Hi, everyone. Welcome. This is the third day of the J.P. Morgan Healthcare Conference. My name is Luka Kachukhashvili. I'm an associate here at the Healthcare Investment Banking group. It's my absolute pleasure to introduce Chinook Therapeutics. With us today is Eric Dobmeier, President and CEO, Eric Dobmeier, the CFO, Tom Frohlich, the COO, Andrew King, the CSO. In terms of logistics, we're gonna go through the presentation and open it up for Q&A after that. With that, hand it over to you. Thanks, Luka. Appreciate it. Good morning, everybody. I'm really happy to be here. When I was preparing for this presentation, I realized this is my 20th J.P. Morgan conference, which just means I'm getting old. It's nothing to brag about. This is the 1st time I've presented in person, so it's great to be here to tell you about Chinook. We're focused on precision medicines for kidney disease. We're focused on rare severe kidney disease, and our goal is to change the course of therapy, because right now there are very few therapeutics that can be used to slow or stop the progression of kidney disease. Most of the effort that's gone on in kidney disease has been focused on dialysis and transplant and supportive care. We want to change that, make this into truly a chronic disease that can be effectively treated and maintain kidney function. I will be making some forward-looking statements in my presentation. Refer to our SEC filings for more information. If you look at chronic kidney disease, it's a huge problem globally. More than 10% of the population of the world has kidney disease. That's 800 million people worldwide and up to 37 million in the U.S. alone. This results in huge costs to our healthcare system. We're spending over $130 billion on kidney disease in the U.S. alone, but very little on therapeutics, mostly on dialysis, transplant, and supportive care. When you think about dialysis and transplant, it's thought to be sort of a backstop. If, you know, if your kidneys continue to progress and you're losing kidney function, well, you can always go on dialysis or get a transplant. These are not good outcomes for patients. They're also not great for the healthcare system. A kidney dialysis costs about $200,000 a year per patient, and these patients don't have a great quality of life. They have to come in to either a dialysis or physician's office about over 150 times a year. Their median survival is less than having metastatic solid tumor. It's less than 5 years if you stay on dialysis, so it's a bridge to transplant but not a great outcome and not a good quality of life. If you look at transplant, there's about 23,000 transplants a year in the U.S. They cost about $400,000 each. There's a four-year wait list. Once you're transplanted, you're immunosuppressed, so you're gonna be at higher risk of infections and cancer during your lifetime. Kidneys only generally last 10-20 years, so you may be in line if you're diagnosed young for several transplants. I talked to an IgAN patient last year who has four kidneys because they had the two original kidneys, they got two transplants. I mean, this is not a great way to treat this disease. If we could stop or slow progression, it would make a huge difference. We think the time is now to really change this paradigm, and there are a number of things that have been changing in this space that are making a difference. We're getting better at understanding disease biology. Instead of just looking at a slide, pathology slide, and saying, "This patient has FSGS, this patient has another disease, and we're gonna give them a RASi, and then, you know, steroids and some other generic therapies," we're able to look at what's causing this disease, what are the causal mutations and biomarkers, the way we can in cancer and other areas. This is resulting in better drug targets, more validated drug targets. The science is really progressing. In addition to that, the regulatory environment is changing. This is very important here that the FDA is now recognizing surrogate endpoints in kidney disease like proteinuria, like eGFR. You really can't do a hard kidney outcome trial in a rare kidney disease. It takes too long. It takes too many patients. The traditional hard kidney outcomes are progression to end-stage renal disease, doubling of serum creatinine. They take thousands of patients, often more than 5 years. It's just, it's really hard, and that's why we haven't seen many drugs in these rare diseases. In contrast, we can now do trials in hundreds of patients. Our trial for our lead program is 320 patients. Many of the IgAN trials you're seeing are in that range, and you can get to your endpoints within short