I'd now like to turn the conference call over to Nicole Anderson, Solid di rector of investor relations and corporate communications. Nicole, please go ahead. Thank you, Operator, and thank you all for participating in today's call. Last evening, we announced FDA clearance of our investigational new drug submission for SGT-212, our AAV-based gene therapy candidate for the treatment of Friedreich's ataxia. The press release outlining this news is available on our website at solidbio.com. Before we begin, I would like to remind all listeners that this call will contain forward-looking statements based on the company's beliefs and assumptions and on information currently available to management. These statements include, but are not limited to, statements regarding Solid's future expectations, plans and prospects, its ambitions related to SGT-212, its planned clinical trials, business strategies, use of capital, results of operations, and financial position. These forward-looking statements involve risks, uncertainties, and other factors that may cause actual results, performance, or achievements to differ materially from those indicated by these forward-looking statements. These risks, uncertainties, and other factors include, but are not limited to, risks associated with the company's ability to advance its SGT-212 clinical program on the timelines expected or at all, obtain and maintain necessary approvals from the FDA and other regulatory authorities, and replicate in clinical trials positive results found in its preclinical studies. For more information on risks and uncertainties and other important factors, any of which could cause the company's actual results to differ from those contained in the forward-looking statement, please see the risk factors section, as well as discussions of potential risks, uncertainties, and other important factors in the company's most recent filings with the Securities and Exchange Commission. Joining us on today's call will be Bo Cumbo, President and Chief Executive Officer, Dr. Gabriel Brooks, Chief Medical Officer, and Kevin Tan, Chief Financial Officer. With that, I would like to turn the call over to our CEO, Bo Cumbo. Bo? Thank you, Nicole, and good morning, everyone. Thank you for joining us on this important day for the Friedreich's ataxia community and Solid Biosciences. Today, we have the privilege of sharing an exciting development in the fight against this devastating disease, a disease that robs patients of their mobility and independence and inevitably their lives. Friedreich's ataxia affects approximately 5,000-8,000 patients in the United States, 15,000-20,000 in Europe, and 40,000-50,000 worldwide. These individuals face progressive neurological degeneration, severe cardiac complications, and overwhelming physical challenges due to a lack of a vital protein, frataxin. The unmet medical needs in FA are staggering, and time is of the essence. It is with immense pride that we are announcing the FDA's acceptance of the IND for SGT-212, the first and only gene therapy to utilize a dual route administration to treat FA. This therapy is not just an incremental advancement. It represents a leap forward in ambition and approach. SGT-212 is designed to reach critical tissues affected by FA, addressing the central nervous system, neuromuscular system, and heart. This approach is designed to address the full spectrum of disease with the ultimate ambition of providing a treatment option to the broad patient population suffering with FA, regardless of a patient's age, disease severity, or organ involvement. Now, as a first step towards this ambition, we will need to establish safety and efficacy data in the initially treated adult patients in our upcoming trial. We are hopeful that this will ultimately be a single treatment available for all patients living with FA. SGT-212 is a paradigm shift in the approach to treating Friedreich's ataxia. SGT-212 strives to address both the neurological and cardiac manifestations of FA through a dual-route administration with contemporaneous systemic intravenous and bilateral direct dentate nuclei, or intradentate nuclei, IDN infusions, using the same therapy but at optimized doses depending on the route of administration. This approach aims to have the treatment reach both the disease-relevant peripheral tissues, for example, the heart or dorsal root ganglia, as well as key affected regions in the brain by achieving restoration of frataxin expression at appropriate levels without overexpression. We consider it a precision multi-system approach for a challenging multi-system disease. This dual-route administration is vital because Friedreich's ataxia affects multiple organ systems, including the cerebellum and Purkinje cells, which are critical for coordination, as well as the dorsal root ganglia and the heart. Most other FA gene therapy candidates in development rely on IV-only administration and either A, focus narrowly on cardiac manifestations of FA, or B, seek to address CNS symptoms by relying on