Good afternoon, everyone. My name is Dae Gon Ha, one of the biotech analysts at Stifel. With us for the next half hour, we've got Rhythm Pharmaceuticals, and joining me from Rhythm is David Meeker, Chair, CEO, and President of the company. So David, thank you very much for your time. Thank you, Dae. Let's start with a broad overview of Rhythm for those of us that are less familiar with the story, and we'll dive into some of your key programs. Great. Yeah, so, Rhythm's a company focused on developing therapies for both genetic and acquired forms of impairment of this melanocortin-4 pathway, which is a pathway which sits in the hypothalamus and governs our hunger and our energy expenditure. So the short biology is we eat a meal, and we signal, our gut hormones signal the pancreas and the adipocytes, and leptin's released. It goes to the brain, and it signals down through this POMC pathway and tells you you're full, and also that there's food on board, and therefore, you can increase your metabolic rate. And conversely, if this pathway is impaired and you're not signaling through the pathway, i.e., you have a deficit of this alpha-melanocyte-stimulating hormone, then the body says, "There's not food on board. I'm hungry, and I need to be seeking food." They also lower the energy expenditure rate, and so the consequence is obesity and often severe obesity. What Rhythm does is we have a therapy, setmelanotide, brand name IMCIVREE, which is an analog of the alpha-melanocyte-stimulating hormone that is deficient, and it's a more potent form of that. Essentially, we're a hormonal replacement therapy for those deficient states. Developmentally, we've focused on, as I said, genetic causes with three different genes approved in 2020. Those were extremely rare, but strong proof of concept. And then Bardet-Biedl syndrome, which was approved a year ago, June, and that's a syndromic complex genetics behind it we could dig into, but we're about 15 months into launch, and both here in the U.S. and increasingly in Europe. And then what was a surprise for the world, a bit of a surprise for us, was an acquired form, hypothalamic obesity, which is an entity which occurs most commonly in children who develop these benign tumors. The tumors originate between the pituitary and the hypothalamus, and as that tumor grows, it often grows into the hypothalamus and impairs signaling through this pathway. Either the tumor itself or the treatment for the tumor, surgery and radiation, damages the pathway, and about 50% of the kids with that problem come out with what they call hypothalamic obesity, which is literally a classic presentation of they're hungry all the time, and they have this rapid increase in their overall weight, and they explode off their growth curves, and that's the characteristic presentation for these kids. Nothing's worked for that group. We think there's about 5,000-10,000 individuals in the United States who have hypothalamic obesity. When I say nothing, I mean, diet and exercise doesn't work, but literally, they've tried all available therapies. I'm sure we'll get into GLP-1s and the like. But there's been many different forms, earlier generations of GLP-1s, which have been used more extensively. The newer forms, of course, are just being tried now. But, but that, that opportunity is very meaningful, and the big difference there is that those patients are all identified, unlike, Bardet-Biedl syndrome, which is a more classic rare disease. You have to do the work to help diagnose the patients and then move them through the system. But the HO patients, because they've been to surgery, are sitting in a care point, again, with a diagnosis and, concentrated in a specialty call point. Great. Let's start with the HO, given you had a recent update from your phase II long-term extension portion of the study that was presented at TOS. Can you just remind us what the trial design was, how long have these patients been followed, and some of the key takes from the presentation? So we ran a phase II, which was an 18-patient open label study. At the end of 16 weeks, we had a mean decrease in the BMI of about 14%. At the end of that period of time, 14 patients went into the long-term extension. Two of the patients stopped because they had an adverse event, one patient was non-compliant, and one patient had lost 10% at the end of the 16-week period, but had a very complicated medical history and was just unable to continue. So, 14 patients went in, and at the, we reported out the 12-month data. We had 12 patients of the 14 who had a full 12 months of data. Their mean BMI decrease was 25%, so a significant you know, further deepening of the BMI decrease from the approximately 14% we saw at 16 weeks. So that was very, of course, reassuring and, positive. But what's been really striking about the HO opportunity and the effect the drug is having is, in addition to a very meaningful patient-by-patient decrease, the consistency across patients. So literally, every patient who's taken the drug has had a response. And the two patients who had intermittently come off therapy, we had their curves on the poster we presented, and what you can see there is that when they were on the drug, they lost weight, and... or their BMI went down, and when they came off it, they regained it. And so again, like many other examples of hormonal replacement, if you use thyroid