So good morning, everyone. Thanks for joining us this morning at the Citi Healthcare Conference. Max Riso here with the Citi Healthcare Investment Banking team. Very excited this morning to have with us Bo Cumbo, CEO of Solid Biosciences, joining us. Solid Biosciences is advancing a portfolio of neuromuscular and cardiac programs, including SGT-003, a differentiated gene transfer candidate for the treatment of Duchenne muscular dystrophy, AVB-202, a gene therapy treatment for the treatment of Friedreich's ataxia, AVB-401, a gene therapy program for the treatment of BAG3-mediated dilated cardiomyopathy, and additional cardio assets. Look forward to having Bo Cumbo with us, and I will pass the mic over to Bo Cumbo. Thank you, Bo Cumbo. Thank you. Thanks, Max. Thank you, Max and Citi. Really appreciate the opportunity to present. I'm gonna be making a number of forward-looking statements today. Please take time to look at our forward-looking statement page on our presentation. Many of the events I talk about today could materially differ from outcomes, which could be out of our control. So please take a look. For those of you online, there is a presentation website on the presentation page on solidbio dot com. With that said, I really do appreciate everybody taking the time to come talk to us today and talk about Solid Biosciences, and our key investment highlights, and our progress that we've made on our program so far to date. On page three, you'll see that we're gonna be talking a little bit about our management team and proven experience from the management team, as well as our diverse pipeline, our manufacturing capabilities, and our capsid library formation. On the next page, in your presentations, you can see on slide four, the management team. We have a very, very experienced precision genetic medicine management team that has been around companies, not only in biotech, but also mainly genetic medicine, and more specifically in gene therapy. Leading with, you know, myself, Ty Howton, Kevin Tan, who's in the audience today, is our Chief Financial Officer. Jessie Hanrahan, who comes from bluebird bio, previously, and AavantiBio, and then Chief Scientific Officer, Dr. Jennie Marlowe. Paul Herzich, who's our Chief Technology Officer, who was, the Vice President of CMC at BridgeBio prior to this, running their gene therapy programs. So from a CMC perspective, we have, excellent manufacturing team. And then Shuli, Dr. Kulak, our Head of BD, and I've just recently, started hiring a CMO, and we'll have that CMO in place, very shortly. That CMO will be a cardiologist, a cardiac background, and you'll see why, because our pipeline is, so robust within, cardiac genetic medicine. On the next page, you can see a strategic outline of what we're building and what we're working toward. This is on page five, and you'll see that we have a very differentiated platform than many other companies. At the top, you can also see that we put delivery at the forefront of everything that we're doing. So it's not just novel capsid and a capsid library, but it's also CMC platform. CMC is the drug, and so everything that we do revolves around CMC and our process. Then, once you look at our programs, you can see very quickly the strategic nature and how we're developing this, and we're leveraging our capabilities and knowledge that we have in Duchenne and FA, and moving it over to our cardiac pipeline. Today, we'll be talking a little bit about Duchenne, FA, as well as BAG3, and we're announcing another program today that I'll be discussing very soon. We're also working on our capsid library, and we're excited about our capsid library. We just had another capsid that was came out of this library this recent week, and we'll be using these capsids for non-dilutive financing down the road. So on page six, you'll see the pipeline that we're working toward. I just talked a little bit about it, and we're gonna go through in depth these programs. So the next section is the neuromuscular programs, and we'll start with DMD. And many of you know DMD because it makes headline news from other companies that are in the space. Obviously, it's caused by a mutation in the dystrophin gene that leads to a lack, an absence of this protein, and we're trying to replace this protein with a functional minidystrophin or a microdystrophin. Now, we talk about Duchenne a lot from an epidemiology standpoint of 10,000 patients in the United States. Realistically, when that's the ocean of Duchenne, and realistically, when you look up under that ocean, there are subpopulations, and every population needs to be treated a little bit differently. When you look at page nine, you'll see the different sections that actually make up Duchenne from our early ambulatory phase. You have about 3,500-4,500 kids that are somewhere in this age, one through eight. You have about 1,500 of those children that have antibodies to drugs prior to being dosed. They'll have antibodies to AAVrh74, to AAV9, to AAV8, to other capsids. Just somewhere along the way, they've been exposed, and we have to find a way to treat these children. We have to find a way to lower their antibodies down to a specific threshold and then dose above that. You have older children, the sort of late ambulatory, they're