Welcome everyone to the 42nd annual JP Morgan Healthcare Conference. My name's Anupam Rama. I'm one of the senior biotech analysts here at JP Morgan. I'm joined by my squad, Grant Grover, [Lorea] Hall, Malcolm Kuno. Our next presenting company is Annexon, and presenting on behalf of the company, we have CEO Doug Love. Doug? All righty. Thank you, Anupam, and thank all of you today. We're delighted to be here to provide an update on Annexon and what promises to be a transformational 2024. This will be the year where we release our first registrational dataset, and just march ever closer towards our mission of helping millions of patients suffering from complement-mediated diseases. I'll be making forward-looking statements this afternoon, and we invite you to look at our materials on file. Annexon is a late-stage clinical company targeting the classical complement pathway to treat a host of different diseases in the body, the brain, and the eye. Unique to our mechanism is that we're targeting classical pathway inflammation right where it starts on diseased tissue, to stop this disease process and produce robust functional outcomes in a host of autoimmune, ophthalmic, and neurodegenerative diseases. On the basis of this data, we've built a robust portfolio of multiple indications, and with two well-developed proof-of-concept datasets, we are now advancing two distinct drug candidates into registrational programs, which we're quite excited about. They have the potential to produce a significant market opportunity by treating millions of patients in the near to mid-term, and we're well-funded to do so with capitalization into Q2 2026. Now, as I said before, our mission at Annexon is to help millions of patients and their families suffering from devastating complement-mediated diseases of the body, the brain, and eye. The unifying principle across all three of these areas is, of course, stopping classical complement inflammation right where it starts on diseased tissue, to provide the most complete protection against this inflammatory disease process right before it starts. We've built, over 10 years, as I said previously, a robust portfolio targeting indications in each of these therapeutic areas, and we've done so in parallel, allowing us to leverage learnings and resources across the board, which has enhanced our overall PTS over the portfolio, as well as these individual programs. That, of course, gives us maximum optionality on how to advance this portfolio as a whole, as well as to monetize it at the portfolio level and at the therapeutic area level. Key to what we're doing, of course, is our science, which was discovered by Annexon scientists more than 10 years ago and has been developed since then with a host of external scientists and folks in the medical community. Excuse me. Our target is C1q, the initiator of the classical complement pathway. It is a recognizing molecule that localizes on a diseased tissue, anchors the classical pathway, triggers its activation, and drives this robust inflammatory disease process, resulting in inflammation and tissue damage in a host of different diseases. By blocking C1q, we're able to block all upstream inflammation and downstream inflammation, including targets at C3, C5, and C9. That, of course, is quite distinct from targeting downstream complement targets like C3 and C5, which do not block upstream inflammation and tissue damage brought on by immune cell recruitment and attack. As a result, we have consistently produced unique or differentiated datasets in our lead indications, including Guillain-Barré syndrome in the body, Huntington's disease in the brain, and geographic atrophy, more recently, in the eye. Based on our science, we've, as I said previously, built a diverse and robust portfolio of complement pipeline inhibitors. There are three things I'd like you to take away with regard to our portfolio. First and foremost, each of our drug candidates have been exceedingly effective in blocking C1q and the entire Classical Complement Pathway down through C9, which, of course, is essential to produce unique outcomes. Secondly, through strong execution, we've been able to advance each of our programs as planned, and importantly, as we've advanced, we've increasingly received regulatory recognition and support to advance to the next stage. And finally, we have a host of proof-of-concept datasets across this portfolio. Notwithstanding that we're targeting three different compartments, the body, the brain, and the eye, it appears that by stopping complement right where it starts, we are indeed stopping this inflammatory disease process before you have too much damage, which is allowing us to generate significant functional data. As a result, we're more encouraged than ever about the outlook of this portfolio, and we're excited to be moving towards our mission again of bringing these therapies to millions of patients in need. First and foremost, however, is dealing with 2024, which, as I said at the outset, promises to be a transformational year for us. Here, we're sharply focused on three core priorities across the portfolio. The first is delivering our first placebo-controlled pivotal dataset in Guillain-Barré syndrome. This is indeed the first placebo-controlled study in GBS in over 40 years. It's our third study in this space and is supported by robust proof-of-concept data, which I'll show you momentarily. The second is we'll initiate a global phase III program in geographic atrophy, using vision preservation as the primary endpoint. This also is a first-in-kind program, supported by robust proof-of-concept data... and allows