Welcome, everyone, to the 44th Annual JP Morgan Healthcare Conference. My name is Anupam Rama. I am one of the Senior Biotech Analysts here at JP Morgan. I'm joined by my squad, Priyanka Grover, Joyce Zhao, and Rati Pinhe. Our next presenting company is Travere, and presenting on behalf of the company we have CEO, Eric Dube.
Good afternoon, everyone, and thank you to JP Morgan, Anupam, and team. My name is Eric Dube. I'm the President and CEO of Travere Therapeutics. It's my pleasure to be here, and I appreciate your time learning a bit more about the work that we're doing at Travere. You can see here our forward-looking statements, which you can find this and other details on our website. For us at Travere, being in rare disease is a deep commitment, and for so many of us, it is personal. There are so many of my colleagues who joined Travere because they themselves have a personal connection to rare disease, whether they themselves are a patient, a mother or a father, or a friend to someone in rare disease, or, like me, a rare cancer survivor. So for us, it is personal, and we bring a patient-inspired approach to everything that we do.
Earlier this afternoon, we provided an announcement around our 2025 performance, as well as some other updates on our three priorities. And we have some very exciting updates for each of our priorities that I'd like to go through. The first is that we reached an all-time high in the number of patients that we reached with FILSPARI in IgA nephropathy. We reached 908 new patient start forms in quarter four, and I'll go into a bit more detail of those dynamics and that performance. We also have achieved 143% growth in our revenue for 2025 compared to 2024. So another outstanding year of execution in being able to reach more patients, and it's another year of outstanding results. We also announced that the FDA is continuing to review our sNDA for FSGS, which I will touch on momentarily.
We also announced that our pegtibatinase phase III program, the HARMONY study, will be reinitiating this quarter, and that's for the treatment of homocystinuria, or HCU. And we also ended the year with a very strong financial foundation. We achieved $410 million in net revenue. That broke down between $323 million for FILSPARI and about $88 million for our Thiola portfolio in cystinuria. We ended the year with $323 million in cash, which we have sufficient funding to be able to support all three of our priorities into the future. Now, with that said, I do want to provide an update on the regulatory engagement for our FSGS sNDA. I can imagine that's on the minds of all of you.
What I can share with you is that Travere is charting new territory within rare disease, and there's no better example than in FSGS, where our understanding of the disease and the understanding of the endpoints used in clinical development are evolving with the evidence, and we're in a very unique position. Tomorrow is our PDUFA day, and this is what I can share with you as of today. Just before the holidays in December, right as we were awaiting a draft label from the FDA, we started to receive a series of additional information requests from the FDA that are focused on further characterizing the clinical benefits of FILSPARI. Importantly, none of those requests were related to safety or to manufacturing.
And as of Friday, just three days ago, we provided the FDA and submitted responses to those questions that we believe should address the questions that they've posed to us, and those responses are currently under review by the agency. Now, I'm sure it's no surprise to any of you that the regulatory delays have become more commonplace over the last year. And while I can't say that that's the case here, what I can say is that the agency has engaged at a high level with us throughout this, and we have engagement with them, including the highest levels of leadership within the cardiorenal division. So unfortunately, I won't be able to share a lot of detail with you today, as our PDUFA date is tomorrow. What I just shared with you is inasmuch as we can, and I recognize you may have questions.
What I will share with you, and the expectation is that when we receive notification from the FDA, we will certainly share more. So with that, what hasn't changed are the three priorities that we have at Travere, and I'd like to go into a little bit more detail with you for each of those. Our goal of making FILSPARI the foundational therapy within IgA nephropathy continues with success. We've seen our strongest quarter to date last quarter and the strongest month since launch last month. Our teams are exceedingly executing very well in reaching patients, even in the face of additional treatment options that have become available. I'll cover further updates on the opportunity and the strength of our data in FSGS, and I'll also cover the opportunity that we have and our phase III program within homocystinuria, or HCU.
With that, let's turn our attention to IgA nephropathy. IgA nephropathy is a rare kidney disease that often affects patients in the prime of their life. The typical age of someone being diagnosed is in their 20s and 30s, and the median time to kidney failure is about 11 years. Over the last couple of years, largely due to ours and others' work, we now understand that this is not a slowly progressing disease. These patients, once diagnosed and if they have proteinuria, are at significant risk. That's now reflected in the recently published KDIGO guidelines. The KDIGO guidelines are the global kidney guidelines for treatments, including for IgA nephropathy, which was updated a few months ago.
