Let's start off with an introduction of yourselves, followed by a snapshot of the company, and touch on the milestones that will shape the company over the next six to 12 months. Great, Pete, thanks so much for hosting us. I'm Marshall Fordyce. I'm the Founder and CEO of Vera Therapeutics. We've been a publicly traded company for the last five years, based in San Francisco, and we're focused on the development and commercialization of novel therapeutics for autoimmune disease. I'm very pleased to be here, Pete, because we have our first drug approval, which occurred on July 7th of this current year. We've been off to a fantastic start on our commercial launch. Pleased to be joined by Dr. Robert Brenner, our Chief Medical Officer, as well as Matt Skelton, our Chief Commercial Officer today. All right. Matt, why don't you give a little bit more of an introduction and your background, because now it's your time to shine since you are the Chief Commercial- All right. officer. I'll kick it off. Good morning, everybody. Matt Skelton. I've been at Vera now for two years. Previous to that, spent a lot of time in the oncology space at Seagen. Previous to that, in the nephrology and oncology space at Amgen, where I worked with this guy in the nephrology space, and we launched a nephrology asset, Aranesp, in the early 2000s. We decided to get back together. Thank you. All right. Before we get into the commercialization, let's sort of start off with the data package that supported the Accelerated Approval, but also highlights Trutakna's competitive clinical profile. Sure. I'll begin, and then I'd like Rob to follow up on the question about the data. What's coming up for Vera, we'll have our first earnings call in November, reporting out on Q3, and that will provide some deeper insight into Vera's first commercial launch of Trutakna. This is a phenomenal step forward for patients. Thinking back to the early days of drug launches in nephrology, we're talking about a wholly different category of medicine. We're treating patients with an autoimmune disease of the kidney called IgA nephropathy, also called IgAN. This affects roughly 160,000 Americans and several million worldwide. These patients are roughly 35 years old at diagnosis, and the fast progressors end up on dialysis by 50 years old, and almost all patients end up needing dialysis or transplant within their lifetime. This is a severe autoimmune disease that takes kidney function and really freedom away from patients. We're the first drug on the market that targets the source of the disease. Both BAFF and APRIL are the signals that overstimulate the B cell compartment to form these immune complexes that clog up the kidney and cause kidney failure in these young patients. We had this hypothesis six years ago. We ran a global phase II trial dose range finding and selected the 150 mg dose. We then furthered that into phase III, which we read out last year. What's important is that we can achieve Accelerated Approval on the basis of a surrogate endpoint, where we can look at protein reduction in the urine. We achieved that, and that is what led to approval. But what is unique about Vera's Trutakna program is that we have two-year GFR data. The actual kidney function over two years was published back in 2024. For the first time in this disease, we showed that patients self-administering Trutakna ended up with stable kidney function over two years. We hope to replicate that in phase III, and we aligned earlier this year with FDA on looking at that data this quarter. We will soon have an update for the public on what that data looks like. The data package you are describing, Pete, is the original one that went into the approval. Rob, you can speak to that and other aspects of the clinical data. Yeah, thank you, Marshall. The clinical program that served as the foundation for the Accelerated Approval was based, as Marshall mentioned, on a readout of proteinuria in patients with IgA nephropathy. They were followed for 36 weeks in a subset of patients that are enrolled in the full phase III. We show that in those 203 participants who were randomized to either Trutakna or placebo, that they had a 46% reduction in their proteinuria in the active group, and the overall placebo-adjusted number was 42%. That was coupled with a very, very encouraging safety profile, where there was no evidence of a different profile in terms of infection risk in patients receiving this chronic therapy to tune their immune system vs those who are on placebo. That is quite different from what we have seen from other agents that are directed against components of the immune system. It lends itself to a chronic therapeutic paradigm that patients would be expected to be on for an extended period of time. Not something that they have to have a time period off that therapy because of the adverse event experience. We were grounded on the efficacy on the proteinuria side, supported by safety, and it was all put together with a very convenient and patient-friendly mode of administration where patients administer a small volume at home once a week, sort