Okay. Well, thank you all for attending this session. I am very excited to introduce our next speaker, James Helliwell at Eupraxia Pharmaceuticals. James, take it away. Thank you very much. Thank you all for being here. Really, really appreciate it. Thank you for Bloom Burton for hosting. We also excitedly have a little bit of fresh data that came out this morning. There'll be no test on this. Apologies for straining your eyes, but we have to do that. This is actually quite a big year for us. Although we had data this morning, we're going to have a lot more data through the year. There's a lot of catalysts that from the programs we're going to be talking about today, as well as some new programs that I'm only going to spend a little bit of time talking about. We're exceptionally now well-capitalized, well-supported to be able to take us through not just this year and all the catalysts that we'll be talking about in this presentation, but a few more we're probably not going to have the time to get through, and take us right through to the middle of 2028. An exciting year for us, and hopefully by the end of this presentation, you'll agree with that assessment. Let's talk a little bit about Eupraxia, what it is that we do, and how it is that we do it. My background, I'm a physician, and I worked doing cardiac transplants at St. Paul's in Vancouver for about a decade in critical care. Precision was incredibly important. Had to get the right drug to the right place and have it in the tissue. That is the aim of what it is that we do here at Eupraxia. What you'll see is these little things called the DiffuSpheres. Essentially what they are is little balloons. They're about the size of a grain of sand. That size is actually really important. It is all about delivering a drug into the tissue and being able to keep it in that tissue for a long period of time, delivering a dose in a stable fashion. You'll see the blue line there. The yellow line is basically almost any other drug that you take, which is that it spikes when you first take it, and it drops off in a logarithmic way over time. What we're talking about here is the ability to actually inject directly into a tissue and have a drug. In this case, we're going to be talking about a drug called fluticasone propionate, you may know it as Flovent or Advair, and have the ability to inject it into a tissue and deliver it for a really long period of time. Really exceptional patent coverage on both the product itself as well as on how we make it and a variety of other things across five patent families deep into the 2040s in coverage. That's what we do. Let's actually talk about where it is that we're seeing the effect here. Eosinophilic esophagitis. When I first started talking about this, almost no one had heard of this. When I went through medical school, this was not a disease. It's a really awful disease if you're a patient. Essentially what it is, it is an inflammatory disease. You get this inflammation. We don't even know exactly why it starts, except for you have this association with eosinophils. It's a Type two inflammatory reaction, basically, you get lots of inflammation, then you end up getting strictures and narrowing and stiffness of the esophagus. You think about now you take some food, what happens? It opens up, and it accepts that food. What happens with this disease is it gets stiff and hard, and it's painful to swallow and difficult to swallow, and it gets worse and worse. This is a progressive fibrostenotic disease. The prevalence of this has grown dramatically. When we first started our program, this was an orphan disease, 150,000 patients in the U.S. In 2023, we went to the FDA, and we applied for an orphan drug designation, and they said, "Nope, 5- 700,000 patients in the U.S." Estimates are closer to one million. This is all about the fact that people are realizing there have been hundreds of thousands of patients who've been misdiagnosed as reflux patients who actually have EoE. The unfortunate thing for patients with this disease, there's not a lot in the way of treatment. Steroids have been the mainstay of off-label treatment for these patients. It's oral. You have to take it twice a day. It's very uncomfortable. You're not allowed to eat or drink afterwards. If you successfully manage to be compliant with taking it works well, but you get left with a candidiasis, a fungal infection in your mouth that occurs more than 25% of the time and up to 50% of the time, which makes people stop. There are other treatment options. We'll talk a little bit about them as we go, but nothing that is really meeting the needs of all of the patients out there. We think that there's an incredible opportunity here in a very large market. Why steroids? I talked a little bit about the complexity here. This is a very, very complex Type two inflammatory market, this slide, I'm going to spend the next 20 minutes on this slide, going through it in great detail. Don't worry. I'm not really. This is basically one of the worst slides to ever put up, but there's a reason