Thanks everyone for joining for the next session with Travere Therapeutics. I'm Ygal Nachmovitz, a biotech analyst here at Citi. For those in the room, please ask questions, just raise your hand and we can take the questions. Also welcoming those listening on the webcast. It's my pleasure to have with me the CEO of Travere, Eric Dube, and the CCO, Peter Heerma. Thank you both very much for coming out and joining our conference. In the last couple of days or three or four days, you've had some very good positive news. I'll let you share that and explain the significance of that positive FDA decision for your sparsentan. Thanks. Yeah, Ygal, thanks so much for hosting us. The FDA recently approved a modification to our REMS. I'll explain what it is and Peter can talk a bit about what that could mean for us moving forward. When we were approved under accelerated approval about two and a half years ago, based on the variable liver safety profile of other endothelial receptor antagonists, we were asked to have a REMS where patients for the first year of their treatment would need to be measuring their liver function every month and then thereafter every quarter. Also, as part of the endothelium class, we had a REMS for embryo-fetal toxicity. Last week, FDA approved the removal of the embryo-fetal toxicity and pregnancy testing REMS and changed the liver functioning testing to every three months, which aligns with how most patients with IgA nephropathy, one, see their nephrologist and two, are tested for their kidney function. This is very much more aligned with how these patients are being seen under standard care. Peter, maybe you can speak about what this could mean. Yeah, the significance commercially for the modification of the REMS is that patients are now monitored like every three months, which is to Eric's point, for most of the patients that are being seen by the nephrologist. There's no additional obligation for patients. I think in particular, two and a half years into the launch, this is really relevant because last year in September, we had a full approval. Within the accelerated approval, we had a label that read for patients that rapidly progress, generally with a proteinuria level of 1.5 g and greater. Since September, with the full approval, there is no proteinuria cutoff. We see a shift to the left to patients that start FILSPARI with proteinuria levels lower than 1.5 g. Many of those patients are not seen monthly but quarterly. I think this is the right time to have this modification. Physicians often are pre-selective in their mindset, like what patients will be compliant on monthly monitoring. I think that will open up right now for a broader patient population, in particular what I mentioned with lower proteinuria levels. We believe that that's where the majority of the patients are. We believe that 70% of the addressable patient population resides with a proteinuria level of lower than 1.5 g. This is where we start to penetrate. I think we have a very strong proposition and the modification of the REMS helps us with quarterly monitoring, which is consistent to other medicine in this market and consistent to how often patients are being seen by their nephrologist. Since it's very new news, just explain how you communicated it to the practitioner base. I mean, you immediately sent out a message, yes, that now you can shift and they're implementing that immediately. We had indeed the next day at 3:00 A.M., we had a call with our full field force to inform them. It's also important to realize it's not only about the REMS. I mean, FILSPARI we believe is a better product because of the consistent nephro protection it provides by inhibiting dual bad actors in the kidney, being angiotensin as well as endothelin. That's the reason the physician prescribes and the ease of access is the contributing factor with the REMS modification. I think there is no reason why a physician shouldn't prescribe it. It's a better product and the modification of the REMS now allows for monitoring that is consistent to other products as well. We've talked in the past about the REMS and going from the monthly to the quarterly as exactly happened. Is there a further plan to go to less frequent or nothing? For example, every twice a year or nothing? Is that in the cards or is that even needed to move things further? Yeah, so our plan has been, first let me take a step back. When we spoke with the FDA at the accelerated approval two and a half years ago, they said, "Look, we recognize that your data safety package and your benefit has not yet been fully established because it's under accelerated approval." We didn't have the full safety data package. They said they are open to revisiting the need for REMS. What we had decided is that a two-step strategy would be the most expeditious for helping patients access. The first step one is what we just achieved, which is to get to quarterly, which is again similar to how patients are being seen in the real world. It's also