us, or it permits us the opportunity to potentially own the entire market. We're incredibly excited about this program. Finally, we'll advance our first-in-kind oral drug candidate, ANX1502, into a clinical proof of concept study. We'll talk more about this, but suffice to say, this is the first oral compound in the classical complement space, allowing us to target a host of antibody-mediated autoimmune diseases, which are currently being treated by every other week IV therapies. I'll talk about each of these programs in turn, starting with GBS. For those of you who may not be familiar with GBS, this is a devastating antibody-mediated autoimmune disease. It really impacts patients who one day were completely healthy, and the next day, had an autoimmune attack that rendered them essentially paralyzed. The picture here is a pic of a patient, a GBS patient, Shane, a 53-year-old financial advisor, who very much could be like you and I. One day, Shane had food poisoning. The immune system or complement kicked on, cleared the body of his food poisoning, and for whatever reason, two weeks later, it turned back on and attacked his peripheral nerves. That rendered Shane in a debilitating state. As you can see here on the left, Shane had to completely learn how to rewalk. He had to learn how to, in effect, get his life back and function over the course of many, many years. And that's what's so unique about GBS. It's an acute monophasic disease that comes on spontaneously and completely changes the direction of patients' lives. Unfortunately, it impacts greater than 12,000 patients a year globally, and there are no approved therapies in the U.S. to treat this disease. IVIG is used off-label to treat the disease because physicians need something to try or to slow or halt this disease. However, notwithstanding IVIG therapy, there's still significant burden on patients. One in four patients are going to progress with GBS to a ventilator. Nearly two-thirds of the patients have significant hypertension, which takes months, if not years, to recover from. 65% of the patients have lasting fatigue, and this is not, "I'm tired." This is: "I cannot perform activities of daily living. I can no longer work or function." And still, 5% of patients here in the U.S. with GBS die from the disease. So it's a really underrepresented disease in the sense that it has not been widely studied, and it's time to do something about it, which we're excited to do. And what we're excited about is what we've done already in our proof of concept study. As I said before, this is the first placebo-controlled study run in GBS in 40 years, and there we showed some very unique outcomes. First and foremost, on the left top panel, distinct from IVIG, which is in blue, ANX005, which is just to the right of the blue line, fully shuts down the classical complement pathway. So we are stopping this inflammation right where it starts and completely and immediately. We're doing that within 24 hours of the infusion of an ANX005, which is incredibly important to arrest this disease right out the gate. By doing so, we saw impact on multiple measures of Guillain-Barré syndrome, including impact on muscle strength. Impact on muscle strength at week 1 is the key prognostic factor for how all patients are going to fare with this disease over the next months and years of their lives, and it was gratifying to see that ANX005 in red had a meaningfully different outcome than placebo in this group. We also had an impact on neuronal damage, as measured by NfL on the bottom left panel. Again, ANX005 in the red showed a 30% reduction, which is important and was statistically significant. But what's even more important is that we sped up the recovery in these patients by reducing this NfL by week 2, so early on in the disease process and allowing patients to then be able to recover thereafter. And all of that translated into a whopping effect on the GBS Disability Scale, the approvable endpoint in this particular indication. Here you can see in the right bottom that nearly a third of the patients showed a 3-point improvement on the GBS Disability Scale, which in effect means that patients who entered, who came into the study on a ventilator, within eight weeks were able to walk with a bit of assistance. These are types of outcomes that have not been seen historically in this disease, and so we're really encouraged for the outlook on our phase III program. Here's an example, or here is the design of what we're doing in our phase III program. This is a robust, well-designed, well-powered, and exceedingly well-executed study. We initially targeted 220 patients to enroll in the study. We over-enrolled the study over to two, to 241 patients, which we're encouraged by, and we were super intentional about the types of patients we allowed into the study. For example, we only allowed patients who had disease within 10 days of signs and symptoms because those are the patients where you have an opportunity to immediately change the course of their disease. We also took patients who are what are considered disabled or severely disabled. As you can see on the disability scale, just under the trial schematic, those are patients who are at 3 or above on the disability scale, meaning they could not walk or needed assistance walking, were bedbound, or on a ventilation. Now, the win on this study is really fairly straightforward. We're looking to show that 2x more patients being treated with ANX005 show a benefit over the course of the GBS Disability Scale versus placebo. We more than exceeded that in our proof of concept study. We powered this program a bit more