Good day, everyone. Thank you for joining the 23rd Annual Needham Healthcare Conference. My name is Joey Stringer, and I'm one of the biotech analysts at Needham & Company. It's my pleasure to introduce our next presenting company, Annexon Biosciences. Joining us today from Annexon is President and CEO Doug Love. For those of you joining on the webcast, if you want to ask a question, please do so at any time. You can submit a question using the chat box at the bottom of your screen. With that, we'll get started. Doug, thank you so much for joining us today. Thanks, Joey. Appreciate you and the Needham team having us here. Great. Well, 2024 certainly looks to be a transformational year for Annexon. Before we dive into the details of the pipeline, what are the top company priorities, and can you briefly touch on the key milestones and catalysts for this year? Yeah, happy to do so. We're super excited about 2024. It's been a 10-year journey for us to get to where we are this year, and we think it has the potential to be really a transformational year. For those who are not as familiar with Annexon, just by way of background, our focus and our thesis is on complement, the innate immune system, and blocking aberrant inflammation that it drives really right where it starts on diseased tissue. As a result, over the last 10 years, we've been really pleased with the suite of drug candidates that we've been able to develop to block this aberrant complement or inflammatory cascade right where it starts in the body, the brain, and the eye, and really are encouraged by the consistent functional outcomes we are seeing in diseases in the autoimmune, neurodegenerative, and ophthalmic space that leads us to where we are here today in 2024 with three primary catalysts for the year, each which we think have the potential to be transformative in and of themselves and combine the potential to drive outsized value for millions of patients and our shareholders. The first is Guillain-Barré syndrome, where we will be releasing data on our phase III pivotal program later this quarter. This is the first placebo-controlled study in Guillain-Barré syndrome in 40 years, so we're really excited by that. The second catalyst for us relates to our geographic atrophy program. That's ANX007. This is the only GA program to ever demonstrate significant preservation against the loss of vision as measured on the key primary endpoint of visual acuity, BCVA 15. It's also the only program to receive PRIME designation. We'll start a large global phase III program in the middle of the year this summer to replicate what we demonstrated in our proof of concept study. And then finally, in the second half of the year, we will be releasing data on ANX1502. This is the first small molecule oral program in the classical complement space, which really affords us the opportunity to hopefully tackle a host of antibody-mediated autoimmune diseases. We previously released data late last year on our Healthy Volunteer SAD/MAD program demonstrating robust effects on the PK measurements, etc. We'll release proof-of-concept data in an indication, cold agglutinin disease, in the second half of the year. I'm sure we'll talk about more of all three of these in detail, so I'll stop there. No, that's a great overview, Doug. We'll dive right into the GBS program. You mentioned phase III pivotal readout coming second quarter, well, this quarter. There aren't any approved drugs for GBS, although IVIG is used off-label frequently to treat. How do you plan to position ANX005 relative to what the standard of care is, and what are the key differentiating features of your TPP? Yeah, really important question. It obviously goes to clinical benefit as well as commercial opportunity. IVIG, as you noted, is the standard of care but not approved, notwithstanding having run multiple phase III programs. The challenge with IVIG is they've never run a program against a placebo, so you don't know its true treatment effect. The general perspective among patients, physicians, and even payers to some extent is that IVIG has a midline effect on patients. When it does have an effect, it's typically on the milder patients. What we are looking to do with our program is completely different. We are looking to fully inhibit the complement pathway to show impact, a robust, rapid impact on GBS, getting patients better sooner and more completely. As a result, we think that translates to significant cost burden benefits, clinical benefits to the patients, such as days in the ICU, days on the ventilator, etc. We intend to position our drug as a model therapy, first-line treatment for Guillain-Barré syndrome treated on the very first day patients show up and see the hospital and hopefully make a meaningful impact in this population. You recently provided some updated incidence numbers for GBS, both in the U.S. and some of the key European markets and countries. Can you walk us through these numbers, and what are the underlying assumptions behind them? Yeah, yeah, we did. So as I alluded to, there's just not been a lot of work done in Guillain-Barré over the last 