It's a very exciting morning. Lots of very exciting companies. I'm excited yet again to introduce this next presenter. We have the CEO and President of Satellos Bioscience, Frank Gleeson. Frank, take it away. Thank you very much. Good morning, everybody. I'm happy this year to be here presenting Satellos as a NASDAQ-traded company. Many of you in the room have been part of the Satellos story from the very beginning. Some days you must feel perhaps you're long-suffering participants on our journey. What I want to talk to you about this morning is where we are, where we're going in 2026, and where we hope to be in 2027. We believe we are now months away from meaningful clinical data and months away from being in a position to pursue approval for a drug to treat a devastating disease. I've never been in a position at this meeting, at this time of the year, to make such a bold assertion. I'm really pleased that I am in a position to do that. Let me tell you about Satellos, those of you new to the story and those that already know the story. Our business is focused on patients like little Charlie here, who's eight years old, is a real person. Charlie lives with Duchenne muscular dystrophy, which means between the ages of eight and 12, Charlie will progressively lose the ability to walk, and from that point on, will begin to lose all of his muscle mass and will not have a very long life as a result of that. Our mission as Satellos is to change the lives of patients such as Charlie and others who have different forms of muscular dystrophies or degenerative muscle conditions. Our business is grounded in revolutionary science out of a Canadian institute at the Ottawa Hospital Research Institute by my colleague and co-founder, Dr. Rudnicki. We're extremely proud to be in a position that we might be able to do something about the lives of these children. Now, why should anyone care about Duchenne muscular dystrophy? This is an investor conference. It's not a self-help conference. I get that. This is a fatal genetic disease. It causes ongoing loss of muscle mass. Imagine losing all of your muscle mass. There are 12,000 individuals in the U.S. and Canada that live with this disease every day of their lives at any one time. One in 5,000 males born everywhere in the world every year suffer from this disease, will be diagnosed with this disease. The standard of care is a class of medicines called corticosteroids. Corticosteroids are pretty nasty drugs. They have very toxic side effects. They have especially toxic side effects on young children who wind up on these medicines, sometimes as young as age five, and generally for the rest of their lives. The most common new therapeutic approaches are genetic in nature. These are the medicines that have held the greatest promise for the last close to 20 years that they have been prominent in clinical development. Some have been approved. They're generally only suitable for specific age groups, either very young or for specific genetic mutations. They come with the potential for quite severe side effects. Even by the most objective standards possible, their functional benefit is minimal. Yet, from an investor point of view, the market capitalizations for companies in this space that are working on these genetic approaches, which are listed here, are somewhat higher than Satellos at $200 million, approximately US. Anywhere from $2 billion, $12 billion, that Avidity was acquired by Novartis. These companies are all focused on muscle, sometimes more broadly than we are, but muscle. They all have a core program in Duchenne muscular dystrophy. The potential for Satellos is enormous from an investment point of view. Now, what is it about this disease that we know that other people don't know? Why can Satellos make the bold claim that we can do something about this disease that others have not been able to do? The first thing is, when you look at this chart of progression, we look at the first part of this chart. Children make muscle. They're born with muscle. They make muscle. They stand. They walk. They can ride their bicycles. Later in life, they're wheelchair-bound. They lose the ability even to sit upright in a wheelchair. They will ultimately lose the ability to move their body at all, and then they stop breathing. Somewhere in this age group, when they're still ambulant, they reach a biological tipping point. In this tipping point, this gain of muscle loses out to muscle loss, and it becomes very quick, it's very progressive, and it's completely unstoppable. We've discovered why this tipping point occurs. That's our contribution to the science. What we've discovered is that during the progression of this disease, children's efficiency at making muscle is compromised. It's compromised because of the genetics that they're born with, and it prevents their body from continuing to make muscle to keep up with the ongoing damage. We're experts in a different area of science, not genetics, but stem cells. What we've come to understand is that the stem cells that are responsible for muscle regeneration, which are called muscle stem cells, oddly enough, are not working properly in these children. There's a way to fix it, and that's what we're focused on. We're focused on