Good morning, everyone. Thanks for joining us here on the third day of the Goldman Sachs Global Healthcare Conference. Thanks to everyone who joined us here as well as online. We're thrilled to be joined today by Richard Pops, Chairman and Chief Executive Officer, and Blair Jackson, Executive Vice President and Chief Operating Officer for Alkermes. Maybe first, just over the last 12 months, you've seen a significant period of change for Alkermes, including validation of the orexin agonist class and acquisition of Avadel, the announced CEO transition. Thanks for joining us, but before we jump into Q&A, I'd love to just turn it to you for some opening remarks on all that progress.
Well, thanks for having us, first of all, and standing room only in this giant room, which is great to see.
You don't know how many people are online.
Yeah. This has been just a fantastically interesting past 12 months for the company. In part, from our perspective, we're smiling because we're doing everything we said we were going to do, and things have evolved in a way that we would have hoped to have predict, but it all of a sudden seems surprising to everybody. That is, we've been working on these orexin agonists now for a number of years. We've been, along with others in the field, slowly elaborating the biology and the chemistry, and I think it's becoming abundantly clear that this is a really exciting opportunity.
With Lilly coming to the space and in many ways validating what we've been saying, now we find ourselves with a drug that we think is really the best-in-class molecule in diseases of hypersomnolence, now enrolling in phase III after a very strong phase II program that answered most of the questions that we all had. Because these weren't underpowered phase IIs. They were very well-powered phase IIs, asking questions about safety and efficacy and tolerability over extended periods of time at a range of doses. The company is evolving really well. I announced that I'm going to move to Chairman. Blair's been shoulder to shoulder with me for the last many years building this company, and we've got ourselves in a position now where I think that if we execute, we can see the valuation of the company really expanding. It's not notional.
At this point, it's in our hands to execute. Blair?
Yeah, I think if you look over the last year, we've really been looking to widen our portfolio and our pipeline in orexin agonism and really laying down a number of different bets over the next little while and programs that are going to report out over the next 12 months. We're in a really exciting moment for the company and a moment of really execution and change. I think everybody in the company is really excited, and I know it's going to be a really interesting data set, both in the sleep space as well as in the neuropsych space as we look at our ADHD and our fatigue programs as well.
What's interesting, we have a $1.7 billion top-line commercial business that drives tremendous profitability and a lot of cash flow, most people don't care at all about it. We care a lot about it because it's the flywheel that powers all this innovation that we've been able to do in a non-dilutive way for our shareholders. We bought Avadel, which brought us into the hypersomnolence business from a commercial perspective with a really good asset with cash. We didn't need to use any stock to do that. We have amazing strategic flexibility that we've been exploiting slowly, carefully, almost quietly, and I think people are beginning to realize that now.
Great. Let's start with the orexin program, and as that competitive landscape continues to evolve, potential approval of the first NT1 asset expected relatively soon, other pharmas stepping into the space. What is your current thinking about how alixorexton is most differentiated, and how does that profile then translate to NT2?
Go ahead, Blair.
Yeah, I think when you look at the space as a whole, this is a disease area that has a number of therapies that are in it right now but has left a really gap in what patients are really looking for. I think with this new class of orexin agonists, it's bringing with it a whole new level of efficacy and opportunity for these patients. We're going to be coming into the marketplace with a drug that has multiple doses to treat different heterogeneity and disease. We'll have a drug with once-day dosing, with split dosing to provide flexibility for patients and their needs, as well as a drug that hopefully works across all three hypersomnolence indications. If you compare that to Takeda's drug, which is coming in right before us, it is a wonderful drug.
It addresses a lot of the efficacy in a subset of patients. It's limited in where it can go. There's not multiple doses, can't go into other indications. We're highly differentiated from the first molecule in the space, and we're really looking to deliver on that data set with our phase III program. Our goal with our TPP is to create a label that's going to be hard for anyone else coming behind us to differentiate from, whether that's Eli Lilly or whether that's anyone else.
Great. Maybe given what we've seen from the data on alixorexton's benefits on wakefulness in EDS in the NT2 population, I think 8- 10 minutes from baseline on the MWT and ESS scores at the upper limit of the normative range. How do your results reinforce confidence in the benefit of orexin in indications such as NT2 and idiopathic hypersomnia, where those orexin levels are not necessarily compromised?
