Ladies and gentlemen, thank you for standing by. Welcome to the Solid Biosciences update call. At this time, all participants are in a listen-only mode. After the speaker's presentation, there will be a question and answer session. Please be advised that today's conference is being recorded. I would now like to hand the conference over to your speaker today, Mr. Tim Palmer, Corporate Communications Manager at Solid Biosciences. Sir, you may begin. Good morning. Thank you, operator. Before we get started, I would like to remind everyone that during this conference call, we may make forward-looking statements, including statements about the company's financial results, financial guidance, future business strategies and operations, and product development and regulatory progress, including statements about the ongoing IGNITE DMD clinical trial. Actual results could differ materially from those discussed in these forward-looking statements due to a number of important factors, including uncertainty inherent in the clinical development and regulatory process, the extent and duration of the impact of the COVID-19 pandemic, and other risks described in the Risk Factors section of our most recently filed annual report on Form 10-K and other periodic reports filed with the SEC. We undertake no obligation to update any forward-looking statements after the date of this call. With me on today's call are Ilan Ganot, Co-Founder, President, and Chief Executive Officer at Solid Biosciences, Dr. Joel Schneider, our Chief Operating Officer, Dr. Cathryn Clary, our Acting Chief Medical Officer, and Dr. Carl Morris, our Chief Scientific Officer. For opening remarks, I'd like to turn the call over to Ilan Ganot. Ilan? Thank you, Tim. Good morning, and thank you all for joining us today. The focus on today's call is to provide an update on our current corporate activities as we continue to progress along our 2021 corporate goals and what our progress means for patients with duchenne muscular dystrophy. First, we'll provide an update on dosing in IGNITE DMD. Two patients were dosed this quarter in IGNITE DMD using SGT-001, produced with our improved manufacturing process and under an amended clinical protocol. As previously reported, patient seven has been dosed safely and continues to do well. Today, we are reporting on an additional patient dosed. Patient eight experienced a serious adverse event, or SAE, but has since been discharged, and as of the patient's 30-day follow-up visit, lab values have either returned to normal or continue to trend towards normal. In a moment, Dr. Cathryn Clary will review this SAE and the steps we are taking to evaluate its cause. Following Cathryn's review of the patient dosing, Dr. Carl Morris will present on encouraging long-term biopsy data collected from the first three patients dosed at the 2x10^14 vector genomes per kg dose. Carl will also be presenting this data later today at the American Society of Gene & Cell Therapy annual meeting. These data provide evidence of sustained microdystrophin expression for 12- 24 months post-dosing and are potentially supportive of the recently reported positive trends in clinical biomarker and functional data from the IGNITE DMD study. To our knowledge, IGNITE DMD is the first Duchenne gene therapy trial to show durable microdystrophin expression out to 24 months. In conjunction with our growing clinical experience, we believe that the totality of the clinical data will establish a risk-benefit profile for SGT-001 that will be meaningful to patients with Duchenne. Today, as Dr. Joel Schneider, Solid's Chief Operating Officer, will share, we are also providing an update on our preclinical pipeline, which includes the nomination of SGT-003 program as our next development candidate and an update on our ongoing collaboration with Ultragenyx. SGT-003 will combine a novel capsid and our proprietary microdystrophin construct to enable a next-generation gene therapy for Duchenne with enhanced delivery to muscle cells. Data from our novel capsid program have also been presented at ASGCT. I'm pleased with our progress on all these fronts as we continue to generate additional evidence to support the long-term potential of SGT-001 while expanding our pipeline of differentiated gene therapies. I'll now turn the call over to Cathryn, who will briefly review our clinical update and the steps we are taking as we progress the SGT-001 program. Thank you, Ilan Ganot. As we reported in March, we've resumed enrollment in IGNITE DMD and have subsequently dosed two patients under our amended clinical protocol. As a reminder, we're working closely with our Data Safety Monitoring Board, or DSMB, to carefully review all the data generated with a built-in waiting period of 45 days minimum between each dosing. We also previously reported that patient seven, dosed at the 2x10^14 vector genomes per kg, was dosed uneventfully and continues to do well. As we do with all patients, we are continuing to monitor this patient and will be collecting additional data throughout the year. Today, we're sharing that patient eight experienced an inflammatory response, which was classified as a serious adverse event and considered by the investigator to be drug-related. This event is described in our investigator's brochure and is not considered unexpected. As of the patient's 30-day follow-up visit, laboratory values had either returned to normal or continued to trend towards normal. We've shared the data related to this SAE with the FDA and also the IGNITE DSMB, and are working closely, both internally as well as with external experts, to further our understanding of the outcome of this dosing and how it may