restoring muscle regeneration. In other words, reversing this tipping point, to put it as bluntly as possible. We're different because we're an oral daily tablet, not a genetic medicine that's needed to be delivered by infusions in a hospital setting. We're safe and tolerable. No nasty side effects so far in any of our work, we've been working on our drug now for years. It's suitable for all individuals with DMD, regardless of their genetic background, regardless of their immune status or their age. It has the potential to be disease-modifying, in other words, to change the course of their lives. What are we doing right now? We have concurrent phase II clinical trials underway, one in children aged seven, eight, and nine called BASECAMP, and one in adults over the age of 16 called TRAILHEAD. Our goal in 2026 is data from both of them, our ambition in 2027 is to pursue accelerated approval for our drug. We have shown effects pre-clinically and clinically already on functional measurements. We've shown in a canine model of DMD, which is kind of the gold standard because canines, believe it or not, can spontaneously develop the same disease that humans do, so we don't have to engineer it into these animals. We showed that we improve the strength of these animals. We showed that in humans as well, in adults, that we saw a doubling of their grip strength after treatment for 28 days with our drug. We showed that in the first quarter of last year. This year, we showed that that gain was durable, and they sustained that doubling of strength. I'll show you this as we go along. Let's go through some of the data. What I want to try here is to convey to you how we look at the path to approval of our drug. What is it that guides our strategy, and what is it we've been trying to do over the last several years of building the dataset to approval? Because our objective is very singular: Get our drug approved and get it paid for. That's our objective. To do that as fast as we possibly can with the minimal amount of capital investment required. What I'm showing you here are images from our canines that we treated with our drug. We treated them for four months. They were nine months old when we started the trial, which means they were sick dogs. What you look at on the left is what tissue, hind leg tissue, biopsy material in one of the animals pre-treated looks like. You'll see in here lots of red. That's the immune system, a component of the immune system, an antibody or a protein called Immunoglobulin G, IgG. It's a signal that tissue is dying and that the immune system needs to come in and basically consume the necrotic tissue and clear it out. That's what causes the muscle loss, and this just progressively gets worse and worse and worse. What you're looking at on the right is a similar type of biopsy of a similar aged animal that's healthy. What you're looking at in the middle is one of our animals after four months of treatment. Which would you rather be? The one on the left or the one on the right? If you can't be the one on the right, the one in the middle looks pretty darn good. We are affecting directly the quality of the muscle, the architecture of the muscle. This is really important because in our BASECAMP study in children, we will be doing biopsy, and it's over a similar timeframe. This was 4 months, in the biopsy in the children, it will be 3 months. We would expect to see some improvement in the architecture of the muscle. The regulators will like to see that if we have that. Our drug in a phase I clinical trial in 72 adults, healthy adults, was safe. We really saw absolutely nothing of any consequence or concern. Our drug has a very clean PK profile. It means it's rapidly acting, and it gets out of the body fast, and we designed it exactly that way. In fact, our chemist is in the room today, this was his sort of pièce de résistance of scientific work, figuring out how our drug would be fast-acting and clear quickly. This is important because that adds huge safety profile to a drug. Now, we know from our work in adults with DMD that our drug acts on muscle. We know it in dogs because we could show you the before and after of the muscle. It's a little harder in the adult humans to take biopsies because they don't have much muscle left. In this case, what we're looking at are proteomic markers. We did what's called a SomaScan analysis. SomaScan is a tool. It's a proteomic tool, company called Illumina, Inc. owns SomaScan, using this tool, you can look at blood samples and look at about 11,000 proteins, then they do these volcano type graphs, and you can spot what's changed. Well, what changed in our case was this handful of established, well-known, well-recognized, validated, used-by-others markers of DMD. In every one of our five participants, in every one of these markers, we saw a dramatic decline in these markers of muscle and muscle damage in DMD. It means our drug is getting into muscle, and it's acting on that muscle. This is of huge importance as we think about our primary goal, which is approval of our drug, because now we'll have markers that we can talk about from a clinical point of view. This is for us, really exciting. This was very quick onset. 