoms resolved without any therapeutic intervention. This participant also had a history of hemolytic anemia of unknown cause years prior to enrolling in DELIVER. Both participants are now home and have fully recovered. There have been no other serious adverse events associated with thrombocytopenia, anemia, kidney injury, or clinically meaningful changes in electrolytes, including magnesium, reported in the DELIVER trial. While we further evaluate these events to understand the underlying etiology, the fourteen participants who were enrolled in the forty mg per kg Q eight-week and Q four-week cohorts are now being dosed at twenty mg per kg. I would also note that the thirty-two participants who have been enrolled in the starting dose cohorts, so the point seven, two eight, and five mg per kg, as well as the ten mg per kg, are all now being dosed at twenty mg per kg, so all participants in DELIVER are now being dosed at twenty mg per kg, and we plan to select doses of twenty mg per kg or higher for our registrational cohorts. One other note. Consistent with our prior updates, we continue to observe a favorable safety profile for DYNE-101 in our ongoing ACHIEVE trial in patients with myotonic dystrophy type one. In ACHIEVE, 56 participants have been enrolled through the 6.8 mg per kg Q8-week cohort, with over 680 doses administered in more than 55 years of patient experience to date. The majority of treatment emergent events have also been mild or moderate. There have been no treatment-related serious adverse events, and no participants have demonstrated persistent anemia or thrombocytopenia. Now, let's turn to the FC data in DELIVER, starting with muscle delivery. Here, we see DYNE-251 drove dose-dependent increase in PMO muscle concentration. We also saw a dose-dependent increase in exon skipping. Here, you see that 20 mg per kg of DYNE-251 resulted in 3.27% exon skipping. We are very enthusiastic about the best-in-class dystrophin data, as measured by Western blot, that we saw with the 10 mg per kg and now in the 20 mg per kg cohort. Furthermore, we see high correlation between levels of exon skipping and dystrophin production in our participants. We are seeing greater than tenfold higher dystrophin levels at six months than what has been reported for Eteplirsen, the current standard of care for exon 51, with a significantly lower PMO dose administered four times less frequent. At the 20 mg per kg dose of DYNE-251, we reached 3.71% normal dystrophin, a change of 3.15% from baseline. This dystrophin analysis is unadjusted for muscle content, and we believe this is an appropriate evaluation of dystrophin. Others in the field have adjusted for muscle content, so we have done that analysis as well. Here, you can clearly see how we have calculated this. AMHC dystrophin divided by percent muscle content. DYNE-251 achieved 8.72% dystrophin at six months. This is a change of 7.37% from baseline. We believe this is the highest level of dystrophin reported for an exon 51 skipping therapy, including peptide conjugates in development. Dystrophin is an important measure, but it represents one muscle, and we know that it builds over time. However, dystrophin is not our ultimate goal. We have always focused on creating enough near full-length dystrophin to generate functional benefit in patients. Because no prior exon skipping therapy has demonstrated improvement in functional endpoints, the entire field has faced two important questions: What level of dystrophin is required for functional benefit? And can you achieve the distribution required to see improvement in all muscle types, including cardiac and skeletal muscle impacted by DMD? This is a remarkable moment in our DYNE-251 program. In our previous updates, most of the discussion was on dystrophin. Now, with multiple cohorts worth of data showing improvement in function in a broad set of patients, we are able to share functional data in greater depth. What is very exciting is that you now see dystrophin levels across two cohorts that are leading to encouraging trends in improvement in multiple functional endpoints that continue with time on therapy. First, let me show you the typical progression of Duchenne. Here, you see placebo-treated patients who worsen across a number of endpoints over time. Now, you see the opposite with DYNE-251-treated patients, and this is inconsistent with the natural history of this disease. Today, we are sharing six-month functional data from the 20 mg per kg cohort and building on what we shared in May from the 10 mg cohort. We now have longer, 12-month data from those participants. These data suggest that the distribution across cardiac, skeletal, and smooth muscle observed preclinically with the FORCE platform is translating into the clinic. Starting with the 10 mg per kg cohort, we saw a continued effect across multiple functional measures at 12 months: the North Star Ambulatory Assessment, time to rise from floor, 10-meter walk/run time, and stride velocity in the 95th percentile. And I'll note that at a time point after 6 months, the 10 mg per kg participants escalated to 20 mg per kg, showing the benefit of higher