40 years. So we really are breaking new ground in this space. We recently completed, earlier this year, a claims pool assessment of patients treated with Guillain-Barré syndrome in the U.S. and Europe. These are patients who are hospitalized and treated. So it's a relatively conservative number. It's not all of Guillain-Barré, but those hospitalized and treated. And there we see 7,000 patients in the U.S. This is based on seven years of claims data as well. So it's a really robust analysis. And then another 15,000 in the EU. Guillain-Barré syndrome is a disease that can happen at any time to anyone, and it really is the incident numbers are driven by populations. That really helped us pull this together, and we are really quite pleased with the robustness of this analysis. Getting into the phase III pivotal trial, can you briefly describe that? There's some subtleties around the phase III program here. You don't have an IVIG comparator arm in the pivotal trial. What are the trial design key endpoints and the development plan here? Yeah, for those who are not familiar with Guillain-Barré syndrome, so this is an acute monophasic disease that can happen to anyone. Typically, it occurs following a preceding infection. So you're completely normal. Let's say you get food poisoning or some other type of infection. Your complement immune system turns on to clear the body of these viruses or pathogens associated with food poisoning. It then appropriately turns off. However, some weeks thereafter, complement turns back on, triggering an autoantibody attack against your peripheral nerves. You, in a matter of hours, go from normal to paralysis in your lower extremities all the way up through your body. One in four patients are going on a ventilator. So a really devastating disease. I say all that to say that you have to treat this disease immediately. So treating these patients as rapidly as possible is hugely important. We've designed our phase III study to do that. So a few things about our phase III study. One, it's a large study, 240 patients, one of the larger GBS studies ever run, which we're encouraged by. Two, we've selected patients who have meaningful disability from GBS syndrome. That means they must be unable to walk without assistance, bedbound, or on a ventilator to enter into our study. So these are really severe patient populations. Three, we required that patients to be in our study have to be treated within 10 days of signs or symptoms. It's important to stop the nerve damage associated with GBS syndrome immediately. And so once patients are too far gone, it's harder to show a treatment effect. So this is the first and only study to do that with a 10-day cutoff. We're really encouraged by that, that we'll meaningfully treat patients even earlier than 10 days, which is really important. Then the fourth, which I think is overlooked in many regards with prior GBS programs, is that we have stratified patients based on their baseline muscle strength. A patient's baseline muscle strength, as measured by MRC, a very objective measure, really is the key prognostic factor for how patients are going to fare with the disease. We wanted to ensure that all of the treatment arms in our study are balanced. We've got two doses in the study. One is 75 mg per kg, and the other is 30 mg per kg. The difference there is just really how long do you want to inhibit complement before you allow your immune system to come back on and to be part of the cleanup process. 75 mg inhibits complement for three weeks, 30 mg for roughly a week. We've powered the study as a standard phase III powering study to win in each of the respective arms. We don't have to win in both. We've given ourselves, in effect, two shots on goal to win with regard to this study. You've got it that the bar for success on the primary endpoint is a twofold shift to improvement or better on the GBS Disability Scale versus placebo at week eight. Can you walk us through why this is and what this means, this twofold shift? You also have provided some guidance on the agency. The FDA has guided that substantial evidence of the treatment effect versus placebo would be sufficient. Does substantial evidence imply that 2x or greater, or is it a little more subjective than that? Yeah, no, that's exactly right. So, I mean, in all phase III programs where you're seeking approval, just kind of the regulatory requirement is that you demonstrate substantial evidence. And working with the regulators, we have some leeway on how to define that. We've used the cutoff of twofold better. And maybe I'll just describe that a bit. So what we are looking to demonstrate with ANX005 is that those treated patients, two, will do two times better on the GBS disability scale at week eight versus a placebo group. What that means is we anticipate that two times more patients will get to a good state of health versus placebo, and less patients will be in a severely disabled state of health versus placebo over the course of the scale. We have the ability, which is the first time also in a GBS study, to use improvement across the entire scale. We look at