conservatively, and so we're encouraged by the outlook that this has the potential to be the first placebo-controlled data set showing statistical benefit in this really debilitated patient population. We're also looking at other measures that we think are quite important for the patients, the physicians, and for the market more generally, which include reducing the number of days in which patients are on ventilation, reducing the number of days patients are in the ICU or in the hospital, et cetera. Now, we'll report out on all of this information in the first half of this year. In fact, we will report out on this data in Q2 of 2024. Now, turning to our second flagship program, geographic atrophy, which is being treated by a separate drug candidate, ANX007. That's a Fab fragment that is injected directly into the eye. As I said before, this is the first and only program that is using preservation as vision as the primary endpoint in this study, which is exceedingly important and candidly near and dear to our hearts. Shown on this slide are a couple of folks who we know quite well. Paul is an 85-year-old patient with geographic atrophy, and Nancy is his wife and caregiver. These are the aunt and uncle of the core team leader for geographic atrophy here at Annexon. So this is a program, again, that lives inside of us, and we're playing with our hearts and minds to try to bring these patients functional benefit who are suffering from blindness. For those who don't know, geographic atrophy is a chronic, progressive neurodegenerative disease that results in vision loss over a period of time. It impacts millions of patients globally and more than 1 million patients in the U.S. alone, and there are no approved therapies anywhere in the world to treat the loss or preservation of vision in this patient population. Really, really important because losing vision in this population that oftentimes is elderly, 80 years and plus, is robbing these folks of their independence. They do not have the ability to function and operate as they did previously. In fact, Paul was an exceptional photographer who can no longer participate in these activities, and so there's a mental and a physical stress associated with this disease that he and Nancy are grappling with. And what are we gonna do about it? Well, I'll come on to that shortly. The measurement we are using for this study is called Best Corrected Visual Acuity 15-letter loss. What's that mean? That's shown here on the left. That represents a patient who has the inability to read 15 letters on the eye chart, on the light, on the left, which shows up as loss of central vision, as depicted here on the right. These patients can no longer see their family and their loved ones. They can no longer cook their own meals. They can no longer drive their own car. In fact, when you have BCVA 15-letter loss, by law, you're required to turn in your driver's license, so it's a significant disease. For us, in assessing this endpoint for veracity, we required that patients demonstrated 15-letter loss on BCVA on two consecutive visits. And I'll show you some data from our proof of concept study that makes us super, super encouraged about that. First and foremost, we showed a statistically significant dose-dependent preservation against vision loss, shown in the top left panel. You can see in the every month group in red, 5.6% of patients lost vision, whereas in the sham treatment group, 21% of the patients lost vision. We also preserved vision over time. When you look at on the top right, over a 12-month period of time, 73-- we reduced the risk of patients losing vision by 73%. That is a significantly high number and very important for the patients who are suffering from the disease. We went further to look at the impact of our drug, ANX007, by studying those patients in the study who had geographic atrophy in both eyes, called bilateral geographic atrophy. We treated one eye, and one eye we treated with sham, so it did not receive drug. And what we see in the sham group, no patients had preservation against vision loss. However, on drug, similar to what we see in the prior endpoint, we had a 74% reduction in loss in the treated eye versus the untreated eye. What's that mean? The drug is having a biological effect. It is preserving against the loss of vision, which is obviously very, very important. And perhaps my favorite part of the data is this last slide here or panel here on the right, where we're showing patients who are not getting drug in the top line. That is the sham eye. As you can see, over 12 months, those patients are losing their vision month-over-month over the course of this study. The patients beneath that in the red and blue lines are the ones getting ANX007, and we preserved that vision, again, that vision over the course of the study. However, once we stopped the drug at month 12 and moved into the off-treatment period, we set a new baseline for the patients, but that preservation against vision began to go away. Another confirmation that that's a biological effect by your drug candidate, and it can't just be chance. So we're excited by this overall proof of concept data, but what we think is only partially important, what we're really encouraged by is that the regulators have also signed on to what they've seen in our data set. In our phase II study or a meeting with the FDA, we have full alignment with them that BCVA 15-letter loss will be the primary outcome in the measure in this study for the first time ever in geographic atrophy. Importantly, there are no requirements on us to study any anatomical biomarkers or other surrogates for