Annexon, Inc. (ANNX) September 2026 Conference Transcript

Good morning, everyone. Thanks so much for joining us. We'll get going here on the next Fireside discussion. My name is Derek Archilla. I'm one of the Wells Fargo biotech analysts. Very excited to have the team from the Nexon. From the company we have Doug Love, President and CEO, as well as Lloyd Clark, SVP of Strategy. So, gentlemen, thanks so much for joining us.

Thanks for having us. Delighted to be here.

Yeah, well, we've got a really exciting year or end of the year for us and for you in terms of some data readouts. So, Doug, do you want to set the stage first and just kind of what to expect? and then we can kind of dig into the bond improvement phase three.

Yeah, happy to do so. Yeah, exciting indeed. So we're in our 11th year here at the Nexon, and more excited than ever about the technology that underpins the company. After 11 years, we've got two major opportunities to deliver game-changing therapies to millions of patients worldwide, the first in Guillain-Barre syndrome, which we'll talk more about, obviously a resounding win on the phase three. We're on file for approval in Europe, and we anticipate filing very shortly for the BLA in the U.S. So that's coming and going, and we're really excited by that. Followed shortly behind that will be the Geographic Atrophy Phase III study with Bon Appearment, a separate drug candidate, where we're really excited about the outlook at month 15, which I'm sure we'll talk a great deal about. And then last but not least is our small molecule program, first-in-kind oral tablet targeting the classical pathway for a host of antibody-mediated autoimmune disorders, where we will update on a proof-of-concept study this fall on that program. So after 11 years into it, one thing we can say consistently is that this platform and this mechanism that we're targeting by blocking upstream inflammation right on disease tissue is really showing very unique functional benefit in patients, which is different from a symptomatic outcome, which we think is really important. So we're encouraged by it across the board.

Got it. So maybe let's start with Vonna Prumance Phase 3. So you guys made an important update, you know, adding the dual endpoint at 24 months. So just tell us kind of, you know, what was the driving decision there? And was this an offensive or defensive move?

Yeah, 100% offensive. So really thrilled by this. For those who are less familiar with the program, this is a 24-month study with the primary endpoint being month 15. We got 12 months through the study, and what we realized is we picked up additional alpha or power over the course of the study. and I'll have Lloyd talk more specifically about how we did that. Anyway, suffice to say, we had the option to either add additional power to month 15 or apply it to a second endpoint, an independent endpoint at month 24. We chose the latter primarily because month 15 is so well-powered. So month 15 is powered at greater than 90%, even higher, I mean really high, plus 90% at the single study level and 90 plus percent at the sub-study level. And so we felt really good about where that endpoint is. And that was our first kind of call to action, was to make sure we do no harm and to protect the primary endpoint of month 15. And then to apply the additional outcome to month 24, really was centered around building a franchise that is dominant, candidly. You know, we recognize that month 15 is an important and an attractive number, But month 24 is even better for the treating physicians, for the patient populations, certainly for the payers, et cetera. And so anyone following us will now need to run a study with 24 months or greater data on an endpoint of BCA 15-letter loss, which is an exceedingly high bar. So we, in effect, were able to build a moat around this franchise by adding in month 24. But maybe, Lloyd, talk a bit about how we picked up power over the course of the study.

Yeah, Doug, we did a 12-month review of the study, and we really found that we had a larger study at the end of the first year than we anticipated due to four factors. First, we made our powering assumptions based on 12-month data, but we extended the trial early in the course of Archer II to month 15, so we had more events at that point. As a reminder, we over-enrolled the study at the outset by 30 patients, which gave us more patients, more time, more events. One of the key factors that we learned during the course of the study, though, was that we had significantly better patient retention than we anticipated, significantly better than our Phase II study, and much better historically than other Phase III dry AMD studies. So again, more patients, more time, more events. And so the size of a study like ours is sort of predicated on the number of sham events that you have in a study. So we essentially found ourselves at the end of the first year with a larger study operationally than we anticipated, which gave us more statistical power. The fourth piece was then looking at that and then putting alpha at month 24. That gives us more time, which gives us a larger treatment effect. And a widening treatment effect is a significant variable to increase powering in a clinical trial. So this was sort of operational statistical power that we recovered with the combination of time as our friend in the second half of the study to give us the opportunity to add a second endpoint.

