Thank you, Tara. Good morning and welcome. I'm Marshall Fordyce. I'm founder and CEO of Vera Therapeutics. We previously shared top-line week 24 results from our multinational randomized placebo-controlled phase 2b ORIGIN trial, which focused on FDA's gold standard analysis intention to treat. Today, we're pleased to share further analyses from the ORIGIN trial that we believe will help put atacicept's phase 2b results in context across the evolving treatment landscape for IgA nephropathy and highlight atacicept's potency and competitive position as we plan for our phase 3 pivotal trial this year. Before we get started, I wanna remind you we'll be making forward-looking statements under the Safe Harbor Act, and as such, we present this disclaimer regarding at-risk statements. I'll begin by providing a brief overview of our program for atacicept and IgAN, then provide detail on the predefined analysis sets in our phase 2b study, a summary of our phase 2b results, and then highlight upcoming milestones for the program. I'll ask Dr. Jonathan Barratt, who leads the renal research group at the University of Leicester, and is an internationally recognized expert in IgA nephropathy, to present the results in detail and put them into context of the evolving landscape for IgAN. I'll then provide further detail on our plans for phase 3, which we expect to initiate in the first half of this year, subject to discussions with FDA, and then we'll open the line for questions. As many of you know, Vera's lead molecule in IgA nephropathy is atacicept, a biologic fusion protein that is self-administered as an injection subcutaneously once per week. Atacicept targets the source of IgA nephropathy by inhibiting two circulating cytokines, BLyS or BAFF, and APRIL, which are both important for the survival and maturation of the B cell lineage and the cells that produce autoantibodies in certain autoimmune diseases. We designed the ORIGIN study to demonstrate whether atacicept's known effects on the upstream causes of IgAN translate into improved kidney function as measured by reduction in proteinuria. We are running a multinational double-blind placebo-controlled randomized phase two B trial to provide the best evidence to demonstrate a clear treatment effect of atacicept in IgAN patients. This study design enables us to assess whether any factors, other than the treatment itself, can influence the primary endpoint, so-called confounders, and make sure that they're well distributed between the treatment and control arms. This study is blinded through 36 weeks and has a primary endpoint analysis of intention to treat, which is the gold standard held by FDA, and we anticipate will be required for phase 3. We also had a pre-specified per protocol analysis of proteinuria to leverage phase 2 learnings for phase 3 success, and that will be the focus of today's discussion. In early January, we disclosed the top-line results from our primary endpoint, intention to treat. This is a conservative assessment that includes all patients who were randomized, regardless of whether they followed protocol or not. In the case of our study, that included 116 patients. As previously reported, these results were positive, statistically significant, and close to twofold better than the 1 approved drug, TARPEYO, at the week 24 time point. Benchmarking our phase 2 primary endpoint against an approved drug gives us confidence that atacicept can hit the primary endpoint of intention to treat in phase 3 and substantially improves our probability of success in phase 3 since our phase 3 study is very similar to our phase 2 study. In order to better understand the full effect of proteinuria, we pre-specified a per protocol analysis. This is defined as all patients who completed treatment according to protocol. The criteria were pre-specified. Independent nephrologists from a third-party CRO conducted a blinded review of subjects to identify major protocol violations. They identified 14 patients across all treatment arms. These patients had changes in their background regimen that are likely to have influenced their proteinuria results. Of the 14, six had a change in RAS inhibition during the study, three initiated SGLT2 inhibitors too close to baseline, three did not reach the week 24 time point, one initiated a steroid during the study, and one had compliance less than 80%. The per protocol analysis was not available at the time of our top-line disclosure. This analysis set really provides a more accurate assessment of treatment efficacy because it minimizes potential confounders for proteinuria. The ORIGIN study met its primary endpoint at week 24 by the gold standard ITT analysis with statistical significance. Proteinuria reduction by per protocol analysis at the 150 milligram dose demonstrated a 41% reduction from baseline at 24 weeks, with a calculated placebo delta of 34%. At 36 weeks, we see continued reduction in proteinuria, 47% reduction from baseline, with a calculated placebo-adjusted delta of 48% through the 36-week time point. As previously reported, patients on atacicept had stable