Yeah, the Global Healthcare Conference at Citi. My name's Geoff Meacham. I am the head of healthcare, global head of biotech, pharma research. Fun, fun. We're thrilled today to have NewAmsterdam Pharma. So we have Michael Davidson, CEO. We have Ian Somaiya, CFO. Guys, thanks a lot for the time. Thanks, Jia. So maybe we'll just do a quick background, Michael. You want to give a couple-minute pitch, just sort of elevator, then we can get into some PREVAIL questions and marketing and sure. Sure. I mean, this has been a great year. 2025, we announced at the end of last year in 2024, our BROADWAY phase 3. We completed our three phase 3 trials, which will be for the submission for regulatory approval across the world, and we had publications this year in New England Journal of Medicine and other very important journals. JACC, in particular, showed our great data on both LDL lowering and tolerability, and I think what everyone got most excited about was our benefit on major adverse cardiac event reduction, MACE reduction of 21% in the BROADWAY trial, which was a large trial, 2,500 patients, well over 100 events, and we saw this early signal of benefit with that 21% relative risk reduction, so we did a lot of analyses based on that, trying to understand what was the reason for this early benefit. We have a drug that we've been differentiating from any other lipid drug for multiple reasons. It lowers Lp(a), which is a very prominent target. It's in development for many therapies trials to read out in the next couple of years. A very, very atherogenic particle that explains premature heart disease and people have progressive disease despite being on statins, because statins have no effect on Lp(a). And our drug lowers Lp(a) by about 50% in that 50-150 range for Lp(a). That's a great benefit. Also, statins increase the risk of diabetes modestly, about 20%, especially on high-intensity statins. And obicetrapib lowers the risk of diabetes. We showed that in our BROADWAY data. Statins also differentiate lower large particles, and they leave the small particles behind. And the small particles are much more atherogenic and stick in the arteries more readily. And then we were able to prove, most exciting, I think, for a lot of the KOLs in the field, because it's a novel finding, is the Alzheimer's prevention benefit. This has been a part of the story from the beginning of NewAmsterdam when I started the company with John Kastelein. We had seen the data from the Mendelian randomization studies showing that when you have APOE4, which is the most prominent Alzheimer's gene, about two-thirds of Alzheimer's patients have APOE4 heterozygote. And then, unfortunately, you have a homozygote, you have tenfold increased risk of Alzheimer's. We saw a very prominent benefit on this really good biomarker, p-Tau217, which is increasingly becoming recognized as a valid marker that changes with improved treatment and very highly predictive. And if you lower it, it predicts benefit. We saw a great benefit in our BROADWAY trial, especially in the APOE4 heterozygote and even more so in the homozygote patients. So at the end of the day, we feel we have a very, very differentiated drug. It's the LDL plus story, efficacy that lowers LDL in the 40% range with 50% with a combination with ezetimibe. But it's the other benefits that really differentiate the drug as a very well-tolerated oral, easy-to-take therapy. So we're in a good place. We've seen, of course, the value being recognized by the community, the medical community. And we also have had some great changes in data from other external sources. There was a VESALIUS trial showing benefit of LDL lowering in a broader population, more of the lower-risk secondary population or primary prevention population. So those are going to modify the guidelines. So, now we're back to this time where we were maybe more than a decade ago where lower the LDL, the better. And now we have even more patients that need or deserve more effective LDL lowering. So, we're thinking we're in a really good spot with our drug and what we've shown and where the unmet need is growing based on new science. So, for us, this is an exciting time, and we look forward to next year. PREVAIL being our key outcome study, it's going very well. We're following the quality metrics very carefully, and we're really, really proud of our adherence to the study protocol. The drop-in dropout rates are low, better than any other trial we've seen or as benchmarks. And so that study will continue to progress in 2026. We have the two-and-a-half-year minimum follow-up will happen around October, which is the first time period where the study could be continued as long as we have enough events, which is the key also. Two factors, time, two-and-a-half years, and then events have to track