Hang on one second. Nope. Which button is it? The green. Great. They are all green. Oh, the big green. Okay. Before I begin, I just need to remind you that during the presentation, I'll be making forward-looking statements, so please refer to our public SEC disclosures. We are progressing through 2025 in a very, very quick and efficient manner, and there is a lot of momentum that is building for the company as I speak today. By the end of 2025, we expect to have four active clinical programs by the end of the year, and we will get into those programs in more specificity. We first and foremost start with our Duchenne muscular dystrophy franchise, and we are rapidly expanding that DMD franchise. For our ENTR-601-44 program, which covers the 44 mutation, we have clinical studies that have been authorized in the U.K., the U.S., and the EU, and we're fast at work on enrolling those studies as I speak. For our ENTR-601-45 program, which goes against the 45 mutation, we have regulatory clearance to proceed to clinical trial enrollment in both the U.K. and the EU. For our ENTR-601-50 program, we're on track to submit our global regulatory filings in the second half of this year. That comprises three of the four. The fourth program really is our Vertex collaboration on myotonic dystrophy type 1, or DM1, which we entered into a few years ago with Vertex. So far, that MAD portion of what is called VX-670 is ongoing, and that's a global study. There's 26 clinical sites that have been initiated, and Vertex continues to make what we believe to be great progress there as they continue to accelerate that. Pretty robust partnership between the two companies and a lot of the traditional milestone payments plus royalties that we do not account for in our current cash runway. DMD and DM1 are obviously two very robust neuromuscular programs and disease areas. However, we are also advancing a preclinical pipeline that's generating a lot of really interesting data, and we look forward to sharing some of that data around our ocular programs by the end of the year. Finally, importantly, within this market, we have a strong financial position with roughly $383 million on the balance sheet and, importantly, a cash runway that goes into Q2 of 2027. Why that's important, besides the fact that we have this cash, is that it allows us to get through a fair amount of very inflective points for the company when we think about the clinical data. Just to take one step back, a lot of companies talk about their mission. The mission is our North Star at Entrada for the 150, 160 people that work for the company, and that's really treating devastating diseases with intracellular therapeutics. That's how the company was founded, on the basis of being able to go after a lot of intracellular targets. This is a picture of different children that have Duchenne muscular dystrophy, and I take a lot of pride in the fact that we're able to communicate and work with a lot of these kids' parents as we design our clinical studies so that we can help them with some much-needed potential therapeutics. Let's talk about these intracellular therapeutics. First and foremost, 75% of all disease-causing targets are located inside the cell, but we just can't really access them efficiently. That's a big number, right? That cuts across a lot of different diseases, and that's where the Entrada solution kind of comes into play. What we are doing is that we're leveraging what we call endosomal escape vehicles, which are a family of cyclic cell penetrating peptides, to not only increase cellular uptake but improve endosomal escape. Once you get out of the endosome, we can then help target the cargo, and I'll put that in air quotes, to the muscle or organ that we need to go to. That's kind of like the secret between Entrada. We really do feel as though we have a potential for best-in-class and first-in-class therapeutics across DMD and DM1, and we are efficiently working at progressing those, as I just mentioned. These endosomal escape vehicles, so here's a bit of a character on slide six around it. Not only do they have a unique chemistry that differentiates these peptides from other peptides, but they also have a structure that's very different. What that allows us to do is not only improve the uptake and endosomal escape, but it allows us to increase the half-life and increase or extend the half-life and increase the stability, which becomes really important. The ability to bind to the phospholipid allows for us to have a very broad biodistribution to all cells. Importantly, the last point here is the consistent and predictable PK. What we've done with our DMD programs and our DM1 program is we've used the same EEV across those programs, and what we've seen is a remarkably consistent translation from murine models into NHP and then into humans now as well. From a pipeline perspective, 75% of all these are intracellular targets, which means that we have a lot of opportunity here, and I think discipline is really important for this company. Beyond our initial focus on DMD and myotonic dystrophy type 1, we do have a pipeline, and we'll talk more about that as the year progresses, but we're talking about ocular programs, we're talking about platform expansion. We're constantly trying to one-up the platform. What does a second generation of EEVs look like? What does the third generation? What are some other programs that we can match these up to? What are some of these programs that do not need EEVs but can use better protein engineering and things like that? Today, as we sit here today, it's very much about focus and very much about pushing these DMD programs further and further into the clinic. Why do we feel as though these therapies have the potential for a best-in-class approach in neuromuscular diseases? Once again, we have these four programs that we want to be activated by the end of 2025. What