Involve assumptions, risks, and uncertainties. Maze undertakes no obligation to update or revise any forward-looking statements. Please refer to Maze's filings with the SEC, which are available from the SEC or on the Maze website for information concerning the risk factors that could affect the company. Joining me on today's call are Jason Coloma, CEO of Maze, and Harold Bernstein, President of R&D and Chief Medical Officer at Maze. Today's presentation will begin with introductory remarks from Jason, followed by Harold, who will review the Phase I clinical data for MZE-782 in healthy volunteers. Jason will then return to conclude our prepared remarks, after which we'll open the call for Q&A. I will now turn the call over to Jason Coloma. Thank you, Amy. Good morning, everyone, and thank you for joining us. At Maze, we are harnessing the power of human genetics to develop precision medicines to transform the lives of patients with kidney and metabolic diseases. With the Phase I healthy volunteer study for MZE-782 now complete, we expect to initiate Phase II trials in both PKU and CKD in 2026. Our Phase II trial of MZE-829, a dual mechanism inhibitor for APOL1-mediated kidney disease, is continuing to enroll, with initial top-line data expected in Q1 2026. As you can see, we have multiple shots on goal, and we are also advancing earlier-stage programs in kidney and metabolic diseases through our Compass platform. In addition, we licensed MZE-001, for Pompe disease, to Shionogi & Co. in May 2024, providing an upfront payment of $150 million and the potential for future milestone payments based on development, regulatory, and commercial achievements, as well as tiered royalties based upon future net sales. With the financing announced today, we are in a strong position to deliver multiple catalysts over the coming months, with expected runway into 2028 based on our current business plan. What sets apart Maze's approach? Our Compass platform is the foundation of everything we do. It is designed to systematically translate genetic insights into medicines. This slide shows how the platform enables us to focus on genetically validated targets and direct our small molecule capabilities by better understanding gene variants in the context of disease. Compass has already delivered multiple clinical stage programs and insights on who the patients are that could best respond to our therapeutic candidates. We are translating genetics into programs that we believe have a higher probability of success and a clear path to value creation. MZE-782 inhibits SLC6A19, a solute transporter of various carbos, including neutral amino acids. The biology is validated and de-risked by human genetics and previous clinical proof of concept data in PKU patients. People with Hartnup disease have complete loss of function of SLC6A19 and essentially model lifelong inhibition without chronic safety issues in the setting of a modern diet. This gives us confidence about the safety of this mechanism. This is the third clinical program to come out of our Compass platform, and we have already shown robust preclinical target engagement with the expected amino acid shifts and disease-relevant efficacy signals. Importantly, MZE-782 clinical development uses established regulatory endpoints, including the reduction in plasma phenylalanine, or PHE, in PKU and a reduction in proteinuria and eGFR slope in CKD. The take-home here is simple: the human genetics support potential safety. The preclinical package supports efficacy potential. Clinical proof of concept data in PKU patients has previously been demonstrated, and the trial readouts map cleanly to endpoints regulators and investors already know. MZE-782 is our opportunity to make a significant impact in both PKU and CKD. Let's start with PKU. Despite newborn screening, more than 60% of patients, especially with classical or severe PKU, remain inadequately controlled. Diets are burdensome, and neurocognitive issues persist. Our goal with MZE-782 is straightforward: to deliver best-in-class plasma PHE reduction with an excellent safety profile. The readout is direct and well-established. Urinary PHE excretion correlates with plasma PHE lowering, so we can move quickly toward endpoints that matter to regulators and patients. In CKD, we are targeting a large segment of patients who are not adequately responding to or discontinuing treatment of the current standard of care, including SGLT2 inhibitors. For example, over 30% of patients discontinue SGLT2 inhibitors within a year. Mechanistically, SLC6A19 inhibition is independent of SGLT2 inhibition and potentially additive. We previously reported the first in vivo proof of concept in a preclinical model. As we started our Phase I study, the nephrology community asked if we could look at movement in eGFR in healthy volunteers, as this would indicate potential future kidney benefit in