Good morning everyone, and welcome to the Sernova Biotherapeutics and Seraxis shareholder and investor webcast. At this time, all attendees are in a listen only mode, and a question answer session will follow the presentation. If you would like to submit a question, you may do so by using the Q&A text box at the bottom of the webcast player. As a reminder, this call is being recorded and a replay will be made available following the conclusion of the event. I would now like to turn the call over to Jonathan Rigby, Chief Executive Officer at Sernova, and Will Rust, Chief Executive Officer at Seraxis. Please go ahead. Thank you very much, Tara, and good morning everybody. Great to have so many people dial in on this exciting day. Before we kick off, I just want to acknowledge that 25 years ago today, the September 11 attacks took nearly 1,000 innocent lives and forever changed the course of history. I just wanted to pause to honor the courage of the first responders and everyday heroes who ran towards it. In our thoughts, may we never forget that. Again, thank you for joining. My name is Jonathan Rigby. I am the CEO of Sernova Biotherapeutics. I will be the surviving CEO of BetaNova Biotherapeutics when the merger is complete. Dr. Will Rust, who is the Seraxis CEO and will be the President and the Chief Scientific Officer of BetaNova. As Tara mentioned, we have a short deck here to run through the science, and then we will turn over the floor to a Q&A session. I know we have a lot of questions coming in, and we will endeavor to do our best to answer them all. If we cannot get through them in the time allotted, then we will reply to those that have submitted their emails. Also on a personal note, as someone who has personally lived with type 1 diabetes my entire life, and I fought it every single day and every single night ever since, I genuinely could not be prouder to be here as part of this Sernova Seraxis merger. Together, we have the chance to write a new chapter in the history of diabetes, and we intend to give everything we have to see that patients and their families finally get to live without it. One more statement actually just came to my mind because of the excitement that I am having. I hope you all share our huge excitement, because BetaNova is and will be the second company on the planet to be entering into a T1D cell replacement clinical trial. I will say that again. We will be the second company in a T1D clinical trial with cell therapy with an FDA-approved IND. For me, that is incredibly exciting. We are now ahead of other known players in the field. If we move on to the next slide. Will, can you move us. There we go. I just want to show folks this disclaimer regarding forward-looking statements. We will be making them today. If you want to take a screenshot of this slide, feel free, and make sure that you read it. The purpose of this merger is that we aim to create a differentiated approach to type 1 diabetes cell therapy by the formation of BetaNova Biotherapeutics. We do have a bold, audacious mission, and that is to create a functional cure for type 1 diabetes. The mission may be bold, as I said, but it is realistic and it is tangible. As a result of this merger, we now have all of the tools in the bag necessary to achieve this mission. We are doing it by uniting what you see on the screen here. If I go down the left-hand side, we are uniting stem cell-derived islets. Seraxis bring SR-02 allogeneic insulin-producing cells. We actually had an IND cleared in April of this year to get them into the clinic. We also have SR-03, which are gene-edited, immune-evading insulin-producing cells. The IND-enabling studies are ongoing, and we plan to file an IND for that program in 2027. We also have an implantable and retrievable medical device studied in a phase I/II clinical trial. A lot of you now are familiar with this. It is the Cell Pouch. It is an investigational device, and we have completed the phase I/II study. We have an open IND, and we will be talking about some of the data on a subsequent slide. But delighted to say that we did meet all of the primary and the secondary endpoints. The third leg to the stool is that we now have and will be deploying an advanced immune management process as we get into the clinic. We will be using co-stimulatory blockers like CD40 ligands as part of an immune tailoring strategy, and we will also include standard of care in that program. On the right-hand side, these are the key upcoming milestones that we believe will translate into increased value for our shareholders and our investors. The merger agreement between Sernova and Seraxis has been executed. We did announce on Tuesday of this week a financing that has been done that enables us to achieve everything that you see on the screen. But we will leave that financing open until the end of September. If you go to the press release that we put out on Tuesday, you will find the names of Nathan and David that you can reach out to with any inquiries that you may have. We will be closing the transaction in November. It is subject to shareholder approval. Also very exciting that we will start recruiting patients for the clinical trial in the fourth quarter of this year. We have a lot of people who send us emails that want to be in the study, so this should not be a problem. The phase I/II SR-02 study will start early in the new year. Given that we expect these cells to be functioning and we will be getting data pretty quickly, we will be in a position where we can put data out in the first half of 2027. We are also working on the SR-03 program and looking to advance that to an IND approval in the second half of next year. It