Good morning, everyone, and thank you for joining us for another session of H.C. Wainwright's 26th Annual Global Investment Conference. My name is Eduardo Martinez. I'm a Biotechnology Equity Research Associate at H.C. Wainwright, and it is my pleasure to introduce Mr. Frank Shannon, Vice President of Clinical Development at Sernova. Mr. Shannon, you have the floor. Thank you. I'm pleased to tell you about Sernova and our regenerative medicine approach to giving patients their lives back. Please see the disclaimers and our instructions regarding forward-looking statements. I will also be telling you about our clinical trial data and a number of preclinical studies that we have conducted to date. Please note that there will be a presentation tomorrow at the European Association for the Study of Diabetes, conducted by our principal investigator, Dr. Piotr Witkowski, where additional data is going to be shared that I will not be sharing at this time, and we invite you to look for that information forthcoming, as well as our ensuing press releases. We believe that we are taking a pioneering approach towards functional cures for chronic diseases. We do this with a platform which is a Cell Pouch transplant system. That system is a flexible, implantable cell containment system that we fill with therapeutic cells, which can be human donor cells. They can also be iPSC-derived cells, such as the islet-like clusters that we are currently partnered with Evotec in the development thereof. Our system creates a vascularized, organ-like environment for the transplant of cell therapies. These cells are then able to sense biological signals, such as increased or elevated glucose, and then produce the missing therapeutic proteins or hormones such as insulin, glucagon, or somatostatin, among others. Our product portfolio includes our lead program, which is our Phase I/II program, Phase I/II clinical program in patients with Type 1 diabetes who are insulin dependent. The insulin-producing cells are implanted into the Cell Pouch in these patients and provides a functional cure for these patients. We have observed this in our trial to date, and I look forward to telling you more about it shortly. We have preclinical programs ongoing in thyroid disease and hemophilia as well. The programs that we have ongoing right now, and these include our Cell Pouch with human donor islets. We also have our Cell Pouch program, which includes preclinical work to date and planning for a clinical trial to commence in 2026 with EVT-3101. That is the title that we are currently using for the induced pluripotent stem cell-derived islet-like clusters with which we are partnered with Evotec. Additionally, we are working towards going into the clinic in the early part of next year with Cell Pouch and thyroid for the treatment of thyroid disease. We are seeking a first indication within diabetes because we feel very strongly that the clinical need has nowhere been met to date. We know that one in ten patients with Type 1 diabetes will die from severe hypoglycemia, but we also know that there are extensive complications that result from the disease as well, including heart disease, kidney disease, neuropathy, blindness, diabetic foot diseases, as well as stroke. Our approach to this functional cure is a two-step approach, the first being with the use of human donor islets that we are putting into the Cell Pouch. Patients who are insulin dependent and who have a history of severe hypoglycemic episodes are implanted with a Cell Pouch, multiple Cell Pouches, and then we fill those Cell Pouches with the human donor islets after a period of four to six weeks. We have observed insulin independence in these patients. Cohort A has been completed. Cohort B is currently ongoing. We have optimized the dose, we have optimized the islet density that is required, and we know that that is of significant concern because islets that are packed too close together will autoregulate one another. We're in the process of demonstrating an optimal immune suppression system, and we will be completing the confirmatory Cohort or Cohort C after we begin later this year. Our next step will be working with the iPSC or induced pluripotent stem cell-derived islet-like clusters that we're developing with Evotec. We're planning a Phase I/II clinical trial to start in 2026. This is going to be for a broader Type 1 diabetic population because the islet-like clusters are going to be an unlimited supply, and therefore not dependent on, deceased donors in order to be able to treat patients. We have already demonstrated preclinical performance in animal models that has demonstrated that the ILCs are at least equivalent to human donor islets in terms of their performance. ILCs can also be cryopreserved, which substantially improves the commercial viability of a product because of inventory management, as well as logistics associated with worldwide distribution. The Cell Pouch is manufactured from highly biocompatible materials that are already used in a wide variety of, implantable devices worldwide. We have demonstrated long-term safety, and we're providing long-term