we have done with our first program, which is ENTR-601-44, is that we ran a phase I healthy normal volunteer study in the U.K. What those data showed were not only thematically a robust clinical validation, but why is that there? There were no treatment-related adverse effects, which is really important for this class of drugs. The target exposure and target engagement, whether it was in the plasma or in the muscle, were fantastic. Importantly, there is a potential to dose these patients in six-week intervals, so the elongated dosing mechanism is actually quite helpful. From a translational perspective, because that is a big question when you look at in vitro to in vivo, from mouse to NHP to human, we've been able to leverage these 44 data within this healthy normal volunteer population to be able to apply the learnings there across our other DMD exons that we're focused on, including 45, 50, and 51. What we're doing there is by having those efficiencies, we're essentially leveraging them to pursue first and direct into patient studies. ENTR-601-44 is the only study that we plan on doing in healthy normal volunteers. We're leveraging that data so that every other study that we run in DMD goes straight to patients, and that's important. We also believe that the Vertex partnership around VX-670 further validates the EEV platform. As I said before, Vertex has completed the SAD portion of the study, and the MAD portion is ongoing with over 20 clinical trial sites that have been activated. When we think about the first phase I healthy normal volunteer study for 44, let's talk about that a little bit. First and foremost, this was a placebo-controlled signal ascending dose study. The way that we ran this, we had 24 subjects and then eight placebos, so a total of 32. What you could see here within the four cohorts is that we started at 0.75 mg per kg and went all the way up to 6 mg per kg. What we were trying to measure, in addition to safety and tolerability, was the evaluation of PK/PD and then target engagement by measure of exon skipping. The key findings on this study were that we had very strong clinical safety up and through the top dose, which we'll talk about in a second, with the potential for best-in-class pharmacokinetics and pharmacodynamics. This was a de-risking study for us with this new modality into a disease population, which is what comes next. From a safety perspective, and once again, for this class of drugs, safety becomes a really, really important factor within oligonucleotides. As I said, there was no treatment-related adverse events within this study up and through the highest dose, and you could see that on the slide here. The most common adverse effect was a headache, and those were even pretty minimal as well too. Really clean, which becomes really important when we start to think about what the patient studies may look like. This slide is really focused on the pharmacokinetics. If you look at the left graph, what we were able to see here is as the dose increases, so does the plasma. There is a direct correlation between an increase in dose and an increase in concentration, and that becomes important because it is a linear relationship. On the right side of the slide, it is a little bit different, right? We are talking about the metabolite excretion. What we have seen here is that for every doubling of the dose, there is more than a doubling of the metabolite, which is important because it implies that there is the potential to increase efficacy without increasing tox. In this class of drugs, the tox is usually seen in the kidney. We're not seeing this here, which means that we have a very broad therapeutic window, which is another significant competitive differentiation for Entrada's programs. When we think about target exposure and target engagement from the healthy normal volunteer study, once again, on the left side, when we look at the skeletal muscle, we've been able to see from 3 mg per kg to 6 mg per kg, a dose-dependent increase within concentration. On the right side, we're able to see a similar dose-dependent target engagement increase when we think about exon skipping as well. What we've shown here actually is placebo and 6 mg per kg, but you can see a statistically significant difference between the two. Once again, all the hallmarks of a very successful healthy normal volunteer study. What are we doing with these studies? As I said in the beginning, the 44 phase I results really unlock a lot of key portfolio investments across the multiple DMD populations. When we think about it for 44, what we've done is we've activated our 201 study, which is approved in the U.K. and the EU, and we are actively enrolling that study, and that is expected in Q2 of 2025, which is still on track. We're also running a study in the U.S., and this will probably be run next year, and it's within an adult population. Now, the adult population is a population that unfortunately is oftentimes overlooked. It's overlooked because the disease has progressed quite a bit, and nobody can really treat that population. We've decided to say, based upon all the data that we've generated to date, we're going to try to address this population, and so we'll run this study in the U.S. next year. On the 45 program, the 45 program is, frankly, a rinse and repeat of the 44 program when we think of what the patient study looks like. Once again, that's authorized in the U.K. and the EU. The only difference is the dosing, which I'll come to in a second, but that study is on the heels of the 44 program and will be initiated in Q3. Our ENTR-601-50 program is on track to submit our regulatory filings in the second half of 2025, and we expect to start the clinical trial soon thereafter. Our 51 program, we've identified the candidate, we've selected the candidate, and it's a little bit more of a staggered approach. What you can see here for a 