of Ozempic-like dosing. We have launched with an auto-injector, and we think that is a terrific presentation for patients. As Marshall mentioned, to gain full approval, we need to show more than the proteinuria. We need to have measures of kidney function, and we are looking forward to reading that information out this quarter. In addition to measuring kidney function, we are also looking at a composite kidney progression endpoint. In phase II, when most of the experience was in open label fashion, or at the early readout of the phase III for proteinuria, we did not have enough experience to start looking at harder clinical outcomes. Are patients dying? Are they going on dialysis? Do they get a transplant? Do they have a very large drop in their GFR, a measure of their kidney function? But in the final readout for efficacy in the phase III, we will have an opportunity to look at a composite kidney progression endpoint. It is something that we pre-specified. We will test it in hierarchical fashion as part of that readout. I think we are poised as a community to move into a new era of treatment for patients who suffer from this glomerular disease, where not only do we see benefits in reduction in proteinuria, we expect to show similar benefits in terms of GFR that we have seen in phase II. But now for the first time, we are showing that we can really have an impact on a hard kidney endpoint progression endpoint. I think that means in the future, the way that physicians are going to be thinking about these drugs will be more like the way they think about other classes and other forms of kidney disease, like ACE inhibitors and angiotensin receptor blockers or SGLT2 inhibitors, which are used because they are kidney protective. People do not walk around with a GFR number in their mind of what the treatment effect is. They just know as a binary outcome, they are kidney protective or they are not. I think IgA nephropathy is heading down a path where for this disease, in the near term, we are going to be thinking about are these drugs kidney protective or not? We are cautiously optimistic that the data will show that they are. Excellent. You also did look at the subgroups. The effect on subgroups, is it broad or is it? Yeah. For the readout on proteinuria, we also had about a dozen pre-specified subgroups that we looked at with care. There is a figure in "The New England Journal of Medicine" that was published last year that shows the tornado plot across all the subgroups. Regardless of age or sex or region in which patients reside, their ethnic background, the presence of absence of higher or lower proteinuria, higher or lower GFR, whether they were on an SGLT2 inhibitor or not, it did not matter. There was preserved benefit in terms of proteinuria reduction. We will see what that looks like when we have the final readout on GFR. Okay. Last year when I hosted you, I asked you, "How's eGFR looking?" You said, "We can't say. Only thing that we can say, it's consistent with the phase II." A couple of weeks ago, last week or two weeks ago, the FDA posted the review documents for Accelerated Approval. In those documents, surprisingly, they did not redact the eGFR data, I think it went out to 72 weeks. Just what did the review show? To be clear, was it your analysis? Or was it the FDA's analysis? Yeah. Thanks, Pete. Some background. While these trials are going on to get to the completion of the efficacy readout, we do have the interim readout, which unlocks the ability to file for Accelerated Approval. At that time, the FDA has been concerned that if the community and the investigators and the patients understand that there is a large treatment benefit for GFR, it could impose a challenge to continue the execution of the trial. When you have an Accelerated Approval, it's grounded on a formal readout later for full approval. The worst thing from a regulatory perspective is to be precluded from getting a clear answer at the end. For that reason, the FDA has imposed on all sponsors a request not to communicate the GFR results while the trial is ongoing. To Pete's point, when the FDA published their review document last month, they included the GFR results that they analyzed using the raw data that we provided. It shows that we were stabilizing GFR out through 72 weeks. Importantly, the question is, why might that have happened? The only thing I can think of is that we aligned with the FDA back in early June on pulling forward the timing of the final analysis. That's going to occur this quarter. As that occurs, patients are going to move from randomized blinded drug to open-label Trutakna for the rest of their experience on the three-year study. Because we're moving away from a randomized period to an open-label period, there was no longer impetus to shield patients from understanding what the results were. We think that might have been one of the reasons, but the FDA didn't let us know in advance that they were going to share it. But the data's out there, it's spectacular. We expect that we'll have similar results when we do the final analysis. All right. How should