Ladies and gentlemen, thank you for standing by, and welcome to the conference call being hosted today by Rezolute Management. At this time, all participants are in a listen only mode. After the presentation, there will be a question and answer session. To ask a question, press star one. Please be advised that today's conference is being recorded. I would now like to hand the conference over to your speaker today, Nevan Elam. Please go ahead, sir. Good morning or good afternoon, depending upon where you are today. I'm Nevan Elam, Rezolute's Chief Executive Officer and Founder. Thank you for taking the time to join us today to learn more about the clinical results from our global multicenter Phase 2b study, the RIZE study in patients with congenital hyperinsulinism. Before we dive in, as a reminder, the information discussed during this call will include forward-looking statements which represent the Company's view as of today, May 1, 2022. We undertake no obligation to update or revise any forward-looking statements to reflect new information or future events, except as required by law. Please refer to today's press release, as well as our filings with the SEC for information concerning risk factors that could cause actual results to differ materially from those expressed or implied by these statements. Now moving on. At the outset, let me just say that we are absolutely thrilled with the results, which definitively demonstrate the efficacy of our antibody, RZ358, in significantly reducing the hypoglycemia experienced by patients suffering with the disease. Before I hand the call over to our Head of Clinical, Dr. Brian Roberts, to provide further granularity with respect to the results, I would like to highlight a couple of key points. First, for everyone's benefit, and as a brief primer, congenital hyperinsulinism is a genetic disease that is characterized by recurrent episodes of hypoglycemia caused by dysregulated excessive insulin secretion. It is the most common cause of severe and persistent hypoglycemia in infancy and childhood. When it comes to managing blood sugar levels and avoiding hypoglycemia, the benchmark really is to, you know, maintain blood glucose values above 70 mg/dL. Unfortunately, those that suffer with congenital hyperinsulinism spend a substantial amount of time below this recommended threshold and even at more severe levels of 50 and even lower. The impact of these low glucose values experienced by patients can be devastating. It can lead to a variety of serious temporary as well as permanent adverse outcomes, including seizures, neurological complications, coma, and even death. Parents, caregivers, and healthcare professionals toil with the intense demand of near round-the-clock management, trying to stave off potentially harmful hypoglycemic excursions. Sadly, there are no approved available therapies that have been developed to treat hyperinsulinemic hypoglycemia. Instead, practitioners really do the best they can by using existing repurposed treatments to blunt the production of insulin. The current standard of care is comprised of a combination of enteral tube feeds, glucagon, and commonly used therapeutics such as diazoxide and somatostatin analogs, and particularly long-acting somatostatin analogs. While all of these treatments help manage hypoglycemia, we know that even when on standard of care, patients still have significant amounts of hypoglycemia. We've previously examined the problem of residual hypoglycemia in a patient population in a natural history study. Now the RIZE study data is further instructive as a representative sample of the hypoglycemic challenge that patients face even when on standard of care. In our study, during the screen-in period, all patients, including those on standard of care, had their baseline hypoglycemia evaluated, and we observed that these patients, on average, still spent almost 25% of the time in a hypoglycemic range. In the RIZE study, we enrolled 23 patients across four dosing cohorts. The average age of the patients was about 6.5 years. The majority of our patients clearly were under the age of 10, and some were all the way down to two years of age. We measured a variety of glycemic metrics based on blood glucose monitoring as well as continuous glucose monitoring to create a robust data set. In the study, target and expected RZ358 concentrations were achieved and dose exposure dependent responses were also observed. RZ358 was generally safe and well tolerated. With respect to our glycemic expectations for the study, we hoped that RZ358 would result in reductions of hypoglycemia in the 30%-40% range relative to baseline, which we believed would benchmark well as a reduction in hypoglycemia of at least 25% should offer a clinically meaningful benefit to the patient. The results from the RIZE study resoundingly and definitively far exceeded our expectations. A starting dose of three mg per kg was chosen primarily to demonstrate safety, as this was the first time that we would be repeat dosing children in a clinical study. We were not necessarily planning for efficacy at this starting dose, and yet we achieved a nearly 25% reduction in hypoglycemia. What we believe is particularly impressive is that in the higher dosing cohorts of six mg per kg and nine mg per kg, the dosing levels that are likely to be taken forward into our pivotal phase three study, the reduction in hypoglycemia was approximately 75%, which is absolutely phenomenal. We believe that these results clearly support the potential for RZ358 to be a highly effective treatment for all forms of hyperinsulinism and potentially to be used as a monotherapy. With that, I would like to turn the