... I should have worn a blue shirt. Okay, well- You know, I just. Oh, that's good. Open mic. Sorry. So, welcome to the Cantor Global Healthcare Conference. I'm Pete Stavropoulos, biotech analyst with Cantor. With us, we have Annexon, a company I cover, and I'm pleased to introduce Doug Love, CEO. So, let's start off with an introduction of yourself, a brief description of the company, and, you know, your therapeutic strategy. Yeah. Hi, Pete, and thanks Cantor for welcoming in Annexon to this year's conference. Happy to be here. I think this is our fifth or sixth in a row, so we're excited by that. So I'm Doug Love, as Pete said, President and CEO of Annexon, founding CEO of the company. We started the company roughly 10 years ago, focused on the classical complement pathway, and importantly, what's unique about our approach is we're targeting the most upstream aspect of classical complement, which localizes on diseased tissue and drives a damaging inflammatory disease process in a host of diseases across the body, brain, and eye. What's unique about what we are doing is all of our programs are first-in-kind or pioneering, and we're really pleased with the consistency in the outcomes we've seen across all of our programs. We're led by three flagship programs. Guillain-Barré syndrome is our most advanced program, having completed a robust phase III program, and we're now in dialogue with regulators across the globe for approval worldwide. ANX007 in geographic atrophy, or ANX007, I'm sorry, in geographic atrophy, is our second flagship program. It's the world's largest GA phase III program, the only program to have demonstrated significant preservation against vision loss, as well as robust protection against photoreceptor cells. I'm sure we'll talk about all of that in the phase II proof of concept study. We fully enrolled the phase III study ahead of schedule, and we're looking forward to reading out on that in the second half of last year, next year. And last, but certainly not least, is ANX1502, first-in-kind small molecule program in the classical complement tech space. This is a translational stage, earlier stage program, but one we're quite excited by, and we'll talk more about how we're walking that down to hopefully bring that to patients. That's... So, you know, why complement pathway inhibitors? So with a number of complement pathway inhibitors approved or in development, you know, why do you see the need for an additional complement pathway inhibitor? Really good question. Yeah, so all complement's not the same. Most of the programs that have been approved in complement target downstream components of the pathway, C3 and C5. The challenge with that approach is, is that the inflammatory process starts at C1q, right at the start, such that by the time you get to C3, C5, you've had this build-up of this inflammatory cascade, which has caused significant inflammation and tissue damage in a host of diseases. So as a result, by targeting C1q upstream, what we're seeing is differentiated outcomes in many, many diseases, including ALS, Huntington's disease, GA, Guillain-Barré syndrome, et cetera. So we really think it matters which node in the complement pathway you target, and starting right at the initiator of the pathway, you can do no better than that. Okay. So, you are developing it in GBS. You know, you did run a phase III study. Just walk us through some of the basic outcomes for this study? Yeah, absolutely. So just a little bit on GBS. This is a really acute neuromuscular disease, number one cause of acute neuromuscular paralysis in the world, a really debilitating disease overnight that just robs people of their lives. Our program is a bit non-traditional in that we've run a really extensive program where we've conducted four studies now, predominantly outside of the U.S., with the aim of running placebo-controlled studies. The standard of care here in the U.S. is an unapproved agent with no well-controlled data, so we're unable to run comparison studies here in the U.S. So we went ex-U.S. to run this study. Suffice to say, we had a robust proof of concept data set, which then led to a robust phase III data set, and in the phase III data set in particular, we saw a really diverse set of outcomes. First and foremost, 90% of patients treated with ANX005 in the phase III program got better by week one. That is a staggering outcome. We know the unapproved drug that is standard of care, patients are still declining at week one, and week one really matters because that's when physicians are making treatment decisions about who goes to the ICU or how long they'll be in the ICU, ventilation, et cetera. And so being able to show improvement, getting patients up and on their feet immediately is really, really important. We also showed really good outcomes on related measurements, such as days on ventilation versus placebo. Our patients spent 30 less days on ventilation a ventilator versus placebo, 30 less days. They walked 30 days sooner. They're in the ICU, you know, 20 days less than on them treated with placebo, so a really profound effect on multiple measures. All right, so, you know, you did mention that you ran this out of the States and EU, but you didn't say why. Like, you did mention that, you know, you can't do a head-to-head comparison, but why can't you do a placebo-controlled study? Yeah, well, it's just unethical to run a placebo-controlled study here in the United States because of the debilitating nature of the disease. The way GBS works is typically, patients are completely healthy. They get some type of food poisoning, their immune system kicks on, triggers complement to