how patients were being studied in our clinical trial in terms of study frequency. The second step would be full removal. We still have not seen any cases of HAIs law in both the clinical trial exposure as well as real-world exposure. Assuming that that continues and we have exposure, the FDA is looking as part of a post-marketing requirement, 3,000 patients follow up for two years. We're well underway to be able to do that. We do have opportunities to go back to the FDA. We'll take every opportunity we can to be able to share the additional exposure data and request full removal. We think that certainly is going to be helpful in ensuring that no patient is left behind to say, "I don't think that this patient can be on FILSPARI because they won't comply with liver testing." It is our goal. While we don't see that the REMS currently is a barrier, we don't want it to also be perceived as a barrier or a perceived safety liability with the medicine. Have you communicated that level of exposure you described? When might you have that in place to make that argument to the FDA? Yeah, we've not specified specifically when because a lot of that is based on the exposure in the real world. We've been very successful with the launch, but it's very difficult to predict with that level of accuracy. We are well underway to be able to do that. We also want to make sure that we're taking every opportunity to go back to the FDA, particularly given that they've approved another medicine within this class without a REMS. We do want to make sure that we're taking every opportunity to go back to them and request the full removal now that we have the modification. Right. Peter, you mentioned the proteinuria levels that are moving now below the cutoff, the old cutoff. Do you track, is that possible to track that in the real world, like what that average tends toward and how it progresses over time? Yeah, we have multiple tools to monitor that, to see what the general proteinuria levels are when you get patients on the market. Patient chart, other data, market research data, etc. You haven't commented specifically on what the numbers are, how it's moving below the 1.5 g or? Yeah, we haven't mentioned a specific number. What we have mentioned is that the median proteinuria level moves to the left and is now below 1.5 g. Okay. It continues to move in the direction that we would like to see. Yeah. Which you would expect with more repeat prescribers because often the first patient a nephrologist is prescribing FILSPARI for is a patient that the physician is most worried about. When the experience is good, both from an efficacy and a safety perspective as well as from a patient experience, I think the high compliance and persistent levels speak to that as well. A physician is more eager to start prescribing also for other patients often with lower proteinuria levels. Okay. Of course, the REMS is important, but that's only one piece of the puzzle. There's another piece of the puzzle, or at least one other piece of the puzzle, which is the KDIGO guidelines, which we've talked about a lot. Can you walk us through what to expect there for the update and you know how you see that driving FILSPARI launch relative to REMS and how they work together? Yeah, it's a great question. Last year, I mentioned earlier that in September we had our full approval and basically no longer had a proteinuria cutoff in our label. In the same week of our full approval, there was also the draft global guideline called KDIGO that actually went for a much lower treatment target for proteinuria. Historically, that was 1 g per day. It was moved to 0.5 g or preferably 0.3 g, meaning complete remission in their draft guidelines. Very soon, we anticipate that the full guideline will be published. I think that will further reinforce one that every patient should be treated towards full remission, but also that there are two categories of treatment options. One that is really focused on protection of the nephron, kidney targeted. That's the space that FILSPARI plays in. The other space is more upstream to go on the immunosuppressive side of the equation. That's the treatment category where you have the steroids, the complement inhibitors, potentially the APOC compounds, the B cells that are coming too, they may come to the market. I think that reinforces the positioning for FILSPARI as well. The third one is the way FILSPARI is being called out in the draft guidelines as the only medicine that has been showed superiority for a maximally tolerated active RAS inhibitor. I'm very pleased with the language that was being used. FILSPARI is also approved in the U.S. and in Europe. I think that that will help us to have a strong position in the guidelines. Is there a specific date when they're getting published, or is it more of just a general statement like, I think it's in October, but that might not be right. It's sometime this fall. I think we're not saying the specific date, but sometime very imminently, yeah. Okay. You