call over to Dr. Roberts and let him take us further on these impactful clinical results. Thank you, Nevan. To those that have joined the call today, we sincerely appreciate the support and interest in our program. I'm extremely pleased to be able to share and discuss the results of the RZ358 uncertain Phase 2b RIZE study in additional detail. From my perspective as a practicing endocrinologist, the efficacy and safety profile we observed from this study are extremely compelling and highly clinically meaningful. I am both extremely pleased and hopeful for the potential for RZ358 to provide a novel treatment for patients and families living with congenital hyperinsulinism. However, before diving in, I'd also like to thank the entire Rezolute team and specifically the clinical operations and regulatory teams for successfully executing this study under the most challenging of circumstances, a global pandemic. Their tireless work over the past couple years has culminated in this outcome, and I'm fortunate to be working with such a talented and dedicated team. Most importantly, I'd also like to thank all of the stakeholders within the congenital hyperinsulinism community with whom we partnered on this study, including our trial sites around the world, but most notably, the patients, families, and their advocacy organizations who carved out more time from their demanding lives to be participants and partners in our study and broader mission. Thank you, and we look forward to continuing this partnership as we move forward. Now let's jump into the study design and results. An overview of the study design is depicted in slide six. Eligible patients received RZ358 in open label fashion in one of four sequentially conducted dosing cohorts of up to eight participants per cohort. The dose levels and regimen are shown in the table. RZ358 was administered as a 30-minute intravenous infusion every other week for an eight -week treatment exposure period. The first three cohorts were fixed dosing levels of RZ358, which is the anticipated dosing regimen. As Nevan noted, the starting dose of three milligrams per kilogram was selected to optimize safety in a pediatric repeat dosing study and was not expected to have significant efficacy. The six and nine milligram per kilogram dose cohorts had shown pharmacologic activity as well as prospect of patient benefit in single-dose Phase 2a trials in adult and teenage patients with congenital hyperinsulinism, including PK/PD modeling of that data. The fourth cohort was an optional cohort, which was designed to explore whether there were any advantages of a fixed titration approach should the first three cohorts indicate a need to do so. The eligible patient population included patients aged two to 45 years with continued and inadequately treated hypoglycemia on stable background therapies as determined by both continuous glucose monitoring or CGM and finger stick blood glucometer or BGM during a robust and extended screening and run-in period comprising a minimum of 10 days of glycemic characterization. This enabled each patient to serve as their own baseline control. I'll provide a further description of the baseline patient characteristics of the enrolled population on a subsequent slide. BGM and CGM were used throughout the treatment period and through day 42 after the final dose as dual methods to assess glycemic control. An additional discussion of the study objectives and the BGM and CGM based principal efficacy endpoints is provided on the next slide. The RIZE study represented the first and longest duration of dosing in pediatric patients with congenital hyperinsulinism. Consequently, safety and pharmacokinetics in this patient population were important objectives. Another important objective of the study was dose ranging, both for level and frequency of dosing. With respect to glycemic efficacy, the objective of this Phase 2b study was to broadly assess several principal and secondary glycemic endpoints across two different assessment tools, namely CGM and BGM, to confidently inform our Phase three registrational study design. Specifically, to do a 360-degree evaluation of RZ358, uncertain activity and glycemic effects across these various endpoints in a phase 2b setting, we are looking at a constellation of findings and a consistency of effect as evidenced by benchmarks such as at least a 25% improvement in hypoglycemia from baseline, a time and dose-dependent response with RZ358, and a subsequent return toward baseline levels of glucose control during the follow-up phase of the study when RZ358 is withdrawn. Importantly, we also wanted to confirm our belief that fixed weight-based dosing achieves optimal benefit and safety across most patients without the need for a titration approach. The RIZE study was conducted globally across 12 pediatric endocrinology centers. Specifically, we worked closely with centers, investigators, and site teams who are experts in congenital hyperinsulinism. Over time, we have built a tremendous network and infrastructure that enabled us to execute the study during the pandemic and should carry over as we begin planning forward. A total of 23 patients were enrolled into the study across the four different dosing cohorts, including eight patients at each of the two key dose levels of six and nine milligrams per kilogram that we had anticipated would be efficacious based on previous studies and modeling. You'll see the breakdown of enrollment by cohort on the next slide. Notably, all 23 patients completed the 8-week treatment and associated efficacy evaluable phase of the study, and more than half of the patients have completed the entire study through the