Alright. Welcome to the second day of the Citi Back to School Biopharma Conference. This is the twentieth annual. We took a little hiatus last year, but I'm happy that's back. I'm Jeff Mitchell. My team's here as well. New Amsterdam. Thanks, guys, for joining. It's gonna be a good dialogue here. So we have Michael Davidson, CEO, Ian Samaya, CFO. So I don't know if you would only kick it off with kind of, like, the two minute pitch. We have tons of questions. Congrats on all, like, the huge phase three progress. I don't know. You wanna give a a quick two minute, and then we can get into questions, or it's up to you? Sure. Sure. No. Thanks thanks for being here, and I I appreciate being included. So New Amsterdam Pharma, we we ended last year with our, you know, fantastic, you know, phase three data, you know, showing great efficacy on LDL lowering and and safety no different from placebo, but we got very excited about the whole, you know, MACE benefit of 21%, you know, four point MACE reduction. We raised did a financing off of that, entered the year, you know, very strong position cash wise. And this year, a lot of other great achievements. We published Broadway paper in New England Journal of Medicine. The fixed dose combination study we published in called Tandem was published in Lancet. We now just published in Jack this this past week and help presented at the European Society of Cardiology, the the pulled MACE data from both our two phase three, Brooklyn and Broadway, you know, showing the the pulled MACE data looking even more than twenty one percent relative risk reduction for the four point MACE. We've had a lot of, you know, tremendous accomplishments on getting PREVAIL fully enrolled and now, well past the one year mark of the last patient enrolled. And so that study is right on track with eight or nine DSMB meetings showing continue on as recommended. And we look to finish that trial late next year. And one of the highlights, of course, this year has been the filing in Europe for the EMA approval just accepted about two weeks ago. And so we're excited about that. And so we're feeling we're in a really good position. And what's exciting about the drug is to kind of as a clinician, cardiologist, what I'm most excited about is that this drug has the benefits of not just lowering LDL, it's the plus benefits, lowering LpLA, lowering small particles, lowering the risk of diabetes. But now this new benefit we demonstrated from our Broadway trial is showing that in APOE4 patients, even overall, we lower pTal217, an excellent biomarker of amyloid pathology in the brain over twelve months. But what's most exciting is that in these eight point four patients, even greater degree of pTal two seventeen reduction. And the homozygotes, e44, which are destined to get Alzheimer's almost one hundred percent, we saw across the board all the biomarkers improve significantly in that subset. So we feel we have a very drug that can provide not just LDL lowering benefits that that translate into MACE benefits, but all these other attributes that make this drug very exciting. And we're we're looking forward to getting it to patients as soon as possible. Awesome. Yeah. Thank thank you for that, Michael. Yeah. So let me ask you. The totality of data for obisetropiv, you know, looks looks great. The you sort of have broken through kind of the history of CTP, but I wasn't sure what the that's probably the view from KOLs that know the molecule and know the data. But in the broader cardiology community, do you still feel like there is, a, you know, a a sort of remembrance of of what happened with old CTP inhibitors, or do you feel like they kind of now view OB as, like, the the the best in class Right. Of the of the mechanism? No. It's it's it's a great question. I think we we always and not we can't take anything for granted, I I would say. But there there there is this class history, and we, you know, purposely deployed our MSLs more than a year ago into the field to start talking to well, you know, well over a thousand, you know, key opinion leaders across The United States and getting their feedback. I think what helps more than anything, of course, is is is clinical data and showing, the benefits of olicitropib this already this proven, this MACE benefit in the Phase III trials. Ultimately, the PREVAIL trial will be the main evidence of benefit showing outcomes in a close to 10,000 patient trials. So we feel we've come a long way. When we do our market research, the vast majority of doctors, 90 are on board already on the LDL plus benefits and all those things, but we still have, you know, some, you know, you know, some skeptics that we have to, you know, get get comfortable with the the class because of the history. But I think they're all even the skeptics now based on our data. You read some of the editorials that we just got published in Jack. The the skepticism is is is is is now turned into great enthuse enthusiasm, but waiting for the outcome study to and that and we we