Great. Good morning, everybody. Happy to be moderating my annual panel where Priya has to listen to me, pepper her with questions for 40 minutes or so with Priya Singhal, Head of Development at Biogen. Thank you, Priya, for joining as always. I am going to kick it over to you to just make some opening remarks on Biogen and give us a snapshot of the development portfolio, and then we can do Q&A. Thanks again, and take it away. Thank you, Paul. Thanks for having me. It's always a pleasure to join you. Before we begin, I'd like to point out that I will be making forward-looking statements which are based on our current expectations and beliefs. These statements are subject to certain risks and uncertainties, and our actual results may differ materially. I encourage you to consult the risk factors discussed in our SEC filings for additional detail. Really excited to be here, Paul. As you may know, you know that over the last two years, we've really focused on efforts to augment the pipeline. The main goal has been rebalancing the risk profile and investing to win in key areas of expected future growth. In 2024, I think we made a lot of progress in our pipeline where we've prioritized key programs, internal programs where we believe that we have the opportunity and potential to win, such as Alzheimer's, where we were able to amend our phase II study, Celia, for BIIB, and accelerate a potential proof of concept readout next year in 2026. We also got a positive phase III outcome with our DAPI phase III trial. We also focused on external innovation. You know we had one M&A with HI-Bio, and we have felzartamab now in our portfolio, poised to have three phase III starts in 2025. In addition, we did the collaboration with Stoke Therapeutics and brought in access really to zorevunersen. That's very exciting because we have the ex-U.S. region and also poised to start phase III in 2025. have also advanced Leqembi. We continue to focus on Skyclarys Pediatrics, which is really the next very important milestone that we are ready to get going on, as well as Spinraza High Dose, where we had a filing already in both Europe and the U.S. Very exciting year. I think as a result of this progress, we have been able to focus now our development efforts on a set of really high conviction, high scientific conviction, mid to late stage assets. If we are successful, you know we could set up franchises in very key areas like Alzheimer's, lupus, as well as rare disease. These, we believe, are really core areas of expertise and capabilities. We are harnessing that low volume, high value sort of portfolio here. Very excited. Yeah. OK, great. We are going to try to take time and go through each of the assets you mentioned and a couple of the key questions. Maybe one more forward-looking question for you just in terms of the whole, where is Biogen going? I guess it would not be a Biogen panel without the token business development question. As it relates to sort of analyzing the tea leaves in your guys' commentary about BD and what you just said, Priya, about shifting the risk profile of your portfolio, how do you think about Biogen's positioning in neuroscience going forward? I think if we rewind, right, you guys had a lot of super cool science, but high risk programs like anti-LINGO, like the LRRK2 program. It feels like Chris now talks a lot more about rare disease and immunology as key areas. Just as it relates to CNS specifically, is this an area you think you'll continue to build out and take on risk in, or is it an area where you feel like your portfolio is full and you're trying to continue to shift elsewhere? Yeah, it's a great question. I think overall, what I would offer are two important thoughts here. One is that neuroscience continues to be a core capability. It's an area we've succeeded in. We've often broken the ceiling there. We'll continue to invest and keep our capability in neuroscience. We've diversified. We're not just going to go after high risk neuroscience programs that will be a decade to kind of get to proof of concept. We are balancing that with immunology and rare disease, both areas which I also believe we have deep expertise. With rare disease, you know we've had one of the best launches and projects with Spinraza. We're continuing to build on that momentum. We broadened Skyclarys. You can see that we broadened Skyclarys, where it's rare, but also neuroscience. What the distinction here is, is being confident in the data, being confident that when we get to late stage, we've de-risked and we have a significantly higher POS and a probability of technical and regulatory success and payer success than we have maybe in the past. That's what I would offer is a key change. In immunology, I think I would say that you know it's really foundational. With multiple sclerosis, everything that we've been doing, immunology has been in focus. We're really the only company now with two different mechanisms of action, both in phase III for lupus, as well as systemic, as well as cutaneous for litifilimab. I think that's how I would think about it. It's not a departure. It's a building around. It's a diversification. Yeah. OK, fair enough. As it relates to taking on risk, what gave you and your team conviction about executing the Stoke deal before phase III? Yeah, excellent. I think overall, you know just stepping back, Dravet is a very serious disease, high unmet need, no