Rhythm Pharmaceuticals, Inc. (RYTM) Earnings Call Transcript & Summary

All right. Good afternoon, everyone, and thanks for joining us at the Morgan Stanley Global Healthcare Conference. I'm Mike Ulz, one the biotech analyst here. It's my pleasure to introduce David Meeker, President and CEO of Rhythm Pharmaceuticals. Before we get started, I just need to read a quick disclosure. For important disclosures, please see the Morgan Stanley research disclosure website at www.morganstanley.com/researchdisclosures. If you have any questions, please reach out to your Morgan Stanley sales representative. And with that, David, thanks for sharing your time with us today, and maybe I'll just hand it over to you briefly to make some introductory comments for people that might not be familiar with your story.

Sure. Yes. No, thanks for hosting us and exciting time for Rhythm. We've been at this for a while. But for the past number of years, our conviction around the importance of the melanocortin-4 pathway, which is the pathway I think governs our satiety signal. We eat a meal and got hormone signal of the fat cell releases leptin, goes to the hypothalamus and signals down to the melanocortin-4 pathway and say you're full and not only you're full, you can increase your energy expenditure. So patients who have a defect in that suffer from inability to feel full. They're constantly eating, constantly hungry. And perversely, because their energy expenditure is kept low, they gain weight and they gain a lot of weight. So what Rhythm's strategy from the beginning has been is to really unravel this, starting with some of the classic known genetic defects that affect this pathway, and those were our first 2 approved indications for POMC biallelic and leptin receptor biallelic and really dramatic responses. It turns out those specific populations are relatively small. We didn't actually put a sales force on the ground in the beginning there, but really powerful proof of concepts. The next indication, which is for Bardet-Biedl syndrome approved in June of 2022. It's a syndrome. So there's multiple signs that you may have this entity. So in terms of getting to a diagnosis that facilitated that. And the size of that population was meaningfully larger. So we talked about 4,000 to 5,000 patients in the U.S., similar numbers in Europe. And our confidence in those numbers has grown over time. And one of the hallmarks of a rare disease, sometimes I think about them as really a desert, you might have epi numbers that say they should be out there, but you just can't find them. And that usually tells you something. Conversely, if you're finding them, that's a pretty good marker that if anything, your epi may be low, not high. And so over time. And those opportunities also, they tend not to plateau. And I came out of Genzyme as many people know. And a number of those opportunities just decades later, more than a decade, they continue to add patients and continue to grow in a slow modest rate, but like I said, they don't peak. So BBS was really important first approval, and you could build a company around that. The -- what people really started getting excited about Rhythm around was this acquired hypothalamic obesity, which is a disease where most often patients who have developed often a benign tumor -- doesn't have to be benign -- but a benign tumor in the area of the brain around pituitary and the hypothalamus, it gets resected, the hypothalamus gets injured. And if they hit the hypothalamus, this part of the hypothalamus where this pathway sits, they come out, they explode off their growth tracks. I mean they're rapidly growing weight. And it wasn't -- the problem was clear. It wasn't clear that an MC4 agonist could work because you're injuring the part of the brain and you're losing some of the receptors, so maybe the ability to respond. But what's really been striking over the past 2 to 3 years of doing the development work in that indication is it's remarkable. And it's remarkable, not just because they lose a quite meaningful amount of weight, or BMI decrease, but the consistency of response. I mean it's -- literally, if you take the drug, most patients, almost all patients have some level of response. And so we're opening that up. We can talk more about that. But that's a really important driver. And then I think there's a lot of other things we can do with this pathway. We've talked about other genetics. We're currently running a Phase II in Prader-Willi. It's early. It's very challenging disease. We can talk about that. But there's a lot to do here, and we think about this area as a product in a pipeline as much as anything.

Yes. Great. Thanks for that introduction. And maybe we could just stop -- start -- sorry, with IMCIVREE. You touched on this a little bit, but your currently approved indications and kind of how to think about the growth drivers today and what that looks like kind of going forward?

