Good morning, everyone, and thank you again for joining us. Before we start the call, I want to take a moment to give heartfelt thanks to the patients who are part of HORIZON, as well as their families, caregivers, physicians, investigators, and Maze employees who are all integral to today's announcement. Before we dive into our AMKD program and the data announced today, I'd like to provide an overview of our work at Maze. We are a clinical-stage biopharmaceutical company harnessing the power of human genetics to develop novel, small-molecule precision medicines to transform the lives of patients with kidney and metabolic diseases. As you can see from our pipeline, the Maze Compass platform has already delivered multiple clinical-stage and preclinical programs in kidney and metabolic diseases. We are also well-capitalized to advance our pipeline and to deliver multiple catalysts over the coming months, with expected cash runway into 2028 based on our current business plan. On this next slide, we provide an overview of broad AMKD, our focus for today. 6 million patients in the U.S. alone have the genetic variants that cause AMKD. Of those patients, 1 million have some form of kidney disease and at least 250,000 individuals could benefit from a therapeutic approach based on the proteinuria cutoff of 300 mg per gram that was set for HORIZON. At a major kidney medical conference late last year, we showed that about 40% of AMKD patients are diabetic, while about 60% are non-diabetic. These data were reinforced by multiple external studies. Despite the prevalence and the severity of the disease, there remains no approved therapy for AMKD. MZE829 stands out as a truly differentiated potential therapy for AMKD due to its dual mechanism, which blocks the APOL1 pore and disrupts pore assembly in kidney cells. This is crucial for treatment as APOL1 pores rapidly turn over in kidney cells, so the ability to disrupt pore assembly has the potential to make MZE829 significantly more potent than other molecules for the treatment of AMKD. Proteinuria reduction is viewed across the field as a key clinical surrogate of disease outcome across a variety of CKD presentations. In terms of numerical measures, a 30% or greater reduction in uACR, or urine albumin- creatinine ratio, relative to baseline is broadly accepted as clinically meaningful and would demonstrate clinical proof of concept in broad AMKD. In addition to its broad use in clinical development across other programs in clinical guidelines, we have previously guided that seeing a uACR reduction of 30% or more from baseline in the HORIZON study of MZE829 would meet the bar for demonstrating clinical proof of concept and, importantly, inform our plans for advancement into a pivotal program in AMKD. To frame the results based on analysis of published results, a different APOL1 inhibitor in FSGS patients demonstrate a mean reduction of about 43% in uACR and proceeded to a pivotal study. Now, I am thrilled to share our positive phase II results. Today's data are the first to demonstrate results in broader, more moderate patients with AMKD, including those with diabetes. MZE829 demonstrated a favorable safety profile and was well-tolerated across patients in the HORIZON study, consistent with prior phase I studies. I'm very pleased to share with you today that we have exceeded the 30% bar, with MZE829 demonstrating 36% mean reduction in uACR in broad AMKD. In patients with FSGS, we showed a 61.8% mean reduction in uACR. The FSGS data we present from HORIZON today reinforce MZE829's potentially best-in-class efficacy in AMKD and differentiation through its dual mechanism of action. In patients without diabetes, we saw a 48.6% mean reduction in uACR. 50% of patients achieved a reduction greater than 30%, demonstrating a meaningful reduction across these patients. Based on the highly promising results announced today, we intend to advance MZE829 into a pivotal program and look forward to providing updates on our regulatory progress and details on our clinical development plans over the course of the year. We are also reporting today some early promising data in patients with AMKD and diabetes. As HORIZON continues to enroll, we will gather more data on these patients to inform next steps and plan to share an update in the future. With that, I will turn the call over to Harold to discuss the positive data in further detail. Thank you, Jason. The phase II HORIZON trial of MZE829 is an open-label, basket design trial that enrolled patients with broad AMKD, including diabetic and non-diabetic patients carrying the two high-risk APOL1 alleles, G1 and G2. The trial is enrolling patients with a range of disease severity with baseline proteinuria of at least 300 mg albumin per gram of creatinine, including those with more moderate disease, to target a broad AMKD population. Now, today we're going to focus on 15 patients with and without diabetes, including patients with FSGS and more moderate levels of proteinuria. Proteinuria in the study actually refers to albuminuria, as albumin is the major protein that passes across the filtration barrier in the kidney in earlier and more moderate stages of disease. The trial design