disease-modifying therapies. The other piece I think to keep in mind here is that these children are often cycling through four to seven anticonvulsant therapies. They really, we know that from the evidence we've seen and we've kind of evaluated, we don't believe these really impact what the decline is from a cognitive, functional, behavioral perspective, as we've seen kind of you know in scales like Vineland 3. What we're excited about with Stoke and with zorevunersen is that we saw the data, although it's a small subset, we saw that in this population that had the background of four to five anticonvulsant therapies, including fenfluramine, more than 50% of the patients were on background fenfluramine. We saw an 85% reduction in anticonvulsant therapy and then out to six months, still durable with about 75%. That itself is very powerful. We did not just look at that. We looked at the natural history that also Stoke ran. They have a three-year natural history data set. We looked at what were the trends on behavior and cognition on the Vineland 3. We believe that this product can actually impact the developmental kind of milestones and the behavioral milestones that are so important for Dravet. Of course, you know it is genetically, it is grounded in genetic evidence, right? Because we know that 85% of Dravet occurs due to haploinsufficiency of the SCN1A gene. You know that then results in the sodium channel NaV 1.1 reduction, which then leads to, you know, an impact on the inhibitory interneurons and the interplay causing seizures. We think that there's not only mechanism of action belief here, but there's a potential data that we've seen in the early phase studies that set us up for phase III. Of course, phase III studies, you do need to get regulator buy-in. That was the other important pivot and anchor for us that Stoke had already discussed their phase III program, had obtained agreement with regulators in the U.S., Europe, and Japan on what the phase III program would look like, how it would be powered. We had a lot of data going in. It kind of goes back to your first question because I wanted to say that what's changed is we are not, it's not like we wouldn't take a risk. The question is, how calculated can that risk be? Are we confident that we've de-risked some things that we would want to with POC? That's the big distinction. I mean, this is like a tremendously interesting program. And just as it relates to epilepsy more broadly, being kind of going through, like it's not a shift because I don't think it's ever going to be broadly like this, but like a subtle shift towards precision medicine. We felt like one of the key questions with this program, and you know obviously given the mode of administration, this would be a big commercial swing factor to the upside, right? If this is successful, is the cognition piece? I was curious you know how you think about this question and whether you even think this question is relevant. If you were developing a drug for cognitive impairment in schizophrenia, right, you'd be pursuing a population that is not acutely psychotic, right? Because the FDA wants you to decouple cognitive benefit and benefit on psychosis. As it relates to the Stoke asset, do you look at that data and think, you know, this impact on cognition is independent of seizure reduction? And then I guess as you think about getting like a label for this and a claim for this and marketing this, like does that matter? Like how should we think about that? Yeah. Another great question. I think it does matter. I think it matters because we, based on our current understanding and all the data that we've evaluated, I don't think it's been demonstrated that just simple seizure reduction will lead to that cognitive improvement. We think there could be some effect, but we think you need to be doing more really in terms of the mechanism of disease. Addressing the mechanism of disease is going to be very critical. That's why we're excited because this is not just anticonvulsant therapy. It's actually going for more than 85% of what we know is causative biology. Plus, I mean, you know just having that data isn't enough because that's what you know from disease understanding. Then we saw in the small data set, granted it's small and it's open label, but I think we have great teams within Biogen and we're able to really dissect these data sets to see whether we have enough confidence that tips us over to know that could this have the potential if the phase III is designed correctly to have disease-modifying therapy. That's what gave us that confidence. We're not just looking for an anticonvulsive therapy. We are looking definitely it has to have impact on seizure reduction. We think that'll be contributing to outcomes. We think it needs to have a distinct disease-modifying therapy, which we believe this product definitely has the potential. Yeah. OK, great. All right, let's maybe just do hits around the whole pipeline. On lecanemab sub Q, can you remind us of just the general timelines there? As it relates to sub Q initiation, you know how has the program evolved over time as it relates to doing more dose work? What would you say the target product profile is, specifically as it relates to ARIA and whether you can get to a lower rate of ARIA? Yeah. So overall, I think very excited about the intravenous Leqembi approval that we got just a couple of months ago because this