Gotcha. So maybe can you walk us through the mechanics of what's going to happen in 4Q? So the DMC is going to give us an update. What will we actually know when?

Yeah, really, really, really good question. And so for us and for the regulators, what's really important is data integrity out to month 24. And so what that means is from a company perspective, we could not unmask ourselves at month 15, yet we still wanted an answer. So we assembled the DMC, which has been running over the course of the studies, a very experienced group of retina specialists. They will look at the data at month 15 and make a determination on whether or not the study is feasible to continue. if we've hit our statistical bar and or to continue. So those will be the three options that they will give us. And so that's all we will know and we will report out at that point. Assuming success at month 15, they will then unmask and look at the sub-studies, which we will have at the beginning of next year. Assuming success on that, the company will then be unmasked as we pull a package together to file for approval while the study is still running for month 24th. So it's a really stepped approach to really align ourselves with the regulators to do this in a way where we protect the integrity of the data.

So STAT-SIG in 4Q on the overall study essentially gets you Europe. Because they are looking at the study at the overall level. And then the sub-study data, which we won't get until the first quarter of 27, that's for the U.S. filing.

At a minimum, yes. So we do know that there's an opportunity with the win on the overall study to also have a discussion in the U.S. for a win there. We know that's the case in the alignment with Europe as we sit here today. But as the regulators have told us in the U.S. as well, the totality of the package will be important if you win on just a single study. We'll look at the secondary analyses, obviously the mechanism, et cetera, which would be supportive of that.

So one of the questions we often get is around the sham control and what you guys have really assumed for the trial. So maybe you can kind of talk to, I guess, the experience from the Phase II learnings and some other contemporary trials in GA and what we should expect there.

Yeah, really important question. I'll start, Lloyd. You should dive in on this. So first and foremost, what's important to note about ARCHER II is this is a vision preservation study. That in and of itself is different in kind from the prior studies that are out there that are RPE structural studies. Why that's important is really we looked at the RP structural studies, particularly looking at lesion location and lesion size and translating that to their sham effects, trying to match up to our study. We were able to then overlay the learnings from ARCHER, which is really, really important, which is, again, visual acuity outcomes. and looking at those measurements, applying those in conjunction with the structural measurements to set up our sham rate as well as the projected treatment effect at 12 months, 15 months, all the way through month 24. Maybe, Lloyd, you can talk a little bit more about that.

Yeah, so we used all of these variables. I mean, we have a tremendous amount of data, both structurally as well as functional data, within the ARCHER database. We certainly started with that, but we also used, you know, So any publicly available data on 15-letter loss event rates to arrive at an appropriate sham event rate to start the ARCHER II study. For the treatment effect, we primarily used as our starting point the treatment effect in the monthly arm of the Phase II study. From there, we took conservative adjustments on both to arrive at what we felt was an appropriate expectation for a treatment delta and then powered the study in terms of the size of the study based on those estimates. And so one of the really reassuring things as we're sort of completing the study, because we're very close to having, you know, we're much farther than 50% of the patients have completed month 15 to date, is that those assumptions have held up during the execution of the clinical trial very well. So it gives us a lot of comfort in terms of our understanding of the disease, which is a very difficult disease, as Doug has been known to say many times, this currently is an undefeated disease. It's a very difficult disease to manage clinically as well as in a clinical trial. Despite that, our assumptions are right on pace, and so we feel very good about our understanding of the disease as well as our expectations for treatment effect.

