Okay. All right. I I think we're ready to get started here in the next session. Thanks, everyone, for joining us again for our inaugural Healthcare Innovation Conference, day three now. I'm Vamil Divan. For those of you who don't know me, I'm one of the biopharma analysts here and cover a number of companies in the renal space. Joined up here from the Guggenheim side, our Cinney Sebbag-Ville, one of the members of the team. And then next up in this room, we have the Vera Therapeutics team. So we have Marshall Fordyce, the Chair and CEO, and Rob Brenner, the CMO. We also have Sean Grant, the CFO, in the audience, and we need to tap into his knowledge at all at any point here. But thanks so much for joining us. Really appreciate it. We had a nice dinner last night, too, so we had a chance to already dive into some of this, but I appreciate the chance to speak to you guys after your very busy October with the R&D Day and ASN, obviously, but maybe we'll just start there, so your views sort of coming off a very big month, the very impressive data that you shared at ASN, sort of how you see yourself positioned now, and sort of the key things you're focused on between now and second quarter next year. Maybe we should get that top line phase III data. Absolutely. Thanks so much, Vamil. Great to have a session this morning with an academic and community nephrologist talking about how this space within nephrology, what I think Rob and I would define as really a revolution in new therapies. Vera is focused on autoimmune disease broadly. First, we're focused on autoimmune disease of the kidney. IgA nephropathy has been our lead indication. Yes, our presence in San Diego at the American Society of Nephrology meeting a few weeks ago was a landmark data set. We think that IgA nephropathy has a very clear pathogenesis, that it's a B-cell mediated disease. Drugs that can target the B cells in a way that is efficacious, safe, and convenient to take it home is really poised to change standard of care. That's why we started this company. Atacicept is the first to demonstrate no decline in GFR over a two-year period. We showed 96 weeks' data. This is the result of an incredible effort by the team to run a gold standard clinical trial, which is also distinguishing in some comparisons. We ran a multinational placebo-controlled randomized trial for a nine-month phase, which is the timeline for a primary endpoint for proteinuria, and then we extended that period over a two-year period. Because of Rob and the team's efforts, we were able to present that data as a late-breaking oral as well as simultaneous publication in a peer-reviewed manuscript. That's important because the details of how we designed and analyzed those data are now in the public domain, and we don't think there needs to be much further debate when you have a peer-reviewed publication, so that's an important tool for us. I think it's important to put that data set into context as we and others carry B-cell modulators to phase III readout and to the market. What's really remarkable is that atacicept has had a very clear disease-modifying effect in a properly controlled randomized trial. The first thing that we would hope is that if you target the B cells by not depleting them, so what we see in the opportunity in atacicept is that we don't think patients with autoimmune disease should be given steroids. We don't think they should be treated with B-cell depleters where patients are immune suppressed for months on end. For example, my father-in-law has antiphospholipid antibody syndrome. He took a dose of Rituxan and couldn't see his grandkids for six months. We all lived through COVID-19. Patients who were on steroids and B-cell depleters were at high risk of severe COVID and hospitalization and death. We know that. That's out in the public domain now in peer-reviewed publications. We ran this phase II trial that you're now seeing evidence on during that time. And there was really no meaningful difference in COVID positivity between atacicept and placebo. And there were no severe infections and no deaths. That is a remarkable result in addition to the GFR stability. That means that we think that the phase II data, and this needs to be supported in phase III, we think that supports the idea that atacicept is B-cell modulating. If that's what we have in IgA nephropathy, if the efficacy is as good as what we think it is in phase II and it looks safe, and this is really the only at-home self-administered B-cell modulator that's been studied in phase II and phase III, we think we're in a very good position to change this disease. It's an Ozempic-like presentation. Patients take a syringe at home. They inject themselves a 1 cc subcu injection on Saturday morning, for example. It's easy to remember something on a weekly basis. That is what the Ozempic profile looks like. We showed over 90% of patients are still doing this in an open-label phase after two years. That's a very high adherence retention number. Lots of highlights from that data set. We are now. We've had a busy fall. We can talk about two other key pieces. One is that we enrolled the number of patients we need to drive the primary endpoint in phase III, so we're on track to read out phase III in Q2 of next year. That enables us to file a BLA in the second half of next year and head to commercialization in 2026, so we're on that timeline and every day counts, and second, Rob and the team shared our thoughts on expansion. Now that we have a very high potential for success in atacicept for IgA nephropathy, what next? And I think what in summary, Rob presented at our R&D day in early October in New York was atacicept in IgA nephropathy is broader than just our phase