renal function as measured by eGFR over 24 weeks. The 150 mg dose showed Gd-IgA1 reduction of 60% at 24 weeks. The safety profile for atacicept was similar to placebo. We've selected the 150 mg dose to advance into phase 3 and expect to initiate that trial in the first half of this year, subject to discussions with FDA. As we look ahead, next quarter, we plan to present an update of the full week 36 results. We're currently preparing for phase 3 and plan to announce initiation of that trial before mid-year. The phase 2b ORIGIN study provides a rich data set, including up to two years follow-up, which we plan to continue to analyze and present in conferences throughout 2023 and 2024. Our expected phase 3 primary endpoint readout is anticipated to be in the first half of 2025, enabling a BLA submission later that year and an anticipated commercial launch in 2026. With that, I'll ask Dr. Barritt to present the results in detail. John? Thanks very much, Marshall. Just a quick reminder on the design of ORIGIN. ORIGIN is a multinational randomized placebo-controlled trial powered to detect a 28% difference between the pooled 75 and 150 milligram doses of atacicept and placebo. The randomized phase lasts for 36 weeks, and today I'm going to discuss the 24 and 36 week data. ORIGIN recruited adults with biopsy-proven IgA nephropathy at high risk of disease progression, meaning that despite being on maximal tolerated ACE inhibitor or ARB, they still had at least 0.75 grams of protein in their urine, with the lower level of eGFR allowed for entry being 30 mils per minute. The primary endpoint was proteinuria at 24 weeks. The secondary endpoints include proteinuria reduction at 36 weeks and eGFR up to 96 weeks, Gd-IgA1 reductions and safety. P lease? It's well reported that a 30% reduction in proteinuria is known to be clinically meaningful in IgA nephropathy. This is based on natural history studies of IgA nephropathy patients, in which a 30% reduction in proteinuria at nine months is associated with a significantly slower rate of loss of kidney function and a potential delay of end-stage kidney disease by over 10 years. As you all know, the first and only drug approved in IgA nephropathy showed an approximately 18% reduction in proteinuria at 6 months and a 31% reduction at 9 months, and was granted accelerated approval for patients with IgA nephropathy and proteinuria greater than 1.5 grams per day. If we go to the next slide. The ORIGIN study is a multinational trial and includes patients in the U.S., countries in Europe, and the Asian Pacific region. As you can see from the graph on the slide here, enrollment was not over-represented by any single country in this study. If we go to the next slide. Of the 210 patients screened, 116 patients were enrolled. Previously, I presented the intention to treat population, which is all 116 subjects that were randomized. Today, I'm going to present the per protocol population. As you've heard already, this was a pre-specified population in which prior to unblinding, blinded third-party physicians determined whether protocol violations had occurred. Those subjects where there had been a protocol violation were excluded, as previously described by Marshall, giving a total population of 102 patients for the per protocol analysis. Because the majority of subjects who violated the protocol were due to changes in background regimen, assessing proteinuria reduction by the per protocol analysis is a more accurate way to compare ORIGIN results to other programs. Just to note again, there was a low discontinuation rate in this study. 2% in the atacicept arm and 3% in the placebo arm. If we go to the next slide. As I previously presented, the study enrolled patients who were at high risk of IgA nephropathy progression and were on current optimized supportive care, allowing us to make a clear assessment of the treatment effect of atacicept compared to placebo on top of what is regarded currently as standard of care therapy in a diverse global population. Average age was 39, 59% were male, 44% of Asian ancestry, and the average eGFR was 63 mils per minute, with an average uPCR of 1.6 grams per gram. Patients were on optimized ACE inhibitor or ARB, but in addition, if a subject was also on a stable dose of an SGLT2 inhibitor without change for at least 8 weeks, they were allowed to enroll in ORIGIN. As you can see, 14% of subjects on SGLT2 inhibitors were enrolled in ORIGIN. If we go to the next slide. Here you can see the change in proteinuria as evaluated by the uPCR, the urine protein to creatinine ratio, from a 24 hour collection. You can see a significant and dose-dependent reduction in proteinuria in those patients treated with atacicept compared to placebo. For the 150 milligram dose at week 24, there was a 41% reduction compared to a 10% reduction on placebo, with a calculated delta of 34% and a P value of 0.025. At week 36, with 38% of subject data available, a 47% reduction was seen compared to an increase of 3% on placebo, with a calculated delta of 48%. We go to the next slide. When we look at a responder