Hi, good morning, everyone, and welcome to UBS Organ Restoration Day. My name is Erick Masanza, and I am one of the SMID Cap biotech analysts here. We're very pleased to have Bruce Culleton from ProKidney with us this morning. And, before we jump in, I'm just going to read a couple of our disclosures. For important disclosures, please see the UBS Research disclosures website, ubs.com. And if you have any questions, please reach out to us or your UBS sales representative. So with that being said, Bruce, I'll turn to you real quickly. Could you give us a brief introduction of ProKidney and your REACT technology? Sure. Well, I'll start with just a thank you for the invitation to join you today. And, I'm delighted to be here, delighted to actually take your attendees through our company, our product and some of the evidence that we have and obviously, our path forward. So, just a brief overview of our company. We're a publicly traded company, we're on Nasdaq. We have about 200 employees, full-time employees. Our offices are in North Carolina, in Raleigh and Winston-Salem. Our manufacturing facility is Winston-Salem. And we have an office in Boston, where some of the executive team sits. We went public in mid-2022. Our primary asset has intellectual property that goes back for over a decade and is based upon well over a decade of preclinical work, but actually origination of the IP goes way back to some work that was done at Boston Children's Hospital. Today, our asset is rilparencel. You may hear the term REACT. We are using the term primarily rilparencel. It's a product that's made from the patient's own kidney cells, and we take a biopsy from patients, essentially transport that biopsy sample to our manufacturing facility, and through a series of steps, from digesting that sample to expanding it, putting it through a series of steps to select out the renal cells that we're primarily interested in. After our harvest of those cells and formulation of those cells into our product, we cryopreserve it, ship it back to the clinical study site. At the study site, it's actually injected back into the outer lining of the patient's kidney, the kidney cortex. Perfect. And, just now, you described rilparencel as a certain cell type that you had selected. How did you go about deciding which cell types to include? And, if you know, how do they each contribute to kidney function? Yeah. So those cells, the selection of those cells goes back to some really early preclinical work, which identified a layer, a series of layers of cells after digestion. And in some of this very early work, it was identified that a certain layer of those cells was more likely associated with improved outcomes in animals, improved kidney function, and less inflammation on histology when you look at the animal's kidneys. So improved survival, improved kidney function, and histology, less inflammation. And so it was based upon that work that the prior team involved, the scientists involved and the leaders of the team before ProKidney went public, actually said, "Okay, well, this is the product that we're going to focus on." And eventually, that product became a fresh product, a fresh manufactured product that was tested in early clinical studies. And over time, now we've gotten to a place where we have a cryopreserved product, and that cryopreserved product is the product that's been tested in a phase II study, and is also now the same product that we're using moving forward in our phase III program. Got it. So it sounds like you had a lot of supportive preclinical animal data that helped you develop this. I also understand that in second half of next year, in twenty twenty-five, we'll be getting an update on the mechanism. What information should we expect to learn from this, and how do you see it helpful from a regulatory perspective? I like to separate, sort of, as we talk about mechanism, two sort of overlapping features or interests. One is a regulatory piece, and that's associated with, primarily our CMC activities. This has a focus, not the only focus, but has a focus on potency and assurance. The second is the biological mechanism. And so that biological mechanism is really trying to drive a better understanding of how actually does rilparencel work when it's injected into kidneys? This is of interest to regulators, but it's really not necessary for approval. And as you and your audience, many of your audience may know today, there are lots of examples of drugs that have been approved by regulators without a really defined biological mechanism. But, you know, despite that, that history, we, we think this is a really important story to evolve, and, we've got some new data that's being presented at the ASN this year that's talking a little bit about our product characteristics and the evolution of that story. I actually think that story is going to evolve over time. We'll definitely have some more data in the second half of next year.... likely presenting that at the ASN. Again, that's sort of our target at this point in time. And I think that'll help us sort of explain, at least to, you know, the scientists that we work with and the physicians and the patients, you know, a better understanding of how this works when it's injected into kidneys. But I also consider this to be an evolving story that likely is going to be without an aha moment. It's not going to be one of those days where we wake up, and we say, "We've solved this." It's probably