Greetings. Welcome to the ProKidney Corporate Update Call. At this time, all participants are in listen-only mode. A Q&A session will follow the formal presentation. If anybody should require operator assistance during the conference, please press star zero from your telephone keypad. As a reminder, this conference is being recorded. At this time, it is now my pleasure to introduce your host, Ethan Holdaway, Senior Director of Corporate Development and Investor Relations. Please go ahead, sir. Thank you, Operator. Good morning, everyone, and welcome to ProKidney's Corporate Update Conference Call. Earlier this morning, we issued a press release that provided interim REGEN-007 phase II trial results and several clinical and operational updates. Today's presentation is now available on the Investor section of our website, and a replay of the call will be available approximately one hour after completion. Joining me today are ProKidney's CEO, Dr. Bruce Culleton, our CFO, James Coulston, and our Chief Business Officer, Nikhil Pereira-Kamath. Following the presentation, we will open the call for questions. Before we begin, I'd like to remind everyone that we will be making forward-looking statements during the presentation today. I encourage you to refer to the most recent SEC filings regarding risk factors associated with these statements. I would now like to turn it over to ProKidney's CEO, Dr. Bruce Culleton. Bruce? Thanks, Ethan. Good morning, everyone. Today, it's my absolute pleasure to present exciting interim data from the phase II REGEN-007 clinical study and several important operational updates. But first, let me tell you a little bit about ProKidney and ProKidney's clinical study program. Our company's goal is to preserve kidney function and have a meaningful impact on the lives of patients with advanced chronic kidney disease. Our product is Rilparencel, also known as REACT. It is a proprietary autologous cell therapy that is generated from a patient's own kidney cells. The patient's cells are harvested via traditional biopsy and expanded in our manufacturing facility. These expanded cells are then cryopreserved ahead of being injected into the patient's renal cortex via a percutaneous outpatient procedure. We have an experienced leadership team with several new faces leading critical functions, as we have announced recently, and we have made substantial progress in the last six months, which we are happy to share with you today. Let's take a step back and review why Rilparencel could be very special. As you can see, chronic kidney disease is a significant problem. While one in seven adult Americans have some degree of CKD, there are more than three million Americans who have type 2 diabetes and advanced stage 3B and 4 CKD. Treatment options for these patients have improved over the last 5 years, but no therapy currently provides long-term preservation of kidney function, and treated patients continue to develop kidney failure. Within this large population, I'd note that more than 135,000 CKD patients in the U.S. continue to progress to dialysis every year. There is a substantial opportunity with REACT®, as we believe we can preserve kidney function to delay or eliminate time on dialysis. REACT® is different than other small molecules in biologics, and we'll walk through new clinical data this morning that will show why we believe REACT® may be able to preserve kidney function and possibly provide greater benefit in high-risk CKD patients. The new data being released today complements the recently announced phase II 002 study results that was presented as a late-breaking clinical trial at the 61st Scientific Congress of the European Renal Association. REACT®'s clinical study program is robust, as highlighted in this chart. We've previously published data showing REACT®'s potential to delay dialysis from the phase II 003 study of patients with stage 4 and 5 CKD. This, combined with preclinical data and interim data from Study 002, we initiated our pivotal phase III program, the PROACT 1 and PROACT 2 randomized controlled trials. As just mentioned, we recently presented final results from the 002 study, where a strong efficacy signal in a subgroup of patients with the highest risk of kidney failure was observed. This data helped inform the decision to amend the PROACT 1 study protocol. Today, we'll be focusing on interim data from our REGEN-007 study. As you can see from the images on the slide, the 007 study uses a cryopreserved REACT cell product, and injections are performed in both the biopsied kidney and the contralateral kidney, thus replicating the approach in our phase III program. Now, before discussing the study results, we are delighted to give you an update on manufacturing and the phase III clinical program. In November of last year, we announced a pause in our manufacturing to address an audit of our manufacturing facility. Importantly, this pause was not due to a clinical safety event. The audit was performed by our contracted qualified person to evaluate our readiness for release and distribution of Rilparencel to the E.U. Certain deficiencies in the documentation of the quality management systems, including improvements and validation of GMP systems, had to be addressed prior to release and distribution to E.U. clinical sites. During this pause, we optimized