was a big debate out there about whether this product has a dual action. Can we actually have a label enabling update on that? I think that was an important milestone because Leqembi is really the only product now where we say, where we know that if you remove plaque, obviously if you remove amyloid, that translates to clinical benefit, but that that benefit can continue and be durable beyond plaque clearance. I think that was a very important milestone for us. The other is that you know we remain in review for subcutaneous maintenance, which I think is going to be very important. We will get an outcome and we have a PDUFA date in August this year. Why is that important? Because this gives optionality to patients and prescribers, could potentially alleviate some of the stress in the health care system. Importantly, there's going to be this bolus of patients who are going to be completing their 18-month therapy or such where they have the plaque reduction and potentially they could transition if we, assuming we get approval for the subcutaneous maintenance. Moving to subcutaneous initiation, what we've said is that we will file that at some point this year. We expect an outcome, a regulator, an FDA outcome before the first half or within the first half of 2026. We remain on track for that. Now, the data, we try to be as driven by data, you know, in every program. Here again, the data has driven us because we saw with the data that the 360 milligrams IV, you know, twice a week, you know, will actually lead to a higher plaque clearance and is much more than we potentially need. The question here is, can we reduce that in some way to make it more optimized or reduce the initiation dose, which potentially could have an impact? We think efficacy will be maintained, but it could have an impact on ARIA. Now, ARIA, I think you know, nobody's fully understood it. I think what's important is two things. One is it has a window of susceptibility, especially for a product that's not titrated. It happens early and you can capture it with monitoring. Most of it is asymptomatic. Serious ARIA really remains below the 1% mark, at least for lecanemab, symptomatic less than 2.8%. We have not seen any differences with real-world data with more than thousands of patients treated now. That gives us confidence, one, that it is kind of replicating what we saw in trials. Physicians are able to manage it. It is something that education really helps with. Second is that if it is lower, that will be a potential advantage, but we are not there yet. You know, I think the data that we are generating is to really look at can a more optimized dose be adequate in terms of efficacy? I think if it provides advantages in terms of ARIA, which we know with subcutaneous is more related to steady state, unlike the intravenous formulation. We will see. I think overall, we believe ARIA continues to be manageable and is replicating for lecanemab as we saw it in the clinical trials. Yeah. OK, that makes sense, Priya. You know, Chris, I've always appreciated his candor about this launch because I think he's not, he hasn't tried to oversimplify it, right? I mean, I think he's been pretty open that this has just been such a complicated, such a complicated launch. Like there's so many factors that play in. I guess now, you know where we are with lecanemab, how would you rank order the impediments to uptake? I would assume, you tell me if I'm wrong, but I would assume sub Q maintenance, you know might have an incremental impact on uptake just because you have to be on the drug for so long. For sub Q initiation, like how much of a game changer is that? Is it still more about everything else, seeing a neurologist, the MRIs, et cetera? Yeah, I think you're right. I think Chris has articulated that exactly right as well. It's a multitude of factors. Some are related to the product, but a lot are related to the infrastructure and the fragmentation of dementia care in the United States, really. I think that we believe there's several catalysts. To your point, I do think subcutaneous maintenance could be just incremental. If we really see a blood-based biomarker hitting the ground in terms of an IVD in 2025, you know FDA approved, that could really be quite important because I think the biggest hesitation, you know, neurologists have is that they have to go through so many steps to even confirm amyloid, right, before they can put a patient on drug. I think that with the advent and sort of upswing that we see on digital cognitive tools, if IVDR comes along, I think the combination of that, the potential of optionality for patients with a subcutaneous formulation, all of this could be really powerful. And then if we can sort through some of those things and we come along with a subcutaneous initiation possibility in 2026, I think that could, you know, really be very important. I think, yes, you're right. It's going to be a series of catalysts and continued education for prescribers. How would you think about the probability of success for a credible blood-based biomarker coming to the market in the next one to two years? I think it's high. I think it's high. Yeah. What should we be looking at? Do you want to just help people? What should we be looking out for? Yeah. We know that Fujirebio is already in review, I think as of September 24 in the public domain. I think this is going to be important because the one thing