Good afternoon. I'm Serge Belanger, one of the healthcare analysts at Needham & Company. I want to welcome everybody to our 24th Annual Healthcare Conference. For our next fireside chat this afternoon, we have the NewAmsterdam Pharma team. With us, we have the company's Chief Scientific Officer, John Kastelein, as well as Matthew Philippe, who's Executive VP and Head of IR for the company. I'll hand it over to John and Matthew here to give us a quick overview of the company, and then we'll proceed to the more Q&A portion, sorry, of our fireside chat. For those listening in online, you do have the option to submit questions via the portal. We'll be taking those as they come in. Gentlemen, thanks for joining us this afternoon, and I'll hand it over to you for a quick overview of the company.
Sounds good. Thanks, Serge. I guess I'll hand it over to John if you just want to maybe give a little bit of a background and kind of, we had a pretty exciting year last year and maybe highlight the phase III results.
Yes. I'll certainly do that, Matt. And Serge, t hanks for this opportunity. Indeed, in a very short space of time, we have finished our entire phase III program with the exception of our cardiovascular outcomes trial. As the FDA stipulates, we have done about a 350-patient trial, a 52-week trial in patients with heterozygous familial hypercholesterolemia, so genetic high cholesterol. We have finished a 2,600-patient trial, also 52 weeks in patients with clinical manifestations of atherosclerosis. We have finished our TANDEM trial, which is our phase III trial for the fixed-dose combination of ezetimibe plus obicetrapib. If we just kind of have the overall results, I would actually like to start with the safety because a phase III is basically so big that you are overpowered for efficacy always. You could very likely do with like 100 patients.
You need the numbers in order to really say and tell the FDA that the drug is safe before it can apply for a marketing authorization. This drug is exquisitely safe. In fact, the discontinuation rate in our phase III program for the obicetrapib arms was lower than for placebo. Of course, you can't be better than placebo, but we like to say that we are at least completely on par with placebo. In fact, there were a number of effects in the obicetrapib arms that had statistically significant lower prevalence of that specific side effect for obi. The most notable one is, in fact, type 2 diabetes. We have this side effect of special interest, which is new onset type 2 diabetes and worsening of glycemic control. We had a statistically significant decrease in the obicetrapib arm.
Furthermore, there was clearly also a disbalance in favor of obicetrapib for renal endpoints. That was actually close to statistical significance. We are currently looking into that side effect to further refine it. Safety was fantastic with an effect on type 2 diabetes and possibly on chronic renal disease. First, the efficacy, we saw an LDL-lowering efficacy of somewhere between 37%-40%. It has to be noted that that LDL-lowering efficacy was just as good in the BROOKLYN trial, so the heterozygous FH trial, the BROADWAY trial, the ASCVD trial, and in the monotherapy arm of the TANDEM trial. If you look at median change from baseline, the LDL-lowering was around 40%. If you look in the TANDEM trial at the fixed-dose combination, the LDL-lowering was, in fact, 50%.
The phase III results reveal for the monotherapy, 40% LDL reduction, for the fixed-dose combination, 50% LDL reduction and spotless safety. On top of that, we saw an effect on lipoprotein (a) and also on small dense LDL particles that we might go into a little deeper a little later. In that sense, we are now at the point in time where this year, we will submit our briefing book to the CHMP in Europe at a certain point in time, and we will enter into discussions with the FDA. Of course, for us, this is a happy time, finished our phase III, ready to go to the regulators and take this drug further. We have, of course, fully enrolled our cardiovascular outcomes trial of about 9,600 patients. We are very soon coming up to the one-year mark.
Also in that outcome trial, everything works exactly as we predicted in terms of event rates, patients staying on drug, safety alerts, DSMB meetings. We've seen eight DSMB meetings, and every meeting they say, "Nothing's wrong. Please continue the trial." We are in that kind of happy zone, I would say. Matt, is there anything that you wanted to add?
No, I think that's a good overview with the kind of, I guess, jumping into the questions.
I think that's a good starting point. For any investor interested in obicetrapib and CETP inhibitors, they have to be aware of the history of this class of drugs. Maybe if you can just start by highlighting the differences of obicetrapib versus prior iterations of this drug class. Coming out of the numerous phase III trial readouts, do you think you've kind of put a lot of issues to bed regarding some of the potential issues that could have come up with this drug class?