neurotrophic capsids in the hopes of penetrating the blood-brain barrier to target all neurons, regardless of whether they are affected with frataxin deficiency or not. We are excited by our novel approach because, in large part, it seeks to address one of the FA community's greatest areas of uncertainty: the life-limiting impacts of CNS and neuromuscular symptoms by specifically targeting and administering to the cerebellum. The dual-administration approach helps to solve for the potential shortcomings of a single systemic IV route administration, which risks being unable to reliably penetrate the blood-brain barrier to fully reach the targeted areas deep into the cerebellum, or requires higher doses and potential toxicities associated with excessive frataxin expression and increased viral load. We've come to this conclusion based on our research conducted over the course of many years in multiple FA programs. During the course of that research, we, along with our collaborators, have dosed over 120 non-human primates, following some out to a year in life post-dose, to ensure we understood how different routes of administration, using different capsids at varying doses, translated into potential toxicity. Because of this extensive work, we have confidence in the potential of SGT-212 and believe that dual-route administration is essential to target both aspects of the disease. Before turning it over, I want to take a moment to recognize those whose dedication made this achievement possible. First, my heartfelt thanks to Jen Farmer, CEO of the Friedreich's Ataxia Research Alliance, or FARA, whose advocacy and partnership have been instrumental in advancing treatments for FA, including SGT-212. I also extend my deepest gratitude to Doctors Jim Wilson, Juliette Hordeaux, and Christian Hinderer, who led the preclinical R&D work for SGT-212 while at the University of Pennsylvania. Their efforts laid the scientific foundations and helped shape the clinical strategies behind SGT-212. We look forward to continued collaboration with Dr. Wilson, now the CEO of Gemma Biotherapeutics, and his team as we advance this program. Most importantly, I want to honor the FARA families, led by Tom Hamilton, who initially funded and collaborated with Dr. Wilson and his team, and worked tirelessly to bring this therapy out of the lab and into the clinic. Their steadfast commitment to finding a meaningful treatment for this devastating disease is extraordinary. To all patients and families living with FA, your courage inspires everything we do. And to our investors and partners, thank you for your belief in our mission and your unwavering support. We hope to continue to bring life-altering therapies to not only the FA community but also numerous other devastating neuromuscular and cardiac diseases. I will now turn it over to Dr. Gabriel Brooks, our CMO, to discuss the scientific foundations of SGT-212 and future clinical plans for the program. Gabe? Thank you, Bo. Good morning, and thank you for joining us on this tremendous day for Friedreich's ataxia community and for our company, Solid Biosciences. Friedreich's ataxia is a debilitating disease affecting tens of thousands of people worldwide. Typically diagnosed at a young age, between the ages of nine and 15, patients face progressive degeneration and see an average shortened lifespan of less than 40 years of age. Early-onset patients demonstrate faster neurologic decline and higher overall disease severity. Despite recent advancement, approved therapies do not address the underlying pathophysiologic cause of the disease, Friedreich's frataxin deficiency, which leads to mitochondrial dysfunction affecting both nervous as well as cardiac tissues principally. Almost all patients with Friedreich's ataxia suffer from ataxia, with the average patient losing ambulation with approximately 10 years of the initial presentation of symptoms. Beginning in the early stages of disease and worsening over time, nearly all patients will endure some form of neurologic debilitation. Dysarthria alone impacts 90% of all patients. Though cardiac complications are the primary cause of death, the vast majority, 80% of people with Friedreich's ataxia, experience either slow cardiac decline or do not present with any cardiac symptoms. It is crucial, then, when we consider the current approved and investigational treatment landscape, that we recognize that patient morbidity principally involves their neurologic symptoms. Approaches that focus solely on cardiac symptoms unfortunately threaten to leave patients' neurologic and neuromuscular suffering unaddressed. At the core of our SGT-212 program is our fundamental belief that, from the outset, therapies must be designed intentionally to meet the needs of patients at any point in their FA journey. It cannot be overstated that patients need and deserve therapies that can address both neurologic as well as the cardiac effects of Friedreich's ataxia. I'm proud to share with you the extent of our work at Solid Biosciences in the pursuit