III population. There's a broader patient population that we think could benefit from atacicept, and we will study that in a study called ORIGIN PIONEER. We also see adjacent autoimmune kidney diseases where it just makes a lot of sense for us to leverage the value we've built in our relationships with sites, investigators, KOLs to go into autoimmune kidney disease like membranous nephropathy, FSGS, and MCD, as we just heard this morning. A good number of those patients are driven by autoantibodies. So we think that those are very reasonable clinical hypotheses to test in the near term. We're starting those studies, and we should have some clinical data next year. So it's a very exciting time for Vera. We're well set up for an eventful 2025. Okay. No, that's great. Definitely want to dive into a lot of that in more detail. One question again, coming out of ASN, we also saw updates from some of the competitors in the space. So how are you seeing sort of those profiles stack up? I mean, I think without question, you guys have the best quality data, randomized placebo-controlled and all that. But just how are you seeing this sort of field evolve, the other sort of APRIL/BAFF approaches, the APRIL-only approaches, and kind of where you're positioned relative to them? Yeah, just I think inherent in your question is narrowing the field already, which is Vera has set the standard with GFR with a normal annualized slope over two years. That's a standard that has to be met. And to our knowledge, there's no other program that has or in the near term will have two-year GFR data. And that's among the B-cell modulators that you mentioned. I think that also has implied that other mechanisms are unlikely to achieve that outcome if you're working downstream in the pathogenesis. So that's generally how we look at the field. But Rob, it would be great to get your thoughts on that as well. I agree with Marshall. I think one of the things that we've done going back now to January of this year is we appreciate that when Marshall and the team designed the ORIGIN program, we really focused on capturing data in four endpoints. One is the autoantigen in this disease, galactose-deficient IgA1. And you expect that if you are modulating the activity of B cells, you'll see a prompt and sustained reduction in that autoantigen, which we've seen about two-thirds reduction over two years. Two, and this is unique in clinical development in the space, getting to your question about competition, is resolution of hematuria. Blood in the urine is a hallmark finding in IgA nephropathy. I think of it as a lens into the magnitude of inflammation that's going on within the infected glomeruli. And so resolution of hematuria using a simple point-of-care urine dipstick is a powerful tool that hasn't traditionally been used in clinical trials, but really helps us put the biologic story together around the mechanism of action. So that's another distinguishing component of our development program. Finally, the proteinuria reduction. And most importantly, to Marshall's point, a change in the annualized slope of GFR loss from one that looks like traditional IgAN in that four to eight mL per minute per year range on conventional therapy to less than one mL per minute at 0.6, which compares similarly to people who don't have kidney disease. So when we put all that together, I think the data package that's been generated to date with atacicept is different. It has set the standard. And so in many ways, I think the question for competitors who are following us is how likely will their data even match what we've already demonstrated? Maybe they'll be able to match. Maybe they won't. We'll have to see. But that's how we see the landscape right now. Okay. And maybe just talking a little bit more on the commercial opportunity here. We didn't get a chance to really talk about this much in the morning session with the KOLs, but just kind of how you're seeing the IgAN opportunity for you at this point, but also your views on just what the new KDIGO guidelines, I think, just clearly increased awareness of being more aggressive in treating IgAN, getting more patients diagnosed and treated to lower levels. What do you see as a sort of potential opportunity patient-wise and if we look out three, four years from now? So I'll start, and Marshall, you can add. Our estimation is there are about 160,000 prevalent patients with biopsy-proven IgA nephropathy in the United States today. To Marshall's point, if we look at the overlap between the inclusion and exclusion criteria in our phase two, phase III program, that would cover about half, maybe 55% of that 160,000. Given the quality of the data that we've generated now over two years, the leadership team at Vera decided to augment our investment at this stage in development to capture patients who represent the broad phenotype of IgA nephropathy, not just those who would meet the criteria for phase III enrollment. So as Marshall shared, we are starting shortly a new program called PIONEER where we're going to enroll patients who would not meet the criteria for our phase III. We can offer that protocol in the same sites where we continue to enroll in the phase III program. So when the coordinators and the investigators and the patients go through a screening process, they can either rule in and be enrolled in our phase III, or we can put them in this complementary program where we can also dose them with atacicept where we think they'll have the opportunity to benefit. That would allow us to go from that 50%-55% of biopsy-established IgAN today to that full 160,000 population cohort that represent all of IgAN in the U.S. Beyond that, I think one of the things that is clear in