Currently, there are about 70,000 patients who we believe are addressable, and that reflects those patients that are diagnosed based on biopsy, that are under the care of a nephrologist, and have proteinuria levels that place them above 0.3. So they're essentially not in complete remission of their disease. And so there is a tremendous number of patients that we believe could benefit from innovation, including with FILSPARI. And this is a tremendous opportunity for us, as well as for others that are entering this space. I'd like to share with you why we believe that FILSPARI is uniquely positioned to be the new foundational therapy within IgA nephropathy. This is a once-a-day pill, and the clinical data that we have generated with FILSPARI demonstrates a very clear differentiated profile.
Our PROTECT phase III program is the only head-to-head study conducted within this space, and we are able to demonstrate not just a profound reduction in proteinuria compared to the current standard of care RAS inhibition, but we also see, and has been very well received by the nephrology community, an accumulation of benefit in kidney function measured by eGFR over two years. And it was with the availability of our two-year data from our phase III that really helped to build further confidence and further use of FILSPARI in the real world. FILSPARI is non-immunosuppressive, and based on the profile, it really gives flexibility for nephrologists to use this in combination, which we continue to see in the real world. And as we look at our performance last quarter, I couldn't be prouder of the execution and the results that my team have delivered.
We have seen the highest level of new patients achieved in the fourth quarter, and again, just as we're seeing new treatment options be available for patients with IgA nephropathy. 908 new patient start forms in quarter four. And that growth is based on both existing nephrologists who have had a good experience with FILSPARI and are looking for other patients to benefit from moving from RAS inhibition to FILSPARI. But we also see some of the greatest growth coming also from new prescribers finally deciding to adopt innovation for their patients with IgA nephropathy, starting to use FILSPARI in their practice. What we're also seeing is a continued decrease in the median UPC level when they start to prescribe, meaning that the physicians are starting to prescribe for earlier and earlier patients. And that's important for two reasons.
One, that's what the guidelines are now recommending, that patients are not safe if they have proteinuria at any level above 0.3. Second, this is where the majority of patients are, those addressable patients. The majority of them are in those lower UPCs. So we're really seeing growth where the majority of patients are. The other aspect of our performance last quarter is that we have finally achieved over $100 million in revenue for the quarter, $103 million, which represents 108% growth versus the same quarter prior year. That's really benefited by not just the growth that we've seen in demand, but also the consistently high compliance and persistence rate. Once patients are on FILSPARI, they see the benefit, and they continue on with therapy.
And as we take a step back and look at the uptake of our revenue over the last three years, I think it really reflects a differentiated profile. When we launched three years ago, we guided that the first year of the FILSPARI uptake will look very similar to other rare renal launches, which is exactly what you see here. But there are two very important inflection points. The first is upon full approval and the availability of our two-year efficacy and safety data, including the two-year eGFR data showing accumulation of benefit versus an active comparator over time.
The second inflection is more recent with the update of our REMS, simplification of our REMS, as well as the final publication of the KDIGO guidelines that strongly position earlier use of innovative therapies, combination use for patients with proteinuria, and a very strong positioning and support for FILSPARI being used, given the head-to-head nature and the superior profile versus RAS inhibition. And when we look at a similar type of chart looking at patient start forms or demand, you can see very clearly those inflections in demand once we had full approval and two-year data, and then more recently when we have the support from KDIGO and from REMS. And if we look in aggregate at the patients that we've been able to reach over the last three years, we still have not even reached 10% of the addressable population.
What that means is that the overwhelming majority of patients are still able to benefit from FILSPARI. They still are on RAS inhibitors and are not at goal, and so there's a tremendous opportunity for growth for us moving into the future, as well as for the other treatment options that will become available for this community, and I'm confident in our ability to grow even with the additional treatment options that are coming because of our understanding of this disease and in the way that it's described by the KDIGO guidelines. Historically, patients have been treated with RAS inhibition and steroids, and that's because nephrologists recognize that every single patient, without exception, with IgA nephropathy really has two diseases. They have an overactivation of their immune system, and that's really what's driven the need to use steroids.