impact our clinical strategy moving forward. While we already had a minimum built-in waiting period of 45 days between dosing patients eight and nine, the complexity of this event requires us to carefully analyze all the data before continuing to dose additional patients in IGNITE DMD. This will allow us to determine what, if any, changes we might make to the clinical protocol to further enhance patient safety, which is always our top priority. I'll now turn the call over to Carl, who will review the long-term biopsy data from patients four through six, which we believe supports the potential of SGT-001 to provide benefit to patients with Duchenne. Carl? Thank you, Cathryn. Today, I'm excited to share our analysis of the long-term biopsy data from patients four to six, which provide compelling evidence that a single dose of SGT-001 at the 2x10^14 vector genomes per kg dose leads to sustained expression of our proprietary microdystrophin construct containing the neuronal nitric oxide synthase, or nNOS, binding domain for up to 24 months post-dosing. The muscle biopsies were collected from patients four to six and taken at 24, 18, and 12 months, respectively, post-dosing of SGT-001. For each patient, the baseline and the last time point biopsies were taken from the right quadriceps, while the day 90 sample was acquired from the left quadricep muscle. Over the next few slides, I will share with you immunofluorescence and western blot data from the long-term biopsies that demonstrate microdystrophin expression remains comparable to the levels observed in the day 90 biopsies for all three patients at this high dose. I will then walk you through results highlighting microdystrophin protein function through the colocalization of a dystrophin-associated protein, beta-sarcoglycan, as well as nNOS. Finally, we'll look at some morphological analyses of the muscle biopsies that demonstrate overall only minimal muscle deterioration since the day 90 time point, with mild active dystrophic pathology observed in the long-term biopsies. Collectively, these data are potentially supportive of the positive trends in the clinical biomarker and functional data, which we shared in March. Slide seven shows immunofluorescence results from patients four through six at baseline, day 90, and at their last time point. As we previously shared, the 90-day biopsies showed microdystrophin-positive fibers in all three patients that weren't seen in the baseline samples. The longer-term data that we are reporting today show the proportion of microdystrophin-positive fibers is maintained for up to 24 months. Specifically, patient four has 10%-30% positive fibers at 24 months. Patient five is seen to have 85% positive fibers at 18 months, while patient six shows 50%-60% positive muscle fibers at 12 months post-dosing. On slide eight, we show western blot data collected for patients four and five in the top panel, and then patient six in the bottom panel. As shown in the table on the right-hand side, patient four's microdystrophin level remains below the level of quantitation of 5% of normal dystrophin, but is still detectable out to 24 months. Patient five's microdystrophin level is seen to be 69.8% of normal at 18 months, compared to 17.5% at day 90. For patient six, an average level of 20.3% of normal was found at 12 months post-dosing, compared to 8% at day 90. Slide nine summarizes the microdystrophin expression as assessed by western blot and IF of the three 2x10^14 vector genome per kg patients for up to two years post-dose. The figure on the upper left shows the western blot I mentioned on the last slide. Interestingly, you can see there is an apparent increase in microdystrophin expression for both patients five and six, that both had quantifiable levels at three months, while patient four's microdystrophin expression remains clearly detectable but below the level of quantitation of 5%. On the right-hand side, we've shown the immunofluorescence results from our validated automated analysis. The results show measurement of stable, persistent microdystrophin-positive muscle fibers out to the 24-month time point that remain comparable to the levels seen in the day 90 samples. Switching to additional functional analyses of the biopsies, we observed restoration of dystrophin-associated proteins to the muscle cell membrane and show colocalization in microdystrophin-positive muscle fibers. The column on the left shows microdystrophin in red, middle column shows beta-sarcoglycan in green, while the right column shows these two images merged with the colocalized proteins appearing yellow. As you can see, these two proteins colocalize to the cell membrane, which demonstrates the capacity of our microdystrophin to recruit dystrophin-associated proteins to the muscle sarcolemma. On slide 11, we show a similar analysis but looking at nNOS activity and localization to the muscle membrane. Again, microdystrophin is shown in red on the left, while the right panel shows nNOS activity using an enzymatic stain, as indicated by dark purple staining at the muscle cell membrane. These results demonstrate both nNOS activity and its localization to the muscle membrane, aligning with the expression of our microdystrophin protein. The continued nNOS activity observed in these long-term biopsies provides additional evidence of the durable functionality of our microdystrophin construct. The next slide shows histological staining of the muscle biopsies from each patient at baseline, 90 days, and at 12- 24 months. Although these muscle biopsies show variable degrees of dystrophic pathology, it is encouraging to see limited disease progression between baseline out to the long-term