obviously had the second quarter numbers, which look good, and you got over this sort of 700 start form plateau. Can you just talk more generally about the momentum on the commercial side, and of course these two drivers, but how do you see the trajectory moving now? Yeah, maybe I'll make a comment generally and then Peter, you can provide a more meaningful response. We've not yet provided guidance for our revenue outlook, but we remain very confident in continued growth of revenue throughout the year and certainly throughout next year based on the very strong demand and based on the opportunity that we have. If we think about the addressable population of our full approval in IgAN alone, there are about 70,000 patients in the U.S. that we believe can benefit from FILSPARI that would be addressable today. When we look at the cumulative patient start forms that we've received since accelerated approval, we're not even penetrating 10% of that addressable population. There are many patients out there that are diagnosed, that are treated with off-label RAS inhibitors. The overwhelming majority of them are failures of RAS inhibition alone and are not at goal. With the KDIGO guidelines, that's only going to accelerate the uptake and the need for something better than these unproven therapies. That's really where FILSPARI comes in. We do believe that there's a strong opportunity for us to continue to grow. There's been a lot of focus on what's going to happen when you have these B-cell therapies come to be available for these patients. As Peter talked about, this is really about the future of combination therapy. We have no evidence to show that patients would benefit from an immune suppressant like a steroid or immune targeted therapy like a B-cell alone. All of those are being studied on top of nephro protection, like RAS inhibition and some of them on top of FILSPARI. The future really is that combination. Our focus is to really upgrade these patients' foundational therapy from being a RAS failure to lowering their proteinuria further by switching to FILSPARI, regardless of whether they're on a combination with an immune targeted therapy and regardless of which one that is. That's really what gives us great confidence in the outlook for growth. At some point, we'll look to provide guidance. At this point, we have a lot of dynamics and catalysts in the near term to be able to work through before we do that. Peter, maybe you can talk a bit more about what you're seeing. Yeah, I know absolutely. Based on the last point that you made, it's a very dynamic market, especially for rare disease. I've not encountered so much new treatment options in rare disease, which I think is a good thing. First of all, it's a good thing for patients. Second, I think it's good for us as well to have more modalities and more companies coming to the market. The biggest challenge we were initially facing was really to reinforce the urgency to intervene earlier in this disease. Historically, IgA nephropathy was seen as a relatively benign disease by nephrologists. It was really till we really invested in registry data, and we had 2,500 patients from the UK in the RaDaR study, longitudinal follow-ups that actually indicated that every patient in that registry did face kidney failure in their lifetime. The average time towards dialysis was 10- 12 years. That was really an eye-opener for a lot of nephrologists. That's also what is now being reflected in the guidelines and why the treatment target is much more aggressive, moving from 1 g per day to 0.5 g or preferably 0.3 g. I think all the new companies that are coming to the market are reinforcing that same message. To Eric's earlier point, we believe that the addressable market is about 70,000 patients. The majority, 70% of those patients, remain with proteinuria levels below 1.5 g. I think those patients are still at risk, but we're underestimating what the real risk was. I think that will help us to further penetrate so the pie will be getting bigger. It's up to us to take a big piece of the pie. I believe we have a very strong proposition with the full approval, with the data, the head-to-head long-term data that FILSPARI has in a very strong position also in formularies and payer plans. Do you have a view on which of these REMS versus KDIGO is sort of more of the bigger driver of further uptake? Are they going to kind of work in synergy? I think it's going to work in synergy. I think it's really difficult to parse out both the very strong profile clinically of FILSPARI, having both superiority data versus an active comparator and having two-year data showing the only drug over two years to be able to have a cumulative benefit on kidney function. We're one of the only companies in this space to have actually disclosed complete remission data. These are really important to nephrologists as they think about why they would choose to select one medication over another. The other aspect, the KDIGO guidelines, as Peter talked