to complete the trial. Yeah. I guess, Michael, let's talk about PREVAIL and the clinical piece, and we can get into kind of the market component. So you mentioned you're comfortable with the conduct of this study. Just want to get maybe an assessment of you. I'm assuming that you retest your assumptions as you see events between the different arms. Maybe talk about what you can do to just ongoing basis to monitor PREVAIL and maybe what gives you maybe the conviction, at least in the timing of it. I know, obviously, you're pretty convinced in the ultimate outcome, right? Right. So again, because BROADWAY was a mini PREVAIL, it was meant to be a way to de-risk PREVAIL for the skeptics because of the CETP, kind of molecule issues. So we wanted to make sure that BROADWAY itself was going to have a lot of events that we could look for and how we also guide the event prediction for PREVAIL. So we based PREVAIL on the FOURIER trial, which is one of the prominent Repatha trials. That's a CHD population. And those patients had an event rate that we basically how we determined our sample size calculation with a 20%, but also risk reduction. So whether it's just because we did a good job predicting, but BROADWAY was exactly what PREVAIL was that one year. It was exactly the same event rate. So we feel that was a good benchmark of event. Now, the thing is, the BROADWAY data was greater than expected relative risk reduction at that time point, so we're tracking that. I mean, if our event rates are falling short of the predicted progression rate, you can anticipate either we're wrong about our projections, which we don't think we are, or the drug is performing better than expected. So we'll also keep a track on that. We'll get back to the community more about the timing of that as we get more events adjudicated. We're doing that on an ongoing basis, but I think the quality metrics are great, and now we'll track the events, and we'll see where we are. I think we're expecting to come back to the medical community, the investor community, in about the middle part of next year with an update on the timing of PREVAIL. Yeah. And then just related to that is the regulatory timelines in the U.S. Because remember, our goal is to really take advantage of the rare opportunity of having outcomes data available at launch. So once we have a better handle on timing of PREVAIL readout, we can also give you an update on when we plan to file for U.S. approval. Yeah. That makes sense. I know you guys have been talking about diabetes and Alzheimer benefits associated with obicetrapib. I'm assuming that PREVAIL has enough power and data points to even directionally assess that as well? Diabetes, for sure. There's enough. Alzheimer's, the part we cannot do is we cannot get cognitive testing in the trial. So we will have biomarkers again. Like p-Tau biomarkers. We'll have PTAL and neurofilament light and GFAP, all the amyloid 42/40s, all the different biomarkers which are showing up as a really good prediction of future cognitive decline. We have those as well in PREVAIL. We'll have APOE4 phenotyping again. But now we'll have a much bigger sample size, and we'll have a longer duration of follow-up. We have promised to get back, again, to the investor community, the medical community. We are planning another study for Alzheimer's, a pre-specified trial that focuses on the patients in BROADWAY who responded the best, which are those that have APOE 3/4 or 4/4 at a certain age. What's really good about the data, we've published it in a very prominent journal, the Journal of Prevention of Alzheimer's Disease, just a few weeks ago. Actually, this got published this week. The data shows, which is what you'd hope to see, is that the drug worked best in those where p-Tau was increasing, and it turns out p-Tau was increasing in those that were older, especially those who were older with APOE 3/4 or 4/4, so exactly what you would expect of a good biomarker for predicting Alzheimer's disease, and that's where the drug showed the greatest effect on reducing that biomarker significantly, as well as neurofilament light and GFAP and amyloid 42/40 ratios were all consistently improved in the patients that got obicetrapib. That was published this week, and also, I think what we also believe is helpful to us, unfortunately, the GLP-1s did not work. EVOKE-1, EVOKE, and EVOKE+ did not work, and we'll see tonight the presentation, but we've heard that there was no effect on p-Tau217 in that trial. And so, again, it gives us, again, a negative showing that you don't improve cognition. You don't see improvement in p-tau. On the other hand, just published this week as well in JAMA was the TRAILBLAZER-ALZ trial showing that the improvement in cognition highly correlated with p-Tau217 changes. And so these