periods of time. Proteinuria at 6-9 months, eGFR at 2-3 years. It's really changing the whole paradigm in these diseases. You can see this is in, you know, resulting in more development. We only had 5 drugs approved for kidney disease in the last 2 years. There are more than 40 in late-stage drug development, so this is a great sign that we're making good progress in developing new therapies here. At Chinook, we have 3 clinical-stage programs. Our 2 lead programs are both for IgA nephropathy. We think we have the potential to have 2 best-in-class drugs. We're going to tell you more about that. We also have a 3rd program called CHK-336 that's for kidney stone disease that's in phase I, and a number of R&D programs behind that focused on rare severe chronic kidney disease. We're going to talk more about each of these elements of the company in the presentation. This is a snapshot of our pipeline. As you can see, atrasentan, our lead program, is in a phase III trial currently for IgA nephropathy called ALIGN. We're going to have a top-line readout from this trial in Q3 of this year. It's coming up quite soon. We're excited about that. We also have a phase II trial called AFFINITY. This is a basket trial. There are currently five arms in this trial in different proteinuria glomerular diseases. We have reported data from the IgAN cohort. We're gonna have additional data from some of the other cohorts later in the year. For BION-1301, this is a monoclonal antibody that targets APRIL. This is in a phase I/2 trial that we reported data from multiple times over the past few years. We're gonna have additional data this year from that trial as we accrue 40 patients. It's a substantial amount of data in the 2 cohorts of that trial. We're moving into a phase III in mid this year. We're currently in regulatory interactions. We've hired a CRO. We're really making great progress towards getting that trial going in the next 6 months. Our third program, as I mentioned, the kidney stone program, is in a phase I healthy volunteer trial that we'll have data from in the first half of this year. We have multiple programs behind that. We haven't disclosed targets or indications for competitive reasons, but we're making a lot of good progress, both through internal development as well as supplementing that with business development. I wanna talk a bit about IgA nephropathy because this is the target disease for our lead, two lead products. It's the most common primary glomerular disease. It's a rare disease, but not that uncommon. There are about 150,000 diagnosed IgAN patients in the U.S., probably more who are undiagnosed because it requires a kidney biopsy to get a diagnosis, and nephrologists don't always biopsy early on in this disease. There are about 200,000 patients in Europe, and there are several million in Asia where it's a more common disease, potentially due to genetic or environmental reasons. The standard of care in front line is RAS inhibition, an ACE inhibitor or an ARB are used in probably 90%-95% of patients, everyone who can tolerate them. They do have efficacy. They reduce proteinuria by sort of 20%-30%. They lower blood pressure. They're kind of... They're always gonna be around as part of the treatment paradigm. If you still have too much proteinuria while you're on a RASi, docs try other things. They're starting to try SGLT2 inhibitors. About 20%-30% of IgAN patients are currently on an SGLT2 inhibitor. That's probably gonna increase over time. They try steroids or sometimes things like fish oil, chemotherapy drugs, Rituxan, none of which are approved, none of which work very well. And the main way to classify patients in terms of their risk profile is proteinuria. We don't have good ways of stratifying or classifying patients due to risk factors other than how much protein are they having in their urine. If they're over 1 gram per day, that means they're at high risk. Even over half a gram per day is considered at higher risk. Normal proteinuria is below 0.3 grams per day. When you look at the whole population of IgAN patients, it's a prevalence population. About 40% of them have more than 1 gram per day of proteinuria while on standard of care. Another 20%-25% have over half a gram. These are the patients that are in greater need of therapy. I think one misperception about this disease is that it's, you know, it's a rare disease, it's a small patient population. What we're talking about here is even 40% of the U.S. population is 60,000 patients, generally young, living currently for a decade or two with their disease and needing treatment. If we can reduce, for example, if you reduce proteinuria by 30%, it extends kidney life