Yes. So what we've talked about for Bardet-Biedl and we talked about it, we don't give revenue guidance. But if there's 4,000 to 5,000 patients in the U.S. for Bardet-Biedl, what's the probability we can get 1,000 patients on drug? It seems high at $300,000 net. I mean that sort of gets you to a $300 million opportunity. You do better than that. I'm talking U.S. only, $300 million, $500 million opportunity. So I think, as I said, our confidence in BBS as a foundation has really grown. So you've got that as a solid piece to build on. HO, we've talked about 5,000 to 10,000 patients. More recently, as we've done more work, we've done some claims analysis. We have individuals in the field now are beginning to profile the disease, talk to thought leaders and treaters in the field. So we're increasingly confident that, that are probably at the top end of that range in terms of the overall opportunity here. We're excited about Japan, where the prevalent numbers on a population basis seem to be somewhat higher. So we talked about 5,000 to 8,000 patients in Japan, continuing to do more work. And so these are -- that's going to be a big part of the growth driving on top of our BBS opportunity, and we have our PDUFA date set for end of this year and so in the U.S., so we'll be ready to launch. And we filed simultaneously in Europe. So we look forward to hopefully getting approval mid next year or sometime Q3 maybe.

Great. You talked about your increasing confidence just in the sort of market opportunity here in the U.S. for HO. And maybe talk a little bit about what drove that sort of thinking? And is it possible that maybe 10,000 is -- could be conservative maybe?

Yes. I mean people -- a lot of people, they're doing work. Everybody is doing work on this. I just -- for me, it's -- so could it be higher? Absolutely. And like I said, this has the feel that there's probably more patients out there. I think -- but we're not going there now. I don't think we need to go there now. I think let's solidify around these numbers. I said 5,000 to 10,000, we're skewing toward the 10,000 side of that equation now, which I think perfectly appropriate. As we learn more, maybe we'll update it. But one of the things that's been apparent as the team has been out in the field is pediatric endos, not surprisingly, are pretty on this. And that's not surprising in that they're seeing kids who may not be so far away from when they had their injury, their tumor and their surgery. And so it's easier for them to connect the dots and the like, whereas if you're an adult endo and you see somebody who had a history of a tumor and resection 20-plus years ago. They've got some pituitary insufficiency, so you're following and they happen to be obese. You may not connect the dots. And this is a disease where, like many things, until you have a treatment, there's also no urgency to make a diagnosis. If you don't diagnose it, so what? I think people tend to react to obesity in general, still amazingly as one disease. So a lot of these patients will have seen GLP-1s. I think we have a pretty good sense about the limitations of GLP-1s here if you don't correct the underlying biology, which is this MC4 pathway defect. So long story short is, yes, I think there's a lot of potential here, but we feel really good about the 10,000 number and we go.

Makes sense. Maybe could you talk a little bit about Japan. You mentioned that as a potential important opportunity for you and maybe some of the dynamics in that market versus what you see in the U.S.

Yes. It's -- so for a reason we don't maybe fully understand, there seems to be a higher prevalence of tumors, these benign tumors, which would lead to the higher diagnosis of HO. There's a pretty -- it's really not dissimilar, meaning there's a small active, knowledgeable expert community there that we're working with, a lot of support from endocrine society and the like. The PMDA, the Japanese regulatory authorities, they are, I think, for the past couple of years, maybe more than that, have been opening up in the sense that they don't want Japan's access to medications to be significantly delayed, which has been historically the case. You have to run special trials or do additional work that you wouldn't have to do. So they've really been incredibly helpful to us. I mean, as you know, we went to them late. We already had our Phase III underway, and we went with a proposal that said, look, can we bring in an additional 12 patients here as part of that trial, would that be sufficient for approval? And they said, yes. So that to me, that was great. I mean that was a real strong indication that they are really motivated to work with you. And like I said, we're not the only company with that experience. So Japan has a lot of positive attributes now.

And maybe if we just move back to the U.S. opportunity and maybe just highlight some of the unmet need or how these patients are treated today or what are their options?

Yes, their options are limited. So they're, not surprisingly, a sick population. And when I say sick, it's probably the sickest population in my career that I've worked on and one measure of that is their medication list is 1 to 2 pages long. I mean they're just the number between all of the different hormonal replacements and they have a seizure disorder and they have other things going on in terms of mood, depression. So it's just -- it's a really, really tough population. So despite that, what they're suffering with hypothalamic obesity is a major part of what they have to deal with. And there are other hormonal deficiencies. If you're hypothyroid, you can place your thyroid and live a pretty normal life. And so this acquired hypothalamic obesity part of their presentation is really dominating their quality of life, the family's quality of life and we did well and very well on the quality of life scores. We did well on the hyperphagia scores. But this really comes through when you read the exit interviews and just know what life was like before and what life is like now. And so yes, it's pretty remarkable how important this is in the current situation.