purposely knew that. I think I take very strong pride in the fact that when we started the company, we started phase three. You know, we started our three phase three trials in the outcome study at the same time. We started the outcome study very early in development, and we didn't have enough money to finish the trials. You know? And now now we do. So we took we took a lot of risk financially to get going on all these trials, and it's paid off now with having the outcome studies happening, you know, right at the launch time frame. That's how we that's how we get around this the the the the the the class history issue. Yeah. Let let's talk about that for a second. So that's always been sort of the intention is to have outcomes at or or or near launch. You know, what's your perspective maybe from talking about, you know, the data thus far with with payers? Do they sort of validate what you're what you're thinking about in terms of having outcomes, you know, meaning better reimbursement, better access? There are lots of proxies in in cardio launches, right, for better access and pricing post outcomes. But I wasn't sure if, like, that thinking has evolved with We're we're we're we are doing a lot of interactions with payers. That's a big big part of that. And and our most payers are comfortable with the data available in the public domain, not not in the label. So we we have that. But I think our objective is to get the strongest label at launch. And so we we we will weigh the the pros and cons of that and the timing of that. But we feel because we started this outcome study when we did, we feel we're in a good position to to know that when we launch the drug, the outcome study will be pretty much in in the public domain or or or in the label. We we the the time difference is not very not very much between the two. So we're we're we're considering how to how to time that appropriately. Yep. Do you think that with the outcomes data and all the data you've had so far, will you will the totality of data in, say, diabetes or in Alzheimer's be enough to, you know, to have a commercial sort of angle on these markets, or is it just the the cardio benefit? No. We think we do think these the plus benefits will have a tremendous effect on on the uptake. And it's gonna speaking as a clinician, I mean, I I can tell you that, you know, most patients don't wanna take a drug. And and it's a it's a sales job to get a patient to take a statin, is an excellent drug, well tolerated, safe. And we we you know, some patients are just very reluctant to take any medicine, and and and and and statins have such great safety and benefits. It's it's still a little bit of a hard sell. So we we believe the other benefits of elbocetropib, especially the LpLA, the diabetes benefit, and now the APOE four Alzheimer's benefit are are are gonna be highly highly motivational. These benefits are gonna what's gonna drive adoption. So we we we we feel that's a very important part of our message and even our commercial story going forward. Yeah. The the diabetes benefit I mean, there's a lot of cardio drugs that have a spillover benefit into, you know, into metabolic disease. The Alzheimer's is is unique, though. How how has that resonated, you know, with with clinicians, since you guys have have accumulated? We're we're just getting started with that. We we have the data from Broadway, but the some some great excitement, but there's also this, like, this is just too good to be true. I mean, the the benefits that we saw were across the board very significant in the entire population, but even more so in the higher risk patients, the eight 8.4, and then the and then the older they were, the greater the benefit. Just consistent with the biology of Alzheimer's, you want to the highest risk patients had the greatest benefits such that the E4 homozygotes had across the board benefit in all the different biomarkers, including neurofilament light and GFAP, pTau-one 181 and amyloid fortytwo 40 ratio. So the benefits were as good, if not better, than the anti amyloid drugs. In fact, the neurofilament light reduction has not been seen with the anti amyloid drug, which is an inflammatory response to neurodegeneration. So the the drug the we're gonna we need to continue to develop the science around that, but was part of our investment. When I started the company with Doctor. John Castelline, we said we believe there's an Alzheimer's benefit here. We want to prove it. Out of $200,000,000 they gave us $1,000,000 to look at Alzheimer's. We think it's very exciting. That's what our Alzheimer's experts tell us. But we'll continue to build upon it. And I think when we have the drug available for patients, we'll have even more data to support this added benefit of obicitropib. And the the mechanism of that is essentially looking at cholesterol in the brain and management. Is that the Well, e e four is a lipid gene. It's twenty five percent of the population. It's two thirds of all Alzheimer's disease. You know, threefold