as an analogy, you take your thyroid hormone if you're deficient, you feel better, you stop your thyroid hormone, you get sick again. And so I think that's what we're seeing, largely here in the HO space. I guess we'll focus on those two patients. You'll. As you mentioned, the graphs were there. Can you just maybe remind us what initially led them to go off drug? We don't have the presentation here, but what was the overall curvature like, such that- Sure Once you reinitiated, what was the magnitude of response, the rapidity of response, those kind of things? Yeah. So not so hard to describe. So, one was a teenage male who had lost 21% of their BMI at 16 weeks, and chose to enter the long-term extension, but was immediately lost to follow-up, and when I say lost to follow-up, for all medical care. About 80%-85% of patients with hypothalamic obesity also have pituitary insufficiency, 'cause the tumor injures both the hypothalamus and pituitary, again, often both the hypothalamus and pituitary, they're both. They sit close to each other. So, this patient came off, like I said, all of their meds, they were lost. We eventually or the investigator eventually located the patient. They were reconsented, and this was, I don't know, four to six months later, and at that point, they had regained all of their weight. So that 21% decrease, they were now back at baseline when they were reconsented. They went much more slowly on the dose escalation, so at the point we had seen them... We We reported it on the graph, I think they were a couple of months in, two, three months in, and they were down at about 10% or 11% weight loss. So they'd started losing again. The other patient was more complicated and these patients, again, it's just they have so many medical problems, again, related to the tumor and the surgery. Their co-medication list can be a page of, you know, different medications that they're on, and this individual had a lot of GI complaints, gastrointestinal complaints, coming into the study. Had a difficult time tolerating the medication, so we were up and down on the medication, and when we went up, she lost weight. 11% was the most that she lost at one point. When we titrated down, she regained, and so she was down to 11%, back up to 6%, off drug again, now she's back on drug. But again, it's just the on/off nature of the response was very clear in both of those patients. I thought it was also unique that you guys also, for the presentation, put not only fat loss, but the lean muscle mass. Some actually gained on it. Can you maybe walk us through some sort of your thoughts, not only in terms of differentiation from some of the GLP-1s that are out there, but what do you think is going on? What's the mechanistic rationale for lean muscle mass increase? Yeah. I mean, for people who are following, the obesity space, which is, an incredibly exciting space, at the moment, the GLPs, that world is paying a lot of attention to the quality of the weight loss. Again, you can, the GLPs can turn off your appetite to an extreme degree, and, and, you lose, weight, but both fat and lean mass, and, not in everybody, but in, you know, a significant percentage of patients, perhaps. So what's interesting, and, the way this is measured, we did DEXA scans, which again, allow you to... It's a, a form of X-ray that allows you to measure, the lean mass and the fat mass, space and quantify that. I think the best example of what we were seeing, a more striking example, there was only one patient of the 17 patients who took the drug, of the 18, one was non-compliant, but there was only one of the 17 who was compliant with the drug, who did not lose 10% or wasn't on track to lose 10% at the end of the 16 weeks. And that patient, at the end of 16 weeks, had lost, like 2.9% or, yeah, 2.9% of their BMI. So a very modest response. At one year, they had lost 8.9%, so the mean was -25%. This patient was at 8.9. So we were struggling to understand, so what was different about this patient, and why, why weren't they getting a more profound response? They were compliant, the doctor said they looked good. So you look at their DEXA scan, and that patient had lost 23% of their fat mass and gained 15% of their lean body mass. So the net, what we were looking at at the BMI, which looked like a very modest decrease in their overall weight, was actually an incredibly healthy physiologic response. So small numbers, but I think in a very sort of simplistic way, what I think we're doing is we're restoring more normal physiology. We're restoring a more normal relationship with food. I mean, what patients describe is, for the first time in their life, they can get up from the table and leave food on the table. When the signaling is impaired, they couldn't do that. They'll just eat everything in sight. But for the first time, they could get up and leave food on the table. But it's not that they weren't interested in food. It's not that they have lost completely their, you know, desire to eat and the like, which is why also, if those individuals on the drug love ice cream and go out and eat a ton of ice cream, they're gonna gain weight. I mean, this doesn't prevent that. This is just restoring the physiology to say, to allow the body hopefully to do what it does. So in that kid, you know, he's growing normally. This is a teenage boy, should be gaining lean body mass, putting