patients. I am proud to say that today we are the first company to report early clinical eGFR data with SLC6A19 inhibition that is supportive of kidney benefit and our mechanism of action. As a result, we plan to run a Phase II proof of concept study utilizing proteinuria as the endpoint. The MZE-782 program has two clear development paths: an efficient PD-anchored route in PKU and a precision add-on or standalone strategy in CKD. Before I transition to Harold, who will walk us through the data in more detail, I would like to preview the key takeaways from our Phase I trial of MZE-782 in healthy volunteers. The data exceeded what we set out to show and gives us the conviction to move into Phase II in both PKU and CKD. First, safety. The safety profile was excellent, with no serious adverse events observed. Second, PK. We saw linear, consistent exposure across both the single and multiple ascending dose cohorts, which is precisely what we want to see heading into our dose selection for Phase II. Third, proof of mechanism. By day seven, we observed up to a 42-fold increase in urinary FE and 68-fold in urinary glutamine. This is well above the 10-fold increase we previously set as our threshold and was publicly reported with another SLC6A19 inhibitor in healthy volunteers. Fourth is kidney physiology. eGFR was an exploratory endpoint in the study, and this is the first time any company has reported SLC6A19 inhibition with this effect. We observed a dose-dependent initial eGFR dip consistent with the hemodynamic effects seen with SGLT2 inhibitors and other approved kidney medicines, a pattern predictive of long-term CKD benefit. It is supportive of our hypothesis and will inform our CKD trial design. As a result of these exciting data, we plan to initiate Phase II proof of concept studies in both PKU and CKD next year. In PKU, plasma FE reduction will serve as a primary endpoint, the same endpoint regulators use for approval. In CKD, initial proof of concept will be focused on proteinuria reduction. We are very pleased with the data, which demonstrated excellent safety profile, predictable PK, compelling PD, and a clear, efficient path into Phase II in both indications. With that, I'll turn the call over to Harold. Thank you, Jason. The Phase I trial of MZE-782 was a randomized, double-blind, placebo-controlled study evaluating single and multiple ascending doses of orally administered MZE-782 in 112 healthy adult volunteers. The study included 56 participants in the single-dose cohorts, 40 participants in the multiple-dose cohorts, and 16 participants in the food effect cohorts. Each cohort included eight participants randomized, six receiving MZE-782 to two receiving placebo. The SAD doses ranged from 30 to 960 milligrams. You may notice that 120 milligrams was administered in two single-dose cohorts as we transitioned from 30 milligrams to 120 milligram tablets. The MAD doses, with dosing once or twice daily for seven days, ranged from 120 to 240 milligrams twice daily and 120 to 720 milligrams once daily. The food effect cohorts evaluated single and multiple doses of 480 milligrams. One food effect cohort included eight participants administered 480 milligrams of MZE-782 or placebo, six to two, with a high-fat meal. The second food effect cohort included eight participants administered 480 milligrams of MZE-782 fasted or with a low-fat meal in a crossover design. The primary objective was to evaluate the safety and tolerability of single and multiple ascending oral doses of MZE-782 in healthy volunteers. Secondary and exploratory endpoints included pharmacokinetics, pharmacodynamic measures of target engagement, specifically urinary excretion of phenylalanine and glutamine as predictive biomarkers of SLC6A19 inhibition and disease control, food effect for different dosing regimens, and estimated glomerular filtration rate, or eGFR. As we can see, demographics for the Phase I study were well-balanced and comparable between the placebo and treatment arms. Of the 112 participants enrolled, the median age was 38 years, 44% were male, and race and ethnicity were diverse, with 39% Hispanic or Latino, 31% Black or African American, and 60% White. We'll look at safety tables in a moment. Overall, MZE-782 was well tolerated across all dose levels evaluated in the SAD and MAD cohorts, with no serious adverse events and no treatment-related adverse events with chronic dosing. Among the 86 participants treated with MZE-782, there were only three treatment-related adverse events in the SAD cohorts, all of which were mild in severity and not seen at the higher doses. As we see here in the safety table, the three adverse events in the SAD cohorts that were deemed treatment-related were not dose-related. There were no treatment-related adverse events in the MAD cohorts. The treatment-emergent adverse events that were not related to treatment included