we actually look and interpret the magnitude of separation between the active arm and placebo from those documents? Yeah. What is the goal here? What are we trying to do as a community with patients? This is a disease where patients have inflammation, fibrosis, and loss of the functional unit of the kidney called the nephron, such that they're on a progressive path towards end-stage kidney disease. Patients in our clinical program have enrolled with a GFR of 65. Not expecting that that number means a lot, but what it does mean is they've already lost 40% of their endogenous kidney function. They're losing about another 10% of their remaining kidney function every year. That puts them on a path to when we can predict when they're going to need a fistula for dialysis, or they need to be listed for a transplant. That's the natural history, and that's while they're on the best supportive care we can give. Maximal doses of RAS agents, ACEs or ARBs, and SGLT2 inhibitors. The goal of therapy is to try and have a transformation of their rate of loss of kidney function so that they're not losing five, six, seven, 8 mL per minute per year, but maybe 0 to -1 mL a year. Where does that -1 mL come from? A healthy 40-year-old who doesn't have kidney disease loses about 1 mL per minute per year as part of normal aging. That's about the best we could do. That would be the asymptote of clinical benefit. Can we change someone's profile from losing five or 6 mL per minute to -1 mL or less? What we've shown through our phase II-B program is we accomplished that. That's as good as we would expect to do. It's what the FDA posted at the time of the interim analysis. That means that on an annual basis, maybe we can get to, I don't know, 5 mL per minute per year of benefit in patients who are receiving Trutakna vs placebo on top of background care. Okay. So moving on. Pleasantly surprised in June when you disclosed that you aligned with the FDA on a revised analysis on eGFR for full approval, like you just discussed a couple of minutes ago. Shifts the timelines forward. This decision partially came out of the NKF workshop in April. Just help us understand what was discussed and the rationale behind this decision. Yeah. It is a great question, and Matt and Marshall are smiling because they know I could talk about 90 minutes on this topic. This began over a year ago, when we first had conversations with the FDA about our interpretation of the interim results. That led to a series of conversations with the agency over the last year that culminated with the agency asking the National Kidney Foundation to host a meeting where they brought in experts from all over the world, clinicians, clinical trialists, patient advocates, statisticians, to all talk about what kinds of analyses and what kind of trial designs would be amenable in an era where we had drugs that had transformative benefit on GFR in a way that we had not seen with previous modes of action. That resulted in us aligning on a new paradigm for how to think about a final analysis from a randomized portion of a study, and that was the basis of the alignment that we announced on June 2nd. Is there any details that you can give us on how this analysis will be carried out in maybe the lower or upper boundary of time patients have been on drug? Yeah. It's a good question. Until we release the results, I'd rather not get into excruciating detail about it. We're still anchoring on readout of a mean change in eGFR vs placebo over time. We're still going to look at the annualized rate of loss or the slope of GFR. Then there's a whole other group of endpoints that we're looking at. What we haven't been definitive on publicly is the time point with which we're going to look. At the moment, Vera's the only sponsor that has achieved alignment with the FDA on something other than every patient going a full two years. That's something that, I think until we disclose, we'll keep to ourselves. The most important part of this is we randomized 214 people to receive once-weekly placebo, self-administered at home, for as long as two years in this trial. What we aligned with the FDA on is we think we've already gotten to the point, without waiting the full two years, to answer the question: Does Trutakna have a benefit in preserving kidney function in patients receiving it vs placebo? If the answer is yes, then I feel like we have a responsibility to liberate all those patients who are receiving placebo to be able to switch to open-label Trutakna for the remainder of the study. So there's nothing that we're more excited about than to complete this analysis, share the results, and execute on that transition from randomized period where half of the patients are on placebo to where all the patients are on active drug. Yeah, I'd like to add to Rob's comments. This is really how Vera has led the field in a frame shift on what standard of care is like. That's why Rob was in the room at NKF. It's why we've been the first, and so far, the only program to ask the question: Should we stop the trial earlier than all 428 patients through two years? These