But now, with more innovative therapies that are developed for IgA nephropathy, we expect an increase in the use of those other therapies, but not at the expense of FILSPARI. FILSPARI is targeting the second component of this disease, the disease that occurs within the kidney, because every single patient has a kidney disease as well. By the time a patient is diagnosed with IgA nephropathy, the average patient with IgA has lost half of their nephrons, and those are not coming back. And so a nephrologist's goal is to protect as much as they possibly can, and that really is where FILSPARI or a foundational therapy comes in.
With our head-to-head data showing superiority over the historical standard of care RAS inhibition and the data that we've generated showing an additive benefit when FILSPARI is used with SGLT2s, we believe that the best approach for protecting those nephrons is with FILSPARI. And the guidelines recommend that FILSPARI should be used in combination. So there's a tremendous opportunity for better treatment and, as part of that, growth with FILSPARI. And it's with this success and our very strong execution in IgA nephropathy that we are equally committed and excited to be able to provide FILSPARI to the FSGS community. And I'd like to go into a little bit more about what drives our commitment and our confidence within FSGS. FSGS is a cruel disease. It is rapidly progressing.
These patients oftentimes lose most of their kidney function, and for some patients, within a year, go from diagnosis to the dialysis clinic, and perhaps most cruelly, those patients that are fortunate enough to receive a kidney transplant, 55% of those transplants fail because the disease comes back. Every single year in the U.S., thousands of patients lose their kidney because of FSGS, and thousands more lose their life. This is a dire need for innovative therapies, and there's been a tremendous amount of attention and work on how best to do that in recent years. The PARASOL Group was formed a couple of years ago, really with this urgency in mind. The PARASOL Group is comprised of the global leaders within FSGS, the patient community, leading statisticians within this space, as well as leaders from EMA and FDA.
And their goal was very simple: how do we best identify the endpoints that would be most effective for the development of medicines in FSGS? Because with the emerging evidence, we've learned that the hypothesis of how proteinuria and eGFR work was not right. It was very different in FSGS than it was in IgA nephropathy. And so by capturing as much of the real-world databases that the PARASOL Group could, they had enough data to be able to assess what was going on with kidney function in FSGS. And these are the conclusions that the PARASOL Group came to. The first is very clearly the evidence shows these patients are at significant risk of kidney failure. They disproportionately represent patients in dialysis clinics, and there is an urgent need for innovation.
The second is that when you look at what's going on with the disease in the kidney, it is a disease of the podocyte. That is the cell that filters the blood and the urine, and over time, you have more of these podocytes that die off, and as a result, you have increased proteinuria, but there's also a vicious cycle that occurs when you have proteinuria that damages any healthy podocytes, which is why you get such a rapid progression of this disease, and so proteinuria became the primary candidate for understanding whether it could be an endpoint. Part of their conclusion was that eGFR is not going to work in a clinical trial setting because it's far too variable, and you would need to have such large sample sizes that it becomes unfeasible for a rare disease to be able to be studied in this way.
And so the work focused on proteinuria and their analyses, which I think is summed up perfectly by the lead statistician's quote here, Abigail Smith, is really that if you can reduce proteinuria within two years for these patients, it is strongly associated with a significant reduction in the patient's risk of kidney failure over time. And so with that in mind, I'd like to turn your attention to the proteinuria reductions from our phase III DUPLEX study. This is the only study that's been conducted in this space as a pivotal study, the only head-to-head study as well. And what you see, let's first look at the gray line with an active control maximum dose RAS inhibition, irbesartan. And irbesartan reduced proteinuria from baseline by 32%.
When you look at the very limited literature of clinical trials in this space, ACE inhibitors and ARBs reduced proteinuria in FSGS by about 30%. When you look at the addition of endothelin, which is what sparsentan does, you see a rapid, sustained, and superior reduction in proteinuria. By the end of this trial, 50% of proteinuria was reduced on average. Now, PARASOL also looked at certain thresholds of response of proteinuria. How much control of proteinuria do you need to have in order to reduce a patient's risk of kidney failure over time? These are the pre-specified analyses from our phase III DUPLEX study looking at those levels of response, comparing sparsentan to i rbesartan, and in every single one of these thresholds, you see that s parsentan helped more patients achieve proteinuria control compared to active control maximum dose i rbesartan.