It's a really important point. I mean, I think what Lloyd is saying is this study is designed to replicate Archer, and it's performing exactly like that, as we see it at this stage in the study. So now it's about, you know, the drug doing its thing, and we've given it a great opportunity to do so.

And, Lloyd, you had a comment there that I want to revisit in terms of, you know, the increased power to the trial based on just a very low discontinuation rate. Why do you think you're seeing such a low discontinuation rate?

I think the community, both in the U.S. as well as the ex-U.S., sees this as a very highly differentiated product. There's a number of key differences here, which gives patients and physicians tremendous hope for this program. Obviously, the ability to offer patients a functional benefit. You know, we are five years into this clinically in the United States. No functional benefit. There are no drugs that are functionally available for patients outside the U.S. So from a functional perspective, highly differentiated. From an administration effect, highly differentiated, small volume, low viscosity, very easy to administer. And in terms of our safety profile, I think it's very, very encouraging for investigators to continue patience in these studies because they have comfort in the ability to offer a highly differentiated product. So there are a number of factors which I think have given clinicians and patients a lot of encouragement to stay in. It makes us feel really, really excited as we complete the study.

And now that you're kind of pushing out the trial to 24 months, you've had to make some probably new assumptions around what the sham could do. So I guess one would assume that they would probably progress more, but what sort of assumptions have you kind of made around that?

Well, there's a number of data points that are publicly available that look at 15-letter loss event rates past month 12, and those events continue to occur for several years. You know, if you're looking for a good data point to look at publicly available, the Lampolizumab studies have 15-letter loss event rates, which go consistently out past year two. So we feel very comfortable that the event rates will continue, which will give us the ability to see an increased treatment delta. Understood.

So I guess, you know, data come out, they're positive. I guess when you think about the overall opportunity, so we have two drugs out there kind of run rating, you know, well north of a billion dollars. But this is still a huge market. So what do you think this really unlocks? And as you were just talking about, this is the only trial that's really run BCVA 15-letter law, so it's novel. But how do you think, as a physician yourself, how do you think this is going to be interpreted?

Well, I think, remember the number 20. So 20% of patients with geographic atrophy are currently receiving treatment today from only 20% of retina specialists in the United States. You factor that in, that there are no available therapies outside the United States for geographic atrophy. So first, this is a replacement therapy for currently available drugs that offer no functional benefit. So that billion-dollar run rate we see as a replacement. This drug is a replacement for currently available C3C5 drugs. But to that 20%, that demonstrates the potential opportunity for really transformative therapies. We saw this in the wet AMD space when you went from, for instance, photodynamic therapy to anti-VEGF therapy. The uptake was dramatically higher once you have meaningful therapy. So we believe that physician activation, patient activation will be quite strong when there's a drug that offers a functional benefit.

We've got some evidence of that, right? When you look at the Phase III, Lloyd alluded to it. We over-enrolled that study by 30 patients almost six weeks ahead of schedule. So there's real pin-up demand. So we think stepping right into the GA market, there's a real commercial opportunity, and we think we can expand the market. I mean, when you look at our data, our drug performs even more effectively in earlier-stage disease. You look, for example, in our Phase II data, LLVD less than 30 represents healthier eyes, 0 out of 56 patients, lost vision versus 17% on sham. That allows you to push earlier in the treatment paradigm, and we know there's a large cluster of patients who are sitting there, an even larger cluster of patients who are sitting there, and you can assess these patients using imaging techniques like EZ, et cetera. So stepping into the existing defined market is really, really large, and then pushing even earlier is really ginormous. So we're excited about this commercially.

Could you talk about kind of mechanistically how you guys differ from the C3, C5s, and why, you know, neuroprotective, you know, kind of agent like Bonaprovement is probably going to be more successful?

