All right. I think we all quieted down. All right. Our final presentation of this session is from Xenon Pharmaceuticals, and we have the honor of having Ian Mortimer, the CEO, here to present to us today. Take it away. Great. Thanks, David. Pleasure to be here back at Bloom Burton. Lots happened at Xenon over the last 12 months, happy to provide an update. Before we get started, I will be making some forward-looking statements, so I do encourage you to read all of our risk factor disclosure as filed with the SEC and on SEDAR+. For those that maybe are less familiar with Xenon, we're a CNS company with really deep expertise of drug and ion channels in the CNS. Today, I'm going to spend most of my time talking about our lead molecule. It's called azetukalner, that's in development for the treatment of epilepsy as well as a number of different psychiatric disorders. We had really strong phase III data in epilepsy just last month. I'll spend some time walking you through those data. That gave us an opportunity to raise additional capital. Today, we have pro forma cash of about $1.4 billion on the balance sheet, which takes us into 2029, and our first commercialization of azetukalner in epilepsy. As I mentioned, we really have this deep expertise of drug and ion channels in the CNS, and you'll see that as a theme that runs through our pipeline. Today, there's really three key messages that we'll focus on. Number one, I'm going to walk you through azetukalner in epilepsy, and we'll spend most of the presentation on that. Second, I'm going to walk you through some data of azetukalner in psychiatry and the work we're doing there, and we have a broad phase III program ongoing in psychiatry. At the end of the presentation, really exciting is some of the early work we're doing. We do drug discovery. We have 80 bench scientists. We just took two new molecules into phase I clinical development last year. I'm going to spend a little bit of time on that. Those are in healthy volunteer studies, but we expect those to transition into pain proof of concept studies later this year. As we look forward over the next couple of years, you're going to see more molecules at Xenon transition into human clinical development. Really, the strategic objective here is to build a fully integrated neurology company. We've been doing drug discovery and drug development for a number of years, and we expect to have our first commercial launch in the next few years. As I mentioned, we really want to focus today's presentation on the lead molecule, azetukalner. This is a Kv7 potassium channel modulator or opener. It's been in clinical development for just shy of a decade, so we know a fair bit about the molecule. Today, I'm going to spend most of the time on epilepsy and on psychiatry. We really have a significant package of efficacy in both those indications and a really well-understood safety profile. The molecule has now been in some patients for more than five years, and we have over 800 patient years of exposure in our lead indication of focal onset seizures. One of the benefits of azetukalner is not only does it have a novel mechanism of action, there are no potassium channel modulators on the market to treat either epilepsy or psychiatry, but it's really these ease of use attributes. It's dosed as one pill once a day. There is no titration, and really no meaningful drug-drug interactions. On patients that are on significant polypharmacy, you don't have to make adjustments. Patients are on a therapeutic dose on day one, which is really unusual in some of these therapeutic indications. Let's focus a little bit on epilepsy to start. Actually, epilepsy is more common than many people recognize. It's the fourth most common neurologic condition. We all have about a one in 26 lifetime risk of developing epilepsy. If we look at the U.S. market, there's just over 3 million Americans that have epilepsy, obviously about 10% here in Canada. The most common form of epilepsy is called focal onset seizures, which is about 60% of the market. That is our lead indication where we just had our phase III data last month, and that'll be our first New Drug Application. We're also developing azetukalner in the most common form of generalized epilepsy, i t's called primary generalized tonic-clonic seizures. That's a phase III clinical trial that's ongoing. We're really trying to address the large parts of the epilepsy market. It is a highly genericized market. There are a number of drugs available to treat epilepsy. More than 20 are commercially available. They fit into a narrow number of mechanistic categories, and so again, a potassium channel modulator has the opportunity to bring a new and novel mechanism to the epilepsy field. Even given this large and significant number of drugs that are available, still up to 50% of patients still need better seizure control. We see that in clinical development, and we see that in the commercial market as well, and the opportunity to bring a new molecule for epileptologists and general neurologists to help their patients. These were the results that we disclosed at the beginning of March. This was our phase III study that we called the X-TOLE2 study. I'm going to walk you through all of the key