150-something company is an immense amount of work in progress from a regulatory perspective that will unlock a lot of clinical studies next year. 2026 is going to be a year of continuous data releases, which is really exciting for Entrada and for the patient population as well too. As you can see on the right here, we think about over 40,000 people have Duchenne in the U.S. and Europe with a profound unmet clinical need, so a very, very significant opportunity here. When we think of the patient study, and this is for our 44 program, our 45 program will be very, very similar. What we're doing is we're running a global two-part study. It's randomized, double-blind, placebo-controlled, all the normal stuff. It's going to be in ambulatory patients who have DMD and who are exon 44 skipping amenable. The two parts really are, one, part A is a multiple ascending dose study, and that will go from 6 mg per kg up to 18 mg per kg, so a very, very wide dose, which shows the therapeutic window. The second really is a phase IIb study. We think the phase IIb study will be the basis for an accelerated approval pathway in the U.S., which becomes really important. The primary objective of this 44 study is safety and tolerability, but the secondary objectives are as important as the primary objectives in that we will be evaluating PK, but we'll also be looking at dystrophin production and functional changes as well too, which is obviously very, very important. There'll be 24 ambulatory patients in this study as well, so pretty robustly designed. Our 45 program is the same exact design. The only difference is that the dosing, instead of 6 mg per kg, 12 mg per kg, and 18 mg per kg, which is what we see in the 44 study, it's 5, 10, and 15 in the 45 study. That's just due to some experiments. That's nothing really to do with the data or the therapeutic window. Once again, a rinse and repeat type of approach. That's from the clinical perspective. Why we think that we can go direct to patients is because of what's written on this slide. There is a robust amount of clinical data that supports what I just went through. 45, one of the things that we're really excited about is that we probably have the most robust preclinical dataset across the canonical MDX mouse model, the DEL44 DMD mouse model, et cetera, et cetera, et cetera. What we've been able to see is this continuous translation of data. Importantly, on the 45 side, on the second bullet point, we've also been able to see complete functional correction. At the end of the day, it doesn't matter how much dystrophin you produce. If the patient can't see a functional benefit, that becomes a challenge. Being able to see this functional benefit in mice gives us a lot of confidence that it will translate to humans as well. Our 50 program looks just as good as our 45 program, and our 51 program is, as I said, a rinse and repeat of our 44, 45, and 50 programs. As I said before, we'll run all these straight into patient studies. 2025, 2026, and 2027 are going to be extremely busy for Entrada when it comes to DMD, and that's just one disease. When we start to think about the pipeline and where else can we go, we will share more on ocular as the year goes by, and that's another tremendous unmet clinical need area with a significant population across a variety of diseases that we're going after. We can do a lot of different things here, right? We have a robust data editing, our gene editing dataset, but the variability of our ability to go after multiple diseases using different tools, essentially, in our toolset is something that we're really excited about. We can look at DNA, we can look at RNA, we can look at proteins as well too. A lot of different optionality around the company as we think of what Entrada 2.0 may look like as well. In closing, multiple near and long-term value drivers, four active clinical programs expected in 2025, which I talked about. Our 44 and 45 programs are in the lead. Those are our two co-leads right now, and they are right on the heels of each other, as I said. 44 is initiating in Q2 this quarter. 45 is initiating next quarter in Q3. 50 is a little bit later in the year in 51. VX-670, our partner program for Vertex, continues to move well. There is a lot of good data that hopefully will come out of that and a lot of milestones that we're not accounting for right now in our current runway. The ability to move beyond neuromuscular. We're building this company so that it has a wide variety of diseases that we can address. The platform is broadly applicable to diseases that target a variety of intracellular targets as well too. We're very cautious, but we're very excited about what our movement beyond neuromuscular and beyond ocular may look like. In today's market, cash obviously remains king, and we still have cash runway into Q2 of 2027. What that allows us to do is get through this patient data, certainly through 44 and 45, and allows us to have very strong inflected points along the way. That's Entrada in a nutshell. Happy to answer any questions with the team here as well. When you say you have cash to go through the 44 and 45, are you accounting for the—sorry, it's so loud in your ear. Are you accounting for the part B as well, the phase II B? Yeah, it's a good question, Preston. I think we'll have to see. We'll have to see how enrollment goes within the initial. I'd like to answer that question when we're a little bit further into the clinic. Certainly a fair amount of it, for sure, but we'll have a little bit more granularity as we get closer or deeper into the studies. Yeah, I think it makes sense. You have such flexibility, you have such great clinical things all coming through. Flip the cards and see what happens. So we're really impressed with the programs. Thanks, Preston. Any other questions? All right, you guys got 8 minutes and 34 seconds back. Thank you for your time.