dose and longer time on therapy. And finally, you see 6-month data for the 20 mg per kg cohort, and again, improvement in the same functional measures. And what's exciting about this is that it replicated another set of patients. While it's great to see the impact across many measures, we want to spend a little more time on SP95C. This is a digital outcome measure approved as a primary endpoint for Duchenne clinical trials in Europe. It is an objective endpoint of ambulatory performance in patients' normal daily environment, where patients wear the device on each ankle for at least three weeks prior to clinic visits. What you see here is DYNE-251 treatment led to clinically meaningful benefit, and the change from baseline met the published minimally clinically important difference, or MCID, by the EMA at zero point one. At six months, we are at the level identified by the EMA, and this is compared to baseline, not accounting for the worsening among placebo. As you recall, SP95C is a real-world measure, and it's not subjected to motivation bias that is seen in other endpoints. This is a level of improvement previously not observed in the field. What is also meaningful about the dystrophin and functional data and across these two cohorts is that it gives us a lot of confidence that we have the opportunity to see benefit in all patients with DYNE-251.... We believe this data set from DELIVER illustrates the promise of FORCE in developing next generation exon-skipping therapies and building a global DMD franchise. We are excited about the opportunity to leverage FORCE to address additional mutations. We have preclinical programs targeting additional exons, including fifty-three, forty-five, and forty-four. There is a significant need for therapies targeting these exons as well. So in summary, we believe these DELIVER data reinforce the opportunity for our DMD exon-skipping franchise, starting with DYNE-251, and we are driving towards a potentially registrational data set based on the strength of the data we have shared here today. At 20 mg per kg Q4 week, DYNE-251 showed a compelling profile with unprecedented level of dystrophin generated, with 3.7% unadjusted and 8.7% muscle content adjusted dystrophin, with encouraging trends in improvement across multiple functional outcomes, including SV95C, which is an approvable endpoint in Europe, and a favorable safety profile, with approximately 675 doses administered, representing over 50 patient years of follow-up to date. All of this reinforces the potential of FORCE in the development of our global DMD franchise. With the strength of these data and regulatory interactions, we are initiating registrational cohorts, pursuing accelerated approval, and plan to provide an update on the path to registration for DYNE-251 by the end of this year. Before I turn things over to John, I just want to say how excited I am about these data and the opportunities ahead for DYNE to deliver truly life-transforming therapies to individuals living with serious muscle disease. It has been a privilege to work on the design of our clinical programs, partner with clinicians, patients across the globe participating in our DELIVER and ACHIEVE trials, as well as our dedicated employees at DYNE. When I step back and think about all that has been accomplished in a few short years, it's truly been amazing. We have shown in DYNE-251 and DYNE-101, two programs with favorable safety profiles, clear improvement in biomarkers that can serve as surrogate endpoints, and functional improvement across multiple measures and multiple time points up to one year. I am extremely proud of the DYNE team, and I want to thank them from the bottom of my heart. I am very excited about DYNE's future and its opportunity to bring truly life transformational therapies to patients. It is a good time for me to hand the reins over to Doug Kerr, who is joining the team. Doug and I worked together for many years at Biogen, and he brings great experience in developing therapies, including rare neuromuscular diseases. Doug, it would be great to hear your perspective, not only on the data we are sharing today, but the opportunity you see here at DYNE. Thank you, Wildon, and really congrats to you and the DYNE team. This is truly remarkable data. You and I have worked together, we've known each other, we've worked on spinal muscular atrophy, and we've really seen the potential of Spinraza to radically transform disease progression and actually lead to improvement in function. So Spinraza has been transformational for patients, and I actually see huge parallels between that and what you and DYNE are doing here in Duchenne muscular dystrophy. I am deeply impressed with the science and the execution that has enabled DYNE to obtain these really important data. As you know, I am a neuromuscular neurologist. I have taken care of people with DMD for many years. The field desperately needs therapies that preserve or improve function in individuals with DMD. As I look at these data, I believe DYNE-251 is potentially transformative therapy with meaningful impact across multiple functional endpoints. I'm excited to be