time point. Out to two years, only mild active dystrophic changes in muscle pathology were observed, supporting the role of microdystrophin in slowing progression of muscle loss. Overall, these new results from the long-term biopsies are encouraging as they demonstrate persistent and potentially increased microdystrophin expression between 90 days and out to 12- 24 months. The minimal progression of muscle deterioration since the baseline provides potential support for the recently reported positive trends in the clinical biomarker and functional data from the IGNITE DMD, as summarized on the previously reported efficacy heat map. As Ilan noted at the start of the call, I'll be presenting these data at 1:45 P.M. today at the ASGCT conference. My full presentation will be posted to the Solid Biosciences website once my talk is complete. I'll turn it over to Joel for an update on the preclinical pipeline. Thanks, Carl. The growing body of evidence supporting the potential for SGT-001 to provide benefit to patients with Duchenne is very encouraging, and we look forward to generating more data for this program as we dose additional patients in IGNITE DMD. While advancing SGT-001 remains our priority, we continue to explore new and innovative ways to improve outcomes for patients with Duchenne and to potentially address the needs of patients with other musculoskeletal disorders. Toward that end, we have been actively evaluating a library of novel, rationally designed AAV9-based capsids. Today, we are announcing our next generation Duchenne microdystrophin gene transfer program called SGT-003. This program is an internally developed preclinical asset that leverages our broad expertise in gene therapy and muscle biology. Data presented at the ASGCT meeting by Dr. Jennifer Green demonstrate that we have successfully developed a library of novel capsids with increased muscle tropism that corresponds with decreases in liver biodistribution and drive improved efficiency compared with AAV9 in various in vitro and in vivo models. SGT-003 is a preclinical candidate that combines a novel capsid designed to enhance delivery to muscles with our proprietary nNOS-containing microdystrophin. We are currently conducting lead optimization for SGT-003, and we look forward to sharing additional data with you as this program advances, with a potential timeline to the clinic in approximately 18 months. This slide summarizes data from a dose-response study exploring AAV9 alongside capsid candidate AAV-SLB101. As you can see, at all doses, our novel capsid led to increased biodistribution and ultimately microdystrophin expression. We will aim to provide additional program and pipeline updates as we progress SGT-003, as well as other candidates which leverage our strong internal research capabilities. In addition to our internal research and development efforts, we also have a collaboration with Ultragenyx to explore other next-generation opportunities to develop additional Duchenne gene therapies. The companies have been collaborating to optimize candidate vectors that leverage our nNOS-containing microdystrophin construct with an AAV8-like capsid within the Ultragenyx HeLa producer cell line manufacturing approach. I am pleased to share that this is a very productive collaboration that has leveraged each company's expertise and resources. Ultragenyx is leading efforts around vector construction, optimization, and creation of the HeLa producer cell line, and in vitro and in vivo screening of the novel vectors has been expedited by routing expression analytics through Solid's research team and leveraging our established assets. We expect to provide an update on this program by the end of 2021. As a company committed to improving outcomes for patients with Duchenne, we believe that having multiple ways to deliver our proprietary microdystrophin construct enhances our ability to make meaningful differences in these patients' lives. We are excited to expand our pipeline with additional opportunities. I will now turn to our Q1 2021 financials. Earlier today, we filed our Form 10-Q for the quarter ended March 31, 2021, which contains detailed financial results and is available on the Solid website. Although I'm not going to review our detailed results during today's call, I do want to highlight that during the first quarter of 2021, we closed a public offering, including the full exercise of the over-allotment option, resulting in gross proceeds of approximately $143.8 million before deducting underwriting discounts, commissions, and offering expenses. This financing further strengthened our balance sheet, and we ended the quarter with $268.5 million in cash and cash equivalents. We expect that our cash and cash equivalents will enable us to fund our operating expenses into the fourth quarter of 2022. I'll now turn the call back to Ilan for closing remarks. Thanks, Joel, Carl, and Cathryn. Before we take your questions, I want to take a moment to review our 2021 priorities and anticipated milestones. As previously announced, we successfully achieved our first quarter 2021 milestones. As Joel just discussed, today we are expanding our pipeline with SGT-003. We remain on track to present additional 90-day biopsy data in the second half of this year from patients seven and eight who were recently dosed. The long-term biopsy results we presented today are encouraging and further increase our confidence in our technologies, in our team, and strategies for making gene therapy a reality for patients with Duchenne. I'll close by reiterating our commitment to the Duchenne community and to working every day to advance therapies that improve their lives and address