partially ambulatory, or they're non-ambulatory. This represents roughly 50% of that population as well, and unfortunately, many of them, yeah, you know, 15%-20% have antibodies for, these capsids as well. So we have not only the adult older population who's weaker, they typically have a fat fraction of greater than 80%. This is why they're non-ambulatory. They have fatty livers. They have decreased pulmonary outcome, decreased ejection fraction. These children are fragile, and you're gonna have to find ways to get the drug to them, and most likely, you're gonna have to find ways to get the drug to them over and over in the heart and the diaphragm. So redosing is gonna play an important role. Unfortunately, there's gonna be a subpopulation that's gonna be dosed with drugs that are currently coming to the market, and these are gonna be suboptimal durability for one reason or another. Either the child didn't get enough exposure or the child has breakdown of muscles, and unfortunately, these drugs are not in the stem cells, the satellite cells, and over time, as the muscle breaks down, they're gonna regenerate dystrophic muscle. So we're gonna have to think about redosing these children. The population, if these drugs are working, and I believe they are, if these drugs are working to increase survival over the long haul, Duchenne gets bigger. It actually doesn't decrease. It actually becomes a bigger, more urgent population. Now, as we're developing these drugs, and we're thinking about the next generation, we have to consider all this and think about the redosing and what it takes to redose. It starts with the actual construct itself, including the capsid and the manufacturing. On the next page, on slide 10, you'll see that we have now, what we believe has created the next generation Duchenne program. We use this transgene that has domains R16, R17 in it without hinge 2. Without hinge 2, you provide increased flexibility, as well as with R16, R17, you are recruiting for alpha-syntrophin as well as nNOS, and that's very important proteins that, for the microdystrophin. We've changed our capsid. We're using a new capsid. It comes out of our capsid library called SLB101. I'm gonna talk about why this capsid is so important. Then we've changed our manufacturing process, and we've made improvements to our manufacturing process, not only in Duchenne, but our future programs, and we're on the cutting edge of really transforming the way we think about gene therapy manufacturing, not only from a yield standpoint, but also from a plasmid and purity. So when we think about Duchenne, it starts with transduction speed, especially in a new world where we have to lower antibodies, and we have a short period of time to dose, transduce, and express. And on the next page, you will see that this capsid, this SLB101, along with our transgene, has done something that we actually have never seen before in Duchenne, where at day 4, we're seeing expression in the MDX mouse. And so what does this mean? This means that we have dosed, we have transduced, and we now see an expression at day 4. We've repeated this study, and we can see expression all the way down to day 2. At day 29, all the animals, regardless of the dose, at the doses that are listed here, they're all at roughly 100% across the board, whether it's the heart, the diaphragm, the quadriceps. The heart and the diaphragm are extremely important, especially in the non-ambulatory boys, because that's all they have left. You don't have peripheral muscle. So you're looking at trying to get to the diaphragm and the heart. And this capsid in our non-human primate study increases microdystrophin expression around 3 to 5-fold in the non-human primates in our GLP tox study in the diaphragm. And that's extremely important when you're thinking about pulmonary function in the non-ambulatory patients. The following slide, we look at the MDX mouse, and we compare it to Solid's original program, which was called 001. How did this program, this next generation program, compare to Solid's original program? And you can see from a biodistribution standpoint, expression standpoint, and from a reduced CK levels, it's significantly different than Solid's original program. In non-human primates, on the second, next page, slide 13, you can see that this, what we saw in the mouse, did translate over to these non-human primates. Now, this is with luciferase. It's not with microdystrophin. It's luciferase. We looked at skeletal muscle, looked at cardiac muscle, and looked at liver. We have completed our GLP tox, and that study started in December. We took down the animals in March at the end of study. All animals from start of trial to the end of trial did very well, and there were no unscheduled takedowns until the end of the trial was completed. We're in the process of writing our IND. We're on track to file the IND in early Q4, and then hopefully, we will be screening and dosing patients shortly after IND acceptance, which should happen roughly 30 days or 40 days post submission. Now, the following program, the next program I'll talk a little bit about is Friedreich's ataxia. That's slide 14. We're very committed to the patients in Friedreich's ataxia. If you don't know a lot about FA, what I'll tell you, the