I'll start, and you should jump in on this. So what's important to note is all complement is not the same. What C1Q does is it recognizes transformations in disease tissue, localizes there, and drives this inflammatory cascade. What that means in geographic atrophy, geographic atrophy is a disease of neurodegeneration where you lose your photoreceptors, which are the neurons in your eye that are responsible for visual acuity. C1Q localizes there and drives the removal of these photoreceptors, i.e. the loss of vision. really, really important versus downstream approaches. So we are blocking C1Q right where it localizes there and protecting this entire process. So we're treating the disease process of geographic atrophy actually earlier than what has been done historically. You lose your RPE cells after you've lost your photoreceptors. You're more advanced in your disease as a result. So we really love this mechanistic differentiation.

Yeah, so the key thing to understand about C1Q is that C1Q in the eye, in the photoreceptors, binds to photoreceptors in disease, but they're still functional, right? So that's the first important step. The second important step to understand is that in geographic atrophy, as a neurodegenerative disease, photoreceptors are lost first before the RPE is lost. And then the third piece is that really the role of C3 and C5 is to clean up dead and dysfunctional RPE cells once they're no longer functional. So that gives you a sense of the time course of this neurodegenerative disease and why intervening at the level of C1Q early in the course of disease is critical compared to C3 and C5 later in the course of disease.

So that's kind of why we see retention or preservation of RPEs with C3, C5, but really no impact on vision, because they're just holding those dysfunctional cells in place. Exactly.

And listen, this mechanism is really, really worn and tried and true at this stage. I mean, it's the exact same phenomenon in GBS, if you think about it, where C5 has been in GBS, or eculizumab with Alexion ran phase two, phase three studies in GBS. Everyone has forgotten about that. Very midland treatment effect. We've come forward with C1Q that's blocking the disease earlier in the disease process. You're seeing very pronounced outcomes as a result. So it's an entirely differentiated mechanism of action. And this is our second time demonstrating it. It's a different compartment in the body versus the eye.

Now, you've talked about, you know, kind of creating this moat with non-approvement in GA. So you've got, you know, 24-month data, the data moat. What other kind of moats can you generate, you know, around this asset?

Yeah, well, I think the asset itself, and Lloyd used to talk more about this, but this is a very different asset than the first-generation approved therapies. First of all, it's non-pegulated. You have low viscosity. The administration is very simple with regard to that. And dosing. So we're initiating with a monthly dosing profile as we're running it in the Phase 3 study. But the concentration levels for vonaprumid is about 25 microliters, about a quarter of what you see with the approved ARPs, Sifovir, and Iservate. What that means is, one, it's easier to administer, but two, by increasing the volume of this drug, if you double it or triple it, we'll be able to dose this drug every other month or once a quarter, if you will, which is a really important life cycle approach without doing a reformulation so it's much simpler so we really are looking to is again build a moat around this and own this franchise outright and you would get new ip on something like that absolutely as is our ip's into 2040 so we've got long ip this is a wholly owned asset we've got a lot of opportunities to fully optimize this asset gotcha i mean well maybe shift gears to gbs so you were bringing it up so you know you guys have now had this forward data that came out, and maybe talk us through that and kind of the near-term

BLA filing.

Yeah, really excited by the forward data. I mean, first and foremost, it replicates what we see in the phase three study. You all will recall the phase three study was run in Southeast Asia to be the first and only placebo-controlled, fully randomized study in the history of GBS. Roughly 90 percent of the patients responded by week one. Yeah, 90 percent response rate is really, really significant. You rarely see that in a disease. Speaks to C1Q in its mechanism of stopping this disease process right where it starts and allowing for rapid recovery. What we're seeing in four thus far in 11 patients that have been treated and reported out is 100% response rate. So 100% of the patients improved clinically, meaningfully by week one in this study. So it's a really pronounced, significant outcome. And from a safety perspective, it looks very similar to placebo. There are a few patients that have a transient rash with the infusion. It goes away on its own. Otherwise, the safety events are attributed to the disease itself. So this is a highly differentiated data set. It's really important to contextualize the Phase III data. One of the topics that have come up from a regulatory perspective is, given that the Phase III was run in Southeast Asia, is it generalizable to the West? Well, for it's being run in the U.S. and Europe, we're seeing 100% response rate. And what's really important, again, just to keep bringing this back to our mechanism of action, is. That's notwithstanding differences in geography, differences in baseline disease severity, age, time to treatment. All of those things matter, but they matter far less than the mechanism of action in blocking C1Q in this disease. And so we really like forward in really validating what we see in the phase three program.