on muscle and leg. That's what was happening. Another example, the six-year-old kid in the trial who was our most rapid and profound, this is a child who was, you know, relatively skinny before they got their tumor, and then they developed HO and started to put on weight. That patient lost 30% plus of their BMI in the first 16 weeks. That patient now at 12 months, their BMI is increasing. So they're in the mean also of that 25% decrease in their BMI, but they're gaining BMI. Now, they're below the 50th percentile for their age. They're completely normal. They're gaining BMI as you would expect and want them to do. Again, this is back to what, you know, I think we're doing in HO. The drug, because the drug is specific for the MC4 receptor, it's teaching us something about the biology here. I mean, that consistency of response is telling us that this melanocortin-4 pathway is fundamental to what's going on in these patients with HO, hypothalamic obesity, and when you correct it, you get the benefit. Great. So we have a lot of that data. Granted, it's a limited number of patients, but really profound results. I guess, you know, the key question is, this being single-arm trial. Y ou didn't have a placebo control here, but in the upcoming Phase III trial, you do have a placebo. How should we think about the placebo effect in HO patients? I mean, are there any other GLP-1 or any other type studies in the HO setting to give you some insights on what that placebo rate might be? Yeah. So, again, just the natural history of this disease is nothing really works. I mean, and certainly, diet and exercise don't work. And so, our expectation is, in the placebo group, they'll—we've modeled it with for no effect. I mean, there won't be a placebo effect in terms of decrease in BMI. Also, just to be clear, we don't have formal diet and exercise counseling. I mean, Lilly and Novo in the GLP trials have, you know, very structured, and they did an amazing job of, you know, you know, formal, intense diet and exercise counseling, and those placebo groups did quite well in this comparison. They did much better on the drug, but the placebo groups did well as a group of just diet and exercise. So we don't have that. But as a rule, these patients have tried everything, obviously, including diet and exercise, without success. So for the trial itself, we expect zero impact. If anything, I would expect some weight gain over the course of a year, just given the natural history of the disease. We're modeled or powered for a 10% difference, 99.5% power to show a 10% difference. And that's, yes, that is overpowered. And the reason we ended up with those numbers, we got into the FDA with a proposal for a smaller, shorter trial. We ended up with this because that's basically the rulebook for developing an obesity medication. It's a 1-year study, and also on the safety side, they absolutely wanted a placebo-controlled, 1-year follow-up, so we ended up at 120 patients, two to one randomization, 80/40. So that's our, that's our trial design, but I think the placebo group, you won't see much. Yeah. Okay, that 99.5 is probably a record when it comes to biotech companies, but- It's not about the powering. This was much more about the safety. They were excited. I mean, I think, you know, it's fair to say, the FDA, I mean, their job is to approve drugs that are gonna make a difference. And you know, when you're in there with a me too, or when you're in there with something that's potentially pretty meaningful, so. Yeah. Just to touch on this, or button this up, the trial is currently enrolling. What was the guidance for enrollment completion, and what are you seeing from the trial centers? I mean, are you seeing bolus of patients that are lining up? Is the enrollment faster than you anticipated? How do you balance the rate of enrollment versus maintaining high-quality patients so as not to kind of, you know, throw your- Yeah, no, that's a good question. I mean, I think when we first started, we knew the patients were out there, and I'll explain why we knew that, and interested in coming in the trial. The biggest issue was getting the sites open, and post-COVID, it's been anybody who's running clinical trials in anything is it's challenging. And these sites are challenged. They're not staffed the way they were pre-COVID. The contracting and IRBs aren't functioning the way they were pre-COVID. It's always a bit laborious in some of these academic centers, but definitely worse post-COVID. So we knew our challenge was gonna be just logistics, getting these trials open. We are looking for 25-30 sites, globally. So we guided to the end of the first quarter. Once we got underway, and we got a better sense of how the site opening was gonna go, we moved that up to guiding to the end of the year to be enrolled. In terms of patients, the way it works is every one of the sites in our trial has a list of patients. Often you're running a trial, and, you know, the center says, "Yeah, great, we'd love to be involved. We'll go out and we'll try to find some patients." But in this case, they all had their lists of patients, and they also obviously knew the inclusion criteria. So they went to their list with the inclusion criteria, and they just called the patients who they felt were going to be eligible. They weren't just inviting everybody with HO unnecessarily. That's shown by the