are important questions for patients, for physicians, and for trial design. A drug is great if the effect size is excellent, if the safety looks like placebo, and if it's easy to take. So we're focusing here on the effect size. We wouldn't be talking about any of this unless we had a massive effect size, which is what we showed in phase II, and that's something that is worth dwelling on when you're talking about shifting standard of care. Vera's now in commercial stage. As I said, this is a large unmet need, even just focusing on the U.S. alone. We're off to a great start on the commercialization front, and I think there are a lot of exciting things happening in the field driven by Trutakna's profile. So, moving on. The label. Highlight what you think matters most. Maybe we ask Matt to speak to the label. Yeah. I think from a commercial standpoint, the broad indication statement. That, I think, really opens up a large addressable pool for us. There's no proteinuria threshold in the label, and that has been well-received in the marketplace so far. So, one area of differentiation is immunogenicity vs the approved agent, Voyxact. Label notes no clinically significant impact on ADAs, on PK, PD, safety or efficacy. How important is that to clinicians? Yeah. It's something that does come up in the field. It's something that we don't focus on, but to more informed physicians, it can be a concern. But we're on offense, as I like to say, with Trutakna, and talking about the benefits of Trutakna. And the reality is when we're in front of nephrologists, we're not spending a lot of time in a competitive detailing, if that makes sense. It's more talking about the number of IgAN patients they have, that they're treating them with foundational care now, supportive care, and the benefits of a B-cell modulator like Trutakna. That's where we're spending our time. Okay. The opportunity, Marshall mentioned about 160,000 patients in the U.S. However, there's a wide bracket. I think Novartis goes up to 185. Otsuka did a claims-based paper and put it at 200. How do you get to your numbers, and do you think you're just being conservative? Yeah. The 160 number is what we've stuck with, and I think that when you looked at those at-risk patients that were in our trials, that was around 80,000- 90,000. But I think with the broader indication statement, it opens it up closer to that 160. We see the opportunity as very large out there. You did launch at $425,000 per year, which was a pleasant surprise, which places it at a premium to Voyxact. How do you think about the value proposition underlying that price? Sure. I think that represents the value of what we're bringing to the marketplace. I think we have a better profile when you look at the profile across. You mentioned it already, Pete, no ADAs, a convenient patient-friendly auto-injector, and the efficacy and safety profile that we bring to the market. We think that represents the value of where we priced it. All right. And maybe, just important to say is, we're in our 10th week, no meaningful pushback from payers. We saw that when Voyxact launched at $390,000 per year, there was no pushback, no really limiting payer policy so far. So we're feeling good where we are. We'll get into some details in a minute. Okay. How many nephrologists are you targeting? With that number in mind, how large is the sales force and what kind of experience do those reps have around like what gives you confidence that it's right-sized for success? Great. There are about 11,000 nephrologists in the U.S. We're calling on about 6,000 of them. That's through doing a lot of claims analysis, a lot of market research that give us that number. We have 82 sales reps. We think that maximizes the opportunity. We don't plan to add or subtract from that number. We wanted to at launch have the right number out there. So 82 we feel really good about. The background of our reps, we've got an all-star team. 90% with rare disease experience, which is really important in this space, and close to 90% with previous nephrology experience. So they have the relationships. We're getting great access to key customers, and so far we're in our 10th week, and we feel really good about the team we have out there. All right. You did launch in July. When did the drug actually hit broadly? When did it enter the channel? Yep. We had drug in channel three weeks after approval. We've been generating patient start forms from day one, but drug was available three weeks in. Right. What are some of the key indicators that you are watching, and we should be watching that determine whether the launch is gaining traction, and what would you consider a strong start? Sure. First, the things that I look at is, "Hey, are our people getting access? Are we getting into the important customers?" We are spending a lot of time focused on those higher decile accounts. We are getting great access. There is a lot of excitement around Trutakna, so we are getting into the right places for sure. As far as saying how are we judging the launch, I think we have talked about patient start forms. Our competitor