three-month post-treatment safety follow-up period. Specifically, no patients have discontinued the treatment or follow-up phase of the study for any reason, which we believe to be one of several indicators of the robust safety, tolerability, and activity of RZ358. On the next slide, the key patient demographics and baseline characteristics are presented for each of the four dosing cohorts and overall for the pooled group of 23 enrolled patients on the far right column. As mentioned previously, we focused enrollment into cohorts two and three due to expectations that these would be the best for performing cohorts or doses. After enrolling the minimum number of four patients to meet the thresholds for an independent dose review committee to review safety, we dose escalated to cohort two. On that particular point, the review committee comprised three respected hyperinsulinism experts and met three times throughout the study to review safety prior to unanimous agreement to dose escalate. Each of Cohorts two and three were enrolled up to the protocol defined maximum number of eight patients per cohort. Cohort four was optional, and we were fairly confident it wasn't necessary from a dose exploration perspective. We made the decision to open this cohort to accommodate patients that were already in screening. The three patients enrolled in the Cohort four certainly do contribute an expanded database and to the interpretation of the safety and efficacy profile of RZ358. I'll highlight a few of the key characteristics of the study population. As Nevan mentioned earlier, a notable point is that the average age enrolled into the study was approximately 6.5 years old, with a range between 2-22 years of age. In fact, 16 of the 23 enrolled participants were between the ages of two to six years old. It's reassuring that we are already able to discuss the safety, pharmacokinetics, and efficacy of RZ358 in this context, inclusive of this young pediatric age group. The same can be said across the other demographics and baseline characteristics. Just under half of patients had known mutations affecting the potassium ATP channel and are therefore largely unresponsive to diazoxide at all, which acts at this channel. The remaining patients had either known mutations affecting other aspects of insulin production or secretion or unknown genetic etiologies. Interestingly, about a third of the patients were reported to be responsive or partially responsive to diazoxide, but nevertheless met our entry criteria for having persistent hypoglycemia on these therapies and were enrolled to add on RZ358. This was an interesting observation as it suggests that there may be an underappreciated addressable need for improved glycemic control in this patient subset beyond just the known safety and tolerability limitations of diazoxide. Slightly more than half of the patients were taking short or long-acting somatostatin analogs at enrollment, while about a third of the patients were managed by other means, such as two or more medications, enteral or tube feeding, or previous partial pancreatectomy. While very likely offering a measure of benefit for these patients, these underlying interventions were not adequately controlling hypoglycemia as per our protocol entry criterion. In fact, as shown in the last two rows of the table, during a robust screening and baseline run-in period on stable standard of care, the average RIZE study patient was hypoglycemic for almost 25% of their overall monitored time on CGM, corroborated by having an average of 16 hypoglycemia events per week by point-of-care blood glucometer. As you'll see in the glycemic results section of the presentation, there was also a significant amount of severe hypoglycemia at baseline, defined in this study by a threshold of a glucose less than 50 milligrams per deciliter. Interestingly, in spite of substantial continued hypoglycemia on their background treatments, we also observed a fairly significant and somewhat unexpected amount of glucose variability and even mild hyperglycemia above the 180 milligram per deciliter threshold in many of our patients. Patients on background therapies may be predisposed to some periods of hyperglycemia through a variety of factors, including the kinetics and counterregulatory responses of these therapies. Mild hyperglycemia is not clinically relevant in this setting in which hypoglycemia is at the forefront of management. In summary of the demographics and baseline characteristics, the RIZE study patients were experiencing significant amounts of continued hypoglycemia on available therapies of study entry, indicative of the unmet treatment need in many patients and exhibited considerable diversity and heterogeneity in their overall patient characteristics. This largely mirrors the epidemiology and heterogeneity of the broader congenital hyperinsulinism patient population, where it is rare to find two patient experiences that are exactly alike. The observed results are extremely reassuring in this context and validate our belief in the potential for RZ358 to be a universal treatment for all forms of hyperinsulinism, from mechanistic hypothesis and now through to real-world results. With this in mind, let's move on to the study results. RZ358 was generally safe and well-tolerated across the studied dose range in age demographics. There were no adverse drug reactions. In other words, no identified side effects or safety risks. As previously mentioned, there were no study discontinuations. A total of three serious adverse events occurred in three separate participants, but all were judged by the investigators as unrelated to the study drug and rather related to the background