about, is going to drive that sense of urgency. I think the REMS is going to be important for a segment of patients that may have been reluctant. I certainly don't like to, you know, get my blood tests, etc., and to do it every month versus every three months. I know what I would choose. It's certainly going to help. I think the broader opportunity is to be able to expand beyond these patients being undertreated by ACE inhibitors and generic steroids for decades. Most, I mean, most if not all of the patients that are starting on FILSPARI have had some other intervention for IgAN. Is that right? Or did you get anyone that's newly diagnosed or that's unlikely? Yeah, we have seen some, but the overwhelming majority of patients that we see as addressable will have been on an ACE or an ARB plus an SGLT2. Yeah. Most of the patients that we see in terms of their journey, they will have been diagnosed or at least treated for proteinuria by their primary care physician before being referred. What I think is important about your question is, one, is twofold. One, the majority of patients are already on ACE inhibitors or ARBs and are not at goal. 90% of the patients with IgAN are on an ACE or an ARB, and 90% of those patients are not at goal. We have about 80% of the addressable population that can be better served by FILSPARI. The second aspect I would answer your question is, we're the company that's conducted the only treatment-naive trial in the space. We have a trial called the SPARTAN trial where we looked at patients that were completely treatment-naive. They were just diagnosed based on biopsy for their IgA nephropathy. Mm-hmm. These patients were not on ACE or ARB. They were not on an SGLT2. They were not on a steroid. Their first therapy for their kidney disease was sparsentan. What we saw was compelling. We saw that there was about a 70% reduction in their proteinuria out to 24 weeks. Nearly two-thirds of them were able to get into complete remission of their proteinuria, and their eGFR was stable for that six-month period. At the end of six months, we did a repeat biopsy. A very intensive clinical protocol, but one that is going to inform us not just on the function but the structure of the kidney when you're treated with FILSPARI. We are seeing a very compelling profile when you initiate FILSPARI early, and it makes sense because when you think about a nephroprotective therapy, you want to intervene earlier. On average, the patient with IgA nephropathy is diagnosed, they've already lost about 50% of those nephrons. Those nephrons are never coming back. What you want to do is everything you can to protect the remaining nephrons you have. To be able to start with a superior therapy like FILSPARI early at diagnosis is going to give the patient the best opportunity to be able to retain those nephrons. We have other treatment options if this patient does need more, for example, the potential for B-cell complement, etc. Is that sort of within the scope of the current label? I mean, a physician could find a new patient and employ FILSPARI from right out of the gates, right? Would there be more work that needs to be done in terms of the label language to kind of carve that out in a more structured way? Yeah, so the SPARTAN data, the treatment-naive data is not within our label. We've not submitted that to the FDA. The indication statement, however, is broad for the treatment of IgA nephropathy. Right. A physician for their own decision can decide whether they want to start with FILSPARI or whether they want to start with an ACE or an ARB and then wait for that patient to fail. That's really up to the physician and for the payer to be able to decide. You know, Peter can certainly speak to what we're seeing in terms of physician prescribing behavior. Okay. Yeah, maybe one point too, like anecdotally what I've heard several times now is that based on KDIGO and based on the RaDaR data set that I was referring to earlier, actually biopsies are being done early on. I heard examples like patients with proteinuria levels like 0.4 g that wouldn't be biopsied historically, but are being biopsied right now. Physicians saw sclerosis, identified IgA nephropathy, and actually started FILSPARI right away. This patient was not on RAS inhibitors. We don't promote that specifically, but I hear anecdotally feedback, and it is consistent to the label that we have right now. You mentioned, of course, being a foundational therapy and the intersection with the B-cell modulators. What about some of the other recent launches like this drug called Vanrafia? How do you see that playing out? Yeah, to Eric's earlier point, you have basically two treatment categories. One is really focused on protecting the remaining nephrons. The other is more upstream on the immune suppression and immune modulation. Vanrafia and FILSPARI are the only two novel medicines in that foundational category. FILSPARI, I think, is differentiated because it is a different mode of action. FILSPARI is inhibiting