Operator
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.
Naomi Eichenbaum
Thank you, Bruce, 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 [indiscernible] 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 Investors 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 [indiscernible] 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 2 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 21, 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?
Eric Dube
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 2 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 IgAN 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 today and comparable to the active control irbesartan. As you will hear from Jula and Dr. Rovin, these data represent a clinically important benefit in 1 of the most rigorous head-to-head clinical trials in [indiscernible] conducted to date. Before reflecting on the FILSPARI journey, I'd like to thank all of those individuals who have helped in the development of FILSPARI, the patients, their caregivers, their 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 5 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 2 years of FILSPARI treatment. The eGFR data over 110 weeks provides a clear picture of the potential treatment benefit on kidney [indiscernible] 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 2-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, CSLB 4, 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?
Jula Inrig
Thanks, Eric, and good morning, everyone. I'd first like to reiterate our gratitude to the patients and their families, investigators and site staff, our 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. And 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 7 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. And recently published data from the rare renal diseases or RADAR study, patients with persistent proteinuria progress to kidney failure in roughly 8 years. However, a 40% to 50% reduction in proteinuria at 9 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 8, you can see the progression of IgA nephropathy to kidney failure is driven by 2 critical pathways, endothelin I and angiotensin II. These are overactivated by abnormal IgA complexes deposited and critical control cells in the kidney. This drives upregulation of endothelin I 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 2 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 9, you can see that a total of 404 adult patients were enrolled globally in PROTECT. Individuals were randomized 1:1 to receive either 400 milligrams of FILSPARI or a maximum dose of 300 milligrams 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 label dose for at least 12 weeks prior to screening and have proteinuria greater than or equal to 1 grams per 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 [indiscernible] 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 2 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 2 years with FILSPARI treated patients achieving a mean reduction in proteinuria from baseline of 43% compared to 4% for irbesartan-treated patients.
At 2 years, the prespecified 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 2-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 end points, 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 flow evaluates kidney function starting at week 6, after any initial potential changes like blood pressure in the kidney have stabilized, and it continues through week 110. Treatment with FILSPARI resulted in 1 of the slowest rates of kidney function decline seen in a controlled IgAN clinical trial to date. Patients on FILSPARI over 2 years exhibit an annual decline of kidney function of minus 2.7 mL per minute per year as measured by chronic slope, and minus 2.9 mL per minute per year, as measured by total slope. This compares to an annual decline of minus 3.8 million to minus 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 per minute per 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 per minute per year in favor of FILSPARI compared to the active control irbesartan with a p-value of 0.037.
On Slide 14, we have included 2 important supportive eGFR analyses. First is the intent to treat or ITT population, which includes all patients irrespective of whether they stopped treatment early during the study. The second is sensoring on patients who received rescue immunosuppression during the study. These analyses are important for 2 reasons: one, the irbesartan [indiscernible] experienced higher early treatment discontinuations due to patient or physician decision. And two, there is more than twice as much use of rescue immunosuppression medication and patients on irbesartan compared to sparsentan. In these 2 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 4 weeks after stopping treatment and resuming standard of care medication. Importantly, we see the 2-year mean change in eGFR of minus 5.8 mL per minute with sparsentan and compared to minus 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 4 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 maintain 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 minus 5 mL per minute per 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 a decline of minus 5.3 milliliters per minute per year. For a patient population like we study in PROTECT, these patients would be projected to face kidney failure in 8 years. But maximal treatment with the active compare to irbesartan, slow the rate of progression to kidney failure. Importantly, these data suggest treatment with FILSPARI utilized long term has the potential to significantly delay the time to kidney failure by up to nearly 8 years compared to routine standard of care treatment and maximal 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 [indiscernible] 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 demonstrate the largest sustained reduction in proteinuria in clinical trials in IgAN, 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. Robin, who is a Medical Director at Ohio State University Center for Clinical Research Management, Director of the Division of Nephrology 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.