or improved many of our capabilities to meet E.U. and global standards for our phase III program and future commercial manufacturing. Effective June 1st, we restarted manufacturing under GMP. We've also been closely working with the E.U. QP auditor, and we anticipate QP declaration of equivalence to E.U. good manufacturing practices by the end of this month. This has allowed us to resume the phase III clinical study program. For PROACT 1 study, an amendment was filed with the FDA in March to enrich the study with more late stage 3B and stage 4 CKD patients. Central IRB approval for this amendment has been received, and sites are now open for enrollment. Just last week, patients were screened under this amended protocol. Sites have also been activated in Europe in anticipation of receipt of QP declaration of equivalence to E.U. GMPs. I cannot be more proud of our internal teams that have delivered ahead of schedule on these critical milestones. We are now advancing our clinical plan. Enrollment is complete in REGEN-007, and you will see interim results today. Additional time is required to allow this data to mature. We expect to present mature data publicly in the first half of 2025. With the resumption of our phase III studies, we are now focused on accelerating recruitment in those studies. Before I share the 007 interim results with you, for background and context, let me share with you a framework for the classification of chronic kidney disease. The foundation of this work started over 20 years ago by the National Kidney Foundation. For the first time, this work provided standard definitions for CKD and an approach to risk stratification. This general approach is now used globally and accepted by guideline committees around the world. If you look at this heat map, the rows represent kidney function, and the columns represent kidney injury. Together, they predict the risk of kidney failure, as shown in the different colors. As a company focused in the highest risk area, patients who have moderate to high kidney injury and moderate to severe decrease in their kidney function, that's our focus. This is where we believe we are distinctly different from many small molecules and where biologics may operate, as shown here with the dashed oval lines. Today, clinical priorities for patients with CKD stage 4 are largely focused on treating comorbidities such as anemia or abnormalities in mineral metabolism and preparing patients for dialysis or transplantation. We also know that payers acknowledge a specific pain point with stage 4 CKD. They know these patients have the highest risk to progress to kidney failure and the need for dialysis. As I stated earlier, this is a goal for ProKidney to reduce or eliminate time on dialysis, which is life-altering for patients and their care partners and costs commercial payers between $110,000 to $240,000 per patient per year for total cost of care. To further support our focus on these high-risk patients, we took a look at several landmark CKD studies that have been published over the last several years, including the FLOW study main results, which were released at the end of May. Here's a selection of them. Of note, three papers involved interventions using SGLT2 inhibitors, all published in the New England Journal of Medicine. There's a paper using selective MRA, as well as the FLOW study, which investigated semaglutide, a GLP-1, in patients with diabetic CKD. As you can see in all these landmark papers, there was little focus on patients in stage 4 CKD. That's our focus. We believe there's an unmet medical need in this population despite the recent advances in CKD therapy. Going into more detail on one of these published studies, specifically the study that looked at the SGLT2 inhibitor dapagliflozin versus placebo that was published several years ago in the New England Journal of Medicine. There are three key points here that I want to draw your attention to. The first, although these new SGLT2 inhibitors are a big step forward, patients still lose kidney function. This is shown on the left panel of this slide, which looks at change in estimated glomerular filtration rate over time. This is also the same efficacy measure in our phase II study that I'll present today. In this panel, here you see the DAPA-treated patients losing approximately 4.5 mL per minute in eGFR by 12 months and 5.5 mL per minute by month 18. We have another slide in the appendix that shows similar results in two of the other SGLT2 inhibitor landmark trials. A second point is that even after two years, there's only a very small difference in eGFR between patients treated with DAPA and placebo, less than one mL per minute per year. Not shown here, but I'd also like to point out that the difference in decline in eGFR is approximately one mL difference per year in the FLOW study of semaglutide versus placebo. The third point, as shown on the right panel, is the fact that patients who are treated with SGLT2 inhibitors or ACE inhibitors or angiotensin receptor blockers or GLP-1s for that matter, a substantial residual risk remains despite the intervention. While the blue line in the right panel shows that DAPA reduces those events versus placebo, it's important to recognize that these patients on DAPA still had events, still ended up on dialysis, and still succumbed to