the history of the studies, again, dating back decades. Typically, the endpoint has been a responder analysis. Percent of patients able to run at week four or week eight has been the endpoint. The challenge with that endpoint is you're not capturing your drug's treatment effect in other aspects of the scale. So for those patients who enter the study on a ventilator, getting them off a ventilator to a condition where they can walk even with assistance is a meaningful improvement for these patients and a key prognostic factor for how they're going to fare with regard to their recovery. Using a responder analysis would not allow you to capture that type of improvement. Doing the proportional analysis, odds analysis that we're doing, allows us to capture that benefit across the entire scale. So it's a very efficient mechanism by which to do that. It's actually given us more power. We were thrilled with the engagement with the regulators on this endpoint and how to analyze this endpoint. And so we're excited to turn over the cards and see what they show. To support the potential BLA submission, you'll also need some comparability data from U.S. patients using IGOS. I guess for those not familiar, what is IGOS, and why did the FDA require this study? Yeah, so really great question and important question. So IGOS stands for the International Guillain-Barré Outcome Study. This is a 2,000-patient prospective registry that is currently being run in all developed countries and many developing countries around the world. And what I really love about this is they are capturing the disease and the treatment effects of the various therapeutic approaches and placebo across the globe. This is a registry that is, in effect, homegrown, meaning it is not industry-sponsored, but in fact, sponsored by academic institutions as well as patient advocacy groups, really with the aim to attract new therapies into the space to treat Guillain-Barré syndrome because of the prevailing view that IVIG is just underwhelming in terms of treating patients with this disease, particularly the more severe patient population. As it relates to the comparability requirement, it's an important aspect of our overall program. IVIG, as we alluded to, is the standard of care in the United States. It has not been approved because they have never run a placebo-controlled study. When we came into the FDA, the feedback we received was that you cannot use IVIG as a comparator for your phase III program and get a label because we don't know its treatment effect. That required us to go to jurisdictions outside of the U.S. where IVIG is just not readily available to run a true placebo-controlled study. We've done that now in Southeast Asia. It's our second set of studies over there with these folks. They've done a really nice job in executing this program, and they've got a really high incidence of Guillain-Barré syndrome over there. In fact, Bangladesh, one of our countries in the study, is the largest contributor to IGOS in terms of patients, even larger than the United States, which is amazing in my view. So a lot of work and experience with GBS in that particular part of the world. Anyway, suffice to say, to bring that dataset back into the United States, we need to demonstrate that the patients ex-U.S. in our study are comparable to the patients in the U.S. Meaning, if you have a GBS score of a three or four in Southeast Asia and a score of three or four in the United States, you're going to progress similarly with regard to your disease. There, we're using IGOS to make this to confirm this comparability by, in effect, assessing patients in the IGOS Natural History Database who are matched with patients in our study. These are Western world patients in IGOS matched with Southeast Asian patients in our study to demonstrate this comparability analysis. We have what we call a real-world evidence protocol that's been aligned with the agency to do so. It's a rigorous analysis. We had to submit it and get it approved with the regulators to be able to do this. I will say that we've already taken a practice run at that, in that we submitted a matched analysis of ANX005 patients from our proof of concept study with IVIG patients in the Western world, in the U.S., and Europe. We submitted that to Europe in the fall last year, where we received an Orphan Drug Designation from EMA. We were really encouraged by that. There, they commented on the quality of the data from Southeast Asia, and they went further than maybe we were even hoping in making a determination that we were likely to be better than IVIG, particularly as it related to muscle strength, days on ventilation, and other things. We've got a lot of experience in doing this real-world evidence matching. We'll do that when we get our phase III dataset. Oh, that's a very helpful overview. I guess in terms of an expected outcome, yeah, of course, on the GBS Disability Scale, but MRC, days on ventilator, those important efficacy measures. What would you need to see when you compare the ANX005 phase III pivotal trial to what is seen for IVIG when you actually fully do the