Good morning. Okay, this is not the first session, but first session for me. So my name is Mohit Bansal. I'm one of the biopharma analysts here at Wells Fargo, and I'm joined by Team Neurocrine. So we have Kyle Gano. He's the CEO-elect of the company, and in thirty-six days, he will be the CEO of the company. Congratulations, Kyle. And Kevin, if you are listening, you will be missed. Congratulations on making a great company. We have Matt Abernethy. He's the CFO of the company, and we have Todd Tushla with us. He's the head of IR at the company. Thank you, team Neurocrine, for joining us today.
Thank you very much.
Thank you.
Great. So maybe I'll hand it over to you, Kyle, because, like, again, you are filling in big shoes of a great man. So, how do you... I mean, like, just talk a little bit about what are you excited about the company, and then what is, how do you see the company in next couple of years?
Sure. No, thanks, Mohit. I appreciate that. First of all, I'll start by saying we'll be making forward-looking statements here, and I'd direct everyone to our SEC filings for the risk factors of the business, but in terms of what I'm excited about for the future, there's a lot of good things at Neurocrine that are ongoing right now. You know, I'll start with, you know, twenty-plus years ago, Kevin and I, you know, our dream was to have a deep, diversified portfolio, and looking at the pipeline today, I see it fulfilling a lot of our dreams that we had in mind and put in place and number of activities to support that over the years. It's diversified by stage and therapeutic area, in some cases, in some of our collaborations, it's risk managed through some of the structures that we have.
So very excited to see that. For the first time since I've been at Neurocrine, I can say that it's sustainable, and it's gonna deliver a lot of data readouts, consistently over time, which is something that we haven't had the luxury of having, in our past. The sustainability piece of it is due in part to the R&D transformation that we have underway, that will take advantage of our own internal research capabilities to move away from a reliance on bringing in things from the outside and being able to discover programs internally. We think that's gonna be the key to our success moving forward. But there's other aspects of that, R&D transformation that are ongoing now, that are gonna help us out in the future.
We can talk about some of those in some of the questions in Q&A. But overall, that profile, the pipeline and the pipeline that we have today is something that's very rewarding to see and very exciting when we think about the future. That's kind of like a high-level type of overview. There are specifics, you know, obviously, you start with INGREZZA.
Mm-hmm.
This is our growing blockbuster that's approved for tardive dyskinesia and the chorea associated with Huntington's disease. We launched the medicine seven years ago. In Q2, we reported $580 million in revenue. That's about a 30% year-to-year growth, 15% quarter-to-quarter growth, and that's all driven by strong demand and some improvements in gross-to-net. But to think about that type of growth seven years into the launch is pretty remarkable. And what we see now moving forward is two-thirds of the patients still aren't diagnosed with tardive dyskinesia, if you think about that particular disease state. Eighty percent of the 600,000 patients or so with tardive dyskinesia aren't getting a VMAT2 inhibitor.
So there's still a lot of work for us to do to reach many more patients, and there's a fundamental opportunity still for the company, and that's also exciting. But that's one leg of revenue growth for the company. We also have another one on horizon, being crinecerfont. This is our first-in-class CRF1 antagonist. We had some incredible data that we disclosed last year in the disease state, congenital adrenal hyperplasia. That led to breakthrough designation in December of 2023 and allowed us to submit the NDAs in Q2 this year. There are two NDAs for two different formulations, one that's more of a pediatric-friendly one, as well as one for adults. We received priority review on that, and we have two PDUFA dates for the two NDAs of December twenty-ninth and thirtieth of this year.
So thinking about early twenty twenty-five, there's another launch for us in this rare orphan disease. And what we see there is a potential blockbuster in the waiting for us, another leg of revenue and revenue diversification, which then you can start thinking about maintaining that profile of a high-growth company, revenue growth, diversification, and that deep and diversified portfolio that I just mentioned. That's a pretty bright future. I'm really excited to build on the momentum that Kevin's built for us. I think we're all sharing that same sentiment. And wrapped around this whole story is a very nice financial position that we're in. Never been stronger with $1.7 billion in cash, and it gives us a lot of opportunity to continue to invest in the company ourselves.