includes an eight-week lead-in period on standard of care prior to MZE829 treatment to minimize confounding by better adherence to standard of care during the trial. Patients received 250 mg of MZE829 once daily for 12 weeks, followed by four weeks of follow-up on standard of care therapies alone. The primary endpoints of the study are safety and tolerability. The secondary endpoints are pharmacokinetics and reduction in proteinuria. This is measured by the percentage of subjects with a 30% or greater reduction from baseline in urinary albumin-to-creatinine ratio, or uACR, at week 12. Now, uACR is a sensitive measure of proteinuria, especially during earlier stages of glomerular kidney disease with more moderate levels of proteinuria, particularly as seen in hypertension and diabetes, and this has been used to assess risk of cardiovascular disease. As Jason discussed, a 30% or greater reduction in uACR is a broadly accepted measure of clinical meaningfulness across CKD presentations that strongly correlates to improvements in kidney outcomes. As we can see on this table, we'll be looking at 15 patients with AMKD, eight without type 2 diabetes and seven with. All patients who received at least one dose of MZE829 are included in the safety analysis. The 12 patients who received at least 80% of scheduled doses are included in the efficacy analysis per protocol. As detailed on the slide, age, sex, and body mass index were fairly balanced across patients, and all APOL1 high-risk genotypes were represented. With this first look at diabetic AMKD patients treated with an APOL1 inhibitor, patients with diabetes had slightly lower levels of baseline proteinuria. On the next slide, we'll look at the distribution of baseline proteinuria for this group. As we can see on this slide, the 15 patients with AMKD with and without diabetes included in this analysis had levels of proteinuria largely in the subnephrotic range at baseline. 10 had moderate levels of 300 mg-1,000 mg albumin per gram of creatinine in their urine. Of the 12 patients evaluated for efficacy, 11 were in the subnephrotic range. This reflects the broad AMKD patient population we've been focused on and is an important feature of demonstrating proof of concept for MZE829. Overall, in the HORIZON study, MZE829 was well-tolerated and consistent with the safety and tolerability profile we saw in phase I. There were no safety or tolerability signals observed. There were no serious adverse events reported, and all adverse events considered related to treatment were mild or moderate. The most common adverse events that were deemed treatment-related, occurring in two participants each, were headache and diarrhea. As seen with the phase I data, treatment with MZE829 demonstrated no clinically relevant changes in vital signs, laboratory tests, or ECGs. Overall, all treatment-related adverse events were mild to moderate in severity. There was one severe AE reported. This occurred in an AMKD patient with diabetes who was noted to have bilateral cataracts on day two of dosing. The patient had previously been scheduled for cataract surgery prior to enrollment. However, the referring nephrologist was not aware of this at the time of screening. As such, it was deemed unrelated to treatment with MZE829. The one discontinuation observed was due to mild nausea. This discontinuation took place shortly before the patient's week 12 visit but met the compliance threshold for inclusion in both safety and efficacy analyses. To date, there continue to be no safety signals of clinical interest for MZE829, which continues to demonstrate a tolerable and safe safety profile in the HORIZON study. We'll now look at this waterfall plot of all AMKD patients with and without diabetes who were included in the analysis based on our compliance threshold. As a reminder, for the efficacy analysis, we've included patients who received at least 80% of scheduled doses of 250 mg once daily. We are very encouraged to see that 50% of patients treated achieved at least a 30% reduction in uACR, and the mean uACR reduction across both subgroups at week 12 was 36%. Next, we'll focus on the effect of MZE829 on proteinuria reduction in those patients without diabetes. As we can see in this waterfall plot, the mean reduction in urinary albumin to creatinine ratio was 48.6% with a response rate of 57%. These are the first data supporting proof of concept for any APOL1 inhibitor in broad AMKD among non-diabetics and specifically for MZE829. In patients with AMKD and diagnosed FSGS, the mean uACR reduction at week 12 was 61.8%. For those interested, the mean uPCR reduction among FSGS patients was 59.4%. This supports the potential for MZE829 as a best-in-class therapy for AMKD. While the data in patients with AMKD and diabetes are early, we are highly encouraged to see this effect in two out of the five patients treated. While we and others had previously reported population-based analyses indicating a role for MZE829 in diabetic AMKD, this is the very first clinical confirmation of the potential benefit. On this slide, I'll go briefly into the details of the two patients with AMKD and diabetes who showed a meaningful response to MZE829. One patient