Gotcha. In terms of the BLA, so, you know, you'll have potentially filing that. And I guess, do you think that's something that we could see a BLA acceptance this year?

Yeah, really good question. So just regulatory package, there's a picture in full. We're on file in Europe. We're through day 120. We anticipate getting a final outcome with regard to this program in the first part of next year. So we're really excited about what's going on with Europe and the engagement there. Similarly, we're having really nice discussions with the regulators here in the U.S. So it's a very open dialogue, which from a rare disease perspective is quite refreshing. We're very much on track to file, excuse me, this year for the BLA and a The question of whether or not it'll be accepted this year really will be depending upon timing from an FDA perspective and the resources deployed to assess it.

We certainly are pushing for that to be the case. So I guess one of the questions we get a lot about this is around the market opportunity in GBS. And certainly the potential EU launch next year, so you can kind of walk us through how you guys are thinking about that. But generally thinking in the U.S., kind of the logistical component to, I guess, this type of product, the hospital product, and then overall kind of pricing, how you view that in context of what IVIG costs.

Yeah, really good question.

We think that GBS is a unique rare disease because it's a blockbuster disease.

As it sits today, 90 to 95 percent of patients get treated with GBS with an unapproved therapy that has a middling effect. And so bringing forward a targeted therapy where you're having a response rate between 90 to 100 percent, you would anticipate you're going to get all of those patients going forward. What we've done is extensive research on where the GBS patients show up year over year across the hospital systems. We know roughly 50% of hospital systems see roughly 50% of patients year over year. So that allows us to have a very concentrated commercial footprint in GBS. The key is making sure you get pricing and making sure you get on formulary. We think the formulary question is really fairly straightforward, given the outcomes of the drug, both from an efficacy and safety perspective, and it's a single administration, which is really efficient. And then just with regard to pricing, we have a really strong value proposition. Some of you all may have seen our health economic work. We know that the impact of GBS on an annualized basis in the health care system here in the U.S. is exceeding $20 billion. I mean, there's a really high mortality rate in GBS. We don't talk enough about it. In the general GBS population, if you're hospitalized, 10% are dying. If you're 65 and older, a quarter of them are dying. One out of four patients are dying. And so by getting patients better within a week, you really are bringing down all of those numbers. So that's the assessment that we're making. And we're doing this work right now on a hospital-by-hospital basis as well as at the system payer level. We're really showing the cost associated with GBS and the potential savings with TAN-Rupal-BARC treatment. And so we're encouraged by that. You can do the math on this with 8,000 patients a year in the U.S. With reasonable pricing, this quickly becomes a really accretive drug. And the cost of goods are really small. I mean, it's a single infusion with a really targeted commercial footprint.

And just going back to your comment around kind of the engagement with the FDA on this. So this has been a program that you guys have been working on for quite a while. I know it's close to you and your heart on this one and getting this one over the goal line. But I guess, you know, has there been a change in kind of the tenor with the regulators? And, you know, it seemed like when you kind of provided the update not too long ago, it seemed like something had changed, and ultimately, like, now you're kind of getting ready to file, and they're accepting of the data. So, you know, I guess, what was that? And, again, it seems like they're more accepting as, like, the EMA has been.

Yeah, I mean, I think it's two things. One, I think as we've engaged with the FDA over time, they certainly have gotten further up to speed on GBS. No fault of their own, but they just have not seen the GBS package in 40 years. So they're just further along on the curve. I think secondly, just from an administration perspective, this commitment to rare diseases is really at the forefront in the agency, and we see that commitment. And so we're really pleased with the way they've engaged with us more recently and the dialogue that we're having on the program. We feel like it's a really pretty straightforward path to getting the BLA filed and making sure it gets reviewed. And, you know, the data has to speak for itself at that point.