IGOS study from a competitive perspective, even though IVIG isn't approved in the U.S.? Would you need to see as good of an efficacy profile there, or would you have to show better efficacy than IVIG just from a potential uptake perspective? Really good question. Look, I think at a minimum, we expect we would be comparable, but candidly, we anticipate we'll be much better. So the reason why comparable is the floor for us in this regard is there are aspects of the drugs themselves that are differentiated. So IVIG used in Guillain-Barré syndrome requires five days of treatment. That's really, really important in a disease where every day matters in stopping this nerve damage so that you can facilitate more complete, rapid recovery. Whereas ANX005, we're fully inhibiting complement in a single dose within a day. So it's a very different treatment paradigm between ANX005 and IVIG. But as it relates to outcomes, and again, where we were encouraged with EMA's determination on our data versus IVIG, we just notwithstanding IVIG, we have not seen a change in the mortality rate with IVIG in GBS patient population in decades. We know that one in four patients are going on a ventilator with IVIG. We know that 20% of patients are unable to walk after one year with IVIG. 40% are still going to the ICU with IVIG treatment. We expect to win on all of those measurements. We consider those very important key secondary measures. We'll be looking at those at week eight and week 26 to make a demonstration that we know is important to physicians, patients, and the healthcare system that we're providing a more complete and rapid benefit to this patient population. And that's how we anticipate positioning it in the marketplace, not just a better mousetrap, if you will, with a more convenient dosing profile that's stopping the disease more quickly, but actually tangible outcomes that are changing the course of these patients' lives. I think you guided for the readout from the comparability results in the first half of next year, but correct me if I'm wrong there. My question is, is that gating to the submission, or could you initiate a rolling submission given you have Fast Track designation for 005? Really good question. At TBD on the rolling submission, the data will ultimately help guide that. So we will go back and have those discussions with the regulators once we have the data. The door is open to have those discussions. So that's the good part of that story. And then, as you alluded to, yes, we have guided to first half of 2025 to complete the matching comparability exercise, and I anticipate filing for the BLA just in time with that. So that's pretty much the timeline for all of that. Great. Last one on GBS, and then we'll get into the GA program. No, it's too early. It just depends on the data. But I want to ask on potential pricing in GBS. I mean, the cost of IVIG, I think, is around $20,000-$30,000 if you kind of do the math. But would you have a potential first-in-class, first-line therapy, how would you think about pricing? And what would give you the confidence that you'd be able to command premium pricing? And then maybe as a follow-up, beyond IVIG, what would be good, potentially good pricing comps to think about? Yeah, no, it's a really, really good question and important question. Look, we candidly see Guillain-Barré syndrome as a blockbuster opportunity. As I alluded to, you've got 20,000 patients between here and Europe. It's important to note that more than 90% of these patients get therapy, IVIG or plasmapheresis. And the reason for that is, and that's irrespective of where they are with regard to their disability when they come into the emergency room, is you do not know who is going to progress to a ventilator when they show up. So everyone has to get treatment. And there's been no detailing in this space at all. So it's really greenfields that you've got a built-in market that is not being detailed or educated on, and so we can come in and really with a large share of voice command a great deal of attention. Importantly, we're positioning this drug as a model therapy, first-line treatment. And so we think that's really, really important to provide differentiated outcomes. All of that leads to our pricing thinking with regard to that. The key cost for tackling Guillain-Barré syndrome is not the cost of the drug. It's actually the cost of care. So what we know from studies done 20 years ago, it costs more than $2 billion a year to treat Guillain-Barré patients in the U.S. alone. And that's because these patients are in the hospital, they're on the ICU, they're on a ventilator, and then you have the recovery period, skilled nursing facilities, physical therapy, etc. Improving upon all of that sooner saves meaningful dollars to the overall cost burden of treating a Guillain-Barré syndrome. And so we think with a reasonably priced drug, we've seen comparables in the neighborhood of $75,000-$150,000 for a course of therapy. We feel like that's quite readily supportable. We're not going to guide your price today, but feel like that's a very reasonable range. When you do the