Yes. So very high unmet need, and you started to touch on some of the data you saw and maybe you can expand on that a little bit. You shared results from the Phase III TRANSCEND study. So maybe highlight some of the key takeaways and data points there.

Yes. I mean -- so that was the largest trial that's ever been run certainly in this disease, 2:1 randomization, so about 80 treated, 40 on placebo. Also the largest placebo control group we had. And so a couple of things stood out. One is we got a very good response in the treated group, 16% and that was imputing data from patients who discontinued during the trial for a variety of reasons. We had less than about a 10% dropout rate overall, which was small compared to and pretty remarkable considering we had a placebo group. It was about half and half between treated and placebo. But if you did drop out, you had your values imputed and the way that whole approach works is you're informing the data, you're imputing based on the trajectory of the placebo group. So in a way, it's the absolute most conservative way of looking at that data. So long story short is we had about a 16% positive -- or 16% decrease in BMI in the treated group, 16.5%. And really importantly, because this is always a question in obesity trials, you can have very significant placebo effects and decreases in the placebo groups. That does not happen in this disease. I mean there is no placebo effect. And those patients, they gained 3.3%. So it wasn't like huge, but meaningful increases in weight from where they were. So our placebo-adjusted effect was 19.8%. So really strong numbers in terms of overall BMI decrease. But the other piece, which I highlighted earlier, which I think was really striking was the 3 age groups, 6 to 12, 12 to 18 and 18-above had identical results. I mean they all had placebo-adjusted rates of 19% to 20%. So again, it wasn't being driven by one sub-population. One of the early questions we had about HO was, well, gee, you're out 20 years from your index event, maybe you're not going to respond as well as a kid who's just had it 2 years ago or is fresh off their injury, and that's not the case. They responded exactly the same. I think the oldest person in our trial was 66 and they responded. So again -- and these patients from an epidemiology standpoint, they tend to live a normal life, relatively normal. So the 80-plus -- so the 20-year survival is like 80-plus percent, again, depending when you born and 50%, 30%, 40%. So yes, it's important to be able to treat them across that full age range, and I think the trial supported that. And then the last piece I'll just highlight back to the GLP-1 is we did allow patients on GLP-1s to come in the trial. They had -- they couldn't be losing weight, actively losing weight on the trial. So we had about 30 patients, half who had been previously on a GLP-1, but were not on it when they started and half who previously been on but continued during the trial. And those who had previously been on stop, they had about a similar response as the others. But those who concurrently were on a GLP-1, they lost 25%. So again, the trial wasn't stratified. It wasn't designed to make conclusions about GLP-1, but you could look at that data and say, well, here's a group of patients who weren't responding to a GLP-1. But once you replace their hormonal deficit, corrected the underlying biology in theory, made them more normal, normal physiology, then their ability, and I would argue to respond to any anti-obesity medicine might be restored. So to the extent that you need additional weight loss, then maybe you're going to get more of an effect. And so again, there are a lot of pieces of the trial, which I think were incredibly helpful. We have growth curves on all 31 of those patients. So showing the effect of when they started the different GLP-1s. The majority of them were on either semaglutide or tirzepatide. So it wasn't like they didn't get the most recent newest generation drugs. And you can see when they started and the pattern is pretty clear. For the most part, you put anybody on a GLP-1, they'll lose some weight. But in this disease, if they're working against this defective signaling, abnormal underlying biology is they tend to regain and they tend to regain again after 6 to 12 months, and that was very much supported by the pattern and the growth curves that we have for the patients in this trial.

Yes. So very promising results there. And as you mentioned earlier, you've already filed with the FDA and gotten acceptance with the PDUFA date later this year in December. So maybe you can just talk about interactions with the FDA and how that's gone just given all the sort of changes in the leadership you've seen this year.

Yes. I mean, reassuringly, from where we sit, our review division seems to be relatively intact. So in terms of people leaving, and that's so apparent. All of our interactions in the process of filing, we had our end of Phase II meeting, which was the first in-person meeting I've had with the FDA in about 5 years. All that was positive. And I'd just characterize it as normal. So we're pleased to get our PDUFA date on schedule. That was exactly when we expected to get it. I know Commissioner McCary yesterday reinforced again. I mean they're highly motivated to meet their PDUFA dates and have "a record number of approvals this year", and hopefully, we'll be part of that.