of this goal. Extensive preclinical work has led to the candidate selection of SGT-212 for first-in-human evaluation. Nine separate non-human primate studies were conducted, including more than 120 animals, to evaluate multiple lead candidates and routes of administration with the goal of identifying safe and therapeutically relevant dose levels to address both cardiac and neurologic disease. Based on this deep library of data and experience, we have come to the conclusion that IV-only administration, irrespective of dose, is unlikely to reach the dentate nuclei, the essential area of the cerebellum implicated in neurologic decline. Importantly, as stated previously, substantial overexpression of frataxin poses an unacceptable risk of fatal toxicity. This liability complicates any gene therapy approach that aims to address both neurologic and cardiac manifestations of disease, relying on systemic gene therapy administration, regardless of the CNS penetrance of the vector. We were pleased to find that NHP studies specifically evaluating contemporaneous IV and bilateral intradentate nuclear injection of SGT-212 demonstrated that the dual administration was safe, well-tolerated, and capable of eliciting no associated toxicity at therapeutically relevant frataxin expression levels. Next, I'd like to share with you the revolutionary dual administration approach we are using to address neurologic and cardiac manifestations of Friedreich's ataxia. With SGT-212, the risk of toxic frataxin overexpression is managed by leveraging the two routes of administration. Through this approach, we aim to deliver frataxin directly to the critical tissues and organs affected by Friedreich's ataxia and achieve therapeutic levels of expression while avoiding potentially toxic overexpression. Based on extensive animal studies, we expect low-dose systemic IV administration to adequately target and treat cardiac complications of Friedreich's ataxia in addition to peripheral tissues, and bilateral intradentate nuclear injections with SGT-212, leveraging real-time MRI-guided delivery technology to exquisitely target and confirm dentate nuclei coverage. SGT-212 uses the AAVhu68 capsid, a capsid that has been used in multiple neurologic disorders, including GM1 gangliosidosis, and has demonstrated tolerability in multiple human patients. Multiple preclinical studies supported the IND package that was submitted to the FDA, including neuronal and cardiac knockout mouse model studies that established proof of concept in each target tissue. On the following slide, I'd like to share with you some of the compelling disease-modifying activity of SGT-212 in neuromotor-affected animal models that gives us confidence in SGT-212 for addressing ataxia in patients with FA. Shown on this slide are the results from two functional assessments evaluated in the neuronal knockout study in mice, the first of which was the NeuroScore test, which was used to assess the severity of ataxia. The NeuroScore results show a dose-dependent improvement in ataxia, with a greater NeuroScore reflecting more severe ataxia. In the plot on the right, we show the results of the Rotarod test, which evaluated coordination and balance by measuring the time to fall for mice that were running on a spinning, progressively accelerating rod. Lower values on the Y-axis indicate greater neuromuscular impairment. All three dose levels tested for SGT-212 demonstrated significant improvement in efficacy versus the disease-controlled mouse. We also saw compelling responses to SGT-212 in animal models of Friedreich's ataxia. In the cardiac knockout mouse study, we demonstrated heart transduction and expression of human frataxin in cardiomyocytes that resulted in improvement in cardiac function and cardiac biomarkers. The left-hand plot shows clear evidence of a dose-dependent cardiomyocyte frataxin expression. Frataxin expression correlated to improvements in mitochondrial function, as demonstrated here by improvement in succinate dehydrogenase activity at the middle and high doses of SGT-212. Additionally, increased transduction of heart tissue translated to a decrease in left ventricular mass at day 30 across all doses tested versus the disease-controlled mouse. Left ventricular mass index is known to be a key biomarker in managing underlying Friedreich's ataxia-associated cardiomyopathy, which presents as hypertrophy and may be a predictor of the efficacy of the therapeutic intervention relative to cardiac function. Observational studies have concluded that increases in left ventricular mass index in patients with Friedreich's ataxia correlate with increased risk of all-cause mortality. These key data give us confidence that IV administration of SGT-212 can lead to a cardiac frataxin protein expression, improvement in cardiomyocyte mitochondrial function, and mitigate cardiac structural changes that are consonant with those seen clinically in patients with Friedreich's ataxia. A critical requirement for SGT-212 to be effective for Friedreich's ataxia is