single events with no dose relationship. All were mild and were classified as not related to treatment by the investigator. The PK profiles for the SAD and MAD cohorts show linear pharmacokinetics. MZE-782's half-life is approximately 11 hours, supporting once or twice daily dosing. Steady state was achieved by day three of chronic dosing. Now, let's look at the data on slide 18 that we find so compelling from this study. As we can see here, MZE-782 demonstrated a dose-dependent increase in urinary phenylalanine excretion. We saw a 39-fold increase in urinary phenylalanine excretion over 24 hours with a single dose of 960 milligrams of MZE-782. We saw a 42-fold increase in urinary phenylalanine excretion over 24 hours at day seven, with chronic dosing of 240 milligrams of MZE-782 twice daily. The gray dotted line indicates the tenfold increase that we had initially set as our threshold, which had been achieved by a competing SLC6A19 inhibitor that translated to a clinically meaningful reduction in plasma phenylalanine in patients with PKU. However, even with 120 milligrams once daily dosing of MZE-782, we still saw a 12-fold increase in urinary phenylalanine excretion, which comfortably exceeds the threshold we had set. We also measured glutamine excretion as a separate measure of target engagement. Here we see that MZE-782 also demonstrated a dose-dependent increase in urinary glutamine excretion. We saw a 55-fold increase in urinary glutamine over 24 hours with a single dose of 960 milligrams of MZE-782. We saw a 68-fold increase in urinary glutamine excretion over 24 hours at day seven with chronic dosing of 240 milligrams of MZE-782 twice daily. This is consistent with the target engagement on the previous slide. Before we share the exploratory eGFR data for MZE-782, I'd like to take a step back and walk you through the potential mechanism of action for MZE-782 in chronic kidney disease. MZE-782 has the potential to improve kidney function through both a pathway that is complementary to SGLT2 inhibition through tubuloglomerular feedback, as well as an independent pathway for kidney detoxification by removing toxic metabolites. As you know, SGLT2 inhibitors reduce glucose and sodium reabsorption in the proximal tubule. This has been shown to ultimately decrease intraglomerular pressure, which has become one of the foundational mechanisms employed by current therapies in chronic kidney disease. There is another transporter in the proximal tubule that we identified through our genetic analysis: SLC6A19. MZE-782, which inhibits SLC6A19, may reduce the reabsorption of sodium and other solutes, like neutral amino acids, in the proximal tubule, with the potential to similarly decrease intraglomerular pressure. In addition, by blocking the reabsorption of additional potentially toxic metabolites in the proximal tubule, MZE-782 may also prevent harmful metabolites from building up inside kidney cells, thereby reducing stress and injury. Importantly, this mechanism doesn't just protect the proximal tubule; it also enhances downstream function. By preventing reabsorption of these metabolites and amino acids, more nutrients reach the distal tubule, which has long been shown to improve distal tubule function, but without the risk of hypoglycemia and urinary tract infection associated with SGLT2 inhibitors. We also have non-invasive biomarkers that allow us to track this biology in patients. As we just saw, increased amino acid excretion in the urine provides a direct readout of target engagement. As with SGLT2 inhibitors, we can use changes in eGFR as a signal that intraglomerular pressure is improving. To explain further how we might assess this improvement in intraglomerular pressure and kidney function, let's review some background on the typical eGFR trajectory demonstrated by other chronic kidney disease therapies. With renoprotective therapies such as SGLT2 and RAS inhibitors, we see a small initial eGFR dip. Although this may seem counterintuitive, we know that dip reflects a transient hemodynamic effect indicating a decrease in pressure in the kidney. The eGFR slope flattens over time versus placebo. Across classes of medicines, this initial dip has been associated with a slower rate of eGFR decline and therefore better outcomes, whether or not patients have coincident diabetes. In fact, nephrologists have adopted the approach of treating through the dip, as they know this predicts a better outcome. This pattern matters for MZE-782 because it provides a pharmacodynamic read-through for potential kidney benefit. An initial dose-dependent eGFR dip would be consistent with a similar long-term benefit to kidney function that we can further explore in a Phase II study in chronic kidney disease patients. Now let's look at our data with MZE-782 on slide 22 in this Phase I study. We can see on the right, even in this limited study with healthy