I think if I can go quite rapidly, the first drug was a Pfizer drug, torcetrapib. It had an off-target effect. It entered your adrenal, and it promoted the synthesis of aldosterone and cortisol. You actually got hypertension from it, and it was pro-inflammatory, which is terrible for anyone with ASCVD. Anyone understands that that is what you test for immediately in mice and rats and human volunteers. Obicetrapib does not have any of those characteristics. That is excluded. The second drug was a Roche drug called dalcetrapib. In those days, people still believed that raising HDL cholesterol would lead to lower heart attacks and strokes. We now know that that is not the case. This drug, this Roche drug, did not lower LDL at all.
We now understand that if you don't lower LDL, there will be no return in terms of less heart attacks and strokes. We actually have shown in phase II that we have median reductions between 45% - 50%. Actually, the fixed-dose combination had almost 60% LDL-lowering. In phase III, we had 40% median reduction from baseline for the monotherapy and 50% for the fixed-dose combination. Our drug definitely lowers LDL- cholesterol. The third drug, which was the Lilly drug, evacetrapib, they actually measured the LDL-lowering with a technique that we now no longer use, which is direct LDL assay. They overestimated their LDL-lowering power. Therefore, they stopped their trial too early. They stopped it after two years. We now know that if you stop after two years with a miserable LDL-lowering effect, you won't see anything.
We have a much deeper LDL-lowering effect. We have stipulated in our outcome trial that everybody needs to stay in at least 2.5 years last patient. Our median follow-up will be around four years instead of two. All the calculations tell you that that will be enough. The last drug, the Merck drug, actually, everybody always thinks that the entire CETP class did not work, but the Merck drug did work. Despite the fact that it was a small LDL-lowering, it actually did result in a benefit in terms of MACE. The only problem with that drug, and that was quite a mistake for a company like Merck, it had a half-life of like three years. It stayed in your system forever. Our half-life is five days.
We have made absolutely sure that we are completely differentiated with regards to the old CETP inhibitors. That is, of course, also the focus of our discussions with the regulators that we have nothing of that old stuff. In fact, the proof of the pudding is in the eating because in BROADWAY, our phase III ASCVD trial, we saw a 21% reduction of MACE. That, of course, is kind of, that's why you do all this. You don't do it for LDL-lowering or for whatever. You do it to reduce MACE. This only after one year early and quite a big signal was for us really, I would say, the icing on the cake that we have chosen the right drug in the right patient population and that we actually already see a MACE reduction.
While we're on the MACE reduction topic here, like you said, we saw a 21% MACE reduction. It was an exploratory endpoint. How should we think about this going forward and how it could change? I guess it won't be from BROADWAY. It will be from the PREVAIL study. Does that give us a preview of what to expect in PREVAIL?
We have specifically designed BROADWAY to be a mini PREVAIL. The baseline characteristics between the two trials are completely similar: LDL, HDL, percentage of patients on statins, percentage of patients on PCSK9s, GLP-1s, SGLT2s. Those two trials are eminently comparable to one another. In that sense, we can definitely see that BROADWAY predicts PREVAIL. And , even more so, at one year, we only would have expected a 9% MACE reduction. The fact that we see much more gives us, I mean, gives us, I would say, the wisdom that this drug is more than just an LDL-lowering drug. The Lp(a) lowering, 40%-50%, small particle lowering, around 90%, the protection against diabetes. The HDL increase is still, it's definitely not bad, but it might actually also deliver a little extra benefit. We are currently looking into that.
We hope to present those data on our R&D Day in New York in June to actually understand what mediates this benefit. You can do very advanced statistics to understand what proportion of this additional benefit on MACE comes from Lp(a), diabetes, HDL, LDL, particles, et cetera, et cetera. We do not have those data yet, but we will definitely have those data in the coming year.
I mean, I think what's important to realize here as well is there's multiple aspects that point to that this is not a sort of a chance finding of MACE, but actually a biologically rational explanation of what should happen. John went through a lot of the, we can't say what the numbers are for Lp(a), the particles, the diabetes benefit, but we know those have benefits. I mean, we'll know for certain with Lp(a) as some of these Lp(a) studies read out. Also, in the individual components of MACE, they were all trending in the right direction, as you would expect. The Kaplan-Meier curve is exactly what you would expect for a biologically rational result where you don't have a separation for the first six months as you have to stabilize the plaques in the arterial walls before you can start seeing a benefit.