Brad Rovin
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 [indiscernible] Medical Center. I have -- 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 to 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. And we do have a lot of that from the community and also from the surrounding areas in Central Ohio in the [ contiguous ] states.
So as you probably all are very well aware, the treatment options for IgAN have been really conservative management lifestyle modification and 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 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 kidney failure. In addition, proteinuria in and of itself may be harmful to the kidney. So it may be a biomarker as well as a mechanism of tissue injury to the kidney. So 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 1 gram per day. And I think that the data that were alluded to earlier, and I think Dr. Inrig showed some of the results from the RADAR study suggests that this treatment goal may be a little bit too liberal in a sense. These data really suggest that patients who have proteinuria well below 1 gram 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 milligrams a day. And beyond that, I would like to see the patients below 300 milligrams 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 2 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 2-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. And 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 a historical perspective, just to show you how rigorous and well done this trial was and 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 2.
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 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 is in your slide set and was just presented is that sparsentan does a superior job to what we would consider as standard of care active treatment with a RAS inhibitor and that's clinically meaningful.
So I would also suggest to you that the total slope data are also very impressive. And 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. And I think that's where these PROTECT data shine. .
So 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 9 months of use. And this is just verified after 2 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. But 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 1 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. But observationally, I knew what his proteinuria did and his proteinuria rapidly decreased. So 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 in 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 drop 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 we've 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 spectacular outcomes with the PROTECT trial and so with that, I'm going to hand the call back to Eric for questions.
Eric Dube
Thank you, Dr. Robin. 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 towards a planned sNDA submission in the first half of 2024. And with the achievement of the confirmatory eGFR end points for the EU, we anticipate, together with our partner, CSL [indiscernible] 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 3 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.
Naomi Eichenbaum
Thank you, Eric. We can now open the line up for the Q&A. Operator? .
Operator
[Operator Instructions] Welcome to first Joseph Schwartz with Leerink Partners. .
Will Soghikian
This is Will on for Joe. 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.
Eric Dube
Well, thanks for that. I think 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 favor FILSPARI compared to irbesartan and as we have 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. And it's our belief that, that did not contribute to narrowly missing statistical significance on total. So I'll turn it over to Jula to provide her thoughts on the total slope endpoint.
Jula Inrig
Yes. 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, so yes, 1 aspect can be the acute effect because that adds to the variability with regards to the measurement of total slope, but we didn't see a large acute effect or 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 [indiscernible].
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 [indiscernible]. So I think some of those put it into context around why we may not have hit statistical significance. But again, I want to reiterate, we saw a clinically meaningful effect on both measurements of kidney function preservation.
Operator
[Operator Instructions] Our next question comes from the line of Anupam Rama with JPMorgan.
Anupam Rama
I know you presented a few analysis here, but can you give us any more color if there are additional subgroups of patients that may have had an outsized or lower muted benefit on eGFR based on baseline characteristics? Or is that kind of work still ongoing?
And then for Dr. Robin, how do these kind of top line 2-year eGFR data update your views on the right or eligible population for FILSPARI in your practice?
Eric Dube
Thanks for your questions. With regard to subgroup analysis, 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 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.
Jula Inrig
Yes. 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.
Eric Dube
Thanks Jula and Dr. Robin, do you want to provide your thoughts on the patients that might benefit now that you have seen these 2-year data?
Brad Rovin
Yes. Thank you. I just start with -- I love subgroup analyses, and I hope that I will continue to be involved when we start looking at the data because that's the most fun part of my job. But anyway, in terms of my thoughts, I actually -- 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. So I believe that sparsentan can be a foundational baseline for sort of the treatment pyramid of IgA nephropathy. And what we generally have used is starting out with RAS inhibition. And this is just so much better as you can see in reducing proteinuria that to me, this drug would be a drug I could use in any IgA patient. Now there's caveats in that. Obviously, 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, these types of things. But in general, for the IgAN population as a whole, I actually think this could be a foundational therapy.