We're going to show a more complete analysis of the NT2 data next week at the SLEEP conference in Baltimore. The feedback we get from opinion leaders in the space is that it's remarkable to see, this is the first agent to show against the backdrop of this very highly variable patient population, not just changes in MWT that are clinically meaningful, but changes in the Epworth Sleepiness Scale, which is the patient's self-reported assessment of their daytime sleepiness, taking people from highly symptomatic to normal. At SLEEP, we'll show the longer-term extension data from the open label phase, showing this is a durable effect that lasts for multiple weeks, coupled with new data on fatigue and cognition, which are part of this holistic benefit that these orexin agonists seem to be bringing patients.
Which is, it's not just the number of minutes your eyes are open in the MWT test or how you report on the ESS. It's what are the components that lead to that feeling of normalcy with respect to cognition and fatigue as well. What people have to understand about the NT2 data is that unlike NT1, it's a very diverse patient population. In a phase II study where you keep people in a particular dosing lane for the duration of the period of time, you get a certain response. In the real world, the patient won't stay in a dosing lane. If they need a higher dose, they'll go to a higher dose. If they need a lower dose, they'll go to a lower dose. Which is why, to your earlier question about differentiation, this program from the outset has been built on differentiation.
The differentiation we see central is range of doses, range of regimens, and range of indications. That the physician and the patient have the ability to flex into whatever duration they want and whatever dose that is most suitable to their disease and their lifestyle.
Right. Maybe you could contextualize for us how clinically meaningful the results you've shown on MWT and ESS are relative to other options currently available in these indications.
Well, no one's ever shown any data in NT2 alone, to my knowledge. When you see the data from the oxybates, for example, it's a pooled NT1, NT2 population. I think it's one of a kind at this level with respect to the various parameters we've measured in the NT2 population. In the NT1 population, of course, if you compare the orexin agonist to previous therapies, I don't think there's any comparison between the MWT changes that you're seeing in the NT1 patient populations compared to the previous drugs.
Yeah. What I'd say is when you look at any of these various indications, there's multiple prisms that we look at with regards to efficacy. One of them is MWT, which we use in NT1 and NT2. I think there's a risk of over-interpreting that result when you look at an average across a number of patients. Especially in NT2, where you have this huge heterogeneity of response. When you lump it all together into an average number, it actually hides what's going on underneath. You may not see certain things that are really there, like dose range and things like that. I think also, though, when you look at these indications, you need to look at it from the context of what patients are looking at within their treatment paradigm, things like ESS.
This is your Epworth Sleepiness Scale, and really gives a sense of do they feel tired or don't they feel tired? What we saw in our NT1 program is that we were able to normalize almost everybody under the ESS scale. We normalized about 70% of them on the ESS scale with the NT2. From a different prism, it shows you a different element of the disease response. The other thing I'd point out, and we're going to talk a lot about this at the SLEEP conference, is cognition and fatigue. One of the things that we're seeing is with these orexin agonists, we can drive improvements in cognition, improvements in fatigue, take patients who were severe to start and pretty much normalize them over the course of the study.
It's really all of those things that contribute to that patient, how they feel, how they're going to respond on treatment, and how they'll move forward with their treatment parameters, once they're on therapy long term.
Right. To that point, what should we look for in terms of the scope of data you'll present on things like fatigue and cognition?
We'll show some detailed slides or graphs on both cognition and fatigue over the course of the study, as well as over the OLE period. You'll get a chance to see, one, the response. What happens when you take a placebo patient on the trial, flip them over into active, and then you'll also get to see the duration of the response in the OLE period as well. It'll be a fulsome data set similar to what we showed with the NT1 prior.
Great. To what extent do we understand those symptoms like fatigue, brain fog, et cetera, to be attributable directly to a loss of orexin tone versus being kind of secondary effects of sleepiness?
It's interesting. When you look at our programs in NT1 and NT2, that's exactly that experiment. NT1 patients don't have orexin tone, and NT2 patients have full orexin tone. What we're seeing is consistent responses regardless of what the orexin tone is. I think that one of the things that we look to do as we move forward with our programs is continue to generate evidence to show that cognition and fatigue are actually both independent of sleep. There is some overlap and some correlation. If you look, for example, at our fatigue study, patients have fatigue for a number of different reasons. It's independent of orexin. It can be from a neurodegenerative process. It can be from a cancer treatment. It can be from a variety of different things.
