Good day, and welcome to the Travere Therapeutics Corporate Update Call. Today's conference call is being recorded. At this time, I would like to turn the conference call over to the Vice President of Investor Relations, Naomi Eichenbaum. Please go ahead, Naomi. Thank you, Ruth, and thank you all for joining us today. Earlier today, we issued a press release announcing the confirmatory data from the Phase III PROTECT study of FILSPARI in IgA or IgA Nephropathy. A copy of the press release, along with the slides that we will be reviewing on today's call, are available on the investor section of our website. Today's call will be led by our Chief Executive Officer, Dr. Eric Dube. Joining Eric will be our Chief Medical Officer, Dr. Jula Inrig, and we are joined by guest speaker and key opinion leader, Dr. Brad Rovin, the Director of the Division of Nephrology at Ohio State University Wexner Medical Center. Dr. Bill Rote, our Senior Vice President of Research and Development, will be available during the Q&A session. Before we begin, I would like to remind everyone that statements made during this call regarding matters that are not historical facts are forward-looking statements within the Safe Harbor Provisions of the Private Securities Litigation Reform Act of 1995. Forward-looking statements are not guarantees of future performance. They involve known and unknown risks, uncertainties, and assumptions that may cause our actual results, performance, and achievements to differ materially from those expressed or implied by such statements. Please refer to the press release today and on slide two of our accompanying slide deck, as well as our risk factors and sections of the risk factors for our quarterly and annual reports on Form 10-Q and 10-K, filed with the SEC. In addition, any forward-looking statements represent our views of today, September 21st, 2023, and we specifically disclaim any obligation to update such statements and to reflect information, events, or circumstances. With that, it is my pleasure to turn the call over to our Chief Executive Officer, Dr. Eric Dube. Eric? Thank you, Naomi, and thank you, everyone, for joining today's call. This is an important day for the rare kidney community, as well as the whole team at Travere Therapeutics. Earlier this morning, we announced the confirmatory data from the Phase III PROTECT study, demonstrating treatment with FILSPARI over two years can lead to long-term kidney preservation by slowing the rate of annual kidney function decline. These are some of the most impressive eGFR benefits demonstrated in patients with IgA nephropathy in a clinical setting. The study showed a clinically meaningful benefit of FILSPARI on eGFR total slope, the confirmatory endpoint for the U.S., but it narrowly missed statistical significance. With respect to the confirmatory endpoint for the EU, eGFR chronic slope, the study achieved statistical significance. In addition, all top-line efficacy measures favored FILSPARI. Furthermore, FILSPARI was well tolerated, with a safety profile consistent with what we have seen across all clinical trials conducted to date and comparable to the active control, irbesartan. As you will hear from Jula and Dr. Rovin, these data represent a clinically important benefit in one of the most rigorous head-to-head clinical trials in IgAN conducted to date. Before reflecting on this FILSPARI journey, I'd like to thank all of those individuals who have helped in the development of FILSPARI: the patients, their caregivers, the clinical investigators, and the site staff, whose support has been invaluable in the development of FILSPARI and the execution of the PROTECT study. From the study initiation five years ago, our Travere team has maintained a commitment to delivering an innovative therapy for patients living with IgAN. It is important to recognize that for years, individuals with this devastating disease have had to rely on therapies with limited efficacy and tolerability challenges. Recent data from the RaDaR study underscore the sobering fact that over 50% of patients on historical standard of care progress to kidney failure or dialysis in approximately 11 years. In February of this year, FILSPARI was granted accelerated approval as the first and only non-immunosuppressive treatment indicated for the reduction of proteinuria in IgAN. Since then, we have continued to hear inspiring stories of how this medicine is making a positive difference for patients. The accelerated approval was based on the impressive proteinuria reduction seen at 36 weeks, which has now been shown to be durable over two years of FILSPARI treatment. The eGFR data over 110 weeks provides a clear picture of the potential treatment benefit on kidney preservation that FILSPARI can provide, and the safety profile remains consistent and comparable to irbesartan, all of which further shapes FILSPARI's profile to potentially become the future foundational therapy in IgAN. With these compelling two-year PROTECT data now in hand, we look forward to engaging with regulators and expect to submit a supplemental New Drug Application, or sNDA, in the first half of 2024 for full approval in the U.S. Together with our partner, CSL Behring, we also anticipate a review opinion around year-end from the CHMP on the conditional marketing authorization application for sparsentan for the treatment of IgAN in Europe. With that, I'd like to turn the call over to Dr. Jula Inrig to discuss the Phase III PROTECT study results. Jula? Thanks, Eric, and good morning, everyone. I'd first like to reiterate our gratitude to the patients and their families, investigators, and site staff. O ur research and advocacy partners, as well as our internal teams who contributed to the success of the PROTECT study. Before discussing the top-line results, I want to shortly walk through some historical background on IgA nephropathy that will place these important study results in context. IgA nephropathy is a rare disease that attacks the kidneys, typically affecting adults in their 20s and 30s. Seemingly healthy individuals can struggle through a long road to diagnosis and subsequent treatment. Unfortunately, even those patients who are considered at low risk often progress to kidney failure and require dialysis or transplantation in approximately 11 years. On slide seven of the deck being used for today's call, you can see the clear importance of how reducing proteinuria in patients with IgA nephropathy can lower the risk of progression to kidney failure. In recently published data from the Rare Renal Diseases, or RaDaR study, patients with persistent proteinuria progressed to kidney failure in roughly eight years. However, a 40%-50% reduction in proteinuria at nine months reduced the rate of eGFR decline and delayed time to kidney failure or death by up to 8.5 years. These data are important to keep in mind as we discuss the PROTECT results and highlight that patients with IgA nephropathy need early and effective treatment options capable of reducing proteinuria in order to preserve kidney health. On slide eight, you can see the progression of IgA nephropathy to kidney failure is driven by two critical pathways: endothelin-1 and angiotensin II. These are overactivated by abnormal IgA complexes deposited in critical control cells in the kidney. This drives upregulation of endothelin-1 and angiotensin II, which work in tandem to cause further damage in the kidney. This cascade causes proteinuria to rise to detrimental levels, resulting in loss of kidney function and ultimately kidney failure. FILSPARI, or sparsentan, is a novel treatment taken once daily with selective antagonism of the endothelin type A and angiotensin type 2 receptors, the two causal pathways critical to IgAN disease progression that I just referenced. FILSPARI is the first and only non-immunosuppressive therapy granted accelerated approval for the reduction of proteinuria in adults with primary IgA nephropathy at risk of rapid disease progression. To evaluate the safety and efficacy of FILSPARI in IgAN, we designed one of the most robust and rigorous pivotal trials to date. On slide nine, you can see that a total of 404 adult patients were enrolled globally in PROTECT. Individuals were randomized 1:1 to receive either 400 mg of FILSPARI or a maximum dose of 300 mg of irbesartan, the active control, once