analysis, and this is a responder analysis of those patients who had an over 50% reduction in proteinuria at week 24, what you can see here is that 33% of those patients on atacicept 150 milligrams experienced a 50% reduction in proteinuria. If we go to the next slide. This is a slightly different responder analysis. Here you can see of those patients who had a baseline proteinuria of over 1 gram per gram, 43% of those patients on atacicept 150 milligrams achieved a proteinuria less than 1 gram per gram at week 24. If we go to the next slide. This is the data presented previously, which is the primary endpoint, which was an intention to treat analysis, looking at the change in proteinuria as evaluated by the uPCR at week 24 of the pooled 75 and 150 milligram dose groups. As you've heard already, that achieved statistical significance and showed a 31% mean reduction compared to baseline, with a P value of 0.037 compared to placebo. The magnitude of proteinuria reduction by this analysis was clearly affected by major protocol violations, as you can see if you compare this data to the per protocol analysis. In this graph here, you now see the 150 milligram and 75 milligram dose effects over time. You can see there's a clear dose dependence and a statistically significant reduction in proteinuria at week 24 for the atacicept 150 milligram arm, with evidence of further proteinuria lowering for 150 milligrams at week 36. If we go to the next slide. Now putting the atacicept phase 2 data into context of the emerging treatment landscape, you can see that the magnitude of proteinuria reduction seen in ORIGIN have the best-in-class potential, especially given the rigor of the trial design and analysis. You can see here the Vera data with the intention to treat and per protocol analysis data presented. Here you can see that we compare the atacicept results to the other multinational randomized placebo-controlled trials, with data at week 24 and 32. Given the differences in study design across these studies and the analyses that have thus far been performed, we believe the best comparison is atacicept and TARPEYO. Although they have not been compared directly in a head-to-head study, the intention to treat and full analysis set analyses are similar. What you can see here is that atacicept shows approximately a 2-fold greater reduction in proteinuria at the week 24 time point. The Novartis study of iptacopan and the Alnylam study of cemdisiran, you can see the data presented on your screen. You can note that there were significantly fewer patients, and at present, the analysis that was being performed is unspecified, and we do not have P values. Notably, the atacicept phase 2 study is the only one of those studies that has allowed patients on SGLT2 inhibitors to be enrolled in the study. If we go to the next slide. If we now look at the comparisons across the multinational randomized placebo-controlled trials, looking at week 36 now, we can see that atacicept's 48% delta is the highest reported in the field, again, suggesting best in class potential. If we look at the data for sipaprenlimab, which was reported at the ASN late last year, which is an APRIL-only approach, you can say that they reported a 43% delta in this phase 2 study of an intravenous infusion. Both of the results that you see at the moment are not specified because the data has not been presented in terms of the analysis that's been performed. If we go to the next slide. What you can see here is the eGFR data. Looking at the eGFR data, both for the intention to treat population and the per-protocol analysis, you can see that there is stability of eGFR for patients on atacicept. That's what we might expect, because at this early time point, we wouldn't expect to see a significant decline in eGFR for patients on placebo. If we go to the next slide. As I've shown previously, the safety results indicate that atacicept was well-tolerated, with adverse events similar to placebo. There was 2% of serious adverse events overall, and none on the 150 milligram arm. There was a 1% discontinuation rate. Infections were similar between atacicept and placebo arms, and there were no cases of hypogammaglobulinemia. Placing into context the efficacy data and the safety data I've just described, I believe these data are very exciting and show a significant impact on renal function as measured by proteinuria and strongly support advancing atacicept into phase three. I'm now going turn back to Marshall to continue the presentation. Thank you, Dr. Barritt. We're now preparing to initiate our phase three program. We have alignment with FDA regarding our phase three design and can leverage our phase two global operations for a rapid start for phase three. Dose selection is complete, and as conducted in phase two, we will test the self-administered subcutaneous formulation in phase three, as we did in phase two. We're positioned well because phase two informs phase three, both operationally as well as from a data standpoint. We're in a strong position to not require much change within protocol and operations. Entry