2 weeks, we saw this effect. Our drug is acting on muscle very quickly. This is data we have shown previously. This is data from a year ago. This is the data in the five adults that we treated. They were on drug for 28 days, and this is their grip strength. We see the grip strength on the average of the five in the left, and we see the grip strength by individual in the right, and on one side of the slide, it's the dominant hand, and on the other, it's the non-dominant hand. Why they didn't say left and right, I have no idea. We did this in Australia. Maybe it's an Australian thing. What this shows very clearly to us is that the drug is having an impact. I want to point out a couple of things. The regulators are not looking for us or anybody developing a drug to cure everybody equally in any clinical trial. They're looking for the balance of probability evidence that there's a significant chance of improvement. I would say, looking at this, we have clearly affected two or three of these adults in a meaningful way. These adults are, in this case, at the beginning of this study, were between the ages of 20 and 27. A typical Duchenne adult in their mid-20s that I have met, many of them, cannot shake your hand. They cannot articulate their hand sufficiently to give it to you to shake your hand. The fact that we're showing improvement in the ability of them to use their hands is amazing. Interestingly, this one's a little bit nerdy science, the greater improvement amongst those patients correlated with their level of muscle, as measured by another marker of muscle called creatinine, and with the amount of drug they saw within that first day. Remember I showed you that PK graph. Patients with a little more muscle saw better results than patients who had less muscle. This makes total sense to us because we're acting on the muscle stem cells that live in muscle. If the muscle's not there, they won't have as many stem cells. This is extremely important for us when we think about our BASECAMP study in children, because children will have more muscle. They will have more muscle than any of these adults. First work that we did, I showed you in the adults, was one year ago in a phase I-B trial. That's plotted on the left-hand side of this graph. We started a new trial with these adults called TRAILHEAD, which, in the case of the patients that are returning, is an 11-month study for a total of one year, and in which we will enroll 25 additional patients for a full year. In between, these patients were off drug for a period of time between 205 days and 328 days. In other words, between seven and 11 months off drug. A study like this is not the ideal planning to do a study like this. This wasn't designed this way. This is the progression of a small company advancing and being able to develop trials. What we showed is that the gains we saw a year ago were sustained. The patients are all one year older. They decline at this age. They were off drug for an extended period. Just to make it clear, that was a two times gain sustained for a year. That's a gain of function. There has been no drug in development that I'm aware of or any of my colleagues are aware of that has ever reported this kind of a result, a doubling and maintenance of that gain over a full year. We think this is extraordinary. When we showed this data at the MDA Muscular Dystrophy Association meeting a few weeks ago, the stock market didn't see this picture. I can't explain that, so I'm trying again today. That is what the data show us. Just to hammer home the point, when we compare this to natural history, there is significant body of natural history related to grip strength in DMD patients, and it is an endpoint that the FDA will consider as part of accelerated approval. This is the natural history for thousands of patients from age five to 30. If you plotted a graph, that would be a downward sloping line that's very steep. Young people gain grip strength until their mid-teens, early teens, then bam, it really declines. What did we do? We moved some of these adults into what is called white space, an area that's not seen because they don't get better. We added to TRAILHEAD other measurements, because we're very curious to see could effects actually radiate out to other muscles. What we saw in 56 days of treatment is that an elbow flexion and shoulder flexion. Oh, that bottom one should be shoulder abduction. That's my bad for doing a cut and paste and not correcting it. We see a clear trend to improvement in shoulders for sure. Again, these are patients that left on their own, cannot move anymore. This is remarkable. When we tease it out between the ones with a little more muscle mass and the ones with less, that gap increases. What's coming up? In TRAILHEAD, as I mentioned, we did a study, the one-month study, which we did a year ago. Those four of the five patients have come back, and in the course of the year, one patient became ill, unrelated to us, just the natural course of their lives. Four have come back and will be on drug. We're measuring a variety of factors. TRAILHEAD will be enrolling starting later in Q2, and we'll enroll up to 25 patients. We're looking at MRI, we're looking at PUL, which is upper body movement. We're looking at dynamometry, which is hand grip and shoulder, and we're looking at safety. We're doing this over a period of time at intervals, which gives us the opportunity to see data and then to decide what we need to do about working with that data. BASECAMP is a bigger, more complex study, more variables, more patients, because this is basically our gold standard study on which we plan to pursue accelerated approval. It's in children aged seven, eight, and nine, an N of 51. 