was younger, earlier in his disease journey, and yet experienced a 47% reduction in proteinuria despite being on a stable regimen of medicines for CKD, diabetes, and hypertension for at least eight weeks prior to initiating MZE829. The other patient was older, further along in his disease with multiple comorbidities stemming from CKD, who still benefited with a 35% reduction in proteinuria despite being on an SGLT2 inhibitor, the recently approved KERENDIA or finerenone, as well as antihypertensives. We believe that this is very promising early data supporting a role for MZE829 in the treatment of patients with diabetic AMKD. We're especially encouraged to see the positive effects of treatment with MZE829 apply across two very different profiles in patients with AMKD and diabetes, and look forward to gathering more data from these patients as HORIZON continues. In summary, from this first data analysis of MZE829 in patients with broad AMKD, we continue to see a favorable safety and tolerability profile. Most importantly, we have established clinical proof of concept for MZE829 in broad AMKD, including patients with more moderate disease with and without diabetes. We observed a 35.6% mean reduction in proteinuria based on uACR across all patients, including those with more moderate disease, patients with FSGS, and patients with diabetes. The observation of a mean reduction in proteinuria of 61.8% in a subset of patients with FSGS illustrates the best-in-class potential for MZE829 across the broader population. We observed a 48.6% mean reduction in proteinuria based on uACR across all patients without diabetes, and so very promising early data in patients with AMKD and diabetes. The data we've shared with you today is significant in the AMKD treatment landscape and reinforces the potential of MZE829 to be a truly differentiated treatment option, bringing meaningful, much-needed benefit to patients with broad AMKD. We look forward to sharing more data from the HORIZON study at a future medical conference and providing further details about our plans for a pivotal program as these develop. With that, I'll hand the call back to Jason. Thank you, Harold. Before we close, I want to take this opportunity to acknowledge the continued value the Maze Compass platform has delivered to patients and our shareholders. In addition to today's positive HORIZON data in broad AMKD and advancing MZE829 to a pivotal program, I would like to highlight some of the recent announcements. Based on the positive data we presented last fall, we continue to advance MZE782 to two phase II trials, one in PKU and a separate phase II in chronic kidney disease. In fact, we now have three clinical programs in development based on the insights from the Maze Compass platform in kidney and metabolic diseases and several preclinical programs that we hope to talk about in the future as they enter the clinic. Importantly, we announced this morning that Shionogi Pharma dosed the first patient in its phase II study in Pompe disease, which, in accordance with our global collaboration agreement, triggers a $20 million milestone payment. Finally, I also want to extend a warm welcome to the newest member of Maze's Board of Directors, Dr. Neil Kumar, founder and CEO of BridgeBio Pharma. We are excited to work with him, especially at this critical juncture for the company, given his experience developing and commercializing multiple genetically based medicines. With the positive data we presented today and summarized on this slide, we are starting this year excited for what's ahead in our mission to improve the lives of patients with broad AMKD. As we advance MZE829 to a pivotal program, we look forward to providing updates on our regulatory progress and details on our clinical development plans later this year. With that, operator, please open the call for Q&A. Thank you. We will now begin the question- and- answer session. To ask a question, you may press star then one on your touchtone phone. If you are using a speakerphone, please pick up your handset before pressing the keys. If at any time your question has been addressed and you would like to withdraw your question, please press star then two. Our first question will come from Anupam Rama with JP Morgan. Please go ahead. Hey, guys. Thanks for taking the question, and thanks for the update. Two quick ones from me. Look, I realize it's small numbers here, but can you comment either on biology or mechanism which might explain the efficacy that you're seeing in diabetics versus non-diabetic patients? Or is this really just be related to some baseline proteinuria levels in this early data set? Then second one, just from a patient accounting perspective, of the seven non-diabetics in your study, what portion were FSGS versus non-FSGS? I guess the reason I'm asking is there's this fear out there that this product or this mechanism really only works in FSGS patients, so how would you respond to that? Thanks so much. Thanks, Anupam. This is Harold. In terms of the biology, you know, we're still working through the data. We do believe that mechanistically, MZE829 is still doing what we predicted based on our drug discovery efforts, which were founded