most important thing is to understand that it is a multi-system manifestations of the disease, and cardiac as well as neuromuscular and CNS. It's extremely important to pull all the patients along when you're treating these patients. It's a very large unmet need, and what we've decided to do, we have a lot of data on cardiac, and we feel very comfortable with the levels and expression and the outcomes we're getting with cardiac. However, we've determined that it is not sufficient to move forward cardiac only, and that you really need to make sure that you address the CNS and neuromuscular manifestations of this disease. When you talk to patients and the patient advocacy organizations, they'll tell you, "Hey, listen, it's wonderful if you can cure cardiac, but if you lose the ability to walk, see, speak, hear, quality of life really does matter." So what we're trying to do is address all the manifestations of the disease by doing dual route of administration. Why is that important? Because it's not just the amount of frataxin expression, it's actually the distribution of frataxin. It's across the DRGs, it's the base of the cerebellum, it's the Purkinje cells, it's the heart. So that's what we're trying to accomplish. On the following page, you can see why we're so confident about cardiac. We've, we've started at the very top, and find that sort of toxic levels of frataxin, and then we work our way down to get to the lowest level, the lowest dose with the best outcome. And you can see that we're already down to 6E12. We can change ejection fraction, we can change survival. And just as importantly, on the far right-hand side of the screen, you see SDH activity. That's succinate dehydrogenase. In patients that have FA, when unfortunately they pass away and you do autopsies, and you look at the mitochondria in the heart, the DRGs, you see succinate dehydrogenase completely depleted. You see the mitochondria in shambles. And so what we want to know is, while we're restoring frataxin, is it functional? And we can restore succinate dehydrogenase level, which is a surrogate for the mitochondrial health, right back to normal levels. We can also, as I mentioned, change ejection fraction, change survival. Now we want to know, can we do this in the CNS model? Can we get to therapeutic levels without creating a toxicity event in the heart? And so on this next slide, Slide 16 is a very large non-human primate studies, 40 non-human primates. This study was done a 6-month period of time to help us understand, can we get into dose therapeutic ranges in the heart as well as the DRGs? And the answer is yes. We looked at multiple different doses and multiple routes of administration: IT only, IV only, IT and IV combination, dual therapy with multiple doses. The outcome is that we can elegantly increase expression by manipulating the dose, and the route of administration, so we can get to therapeutic levels in the DRGs as well as the heart. Now, what are we going to do next? We're gonna take these learnings, and we're gonna look at our non-human primate study to understand, are we getting enough frataxin in the cerebellum to make a difference? We're gonna be talking to KOLs about this. We're also working on a CNS mouse model to understand, can we change the outcome in the CNS model, similar to what we did with the cardiac mouse model? More to come on timelines to an IND for this program, and I'll update you further as we move forward. Now, I'm very excited to start talking about cardiac programs. And you saw in our first two slides, we have a whole host of cardiac programs that we're building in a very strategic manner. Our first program is called BAG3. And then, well, let me talk a little bit first about slide 18, of why we're going into cardiac. Really, when you think about cardiac, you look at CNS, you look at neuromuscular, you look at all the companies that are, that are out there are really attacking these, rare and fatal diseases. Cardiac has been largely untouched. This is going to be a huge opportunity for companies that are in the space. Projected, societal cost is going to be $1 trillion by 2035. Heart failure rates are 40%, heart failure mortality rates are 40% after five years, so even more so when you think about some of the programs that we're trying to tackle. These are big disease states. Dilated cardiomyopathies, BAG3, more specifically, which is our first program, is 29,000 patients. CPVT, and I'll talk a little bit about that, 33,000. And then hypertrophic cardiomyopathies can be up to 600,000. These are huge opportunities, and we'll talk about why we're going into them later. BAG3 is our first program. If you don't know BAG3, you should get to know it. It's called, it codes for this BCL2-associated athanogene 3 protein or BAG3. When you have reduction in this protein, you're going to end up in cardiomyopathy, and you're ultimately going to end up in heart failure. Males decline a lot faster than females, and once you're symptomatic, your quality of life is shot. You're in heart failure. You're not moving around. You're not active. Eventually, heart failure sets in, and mortality sets in. 25% in the first year, once you're symptomatic, 50% in five years. Now we're delivering. We worked on multiple different constructs. We