fact that we're about two-thirds of the patients are either enrolled or actively in screening, and our screen failure rate is only four out of that two-thirds, which is 80-ish patients. So again, a very strong indication that they are they have lists to choose from, and you know, they, they've picked patients go. I think the total number, when you go to each site and you ask how many patients they think could be eligible, it was basically 2x what we're looking to enroll. So the 120, you know, these sites easily had access to, you know, the 240, 250 kind of patients. And then, in terms of finishing the trial, you know, we're about two-thirds actively in screening. The others, the vast majority of the balance to get us to 120 are in the process of scheduling their visits, so they've been identified. So again, I think we're. My bigger concern, to be honest with you, is just managing what is going to be, I think, a bit of a rush at the end, and not every trial you over or you often over-enroll a little bit. It's not to too over-enroll it to too great a degree. So, we're gonna aim between 120 and 130, and we'll shut it off as soon as we can when we hit 120, but anybody who's in screening, we'll obviously allow them to enroll, so. Okay, so sounds like the runway is already pretty visible. The runway is totally visible. Yeah. Yeah. Okay. Okay. Just remind us of this market opportunity. I know this is more of a triangulation prevalence estimate. Can you remind us what your updated thoughts are, and, you know, when you start thinking about other tumor types versus the two that primarily led to your prevalence estimate? Like, how should we think about the total addressable market? Yeah, I mean, epidemiology is mostly annoying, I guess, all of you. I mean, ultra-rare disease is extremely difficult, so literature tends, because it's rare, tends not to be terribly robust, and you don't know... But in this case, actually, we triangulated on the BBS numbers, so we can come to that. The way we got to the hypothalamic obesity numbers, which we've estimated at about 5,000-10,000 in the U.S., and a similar number in Europe, is what's known about this, and there is more literature here, the craniopharyngiomas are by far the most prevalent tumor type. So about 70% of HO cases have craniopharyngiomas as their origin, and there's tumor registries and the like, and so you have a pretty good feel for that. What creates the... And then the other tumor is astrocytomas and glioblastomas. I mean, there are some other, you know, much more rare tumors that you know, occasionally will involve this area of the brain and non-tumor types. At a recent meeting, you know, a physician came up and had a patient who'd had a gunshot wound to their head and had survived it, but had classic HO. And so again, it's just the injury itself that's really the factor. The biggest variable in trying to figure out, you know, how do you get to the what's the right number in terms of epidemiology is, about 50% of the patients who have this tumor or a tumor goes to surgery develop HO. But if you look at the different cases and series, it sort of ranges from, like, 20%-90%. I mean, that's the range. So I would say the world more or less agrees that 50% is a pretty good number, but that is the variable piece in terms of you could have sort of wildly different sort of overall prevalence numbers. I think 5,000-10,000 is not bad. I also think, like, with most diseases, this one a little less, there will be a group of patients who have not been recognized as having HO, and once there's a therapy and more attention, you know, they will get to a more formal diagnosis, so. Any questions from the audience on hypothalamic obesity? Okay, let's pivot to BBS and your rest of the commercial portfolio. What was the most recent 3Q update that you had as it pertains to BBS? And as you mentioned, you're now past the one-year anniversary of launching in the U.S. What are some key learnings and sort of the remaining pushes and pulls as it comes to commercial? Yeah, I mean, I think when we launched a year ago, like, the world, I think, you know, wondered, can you get this working in a meaningful way? You've got a ultra-rare disease drug and priced at a price point, where rare disease drugs should be priced based on rarity, and this is ultra-rare, and so we're at a $360,000 annual analyzed cost for this therapy, so obviously a significant price point. You know, could you find the patients? Could you get them through the system? Would the different payers pay for it? You know, when I say this is a classic rare disease, it was classic in every sense. I mean, obesity is common, but this Bardet-Biedl syndrome, specifically, no experts. We had one center of excellence in the United States, little awareness, no testing, and again, in rare diseases, that's often the case. There's, because they're rare, and if there's a specific test, particularly if it's genetics, it's not available commercially, for the most part. And so the company has to develop it and provide it, and provide it for free, and that's what we had to do. So we had to put all those elements in place, and the question is: Could you get it working? And I think where we are now, you know, 15 months plus into the launch, is the answer is yes. You know, a resounding yes. And you know, the striking things are not so much... I would say the development