I mean, do you think this is a program that warrants an adcom for, like, more, like, educational purposes? Or what's your kind of thoughts on adcom and priority review?

Yeah, listen, I mean, I have to say from a company perspective, first of all, we like priority review. We have all the bells and whistles, and so we will be filing for priority review. We like the idea of an adcom. I don't know if it necessarily needs one when you have this. I have a response rate coupled with the safety profile. But educating on GBS in the marketplace is order business number one for us. We're doing so many things out there. You guys can go to our website. We've got gbs4.com where we are out educating right now on the disease, various aspects of it. We're in partnership with the Patient Advocacy Group with a 110 campaign. This is the 110th year in which GBS was discovered. So we're videotaping 110 patients around the country, actually around the world, to tell their story on GBS, et cetera. And you'll see a lot of that out in the atmosphere over the course of this fall. So an adcom would just further educate on the need to treat GBS immediately and with a therapy that provides really rapid benefit to patients.

And then I know in the EU you've kind of talked about partnering and kind of looking at that aspect. So I guess what's the plan post-approval in the first half of next year? Is it to go seek a partner or is it to kind of launch in a couple select countries yourself? What would you kind of execute on?

Yeah, so we've got term sheets for partnership deals. We have not executed on those yet. Just looking at the whole MFN landscape has really given us pause with regard to that. That being said, we're not going to commercialize the drug ourselves. We will be announcing at some point before the end of the year an approach where we're able to commercialize in Europe where we provide some oversight, but we're not providing boots on the ground, if you will, with regard to that. And look, we're really encouraged by that because we will be doing that with folks who are really experienced at doing this, I mean, getting this out to patients across the world, which is really important to us as quickly as possible. Gotcha.

I guess when you think about, you know, the current, you know, education you'll have to do around Tanner Poupart and all that, it does sound like there's been some more interest around other types of, you know, acute neurodiseases. What would those be where you could get out?

Yeah, no, listen, we think that this is a pipeline and a product. This drug works. There's no question about it, right? And it works rapidly, and it appears to be relatively safe. There are a host of other acute types of diseases. For example, MG crisis, Mycenae-Grivis crisis. Still a problem out there. These are the same treating physicians. And then there are one or two other diseases that are hospital-based, acute, that we're going to hold in our back pocket. But we anticipate, with approval of Tanner Rupert Bart for GVS, that we will be able to launch into additional related diseases that really fit the profile of a GVS-type opportunity to further just kind of advance this therapy. And, look, this is another wholly owned asset with IP that runs quite a wild force, and so we really want to optimize it.

Got it. And maybe the last asset, 1502, so Oral-C1S, maybe just a little bit of background on that program and where you guys are in terms of the development.

Yeah, this program's been a bit of a windy road, but one we've learned a ton about and we're still highly encouraged by. So this is the first ever small molecule turn in classical complement pathway targeting a host of antibody-mediated diseases like MG, CIDP, et cetera, et cetera. We've learned along the way this asset does have really meaningful drug activity. That being said, we've run into some formulation challenges. We know that the enteric coded on this asset has begun to break down in certain conditions. So we want to optimize that. We will release the phase two proof of concept data and then make a determination on the next step. I've not seen the data yet. We're waiting for the PD data. It's now in-house. The team is analyzing. I'm sure we'll see it shortly. And all of that is done at the same time. So that's why we don't have that data. This is an open-label study. Typically, you would see everything along the way. but PD is all done in this particular instance at the same time. So that's coming on that, and at that point we will announce next steps with regard to that program.

What should we be taking away from that program in terms of whether it be the PD effect, the efficacy, what will translate, particularly if you're going to have to do some reformulation work?

