Good morning, everyone. Let me begin by thanking our organizers for the H.C. Wainwright BioConnect Conference for the invitation to present and to those attendees attending. We're excited to be able to introduce our R&D programs and plans for late-stage clinical trials in chronic kidney disease and in acute kidney disease. During the course of this presentation, we plan to present forward-looking statements, projections, estimates, and expectations, and as such, we seek safe harbor. Our mission as a company is to develop therapies for kidney disease using our experience in developing oral formulations with unique drug development programs specifically targeted at treating chronic kidney disease and autosomal dominant polycystic kidney disease, but also acute and emerging chronic kidney disease associated with COVID-19 infection. To put things in perspective as we look at the global market for end-stage renal treatment, really the best estimate of the market at present is the number of treatments administered to patients with diabetic nephropathy or with end-stage renal disease and dialysis for chronic kidney disease. We know that the rate of diabetes growth and so associated diabetic nephropathy and the rate of chronic kidney disease that's emerging because of coronavirus infection is driving the compound annual growth rate for the renal disease market in a way that we expect it to double within the next eight to 10 years and potentially double again in the decade following that. Our focus as a kidney drug development company and our R&D focus is really to develop unique proprietary programs in autosomal dominant polycystic kidney disease, but also in acute kidney injury associated with COVID infection. In many cases, especially where kidney disease is involved, there are very few therapeutic options for physicians and patients, and so we see an enormous opportunity in a variety of kidney diseases that extend beyond autosomal dominant polycystic kidney disease and acute kidney disease into type two diabetic nephropathy and other areas. We have a number of patent families, issued, granted, and in the application and provisional form that cover off a number of our proprietary formulations in terms of composition, in terms of use, and in terms of manufacturing processes. Our lead program is XRx-008 in polycystic kidney disease, where we see that program and our efforts advancing into a single registration trial prior to marketing approval later in this year, the H2 of this year. With respect to our second program, and equally important, XRx-101, this is a combination of therapeutics aimed at decreasing high uric acid in hospitalized patients with COVID infection and decreasing the risk, removing the accelerating risk on acute kidney injury to those patients that are hospitalized. Our team is composed of a number of individuals who have extensive drug development experience, both from manufacturing through formulation work, non-clinical research and clinical research, as well as applications such as NDAs for marketing approval. The pipeline for the company, for XORTX Therapeutics, is focused on advancing XRx-008, a xanthine oxidase inhibitor formulation that's proprietary to the company, through 505(b)(2) FDA development pathway into a single phase III study in the H2 of this year. For the XRx-101 program for acute kidney injury due to COVID, we're also looking to initiate a phase III trial later in the year, and we see that as being developed under the 505(b)(2) pathway. The reason why this is possible is oxypurinol which is core to both of those programs, although the formulations are unique to each program, has been largely developed through an NDA stage filing and an approvable letter. While it's never been approved anywhere for marketing in the world, it's ideally suited for positioning in these diseases. Secondarily, we have a new chemical entity program for diabetic nephropathy where there is good evidence that lowering uric acid and decreasing aberrant tissue purine metabolism can be beneficial. Our focus is on developing new oral therapies that focus on xanthine oxidase. Xanthine oxidase is essential for creating uric acid and excreting purines within our metabolism that build up. However, it has a pathological role that's well characterized, and we see the development of xanthine oxidase inhibitors, especially in the kidney disease space, as ideally suited to reproduce the many independent phase II clinical trials that have been completed and show benefit in patients ranging from autosomal dominant polycystic kidney disease that I'll present in the course of this talk, but also in type 2 diabetic nephropathy and in chronic kidney disease. We can rely on the references and the methods to succeed that are outlined in those clinical trials as part of our development program. That places us as a company in two late-stage clinical trials and hopefully single registration trials that will lead to marketing approval in the future. A survey of peer-reviewed publications shows that uric acid when it's saturating, so above six mg per deciliter in the circulation, can lead to a number of drivers of pathological conditions and represents in its own right a mechanism of injury. Those injuries can include injuries to the blood vessel lining, the endothelial layer to circulating blood vessels, and importantly, to the formation of kidney stones that come in either the form of oxalate, which uric acid crystals can seed, or in