by 10 years. As we get better therapies, we're gonna have patients living their lifetimes, hopefully, on different therapies. This is not a winner-take-all scenario. There are multiple therapies that are gonna be needed in these patients over their lifetime to keep their disease in check. Looking quickly at the pathophysiology of this disease, often patients get IgA nephropathy after a mucosal infection. We don't know exactly why some people may be genetically predisposed to it. What happens is these patients get an infection, and they react by producing greater levels of these aberrant IgA molecules called Gd-IgA1, galactose-deficient IgA1. This is hit 1 in the disease. Hit 2 is when the immune system for these patients reacts, forms autoantibodies that then bind to these Gd-IgA1 molecules and create immune complexes, which is hit 3. These immune complexes circulate, end up in the kidneys, and cause damage. What they cause is inflammation, fibrosis, they cause mesangial cell activation. Ultimately, it causes damage that results in greater proteinuria and loss of kidney function. I'm gonna move on now to talk about atrasentan, our lead program. This is a potent and selective small molecule inhibitor. This is a key target in across chronic kidney disease, not just in IgAN, but in IgAN, it does have unique properties in that by reducing mesangial cell activation in the kidney, this is the initiating event of the disease. If we can really target that, you can have effects on inflammation, fibrosis. There's also some hemodynamic effects and ultimately proteinuria lowering effects. It's an important target here. We also think it could have application really across any chronic kidney disease 'cause it's addressing the final common pathway of kidney function decline and proteinuria driven by proteinuria. This is data. This is the phase II AFFINITY trial that I mentioned. We've presented data from this trial from the IgAN cohort. This is 20 patients with IgA nephropathy. They have slightly lower starting proteinuria levels than the patients in ALIGN. Their average proteinuria was 1.2 grams per day. We think in the phase III trial, it'll be more at like in the high ones or closer to 2. Other than that, very representative patient population. What we saw from that cohort is proteinuria reductions of greater than 50% when you get out to 24 weeks, which is the primary endpoint for a phase III trial. We're really happy to see that. It's been well-tolerated. No related, treatment-related severe AEs, and we haven't seen much evidence of fluid retention either. We've seen no weight gain. We had 2 patients with minor peripheral edema that resolved within a week on low-dose diuretics. Within this patient population, which is a young, healthy population, we're really seeing a well-tolerated drug that's having a significant impact on proteinuria. We're also conducting this trial in 4 other cohorts. We've got 2 cohorts in FSGS. We started at our current dose of 0.75 mg in FSGS, and what we saw is lower exposures in this disease compared to the other 3 diseases. We don't know exactly why this is the case, but we like the data we saw at the lower dose, but we're dose escalating to 1.5, and we hope to see even better efficacy. We could potentially have some data from that cohort later this year, depending on how quickly it enrolls. We also have a cohort in Alport syndrome. This is a genetic kidney disease, often manifests in children. There are no approved therapies at all. It's a huge unmet need. If we could reduce proteinuria significantly, it could be a, you know, a really important opportunity for these patients. We did do a cohort in DKD combined with SGLT2 inhibitors. I'll talk more about this later. We do have a strategy to inform docs on how to use our drug with SGLT2 inhibitors. We did this cohort in DKD because at the time we started the trial, there was no use of SGLT2 inhibitors in IgAN. There is now, we've got some other trials underway. We've reported this data several times to ERA and ASN last year. We'll have some additional data from this trial likely later this year as well as into next year. The phase III ALIGN trial is enrolling well. We'll have data in Q3 of this year on the top line proteinuria endpoint, which we believe could support accelerated approval. The trial design is pretty straightforward in terms of IgAN phase III trials. This is all biopsy proven IgAN patients. They're all on standard of care RASi. They have proteinuria over 1 gram per day and eGFR greater than 30. It's a 320 patient trial. It's actually 270 patients for proteinuria, 320 for eGFR, 1-to-1 randomization. We're conducting it in 15-20 countries, up to 