are all starting to line up to give us a lot more. We've always had the confidence, but a lot more of addressing the skeptics that all you showed was biomarkers getting better. Is it really going to matter at the end of the day when it comes to preventing Alzheimer's disease? And we believe that the data is continuing to strengthen our argument that our BROADWAY data is very compelling. We know that a lot of the KOLs believe that already. But as we get the other study underway and continue to highlight this benefit, we believe this will be another really great differentiator of obicetrapib compared to any other LDL-lowering drug. And we'd like to ultimately see it approved for Alzheimer's prevention. That's our goal. So is the idea that you see rising p-Tau levels, Tau correlating, I think, with more cognitive declines, meaning like moderate to severe? Is that a fair characterization of the baseline that you were the patients that you saw in BROADWAY in BROOKLYN? Right. Well, for example. They were clinically diagnosed? We know. Unfortunately, we don't have cognition. It's just a very cognitive testing is something that requires a lot of expertise. We just didn't have that in the trial. So we will be doing that in our upcoming trial. We'll do cognitive testing. But what we, again, believe is that nothing predicts better the conversion of normal to MCI or MCI to later stages of Alzheimer's than p-Tau217. And there's been 10 publications in the last few weeks to continue to strengthen that argument. So we believe that over time, this will become something that will really highlight the differentiation of obicetrapib from any other drug out there. Again, the other benefits are safe, well-tolerated, easy to take. So those are the things that are going to make it even better uptake among those that you might have concerns about taking an anti-amyloid antibody, which can have serious risk factors, social safety issues with it. I guess let me ask you, when you think about from PREVAIL, if you had the same trend, and let's say, but you saw, obviously, a stat sig MACE outcome, so that's a home run. You can file with that. Would you want to what would be the range of outcomes? Would you have descriptive data on p-tau levels and the label? Would you ask payers to would you want more value for it if it had a trend on Alzheimer's? Obviously, no cognitive data. Right. I just want the range of outcomes. Yeah. We are going to look exactly to that point. We do believe with this type of trial, we can look at certain functional outcomes, conversion to people going on drugs for dementia, those kind of things in our whole overall. As you do all these outcome assessments, you look at a whole variety of things that go along with the traditional MACE benefit. You can look at the same thing for the diabetes benefit. We'll see. We already saw that in BROADWAY, a decline of people going on the new drugs for diabetes, for example. So we can see similar things in Prevail. But the key will be our own prospective trial, which we are starting sometime next year. That'll be the basis for a population that we think is well-suited for obicetrapib, which are those that have a certain age and they have APOE4, either homozygote or heterozygote. Is this a phase 2B? Phase 2B. Yeah. We're calling it phase 2B. But we believe there's a chance, very low chance, but there's a chance it could be a basis for accelerated approval, so. Is there a scenario where you could maybe get another entity to fund a large-scale phase 3? That way, you don't have to take the financial risk, but you, obviously, if it works. There are, like, the Gates Foundation. We're looking at all kinds of things. Okay. You're creative with. Obviously, Bill Gates had a father who died of Alzheimer's. That's an example. These are things that we could look into. We feel that there are. But at the end of the day, though, because the population we chose is such a high risk to convert to Alzheimer's, it's not what people think when it comes to cost. And so we feel that after PREVAIL, when we're a company that has a cardiovascular drug with well-proven benefits, we can proceed with a true outcome study on our own if necessary. Yes. We had Marty here yesterday from FDA. He was talking about creative ways to accelerate development to remove kind of the white zones where there's just sort of dead time with the regulator. If this works in PREVAIL and you see the Alzheimer's benefit, are there ways to convert your phase 2B to a pivotal? That's how we're looking at it, actually. Yeah. Okay. Yeah. I mean, it would be the phase 2B. That's how we're phrasing it. But we also have all the supportive data from PREVAIL, so. You'll have baseline sort of cognition and all that. Right. Okay. Yeah. That makes sense. Awesome. Has there been science