Vera Therapeutics, Inc. Class A Common Stock 12th Annual Cantor Fitzgerald Global Healthcare Conference

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 5 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.

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.

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-milligram 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 2-year GFR data. The actual kidney function over 2 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 2 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 versus 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.