is approximately a year behind the SR-02 slides. We are working diligently right now to be ready to be NASDAQ-ready by the end of this year. And we plan to list the company on NASDAQ in the first quarter of next year. Very exciting times. With that, I'm going to hand over to Will to go through our science. Over to you, Will. Thank you. Thanks, Jonathan. As Jonathan said, my name's Will Rust, I'm the CEO of Seraxis. I'm going to talk to you about the science underlying this very exciting program. Let's start off with the cells. These are different from what you've heard about before. They're not embryonic stem cells. They're not iPS cells. They're unique to our effort. If you focus your attention on the image on the left side of your screen, this describes where the cells come from, how we made them. We acquired a pancreas through the organ donation network and then harvested the islets and reprogrammed the islet cells to gain a stem cell phenotype. The goal in doing this was to find a stem cell that would grow, but despite that, still maintained some identity of being a pancreatic islet, and the purpose was that they would simply be better as a manufacturing basis for making more islets. We screened the cells to find that one. We found it, we expanded it, and made the cell banks, and those cell banks are the foundation of the manufacturing and the clinical study that I'm going to introduce for you in just a minute. Again, this is different from embryonic and iPS cells in that they have a bias of a pancreatic identity. If you focus now on the right side of the screen, the consequences of that bias are is that they're simply very potent. In vitro, when we take the manufactured islets, we can show that they secrete quite a lot of insulin, and that secretion is glucose responsiveness. That's one very important detail. Next, when we started this program, we had always intended for this to be a therapeutic product, so we chose as a donor for this tissue, a donor who was highly compatible. In our upcoming clinical study, there are no exclusion criteria due to compatibility with the graft. Another consequence of having this pancreatic bias stem cell line is that the manufacturing is just simpler. It's streamlined. We don't require a sorting at the end, and that means that at the end, we have quite a stable product. In addition to that, the last point I'll make is that because of this process, this cell is proprietary to us. We have patents around the world to protect that. I am going to now show you some of the glucose responsive data. This was generated independently by another group testing our cells. If you look on the right side of those two graphs, this is the response of human islets to differing levels of glucose. If you look at the bottom, what it is showing here is the amount of insulin that is secreted into the media in response to those glucose. If you now look on the left, you can see that the profile of our manufactured islets is very similar to what native human islets can do in the lab. This is remarkable. Those islets came from a patient who was over 30 years old, in comparison to our manufactured islets that are 30 days old. There is quite a lot of similarity between what we manufacture and a native human islet. If you look at the top, this is the mechanic of insulin secretion, influx of calcium, and you can see that those profiles are also very similar between our cells and a native islet. These are highly potent, very similar to a native islet that has been harvested from an adult pancreas. What we are looking at now is some of the animal data that we generated to demonstrate that these work. On the left shows that we are able to rescue diabetes in animal models. On the right, what we see is what the cells looked like before they went into the animal, and then what the graft looks like when it is removed. On the top, we can see a low magnification image of islets that we have manufactured. The next one is what an individual islet looks like. What is remarkable here is the distribution of, similar to a native islet in the right proportions. These go into the animal and form a graft that can be functional enough to rescue diabetes. Then when they are removed, what is remarkable is they look like human pancreases that are removed from these animals. They have the structure of a pancreas. They have the hormone-secreting cells in the correct distribution as a human pancreas. We are able to make an extra-pancreatic functional pancreatic organ in the animals. I want to just spend a minute talking about our immune suppression strategy. I know this is very topical today. The first thing I would like to say is that modern immune suppressants are changing the landscape of solid tissue transplant. We are very confident that the clinical record shows that if we were to pair our islets, which are already a very compatible tissue as a donor tissue and has no vasculature from the donor, with these modern immune suppressants, that the likely clinical outcome is that these patients will need only a minimal dose of these low-toxicity immune suppressants. I also personally believe that there is strong clinical evidence to suggest that over time, with the right immune suppressants, some of these patients will be able to reduce that immune suppression burden to nothing. They will be able to establish tolerance to the graft. We intend to initiate an analysis of this immune suppression in our clinical study. The next strategy that we're deploying to reduce the immune suppression burden is we've got a version of our cell line, SR-02, that has been genetically engineered through a loss-of-function strategy to be even more compatible