that I put it up there. I put it up there because what this is doing is showing how everybody else has tried to tackle this market, from Pfizer to BMS, Celgene to Allakos to Cellex. What they've said is, "Hey, I'm going to make an antibody to one thing that's happening here, and I'm going to look at that one thing and try and stop it and hope it turns everything off." Well, it turns out that hasn't worked. They've been able to make eosinophils go down. They've been able to make mast cells go down. What they haven't done is make patients feel better, and the most important thing you need to do in this disease is make patients feel better. Steroids, very luckily, hit everything you see on the screen here, and they do so directly. The problem with steroids is, as you know, when you give them, and you take them all over your body, you get lots of side effects. What does Eupraxia do? We deliver really locally, and because we deliver really locally, it means that we can actually deliver directly into the esophagus with an injection, and I know that that sounds painful. I promise you it's not. Having the scope going down, not particularly comfortable. The actual injections themselves, patients actually can't feel them. There's no nerve endings for that. Otherwise, you would feel every little bit of food that went down, and it would be very uncomfortable. These injections, they don't take very long for a physician. You can see in the bottom left-hand corner, they're basically injecting directly underneath, and this is a procedure that physicians are really used to doing. Our delivery tech allows us to actually get this into the esophagus and deliver it over a long period of time. You may be wondering, okay, this sounds like you have to now go and do a scope and give an injection. Well, this happens to work out really well. Once you are diagnosed with this disease, you are supposed to go by guidelines all around the world, go see your gastroenterologist once a year for an endoscopy and biopsies. 60% of patients actually show up and do this. The other 40% don't really. Why? They're not sure why they're supposed to go. All they get told is, "Your disease is getting worse, and I have no other treatments to give you." For the gastroenterologist, we want to be able to move the 60% closer to 100% by tying therapy to that visit. It is not just about monitoring and screening, it is in fact, actually also about therapy. Imagine if you're a patient, you go from a twice-a-day oral drug, or a once-a-week injectable drug, to a once-a-year drug. That's our goal, once a year. It is tied with your visit here. From a commercial perspective, this is a really big opportunity. We talked about the number of patients being close to a million by the time we're actually launching this. There are only two therapies that are approved in the United States right now. One of them only for 12 weeks of use, that's priced at a WAC of $22,000. The other, which is a once-a-week injection for most people and has a wholesale acquisition price of $109,000 a year. Neither of those is providing all of the therapy that patients and providers and payers are looking for. We think that there is a really big opportunity here, provided that we can provide therapy that is at least as good as the competitors that are out there, and to be able to do so with good safety and importantly, the durability and being able to provide that really long-term relief. You imagine if there is one million patients and you look at pricing in the median part here, if you are getting 50,000 patients a year and you are charging $50,000 a year, you have now established yourself a very big market. There is more places for us to expand in GI beyond EoE, and I will come back to that on the back of data. We have got some data to show you today. This is from a RESOLVE trial. This is a two-part trial. I want to first define what success is. When we are looking at this, what does this data mean? Success in this, and we have tested this with payers, we have tested this with physicians, we have tested this with patients. Success is we have to make the patient feel better. That means that about 40% of the patients need to reach clinical remission. That is the bar by which everything is judged today because of other therapies that have been available. We also need to make sure, again, this is lasting a year and that we see some histologic difference. We are going to talk about histology and come back to this, but that we are actually seeing change in inflammation and fibrosis on biopsy. This is the trial that we have that is ongoing right now. This is a dose escalation trial, and it is the first part of our phase II trial. Essentially what we did is we tested a whole bunch of different injection patterns and also a whole bunch of different doses. We are going up slowly a number of injections and doses as we go, and we are looking at patient symptoms, we are looking at histology, we are looking at durability. What have we seen? First, let us talk about pharmacokinetics. This is plasma. This is