volunteers, an initial dip in eGFR similar to what has been seen with other kidney protective therapies, as we're showing here for the approved SGLT2 inhibitor, empagliflozin. We also saw, as shown on the left, that the magnitude of the dip is dose-dependent, and it reverses within days of stopping MZE-782. This means that the initial dip in eGFR is the direct result of treatment with MZE-782. In fact, we believe this is the first clinical demonstration of the potential benefit for MZE-782 in chronic kidney disease. In closing, MZE-782 was well tolerated at all dose levels with an excellent safety profile. We saw linear PK and an approximately 11-hour half-life, which supports once or twice daily dosing. There was a moderate positive food effect after a single dose, but with twice daily administration, steady state plasma exposures were similar, fed or fasted, allowing for a potentially more practical regimen for patients. We observed consistent and dose-dependent increases in urinary phenylalanine and glutamine with exposure, up to a 42-fold increase in urinary phenylalanine and a 68-fold increase in urinary glutamine by day seven, confirming SLC6A19 inhibition. For PKU specifically, this anchors our Phase II plans to utilize plasma phenylalanine reduction as the efficacy endpoint. We also saw an initial dose-dependent eGFR dip, similar to SGLT2 and RAS inhibitors, a transient hemodynamic effect that tracks with slower long-term decline, which we will evaluate closely in Phase II. Our Phase I results, demonstrating an excellent safety profile, predictable PK, robust on-mechanism PD, and an exploratory signal consistent with kidney protection, support advancement into Phase II in both PKU and chronic kidney disease. Thank you, and I'd like to hand the call back to Jason for some final remarks. Thanks, Harold. Our Phase I results position MZE-782 to advance into Phase II in both PKU and CKD in 2026. In PKU, we plan to run a proof of concept study with plasma phenylalanine reduction as a primary endpoint. In Phase I, we demonstrated up to a 42-fold increase in urinary phenylalanine excretion in healthy volunteers, confirming target engagement and SLC6A19 inhibition. This is well above what has been seen with other approaches and leads us to believe that this will translate to best-in-class plasma phenylalanine reduction in patients. This activity is expected across all patients, including classical PKU that is not responsive to PAH activators, which is important as these patients currently have limited treatment options. Plasma phenylalanine reduction is the approvable endpoint in registrational studies, and we plan to design our Phase II trial to utilize the clinically validated link between urinary phenylalanine excretion and plasma phenylalanine reduction in patients. We expect to finalize trial design details and initiate the Phase II trial in 2026, subject to regulatory input. Shifting to CKD, we plan to design our Phase II trial to evaluate proteinuria reduction as the endpoint to demonstrate clinical proof of concept. MZE-782 could represent a new mechanism for patients who do not respond adequately to current therapies, including SGLT2 inhibitors. Importantly, we saw the initial eGFR dip in Phase I, which is a mechanism consistent with renoprotective drugs and gives us a potential read-through to longer-term benefit. Registrational studies will potentially evaluate proteinuria and eGFR slope, with the potential for accelerated approval if we show a meaningful effect. I would like to close by saying that MZE-782 offers two exciting mid-clinical stage opportunities, each with well-established regulatory endpoints. The MZE-782 profile and data enable us to explore multiple and potentially different doses for PKU and CKD. Backed by a team with the experience and track record to deliver, we're confident in our ability to execute, and we look forward to creating additional value for patients and shareholders with programs that have the potential to be best-in-class across indications with high unmet need. I will now turn the call back to Amy to lead the Q&A, and we are also pleased to have our new CFO, Ms. Patahir, join us for the discussion. Thank you, Jason. At this point, we'll open the line for Q&A. Operator, please open the call for questions. Thank you. At this time, I would like to remind everyone, in order to ask a question, press star, then the number one on your telephone keypad. Your first question comes from the line of Anupam Rama with J.P. Morgan. Please proceed with your question. Hey, guys. Thanks so much for taking the question. Just two quick ones from me. Based on the totality of the data that you're seeing, do you think you'll be most likely moving forward with a QD dose, or is it worth exploring a BID dose in PKU and/or CKD patients? Is there a difference on how you think about it between the two indications? Second