just a story that's going to evolve over time, and we'll have more of that data next year. Perfect. We'll be looking forward to seeing that for sure. So the parenchymal cell technology described, it's being leveraged for diabetic chronic kidney disease. Could you tell us a bit more about the standard of care in that disease and how that might be evolving? Sure. Well, I mean, if you're a patient today, and you've got, you know, unfortunately, you have chronic kidney disease due to your diabetes, you are in a way better place today than you would have been five years ago with regards to your treatment options. And so there's been a real advance in care of patients who have diabetic kidney disease, not just slowing progression, but also treating comorbidities. And some of the classes of drugs that, you know, are now available for patients include, you know, renin-angiotensin system inhibitors. They've been around for fifteen to twenty years, and they were really the mainstay of treatment until twenty twenty-one, when the first SGLT2 inhibitor got approved in the U.S. for, or at least got a label for a kidney indication, and that's expanded to other SGLT2 inhibitors. We have data from finerenone, non-steroidal MRA, and now even more data on GLP-1s all around they're not just renal protection, but also cardiorenal protection, much broader. So if you're a patient, you've got diabetic kidney disease, clearly you should be on one or some of, or both of... one or many of these agents. The guidelines often are a little bit slow to evolve. You know, the data comes first, and then the guideline committees start coming out with their opinions. There's a general feeling that we're living within an era of four pillars of care, and those four different agents that I just talked about. That's great for patients. What does that mean for us? I mean, that's a question that pops up all the time. You've got this evolving landscape. What does that mean for a cell therapy company that's also in this space? We recognize that, A, you know, these agents are either drugs or agents that patients can easily take at home, not as complex as what we have for ProKidney and our cell therapy. We're likely going to be sort of after those agents are tried. We see ourselves in a position where the data will show, the data continues to show that some patients continue to progress. You know, these four pillars of care are not a cure, despite the advancements that have been made. Patients will continue to progress, and we see ourselves in that niche of patients have continued to progress, and now they're at a point where, you know, their providers are talking to them about needing dialysis or needing a transplant, their GFR is often less than 30, so they've lost over 70% of their kidney function. That's where we see, you know, should our phase three program prove itself out, that's where we see as almost like a rescue therapy for those patients, and not only is that important for patients, but providers are telling us that they've got nothing else to offer those patients, so it meets the provider need, too. I think it's really important for payers as well, because payers want to keep people from going on to dialysis, and that's high cost for them. So it does meet the needs of not just patients, but providers and payers as well. And we think there's a real unmet need for patients by focusing on that late-stage chronic kidney disease population. Got it, and you've previously presented some of this data in the CKD setting. I wanted to discuss briefly the phase two trial, RMCL-002. For our audience, could you quickly go over that trial and the design and your insights from there? Yeah. Yeah, happy to. So, the 002 study was a study that was conducted. I think it started in 2016, and the last patient, last visit was at the end of 2023. It was conducted through COVID, right? Which a lot of the data was collected actually during the COVID period and all the challenges that came with that. But in essence, it was a study that looked at patients with type 2 diabetes, with a GFR between 20 and 50 mL/min, and those patients were randomized into two groups. The first group was a group that after they had their kidney biopsy done, and the cells were made in our manufacturing facility, they got injected. The product got shipped back to the site. It was a fresh product, not the frozen product that we're using now. It was a fresh product. It got shipped back to the site, and the initial injection went into the same kidney that was biopsied. And then six months later, a second injection was given in that same biopsied kidney. So that was group one. And then group two was, if you got randomized to group two, you essentially didn't get an injection, you got a biopsy, you made your cells, and you didn't get injected until a year later. And so that was a year of standard of care. All the sites, all the PIs, the investigators were told, "Please treat your patients according to standard of care, good glycemic control, good blood pressure control, renin-angiotensin system management treatment," and there were primarily no SGLT2 inhibitors approved for kidney disease, but they were available for diabetic control, and so some patients got SGLT2 as part of that standard of care, so you had two groups, and those two groups were essentially active treatment or deferred treatment. In the second group, after that 12 months, those patients ended up getting treated, and then we followed