not measuring what is in the tissue, but we know from all the work that we have done that our tissue has about two orders of magnitude. Not two times, two orders of magnitude more in the tissue than it has in the plasma. But if you look at that delivery, remember, this is from a single injection given at day zero. There is about a 24-hour equilibration period, and then after that is a flat line in pharmacokinetics. That is zero-order kinetics running out to 52 weeks. That is across all our doses. You will see the red line up there. If you know people who have COPD and asthma, they very likely take fluticasone. They take it either as Flovent or Advair, which is the most common as a discus. That red line is what they have in their blood every single day. The regulators know that is safe, the patients know that is safe, and we are well below that. That allows us to follow a 505(b)(2) pathway and really put to rest a lot of systemic safety issues that you often have when you are developing a drug. We will also show some data confirming that. PK is great. What about efficacy? Here what we are doing is we are showing you, and we are actually combining a bunch of doses here. Even though as we go up in dose, our higher doses tend to do better, this is to allow you to see really some depth of data by putting some of these cohorts together. This is the Straumann Dysphagia Instrument. It's measuring the severity and the frequency of how often you have difficulty swallowing. If you imagine this from a patient's perspective, this is taking some food gets stuck, maybe you have to run to the washroom to try and get rid of the food, you have to go to the hospital, or you just find you can't eat properly. These are really debilitating symptoms. What we know is the line we have to get to is about 40% clinical remission. That has been achieved by others by getting there at 10 weeks. We're achieving that within two weeks, which is our first measurement point. At two weeks, 40% of our patients are in clinical remission. By 12 weeks, we're close to 60%. By 24 weeks, that's close to 80%. Then we see durability running all the way out to 52 weeks in that sort of mid-60s percent. You'll notice the numbers are dropping off. Those are not dropouts. That's because the patients haven't reached that point. When I talked about a lot of data coming this year, we're going to be filling out all of that all the way through to the end of Q3. Lots of more data coming on this trial throughout the rest of this year. Why though, do we go from 40% clinical remission at two weeks to 80% clinical remission at six months? What's happening? It's really interesting. These patients have two things going on. One is inflammation, the other is fibrosis. In other words, they're actually developing scar tissue in the esophagus. It's getting rigid, it's getting hard, and it's getting narrow. We can measure that on biopsy. The EoE HSS is the histology scoring system for EoE. What that's doing is it's looking at eight subscores, and these are all centrally read, so they're taken at all the sites that we have around the world, sent to a central reader. There's a standardized way to do it. Everybody is blinded, and there has never in this been a placebo response in any trial of anybody looking at EoE HSS. This is hard data. When we look at what we're seeing here, we're looking at three different dose groups, 4, 6, and 8 mg. You'll notice at 36 weeks, we don't have the six there. That's just because they haven't reached that time point yet. The best that people have seen here on this scale is about a 0.2 improvement. Most people are entering at about a 0.55 as a mean entry point. At the 4-mg dose, we're actually doing as well as we need to do to be a successful commercial product. As we go up in dose, we get dose responsiveness. We're getting about a 70% improvement from baseline at 6 mg and a north of 90% improvement at the 8 mg. That improvement is seen early and is seen all the way to nine months. If you think about that, a patient got dosed once. We've controlled their symptoms as you just saw. The other thing that we're doing is we're actually reversing inflammation, and we are reversing fibrosis. I'm going to take a slight deviation from EoE here and say this is very unusual to the KOLs. Normally, when they see scar tissue, scar tissue stays forever. Some of these patients develop strictures in EoE, that means a really tight narrowing. The only way to treat it is you go down with a balloon, you actually physically tear it open. There's about one million patients in the U.S. who have benign esophageal strictures. Only 5% of them are from EoE. The physicians have come to us on the back of this data and said, "We have no drugs available to treat this, no one is working on it. We would like you to use your drug in benign esophageal strictures because we think it will make the difference for these people having to go get ballooned all the time." We're going to be launching a trial in late 2026 in that indication. Let's also look at histologic remission. This is