that people need to remember, and prescribers, you know, also need a lot more education on this, is that there are lab-developed tests, which are not FDA approved. Then there are IVDs, which are, you know, potentially FDA approved. Fujirebio is definitely in review. There may be one or two more players who will get in there. I think that'll be good momentum to have. The difference is the sensitivity and the specificity. This is important because this is a serious diagnosis, high on unmet need, but a serious diagnosis with implications for both the patient, the caregivers, and the prescriber. I think that prescribers are looking for concordance with PET, amyloid, as well as CSF. That is going to be important, which I think the specificity of an IVDR is poised to deliver. That is number one. Number two, it needs to get reimbursed. I think having IVDR status is likely to potentially garner, I hope, a reimbursement, which is pretty important. It is not big dollars in the big picture. I think it is just about getting the data right. Finally, they need to scale up. I think that is going to take the entire infrastructure. I do think that next one or two years, this is likely. I think it could be a game changer along with all the other momentum because on its own, a diagnostic test does not mean much if you cannot do anything for the patient. Now, with the advent of products like Leqembi, we believe the physician actually has something to offer. There'll be a lot of momentum, you know, in the future. I think PCPs could be using the blood-based biomarker. But, you know, I think that might take a little bit of time. Things move fast when you get to this stage. There's a tipping point. Yeah. Yeah. OK, very interesting. Let's talk about the tau program. You know, I think the natural question, and you guys have some data to address this, but the natural question for me for any of these intrathecally administered products, be it, you know, antisense oligonucleotides, RNA, gene therapy, is, you know, are you getting enough target engagement across the key areas of the brain? You know, I think it's complicated, but I think as we've tried to bridge from the early successes in spinal muscular atrophy to other diseases, like, the success rate has been very mixed. Again, it's nuanced. One of those is, one of the reasons I think is biodistribution. To that point, can you just review for everybody the target engagement data you've generated and your level of conviction that you are reducing tau levels in the brain areas that matter in Alzheimer's? Sure. I think there are two lines of evidence I'm going to offer. One is preclinical data. I think you know tau has been a long-time focus for Alzheimer's drug development. We know a lot of attempts have failed. We ourselves have failed with BIIB092 or gosuranemab, which was an antibody. I think what we've learned from everything that we've done and evaluated is that you need to be able to knock down intracellular and extracellular tau. I think that's the beauty of the ASO platform. That's what it's given us, the opportunity to knock that down. When we looked at really our preclinical models, we saw that we were getting sufficient exposure across the key brain regions. That really is the most direct evidence of target engagement for BIIB080. Now, we've looked at BIIB080's effect on tau expression in brain tissue of mice, rats, non-human primates. And consistently, we've seen a robust reduction of the MAPT mRNA or tau protein levels in brain regions where BIIB080 was detected. Now, that's not enough, right? You've got to do the human experiment. We converted that phase I study into a phase Ib study. We opted in early. This was our wholly owned now Biogen program where we saw effects on tau pathology and clinical outcomes. This was more than what we might have expected, right, which is more than just PK data. I think what is most attractive about BIIB080 in terms of, you know, how do you kind of get to proof of concept and what gives you the confidence to continue to invest or invest to win, as that's the category the program's in. It is the fact that we saw a confluence of the fluid biomarkers, tau PET, which we believe is very critical to observe. Can I clarify something with you? Have any of the antibodies that have failed shown an effect on tau PET to your knowledge? Not to my knowledge. Not to mine either. Yeah. That's the piece we're always looking for. In fact, it's become very simple for us to look at exciting programs because we're looking for that piece of data. Yeah. Yeah. That's critical. Also, I would say unexpectedly, we saw an emergence of clinical outcomes that was very exciting. Granted, it's a small data set. It's a mad study. We saw that these were durable several weeks after drug. That was another very exciting piece of information. That's the confluence that gives us excitement, you know, gives us the impetus to kind of keep going. We looked at that data. Our Celia study, which was our phase II study, was already ongoing. We went back. We reevaluated what was the power we needed for Celia. We actually cut that study in half. Yes, like you, I was concerned about intrathecal delivery and acceptance, right? You'll be surprised to know the study enrolled very fast. We completed enrollment in 2024 ahead of our sort of expectations, I would say. Very exciting. You know it's anecdotal, but when I've talked to investigators, they