criteria and study conduct will be very similar in phase three, and we have the additional ability, using subgroup analyses and other insights from our global phase two program, to make slight modifications to maximize efficacy in phase three and ensure strong results. The phase 3 study design will be another global randomized placebo-controlled trial of atacicept, this time single dose, 150 milligrams as a self-administered 1 milliliter subcutaneous dose once weekly, compared to placebo. The primary endpoint will be proteinuria reduction at week 36, with a confirmatory secondary endpoint of estimated GFR at 104 weeks or 2 years. Entry criteria for phase 3 are very similar to phase 2. Turning next to our development timeline, we project primary endpoint readout for the phase 3 study in the first half of 2025, and we anticipate submitting our BLA later that year. With that, I'd like to open up the lines for questions, Dr. Barritt, Celia Lin, and myself will be available to respond. Tara, happy to open the lines up now. Hi, everyone. This is Priyanka on for Anupam Ramaa. I had a couple of questions. What medical meeting are you targeting? On slide 24, you talk about the subgroup analyses that will be performed to guide phase three. Will these subgroup analyses be presented at an initial full medical conference presentation? The other question I had is, what is your level of confidence that the 36-week data are replicated in the full analysis in 2Q, and what gives you this confidence? Thank you. Yeah, good questions. Just first, to the first question, we will target the major renal meetings, both European Renal Association as well as Kidney Week, and we'll provide specifics as those dates get closer. Number two, about subgroup analyses. These are important insights from phase 2 informing phase 3. I can share that at a high level, we're confident in atacicept's efficacy, according to proteinuria in all subgroups. It's not yet decided whether we'll share that data in detail in a public forum. Those, these are important insights that set us up for phase 3, operations, protocol, and conduct. Then finally, we are confident in the week 36 data. This is a portion of the data, 38% of all subjects, who are representative of the average that we see at week 24. Of course, we'll provide an update when the full data set is in. Thank you so much. Hi. Thanks for taking the question. Marshall, can you go through some of the reasons for protocol violations, and in particular, the change of RAS inhibitor medications? Like, why would that affect, you know, proteinuria in a negative way? It seems like when we did our back of the envelope, it was at about a 10% change for those 5 patients that were taken out of the analysis. Why would changing that medication, for example, and some of the others are a little obvious, but that seemed to be a big one, and I was curious. You know, my next question is just around what you can do with phase 3 to try to, you know, kind of reduce as much as possible these protocol violations. Thanks. Good question. I think it's well known that changes in RAS inhibition, ACE inhibitors, angiotensin receptor blockers, can have an effect of tens of percents on proteinuria. One could imagine, regardless of treatment arm, both an increase in dose or a decrease in dose, having that effect in individuals. It's important to protocolize background regimens, not only in IgAN clinical studies, but in other studies, changes in background regimen can threaten the primary endpoint. This was an approach that we took in phase 2 to recommend stability of these treatments. I can say that it's several changes we can make going from phase 2 to phase 3 can optimize the intention to treat number going into phase 3. You know, these are protocol violations that were identified. These happen at this rate. Similarly with a study of this size, with about 30 subjects per arm, you can imagine 3 to 5 subjects having a significant impact on the primary endpoint. This is all within our expectations of what we'd expect to see. Thank you. Hi, Thanks for taking the questions. Dr. Barritt, question for you. How would you expect these immunomodulatory drugs to behave as you think about different baseline characteristics? I think as we look at some of these trials that are on slide 19, there were different baseline uPCRs. Would you expect, I guess, a greater benefit or less of a benefit as you sort of go down that grams of protein? A corollary, Marshall, for you. I believe since you are changing that uPCR from the phase 3 to the down in the phase 3 versus the phase 2, what do you expect baseline to end up? Thanks. Should I go first, or Marshall? No. Go ahead, Dr. Barrett. I think this approach of targeting the production of pathogenic IgA is going to be fundamental to any treatment going forwards in this disease. We know that the background therapy with RAS inhibitors, with SGLT2 inhibitors is protective to proteinuric kidney disease, but it does nothing to the underlying pathology of this disease in terms of stopping IgA depositing the kidneys. That's the rationale for this