daily. All patients were required to be on a stable dose of maximum tolerated ACE or ARB therapy, which was at least 50% max labeled dose for at least 12 weeks prior to screening and have proteinuria greater than or equal to 1 g/day. Notably, the baseline characteristics in the study demonstrate a representative IgAN population and are well-balanced between arms. The primary endpoint in PROTECT was the change from baseline in proteinuria, measured by the urine protein-to-creatinine ratio, assessed at the 36-week interim analysis. As you can see on slide 11, at the interim analysis, we reported a statistically significant reduction in proteinuria for patients treated with FILSPARI compared to the active control irbesartan, as published in The Lancet earlier this year. Specifically, FILSPARI demonstrated a rapid and sustained reduction in proteinuria from baseline of 49.8%, compared to 15.1% for patients receiving the maximum tolerated dose of irbesartan. These data supported the accelerated approval in the U.S. in February of this year. Today, we are pleased to present the confirmatory Phase III PROTECT study results that build upon the interim analysis and continue to demonstrate that FILSPARI has a durable effect on proteinuria over two years of treatment. In fact, as you can see on slide 12, this is the largest magnitude of sustained proteinuria reduction shown in a pivotal trial over two years, with FILSPARI-treated patients achieving a mean reduction in proteinuria from baseline of 43%, compared to 4% for irbesartan-treated patients. At two years, the pre-specified statistical analysis plan called for a hierarchical assessment of the key secondary confirmatory endpoint of kidney function over time, prioritizing total eGFR slope for U.S. regulators and prioritizing chronic eGFR slope for the European Union. On slide 13, you can see that both of the two-year confirmatory secondary endpoints show a clinically important benefit for FILSPARI on long-term kidney function preservation in patients with IgA nephropathy relative to irbesartan. When evaluating the secondary confirmatory efficacy endpoints, we look at eGFR total slope and eGFR chronic slope. Total slope includes all treatment measurements of kidney function, starting at treatment initiation through week 110. Chronic slope evaluates kidney function starting at week six, after any initial potential changes like blood pressure in the kidney have stabilized, and it continues through week 110. Treatment with FILSPARI resulted in one of the slowest rates of kidney function decline seen in a controlled IgA nephropathy clinical trial to date. Patients on FILSPARI over two years exhibit an annual decline of kidney function of -2.7 mL per minute per year, as measured by chronic slope, and -2.9 mL per minute per year, as measured by total slope. This compares to an annual decline of -3.8 to -3.9 mL per minute per year for patients on irbesartan in the study. These measurements suggest that treatment with FILSPARI allows patients to maintain more of their kidney function over time compared to Irbesartan. The annualized treatment difference on kidney function, measured by eGFR total slope, was 1 mL/min/year in favor of FILSPARI, which narrowly missed achieving statistical significance with a p-value of 0.058. When looking at long-term kidney function assessed by eGFR chronic slope, the annualized treatment difference was 1.1 mL/min/year in favor of FILSPARI compared to the active control Irbesartan with a p-value of 0.037. On slide 14, we've included two important supportive eGFR analyses. First is the intent-to-treat (ITT) population, which includes all patients, irrespective of whether they stopped treatment early during the study. The second is censoring on patients who received rescue immunosuppression during the study. These analyses are important for two reasons. One, the Irbesartan arm experienced higher early treatment discontinuation due to patient or physician decision. Two, there is more than twice as much use of rescue immunosuppression medication in patients on irbesartan compared to sparsentan. In these two sensitivity analyses, you can see further evidence of kidney function preservation, which is favorable for patients on sparsentan versus irbesartan, as measured by differences in both chronic and total eGFR slope. On slide 15, you will find additional kidney function endpoints from the study. Here, we assess the absolute overall change in kidney function from baseline to the end of the study, as well as from baseline to four weeks after stopping treatment and resuming standard of care medication. Importantly, we see the two-year mean change in eGFR of -5.8 mL per minute with sparsentan, compared to -9.5 mL per minute with irbesartan, with a mean difference in eGFR of 3.7 mL per minute favoring sparsentan. This effect was durable, with an absolute mean difference in eGFR from baseline to four weeks post washout of 2.9 mL per minute, favoring sparsentan. We've also evaluated the combined composite kidney endpoint of confirmed 40% reduction in eGFR, end-stage renal disease, or death, which are trending in favor of FILSPARI, with a lower incidence in participants on sparsentan than irbesartan, 18 versus 26, respectively. In summary, all of the kidney function endpoints show that patients treated with FILSPARI maintained more of their kidney function over time compared to irbesartan. Now, let's put this data into context. To fully appreciate the study results, I will guide you through the clinical application of eGFR slope from PROTECT for patients and clinicians. eGFR slope serves as a measure of kidney function over time and the rate of progression to kidney failure. A higher slope value, like the natural course of an IgAN patient of -5 mL/min/year, roughly translating to losing about 5% of kidney function per year, indicates a quicker progression to kidney failure. The objective of treatment is to minimize this eGFR decline or reduce the slope value to delay the time to kidney failure. As you can see on slide 16, in recent clinical trials in IgAN, patients on standard of care typically exhibit an annual kidney function loss or decline of -5.3 mL/min/year. For a patient population like we studied in PROTECT, these patients would be projected to face kidney failure in eight years. But maximal treatment with the active comparator, irbesartan, slowed the rate of progression to kidney failure. Importantly, these data suggest treatment with FILSPARI, if utilized long-term, has the potential to significantly delay the time to kidney failure by up to nearly eight years compared to routine standard of care treatment and maximally titrated irbesartan. For IgAN patients that are typically young and relatively healthy and faced with limited, safe, and effective, and approved therapies, this represents a significant medical advance. As shown on slide 17, the safety profile of FILSPARI continues to support long-term use. The results from PROTECT show that after 110 weeks, FILSPARI was well tolerated and has shown a consistent safety profile across clinical trials conducted to date. Notably, when we look at the adverse event of interest of liver test elevations, or ALT or AST, of at least 3x the upper limit of normal, the data are in line with the interim results and less frequent in FILSPARI-treated patients as compared to patients on irbesartan. Additionally, to date, there have been no reported cases of drug-induced liver injury, or DILI, or Hy's Law with FILSPARI. These findings build on earlier reported trial results, suggesting that FILSPARI is generally safe and well tolerated. Overall, we are pleased with the Phase III PROTECT study confirmatory results that show treatment with FILSPARI demonstrated the largest sustained reduction in proteinuria in clinical trials in IgA nephropathy, which correlates to an important clinical benefit on slowing kidney function decline. As a former practicing nephrologist who treated patients for more than 20 years, I am excited about what these results represent for the treatment of IgA nephropathy patients. These results further support the clinical and safety profile of FILSPARI, and we look forward to the next steps of engaging with the regulators regarding our planned submission of an sNDA in the first half of 2024. Now, I will turn the call over to Dr. Rovin, who