Good afternoon, everyone. Our next presenter today is Allen Davidoff, the co-founder and CEO of XORTX Therapeutics. Take it away. Thank you. Well, welcome everyone. XORTX Therapeutics is a company that is focused on developing therapies for progressive kidney disease. Our focus, as our name indicates, is on inhibiting the xanthine oxidase enzyme. This is an enzyme that's essential to the breakdown of DNA and purines in the circulatory system during the course of life, from the time of conception until death. And, in the case of this enzyme, what we're observing through our pioneering work is that the overexpression of this enzyme in the case of kidney disease is driving the progression of disease, acting like an accelerant, if you will. So I'll talk today about our three programs, but very specifically about the polycystic kidney disease program that is in late-stage clinical development and we think is the greatest potential creator of value over the course of the next three years. For this presentation, we seek safe harbor. There are forward-looking statements, estimates, and projections within this presentation that may or may not become true. Our management team is composed of individuals with a substantial amount of experience, including myself, with over 20 years of drug development and senior executive experience. Individuals such as Stephen Haworth, who has worked with large and small pharma companies in the drug development space and has a specialty in regulatory and clinical trial development. Dr. Taryn Boivin, who's the head of our chemistry and manufacturing group, James Fairbairn with extensive public markets experience, both in Canada and in the United States, and Dr. Stacy Evans, Chief Business Officer and consultant with extensive licensing and business development experience with companies such as Pfizer. We also have a board of directors that includes a number of individuals who've seen successful exits in drug development programs, including our chair, Anthony Giovinazzo, who recently—as recently as 2016, exited his company, Cynapsus, with an $841 million deal. I've been exposed to and experienced exits in the three companies that I've been involved with, Cardiome Pharma, where there's a drug developed and marketed across Europe at present, with Trillium Therapeutics, where the company was recently sold to Pfizer for $2.2 billion, and we hope it's the case with this program for polycystic kidney disease, that it is in a position and will be in a position over the course of the next two years for a partnership. Dr. Raymond Pratt is a trained nephrologist and an expert in drug development. Paul Van Dam and Ian Klassen have experience in public markets and governance at the board level, and William Farley has extensive business development experience with a number of, of companies. So a very experienced group. We work as a company focused on developing these three kidney disease programs. Our focus, as a company in the last year and a half, has been to bring along two programs. One primarily is in the polycystic kidney disease space, but all of our programs are really focused on kidney disease because there are very few therapeutic options for individuals. We continue to grow our patent portfolio with recent patents in 2020, 2021, and 2022, and have others under development that will create both longevity in terms of patent protection and product protection, but in terms of breadth. Much of the pioneering work we're doing today is allowing us to understand and observe the injurious properties of an overexpressed xanthine oxidase enzyme in a number of disease areas. We have, because of our late stage of development for the polycystic kidney disease program, focused on the development of this program to the point where we have FDA advice that we can begin a single phase III registration trial. That, we believe, would lead us to accelerated approval in 2026, early 2027. As a result of a number of partnership discussions that have been ongoing, we solicited an independent commercial review that has very conservatively estimated peak net sales at around $1 billion per year for the polycystic kidney disease program, which is an orphan disease program. Our focus is on developing three drugs in separate areas. Those therapeutic approaches for ADPKD, which is autosomal dominant polycystic kidney disease, XRx-101, which is for acute kidney injury due to respiratory virus infection, and XRx-225, which is early-stage development for Type 2 diabetic nephropathy, are advancing as follows. Our lead program, where we think the greatest value creation is available to us in the next three years, is in the autosomal dominant polycystic kidney disease space. We have met with the FDA in the fall of last year and in the spring of this year with respect to the design of that clinical trial, and their guidance is we can conduct a single phase II, III clinical trial that would be a registration trial and available for accelerated approval. Our XRx-101 program at present is moving slowly because of the value creation opportunity in the first. With respect to the disease, autosomal dominant polycystic kidney disease, there are a number of symptoms as a part of this syndrome for individuals. Most notably, half of individuals lose their kidneys due to this rapidly progressing disease by their mid-50s. But in the course of their diagnosis and the progression of their disease from diagnosis in the early 20s, we see that a number of factors are occurring and associated with the disease. Pain and discomfort, because kidneys, which are normally the size of your fist, are expanding over the course of this disease. By mid-30s, those kidneys that are normally 300 milliliters are now in a 1-liter to 1.5-liter range, quart to 1.5-quart range. And by the time many of these individuals lose their kidneys to failure in their mid-50s, their kidneys are the size of a gallon jug, often. About half the time, their livers are also involved. And so this is a very serious disease associated with a distended abdomen, a lot of pain associated with compression of other organ systems, back problems. Notably, the occurrence of aneurysms in these individuals because of this disease is about 10-fold higher. We think by lowering uric acid, we can have a direct benefit on the formation of kidney stones, hypertension, slowing the decline of glomerular filtration rate, and I'll talk about our approach in this process as we go forward. So this disease is typified, as I explained, by expanding kidneys due to the genesis of cysts and their expansion