on the N264K protective variant. We don't think mechanistically it's working different. We do recognize that diabetes has its own pathophysiology, so we're really looking into the data to try and understand better whether, and even if there's a difference, in the effect. Now, as far as the non-diabetic cohort, four of the patients included in the efficacy analysis did have FSGS. I think it's important to recognize that three of the other patients who did show a good response did not have FSGS. One who fell into the non-diabetic category and two patients who actually had coincident diabetes. I think that gives us a level of confidence that we really are seeing an effect of MZE829 that's clinically meaningful across the what we're defining as broad AMKD, including patients with and without diabetes, as well as those with non-diabetic FSGS. Thanks so much for taking the question, and congrats on the update. Thank you. The next question will come from Debjit Chattopadhyay with Guggenheim Securities. Please go ahead. Hey, good morning, and congrats on the update here, three medicines from the Compass platform right now. I just was wondering if enrollment in the pivotal study would mimic HORIZON with respect to FSGS patients, and if you are planning on a 48-week GFR as a primary endpoint, and if so, what kind of effect size are you likely to power the study for? Thank you so much. Yeah. I'll take the first question, and Harold can follow with the second. I think what, you know, this is the first time anyone has really been able to demonstrate clinical proof of concept in broad AMKD. I think just to reiterate what Harold had discussed, you know, we're seeing response in more moderate proteinuria patients. We're seeing responses in those that don't have FSGS, showing data for the first time in diabetes. We're gonna continue to enroll, and I think the thing to keep in mind is that with this data in hand, Debjit, we're gonna be able to engage the AMKD community, including the patients and the nephrologists. As the increased awareness occurs in AMKD, I think we're gonna take the learnings from HORIZON and expect enrollment to pick up as we move towards the pivotal. We've seen that in other sponsored studies. I think the other thing to kind of keep in mind is, you know, if we look at analogs and corollaries to this, as awareness and treatment options become available, you know, we see these kind of trends increase. You saw that in ATTR cardiomyopathy as well, where with treatment options and more awareness about the disease, you can only bring even more people into the community and think about improvements on enrollment rates. You know, in response to your question about what a pivotal program would look like, just to add to what Jason said, I think, you know, the recent approval of new ICD-10 codes for the diagnosis of AMKD will also really improve identification of patients and subsequently recruitment and enrollment. We're only seeing awareness grow, and that's going to make it, you know, easier to run these studies. I think in terms of a pivotal program, you know, this data is fresh for us. We're still thinking about what a pivotal program would look like, who the patient populations would be, what doses we would select for those. We'll have more information about that as that develops. Based on these data, you know, we're really excited and we're gonna be working very hard going forward on defining exactly what that program's gonna look like. Thank you. Thank you. The next question will come from Joseph Schwartz with Leerink Partners. Please go ahead. Great. Thanks so much, and congrats on the exciting results. I was wondering if you can describe the general trajectory of the proteinuria reductions over the 12 weeks, and what have you seen beyond week 12 in any patients that are still on therapy? Thanks, Joe. I'll direct that one to Harold. Thanks, Joe. We saw a steady decline in proteinuria, and a return towards baseline proteinuria after the 12-week treatment period. This actually gives us confidence that the patients we're enrolling had been on stable regimens of their CKD therapies before starting MZE829, and that the effects we're seeing on proteinuria reduction are in fact due to MZE829 treatment. You know, we did that by design by including this requirement that patients be on a stable regimen of their CKD, and for the diabetics, their diabetic medications for eight weeks prior to starting MZE829. That together with what happened after they went off MZE829 gives us confidence that the effect we're seeing really was due to MZE829. Yeah. I'll just add, Joe, that it's an important point that, you know, we had this particular eight weeks of them on standard of care, and to see the type of responses we had with people on GLP-1s and SGLT2s, which hasn't been described in the literature before, that's highly encouraging because we can see that a 30% drop in these patients is clinically meaningful. I think if you look at the diabetes case studies, you can see that pretty clearly that, you know, heavily pretreated and had, you know, not only the SGLT2, but the MRA, which indicates that, you know, we're seeing a 30% drop despite the fact that you have