them in the same way, and then we followed them over time, so phase two study, here are the takeaways from my perspective, two big takeaways. One is, in the patients who were initially exposed to standard of care and then got treated, in that sort of 12 months of standard of care, there was a decline in their kidney function. What happened then after 12 months, when those patients got injected, that decline in kidney function actually stabilized, and it flattened out over the next 18– 24 months. And so that was a signal to us in this population that there was a potential efficacy signal because we saw that layer of decline and then a flattening of kidney function in those same patients. The other thing that perhaps had the most meaningful impact on us, and it certainly affected how we made a change to our Phase III program, was when we looked at those patients who had the highest risk of kidney failure, their GFR was less than 30, and their UACR, or their albumin excretion, was greater than 300 milligrams per day, highest risk of kidney failure, generally accepted in the literature that these people are at the greatest risk. When we looked at those patients, what we saw was a real clear separation in patients who were treated with rilparencel versus patients who were not treated with rilparencel, sort of that active treatment versus deferred treatment. And then what we also saw, which was impressive, was those patients who got deferred treatment, standard of care, initially. They lost about six mL per minute per year of kidney function, a lot, and then when they got injected with rilparencel, we saw a real stabilization of their kidney function. So to us, that meant, you know, there's something that's working here, and we've got some clinical data to support it. And so those were the two big takeaways from that Phase II study. And then I'll just skip forward. So that data, we saw that data around this time last year. We presented it publicly, I think, around mid-November. We presented final data at a nephrology congress in Europe at the end of May, and we used that data to inform our Phase III program and our Phase III study, a study called RMCL-006. We used that data to narrow the inclusion criteria so that we're more focused on patients with advanced chronic kidney disease. Got it. So it sounds like you saw an efficacy signal. It helped you hone in on a specific subset of patients that you think will have the most benefit, and you've helped use that information design around your phase three. Great summary. Um- You said it a lot more concisely than I did. One thing I do want to touch on that real quick, what, what did you learn on safety and tolerability from that trial? That's a great point. So, we didn't see any serious adverse events related to the drug itself, which was good. What we did see is we saw some serious adverse events related to either the biopsy or the injection. And that wasn't unexpected for us. You know, you're putting a needle into a patient's kidney, someone with advanced kidney disease, and whether it's a biopsy needle or an injection needle with the drug. And so, you know, even with the best training, you're going to see some events happen, mainly local hematomas or local bleeding events. What we did see was the rate of those events is very, very similar to what's been described for kidney biopsies in the literature. In fact, if you take a really critical look at our overall safety profile, of all the patients that have been injected, of all the patients that have been biopsied, our serious adverse event rate is actually a little bit lower than what you'd expect based upon reports from the literature. And I think that just comes with, you know, patients who come into studies are typically a little bit more stable than patients who aren't coming into studies, and also the fact that, you know, we've got a training program that's wrapped around this. And so that training program, I think, also limits the serious adverse events. Got it. Very helpful. Separately, you had another phase two trial, REGEN-007. Could you tell us a bit about that trial design and some of the interim data that you presented on that? Yeah, of course. REGEN-007 is an interesting study for us because it was the first time patients were exposed to our cryopreserved product, which is now being used in our Phase III program. And also the first time where we, as a company, but also the FDA, got comfortable with injecting both kidneys because we had the safety data from our prior experience. So now, instead of just injecting the kidney that was biopsied, in 007, we were injecting patients in the biopsied kidney when the product was available, and then in the contralateral kidney, three months after the initial injection in the first kidney. Not six months, but three months after. So cryopreserved product and that treatment of injecting both kidneys. Now, 007, type 1 and type 2 diabetic patients, so both type 1 and type 2, the GFR was from 20– 50. There was a cap on UACR of 5,000, and again, we learned something from 007. Patients who have, like, really substantial amounts of urine protein loss are less likely to benefit, I think, from almost any treatment. They're certainly a more challenging population, so we capped it at 5,000 milligrams per day, milligrams per gram, and those patients were then randomized into two separate groups, and just to be clear, there was no control group, so this wasn't a randomized controlled