is Director of the Division of Nephrology at Ohio State University Wexner Medical Center, and steering committee member for the PROTECT Clinical Trial. He will share his perspective on what he sees in clinical practice, the urgent need for effective treatments in IgA nephropathy, as well as his experience treating patients with FILSPARI. In addition, I'll ask him to touch upon what these results from this study could mean for the treatment paradigm in IgAN. Thanks very much, Jula. I'm really happy to be here and to comment on these outstanding data from the results of the PROTECT trial. As you heard, I'm Brad Rovin. I'm a professor of medicine and pathology, and I am the director of the Nephrology Division at Ohio State University Wexner Medical Center. My entire career has been in glomerular diseases. I have a big clinical trial program here. We have created a glomerular diseases clinic and fellowship for advanced training of nephrologists, and I also run an NIH-funded translational research laboratory. As was mentioned, I do have a considerable experience in treating all glomerular diseases and of course, IgAN. Our group has been involved in most of the major clinical trials of IgAN, including being an investigator on the PROTECT trial. But we also have engaged with the other trials in which the mechanism of action of their potential medications are different. Our practice overall sees probably 25-30 new IgAN patients per year, ranging in severity from newly diagnosed with hematuria and proteinuria, to really patients far along their course, referred from other nephrologists who have very few options left or who are referred to be put into clinical trials. We do have a lot of that from the community and also from the surrounding areas in Central Ohio and the contiguous states. As you probably all are very well aware, the treatment options for IgAN have been really conservative management, lifestyle modification, and it's sort of a foundational principle is use of Renin-Angiotensin-Aldosterone System inhibition or the use of ACE inhibitors or ARBs. And the idea behind that, of course, is to reduce proteinuria. We know these medications are helpful for some patients, but they also have limited utility. And what we see often over time is that proteinuria reduction is either insufficient or not durable. The underlying disease often continues to proceed in the background, and these patients show a decline in kidney function. So when I think about treating IgA nephropathy, my goal for these patients is to reduce proteinuria as much as I possibly can. You've heard and you know that proteinuria is a marker, of, of prognosis in patients with IgA nephropathy. Proteinuria reduction has been shown to preserve, glomerular filtration rate, which is kidney function, and I'll use those terms interchangeably, and delay time, to, to kidney failure. In addition, proteinuria, in and of itself may be harmful to the kidneys, so it may be a biomarker as well as a, a mechanism of, of tissue injury to the kidney. When we think about the current guidelines or general, ideas in the nephrology community, the consensus for many years has been that we target reducing proteinuria in IgA nephropathy below 1g per day. I think that the data that were alluded to earlier, and I, I think, Dr. Inrig showed some of the results from the RaDaR study, suggests that this, this treatment goal may be a little bit too liberal in a sense. These data really suggest that patients who have proteinuria well below 1g per day continue to progress to end-stage kidney disease or death. And so in my opinion, clinically, we try to get proteinuria, as I said, as low as possible, certainly below 500 mg a day, and beyond that, I would like to see the patients below 300 mg of protein a day, if that's possible. And the idea is that we're using this to sort of indicate to us that we're going to have a beneficial effect on kidney function over the long term. So that really brings me to the FILSPARI sparsentan data, and forgive me if I use the words interchangeably. They're really impressive in that respect, and they really reinforce my confidence in using sparsentan for my patients with IgA nephropathy. So first of all, again, compared to the active comparator arm, which is irbesartan and ARB, what we see is this really incredible sustained 43% reduction in proteinuria over the two years. And that, as was mentioned, is really the biggest decline in proteinuria from our recent trial experience. And this is absolutely what we need as practicing nephrologists because, as I said, getting proteinuria as low as possible really seems to be the key in preserving kidney function in these patients. Now, the follow-up data that were just presented, the two-year data, are very exciting because we're actually measuring GFR in these patients. Unfortunately, in both groups, GFR declines, but the treatment with sparsentan reduced the annual decline of GFR significantly and in a clinically meaningful magnitude. I think this is really important to understand that proteinuria is great, but we want to see attenuation of the decline of kidney function, because what we don't want is our patients, in their expected lifetime, to progress to needing renal replacement therapy with dialysis or transplantation. Now, a little bit of historical perspective, just to show you how rigorous and well done this trial was, kudos to the investigators. We participated, my team participated, as did many people around the world. The decline in the control arm, the active comparator arm, was really a lot less than we've seen in recent trials, and I think that's a testament to how well the patients were monitored and treated with the Irbesartan. So keep that in mind when we look at the comparison of the two. So when I look at these data... And again, I want to reiterate, I'm not a statistician. I appreciate the importance of statistics and p-values, et cetera, but when I'm looking at the data, what I want to see is the long-term effect on kidney function, okay? And that translates to the chronic slope, is what we really consider as we're practicing. Drugs like sparsentan and the RAS inhibitors, ACEs and ARBs, have a hemodynamic effect right off the bat when they're given to patients, and that reduces glomerular filtration rate acutely, okay? That is absolutely expected. We see that with almost all of our drugs that we consider kidney protective over the long term. And the decline, the initial decline in GFR, doesn't bother me. What I want to see, and what we do see in this trial, is that after that initial period, there is no further rapid decline in GFR, and it stabilizes or it slows down. And what you see over the long term in chronic slope, as is in your slide set and was just presented, is that sparsentan does a superior job to what we would consider standard-of-care active treatment with a RAS inhibitor, and that's clinically meaningful. I would also suggest to you that the total slope data are also very impressive. I realize that the p- value is just a little bit off from what we consider statistical significance, but we really should be looking at this with the totality of data and its clinical significance. I think that's where these protect data shine. The other thing that's very important is that we can use this medication safely, and I'm very pleased with the safety profile. We knew that the drug had a very good safety profile from the first nine months of use, and this is just verified after two years of continuous use, showing that the adverse event profile is really no different than that of irbesartan. Specifically, adverse events of interest, which was liver functions, really didn't pan out, as some people had suggested, and of course, why the drug was given a REMS designation. I believe these data are very supportive of the fact that the drug can be used safely in the long term. I'll just give you one anecdote. One of my patients is in the PROTECT study, and of course, I'm blinded. I didn't know what medication he was getting. Observationally, I knew what his proteinuria did, and his proteinuria rapidly decreased. I sort of assumed he was getting sparsentan, but I didn't know. And then he to get enrolled in the open-label extension, he came off the medication, blinded medication at 110 weeks, and his proteinuria actually went up again, and I