their disease. In fact, 19 patients need to be treated with DAPA to prevent one primary outcome event, highlighting the fact that there remains a residual risk, a big unmet need in this population, and a gap that we believe we can fill. Now that we've clearly articulated the background and the opportunity for ProKidney, let's walk through the latest update on our phase II REGEN-007 clinical trial. Let me take you through the design of REGEN-007, a phase II study. The study began in 2021 and completed enrollment in Q2 of 2023. Patients with CKD caused by diabetes were randomized after kidney biopsy to one of two treatment groups. Group one replicates our phase III clinical program dosing regimen. Initial injection of cryopreserved product into the biopsied kidney and the second injection three months later in the contralateral kidney. The study is designed for follow-up visits every three months out to 18 months following the second injection. Group two followed an exploratory dosing regimen in which the second dose was provided only after a physiological trigger was hit. In this case, either a sustained decline in eGFR more than 20% from baseline or a sustained increase in urine albumin excretion of more than 30% from baseline. The focus today is Group one because we believe this treatment schedule gives us an early window into our phase III clinical study program. We will not spend time on Group two today, but I will say that 25 patients received one injection in this group, and 12 patients received the second injection anywhere from 5 to 15 months after the first. Nine of these second injections followed the UACR trigger, and three followed the eGFR trigger. Although this data is also maturing, it does appear that we shouldn't wait this long for patients to receive the second injection. This data supports our prior decision to schedule a second injection three months after the first injection, as we have done in our phase III clinical study program. As we've stated over the last six months, the primary reason for this interim analysis is to assess efficacy in Group one patients who've had 12 months follow-up after their second injection. We wanted to have a high degree of confidence in this analysis, so we waited until at least 10 participants met this criterion. We also assess safety in all subjects that received at least one injection. Here's a description of the flow of subjects in Group one to get our reasonably mature data set for our primary interim analysis. 26 subjects in Group one were biopsied. Two biopsies had insufficient cellular material, and these subjects didn't continue in the study. 24 subjects had an initial injection with Rilparencel, and 23 subjects had a second injection, with one subject developing a bleeding risk and contraindication prior to the second injection. Of the 23 subjects that received two injections, one subject has died from a cardiovascular cause that was unrelated to Rilparencel or the procedures. As of today, we have only this one early termination in Group one, which provides us even more confidence in the data. 13 subjects have completed at least 12 months follow-up after the second injection. These subjects are the focus of the analysis today. Of note, we anticipate that nine more subjects in this group will have 12 months follow-up after the second injection in the coming 12 months. We will continue to follow all of these subjects for 18 months after their second injection. The characteristics and demographics of the study population are presented on this slide. Data from all 13 subjects are shown in the middle column. In the right column, data from 10 subjects who met key eGFR and UACR inclusion criteria from our phase III program are shown. Please note, these 10 participants are a subset of the 13. The average baseline eGFR was approximately 30 mL per minute in the 13 subjects and somewhat lower in the 10 subjects meeting the phase III inclusion criteria. Urine albumin excretion was also a little worse in these 10 subjects. Of note, less than one-third of subjects were using SGLT2 inhibitors at baseline, which reflects the slow adoption of these drugs in patients with advanced CKD in the 2021-2022 timeframe. Six patients were treated with a GLP-1 at baseline. three of these patients stopped taking this therapy within four months of the first injection. REGEN-007 had no within-study control arm. To help contextualize the results, we looked at published data from recent landmark trials, as we presented earlier. In these reports, average eGFR declined from 3 mL to 6 mL per minute per year for the first year in the active treatment groups and placebo-treated patients. It varied study by study and by study population. So we also explored how kidney function would change in matched controls of these 13 subjects in this analysis. In partnership with Dr. Navdeep Tangri, these 13 subjects, one by one, were matched approximately 10:1 with diabetic patients from recent CKD landmark trials. Dr. Tangri and team matched each of the 13 subjects with control subjects using overall kidney failure risk for matching criteria and SGLT2 inhibitor use. On this slide, we provide additional information on Dr. Tangri and the ClinRisk founding team. As you can see, Dr. Tangri is a global leader in risk prediction within the kidney space. The analysis of the data by ClinRisk was independent of ProKidney. Here are the results of the matched analysis. 