170 sites. It's truly a global trial. The primary endpoint is 6-month proteinuria. The full approval endpoint is eGFR at 2.5 years. As I mentioned, we're also doing some work to generate more data in combination with SGLT2 inhibitors. Our goal with atrasentan is to be the drug that can be combined with whatever SGLT2 inhibitor you want, whatever RASi, either ACE or ARB that you want. What we're doing is we've added a stratum to the ALIGN trial of up to 64 patients who are gonna be on RASi and SGLT2 upon entry, and they'll be randomized to placebo or atrasentan. This will allow us to get some eGFR data as well as proteinuria, but we really wanted to do it in ALIGN because this is a way to get some randomized eGFR data at the end of the trial. We're also doing a phase II trial that'll start in the first half of this year that'll get us proteinuria data around the time of launch. This trial will start pretty soon, and it's a randomized trial to really look at what kind of benefit can we get on proteinuria, how safe is it, in combination with SGLT2s. Moving on to BION-1301. This is an anti-APRIL monoclonal antibody. We're really excited about the disease-modifying potential of this approach. Most drugs in kidney disease are really treating the symptoms or the damage in the kidney rather than the underlying cause of what's going on. With APRIL, we can actually target a really key target in the disease progression. APRIL is a TNF family cytokine. It's involved in B-cell signaling, and it drives IgA production. It's expressed on mature plasma cells. There's a number of correlations between APRIL and higher, Gd-IgA1 secretion, higher, proteinuria, lower eGFR, and increased risk of progression. It's a really key target here. We think that a pure APRIL approach is the best way to go on this disease because we can actually knock down HIT 1. We don't have as much of the Gd-IgA1 circulating, so we're not gonna have as many immune complexes, and hopefully, we can kinda turn off the spigot on the disease. We've got a lot of data from multiple trials with this drug already. We did a non-human primate work. We did a healthy volunteer study. There was a multiple myeloma trial where it was very safe and actually depleted APRIL really well. It just didn't have much impact on the disease. We've got our phase I/II trial that's underway, and I'll show you some of that data. You can see here, what we've been really impressed with this drug is the consistency that we're seeing. We're seeing free APRIL go down very significantly, followed by IgA and Gd-IgA1, followed by proteinuria. It's been very predictable. We've got really narrow confidence intervals on this data. We've got 2 cohorts in this trial. The first cohort was an IV cohort at 450 milligrams every 2 weeks. We, based on the bioavailability data, we switched over to a subq cohort because that's what we wanna use ultimately in phase III and commercially. Excuse me. What you can see here is really consistent data between cohorts one and two, both on IgA and Gd-IgA1, as well as other biomarkers. It's been really well-tolerated. We don't have an MTD. There's no deaths, SAEs or AEs. We haven't seen any ADAs as well. It really looks like a great profile so far. These reductions in biomarkers have translated into really impressive proteinuria reductions. Recall, in this disease, 20%-30% reduction in proteinuria on top of a RASi is considered clinically meaningful. What we're seeing is 50% out at 24 weeks, and then in cohort 1, continued lowering of proteinuria out through a couple of years. We're gonna have more data from this trial. We've enrolled 40 patients, so we'll have more data this in the first and second halves of this year from this trial as these patients stay on treatment longer. What you can see, too, is that it's really consistent. At week 52 in cohort 1, 7 of 8 patients had greater than a 50% reduction in proteinuria. This is just, you know, really remarkable data. We're thrilled with what we're seeing, and that's why we're currently moving towards phase III as quickly as we can. We've selected cohort 2, the 600 mg every 2 weeks subq dose for phase III. We're currently aligning with FDA and EMA and getting consolidated advice, then finalizing the protocol, doing all the study startup and feasibility work and finishing up the PFS. We're gonna use prefilled syringes in this trial, so we're doing all the CMC work needed to take that into phase III by mid-year. The design of the trial, it's not completely finalized, but I don't think you should expect anything unusual here. It'll be a several hundred patient trial, likely between 200 and 300 patients. Similar inclusion criteria to what