trial, this was a randomized trial, and group one is the group that we've got most interest in because it's very similar to our Phase III study. Group One, in essence, patients, if you got randomized to that group, you got a biopsy. We made a product, injected into the biopsied kidney, and three months later, we injected into the other kidney. It's a treatment paradigm, which is the same as our Phase III program. Mm-hmm. If you got randomized to the other group, you actually got a biopsy, and you got a product made. That product was injected into your biopsied kidney, and then we waited. We waited for a trigger, and one of those triggers was either a decrease in GFR to a certain degree or an increase in UACR to a certain degree that was sustained, and then you got a second injection. And so what I can tell you right now is that, you know, everyone's been enrolled. I think we enrolled fifty-three people. We presented interim data, with a focus on group one, because that mirrors our phase three population, but really a focus on group one. We really wanted to see, you know, what was the effect on eGFR after someone had been given two injections and stayed on and had a follow-up for at least twelve months. We were really keen on seeing that follow-up for at least twelve months. Mm-hmm. What we saw in group one was in 13 patients, so, you know, we've talked about this before. Obviously, we're gonna have bigger numbers next year, so this was an interim analysis. We had 13 patients, and what we saw was really a flattening of the eGFR. Again, no control group, so the eGFR change was preserved, we thought, over the course of 15 months, and we're still following those patients, but you know, we asked ourselves, like, you know, there's no control group here. What does this actually mean? We tried our best to find a synthetic control group, an external control group that was outside of the study. We worked with Dr. Nav Tangri, who's an expert in kidney failure risk prediction. He's a globally recognized expert, spends time on a lot of guideline groups, works with hospital systems and other companies, and so Nav was able to find us about 10 patients for every one patient in that group of 13 patients. Mm-hmm. They were matched into a database that he had, which was a database involving patients who were previously recruited into SGLT2 inhibitor trials. Mm-hmm. He came out with about 125 patients who were really well-matched to those 13 patients. What he saw was, over the course of 12 months, those patients, as you'd expect, this high-risk population, they lost about four mL per kidney function, and our patients lost just under one mL per kidney function or thereabout. We saw, at least in a synthetic control group, it gave us even more confidence that we're seeing an efficacy signal with, with patients treated with rilparencel. Gotcha. And, what were the safety and tolerability that you learned from that same interim data? Yeah, I mean, same thing, right? So same kind of picture that, you know, there were some SAEs related to small numbers, related to the injection or the biopsy, but nothing related to the product itself. Got it. And what do you expect to see with the full data? And what's the benchmark for clinical efficacy there? Yeah, I mean, the full data we expect will have full data in the first half of next year, latter part of the first half of next year. We're looking at eGFR and change in kidney function based upon eGFR. And, you know, my hope is that we continue to see, you know, a reasonably flat line with regards to change in kidney function. I don't expect an upswing. I'm also not expecting, you know, a precipitous decline, so I am looking for something that's hopefully around, you know, what you tend to see with just normal kidney function loss in patients- Mm-hmm. As you get older, and that's around one ml per minute per year. That would be, that would be my hope. Got it. Got it. And so with all that being said, I know you briefly touched on the PROACT 1 Phase III trial and some of the trial design, but just a quick recap on what that looks like now and, what the endpoints you're looking at are. That's a Phase III study, as you said. It's focused on patients with type 2 diabetes and a GFR between 20 and 35 mL per minute. We've really narrowed that GFR range to patients with the most advanced kidney disease. We're, you know, expecting the sites to follow standard of care before patients come into the study. The patients are then randomized to receive rilparencel or a sham placebo, right? I'll explain that in just a little bit more detail. The patient's blinded, principal investigator is blinded, the radiologist, the interventional radiologist is not blinded. And if patients are randomized to rilparencel, we make the product after the biopsy, and patients get injected twice in the same way that I just described for the REGEN-007 study. If you're randomized to sham or placebo, then it's really important that we try to protect that blind. So patients actually go to an interventional radiologist, primarily an interventional radiologist. They get a sham biopsy, so as far as the patients are concerned, there's a little nick in the skin, some pressure applied. Procedure takes 20, 30 minutes, so patients actually think they're getting biopsy. And the patients leave, and they're monitored just as if you got a kidney biopsy. Mm-hmm. In eight to twelve weeks, they come back, and they get a sham procedure. This speaks