125 similar subjects from prior landmark studies were identified. 12-month decline in eGFR was 4 mL per minute, and 18-month decline was just greater than six. This triangulates nicely with historical published data in diabetic patients with CKD. Please keep -4 and -6 in mind as we present the REGEN-007 data. On this slide, we show the main efficacy results of the interim analysis of REGEN-007. The top panel shows the average eGFR change from baseline, and the bottom panel shows average eGFR at each time point. Month 0 is at first injection. Month 15 is 12 months after the second injection. We also have 3 months of additional follow-up in 12 subjects that we are showing here as well. This takes the data out to 18 months after first injection. As you see, the average decline in baseline with 18 months of follow-up was -1.3 mL per minute. As a reminder, in the matched control analysis, the 18-month change was -6.2. The lower panel here tells the same story, and the curves are almost superimposable. We believe this data reflects the potential to preserve GFR in patients with diabetic CKD-treated patients with Rilparencel. This slide is presented in a similar way to the last, but now for the subset of 10 subjects that would have met the eGFR and UACR inclusion criteria in our phase III program. Numerically, the average eGFR change from baseline is less in these 10 subjects than the full 13-subject analysis. But really, this tells a similar story and is one reason why we feel confident in our phase III program. As you can see, the average eGFR change from baseline in these 10 subjects at 18 months since the first injection was 0.6 mL per minute. This level of decline in kidney function over this time period is similar to what one would expect as part of the normal aging process in older adults. For full transparency on this slide, we show results for all the subjects in Group one that received at least one injection. This shows average eGFR change from baseline in all subjects in the top panel and phase III eligible subjects in the bottom panel. Please note the declining number of subjects over time. This is due to subjects that continue to be followed up as they progress through the study. The number of early study terminations has been limited to one subject who died of a cardiovascular event four months after their first injection. Although this data is immature, we're not seeing anything to make us believe our overall assessment will change. Finally, here we present a summary of the serious adverse events as of May 2024. All subjects biopsied and injected are shown here. These results are consistent with their existing safety profile and are similar, if not better, than kidney biopsy safety reports in the literature. In summary, in Group one participants who had at least 12 months follow-up after a second Rilparencel injection, kidney function was preserved for 18 months. Similar results were observed in participants who were evaluated under phase III inclusion criteria. Our bilateral dosing of cryopreserved product showed safety profile consistent with prior studies and comparable to a kidney biopsy. We look forward to providing full results in the first half of 2025. I'd now like to hand this back to the operator. Thank you. Thank you. We'll now be conducting a Q&A session. If you'd like to ask a question at this time, please press Star 1 from your telephone keypad, and a confirmation tone will indicate your line is in the question queue. You may press Star 2 if you'd like to withdraw your question from the queue. For participants that are using speaker equipment, it may be necessary to pick up your handset before pressing the Star keys. One moment, please, while we poll for questions. Thank you. Thank you. Our first question is from the line of Justin Zelin with BTIG. Please proceed with your questions. Hi, team. Congrats on the very impressive results here. It's great to see stabilization after 18 months. Just was wondering about the phase III PROACT studies. How should we think about the control arm performance here among the patients? Is there any good data to look towards, and when might you look to see separation of curves in those studies? Thanks for your question, Justin, and your comments. In the phase III program, our primary composite event is time to onset of sustained dialysis, kidney transplantation, renal or cardiovascular death, or a greater than 40% decline in eGFR. So obviously, in 007, we looked at a decline in eGFR, which we are very happy with our results in this study. Certainly, if these results are to continue into our phase III program, then we expect this benefit on decline in eGFR to have a direct impact on several components of our primary composite endpoint, including time to dialysis, time to transplant, and the 40% drop in eGFR. Justin, this certainly gives us a lot more confidence that we will hit our predefined hazard ratio for Rilparencel versus our placebo group. So it certainly gives us a lot more confidence, and I think de-risks the overall phase III program. That makes a lot of sense to me. And if I could just ask about the patient that experienced in the study that unfortunate event, could you just elaborate just why you think it was not related to