I think we can get going since it's exactly 10:30 A.M. So welcome everyone to the next session of the Citi Biopharma Back to School Summit. So we are literally back to school, checking up on all the companies. So the next one is my pleasure to introduce the management from ProKidney. We have Bruce Culleton, the CEO, and Ethan Holdaway, who's the head of the Investor Relations Group. So welcome. I'm Yigal Nochomovitz. And for those of you in the room, if you're interested in asking questions, just you know, chime in. There's microphones. And also welcome to everyone listening on the webcast. So Bruce, obviously you've had a very, very busy summer with some pretty important data that sent the stock up quite a lot, actually. So tell us about the data.
Tell us about the platform, I guess, maybe to start with, and how you got to this point.
Sure. So I think my mic is working.
No, you gotta push. There you go.
Okay, great. Okay, thanks. First, Yigal, thanks for having us here. We appreciate the opportunity to talk and answer any questions as well. You're right. We had a busy summer. We announced the results of one of our phase II trials, top line results, in July. Just as a background, ProKidney is an autologous cell therapy company. We have a single asset that's called rilparencel . It's directed at preserving kidney function in patients who have type 2 diabetes and advanced chronic kidney disease. Our company's headquarters are in North Carolina, where our manufacturing is in Winston-Salem. We have a clinical office and an R&D office in Raleigh, and we have more of a corporate office just one block that way.
You don't have to go far.
Ethan and I just walked down the street, which was good. So we did announce our phase II results top line for a study called REGEN-007. And then a short time after that, we announced an update on our regulatory discussions with the FDA, which we'll get into today, I'm sure, as well. So from a top line data perspective, I'll just talk quickly about the design. So REGEN-007 was a randomized, open label study. Patients with advanced chronic kidney disease and type 2, and diabetes, type 1 and type 2 diabetes in the study, they were randomized to get a scheduled regimen of rilparencel, which consists of two injections, one injection in each kidney separated by three months, or randomized to group two, where they received one injection of rilparencel.
And then those patients in group two waited essentially for either a decrease in kidney function measured by eGFR or an increase in kidney injury measured by UACR. Once they reach those triggers, then they will get a second injection. The overall sample size was 49 subjects, and we followed patients for up to 18 months after their last injection. Just getting to the top line data, we didn't release all the data because we wanted to preserve potential embargo for a late-breaking trials presentation at ASN coming up in Kidney Week coming up in November. From a top line efficacy perspective, in patients in group two, in group one, sorry, and group one is really important because they're very similar to patients being enrolled in our phase III program.
So patients in group one, the patients who received two injections, their pre-injection slope of loss of kidney function was minus 5.8 mL per minute per year. And after their second injection, their slope for the next 18 months, their annualized slope was -1.3. So essentially what that works out to was a 78% improvement in decline in kidney function for those group one patients who got two injections. Now, we also saw less of a benefit in group two, and not everyone got a second injection in group two. I think 15 or 16 people out of the 25 got a second injection, but they also had a delayed second injection, even those that got a second one. But we did see a 50% improvement in kidney function decline in group two. So not as substantial, but still we saw a signal of efficacy in that group as well.
It wasn't statistically significant in group two, but we did see a clinically important and statistically significant difference in group one.
So for the ones that didn't get the second injection in group two, that they just didn't hit the trigger or?
Correct. Yeah, they, they didn't hit the trigger.
Okay. So that wouldn't suggest that they benefited enough or substantially from the first one? Or is it not that simple?
It's probably not that simple. It may simply be that their decline was not substantial to begin with. There's some patients, 'cause there's a lot of variability in decline. Or you're right, you know, presumably they received some benefit from the first injection as well and didn't progress as you say.
Yeah. Yeah, so very interesting design. And this, I don't think I've ever seen, well, a cell therapy in kidney cancer and kidney disease, you know, we haven't seen that before. So, and then this design is interesting given the staggering and the bilateral. So what exactly are you going to show us? 'Cause you have kind of described it qualitatively, but we're waiting for graphs and charts.
Absolutely.
So, what's gonna, what are we gonna get at ASN? Can you, like, how much detail is gonna be discussed there?
Yeah. So ASN Kidney Week, again, is coming up in early November in Houston. So we, we're submitting an abstract this week for late-breaking trials.
Okay.
So that abstract is going in. I think the deadline is September 9th. So within the next six days, we'll have that submitted.