a part of the team that will drive this program forward and hopefully enable this to get approved globally. Great. Thanks, Doug. I will be at DYNE to help support the clinical execution through the end of the year, and we'll work closely with Doug as we continue to drive these programs forward. With that, I turn it over to John. John? Yeah. Thank you, Wildon. And, you know, just first, I just want to thank you, Wildon, for really a phenomenal job here at this company. It's been a pleasure for me to work with you. I'm glad you're staying on through the end of the year. And I've really enjoyed working with you and appreciate all that you've done with the team. And I also want to welcome Doug Kerr. I've known Doug for years. He's a renowned clinician in this area, very creative, and I think both Wildon and I would agree that he's really the perfect person to take these programs to registration, to the next step. Today's data continue to highlight the opportunity we have to change the treatment paradigm in these two diseases and the potential of the FORCE platform in the development of targeted therapies for other muscle diseases. We have now shown data at higher doses and longer time points across both DM one and DMD programs. In Duchenne, we continue to see unprecedented impact on dystrophin. But dystrophin alone is not enough. We are now seeing functional improvement where this has been very difficult to achieve. We are continuing to pursue expedited approval pathways, and we are initiating registrational cohorts in DELIVER. In ACHIEVE, we fully enrolled the 6.8 mg per kg cohort. We continue to pursue expedited approval, and we have the opportunity to share additional data in the DM one trial, as well as an update on the path to registration by year-end. Finally, we are building the team to plan for potential registration and commercialization. As Dyne enters this next chapter of becoming a fully integrated biotech company, I'm pleased to welcome Doug Kerr, CMO, Johanna Friedl-Nader as Chief Commercial Officer, and Lucia Celona as our Chief HR Officer. I have worked with each of them for years. They bring to Dyne tremendous experience in launching rare disease therapies globally, all while building and leading teams with proven expertise in these areas. This will be invaluable as we prepare for potential expedited approval, registration, and commercialization, starting with our DM1 and DMD programs. Together with all Dynamos, we will build on the progress the team has made and continue to move with a sense of urgency to deliver new hope for patients with serious muscle diseases. Thank you all for joining us today, and I'll turn things back over to Amy to open things up for Q&A. Great. Thanks, John. Why don't we start with Wildon? Question for you, can you provide any additional detail on the SAEs observed in DELIVER, and is there any read-through at all to the platform? Yeah, thanks, Amy. So first of all, I just wanna again restate that we are very pleased with the overall favorable safety profile for both DYNE-251 and DYNE-101. We don't view this as platform related at all. The two participants with these SAEs, they both had multiple potential confounders. The one participant had clinical course very consistent with infection. Both events occurred in one country in Europe. We continue to follow these events. We feel quite comfortable with the clinical course. Both participants are now at home doing well. We continue to monitor the participants in DELIVER. We've not seen any consistent similar phenomenon to what was observed in these participants, so we feel good about where things are with the trial. Out of an abundance of caution, we down-dosed to the 20 mgs per kg. All participants are now at 20 mgs per kg, and we continue to follow them going forward. We do believe we have the opportunity to pursue registrational cohorts now, and that is what we will begin to do at 20 mgs per kg or higher. Great. And another one, Wildon, you know, what was the FDA or other regulators' reactions to the SAEs? Did they influence the decision to dose at 20 mg per kg in DELIVER for all participants? Yeah, so we've been working very hard to understand the etiology of these events. We've shared all of this information with regulators. They've been very comfortable with our approach. They've agreed to the plan that we've put in place. It has been a very good collaborative relationship. Again, we continue to provide them with updates. They continue to be very pleased with the progress that is being made in understanding these events and are very happy to follow our lead as we continue to monitor and continue to follow these events going forward, so we've had a very good relationship with regulators on these events, and we plan to continue that going forward. Great. Wildon, staying with you, you are initiating registrational cohorts. You know, what dose can you go up to 40 mg per kg? Yeah, so we really believe the data at the 20 mg per kg is transformational. To be able to see the highest level of dystrophin for an exon 51 skipping therapy, and then to see that translate into functional benefit for patients is