delivery to the dentate nucleus of the cerebellum, the organ responsible for coordinating voluntary motor commands. When the dentate is damaged by the disease, as is the case in Friedreich's ataxia, patients manifest ataxia and bulbar dysfunction. As mentioned earlier, we were able to demonstrate therapeutically relevant frataxin expression in NHPs without treatment-related toxicity. Precision MRI-guided intradentate nuclear injections were able to elicit safe, sufficient, and properly localized frataxin expression in the cerebellum of NHPs at low doses anticipated to be clinically relevant. The left-hand plot shows that using bilateral injections, each NHP saw frataxin expressions in both dentate nuclei, right and left, with localization captured on the image on the right. Of note, quantification of frataxin expression in NHP4 was limited due to a small amount of dentate nuclei area available for analysis due to requirements for other analyses, such as histopathologic tissue state. We are proud to share with you our plans for the first-in-human study of SGT-212. As approved by the FDA as part of our IND submission, SGT-212 is now clear to begin first-in-human clinical evaluation. We expect to initiate a phase 1b study in the second half of 2025, pending IRB approvals, which we are working towards now. The phase 1b study has been designed to evaluate the safety and tolerability of SGT-212 using contemporaneous systemic IV and bilateral intradentate nuclear infusions in adults with Friedreich's ataxia. The study is designed to evaluate older and more severe patients, both non-ambulatory and ambulatory. As we establish safety and early signs of efficacy, we aim to expand the age criteria to the study of the safety and efficacy of SGT-212 in individuals of all ages and disease stages who are suffering from Friedreich's ataxia. Beyond initial safety and tolerability, this first-in-human study of SGT-212 will also assess key exploratory objectives to determine the impact of dual SGT-212 administration on frataxin expression, motor function and disability, cardiac function, and speech function using various methods of measurement post-treatment. We are eager to advance into the clinic later this year as we firmly believe that SGT-212 has the potential to be a singular treatment for all patients in need. We look forward to sharing further updates on the phase 1b study as they become available. We are deeply grateful to the FARA patient community, our collaborators, and our team at Solid Biosciences, all of whom are essential elements of today's news. With that, I will hand the call back to Bo. Bo. Thanks, Gabe. In closing, I once again want to acknowledge and express my deepest gratitude to Jen Farmer, Dr. Wilson, the Gemma team, the University of Pennsylvania, and the original program founders, Tom Hamilton and others. I know your contributions to the FARA community are deeply appreciated. We'd also like to recognize the University of Florida for their commitment to FA and the tireless work conducted on our behalf in support of patients. To everyone living with FA, their families, and investors, thank you for your trust and support as we continue this journey. Before we turn to questions, I'd also like to take a moment to acknowledge the Solid Biosciences team. Your vision, innovation, and persistence are paving the way for a new era in FA treatment. Today, with the FDA's acceptance of the IND for SGT-212, we stand on the threshold of a new era for both Friedreich's ataxia treatment and for Solid Biosciences. This IND acceptance is not just a milestone in the evolution of our company. It's a beacon of hope for patients and families worldwide. We look forward to keeping everyone updated on the progress of our clinical trial as we work to bring this groundbreaking therapy to those who need it the most. But this is just more than a single step forward. It marks the turning page for Solid Biosciences. In December 2022, Solid Biosciences embarked on a bold new chapter. At that time, the company was known primarily for its focus on a single area of genetic medicine, Duchenne muscular dystrophy. However, with a renewed vision and commitment to transformation, Solid began an ambitious journey to redefine its mission and broaden its impact. Today, we are proud to say that Solid Biosciences is no longer a single program company. With SGT-212 plus SGT-003 moving forward in the clinic, we have now cleared two INDs in the past year and a half, and we are poised to submit a third IND for SGT-501 targeting CPVT by mid-2025, and we have another program, SGT-701 for TNNT2, that is now moving toward GLP studies with an IND anticipated in 2026. The transformation of Solid Biosciences was not merely about adding programs. It was about strategically building the key platform technologies required to deliver on the hope of gene therapies, including next-generation capsid technologies, novel promoters, immune modulation techniques, and manufacturing purity to create medicines with the potential to address a wide