say that patients really want to try it. They really want to try it. The patient today is really well educated. This is also targeting MCI and mild. They have an understanding of, you know, the phase I data. They've seen the information. I think they want to give it a shot. It's been very exciting. Yeah, I'm excited. We'll get a readout in 2026. Yeah. No, I'm very excited about that program too. Can you maybe some of the other just biological questions that I think come up with TAU? I mean, one is you know the right time to intervene or the right window for intervention. Maybe you can comment a little bit on that when we think it plays a role in the disease. The second is just you know TAU, if you just read about it you know at a base biology level, right? I mean, it's evolutionarily conserved. It's talked about as an important cytoskeletal protein. Like how confident can we be that knocking it down is not going to have some sort of safety down? Yeah. We looked at this question very carefully. I'll offer a few points here. The first one is that the current understanding of the biology of tau is that there are lots of redundancies in the biological processes that tau participates in, such that the tau knockdown has an impact on the pathologic gain of function, but not on physiologic function. This has been published. I think it's an important line of evidence. The other is that when we looked at animal models in mice, we looked at complete knockout of tau. We saw that that's tolerated, and animals are viable. That's like, you know, it's not a very high bar, but animals are viable. Multiple tau, different tau knockout mouse lines have been generated and phenotypically characterized. In these lines, the complete TAU knockout had normal development and cognition with a minor motor phenotype developing later in life. You know, potentially mitigating the safety concern that it would be a devastating outcome, right? That is one, two pieces. Now, for humans, the way we have tackled this is we have had access to the U.K. Biobank samples. Our team, our translational medicines and translational sciences team, did a lot of work on this question. They saw that these really, you know, genomic data that was available showed us that heterozygous loss of function of TAU in humans is actually very likely tolerated, highly compatible with life. That tells us that about a 50% reduction in TAU may not be associated with gross neurological defects. We see that also in the data that we saw. Now, in the BIIB080 trial, granted, it's a small trial and small number of patients. We have seen that we saw dose-dependent and sustained reductions in tau, reducing it to about 50% in CSF. And we have an acceptable safety profile. We think that this supports ongoing development. You can never be sure. You need to continue to test it. That, I think, is something that we are looking at very carefully in phase II. So far, all the lines of evidence tell us that this is really compatible. The other question you had is, what's the right time for intervention? As you know, I mean, everything we know about Alzheimer's tells us that you've got amyloid buildup for years, probably decades. Then you've got this penultimate sort of tau buildup. Yeah. You kind of have that tipping point a few years later of getting into symptomatic zone. We are targeting that same population, the MCI and mild. We continue to look at the spectrum and think about, are there other areas for intervention with TAU? We are being very systematic about what do we want to first prove and then what does that unlock in terms of development. I think BIIB080 could be really powerful in so many other avenues, right? Primary tauopathies, potentially moderate AD. These are all areas we are exploring. We remain very focused on how do we accelerate once we get that confirmatory POC, which hopefully will have a readout. It will tell us, we will learn a lot because we have got TAU PET. We have got all these markers in the Celia study. Yeah. Yeah. OK, great. What are you powered for from an effect size perspective? And do you think the effect size for something like this, given the IT administration, has to be bigger? How do you think about the clinical hurdle? Yeah. I think one big thing to kind of keep in mind is, you know, we are looking at three doses and two dosing paradigms. We built this based off of the data that we had from phase Ib. That's the number one thing. We're thinking about burden. We're thinking about adequate PK/PD sort of exposure and all of that and biodistribution, as you rightly pointed out. We saw durability of tau reduction. That's going to be important for us to nail. The other thing is, yes, we're going to look for effects on fluid biomarkers. We're going to look for tau PET. We're going to look for clinical outcomes. We have the same primary endpoint, which is CDR-SB, because we want to anchor it on a validated registrational endpoint. Now, obviously, we have a lot of other secondary and exploratory outcomes. We'll be looking to learn deeply. We are anchoring this on what we know has evolved, you know, with the anti-amyloid space. We are anchoring it on CDR-SB. What do we need to see? I think it depends a little bit. I mean, we believe we've powered it to see an effect. I think it depends because remember, tau is not necessarily, or we hope it's not going to be associated with ARIA. What's the benefit risk? How