rate. We believe, based on pioneering observations in models, in animal models of disease, that there is an overexpression of xanthine oxidase, the enzyme that creates uric acid, in these kidneys during the course of the disease, and that's playing a role in the decline of filtering function, but also in accelerating the rate of expansion. And so anytime you have a tissue that's expanding rapidly, it squeezes the tissue in the surrounding location, and that can cause secondary lack of oxygen, lack of metabolic exchange, and so we see that as a driving factor. We have observed and reported last year at the American Society of Nephrology, and again in November this year, evidence to show that this is a driving factor. It suggests that anytime you develop a therapy, you need a therapy that will penetrate the kidney tissue. What we believe and what we speculate is the overexpression of this xanthine oxidase enzyme in these kidneys is acting to increase intracellular uric acid and intracellular oxygen-free radicals, and so the kidney in this disease is digesting itself inside out. Both of those factors turn off the mitochondria, which tends to trigger apoptotic cell death, programmed cell death, if you will. So we believe by inhibiting this enzyme, xanthine oxidase, with a drug that will penetrate the tissue, this is one of the optimal ways to slow this progression. To that end, lowering uric acid in the circulation, but also inhibiting the enzyme in the kidney tissue, can be done with a variety of drugs that are xanthine oxidase inhibitors. We believe oxypurinol is the ideal drug because it's not metabolized. It doesn't need to be metabolized to work. It's absorbed as oxypurinol and excreted as oxypurinol. And so for a drug that we believe is necessary to be taken at the first day of diagnosis through the end of life to slow the accelerating progression of disease, that this drug is ideally situated. We've done, formulation work, extensive formulation work, to identify formulations of a drug that will deliver it at a high rate across the full therapeutic range for individuals with progressing kidney disease. And so we propose and are developing a single once-a-day tablet for individuals with polycystic kidney disease. That has led us to a state where we have oxypurinol, a drug that's been largely developed through phase I and phase II trials, that's ready for a single phase III, pivotal trial, in the upcoming years. So the drug is ideal because it has a very clear-cut safety profile that's superior to the other drugs of this class. It's not metabolized, so it doesn't involve the liver. And the reason why that's important is liver enzyme elevation is one of the major reasons why drugs are poorly tolerated and have poor side effect profiles. So we see this drug as ideal and are developing it for this purpose. What we believe we have at this point, based on the evidence that's been published by independent studies and by ourselves in our pioneering exercises to develop oxypurinol for polycystic kidney disease, is a therapy that can slow the progression of kidney disease. So in most cases, whether it's polycystic kidney disease or diabetic nephropathy, kidney disease is accelerating, especially in the latter seven or eight years. Each year, you see an increasing decline in the filtering capacity. Normally, our filtering capacity is 100 milliliters per minute of glomerular filtration rate if we're healthy. For many individuals with mid-stage 3 kidney disease, their filtering capacity is in the 50s. By the time their filtering capacity drops to the 20s, they're ready for dialysis or transplantation. We believe we have a therapy that can stop this accelerating effect of xanthine oxidase and uric acid and flatten out that trajectory. The data, which I'll talk about briefly, suggests that for every year of treated, we can maintain healthy kidneys at that status, and that has enormous implications for not only quality of life, but also the dialysis market and for kidney health for these individuals. We've recently completed an FDA review of an orphan drug status, the package that we submitted and received orphan drug status for this oxypurinol formulation. That included a demonstration that the xanthine oxidase overexpression in the kidneys of two animal models seems to be accelerating the decline in filtering capacity and increasing the expansion rate of which these kidneys are expanding. We were also separately able to demonstrate that if you increase circulating uric acid in the system, that tends to accelerate the expansion of kidneys and accelerate the decline, the filtering capacity. But most importantly, with our drug and our formulation, when we administer it consecutively with these, in these animal models, both rat and mouse, we can turn off this expanding process for total kidney volume, but also the declining filtering capacity. So this clear-cut demonstration of a mechanism of injury that seems pertinent in polycystic kidney disease and the effect of this drug at slowing that progression, we believe will result in a clinically meaningful result for patients with this disease. We have, over the course of the last year and a half, been engaged in over 50 discussions with pharma partners and interested parties with respect to this program. To date, we have ongoing discussions with a number of those. In parallel with those discussions, we've also launched a commercial assessment of the XRx-008 program for polycystic kidney disease. That commercial assessment, which was very conservative, suggests that of those individuals who are diagnosed with PKD in the United States, 160,000, those individuals with Stage two, three, and four polycystic kidney disease count about 100,000 individuals. Of those, individuals with Stage 2 kidney disease have high uric acid about 15% of the time, moderate uric acid about 55% of the time, and high uric acid in Stage four, about 97% of the time. So there's an increasing exposure to uric acid, and so indirectly, xanthine oxidase, the cause of rising uric acid, we can treat it with a xanthine oxidase inhibitor to turn down the production of uric acid. And when we estimate the addressable market, and so the potential projected peak net sales for this program, very conservatively, we can use two numbers to get to a range of revenue. In the United States today, if you have failed kidneys and you're on dialysis, the U.S. government pays about $90,000 per patient per year. There are estimates up to $100,000. These individuals, when they have kidneys that are failing, are also sufficiently