of the experts, the interest, the willing to write scripts, all of that, I would say, has gone the way I would have hoped, and the way you would expect a solid rare disease opportunity to go. The payer world, I was really pleasantly surprised. It was super positive. And why I say that is that, the GLPs were out. They understood that this was a rare disease. It was apples and oranges. We weren't. It wasn't that, you know, all obesity drugs are the same and, you know, it's just weight, and you just gotta get the weight down. It was recognized as a distinct disease. It needs a very specific solution that's specific for what's driving that early onset obesity and hyperphagia in patients with BBS. So that was successful. Two, about half of this population is Medicaid, about half of it was commercial, and then, you know, about 10% of it is Medicare. So Medicare does not cover, by statute, doesn't cover the GLPs, doesn't cover us, and so Lilly and Novo are working that. We're wishing them a lot of success there. I think that's will be positive for everybody. So we'll see where that goes. But, on the Medicaid side, and, you know, Medicaid is a challenging payer point, and 80% of the Medicaid lives in the U.S. essentially have access to our drug. The last 20% are states where it's, you know, I'm not sure we'll ever get there, but you, you never get up. It's just a work in progress, and you keep working it. But 80% is a pretty remarkable level of coverage. So, you know, that was the part that I felt probably best about in terms of what we learned in the first 15 months. And beyond that, you know, again, it was just reinforcing lessons on rare disease worlds. What works? What doesn't work? You have to... You know, one of the concerns was, okay, Rhythm, you know, you've, when you started, before you launched, you said you had about 350 patients you knew. There was this registry that had about 600. When you exhaust that, you're done, right? And the other part was, no. I mean, we've been able to find patients and just... And in finding the patients, you know, there's things we're doing that are working, and, you know, we're working ICD-10 codes, we're doing non-personal promotion, we're looking for the nodes. And when I say nodes, these complex diseases all have referral patterns, and so if you can find the node, then you can break down the referral patterns and map it and figure out sort of where, you know, the different people sit, so or different prescribers may sit. So all of that was playing, you know, more or less as expected there, and... So again, I think there weren't necessarily huge, huge learnings in that. It was just a reinforcement of what many of us who've worked in, rare diseases knew, should work, but they turned out they were working here. Mm-hmm. So it's been a fairly consistent quarter-over-quarter of new start forms being in that 120, 130, 140 range. We on this side tend to love to see that kind of trajectory and model it out. How should we, looking forward, think about the growth trajectory 15 months in? You just pointed out one of the key pushbacks, which is, hey, they talked about the 350, they've exhausted it, we're getting close to the ceiling, if not already surpassed it, so they've, like, exhausted the patient population. What are you seeing, or what are you hearing from boots on the ground of patient identification efforts and new patient diagnoses? No, I mean, you know, go back to, you know, when you said triangulated. I mean, to get to our prevalence number of 4,000-5,000 patients, A, we think the, the prevalence in Europe is probably similar, you know, 4,000-5,000 patients in Europe overall. It's a larger population, but, you know, more or less the same. If you, if you take France, so there's, you know, 700 patients identified in France, easily, you know, over 1,000 patients, if you include the non-diagnosed, and you correct the French population, 66 million for the U.S., I mean, you get to 4,000-5,000 type of number. If you take our URO testing, about 0.2%-0.3% of our URO test, this is our genetic panel, which has the 23 BBS genes on it, 0.2%-0.3% will come back biallelic for a pathogenic mutation in BBS. The number of patients in the United States that should be screened, who have a, i.e., the, that is, those patients who have a history of early-onset obesity, is about 5 million. So 0.2%, 0.3% times 5 million, would say that's 10-15 thousand patients in the U.S. The math on the French population gets you to sort of this 4-5. And so we think that 4-5 is a pretty robust number, and then the last, which is sort of a gut check, is, can you find these patients? And you know, there's patients, and I've worked in some of these, which are, they're just so you just almost impossible to find. And that's not the case here. If you look for BBS patients, if a physician starts looking for BBS patients, you will find them. And so all of those things together, like I said, I think we're working with a pretty robust number here, and you know, quarter on quarter, we're just finding more patients, and we'll continue to find them. They're out there. One of our salespeople, I asked what what. On the ground, what they say is, they're not out there looking for patients so much as they're out there looking for a physician who's interested, willing to take a little bit of time and start looking for the patients, because you get that physician who's interested and they're looking, they'll find them. That's how this has worked. One other, I guess, evolving or developing angle to this is ex-U.S. Yeah. And so you talked about several of the geographies, like France being one of them, where patients are identified. Their healthcare system is a little bit more centralized compared to the U.S. So what's sort of your expectation of EU launch compared to what we have seen in the U.S.? So country by country, it'll vary. And part of the strategy, again, just to highlight, from the very beginning, you know, the leadership at Rhythm, and we've had experience with this, has been thinking globally. I think the mistake many rare disease companies make is that they say, "Well, we're just gonna focus on the U.S. 