treatment? Yeah. We obviously went back and looked over that data, Justin, and so did the primary investigator at the site. And the cardiac event occurred a month after the second injection, four months after the first injection, and we couldn't see any direct relationship with our therapy or with the procedures. I would like to point out that cardiovascular disease in patients with diabetes and chronic kidney disease is a very substantial problem, and the risk of cardiovascular events is compounded even more when you combine both diabetes and chronic kidney disease. Great. Thanks for taking my questions and congrats again. Thanks, Justin. Our next questions are from the line of Jonathan Miller with Evercore ISI. Please proceed with your questions. Hi, guys. Thanks for taking my question, and congrats on getting to this date. It's a really important milestone. I'd love to follow up on that question about the phase III. Obviously, we've seen a lot of results recently from GLP-1s, from SGLT2s that are not fully reflective in this patient population. You mentioned slow adoption of those in recent years. But what are your expectations for background GLP-1 and SGLT2 treatment in the phase III populations, especially ProAct 1 enrolling in the U.S.? So John, thanks for the questions. So we do expect a greater background use of GLP-1s and SGLT2s in this population, despite the fact that we're studying a more advanced CKD population where some of these agents have yet to be indicated. We understand that that's probably going to reduce the overall underlying risk in both the placebo and the intervention group. Now, when we consider that and we go back through all the data that we could possibly scrub to understand what the underlying baseline risk is, we still think the event rate is going to be high. We still have, I think our assumption is around 13 events per 100 patient years being treated. So we expect that's still going to remain high, largely driven by some of the residual risk despite the background advances in therapy. Certainly on our mind, John, certainly something we've dug into, and we think we're in a good place and perhaps an even better place looking at this data. That makes sense. And I know the focus today, obviously, is on Group one, but for Group two in 007 that you didn't show, one injection clearly didn't prevent decline entirely, given that there are nine patients still getting a second shot. But qualitatively, can you at least say that the slope of the eGFR decline in that Group two is less than that negative four to six from the historical controls that you were citing? Yeah. So John, just for your information, we have added an analysis of the Group two data in the appendix of the submitted 8-K deck that's on our website. What I can say about that is that in patients who got one injection, their change in eGFR seems to be somewhat in between those that got two injections in Group one and what we'd expect from a placebo. So it seems to be somewhat in between. But it's also obvious when we look at that data that there's really no need to wait for that physiological trigger. It seems like we're on track with regards to our treatment schedule in our phase III program. That makes sense. Then maybe just one final one. Obviously, this is something that you've talked about in the past. Could you just remind us, when we look at the SGLT2 trials, what's driving the immediate drop in eGFR in the first measured period? Obviously, we see an immediate drop, and then it looks like the slope moderates in the SGLT2s. What's driving that initial drop? Yeah. I know there's more detail behind what I'm going to say, John, but I think it's similar to renin-angiotensin system agents too, where there's a hemodynamic effect that has almost like an immediate perfusion, creates an immediate decrease in perfusion within the glomeruli. That leads to an early drop, but a protective impact over time. That's my understanding. Yeah. Makes sense. Okay. Thank you very much. Our next questions are from the line of Kelly Shi with Jefferies. Please proceed with your questions. Hi. This is Claire on for Kelly. Thanks for taking my question. So just looking at the eGFR curve, the curve starts trending up at 15 months and back down at 18 months, and it says it's influenced by one patient that recovered measurements at months 15. Could you provide more color on this patient, and have you done any analysis on what the curve might look like without that patient? Thank you. Yeah. Hey, Claire. Thanks for your questions. So we were obviously also interested in this time point when we first saw the analysis. And when we dug into the data, it was driven by one patient who had a substantial variability in his eGFR around that time, an abrupt decrease in his eGFR, and then an increase in the following months. And given the small sample size, these outliers have more of an impact on summary estimates, like the average change in eGFR. It's not uncommon in patients with kidney disease and diabetes, but kidney disease in particular, to have abnormalities of their left ventricular function. And when this happens, should that left ventricular dysfunction worsen, then that has a direct impact on the kidneys because the kidneys rely upon the heart for perfusion. This is something that you see clinically on a pretty