Importantly, PARASOL showed us that if you're able to achieve these levels of control, a patient's risk of kidney failure over eight years is reduced by 80%-90%. These responses are incredibly powerful in the context of what PARASOL has showed us. When you look at the most rigorous level of proteinuria control, complete remission, which here is represented as 0.3 grams of protein or less, patients on sparsentan were two and a half more times likely than active control i rbesartan to achieve complete remission, conferring a substantial potential reduction in kidney failure over time. Now, there was an additional threshold that PARASOL introduced, which is 0.7 g of protein. Here you can see a similar analysis. This was not pre-specified because it historically was not a threshold that was considered.
PARASOL wanted a threshold that not only conferred reduced risk over time, 0.7 g if you achieve 0.7 g of protein or less, a patient's risk of kidney failure is reduced by 85%. But they also wanted one that was able to be clinically meaningfully reduced from baseline. And typically, you would expect to have a patient at baseline have a proteinuria level of 1.5 g. So to go from 1.5 g to 0.7 g is a meaningful reduction. In our two-year trial, you can see that those patients that were able to achieve this level of response, this level of control, had a substantially lower risk of kidney failure in two years. So not projected, but actual hard events in our trial. That's represented by the blue bar of 3.6% of patients versus those that were not able to gain control, 11.2% of patients hit kidney failure.
When we look at the overall rates of kidney failure in our DUPLEX trial, 6.5% of patients on sparsentan reached kidney failure compared to 11% of patients on irbesartan. When you look at some of those large databases, the real-world databases in FSGS, the two-year kidney failure event is 11%-14%. So very comparable to what we saw in our control arm. It suggests that with the better proteinuria reductions that you get with sparsentan, it may confer a reduced risk of kidney failure over time. We did an additional analysis that was recently presented at the ASN this fall. What we looked at was the reductions in proteinuria over the two-year period. You can see here the 50% and the 32%.
We said, "What would that confer looking at a matched sample from these large, long-term real-world evidence databases?" That difference of 50% versus 32% confers an additional 26% reduction in the risk of kidney failure based on the treatment effect of sparsentan. Certainly a meaningful one in the context. As we've done all of these analyses, it further strengthens our confidence in both the consistency of benefit, the consistency in the relationship between proteinuria and actual hard endpoints, and also the consistency with the findings from the PARASOL Group. With that in mind, we remain very confident that sparsentan should be approved in FSGS. Whether it is approved on time or whether it is approved on a delayed timeline, our teams are ready.
We will take all of the relationships, all of the momentum, and all of the learnings that we've had in the success of launching in IgA nephropathy and take that to FSGS for what we believe should be an even more rapid and stronger uptake. And that's for the following reasons. The first is that patients with FSGS have an urgent need. There is no arguing with any nephrologist that this is an urgent need to treat. The second is that there is a growing awareness, but more importantly, growing clinical use of FILSPARI in nephrology practices. That success that we've seen in the uptake of IgA nephropathy, these are the same physicians that are treating FSGS patients. So the awareness and the overlap is there.
We also expect that because these patients are being seen so frequently by their nephrologists, that there will be a very rapid uptake if approved. So with that, I will turn our attention to our third program with pegtibatinase for classical homocystinuria or HCU. We announced that we are reinitiating our phase III HARMONY study this quarter. HCU is a genetic metabolic disease. These are patients that are born with a defect in their CBS enzyme. And the CBS enzyme is responsible for metabolizing certain proteins in our diet. And because of the defect that these patients have, they get a toxic accumulation over time of homocysteine. And that accumulation of homocysteine leads to a whole constellation of symptoms. It leads to vision problems often occurring in childhood. There are cognitive and psychiatric symptoms that occur. There is bone malformation.
Most alarmingly to many patients, 25% of these patients have an ischemic event before they are a teenager, and 50% of them have an ischemic event before they turn the age of 30. Sadly, even though HCU is part of the newborn screening panel in the U.S., 50% of these babies are missed on newborn screening. There is a tremendous opportunity that we have to be able to help this community. The current way of treating these patients is a very, very strict protein-limited diet, as well as the use of betaine and vitamin B6. Unfortunately, most patients are not responsive. There's a real urgent need for a therapy that is disease-modifying, like pegtibatinase and enzyme replacement therapy.