got really concerned. And fortunately, we were able to get him into the open-label extension, get him back on the sparsentan, and remarkably and very rapidly, his proteinuria dropped back down, and I'm much happier now. That's the other thing I think we need to point out. If you look at the proteinuria data that was shown to you, it's just a remarkable decline in a very short period of time, and that is not what we see with routine RAS inhibition. So, I am really happy to be here. I'm happy to answer any questions you might have regarding these really, really spectacular outcomes with the PROTECT trial. And so, with that, I'm gonna hand the call back to Eric for questions. Thank you, Dr. Rovin. We appreciate your deep insights and the work that you're doing within the rare disease community for patients. And we're really proud of the PROTECT study's confirmatory results, showcasing a clinically important benefit on long-term kidney function preservation in patients with IgAN, as evidenced by the difference in eGFR total and chronic slope versus irbesartan. These additional data from the PROTECT study continue to support our belief that FILSPARI's profile can enable it to become a new treatment standard in IgAN. Given the totality of data favoring FILSPARI, we are looking forward to sharing these data with the FDA as we work toward a planned sNDA submission in the first half of 2024. With the achievement of the confirmatory eGFR endpoints for the EU, we anticipate, together with our partner, CSL Vifor, a review opinion by the CHMP on the CMA application for sparsentan for the treatment of IgAN in Europe around year-end. As we move forward, our focus remains on three priorities. First, achieving full approval for FILSPARI in IgAN. Second, the continued successful launch of FILSPARI. And third, advancing our pipeline. We have a very strong financial foundation and the internal talent to continue executing on these priorities. We look forward to providing updates through the balance of the year, and I want to thank you again for joining today's call. I will now hand the call over to Naomi for Q&A. Thank you, Eric. We can now open the line up for the Q&A. Operator? Thank you. If you would like to ask a question, please signal by pressing star one on your telephone keypad. If you're using a speakerphone, please make sure your mute function is turned off to allow your signal to reach our equipment. Again, please press star one to ask a question. We'll pause for just a moment. We'll go first to Joseph Schwartz with Leerink Partners. Hi, all. This is Will on for Joe. Thanks for taking our questions today. So first for us, what do you think drove the miss for total slope here? Did you guys see higher variability among patients than you had expected? And can you compare the acute effect seen in DUPLEX and PROTECT? And then I have a quick follow-up. Thank you. Will, thanks for that. I think, you know, what I have to say, I'll take the first or the second question on the acute effect, and then I'll turn that over to Jula to be able to provide her answer to your question about total slope. I think first, if we look overall at the data, all of the efficacy results favored FILSPARI compared to irbesartan. As we've expected all along in the way that the trial was designed, we would have expected an attenuation of that acute hemodynamic effect. We would expect some, but not to the degree that we've seen in FSGS, both the DUET and the DUPLEX trials. It's exactly the pattern of results that we've seen here in PROTECT. It's our belief that that did not contribute to narrowly missing statistical significance on total slope. I'll turn it over to Jula to provide her thoughts on the total slope endpoint. Yeah, thank you. I want to reiterate, we saw meaningful preservation of kidney function as measured by both total and chronic slope. With regards to not hitting statistical significance on total slope, yes, one aspect can be the acute effect, 'cause that adds to the variability with regards to the measurement of total slope, but we didn't see a large acute effect, nor a very large difference between Irbesartan and sparsentan. I think we provided some data around our sensitivity analysis that may have impacted our ability to achieve statistical significance that I mentioned during the call is, one, we had a greater number of patients early discontinue the study treatment on Irbesartan versus sparsentan, and when we account for that and look at all patients on treatment, we exclude the null. In addition, we had higher rescue immunosuppression treatment on patients on irbesartan compared to sparsentan, and when we take that into consideration as well, we exclude the null. I think some of those put it into context around why we may not have hit statistical significance. Again, I want to reiterate, we saw a clinically meaningful effect on both measurements of kidney function preservation. As a reminder, if you do have a question, that is star one. Please limit yourself to one question. If you do have another question, please rejoin the queue. Our next question comes from the line of Anupam Rama with J.P. Morgan. Hey, guys. Thanks so much for taking the question. I know you presented a few analyses here, but can you give us any more color if there are additional subgroups of patients that may have had, you know, an outsized or more muted benefit on eGFR based on baseline characteristics, or is that kind of work still ongoing? And then for Dr. Rovin, how do these kind of, you know, top-line, two-year eGFR data, you know, update your views on the right or eligible population for, for FILSPARI in your practice? Thanks so much. Thanks so much for the questions. With regard to subgroup analyses, I'll turn that over to Jula, but we are providing today what we believe is a pretty extensive view of the top-line results, and as you can imagine, we've got a lot more data to analyze, but we've provided a pretty extensive view. Jula, do you want to comment on subgroup analysis and perhaps what we saw at the interim that may inform our thinking as we move forward? Yeah. As I just mentioned, we are impressed with the amount of kidney preservation that we see overall. We have not looked at any subgroup data to date. I would say importantly, to Eric's point, when you look at the magnitude of proteinuria reduction across subgroups, which we did publish in The Lancet, we see a consistent treatment effect on proteinuria across all subgroups. I would anticipate that would translate into a consistent treatment effect on kidney function preservation, but again, we have not done that analysis yet. Thanks, Jula. And, Dr. Rovin, do you want to provide your thoughts on the patients that might benefit now that you have seen these two-year data? Yeah. Thank you. I, I, I'll just start with, I love subgroup analyses, and I hope that I will continue to be involved when we start looking at the data, 'cause that's the most fun part of my job. Anyway, in terms of my thoughts, I actually... You know, I've been thinking a lot about this because I'm thinking about all the different mechanisms of action of the drugs for IgA nephropathy that are becoming available and/or are in later phase trials. I believe that sparsentan can be a foundational baseline for sort of the treatment pyramid of IgA nephropathy. You know, what we generally have used is starting out with RAS inhibition. As you can see, in reducing proteinuria, that to me, this drug would be a, a, a drug I could use in any IgA patient. Now, there's caveats in that. Obviously, you know, if a patient has very, very low blood pressure, they may not tolerate the full dose. We sometimes had to titrate the dose for hypertension, you know, these, these types of things. In general, for the IgA population as a whole, I actually think this could be a foundational therapy. I'm gonna go one step further, and I, you know, I'm not speaking on behalf of, of, of Travere at all. I'm speaking on my interpretation of the current state of data. Generally, if a patient has an IgA diagnosis, no matter what their proteinuria level is, I will start them on RAS inhibition if they can tolerate it. Some patients do have low or normal blood pressure, so they may not. But I would likely do the same thing here because of now, the accumulating data that suggests low level of proteinuria is still