Sounds good. You're also planning an investor event in a couple of weeks to kind of maybe shed a little bit more light on how you're thinking about the opportunity and launch. So maybe just talk a little bit about what things we should expect there.

Yes. I mean we did one when we -- several months in advance of getting BBS approval. So the goal will be to share very North American focused. So we'll have a couple of experts. One is pretty well known to the community, one maybe a little less known, but follows a very large population of HO patients. So I think we'll have 2 nice perspectives there, which will be educational in terms of what they think about the data and how they see this world evolving. And then we have our teams, as most companies are at this point, where the build-out of our sales force is well underway. And we've got a good number of people who are in the field now interacting with endos and profiling and the like. And so we'll share a lot of those learnings. So that's, I think, more or less what you'd expect here. I don't expect us to revisit the epi. I know there's always a lot of interest there. But I think we're in a good place on the epi. So we'll probably sit tight on that.

Can you talk a little bit about your current sort of infrastructure and how you leverage that? And like how much of a lift is this to sort of loop in HO?

Yes. It's -- I mean it's always a lift in the sense of a launch. But I'll just make a general comment. I mean it's much harder to develop a drug that works than it is to build a sales force. So I mean, the heavy lifting is done. The teams that are out there, I mean, we've done a couple of things. We've directed our MSL medical affairs group very much around this HO in the recent past and upcoming near term. We had a group of individuals, we call it ADMs, area district managers, whose prior job was to really support our genetic testing and clinical trial enrollment. Now EMANATE is fully enrolled and the like. And so they've been redirected to disease awareness and working to understand ends and the like. And some of those individuals will then convert over to becoming salespeople once we get closer to launch. And then, of course, we're building out the total number. So we work it on multiple fronts we're well underway.

Great. And you're also sort of in discussions with Europe and filing there. Maybe just sort of give us any updates.

Yes. We did a simultaneous filing literally. So we got in a good time. As I said, expect maybe a Q3. I don't know if we've guided, so I'm probably guiding here. Hopefully, that's what happens. And then too early for feedback, but I don't -- they've been very receptive overall to all of our programs, I would say. And so again, I'm not expecting major issues in Europe, but we'll see.

Yes, makes sense. Maybe I can just go back to Japan, and we spoke about the opportunity there, but you're going to have some data on those 12 patients coming up, I think, early next year, if I remember. How do we think about that data? Or any reasons to think that those patients may be responding differently? Or is there any impact of like baseline characteristics or things like that?

Yes. No reason to expect it. And I think that was part of the PMDA agreeing is that, obviously, at 12 patients, we're not powered to prove anything based on the Japanese cohort as a stand-alone. But from a biology standpoint, there's really not any reason to believe this is different. I mean the way they present is similar. It's the same. So again, I would expect the response to be similar.

Got it. Maybe we can shift gears a little bit to your next-generation MC4Rs, and you've got 2. So maybe at a high level, just walk us through those 2 programs and what's different about them?