And I'm going to go 1 step further, and I'm not speaking on behalf of [indiscernible], I'm speaking on my interpretation of the current state of data. I 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 lower 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. So I think that can benefit all patients.
Operator
We'll go next to Greg Harrison with Bank of America.
Greg Harrison
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?
Eric Dube
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 precedent, there really is an emerging area where FDA is looking at eGFR within these rare kidney diseases. And so I think rather than rely on 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 how we'll approach the FDA.
William Rote
On mute, of course. Thanks, Greg. The agencies 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 data set 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. .
Operator
We'll go next to Maurice Raycroft with Jefferies.
Maurice Raycroft
I was going to 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?
Eric Dube
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 EMA and 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 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.
William Rote
Yes, 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 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, 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.
Brad Rovin
Yes. So as I mentioned, to me, this is the key because we're not focused on treating the patient just for a year or 6 months, 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 the SGLT2 story, and you can easily see that the acute effect on GFR with the SGLT2 inhibitors is a decline. And then the 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 much as what Eric and Bill just said, 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 that 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. .
Maurice Raycroft
Thank you, Dr. Rovin. I know you've been looking quite a bit at all of these different classes of medicine and trials looking at IgAN. Do you want to comment any further about your assessment as the nephrologist as well? And particularly also on [indiscernible] versus total?
Jula Inrig
Yes, I think it is important. But 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 1 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. .
Operator
We'll go next to Liisa Bayko with Evercore ISI.
Liisa Bayko
Can you just kind of give us any color on conversations you've had with FDA on chronic versus total slope? And what you anticipate the 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 the total slope. And I'm just wondering kind of just your sense on their ability to be flexible based on any conversations you've had. Obviously, the outcome of the study was 1 possibility might have contemplated with them.
Eric Dube
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 2 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 .
William Rote
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 primary. And the comments were made, 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, 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.
Operator
We'll go next to Laura Chico with Wedbush Securities.
Laura Chico
I guess I just wanted to clarify really quick, Jula, on 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 2-year data change your views, I guess, if you're trying to decide between using something like budesonide, extended release or FILSPARI, does this 2-year data change anything from your view?
Eric Dube
Thanks, Laura. Jula, we'll turn to you first and then go to Dr. Rovin.
Jula Inrig
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 [indiscernible]. So if we had alpha to give to that you can imagine that we 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.
Brad Rovin
So your question is really, really relevant because my colleagues and I are really thinking about how we can use all of the new medication and 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. And then I have, on top of that, the ability now to go to a drug [indiscernible] that may actually target the pathogenesis of the abnormal IgA formation. So these drugs, to me are not competitors, they're synergistic. And 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 2-drug combination, if not multipical.
So in other words, I don't know how far this can go. And of course, now many of us in the community are interested in how we would design and use multi-targeted regimens or IgA nephropathy, much as we're doing in other glomerular diseases. I think it's naive to assume that 1 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 itself -- themselves to the possibility of combinatorial treatments and 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.
Operator
We'll go next to Vamil Divan with Guggenheim Securities.
Vamil Divan
Great. Maybe just follow up on a couple of these points that were just great. So 1 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 the [indiscernible] and also on the SGLT2 side, does this data any way you sort of change how you might think about when you're at [indiscernible] this sort of change treatment through landscape?
And then 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 were taken out of the analysis when you did the -- the second [indiscernible] I realize there wasn't any stats that you can do there or any p-value you can provide, but just curious what number of patients we're talking about that were excluded?
Eric Dube
Vamil, thanks for your questions. Dr. Rovin will turn to you first and then Jula, you can take the question about the sensitivity analysis.
Brad Rovin
Yes. Okay. So the data today, don't really -- they confirm sort of my initial impression of how I would use sparsentan in sort of the treatment paradigm. So early on, 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 where we've been talking about IgAN 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 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 are 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? And so as I said, what I visualize for most IgAN patients is a foundational treatment with sparsentan, for example. And then I would like to add a treatment that would focus on 1 of the pathogenic mechanisms of the immune disease of IgA nephropathy. I think we've been very clear. And importantly, 1 of the benefits of sparsentan that allow its long-term use is that it's not immunosuppressive. So we're not immunosuppressing a person forever like we do in transplant patients.