the challenges of this horrible disease. This commitment, for obvious reasons, is a deeply personal one for me. What makes Solid such a special company is that every one of our employees is as committed as I am, and we see these boys with Duchenne for who they are today, kids who just want to go out and have fun with their friends. We also know what the future holds for them without an effective therapy. What inspires all of us at Solid every day is the prospect of giving them a different future. This commitment is what guides us through the challenges and drives us to build on our successes. We thank the Duchenne community, our employees, and our investors for their continued support and dedication to our shared mission. I look forward to updating you as we continue to make progress in our clinical and pre-clinical programs. We'll now take your questions. As a reminder, to ask your question, you will need to press star one on your telephone keypad. To withdraw your question, press the pound key. Please stand by while we compile the Q&A roster. Your first question comes from the line of Joseph Schwartz with SVB Leerink. Everyone, congrats on all the progress. My first question is on the longer-term expression data, which it's encouraging to see those delayed kinetics, and it seems like they correspond or correlate most closely to six-minute walk and FVC clinical benefits as opposed to an NSAA. I was just wondering, how are you thinking about being able to take advantage of this observation, if you agree with that, and try to establish whether these clinical endpoints or a composite of these, with or without an NSAA, might improve the chances to get microdystrophin gene therapy such as SGT-001 or three across the goal line with the FDA? Great question, Joe. Good to hear from you. I think Carl will start and Cathryn will finish. Yeah. Pretty good that you picked that up so quickly. Yes. There seems to be an apparent correlation, but it's an N of three. As you know, you can sort of make any associations you like. I think we're encouraged by the data overall. There is variability expected in these biological assays. We took them different muscles at different time points. We are sort of quite happy about it. It's not unexpected that we would see an increase in expression over time. We need to get more data from more patients to really sort of start trying to look at specific relationships. I'll turn it over to Cathryn to talk about the clinical trial and how we might be thinking based on that. Sure. Yeah. Thanks a lot for the question. We were certainly very encouraged by these long-term results. I think you asked a question which really gets to the heart of what we're thinking about as a company in terms of designing our registration trial. Which outcome measures do we use? How can we find the most robust way to measure functional benefit in patients in such a heterogeneous disease? As Carl said, this is a small data set so far, we're encouraged by it. It's a bit early to start doing correlation analyses, although we're certainly thinking about that. We look forward to getting the data on our two additional patients and others so that we can make those decisions. Okay, great. I appreciate that. As far as dosing additional patients in the future, I was just wondering, what does that path look like for you from here? Could you characterize the SAE, which I heard you say was not unexpected but had some complexity? Was this triggered by lab and/or clinical findings? What can you tell us about the last patient to be treated with SGT-001? Cathryn, Yeah, keep going. Sure, I'll just keep going. As I said, the patient had an inflammatory response with elements similar to some of our other patients, which is why it was not unexpected. However, the severity of the event was less severe than patient six. We still are really looking at all the components of it from a causality perspective, the patient course. We're working both internally and with external experts to fully understand it so that we can move forward in a way that will ensure patient safety. You asked about the path to dose the next patient. We are working, of course, with our DSMB. They've reviewed the case, and we'll be going back to them with the results of our investigation. They will need to approve dosing the next patient. We'd already built in a minimum of 45 days between patients eight and nine. While we can't speculate on exactly when we'll dose patient nine, there was going to be a bit of a delay. Then we're working with FDA as well. Thank you very much. Your next question comes from the line of Gena Wang with Barclays. Thank you for taking my questions. I have three questions. The first one also regarding the patient eight inflammatory response. Wondering, any additional color you can give regarding this patient? You did present at the ASGCT, showing the seropositive AAV9 is related to complement activation. I think Pfizer also shares some additional color on their understanding of the safety. If you can give a little bit more color on this patient and what exactly that inflammatory response was, and what kind of baseline characteristic from this patient, like seropositive, also the platelet count, any other information you can give. That's the first question. My second question is regarding the SLB 101. Did you test in non-human primates? What does the safety look like in non-human primates? Also, which backbone was derived for SLB 101? My last question is more the future direction. You do have your own internal SGT-003, but you also have a rare collaboration. How do you prioritize? Do you see this as internal competition? Awesome questions, Gena. I think