took our time with this to understand constructs, promoters, the combinations, plus manufacturing, and we landed on rh74 with a very specific cardiac promoter, with triple transfection manufacturing platform that we're using across all of our programs. And we have a great collaborator in Dr. Eric Adler out of UC San Diego. We're working with him, and you can see on the next slide, slide 20, we're utilizing his mouse model. And this is a great time-dependent mouse model that's very predictive. And this will be the program that we're working on. We've also created a construct that is very specific for the heart, as you can see on the right-hand side of the page. It goes to the heart, it doesn't go to the gastric, it doesn't go to the quad, it doesn't go to the liver. So we're very excited about this. On the next page, you can actually see on slide 21, two of our constructs that we created compare against each other, one rh74, one AAV9, with a ubiquitous promoter on AAV9 and the cardiac-specific promoter that we haven't disclosed. and you can see we're getting to the heart, we're getting to the endogenous levels that we actually need to. However, it's not going to the liver, it's not going to other muscles, and so this is going. We're very excited about this program. Equally important, on Slide 22, when you look at cardiomyocytes, when you actually look at the heart muscle, you can see that 80% of the cardiomyocytes are gonna be positive for BAG3. This is huge. We don't believe that we need anywhere near 80%; however, our drug is getting to the heart, getting to the heart well. Now, our next program, we're very excited about this program, and we're working with a collaborator that's one of the world's leading experts in this. It's a catecholaminergic polymorphic ventricular tachycardia, CPVT. It's a fatal disorder. It's actually two disorders. It's called CASQ2 and RYR2, and this program we're extremely excited about. It's a large population. Now, CASQ2 is relatively small, about 2,000 patients in the United States. However, RYR2 is 20,000+ patients in the United States and extremely fatal. When you look at RYR2, and that's gonna be our lead program with the CPVT. When you look at RYR2, these kids are diagnosed young, aged 7-12. They end up with ventricular tachycardia, and many of them die, present with their first instance of ventricular tachycardia, they end up unfortunately passing away. You see this in a lot of sports at kids that are playing sports that unfortunately, eventually, you know, fall down and die or have to be treated. Also, it's, you know, when you think about the program, what they are on, there's really no drug to treat the underlying cause of this disease. And we believe that we have an approach that will do that, and so we'll talk a little bit about this. And what we're planning on doing is delivering and overexpressing the CASQ2 transgene and overexpressing calsequestrin. And this will inhibit the arrhythmias in RYR2, and we have the animal model to prove it. Now, on the next slide, slide 24, you can see, as I mentioned before, how big of a population this is, and I've already told you that BAG3 is gonna be roughly 30,000. Our next program is gonna be roughly 20,000 in the United States. It averages, so 80%-90% of the mutations will be adaptable to our program, and there's no therapies currently. The current options for these children are exercise restrictions, so you just tell them, "You can't move, can't run around, can't do anything." Beta blockers, but the beta blockers are very important to take on a very timely manner. If they miss a dose, they could have an event, and they could unfortunately pass away. And so the outcomes are not very good for this, and so this is a perfect disease state for us to go into, and I believe we're the only company that is doing this currently. So on slide 25, you can see what we're trying to accomplish here, the normal signaling on the far left, what's actually happening in the RYR2 mutation in the middle, and then following, the overexpression of the CASQ2 or the calsequestrin, we're binding up all the calcium, and this gets us a normal rhythm in the RYR2 channel. On the following slide, you can see our results on slide 26. And we have two different mouse models. We have the RYR2 mouse as well as the CASQ2 mouse. And you can see both in the low dose, the medium dose, and the high dose, that we can pretty much eliminate all arrhythmias in this mouse model. So we're very excited about this program. We're gonna be moving this from a research-grade material into normal, you know, FDA-approved type of material, getting away from the low empty to fulls. We're also gonna be moving this over to a capsid that we're working with internally. More to come on that. We'll announce which capsid in short order. But we're very excited about this program, and we're gonna be moving it forward very quickly. So the next slide, we'll be talking about our platform, and it's extremely important if you're going to be a next-generation or a genetic medicine company in the gene therapy space, you really need to focus on delivery. And delivery comes in multiple forms, and the two most important forms are capsid delivery and CMC. So let's focus on capsid delivery first. We're in the