on the mechanism of CETP? And is it classic sort of anti-inflammatory? It's anti-inflammatory in that it removes the inflammatory stimulus, which is the oxidized hydroxycholesterol. So in other words, we know that inflammation is a big factor in Alzheimer's disease, as is in atherosclerosis. The analogy I like to give is you got a splinter in your finger, and it's inflamed. What's the best way to get rid of the inflammation? It's to take out the splinter. I mean, the same thing is true for the brain. If you have inflammation due to hydroxycholesterol, the best thing to do is remove the hydroxycholesterol, which is what HDL does. So we feel that is the core pathology behind APOE4 that we address with CETP inhibition. Maybe this question for you. When you look at sort of consensus expectations for OB, to what degree do you think they bake in kind of Alzheimer's and diabetes benefit? Is it just MACE and cardiovascular sort of success blocking and tackling, or there is another dimension to what you think the street expectation is? Geoff, that's a loaded question. I could turn that right back to you and ask you what you're assuming in your model, but if you look at consensus, it's hovering around $2-3 billion in peak sales. During our R&D meeting in the summer of this year, we obviously shared with you what we think peak sales potential is, and it is $8 billion plus, so there is a disconnect. And depending on the model you look at, there are obviously many sources of variability. None of those models assume any value for Alzheimer's, and I think, as we've said to you before, the value in MACE is having a positive study. It's really less to do with the number. As long as we have a successful study, we have a validated mechanism, and we inherit the class label, and this is an important point. The FDA has harmonized labels for lipid-lowering therapies, so we benefit from that. I just don't want to be in a situation where you have a positive MACE outcome and then the Alzheimer's stuff is trending, and then that's a disappointment, right? No. Look, I don't think it's. It could be. It's possible, but look at our data from BROADWAY. It's. Unequivocal. Unequivocal. The P values are 0.0002 or something like that. Yeah. So it's unequivocal. Yeah. You can get to seven or eight without any diabetes or Alzheimer's benefit. Our 8 billion plus is entirely predicated on CV. Yeah. Okay. Okay. And I know you've talked to, you spent a lot of time probably talking to U.S. payers. What about the global? What sort of leaps do they have in terms of how they, I guess there's a clinical history with CETPs that you guys are sort of undoing. That's mostly a U.S. phenom. Is there anything outside the U.S. that you have to overcome with regard to CETP attitudes or? Yeah. I can take that, I guess. I think we've deployed MSLs in the field for two years now because that is an issue we had to address, and I think they're making a lot of headway. Of course, the data itself is the best way to get the skeptics on board, and our JACC, the Journal of the American College of Cardiology paper, I think, which was the subset of BROADWAY that showed that MACE benefit more clearly, was a very well-received publication showing the statistical difference. After six months, it was like 0.003, a very statistically significant difference in MACE in that study, so that's a big factor. In Europe, we also have a lot of KOL support, many publications. One of the things that NewAmsterdam excels at, because that's our background, I mean, both John Kastelein and I are academics. I'm still seeing patients at the University of Chicago. So we're very embedded in the academic community. And that's where we are. That's, for us, is our home. So if you look at what we've done on the publication side, New England Journal of Medicine, Nature, JACC, JAMA, all these things have really, I think, impacted the medical community and where we're going with obicetrapib. And so Europe, we have our Menarini partner also engaged with very much outreach with their MSL network, already meeting with KOLs. And so they're preparing for the launch. And what's great about Menarini is it may not be that well-known in the U.S., but in Europe, it's very well-known. It has the largest footprint of any company when it comes to cardiovascular medications. And so we feel we're well, we have a great partner there to help us in the launch. That's awesome. I mean, just to share some numbers with you, Menarini has 6,000 sales reps in Western and Eastern Europe. That's a sales organization that we could never imagine being able to build on our own. And given the economics that we have retained on the drug, with royalties going up to mid-20% and milestones that are still owed to us, which are north of EUR 800 million, and a deal that was struck