endpoints on subsequent slides. This is really just a summary slide where we met the key primary endpoint. In all of these epilepsy studies, what we're trying to show is seizure reduction from a baseline period through a double-blind period. The primary endpoint is what we call MPC or a median percent change of seizure burden on a monthly basis. We also look at things like responder analysis, so the percentage of patients that have a 50% reduction in their seizure burden as well. As you'll see on subsequent slides, the study was highly statistically significant across these seizure reduction endpoints. The other thing, because the drug isn't titrated, meaning you're on a therapeutic dose on day one, we also looked at the rapid onset of efficacy. What we see at the high dose of 25 mg is we have a statistically significant separation at week one. We don't titrate the drug. You're on your therapeutic dose on day one, and we're seeing seizure control almost immediately with this therapy. I'm also going to show you some open-label extension data, and what it looks like is the response deepens over time. Those patients that are on the drug for a longer period of time do even better and have longer periods of seizure freedom, and I'll walk you through those data. As I mentioned, in terms of the safety and tolerability profile, I think we have a really good comfort around the profile of the drug, given how long it's been in clinical development. The phase III study design, again, a very standard epilepsy study design, standard endpoints. This was a three-arm study, a 12-week double-blind period looking at two active doses of azetukalner, 15 mg and 25 mg versus placebo. It was designed to randomize about 360 subjects or 120 subjects per arm, and we over-enrolled just slightly, randomizing a little bit more than 360 subjects. This is the primary endpoint of the study, which as I mentioned, I walked you through what an MPC is, this reduction in seizures. What you'll see from this slide is there's a small reduction for the placebo patients, those randomized to that arm, and then we see a clear dose response. I think one of the things that we're very comfortable with this mechanism and this molecule is we're seeing clear dose dependency in almost a linear fashion, so as you go from placebo to 15 mg- 25 mg. You can see the p- values there on the slide. If we look at the 25-mg arm and we look at what we call the placebo-adjusted efficacy, so if we look at the 53.2% and we subtract the 10.4%, that's the 43% placebo-adjusted MPC. This is the best efficacy ever seen in a focal onset seizure study in the most severe patient population ever trialed. It's really a massive step forward for the field of epilepsy and for patients with focal onset seizures. I'll put those data into context in a few slides versus the other drugs that are currently available. This slide we've looked at both. We had a very positive outcome in our phase II study, which we called the X-TOLE study, and then we followed on with X-TOLE2, which as I mentioned, we disclosed last month. Going from left to right, this is every dose that's been treated or has been tested in an efficacy study, starting on the left at 10 mg and on the right at 25 mg. The discussion that we've had with FDA is to get four doses approved, so we're going to apply for approval at 10 mg, 15 mg, 20 mg, and 25 mg. What you can see from this slide is as patients are randomized to different doses, as they go from 10 mg up to 25 mg, the data gets even better, so you're seeing a clear dose response. The other thing is the phase II study was an eight-week study. The phase III study was a 12-week double blind. If you look at certain doses, if we look at the eight-week time point or the 12-week time point, as I mentioned, the response deepens over time. These patients are doing even better, getting better seizure control the longer they're on therapy. In terms of safety and tolerability, this is a very active drug in the CNS, so I haven't gone through the mechanistic rationale, but the potassium channel is really looking to break hyperexcitability. We're trying to dampen hyperexcitability in the brain. Anytime we try to do that with a molecule, you're going to see CNS adverse events. The most common adverse events is what we would expect, things like dizziness, somnolence, fatigue, and headache. Other adverse events are less rare, and we see those in a handful of patients. Very few serious adverse events or SAEs and reasonably well balanced across the treatment groups. Now that we've had this molecule in patients for over five years, we're seeing a really consistent adverse event profile and safety profile that you would expect as a treating physician if you're an epileptologist or a treating neurologist, and we see a consistent safety profile both in the short term, so that's in the double-blind period, but also in the long term. As I mentioned, we now have patients that have been dosed more than five years on therapy. This is the open-label data that I had mentioned. As that response is deepening over time, this is our phase II data. All patients that finish the double-blind period, either in phase II or phase III, have the opportunity to go into open-label extension. Those