efficacy for these products as well. We have demonstrated functional support for the islet grafts, and very importantly, we have demonstrated that these devices provide complete containment of the therapeutic payload and also allow for complete retrievability of the device and the payload, should it be necessary. How the system works? If you look at the left-hand panel, a Cell Pouch is placed deep beneath the surface of the skin, between the skin and the muscle. It is allowed to reside there for a period of four to six weeks, while tissue integrates, vascularized tissue integrates into the mesh and around the non-adherent plugs that reside within each of the individual chambers of Cell Pouch. After a period of four to six weeks, the operator then returns, reaccesses the device, removes the plugs, resulting in tissue chambers that have been formed that are well vascularized, native tissue chambers of the patient, and provide an organ-like environment into which the cells are then infused. The device is closed through a self-sealing closure zone, and those therapeutic cells thereafter become responsive to endogenous regulation by detecting the biological signals and correcting biological dysfunction by releasing the otherwise missing proteins or hormones for the patient. In the case of Type 1 diabetes, we know the pancreatic islets are the victim of the onset of Type 1 diabetes. It is important to recognize that islets are not themselves cells, but clusters of cells that include beta cells that secrete insulin, alpha cells that secrete glucagon, that actually raise blood glucose, and then delta cells that secrete somatostatin, which will lower insulin and glucose. These three cells in concert are what maintain glucose homeostasis in patients. Today's current treatment really lacks that overall hormonal control. It is a focus on the administration of insulin to lower blood glucose. However, we do not have automated provisions of glucagon or somatostatin within the technologies available today. However, that is available through cell therapy technologies, as we're talking about right now. In our Phase I/II multi-cohort trial design, we currently have 13 patients enrolled in this trial. The inclusion criteria are that patients have to be long-term Type 1 diabetic patients who've been receiving insulin or dependent on insulin for at least five years, recent history of severe hypoglycemic episodes, and impaired awareness of hypoglycemia, meaning that they do not detect the physiological onset of hypoglycemia. These patients have no stimulated or no detectable stimulated C-peptide in response to a mixed meal tolerance test, and just for clarity, C-peptide is released into the blood simultaneous with insulin and is therefore a surrogate marker for insulin being produced endogenously. In our Phase I/II trial, we added Cohort A. Our enrollment is complete, and that used an eight-channel Cell Pouch that was placed subfascially, as I mentioned earlier, and requires systemic immunosuppression. Seven of 10 patients have now been recruited into Cohort B. We use a larger 10-channel Cell Pouch in this Cohort, which has 50% greater capacity than the 8-channel, and we also employed systemic immunosuppression. On the first day of enrollment, patients have their Cell Pouches implanted. By week three, immunosuppression is initiated, and by week six, the first islet transplant to Cell Pouch occurs. By approximately month five to six, a second islet transplant to Cell Pouch occurs. The reason for two transplants is that there are limitations in terms of the number of islets that can be derived from a single donor pancreas. If patients do not achieve complete insulin independence after six months following their second transplant to Cell Pouch, they will be permitted to receive a supplemental dose via the portal vein. In our first Cohort, excuse me, five of six patients received, who received two islets to Cell Pouch as well as small intraportal supplements, achieved insulin independence, with durations ranging from nine months to more than four years. Through this Cohort, we have actually determined the optimal islet dose, the optimal islet density. We have seen positive stimulated serum C-peptide in three of six patients, and we saw antibody-mediated responses in the remaining three patients. It was the observation of the antibody-mediated rejection or donor-specific antibodies that really drove us to further adjust the maintenance immunosuppression regimen. This is an illustration of the doses that each patient in Cohort A received. The blue bars, the blue segments represent the doses of islets that were administered to Cell Pouch. The gray bars represent the doses that were administered via portal vein. It is clear from this diagram that the more cells, the more islets that were placed via the Cell Pouch, the fewer that were required in the portal vein. And I do want to point out that five of these six patients achieved insulin independence, and we determined that the threshold is approximately 14,000 IEQ per kilogram. IEQ meaning islet equivalent dose. You can also see from the blue band at the top, that