vision. What matters for this elderly, vulnerable patient population is vision. The FDA globbed on to that, and that's what we'll be doing in our phase III program. We're also pleased to receive PRIME designation in the E.U., submitting this data set there as well. For those who are not familiar, PRIME designation is akin to breakthrough designation in the U.S., and you can see the quote here in the award of, granting of designation of, of PRIME designation for this program. Really, the consistency of the data, the robustness of the data, and preserving vision is what the EU globbed on to, and so we're really quite encouraged that we have not only a strong clinical data set, we have regulatory support to advance this into a phase III program. That's just what we're doing. In fact, we're not running one program, we're running two programs. The first program is our ARCHER II study. That is designed to replicate almost exactly what we did in the proof of concept study, which is called ARCHER. This is ARCHER II. The primary endpoint being BCVA 15-letter loss. The endpoint, time point is 12 months. That'll be the primary readout, and we will follow these patients for another 12 months of additional treatment to build a robust safety database with regard to this program. The second study is an injection comparator study, and we will run that second. That is a study that we will be running against SYFOVRE. That is one of the approved therapies in the GA space, which have been approved on a surrogate biomarker for vision. So fundus autofluorescence, slowing or lowering of lesion growth. We're quite encouraged to go against this drug in a head-to-head contest so that we can make very clear to the patient population that we are trying to do something to change the course of their lives. We know a lot about SYFOVRE. It's a great drug for treating lesion slowing. However, in three studies, in more than 1,400 patients, it's had no impact on vision, and so we feel quite optimistic about our opportunity in this program. Our aim, candidly, is to treat every patient who can benefit from this drug and preserve their vision at a vulnerable time in their life. Finally, our third flagship program, ANX1502, the first-in-kind oral small molecule program. Now, one thing I failed to say with GBS and GA, and I'll say here, all of our programs are stopping complement right at the start. Please keep that in your mind. If inflammation is driving the disease process, it's far better to stop it right where it starts before the train gets going. We're doing that here, too, with ANX1502. As a small molecule, we're targeting part of the C1 family, activated form of C1s. What we like about that is we're only targeting complement that is activated in part of the disease process. Other aspects of complement we're leaving intact, which we think is important from a safety perspective, and affords, and of course, it's an oral compound with twice-a-day dosing. We recently completed a healthy volunteer study, and it met all of our objectives. It was safe and well-tolerated, with no serious adverse events and no significant clinical lab findings. And importantly, in those healthy subjects who had elevated complement, we were able to reduce that complement rapidly in a pharmacodynamic assessment, which is quite encouraging. And perhaps most importantly, in a multiple ascending dose, all three of the doses that we took forward with repeat dosing in this study exceeded the target drug levels that we had for a pharmacokinetic perspective. In fact, the top dose is almost fivefold higher than what our goal was in this study. ANX1502 is looking like a robust therapeutic that we're really intentional about advancing. The next step for this program is to initiate a proof of concept study in patients, in cold agglutinin patients, to quickly validate our impact on active complement in a diseased patient population, which we'll initiate the first half of this year with data in the second half of this year, and then onward from there. What we're continuing to do with this molecule is to attack a range of autoimmune conditions, starting initially with neuromuscular conditions that are really difficult for patients to live with. In fact, they have a hard time getting out of bed. Many of them cannot work and function, can't go to church, et cetera. We're going after these drugs. Many of these drugs have approvals with downstream complement approaches, and so we think we have the potential for two advantages over these. One, by blocking upstream, we think we have a more efficacious approach. We've seen it in other diseases. We expect to see this here, too. And two, we're gonna offer them a pill so that they can get the treatment in their home, in a comfortable, confident setting. So we're really encouraged by that, and we look forward to getting started on these studies after completing our proof of concept study. So let me bring you back to our mission. We're doing quite a bit, and it just plainly is. We're playing with our hearts and mind to help millions of patients suffering from complement-mediated diseases of the body, brain, and eye. We've been at this now for a decade. We know as much about this pathway as anyone in the world, and we've been in more diseases than anyone in the world with regard to this target, and we're well-positioned to do so. 2024, as I said before, promises to be a transformational year. We're well-funded to achieve all of the objectives you see here on the right. In the first half of the year, we will have GBS data in Q2. We'll initiate our GA programs in the middle of the year, and we'll have the