truly, truly remarkable, and so we're very excited by this data set. We do believe that we can initiate the registrational cohorts at 20 mg per kg or higher, and so that is what we're beginning to do. Great. And, Wildon, maybe you could start, and then Oxana could chime in. Are you surprised to not see more of a linear progression on dystrophin? No, not at all. Look, again, we're very pleased with the dystrophin results that we see in DELIVER. To be able to see the highest level of dystrophin ever reported for an exon 51 skipping program is truly remarkable. Just recall, this is one snapshot in time. This is one muscle. We know dystrophin continues to increase over time. We know that with more drug, there's the opportunity to see even more benefit. What is truly remarkable is this functional benefit that we are seeing with DYNE-251. First, we presented the data on 10 mg per kg at six months, and now, with this data showing functional that continues, out to one year to show additional, functional benefit in the 20 mg per kg, that is what matters to patients, is functional, benefit, and that's what we're excited about. Oxana, anything to add? You know, I mean, your perspective, you know, in terms of the platform and what do you know about, you know, distribution based on the delivery we're seeing and concentration? Of course. First I'd like to echo Wildon to say what we are seeing is quite expected. What we are seeing actually is the clinical translation and validation of our FORCE platform, particularly its ability to enhance delivery therapeutic payloads to muscle, thereby driving changes in both biomarkers, skipping dystrophin, as well as functional outcomes. Ultimately, functional outcomes matter to patients. I just want to remind you that we have shown previously with our preclinical data in Duchenne muscular dystrophy models, that we can see the ability of FORCE to deliver to different muscle types: limb muscle, skeletal muscle, but also diaphragm muscle and cardiac. I would like to particularly name cardiac and diaphragm as key tissue that we absolutely need to treat in order to see benefit, functional benefit in Duchenne muscular dystrophy patients. It is very hard to move far if your heart, diaphragm, or even CNS is not working. From the fundamental design of our platform, we included selection of fab to target transferrin receptor 1, and the idea was to aim at achieving uniform, deep tissue distribution of our molecules into the muscle, and I'd like to mention again, also CNS. So as a result, what we see is functional benefits in DMD patients, and we are seeing it at a very early time point in our delivery trial. So I just wanna say that this is exactly what we saw preclinically, and now we are seeing it being translated into the clinic. Super. And then Wildon, another one for you is, you know, was there a bar, say, you know, 5% or so for distributed expression that you had in mind for the 20 mg per kg cohort? And based on the data so far from 10 to 20, you know, did you anticipate to see similar or greater, you know, dose response in exposure, skipping dystrophin, et cetera? Look, the goal in DMD has been to develop therapies that can improve function. There has been a thought that levels of dystrophin of five to 10% may drive a functional benefit. What we're seeing here now is levels of 3.7% dystrophin driving truly meaningful functional benefit for patients, and so we do believe that dystrophin can increase with time on therapy. We do believe that we have the opportunity to continue to follow patients, so we may be able to escalate the dose even further. Again, we're initiating the registrational cohorts here at 20 mg per kg or higher, and so, you know, we do... Are very excited by this functional data, and that is what we aim to bring to patients in the future. Great. And Doug, one for you would be, is there anything in the baseline characteristics in the, you know, 20 mg per kg that you see that contribute to the results that we're seeing here? You know, it's totally expected that across cohorts there would be subtle differences from one to the other, for example, age or BMI or even functional status at baseline. And indeed, that's what we see in DELIVER. What is actually really encouraging is that there is an apparent benefit across multiple, multiple cohorts that have distinct baseline characteristics. So this does not seem to be a narrow response within, for example, the 20 mg per kg cohort. We see it in the 10 milligram per kilogram cohort, and in fact, every single patient responded with a higher level of dystrophin, and this is translating to the functional benefit that Wildon talked about. I'll also say that this is exactly what has been seen with DYNE-101 in myotonic dystrophy. That with higher doses, you see higher levels of improvement at a molecular level, but also a more consistent functional response. And so I think if you take a step back, look across potentially transformational therapies in neuromuscular disease, here, what you see is this is not narrow.... This is a broad impact across multiple cohorts, multiple doses of drug, multiple time points across