middle of our building out our capsid library. I've already mentioned that we're using SLB101 for our Duchenne program. That was our first capsid that came out of our capsid library. We actually have another capsid we're working on internally called SL34, and it bypasses the liver altogether, and it goes specifically to the heart. We're very excited about this new capsid that's coming out of our library, and we'll be moving that forward and talking more about that in the future. We're already through our second round of non-human primates, as well as pigs, in our overall capsid library. We've already taken down the animals, and we'll be working on identifying 10 capsids to move into further rounds of non-human primates and pigs, as well as mice. More to come on that. The next slide is around manufacturing. Everything we do revolves around manufacturing. We have the ability to scale up to 500 liters in-house. So in our process development team, in Charlestown, right down the street, about 100 feet from where I sit, we can go from a shaker flask to 10 liters, to 50 liters, to 250 liters, to 500 liters. Feel free to come by, and we'll give you a lab tour, and you can see the labs yourself. It's extremely impressive. We also have a vector core down in North Carolina that makes all our small-scale materials. So any material that's for, you know, non-human primates or mice can be built out of our vector core while we hone in our process at the 500-liter level in Cambridge. We've also make improvements. We've already made improvements for our Duchenne program. We're making improvements for our BAG3 program. We're moving from a triple plasmid to a dual plasmid platform, which was, you know, not many companies are doing. We believe that we can make multiple other improvements that we've seen in the labs in our process development team right now, and we can scale up and increase yields by about 15 times, lower the COGS, increase purity. We definitely focus on the full to empties, and most of our drug is close to that 80% true full, so it's very, very important. The next two slides, really driving to the future. So slide 31, the overall, what is our foundation going to be built upon? Obviously, I mentioned this new management team that came in during the merger of AavantiBio with Solid. We now have a very diversified but strategic platform and pipeline that you can see we can build off each other. So the knowledge that we gain from BAG3 or CPVT or FA can really work all synergistically together. And you also saw that we have multiple other cardiac programs that we'll disclose in short order, and these programs continue to build. It also provides a lot of confidence for the KOLs that we speak to, that they know that we are committed to the space, and I think it will be a major driver and player in the cardiac space. We have our next generation Duchenne program. That IND is on track, and so So it's September, I said early October, we'll have an IND early Q4, we'll have an IND. And so we feel very comfortable with the timelines there. And we'll be dosing patients as soon as we can get IRB approvals and screen patients post IND acceptance. We have thought leaders that are working with us around the world. Not just University of Florida, but we have Wisconsin, University of Wisconsin that's working on one of our cardiac programs, UC San Diego. As I mentioned, Dr. Adler is working with us on our BAG3 program. We have Iowa, that's working on one of our dilated cardiomyopathies. We're working with Phlox on a rare dilated cardiomyopathy. And we have so we have leaders across the world that have collaborated with us now, we're really building a great network. As I mentioned before, platform, where you have a lot, capsid library, that is already pulling out multiple capsids that are very unique. We have our CMC platform, where we can scale up, up to 500 liters in-house, really refined product, trying to focus in on that 80% true full, not partials, true fulls, and it's extremely important, CMC is the drug. What are our anticipated milestones? This is the last slide on slide 32. As I mentioned, Duchenne, coming real soon to you for an IND. Capsid library, dosed already, non-human primates and pigs. Second round, third round's coming up at the end of the year, early next year. AVB-401, that's our BAG3 program. Dose range finding is underway, then we'll move into GLP tox and other preclinical studies early next year. And then for CPVT, we have CASQ2, as well as RYR2. Drug candidate selection is underway, as well as preclinical studies will happen early next year, and then we'll move forward with that. We have $160 million in cash, as of June thirtieth. That will take us into 2025. And with that, I'll turn it over, back over to Max. But thank you very much for your time. I really do appreciate it. Thanks, Bo. Maybe we can have a seat. Where would you like me to sit? There, you sit there. Musical chairs. Well, congratulations to you and the team on all the progress you've made, and exciting to hear about the new program. What I thought we'd do for the remainder of the time here is maybe just spend a few minutes, you know, peeling back the layers to the onion on some of the points you made during the course of the presentation. You know, maybe