So 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 the auto antibody against the [ aberrant ] IgA as an example.
And then when I treat the immune disease, and I would probably -- I don't like to keep patients on immunosuppression forever if it's not necessary because of the risk of immunosuppression. What I'm done with that, and I have the proteinuria controlled as best as I can with against 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. So I think the 2 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, especially in IgA, if you look at the subset of [indiscernible] from Dapa-CKD and [ ampakidney ]. These are our 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 -- and would add 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 product kidney disease that's progressive. I do a kidney biopsy. I verify there's no more activity and then I add an SGLT2 inhibitor. And I realize there are no data for lupus or some of these other diseases ye with the SGLT2 inhibitors, but that gives you an example of how I visualized using the drug in IgA nephropathy as well.
Eric Dube
Thank you, Dr. Rovin. And Jula, would you like to take the question about the additional data from the analysis of [indiscernible] an early stopping of treatment?
Jula Inrig
Yes. So our primary analysis for both of our eGFR endpoints was prespecified 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 [indiscernible] 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. And 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 stop study treatment early because they just didn't feel like they were doing well or their physicians felt like they were progressing. That's the ITT analysis. It's all patients, kidney function over 2 years.
The steroid censoring or the immunosuppression sensoring is once patients get started, we sensor their data thereafter. We'll provide more details around that, again, as I said, at an upcoming meeting.
Operator
[Operator Instructions] We'll go next to Carter Gould with Barclays.
Carter L. Gould
I appreciate Dr. Rovin hopping on his commentary has been helpful. I guess 1 really kind of, I guess, straightforward and simple question for Eric and Jula. You mentioned that the pre-NDA meeting is set for 4Q, 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 output of that meeting on IgAN before year-end?
Eric Dube
Thank you, Carter. So we are on track to provide an update on our FSGS discussions this fall. So I'd say 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 we -- as our practices, 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. .
Operator
We'll go next to Tyler Van Buren with TD Cowen.
Tyler Van Buren
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 to $40 million?
Eric Dube
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, we certainly see that there is a pretty tight range of first year revenue with regard to recent rare renal launches. And 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 6 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 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, we'll focus on what we shared on Q2, which is 1 of the strongest starts to a rare renal launch, and we have an ambition and certainly, we can't discuss the 2-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.
Operator
We'll go next to Mohit Bansal with Wells Fargo.
Unknown Analyst
This is [indiscernible] on for Mohit. Firstly, could you just talk about why you may have seen a discount between the proteinuria effect that you saw with sustained reduction and the expected eGFR response you would see. And then secondly, at the interim review that supported a great approval I was curious to see what kind of changes there were between the first year [indiscernible] data you saw in some patients [indiscernible] the second year because I understand that the FDA was reviewing some of that data and ensuring that there was adequate powering to support a positive trial on that hard outcome?
Eric Dube
Thank you for the questions, [indiscernible]. Jula, I will turn those questions to you.
Jula Inrig
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 2 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 and even greater with FILSPARI.
Operator
We'll go next to Tim Lugo with William Blair.
Tim Lugo
Do the data confirmed 40% reduction of eGFR, ESRD and [indiscernible] obviously, FILSPARI, but if you only look at ESRD and death, is that also skew towards percent in use, and there was -- it did look like there was more [indiscernible] group then irbesartan -- was there anything of note there?
Eric Dube
Jula, I will turn that to you.
Jula Inrig
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 comfortable between both treatment arms. .
Operator
We'll go next to Alex Thompson with Stifel.
Alexander Thompson
Great I guess clearly, the [indiscernible] 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?
Eric Dube
Alex, thank you for the question, and I will turn that 1 over to Bill.