Okay.
We also have a manuscript that's written that will be submitted to JASN for simultaneous publication. Now, all that depends upon the reviewers. So we can't say that all that's gonna happen, but that's our goal. And what you'll see if should we get late-breaking trials acceptance and manuscript as well, you'll essentially see everything in the way of graphs and figures and tables. The tables will outline sort of a really good description of what the patient's baseline characteristics are. You'll also see secondary endpoints, which would be things like time to dialysis in each group, time to death in each group, small numbers, but all that was part of a secondary endpoint analysis.
I think a lot of people are interested in subgroup analyses, you know, what happened to patients if you were on an SGLT2 inhibitor at baseline or you were not? What happened to patients if you're on a GLP-1 at baseline, GLP-1 agonist at baseline or not? What if you're type 1 versus type 2 diabetic? So those types of things will have more of an opportunity essentially to produce all that data and reveal all that data in either the abstract presentation or the manuscript. The other thing just for clarity on this is we talked about top line safety as part of our press release in July. You know, all the adverse events will be described and serious adverse events and sort of that just broad, you know, safety analysis would also be part of that presentation.
Okay. And so you mentioned some of the changes in the slope, which were profound, well, for sure in the two injections three months apart. What about just sort of the, who are these patients? I mean, what stage of CKD were they? 'Cause there's a big range.
Yeah. So the entry criteria into this study was the eGFR 20-50. So that encompasses stage four patients and some stage three patients. Now, the average eGFR I think was around 30, 29 or 30. So primarily patients with more advanced stage three and some stage four patients were part of the study.
Okay. Now you had done a lot of work over the past few years to sort of determine where this therapy would potentially have the greatest impact. And so I guess this just sort of gets into mechanism of action and how it works in terms of the action on the podocytes. Yeah. So can you talk about, you know, the MOA and how you believe this is working and why it may be, you know, better suited for a certain segment of the CKD population versus another?
First, I think, Yigal, I believe it works in patients who've got less severe kidney dysfunction as well. Even though we're targeting in our phase III study patients who have a GFR less than 35, there's a reason why we're targeting patients with more advanced chronic kidney disease. There's several reasons, but I'll just say that, you know, I do think it works in patients who have less severe kidney disease as well. It just may not be an easy market for us.
Yes. Yeah.
Partly because if you look at someone with, let's say, a GFR of 50, for the most part, you know, that patient's risk of dying of something other than kidney failure is maybe a hundred times higher. Right? And so the real benefit to that patient in treating them and preserving their kidney function is maybe not something that the patient would want to go through, that their physician may not want them to go through, and a payer may not pay for it. Right? So our current approach within our phase III study is to really look at patients with more advanced kidney disease, those that, you know, have unfortunately progressed to a GFR of less than 35, many of them with an eGFR less than 30.
The nephrologist may have already started discussions around what type of dialysis you may want or if you're suitable for transplant, et cetera. So it's on a patient's mind, it's on the family's mind, it's on care partners' minds. And it's also something that, you know, economically becomes a lot more attractive to payers because they don't want these patients ending up in dialysis clinics because they know, you know, they know the cost of that. It's, you know, $125,000-$250,000 per year. So that's something that they want to avoid as well. So just getting back to the MOA, so we've invested a lot in the last 12 months to sort of revamp our thinking around the mechanism of action. ProKidney's got a pretty rich history.
And in a version of ProKidney before ProKidney went public, the previous leadership at ProKidney invested in R&D, but stopped really investing in 2015. And the reason for that sort of stopping real investment in R&D in 2015 was, A, I think they felt like they had the answer that they wanted. And B, you know, they wanted to use what funds they had to start phase I and phase II clinical studies as opposed to continuing R&D investment. Now, from 2015, when they stopped the research, which suggested that rilparencel had an effect mainly through antifibrotic and anti-inflammatory mechanisms, when they stopped the research in 2015, you know, the advances in new tools and how to demonstrate mechanism of action continued to advance independent of ProKidney.
All our understanding around multi-omics was something that evolved over the course of that period of time. We've really, in the last 12 months, and you'll see some of this at ASN as well, we've really started to focus a lot of our efforts on, you know, from a multi-omics perspective, what happens when rilparencel is injected into patients' kidneys. That's where our efforts are focused today.