to kick us off, I was just wondering if you could comment a little bit more on how you see the SGT-003 program being positioned in the Duchenne market? Yeah. Yeah, as I mentioned, Duchenne is a... Unfortunately, it's a traumatic disorder, and it's very complex, and every patient is different. It's a very heterogeneous population, as I tried to show you on that one slide, but really, that slide doesn't even give it justice. You have so many patients that are sort of early ambulatory, late ambulatory. Late ambulatory has multiple layers within it as well, because these kids are fragile. You have a decent amount of kids, 15%-20%, sometimes, you know, it could be greater, depending on the capsid, that have antibodies before they've been dosed. Duchenne's gonna be here for a long time. If these drugs, by the way, work, and I believe they do, Duchenne's gonna get bigger. We're gonna have to find ways to redose, as I mentioned, for the, you know, not only the kids that already have antibodies, but for the older children that can really only get to the heart and the diaphragms. You have to have a capsid that really drives expression in the diaphragm and the heart. Then, unfortunately, you're gonna have a lot of children that don't get the response that they truly need, and you're gonna have to find ways to lower antibodies and get to them. I think what we have done is we've created a next-generation program that can get to, and transduce, and express very quickly in that four-day window. So once we're able, and once the scientific community is able to lower antibodies down to a certain threshold, and we're working on that internally, right now, then we can dose, transduce, and express. We also know that this capsid gets to the diaphragm a lot better than AAV9, our old program. And so that's what you're gonna have to have for these older kids, right? Get to the diaphragm and the heart. It was already expressed in the heart very well, AAV9 does, but the diaphragm is always lower. This program in our non-human primates is getting about 3- to 5-fold higher than AAV9, and so we feel that it's positioned well. Unfortunately, you know, these kids, these drugs, all drugs, so it doesn't matter which one you wanna talk about, they really don't get into the satellite cells, the stem cells, and unfortunately, these little boys start acting like little boys again, and they're gonna run around, they're gonna tear down the muscle. You can see the CK rise, and you know that microdystrophin drugged muscle is gonna turn into dystrophic muscle after it's regenerated. So we're gonna have to find ways to get to it. So I think it's positioned very well as a second-generation drug, where we can get to older population as well as the younger population, naive as well as redosing. Now, we gotta work on the science to get the threshold antibodies down to a certain threshold so we can dose, and that's what we're gonna do. Unfortunately, Duchenne's gonna be around for a very long time. Thanks for that, Bo. Moving over to cardiac, and I know you touched upon this a little bit in the presentation, but, you know, anything else to note on, you know, why you've chosen, you and the team have chosen cardiac as the next space to make an investment, but more importantly, you know, the indications that you've selected? Yeah. I think, one, we are one of the leaders in cardiac space, and we started out working on cardiac many years ago at AavantiBio, and AavantiBio was actually purchased by Solid Biosciences last December. And so we brought over all the programs from AavantiBio. So we've been in the cardiac space from the day AavantiBio started. And why? It is the next frontier. And you can actually see some follow-on program companies jumping into the space recently because they know that we're onto something. This is going to be a huge market. Neuromuscular and CNS, they were the first, and genetic testing started, you know, really ramping up, you know, 2010, 2011, 2012. I ran a genetic testing program for, one of my previous companies I worked for, for a very long time, and you saw the increase in genetic testing. You did not see that in cardiac. You're seeing it now. Cardiologists are jumping onto it because they're realizing there's so many reasons for these, ventricular tachycardia—I mean, arrhythmias, for dilated cardiomyopathies, hypertrophic cardiomyopathies, and they're jumping on it now. They're dosing, they're genetically testing over and over. So these populations are going to explode, and no one's in the space, or not many companies, just a handful, and Solid is leading the frontier. You don't have a, you know, a lot of turnover in the muscle. So... And you can use a promoter-driven expression right to the heart, as I showed you with CPVT, as I showed you with BAG3. So we can go right to the heart. You're not having turnover. You know, there, there's other, there's other reasons. It's huge unmet need, $1 trillion by 2035, as I mentioned. And I think what's also important is you see our strategic pipeline and how we're building it. We can piggyback our knowledge off of it, so our program 401, 501, 601, they all start to add up. And so, I think strategically it is the right move, and, it's positioned very well. Importantly, you know, when we talk about