than the parent line, and that one is called SR-03. This will follow up SR-02 in the clinic. It'll have the benefit of the safety profile and the dose response information that we generate from SR-02, and the goal here is to determine if we can reduce the immune suppression even more and get to the point of elimination. The non-clinical data in animal models with SR-03 is very promising, showing that we can remove immune suppression. However, there's no adequate model for the autoimmune component of type 1 diabetes, and this really is something that we're going to have to determine empirically in our clinical study. It very well may be that SR-02 could outperform SR-03. We're going to have to find that out. We have both of these programs. I want to just show you some of the data about our immune-evading cells, SR-03. What I'm showing you here is that SR-02, when implanted into an animal that has a humanized immune system, so has human immune effector cells, that those quickly recognize the graft and form antibodies against it. Whereas when we put in SR-03, it does not, demonstrating that it is not recognized by the human immune system in those animals and is unable to generate an antibody-mediated response. Moving on. Last detail about our cell program, but an important one, is that we have built out in-house full GMP manufacturing to support our clinical study. I mentioned earlier that it's efficient and streamlined because our cells are very good at making more islets. We are only using scalable materials, and we're already working to outsource this to do larger-scale manufacturing. On the bottom is a little graphic that shows the process. It's very simple. We take a cell from our frozen cell bank, an aliquot. We expand those. We then cause them to mature to the islet phenotype. They pass QC, and the final fill and packaging is complete so that they can be distributed to the point of care. At that time, they're very stable, so the logistics in distribution to the point of care is very straightforward. All right, I'd like to shift focus now and talk about the implant device specifically. The purpose of the implant device is to create a niche in the human body that has all the specific requirements for an islet cell to survive and to be able to regulate blood glucose. Key among those properties are that it must be highly vascularized. It must not suffer from fibrosis that would choke off the cells from the blood supply that it needs to regulate, and it needs to be retrievable. This device, the Cell Pouch, has already completed a phase I/II study using cadaveric islets, and it demonstrated all of those points. I'd like to highlight that it is the only device to have demonstrated each of those objectives in a clinical study. Specifically, the others had failed out because of the formation of fibrosis. That's very important here. In the course of conducting that study, over 30 years of patient data cumulatively has been generated that demonstrates. I'm going to show you what it looks like. If you first look at the middle of your screen in that white square, this is the Cell Pouch, and those horizontal lines are actually rods. After implant, those rods are removed, creating little tunnels, and in the void space of those tunnels is the vascularized environment where the islet cells are distributed. That is the space where they can thrive and function to regulate blood glucose in the patients. On the right side of your screen is what one of those pouches that housed cadaveric islets looked like upon removal five years later. You can see here that it is a highly vascularized, healthy, non-fibrotic tissue that came out even after five years of being implanted in the patient. Another thing, in the course of doing that, it was proven that this was fully retrievable and retrieved all of the implanted cells. If we move on, this is what a Cell Pouch looked like after years in the patient. What we're looking at is the histology on the top, where it's just H&E, and each of those circles represent one of the void spaces where the islets were living. On the bottom is immunofluorescence microscopy, so you can visualize those islets. What's colored in red is the insulin, so you identify the cells that are regulating blood glucose, and in green are the blood vessels. You can see that the elements for rescuing diabetes are there. We have the stable insulin-creating cells, and we have very close association to the vasculature. With this unique data set, we are very excited to combine our cells with this niche that will enable their survival and also their monitoring and retrieval from the patient. This aspect, this point I'm making about retrieving, we feel is very important. There's a reason here. This is not a drug where patient takes it, and over time it goes away. This is intended to be a graft that will survive in the patient for years or decades. The number one concern among regulators is that long-term stability of the graft. What should happen if something goes wrong? It is highly favorable that the implant be monitorable and retrievable for that reason. It shifts the safety profile strongly in favor of implanting this therapeutic device. You can imagine that this Cell Pouch, which you see on the right, has a therapeutic dose of islets, which we've already established through our dose response study at that time, that would provide independence from insulin. If it ever should be removed or replaced, that can be done in a simple surgical procedure. All right. Those are the points I wanted to make sure we got through and stay in time today, and I think I've done that. Jonathan, I will pass it back to you. Thank you so much, Will. That