looking at peak eosinophil count. This is the number of eosinophils that you actually have in your tissue. Turns out in this disease that you can get rid of eosinophils and not make patients feel better. Why does this matter? This matters a little bit because people like to see it, matters a little bit because the regulators want to see us actually get rid of these eosinophils. It also matters because eosinophils only live about 72 hours. Remember I was showing you earlier that we were having the plasma level of drug. This is actually a surrogate for us saying how much drug do we actually have present in the tissue itself. Because we know that fluticasone stops the eosinophils only last 72 hours, this tells us the drug is still there. As you can see, we get a really good dose response in reducing eosinophils and putting patients into remission out into the 60%, all the way out to nine months. Again, we're also when we flip that and look at how much are we reducing from baseline, the answer is we're reducing from baseline a lot for a long period of time. Overall, we seem to be getting a really good clinical response. Patients are feeling better, that's number one. We're making a histologic difference, doing so, we think, in a very dramatic way, also getting durability. The last piece of this puzzle is safety. We now have 230 patient months of follow-up. There have been no drug-related SAEs, I talked a little bit about the oral steroids. The most common thing that leads people to discontinue that treatment, even though it often works, is that oropharyngeal candidiasis, the fungal infection in the mouth. We've had zero patients who've had oropharyngeal candidiasis in this trial, that's really important because that becomes a real barrier to compliance and long-term compliance. In addition to that, the only real sort of adverse event that patients have reported in this trial is a bit of a sore throat. About 20% of our patients get a sore throat, lasts a day or two. Turns out that's how you feel when you get an endoscopy. About 20% of patients have a sore throat for one or two days afterwards. We don't seem to have any difference in that, our procedure doesn't seem to be making much of a difference. No change in cortisol, we often think of that, and glucose when we think about steroids. No change in either, including in patients who are diabetics in this trial, haven't made a difference. Just a really well-tolerated drug. What's next? What's coming is lots more data from that phase IIa all the way through Q3. This is our phase IIb trial that is currently ongoing. We are well through the halfway point of recruitment here in this trial, and, essentially what we have is the top two doses. Of that phase IIa trial, we took the top two doses. They're being tested here. This is a very well-powered study. You'll also notice the placebo only runs for about six months. That's because they do a blinded crossover at that point. The patient thinks that they're just going in for getting their endoscopy, and in fact, what's going to happen is they're going to be given drug if they were placebo into one of the two groups there. We're going to be looking at patient symptoms, both SDI and DSQ, the Dysphagia Symptom Questionnaire, and we're also going to be looking at all the histologic measures that we just ran through. It's very well powered across all of those measures, and we're actually going to be doing an interim analysis when all the patients have reached three months, most of them have reached six months, some have reached nine, and some have reached 12. We've also had a number of patients who've done a crossover. The reason we're doing that interim analysis is that internally, we really want to ensure that we are setting ourselves up for the optimal phase III design so that we get all of the right things we need from a regulatory perspective and from a commercial perspective, driven by phase IIb data. That we're going to have available for us internally as well as the regulators, as well as for the market in late Q4 of this year. All of that data we really are anticipating, and we know a lot of our investors are as well. The development path, essentially, once we get that phase IIb interim data, that we're then going to go for an End of Phase II meeting. We anticipate then moving to our single registrational phase III in mid-2027, with a size of about 300 patients. Other things, that are not EoE, I talked about benign esophageal strictures. Benign esophageal strictures, again, we're going to be launching that trial in 2026. Physicians have also come to us, the GIs, and said, "We have another really big problem." They actually come to us with quite a few. This other one is fibrostenotic Crohn's. Fibrostenotic Crohn's is a very big problem. It affects about 45%-50% of all Crohn's patients. What happens is in the proximal colon and the terminal ileum, that they actually get lots of inflammation. A stricture develops, and they get a bowel obstruction. When they get that obstruction, it often leads to surgery. Once they've had