harmful to the IgA patient. And I've seen that in my own practice, where we have patients who come in with impaired GFR. They have hematuria that's glomerular in nature, and they have no proteinuria, and they haven't had proteinuria, at least by what I can tell from medical records, and they have IgA nephropathy. So these patients have progressed with very little clinical demonstration that they were going to progress. I think that can benefit all patients. We'll go next to Greg Harrison with Bank of America. Hey, good morning. Thanks for the update and for taking our questions. What is your sense of the weight that the FDA will place on chronic slope, based on your discussions to this point? And can you point to any other drugs that have been approved within renal indications that may have slightly missed on their primary endpoint on the p-value? Greg, thanks for the question. I think, what's important is for us to be able to sit down and speak with the FDA. In fact, we have a pre-NDA meeting scheduled with the FDA in the fourth quarter, and we're really eager to sit down and review these data with them. I'll turn it to Bill in a moment, for his thoughts on chronic slope. With regard to precedence, you know, there really is an emerging area where FDA is looking at eGFR within these rare kidney diseases. And so I think, you know, rather than rely on, you know, what FDA has done with others, I think it's important for us to share the data that we have from the PROTECT trial, and Bill can provide his comments on, you know, how we'll approach the FDA. On mute, of course. Thanks, Greg. The agency's aware that there are multiple ways to look at eGFR and how to quantify renal protection in clinical trials, and we've had discussions with them over the course of time, and they are interested in all the different ways of measuring GFR over time. And I think what's important to realize that the dataset coming from the PROTECT study shows that every way we look at, every measurement that we employed in the study, favors sparsentan. And I think that that's really where they're going to focus their review on, and they recognize the physiologic effects of any drug that lowers blood pressure and what that has to do, and I'm certain that they're going to take that into account, and I look forward to reviewing the data with them. We'll go next to Maury Raycroft with Jefferies. Hi, good morning. Thanks for taking my question. I was gonna ask a follow-up on chronic slope as well. I guess since you're yet to get clarity from FDA on the use of chronic slope and the total data, can you talk about how you reached alignment on use of chronic slope in the EU? And maybe if Dr. Rovin can comment on how his colleagues would perceive having chronic slope in the label versus total slope, if that matters commercially, and how they would use the drug. Thanks, Maury. Let me start by saying that we've really focused our efforts throughout this entire program, including how the trial was designed, by aligning with how the nephrology community monitors patients with IgA nephropathy over time. And that certainly is chronic slope. As Dr. Rovin mentioned, nearly all medicines that have this acute hemodynamic effect have been demonstrated to be cardioprotective in the long run. And so our belief all along has been that chronic slope is the right measure of kidney function over time. I think that's certainly reflective of the discussions that we had with the EMA and you know certainly invite Bill to provide his comments if there's anything further. But really, fundamentally, I think it's important to reflect on our view and, you know, our reliance on the nephrology expert community and how they have over time evaluated these patients. Bill, do you want to provide some comments, and then we'll turn it to Dr. Rovin on his view of chronic slope and how he might think the nephrology community will view these results? Yeah, certainly. The EMA, when we met with them over trial design, their focus was on the totality of data, but with chronic slope as the top and primary measure, accounting for the physiology and the pharmacology of sparsentan, along as they would with any of the drugs that have any differential acute effect. They also are going to look at all of the different measures because none of these studies is complete without all of the data. And I think that's any regulator is going to look at it that way. I'll hand over to Dr. Rovin to discuss how he views chronic slope. Yeah, so, as I mentioned, you know, to me, this is the key because we're not focused on treating the patient just for, you know, a year or six months. We... It's a long-term perspective. And to directly answer your question about how the nephrology community will adapt to this, let me just raise, you know, the SGLT2 story, and you can easily see that the acute effect on GFR with the SGLT2 inhibitors is a decline and then a stabilization of the GFR over the long term. And you're probably well aware of how rapidly the nephrology community has taken up the use of SGLT2 inhibitors in patients with chronic kidney disease that's progressive. So I think, you know, much as what Eric and Bill just said, you know, we look at the totality of the data, and use that to make an assessment of how well the drug works. And I know you guys today was just the top-line data, but we're working on bringing this whole thing out in publication, of course, you know that, and the totality of the data is very impressive. Thank you, Dr. Rovin. Jula, I know you've been looking quite a bit at all of these different classes of medicine and trials, looking at again. Do you want to comment any further about your assessment as a nephrologist as well? Yeah. Particularly also on chronic versus total? Yeah, I think it is important that, as Brad mentioned, most of the drugs that we use that are kidney protective over the long term do have some sort of an acute effect, but we know that's beneficial. And it is important, as he mentioned, SGLT2 inhibitors, when we look at the DAPA-CKD trial, that study didn't show a statistically significant effect on total slope, but it did on chronic slope and overall was nephroprotective. That is very consistent with what we see with drugs that work in this mechanism. They may not hit statistical significance on one measurement because of the potential for an acute hemodynamic effect, but have long-term kidney preservation. And we know SGLT2s are increasingly being utilized across the spectrum of patients with kidney diseases. We'll go next to Liisa Bayko with Evercore ISI. Hi there. Thanks for taking the question. Can you just kind of give us any color on conversations you've had with FDA on, you know, chronic versus total slope, and, you know, what you anticipate their flexibility might be in this particular case? I mean, given the totality of the data, I hear what you're saying, yet they still chose, you know, the total slope, and I'm just wondering, you know, to kind of just your sense on their ability to be flexible based on any conversations you've had. You know, it obviously the outcome of the study was one possibility, might have contemplated with them. Good morning, Liisa. Thank you for the questions. I'll provide my brief comments and then turn it over to Bill. I think it's important for us to remind that all of the measures of efficacy at two years favored FILSPARI. And when we look at the weight of the evidence from these top-line results, including both the benefit that we see, as well as the safety and tolerability profile, it's clear to us that this is a clinically meaningful set of results. Bill, do you want to comment on the conversations with regard to looking at both total and chronic? Certainly. This was a point of discussion around trial design with both DUPLEX and PROTECT trials. And with PROTECT, in particular, we started the study with chronic slope as the primary endpoint, and it was only after extended discussions with the FDA, where we were required to shift it to total slope as the, as the primary. And, you know, the comments were made, "It's, it's a shame that we have to pick one," but the agency, I believe, was looking for consistency across trials and a measurement that would work in all clinical studies. And I don't think that, you know, that may be a tough item to find. I think as we look at trials going