conditions of the patients. Overall, 15 study patients experienced a total of 43 treatment emergent adverse events, or TEAEs. These were generally mild in clinical severity, unrelated to RZ358, and did not exhibit a dose response. Furthermore, the TEAE event rate was comparable on a time-adjusted basis to the non-TEAE rate of 15 events in 10 subjects, or 43%. three patients experienced mild AEs that were judged by the investigators as related to study drug, including one patient who was described as exhibiting hyperactivity due to improvement in hypoglycemia. One patient experienced transient dizziness, while another had a transient localized rash at the infusion site. No other subjects had infusion site reactions, and no subjects experienced any systemic infusion reactions. In this patient population that is predisposed to some hyperglycemia on their background therapies, we observed a modest increase in mild hyperglycemia above the 180 milligram per deciliter threshold in conjunction with overall glucose increases, but no increase in clinically relevant hyperglycemia and no hyperglycemia adverse events or adverse metabolic changes. As you'll see shortly, this was indeed a case of a rising tide lifting all ships. The remainder of our comprehensive safety evaluations, including hepatic monitoring, physical examinations, and electrocardiogram monitoring, was unremarkable. Continuing with the safety, an overview of adverse events is reiterated in the table on the next slide. As you can see, the number of subjects with adverse events was comparable between the treatment emergent period and the pre and post-exposure periods, and there was no dose response. The higher number of treatment emergent adverse events at the six milligram per kilogram dose was primarily driven by two patients who reported several AEs that were mild and unrelated to study drug, and the incidence of subjects who experienced adverse events at the nine milligram per kilogram dose level was the same as the three milligram per kilogram dose level. Thus, as previously stated, no identified safety risks or adverse drug reactions were attributed to study drug. In terms of the pharmacokinetics, as a function of the IV route of administration, RZ358 exposure levels are highly predictable, and intrinsic variables or factors that are relevant to this congenital hyperinsulinism patient population, such as absorption kinetics, gastrointestinal tolerability, and food aversions, would not be expected to compromise exposure to study drug. The observed RZ358 concentrations in the RIZE study were extremely comparable to simulated exposures, were dose proportional, and exhibited low intra and inter-patient variability, including no apparent age dependencies. The half-life supports the dosing interval of every other week. While the observed concentrations reached modeled or target efficacious levels, they remain well below the concentrations that were safely tested at the highest doses in our chronic non-human primate toxicology studies. Moving on to the glucose results, as a top-line summary, we're extremely pleased to have demonstrated that the predictable and stable concentrations we achieved with the aforementioned dosing regimen resulted in highly clinically significant and dose-dependent improvements in hypoglycemia that exceeded our expectations for the study. At the three mg/kg starting dose, which as I mentioned previously, was selected primarily for safety and enrolled only four participants, a clinically relevant improvement in hypoglycemia of approximately 25% was still observed. Improvements in hypoglycemia of approximately 75% were seen at the six and nine mg/kg dose cohorts. Importantly, there was a very high patient response rate, and the improvements were corroborated and comparable between blood glucometer, measuring hypoglycemia event rate, as well as continuous glucose monitoring, measuring hypoglycemia time. Increases in time in range, between the range of 70-180 mg/dL by CGM in the RIZE study increased 8% across all doses and 16% at the top dose. The time and range changes were not as pronounced as the improvements in hypoglycemia because the average patient coming into the RIZE study had a somewhat higher time and range, as well as some hyperglycemia at baseline on their background therapies, in spite of their significant hypoglycemia. Unlike in our previous Phase 2a study, where background therapies were washed out for RZ358 monotherapy administration, in this present study setting, add-on of RZ358 corrected hypoglycemia substantially, modestly increased mild hyperglycemia, as previously mentioned, and increased time and range modestly. Consistent with this observation, time and range increases were more substantial and exceeded 25% in patients without baseline hypoglycemia and/or who were not on background therapies, thus mirroring the improvements in hypoglycemia. We believe this demonstrates the potential for RZ358 to be a standalone therapy, particularly in cases of diazoxide non-responsiveness, responsiveness or intolerance. These combined observations, as just summarized, are very compelling to us and speak to the consistency, robustness and broad patient applicability of the response. We believe the results demonstrate the clear potential for RZ358 at fixed dose levels to be an effective combination or even monotherapy across a broad range of patients with congenital hyperinsulinism. To dig into a bit more detail, in the graphical representation of the data in the pool group of patients across the entire dose range of RZ358, you can see highly, clinically and statistically significant reductions in hypoglycemia events on BGM and hypoglycemia