does that change? I think a lot of these factors will be part of our overall framework as we think of developing a go-no-go framework. A go-no-go means, you know, are we going to go beyond AD? Are we going to do more other exploratory trials? What are we going to do? Are we going to double down just in AD, mild AD, MCI? I think all these things will matter. Overall, I think we're powered on, we believe we're powered on CDR-SB. We've got a bunch of other things we'll be learning. We'll be looking at tau PET very carefully. We believe it's very critical, and the fluid biomarkers. Yeah. Yeah. OK. Last question here. And it's really just on the oligo brain space in general. Do you have a view on the brain shuttle approaches? You know, I think we've seen these approaches in the brain validated with, you know, antibodies, proteins, enzymes. And then in the muscle space, right, also with transferrin, we've seen that oligos are a viable cargo you can deliver to the right part of the cell. And I know there's interest with this TAU target specifically with brain shuttle approaches, which, you know, again, super early, higher risk, but you know could be IV. Is this something that Biogen has on its radar? Very much. Jane and her organization, and we are partnering on this. We continue to believe that the brain shuttle delivery to the brain is a primary goal. Yes, the short answer is yes. This remains very exciting. We've got a lot of work internally. We believe we've made headway. We have some real important areas that we think we're making rapid progress. Yes, continues to be very important. We are continuing to work on it. It's really the third pillar for us. Yeah. OK. OK. All right. Let's talk about lupus a bit. And then we can maybe talk about Felzartamab and Biogen and the transplant space as well. But you know, just as it relates to lupus, it's interesting, right? Because I feel like Biogen's stock doesn't get much credit for dapirolizumab or litifilimab. And I think the things that hold investors back, you know, one is that in the dapirolizumab phase III, right, the study was positive. But you know, the p-value was close, right? So there's a question on how much margin is there, you know, for the next study? Can we be confident in the replicability of it? And then just the second question more broadly is that it's weird. On the one hand, lupus feels like it's this big unmet need. On the other hand, it feels like it's a competitive space, right? I mean, there's a lot of stuff in development. I think it's hard for people to kind of figure out where, you know, different assets fit in. I realize that there's multiple questions there. It'd be great to kind of get your snapshot on, you know, both the clinical risk side and then just the positioning side as well for your two assets. Yeah. You are exactly right. I mean, I think two points that you made I'll reiterate is very high unmet need, extremely high, and a lot of competition. Absolutely true. I think that when you look, when you step away from those two points, you realize that there've only been ever two products that have been approved. It's been a graveyard for trials. I think a lot of people did not expect dapirolizumab pegol to be positive. We believe that the broad mechanism was going to be impactful on the T and B cells. We understand the area really well. We've worked very closely with UCB on the partnership. We believe that the modality and the target are very important. We were really delighted, not only with the primary endpoint, but Paul, I want to call your attention to the fact that 50% reduction in severe flares, steroid sparing. I mean, these are the problems that these patients face every day. I mean, really having that positive primary endpoint on BICLA, and this was a global trial. I think that's the other piece. Do I think that we have a good chance of it replicating? Yes. We are working very hard. Before we actually, when we announced results within literally months, we were able to dose our first patient. We were already behind the scenes very bullish on it. That should tell you because we did not lose any time in getting going on our second phase III. Now, the piece that I think we have appreciated over the past many years, and we've called in a lot of patients, we have patients who advise us on trial design, you know what matters to them, as well as sort of, you know, we are on a lot of private-public consortia and such for lupus. What's really become very clear is that only 20% of patients are treated today. All modalities are important. Very few biologics are available. And patients need more therapies. One of the key points that we've learned from our patient engagements is what patients tell each other. They tell each other that this is heterogeneous. Your lupus is not my lupus. We actually keep this in mind. That is why we're so excited about dapirolizumab pegol attacking from a B anticellular perspective, high upstream mechanism, and then litifilimab going up after the sort of BDCA2 type 1 interferon signature. I think that's what's making us really excited. You know, you see that now we're in, I think, the only company, the third product ever to have a phase III positive is dapirolizumab pegol, and then the only company with two programs with different mechanisms of action in phase III. It is competitive. Our teams are doing a fabulous job keeping us on track with enrollment and