forward, we're going to see different endpoints and different measurements. What's important is that they understand the value of all the measures of eGFR, and clearly, the data here show a renal protective effect with sparsentan, sustained deep and durable proteinuria reduction, and a safety profile that allows the regulators to very quickly get to a positive benefit-risk evaluation. And I look forward to having that review and those further discussions with them. We'll go next to Laura Chico with Wedbush Securities. Thanks very much for taking the question. I guess I just wanted to clarify really quick, Jula, on the, the ITT analyses that you shared. Would those GFR changes be statistically significant? Just to clarify that. And then for Dr. Rovin, how would you... how does the two-year data change your views? I guess if you're trying to decide between using something like budesonide extended-release or FILSPARI, does this two-year data change anything from, from your view? Thank you. Thanks, Laura. Jula, we'll turn to you first and then go to Dr. Rovin. Yeah, thanks. With regards to the intention to treat analysis, we did have a hierarchy of testing. So once we miss on any of the eGFR tested above that, we don't have any alpha left to spend. However, you can see the confidence intervals around that, that exclude the null. So if we had alpha to give to that, you can imagine that we'd have a statistically significant p-value. However, we do not. If you can imagine if we had put that as our primary endpoint and so had assigned alpha, then yes, that would have achieved statistical significance if that was assigned as our primary endpoint in the hierarchy. Hopefully, that answers your question. Your question is really, really relevant because my colleagues and I are really thinking about how we can use all of the new medications. I will tell you right off the bat that sparsentan and budesonide, and others as they come along, but right now we only have budesonide. What I'm looking at is using them together, to tell you the truth. The idea for me is that I get control of proteinuria as quickly and as deeply as I possibly can, and of course, sparsentan can do that. I have, on top of that, the ability now to go to a drug and add it on that may actually target the pathogenesis of the abnormal IgA formation. These drugs, to me, are not competitors. They're synergistic. These data, with the reduction in the attenuation of decline of GFR slope, I think will be, at the very least, additive. In other words, we'll get a boost if we use two-drug combination, if not multiplicatively. So in other words, I don't know how far this could go. And of course, now, many of us in the community are interested in how we would design and use multi-targeted regimens for IgA nephropathy, much as we're doing in other glomerular diseases. I think it's naive to assume that one drug is the only drug that would be used for all patients and take care of everything. I think these are complicated diseases with multiple steps in pathogenesis and multiple steps in kidney injury that really lend themselves to the possibility of combinatorial treatments. So to me, the question is relevant, but it's really in a positive way. I would suggest using both together as a way to treat IgA nephropathy. We'll go next to Vamil Divan with Guggenheim Securities. Great, thanks for taking the question. Maybe just to follow up on a couple of these points that were just raised. One, for Dr. Rovin, maybe you could just comment, I think, to the last question. Is there anything in the data here today that sort of changes your view, around how you would use this, maybe in combination with budesonide? Also on the SGLT2 side, does this data in any way sort of change how you might think about when you add SGLT2s, or how this sort of changes the treatment sort of landscape? The other question I just wanted some clarification on is that analysis you showed with the higher rates of, treatment discontinuations and patients receiving immunosuppression. On slide 14- Can you provide any numbers in terms of the number of patients in each of the arms that, you know, that were taken out of the analysis when you did the second—I realize there weren't, wasn't any stats that you can do there, or any p-values you can provide, but just curious what number of patients we're talking about that were excluded? Vamil, thanks for your questions. Dr. Rovin, we'll turn to you first, and then, Jula, you can take the question about the sensitivity analyses. Yeah. Okay. The data today don't really... So, they confirm sort of my initial impression of how I would use sparsentan in sort of the treatment paradigm. So early on, you know, when I became involved with this trial and the drug, understanding the mechanism of action, et cetera, I had really sort of started forming the idea that it would be a foundation upon which other therapies would be compatible and additive. And these data confirm that. So it doesn't really change to me how I would use it, but really just provides more support for what I've thought and actually have said in public meetings, you know, where we've been talking about IgA treatment management. So, now, where we put the SGLT2 inhibitor in the paradigm is very interesting. So SGLT2 inhibition, and we don't know the exact mechanism of how it's providing renal preservation. I realize that the SGLT2 also has a hemodynamic effect on glomerular hypertension or glomerular pressure, if you will. But, you know, all of the SGLT2 studies have been done on presumably optimized RAS inhibition. And so the additional benefit of that on glomerular hypertension is not necessarily how I think this is working. My assessment of the current state of affairs with SGLT2 inhibitors is that they're probably affecting energy utilization in the tubules. And by reducing the need for energy utilization, it preserves the tubules over time. So then how do I feel I would add an SGLT2 inhibitor into the treatment regimen? As I said, what I visualize for most IgA patients is a foundational treatment with sparsentan, for example. I would like to add a treatment that would focus on one of the pathogenic mechanisms of the immune disease of IgA nephropathy. I think we've been very clear, and importantly, one of the benefits of sparsentan that allow its long-term use is that it's not an immunosuppressive, so we're not immunosuppressing a person forever like we do in transplant patients. I would like to then add something that would interrupt, for example, the generation of the aberrant IgA, so that would, at this time, potentially be budesonide. I would consider some of the drugs that are in development, which would be B-cell inhibitors, which block the formation of the IgG. That's, you know, the autoantibody against the aberrant IgA, as an example. When I treat the immune disease, I would probably... You know, I don't like to keep patients on immunosuppression forever if it's not necessary because of the risk of immunosuppression. When I'm done with that, and I have the proteinuria controlled as best as I can with, again, sparsentan, then at the very top of the pyramid, I add on the SGLT2 inhibitor, and I think that, again, this is a drug that would be readily compatible with the sparsentan in terms of renal preservation because it's working almost certainly by a different mechanism. I think the two could be, again, additive. Why do I say I would do all these other things first? Well, the data we have so far with the SGLT2 inhibitors is especially in IgA, if you look at the subset of IgA from DAPA-CKD and EMPA-KIDNEY, you know, these are patients with far advanced disease that's really very chronic. So I want to get the active IgA, the active immunologic disease under control, and then when that's done, I would consider adding the SGLT2 inhibitor. My example might be, just to put this in context, I treat a lot of lupus patients, and when I'm done with treating the active disease, if there's no more active disease left, but they have chronic kidney disease that's progressive, I do a kidney biopsy, I verify there's no more activity, and then I add an SGLT2 inhibitor. I realize there are no data for lupus or some of these other diseases yet with the SGLT2 inhibitors, but that gives you an example of how I visualize using the drug in IgA nephropathy as well. Thank