I think for us, there's a lot of things that each one points in the right direction and that each one gives us greater confidence outside of just finding a single finding of a 21% MACE benefit. One of the more important ones as well is, as John alluded to before, were these second CETP to show us MACE benefit. Anacetrapib did show one. Although it was small, it was above the line as well. They had an Lp(a) benefit, roughly half of us, but they had the diabetes benefit. They most likely had the particle benefit. There's another CETP drug that has done a trial and also shown an above the line or higher than LDL alone would have explained MACE benefit. I think for us, this has given us a lot of comfort going forward into PREVAIL.
Okay.
Absolutely.
When investors ask for examples of products that have shown an increase in CV outcomes in terms of MACE reduction over time, what drug or data can you point them to?
I don't understand. Sorry, Serge. I think I'm not understanding completely what you're asking.
Yeah. No worries. I'll try to clarify. When investors ask for examples of drugs that have shown a MACE reduction at one year that continues to increase going forward at two years, three years, or four years, what drug or data can you point them to to get them comfortable?
First of all, the best example among the statins is Crestor, rosuvastatin with the JUPITER trial, where the JUPITER trial over time showed ever-widening curves. In fact, that drug worked so extremely well that that trial was stopped prematurely. The result was like over 40% MACE reduction. Also, both PCSK9 injectables, actually Praluent and Repatha, showed a benefit in their one-year phase III lipid-lowering trials. Actually, afterwards showed a real benefit in both ODYSSEY outcomes and in FOURIER. Of course, inclisiran also showed a benefit in its one-year trial program. Eight actually was 18 months. In its 18-month program, unfortunately, the outcome trial of inclisiran or LEQVIO or ORION-4 completely tumbled because of the COVID pandemic. Novartis has actually started a new outcome trial called VICTORION-2-PREVENT. That trial has not read out yet.
There are examples of other lipid-lowering drugs who showed a benefit in their 12 months or 18 months phase III lipid-lowering trials that later translated into an outcome benefit.
Okay. In terms of data for this year, any medical meetings where we'll see additional slices of data?
We have a very hefty program. We will present all our phase III trials with the exception of BROOKLYN because BROOKLYN was already presented at the American Heart Meeting last year. At EAS, which is the first week of May this year in Glasgow, we will present the other phase III trials, BROADWAY and TANDEM. We will have a lot of additional science that we are doing to better understand, especially the HDL part of our drug. We will specifically address the diabetes benefit with extensive data also again at NLA, which is the last week of May, first week of June. We will go into the European Society of Cardiology at the end of August. There we will present our extensive phase III MACE analysis because we have MACE reduction not only in BROADWAY, but also in BROOKLYN.
We will pull the data to better understand the Kaplan-Meier curves and also the mediation analysis. What exactly determines the benefit in MACE? That will be something for the ESC in August. In November, we'll have the American Heart Meeting where we will publish background therapy, statin intolerance. It will be a very information-dense year for us with four meetings, four major meetings to come with novel data that we've not shared with anyone until now.
I mean, Serge, just to caveat a little bit, this is the target. Obviously, several of these conferences haven't taken place yet. We are not 100% positive. Some of the data may be put in a different conference, but that's the plan is to get all of these incremental data that just continue to offer the differentiation of obi versus everyone else.
Yeah. And then on the PREVAIL outcomes trial, I know it's an event-driven endpoint here, but we're still a late 2026 or early 2027 readout. Is that the right way to think about it?
Yep.
Okay. I think in April or later this month, you have the opportunity to look at blinded data for the trial.
It is our intention to publish and present the baseline and design criteria for the PREVAIL trial. That will be an extensive paper where, of course, it's all about blinded data, but you can publish the baseline data, what exactly, et cetera, et cetera, what exactly is LDL, I mean, particle distribution, et cetera, et cetera. We can also, also the first year, we'll have a very accurate event rate over the first year because in April, end of April, everybody will be in the trial for at least a year. I can tell you already, as we've publicly said multiple times, that events are exactly on track. Our predictions for the closure of PREVAIL still stand.
Okay. Yeah.
We do not want the expectation to be that what we do internally is something that is going to be expressed externally. Really, what investors should expect is once we do this analysis, that our point still remains that we continue to be on track. As John has mentioned, we have already had eight DSMBs. We do see sort of blinded event rates going on. As of today, nothing would point to us to have to alter that timeline.
Okay. This April event, I guess, is just a look at the blinded data. There's no decision to be made to go one way or another for.