rid the body of these cells that are associated with food poisoning. The immune system is then supposed to shut off and perform its normal function. Unfortunately, in GBS, it aberrantly reactivates, attacks peripheral nerves, and overnight, you can't work the remote. By day two, you may not be able to get out of bed. By day three, you could be on a ventilator. So it's a really debilitating disease that robs people of their lives. Not giving them any treatment was deemed unethical by all of the IRBs and treating physicians around the globe, candidly, when you had the standard of care available to give them. Okay. So that's why we're unable to run a placebo-controlled study here in the U.S. Okay. So I guess another question is, you know, that we've spoken about a number of times, is the neurotype observed in a Bangladeshi population is similar to the Western population, you know, namely, AMAN versus AIDP. Yeah, so there are two neurotypes for Guillain-Barré syndrome, and it really relates to which aspect of the peripheral nerve is being attacked by complement, but the diseases are the same. They're all antibody-mediated diseases for which complement is the key effector. You stop complement, you have the same outcomes. I will say that AMAN appears to be more of a severe disease, and typically, it's all gradient, typically more severe than what you see in AIDP. In the United States, the preponderance of patients have AIDP. Where we ran the study, the preponderance of the patients had AMAN. So we, in effect, had a higher bar to go against because these were more severe patients that we saw here in the U.S. That being said, when we looked at the patients in our study who had AIDP, the less aggressive form of the disease, our outcomes are even more pronounced than what we saw in the full phase III data set, and so on every measure, so we're really encouraged that not only can we treat patients who have a very severe aspect of the disease, we can treat those patients with a milder form of the disease and see even more rapid and durable outcomes as a result. Okay. And so, you know, I guess, some of the outcomes was... You did have two doses, thirty and, seventy-five, and, thirty outperformed seventy-five. Rationale for that? And, you know- Yeah ... you have shown some graphs. Absolutely. Yeah, really good, really, really good question on that. So with regard to two doses, thirty and seventy-five, it relates to duration of inhibition of the complement pathway. Both doses fully inhibit complement. Thirty inhibits complement for about a week, seventy-five inhibits complement for about two to three weeks. What's important about that disease, GBS is an acute monophasic disease. The disease process lasts from somewhere between one to three weeks. What we learned, and we see this now in multiple studies from others, as well as with IVIG use, is that you really want to inhibit complement for a limited period of time, just so long enough to stop the disease process, and then you want complement to come back and be part of the repair process, which is its normal function. What we learned in our proof of concept study, which was replicated in the phase III study, is that shorter inhibition is better. IVIG has seen that in the studies they've run, where they've done two doses of IVIG treatment. One dose of IVIG treatment outperforms two doses as well, so it's a very consistent outcome. Limited inhibition of complement, then allow complement back to help with your recovery. Okay. So, you know, for an approval, you need to conduct a real-world evidence study, I guess to do comparability. Just describe the real-world evidence study and, you know, how it was conducted. Yeah, absolutely. So, as I said before, we ran this program ex-US, outside of the U.S., because we cannot run placebo-controlled studies here. The study was run in Southeast Asia, in Bangladesh and the Philippines, where standard of care IVIG is not readily available, so it was deemed ethical to do so. We knew at that time, per agreement with the FDA as well as EMA, that to get an approval, we needed to demonstrate two things: one, substantial evidence on the phase III study, and then two, that the data that we generated in the phase III study was generalizable or comparable to what we would expect to see in a U.S. patient population. To do that, we ran a real-world evidence study in well, globally, where we looked at patients from our study, and we matched them with patients from a 2,000 patient natural history dataset called IGOS, International Guillain-Barré Outcome Study, that's out of Erasmus in Europe. There, we did a propensity score matching to match patients based on their baseline disease severity, which is the key prognostic factor for how patients are going to do. How severe is your disease at baseline? We were able to match every patient in our 30 mg per kg dose, the dose we're moving forward, with patients in IGOS to really satisfy that we had a comparable patient group to what we would see in the West. We went the additional step of also comparing outcomes with these matched patients versus those patients in IGOS who got IVIG, and there we showed benefit against IVIG on every measurement that we looked at, including the primary endpoint. All right. What are some of the key clinical and efficacy outcomes when you compare it to IVIG and plasma exchange, and, excuse me, which seems to be the more effective from the data you generated? I mean, you just did mention that you beat IVIG, but- Yeah. - a little bit of detail. Yeah, yeah. Go on to tell a bit more. Yeah, happy to. So starting always with week one, which is where we start, because