uric acid kidney stones themselves. Kidney stones alone are increasingly prevalent in a number of kidney diseases, certainly in the case of autosomal dominant polycystic kidney disease, and can lead to end-stage renal disease that results in the failure of kidneys and the need for dialysis or transplantation. There are other insidious forms of kidney injury, both at a structural and functional level that are occurring. We know in the polycystic kidney disease patient population that there is a transition that happens from a pink, fleshy, well-functioning kidney in early age in the teens or twenties to a kidney that is increasingly fibrosis, has increasingly less functional kidney units, nephrons, if you will. This process of increasing the number of cysts and the growth of those cysts, and certainly the pace of growth of those cysts, creates microenvironments around the area of the cyst, which causes dropout of the filtering units of the kidney. By about 55 or so years of age, about half of all individuals with polycystic kidney disease will have lost their kidneys. That leaves them with few therapeutic options, really dialysis or transplantation. Our programs are focusing on slowing this process, so patients take a longer time or may never reach a need for dialysis or transplantation. Our most recent work as a result of the funding rounds that we've completed in 2021 has led us to a number of key discoveries that suggest a new mechanism of injury in these, in these models of progressive kidney disease due to autosomal dominant polycystic kidney disease. Our first results have emerged from an independent lab with polycystic kidney disease specialization. In this lab, they show in rats the Han:SPRD model of rats that by the time rats reach middle age, there's increasing expression of xanthine oxidase, which is statistically significant and increased, and increased activity of that new expressed enzyme in kidney tissue. This is a new mechanism of injury that's not been identified before and we think is fundamental to disease progression. In addition, as we ask the question that is similar and parallels the human condition, where about half or more of all individuals by middle age have hyperuricemia, we see that uricase inhibition of uric acid metabolism can lead to high uric acid levels. In that scenario where uric acid is high, we see that there are demonstrable structural and functional deteriorations, changes to the way that these kidneys are functioning, including increasing total kidney to body weight volume in a statistically significant way, and also increasing the buildup, the accumulation of creatinine in the circulation. Creatinine is typically a marker of decreased filtering capacity. In both cases, this aberrant tissue-related purine metabolism in polycystic kidney disease and the driving factor, the accelerating effect of uric acid on kidney function, can be managed through the drug programs that we're developing and certainly the new mechanism of injury and addressing that new mechanism of injury with a therapeutic program. For us, the XRx-008 program, which is a xanthine oxidase inhibitor, so slows the production of uric acid, is ideally suited to address the progression, the rate at which kidney function is declining and structure is being eroded in a way that we feel as we take these developmental steps, can slow that harm to the kidneys and extend the time that it takes for a patient to reach dialysis. We know that dialysis while it saves life on a week-to-week basis, is onerous in terms of the time commitment required, but it also comes with a poor prognosis. If you or I were to start dialysis today, we would see the quick decline in our kidney function and our longevity, so cumulative survival over time, such that by two or three years, the prognosis becomes quite poor. In our case, there are many lines of evidence, peer-reviewed publications within the literature that suggest uric acid is high early on in individuals, that it can accelerate the process, perhaps that uric acid is a special condition for ADPKD patients. In this study by Mejias, if you compare ADPKD patients with a similar stage of injury, similar stage of chronic kidney disease to CKD patients, ADPKD patients show higher serum uric concentrations than what is observed in chronic kidney disease. It is also notable that higher serum uric acid in ADPKD patients has been associated with increased kidney volumes, much like the mouse model we just demonstrated, and with increased end-stage renal disease, suggesting that there's an accelerating effect of uric acid when it's present in the circulation. Now the suggestion is that it's also present in kidney tissue. Uric acid is strongly associated with endothelial dysfunction, and importantly in this study by Kocyigit, there is a strong indication that if uric acid levels are high, they can influence as an independent risk factor the decline rate of glomerular filtration and the presence of endothelial dysfunction. Perhaps the best of the independently run phase II clinical trials that have been conducted is this study by Han in ADPKD patients. It's notable that this result has been demonstrated in chronic kidney disease but also in type 2 diabetic nephropathy about a dozen times, suggesting that this is very much a similar result that could be expected. In this case, patients were carefully selected for declining progressive kidney deterioration over a one-year period. Their uric acid was lowered