risk if you're e three, e four, ten times risk if you're homozygote e four. Very, very the most important gene for by the way, other genes, a b c a seven, TREM, they're also lipid genes. So there's a there's a there's definitely a lipid angle to Alzheimer's. There's no LDL in the brain. It's only apo e four. It's only apo e, and there's and there's HTL. HDL is the one lipoprotein that can transfer us to blood brain barrier or at least interface the blood brain barrier to remove excess junk out of that's what HDL does. And so we the high HDL increase that we get a 125%, you know, we believe that is what we move. We know it removes the amyloid from the brain. We know it removes toxic sterols. It also can can add positive things like antioxidants and DHA to the brain. So a lot of things about HDL and interfacing with the brain histology and, you know, pathology are are potentially benefited by elbocetropiv. Is there when you look at some of the totality of data for PCSK9 or for LP or whatever cardio mechanisms, is there have they even have they looked at neuro or Alzheimer's? We know that stands don't work for outside. We we know that stands don't work. And so so we think we have a real differentiated thing here. PCSK9, by the way, just step back for a second, the reason why we got interested in Alzheimer's for CTP inhibition is the genomics were there, genomic validation. We had animal data supporting it. Persist kind inhibitors don't have that genomic validation. They don't have any so we have a lot of science even preceding our clinical data that showed a benefit. So we believe this is unique to opacetropin and it's related to the HTL raising effects. Great. Thanks. So maybe since we're on the topic of AD for opacetropin, could you please I know you guys gave us a quick overview of some of the findings you had presented at AIC. But maybe just more broadly, how do you think these data inform the ongoing development strategy of OB and AD? Right. So we see this as part of the LDL plus story, in other words. If you're ApoE4, which is 25 of the population, you also have high LDL and high LpLA. So it's at least a quarter or more of the lipid high lipid population. So we therefore, you put that into the precision medicine approach where you have a drug that can lower their LDL and LPLA, but also potentially mitigate their Alzheimer's risk becomes a real important motivator for these patients. If you have I see I measure APOE genotyping for everybody in my patient population, if they want it. I mean, some people don't want to know, but if they want to know, we look at it and we give them advice about what to do because it is actionable. You can obviously know you have increased risk. You can do a lot of other things that might mitigate risk like good lifestyle and so forth and not not have diabetes or not smoke and things like that. But but but but what you can do as far as true benefit on on now with lowering pTal217, which you can now also measure clinically and see what you're doing, I think this is the future. I mean, having a drug that can actually treat the underlying disease pathology is something very exciting. Now we're getting we need to build upon this data with more more information, you know, more validation. But even this data alone, we know, is is gonna be quite powerful to get the message out there that we can, not just lower LDL, but have this other benefit as well. That's that's our that's our focus right now. I guess we should also speak about the PREVAIL study. Yeah. Right. So PREVAIL, we have we do we do have the ability to measure the biomarkers again, longer, much bigger study. We are going go to the FDA with this data and discuss, you know, what another study would look like. We think that we first want to confirm it with a smaller study. And I think what we've we're trying to also recognize that we are a company that has a lot of cash available right now. We're going to need that cash for the launch of the drug. And so we're to be very wise with our cost considerations. But we think we can without spending significant dollars at all, we can further validate this either with with Prevail plus maybe another study that's not very expensive that we can then build upon that for follow-up studies with whatever the FDA believes is the right analysis or type studies to do to get the the indication for prevention of Alzheimer's disease. Is there a way to maybe partner this and and share the risk do that? Yeah. Because it's it's a hard yeah. It's a Are you gonna be marketing, though? Like, let's say the best case scenario and you do have a a benefit is is New Amsterdam gonna be having a neurology sales No. No. But I I think we it's hard to do indication splitting for for that, but it but it like I said, this is such a we have if you if you have eight o e four, you're just very motivated. I mean, just you're you're just very motivated to get something that helps. And so I don't think it's gonna take a lot of effort to get patients that and then and then