patients. Now, the magnitude of benefit will vary depending on the individual patient, but it's broad, and we're very excited about that. Great. Super! Next one, for Wildon. You mentioned the possibility to dose higher than twenty mg per kg in the registrational cohort. What gives you the confidence in going to, say, thirty, but not forty? And what would give you and regulators confidence in being able to find the right dose above twenty mg per kg? Yeah. So again, first of all, we're very comfortable with the safety profile that we see overall for DYNE-251. This is a profile that is based upon over, you know, 670 doses, over 50 patient years across a broad spectrum of patients living with DMD. So we're comfortable that we have a safety profile that allows us to continue to pursue 20 mg per kg as a registrational dose level, and potentially higher doses as well. We will continue to monitor as we have for safety. We are very diligent in that. We want to make sure that we understand the risk profile. What we're seeing with the potential benefit in DYNE-251 is important, and it is something that patients have been asking for a very long time. They know that this disease is not just a biologic dystrophin deficiency. This is a disease where there is huge unmet medical need. They are looking for improvement in function. And here with DYNE-251, we're showing a therapy that allows participants to increase dystrophin and potentially increase function as well. So this gives us high confidence based on the safety profile we've already established and the monitoring that we're continuing to do, that we can continue to pursue 20 mg per kg or higher as our registrational cohort. Great. John, one for you on sort of the competitive landscape in Duchenne. You know, how does the data and update we're providing today compare with others in the field, you know, particularly in the context of the functional data and the approved gene therapy? What line of therapy would you expect DYNE-251 to play? I mean, I think if you look at the functional data, it's hard to imagine it not being a first-line therapy, and it ought to be. We've talked about the unprecedented dystrophin levels, but as Wildon has emphasized, if you're looking at function, what caught my attention when we first saw this data was that it was not just a slowing of progression relative to natural history of placebo. We saw what appeared to be improvement on multiple measures, and that's what patients are looking for. So, I have not seen anything out there, whether it's gene therapy or some of the other exon-skipping approaches that have presented data that's quite that fulsome and meaningful. So we'll see how this plays out, but we certainly see whether it's a 20 mg per kg cohort or other doses, we certainly see ourselves having an opportunity for something. Great. And, John, I'll stay with you for this one. How quickly can you advance, you know, the other four candidates for the other DMD exons into the clinic? Listen, Oxana and her team have been working on multiple exons in preparation. We really wanted to see whether we could get this kind of data, and this quickly. You know, Oxana's thesis has always been that the preclinical data she talked about led to distribution broadly to muscles that matter in this disease. And if you started treating all of those muscles, you might see a response or functional benefit, faster than one otherwise might. And that thesis seems to be holding true, and that gives us a lot of confidence to quickly move into the other exons, and we're gonna. We fully intend to do that. Great. Doug, you know, given the DMD functional data, do you still plan to go for accelerated approval? Oh, absolutely. I mean, we will continue to pursue expedited approval both in the US and globally. We are obligated to get DYNE-251 to patients as quickly as possible, and we know that dystrophin is a surrogate endpoint for expedited approval, and we plan to avail ourselves of that option. You know, just as a reminder, and John said this, there are no approved therapies in Europe, and this is why we are looking at multiple functional endpoints, including these pretty dramatic data on SV95C, which the EMA has qualified as a primary endpoint. So expedited pathways, full pathways, dystrophin, and multiple functional endpoints is really how we're going as quickly as possible. Great. Wildon, can you provide a general update on where we are in the clinical trial for DYNE-101? Saw that we had, you know, updated the safety table for ACHIEVE. Maybe if you could speak to that, that would be great. ... Happy to. So with DYNE-101, the ACHIEVE clinical trial, so what we have described is, we have enrolled through the 6.8 mg per kg eight-week cohort. We in May shared data through the 5.4 mg per kg cohort at three months. And so we're waiting on data from later time points for 5.4, as well as data at all in the 6.8 mg per kg cohort. So that data will be available later this year. As we described, you know, the safety profile for DYNE-101 continues to look favorable. We continue to monitor very closely just as we have in DELIVER. We don't see the same events in ACHIEVE