time on CGM of more than 50%. Notably, severe hypoglycemia, which is particularly problematic for obvious reasons, was improved by 60%-70% across the combined doses. Since this depiction of the data includes patients in cohorts one and four who received lower doses as previously mentioned, this represents a fairly conservative depiction of the average hypoglycemia improvements. The magnitude of response was even greater at the individual six and nine mg/kg doses as mentioned previously and highlighted in more detail in the next slide. The table here presents the same pooled data as the previous slide in the far right column, but also shows each of the same hypoglycemia endpoints by dose cohort. This shows the highly significant and dose-dependent response to RZ358. While an unexpected clinically relevant improvement of approximately 25% was observed at the three mg/kg starting dose, average improvements in hypoglycemia, including severe hypoglycemia, reached approximately 75% at the top doses across both BGM and CGM assessment methods. The CGM magnitude at nine milligrams per kilogram is attenuated somewhat because of two patients in that group with problematic CGM placement and sensing. These same two patients checked blood glucose by glucometer regularly and had a better than 80% improvement in hypoglycemia events by that measurement, which is reflected in the clear additional step up in response between the six and nine milligrams per kilogram cohorts as assessed by BGM. It's also noteworthy that the few patients enrolled into cohort four at a fixed dose titration had a magnitude of hypoglycemia improvement that was a blend of the other doses, providing further evidence of robust dose-responsive drug effect. The next slide presents an alternative way to look at the hypoglycemia improvements, utilizing a responder analysis at different clinically relevant thresholds of improvement from baseline, starting with a clinically significant improvement of 25% and through greater magnitude improvements of better than 50% and better than 75%. Each of these different benchmarks shows the patient response rates for overall hypoglycemia as well as severe hypoglycemia levels. What this demonstrates again is a clear dose response and a very high response rate across the study. Notably, at the top dose, all patients achieved at least a 50% improvement, and all but one patient achieved at least a 75% improvement, which is very compelling. This indicates that the substantial reductions in hypoglycemia observed on average were nearly universally experienced by the very patients that were enrolled into the study, and therefore the potential for RZ358 to be an effective treatment for all forms of congenital hyperinsulinism. I'll end my portion of the presentation today of the RIZE study results with a slide that brings the individual patient experience with RZ358 a bit more to the forefront. It also highlights the potential for RZ358 as a standalone therapy. The patient at the top of the slide is a 2-year-old boy receiving somatostatin analog injections because of lack of responsiveness as well as intolerance to diazoxide. His family reports he experiences 4-5 episodes per day of symptomatic hypoglycemia that require intervention or assistance. The patient at the bottom of the slide is a six-year-old girl who has failed to respond to all other available medications and had more than half of her pancreas removed to try to combat hypoglycemia and may unfortunately be destined to have the remainder of her pancreas removed without the prospect of other therapies. The left-hand side of this slide shows the aggregate CGM data from each of the two patients over an approximate two-week baseline period, having exhausted available medical management and with about 40% of overall time in hypoglycemia. While the tracings on the right-hand side show the aggregate CGM data for the full two-week period following the final dose of RZ358. The difference is clearly striking. In these patients with predominant hypoglycemia and with an absence of hyperglycemia on standard of care at baseline, a profound improvement in hypoglycemia of better than 90% is accompanied by a correspondingly larger improvement in time in range between 70-180 milligrams per deciliter, as depicted by the cumulative ranges in the bar graphs on the far right. As discussed previously, similar magnitude improvements in time in range were observed in our phase two monotherapy trial in which background therapies were washed out. In summary, the combined safety and efficacy data from the RIZE study highlighted by these two patients demonstrate the real-world potential for RZ358 to be a difference-making monotherapy for the treatment of congenital hyperinsulinism. We are extremely excited by the results and we believe they enable phase three and are very much looking forward to advancing this program. Thank you, and now I'll turn it back to Nevan. Thanks for sharing the detailed analysis of the RIZE study, Brian. I'll end the call by reiterating how enthusiastic we are about the study results, and we believe that this enthusiasm is really shared by the key opinion leaders, patient advocacy groups and the families that participated in the study, as well as the broader congenital hyperinsulinism community. Frankly, having worked in the pediatric therapeutic space for many years, I've always believed that there's something particularly special about developing impactful therapies for children, especially the therapies that will help the most vulnerable within this population, therapies like RZ358. With that, I'll turn it back over to the moderator, and we welcome your questions. Thank you.