approach. My view is that this approach is going to be important in all patients with IgA nephropathy, whether you have high levels of proteinuria or you have lower levels of proteinuria. In my view, and we will have a publication coming out shortly, looking at over 4,000 patients with IgA nephropathy in the UK Rare Disease Registry. We're going to start to make arguments that actually we need to lower the threshold at which we treat patients because we've got to prevent them from developing kidney failure in their lifetime. For me, an approach that targets the fundamentals of this disease in terms of turning off the production of pathogenic IgA is going to be critical in all patients with IgA nephropathy. Not only those with IgA nephropathy in their native kidneys, but also those with IgA nephropathy and the risk of developing recurrent disease in a kidney transplant. I think the baseline characteristics help you risk stratify, but in actual fact, they, for me, are not relevant to which patient with IgA nephropathy justifies an approach like this. Any patient who's had a kidney biopsy who has IgA nephropathy requires a drug that is going turn off production of pathogenic IgA. I'll hand over to Marshall. Thank you, Dr. Barritt. I think the comment from or the question from Ritu is how are we changing baseline proteinuria going from phase 2 to phase 3? That's a slight modification. In phase 2, we used 0.75 as the cutoff, as we go into phase 3, we'll use 1 gram per gram as the entry criteria. Of course, you know, even with the 0.75, we ended up enrolling an average proteinuria of 1.6 grams per gram over time, now we have data on efficacy in both patient population above and below that threshold. We're confident in the efficacy that we see here being replicable in phase 3. Marshall, would you expect the baseline to then be pretty much equivalent between phase three and phase two? I would. I think these are minor modifications. Great. Thanks for taking the questions. Hey, guys. Thank you for taking my questions as well. I guess I may be extrapolating a bit, but it looks as if proteinuria reductions with the 75 mg dose have started to plateau at week 36, while the 150 mg dose continues to decrease over time. Was that a consideration when deciding on the dose for the phase 3 trial, and do you expect proteinuria to kind of continue to decrease beyond the week 36 time point? Secondly, did the protocol violations occur at a few specific clinical sites, or were they distributed across geographies? Great. Both good questions, Rami. The second one first. No, we did not identify a specific site that had these. These were distributed across the global sites involved in the trial. We agree. I think looking at the dose response, we're pleased to see that 150 milligrams outperformed 75 and agree that 150 milligrams has deepening proteinuria reductions going from baseline to week 12 to week 24 and now week 36. I think We do not yet know what the kinetics are of a proteinuria reduction with the dual inhibition of blisapril, as we have on these doses. Agreed that, you know, there seems to be a plateauing effect at 75 milligrams, but a deepening effect at 150. Expectations beyond that, I think sometimes, B-cell modification has a longer-term benefit that one can see. That's certainly been seen for the belimumab or Benlysta of programs in other diseases. I think, you know, targeting the source of the disease and having a disease-modifying effect over time, as we've shown previously in 2022, atacicept actually reduces Gd-IgA1, reduces autoantibodies, and reduces immune complex. We've shown that in the prior randomized trial in phase 2A. Now we're showing that that translates into proteinuria benefit, and we'll see how that continues to translate beyond week 36. Thankfully, ORIGIN will be run for 2 years, so we'll be able to have ongoing data trying to answer that question. Thank you, guys. Hi, good morning, everyone. Thanks for taking my questions. I was wondering for the per protocol analysis, can you clarify what cohorts the 14 patients were in? Is there anything additional you can say related to setting expectations for the full 36-week data? Potentially comment on eGFR expectations specifically. Yeah, good question, Maury. you know, I think we've shown what the reasons are, the five reasons that we've listed for major protocol violations, which I think are reasonably tied to an effect on proteinuria. They're distributed across all three treatment arms. you know, we provided both the per protocol and ITT analyses in the slide deck that delineates which patients as well are in each analysis set. I think that's all in good shape. We've got, you know, a sense that as we move to week 36, these are representative of the full patient population. We don't expect that number to change substantially. Anything you can say for eGFR expectations? When you get the full 36-week data, will you have to get final clarity from FDA on the protocol? Is that basically the next step for getting that final FDA feedback? Sorry, I missed your question on the GFR. Yeah, you know, our expectation