to, and I think in many ways, we've seen this in other disease states, it speaks to the power of placebo. Our regulators see the power of placebo, and that's why they want us to actually sham treat half of our randomized patients. Then just from an endpoint perspective, this is a time to event point study, and it's time to cardiovascular death, renal death, dialysis or transplant, or a greater than 40% decline in eGFR. Those are, you know, accepted, commonly accepted composite endpoints, and that's how the study is designed from an endpoint perspective, time to event point. So we anticipate we're gonna need somewhere between six hundred and seven hundred subjects enrolled, and our goal right now is six hundred and eighty-five, but again, it's time to event, so that might change- Mm. Based upon the events and the event rate that we actually see. Got it. And I guess just to quickly summarize all the learnings from the previous phase twos, there's the cryo product now versus the fresh product. You are now injecting both kidneys- Correct. instead of just one, and the injections are three months apart instead of six, correct? Correct, and we've narrowed the population, so that we've got patients with even more advanced kidney disease that we're enrolling in the study. Got it. Perfect. Now, with PROACT 1, as you touched on briefly, there were some protocol amendments. Could you explain what those changes were and why they were made? Yeah, so we made those changes in the first quarter of this year, and we submitted to the FDA, I think, in April, and received IRB approval in March. Mm-hmm. We actually enrolled patients under this version of the protocol starting in, I think it was starting in May or early June. We continue to make some progress on enrollment. Mm. The reason for the change was primarily around limiting that eGFR criteria, learning from our phase two study, but we also took advantage of, if we're gonna go in and change the protocol, we took advantage of a lot of other things just to make the protocol easier, easier to understand, easier to execute. Just some good housecleaning, I would say, that you'd normally do. Mm-hmm ... if you're going in and changing your protocol. Got it. I know you mentioned briefly, both in the press release and in today's call, that the goal for the Phase III is disease stabilization. In this context, does that mean like zero milliliters per minute lost annually? Is that the target? So no. You know, the target is to keep people off dialysis or to keep them alive without being on dialysis. So that's really the target of the study. Now, the actual change in kidney function as measured by eGFR, that's a secondary endpoint. We will look at that, and you know, we hope to see that we stabilize the kidney function. That doesn't mean zero, but it means doing a better job at preserving that kidney function for a longer period of time. And that might be a loss of, you know, one ml per minute per year, for example, but I think the more meaningful thing there would be if we could demonstrate that we can keep people off dialysis or alive longer and not end up on dialysis. Got you. Got you. So delaying dialysis and trying to keep that as long as possible. Right. With that in mind, what kind of durability do you hope to see with the PROACT 1 results? Yeah, we're not changing the underlying cause of a patient's kidney disease. So if you're a diabetic patient, and you've got, let's say, poorly controlled high blood pressure, we're fundamentally not changing that. So we don't think we're actually gonna cure someone's kidney disease. But what we're hoping to see is that we see, with our treatment, an effect that is, you know, eighteen to twenty-four months in duration, and some patients may eventually... we need to understand this. Some patients may eventually need to get an additional dose down the road if we see a change in their kidney function. That's not part of the study. We're actually trying to understand, in this study, what the duration of treatment effect is. Mm-hmm. And I'm assuming there's gonna be an open label extension period after to just track patients going on? We don't have that built in yet, but that's certainly something that we've been talking about, and we'll be engaging with the FDA on that to do something like that in the future, I hope. Got it. And, how do you expect clinicians and patients to view these results? What are they normally looking for when they speak with their doctor? I think, so if you're a nephrologist, I'm a nephrologist. I haven't been in practice for a while, but I certainly remember seeing a lot of my patients with a GFR less than thirty and talking to them about, you know, the options, which are limited and typically involve what type of dialysis do you want to have, these are the benefits of different choices, or, you know, do you have a relative who might be able to donate a kidney? Those are the discussions that will continue to happen, but we're hoping to limit those discussions by providing another option for patients. And then from a patient perspective, you know, I'm always a little bit hesitant to talk about, you know, how patients feel about things, but I would say, because that lived experience is just so important. But I will say that an eGFR number is less meaningful to patients than avoiding dialysis. I mean, dialysis itself has just an enormous impact on a patient's life, and it's not just the patient, but it's their caregivers, and