medicine is when physicians are provided with new tools that unlock the ability to provide disease-modifying therapy in affected patients, they'll be more aggressive with their diagnosis. Because at the end of the day, we want to provide a solution for patients that really matters. So our expectation is in the future, with the availability of atacicept in the market, there will be a natural driver to encourage physicians not to just say, "Okay, I think this patient may have IgA nephropathy, but they could have something else. I'm going to treat them with an ACE inhibitor or an angiotensin receptor antagonist, maybe an SGLT2 inhibitor, and call it a day." I think once atacicept's approved, they'll have added ammunition to say, "You know what? I want to take this patient to the biopsy suite. I want to prove that they have IgA nephropathy because if they do, I will now have a disease-modifying therapy." Maybe they'll have something else, and maybe we can or can't treat them with the same fidelity. But if they have IgAN, we're going to have the right solution for them. I would echo that. And I did get to catch the community nephrologist who spoke this morning and asked him about whether he thought IgA nephropathy and additional autoantibody-driven renal diseases are underdiagnosed. And he said, "Without question. I think there's a big opportunity beyond the baseline prevalence that Rob is describing. Biopsy-proven IgAN, that's a hard number you can get." And the question is, what do you see in a therapeutic area that at a certain stage has a standard of care that's only supportive and doesn't address the disease cause and can't change outcomes? And what happens as you move from that standard of care to an improved standard of care where you're actually changing outcomes? And remember, these are young patients. They're 35 years old, losing 10% of their kidney function a year. They're on dialysis before my age of 51. And if you're preventing that, yes, there's going to be a real motivation across the board in terms of diagnosing more. So I think the opportunity is substantially larger than we currently estimate. I think it's responsible to make sure that we have conservative estimates at this stage. But as we pattern recognize where this renaissance in renal drug development is and where we are leading that change, we see a much larger opportunity than is currently appreciated. Okay. Let me turn to Arsenio to dive deeper in some of the other work you're doing around expanding the population. So maybe that's a great point to explore. What conditions, what other renal conditions you're thinking of going after, and what are the sizes of those patient populations? So let's talk a little bit about the biology of other forms of autoimmune kidney disease. So if we start with IgA nephropathy as an example, we have a clear autoantigen, this galactose-deficient IgA1. And then we have antibodies that bind to that autoantigen and form immune complexes that drive inflammation and nephron loss in the kidney. But there are other flavors of autoimmune kidney disease where we have a known autoantibody that is binding to a glomerular antigen. One of those is called anti-PLA2R, and another is called anti-nephrin. PLA2R and nephrin are both locally expressed antigens by glomerular cells that drive an autoimmune response. And we know that the autoantibodies are produced by B cells. Since we have a wild-type atacicept fusion protein that binds the two cytokines that promote B cell activity, we have a natural approach to attenuate the production of those autoantibodies and not drive the autoimmune process. Among the autoimmune renal diseases that would be characterized as having an autoantibody that's B cell derived, one is called membranous nephropathy, and the majority of patients who have membranous nephropathy have demonstrable high titers of anti-PLA2R antibodies, and we'd be appropriate for therapy. Second, there's another group of patients who have either biopsy-proven focal segmental glomerulosclerosis or its sister biopsy disease called minimal change disease where they have a certain titer of anti-nephrin antibodies binding to the nephrin antigen. Both of those two populations, the anti-PLA2R positive and the anti-nephrin positive populations represent individually about 35,000 patients in the United States, so in aggregate, another 70,000 patients. Because we're in these sites with the PIONEER study and ORIGIN 3, those same sites treat other flavors of autoimmune kidney disease. In the PIONEER study, we can add cohorts for anti-PLA2R positive membranous and anti-nephrin positive FSGS and minimal change disease and accommodate those patients in the same protocol where we're studying a broader population of IgA nephropathy. That's all part of the PIONEER study. It starts in 2025. In aggregate, it means we've gone from a previous expectation of a theoretical addressable population of, let's say, 80,000 patients to the full IgAN population of 160,000 patients. And if you add the 70,000 from anti-PLA2R and anti-nephrin, we're now just shy of a quarter of a million addressable patients in the United States. So maybe we can zoom in a little on FSGS and the importance of anti-nephrin antibodies there. One of the scientific discussions I felt at ASN this year was around how prevalent that anti-nephrin population is. I think physicians and researchers generally feel that it's the minority of FSGS patients. But there is also the opinion that some patients who don't show these antibodies in their blood still have anti-nephrin disease. It's just in the kidney. And in that regard, I thought it was very interesting what you shared at R&D day that potentially you would be looking to do a study