math on that, recognizing that virtually all patients have to get treatment, you can see very quickly the numbers add up, and this becomes really quite an attractive commercial opportunity for us. Fantastic. Well, let's turn to your ophthalmology program and Geographic Atrophy. You've reached alignment with the FDA on a phase III registration program. You're set to start the phase III program middle of this year. You've got a couple of phase III trials planned. So can you briefly describe the phase III program design? Yeah, absolutely. We've got, as you alluded to, two phase III programs. We don't necessarily need to. Two different scenarios. So one, our global large program, which we're calling ARCHER II, the proof of concept study was ARCHER I, really is designed to replicate our proof of concept study. So this will be a sham-controlled study run globally in the U.S., in Europe, with very limited changes from what we did in our proof of concept study. And we'll talk more about kind of some of the data there, I suppose, and more data that we'll be releasing on that program, which we're quite encouraged by. The second study is what we are calling a comparator study, something that the FDA in particular is looking to move companies into getting away from sham-controlled studies and running studies against injection comparator. It could be a saline, or it could be a therapy. Felt like saline would be unethical for patients to poke them in the eye. So we're running this second study, which we're calling ARROW, in comparison with SYFOVRE, the Apellis therapy that's been approved recently. And there, that right now is currently designed as a U.S.-only study. We'll wait and see what happens with regard to SYFOVRE in Europe and approval there. If they get approval, we will expand it and make it a global study. If not, it'll be a U.S.-only study. ARCHER II will start in the middle of year, and the ARROW study will start later in the year thereafter. Of course, there are two approved drugs for GA, SYFOVRE and Izervay. Do you think there's room for three-plus GA drugs? And how do you plan to position ANX007? Yeah, absolutely. I mean, well, so first and foremost, I think what's important is what we are looking to demonstrate in our study. So we are looking to demonstrate preservation against visual vision loss, so visual acuity, which is the key assessment for anyone who you will talk to, whether it's a patient, physician, payer, etc. In fact, you know when you show up at the DMV, they're never asking you about lesion growth. They're asking you about your vision. And we know that over the course of the year, using an endpoint of best-corrected visual acuity, 15-letter, represents a loss of 50% of your vision over that period of time, and in which case you have to turn in your driver's license. So our positioning for our program in the marketplace is just very straightforward. We are looking to provide functional benefit to a vulnerable elderly patient population who want to maintain activities of daily living, the ability to read, to be able to cook, to be able to engage with their loved ones, etc., and to see them. So we'll position it as such. For the comparator trial, Doug, why is it SYFOVRE and not Izervay as the comparator drug there? Really good question. Yeah, we thought we could go after either in that given that neither has shown any benefit as it relates to visual preservation, notwithstanding 2-3 years' worth of data. Now, we selected SYFOVRE candidly because we just know so much more about the program. So our program is looking to treat all GA patients, both foveal and non-foveal. SYFOVRE did that. We also have information on their mean BCVA 15-letter loss, etc. So we had a lot more information than we have versus Izervay, which only treated non-foveal patients. And so we just took a, you know, the better or more informed approach to going against them in this study. In terms of EMA registration requirements, any updates there? What's the latest? Yeah, well, so the EMA has been, I'd say, perhaps more straightforward than our discussions with the U.S. in that BCVA 15 is the only endpoint that EMA has ever recognized as an approvable endpoint for geographic atrophy. Whereas in the U.S., we obviously recognize lesion growth and fundus autofluorescence. So it's been a very straightforward discussion with regard to them and our program. And they've been really quite collaborative. We have PRIME designation there. I may have alluded to that before, the only program to receive, in effect, breakthrough designation in Europe. And as a result, we've got a special rapporteur assigned to us. We've already been engaged with them in face-to-face meetings. So we're really thrilled with the way that program is coming together. Could you potentially file on the 12-month data, or do the regulators need to see the 24-month data? Yeah, good question. No, the primary endpoint is 12 months. So very much similar to SYFOVRE and Izervay, we will roll in the 24-month data. The 24-month data requirement is a safety requirement and not an efficacy requirement. Got it. Makes sense. Looking