question, in terms of next steps, I know the broad guidance here is PKU, CKD in 2026, but any comments on sort of gating factors and the cadence of these trial initiations next year? Thanks so much. Thank you, Anupam. Good morning. I'd like to direct a question to Harold Bernstein. Harold? Yeah, thanks. Thank you, Anupam. With regard to dose selection, we're still in the process of working through all the different aspects of which way to go with dose selection. Clearly, I think from the results, we have a number of different doses that we can consider. We'll have more information about that as we finalize our Phase II study design, as well as after seeking regulatory input. With regard to the second question that you had about sequencing, I'll turn it back to Jason. Yeah, Anupam, we're looking at all different options. Obviously, very excited about the data in front of us, and I think we'll have additional guidance in terms of that as we process the data and closer to the end of the year. Thanks so much for taking our questions, and congrats again. Thank you. Next question comes from the line of Joseph Schwartz with Leerink Partners. Please proceed with your question. Great. Thanks so much. I'd also like to add my congrats. Can you talk about how the amount of amino acid excretion that's required to produce a desired effect in PKU might differ from CKD? Is there the same relative mechanistic rationale in each case, or does it differ at all? If so, what would this suggest about the relative degree of doses that are required in each indication, and how do you think the ultimate product profile could look based on our understanding of these relationships and the data that you've produced so far? Thanks for that, Joe. Appreciate it. I'll direct a question back to Harold. Thanks, Joe. In terms of what we're going for, for PKU, clearly the goal is to reduce plasma levels of phenylalanine. What we know based on a competing development program, they showed that with a reduction of about tenfold in urinary phenylalanine or increase in phenylalanine excretion of about tenfold in healthy volunteers, when they took those doses into patients, they saw about a 44% decrease in plasma phenylalanine. Here we're showing with our highest doses a 42-fold increase in urinary excretion. We feel that for PKU, we want to achieve as much of a reduction in plasma phenylalanine as possible to provide the greatest benefit to patients. Also just note that because of the mechanism of SLC6A19 inhibition, this will work independent of any residual enzyme activity that's really required for all of the other oral therapies that are available. Now, for chronic kidney disease, our genetic analysis shows us that 50% inhibition of SLC6A19 drives a significant kidney benefit. When we've taken this into the preclinical setting, we've seen that with this degree of inhibition of the target, about 50%, we get a substantial reduction in proteinuria. In fact, this is additive on top of clinical doses of SGLT2 inhibition. I think that the takeaway here is that there are probably different dose requirements for each indication, and that's what we'll be exploring in two separate Phase II studies for each indication. That's very helpful. Thank you. As a follow-up, can you help us understand how you're able to have a more potent compound mechanistically or pharmacologically? Is MZE-782 capable of more intense inhibition of the channel, or is it prone to less exposure saturation, or is something else at play? Thank you. Yeah, Harold, can you answer that, please? Yeah, of course. The information that we have is that preclinically, based on an in vitro transporter assay, where we've been able to compare MZE-782 to a synthesized version of a competing compound based on publicly available structures, we see that MZE-782 may have up to four-fold more potency than the other compound. This is based on an in vitro transporter assay. Clearly, we're really excited to have seen that even at some of the lower doses that we studied in our first in human trial, we are achieving fold increases in urinary phenylalanine excretion that exceed what's been shown at the potential clinical doses that the competing program is taking forward. Thanks for the insights. Thanks, Joe. The next question is from the line of Tyler Van Buren with TD Cowen. Please proceed with your questions. Hey, guys. Congratulations on the stellar results. A couple for you. First, curious why you did not go to a BID dose higher than 240 mg, given the SAD data with increasing efficacy at higher doses and the clean safety profile. Are you still exploring higher BID dosing? The second question is, can you elaborate on the magnitude of the dip or benefit in eGFR that you're seeing here early in healthy patients with the 240 mg BID dose compared to what is seen with SGLT2 inhibitors? Please discuss what benefit that might translate to with