51 divides by three for those of you that are good at math. It's a placebo-controlled, double-blind study. Two dose levels of our drug, low and high, plus placebo, randomized one to one to one, then a crossover nine-month follow-up study where placebo goes on to drug. 25 clinical sites across eight different countries. Safety and biomarkers, muscle fat fraction, muscle morphology, all the physical measurements I've been talking about. Patients will be enrolled who are on steroids as their standard of care prescribed medicine. We will enroll patients who've previously received gene therapy, we'll enroll patients who have previously received exon skipping. We're doing this because it's not only the regulators we need to be thinking about, it's the payers. The more evidence we can build that our drug, even with others that have previously been delivered, shows benefit, then we can broaden the payer complement as well. We're thinking as strategically as we can. This is what BASECAMP looks like over the 3 months on drug. It's a 12-week study. Generally speaking, once we start screening a patient, it takes 4 to 6 weeks to get them fully qualified and get the hospital moving them through their system and so on before they first get on drug. I made the unfortunate mistake of not fully understanding this length myself in a comment I made at a previous meeting a while back. I got mixed up between enrollment and first dose. Once patients are on board at the beginning, we do biopsy, we do MRI, we do NSAA, which is all of the lower body movements. We do PUL, which is the upper body. We do dynamometry, which is shoulder, arms, hands. We do stride velocity, which the Europeans really love, and we do safety and biomarkers. These patients come in. It's a hospital visit. They're very busy. They actually can get tired during the day. That's the first dose. We check safety after one month. At the end of 3 months, we bring them back in and we do all of those tests again. From that, we build our database. Inside Satellos, we've passed Q1. Thankfully, we've made great progress in Q1. We've got our trial up and running. We're now in Q2. We've got roughly one-third of all the clinical sites up and running. We've got many patients on drug now. We don't know if they're randomized to drug or placebo, so I just say on drug, meaning they're in the study, they're being dosed. By Q3, we plan to have the study fully enrolled. By Q4, we plan to have data. We will be opening up a TRAILHEAD in the U.S., as I mentioned, in Q2 at some point. We will be planning to launch a trial in a new field of FSHD, another disease area. That wraps us up. Our financial summary is we're on NASDAQ as MSLE, not to be confused with MLSE. I am not a Leaf fan myself personally. This has been pointed out to me. MSCL on TSX, our market cap, fully diluted shares. We have considerable analyst coverage of some pretty big names, plus we have others coming on board. You'll get to lunch on time. We have a few minutes for questions. Thank you very much. Thank you for that talk, Frank. We have time for a couple of questions. Any questions from the audience? Looking around. We got one over there. Let me pass the mic. Hi, Frank. Thanks for the presentation. I was wondering, I'm sorry if I missed it. Is there any form of physical therapy that the patients go through while they're on this treatment, or is that left out of the scope of the study? No, there's not physical therapy in parallel to the trial. Okay. Got it. Thank you. Okay, we got one more. Thank you. Thanks for the presentation. Happy to see you're thinking strategically about payers down the road when you design your clinical trials. They're enrolled if patients are on corticosteroids, I think exon skipping and gene therapy. Any concern that the payers might reserve your treatment for patients who have failed on those instead of de novo or add-on therapies? I'm assuming you're including HDAC inhibitors in the trial design as well? Yeah, givinostat's allowed in this trial. Okay. No, we haven't actually developed any reason to be concerned about that perspective from payers. Fundamentally, these patients fail every treatment, right? They'd all die. Any other questions? There's one at the back. That's okay. What is the cause of the disease? It's a genetic disease that's caused by a mutation. The cost. The cost? He's saying, what is the cost of the disease? Oh, the payer cost. Well, the various drugs, the exon skipping drugs, they're all projected to be CAD 1 million a year annually. Gene therapy is over CAD 3 million. That the payer is experiencing now? Correct. The payers are paying that, and I'm not forecasting anything about Satellos. I'm just telling you what the market evidence is. Any other questions? No? Okay, well then, please give Frank a very warm- Thank you.