both bad actors in the kidney that are actually causing damage, being endothelin as well as angiotensin. You want to suppress both simultaneously. Atrasentan is the other product that you are referring to. It's a single endothelin inhibitor, but it's kind of like dependent on RAS inhibition. We know that generic RAS inhibition in clinical practice is often suboptimal. You basically see that in all long-term compliance and adherence trials. We often hear that from the community as well. My hypothesis is, and it's my personal hypothesis, that may be the reason after nine months you saw less of an absolute reduction in proteinuria with atrasentan relative to FILSPARI. FILSPARI has the long-term benefit that we have shown, published, and is being reflected in our label as well. I do believe based on the consistent nephro protection that you have by inhibiting two bad actors in the kidney, together with the long-term data and the superior effect versus a maximally dosed RAS inhibitor, that we have a very strong position versus atrasentan. The only aspect that they could say like, we are better in that is the REMS that you asked earlier about. I think the modification to now three months monitoring is consistent to what they actually have in their label as well, even though it's without the REMS. Okay, we could keep going on IgAN, but we want to talk about the other indication, which is an important one, potentially the first approval if it happens, which is at Purdue for coming up in January 13th. Of course, this is, I'm referring to FSGS. Tell us about the work there, about the phase III work, as well as the work with this PARASOL working group and the plans for which an expected ad come later in the year. Yeah, so this is a story that I think we've seen previously within rare diseases where oftentimes you need to design a trial, select an endpoint, and power a trial without having a rich literature to base it on. In FSGS, when we designed our DUPLEX trial, the only data that we had was from our phase II DUET study, which showed a superior profile in proteinuria over maximum dosed irbesartan. Like many other kidney diseases, we were basing our view on reducing proteinuria in a trial can improve the eGFR over time or can stabilize eGFR over time. What we learned when we completed our DUPLEX study was that we showed a profound reduction in proteinuria that was superior to irbesartan, and we showed a clinically meaningful difference in the chronic slope of eGFR of about 0.9 mL per minute per year, but that was not statistically significant. The eGFR difference was not statistically significant. We were not able to file an sNDA for this indication. FDA told us at the time, don't file based on eGFR data, continue to do work with the FSGS community for us to better understand these results. That's really where the PARASOL initiative was born. PARASOL was born out of a public-private partnership with the FSGS KOLs globally, the patient community, as well as global regulators, including FDA. We were not involved in PARASOL, but the real objective of PARASOL was to identify what the right endpoints were for this disease because I think our results really shocked everyone that you were able to get a 50% reduction in proteinuria that did not translate into a benefit in kidney function within two years. What PARASOL did was they asked KOLs around the world with FSGS data to donate their registry data. 26 registries were donated to be able to pool and look at these patients over time to see what we were missing in studying this disease. The first conclusion that came out of their analyses was eGFR is, of course, important. It's a measure of kidney function. It's just not feasible in an FSGS clinical trial. That's because the variability is too high. The variability in FSGS is high for two reasons. The first is it's a heterogeneous disease. Unlike IgA nephropathy, where the etiology of the disease is very well defined and it's singular, in FSGS, you can have FSGS that is immune mediated. It could be genetic, and within genetic, you can have different genotypes, or it can be of unknown cause, or it could be secondary to another disease. In addition, you could have variability within a single patient, where over time, this is a relapsing and remitting disease, and so the eGFR can be highly variable. That contributed in our trials to variability in our FSGS trial that was more than double the variability that we saw in our IgAN trial. The PARASOL initiative really basically explained what we saw in our programs. The second conclusion from the PARASOL initiative was to say, if it's not eGFR, what possibly could the endpoint be? They looked at what is biologically plausible with this disease. Regardless of what type of FSGS you have, if you have FSGS, you have a disease of the podocyte. You have a podocytopathy where over time, the podocytes, which are the filtering cells within the nephrons, begin to die. They begin to slough off, and that is what contributes to progressive