We're gonna get some of that, I assume, biomarker or, and/or functional data coming?
You'll get some of that. You'll get hints of some of that data at ASN. You know, I don't believe there's gonna be a light bulb moment where all of a sudden, you know, it's Eureka, we figured this out. I think it's gonna be an incremental story that will essentially come to a point where we say, look, this is how we think it's having an effect on, you know, tubular interstitial cells. We believe those cells talk to glomerular cells, for example. I think that's just gonna be an evolving story, but we're gonna continue to produce data until we feel pretty comfortable about what the story is as well.
Okay. You mentioned in the 07, the range was 20 to 50.
It was. Yep.
Right, but and then in the PROACT 1 , which we can get into more detail, that's restricted to the lower half of that.
Correct. Yeah. We've really narrowed that. So PROACT 1 was originally designed with an eGFR of 20-50. And about just a little over a year ago, we narrowed that range to 20-35, partly because of, you know, the changes in the therapeutic approach to chronic kidney disease and diabetes with the advent of, you know, SGLT2s coming into the market, non-steroidal MRAs, GLP-1 agonists, like the four, we talk about the four pillars of care now in chronic kidney disease and diabetes. That's really been beneficial for patients, but there's not a lot that's been done to study patients with more advanced chronic kidney disease. All those studies have been primarily in patients with less severe chronic kidney disease. We're focused on those patients with the greatest, what we think is the greatest unmet need at this point in time.
Right. So what I guess I was driving at was, when we see the ASN data, are we gonna have a view into the efficacy in that 20 to 35, which will obviously everyone sitting here and listening is gonna be very curious about that set of data?
Yes. Yes. So that'll be part of the subgroup analysis as well.
Okay. Yeah. Well, then, speaking of the PROACT 1, so what else is there to say? How far along is that study? When could it read out? Have you discussed that?
Yeah. So, PROACT 1 , just as a reminder to everyone, it's a randomized, sham-controlled, multi-center phase III clinical study. And for a cell therapy, this is a big trial. Our target, the primary endpoint for the confirmatory analysis, it's a time to event study, and we expect we'll need six to 700 patients enrolled in that study to accumulate those events over a desired period of time. For a cell therapy, that's a huge clinical study. I mean, in listening to an earlier session this morning where there's, you know, for rare diseases, it's, you're still looking at single-arm studies that are small and uncontrolled. This is, I would argue, one of the largest cell therapy studies currently enrolling patients.
That study was designed with an eGFR of 20 to 50, as I said, and we've reduced that now from 20 to 35. We've made some real good progress around enrollment. Recently we said we're over 50% enrolled for our accelerated approval readout, which we expect in Q2 of 2027. We had a really good August for enrollment, a really good July for enrollment. We're well above 50% enrollment for that accelerated approval.
What endpoint is gonna give you that path, accelerated approval?
We are looking at a difference in eGFR slope between the two treatment arms, so the interventional arm and the sham control arm.
Okay.
We're looking for a difference of at least 1.5 mL per minute per year of change in eGFR slope.
Okay, and then assuming you check the box on that, then the full approval would be based on outcomes. What would be the full approval?
Correct. So the full approval is in the same study. So we're using. We have a single phase III study. The interim readout will be accelerated approval readout, and the confirmatory analysis will be based upon clinical events. And those clinical events are time to initiate dialysis, time to transplant, time to renal or cardiovascular death, or time to more than a 40% drop in eGFR, sort of accepted clinical harder endpoints. And that would be for the confirmatory analysis. We haven't said. We haven't issued new guidance on when we think that confirmatory analysis will be, but we expect we'll announce some new guidance on that early next year.
So when you do the Q2 2027 for the slope difference, that doesn't and at that point you won't by default in the protocol analyze for outcomes. It's not.
Correct.
That's not how it's gonna work.
That's not. So we will analyze for outcomes when we achieve, I think, our target number of events is 122 events that will trigger the endpoint confirmatory endpoint analysis.
Which presumably would be obviously after that endpoint.
Correct.
But you haven't said, you don't know yet 'cause it's, it depends on the timing.
Correct. It does.
Yeah. Okay. So that's the key phase III trial. Is there a different one or is that the main one?
That's it.
Okay.
Yeah. We so just for clarity as well, we had another phase III program that we ended up stopping before we enrolled any patients. We stopped that around this time last year. And the reason we stopped that is because we didn't need it. We have an RMAT designation through the FDA and a single phase III study is sufficient for approval.