ANX1502 CAD data in the second half of the year. So plenty of catalysts over the course of this year to continue towards achieving our mission. And we have a robust set of next-wave programs, and one of the things you will notice about all of our programs, these are devastating diseases, folks. Most all of these programs do not have disease-modifying therapies that change the course of a patient's life. We have really nice data in Huntington's disease that show a differentiation in blocking complement upstream versus downstream. Really encouraged by that. We'll release data in ALS later this year, and we have early data in lupus nephritis. These next-wave programs provide us optimal optionality on how we want to advance them, whether we do this ourselves or we do this in collaboration with others. And we'll be pursuing those discussions over the course of the year to do what's most effective in getting these drugs to patients as effectively and efficiently as possible. And so I'll close here. We're, we're excited as any time we've been in this company. You know, drug development is a hard road, and after 10 years, we're still standing, and we're standing stronger than ever, and it's really because of a few things. One, it's our approach. We're stopping this pathway right where it starts, and there's no question that inflammation is bad, right? So you want to stop this train before it gets going. Two, we've got an awesome team. We've got hundreds of years of drug development. Unfortunately, everyone pretty much looks like me with gray hair and a little haggard. But... and three, we're having a little fun. This is a thrive year for us. We look to really reshape this entire marketplace with what we're doing. And so with that, I'll close, and thank you for your attention. Thanks, Doug. So for the audience, live and on the webcast, I just wanna remind folks of three things. There are three ways to ask a question, right? Live, you can raise your hand, and I'll call on you. That's old school, right? There's a new school way. If you have access to the question portal, you can submit a question. It'll show up on the iPad, and I'll ask it for you. And I guess there's, like, an intermediate approach where you can just email me, and I'll ask you the question. So, but I will start. Okay, please. Yeah. Doug, so on the GBS pivotal study, maybe could you describe the primary endpoint, how it's measured, and how it—what it's power to show? Yeah, absolutely. So the GBS Disability Scale, and I'll see if I can click back to it while I'm answering the question, is a seven-point scale. Zero is normal, as you can see here, and each step on the scale is a very discrete scale, a step, right? So one is running, two is walking unassisted, three is walking assisted, four is bedridden, five is ventilated, and six, unfortunately, is mortality. What we're looking to do is to show that 2x the amount of patients on ANX005 versus placebo statistically got better across the shift, the scale. So we call it 2x higher proportion of patients improved with our treatment versus placebo. This is an approach that we did in our proof of concept study, again, as I said, where we were able to demonstrate this. We also have briefed similar data like this that we submitted to the EU, and we were granted in late fall orphan drug designation by EMA, based on an analysis of this, of this sort. Okay. And then remind us of the severity of these patients that are being enrolled, and I guess you kinda told us what's clinically meaningful in your opinion, which is 2x getting better. So how quantify that for us. The patients who are in our study are 3s, 4s, and 5s, and so what we're looking to do is to shift these patients to better across the scale. So if you came into the study as a 4, we're looking for 2x more patients moving to a state of good, so perhaps a 0 or a 1 or a 2 or 3 versus a placebo in the study. Got it. Hi, thank you for the great presentation. The medical rationale of the recent diagnosis criteria of less than 10 days makes a lot of sense. I was wondering if you could expand on the logistical or the implementation side of that. Like, how do you think that it might... how that might affect the label, and if it meaningfully affects the addressable patient population in any way? Yeah. I have a follow-up question on GA later. Okay. Really, really good question, and a really important question because time from symptom onset is a key prognostic factor for how patients will fare with GBS, second to baseline muscle strength. The thing about GBS is it's such a devastating disease that when patients who are otherwise healthy begin to have tingling sensation in their lower extremities and are no longer able to move their limbs and many times lose their ability to breathe, they immediately show up in the emergency room. So in the West, patients show up in the emergency room within three to four days, and outside of the West, Western population, it's typically around six or seven days. So we have no trouble getting these patients immediately, but we still go through a very rigorous validation process to do so. We both interview the patients, or the physicians interview the patients, and separately interview the family members to really understand when did patients first starting having signs and symptoms of an inability to, in effect, move, to get out of bed, to be able to walk. Do you expect that this will be incorporated into label, the final? It's hard to say at this point. We haven't had detailed discussions with the regulators, but I will say that globally, GBS is treated earlier than not. If you wanna have an opportunity