CKD patients. Thank you for that, Tyler. For both of those questions, Harold? Yeah, hi, Tyler. Thank you. With regard to what limited our dose progression in the Phase I, we went to the top of the exposure range that we were able to, based on our preclinical tox. We were able to dose all the way up to the no adverse effect level in our GLP tox studies. With regard to the magnitude of the eGFR dip, as we indicated there, for the clinical dose of empagliflozin in a very large Phase III population, they saw approximately a 5 mL per meter squared decrease or dip in eGFR. This is a very small study. We were able to look at 12 participants, and we saw, with some variation, about 11.5 mL per meter squared dip. We think that signals that with that and maybe even some of the other doses, we will be in the same range as has been seen with SGLT2 inhibitors. In preclinical studies, we showed that with a dose that was only 50% inhibiting of the target, we were still able to see an additive effect of SLC6A19 inhibition on top of the clinical dose, in that case, of dapagliflozin. I think we're really encouraged that we see an early indication of a potential long-term benefit with SLC6A19 inhibition in patients with kidney disease. Thank you. Tyler. The next question is from the line of Rai Forces with Guggenheim Securities. Please proceed with your questions. Thanks for taking our question. Our first question is on the food effect. I think you reported that it was modest. Was that mainly on Cmax or AUC? Does this really present a challenge for using, you know, BID or QD dosing? Our second question has to do with, you know, given the dynamic range you've been able to access in terms of urinary fee reduction, does this imply any flexibility for your later-stage development programs in terms of how you could think about segmenting patient populations based off of, you know, particular requirements for dosing and your target, you know, plasma fee reduction? Okay, Harold, can you answer that, please? Thank you. Thank you, Rai. With regard to the moderate positive food effect, we saw that with single doses, but with dosing more frequently at twice a day, that really mitigated the food effect. Clearly with PKU patients, we're going for maximum efficacy that can be achieved, as well as, in these patients, they're on a very restricted, fairly onerous medical diet. Anything that we can do to liberalize their diet, I think, would be most appreciated. Being able to take MZE-782 independent of whatever they're eating would be a real benefit. That's the feedback that we received. I'm sorry, can you repeat for me what your second question was? Yeah, my second question had to do with the flexibility you have around dosing and the dynamic range you can achieve in terms of Phe excretion in the urine and sort of the implications it has for plasma Phe. Given that flexibility, would you envision that any of your future development efforts would include any patient stratification based off of particular demographic needs? Right. I understand the question. Certainly, that's something that we're going to explore in Phase II, where we have an opportunity to test multiple doses and even multiple dosing regimens if we desire. We're still working that through, but that's a really good point, and that's something that we're interested in looking into. Thank you. Thank you, Rai. Our next questions are from the line of Laura Chico with Guggenheim Securities. Please proceed with your questions. Good morning. Thanks very much for taking the questions. One on PKU and one on CKD. I just wanted to clarify, how should we think about the target level of plasma phenylalanine lowering you're hoping to achieve in the PKU setting? I realize you're trying to maximize the benefit, but, you know, relative to what Janus Henderson Investors saw in a decrease there in their 28-day study, is that the benchmark as you move into PKU patients? Just trying to get clarity around that. On the CKD setting, wondering if you could just comment a little bit more about the patient population that you're looking to target in the Phase II study. Would this be kind of a refractory population after SGLT2 inhibition, or are there other parameters that you're considering? Thanks very much. Thank you, Laura. Good morning. I'll take the first question. I think what we know about the PKU patients, of course, those especially that have severe or more classical form of the disease, that's clinically defined as those that have greater than 1,200 micromolars per liter of phenylalanine in the plasma. The idea here with SLC6A19 inhibition could be that it can work across the entire spectrum, including those that have severe classical form of the disease, which is the majority of the patients, as you know, Laura. The idea that you would need to be able to reduce those individuals below a particular threshold that allows them