everything. We'll have a readout with SLE in 2026. You know, we put that up at JPMorgan about the fact that we expect a readout in 2026. Yeah. OK, great. We only have a couple of minutes left. I just want to try to cover Felzartamab and anything else to close. Just as it relates to the HI-Bio deal, you know, there's data in IgAN. There's work going on in AMR and PMN. I think, again, like, you know, we think about what holds investors back from ascribing value to these assets. I think people have a hard time understanding, like, in what area is this the best drug, right? Or which indication is the flagship indication? How would you answer the question about where you're most excited for this? You know, I want to say that I actually am excited about all three. And I'll tell you why. Because it's rare to have the same product with an established mechanism of action with three POCs simultaneously. That's what excited me personally a lot when we were doing the diligence. And I'll just give you some snapshots of the data that were so compelling and really made me an absolute believer. One is the anti-CD38 in the specificity that felzartamab has to protect sort of immune protection with going after the plasma cells that are releasing these autoantibodies. And in the AMR data, this is like a serious situation. They've got orphan disease designation. So they've got a lot of external validation, which is also very important and you know not to be, I think, minimized. I think it's very important. In phase II, they saw two things that I don't think other products have shown. One is nine doses over five months resulting in a greater than 80% AMR resolution by biopsy at week 24, and then 20% for placebo. And 67% of responders remained resolved. That 52 weeks, that's pretty compelling, you know, published in NEJM, as you know. IgAN is an important area because it is competitive. This mechanism of action is unique. I think that's the other piece, that this is the only product that offers you that UPCR sort of reduction, which we know leads to durable eGFR stabilization. Importantly, you have durability out 18 months after the last dose, out till 24 months. I mean, how important would that drug holiday, could that drug holiday be for patients? I think it would be pretty powerful. Finally, with PMN. Is that like the counterpoint to, you know, when investors, I think, make a table of these drugs and they just compare a% change in protein area, like, this doesn't rank at the top of the list. Is it more about the dosing holiday that got you comfortable with that or got you excited about this in IgA? I think it's both. I think it's 50% UPCR, 50% UPCR. That is important because I think they're all in that range. These are small studies. You know, the variability that could be there, we know it's distinctive, right? We know it heralds the eGFR outcome. That's one good thing. I mean, you know, this is a wonderful space to be in because for once, I find that, you know, the accelerated approval endpoints, surrogate endpoints are all established. It's exciting. Number two, yes, the durability is pretty powerful, right? I mean, think about it. In the future, I think there's also this potential of combinations and other things where we believe this is going to be a unique mechanism. I think it's important. With PMN also poised to start phase III in 2025. I think that we observed rapid partial and complete immunologic responses in both newly diagnosed and relapsed patients. And as you know, as well as people who were on immunosuppressive therapy. As you know, PMN is the largest cause of nephrotic syndrome. I mean, this is really high unmet need. Yeah. Yeah. OK. I am just looking at a couple of questions that came in because we only have a minute left. You know, one asking for, and we'll see what we get Priya, but a comment on anything Sage, right? You know, and then just any updates on development work with Spinraza. And then we can close. Yeah. I think Sage, I will just say that Zurzuvae, I remain really excited. We see a lot of momentum in our launch in how patients and prescribers are responding to the option that Zurzuvae offers women with PPD. I think it has really been a wonderful story. We have so many stories. I could spend the next hour. That is what I am going to comment on. I think very excited. Teams continue to work very closely together on this launch, which we think is really important. On Spinraza, high dose, very excited. We have, you know, submitted both in Europe and the U.S. We are working through, you know, we will soon be in that review period. We have a PDUFA date of September in the U.S. We remain on track for that. We think this is going to be very important. I mean, I think that the data that we've seen is very compelling. I will draw us to the neurofilament data that we observed at day 64. We think this is really, really important. Coupled with the data that we've generated from Respond, which is post-gene therapy and all of that, we think Spinraza remains a cornerstone for spinal muscular atrophy patients across all age groups. We are very excited about what this does for Spinraza. Great. All right. We're one minute over. I want to be respectful of your time. Thank you. Thank you, Priya. This was an awesome discussion. I think we covered a lot of interesting stuff. I appreciate you joining us. Thank you for the great questions. Take care. All right. Bye. Bye. Bye.