I think, course, you know, if you look at clinicians out there, how many are actually looking at 8.4? It's a very small number right now. But once once you have a therapy that might make a difference, that that chain that chain is dramatically. And so we we do believe the future is is is is is two things. One is now a good a good biomarker, p tau two seventeen, which can predict disease twenty years in advance. And and secondly, it would be a therapy that can make a difference. And and and these two things, we believe, is where we could, you know, have an important role to play in the future. And I think right now, people are skeptical. I I I understand. But when when they chance to see our data, understand the biology behind it and the science behind it, I think we're gonna get a lot of people enthusiastically supporting using obocetropin for an LDL or a drug that has this other benefit. Post your FDA meeting, what's kind of the bookend of what, you know, could could happen? Is this, a pilot study of a few 100, like, say, sub 500 or That that that that that's kinda how we're thinking about it right now. We yeah. Could I mean, the the the response we're getting is it's just too good to be true, and we need to you need to confirm it. So we're we're but, again, at at the stats, the the this you look at the the data itself, you'll see this is not a this is a very statistically significant benefit that is makes a lot of sense when we look at the the risk of the patient. So we'll we'll confirm it with the like you said, and then we let's see what the FDA has to say about accelerated approval for something like this. Sorry. I think earlier you mentioned you guys have the ability to measure a biomarker and prevail. Just wanna make sure it's it's p two seventeen. Yeah. Yes. Yeah. For all patients, all 10,000. Well Yeah. Well, we we we can As many as we can. As many as we can. Yeah. I mean Yeah. Because the blood samples are not gonna be available for every patient, but Gotcha. We think we can get the most. Yeah. But but there are there are there's also other p tau type biomarkers that are even are coming as well. I mean, the mark the field is changing dramatically now with these biomarkers. And so we feel we're in a really good spot to to be able to assess, you know, what to do for prevention of Alzheimer's disease. There's there's no imaging, though, in in though. There's no there's no imaging. No. No. But but that's the thing about these biomarkers that that we're hearing is that they're as good as imaging. They are that's what the that's the benefit they are as good as so with whether we have to do imaging or not for this other study that we're thinking about, we're we're we're we're we're gonna maybe do that in a in a a of patients maybe, but not but not in PREVAIL. It would be a separate study. Right. I think it was really interesting earlier you mentioned, you know, opisotropin could have the potential to to treat AD pathology, which honestly is could be, you know, truly transformational. So thinking about, you know, the current two approved assets that are on market that target, you know, anti amyloid, how do you envision OB, you know, fitting into that landscape of AD treatments and also take into consideration the complex pathophysiology of the disease and and maybe other emerging therapies that are in the pipeline? So you're you're talking to a cardiologist, so I'm not but I I'll tell you one thing I in cardiology that we we feel that has been the kind of the the paradigm, which is if you have a patient who has high LDL, has not yet had a heart attack, you give them a LDL lowering drug. It prevents that first heart attack really well. Once they are once they've already had a heart attack, it does prevent the second heart attack pretty well. But once you have heart failure, LDL lowering has no benefit. So we feel these anti amyloid drugs that are that how that how they're being used now when there's already neurocognitive decline. You know, the as you you've heard that how they describe the benefit, you can recognize your family members four months longer with these at the best case scenario. But in the APOE four homozygous, it does not work at all. And and and and they also have a higher risk of ARIA if you're any four, any three four or four four. And so, you know, we we, in some ways, with elbocetropib, the data we have already with with that, we we would be a a therapy for the e four e four homozygotes, which, again, you're not it's contraindicated to use the anti amyloid therapies. And so we also feel that and we we hope the field does move more towards the prevention side of things using these these exciting new biomarkers away from this waiting for cognitive decline before you start treating and moving more towards a prevention approach, which is what how LDL got got established as a truly modifiable risk factor. PTel is different. It's not a it's not a risk factor. It's a it's actually a disease pathology marker. And so we're see, it's what you know, the