you, Dr. Rovin. Jula, would you like to take the question about the additional data from the analyses of IST use and early stopping of treatment? Yeah. Our primary analysis for both of our eGFR endpoints was pre-specified to be on-treatment eGFR, with the assumption that we would have equal amounts of patients staying in the study over time and equal amounts of rescue treatment, meaning that data would just be missing at random. However, as you saw, we saw a significant treatment effect on proteinuria. What that, with FILSPARI versus irbesartan, what that translated into during the study is more than twice as many patients getting rescue treatment with irbesartan versus sparsentan. We'll release that data in an upcoming meeting, what that looks like. In addition, a greater number of patients stopping treatment early due to either the physician or the subject deciding, and what that means is they felt like the treatment wasn't working on the irbesartan versus sparsentan arm. Irrespective of either of those decisions, we measured kidney function in more than 90% of patients for the full duration of the study period. That information is what we can provide in the intention to treat analysis. All patients, what their kidney function does over time, irrespective of whether or not they stopped study treatment early because they just didn't feel like they were doing well, or their physician felt like they were progressing. That's the ITT analysis. It's all patients' kidney function over two years. The steroid censoring, or the immunosuppression censoring, is once patients get started, we censor their data thereafter. We'll provide more details around that, again, as I said, at an upcoming meeting. As a reminder, if you do have a question, please press star one. Please limit yourself to one question. If you do have a follow-up, please requeue by pressing star one. We'll go next to Carter, Carter Gould with Barclays. Good morning. Thanks for taking the questions, and I appreciate Dr. Rovin hopping on. His commentary has been helpful. I guess one really kind of straightforward and simple question for Eric and Jula. You mentioned that the pre-NDA meeting is set for Q4. We're of course also waiting on the FSGS update from those regulatory engagements. I guess clearly what can investors expect in terms of commentary from you guys on the status of those regulatory engagements before year-end? And specifically, will we hear the outputs of that meeting on IgAN before year-end? Thank you. Thank you, Carter. So we are on track to provide an update on our FSGS discussions this fall. So, you know, I'd say no, no change in terms of that timing. With regard to the pre-NDA meeting, as I mentioned, we do have that scheduled. We are eager to review the data with the FDA, and thereafter, we would certainly provide an update on those discussions. And I think you can expect that that could be done by the end of this year. And, as our practice is, we wait until after we have the meeting, and we don't share more specifics of the timing of our meetings. What I would say to your point is that you should expect to see a meaningful update on both of those by year-end. We'll go next to Tyler Van Buren with TD Cowen. Hey, guys. Thanks for fitting me in. There's been a lot of discussion around the results already, so I wanted to ask about the ongoing launch. Are you guys still confident in the FILSPARI launch, achieving first-year sales that are akin to what you see with some of the better renal launches, as you stated in the past, of $30 million-$40 million? So, Tyler, thanks for the question. We're really pleased with the launch so far, and as I mentioned, I think our focus remains on a continued successful launch through the remainder of the year. We've not provided specific guidance, but as you mentioned, you know, we certainly see that there is a pretty tight range of first-year revenue with regard to recent rare renal launches. And, you know, as we look at the demand that's been generated so far, we've been incredibly pleased as we've commented through the first half of the year, which represents just under six months of launch. We're seeing some of the highest rates of patient start forms. And so we don't see anything that would change that trajectory of showing high demand and, you know, further pull-through now that we continue to see growth in payer coverage. So that certainly should translate to an increase in revenues in the second half of this year. We're really eager to be able to share with you third-quarter results. At this point, you know, we'll focus on what we shared on Q2, which is, you know, one of the strongest starts to a rare renal launch. And we have an ambition, and certainly, you know, we can't discuss the two-year data yet until it's in the label. But we believe that even with the 36-week proteinuria data, it is a deep and durable effect that we're seeing a positive response by nephrologists. So, stay tuned, and our focus again is on continued strong execution of the FILSPARI launch. We'll go next to Mohit Bansal with Wells Fargo. Hey, this is Emory on from Mohit. Firstly, could you just talk about why you may have seen a disconnect between the proteinuria effect that you saw with, with sustained reduction and the expected eGFR response you would see? Secondly, at the interim review that supported a great approval, I was curious to see, you know, what, what kind of changes there were between the first year proteinuria data you saw in some patients and the step to the second year. Because I understand that the FDA was, you know, reviewing some of that data and ensuring that there was adequate powering to, you know, support a positive trial on that hard outcome. Thank you for the questions, Emory. Jula, I will turn those questions to you. Thanks. I would reiterate that we see a consistent and durable effect on proteinuria that starts early. We achieved a significant separation at 36 weeks, and we maintain the same magnitude of separation at two years with a 40% treatment effect, and we see a preservation of kidney function. With regards to the magnitude of treatment effect on eGFR slope, again, we see preservation of kidney function in both arms, but even greater in the irbesartan arm versus what we've seen historically. So I would say we see a significant benefit with both treatments, but even greater with FILSPARI. We'll go next to Tim Lugo with William Blair. Thanks for taking the question. Do you know the data on confirmed 40% reduction of eGFR, ESRD and death looks impressive and, you know, obviously favoring FILSPARI. But if you only look at ESRD and death, does that also skew towards sparsentan use? And there was... It did look like there was more SAEs in sparsentan group than irbesartan comm-- Was there anything of note there? Jula, I will turn that to you. We don't have all the breakdown of the subgroups for the composite at this time. Again, we'll have more data available at a publication or a scientific congress. With regards to SAEs, we see actual, fairly comparable numbers of SAEs between both the irbesartan and sparsentan arm, 35% and 37%. So nothing that we see with regards to serious adverse events that's different. Very comparable between both treatment arms. We'll go next to Alex Thompson with Stifel. Hey, great. Thanks for taking my question. I guess, you know, clearly the totality of the data suggests that there's potentially a signal here. I'm curious, though, if FDA does hold a hard line on total slope and disagrees with that analysis, what are the potential outcomes next year? Is there a possibility that sparsentan gets pulled? Curious on your thoughts there. Thanks. Alex, thank you for the question, and I will turn that one over to Bill. I think that with the data that we've presented today and the strong outcome that we have on two-year data extending what we showed at interim, there isn't a case to be made that the drug should be pulled from the market. I think that we look forward to having the engagement with the FDA, but I don't see that as one of the potential outcomes from those initial engagements. The So let me- Data Go ahead. Sorry, Bill. Please, please continue. No, go ahead, Eric. Yeah, no. Let me unequivocally say, we firmly believe that there is a role that FILSPARI plays. And when you look at the data from PROTECT, you see one of