these co-medications. Highly encouraged, early promising data that we're gonna be able to dig into and really sort of guide the way that we're thinking about this going forward. Okay. Thanks. Then if I could just follow up on what you were alluding to with the diabetics who are treated. Do you think it makes sense to treat patients with diabetes earlier in their disease? Would they respond better than patients who are later in their course? What about does it make sense to have higher doses for patients with diabetes? Yeah. Thanks for the follow-up. In terms of treatment, I think in general, because AMKD, as with other forms of kidney disease, is a progressive disease with progressive loss of kidney function, it would be important to treat patients across the board earlier. I think that goes beyond just the diabetics. I'm sorry, can you remind me what the second part of your question was? Yeah. Thanks. I was just wondering if you could talk a little bit about the dose response picture that you're seeing now in HORIZON and everywhere else, and whether maybe it might make sense that diabetics could need higher doses of MZE829. You know, we originally chose doses based on the predicted effect, and so we were above EC90 on the translational PK/PD curve. You know, according to regulatory guidance, you know, we're compelled to try and find the lowest dose that has the maximum efficacy. You know, based on what we've seen here, of course, and the fact that our phase I data gives us some leeway in that regard, we're gonna be thinking about dosing, and we'll have more to say about that as we develop our plans for the pivotal program. Great. Congrats again. Thanks, Joe. The next question will come from Tyler Van Buren with TD Cowen. Please go ahead. Hey, guys. Good morning. Congrats on the data. Great to see the uACR reductions. Just as we look at the waterfall plot, curious, obviously some, again, some great reductions there, but on the non-responders or, like, the three diabetic patients that didn't respond, curious if there's something about the baseline characteristics or something about their disease that may have made them less likely to respond and how you're thinking about future pivotal development in the diabetic population relative to FSGS and non-diabetic. Maybe just as a follow-up to, I realize it's small patient numbers, but broadly across all patients, did you see any differences in efficacy among the different genotypes? Thanks, Tyler. Two areas that we're thinking a lot about. In the case of the patients who didn't show a robust response. You know, initially we've dug into those who did show a response, so the two patients that we detailed in the presentation, you know, really if you look at them, they present sort of two very different, you know, phenotypes if you were different sets of background medications, different stages of disease, and in fact, even different baseline levels of proteinuria. In fact, you know, it was instructive that the patient who had the lower level of baseline proteinuria actually had a deeper response than the one with the higher level of proteinuria. We're still in the process of looking through the patients who didn't have the response, and of course, we'll try and get as much information as we can out of that, as well as, you know, we're continuing to enroll in HORIZON, and so we'll have additional data to help inform how we might approach enrichment as we go forward into a pivotal program. Next question will come from Salim Syed with Mizuho. Please go ahead. Great. Good morning, guys. Congrats on the data. Just one for us. I wanted to focus a little bit on the FSGS comparison, because I think that's really the data point here that if we wanted to get something a little bit more apples- to- apples versus the Vertex and Axsome compounds. You guys put up 62%. They put up 43%. I think you guys both used the 80% cutoff. Both of those were geometric means. Three out of the four FSGS patients that you had in your trial with evaluable efficacy were showing north of a 55% reduction. Just curious, in your mind, when you look at this, is there anything in your mind here that you would think would take away from having that best-in-class potential? Is there any? You know, outside of the small end here, is there anything else that we should be focused on that could rule out a best-in-class potential? Thank you. Yeah. Yeah, no, I think. Thanks, Salim. I think it's clear that there's a signal both on uPCR and uACR. I mean, just to make that point again that you made. uACR, we were 62%, and they were 43%. And then from a uPCR perspective, you know, we were at 59% reduction, which Harold pointed out, versus the 47. So clearly, you know, improved data there. The other thing to kind of point out, which you kind of dug into, is that all responded, you know, with the one exception not getting, but approaching the 30%. So we actually had response in all the FSGS patients. And the three that did get below the 30% had greater than 50% reduction, right? I think, you know, what's really encouraging to see there is that it does reinforce what we were expecting from the preclinical data, which was the increased potency should see better