was a great overview of our respective science. We are putting together something very special here. As I said at the beginning, if you have any further inquiries or you want to chat, please do reach out to David. He is our VP of Investor Relations, and his email is on the bottom of the slide. Tara, we can actually drop the slides now and go onto full screen, if you like, and then I will let you moderate. I know we have a lot of questions coming in, a lot of excitement, and I would be happy for you to go through those. Great. Yes. Thank you both, Will and Jonathan. We do have a lot of questions here. If we do not get to your question, we will follow up via email to answer. The first question here, why did Sernova and Seraxis decide to combine forces now? I would be happy to take that one. I have been asked that question a lot this week, which is a good thing. Quite simply, by merging to form BetaNova, we are bringing together several critical capabilities in-house to develop our mission, a functional cure for T1D. These include an in-house source of insulin-producing cells. Will mentioned SR-02, the allogeneic stem cell-derived pancreatic islet cells. He also mentioned SR-03, the hypoimmune gene-edited cells. We also have in-house cGMP manufacturing in Germantown in Maryland. As Will just went over, we have the implantable and retrievable cell containment device, i.e. the Cell Pouch, that has clinically been proven in a phase I clinical trial to support islet function engraftment. Each of these capabilities that I just mentioned actually addresses a different part of the islet cell replacement challenge. It really is a trifecta. By bringing them under one company, we can develop the cell source, the manufacturing process, the implantation strategy as part of a coordinated clinical program, rather than doing this separately. That integration is one of the fundamental reasons this is so compelling. Next one, please, Tara. Yes. So what exactly is being created here, and who owns what? Okay, I'll take that as well. Sernova and Seraxis are combining our businesses under a definitive merger agreement. That has happened, and we're forming a new U.S.-domiciled clinical-stage company called BetaNova Biotherapeutics. As mentioned, it will be headquartered in Germantown in Maryland, and it has its own integrated research labs there. We have cGMP manufacturing capabilities there. As the company grows, the cell manufacturing that we have in-house will, of course, as is normal, be transferred out to a contract manufacturing organization for manufacture of commercial sale. The little bit on the ownership structure, this is a true merger of equals in economic terms. Upon closing, the existing Sernova shareholders and the existing Seraxis shareholders will each end up owning approximately 50% of the combined company. For Sernova and Seraxis shareholders, we see this candidly as an opportunity to take the progress and foundation that both companies have already been building, and we combine them with our capabilities needed to move forward a more complete and scalable T1D cell therapy solution. By combining the two companies equally, shareholders will notionally maintain the value of their shareholdings prior to and post the merger. Next one please. The next one, how does the convertible note financing work, and is it still open to new investors? Good one. Good question. The notes that are being offered will automatically convert into common stock of BetaNova once the merger closes. Note holders aren't making a discretionary choice about whether to convert. It will happen by design on closing. And yes, the current round will remain. We have the capital committed to do all of the things that we've mentioned in this presentation. But we do plan to keep the round open until the end of this month. As I mentioned, if you do have interest, please do reach out to Nathan or David. If you can't find their contact details, they are in the press release that we made on Tuesday earlier this week. Let's move on. Great. The next question, what is BetaNova's lead product candidate and what is its development timeline? One for you, Will. I can jump in on that one. I'd like to point out first that this is IND approved. We are actively launching the clinical study with the goal of enrolling patients soon. As Jonathan mentioned earlier, we will be treating patients in the first quarter of 2027 and have data distributed, made available as early as we can, which will be in the first half of 2027. This study is an evaluation of the dose response and safety of SR-02 alone. This is not yet the combination of the SR-02 with the Cell Pouch. We are quite risk averse. We're not going to combine two experimental programs immediately. First, we're going to develop that safety profile with SR-02 and get a very good understanding of the patient experience, the dose response. Then we will, with that knowledge, we will then combine that with the Cell Pouch, as the implant device. Great. Thanks, Will. Thank you, Will. Yeah. Sorry, Jonathan Rigby. Our next question, could you help us understand how BetaNova's approach is scientifically differentiated from other companies pursuing islet cell replacement for T1D, such as Vertex Pharmaceuticals, Sana Biotechnology, and Century Therapeutics? Yeah, I'll jump in on that one as well. There's several ways that we are differentiated and our program is different from those programs that you mentioned. The first one is a different cell type. I spent some time during the presentation today describing why it is different. The main consequence of its difference, of course, is that the islet product, we believe is more potent and the