rare disease, we're – I'm still in rare disease, but now I'm into patient populations that are 20,000, 30,000, 50,000. And so from an investor standpoint, when I hit a milestone, it's gonna be significant. It's. And I, I think that's very important as well. Thank you. The capsid library, very important part of the Solid story. Can you just explain to us a little more about the value of the work you and the team are doing there? Yeah, look, you know, it, it's everything. We believe everything in gene therapy and precision genetic medicine is gonna revolve around delivery, and delivery takes sort of multiple roles, right? It's the CMC, making sure you have a very clean and pure product and try to drive the yields up. It's also then delivery from a capsid and promoter standpoint, and we focused in on capsids because, you know, there's a lot of capsids that have been tried and true, but they have some flaws. We think that we can do a better job of delivery, specifically to the heart, and then try to bypass the liver. So we've been building these capsid libraries for an extended period of time. We're actually starting to see major results. So obviously, our first capsid came out of it. It's SLB-101. That's the capsid we're actually using in our Duchenne program. We have another capsid that literally we just received the data on this past week, called SL34, and it completely bypasses the liver. We're gonna use this-- we're looking at using these types of capsids for our cardiac programs in the future. This capsid goes straight to the heart, bypasses the liver almost altogether. What we want to accomplish is we want to build a whole portfolio of capsids like this. We're already through our second round, as I mentioned, non-human primates and pigs in our capsid library. We did first round was mice and non-human primates only. Second round was mice, non-human primates, and pigs. Now we're going to take it down to about 10 or so, 10, 20 capsids, and then really develop those capsids. We'll use these capsids for our own pipeline, but we'll also use them for non-dilutive financing for people who want to work with them. So very excited about the capsid library, and if you really want to be a precision genetic medicine company leader in the space, you've got to get delivery down, and that means CMC as well as capsid/promoter. Great. Thank you, Bo. And on that end, you know, you and the team have also made significant investment on the manufacturing end of things. Can you talk a little bit to us about, you know, what you've done there and why you view it as so important? Yeah. So we have a full process development, analytical development team in place, and as I mentioned, in Charlestown, where, you know, Kevin and I sit about 100 feet. Our process development team can scale up from shaker flask all the way to 500-liter. So, you know, they go from shaker flask to 10, to 25, to 50, to 250, to 500. So we lock down our process, and we make, we modify our process, we continue to modify our process for future programs. Once you lock down your process for, like, Duchenne or BAG3, it's locked. Don't make any changes because the FDA won't like that, and it'll just send you back. But you continue to modify your process, make your own process, by the way, that is proprietary to us and how we do things. And then we believe, based on the data that we have, that we can potentially get up to 15 times greater yields by making tweaks along the way, and we're going to continue to do that, modify it, file our patents, and, and keep it as a trade secret. We're already moving away from triple plasmids to dual plasmid design, that increases our yields as well as decreases our COGS. And so process development is everything. Now, we have a vector core down in North Carolina, so they're full-time busy, and they're, they're backed up for, like, months just working on making material for mice, rats, non-human primate studies. So our PD team stays there, and then our vector core. It's very important for you all to know that we have two other teams that not a lot of companies have. We have a CMC regulatory team that's embedded in everything we do. And so these are regulatory experts that focus on CMC only. So they're not regulatory strategy type of teams. They're people who understand CMC from the very smallest of molecule and changes, and how that affects regulatory. They're embedded. We have a medical manufacturing science and technology team. And why is that team very important? Because when you create your own process, and then you have a CDMO that's making your commercial-grade material for you, you don't want them to mess around with your process. You don't want them to make changes. So we embed this MS and T team in the CDMO. They sit on the floor. They're solid employees, but they're embedded in that CDMO, and so you don't make any changes. It's extremely important if you want to get it right. Thank you. I know we're coming up on time, but maybe if there's any questions from the audience? Okay, great. Well, Bo, on behalf of Citi, it was a pleasure having you up here today. Congratulations again on all the progress, and look forward to seeing more. Yeah. Thank you, Max. Thanks, Citi, for the invitation. I really do appreciate it. Thank you. Thank you.