the pTel in the blood is what's, you know, this explaining amyloid in the brain. And so, you know, showing that decline progression of amyloid with p tau is really showing a disease modifying effect. And so we think, you know, prime prevention is is someone who already has no amyloid or a little bit of amyloid preventing it from getting higher amyloid. That's what we're focusing on with with obicentropib. The combinations so stick with combinations, but back in in cardiology, talk a little bit because your your data has been impressive just as a monotherapy. Talk a little bit about how you view the market, you know, from a polypharmacy context, So combinations with PCSK9s or LP. Would you view OBI as sort of the foundational therapy and then maybe depending on the subpopulation add other mechanisms? That that that's how we we see it. We we, you know, we have if you dig into, we have combinations with SGLT two IP and genomic validation of the two for preventing diabetes. Of course, we have the the the the trial combining obacetropir with Repatha for LPA lowering. So that's that's also underway. And the Vinson trial. So that that is our strategy will be, like, almost like a pipeline and a pill. This is a what's great about elocentropin, which, again, we we don't get a lot of credit on the value side. This drug is very good. It's a small little pill. It's the size of a baby aspirin. You can combine it with almost anything. And so for those companies that are looking for a cardiometabolic, you know, kind of combination, you know, we're an ideal drug to combine with with any other other cardiometabolic drug. An oral an oral GLP one, we have great we think we have great validation for that combination, and we're working on ways to further that science as well. And same for LPA lowering drugs that are oral. Don't lower LPA as well as the injectables, but maybe in combination with obicitropin, we can have an LPA oral that now has greater LDL and LPA lowering benefits when you combine the two together. So we see this as a we were well positioned to be a combo to add to a lot of these other cardiovascular drugs that that need, you know, another another different approach or additive approach to reducing risk cardiovascular risk. The Vincent study is is this calendar year still? Or is We we we decided to expand it. Okay. And so it won't be this year, but it it'll be next year. So Sometime in '26. Yeah. Right. We got it. So but we but it's again, it's all about combining it with the PCSK9, oral PCSK9. It's more of a strategic study Yeah. To look at the, you know, the oral the oral PCSK9 is available. So we're looking at it as a as a as a way to to validate that combination going forward. In a way, I mean, with pretty good reimbursement now with PCSK9s, you're sort of trying to connect all the dots around getting better payer access by, you know, combining with that. Is there a step function, though, in terms of efficacy that you feel like would, you know, would be what's it between clinically meaningful, numerically better, you know, meaningful better. I don't I don't know what the what does a win look like in in in Vincent? I think for for us, I think we we you know, I I I think I I put my clinical head on here too. I think that we have the type of drug profile where where you're on a statin, and it's either not enough or you cannot take a statin, and so you need another drug. And you want an oral agent and either have obicitripip alone or obicitripip with ezetimibe to fix those combination. We know from our studies that ninety percent get a goal with that, with either of those options, either alone or in combination with ezetimibe. And so we feel we could become the next go to option for any any patient. If you need more than that, you have a you have a you have a PCSK9, which has, you know, good LDL lowering efficacy and and and and potential safety. But we have a drug that has incredible tolerability. You know, no different from placebo and excellent safety and a lot easier to use, at least based on the oral PCSK9 for Merck. We we see that becoming the next go to agent for the majority of patients overall. So we we feel that fits very well into the to the majority of patients. So the p s k nine options are are gonna be nice to have also. But for primary care doctors, you know, what they really want more than anything else is they know that they they know statins now, another oral agent that they can add, and that's all they need to think about. They don't need to think about four four or five other drugs to consider this. One one simple I don't wanna get calls in the middle of night from a patient with side effects or they they they can't they have to take the drug without any food for for eight hours and can't take any other pills within thirty minutes or so. So it's a very simple, you know, well tolerated, and I think that's what primary doctors said it'll be very, very accepting of this approach as the next go to agent after after statins. But I would what I would