manufacturing more straightforward, ending up with a genetically stable, and more durable product. So that's one way that it's differentiated. Another way that it's differentiated, of course, is the implant device. As I mentioned, we're the only ones that have the opportunity, and the long clinical history and knowhow to be able to pair a stem cell generated device with I'm sorry, a stem cell with a device that creates a niche for those cells to survive inside the body. To be able to replace that is invaluable in terms of giving the best, most practical, and safest therapy for patients who suffer of T1D. So that's another one. The third one I'd like to bring up is our differentiated strategy in immune suppression. I know that there's a lot of talk about just gene-edited cells. We feel that the best strategy is two-pronged, to evaluate intolerance mechanisms and be evaluated in comparison with modern low toxicity immune suppressants in addition to gene-edited strategies. So that's we think much more conservative, higher outcome of clinical success following that strategy. Embedded within that is that our philosophy about gene editing is different. Our gene edits to the cells are different from the gene edits that they're currently using. We've done a lot of in-house evaluation, and we're confident that our gene edits are superior. Great. Thanks, Will. The next question, is BetaNova going to list on NASDAQ and when? I'm happy to take that one, Tara. The short answer is yes. This will be the fifth NASDAQ listing that I've been a part of. So we do intend to list on NASDAQ in the first quarter of next year, early next year. However, this is conditional. It's subject to satisfaction of applicable listing requirements and approvals. So it's an intention and it's a target. It's not a guarantee, but we fully intend to do this. NASDAQ listing requirements typically include a minimum share price, a certain market capitalization, a certain public float, and requires corporate governance standards that are very high. I can let everybody know now, we are great believers and maintainers of very high corporate governance. So shareholders should understand that BetaNova will need to actively work toward meeting those thresholds. We are super confident that we are doing the work now and we're doing the work for the remainder of the year, that we can meet all of those thresholds and list this organization on NASDAQ. Great. Thanks, Jonathan Rigby. Next one, please, Tara. Yes. How is SR-03 different from Sana SC451? All right. We're going to get into the specifics of the science here. The Sana approach, and others in the field, Century, is what can be considered a gain-of-function, right? There's some complex expression cassettes that must be introduced into the genome of the cells. And those expression cassettes are tricky because they can cause off-site mutations, some of which can be cancerous. One of the concerns here is that those gain-of-function mutations need to be stable, not only just over many, many generations of cell passaging during the manufacturing process, which is already a challenge, but they need to be durable over decades of implant in the patient. From a practical and logistical perspective, that's challenging. We did evaluate that strategy in our lab and compared its efficacy against what we ultimately chose, which was a loss-of-function strategy. In this case, we're removing the determinants that could trigger immune rejection. By not having gain-of-function, rather only removing expression of certain genes, the end product is something that doesn't have the risk of off-site mutations, and it has a much better stability and durability profile. With that, we can generate 100 passages of manufacturing capability in our process without any loss of stability or durability of the character of those cells. And we anticipate that the same would be true after implant. The graft would be a stable graft within that patient and provide very predictable performance outcomes and safety profile for the patient. That's a distinct difference between our philosophy towards the gene editing and their philosophy. Thanks, Will. The next question, the Cell Pouch is described as both implantable and retrievable. Can you explain why retrievability matters clinically and what safety or engraftment data supports it? Sure. With the retrievability, we couldn't have a stronger data package. As indicated, a phase I/II study has been fully enrolled. All those patients have already been treated. We know exactly what it takes, how safe it is, and how easy it is to remove the graft. We know that the graft was removed in its entirety. We know that there aren't morbidities associated with that in the patient. That is very strong contributor to the argument that this strategy is safe for the patient. The device can easily be visualized using scanning techniques, a CT scan, or ultrasound scans to follow the graft. That gives it a very high safety profile. We think that safety profile is incredibly important because we're very soon going to approach the agency and say we'd like to implant into patients cells that are genetically modified, right? That's breaking new ground in human medicine, a permanent graft that is genetically modified. Being able to say that this is retrievable raises the safety profile. We know the FDA has already communicated that that is an important element of this strategy, the ability to remove it if something should go wrong. We think it's very important. The safety- Will, yeah, if I could just chime in there a little bit. As mentioned, I've had type 1 diabetes all my life, and let's assume even if we say all cells are equal, if