we're going to start with Cathryn to talk a little bit about the SAE, and then she can hand it over to Carl to finish that off, and then talk about SLB 101, and I'll talk about the priorities at the end. Thank you, Gena, for the question. As I mentioned, patient eight eight did have an inflammatory response with elements that were similar to what we had seen in some of the other patients. You asked about complement activation. It's interesting, complement activation is part of the innate immune response, we've actually seen laboratory evidence of complement activation in all eight of our treated patients. Patient seven, as we reported before, had some complement activation in lab, it was lower than what we had seen in some other patients. We're still really evaluating the elements of patient eight. Every patient appears to be somewhat different, we haven't really identified a common factor with our SAEs, we're still examining certain elements of it. Once the results of that investigation are done, we can provide some additional information. Hi, this is Carl. The ASGCT poster is highlighting that in the presence of antibodies, AAV, and it doesn't matter if it's AAV9 or AAV8, we showed both can activate the complement system. We think this is an effect that will be seen within different programs. I think we're getting a better handle on it. Other companies are seeing that as well. Regarding SLB 101 and SGT-003, the capsid is derived from some rational design that we did internally. Rather than going through a computational analysis like a number of companies, we sort of went from the other way and looked at using our muscle expertise to think about how best to target muscle specifically. We identified a number of capsids that look promising. It's very early on in the plan, and we're still in sort of lead optimization right now. We haven't sort of finalized the candidate, but we plan to be moving into IND-enabling studies as soon as possible once we've identified the specific capsid and specific transgenes as well that we're using. I'll pass it back to Ilan. Just to say that we're actually making good progress with Ultragenyx. I enjoy seeing the two teams collaborate. There's some real complementary skill sets here when you think about doing DMD, with another manufacturing system. It happens to be that their gene therapy people are here in Cambridge, too. I think there's a lot of good chemistry and very good people involved from both companies. I think they'll probably be leading the communication on the next steps there. We are committed to really helping in any way we can advance that program. Gena, you've heard me say this before. I don't think there could ever be enough programs there for DMD gene therapy. There's just so many patients and such a massive unmet need. I would just say that there is the potential to consider other musculoskeletal disorders as well as additional next-generation gene therapies like SGT-003. Carl keeps confusing me with those numbers. I look forward to continuing to update on the existing and more programs in the future. Thank you very much. Thank you, Gena. Your next question comes from the line of Salveen Richter with Goldman Sachs. Hi. Thanks so much for taking our question. This is Sonia on for Salveen. I know you're currently evaluating what caused the inflammation in patient eight. Do you happen to have any initial hypotheses on why that might have happened? Our second question was just when are we going to see any additional functional data from patients seven and eight? Thank you. Hey, thank you, Sonia. Cathryn? Thanks very much for the question. I don't want to speculate right now on causality because we are looking at several things. As we reported, our principal investigator did deem the event to be drug-related, and it does have some elements that are similar to our other patients, but less severe than we saw in patient six. patient seven, of course, dosed under our new protocol, had a very safe dosing. We're evaluating a number of different factors. As I said before, we'll definitely get back to you when we have a better handle on exactly what happened and what some of the causes were. In terms of the functional data, patient seven is approaching a 90-day visit. It'll be a while. We don't really look at functional data at 90 days or report it because of the steroids still lingering in the system. It'll be a while before there'll be additional functional data, and we haven't actually guided to that. Again, if you would like to ask a question, simply press star, then the number one on your telephone keypad. Your next question comes from the line of Gbola Amusa with Chardan. Hi, thanks for taking my call. Just wanted a couple questions about the long-term data on patients four to six. It's pretty noteworthy stuff, and I know it's N equals three. There's variability in assays, et cetera. We can't make easy conclusions, but could you update us on any hypotheses you might have on what factors could be at play that create a difference for what you see in patient four versus five and six? Is there anything you can do going forward to encourage results that are more like those seen in patients five and six? Again, I know it's early days here. Hey, Gbola. It's good to have you. This is a Carl question. I know because I asked it to him just two days ago. Yeah. We just sort of pulled these data in and started analyzing very recently. It is very early, but we do have confidence in our assays. Given that we're seeing good results from all these different sort of orthogonal type assays, it does look as very encouraging, the way this dose is sort of a good dose, and we're generating improved