routine basis, at least in subspecialty clinics where a lot of these patients are followed. It's really related to heart function and kidney perfusion that drives quite substantial, at times, variability in kidney function. Okay. Got it. Just a quick follow-up. As you start resuming phase III, ProAct 1 and 2 study, would you expect an increased number of patients who are GLP-1 experienced? And also, do you allow GLP-1 use along with the REACT cell therapy treatment? Just kind of want to get your thoughts on whether the outcome might be confounded by the concurrent GLP-1 use? Yeah. So first, on that second question, Claire, we did look at the impact of GLP-1s on our data, and we saw no clear evidence that our results were impacted by GLP-1s. We also, as I think I noted in my comments, of the six patients who were on baseline GLP-1s in our data set, three of them actually stopped taking the GLP-1 within four months of starting their first injection. So we don't think it really played any role in the long-term benefit that we reported here. I will say as well that that discontinuation is also something that I think we all see with GLP-1s and may be related to side effects or market access issues or even potentially the patient doesn't feel like they need them anymore. With regards to our phase III program on GLP-1s, we do not have a stratification system in place for GLP-1s. We do have that in place for SGLT2 inhibitors because SGLT2 inhibitors are now part of standard of care and are in clinical practice guidelines and also have an approved indication for this. Now, with the FLOW study coming out, I'm not sure where the indication for kidney disease will actually land because the use of standard of care in the FLOW study was pretty low from an SGLT2 inhibitor perspective. In fact, in the FLOW study, I think only 13% of all participants were taking an SGLT2 inhibitor. So I would say, Claire, for us, we're going to keep a close eye on this in our phase III program. If we see anything trending in an unusual way with regards to, A, a discrepancy between the two groups and how they're being treated with GLP-1s or early prescriptions of GLP-1s before patients get entered into the study, then we're definitely going to keep an eye on that, and if needed, we'll make the appropriate changes. Thanks for the question. Got it. Got it. That's super helpful. Congrats again on the results. Thank you. Thank you. Our next question is from the line of Yigal Nochomovitz with Citigroup. Please proceed with your questions. Hi, Bruce and Tim. Congrats on the data. I just had a question on the synthetic control that you constructed with the ClinRisk group and Dr. Tangri. Could you just talk a little bit more about the validation of that approach and where else that has been used to construct these types of synthetic controls? Thanks. Sure. Thanks, Yigal. I think we talked about internally how best to approach this, and we had some thoughts around propensity matching with real-world evidence. And at the end of the day, we felt it was important if we could match against patients who are enrolled in clinical studies, partly because it sort of raises our comparison, if you like, to a higher bar. We know that patients do better even on placebo when enrolled in clinical studies. So we did want that sort of higher bar for comparison. At the end of the day, after talking to Dr. Tangri, rather than a propensity match, we felt the best approach was using the kidney failure risk equation, which obviously he's validated now for several years across, I think, across over a million patients, the KFRE. So we felt that this was a better approach. Now, the specific analysis that we did, obviously, is not an analysis that we would specifically validate it, but I will say the KFRE itself is an algorithm that has been validated around the world in millions of patients with different types of kidney disease and different ethnic backgrounds. Okay. Got it. And then just a couple on manufacturing. You didn't spend a lot of time talking about doses. Did all these patients in the Part one receive the same dose within the manufacturing specs, or was there some variability between the first and the second one? I just talked about dosing for a second. Patients are dosed based upon their kidney size, and their kidney volume is calculated using an MRI. The bigger the kidney, the more cells we think we can accommodate as part of the injection. I'm not aware of any difference in dose between injection one and injection two. Certainly, there was no protocol-driven reason for a difference in dose between injection one and injection two. Okay. And then just one clarifying question regarding the audit of the manufacturing you mentioned for release for the E.U. Just wanted to clarify. Did you mean deficiencies in the GMP system's documentation or actually in the GMP systems themselves? It wasn't clear. Thanks. Oh, I'm sorry. So from our perspective, if you don't have the documentation, then that obviously raises questions around your GMP system. But a lot of this was really driven by our documentation. Almost all of it was driven by our documentation, quite frankly. It had nothing to do with the processing of the cells. So it was things like having our standard operating procedures written and updated. It was validating our computer systems that