I go to my doctor, and she's a wonderful lady, and she says, "Jonathan, we can give you cell therapy to get rid of your diabetes. Would you want it?" She would say, "You have two options. We can either put the cells in your liver where we can't get them back, or we can put them in your forearm where we can't get them back, or we can put them in this little device called the Cell Pouch, which is retrievable." I don't need to say which one I would choose. I think it's pretty obvious. Okay, let's move on. Great. The next question, how is this being funded, and is it enough to reach key milestones? Okay. I'll take that one. Yes, we have secured commitments for up to $10 million in a non-brokered convertible note financing. The money has been put up by insiders of both Seraxis and Sernova. Our objective is simply to deploy this capital very efficiently to advance BetaNova through all the key milestones that you've heard today. As a reminder, the finance is intended to support the cGMP manufacturing of SR-02, which is going on as we speak. We are selecting sites and getting them contractually tied up with us, and we are looking to enroll patients this year. Then, as Will Rust said, we will be dosing early in the new year, which is super exciting. We'll be the second company doing this behind Vertex Pharmaceuticals. We will be getting data the first half of the year, and we will let all of our investors know how that data is showing the performance of the islet cells. We are also using the capital to list on NASDAQ, as we have discussed. There are also lots of preclinical preparatory work going on to advance SR-03, the gene-edited cells, to an IND submission, and hopefully approval in the second half of next year. Our goal is to reach these value-creating milestones with this capital, with as mentioned, a continued focus on being capital efficient. Frankly, the way that we have done it here, we were sensitive to minimizing dilution to current shareholders. There were other term sheets that we could have gone with, which would have been more dilutive, so we have opted not to do that. As with any clinical stage biotech, we need future financing as the programs advance. The important point for shareholders is the current financing is specifically structured to get BetaNova, as mentioned, through several significant near-term catalysts. I think hopefully that answers the question. Great. Thanks, Jonathan. When is the merger expected to close, and what needs to happen first? Okay. We are targeting a special shareholders meeting in November, and the shareholders need to approve this merger before it is final. We are super confident that we will get that. The press release that we put out earlier this week did not lay out the full mechanics. We did not talk about the record date, the proxy timing, the required vote threshold, et cetera. The shareholders should watch for a forthcoming proxy statement, or a circular as it is otherwise known. That should be coming out to you all in October, and that will have all of the details of the financing of the merger, so that you can make an informed decision as to how you cast your vote. Again, this should happen in November. This is our target. It is not a certainty. As with all things, timing could potentially slip, but we're gunning to get this done in November. Then we'll be free to get into the clinic and we'll be a potent force. Great. Thanks, Jonathan Rigby. The next question. Sernova invested significant time and capital in its prior cadaveric islet program. What specifically makes Seraxis SR-02/SR-03 platform a better path forward, and what data supports that decision? Is there a pipeline beyond SR-02? Yeah. That question's probably been answered in the presentation, but I'll take a stab and then Will Rust, if you want to chime in with anything else, feel free. Yes, Will talked about the prior Sernova clinical trial, and it generated very important data for sure, and helped to advance our understanding of what is required for an effective cell replacement therapy. We are building on that experience. We are not walking away from it. We're building on it. The decision is less about saying one cell platform is categorically better than the other. It's about choosing the option that has the most direct path to the clinic. It's about choosing the option that has the ability to develop the cells at clinical scale. It's about establishing the GMP manufacturing. We have the capacity now for the phase I/II clinical trial. We will need to scale up externally, and that will need an immune protection strategy as an integrated part of our plans. That's what we're doing. There was a question about the pack beyond SR-02. Yeah. Beyond SR-02, we'll talk about SR-03. That provides a logical next step. It's mechanistically different from SR-02. Rather than pairing with immunosuppressant drugs, it incorporates gene edits, as Will described, which are intended to help the cells evade the immune detection which could potentially reduce or eliminate the need for chronic immune suppression. For those cells, as mentioned, the IND is expected to be submitted in 2027, meaning it's roughly a year behind SR-02. I hope it came across clearly that BetaNova is unique, that we have two cell types plus an implantable retrievable cell containment system, the Cell Pouch. But we will follow the science, and we will follow the data to make informed choices as we progress. Did I get everything there, Will? Yeah, that's great. Thanks. Good. Okay, next question. Yes. Can you speak to the immunosuppression regimen plan for SR-02 and how it's expected to differ from the standard of care immunosuppression used with therapies like