to move towards liberalizing their diet, which we've been receiving the feedback is around that 360 number. Even just doing the arithmetic there, you would have to get to a certain% decrease in plasma phe. I think while it's great that the Janus compound had shown clinical proof of concept, being able to lower plasma phe, what's great is that given what we see in the early data here, we might be able to exceed that threshold and move as many of those patients that have more of the severe classical form of disease into that area where we might be able to help them liberalize their diets. Harold, can you take the second one, please? Yes. Hi, Laura. Thanks for the question. With regard to the populations that we can focus on moving into Phase II, on the one hand, based on our preclinical data, we would envision in those patients who have perhaps an incomplete response to SGLT2 inhibition or other standard of care, to evaluate the impact on proteinuria reduction with MZE-782 on top of standard of care. As we indicated earlier in the talk, there is a portion of patients who either don't tolerate or don't really respond to existing standard of care. In those patients, especially based on this preliminary exploratory biomarker data with eGFR, there may be an opportunity to test this as a monotherapy. We're still working through how we're going to proceed with Phase II, but some of those are the issues that we're considering right now. Appreciate your question. Thanks, guys. Thank you. Again, if you'd like to ask a question, press star, the number one on your telephone keypad. The next question is from the line of Anand Dakosh with H.C. Wainwright. Please proceed with your questions. Hey, Harold. Congrats on the great data. I have a couple of questions on the eGFR part or the CKD part of the study. Maybe I'll just go through the questions. I'm happy to hear your perspective. To start with, just wanted to understand what were the baseline eGFR values in those, you know, the 2S patients? Are there ways to measure hemodynamic dip other than the eGFR, or are there other biomarkers which you looked into, such as cystatin C, or the kidney injury markers which you looked into the preclinical dataset? Did it replicate the way you saw in the preclinical elements? The last one is, given the dip, how to interpret the dip with respect to the preclinical data where you saw additive effect with the SGLT2 inhibitors in the preclinical elements? Thanks, Ananda, for the question. Maybe just to clarify the second one, are you asking did we see eGFR dip in the preclinical model? Is that the question? How do you interpret the data with respect to the additive effect which you saw in the preclinical data with respect to today's dip? As you think about the Phase II design. I see. Okay, just reconciling the preclinical data with the eGFR dip. Right. Harold, can you answer that one, please? Yeah, sure. Thanks for the question. As far as baseline eGFR values, this is a normal population, and we only included participants with eGFR in the normal range. The second part of your question about whether or not we explored cystatin C and KIM-1 and other biomarkers. We actually use serum creatinine as our way of calculating eGFR, and we had no other indication that serum creatinine would change due to sort of non-renal mechanisms. There was no evidence of any sort of myostatic effects. As far as other indicators of kidney injury, these were normal volunteers, and we wouldn't expect to start off with elevated levels of biomarkers like KIM-1 that are usually elevated when there has been some acute proximal tubule injury. We wouldn't expect to see a change there. Finally, in terms of how to interpret the additive effect that we're seeing in the preclinical studies, there are a couple of ways that we've thought about this, and I appreciate you asking that question. One, of course, is that although the tubuloglomerular feedback that we are talking about that may be driving down glomerular pressure based on SLC6A19 inhibition is also likely due to delivering more sodium to the distal convoluted tubule, similar to SGLT2 inhibitors, it's through this different path. The simplest explanation is that it's additive because you're increasing the amount of sodium delivery. However, we looked at proteinuria reduction in our preclinical models, which really is a summary of all the potential effects that an SLC6A19 inhibitor may have. The fact that we're seeing an additive effect could also be due to some of the other potential mechanisms of action that we described earlier, including detoxification through removing toxic metabolites, as well as delivering more nutrients like amino acids to the distal tubule. Bottom line, we were really encouraged to see that not only did we have this nice impact on proteinuria reduction in preclinical models, but that it was additive on top of what we saw