you saw for the ALIGN trial. Double blind, placebo-controlled, 1-to-1 randomization. We'll probably use 9-month proteinuria instead of 6-month because this mechanism takes a little longer to manifest. The full approval endpoint of eGFR, we'll likely do it 2 years instead of 2 and a half. This is just all based on size of trial, powering assumptions, variability, all that sort of thing. We'll probably also allow patients on this trial who are already on an SGLT2 inhibitor or an ETA inhibitor because that's where the market is going. Those are slight nuances from ALIGN, but in overall, it's very similar design to what you've seen with other drugs. Moving on to CHK-336. This is our first internally developed program. Atrasentan was in-licensed from AbbVie. BION-1301 came in through the merger with Aduro. This program originated in our labs in Vancouver. It's an oral small molecule, targeting towards kidney stone diseases or hyperoxaluria. There are several forms of kidney stone disease. There's the genetic form, PH 1 through 3. PH1's the most severe, where patients often progress to kidney failure by the time they're in their late teens or early 20s. It's caused by genetic mutations, liver enzyme deficiencies that result in overproduction of oxalate by the liver. We're really focused on that segment of the population. There are also patients who get frequent stones due to gastric bypass surgery or absorption issues in the gut. We're not focused there. We're really focused on the metabolically-driven or genetically-driven diseases. There's about 5,000 to 7,000 PH1 patients in the U.S. and Europe. There's only one therapy approved. It's an siRNA from Alnylam that targets a different target called GO. That target is not applicable to PH2 through 3 or idiopathic hyperoxaluria. We're looking initially to go into PH. It's a rapid approval pathway there. Alnylam got approved on 30 patients in a single-arm trial, looking at 6-month urinary oxalate levels. We wanna broaden out into these other diseases, PH 2 and 3, and then the idiopathic hyperoxalurias. There are a lot of people that get frequent stones. Sometimes they don't know why. We're not doing enough genetic testing to really understand. Some of them may have PH 2 or 3 or even PH 4 through 10. There's a lot of speculation in the field about that. There are many patients who get frequent stones. I've never had one, but I hear it's not a fun experience, and I think if you could take a once-a-day pill and reduce those stone events, it would be pretty compelling. That's something that we're looking at currently in terms of a strategy there. There's not a defined regulatory pathway. It would likely need to be not just urinary oxalate, but probably also some kind of stone events. It's something we're pursuing in parallel with doing currently the phase I trial. When we think about this target, we really like it because it has broader applicability than GO. It's really the final common pathway in the formation of oxalate and that gets deposited in the kidney and elsewhere in the body. It could be applicable across a wide range of disease. We've got some great preclinical data in models of PH 1 and PH 2. We're currently doing a phase I healthy volunteer trial. It's a SAD/MAD trial. We're looking at safety PK and a kind of a unique target engagement assay that they're working on. We should be able to report that data in the first half of the year, and then hopefully move into POC trials in both PH and IH. We haven't given timelines on that yet, but we will give more details once we finish the SAD/MAD trial. Our R&D programs. Andrew King, our CSO, is here, and you can ask him questions. He probably won't answer a lot of them about which targets or diseases we're working on for competitive reasons, but we've got a really robust effort to develop new drugs in rare, severe chronic kidney disease, ideally with defined genetic or molecular drivers. We've got a systems biology approach to do target ID, target validation and patient stratification. We have a collaboration with Evotec and have access to the NURTuRE database, so this has been a really rich source of data to help us validate targets we're interested in and also look for new therapeutic targets. We're building better translational models that really are more predictive of human disease. This has been a challenge, I think, across our industry, but we're looking at disease mechanisms, additional target validation, and getting deep biological insights. We really wanna get away from the diagnosis of a disease based on what it looks like on a slide. You know, you think about the way breast cancer was diagnosed and treated 30 years ago, it's