So that one that was paused or stopped was a sort of like a replicate of this one or?
It was.
It was just a replicate.
Yeah. It was very, very similar. Yeah. It was primarily being done in Europe and Asia.
Okay. Yeah. By the way, some people have asked me, you know, since you amended the enrollment criteria to look at the 20 to 35, what, how do you analyze? There were maybe some that got in that were over between 35 and 50, right?
Correct.
Did they, did they get analyzed in some way or how did they get dealt with?
So they're all part of the primary analysis. So they'll all be part of the primary, modified intent to treat analysis, and, and the overall safety database as well.
Okay. And then commercially, if this study works, then that would be the regimen would be this. Well, we didn't even talk about that yet. Let's. Can we go through? We kind of went backwards. The manufacturing and how the cell product is prepared, and yeah.
Yeah, of course. Yeah. So, it's an autologous cell product. So we, how we obtain kidney cells from a patient is through a percutaneous kidney biopsy. That is a pretty standard procedure that's done throughout the world. It's essentially done under a local, mild sedation and local anesthetic. What we do for the clinical study is, an interventional radiologist primarily, although nephrologists are also trained to do this. Interventional radiologists use a standard kidney biopsy needle and we take a couple of samples of the kidney biopsy, mainly from the outer cortex of the kidney. Those samples are then shipped back to our manufacturing facility in Winston-Salem, and over the course of several weeks, those cells are expanded and we select out certain types of cells, which are primarily tubular interstitial in nature, tubular epithelial in nature.
And those cells make up the final product of rilparencel. Before rilparencel, or after rilparencel is actually produced, it's cryopreserved. We typically make anywhere from two to five doses per patient, although we only inject two doses in a patient in the trial. We hold on to the others if there's any vials that are still available. And that cryopreserved vial gets shipped back to the clinical study site where it's thawed and under CT guidance is injected back into a patient's kidney. This is the REGEN-007. The phase II data was the first data that we showed injections in both kidneys. And the phase III trial is also designed to inject rilparencel into the biopsy kidney and three months later into the other kidney.
I actually hadn't thought about this before, but when you do the biopsy, then it doesn't matter which kidney, right? I mean.
It does not.
And then with the one that gets injected first, doesn't matter whether it was the one that had the biopsy or not. I guess it doesn't matter.
It doesn't, but we do go back into the biopsy kidney for the first injection.
Oh, you do. Okay.
And then the other kidney for the second injection.
Okay. And then you mentioned the sham procedure. So that's always, you know, I guess a delicate topic because it's a question of how much sham for, you know, some of them are a little bit, some are. What? Just describe exactly what happens.
You know, from the perspective of making sure that this trial has internal validity, like we're doing a phase III program and we wanna make sure it's controlled, we have taken extra careful steps, I would say, to ensure that the patient doesn't know and the principal investigator doesn't know which arm of the study the patient has been assigned to. And for the sham, how that works is the radiologist and the team inside the radiology suite, they're all trained to deliver the same experience to a patient, whether they're getting a biopsy and rilparencel or a sham biopsy and sham injections.
The only thing that happens that doesn't happen in the sham is we actually don't go into the kidney for a biopsy and we don't insert a needle into the kidney, but the patient does get a nick in their skin. The radiologist says the same thing to those patients who are in the sham controls. They put pressure over where the needle goes in. It's everything's explained to the patient. There's a script that the radiologist follows. For all intents and purposes, the patient leaves that room, goes to a recovery room for six hours and stays there assuming that they've gotten an injection with rilparencel or a kidney biopsy. Everything is followed the same way.
So even with the biopsy, they wouldn't know that they didn't have the.
Correct.
Tissue excision.
Correct.
Yep.
Okay. There's a nick in the skin. There's local. They're given a local, a sedative, and local anesthesia, the same thing as if they were getting a kidney biopsy.
Okay. Now, I mean, a very sort of conceptual question is, you know, there's obviously you were at the session earlier and I've covered a lot of cell therapy. Usually it's not in the sort of solid organ situation. It's in other areas, right? Like, you know, lymphoma or leukemia. So you're kind of a pioneer, I guess. You know, how do you see that? And I also wanted to ask, you know, you're looking at CKD, but that's a big market, obviously. But there are a lot of rarer kidney diseases where something like this could potentially have applicability as well. For example, like, you know, FSGS or others, but I just wondered how you think about all that.