is that GFR is really going be stable through 36 weeks. We would not expect, you know, it's an early time point to start to expect significant decline in placebo. So far at week 24, the data looks stable on both atacicept and placebo, and then, we do expect that to continue into week 36. Okay. Thanks for taking my questions. Just to interrupt here, Tara, I've got a question online I'd like to address. One question was, what do we mean by pre-specified, and when was the analysis added? This analysis was a part of the statistical analysis plan that was clearly, you know, those need to be in place with criteria and predefinition prior to unblinding. This was pre-specified prior to the unblinding of the study in unblinding of this analysis in December. Happy to take the next question, Tara. Good morning, guys. Thanks for taking the question. I apologize. I think I missed this earlier, but with respect to the protocol violations, why were these not uncovered, I guess, in the initial QC of the data? I think you mentioned this is a blinded third-party CRO. Just trying to understand why these weren't originally raised earlier. Then one question on the expectations around the presentation of the full data set. Will you be including the 25 mig cohort in that? Then final question, I think, serious adverse events were actually higher in the placebo group relative to the treatment group. Just wondering if you could characterize those at all. Thanks very much. Sure. I'll try to grab each of those. actually, Laura, can you repeat the first question? Sure. Too many at once. Just with respect to the protocol violations, I think I missed this earlier, but why wasn't this? Originally raised in the initial QC? ...in the initial Q.C.? Thank you. Just to be clear, you know, intention to treat just provides an analysis of all patients randomized. That doesn't require any work by the CRO to identify a protocol violation. We simply didn't have it when we initially presented the data. It takes time and this is a recent analysis that, you know, takes time to produce the analysis. Didn't have it at the time. Second question, I guess, was around week 36 data and will we present both ITT and per protocol? Absolutely. We'll continue to share both. Also the 25 mg cohort, will that be included? The 25 milligram cohort in, you know, that was an underpowered arm. It had half as many subjects and had a variable proteinuria endpoint that wasn't significant at week 24. From a proteinuria standpoint, we don't feel like it's informative, and we'll continue to show the 75 and 150 milligrams over time. Just lastly, serious adverse events looked like they were a little bit higher on the placebo group. Just wondering if you could share any color around that. Thanks very much, guys. You know, we can provide a list. I think at the previous presentation, we had a list of the common infections that we're seeing, upper respiratory tract infection, pharyngitis. These are commonly seen in clinical trials of any kind. We did have some COVIDs as well, but not serious adverse events, distributed really across various adverse event categories. Thanks very much. All right, great. Thanks for taking my questions. First, Marshall, one for you. If the ITT analysis, as you mentioned at the beginning, is the standard by which the FDA reviews this, how will the agency interpret the Per-protocol analysis? Have you had discussions around that? When could you expect any clarity on that, in particular for the phase three? Secondly, for Dr. Barritt, given the clear dose reductions that we've seen so far, would you expect a similar incremental increase, which is now stands at 47%, you know, at the full 36-week readout next quarter? Thanks so much. Sure. You know, we won't provide detail on the regulatory communications, but I can say that there is, you know, an approved drug in IgA nephropathy, and intention to treat was the analysis that was required in the pivotal trial. I think that's the right expectation, is that in phase 3, we expect that ITT will be the primary endpoint analysis. I, and I have... As I've mentioned, Ed, it's important to understand the difference and adjust and optimize the phase 3 protocol to get the best efficacy and minimize confounding going from phase 2 to phase 3. John, happy to ask you to answer Ed's second question. I think the question was, do I expect with the full patients through week 36 that magnitude of proteinuria will be similar? Is that the question? Yes. Correct. I mean, I see no reason why it wouldn't. I think, as has already been alluded to by one of the people asking the questions, that what I'm more interested in is trajectory. If you look at the trajectory of the proteinuria in that 150 milligram group, it's still going down in my view. I would hope that we're going to see even more proteinuria reduction, which will translate through to better kidney function protection. Looking at the data, looking at the variability of those results around week 36 with the small number of patients, I don't have any reason not to suspect that that magnitude will be similar. Looking