back at the phase II data, specifically, this is from the ARCHER trial on BCVA. In particular, we wanted to focus on the sham response on BCVA. It was, I think, I have my notes around 21% progressed. Was this in line with what was seen in other phase II or phase III GA trials? Yeah, very consistent. So interestingly, not everyone has released their sham rate as it relates to BCVA 15-letter from their studies, probably because they just haven't shown an impact on BCVA 15. That being said, when you look at the programs that have, this is very consistent. The largest dataset, and the one we use most often, is the lampalizumab dataset out of Roche, more than 1,500 patients in that study, so this in that program. So this is a massive program, the largest program in geographic atrophy. And there, their numbers were virtually equivalent to what we saw in our study. So we're really confident in what we've seen from a sham rate in the ARCHER II study. We have been more conservative from a powering estimate perspective in setting up our phase III program. We were really pleased to see that as very consistent with the other programs that are out there. Doug, you presented off-treatment data at the AAO meeting last November that we thought was pretty interesting, I think, perhaps for two reasons. One, once patients got off of ANX005, they regressed on the BCVA response. And then second reason is the effect, so the slope of the line from 12-18 months was similar to sham. So with those kind of observations as background, how would you address potential concerns around the variability of the BCVA data and maybe variability in the BCVA endpoint in general? Yeah, no, it's a really great question. The first thing I will say is BCVA as an endpoint is a well-established endpoint for visual acuity in all ophthalmic diseases. In fact, it is the standard, the gold standard for visual acuity, whether you're in wet AMD, diabetic retinopathy, or retinitis pigmentosa, and geographic atrophy. Again, an exception was made for an anatomical biomarker in GA, but that is the exception, not the rule. When you think about BCVA, best-corrected visual acuity as an endpoint, it's important to think about the letters of loss that are associated with it. So when you see variability with that as an endpoint, typically that's at five letters or one line of reading, a bit less variability, but some at 10 letters or two lines of reading. We see very minimal variability at 15 letters or three lines of reading loss. That is why 15-letter BCVA 15 is the standard for the approvable endpoint. We sometimes hear companies or others talk about BCVA generically and talk about variability. That's probably reasonable to do when you're thinking about five-letter or 10-letter. But you don't hear them say that at BCVA 15-letter. It's too well established. The other thing I'll say just with regard to the variability topic is in our proof of concept study and what we will also be doing in our phase III study is we assessed it on two consecutive visits. So you needed to have BCVA 15-letter loss on two consecutive visits to ensure the veracity of what we were seeing. So it was not an anomaly, one visit, and you know, you woke up one day and saw a bit better. We really made sure with belt and suspenders that we were getting a true read on this endpoint, which, you know, the regulators have appreciated. Great. Well, that's a fantastic overview of the GA program. Want to move lastly to ANX1502. A lot of investor interest in this program. I think anytime you say the words, you know, oral complement inhibitor, investors get certainly excited. So it's early stage. You report some phase I SAD/MAD data, PK/PD, last December. Can you talk about the key takeaways from this data? Yeah, look, we're really encouraged by this program. And this is an important program for us. I can tell you, we started this program more than six years ago. And certainly, some said we were crazy. Why are you doing this? You know, you've got a suite of antibodies. But we had looked ahead, and we looked at this autoimmune space, and we looked at the potential indications where you can be really effective and thought that, one, it would be hard to get at all of these indications with an antibody in IV or even in a subcu given the debilitating nature of the disease. And two, it's going to be super crowded. And, you know, a better mousetrap is probably the way to go. So this has been quite a journey. We've got the lead program, ANX1502, with a full robust backup program behind that. And so we were encouraged by what we saw last year with our SAD/MAD study. There, we demonstrated a few things. One, safe and well-tolerated, which is really, really important when you're dealing with an oral thus far. Secondly, we were able to achieve what we think are really conservative targets for drug levels in this patient or in this SAD/MAD study. So we set the bar very conservatively, and we more than achieved that and have plenty of headroom from a dosing perspective with regard to this program from a PK perspective. And then third, we took a peek or got a glimpse at a potential