'cause that's the most valuable market." And that's not really how you build a strong, significant rare disease business. You need to be thinking globally. It's doable. It's doable in a highly efficient, cost-effective way. You don't need a huge number of people. You need a small number of people who are experienced, who know what they're doing, and that's what we have. And so they've been opening up by, you know, country by country. Germany is the first one that we're fully open with, pricing established, and we have a full team on the ground there. But what we've explained is, you know, Germany, before we got our pricing settled and the like, we had two people. Once we got market access fully open and operating, we're at eight. And that's a meaningful opportunity. So that's how Europe will come on. And the other thing is, as people look at Rhythm quarter-over-quarter and do their modeling, which we discourage modeling, as you know, so yeah. You're not firing me, are you? I know. But it's... No, it's just that it's hard to model rare diseases early on, and that's why we discourage it, because it's, as you said, you can look quarter on quarter here, and there seems to be a pretty steady pattern in the first few quarters, but it'll vary in just the nature of it. But what smooths it out is, as you get your numbers up, and as you get by having multiple countries, you know, any given country, the U.S. could be down a quarter, and Germany could be up, and then, you know, the net all of it is that this opportunity just continues to march forward, and that's what we would expect to happen. I think what's exciting about Europe, in addition to being a little more centralized and organized and having experts, and actually, it's not just the patients they contribute. I mean, there truly are more experts there, and they're real leaders, thought leaders in the world. And so, you know, they're writing, you know, papers and helping, you know, articulate and help the world understand how to think about this particular disease and set of diseases. So valuable there. And the last thing I'll say on Europe is France. France is a really interesting story. So France is very progressive in terms of their healthcare system and providing early access to medicines. They have what they call this AP1, AP2 process. AP1 is before your drug is approved. So we went there with our HO data. So think about this, 18-patient HO data and Phase II data, open label, and we got early access. Within one month of submitting that thing, which now it'll come on slowly 'cause the process is a bit bureaucratic in terms of the number of patients getting onto therapy. But the point is the system, A, recognized the need, and B, the potential impact of the drug. So again, reassuring, early, but positive. Cool. So with the closure, let's focus on the cash runway, and I know you have an R&D day coming up. Any teaser you would like to share with us? Yeah, cash, so we finished with a little less than $300 million. That, what we're guiding to, is that'll take us into 2026. So we feel like we're in a good, strong, secure cash position. As Hunter, our CFO, likes to say, we've pretty much peaked in terms of our R&D spend, or we will peak in 2024 with two large phase III's running, and those, as they wind down, they won't be replaced by comparable activities. So that's our cash position. And then, R&D Day coming up on December sixth will be a few things. One is we'll have a KOL, one of the five who participated in our phase II HO study. We'll have the mother of a patient with hypothalamic obesity, who founded the Raymond A. Wood Foundation. We'll talk about our phase II DAYBREAK study, a bunch of the genes and the open label portion of that. This is midway through that, which should be interesting. We'll have our pediatric data, patients two to six. We're in the process of filing there. That's a small number, about 10 to 12 patients, but it's BBS, POMC, and leptin receptor. And then we'll last and importantly provide the insight into the preclinical data, which is behind our weekly formulation. So this is our 718 weekly formulation, which is MC1 sparing, so we've eliminated the hyperpigmentation, which is a side effect of our current drug. Not a health problem per se, but it's a significant issue for many patients, so we definitely want to get rid of that. And we're really excited about where that 718 program is going, and another feature of that is, that's something fully Rhythm-owned. It's a new chemical entity with IP out to 2041. Great. And with that, we can, we can wrap it up. Thanks so much, David. Thank you.