So I'm, I'll talk about FSGS and other kidney disease in a second, but I'll ask Ethan, I'll give Ethan some ear time to talk about the size of the kidney market.
Okay. Yeah. Go ahead.
Yeah, sure. So, it's a pretty big indication, you know, to your point, Yigal. And, I think if you look at our potential TAM, you know, relative to other cell therapies out there, it's, you know, around 500,000 to 1 million patients. And so, while yes, there could be applicability for our product, and other indications, FSGS, you know, there's, there's plenty more. I think initially we're focused on what is the largest, market within CKD, which is, you know, diabetes and, and advanced CKD. So, you know, we're focused on running the PROACT 1 study, and we'll, you know, assess other potential indications, I think, as we, as we move this along.
And if you, getting back to the MOA, we don't think that the product is unique to just patients who've got type 2 diabetes and advanced chronic kidney disease. You know, if it truly does work on some form of antifibrotic anti-inflammatory mechanism, then, you know, even our steering committee has brought this to us as well, our external steering committee, and they said, look, you know, this might be an umbrella therapy for patients who've essentially failed everything else and have progressed on to stage four `kidney disease where there's nothing else for them other than dialysis or a kidney transplant. So conceptually that makes a lot of sense. But, you know, then there's a practicality of it, like we're in the middle of a phase III study and we're focused on patients with CKD and diabetes.
That's our absolute focus is to execute on that study and be ready from a commercial and manufacturing perspective. There will be a day when I think we'll want to explore other potential indications.
I mean, will PROACT 1, it's both type 2 and type 1 or just type 2? Type 1 is another study later, even though in the 007, didn't you have some of them?
We did have some patients, we had a small number of patients with type 1 diabetes in REGEN-007, and we'll show you the data at ASN, how the type 1 patients did versus the type 2 patients.
Okay. All right. Now another interesting thing is, you know, usually with some of the cell therapies, you know, it's a rare disease and obviously price point is high. We've seen. We know what those examples are. In this case, you know, you point out $500,000 to $1 million. So. And you have to. It's personalized, it's patient specific. So, of course, I'm sure you've been asked this, you know, in terms of the manufacturing, gateway to if you have that sort of volume, how do you keep everything organized so that, you know, every patient is its own therapy? It's not. It's specialized. So how do you do that in Raleigh or wherever you do it?
Yeah. So we have tools in place to ensure that from the time the biopsy is done until it gets back to our manufacturing facility until it gets back into that patient, we have tools in place to make sure that only gets to the right patient, and you know, I wouldn't say there's anything proprietary in what we're doing. It's just part of cell therapy to ensure that whatever product you're making gets back to the right patient.
Right. Right. So barcoding and other control.
Yeah.
But what is the right, as of today? I mean, you're doing a pretty big phase III, as you pointed out, for cell therapy, but that's still a drop in the bucket compared to what you would need commercially. So what is the current, like, what kind of capacity would you expect to have at launch for the product? Ethan, you want to?
Yeah. Yeah. Yeah, sure. So we can supply our phase III study today and over the next few years, and this is all baked into our cash runway guidance and all that. We're continuing to expand our manufacturing footprint. We plan to have sufficient capacity for the first few years of launch.
I will say, Yigal, though, if we see similar results to what we saw in our REGEN-007 data, where we saw that 78% improvement in eGFR decline, we expect that demand will outstrip our ability to supply the product.
Yeah.
And we are expanding manufacturing capabilities, as Ethan said, so that, you know, shortly after commercial launch, we would be able to expand in sort of a more of a modular way. But, you know, if we do see the benefit that we saw in REGEN-007, then I, I don't think we'll be able to meet the demand for the first few years.
And when you start to think of, I mean, you mentioned, you know, dialysis and cost savings associated with preventing dialysis, which you mentioned some of the numbers and those could accumulate quickly. So, but, you know, it, cell therapy tends to be on the higher end, obviously, but this is a large market. So when you think about the pricing, how does it all get assembled into a final?
I'll piggyback off of what Bruce just said. If we do see similar efficacy results in the phase III, if we see that benefit, or sorry, excuse me, in the phase II, if we see similar benefit in the phase III, I think we're very confident in our ability to price the product, in a way that where we have sufficient spread between the cost of goods and the price.