That is sort of the future of orexin and where you can take it, is to go after some of those really debilitating indications.
Is there any other efficacy data we should anticipate? For example, could we potentially see any additional MWT analyses across patient subgroups to better understand kind of the efficacy given the heterogeneity of NT2 patients?
Well, I think for the time being, we want to share what's relevant for people to understand the molecules. A lot of the stuff that you're asking for is, it really came out of all the phase II program that we've done to date and really has informed on our dose selection, our development strategy, and things like that. We want to maintain that proprietary for the time being and not reveal that to the rest of the world.
Understood. Maybe turning to idiopathic hypersomnia, you mentioned, I think, on the first quarter earnings call that you've initiated enrollment in a split-dose cohort of the ongoing phase II, and that's on track to complete in the fourth quarter. What should we expect in terms of nature of disclosures here relative to what you've already shared in NT1 and NT2 patients?
I think with the IH, it's going to be very similar to what we disclosed with NT2 and how we proceeded with that. We'll share with the top line. I think what'll be different about the disclosure on IH with Vibrance is that we've introduced the split dosing into that program. That was one of the key learnings we had from our Vibrance-2 study, where we showed that some patients would benefit from having enhanced efficacy in the latter half of the day, and patients were looking for some flexibility, ability to maybe push out their dose later into the evening. This will be the first embodiment of that in the clinical program to show how that impacts their responses, both on ESS and IHSS, which are the endpoints for IH. That's different from NT2 and NT1. MWT is not a component of that disease.
That being said, we do have MWT as part of that, so we will get to see how the split dosing affects the MWT in that patient population.
Great. Can you share how you're thinking about the target product profile for alixorexton in idiopathic hypersomnia?
It's interesting you ask that because when you think of how we design this and what we talked about earlier, the idea that we have alixorexton to be able to provide benefit across all three indications, they really share a TPP. From a physician perspective, the belief is that you could go into that doctor's office, that doctor has a patient who may have one of these diseases, and as you know, the diagnosis is a little bit gray. There's a little bit of back and forth. Sometimes NT1s look like NT2s. A lot of time IH and NT2 overlap. The differential diagnosis won't matter if we have all three indications. The idea here is, can you address those three indications? What are the appropriate doses for each indication as a starting dose?
You can move around wherever you need to be, whatever that patient has. In fact, you might actually use this as diagnostic criteria. You could by dosing low, if the patient responds, you know they'll be NT1. If they don't, you could move them up the dosage curve, and maybe they're NT2, maybe they're IH, et cetera. It provides a lot of opportunity downstream to really provide just a more appropriate treatment for this patient group.
Great. You recently initiated the phase III Brilliance program last quarter. I think the NT1 and NT2 studies are underway. Could you provide an update on enrollment and how that's progressing in the studies? As well, could you just characterize patient physician receptivity to those trials?
You're on a roll. Keep going.
Yeah, you're right. We've initiated these programs. We've moved very quickly. We went and met with the FDA after our phase II, talked them through the data and our approach to building this program. We really have three studies that are part of our Brilliance. We have two NT1 studies and a single NT2 study. Across the programs, we have one-day dosing, and we have split dosing. Across both indications, it'll provide a lot of flexibility downstream. What we're finding is as we introduce these clinical studies, we're getting a tremendous response from patients and physicians. I'll contrast that to when we started, no one really knew Alkermes. We were bringing a new molecule into the space. Takeda was the big fish people. Those were the studies people were really interested in.
We're a little bit more now the belle of the ball. I think people are recognizing that we have a molecule that really can help people, so there's a lot of interest in joining these programs. We're actively enrolling in the studies. Europe is coming on board and turning on. As you know, that takes a little time on a country-by-country basis. That's going really well. I think we're exactly where we had hoped to be at this stage in the development, and if we enroll strong leading into the summer, I think we're in good shape.
Great.
The virtue of running a big phase II program is that it prepares you for phase III.
With the sites and all data set that you can bring in phase III now, when a physician is sitting with a patient, you can say, "If you want to enroll in this study, we know the agent works." The only risk for the patient really is in the randomization. Do they end up on a placebo? They know they can go in the open-label phase later and get access to drug. Whereas in phase II, in the early days, it's an experimental medicine. You don't know whether it's safe or tolerant.
Right.
Now we have that flywheel that began spinning in phase II that rolls really well into phase III.