changed dramatically based on the markers that we've identified, and it's really different diseases, and we think that's where kidney disease is gonna go as well. We translate that into development candidates. We're looking for first in class or best in class, and we've got a really strong chemistry, biology, and, you know, across the board group up in Vancouver that originally came from Inception Sciences, which was a group formed by Versant Ventures, and then, prior to that, often trained at Merck and other big pharmas. A really strong team, and we think there's a huge amount of opportunity in this space for new drugs. Financially, we're in great shape. We had almost $400 million in cash and investments at the end of, at the end of September. This funds our operating plan into 2025 based on our current plans. That includes all the work we're doing across our lead programs and R&D programs. We also do have a joint venture in China that we formed a little over a year ago, I believe. It covers atrasentan and BION-1301. Before we partnered with Pivotal bioVenture Partners China and Frazier Healthcare Partners, two venture capital groups, to form this joint venture. We own half of it, and they have rights in China, Taiwan, Hong Kong, and Singapore to our two lead drugs. They've been really a great partner for us on ALIGN and done a lot of good work on enrolling that trial. They've... They're submitting an IND and are gonna be involved in the BION-1301 phase III as well. It provides local execution and access to these patient populations in Asia, which are often quite large, so it helps with enrollment and execution. There's also a financial element to this. We own originally half the company, and we also have milestones and royalties built into the deal, as well as a reciprocal right of first negotiation for either products that we take through phase I or products they bring in so that we could get rights in our respective territories. It's also a source of new programs for us and for them. Finishing up on catalysts. For atrasentan, we'll be starting the phase II SGLT2 inhibitor combination trial in the first half and then reporting top line ALIGN data in the third quarter. We'll also have additional data from the AFFINITY trial in the second half of this year. With BION-1301, we'll have data from the ongoing phase I/II trial, the 40 patients of data that we're generating, in both the first and second halves, most likely. The conferences we target generally are the 3 major nephrology conferences, WCN in the spring, ERA in June, and ASN in the fall, usually November. We'll have more data, and we'll also be starting our phase III trial with BION-1301 mid-year. For CHK-336, we'll have some healthy volunteer data from the SAD/MAD trial. I don't know if it'll be the full trial. Depends how many cohorts we do in the MAD section, but should be a lot of data in the first half and then moving towards initiation of the phase II POC trials by the second. Thank you for your attention. With that, I think we can move to Q&A. Do you wanna come up and join me on the We've got two seats here anyway and Yeah, definitely. Thank you for the presentation. If anyone has a question, raise your hand. We'll bring a mic around and... Grab a seat. Yeah. Yeah. Just a question, Eric, about the failure of Rituxan. Can you give us a refresher on what those data were, how they were tested? Given that it's IgA and IgG mediated, you think that Rituxan would work well. although Rituxan has failed in a lot of B-cell mediated diseases where you would think it would work. What was sort of the history there? How'd the data look, and how do your candidates differentiate? Yeah. Yeah. Broad-based B-cell depletion hasn't worked in IgA. Maybe Andrew, do you wanna talk a little bit about your thoughts on that? There was a randomized clinical trial. There was a randomized clinical trial of Rituxan in IgA patients. Rituxan depleted B cells effectively, as you'd expect, but failed to reduce galactose-deficient IgA1 or the autoantibody because those are produced by differentiated plasma cells that don't express CD20, so it's unable to deplete the pathogenic drivers of disease. That's why we think targeting APRIL, which is specifically targeted to those plasma cells secreting gD-IgA1, is a more effective strategy. Other questions. I have a question as well. I'm looking forward to the top-line readout from ALIGN in the third quarter. I was curious what success there looks for you. Is this translatable to the 24-week data from the AFFINITY IgAN cohort? Yeah. In the top-line data release, we won't be able to say a lot because the FDA's been really clear about not skewing the integrity