I mean, it's really, so if you think about it, it's the first time, it's the one-year anniversary of the completion of enrollment. That's a good time point to look at because what you understand is that sort of the confidence interval on the event rate is pretty wide during the first year of therapy. After that year, those error bars really come in pretty tight. You can have a better prediction of where you're going to be. Based on what we're seeing today, there's no change in that. We want to take it with a fresh set of eyes with everyone in the trial one year. Remember, just because this is April, that's the last patient in has been on study for the year, but many patients have already been in the trial two years or longer.
We'll have a pretty good idea of where this event rate is tracking. It is just a way for us to take a fresh look. For the investment community, the expectation should not be a look at blinded data. It should be a continued echoing of our statement that we remain on track.
Okay. You will get the June event.
Yeah, exactly.
Also, Serge, normally, you're a bit anxious to look at even blinded safety because there can always pop something up. But since we already have almost 3,000 patients for 52 weeks where side effects were actually less in the obicetrapib arm than in the placebo arm, for us, the safety is beyond any doubt. We are indeed mostly interested in the exact event rate because that'll track into the future.
Yeah.
Yeah. Yeah. To clarify, even though it's a June type event, the one-year anniversary is the last day of April. It only gives us a month to actually look at the data.
Sure. Clearly, the PREVAIL outcome study is a key part of the development of this drug and will provide very important data. Maybe just highlight what the, in terms of regulatory timelines for obicetrapib , I think you're in a position to file without the PREVAIL outcomes trial. Just where the timing is for all that.
Yeah. I mean, what we've said is for Europe, it's a little more straightforward. The plan is for our partner, actually, Menarini, to submit the filing in the second half of this year. Hopefully, second half of next year, we have a European approval. In the U.S., the FDA has always said, once you have your phase III data, come and have a conversation with us. We're preparing for those conversations. Ultimately, what we want to do, and this is why we're not in a real rush, is we want to have the outcomes data available at the time of launch. If we expect outcomes data at the end of 2026, we'll work backwards from there.
That kind of tells you, hopefully, in the U.S., we can have a first half 2026 type filing so that we can launch in early 2027 with that outcomes data available.
Okay. Makes sense. You have other trials that are also ongoing besides PREVAIL, I think REMBRANDT and VINCENT, all these Dutch painters.
Yeah. Right.
Some of the influence is coming from there, but maybe just highlight what REMBRANDT and VINCENT are seeking out to do here.
REMBRANDT is a trial that's very close to my heart because it uses CT scanning and angiography as a way to assess lipid-rich plaque and see whether the therapy is able to regress plaque. Now, the therapy in this case is the fixed-dose combination of obicetrapib and ezetimibe compared to placebo on top of standard of care, so to speak. This is kind of basically our mini outcome trial for the fixed-dose combination because, of course, there are patients on ezetimibe in PREVAIL, but we don't test that against placebo. We test it against itself. Therefore, I'm very happy that we have a placebo-controlled trial for the fixed-dose combination. Of course, images are always very, very powerful. I was an imager in the old days.
I was very, very often involved in the Cleveland Clinic IVUS trials, in the carotid IMT trials. Those are all kind of old-fashioned techniques now. CT a ngio, which does not require you to go into a coronary artery, is a really interesting technique where you can do virtual histology, and you can look at the inflammation in the arterial wall, et cetera, et cetera. That trial is currently enrolling, and it is expected to read out around the time when PREVAIL reads out. That is for it. VINCENT is interesting because our drug, as I said, not only lowers LDL, but it also lowers Lp(a). In fact, it lowers Lp(a) about 2x as good as a PCSK9 inhibitor. PCSK9 inhibitors are very good LDL-lowering drugs. The question then becomes, what if you add the two together? Will the LDL-lowering be additive or synergistic?
What will happen to the Lp(a) lowering? We have designed this trial to precisely answer that question. It is also enrolling currently, VINCENT. It is the shorter trial, and we expect that readout, in fact, around, Matt, New Year?
Yeah, towards the end of the year.
Towards the end of this year, which so therefore also even after the American Heart in November, we potentially will have another readout at the end of the year, which is VINCENT. Yeah.
Could this be a preview of a potential oral PCSK9 and oral obicetrapib combination?
I don't know whether I'm allowed to say anything, but that doesn't seem a stupid idea. Yeah.
It does not, no. Okay. Maybe just highlight the market opportunity. Clearly, obi would play in the non-statin space, but where it could fit in given what we've seen so far from the data?
I'll let Matt handle that.
Yeah, sorry. You cut out on mine. Just what was it?