responses, in particular in patients like this. It is pleasantly surprising, you know, as we were looking at the data. Obviously, we were enrolling in that cohort non-diabetic patients, but we allowed for FSGS. What happened is we had enrolled a number of non-diabetic patients, and then we looked back, and it just happened to be that they had FSGS. I think what's really great going forward to really kind of think about this is that, you know, we do have a group of patients in a non-diabetes patient population where you have a really good signal, and that's what we can carry forward. As we think about the pivotal where you had, you know, almost 60% of those patients get to the above that 40% reduction, right? I think all totality of that data, it really leads us to believe that you can really push forward in thinking about, in particular for the non-diabetes patients. Super helpful. Thanks so much, and congrats again. Thank you. The next question will come from Laura Chico with Wedbush Securities. Please go ahead. Good morning. Thanks very much for taking the question. I guess a couple questions, just related to the pivotal and then one on the remaining HORIZON data. Do you plan on providing an update on eGFR responses? Again, I know it's early, it's only been 12 weeks and small n, but as you continue to accrue, should we anticipate any updates related to changes in eGFR? Then separately on the pivotal study, I'm wondering if you can talk a little bit more about kind of next steps and specifically, what additional data do you need before engaging with regulators? I guess I'm trying to also understand what role do you see PARASOL playing in assisting on endpoint selection. Thanks very much. Thanks, Laura. This is Harold. In terms of eGFR response, you know, we've obviously monitored serum creatinine from which eGFR is derived as a safety lab, and we didn't see anything, you know, in that. That was reassuring. In terms of, you know, for example, an initial eGFR dip that you see with certain therapies that have been shown to be protective for the kidneys, we don't anticipate based on the mechanism of action of an APOL1 inhibitor to see a renal hemodynamic effect in that way. You know, of course we'll look, but we're not expecting to see an eGFR response over a 12-week period. In fact, you know, based on the meta-analyses of how quickly you might expect to see even a change in slope of eGFR decline, you're talking about at least one to two years for that. In response to your questions about the pivotal, you know, again, I think, you know, next steps are, again, this is our first look at the data. I think we're coming away from this seeing, you know, a path forward to think about what a pivotal would look like and start to engage with regulators to discuss that, especially in the non-diabetic population. We'll be doing that. In the diabetic population, I think, you know, in order to approach those discussions, we'd like to see more data in diabetics and, so HORIZON continues to enroll, so we'll be looking at that. Then in terms of PARASOL, you know, our understanding is the PARASOL initiative is now looking at the possibility of using other surrogate endpoints, including reductions in proteinuria in broad AMKD. You know, we're eagerly awaiting, as are others, to see, you know, what they find in their analyses. Assuming the timelines that they've relayed publicly, that should dovetail nicely with our plans for designing our pivotal program. More to follow as we all learn more from their initiative. Thank you. The next question will come from Ananda Ghosh with H.C. Wainwright & Co. Please go ahead. Hi. Good morning, guys, congrats on the data. Thank you. One of the questions I had was, given the, you know, given the 30% reduction you were seeing in the diabetic cohort and given the fact that, you know, those are probably the most challenging patients you had, considering the baseline proteinuria and the added background therapy, does it change the way you have thought about the DKD population? And, you know, how does it change your approach for the future HORIZON enrollment when you are thinking about the criteria for responder and non-responder? And a follow-up question will be given the impressive FSGS data readout, how are you thinking from the regulatory perspective as, you know, as you're anticipating Vertex's data readout later part of this year? Thanks. Yeah. No, thanks for that question, Ananda. I think, you know, it's probably important to kind of understand again that this was the first clinical data showing any signal in diabetes. I remember that before we published our paper on N264K, the previous literature predicted that there should be no effect in diabetes patients and the fact that, you know, HORIZON was the experiment that really allows us for the first time to demonstrate that particular signal. We're not exactly at the data threshold we wanna be yet and but given the early promising signal, you know what we're seeing, of course, is that even the people treated with GLP-1s and SGLT2 inhibitors, you know, we're seeing that response. I think what we're, a s Harold kind of pointed out, we're gonna continue to enroll patients, and as