range of underserved genetic neuromuscular and cardiac diseases. This is the Solid Biosciences of today: innovative, dynamic, optimistic, and committed to delivering life-changing therapies for patients worldwide. Thank you for your time today. And with that, I'll turn the call back over to the operator for questions. Thank you. We'll now be conducting a question-and-answer session. If you'd like to be placed into question queue, please press Star 1 on your telephone keypad. A confirmation tone will indicate your line is in the question queue. You may press Star 2 if you'd like to remove your question from the queue. For participants using speaker equipment, it may be necessary to pick up your handset before pressing Star 1. One moment, please, while we pull for questions. Our first question today is coming from Anupam Rama from J.P. Morgan. Your line is now live. Congrats on the update. Wasn't expecting this, so it's great to see. The initial study here starting in the second half of 2025. Any other gating factors to starting the study beyond sort of getting IRB approvals, which you mentioned in your opening comments? And then are there any sort of KOL education considerations here we should be thinking about given the sort of novel dual dosing administration strategy? Thanks so much, guys. Thank you, Anupam. This is Gabe Brooks, CMO here at Solid Biosciences. And I'll take the second part of your question first, which is about KOL education with regards to this route of administration. Though an IV and intradentate nuclear injection, dual injection is novel, and we hope will be revolutionary for Friedreich's ataxia. For neurologic rare disease, direct intraparenchymal injection has been used in multiple different programs, with actually this type of technology being used in over 10 different gene therapy programs. So in terms of the really leading investigators in which we are engaged with, they should be well familiar with this type of approach. And I think that the team of neurosurgeons that we've assembled to further refine our process, I think we'll certainly be learning lessons from them and be able to promulgate that to KOLs, as you've indicated, as we move forward. In terms of the study startup, this is absolutely, as you indicated, really about site engagement, engaging with the IRBs, and is really kind of the standard process here. And what you're seeing is the timelines between IND opening and study start. We are, of course, in the background, working hard on the program and making sure that all of the pieces are ready to go. But what you're seeing is a standard startup timeline for industry. Great. Thanks so much for taking our question. Thank you. Next question today is coming from Maury Raycroft from Jefferies. Your line is now live. Hi. Good morning. Congrats on this update, and thanks for taking my question. Just wondering if you can contextualize the mouse cerebellum expression data that you're showing that you showed in the slides versus what's seen with normal frataxin expression. And is there anything additional you can say about the promoter or construct that's being used to optimize expression? So in terms of the mouse data, what we see, and given that the kind of vast library of data that we had looking at the necessary amounts of frataxin to be expressed in neuronal tissue, we leveraged that across our portfolio such that when we saw what we believe is compelling data on slide number seven, demonstrating disease modification in the neuronal mouse models, we were able to understand exactly the amount of frataxin that we would need to express. So it's not just leveraging these experiments, but actually leveraging that vast library of data that we had alluded to. And in terms of the vector construct, I don't believe that we've shared publicly beyond the capsid, which is, again, the HU68 capsid, which has been used in multiple different neurologic indications to date. Got it. Thanks for taking my question. Thank you. Next question is coming from Sami Corwin from William Blair. Your line is now live. Hi. Thanks for taking my question. Congrats on the update. Could you discuss the doses you plan on using both for the IV administration and the ID administration, and what levels of frataxin expression you expect those to confer in both the heart and cerebellar dentate based on your preclinical studies? Thank you. Thank you so much, Sami. I appreciate the question. Again, Gabe Brooks here, CMO at Solid Biosciences. In terms of the doses, we haven't shared the precise dose at this time. I can, however, share very clearly that the IV systemic dose is a very modest dose when we talk about IV systemic dosing, and I think that that has to do with the intrinsic tropism of this particular class of clade of viruses to the heart. In terms of the dose in the intradentate nuclear injection, this is an extremely modest dose that, because we're so selective in the targeting using real-time MRI guidance, we can exquisitely and selectively target the dentate nucleus, so really