Yes. So this is critical to the long-term success of Rhythm. One, just from an IP standpoint, those 2 programs, each of them will take our IP out to 2040 plus. So it gives us a good long runway to continue to work all the opportunity we think is associated with this pathway. One is an oral, that's the bivamelagon. We just completed the Phase II, and we're assuringly in this 14-week trial. It was -- and the results were very similar to what we saw at a similar time point in our Phase II and our Phase III studies. So that was highly confirming. The other thing which was reassuring and incredibly helpful was that we saw a clear dose response. So the 200 milligram, there were some responders in that group, but it was clearly less than the 400 and 600 milligrams. So I think we're in range. I don't think we need to do more dose work. And we will run a Phase III with the same general approach that we've used for our setmelanotide development, which is we're not testing a dose per se, we're testing a dose range. So for setmelanotide, it was 1 to 3 mgs, started 1 dose escalate, most patients go to 3, here will start at 200, those escalate to 600 and as tolerated and we'll see and I think most patients will be in the 400 to 600-milligram dose room. So I think we learned a lot about what we need to do to go ahead and set up a Phase III. The other programs are weekly injectable. And historically, when people asked before we had any data between the 2, which do you think is more likely to be successful the answer was always well the small molecule has more unknown, so maybe that's higher risk. Weekly is a 7 amino acid cyclic peptide and setmelanotide is an 8 amino acid cyclic peptide, preclinical data was highly similar, almost milligram per milligram. So based on all those factors, I would have considered 718 to be a lower risk program. So we'll see. That's to say now we have positive data on biva. I still think 718 is a high probability of success. But our strategy overall was not -- would you prefer a weekly or an oral daily oral. The answer is we don't care as a company. Our goal as a company is just say, look, we want to provide a full portfolio of options for the patient and physician. And I think those 2 do it. The other part, which is it's important. I mean it hasn't been a major limitation for setmelanotide, but the MC1 agonism, setmelanotide is a little less specific, which causes hyperpigmentation. Both of those next generations were designed to have less. It looks like and our confidence in this statement is growing that the bivamelagon had really minimal. I think there was a very clear signal that, yes, we saw a little bit, but it was minimal. And patients all rolled over in an open-label extension. And the best of my knowledge, we really haven't had any more updated events from what we originally reported. So I think there may be a slight signal darkening of nevi where there's a concentration of melanocytes. But in terms of the general increased pigmentation that was concerning to patients, it doesn't seem to have that. And then 718 is even more specific for MC4 over MC1. So I'm counting on and expecting that to be even less of an issue. So -- and we do get 6% of our patient population discontinuing and maybe even a higher percentage where that's not their primary reason for discontinuing, but maybe it's in the mix. They're just not so happy with X, Y or Z, but also the pigmentation isn't helping. So I think that will be a meaningful added feature here. And of course, the tolerability is much better.

Maybe I could just ask a follow-up on the hyperpigmentation. And maybe you could just describe what it -- how it presents in -- with setmelanotide and then maybe contrast that to what you saw with bivamelagon.

Yes. Well, setmelanotide, as I said, it's less selective. So you're hitting the MC1 receptor more uniformly. So it's a uniform increase in pigmentation. And the way our bodies work is between the eumelanin and pheomelanin, eumelanin is darker. So darker you are, the darker you get. And so many patients hardly notice it. Some patients like it. And some patients it's quite concerning for them. So -- but it's uniform. And what we saw with bivamelagon, as I said, was in a couple of patients where I'm pretty convinced the signals -- I haven't seen any pictures, to be honest, and that wasn't part of it. But what resonates is real, as I said, is in these areas where maybe you have increased melanocytes and potential for increased melanin release. So the nevi, sun-exposed areas, back of the hands and neck. There's also some reports that make no sense to me, like the right thigh, non-sun-exposed area, the right side of the tongue. And we had one placebo patient who reported increased pigmentation. And I think how does that happen? It's just -- we had a hypervigilant patient and investigator group because they were looking for it. They were instructed to look for it. And as I say often, if you look at your hand one day and then say, tell me the next day if it's darker and that, that can be kind of a hard call. So I think -- I just -- back to what I originally said, I'm quite confident we've got a significantly decreased signal here, and it should be quite a different experience for the patient.

Yes. Makes sense. Earlier, you talked about the bivamelagon sort of Phase III trial design and kind of what you're considering there? I guess maybe talk about when you can start that? And what are the next steps to actually getting that started.

Yes. So we're preparing a briefing document now. We'll get hopefully our end of Phase II meeting before the end of the year and start -- we've got to get our formulations, new formulations done. So it will be hopefully a first half start next year. A bit of a news flash here. I've talked previously about my wish list, which included maybe doing a trial with an external control. In other words, using the control group from our Phase III study, which would mean every patient in our bivamelagon trial could be on drug. As we dug into that and the team had some good pushback on my wish list. And the challenge is that if we do that, then we really need to run the trial in a virtually identical way because that's your control group, you can't be making the changes in the treated group. We've learned some things, different questionnaires, which we want to incorporate, thinking about market access in Europe and some things that might be useful. And so I think where we're likely to net out here, no final decisions made is we probably will run a double-blind randomized controlled trial. It -- the wish list, again, will be a much smaller size. I think we'll make the case. The FDA is pretty very bought into, I'd say, the biology and the mechanism here. So I hope we get a receptive year to smaller numbers, but we'll see. So that's makes sense. or in progress.