that we've reported in DELIVER. We continue to monitor very closely for all safety-related events. Again, the safety profile continues to be very favorable there with over six hundred and seventy doses, over fifty years of patient experience. So, more to come, but again, we've committed to providing a regulatory update on DYNE-101, as well as two fifty-one, by the end of the year. Great. John, can you maybe speak to a little bit in terms of, you know, next steps for DYNE-251 and, you know, DYNE-101 in terms of what should folks expect for the remainder of the year? I think, I mean, we've been quite clear about the guidance in terms of providing regulatory clarity by year-end in both of those programs. I think that's the next step. We've indicated that we should be prepared with more clinical data on DM1. We have obviously accelerated some of the review here in terms of DMD. We're initiating cohorts with DMD. So everything that we had wanted to do this year is what we're executing on, and I'll mention that, you know, we also made some announcements that we're adding some people to the team, like Doug. But you know, also just building some capabilities because you know, if you think about expedited approvals, both programs looking like we could move forward in that direction with expedited approvals, that means you know, commercialization is not that far off in the future, and we need to prepare, and we need to build for that. So we'll do that in a very steady and conservative way, and bring in a few people like Johanna Friedl-Nader, as well as Sheila Solano, who have helped me in the past launch products in rare diseases. Great. And, you know, there were a couple of questions about the leadership appointments announced today. So, John, maybe you could talk a little bit more about, you know, why making these appointments and changes now, and can we expect any adjustments to the overall strategy, you know, across the pipeline of the company as a result? Yeah, listen, I think the, in terms of a strategy, the strategy has been to prepare this company for the launch of a couple of potentially game-changing products in areas where there's huge unmet need. That strategy hasn't changed, and the strategy has also been to become a leader in muscular diseases, and we're building a pipeline to do that. So that strategy, I think, is consistent. You know, in terms of some changes, we have a terrific leadership team here at Dyne. I love the team. Wildon, Susanna, Jonathan have been fantastic. This leadership team, much of it remains and has built a great company to date. But I think it's very normal for there to be a transition as we start to turn the company from a company trying to get to proof of concept in humans, to a company that registers and prepares to launch. And we'll be building some capabilities, going forward, as I mentioned. Great. You know, Doug, you touched upon this a little bit, in your remarks, but, you know, anything else do you wanna add in terms of, you know, why you're joining, Dyne and the opportunity you see in the company? You know, only that I've worked in neuromuscular diseases my whole life, spinal muscular atrophy, ALS, DMD, DM1. I have constantly looked for potentially transformational science that could really address these diseases, and I think that's what Dyne has and I'm really excited about the scientific underpinning of this, and then the execution of this into actual clinical patients with actual clinical improvement so these data today, the DM1 data that we hope to share later, you know, I'm really excited to be a part of this team that is driving these programs forward as quickly as we can to patients. Super. Great, and maybe one last question, John, for you would be, you know, any updates you can provide in terms of the rest of the pipeline, you know, at this point? Yeah, so, you know, one of the reasons I joined this company is because the company, Dyne, has had this platform based upon the Fab technology and the linker, to which they could attach a variety of payloads. So we have a number of programs now with new payloads. That includes FSHD, and that was preclinical work that we have presented, and we've done the same thing for Pompe. So the pipeline is building. We already mentioned before that we'll be pursuing additional exons. And as I think Wildon alluded to, exon 51 is... although it affects a significant proportion of the patients, it's also one that's most severe in terms of disease. So we've taken on the toughest, and we've shown some very promising results. And so all of that tells us that we're in a position, I think, to rapidly build a pipeline right behind the two products that we'll be trying to get registered. Great. I think that covers it for the questions. John, any additional comments you wanna make to close things out here? Thank everybody for the good questions today. As you can tell, we are absolutely thrilled about what this update means for patients living with DMD, and we are more committed than ever to get Dyne two fifty-one, as well as the rest of the portfolio for patients as quickly as possible. Thank you all for joining us today.