And what, I mean, I know for, you know, for some of the CAR Ts and so forth, cost COGS can be a big number. Is it different for your process or similar?
It's, we don't know exactly, you know, what the cost of goods is for the various CAR Ts, but we actually have a cross-functional team working on manufacturing cost of goods, you know, today and what we think at scale. It's guidance that we, you know, intend to refresh at some point in the future because as we progress through our phase III and get closer to a readout, we're obviously getting a lot more questions on it and know it's a huge area of focus. But I think for us, it's just gonna be kind of balancing the size of the market, which is very large for a cell therapy, compared to others out there, the cost of goods, the fact that it is an autologous cell therapy and, you know, patient demand.
I'll also say that, you know, I'm pleasantly surprised where we are with COGS today, and I do think we'll have a profitable, sustainable business, even if we were left with a sort of COGS projections that we have today, but we also have opportunities to lower that substantially more, and we'll be able to talk more about that, I think, next year as we get closer to commercialization, but, you know, right now, a big piece of that COGS is people, 'cause it's a very manual process and there's opportunities around automation that we're looking at as well.
You have a few. I mean, we hit on the big topics with the phase III and the ASN data, but you do have some other studies as well that you can comment on that are still in some state of being prosecuted? Like, there was one called REGEN-008. What was that one? And is it still relevant or not really?
Yeah. REGEN-008, I would think about that as more of a study that's designed to look at long-term safety.
Uhhuh.
Patients that were enrolled in prior phase II trials primarily have been rolled over, like REGEN-007 patients. They've been given an opportunity to essentially roll over into a long-term safety follow-up, which is REGEN-008.
Okay. Okay.
So, we'll, you know, obviously present that data when we think there's sufficient data to present, but there's no more injections in that group. They're just really being followed for long-term follow-up safety. We will collect eGFR as well, and we'll collect data on if they die or on dialysis and things like that. So that's part of the dataset that we'll eventually present publicly as well.
Then you would have further follow-up on those 007, I mean, beyond these 18-month point.
Correct. We will have further follow-up, not on everyone, because not everyone wanted to.
Yeah.
Join that follow-up study. So, but we will have follow-up on those patients that decided to join 008 and continue to have follow-up, I guess.
Okay. And when will, so you're submitting it on the ninth, and then when the conference is in the?
The first week of November, first full week of November, it's in Houston Kidney Week, and we submit the deadline for the late-breaking trial submission, I think it is, September 9th, and so we'll have things submitted for that, this week. I think we get notification early October.
I mean, you would think that would be something that the conference organizers would like to feature given the big thing.
I would think so. Yeah.
But I guess we'll find out. Okay.
I, you know, I'd be surprised knowing ASN. I mean, they do like to present some of the latest science, so I'd be surprised if it wasn't featured in some way or another.
Yeah. Okay. All right. And then if you could spend a little bit of time just talking about, outside of the United States, I mean, ProKidney, is this a study product one that could be used to file for an approval in Europe, or would you need something different?
I think it could serve as a basis for filing in Europe.
Mm-hmm.
But, you know, we're probably gonna need some European data as well. At least that would help with market access. It may not be even required for regulatory approval, but it certainly would be needed for market access. That's not something that we are focused on today. You know, we decided last year to focus on, you know, the biggest market where we have a presence, where we understand the regulatory path more clearly. And with that said, you know, for the right opportunity, right level of interest, we'd be more than happy to explore opportunities outside the U.S. as well. We just don't have any focus there today.
Okay. And then as far as, you know, the management of the cash and the runway and all those things, where is it today?
Yeah. Yeah. We had, as of June 30th, $295 million of cash on the balance sheet, and runway into mid-2027 as of today.
Okay. So that would be enough to get you, as you point out, to the accelerated approval look.
Yes.
But then, for the outcomes for product one, clearly you would need additional funding.
That's correct. Yep.
Okay. All right, and then what about, you know, the, just on the IP aspect, 'cause it's a, you know, there's multiple factors. How does the patent protection work?
We have multiple patent families, a very solid patent portfolio that we're quite comfortable with at this point in time.
Okay. Great. Well, look forward to ASN. Good luck with the reviewers.
Yeah. Thank you. Thanks a lot.
We'll see the data there.
Yeah. And thanks again for the invitation.
Okay. You're welcome. All right.