the crux of the organ that's affected here with Friedreich's ataxia, and we can confirm real-time coverage of the dentate nucleus. And so when we think of overall doses for even for CNS indications, this dose is extremely small because it is so selective, but the coverage can be so exquisitely confirmed at the time of delivery. And I think I've forgotten the second part of the question, Sami. What levels of frataxin expression you expect those doses to confer in the respective areas? Right. So the levels of frataxin that we've been able to really study, what is the maximum level where we would start to see toxicity, as we have alluded to before, these proteins can be toxic to tissues when expressed overabundantly. And so in the brain, we are a log lower in terms of the doses to when you start to see that level of toxicity. So we have quite a robust therapeutic range, meaning that with what we saw with disease-modifying in the animal model, we are still really far away from when you start to see protein toxicity. And in the heart as well, we have what we believe is a really compelling safety margin, again, given not just this particular program, but looking at the totality of the experiments that we've conducted. In terms of the precise number and the protein expression, I think we'll be glad to share that at a later date. Yeah. Thanks, Sami. This is Bo. I think just to add on to that, I mean, we'll share the ultimate doses that we're going to be going in the clinic in the next couple of months as we move forward. But this is why we did this is why we firmly believe the dual route administration is so important. We did all the studies. We were able to coat the dentate, it's in the slide, I think it's like slide eight of the presentation, we were able to coat the dentate in the cerebellum with a very, very low dose in non-human primates. And the IV dose for the cardiac manifestations of the disease, as well as the dorsal root ganglia, are very similar to what you would see where Lexeo started in that range. So we're able to come in at a very low dose. And all of this is capable because of the dual route administration. And we just, after doing, I think, nine different non-human primate studies over 120 animals with multiple collaborators, whether it's at UPenn, UF, Florida, or internal, it really all comes back to making sure that you get to the right organ in a very specific manner. It's an elegant design for a complex disease. And so that's why we're very excited about the dual route administration. Great. Thank you very much. Thank you. Next question today is coming up from Joseph Schwartz from Leerink Partners. Your line is now live. Great. Thanks so much. Congrats on this important program. I wish you all the best with it. I have a couple of questions. First, could you talk about how quickly the study can progress with patient enrollment and evaluation of subjects to confirm that the dosing and exposure is as you'd expect it to be based on your preclinical data? Do you need to confirm that you're seeing what you hope to see in a group of sentinel patients before you can enroll additional patients? At what point do you expect to be able to report the first data from patients treated with SGT-212, and what quantum of data might that encompass? Gabe Brooks, again here. Thank you for the comment at the beginning of the question. Indeed, we believe this is an important step for Solid Biosciences and for the community. Thank you for acknowledging that. There was a lot to that question. I think it had to do with cadence of enrollment and the data that would then be coming out from this study, and what I can share with you is that we're really thrilled with the partnership we had with the FDA. I think it really speaks to the strength of the package that ultimately, in the sentinel dosing, which is really common for these types of studies, that we were able to agree on a very short period, frankly, between dosings. Or how I should say that is, it's an adequate safety, but it's not a prolonged safety between each patient dosed, and so what we're talking about is within the range of around four weeks between patients is what we're looking at, and then what is the data that we're going to be looking at? We're focused here on safety and tolerability, for sure, and as we shared, this will be in the context of three cohorts, starting with non-ambulatory, going into ambulatory, and then going into a combined cohort for extension thereafter. Between cohorts, we absolutely will be looking for signs of that we have the drug where we need it to be, and here, the tissue that we can access is using endomyocardial biopsy, the heart through a minimally invasive approach, as well as we will be looking at the muscle, so we'll be able to see signs of, yes, Frataxin expressing, and we hope to see biomarker evidence of that as well, so with that, I think we'll be able to share that initial success of biodistribution and pharmacodynamic action and activity of the heart. I want to just also say that the