proteinuria, which led them to their third conclusion, which is, can proteinuria be independently predictive of a patient's risk of kidney failure over time? What they saw is that for patients that are able to lower their proteinuria to certain thresholds, you're able to reduce a patient's risk of kidney failure at eight years to 85% to 90%, which is what led the PARASOL initiative to say proteinuria really should be the endpoint for FSGS trials. With that in mind, when those conclusions were reported out, we went back to the FDA and said, are we able to then submit an sNDA evaluating the benefit of sparsentan in our phase II and phase III, showing a robust and consistent reduction in proteinuria? The FDA said they are open to that submission, and they now are reviewing the program. They said that they're planning to have an advisory committee to review our results, and we've not yet seen that in the published register, so we'll see what comes of it, but the engagement with the FDA has been consistent with our experience with our IgAN review. How do you expect the discussion to go, assuming there will be an AdCom? You're going to make essentially the same points, the same conclusions that the PARASOL initiative came away with? You're going to reiterate those at the AdCom, or will there be additional analyses as well? How will that work? Yeah, so we don't yet know what FDA would focus on for the advisory committee, assuming they have one. What we can go on is based on what they shared with us at our type C meeting, which they said our review of this file is essentially going to be understanding the benefit of proteinuria in the context of the PARASOL initiative. We do believe that PARASOL is going to be a very important aspect to educate the panelists on why does eGFR not work, why did we miss our endpoint in a trial that was well designed, well conducted, and clearly showed this benefit on proteinuria. I think that's going to be an important context setting. What's important also is to remind everyone we did not contribute or donate our data to PARASOL. We wanted to retain the independence of our data set so that FDA can independently review our data in the context of what was recommended as an endpoint for PARASOL. What we believe is going to be important is to show that what PARASOL would predict you actually see in the first clinical trial, the first phase III interventional trial done in this disease, which is if you can lower proteinuria, you actually have a benefit on hard endpoints. We had an analysis that was presented at the European Renal Association meeting this year from our phase III study. When you look at patients in our phase III study, they were able to achieve either partial or complete remission. Their risk of hard endpoints, so kidney failure, renal replacement, their eGFR is less than 15 mL per minute, so essentially kidney failure. The risk is reduced within a two-year timeframe by 67%- 77%. That is incredibly meaningful when you think about the progressive nature of this disease. It does replicate for the first time in a clinical trial setting what we're seeing in PARASOL. That's really what we're preparing. Of course, we'll look to learn more from the agency on what they want to ask at an advisory panel, but that's the focus of ours given what they shared with us at the type C meeting. For that analysis you just described, it was sort of like you picked a point, but below which you saw that much improved risk profile. What we looked at was the way that the PARASOL initiative analyzed the data is they looked at patients between week or month 12 and 24. If patients were able to achieve certain thresholds of proteinuria control within that 12-month period, they then looked at what happens at seven to eight years. The hypothesis is if you can get proteinuria below a certain point, that's going to have some kind of effect longer term. What we looked at is within our 12 or 24-month trial for patients that were able to achieve those, what happens within that same 24-month period because we didn't yet follow them longer than that. Even within a two-year period, we were able to show that very meaningful reduction in the risk of hard endpoints. We have other measures that were pre-specified like our partial remission endpoint showing that there's a very consistent treatment effect, whether that's measured at nine months or two years or at any point in that two-year trial, showing a consistent 1.5 times greater proportion of patients that achieve partial remission. There are a number of different ways that we can look at proteinuria. When you take a step back, what's important is it doesn't matter. Every single way that we look at proteinuria, you see a superior treatment effect compared to maximally tolerated RAS inhibition. I guess what I was getting at is, I mean, there was a specific proteinuria, there was a number that you went above and below that showed this risk stratification. Did you do that in, you know, kind of like as