say is the clinical learnings are now more limited because we had many patients on that combination, PCSK9 and and OB in our LDL studies. So it's really the value is strategic. And that's so that's why we describe Vincent as a proof of concept study. It's not the plan isn't to develop a a repath that will be combination in the future. The future is an oral PCSK9 plus OB. Yeah. Yeah. It makes sense. And then just on the down the road, obviously, could coformulate. That would be, you know, pretty straightforward. But you can also Yeah. Yeah. Coformulate in SGLT two as well. Yeah. Mhmm. Talk a little bit about the, you know, the potential development path. Yeah. We we have a patent, and we have we have already published Mandylion randomization data showing that they together, they they prevent diabetes better. But this is not something we're focusing on as a commercial story yet right now. We we're we're limited. Obviously, we're not we we don't we we don't have unlimited support to do a lot of these things. But it would be a trick you know, I think that's these are great drugs. S t l t twos are great drugs. This is their oral. So we we see as a future there, but it's it's not something we're working on on a in a formal way. Yeah. But but we are in a very unique position because we're the only company with a CTP inhibitor. And when you look at the the landscape of drugs, whether it's targeting l p o l a, GLP ones, and and other mechanisms, it's a commodity. And and that's the the marketplace we wanna take advantage of. Yep. Thank you. By highlighting GLP one, you kind of segue to my next question, which is, you you know, a lot of the data that you demonstrated in phase three kind of suggested that you could OB could have a diabetes prevention type of moiety. And, you know, think about its combinability with other oral agents, perhaps the GLP one, which also has shown, you know, proclivity to to decrease diabetes progression. You know, how how do you think that could inform docs going forward, and and where do you think that might take future development pathways? So, yeah, we we are working on that. We have preclinical studies underway with GLP one with obacetropib on on exactly that that that science. We we feel this is like, I I'm a prevent I'm a I'm a I'm a preventive cardiologist. I so I see that, you know, the way to really make a major effect on heart disease is is prevention. You know? And I I see that GLP one, SGLT two, you know, CT inhibition, you know, those three targets are are all kind of circling around where we can if we just start early enough in life, we can we can cure we could prevent heart disease entirely. So we do we do see as these are excellent combinations to think about. And we and and and there is there is interest there. We we we'll we'll we'll consider that when when we have a drug on the market. But right now, we're we we're doing the all the preliminary work to get those type of combinations ready. We are we are working on those kind of things. It is interesting that, you know, the I mean, Jarvis White, I think the tirzepatide showed, like, a ninety four percent reduction in the progression risk of progression of diabetes in the prevention study. But if you if you sort of talk to payers about that, they're like, there's no effing way we're gonna pay for that. You know? And so it's a higher bar, I think. But I agree, like, that, you know, that's gonna be maybe maybe you need a cardio benefit as well as a metabolic benefit to be persuasive to Medicare, to commercial payers to kind of change the the dynamic. We're in an administration now, though, that does talk more actively about prevention than prior I I I hope so. I mean, it's been talked about by a lot a lot of administrations. But right now, it's a tough it is a tough regulatory environment also. So we we we recognize that. And so we that's why I say our focus is LDL plus, and we we feel that the LDL lowering benefits is the cornerstone of the drug and the safety tolerability. And all these other all these other plus benefits are gonna really drive adoption. And to your point of all these plus benefits driving adoption, you know, I mean, they touch on cardiology, endocrinology, maybe even neuroscience potentially one day. You know, as you as you look forward to maybe commercialization paths in the future for OB, you know, how how do you anticipate communicating to all of these different plethora of doctors? Right? I I'd imagine the approach is probably very different for for each segment. Love to hear from that. We're we're thinking about a lot you know, it's a great opportunity and question, and we we feel that we have been thinking a lot about just addressing exactly what you thought about. We we we hired an AI person already to to help us get these messaging, and I'm using AI all the time in my practice as well in my clinic. I feel that's gonna help a lot to to get a lot of these messaging out there, you know, more effectively. And and so we're we're at the very beginning