Yeah, we need to see drug activity. So we need to know that the drug's getting to the target and it's having an effect on the target. We would want to see some movement in some of the measurements as it relates to the PD market, at some of the downstream complement measures, as well as we continue to look at things like bilirubin, et cetera. So we want to look at some of the efficacy measures. None of that has changed from our perspective. And so what is encouraging is that notwithstanding seeing some of this compromise, the compromised enteric coding, we are still seeing some treatment effect, right? We're still seeing some drug activity. Whether or not it's enough to pass our bar, I have to see the PD data before we can make that determination. Gotcha.

And I mean, you know, to my knowledge, there's not very many, if any, other oral complement programs out there. So what's been, you know, kind of the secret sauce, or how have you guys been able to kind of figure this out, particularly given for, you know, it's a pretty ubiquitous target out there, you know, from your platform?

Yeah, it's a great question. It's a stepped approach, folks. So we started with monoclonal antibodies, which everyone does in complement. We're first in kind of the classical pathway, as you all well know. We've created more than 50 de novo assays assessing every component of the classical pathway, and we've made drug candidates against all of those. We did all of that before stepping into an oral construct. So taking those learnings really allowed us to really figure out how to advance an oral program into this space. And so now it's just making sure we can optimize this oral asset in a way to bring it forward. I mean, our focus from a company perspective is still the two late-stage programs, GBS and Geographic Atrophy. But we see, as you look out five, 10 years, that an oral and a complement space is absolutely going to be essential. And it's very much like MS or rheumatoid arthritis, et cetera. You see the advancement over time. We see that here. And so we're encouraged to be out in front. We're encouraged with the learnings that we've taken thus far and where this is going. Gotcha. And is there specific indications that you guys have thought about for oral C1S? Yeah, some of which I can disclose. I mean, we obviously like neuromuscular indications where C1S has been clinically validated, so that's the higher PTS opportunities. But I have to say, given the work we've done, as I alluded to, some of the assay work we have, we like some of these larger antibody-mediated autoimmune disorders in which a subset of the populations are being driven predominantly by classical complement activity. And so that allows us to get into areas that other C1S components have not gotten into or even FCRNs, et cetera. And so there's a wide swath of indications we can tackle with this asset once we optimize it.

And then maybe just talk about the kind of funding for you guys and where you guys are in terms of cash position and what's kind of currently funded.

Yeah, so everything's funded, as we sit here today. So we're funded into 2028, runaway into there comfortably. And that includes, obviously, the phase three readout with geographic atrophy through month 24, really important. We also announced an open label extension study, which is also funded as part of this runway. GBS, and the initial commercialization in the U.S. is also funded, which we're encouraged by. And then, of course, the small molecule through proof of concept. The small molecule after that, as well as the reformulation work, after that, the small molecule's got to pay for itself. So we've got to see how it performs. So we like where we're sitting. We also like that we're wholly owned with all of these assets. So we can be opportunistic and even offensive-minded in how we continue to bring in capitalization to continue to fund the company. And we like other indications, too. So, again, we will be looking to do various things with a win on GBS or GA at the end of the year, not wood, as well as getting GBS on file and approved, et cetera. This platform is delivering data. If you're going to be in the biotech space, you have to deliver data. That's what it's doing. And so we want to get it to as many patients as possible, and we look forward to doing that kind of with our next set of indications as well.

And I forgot to ask, so in terms of GBS, like, the footprint that you need in the U.S. from a commercial organization standpoint, because it sounds like you're doing a lot of education and awareness. What do you actually need on the ground in terms of sales and MSLs?

It's predominantly MSLs and then field-based market access folks. Again, you've got to get on formulary. You've got to get pricing. We will have a small sales force for key accounts, et cetera. All in, our commercial footprint is roughly 50 FTEs. So a very efficient commercial footprint for what we think is a blockbuster opportunity.

Well, Doug, I think we'll leave it there. Lloyd, thank you so much.