that finish the studies, we get about a 97% rollover rate, so almost everyone goes into open label, and then we can follow those patients over a longer period of time. These are data that we presented at the American Epilepsy Society meeting last December. This was our four-year data from our open-label extension. What you can see is that we're looking at reductions in seizures, and you can see over time, we get a deepening of response. Where those patients in the double-blind had about a 50% reduction in seizures, now if we go out four years, the population's having close to a 90% reduction in their seizure burden. Also, if we look at less severe patients in this study, so those that were only on one or two background medications instead of three, they have 100% reduction in their seizure burden, so they're doing incredibly well. I mentioned that on a placebo-adjusted basis, this is the best data ever seen in an FOS study. It's in the most severe population ever trialed. We look at severity based on three measures. We look at the number of drugs that these patients have failed, the number of background medications they're on, and their baseline seizure burden. The median patient in these studies have failed five to six drugs. They're on three background medications, so this is the ninth or tenth drug that they've had exposure to. They're still having 13 seizures per month, so that's per 28 days. They're having a seizure every other day, so that's the severity or the refractoriness of the patient population. We're really seeing how these patients are doing over time. This data we're incredibly proud of, and it's actually quite remarkable. For patients that have been on the drug for more than four years, about two in five, or almost 40%, have 12 months or more of seizure freedom, no seizures at all. You have patients that are coming into the study having a seizure every other day, and now they're getting long periods of seizure freedom. The reason that we look at periods like six months and 12 months, I'm going to focus on 12 months, is in almost every jurisdiction if you've had no seizure for 12 months, you can drive again. It's a huge mark of independence for these patients. These are patients that are incredibly refractory. They've seen every therapeutic option out there, and we're now getting this subpopulation of patients that are getting seizure freedom for long periods of time, having a meaningful impact on their quality of life and their independence. As I mentioned, this is a cross-trial comparison, so obviously with all the caveats that comes with. What we've looked at is the labels of all of the more significant branded drugs in focal epilepsy, and we've looked at their best study. In most labels, they have multiple studies. We've looked at their best study, and we've looked at placebo-adjusted efficacy, and this is the data that supports my statement that we see for azetukalner in X-TOLE2, the best placebo-adjusted efficacy ever seen in a focal onset seizure study. This is comparing to some of the largest epilepsy drugs that we've seen commercially over the last number of decades, drugs like Keppra and Lamictal and Vimpat. Again, bringing a novel mechanism to the field, we're seeing a really strong efficacy both in the short term and in the long term, and we're excited to get this medicine to patients. Outside of focal onset seizures, we're also expanding into the most common form of generalized seizures. This is called primary generalized tonic-clonic seizures. What we used to call in the old nomenclature, this was the old grand mal seizure. It's the same thing. These patients are often unconscious. They have the stiffening and jerking that is consistent with the tonic-clonic seizures. Obviously, if it's a seizure that provides a patient that goes unconscious, often you see accidents and falls, actually an increased risk of death in these patients as well. The first New Drug Application that we'll file later this year will be in focal onset seizures, and then we have this phase III study ongoing in primary generalized tonic-clonic seizures and hope to read out this study in the coming years. That's the update for azetukalner in epilepsy. Obviously, we've had two incredibly positive studies in X-TOLE and X-TOLE2. As we've guided publicly, we're now writing our New Drug Application, which we look to file in the third quarter of this year, which is the final step as we move this molecule to commercialization and available for patients. In addition to the work we're doing in epilepsy with the same molecule and the same mechanism, we believe it has antidepressant effects, and we have a large program ongoing in psychiatry. I'll walk you through the work we're doing in psychiatry with our first phase III clinical readout in the first half of next year. Again, I won't go through the mechanistic rationale of using potassium channel modulation in psychiatry, but it's involved in reward circuitry. We ran a proof of concept study. This was a smaller study, underpowered. It was called the X-NOVA study, where we were really trying to interrogate two different doses of the drug versus placebo on clinical scales of depression and anhedonia. Anhedonia is a key comorbidity for