sick that they have medical costs probably matching that $90,000 per year. The one drug that's approved in the United States today is tolvaptan. It currently retails for $156,000 per patient per year. So we can use this as a floor and as a ceiling to estimate a range of revenue to address these 36,000 individuals. That gives rise to a number between $3.2 billion-$5.7 billion. If we take one more conservative step in this estimate, an estimate that we only ever reach 30% penetration, that gives us a $1 billion per year peak sales revenue for this program. In the polycystic kidney disease environment today, there are very few therapeutic options, as I mentioned, blood pressure treatment being the predominant one. There is a single drug approved, Jynarque or tolvaptan. It has a serious liver side effect and a black box warning accompanying that. What that means is its use is very limited to about 5% of all individuals with a diagnosis. These individuals, about 7,000 of the 160,000 who are treated in the States, 5%, have given rise to peak sales four years after the orphan designation of about $1 billion. We believe we can treat about 5-7x as many individuals with this very well tolerated drug, oxypurinol. Tolvaptan is approved in this market, comes off of orphan drug designation in 2025. For a number of other late-stage programs that were under development last year, they have been withdrawn for safety reasons. Lixivaptan, developed by Centessa Pharma, was withdrawn in the spring of last year, and in April, bardoxolone was withdrawn by Reata Pharmaceuticals. That leaves us as the singular phase II/III ready program that can lead to a drug introduced into this market in the near term. There are a number of phase I and phase II studies in this space, but we project them out at somewhere between 10 and 15 years to market. Our plan, based on our FDA discussions, two of which occurred in the fall and spring of this year, have led us to the conclusion that we can run a small clinical trial studying individuals with progressing kidney disease due to polycystic kidney disease, 60 placebo and 60 treated, and look at the ability to slow the glomerular filtration rate decline in these individuals. We have planned an interim analysis for the early part of this study that will read out around 2024. We expect that to be positive. Then the final GFR readout somewhere towards the end of 2025. That should facilitate the preparation of a new NDA, new drug application, for marketing approval. FDA guidance to date for accelerated approval, which we've confirmed with the FDA, should take between six and nine months to review. That could, in a best-case scenario, lead to XORTX becoming a cash flow positive company by 2027. So a number of endpoints, including a potential partnership that can drive value for this company, as we move forward with that development program. We also, in order to prepare for commercial readiness, will need to start producing commercial drug supply, in addition to the clinical drug supply that would service these two accelerated approval and then secondary follow-up study that are necessary by the FDA. So we have, over the course of the last year, made a number of important steps in our developmental program, including a pharmacokinetic bridging study, a Type D meeting with the FDA that confirmed accelerated approval eligibility for this program, and orphan drug designation. We have a similar European Medicines Agency orphan drug designation that we believe we'll have in hand in the December timeframe, and we look forward to initiating those clinical trials. As of June 30th, we had about $6 million in the bank for our developmental programs. We currently have the following share structure: About 1.5 million out of it, out of 17.9 million shares are owned by insiders. We have 16.5 million shares roughly issued in common shares. We have a warrant overhang of about 10.5-10.6 million shares, with exercise prices around $2.15 averaged for strike price, and a 10% rolling option plan, of which about 4% are issued. So about 40% of the option pool are issued. That gives rise to a fully diluted share count of around 30 million shares. Our clinical advisory board, who are advising us on the design of those clinical studies, is composed of four nephrologists, who are well known and U.S.-based, and two cardiologists. So we're working in a space where there are very few therapeutic options. We think we have an opportunity to lead, pioneer the development of this class of drugs and be the first of this class of drugs to be applied in the next three years for polycystic kidney disease. But we think we can address the growing 12 million or so individuals with diabetic nephropathy with our follow-on programs. We believe that a short-term catalyst for the company are partnership deals, and we have a number of those discussions ongoing, which we think will be catalyzed, upon the start of this clinical trial and as we approach that, approvable top-line result. I'll leave it there. Happy to answer any questions, if there are any. Please. You just announced today that you're having an emergency shareholder meeting to talk about? Yeah. a reverse split. Do we know, kind of, what we're looking at or-? Yeah. So, like a huge swath of the biotech sector in the last two years, we've been trading for about nine months under $1. So, in June, we asked for an extension, which we were granted by the Nasdaq, but this extension runs out November 10th... November. So at some point, we need to prepare to have a reverse split. The scale of the reverse split will be dictated by where our share price is at the time, and so, you know, by inference, our market cap. We have an obligation to call that meeting to go through the process or to delist. We don't feel that delisting is the best choice, and so we're going through the steps at this point. We don't know the details because they'll be dictated at the last minute. But even after the vote is cast, there's no obligation to complete it, although, you know, we would. So if for some reason a partner stepped up and bought the company or share price was greater than $1 for 10 days, then it becomes moot. We don't have to go through the process, but we're doing what's necessary to get there. What is the $6.2 million in runway? How much runway do you have with that where you are? Well, right now, we're slim and trim. That runway will get us through the end of 2024, although it doesn't facilitate the start of the clinical trial. Yeah. I'm being given the stop sign, so thank you all for your attention.