Vertex's zimislecel? One of the objectives of our program is to provide data that can demonstrate the potency, demonstrate the safety, patient experience of the implant. For that reason, we do want to compare to what Vertex has achieved. Vertex, it was remarkable the progress that they pushed the entire field forward with in their program. We think it is important to be able to compare our clinical results with those clinical results to provide a benchmark for the industry. Including standard of care is important here. We want to eliminate all the variables that we can towards demonstrating safety and potency. However, it is not our goal to have standard of care today. I am going to say that it really is unknown what the immune suppression requirement will be for a highly compatible stem cell-derived islet that is not carrying any blood vessels from the donor and implanted deep into stable engraftment site within the host. We do not know what that is, and it might be very low. What our goal is to do is to pair this with the modern immune suppressants that are available, and there are several in clinical studies now, and there are others that are already approved for use that are really transforming the experience of patients with solid tissue grafts. The clinical record using those and other solid organ transplants is very clear. When the graft is highly compatible, the patients most likely can maintain their graft with a monotherapy that is at a low dose with minimal toxicity. We think that that is a probable outcome. We are going to be including an adaptive study wherein we can evaluate those immune suppressants and land on what is best for the patient. I anticipate that is going to be quite low and that the immune suppression management will be favorable over daily insulin management. Great. Thanks, Will. The next question, do you expect SR-02 to eventually be delivered using the Cell Pouch or do you expect to continue with the omental approach for SR-02 and potentially use the Pouch for a later program? We're working on ways to integrate the Cell Pouch as quickly as we can. These are two open IND programs, and we need to be very careful about that. But the ultimate goal, of course, would be to have a therapeutic dose in a Cell Pouch as a single therapeutic implant product for a patient that provides total independence from insulin and total loss of the comorbidities associated with hypo and hyperglycemia in those patients. That's the goal. Great. Thanks, Will Rust. What remaining duration has Seraxis' main patent? I'm sorry, can you repeat? I didn't- What's the remaining duration for Seraxis' main patent? We have maintained our patent portfolio. We are constantly adding to it. We cannot just simply say, "Oh, the original patent is expired, and this is public domain material." It is an evolving process. The patent family is quite large. We have, I think, 50 granted patents worldwide, some of which are derivative of older patents. We have another 50 outstanding. I think that for the foreseeable future, we have adequate protection. I would like to say just one more thing about it. The claims in those patents do not cover just this idea. They are compositions of matter. The cells belong to us. The method for making the cell belongs to us. The method of using the cells to relieve a patient of daily insulin management belongs to us. We think that we are quite well protected. On the Sernova side, it is a similar story. They have an independent patent portfolio that covers the use of that device for this purpose. We intend in the future to continue generating intellectual property as we merge these together, and continuing generating intellectual property with our SR-03 program and immune management. Yeah. We both and together fully understand, appreciate, and value the need to continually prosecute intellectual property. This is a competitive field. We are now one of the leaders in the field, so the importance of filing new IP, of which I am sure there will be lots, is certainly not gone unmissed here. Great. Thank you both. In USD gross from new funding to achieve the milestone. Well, I think we've touched on this one a number of times. But the funds will be used for general corporate purposes as well. But mainly, it's to complete and continue. The cell manufacturing is a 24-hour, seven-day-a-week process. At the headquarters in Germantown, there are people there every single day, Christmas Day, Boxing Day, Thanksgiving Day looking after and working with these cells. So we will continue to do that. We are engaging clinical sites as we speak. We have incoming emails frequently from patients saying, "I've heard all about this. I'd love to be a part of this clinical trial." So we will be screening patients this year and then dosing early in the new year. And on the practical side, getting ready to be a NASDAQ-listed company requires certain PCAOB audits of our financial statements going back a number of years. We have started doing that. That's coming along quite well. Our finance team, I think they're working 24 hours a day as well to get that done. So that's what we're doing. And we are committed to getting it done 100%. Great. So the next question, how do your cells compare to Vertex cells in terms of efficacy and manufacturing? The manufacturing part is easy. There's a lot of published information about that, so we can compare head-to-head. We believe our manufacturing is much more streamlined, straightforward. The key difference is that we don't select at the end of the process, so we don't need to weed out the unwanted cells and then keep the wanted cells. And that's an important differentiator. One of the main reasons