phases of that educational effort. Both both the the work the medical community itself, but also us as a company, we're we're starting to think about how to get all these plus benefits understood by clinicians and how that impact their utilization of the drug. Michael, do you spend a lot of time in a lot of larger cap companies spend a lot of time in Washington, you know, for various, you know, pharma tariffs, etcetera. But I asked another company on this earlier today, but the pill penalty is is unduly, you know, impactful to to you guys and to really all companies that have oral oral medicines. Is there any sort of evolution of that conversation over the course of this year? We we have not been involved politically, but we have heard, I mean, as you you know more than as much as a bit that that they are trying to get rid of the pill panel. So, yeah, we you you you've you've heard that. But we have a strategy no matter what. I mean, our strategy is that we do have the fixed dose combination with ezetimibe. So that's two separate pills. So they're they're not they're not pulled when it comes to the the the the renegotiating, you know, the there's the treated separately. Yep. And so that that helps. Again, that's why the combo idea for us has been part of our strategy to deal with IRA. We hope the pill penalty does go away because it's not it's not a fair way to judge, you know, how drugs are looked at. We think it will be you know, I you you we we we gotta look at the political landscape and see how that plays out. But but we we we have a a plan in place. So we have good IP protection for the drug till 2043. So we wanna we wanna obviously fully get the value of that protection across our lifespan of the drug. So we have we have a lot of we have a strong IP estate across the board for a lot of these other combinations as well that we're we're gonna hopefully you know, be able to deploy when when the time comes. It definitely feels like the plus indications kinda give you an opportunity to life cycle manage. You know, you don't have to immediately do a study in diabetes or Alzheimer's anytime soon. Right? But that can buy down the road five years from now, can buy you a line extension or a new co formulation, right, that has different IP and treated differently. Right. That's how we're that's how we're looking at it right now. Yes. Yeah. I think, you know, now that you mentioned that you're filing in the EU has been accepted, you know, we're all cognizant of your partnership with Menarini. I think you've previously said that you're confident in going alone in The US, but, you know, given that you still retain the rights to Japan and China and other OUS geographies, you know, maybe could you give us a sense of your, you know, various strategic considerations and and perhaps willingness to to partner out? Yep. So the so we are committed to launching the drug in The US on our own. We believe that's the the single best way to deliver the greatest value to the company and to to shareholders. Japan, China, or Asia more broadly, again, significant opportunities, but where we are unlikely to to sort of go it alone. So those are geographies that where we're going to actively pursue partnerships. And I think the the benefit of the the clinical trial program that Michael, John, and the rest of the team have have designed and executed on, it allows for a global filing. So the trials dataset that you've seen will allow for us to pursue regulatory filings in in China and Japan. So so that's something that, you know, we are going to be considering. And then perhaps that is an extension of that, you know, as you look for partnerships and and the LDL plus kind of profile of OB, what what do you be looking for in a in a large larger partner? You know, what what type of concentration or expertise would be important to you as you take those into consideration? You know, obviously, it's it's having that cardiovascular footprint. You know? Menarini is known in Europe for it's it's one of the top, you know, cardiovascular players, but especially in the primary care cardiovascular area, which is, you know, where a lot of these drugs are written. So we we we we we try to find a partner that has that type of kind of ranking, you know, on the cardiovascular benefit, especially in the primary care cardiovascular. Yeah. That's the type of profile that we're looking for. Yeah. But but the stage we're we're at in terms of nearing completion of our clinical programs, we don't need a development expertise. Right? We don't need anyone that helps could help us design, execute on a clinical trial. It's really the focus on commercializing commercializing. And and that's in part focusing on the cardiology community, but also on the primary care. So we want cardiovascular presence, but but we also want sort of the broad reach that a primary care Salesforce and organization provides. Michael, Ian, thank you so much. Yeah. Great dialogue. Thanks for your time. Thank you. Thanks for inviting us. Thank you.