we collect more data, that's gonna give us the opportunity, since this is one of the first studies to actually collect data like this, that we can look for ways to enrich in a pivotal study, right? I think going forward, as we think about, you know, continuing to enroll patients, we're gonna learn a lot more. I think this just definitely moves the field forward because I think, you know, a few years ago, people should have looked at the literature and said, "We shouldn't see any impact." What we're seeing, even with eight weeks of, you know, standard of care, including some of the things like the SGLT2 inhibitors, we're seeing some pretty good responses. Right? I think that's the way to kind of look at the data in totality, and we're gonna learn more as we enroll more patients. Got it. Thanks. The next question will come from Rami Katkhuda with LifeSci Capital. Please go ahead. Hey, guys. Thanks for taking my questions as well and congrats on the update. Once again, I know it's a small sample size, but did you observe a correlation between baseline proteinuria and the magnitude of reduction in any of the subgroups? Maybe going off a previous question, do we see a plateauing of proteinuria reduction in any of the responders by week 12, or does it continue to go down over time? Right. Thank you. You know, those are two things that we've you know, looked at high level. We'll have more to say about it as we go forward. In general, in terms of the relationship between baseline proteinuria and response, we've basically seen, you know, those with lower proteinuria have bigger responses, and those with high proteinuria have lower responses and everything in between. It could just be the fact that we have small numbers. I mean, a good example are the two diabetic cases that we featured, which I think I mentioned earlier in the Q&A. I don't think we have a clear view of that at this point. In terms of the sort of what the reduction in proteinuria looks like over time, again, overall, we saw an initial response and then really a steady decline in proteinuria across all patients who you know met the 30% criteria. Actually, we didn't necessarily see a plateau, suggesting that you know perhaps with a longer treatment period, one would see even further reduction, but you know we don't have data yet for that. Got it. Thank you, guys. The next question will come from Martin Auster with Raymond James. Please go ahead. Hey, guys. Hey. Thanks for taking the question. Congrats on the data update this morning. Just curious if you're contemplating any modifications to either the size of the cohorts or entry criteria, how you plan to kind of enroll HORIZON going forward based on the initial data and kind of the experience of the trial so far? Thanks. Thanks, Martin. You know, for right now, again, you know, the enrollment, the way we've you know, planned it and per protocol has really given us the greatest opportunity to look at this broad AMKD population. You know, of course, we're gonna think about whether we might wanna make some changes, but nothing for right now. What I would say is that, based on the safety and tolerability that we're seeing, you know, there are no new signs of clinical interest, no new signals that we hadn't seen previously. In that regard, we don't feel we need to make any adjustments there. Yeah, and of course, if we decide, you know, based on having a longer look at the data to make changes, we'll be clear about that. Just as a brief follow-up, I know it's obvious to ask, but will you be able to engage with regulators sort of on a rolling basis, or do you tend to kind of complete HORIZON before kind of having formal end of phase II discussion about next steps? I wasn't fully clear from that on that. Thanks. We're still in the process of thinking about what the best timing for an end of phase II discussion would be and then seeking scientific advice for European health authorities. Again, we'll have more guidance on that as we've had more of a chance to think about these data and what our plans would be for the pivotal program. All right. Super. Thanks so much. Yeah. Thank you. The next question will come from Julian Harrison with BTIG. Please go ahead. Hi. Congratulations on the data. Thank you for taking the question. Thanks, Julian. Are there any good natural history references to give us a sense of what the uACR and uPCR increases would have looked like in the key patient populations here, especially among diabetics, if they were not on an APOL-1 targeted therapy? Harold, do you want to take that one? Sure. Yeah, based on the literature, and actually even some of the data that we presented just last year at ASN and was corroborated by others, looking at rate of progression in patients with the high-risk genotype versus those with CKD without the high-risk genotype, we can definitely see this accelerated rate of progression. You know, you know, if we compare that to what we're seeing in our you know, open label trial, we do think that a 30% reduction in proteinuria over 12 weeks would reflect or has the potential to reflect a significant change in that rate of progression. That's where we are with this. We'll have to see. Of course, you