There are about 7,000-10 ,000 patients in the U.S. About half of those, we believe, are addressable today. But with greater awareness, greater education, we believe that those rates will certainly grow. You can see here a profile of pegtibatinase from our phase I/II study. There's a very clear dose-response relationship. And at the dose selected to go into phase III, patients achieved a mean reduction in their total homocysteine levels of about 67%. Perhaps to put that into context, 100% of the patients on pegtibatinase were able to achieve levels of homocysteine that got them below the current treatment guidelines. And we have one patient, one young man, who normalized their homocysteine levels so that they were able to actually eat a more normal diet. And so we're looking to replicate this in our phase III program.
Importantly, it was generally well tolerated in our phase II as well. Let's turn our attention to the phase III HARMONY study. We're looking to essentially have a similar primary endpoint, which is the average change from baseline in total homocysteine level, a biomarker between weeks six and 12. We'll continue to follow those patients beyond week 12 out to week 24, but the primary endpoint is the reduction between six and 12. Perhaps most exciting to this community is our phase III-B study. There are two really important components that are different from our phase II study. One is that we'll be testing self-administration to make sure that these patients are able to give themselves pegtibatinase at home, and the second is to be able to go beyond clinical control of this disease, which is really important to regulators and important to the treating physicians.
But when we listen to patients and their families, the number one thing they want is to be able to have a meal with friends and with family, to not have to feel isolated, to not have to just only eat a handful of vegetables and to really worry about everything in their diet. And so in a very innovative trial design, we are looking at those patients that are able to achieve control of their homocysteine level in the double-blind period and look at a protein tolerance to see how much protein they can increase in their diet and still maintain control of their homocysteine levels. So we're very excited to be able to reinitiate this trial this quarter. We've been working in parallel with the manufacturing scale-up, as well as activating and identifying sites globally.
And we've been working very closely with the HCU community to ensure their readiness and willingness to enroll in this clinical trial. So we want to move quickly in this space. As I take a step back and look at our financials, you can see a snapshot here. Again, I won't go through the revenues as I did before, but we're in a very strong position. We do not have a need for additional capital to be able to support our three portfolios. We have what we need to continue the strong launch in IgA nephropathy, a very rapid launch in FSGS, and the continued progress of developing pegtibatinase. And we've done a very strong job last year of further strengthening our financial foundation. What I'd like to do is close by introducing you to Jennifer.
Jennifer is a woman that I met last year who, at the age of 22, just graduating college, starting her career and starting a new relationship, was diagnosed with FSGS. Within six months, she was in a dialysis chair in kidney failure. She describes her journey with this disease as devastating, not just because of the disease, but she describes in great detail the effects that she's had of having chronic steroid use, the weight gain, the isolation, the depression, all of those elements of what is unfortunately the standard of care for so many patients. Her story is so similar to many that I've met in the eight years that I've been at Travere. What really struck me with Jennifer is two things. One, she's had four kidney transplants. Three of those have failed because the disease came back.
And the second is she is the greatest optimist that I've ever met. In fact, she is the author of a book called The Incurable Optimist that describes her journey living with FSGS. And she is a beacon of hope and optimism for the FSGS community. And her story, while may be very similar to many in the FSGS community, is unique in her ability to bring hope. And I can tell you that every single one of us at Travere takes her example, and we will offer a beacon of hope and a complete commitment to making sure that we have a better future for those patients that are affected by FSGS. On that note, thank you all. I'll take question.
Thank you, Eric. I wanted to just start with just thinking about tomorrow in FSGS. So I see four outcomes, and three of them are pretty binary, right? Approval, CRL, extension, and then you just don't hear, right, which has happened. Is that a fair assessment? And how would you communicate in that last scenario to us what's happening?
Yeah. Tomorrow is our PDUFA date. We do want to make sure that we provide a meaningful update. We have been planning for a communication tomorrow. We're assuming that we will have a notification from FDA, and we will be sure to communicate once we have something meaningful. We want to make sure that that is something that is based on what we hear from the FDA.
Just as a confirmation, when you heard before the holidays from the FDA, that communication, was it a deficiency letter or just needing more information on what you've already filed?
It was not a deficiency letter. Let me go back to what I shared at the beginning for those of you that may have joined after. It was a series of information requests that the FDA had about the characterization of clinical benefit for FILSPARI.
And then those characterizations, was it related to proteinuria? Was it related to eGFR? And as a clarification, did you present the FDA with some of that 0.7 g data in the filing that was critical in the PARASOL assessment?