you want to arrest this disease right out the gate, we showed a ten-point improvement on IVIG, highly statistically significant. As I said before, 90% of the patients got better at week one. At week one with IVIG, patients are still declining. So really important finding, there's not a lot of data on IVIG. And one thing I should note, this real-world evidence study was actually not done by Annexon. We sponsored it, but it was done independently by Erasmus and the university there, who's presented this in, you know, medical conferences, and they're in the process of publishing it. So they're fully standing behind their work there, and we quite like it as well. Anyway, so at week one, we showed 90% of patients getting better, IVIG still getting worse. Whereas at week four, week eight, we're showing on the disability scale that we significantly improve people's function and disability at those time points, whereas IVIG has a midline or mild effect there. And then we showed a durable outcome out to week 26, where nearly two and a half times more patients got back to a state of normal by month six versus IVIG, also statistically significant. So every measurement from a functional strength perspective, we outperformed IVIG. We also performed them as it related to kind of hospital value-based measures. So we got patients out of the hospital almost two weeks earlier than IVIG. We got them off the ventilator almost two weeks earlier than IVIG, less than... We got them out of ICU almost ten days earlier than IVIG. So really robust outcomes, and it stands to reason. So this is a targeted immunotherapy approach that we're pursuing here in Guillain-Barré syndrome. Very much like what you see in CIDP or myasthenia gravis, whereas IVIG is a nonspecific mechanism, and so their outcomes are a bit, you know, wobbly, I guess one would say. Why not combine the two? ... What's that? IVIG and, No need to do it. I mean, you see 90% of patients getting better, one, with our drug. Two, IVIG is five courses of treatment over five days of infusions. We're a single infusion, so it's super efficient for the patient as well as for the hospital and administration staff. And three, IVIG actually carries a black box warning, and really, when you look at our safety profile in our phase III program, looks very similar to a placebo. So the drug is really well-tolerated, and it's, you know, relatively safe. Whereas IVIG with the black box warning, you know, 12%-13% of these patients get thrombosis. Mm-hmm ... in Guillain-Barré syndrome. So we don't want to take that risk, given the outcomes we're seeing, and we're a relatively safe compound. Okay. And then, you know, sort of what are the expectations from the regulators? You know, what does the FDA want to see? What does the EMA want to see, you know, from the RWE? You know, what are the key analyses, each regulator wants for an approval? Yeah, maybe I'll start with EMA first, EMA for the MAA approval, since we're further along in those discussions. As I said before, for both jurisdictions, they're very consistent in that both want you to demonstrate substantial evidence out of your phase III program, as well as demonstrating this generalizability analysis in your real-world evidence work, that we've done. With EMA, we're further along in that we've had multiple discussions with them on the specifics of our programs. This dates back to our proof of concept study, where it was a placebo-controlled study that we won on. There we sought orphan drug designation in Europe with a higher bar there because IVIG is actually approved for Guillain-Barré syndrome on a compendium, not because they ran a study. And to get orphan drug designation in Europe, you need to demonstrate three things in our particular case. We need to demonstrate that the study that we run in Southeast Asia was adequate and well controlled and met the requirements for substantial evidence, which EMA agreed with. We also need to demonstrate that the real-world evidence generalizability analysis we did was appropriate to establish comparability or generalizability between our patient population in Europe, which EMA also agreed with. And then finally, we needed to demonstrate that we were likely to be substantially better than standard of care IVIG in that phase II proof of concept study. EMA also agreed with that. They wrote a 20-page, single-spaced document, really detailing the disease as well as our outcomes, both on the efficacy side as well as the generalizability side. So they have a rich background in what we're doing, and that's really important as we move forward there from a regulatory perspective. Once we got the phase III data, we then went out and did country-specific meetings with the local regulators across Europe, which really were quite productive. In fact, one of the meetings we had was with the Netherlands, really deep in the GBS space, Erasmus is there, et cetera. They do have a lot of research in this space. That meeting went exceedingly well, and the head of the regulatory group there actually raised his hand to be a rapporteur for the program. So we were delighted to see that he's been named as the rapporteur for this program. And we, of course, already have a written opinion from the Netherlands, and the second chair is Poland. So we're in really good position with regard to where we are in EMA and moving that forward, and we're excited. Looking forward to file the BLA or the EMA by Q1 2026, so all systems go there. Similarly, in the U.S., we've had I think 10 meetings with the FDA over the last 10 years on this program alone. This is a first-in-kind program. The FDA had not seen a program in