when we had phase 2 data. So to have that quality of a deal with a partner with this level of capabilities, and Michael mentioned, they're amongst the leaders. They're number one in primary care. They're number one in cardiovascular care. And they're top three in the endocrinology community. Yep. That's helpful. Let's talk about—so we had a session with Merck earlier, and they were talking about their oral PCSK9. And there's a bit of a mixed view of that, just given the food effect. But I think the data are good. But there's a discussion of statins are not enough, I guess. We would probably most people agree with that, right? So what are maybe some of the range of guideline things, assuming that you do have some success in PREVAIL? How would you imagine guidelines playing out with respect to PCSK9s as one vertical, CETP as another, maybe Lp(a) as another, looking out a couple of years? So I think VESALIUS was a big help because it opened up another large segment of the population, proving that getting LDL levels below 55 reduces mortality. I mean, that was the key thing. And so that mortality benefit, which was not seen in FOURIER because it was shorter, it went longer with VESALIUS. It went to almost five years, which is quite long. And they saw the mortality benefit there significantly. So that means the guidelines are very much affected by that type of data. So what we're going to see, basically, anybody with atherosclerotic disease, and it could be as early as you have a calcium score. You had a calcium score. You went to your doctor. You're 50 years old. You have a plaque in your arteries. You now need to have your LDL below 55. What does that mean for the population? It is a huge change in the number of people that need to be more aggressively treated, and statins alone are not going to be enough, so that brings us to what we need to add to statins, and we'll have LDL lowering around 40% and then a fixed-dose combination around 50%. Merck, with the oral PCSK9, will be in that 55% range. The injectable is similar, so they'll have LDL lowering, but we're still in the same range, and the advantage that we would have, of course, is we don't have the food effect or the taking it without eight hours of fasting. It's like Rybelsus, and you can't take any other drugs with it, so that becomes problematic, but I see it more being utilized for those that don't want to take injections on Repatha, more of that type of patient. If you want a CETP inhibitor and all it brings, you don't really compromise the LDL-lowering efficacy because you have a 50% combo pill lowering LDL, but what really drives the benefit, based on all our research, is the other benefits: the Lp(a), the small particles, the diabetes reduction, and now the Alzheimer's benefit. We become the dominant go-to drug after statins, and for the majority of patients who are on a statin, if they get obicetrapib or obicetrapib with ezetimibe, 90% plus are at goal of below 55, and I think that's the message we want to get out there. These are all great drugs. They all have a role to play. But when you have that individual patient in front of you, you think about where I need to go to get them to goal and what else I can provide benefit-wise to them. We believe obicetrapib will become the go-to option for those patients, especially because of the tolerability and safety, which for most patients is the number one issue. They want ease of use. They don't want any side effects. And for them, that's the most important thing. And when you can tell them you can lower their Lp(a) and you can lower their risk of Alzheimer's, you got a much more motivated patient as well. And maybe, Michael, talk through the Lp(a) trial you guys are running with PCSK9. So how should we view that in the context of kind of the body of work on obicetrapib? We already have a lot of data on Lp(a) from our BROADWAY and BROOKLYN and our TANDEM study, all showing this 50%. We published the pool data, 50% Lp(a) lowering in that 50-150 range. And so that is a benefit you cannot do with any other oral agent. And we won't have an oral agent that can lower Lp(a) to that degree until maybe the Lilly drug comes out, probably five years from now, five, six years from now. So we'll be the go-to oral agent for lowering Lp(a). And then hopefully, we're going to have the injectable Lp(a) drugs that are serving the over 150 Lp(a) patients that have already existing heart disease. And that will be specially priced, probably, because that's how they were set up. For the other patients who have high Lp(a), which is the 90% of the other high Lp(a) patients that have Lp(a) below 150 or they already do not yet have heart disease, we see obicetrapib as being the go-to therapy for those patients predominantly. So we see this as a really important