William Rote
I think that with the data that we've presented today and the strong outcome that we have on 2-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 1 of the potential outcomes from those initial engagements. Let me -- go ahead. .
Eric Dube
Sorry, Bill, please continue. .
William Rote
No, go ahead, Eric.
Eric Dube
Yes. 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 1 of the most profound reductions in proteinuria that is durable over 2 years and all efficacy measures favor sparsentan, favor FILSPARI. So we do not see that there would be a 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 just received the data, but we will provide an update once we've met with the FDA.
Operator
We'll go next to Ed Arce with H.C. Wainright.
Antonio Arce
I just had a question I wanted to ask for both management and Dr. Rovin. You look at the 2 arms and they start with nearly identical baseline proteinuria. And as you've mentioned before, the end change in eGFR at 2 years was unusually low at 9.5% versus the 12% for the [indiscernible] study at 2 years. And I'm wondering if you can discuss that and perhaps 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 -- was at the eGFR over the next 4 weeks actually improved by 500 milligrams there. And any comments there would be helpful as well.
Eric Dube
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 [indiscernible] blockade and then randomized to an active control. And I think that that's quite unique to any of the trials that have been or are being done in this space. And 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.
So to your question around 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 eGFR decline in the control arm, let alone even better rates that we see in the sparsentan arm. Jula, I'll turn to you first and then we can turn to Dr. Rovin for his thoughts.
Jula Inrig
Yes. 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 [indiscernible] trial. To your point, they progressed closer to 11 to 12 mL per minute per 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, [indiscernible] incrementally significantly better at whichever measurement you look at, chronic slope, total slope. And to your point, the absolute difference at steady end whether or not you look at 2 years or you look post the 4-year -- or the 4-week washout. Yes, I think you're noting that there is some variability after the 4 weeks. 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 2-year time period when you look at that absolute change to 2 years or 2 years post washout.
Brad Rovin
I'll just be brief. 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, 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. And again, like I said at the beginning, I think this is really a testament to how well the trial was run. But the difference was not bigger, but the patients I think the patients benefited from being in the study in both arms.
Eric Dube
Thank you, Dr. Rovin. And I think as we look at the data and overall, what the absolute eGFR level is, we were able to get patients on FILSPARI below 3 milliliters per minute per year. 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.
Operator
We will take our next question as a follow-up from Joseph Schwartz with Leerink Partners.
Will Soghikian
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 eGFR total slope endpoint was going to be evaluated with a one-sided alpha of [indiscernible]. So any color there would be helpful.
Eric Dube
Certainly. So Jula, would you like to take that? .
Jula Inrig
We had an alpha of 0.05 assigned and then a hierarchical testing thereafter.
Bill, correct me if I'm incorrect on that.
William Rote
Yes. No, you're correct. And it's -- for the U.S., it's 0.05, and it's a 2-sided alpha.
Operator
We will go next as another follow-up from Liisa Bayko with Evercore ISI .
Liisa Bayko
I'm just wondering if you can speak a little to how you think this data will impact the trajectory of the launch over the next sub-4 quarters as we wait for full approval. I know you were initially guiding to sales starting to accelerate towards the end of the year into next year? And does that still hold in the context of these data?
Eric Dube
Liisa, thank you for the question. I think as we look at all of the information that we have, both the 2-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 kidney loss. And I'll turn to Dr. Rovin to get his comments on how he thinks about how patients with IgAN might be treated over the next year. But fundamentally, Liisa, our confidence in the outlook of the launch remains high. .
Brad Rovin
Just, I'll just speak from a person in a very active glomerular disease clinic, of course, at an academic center. We discussed 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 [indiscernible] to get patients up and running on the medication. And I think this will only continue to provide fuel for that fire.
Operator
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.
Eric Dube
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 5 years in bringing innovative therapies to the IgAN community. 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. .
Operator
This does conclude today's conference call. Thank you for your participation. You may now disconnect.
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