it's their extended family, and it has implications on how they feel, what they do every day. You know, can they continue to work? Can they continue to study? Mm-hmm. Some families go bankrupt because of the copays. Right. I mean, it really does have a substantial, significant impact on, on patients' lives, and we'd like to be part of that solution. When might we get data readouts on this PROACT 1 trial, and what will be communicated when that data comes out? We expect top-line readout in 2027. That's what we're working on right now. Mm-hmm. So that top-line readout involves primarily the primary efficacy endpoint, which is the composite endpoint. Then that would form part of our overall submission to the FDA. We don't, you know, we don't think, as I think we've made public recently, we don't think we need two studies for approval. We feel very confident that one study with this composite endpoint is sufficient for traditional approval as a cell therapy. We have ongoing discussions with the FDA on other options that we're entertaining as well that we'll probably communicate at some point later this year or early next year. Got it. So top-line data in 2027. And, just one quick question on that. Will there be any interim data? So, not today. So based upon what we've communicated so far, is that we're actually not doing an interim analysis for efficacy, and there's a- Mm. ... there's a reason for that. If you think about the composite endpoint, if we do an interim analysis on the composite endpoint, we actually do burn alpha, so that affects our overall alpha in the study. It also, we'd have to do that interim efficacy analysis when we have at least some confidence that we'd see a differential effect of treatment versus placebo. And if our desired number of events, for example, I'll just round off, our desired number of events for the effect that we expect would be an overall number of events of, let's say, a hundred and twenty events in the study. We would want to do that interim analysis at, you know, sixty events or seventy events or eighty events. So having some degree of like comfort that if there is an effect, we're gonna see it after those number of events. If you then ask yourself, okay, if we waited until 70 events, for example, where are we in a study execution perspective? Well, by that point in time, we'd have enrolled everyone in the study. Mm-hmm. and we'd probably be six months away from having the total number of events that we would want to see. So just from a timing perspective and the alpha spend in doing the analysis, it just didn't make sense. Gotcha. So that's- Okay. That's where we are today. Mm-hmm. And is the same true for a futility analysis? No, it's not. It's not really. I mean, we could do a futility analysis earlier if we wanted to, but as you know, anytime you do this, if you do a futility analysis even earlier, then you're risking walking away from a product that's potentially beneficial. Mm-hmm. And that's not something we wanna do, just given what we've seen in our phase two data. Got it. And you touched on this briefly, but I just wanna get a little more context. So previously, you were running two Phase III trials, but you discontinued one of them. Can you compare the two Phase III trials and how you came about the decision to discontinue? Sure. So, I mean, the two phase three studies were actually very similar. The RMCL-006 study, which we're continuing, is primarily conducted at U.S. sites, and the RMCL-016 study, which we stopped, was primarily being conducted outside the U.S. They were really similar. There were some minor differences in inclusion criteria, but honestly, for all intents and purposes, I'd say they were pretty similar. We decided to stop RMCL-016 and made that announcement, I think it was in August or early September. The reason why we made that, I'd say part of it is related to just the reset of the company. I mean, as you know, I started at ProKidney last year. I started in the CEO seat in November, and we went through a lot of changes, you know, at the leadership level. We paused manufacturing to get us into a more GMP-compliant position. We amended the clinical study protocol after we paused the clinical study. I think that positions us way better off in the future. And then, you know, the other big strategic decision was stopping RMCL-016. Mm-hmm. And that came about really around some internal discussions we had starting in April, May, around, okay, you know, we have an RMAT designation. Are we really using it to its benefit? And it felt to me and some others that, look, we're really following more of a traditional path forward, despite CBER, you know, showing to other companies a substantial degree of flexibility in how they think about clinical study design. So we talked to, you know, our regulatory team internally. Obviously, we're part of these discussions. We talked to some external experts. Personally, I talked to a lot of people who had worked with CBER, and talked to other external regulatory experts, and really came to a lot of confidence in saying that we didn't, we didn't need two studies. We ended up stopping RMCL-016, based upon that internal and external assessment and our knowledge of CBER and some of the decisions they've made over the last couple of years. That was obviously a big decision for us because it allowed us to focus on one study. It also saves us somewhere between $150 and $175 million, which pushes out our cash runway into 