depressed patients, where they don't get the enjoyment or the pleasure that we do in their lives. We've looked at both measures of clinical scales of depression, but also anhedonia as well, based on the mechanistic rationale of potassium channel modulation. This was a phase II study that we read out a few years ago. It was called the X-NOVA study. Two active doses, 10 mg and 20 mg of azetukalner versus placebo. What we found, I'm going to highlight a few data slides here. This was on the primary endpoint, which is called MADRS. There's two endpoints that we use in clinical scales of depression. It's either the Montgomery scale, which is MADRS, which you'll see on this slide, or the Hamilton scale, which is called HAMD17. What we saw in this was a clear separation between active and placebo and a dose response. Patients that were on 10 mg did better than those placebo patients, and those randomized to 20 mg did better than the patients on 10 mg. We had a clinically significant three-point separation on MADRS. This is what we would expect. We narrowly missed statistical significance, really just based on the sample size and variability of the study. When we looked at the other clinical endpoint of depression, which is called HAMD17, we also had a three-point separation that had a nominal p- value of less than 0.05, and that's because we saw less variability in this endpoint. We saw clinical, we saw separation both on MADRS and HAMD17, but we think that this is the better endpoint for this mechanism and this molecule. This is the endpoint that we've moved into phase III clinical development. As I mentioned, we wanted to look also at anhedonia based on the mechanism. There's a scale that measures anhedonia, which is called the SHAPS scale. Again, we saw a clear separation between active and placebo, a clear dose response, and a nominal p- value also less than 0.05 in a small proof of concept study. Again, this will be one of the key secondary endpoints in our phase III clinical development. Safety and tolerability in psychiatry, again, what we would expect for a drug that's active in the CNS. We saw the same adverse events that we see in epilepsy, but at a lower rate, which is actually quite interesting to us. As we went into psychiatry, we actually thought we may see the reverse, but it looks like this mechanism is better tolerated in a cross-trial comparison in the psychiatric patients when we compare them to the epilepsy patients. We don't entirely understand why. We do know that the epilepsy patients are on a number of background medications, whereas in the psychiatry work, we're doing it as a monotherapy, so that may have an impact on the adverse event profile. Quite a benign adverse event profile in psychiatry, and also very different when we look at the other drugs that are used in depression. We've all heard of the drugs, the SSRIs and SNRIs. The challenge with those drugs is, one, they take some time to work, and two, they often have these adverse events of weight gain and sexual dysfunction. We think for a potassium channel mechanism in psychiatry, we really bring a novel mechanism that works quickly. The patients that do well, you see that immediate reduction in their clinical scales of depression. We see that in epilepsy with seizure reduction. We see it also in psychiatry, and we have a very different adverse event profile, and we also have the opportunity to have an impact on anhedonia. Really a very different approach to treating major depressive disorder than the SSRIs or SNRIs or the atypicals that are currently available to help these patients. We've moved this into a large phase III program. We currently have three phase III clinical trials ongoing in psychiatry, two in major depressive disorder, which we call X-NOVA2 and X-NOVA3. We've taken all of the learnings from our phase II proof of concept and made significant changes into the phase III program. As I mentioned, we're looking at HAMD17 as the key primary endpoint. We're using one-to-one randomization, and we've increased the sample size materially as we move from that proof of concept study to our registration program. These studies are ongoing. They were both started over the last 12- 18 months. We'll have our first phase III psychiatry readout, X-NOVA2, in the first half of 2027. We're also expanding into bipolar depression, and have a phase III trial ongoing. This just started towards the end of last year, so will take a little bit longer. We are looking at 20 mg of azetukalner in bipolar depression. That study's ongoing as well. I'm going to move to, as I mentioned, the third key message today. We talked about azetukalner in epilepsy and psychiatry. Now moving to some of our earlier stage programs, which I think are incredibly exciting and work that we've been doing for quite some time. Again, these are ion channel programs, both sodium and potassium channel. I'm going to focus first on our Nav1.7 program. I know there's some familiar faces in the room. People know that we've been working on this target for many, many years. We were actually one of the companies that did some of the early genetics work on Nav1.7. It's absolutely a remarkable target, but one of the most challenging targets we've seen in pharmaceutical