differentiator from any other drug, including the PCSK9 inhibitors do lower Lp(a) by about 15%-20%, 25% maybe in some studies. But we're double that with our data. So we feel that if you're looking at an Lp(a) patient before you, which is now my leading referral in my clinic, is high Lp(a), these patients really want something done because, unfortunately, a lot of them have very bad family history. So they know basically the risk and the complications of high Lp(a) for their own personal reasons, that they're going to really be motivated to take obicetrapib for that reason as their option. That's the one thing is that you guys don't have to worry about baseline Lp(a). You don't have to worry about there's a lot of things that you don't narrow the opportunity for your drug. Some of the Lp(a) drugs have to worry, have to focus on just tiering, right? Right. Especially for the payers. I mean, payers are going to say, "Do you have established cardiovascular disease? Is your Lp(a) above 150?" Because, again, they will be specially priced. So they'll go through prior authorizations. If you don't hit those criteria, the payers aren't going to pay for it. And so. What's your view of the? I guess there are two sort of cynical cases. We had a Cleveland Clinic with Steve Nissen, who was unbelievably bullish about Lp(a), but he's like, "I don't know the actual percentage in the real world of who this is because people that come in to see me have known cardiovascular disease. So if you take 1,000 people, I don't know how many you're going to read negative." And diagnostics is an issue. And the other thing is you can live for 30 years with higher risk and maybe not have an outcome. And so you have to just focus on the people that have comorbidities and high Lp(a). Right, right. Those are some of the nuances. Again, none of them affect you from a clinical. Right, right. Exactly. Yeah. I mean, that's true for anything, but yeah, you're right. The patients with high Lp(a) that do the worst, those that also have high inflammation, high CRP, they have diabetes, those are things that you also know increase their risk. The other genetic factors involved that I'm interested in that may make the Lp(a) risk double or triple what it otherwise would be. So those are all things we can do precision medicine better to select the patients that are most likely to benefit from Lp(a) lowering. But that's again, the beauty of obicetrapib is you'll be using it anyway for LDL lowering. So why not get the benefit of that Lp(a) lowering with your therapy, which is kind of like a bonus. It's a bonus benefit. You can make that statement quite broad because there are many reasons to use obicetrapib. There are really none to choose something else. Yeah. That's exactly right. Just in that maybe commercial context, Ian, so when you think about the companies that have gone through the White House this year and gone through kind of the MFN scrutiny, I know you guys are not ready to have those conversations. But when you are, how do you think about a drug like obicetrapib, which has global appeal, but to try to harmonize the OUS and the US kind of net price? Yeah. So you hosted a very interesting lunch session where we really got to hear about the goals for the administration. And I really liked the overarching goal is to harmonize pricing globally. That doesn't mean just simply bring U.S. pricing down. It's really to bring international pricing higher. And as you think about the steps that companies have taken, so obviously, there were 18 companies that were given letters from the administration, right, and were asked to come to the negotiating table. Well, we'll benefit from learning from all of them. We're not going to be the ones. We're not going to be the trendsetters here. We're not going to be the company that establishes a new algorithm for pricing on a global basis. What we can say is the drug delivers a lot of value that goes above and beyond LDL. Our overarching goal is to make sure we have broad access at the time of launch. I think we have all learned from the critical mistake when the PCSK9s were first introduced to the market from a pricing and discounting standpoint. So that's been corrected. We just want to simply participate in that pricing paradigm. Yeah. To what degree is this mostly you guys taking a leadership position, or does Menarini help inform the OUS initial pricing? I know they're obviously there for commercial distribution, etc. So contractually, they will set the price in Europe. But we have a great working relationship with them. So we're working together on the global branding, the initial strategy, the commercial strategy. And obviously, there's a lot of data that supports pricing decisions, which they're very well versed in. The reality is there is differential