of an ongoing trial. It'll be probably proteinuria, comment on safety and, you know, P value, that kind of thing. We won't be able to comment on eGFR. When you think about this disease, 20%-30% reduction in proteinuria is clinically meaningful. It's probably needs to be closer to 30% to get approval as an accelerated endpoint. I think TARPEYO is in the high 20s. And then, you know, the higher the better honestly. You know, over 30% would be, I think, an approvable drug and meaningful for these patients. We are seeing, you know, close to 55% proteinuria reduction in phase II. It's a single arm trial. There's no placebo arm. It's a small patient population, and the patients look very similar to ALIGN other than being a slightly lower proteinuria, so we're really encouraged by that. Ultimately, you need to run the phase III trial and see what data you have. We're really happy to see what we saw in AFFINITY, and hopefully we can get, you know, that translating into a strong result and, you know, well over a 30% reduction in proteinuria in ALIGN. Any questions? Yeah, I have plenty of questions. If you don't mind. All right. I'll keep going. You've got 10 minutes. Yeah. Yeah. I was wondering, how are you thinking about a potential liver monitoring REMS program for atrasentan? Is this something that you have been discussing with the FDA, will discuss or any light there? We have not yet discussed it with FDA. It just really came up a few months ago when Travere had the delay to their PDUFA date. We do plan to have a discussion with the FDA. There are several differences between sparsentan and atrasentan that we think may give us a good argument not to have a liver REMS. First of all, we don't have a sulfonamide in our chemistry, which has been associated in the past with some idiopathic liver tox. It's a different chemistry. We have a much lower dose, which is also a benefit here. We have a 0.75 milligram dose versus 400 milligrams for sparsentan. Probably most importantly, we have over 5,000 patient years of data from the SONAR trial without a liver tox signal. I think we can take that to the FDA and argue that we shouldn't be lumped in with the other ERAs on that. AbbVie did talk to FDA 10 years ago before they started the SONAR trial, and they also talked to EMA and Health Canada and said, "If we don't see a signal in SONAR, do we need to have liver monitoring?" All three agencies said, "It seems reasonable that you would not need liver monitoring if you don't see a signal, but it's a review issue," which they'll always say. We think we have a good argument, and we plan to engage with them this year. You know, it's not a given, and we're not gonna take it for granted. Yeah. I'm also curious about BION-1301. It's great that you guys are initiating the phase III study this year. Is there any additional information, details that you can offer us other than what you shared previously? What are the remaining gating items? Yeah. Andrew, you wanna talk about that one? We are excited to move quickly into phase III for BION-1301, given the exciting clinical proof of concept data Eric shared and the potentially disease-modifying mechanism of action. We are on track to initiate the study in the middle of this year. They're currently finalizing regulatory interactions with both the FDA and EMA to have a unified protocol for a single global phase III trial for registration. It's really just the traditional startup activities that are ongoing. We have a CRO. We're doing site feasibility, finalizing the prefilled syringes from a CMC perspective and ready to move forward quickly beginning in the middle of this year. Great. Kind of to follow up on that, is there any background meds that will be allowed excluded from the phase III study and any light there? Yeah. As Eric mentioned, IgAN's an evolving treatment landscape, particularly with the emergence of SGLT2 inhibitors, being used currently in 20% to 30% of IgAN patients, and the potential for endothelin receptor antagonists to be approved in February with Travere's PDUFA and then hopefully atrasentan following the ALIGN readout. It is important that you demonstrate efficacy on top of emerging treatments available for these patients, so we'll likely enable individuals who are unstable of background therapy with RAS inhibitors, SGLT2 inhibitors, and/or ERAs, to be enrolled in the study. We will need to exclude the use of immunosuppressive agents, like steroids or other B-cell agents, to ensure the safety of the patients, given BION-1301 is immunomodulatory in targeting plasma cells. Thank you for that. Any other questions? If not, I think we can call it. All right. Thanks again. Thanks a lot.