GBS in 50 years, which is again different than EMA from that perspective, so we've spent a great deal of care in working closely with them. They've been really engaged and quite productive in the discussions and just first understanding the disease, Guillain-Barré syndrome, and why it's different from most any other disease one will see, and then two, our development program, including the alignment on substantial evidence for the phase III study in Southeast Asia and the real-world evidence analysis, so that's what they're looking for. Similarly, we've had good discussions with them on both. More recently, we met with the FDA in June, towards the end of the month, on the real-world evidence discussion. We'd already talked about the phase III study, and that was really a quite productive meeting led by Teresa, Dr. Teresa Buracchio, who is the office head for the Neuro Division. So really strong engagement from up high, and we really appreciate their collaboration on it. Quite a productive meeting. Once we got the meeting minutes, however, a bit surprised in an aspect of it, in that there was post-meeting comments that reflected meetings that occurred internally within the FDA, outside the purview of the company. And so some of the comments we're going back to them on just to make sure we are really clear on what they're thinking and what... You know, and whatever it is that they would be looking for as a result of that. So that's our next steps. We'll be back with them this fall, to really address these post-meeting comments that we just weren't a party to for those discussions. Sort of, what's the nature of it? It's all around generalizability. I'm sorry, I should say that. Yeah, so all of those post-meeting comments and even all of the meeting minutes from the June meeting are all related to generalizability, and I can say what they don't say. So what they don't do is call into question what we did from a phase III perspective or call into question our generalizability analysis. It appears that there could be a larger policy question in terms of what type of information would you want from programs that are run outside of the U.S. under today's kind of, you know, FDA leadership? Is it changing? So I believe there was guidance last year or two years ago. There's been guidance. There's guidance in the Federal Register on this. There's international guidance that companies follow,[crosstalk] and then we have- Specifically from the agency. Yeah. Yeah. Specifically, and then we have specific guidance on this program before initiating the phase III. And so whether it's changing or not, it's too early for me to say, before we have a discussion with them. All right. Have hands switched in terms of dealing with Annexon at the agency? No. Well, Dr. Buracchio has been with the program for the past two years. She started off, I think, 10 years ago. We first met with them. I think she was the clinical reviewer on the program, and she's matriculated up the organization, so she's been there. But of course, like most organizations over the last 10 years, there's been some ins and outs, I imagine, in that Neuro Division. So... All right. So you do have the FORWARD study, open label study, conducted in North America and Europe. Just, you know, walk us through the design, you know, how many patients you expect to enroll, and the rationale for conducting it. Yeah. So the FORWARD study is the first U.S. study in Guillain-Barré syndrome in, in forty, fifty years. We're super excited by it. The reason we're able to run this study is it's an open label study where everyone gets treatment, ANX005, and that's on the basis of the strength of our phase III data, where the physician population, the IRBs, et cetera, are really excited to give patients an opportunity with this drug in the U.S. Our purpose for doing the study is twofold. One is to get patients and physicians in the U.S. experience with our drug prior to launching in what we think is a very meaningful commercial opportunity. The second is it checks the box of we expanded the study to allow pediatrics into the study. Okay. So it allows us to pick up patients earlier, which is an important element for an EMA filing, that you actually have a study ongoing that allows pediatrics to be treated as well. So twofold, we love what we're seeing so far in the study in that we are really bringing sites online and really helping to harmonize their approach to treat GBS. GBS is very different than any other acute disease you will see, like stroke or something or another, where there are really robust protocols and consistency in how it's dealt with in institutional level and across the United States. That's not the case with GBS. We see that every institution does it differently, and so being able to harmonize how you treat GBS is important. In fact, one out of four patients are diagnosed with GBS upon first presentation, and time is nerves. You need to treat this disease as quickly as possible. Part of that is that there's never been an approved drug with, you know, sales reps, MSLs, and companies coming in to educate and to help assist- ... in kind of harmonizing how it's managed. So we're doing that as part of this study, and it's been really great to see. Have you enrolled any patients yet? We're gonna just hold off on... We've initiated our sites. We will do an update on the patients once we have a cohort that answers the question for us. Okay. Questions we want to answer is PK/PD. One, does ANX005 perform the same in the West as it does in Europe? In Southeast Asia, antibodies perform 99% the same. Geographically, it doesn't really matter, but we need to demonstrate- Not