pricing in Europe for the lipid-lowering class. And we should expect that for our drug as well. I think there are steps legislatively that have been taken where, and I'm specifically referring to Germany now, where the net price is not disclosed. So I think it's the same situation as we find ourselves in the U.S., where we're all aware of what the gross price is, but what's been negotiated is often unknown. The good thing for you guys is, though, like you said, I mean, you're not, and you said it well, you're getting all the other benefits for, I'd say, minimal, depending on where you price it, but less you're getting a MACE benefit, in theory, locked in. Right. No, you're exactly right. I mean, if you think about health economic studies, and we're obviously working on those now, the benefit we provide goes above and beyond other therapies, and there's a real dollar value, real dollar savings that we're providing with our drug. I'm assuming with Prevail, you have all those economic outcomes also. Yeah. Yeah. We're going to definitely get that. That's a big part of what we're going to do. We're already doing that with BROADWAY, too. We're going to look at economic outcomes. Yeah. I've always been a big fan of that. Other studies that I've done, I look at economic benefits that you achieve by lowering LDL cholesterol. Yep. That's also a big part of your payer argument, too. Yeah. So Alzheimer's phase II, you have the Lp(a) trial. Are there any other studies? Yeah. We have the RUBY study. We hope to get done by the end of next year, which is a diabetes study. The other ones are the HORIZON trial for Lp(a) that should read out in the first half of next year. The one thing that Michael mentioned earlier, the impact of ASCELSIUS in terms of the updates to the treatment guidelines. I think that's one of the most understated milestones and drivers next year because it could literally increase the market by either 50%, 60%, or 100%. Do you find that when you talk to KOLs, maybe some that are more academic and run trials versus those that are more guideline-driven? I think BROADWAY, I mean, PREVAIL is going to obviously dictate the sentiment, right? But do you have sort of a situation where the BROADWAY and Brooklyn data are enough to say, "Look, CETP, we're good with the prior baggage," or do you? No. I think no, no, no. We know that for 90% of doctors, they're believers, but we have the 10% that need PREVAIL. So that's why we're not launching without PREVAIL data. Because it is the minority, but it could be a vocal minority. We don't want any issue to be involved when we launch the drug. So that's. But none of the KOLs are thinking like Alzheimer's or any sort of neuro or metabolic benefit on diabetes. For us, you mean? Yeah. No, they are third. They're the owners. No, they're not. But as far as I would tell you, though, again, I know they're lipidologists or cardiologists, but they're actually extremely excited about the Alzheimer's benefit. And so the neurologist is a little bit more on the skeptical side because they've been such a big advocate for the amyloid hypothesis. And it's kind of like been driving the thinking for more than a decade. But if you go back, it's interesting. When you look at the literature because if you went back another decade before that, almost all the literature was about the lipid metabolism in the brain and how that affected Alzheimer's. And then they went over to amyloid, not realizing, I think, that the amyloid production was stimulated by the abnormal cholesterol in the first place. And so taking the amyloid out, you might have some benefit. But the best thing you can do is improve the lipid metabolism, which is what obicetrapib does. But nevertheless, we believe that the lipidology, cardiology community are really embracing the Alzheimer's benefit in a big way. We're seeing the brain-heart-health continuum really coming together. As you know, stroke is already an LDL-driven dementia risk. So LDL lowering is one of the key things for dementia prevention already for stroke reduction. Have you looked at other benefits like renal clearance? There is. Yeah. We already have. We published on that, too. Renal improvement is also evident. We'll have more data on that. We're looking at, of course, PREVAIL will be a much bigger sample size for that. So that's other things about obicetrapib that are really differentiating it across the board as far as, and it's not surprising because one of the most prominent longevity genes is the CETP loss of function. And so if you look at all the different longevity genes that are out there, that's one of the top. So it's not surprising that it affects a number of other all the organ systems that are involved with aging. Okay. Michael, Ian, thank you very much. Okay. Thank you. Yeah. Thank you.