a ladder, like as you progressively lower the proteinuria, you continue to see even better long-term risk? great question. That's what I'm getting at. Yeah. For context, the PARASOL initiative showed that the lower you get, the better. It's incremental. You basically, you know, once you get below one, you're getting most of the risk reduction from that trial. When you look at the data from DUPLEX, when we look at partial remission, which is less than 1.5 g of protein and a reduction of greater than 40% of proteinuria from baseline, you see a 67% risk. Okay. In hard endpoints, when you get further down to complete remission, which is less than 0.3 g of protein, that risk reduction further improves to 77%. You do see that step rise. Right. You're getting two points on the line. That should be quite a strong argument, right? I mean. We think so. We're certainly working with many of the experts to make sure that we are able to provide a very cogent and robust description of our data, particularly in the context of the PARASOL findings. Okay. Okay. We have three minutes. One more, a somewhat unrelated program, pegtibatinase. Can you talk about that one, please, quickly and how that ended up being part of Travere and what the origins of that were? Also, what are the plans given now you're restarting the manufacturing? Yes. We are very excited about our program with pegtibatinase, which is for classical homocystinuria or HCU. This is a program that came out of the University of Colorado. HCU is a genetic metabolic disease. It is a disease that for half of the patients is diagnosed upon newborn screening. The other half of the patients are missed but continue to have a toxic accumulation of homocysteine that manifests then symptomatically within oftentimes their childhood and teenage years. By the time patients are a teenager, about 25% of them will have an ischemic event. Before their 30th birthday, half of them have an ischemic event. It is a very significant disease. The current standard of care is really inadequate nutraceuticals and a very, very strict protein-restricted diet. That is the worst part of the disease for many of these patients. This is a humanized pegylated enzyme replacement therapy and would be the first disease-modifying therapy that really addresses the enzymatic defect for these patients. We showed in our phase II a profound improvement of 67% reduction in homocysteine levels, and 100% of these patients were able to get below the guideline target of 100 micromoles of homocysteine. 50% of them were able to get below 50, and some of them had been able to normalize their homocysteine levels. The key of our phase III, which we are in, is to be able to replicate those, but also as part of a sub-study, demonstrate what patients want most, which is keep control of the disease, but allow me to eat a little bit more protein. Allow me to normalize part of my diet. That is where we are. We ran into a manufacturing challenge when we moved from clinical scale to commercial scale. We paused enrollment to make sure we were able to resolve those. We have made very good progress in resolving those manufacturing scale-up challenges, and our target has been to reinitiate enrollment of our phase III next year. We are well on track to be able to do that, and we will look to provide further updates as soon as we can. We want to make sure that we are able to move very quickly in phase III because these patients have been waiting very patiently for what could be the first therapy approved in decades for their condition. It fits with us, we are a rare disease company. We've had other therapies, some of them we've out-licensed or divested to Mirum that really is very similar to the capabilities within HCU, but also, you know, core to what we've been doing with sparsentan is identifying these patients, working with regulators and thought leaders to identify the right endpoints, particularly where there have not been a regulatory pathway, and to be able to enroll these trials that have been very challenging. Peter's team has done an amazing job with the launch of FILSPARI. We continue to have a cystinuria treatment, Thiola, that is the gold standard for that condition, and we'll take a lot of those learnings to get to the commercialization of pegtibatinase. You'll take that one to commercialization yourselves. That's our plan. Okay. That's our plan. It's a very meaningful opportunity for the company and certainly for this community. Do you have the global rights from the University of Colorado? That's right. Okay. That's right. Okay, that could launch sometime, I guess, when? What are we talking about? We've not provided the timing. We want to make sure the gating factors really to resolve the manufacturing scale up. Once we get through to phase III, that's typically when we'll have better line of sight to that timeline. Okay. Excellent. All right, thank you so much. I appreciate it. We'll be chatting again soon. Thank you, Ygal. Thank you. All right, welcome.