know, you raised a question that's an important consideration in how we think about a pivotal program and how long we think it would take to see a change in slope of eGFR decline, based on these findings. We'll have more to say about that as we go forward with planning for our pivotal program. Got it. Thank you. A follow-up, if I may. The two diabetic patients with the proteinuria increases over 12 weeks, are those changes generally in the realm of your understanding of the natural history for those patients specifically? We haven't looked at it in that context, so we're still exploring, you know, what might be going on with those patients in particular. Don't really have a conclusive answer for that yet. Thank you very much. Our last question will come from Sadia Rahman with Wells Fargo. Please go ahead. Hi. Thanks for taking the question. Congrats on the results. A couple from me. Sure. Can you help us understand why a large proportion of non-diabetics that were enrolled had FSGS histology, given that FSGS is thought to comprise population of AMKD? As far as the responses that you're seeing, do you think there could be any explanation or rationale for why this mechanism would work only in FSGS or better in FSGS patients versus the broader non-diabetic group? I'm not sure why that would be, but wondering if you have a perspective on that. Yeah, no, just thank you for the question and appreciate it. You know, take a look at what we did in HORIZON, in particular in that cohort of non-diabetic. What we did is we allowed for more moderate disease and, you know, allowed for FSGS patients. I think the order matters in terms of questions 'cause we enrolled non-diabetics, and then we went back and looked at whether or not they had been diagnosed with, you know, confirmed with FSGS. It was interesting, and I think we were pleasantly surprised that we actually saw activity of that degree in FSGS patients. All right. I think what's really nice about that particular cohort is we did see responses in non-diabetic patients, pretty significant, in fact. I think it's clear that, you know, a couple things kind of emerged from that data, which is in the non-diabetes patients, you know, thinking about that going forward in a potential pivotal, you know, you have a pretty high probability of success criteria of seeing a pretty deep response with uACR, particularly in those patients. Then what we can kind of think about is what we had in terms of what we were pleasantly surprised is that because they had FSGS, it allowed us for the first time to really be able to try to compare with another sponsor's therapy, which, you know, I think clearly it reinforces what we think we have in terms of a best-in-class molecule. I think for us, you know, we can see a couple things emerging from the data where we're seeing response from more moderate patients, more moderate proteinuria patients. We're seeing responses in non-FSGS patients, and we're seeing that early signal in diabetes patients, particularly those that have been treated with GLP-1s and SGLT2s. And again, as we collect more data and enroll more patients, I think we'll look for ways, in particular for the diabetes patients, to kind of think about what are some enrichment strategies we can carry forward in terms of, the next study. Got it. That's helpful. You mentioned you're enrolling more patients. I'm curious if we might see a later data cut, particularly with a larger sample size might help to clarify the responses that we could see in non-FSGS non-diabetic patients. Do you think that you might need to see that data to help design a pivotal trial to think about any enrichment that's needed and baseline characteristics in a pivotal study? Maybe I'll follow up with your question. You know, in terms of sharing another data cut, we expect to present additional data from HORIZON at an upcoming medical conference later this year. You know, we'll give more guidance as we can clarify when that will be. In terms of how we're gonna use the additional data as HORIZON keeps enrolling, I think it's pretty clear to us that, you know, we have a potential medicine for broad AMKD, and we're certainly going to work towards, you know, a pivotal program for MZE829. I think we'll use the additional data to help further sort of clarify the specific population that we'll study in phase III, as well as to see if there are any enrichment strategies we might be able to use as we get more information, specifically in the patients with diabetes. More to follow. You know, your questions, you know, really raise the important issues that we're actively thinking about even as we're getting this first look at the data. Great. Thank you and congratulations. Yeah, thank you. This will conclude our question- and- answer session. I would like to turn the conference back over to Mr. Jason Coloma for any closing remarks. Please go ahead. Thank you again for joining us today. We look forward to presenting the MZE829 data at a future medical meeting and keeping you updated on our continued progress. We hope that you have a great rest of your day. Thank you. The conference is now concluded. Thank you for attending today's presentation. You may now disconnect.