Yes. So a lot of opportunity for your next-gen MC4Rs. And maybe we can shift gears and talk a little bit about Prader-Willi. You've got a Phase II study ongoing. Maybe talk about the design there and what you learned from your prior experience in Prader-Willi.

Yes. So Prader-Willi is a tough disease, as we all know. So what do we know? There's no news here today. What I've said is I think there's about a 50-50 chance. The biology is really clear in the sense that this -- 2 of the genes in chromosome 15 that are affected here are MAGEL2 and this SNORD115. Both of those have impact on melanocortin-4 signaling. And we know from our Phase II DAYBREAK study, where we studied patients, one of the groups were patients who had variants in the MAGEL2 gene. For those patients who had confirmed loss of functions, they had a good response to setmelanotide. And we know the mouse models, hypersensitive to setmelanotide. And so the biology around MAGEL2 specifically is very clear. 90% plus of patients have involvement of those 2 genes and the 20-plus genes that are affected in Prader-Willi. So I'm sure about the biology, and I'm sure to the extent you can be, we can make the biology better. The challenge with Prader-Willi, of course, are the behaviors and the noise. And so it's one thing if you can correct the biology, the next is can you show it clinically. And one of the things that everybody has to deal with is the obsessive compulsive disorder part of this. And what really resonates for me is like think about this is if you correct the underlying biology, but you're hardwired based on your obsessive compulsive part of your disease to have a snack at 10:00 a.m., you want your snack and you're going to eat it and has nothing to do your food. There's nothing to do with whether you have a drive to eat and the like. And so that's the world that all the companies trying to develop are working in. It creates a lot of noise and Soleno, to their credit, got through and almost heroically, but even their trial design had a lot of challenges with COVID came and disrupted things. And so that's the challenge of clinical development in Prader-Willi. So the design, long story short is we've run a trial in 2018, '19, which was designed based on what we knew at that time, short crossover periods and the like, looking for quick changes in hyperphagia, which clearly is not appropriate for Prader-Willi. And our maximum dose was 2.5. And so our strategy here is to go to 5 mgs, titrate all the patients up to 5 mg as tolerated to as best we can take off the table the possibility, gee, if we've gone a little higher, maybe we would have seen something. So -- and I don't think there's a lot of room, to be honest. And for most patients above 3, I think 3 probably gets us most of the efficacy if there's -- but we want to remove that this possibility. And the other thing is, for whatever reason, they may just take longer to respond back to these behaviors. So 6 months, so minimum for these patients. And the other thing we're allowing is we're allowing patients to be on as long as they're stable on whatever meds they're on, which would include the long-acting diazoxide [indiscernible]. So yes, we'll see.

Yes. So you plan to give an update by the end of the year. And will you have...

That's our goal. Qualifier.

Okay. Goals. But when -- I guess when you eventually share the data, maybe how many patients, how long will it all be followed up post 6 months? Or what does that look like? And then what are you looking to see to sort of say, okay, move this forward?

Yes. So the goal here, the endpoint is weight loss. I mean we're not -- I know several companies are pursuing hyperphagia based on the Soleno experience, but we should get weight loss if it's working. And so -- and the bar for the weight loss, we think, based on FDA's published guidance for weight loss drugs is 5% -- and I don't think -- we haven't had conversations with the FDA about this yet, but that makes sense to me. I would be surprised if they didn't agree with that. So that's the bar. So what we're looking for is confidence -- reasonable level of confidence that we could run a 52-week trial and get people to 5% or more weight loss. So our goal in this Phase II open label, we don't have a control group. The advantage of working with a single site and a very experienced knowledgeable investigator is that hopefully, she can help us understand the data through the noise, and she really knows the patient. So if it works in person, okay, that may be clear. If it doesn't work in somebody, why not? And maybe there are circumstances in the family at home, other things that may allow us to interpret the data. And we'll present it the same way we have all of our studies or most of our studies, which is the individual patient responses, and you can see, and hopefully, we'll have a story for what's going on around that. And the qualifier, the goal is to get 10 to 20 patients. I'd like to have some patients who are on diazoxide and some who are not. And the hedge always is you work with a single site and the recruitment is not always reliable. So she goes on vacation, she gets sick, or study coordinator doesn't show up. I mean these are things. So that's just left. But anyway, that's still our goal based on where we're there.

Okay. Great. It looks like we're just about out of time. So why don't we end it there. Thanks so much, David. I appreciate your time.

Thank you.