disease, but I mean, you did run the Huntington's disease- We've run multiple programs here in the U.S. with ANX005. Would the PK be any different? This is an acute disease. The studies we've run here in the U.S. historically have been chronic diseases, so we don't anticipate it'll be different- Okay ... but it's a box checking, and we want to make sure we do that, the PK and PD. We'll also look at efficacy. We want to carry through the, what we've seen in the two prior studies of 90% of patients getting better at week one. It's a really important finding and certainly will help as we commercialize this drug post-approval. So those are the two primary things we're looking for out of the FORGE study. Okay ... in addition to the experience aspect of it. All right. Does any of this have to do with generalizability, with the FDA? It hasn't yet, but we will see. TBD. We'll come back on that. All right, so did you initiate it, or did the agency ask you? No, we initiated it. Yeah, we had no interactions with the FDA with regard to the FORGE study. We did that on our own. Of course, we went through the normal channels and submitted the protocol, et cetera, received no comments or anything, but that was not a mandate when we initiated the study. Okay. Yeah. All right, commercial prospects. Yes. Just run us through it. Let's go. Really excited about this. So there's a minimum of 7,000 patients treated every year, and I say a minimum because we're just completing our health economics work, which we'll release in the fall. No one's done any extensive analysis of Guillain-Barré syndrome ever. Forget about it, bar none. And we're seeing that it's likely more than that. We're also seeing that the cost to the healthcare system is dramatic. I mean, it's in the neighborhood of $3-$4 billion a year to treat 7,000-9,000 patients, so it's a really significant burden. What we like about it from a commercial perspective is it's a super efficient commercial footprint. 175 physicians or Right ... 175 hospitals control 60%- ... of the patient population, which we love. So this is an incidence-based disease. It's really driven by population, so we know exactly where to go. In fact, 26 hospitals control 20% of the population. So with a really crisp sales force and MSL group and then field managed care, we think this is a real blockbuster opportunity. The one thing I left out is 90+% of patients get treated for GBS. Many of them are getting treated too late, so we need to move that up, but everyone's getting treated, so it's a ready market right there for you. The other thing I will note is that from a payer mix perspective, while this is a hospital-based disease, two-thirds of patients are reimbursed with commercial payers. That's really, really important. When you think about CAR T's, for example, they're charging millions of dollars in the hospital. How does that work economically? They're commercial payers. It's the same paradigm for GBS. We do not anticipate charging anything near that, but, we like that we have a real robust path to reimbursement, with regard to this program. Okay. We have about six minutes or so left. Oh, I'm sorry. I'll go- Let's quickly just touch on a molecule, which is, you know, I think there's a lot of interest in it and in the pathway, ANX1502. Yeah, ANX-1502. Yeah, first small molecule program, the classical pathway. I'll be quick about this. This is a program that we started eight, nine years ago, really to bring forward kind of the first oral approach to a host of autoimmune diseases. When you think about, for example, rheumatoid arthritis, MS, you can see how those fields evolved, where they started with, you know, monoclonal antibodies, infusions, they moved to subQs and then ultimately to orals as competition has exploded. We're seeing that in MG, CIDP, and other indications where you see a lot of players that are trying to differentiate on the margins between an infusion or a, a subQ. We've gone hopefully towards the front of the pack with an oral.... full stop. We started a preclinical program where we did a CH50, where we compared our molecule with approved drugs targeting C1s in the space, and sutimlimab in particular, to really establish our target drug levels and exposure we need to see to demonstrate efficacy. From there, we ran a suspension study in phase I to show PK tolerability. That went well. We then moved to a film-coated tablet. We ultimately want to be in a pill form. That also went well from a PK exposure perspective. Saw some tolerability in that study that we thought was related to emesis and nausea that we could bypass with an enteric-coated formulation, which we were able to successfully do. We moved to enteric-coated, ran another healthy volunteer study. There, we demonstrated similar or better PK profile, but really more or less minimized the tolerability topic. So that was really quite encouraging. We are now in our first proof of concept phase study in patients. What's important about that, these are patients where complement is really highly elevated. This is also the first group that we've run a study in where patients are not fasted. So in the healthy volunteer studies, all of the subjects were fasted. What we've seen thus far in the proof of concept study is in patients who are fasted, our exposure levels are fivefold higher than what we want from a target perspective. Like, we're super excited about what we're seeing. On the other hand, and when patients are taking the drug with food, it's washing out, the drug in the stomach before it gets to the intestines. As a result, our exposure levels are minimal. Notwithstanding. And this is BID dosing, so