That's super helpful. Maybe you could speak to the Takeda approval for, I'm going to leave that one. Oveporexton, in terms of how it might impact your kind of enrollment ability, particularly in the NT1 population where it's relevant.
Well, look, I think in any development program, there's a number of things that people do to provide treatment for their patients and to keep them on therapy while you're getting ready to commercialize. Takeda's done the same thing. They have a number of people in their extension programs who are likely going to be some of their early customers as they move forward. If you actually look at the true overlap of where we are in enrolling our studies versus their launch, I think we're in a really good place. One of the things to keep in mind, too, we're in a number of different countries around the world. There's U.S., there's a number of countries ex-U.S. In fact, some of our best sites come ex-U.S.
Yeah.
I don't see their launch really impacting our enrollment in this program.
The contrary, we're probably the biggest fans of a strong launch from...
Yeah
... Educating patients to the new mechanism, recruiting doctors to understand the mechanism so they feel comfortable prescribing to the patients.
Great. What can you share regarding the powering assumptions across the three studies and the magnitude of improvement that would be both statistically but also clinically or commercially meaningful?
It's actually a really interesting question because I think this disease area is different than what a lot of people are familiar with. I think a lot of times, if you're talking about a depression study or schizophrenia study, that power calculation is so critical, and it's so important. I think what we're finding here, given the effect size of these molecules in efficacy, is that the power is not your real key question. Your key question is really about your clinical effect size and how that compares competitively to the others in the group. I'll point to the fact when we started our NT1 study, and we did our multi-dose, we had four patients that drove statistical significance. When you have a 90-patient study, 150-patient study, it's not the P value. You kind of leap over that.
In fact, one of the things we showed in our NT2 program, despite all this patient heterogeneity, despite some patients responding, some not, variability in how the tests were run, the efficacy of the drug just shines through. For us, it's about standardization. It's about making sure that we're enrolling the right patients. You don't want an NT2 patient in your NT1 study.
Yeah.
That'll mess up your signal. You want to make sure your cataplexy is standardized, so you're counting them the same at any treatment site so that you can actually have as much fidelity in the data as possible and get rid of some of that noise. I think one of our key learnings as well in our Phase II program was that the MWT, which I think a lot of people felt was a very standardized objective test, has a lot of art to it, how people do it, whether people determine whether the person's asleep or not, how all that happens, requires a lot of attention. I think doing that and applying that care into the Phase III is going to enhance our signal that much more so that we have a really strong label as we go into the market.
You mentioned measuring cataplexy in the NT1 studies. I think you've recently revised the assay that you'll use to measure and report those events in Phase III. Remind us how that new methodology differs from prior ones in terms of standardization.
Sorry, this is cataplexy?
In cataplexy.
Yeah. I think one of the things that was a surprise a little bit is that even within treatment specialists, how they recognize cataplexy and how they count it somewhat differed, especially as you went across different locations and things like that. Cataplexy is really a spectrum, and it can be anything from a patient losing full muscle tone to almost a tweak in the cheek or an eye, and it sometimes becomes hard to recognize for both the patient and the physician. One of the things that we did is we put very clear criteria on what is considered cataplexy, making sure they were trained to understand it, making sure that was consistent across our study. Consistency is key. The other is counting them. A patient could be watching a comedy and then all of a sudden have a cataplectic event.
Maybe it's their leg twitching, and their leg, in the course of a short time, twitches 10 times. One doctor might call that one cataplectic event. Another might call it 10.
Right? You can't have that. That really messes up your score.
Big difference.
It's all those little things and making sure they're trained, making sure that we're certain they were trained, making sure the patients understand how to do it as well. That's what's going to drive the effect as we move into phase III.
Great. You kind of alluded to this already, how confident are you that the effect sizes seen in phase II will translate and hold up into phase III? Would there be any reason to expect compression in a larger patient population or a longer duration trial, or is it the reverse?
Yeah. I think, again, this area is a little different when you have an asset that actually has an effect size like this. It really mutes a lot of those effects. A lot of times when you see compression of effect, it has less to do with the active drug and more to do with placebo.
Yeah.
There's not a lot of placebo here. What you find is, if you look at MWT, look at ESS, placebo's flat on the bottom. It doesn't tend to move.