one surgery, they tend to have a lifetime of surgeries. Right now, physicians have nothing to treat fibrostenotic Crohn's. They've come to us and said, "We scope these patients. We see the stenotic lesion developing. We want to inject it with your product and see if we can stop that." We look to be launching a trial on that in 2027. We are funded to be able to do all of that. I've talked to you only about GI products and primarily EoE today. Remember where we started, we started with the DiffuSphere, which was the technology that actually allows us to be able to deliver a drug locally and to be able to get it right there. You can start to, if you let your mind wander, what would you do if you could do that in oncology, in CNS, in other places where you don't want off-target effects? You only want to be on target. We have our expert team who built EP104, are busy working on other assets. We will come to the market with them later, but they are very busy in the lab working, developing more IP, and really building the future of Eupraxia beyond EP104 and where we are in gastroenterology. Little bit about the market data. You can see our recent share price, our market cap. There's been a few interesting things. Our cap table is cleaning up. First, we're very well-financed. We've had two series of warrants, which were our only warrants that were held by investors. Those have all now expired, so there's none left. They brought some additional funds. We have about $ 143 million as of today, and that's because of all that warrant exercise, plus two financing rounds. We've been very, very pleased with the investors who've been coming in and sponsoring us as we've been going forward. I also want to point out just the board and management ownership. Management, myself, other members of the senior leadership team, we've really put our money where our mouth is, and the board has done the same. We are very, very aligned with investors. We're very aligned with patients, getting these products to patients. We really look forward to an exciting 2026, and a very busy 2027 on the back of that. With that, I will stop and say thank you all very much for your time and attention today. Really appreciate it and appreciate Bloom Burton. Thank you. All right. Thank you for that great talk, James. We have time for some questions from the crowd. Got one over here. Here, I'll pass you the mic. In talking about the total addressable market of the esophagic stuff. If that's a unit of one, then how does the benign version of that compare? Yeah. In EoE. Also, sorry, one other piece that's tied to that as well, and Tim, is when you flip over to the 50% of folks with Crohn's that may end up having to go under the knife, how big is the Crohn's opportunity relative to what you're doing in esophagus? Yeah. Great question. Really all about that market. First I'll start with EoE. The EoE market right now is about one million patients, and all of those patients are needing some kind of treatment. About 400,000 of them right now are started on a proton pump inhibitor. The problem with that is that while it helps symptoms, it does not stop the progression of the fibrotic disease. Patients are actually needing something more there. The total addressable market is really if you get that balance of making patients feel better, stopping fibrosis, there is the potential that you are looking at sort of almost everybody in that space. It is a very, very large total addressable market really being driven by the data. The benign esophageal strictures, there is one million patients with doctor-diagnosed strictures. Most of them are reflux patients, and patients with Barrett's esophagus. There, the numbers get smaller when you actually look at those that you'd be treating. There's about 400,000 patients who are actually getting balloon dilations, and there's about 200,000 patients that are getting balloon dilations quite frequently. Imagine going in every sort of week to two weeks to three weeks. Those are really where we'd be focused at the beginning of that. That's another couple hundred thousand patients. Crohn's disease, basically what you'd be looking at there is of all the Crohn's patients, and again, those numbers are slightly north of one million. You're looking at the half of those patients that have fibrostenotic Crohn's, and we'd really be looking at those who are pre-obstruction. Once you've got a bowel obstruction, I don't think we're really going to be of much help at that point. You're really down the surgical path. It's finding those patients that are earlier. It's a few hundred thousand patients who are really the focus of fibrostenotic Crohn's. The great thing for us is a commercial asset, same doctors, same sales force, same call point, same drug, same dose, same delivery method. Really building a gastrointestinal franchise there. That was a great answer. Any other questions from the audience? We got time. If not, please help me in giving James a very warm round of applause. Thank you. Thanks very much. Appreciate it. Awesome talk. Thank you.