with an approved SGLT2 inhibitor, dapagliflozin. Great. Thanks very much. That was very helpful. Thank you, Ananda. The next question is from the line of Julian Harrison with BTIG. Please proceed with your questions. Hi, good morning. Congrats on these impressive results, and thank you for taking my questions. I have two. First, Jason, just to follow up on an answer to a prior question, are you able to maybe start framing expectations for the proportion of classic PKU patients you would expect to achieve or go below the plasma Phe threshold associated with diet liberalization? You mentioned that's easily translated or modeled from the results today. Second, it's great to see formal Phase II plans both for PKU and CKD. I'm wondering if you could talk now about any relative priorities there, if any exist between these two opportunities, and could that maybe be contingent on future data? Is there an opportunity to address both of these markets simultaneously with 782? Or do you maybe envision a fork in the road for future development? Julian, thank you for the question. I think, on the first question, this data is pretty fresh, as Harold kind of described. We have to look at the way that we're going to design our Phase II and what we would define as success within that Phase II. I have no current guidance in terms of how we think about that because we'd like to get the study designed and think about getting some feedback from patients as well as the regulators in terms of that. I think, going forward, what's nice, of course, is that we have a range of different options, just to answer your second question, given the fact that we can think about development paths in both of them. What we've described today is that we're going to be taking the data in, get some feedback, including those from some of the regulators, and we'll have more news and guidance on how we would think about those studies. What's nice, of course, is that we have clinical proof of mechanism on both of these with a well-defined path to how we can define success with Phase II. Excellent. Thank you. That's very helpful. Congrats again. Thank you. Yes. Thank you. The next question is a follow-up from the line of Laura Chico from Wedbush Securities. Please proceed with your questions. Hi, thanks so much for taking the follow-up. I apologize. One more on the PKU data. Could you speak at all to any preclinical data that you've obtained on doing 782 in combination with perhaps like Kuvan or something along those lines? Could you speak to the potential for combination therapy? Thanks very much. Do you want to take the first part, Harold, please? I'll take the second. Sure. Thanks, Laura, for the follow-up. We've essentially, in preclinical models of PKU, really just looked at plasma phenylalanine reduction aligned with urinary phenylalanine excretion. We haven't generated data with regards to other therapies in that model. Jason, do you want to take over? Yeah, it's a good question. I think we can now, with this type of data that we haven't had, and clearly the excellent safety profile that we have, there could be ways to think about developing a TPP in combinations. I think we would take that into feedback and talk with different folks in order to think through that. At the end of the day, as you are alluding to, what we want to be able to do is help in the sense of maximizing the efficacy with plasma phenylalanine reduction such that the patients can be liberalized from their diet. If the combinations end up being one form of that, we would explore it in further development. Thanks. Of course, thanks for the question. Thank you. There are no further questions at this point. I'd like to turn the conference back to Jason Coloma for closing remarks. Thank you, everyone, for joining us today. This today marks an important milestone for Maze Therapeutics as we share this data. What we see is compelling and continuing the development and advancing MZE-782 for patients. Before we close, I did want to express my deep gratitude to the Maze Therapeutics team. This program has been years in the making from our foundational work in genetics to identifying the right molecule and now to generating strong clinical data. I'm incredibly proud of what we've accomplished as a team. Looking ahead, we're very energized by the prospects and the next phase as we move into patient studies in both PKU and chronic kidney disease, two areas where we believe MZE-782 can make a meaningful impact for patients. Thank you again to the analysts and investors who joined us today. We look forward to continuing the conversation in the days and weeks to come. Thank you. Ladies and gentlemen, thank you for participating in today's webcast and conference call. This call was recorded and will be available shortly for replay in the investor section of Maze Therapeutics' website. This concludes our call. Have a good day.