effect from a pharmacodynamic perspective. Measuring PD in a healthy volunteer population in complement is difficult to do because complement levels are generally normal in healthy individuals. That being said, we were able to ferret out a group of healthy individuals who had elevated complement levels. We consistently, in every one of those subjects, lowered their complement in the order of magnitude that we would hope to have a PD effect. We are now moving forward to confirm that in a patient study, in a true proof of concept study. We were encouraged where we are with this program thus far. So kind of all systems go as we sit here today. Is the PK definitely supportive of BID dosing, Doug, or do you think you can get it down to a once daily if you go to a higher dose? Yeah, it's definitely supportive of BID dosing, again, at conservative levels that we've set in this study. One. Two, we've done no special formulation work on this drug candidate. So this is our first presentation of it, really just to demonstrate its capabilities. There are opportunities to optimize this drug candidate, without a doubt. And so as we get through the proof of concept and validate what we saw in the healthy volunteer study in a patient population, we'll get going much more in earnest with regard to those activities. You mentioned that, you know, a lot of opportunities here with this molecule, potential indications. You mentioned that you initially planned to start in cold agglutinin disease, CAD. Correct. I guess the question is, and Enjaymo is the only approved drug for CAD. This is maybe a bigger picture question on C1s inhibition, but why didn't Sanofi pursue more indications for Enjaymo beyond CAD? And is there a biological reason or risk based on C1s inhibition? What does that mean for your approach? Yeah, no, not with regard to CAD. CAD is a really straightforward antibody-mediated disease for which the classical pathway is the key effector. So it's really well elucidated in that regard. My sense is they have not pushed forward with more indications with Enjaymo because they've developed additional mousetraps, candidly, that I think they like better. So you can see they're using different drug candidates, for example, in CIDP and other antibody-mediated autoimmune diseases that you would otherwise take forward with Enjaymo. Enjaymo is a solid drug candidate. We see some strengths there, but we also see some opportunities just with regard to full inhibition, particularly in high-stress circumstances. So depending upon the disease, you may even run into breakthrough. We don't know that. It's a complete hypothesis. But we do note that they're not moving it forward into other indications, and they're looking at other drug candidates to do that. CAD is a small indication, but it's a really effective indication in proving out a complement therapy's capability, drug candidate's capabilities, because of the objective measurements of its endpoint. So you're really looking to have an impact on hemolysis, things like bilirubin that are super, super objective, and you can move in a matter of weeks. And you only need a small number of patients before you know that. And that's how we're using the indication. We don't necessarily see CAD or cold agglutinin disease as a major commercial opportunity. And you've got Enjaymo there. But for us to fully validate our small molecule and then move into a host of other neuromuscular diseases and other indications, that's really our strategy. Got it. And you mentioned the proof of concept trial in CAD. Just any insight into the trial design and important endpoints there? Yeah, small study. It'll be, you know, no more than six patients, if that, because it doesn't need to be to establish pharmacodynamics. And there, we're just looking to really continue to, you know, we're super hypervigilant about safety and tolerability. So we're really focused on that. We've got a new tablet formulation, which we will be introducing into that study, so one that we think will play really well for multiple other indications, and then showing an impact on the key measurements like hemolysis, hemoglobin, etc. Two more questions from us, Doug. What would trigger the advancement of ANX1502 into other autoimmune indications? Yeah, safety and tolerability coupled with, you know, robust target engagement, PKPD. What's your current cash position? What's your expected cash runway? Yeah, so we're pleased with the finance we did late in the year last year. And we're cash runway well into the middle of 2026. So it'll get us through multiple catalysts, including importantly, the GA ARCHER II study. So that's really important for us is that we were financed through GBS and some of the pre-commercial, commercial activities, as well as our GA program and then the ANX1502 proof of concept study and some additional work there as well. Great. Well, Doug, thank you so much for participating. It was a great discussion. Thanks so much, Joey. We always enjoy speaking with you all. Thanks, everyone, for joining us on the webcast. Everyone, have a good day and a good rest of your conference.