for a one-year period. During that time, that patient group that was losing about 4.5 mL/min/year of filtering capacity and would be expected to lose at least that much and probably 50% more in the year following showed after a year of treatment a reversal of that decline. In fact, in this study, again, what one can generally say in this case is that there is a slowing of the progression. This study suggests that for every year of treatment, there's an opportunity for a year off dialysis, which for any patient is an enormous gain compared to where therapeutic options sit today. We feel that starting with oxypurinol and formulations of oxypurinol that are unique and proprietary and boost oral bioavailability are ideally suited. This drug has a very good tolerability profile. It has received an approvable letter for allopurinol in gout in the mid-2000s, so it's eminently approvable in our opinion. It's eligible for orphan drug designation, and we will work with the FDA on negotiating a special protocol assessment that should more closely and more discreetly define the steps we need to accomplish in order to gain marketing approval. The drug is also, from a pharmacologic standpoint, ideally suited. It's minimally metabolized. It's excreted unchanged, which means its effects on liver are decreased. We know that it acts both extracellularly to decrease uric acid in circulation. Importantly, based on the information that I just presented, it should act at the intercellular level to decrease the harmful effects of that localized kidney tissue mechanism of injury. In the autosomal dominant polycystic kidney disease space, there's a single drug approved. It was approved in 2018. It's reaching its peak of sales for that seven-year orphan period and will address about 7,000 individuals with autosomal dominant polycystic kidney disease. That represents about 5% of individuals, 5% of the 140,000 individuals who have polycystic kidney disease. Despite the fact that there's an approved drug here, limitations to tolerability and to liver enzyme liver toxicity issues have limited the number of patients who can tolerate and access this drug. We think that we are ideally suited to enter the market with few competitors. At the present time, the competitive landscape is composed of tolvaptan, the single drug that's now helping 5% of the population. The other 95% of the population may be aided in their battle with polycystic kidney disease through the development of lixivaptan. Although because it's in a similar class of drugs, we would expect this side effect profile to at least approximate to some extent the tolerability issues. Those are yet to be defined in phase III trials. Bardoxolone and venglustat have had their developmental challenges, and at this point, we can't predict whether or not they remain competitors. We see ourselves as ideally suited to introduce a new class of drugs, a first-in-class of drugs to the autosomal dominant polycystic kidney disease space and enter the market as tolvaptan is leaving the orphan drug designated protection that they have at present. We see this year as being an exciting one with important milestones, including pharmacokinetic studies one and two, and the launch of phase III trials in polycystic kidney disease and in acute kidney injury due to COVID later in the H2. We have a strong and growing patent portfolio that includes granted applications, partially granted applications with European grant and U.S. pending, and other applications in the form of PCTs or provisional patents, and we continue to grow on a number of levels, this patent portfolio. We also see that orphan drug designation provides additional layers of exclusivity and premium pricing for the ADPKD program, so that's ideally suited to advance. Currently, after our reverse split and Nasdaq uplisting, we have about 12 million shares as the trading float for the company, including outstanding warrants and options outstanding. We have about 18.5 million shares fully diluted with what could be fairly represented as a tight closely held stock equity portfolio. Management team is composed of myself, Allen Davidoff, and Dr. Stephen Haworth, and about 20 other individuals who have a substantial amount of experience in developing drugs through NDA filings, but more specifically in developing xanthine oxidase inhibitors and oxypurinol for the market. We're working in an area, renal disease, where there is substantial growth over the next decade that's projected. There are very few therapeutic options for patients with autosomal dominant polycystic kidney disease, and very few therapeutic options for individuals who are hospitalized with preliminary evidence of acute kidney injury and the driving factor of hyperuricemia in those patients. We are addressing a unique mechanism of action in both of these disease cases, and certainly we see the opportunity to slow the progression and decrease over time the severity of progressive kidney disease in both of these indications. Certainly with respect to the autosomal dominant polycystic kidney disease patient population and XRx-008, we think that a single registration trial, a phase III trial, if you will provide the optimal information that we need for registration of this for marketing approval, both in the U.S., but we're also working diligently behind the scenes to bring this program along for the European markets as well. I thank you for your attention and look forward to fielding questions.