at the trajectory, I think that if we looked out a little bit further, it would be, the proteinuria would be falling even more. I think that's what we would expect from a drug that is reducing pathogenic IgA. We know in those examples where patients have been transplanted with a kidney that contains IgA, that actually repeat protocol biopsies show that it takes a while for the IgA that's in that kidney to actually be resolved and for the kidney to remodel. The magnitude of response we're likely to see in the timeline for an approach really targeting the very pinnacle of the pathogenic cascade is going to take some time to reach its maximum effect. I'm going be really interested between the 6 and 12-month mark to see what continues to happen with proteinuria. We'll be looking clearly then at GFR. Great. That's helpful. Thank you so much. Thanks for taking the follow-up. Dr. Barritt, another couple of questions for you. One, just going back to slide 19, we on the, I guess, investment side have been looking pretty closely at the comparability of the analysis across the different data sets presented on this slide, and we've just got a bunch of questions on Otsuka and the comparability of that analysis. As far as what you know, is that also a sort of modified intent to treat or per-protocol analysis? I guess, what's the best comparability set to the atacicept data as we see it on this slide? I have a follow-up. Sorry, that was a question for John, Ritu? Sorry, I didn't unmute myself. The sibeprenlimab data was presented at the ASN meeting, and the abstract and the poster do not state the statistical methodology used. I think, you know, the poster is freely available to see, the data is presented, at the moment we need to wait for the manuscript to understand the analyses that have been performed. That's where we are. We can't comment because there is no data in the public domain that describes that. Fair enough. As we think about placebo effects going forward, there's a range again also on slide 19. Is there any potential mechanism for real uPCR reduction in placebo, or should we just think about, you know, the 3 minus 4, minus 5, minus 15 as the variance of the measure? No, I think that the one that you need to discount, and I'm not saying this as a negative way, is the sparsentan data. If you look at the variability in the proteinuria response in each of the others, where background or RAS inhibition has not been modified, that's where you're looking at anywhere between a 1% and a 5% reduction in proteinuria. Mm-hmm. The difference with the sparsentan study was that all patients were randomized to either irbesartan or to sparsentan, and then the dose of irbesartan or sparsentan was protocolized and uptitrated. What you're seeing here, in my view, is that -15% is because people had their background medication changed, i.e., they were on a certain dose of ramipril, for instance. They were randomized to the irbesartan arm, and then they had that irbesartan dose increased, and they therefore got more renin-angiotensin system inhibition, and that's why you see the -15%. I think touching on Marshall's response to one of the earlier questions, you absolutely can see significant changes if someone changes your background RAS inhibition that will really confound the proteinuria changes. If I take a lady who is on a RAS inhibitor, and she wants to get pregnant, and I stop that RAS inhibitor, they can go from having no proteinuria to having a gram and a half simply by stopping the RAS inhibitor. Even smaller dose reductions or dose increases can impact on proteinuria. That is what I think you're seeing in the placebo arm of sparsentan, is that they protocolized the RAS inhibition arm. Very helpful. Thank you. Hi, everyone. Thanks for allowing me the follow-up question. First one is on GFR. When do you think would be the right time to look at GFR for this mechanism? Dr. Barrett, would you take that? I mean, I think if I wanted to look at GFR, all the trials are looking as an approvable endpoint at 2 years. We've published a paper looking at 12-month GFR changes, showing that they are highly predictive of what is likely to happen at 2 years. I would be waiting for at least 12 months before I start trying to interpret the impact on GFR. That's where and that's why the data that I've just presented is it's reassuring that we're not seeing a decrease in GFR with treatment, not that we were expecting to, but we really need the 12-month data to start getting a really concrete idea about what impact there is on GFR slope. Okay. Then, I was looking at the TARPEYO label, and they indicate, you know, patients should generally be treated if they're over a gram and a half. I know you're going be including patients with over a gram. Should we expect, like, forthcoming labels to specify patients having, like, a gram and a half? Like, why do the labels suggest, like, you should have a gram and a half, and in fact, like, patients with lower proteinuria were included, and the idea is if you're over a gram, you should be under a gram. Why this gram and a half as a cutoff