ability to contextualize the urgent need to the patient and the robust package that we were able to submit to the FDA could not have been made possible without the partnership of Jen Farmer at FARA. So I think it's incredibly important that we acknowledge their enduring and tenacious activities towards treatments for this disease. That's very helpful. Thank you. And then to what extent do you think that you can rescue the phenotype that's already present in FA adults who have the disease by restoring frataxin after the disease has been underway for a while based on what's known about frataxin and its function? You've done a lot of great work in animals. Are any of these models informative about the ability to produce a benefit on clinical endpoints such as LVMI and mFARS in the types of patients that will be enrolled in the phase 1B study? Yeah. This is Bo Cumbo. I'm going to turn it over to Gabe in a second to answer the clinical questions. But one of the most important, when we were designing these programs, we started working on this many years ago. The main goal was to try to bring a drug to the patient where they are in their journey. Obviously, we've been in these disease states, meaning these CNS neuromuscular cardiac disease states for many years, and we've learned a lot of lessons. And obviously, time is muscle. Time is neurons depending on the disease state. We understand that it's going to be very challenging to reverse disease that has been progressing for many, many years. Our goal with this program, and I'm going to turn it over to Gabe in a second to answer your question specifically. Our goal with this program was to if there's a 40-year-old that has CNS-only manifestations, there's a drug for them eventually. If it's a 20-year-old that has both CNS and cardiac manifestations, then we have a drug for them eventually. And if it's a two-year-old that has no idea the progression of her or his disease, we have a drug for them. And we've left no patient behind. And that's the type of drug that we believe that we've created here and worked with Tom Hamilton, FARA, UPenn, University of Florida, all our collaborators over many years. And so we're very excited about it. Now, obviously, it's going to be challenging to halt the course or reverse course for patients that have severe disease. But I will turn it over to Gabe for more clinical update. Thank you, Bo. And Joe, I think that in the first instance, we really want to do everything we can to preserve the quality of life that patients have. And if we can come to patients and say that we can help them forestall or to eliminate further decline, I think that that would be very meaningful to patients. I think that it's really difficult, although attractive, to think about could there be some sort of recovery. I think we have to remain humble at this stage and really try to preserve the quality of life that patients have to the best degree possible. That makes sense. Keep up the good work. Thank you. Thank you. Next question today is coming from Arthur He from H.C. Wainwright. Your line is now live. Hey, good morning, Bo and team. And congrats on the treatment milestone. I had two quick questions. So, Gabe, regarding the mouse study, do you guys have any data regarding the in-group mouse model? How the treatment impacted lifespan of the mice? Arthur, thank you so much for asking the question. And we are today sharing a small sliver, I think, of the data that we have generated to date. And your question is very apt. And I'm very pleased to share with you that indeed, these therapies increased the lifespan significantly of the mice. And also, the overall health of the mouse was better in the models. And we know that because they maintain their weight. And so if we just kind of look at the organism itself, we were really pleased to see that this seemed to be very effective in preserving the life and health of the animal, not only through the specific scores that we've shared, but just globally as well. Awesome. Thanks for that, Gabe. And my second question is actually regarding the manufacturing side. So could you tell us more about the readiness regarding the manufacturing of the 212 for the upcoming clinical trial? Yeah. So it's a great question. This material was manufactured at an undisclosed CDMO. It was not using Solid's original process development that we have with CPVT as well as with 003. But we plan on moving that forward. We do have drug in the freezer, and we're going to be putting it in vials and making sure that we have adequate drug for the patient trial that's coming. So we already have drug available. It's already been manufactured. And now we're going to be moving that toward our purification process for the phase II. Thanks, Bo. And congrats again. Thanks. Thank you, Arthur. Thank you. We've reached the end of our question-and-answer session. And that does conclude today's teleconference and webcast. You may disconnect your lines at this time and have a wonderful day. We thank you for your participation today.