2027. That wasn't the purpose, but that's, that was a really nice side effect, if you like, of stopping the study. We've got engagements with the FDA, and we will communicate as appropriate, probably sometime this year on how those interactions are going with the FDA. Got it. So just to be super clear on our end, have you already heard regulatory feedback on this strategy? We haven't disclosed that yet, and we'll communicate that sometime this year. Got it. And, I guess any other potential interactions, regulatory bodies going forward, one, should we expect communication? And two, if so, what channel should we potentially anticipate that through? Yeah, I think, you know, we'll. So first, I'll just take a step back. You know, we do have the RMAT designation, and as you know, that RMAT designation does give us some benefits. You know, it gives us an accelerated development and review process. All the benefits, essentially, of the fast track approval process, the priority review as well. But I think in some ways, even more importantly, it allows us to have ongoing collaborative interactions with the FDA and the review team. And so to me, that relationship that we develop, that collaboration we develop with the FDA review team is critical. I can say that is positive, really positive, and we will interact with them around CMC moving forward into next year, and some other things that we have planned around the study design and study analysis and things like that. Got it. Got it. And, you touched on the RMAT designation already. Another thing that you've mentioned is an accelerated approval approach for rilparencel itself. Could you tell us about your thoughts on that and what gives you confidence in this approach? All I'll say on that approach is that by having RMAT, it allows us to take advantage of an accelerated approval pathway. Right now, what we've communicated publicly as of today is that we're doing one study, and we think that one study, if our composite endpoint is positive, will allow us to get full approval. That's where we are today. We are working with the FDA to determine what that accelerated pathway will look like. Nothing to share today, but we'll share some things in the future. Okay. Well, we will be anxiously awaiting to hear the updates. So I guess stepping back and looking a bit more broadly at other cell therapies and the regulatory experience there so far, we've seen other companies struggle with some CMC issues in the past, and you briefly touched on that with some of the mechanism discussion earlier. What strategies will ProKidney use to ensure there's no CMC or quality issues? I think it's all around mitigating our risk. Like, I don't think I could stand here and say, we're going to ensure that there's no issues, but I'll tell you some things that we've done. We're being proactive. As you know, we stopped manufacturing last year, so we really moved our facility from operating like an R&D phase II facility to really being GMP compliant from a phase III program. Mm-hmm. And so that operational compliance is very close to commercial compliance from a GMP perspective. So we definitely used that pause to put us in a much better position from a GMP compliance perspective. And then, more broadly speaking, around CMC, obviously the FDA is very interested in this for cell therapies and gene therapies. Mm-hmm. And we're learning with them, but to our advantage is they have put out a guidance document to help sponsors, right? So we definitely understand that guidance document. We have this collaboration with the FDA, and we'll be talking to them about our CMC plans in the new year, in 2025. And we hired a new head of technical operations six months ago. And Dr. Ulrich Ernst led technical operations at Iovance and took Iovance through their CMC complicated CMC process. But we also, so that means we have got that sort of, that internal knowledge of a leader who's already done this. Mm-hmm. Even though that was a complicated process, second time around, and all the learnings that Ulrich had during that process, he brings to ProKidney. Got it. Got it. And I'm sure he'll have a lot of very helpful advice and tips going forward. So we're looking forward to having him on the team as well. Well, I guess just in our last few minutes here, as we come up to time, what catalysts can we expect over the next 12-18 months, and what should excite investors going forward for the rest of 2024 and 2025? So, I mean, I think what we've said is, evolving story of mechanism of action. Probably no aha moment, but we're going to keep telling that story and evolve that story. Final results of REGEN-007, you know, our phase programs, that's coming up next year. And then, you know, obviously, if we have any regulatory updates, then, depending upon the importance of that update, that could also be seen as a catalyst. Got it. Well, thank you so much for taking time to walk us through the ProKidney story and share some of your previous data and experiences and some of the exciting catalysts coming up. Is there anything else that you think we should have touched on that we didn't? No, I mean, forty-five minutes, I think this was a great, great Q&A. Thank you for the great questions. Also, just being part of, you know, this event, Organ Restoration Day, I think that's what you're calling it. So just being part of this event today, thanks for the invitation. Absolutely. Yeah, it's an exciting space, and we're very happy to have you.