We feel pretty good as you go to bigger sizes. It's not so different. The other thing to keep in mind is that your phase II trials are similar in size to your phase III trials here. You're a rare disease. We were 90 patients in our phase II trial, and we were like 150 in our phase III trial. You're not that much bigger.
Yeah
This idea of dilution doesn't really come into play.
What about the decision to evaluate the cognition endpoints BC-CCI and PVT in the phase III programs? Could you speak to which, if either, is more kind of clinically meaningful?
I think what's interesting is, we've used BC-CCI consistently through the program, and I think as a tool, it's really good for measuring cognition holistically. Cognition is how is that patient interpreting things? Do they have memory? Are they able to engage in tasks? Things like that. I think it's a true sense of how the patient feels. PVT is a little different. That's a vigilance test, essentially, and it's actually more of a behavioral test. It's akin almost to do you have attention? Are you able to respond in a task situation? I think they measure very different things.
I think we're really expanding in the cognition side with regards to these assets as well. I think as we go to the vigilance side, we'll be doing more of that with the ADHD program as we think of some of the attention and things like that we're doing there. We decided to measure PVT as part of our program in phase III. We do know others are doing it. We want to make sure we have a rounded data set to show the benefit of our drug. We'll have both BCCI and PVT to round it out. I think most of the data that we share with you and you've seen before is really around that cognition piece, because we know that's a key driver of patient satisfaction.
When you talk to patients with narcolepsy, they don't talk about MWTs or even ESSs. They talk about brain fog, and they talk about fatigue.
What we tried to do from the outset was build these instruments into the clinical trial using instruments that are recognized as having validity, despite the fact they haven't been used historically in narcolepsy, because we know that patients care about those things. It's also beginning to increase the dimensionality of what an orexin agonist does. First principle is when you think about what this circuitry does in the brain, it drives wakefulness. Wakefulness is more than just the amount of time your eyes are open. Wakefulness is about mood elevation. It's about focus. It's about vigilance. It's about cognition. All these things that turn on in the beginning of the day, that, well, you just sustain through the day and then wind down at night so you can sleep.
It's not surprising that an orexin agonist would have an effect on these various domains, and what we're trying to do is bring light to that through data. Whether or not it ends up in the label at the outset, I think ultimately it will.
Yeah
It's important to differentiate these from mechanisms that preceded them.
Yeah. Can you speak to any new learnings on the safety front in the open label extension study, or as you kind of gather feedback from physicians on what they're willing to tolerate? Maybe related to that, can you provide an update on whether you'll be conducting ophthalmic exams to assess visual changes in the phase III?
Yeah, as we look at the open label, I think what we're going to show, and you'll see it at SLEEP, is a lot of consistency on tolerability of the drug. A lot of the key sort of AEs that you tend to see with this are things like transient insomnia. You'll see polyuria. What's interesting is as you move into your OLE period, longer term treatment, it doesn't come up that much. Even as patients move to higher doses, you don't tend to see that many additional AEs. Highly tolerable program, to what Rich said earlier in the study. With regards to ophthalmic exams, that was only done as part of the phase II. As you know, we had a couple AEs related to vision. We wanted out of abundance of caution to understand that, to make sure there wasn't anything going on.
That was confirmed as part of our phase II program, there'll be nothing in our phase III.
Great. Beyond alixorexton and hypersomnia, there's also a growing investor interest in your Project Saturn programs. Maybe starting with ALKS 7290, you have a phase I-B study in ADHD patients coming in 4Q. How translatable do you think the preclinical mouse data are in this setting?
We use the five-choice serial reaction model as our preclinical model. It's quite a robust model that's been used in the community. It allows you to kind of compare assets on a rank basis, but also on an effect size. We went through rigorous testing of these therapeutic class within these models. We feel really good that we're engaging that circuitry. We also know that we did a number of other things, too. We did EEGs. We did microdialysis, neurotransmitter expression in the brain. We think that if you look at all of the indications that you could take orexin agonism, anywhere alertness goes, all these different things, ADHD is probably the most proximal next to sleep. You do your hypersomnia. ADHD has the highest probability of success, and then you kind of move out from there as you look at other indications.
The real question for us, and this is part of why we're doing our I-B, is that no one's really taken orexin agonism into ADHD patients before, and they may provide additional benefit beyond what the existing therapies do for ADHD patients. It's not just about your ACE-R score. What about cognition? What about fatigue in those patients? What about other elements that they may feel on this drug? That's part of what we want to explore in that early study.