for TARPEYO's label, and is that something we should expect going forward? Marshall, do you want to me answer that? Yes, please. Okay. The TARPEYO label in the U.S. doesn't stipulate 1.5 grams per gram. It simply says in patients at high risk of progressive kidney disease, typically those with above 1.5 grams per gram. There's a Kidney International publication that we have produced from the Part A of the NefIgArd study. I think what the FDA have done is they have looked at the proteinuria change, and they have looked at the associated GFR changes, and they have felt that proteinuria was a good surrogate for those patients who had a higher proteinuria to start with because they had a more rapid rate of decline of GFR. At the time they reviewed the data, they were starting to see an impact on GFR. I would defer you to the KI manuscript, which has some very nice graphs in there, that explain, I think, why the FDA have taken their approach with an accelerated approval. What I think is really important is I have absolutely no doubt that patients with less than 1.5 grams per gram will benefit from treatment, and by targeting production of pathogenic IgA. Because the rate of decline of GFR in those with the lower levels of proteinuria is so slow, it's really challenging to look at any impact of treatment at nine months 'cause the GFR is only changing very slowly in the placebo anyway. I think for those groups with lower proteinuria and lower baseline rates of decline of kidney function, we are going to need to wait for two years, and I am pretty confident in my own mind that at two years, for those lower proteinuria patients, we will see the benefit of treating IgA nephropathy, and we will see separation of those GFR curves. With small numbers of patients at an early time point, it's virtually impossible to see any impact of any treatment because the proteinuria in the placebo groups is just not changing very quickly. Does that answer your question? No, that's very helpful. Thank you. Just final question, this is just a small thing, but I noticed your placebo-adjusted numbers like the... you know, it's not a simple matter of subtraction of the placebo to get the placebo-adjusted. You know, how is that math done? If you could just enlighten us. I'll defer to Marshall here because this is statistically appropriate, but needs a bit of explanation. Yeah, Lisa. The proteinuria reductions are expressed as a geometric mean by us and others in the field as well as FDA. There needs to be a log transformation of those numbers prior to demonstrating a delta. It's not a simple arithmetic subtraction. That's an important point. Thanks for raising it. Thank you. A couple of few other questions I'd like to address, one from Farzin at Jefferies. Will you need to request additional feedback from FDA after week 36 data to start phase 3? The answer is that's ongoing, but we do not need to wait for week 36 data prior to starting the phase 3. There are a few additional questions around baseline proteinuria, one from Dr. Tesař in Prague. Dr. Tesař, we do not see a significant difference in terms of response based on degree of proteinuria. Atacicept's proteinuria effect is strong in across those subgroups. There was a question, why are we not comparing to BION-1301? We believe that it's important to compare apples to apples when you consider study design, it's important in our view, that we're looking at multinational randomized placebo-controlled trials, and we're not aware of that data from that program yet. That's particularly important for the reasons that we've discussed this morning. You know, confounders such as changes in background regimens clearly have a significant role in proteinuria response. We believe that attention to study design as well as analysis type is critical when comparing across programs. Additional questions from Dr. Solomon in the University of Vermont. Some other trials have a lower uPCR inclusion of 0.75. We considered lowering the inclusion to expand the patient population for this trial. Just to be clear, in phase two, the data we're presenting this morning, we did have an entry criteria of 0.75 grams per gram that's consistent with KDIGO guidelines. You see that's the entry criteria, but our baseline proteinuria was 1.6 on average across all study arms. We will go to one gram per gram in phase three, and this is really to align with FDA's desire to demonstrate efficacy in patients at the highest risk of progression. One other question regarding the impact of SGLT2 inhibitors. We do have a unique data set in which we're demonstrating atacicept's proteinuria effect on background regimen, which includes up to 14% of patients with SGLT2 inhibitors. We do have data in both with and without SGLT2 inhibitors, and we're confident that we can demonstrate that difference in phase three. With that, I don't see any other questions, so I will ask that we close the call. Dr. Barrett, thank you once again for describing our data and putting it into context. Very thrilled to share this broadly. This can remain because it is a speaker closing statement.