I'm not going to be able to go into details on the information requests. I want to make sure that I maintain the consistency of not going into detail when it's an ongoing engagement. What I would say is that our original filing included all of our data in the pre-specified endpoints. That 0.7 g was not pre-specified in our trial because it came out of the PARASOL work, not in our SAP originally with the filing or with the trial, sorry.
Okay. Let me see if there are any questions from the audience. Yep.
You characterized that you submitted the data Friday. Was this an ongoing? Did you submit several other iterations of the data along the way, and Friday was the last submission of a piece of the data that you were able to gather, and have you responded to all of the requests, in your opinion, now by last Friday? Were there several different submissions, and Friday was the last one, or did you put a package together that they saw on Friday?
What I would say is we received a series of information requests, so a number of different questions. I'm not going to get into the timeline of when we did it, but what I would say is that as of Friday, we believe that FDA has everything that they need.
Was there one submission on Friday? What I'm asking is, was there one package on Friday that you took all the submissions, put them in one package, or have you been sort of in ongoing dialogue with the FDA along the way?
Yeah. So I won't go into the specifics of what was submitted and when. What I would say is that we've had ongoing dialogue and strong engagement with the FDA. Yeah. And again, I think the important aspect is we believe that as of Friday, the FDA should have everything that they need to answer the questions that they've submitted to us.
Yeah, go ahead.
Thank you so much. Could you characterize if it was new data that they didn't have or a reanalysis of data that was in the file?
So what I would say is that it's information that we had. Most of that is in the file. Typically, what you get for information requests is analysis, sensitivity analyses, reanalyses of information that are there. But I don't want to go into detail of what specifically was requested or what we submitted.
Could you comment if Aliza Thompson was part of this information request? She was the internal champion, we had assumed, so.
Yeah. When I said we've got engagement with the highest levels of leadership in cardiorenal, it certainly would include Dr. Thompson.
Is all of the PARASOL data now with FDA to review that was included with FILSPARI?
PARASOL was a separate initiative, and we do not have the data from PARASOL. What I would say to make sure I understand your question, they would have access to PARASOL independently. If there were any additional analyses that came out of PARASOL, for example, the analysis of 0.7, that certainly could be part of our overall package if they want to analyze the data at that cutoff.
Okay. Questions from the audience? Go ahead.
All right. Trying to slice the apple a different way. PARASOL and KDIGO, you have the FDA with those in there. Were they potentially asking for different cuts of your data in order to kind of align them with pre-you submitting your NDA or your sNDA? Were they potentially looking just to say, "Okay, did these align with the current guidelines?" Guidelines have changed since you folks have talked with the FDA the first time around. Is that probably a fair characterization of it?
So the KDIGO guidelines that were recently updated were for IgA nephropathy. So we've not seen updates for FSGS for a number of years.
But they're likely going to use that kind of as cheat sheet.
I can't speak for the FDA and what they're looking at. I want to make sure that I don't go into detail on the specific analyses that they may have requested. What, again, I'd say is they should have everything they need to approve FILSPARI.
Okay. Can I ask a follow-up on PegT?
Sure. Go ahead.
Yeah. Peg tibatinase?
Yeah.
Okay. HARMONY, why 6-12 weeks for the primary when you've got to go out to 24 anyway?
Yeah. So we saw a very rapid reduction and very consistent response in our phase I/II where the majority of the benefit we saw early in the trial. So six to 12 weeks should give us sufficient time to be able to see that. We want to be able to follow up longer for safety and for durability. The other aspect is a large part of our design of this program was to minimize variability that patients could have if they have a cheat diet. The longer you go, the more likely you're introducing that risk that patients are not compliant with their diet.
Back on FSGS, just quickly, had you at any point entered into labeling negotiations for the product in FSGS?
We received those information requests at the time we were expecting our draft label. What I would assume is typically you would get a draft label once those information requests are and the review of those are complete. In other words, we would expect that.
So then you would have entered into label negotiations once you got your draft label?
That's right. That's right.
Final question in the back? Okay. Thank you, Eric.
Okay. Thank you. Let me leave you with our commitment to the rare disease community. We are ready for an approval, and we believe that FILSPARI should be approved in FSGS. And we are committed to redefining the standard of care in IgAN, FSGS, and HCU. Thanks so much for your attention today.