is not only do we save on economies of scale because we're not throwing away a good portion of our manufactured product, but because they never have to go through that process of sorting, they're more stable. The clusters of cells, they remain adhered to one another. So at the end of the process, we can literally, according to our testing, leave them out on the lab bench at room temperature for a week, and they don't lose their potency. We can throw that in the refrigerator and ignore it for three weeks, and they don't lose their potency. Just to demonstrate the stability of the manufactured product, right? I think that is important because it's not whether we can make cells that secrete insulin. That's almost irrelevant. What's relevant is can we make enough to be beneficial to patients? Can we commercialize it? Can we distribute it? Can we make a meaningful impact in the patients who need it? This focus on manufacturing simplicity and stability is incredibly important, and we think a big differentiator. The other differentiator, which I mentioned at the beginning, was the cell source. These are not embryonic. The Vertex cells are embryonic stem cells. The embryonic stem cells used by Vertex also came from a patient that limits the patients that could receive it due to host incompatibility issues. We don't have those issues, right? We intended from the very beginning that this was going to be transplant therapy, and therefore, we chose a donor that had a highly compatible universal donor blood type, for example, to avoid those issues. There are two big distinctions right there. I mean, look, at the end of the day, there are many tens of millions of people with T1D world over. The number is growing and growing and growing. People sometimes say to me, "Jonathan, you have an insulin pump, and you have insulin, and you have a continuous glucose meter. Diabetes is fixed." I find those statements to be quite comical because it's far from being fixed. The comorbidities associated with badly controlled T1D are gigantic. There's a lot of patients is my message, and we want Vertex to succeed. We want Vertex cells, we want BetaNova cells to be approved and be available to people suffering from this condition that where the clinical need certainly has not been met. Next question. For SR-03, what are the biggest remaining preclinical questions you need to answer before the IND, particularly around immune evasion, durability of engraftment, and recurrent autoimmune attack? We have answered all of our questions with regards to the animal models, the gene edits. We are not changing those. We have the master cell banks. They are already done. Our strategy is defined, and we know the path forward. All that needs to be done is completing the non-clinical studies and putting together the package for the regulators to review. We think that is going to be very straightforward because we have just accomplished it. We have already done that. We know exactly what to see. We can draw on the data from the parent one. It will be incredibly advantageous for us to have the safety and dose response data from the parent when we submit to the agency an application to use essentially the same cell line, same manufacturing, same lot release criteria, same fill finish, everything the same except for the incorporation of loss of function mutations in the genome. The path ahead of us, we think is defined. We know how to accomplish it. I think our timelines are realistic, and I am confident we are going to achieve them. That is all it is, it is just checking the boxes, finishing the package to submit to the agency. Tara, I see that we have three minutes left, so we can probably squeeze in at least another one before we close. Yes. Our final question, ahead of moving into clinical study, Cell Pouch and the SR-02 asset. That's probably got a scientific and a business answer. I'll just quickly give the scientific answer. Combining the Cell Pouch and our cells is already being accomplished in animal models. We've done those implants, and we're already tracking the progress of that combination, which is super exciting. Aside from that, we need to communicate with the agency and determine what the regulatory path towards combining the two, the favorable path is, what's the shortest path, what's the best path, and we're working that out with our consultants and in communication with the agency. Yeah. If you stand back and look at the respective companies, Sernova and Seraxis, it was abundantly clear to me from when we started the discussions that we have complementary skill sets. There's very little overlap. It's very complementary, and our technologies are, of course, extremely complementary, and I think one of my first slides said the goal here is to be the differentiated player in the T1D cell therapy place. I'm personally convinced that is going to be achieved. I know Will is convinced, all of our respective employees are convinced, and hopefully, we've done a good job today of convincing the over 200 people that are listening to me right now and listening to Will. I think it's a very timely segue to thank everybody for dialing in. I sincerely mean that. As mentioned, we have a raft of additional questions we could have gone through, but time didn't permit. But for those that did provide an email associated with those questions, we'll send you a response. Will, do you want to have any parting comments? No, thank you. You wrapped it up quite nicely. I appreciate everybody who took the time to listen to us. Thank you very much, everybody. Tara, it is time to adjourn the meeting. Great. Yes. Thank you both. This concludes today's event. You may now disconnect.