responses over time. It's not unexpected, I guess, if you think about the just sort of continued production over time and then finding sort of more spaces to fill in on the membrane and stabilize the overall muscle. It's very encouraging. We're going to obviously spend a lot of time thinking about mechanisms to look at this. Patient four started, unfortunately, like with all drug trials, you have responders, non-responders, and unfortunately, patient four had lower levels and below the level of quantitation, still very detectable levels. There may be some threshold effect here that we are just not aware of. Importantly, patient four did see a trend with functional improvements that we presented back in March. I think even with less than 5%, there's sort of really promising results coming out. The overall sort of apparent increase is something that we're definitely going to be looking into. I would just add, Gbola, that this notion of long-term durability, we got a little lucky here because this was supposed to all be one year of biopsies that ended up being delayed because of COVID and because clinics were closed, patients couldn't show up. The one-year visit ended up being a year later. Now we have two-year data. I think when you think about gene therapies, as you obviously do all the time, the notion of duration, the notion of continued or even improved durability is clearly going to feature. In a disease like Duchenne, that is so hard to measure the functional outcomes, I'd like to hope that such biomarkers are going to provide us with a lot of confidence that this is not something that just disappears after, I don't know, three or six months. Got it. Just another one really quickly. I think earlier in the call, someone referred to delayed kinetics, and I know we have seen that elsewhere in the AAV space. The magnitude of change seems greater here for Solid, and I know it's apples to oranges and N equals three, et cetera. What's the state of art on biological reasons why there might be delayed kinetics, or is there a reason, an explanation that we can sort of latch onto to feel like maybe this is a real phenomenon going forward? I'd love to talk to you for a while about this. If the muscle becomes more stable and sort of healthier, there may be sort of a more consistent production of protein production that's occurring. More myonuclei being fused in as the muscle can grow and build, and therefore, every time we get a positive SGT-001 positive nuclei in there, it could produce more protein. Again, it's all speculation. Kinetically, we generally see stabilization after about 28 days in our preclinical models with sort of a continued, but very slow increases. We do see an apparent doubling in patient six and a threefold in patient five, again, apparent. We don't know. There could be other things happening. Actually, importantly, someone asked about age, and could age be a factor? patient four was older. We really hope not, but patient four was about 11 years of age. That's something that we really need to be thinking about as we move forward. Okay. Your next question comes from the line of Maneka Mirchandaney with Evercore. Great. Thanks for taking the question. Based on what you're seeing for patient eight, do you think there are any additional potential changes in the protocol that might be able to further decrease the risk of these inflammatory events, like changes in the dose of the immunosuppressive drugs or timing or other factors, and what might that look like? Thanks. First, obviously Cathryn will take it, but I'll just say, Maneka, that again, we learn so much from every patient, and the idea here is to identify a long-term solution to a pretty serious problem. I feel that if things need to be tweaked, that's a great thing, and hopefully arrive at a very happy place at the end. Other companies are hopefully doing the same, and I'll have Cathryn add if she's got some. Sure. Thanks, Maneka. It's such an important question. Obviously safety is really our first concern with these patients. Probably one of the biggest questions we are grappling with right now is to understand the event so that we can potentially modify the risk mitigation profile in a way that we think will optimize safety. We're still really in the middle of that investigation, including consulting with some external consultants who are experts in this area. I can't really tell you what our hypothesis is at this point because we're still really exploring different options. We will certainly share that with you if and when we do decide to make protocol changes. Of course, those will need to be approved by our DSMB and shared with FDA as well. I think you also asked the question about the doses. That is one of the things we're looking at, is dosing, but potentially other options. Got it. Thank you. Okay. Your next question comes from the line of Anupam Rama with JP Morgan. Hi, guys. Thanks so much for taking the question. Just a clarification question here. Has the patient eight SAE and sort of clinical profile of this patient been shared with FDA and the DSMB? What are the timelines for feedback from both of those groups? Yeah. Yeah. Hi, Anupam. Absolutely. Shared with FDA and with the DSMB. We have ongoing dialogues. We are not really able to project timelines. Have been shared and discussed. Got it. Thanks so much for taking our question. Thank you. At this time, there are no further audio questions. Are there any closing remarks? Look, thanks everybody for dialing in. Have a great weekend, and we look forward to talking again soon. Thank you. Thank you. This concludes today's conference call. Thank you for your participation. You may now disconnect.