drug development. The reason that it's so remarkable is the genetics. If you are homozygous loss of function for Nav1.7, which means you don't have any of the protein in your body, you don't feel any pain, regardless of noxious stimuli, and the case studies are absolutely remarkable. Not only do we have loss of function in the channel, but there's also gain of function in the channel. Those that have too much activity in Nav1.7 feel too much pain, and they feel spontaneous pain. We have this really unique genetic story, incredibly elegant genetics, where we have both loss of function and gain of function. We and others have been trying to drug this target for the past 20 years or so, and I think we have a really novel approach now, and we've moved our first molecule into human clinical development last year. We felt some of the early approaches were really challenged based on the biodistribution of the molecules, the free fraction, as well as the selectivity and potency profile. The chemistries that we're working on now that we've moved both into human clinical development and we also have pre-clinically, I think are clearly differentiated from what the field has been doing historically, and we're now in a phase I healthy volunteer study. We had announced earlier this year that we've already gotten to doses and exposures where we're seeing receptor occupancy of Nav1.7 where we would expect to mimic the human genetics. We've actually already achieved a lot in the phase I study, and we're excited to move this molecule into a phase II proof of concept acute pain study later this year. In addition to Nav1.7, we also have a Kv7 drug in phase I clinical development as well. This is called XEN1120. Very similar timeline to our Nav1.7 drug, just finishing off healthy volunteer studies this year, and that will also move into a pain proof-of-concept study. In summary, a huge amount happening at Xenon. We've accomplished a lot over the last 12 months and really exciting next couple of years as we transition into being a commercial organization. I think we really have best-in-class efficacy in epilepsy. I've walked you through those data. The best placebo-adjusted efficacy ever seen in a focal onset seizure study. That's going to form the basis of our New Drug Application that we'll file later this year. We're expanding azetukalner both into primary generalized tonic-clonic seizures, as well as into a broad psychiatry program. Really a nice maturing early-stage portfolio, starting with our pain programs, Nav1.7 and Kv7, and you'll see more molecules transition into human clinical development over the coming years. Thank you very much, and I'm happy to take any questions. Thank you very much, Ian. Really compelling data in epilepsy, and looking forward to seeing in other indications what this drug can do. Let's start with Alfred. Thanks. You've had phase III accepted by the FDA? If not, what's the timing of their response? Yeah. After our phase II study, our phase II-B X-TOLE, we did an end-of-phase II meeting with FDA. At that end-of-phase II meeting, that's where we talked about our phase III program and had them sign off on the phase III program, and obviously they signed off on the protocols. We've now, as I just mentioned, last month, had our phase III data, X-TOLE2. We'll have a pre-NDA meeting as the next step in terms of interaction with FDA. We'll do that in the coming months, and then we'll get ready to file the New Drug Application. Thank you. Ian, congratulations on the data. I've been, I guess, a long time Xenon shareholder, so I've been very pleased with the results. What's the commercial opportunity, and how will the pricing compare to your competitors? Yeah, thanks. That's a good question. As I mentioned, there are a number of generic drugs that are currently available, but still up to 50% of these patients are not getting good seizure control. If we look, just if we focus on the U.S., because that's going to be our first approval and our first registration. As I mentioned, with 3 million Americans, if you look at then those that have focal epilepsy and those that are having breakthrough seizure, if you look at some of the adolescent and pediatric patients, that could be upwards of 1 million patients that still need better seizure control in the U.S. Still a significant commercial market. In terms of the payer environment, this is a protected class under Medicare, so it will be covered both commercially as well as under government programs. We're starting to build that commercial infrastructure now. We have about 15 people. We have all of the commercial leadership roles already in place, including our Chief Commercial Officer. All of those people have experience in epilepsy and will be building out their teams and getting ready. Obviously, in terms of competition, as we think bringing a novel mechanism, this drug is going to be used therapeutically in combination with other drugs like levetiracetam or lamotrigine, that have different mechanisms. There are a number of other companies that are in development for focal onset seizures. I think we've set, obviously, an incredibly high bar. All right. Well, if there's no more questions, we can thank Ian one more time. Thank you.