Great. I think you're starting a phase II study later this summer. I guess, could you talk about your conviction to move into that ahead of seeing phase I-B data, how you might be able to incorporate any learnings out of the phase I-B into phase II design?
The phase I-B is about rounding out, making sure we are hitting the targets, making sure we are rounding out some of our signals, understanding the benefits of the mechanism. The phase II is a traditional dose ranging phase II study, where we set a range of doses that we are going to look at, and we are really trying to put ourselves in a good spot to design our phase III program for efficacy. It is a much longer study. It is going to use the ACE-R test as a statistical test. It is 300 patients. We will have that AE. The things that overlap. There is an opportunity to adjust on the edges, but we feel pretty good about where we are in our dose range and our target engagement that we do not need to wait to do phase I-B and then move into phase II.
Great. Briefly we can touch on the Avadel acquisition and LUMRYZ, which you talked about as being complementary. That transaction has closed, what are kind of the key next steps in terms of integration?
It is interesting. This transaction really addressed a number of different issues for us. Not issues, but actually benefits for us. It brings with it just an incredible asset with the LUMRYZ and the oxybate class. It actually bolsters our commercial business as a whole, revenue-wise, profitability-wise, and it prepares us for the launch of alixorexton. It really gives us that step into the sleep space with a commercial group that is highly experienced, knows the patients, knows the payers and the physicians. What is interesting about it too is in many ways it was a bolt-on. We brought over more than 90% of the commercial business, which was actually most of Avadel, frankly. We brought that group in. They are part of our team. We are having a lot of discussions with them.
Interestingly, this transaction has opened up a lot of discussions with the treatment community on how can you use orexins in the morning and perhaps oxybates at night. There is a lot of discussion now about how can we generate data to show the benefits of doing those things. From an integration perspective to your core question, they are pretty much integrated. We have hit the ground running. We are having just a great response having them as part of the team, and they are going to benefit from our scale and some of the things that we have, patient engagement and all these other things. We are going to benefit from some of the things that they do really well, like some of their market access and pull through and some of the stuff we are doing on alixorexton. It has been great for us.
You're sort of alluding to it, but could you expand a little bit on the way that your work with LUMRYZ could lay the groundwork for potential launches of alixorexton?
Yeah. It's interesting. When you go to launch one of the drugs in a new space, it's sometimes tough. You have to go in a doctor's office, you're a new company, they don't know who you are, you don't know who they are. You don't know if you're supposed to talk to the doctor, the nurse, who their payer is, what systems they're using, all these things, and that takes time, and it takes time to burn that in. With this transaction, we bypass all that. We're right now talking to most of the doctors that we're going to want to talk to for alixorexton. We're out there. We know the nurses. We know how to wire that office. As we come in with alixorexton, it's going to be a face they know. We're going to have a reputation.
As Rich said earlier, we're going to be at SLEEP in a pretty profound way this year. Avadel was going to be there in force, as were we. Together, we have many posters. We're going to talk to all the KOLs, all the physicians. We're known to those offices, that can only help your launch as you move into a new space.
Right. In our final minutes here, I wanted to just touch on the CEO transition. Rich, I think you're moving away in August after more than three decades at the company. What are you most proud of throughout your tenure at Alkermes, what's the legacy you kind of hope to leave behind?
The thing I'm probably most proud of is the fact that over 200,000 patients will get Alkermes medicines this year. We've been sort of quiet about it, but we've chosen to work often in places where Big Pharma has not spent as much time, serious mental illness, addiction. In doing that, we've created a culture at this company that is a really lovely company because it's animated by this idea of helping people. This most recent progress in narcolepsy, you can see that being brought over, like when Blair talks about the Avadel team coming in, and what we get with them often is just that connection to the patients and the physicians. That's really exciting for a company like ours that sees the translation of what we do in the laboratory into patients' lives, and it isn't theoretical.
We've been doing it, and that's a really good feeling. If you can spend your professional energies doing things like that, at the end of the day, if you're successful and it's hard, it translates into people's lives getting better. That's a pretty satisfying experience, and I'm really proud of handing the baton to Blair, who's obviously been integral in building it to where we are today. I think we're going to make that transition without a hitch.
Okay. I think that's a great place to end. We're officially at time, thank you so much.
Well done.
To you guys. Appreciate it. Thanks to everyone who joined us here and online.
Thank you.