to repair these patients, it's pretty well known. And again, there's nothing like it. You know, it affects people of all ages. You're normal one day, and the next day you cannot move, so you're going to the hospital. Whether it's in a label or not, we anticipate it'll be used that way. Thank you. And on the GA slide, the competitor with the SYFOVRE has mentioned that they will prioritize Germany as the initial, like, launch site. How will the upcoming EU regulatory decision on that end? Would that possibly affect how you approach the sham study? It won't affect the sham study at all. The sham study will be global in nature. It'll be both Europe and the U.S., but it could affect the ARROW study, the comparator study against SYFOVRE. If they get an approval in Europe, then we will run a study that's in both Europe and the U.S. If they do not get an approval in Europe, meaning you can't get drug there, it'll just be a U.S.-only study. Okay, thank you. Thank you. Good questions. Following on the geographic atrophy question, strategically, why even run ARROW? It's a head-to-head study. There's probably some risk there. It's not like SYFOVRE has shown prospectively any type of vision benefit or loss of vision decline. Yeah, really good question, and listen, we like SYFOVRE as a drug. We think it's an effective therapeutic to the extent it is slowing lesion growth. But the key question with that is: What's that mean with regard to vision preservation? And we just plainly have not seen any impact on vision across three studies in 1,400 patients. And I just... Candidly, this is a vulnerable patient population. This is an elderly population that's being robbed of their ability to function, and so we think it's important that everybody gets a drug that gives people an opportunity to get their lives back. A couple onto that, the regulator, FDA's in particular, would love to have an injection comparator in one of the eyes, and the study with SYFOVRE meets that objective as well. Questions from the audience? Just quickly on GBS, going back, there are no U.S. patients in the pivotal study, so how do we think about a U.S. approval process versus global? Yeah, excellent question. So the GBS study is a study of ANX005 against placebo. So it is not against the standard of care in the U.S., which is IVIG. And the reason for that is IVIG is not approved in the U.S., and IVIG will not be approved in the U.S. because they have never run a phase III program against a placebo arm. They've run multiple phase III studies, and the FDA has never given—granted approval because they don't have a true comparison. So the regulators required that we ran a study against a placebo so that they can know our true treatment effect, which required us to go to jurisdictions outside of the U.S. where IVIG is not readily available. It would be unethical to withhold IVIG in the West. and so the discussions with the regulators have been relatively straightforward, in that what we need to do is demonstrate comparability between patients in the U.S. with those patients in our study in Southeast Asia. And the way to do that is really based on a patient's baseline muscle strength as measured by MRC. This is called mEGOS. There's a ton of published literature on that. A patient's baseline muscle strength sets the course of their trajectory with this disease wherever they are in the globe. And the way we're able to validate that is through a 2,000-patient natural history study called IGOS. This is a prospective study in virtually all developed countries and most developing countries, which has allowed us to mine that data to assess how similar the patients are outside of the Western world with the patients in the Western world. As part of our submission for a label, we'll submit both the outcomes from this study as well as this analysis on comparability, which we're calling a real-world evidence analysis. Questions from the audience? Maybe on ANX1502, you mentioned in your presentation that cold agglutinin disease is really a proof of concept in indication. So I guess when you look at the whiteboard of options, what are the key levers for understanding how... what indication or lead indications you might select? Yeah, really good question. So we're looking, of course, for antibody-mediated autoimmune diseases. That's where complement inflammation is the key effector and driver of the disease process, so that's first and foremost. And then after that, we're not trying to be the smartest people in the world. We're going after indications where targeting classical complement has already been clinically validated. In many instances, there are even approved therapies out there. But as I said before, these are approved therapies that require patients with severe disability to come get an IV every other week. In maybe one instance, it's once a month. So it's a really significant circumstance. I say all that to say we're gonna start with indications where the mechanism has already been validated and offer what is a pill formulation. From there, we will fan out. We have a host of different additional indications that we like. They're antibody-mediated disorders. We've been doing this for 10 years. I'm gonna say that one more time, and I won't say it again. Sorry. We started with GBS 10 years ago. We ran three studies there. Along the way, that's an acute indication. Along the way, we've been building a portfolio of data around a host of different chronic indications, and so we're excited to really bring this to as many patients who can benefit in the autoimmune side as possible. Any final questions? Thanks so much, Doug. Thank you.