every patient is their own individual control, if you will, with regard to that. Notwithstanding that, we're still seeing very nice trends on bilirubin, et cetera. So what we are doing is we're taking a handful of patients, re-treating, and a couple of new patients as well, and we're looking at them fully fasted on both doses to really confirm what we've seen thus far. Once we have that data, we'll release it and hopefully, you know, knock wood, everything plays out. We're just walking this down. It's a first-in-kind approach. I tell people all the time, it is not off the shelf. People talk about timelines, et cetera. You can't really do that with a translational program of this nature. I think the question we should be asking is: why isn't everyone going after a pill in this space? And they are not. It is not for the faint of heart, but complement's what we've been doing over the last ten years, and our research goes back twenty-five years, so we know complement pretty well. Right. So, are the patients that were originally on it staying on? I don't know if I just misheard you. It's a four-week study, so they're off. It is. Okay. Some of those we will bring back- You will ... and retreat with this new fasted for both doses paradigm for four weeks. All right. I know you just said, you know, timelines. But timelines? No. No, listen, we're taking learnings all the way, along the way, which we're excited by, and we anticipate updating on this by the end of the year. Okay. Yeah. I guess, what indications would you go after? We like all the neuromuscular indications, of course, but we like more than that. I think with an oral, gives us an opportunity with the dosing flexibility and other aspects of it to go into a range of diseases that some of the programs from an IV perspective aren't in yet, so infused perspective. Right. When you think about, like, the need to inhibit complement, you know, for different diseases, it's to a certain degree, right? So for MG, you can get away with 90%, you know, inhibition and so forth. Our approach is full inhibition. I mean, if you can get away with less, we will be able to do that with the pill because you can titrate the dosing. But we're starting off with full inhibition because typically, complement-mediated diseases, you want to knock all the way down. We are seeing some more recent data that suggest maybe that's not required. We saw some data released last week, with regard to that, which- I was gonna ask what's your take on that? It's a little tricky. It's a little flute- It's interesting. or is it actually... It's hard to know. What do they have? 75-78%. Seventy-four, I think it was. Yeah, 74, yeah. So it's a little hard to know. I mean, that aspect of it is not complement, though, right? As from an inhibition perspective. And I mean, the question I'm still asking is: how much better do you need to see from an efficacy perspective with a second, third, fourth, fifth subQ program in this space to win from a commercial perspective? I think we're not having the right discussion. I think that these drugs are gonna have similar efficacy. I mean, that's the hope anyway. It's been validated with the prior target. But how are you gonna win on the commercial side as the third or fourth subQ? I don't know the answer to that, but that's gonna be the fight. I've seen how that's played out in RA and MS, and you need an oral if you want to win it, is what I've seen, so. Oral, and, I think where you're inhibiting, no black box. And no black box. Safety's very important. Absolutely agree. All right, we got one minute left. Just zero, zero, seven timeline. Kind of talk about that in one minute. So ANX007, so this is the phase III program in geographic atrophy. World's leader. It's a blockbuster. We love it. We're super excited on the data on the functional side as well as on the structural side. The phase III enrolled two months ahead of schedule, more than 30 patients, over-enrolled globally. Physicians are on board, and, you know, well-run studies tend to do better, so we're super excited by that. We'll have data second half of next year, and hopefully get this out to the 8 million patients around the globe impacted by this disease. Right. Are you thinking about keeping it in-house or...? We're keeping this thing as long as we can keep it. All right, then. We like it. And look, there's a paradigm. I mean, there's precedent for that, right? Of course. We saw with the other approved GA programs, which has really helped make the market. So coming in now will be a bit of a more efficient approach to commercializing with a very differentiated profile. Okay. And, if we're sitting here a year from now, what do you want to say that you accomplished? Listen, GBS needs to be approved. Mm-hmm. Let's get that out to the patients around the world. I mean, these patients are really suffering from that disease. GA, let's turn over the cards and crush that thing, right? Like, and again, we're preserving vision in an elderly, vulnerable population. Don't get me going on that, but it's really important that we protect this population, and the world is aging, right? And then we want to get this small molecule going in a range of different diseases. We think we can help a lot of people in a way where they can take this from their home in a very comfortable, safe way, where they don't have to deal with needle phobia, they don't have to go get an IV, et cetera, and get them back and helping them live their best lives as well, so. All right. Well, thank you very much for attending our conference and the fireside chat, and look forward to all the updates. Thanks, Pete. Thanks for having me.