the maximum capacity range of the ten-channel Cell Pouch allows for additional islets to be transplanted to the Cell Pouch if required. In Cohort B, these patients started with a modified immunosuppression regimen. Patient A, the very first patient to be entered into this Cohort, developed severe neutropenia almost immediately following their first transplant to Cell Pouch. Therefore, their immunosuppression was reduced, and subsequently, because their neutropenia did not resolve, they discontinued the immunosuppression in this individual. Patient B was started at approximately the same time. This patient continued to receive the same immunosuppression regimen for about 90 days, until the point in time where it was determined that patient A's immunosuppression was potentially toxic, and therefore had to be reduced. After that time, patient B's was reduced. Nonetheless, that patient developed a positive fasting serum C-peptide, and as well became insulin independent after one transplant to Cell Pouch, and a very small top-up to the portal vein. In fact, you saw earlier that we had achieved an estimated islet threshold of about 14,000. This patient received a cumulative islet dose of less than 9,000. Patients with reduced immunosuppression regimen, that being patient C, D, E, and F, had no detectable C-peptide. When we did a quick deep dive, we realized that the optimal immunosuppression was what had been received by patient B, and at the request of patient A, as well as the other patients, they were all re-challenged on the optimal immunosuppression regimen. What we ultimately learned is that patient A, themselves, had a severe sensitivity to one agent within the immunosuppression cocktail, and it was just a stroke of unfortunate luck, if you will, that that was the first patient in the Cohort. We have now determined what the optimal immunosuppression regimen is, and we have recently enrolled patient G. That is the seventh patient in the Cohort, and that patient is awaiting a pancreas for their first transplant to Cell Pouch. We have also gone back to the FDA and immediately received authorization to add a few additional patients into this Cohort in order to be able to demonstrate the efficacy of this optimized immune suppression regimen. HbA1c is an estimated measure of the average control a patient has over their glucose in the preceding three to four months prior to their test. What you're seeing in this particular chart is that the blue represents their HbA1c values prior to treatment in the trial, and the gold represents their HbA1c subsequent to treatment in the trial. It is clear, if you look at patients D and B, that there were dramatic improvements between their pretreatment and the posttreatment events. What's more important, though, is to recognize that the patients prior to treatment in the trial were on an optimized diabetic treatment, so they were all under the care of an endocrinologist. They all had intensive insulin therapy at that time. So it was expected that they would have well-controlled glucose levels. Those well-controlled glucose levels were at least sustained, if not improved, after the completion of their therapy in this trial. I'd like to talk a little bit about our partnership with Evotec, with whom we are developing induced pluripotent stem cell-derived islet-like clusters. We have conducted multiple studies, including preclinical animal models, testing the ILCs in Cell Pouch in induced diabetic mice. Excuse me. You can see in the image on the left, the mice who were first implanted with Cell Pouches, they were then induced with STZ to become diabetic, or as a diabetic model. Thereafter, they were further transplanted with the ILCs, the islet-like clusters into the Cell Pouch, and you can see that over a period of sixty days, their glucose control improved to the point where after sixty days, it normalized and was sustained. This was one study that we did. As I said, we have done multiple, and we have the identical results extending out beyond six months. In the top right-hand, what you can see is that the human C-peptide levels that are provided by the ILCs at during the still immature stage of two weeks and six weeks post-transplant, you can see that there's a rise in the human C-peptide during that time as the ILCs mature. Moreover, you can see that though they are acting identically to human donor islets that are implanted into the into the kidney capsule of mice in a similar trial. Looking to the bottom, you can see that we have efficient glucose clearance by not only the human islets, but virtually complete overlap in an oral glucose tolerance test of the glucose curve for the ILCs in Cell Pouch compared to the human islets. I wanna leave you with a quote from our very first patient in our clinical trial. As an example of the efficacy of the product that we have seen to date and our efforts towards giving patients their lives back, please note that this patient actually achieved insulin independence that was sustained for greater than four years. Thank you. Thank you so much, Mr. Shannon, for sharing the exciting work that's going on at Sernova.