The market opportunity for obicetrapib in the non-statin space and kind of where it would fit right now.
Yeah. I mean, I think the one thing we would think about the opportunity is, one, all patients will be on statin. We are not talking about statin intolerance space, but it is more sort of adjunct to statin therapy is really where we are looking at here. Our goal is ultimately, given the product profile that we have, it is basically the next step post a statin therapy, which, as you can appreciate, is a very big market opportunity. Roughly 30 million patients in the U.S. are not at their goals, and about 20 million of them are more than 20% from their goal. We are seeing a lot of positive dynamics that showing patients are starting to look for better therapies that are available or becoming more compliant with existing therapies. Branded therapies are growing 30%-40% + in terms of volume.
Even generic ezetimibe is growing 20% +. We are seeing this very positive tailwind in overall market dynamics that could really support this. Ultimately, what we are trying to do is really basically change the way you define LDL efficacy now. It used to be that LDL-C lowering was enough. Once we are available with all these other ancillary benefits, that is where we really think we can shine. Because if you think about it today, what are the concerns with statins? They increase your diabetes risk. They increase your Lp(a), and they disproportionately affect your large LDL particles. Wouldn't it be great if you had a therapy that could sort of offset or negate some of those effects? Fortunately, that is obicetrapib. We reduce your risk of diabetes. We reduce your Lp(a), and we eradicate your small particles. It is the only therapy that has that profile.
On top of that, it's extremely safe, well-tolerated in a tiny single oral pill once daily. We think it's in a very good position competitively. That said, this is a market that has been underpenetrated for a long time, and it will take multiple players in this market to drive ultimate success. There's a reason statins were doing $30 billion, $40 billion, $50 billion a year. It's because you had five different companies in the market talking to physicians about what are you doing about your patient's cholesterol. We need to get back in that scenario. Ultimately, we think obicetrapib will be the preferred product because if you have a patient who has high LDL-C, but they also have high Lp(a), then you'll grab obicetrapib off the shelf.
If they have high LDL-C and they're prediabetic or have diabetes, you grab obicetrapib off the shelf. You start seeing all these really subsegments of where could our drug be used. You start realizing those are very big patient population segments that are active and are actively looking for a new therapy. I think one of the interesting things about generic ezetimibe use is that is a generic. It only works 20%. You know most of the patients who take ezetimibe still are not getting to goal. It tells you if you have patients who are taking another therapy, they're most likely compliant because you don't take a second therapy if you're not compliant with your first therapy, and they're not getting to goal.
There is a lot of easy patient populations that we can start to look at and say, these are ones where we should penetrate very easily. At the end of the day, what's good for us is they're all very large patient populations. I think we're in a good position in terms of market opportunity. It's the question of how do we get more patients on drug? I think having a profile like ours is a very good first step.
Are we starting to see an appreciation of the impacts on Lp(a) and some of the other lipids beyond LDL-C reduction? I mean, do we need to or do we need to see more data and more?
I think it's interesting. Michael will always say he still sees patients 4x a month. One of the highest referrals he gets is for high Lp(a). More and more patients are familiar with that, especially patients who have a familial history of heart disease. A lot of them tend to have higher Lp(a) or get checked regularly because they're concerned about early events happening. They're well aware of this. I think there's a good opportunity there. What's interesting for us as well, and this works in our favor, is the fact that as HORIZON reads out, and hopefully it's positive, they'll read out and there will be a validated mechanism in the market, but no available therapy.
Now, ultimately, obi is not an Lp(a) therapy, but what it is, is that's a differentiator in our product profile that would hopefully get more patients who have high LDL-C and high Lp(a) onto our drug. We can see where they go from there. Lp(a) is clearly very topical. It's probably one of the biggest sections talked about at the cardiology conferences lately. It's really Lp(a) is a new exciting area for a lot of physicians and patients.
Okay. In terms of potential future competition for obicetrapib, are the oral PCSK9s kind of the main focus? Is that what you hear from investors or how you view it internally also?
Yeah. I mean, I'll let John kind of dive into the scientific aspect, but I think from a business perspective, they are the only competition. Nothing else is really being developed for LDL-C outside of us and the oral PCSK9s. Fortunately for us, there's a lot of PCSK9 alternatives now. You have the injectable PCSK9s. You have siRNA PCSK9s. You have oral peptide PCSK9s, small molecule PCSK9s, but you have only one CETP inhibitor in obicetrapib. And what we appreciate is physicians and payers like choice because they don't want to have to say, "Well, I'm going to decide on a PCSK9." Now they can say, "Well, what's better? Is it a CETP or a PCSK9?" We think ultimately we'll win that battle between the PCSK9s given the overall profile.