we're using for batch release and batch tracking during the product development. It was environmental testing that we'd been doing but hadn't been doing it in a true validated test manner. So it was all of these things that we've the undertaking, I would say, was pretty enormous, and the team involved really collaborated cross-functionally in a way that I had not seen before. I'm so proud of what they accomplished in such a short period of time. Okay. Thank you. You're welcome. Thank you. Our next question is from the line of Judith Romer with Morgan Stanley. Please proceed with your questions. Yeah. Hi. Thanks for taking the question, and congrats as well on the update here. Most of my questions have been asked, but I just wanted to follow up. Obviously, it's a small number of patients. In the patients that did stop GLP-1s, I think you said within four months of the first injection, what was the decision-making process there? Was there any input from investigators? Was that a patient decision with potentially one of their own physicians? How did that go? I guess, how much information do you have around those decisions? I have very little information. I'm sorry. It's only speculative from my perspective on what may have led to the stopping of the GLP-1s in those patients. It would have been something that the patient and probably their own nephrologist or some other provider would have made that decision. It wasn't something that we drove as a sponsor. Okay. That's helpful. Thank you. Yeah. Yeah. Thank you. The next question is from the line of Jason Gerberry with Bank of America. Please proceed with your questions. Hey, guys. Thanks for taking my questions. 2 for me. Just going back on a previous question that was asked about the single patient outlier in group one at months 15, 18. Just wanted to confirm. So when you take that patient out of the analysis, you're still seeing disease stabilization at those time points. And just to remind us how you define disease stabilization. And then on the phase III, how does data inform your thought process around the REACT event rate? And the question that you get often about when and if you would do an interim analysis on that study. Thanks. Yeah. Thanks, Jason. So I'll address those three questions. So I actually we haven't done an analysis where we kick that patient out of the data, but I have looked at the data on that patient. And so I know visually what happens if we actually remove that patient from the data. And it is a pretty flat line. You avoid the dip, and the patient also rebounds a little bit higher at month 15, and so you avoid that peak. So it's actually a pretty flat line. From a stabilization perspective, our goal is to have an eGFR decline of 1 mL per minute per year or less in keeping with, especially in older adults, in keeping with age-related change in kidney function. So that's our goal. That's how we're thinking about stabilization and preservation of kidney disease. As you know now and what we've shown you here today, that's substantially less than what's seen with some of the newer agents as well as placebo. Jason, getting on to your other questions around events and interim analysis. I think I answered part of this with Jonathan, but we're not going to go back in and change our assumptions with regards to our event rates in our phase III program at this point in time, though I would say this gives us a lot more confidence. I will also say that from an event perspective, which also gives us more confidence, is that in cohort one, we had about 25 patient years of follow-up, and we had one death. We had one event, essentially, in 25 patient years of follow-up. That is small numbers, right? I don't want us to get too excited about that. But that works out to, as the quick math here, 4 events per 100 patient years, which is well less than what we have built into our program. But not to get too excited because the numbers are pretty small. Then on the interim analysis perspective, so the way we've looked at the interim analysis is that in order to do an interim analysis for efficacy, we would want to do it at some point in time when we've accumulated 70% or 75% or 80% of our outcome events. And when we look at when we do the modeling on that, and let's say it's 75% of the outcome events, by that time, we would have enrolled both studies completely. And we would be maybe 6 months away from actually having all of the events because they accumulate much more rapidly towards the end of the study. In fact, we would be taking an alpha hit on our analysis and saving just a few months and really not saving much money at all because of the fact that all the patients were fully enrolled. At this point in time, we don't have a plan for an interim analysis. Thanks, Jason. Thanks so much. Yep. Thank you. At this time, we've reached the end of the question-and-answer session. I'll hand the call back to Bruce Culleton for closing remarks. I'd like to thank everyone for joining us today and for, I think, the many great questions that we received during the Q&A. We're really looking forward to providing you updates on 007 next year when we have more complete mature data. Thanks again for joining us today. Thank you. This will conclude today's conference. You may disconnect your lines at this time. Thank you for your participation.