has talked about patient start forms. So that is what we are keeping a really close eye on. We know at five weeks into launch, Otsuka reported 180 patient start forms. That is a benchmark we have. At the five-week mark for us, where we were with patient start forms, we feel really good. That is one indicator for us. All right. You did launch in the summer. Any possible seasonality factor and may impact initial uptake? Expectations, can you help set that for us? Yeah. At least in my experience, traditionally Q3 is a little soft. It can be. A lot of vacations in August from physicians and patients. Okay. We'll see. But I don't think it's played a major impact so far. All right. How should we think about patient start forms vs actual patients on therapy to ultimately revenue conversion? Yeah. That's something we're spending a lot of time focusing on. Patient start forms are great. If they don't convert into patients on drug revenue generating, then that's a major leakage point. That percentage will increase with time on that conversion rate. We've seen higher than anticipated conversion rates with Voyxact, upwards of 65%-70%. I think that's a good benchmark that's out there that we'll strive for. All right. Can you just touch on. Actually, just set the benchmark for us. What should we expect to see in November, and should we be looking at Voyxact as a benchmark for you? Yeah. I think that's fair to a certain degree, but I'd also say there is an advantage of being the first mover. So, give us time to catch up. But I think we saw that publicly released data from Otsuka and how they were tracking and what they've announced, and we feel really confident the way we're tracking with our patient start forms relative to that. Okay. I look forward to telling you more about that later. I think we're all waiting to hear. Are you going to make us wait until November? We'll see. All right. Payer mix in IgAN. What proportion of diagnosed patients are actually commercially insured? Yep. We think over 70% are commercial pay, which is one of the higher percentages I've seen in my experience. Again, keep in mind, Rob mentioned it, when these patients are diagnosed, they're in their mid-30s or early 40s, so predominantly commercial pay. Can you touch on the TRU SUPPORT program? What's its function, and should we look at it as a white glove service? Yep. It's our patient hub. These specialty drugs are not like you get a prescription written, you go over to CVS, and you get it filled. That's not it. Our distribution is through two specialty pharmacies, and then we have our patient hub, and that is the hub that helps the physician offices work through the prior approval process. There's run our co-pay assistance program, all of those things that help offices and patients get the drug. We've resourced that to a level that is super competitive with what's already out there in the IgAN space. So far, so good on those services. All right. We're running out of time. Robert, where are we with possible different formulations? Well, I would begin with, Matt can talk about it, we really are encouraged by the reception of our dosing algorithm in the community. I think Matt has it with him. This auto-injector, small volume, self-administered once a week, has been really well received in the community. So, we believe that we already have a great presentation. That said, we recognize that for some patients, alternative dosing frequency could be worthwhile. A year ago, we began a dose range-finding study looking at three different potential monthly doses. That program continues. It's designed to end next year. We've been looking at the data. We're going to continue to look at it this fall. If we identify what we think the right dose is, we'll be able to talk to the FDA and navigate the path forward to achieve label claims. All right. Last question. We are sitting here a year from now, and I ask you the key value creating accomplishments for the company over the last 12 months. What would you like to say? I think look, it is continued leadership. Vera Therapeutics has been the leader in the nephrology space as we focused on today, really shifting standard of care, in dialogue with physicians, guidelines with FDA. So, continued leadership, and I think that should be reflected in a strong commercial launch for our offering, Trutakna. The strongest data package that has been out there, and I think as a program that has run two global randomized control trials successfully with outstanding efficacy, placebo-like safety, and a convenient dosing algorithm. We are in the position to really lead a revolution in how these patients are treated. For me, personally, this is so satisfying to now deliver a new tool to physicians. I have been out there in the field, and the kind of traction that we are getting is incredible. So, we should be in a leadership position the same way we are today next year. All right. Well, thank you very much for taking the time and participating in the Cantor Fitzgerald Global Healthcare Conference. Looking forward to updates, and best of luck. Thanks, Pete. Great. Thank you.