Maybe I'll turn it over for John if he wants to talk about sort of any product attributes or differentiators there.
We expect the first phase III trial for the Merck peptide to be good. We expect the same LDL-lowering efficacy that they've indicated before. We should always realize that it's a large pill. It is a permeation enhancer with, I think, 20 mg or 30 mg of the actual peptide. That leads to all sorts of household difficulties. You have to be fasting for an entire night. You have to take the pill, and then you have to wait for your other drugs for half an hour, your coffee, your eggs, and your bacon. It's a bit of a hassle. The oral drug, so the AstraZeneca, the small molecule drug, was published in JACC and presented at the ACC. I have to say that presentation and also the publication was what they call ideal analysis.
It's even more kind of ideal than an on-treatment analysis because everybody that didn't really fit into the treatment paradigm was thrown out of the trial. There were 29 patients thrown out of the treatment arms and two out of the placebo. What you'll get is a little overestimation of your LDL-lowering effect. On top of that, they used a direct LDL assay, which overestimates, as I said before, the LDL-lowering. If you take the placebo away, the drug did 46.6% LDL-lowering. Taking the rest into account, it'll be in phase III less than what was reported in phase II, as, by the way, for every lipid-lowering drug. Of course, there'll be competitors, but they'll just compete on the LDL-lowering effect. They cannot compete on the diabetes protection.
They cannot compete on the lipoprotein(a) or the fact that we are a 10- mg a day tablet that you can take with food, without food, in the morning, in the evening, very easy to swallow, and has no side effects. In that sense, we are not afraid of that competition. In contrast, as Matt was saying, we need other players in this market to kind of ruffle the feathers.
Yeah.
I think what's important too is given that the LDL-C efficacy is roughly similar amongst all of them, it really comes down to those other product attributes, specifically safety and tolerability. It doesn't matter if you have higher efficacy if patients don't take the therapy or if they feel discomfort when they take the therapy. I think for this kind of opportunity, you can't understress that enough, that safety. If you look at it today, the reason ezetimibe is doing so well despite the low efficacy is it's considered a very safe drug. I think our overall profile will lead there. Given that amongst all three of those competitors that we talked about, including ourselves, we're getting the same proportion of patients to goal. Once your patients to goal, you start looking at these other issues.
I think the fact that we get everyone to goal in the same proportion, that really leads to the next question is, okay, I got my patient to goal. What's the safest way possible to do that and the most convenient way possible for the patient? Oh, and do I get other? I mean, it's very rare where you get all these other ancillary benefits of the diabetes, the Lp(a), the particles without any increased safety profile. So you're getting all these benefits without having to give a trade-off for safety, which is a very powerful statement for both physicians and patients as well as payers.
Okay. I think we only have a couple of minutes left. Maybe to end here, just a financial overview and where you are in terms of cash balance and projected runway.
Yeah. At the end of the year, we had over $835 million in cash. We kind of get away from providing runway guidance given we can make that cash last a very long time. What we have said is, what does that cash get us? Even before the financing we did back in December, we had sufficient cash to complete all of the ongoing clinical studies, the pre-commercial activities, the inventory buildup, and really the $480 million-$490 million we raised back in December will fund all of our commercial launch activities. We feel like we're in a pretty good position to launch this product into market with the cash we have on hand.
Yeah. A good place to be given the current market environment.
Yes, definitely.
Maybe just to wrap up here, anything that you feel is underappreciated or misunderstood about the drug or the NewAmsterdam story?
What's underappreciated, I would say, I mean, I did clinics too, like Michael, until very recently in Europe. In Europe, there are also 30 million patients not at goal. Together, these two sides of the Atlantic. The most important thing for a physician is that the patient, after you treat him, does not come back complaining about side effects. That is the key issue. You want to treat; you don't want to have a negative conversation in three months, in six months, and in t12 months. You just want to say, "Okay, listen, I've got the solution for you. This is it." Everybody goes home happy. That is underappreciated, how safe this drug is and how easy to take 10 mg. It's like a little baby aspirin.
Yeah. Okay. I guess we got to wrap it up here. I want to thank you both for spending time with us this afternoon. We've got a lot to look forward to for the rest of 2025 here.
Thank you, sir. Appreciate the time. Thanks for hosting us.