where you sort of experimentally treat a patient with atacicept who is suspected to have anti-nephrin disease or antibody disease. So maybe you could expand a little on that and your plans there. So it's a very interesting question. And it is truly from a drug development perspective and from thinking about where medicine is practiced today to where it could be in the future and trying to forecast that, it is an incredible opportunity to think about the tool that we have, this reagent that we have in atacicept. So I recognize that in nephrology, we have been beholden to tissue biopsy as a tool for defining what disease patients have in terms of the optics of what things look like in a picture. The challenge is in diseases like focal segmental glomerulosclerosis, the heterogeneity in pathophysiologic underpinnings of that histology are vast. You can get an FSGS profile if you have loss of kidney mass, renal ablation. You can get FSGS if you've got diabetic kidney disease. You can get FSGS if you've got hypertensive kidney disease. You could get FSGS if you're unlucky and you have the wrong genotype for APOL1. And you can get FSGS if you have an autoimmune component that includes an anti-nephrin antibody to nephrin. But the intervention for each of those might not be the same because the pathophysiologic underpinnings of the disease are different, even though the histology is identical. So where I think the field is moving in the future, and if Vera has a contribution to this conversation with the community, which we do, is where do we think it's going? And with a tool like atacicept, we can think of defining patients not based on their biopsy, but based on whether or not they have a B cell modulatory responsive autoimmune kidney disease. How could we interrogate that question? We could give patients who present with phenotype of nephrotic syndrome a challenge of atacicept over, let's say, 10 or 12 weeks and see if they respond or they don't. If they do, they could be categorized as having a B cell modulatory responsive autoimmune kidney disease because of the mechanism of the drug. We've done this for 50 years with steroids with a blunt instrument that's poorly tolerated that can't be given chronically, and we say, "Oh, they're steroid responsive." But wouldn't it be more elegant to have that definition of their disease be defined by more precise B cell modulation to understand that the B cell is producing a panoply of autoantibodies that are driving antigen-based disease in the kidney? And there we also are able to treat them chronically. That's the difference with what we've done historically with steroids. This phenomenon is not new, but it is new in nephrology. I do think that there is a long-term opportunity to help not only define disease based on histology, but based on the presence of autoantibodies in autoimmune conditions. Most importantly, use a new tool like atacicept to help define who those patients are and therefore what the roadmap is for the precision tool that can help change their outcomes. I want to add to what Rob said. This is what Rob presented at the October 2nd R&D day. You saw this Monday we announced a collaboration with the University of Michigan and the NEPTUNE Network. Vera is going to lead this. We think this is a space that we can own. And there's a middle step between biopsy-proven diagnosis and diagnostic as a response to therapy. And that's non-invasive diagnosis. And as you continue to learn about these different autoantibody-driven kidney diseases, maybe PLA2R and membranous nephropathy is the furthest along in terms of it's there is a clinically used serology to diagnose and understand response to therapy. That doesn't quite exist yet in IgA nephropathy. It doesn't quite exist yet in anti-nephrin disease. We have recognized this opportunity very early on, and we're going to be the leaders in that change. Well, yeah, so maybe just a couple of minutes left here. So just obviously top line phase III data, second quarter of next year is a huge event. Maybe you can walk through the other catalysts with some of these other programs that you're working on over the next 12-18 months that investors should be looking at. Yeah. So I mean, the major events next year will be our lead program. Q2 of next year, we'll have top line phase III results that enables a BLA filing in the second half of next year. I have not been externally more precise about timelines, and that's where we are today, and then we will have the two studies that Rob and the team announced in early October, ORIGIN Extend, which starts to explore atacicept as chronically dosed not only after the first two years, but for many patients a pause, what happens to their markers of disease to Gd-IgA1, to hematuria, to proteinuria, to GFR, and then we restart them and are going to follow them over the long term. That's going to be a really interesting data set. We hope to share that next year in 2025. Haven't been more specific on timing. And same with the PIONEER. That's an open label enrollment of a variety of cohorts. So we will see how that evolves. And as soon as we see interesting data that we want to present, we'll do so. And then lastly, maybe just on the capital side, you guys have done a raise recently. Maybe just update on kind of the cash position now and the runway? Yeah, cash. We've been very lucky to have enthusiasm in the investment community, have made great progress in capital formation. I think we're just shy of $700 million in cash. And we're well funded through 2028 and beyond for our activities. Okay. I think we're just about out of time. So I think we'll have to leave it there. Thanks so much again for joining us. Thanks for the great coverage. Thanks.