the most profound reductions in proteinuria that is durable over two years, and all efficacy measures favor sparsentan, favor FILSPARI. So we do not see that there would be rationale for any action like removing the authorization. So we're eager to be able to meet with the FDA and walk through the body of evidence here. Certainly, we cannot speak for the agency. We've just received the data, but we will provide an update once we've met with the FDA. We'll go next to Ed Arce with H.C. Wainwright. Thanks for taking my questions. I just had a question I wanted to ask for both management and Dr. Rovin. You look at the two arms, and they start with nearly identical baseline proteinuria. And as you've mentioned before, the end change in eGFR at two years was unusually low, at 9.5 versus the 12 for the TARPEYO study at two years. And I'm wondering if you can discuss that, and perhaps, you know, in discussions with the FDA and any particular issues with regards to the trial setting that may have had an impact there. And then related to that, I'm just curious why it was that the eGFR over the next four weeks actually improved by 500mg there. And any comments there will be helpful as well. Thank you. Thank you for the question. Maybe I'll start just by reflecting on the unique trial design and the rigor that we have in the PROTECT trial, and then I'll turn it to Jula and Dr. Rovin for their comments. This is a trial that was done in all patients were required to be optimized on background RAS blockade and then randomized to an active control. I think that that's quite unique to any of the trials that are, that have been or are being done in this space. I think that that's an important context to keep in mind when we think about the benefit that we see over time, both on proteinuria and kidney function preservation. To your question around, you know, what is how is the trial design influencing? That fundamentally is a really important aspect, and Dr. Rovin mentioned that that's perhaps why we see some of the lowest rates of, of eGFR decline in the control arm, let alone the, the even better, rates that we see in the sparsentan arm. Jula, I'll turn to you first, and then we can, we can, turn to Dr. Rovin for his thoughts. Yeah, I think it's a very important point, which is why we showed in the deck the rates of progression in patients, both with irbesartan, who did better than the control arms of historical trials, including the TARPEYO trial. To your point, they progressed closer to 11-12 mL/min/year. That's similar to the control arm of most of the clinical trials that we've seen to date in IgA nephropathy. Both of our treatment arms did better. Irbesartan did better. They were taking nearly 100% adherence of the medication, and we got them to the max dose. All of this information needs to be taken into context about the treatment effect of what we saw. However, FILSPARI did incrementally significantly better at whichever measurement you look at, chronic slope, total slope, and to your point, the absolute difference at study end, whether or not you look for at two years or you look post the four-year or the four-week washout. Yes, I, I think you're noting that there is some variability after the four-week, and it's not a true washout. Patients resume whatever standard of care measurement or medication they were previously on. But importantly, you see in the FILSPARI arm a durable kidney function protection over the two-year time period when you look at that absolute change to two years or two years post-washout. I'll just be brief. You know, I don't think the populations were substantially different. I think the rigor of the trial design and the optimization of RAS inhibition really lent itself to the slower decline that you see in the control group compared to historical control groups. And of course, you know, patients in clinical trials are motivated to a large extent, and adherence is often very good, and pushing the drug to the maximum, which is what we try to do clinically to benefit the patients as best as we can, really probably did benefit the control arm as well, compared to what would happen in other situations. I, again, like I said at the beginning, I think this is really a testament to how well the trial was run, that the difference was not bigger, but the patients, you know... I think the patients benefited from being in the study in both arms. Thank you, Dr. Rovin. And I think, you know, as we look at the data and overall what the absolute eGFR level is, we were able to get patients on FILSPARI below 3 mL per minute per year. That's, that is a pretty outstanding effect when we think about the natural progression or even the progression of patients that are in kind of the real world, considered optimally treated by RAS blockade. So I think when we look at the absolute eGFR and kidney function, these are really impressive results. We will take our next question as a follow-up from Joseph Schwartz with Leerink Partners. Hi again. Thanks for taking the follow-up here. This is Will on again for Joe. Could you just briefly remind us of the powering assumptions for the study? We were under the impression that the eGFR total slope endpoint was going to be evaluated with a one-sided alpha of 0.02. So any color there would be helpful. Thank you. Certainly. So Jula, would you like to take that? We had an alpha of 0.05 assigned and then a hierarchical testing thereafter. Bill, correct me if I'm incorrect on that. Yeah, no, you're correct, and it's for the U.S., it's 0.05, and it's a two-sided alpha. That's right. We'll go next as another follow-up from Liisa Bayko with Evercore ISI- Hi there. I'm just wondering if you can speak a little to how you think, you know, this data will impact the trajectory of the launch over the next, you know, several quarters as we wait for full approval. I know you were initially guiding to sales starting to accelerate towards the end of year into next year, and does that still hold in the context of these data? Thank you. Liisa, thank you for the question. I think as we look out at all of the information that we have, both the two-year data, the launch performance to date, as well as the research that we have from both patients and nephrologists, there's nothing that we see that changes our outlook for the launch, both in the short term as well as the long term. And if we think about over the next year, these patients still have very few treatment options to address fundamentally what they and their nephrologists are looking for: a reduction in proteinuria and a slowing of their, their kidney loss. And, and I'll turn to Dr. Rovin to get his comments on how he thinks about, you know, how patients with IgAN might be treated over the next year. But fundamentally, Liisa, our, our confidence in the outlook of the launch remains high. Just, I'll just speak from a person in a very active glomerular disease clinic, of course, at an academic center. We discuss adding FILSPARI to almost every IgAN patient that we haven't put into a trial. Now, that's not a huge number of patients because we are trying to put patients into trials, but this comes up every week. We're utilizing, working closely with Travere, to get patients up and running on the medication, and I think this will only continue to provide fuel for that fire. This does conclude the question and answer portion of today's call. I would like to turn the call back over to Dr. Eric Dube for any closing remarks. Excellent. Well, thank you all for the time this morning. We were very excited to be able to share the top-line results from the PROTECT study, a passion of ours for the last five years in bringing innovative therapies to the IgAN community. You know, perhaps it's best summed up by what Dr. Rovin said, which is that these are impressive results, and they really provide even more support for the foundational role that FILSPARI can play, in treating patients with IgA nephropathy. So we look forward to providing further updates, and certainly, Jula and her team will be working feverishly to submit a manuscript as well as to present data at further medical meetings. So certainly more to come from us in the near future. And again, thank you all for your time and your questions today. This does conclude today's conference call. Thank you for your participation. You may now disconnect.