The end game here, of course, is develop many more medicines for patients in the future. Maybe I'll stop there and see where we go in terms of questions.
Great. No, I mean, there are a lot of layers to go through here, but one thing I do want to ask you about, because, like, you I mean, as of now, you're donning the hat of a business development officer, and companies in your position, where you have had success with first asset, and then you are looking for something else, because that's where, like, in last couple four years, Neurocrine was at. Often people look for easy route of BD or buying something big and then trying to fill a hole. You actually did not take that route. You tried some early-stage deals, but you went for internal pipeline and working something in-house, plus licensing deals.
So just walk us through that thought process there, because it is like, like, you—I think you did not go for easy or quick fix there. So how did you think about it? Tell me about that, and... And how do you think about ROI and those kind of stuff on that?
Yeah, I think from a business development perspective, for those of you that have followed the Neurocrine story, there have been times where we've been down.
Right.
And in those moments, you usually, you typically use that time for reflection, studying, and learning from others on what works and what doesn't work in our industry, and I certainly took advantage of that at Neurocrine. I think when it comes to business development or externally derived assets versus internal research, I think where you land is that you gotta have a little bit of both. And the reason for that, and this is something that I tell members of my team, and I think they appreciate that now, is that business development actually has a higher attrition than internal R&D. And the reason for that is you have your typical R&D attrition that's tied to the assets that you're interested in. But there are things like competition, or there are things like you can't afford the deals-
Right
... that you want, or if you need a phase II asset and there's no quality phase II assets, you're stuck. So you really need to have that internal R&D engine also adding to the portfolio, so you can deal with those moments in time where you can't do things from a business development perspective. Otherwise, you have a huge gap in your portfolio. So I think what we've tried to do over time, starting with the approval of INGREZZA, is we tried to, first and foremost, build out the pipeline. We did that first. We did that as our initial kind of next step after commercialization. We built out the clinical group to develop those assets we brought in from the outside.
But ultimately, it was reinvesting the dollars into scaling our research organization, so they could step up and bring the programs that we needed from our internal labs into the pipeline. And that's where we are today. We're gonna start seeing some fruits of those efforts, more over time. We've seen a little bit about that, that area the past couple of years. We have five programs in phase I. We're gonna see gene therapy entering the clinic, next year, from some of our efforts, internally, as well as with our collaborator, Voyager, who brings in capsids to the equation. But this will expand us into new areas, different modalities that will take us into disease states we think are important for neuroscience, namely, moving away from just the treatment of the symptoms of disease, but disease modification and curative therapies.
These are all part of the things that we'll be looking at, moving forward. So I think it's the right mix of business development and internal research.
The only thing I'd add, I mean, we're in a really fortunate position right now to be able to have crinecerfont coming, two great phase III programs in psychiatry with the AMPA and then also the muscarinic. We don't feel like we have a gap in our portfolio.
Right
... that we absolutely have to fill. As Kyle mentioned, we have $1.7 billion in cash at this point. We have EBITDA. We could take on debt if we really wanted to, to acquire something. But right now, the focus is really on pushing forward those assets that are really high quality. We feel fortunate when you do look across the landscape and say: Who else has a pipeline like ours that has quality assets coming behind a major blockbuster? Not very many.
Right.
So we don't sit here today thinking we absolutely have to do something. That doesn't mean we won't deploy our capital if we see something that will add value over the years ahead, but we are in a very fortunate spot.
Got it. No, that's, that's fair. Super helpful. Let's just dive deeper into some of the assets. So of course, muscarinics are have... Todd was expecting it to be
I was hoping you'd go there.
Let's just talk about muscarinic. You have had some data. I mean, Street seems a little bit mixed on that data at this point. Let's just put the data in context, what you wanted to see versus what you saw there, and how do you think about the data at this point?
Sure. So last week, we announced phase II results for our selective M4 agonist. This is NBI-568. We announced positive phase II results with a 20 milligram dose, and at the primary endpoint. So if we drill a little bit down into the phase II trial, this is really a signal-seeking study, very similar in the approach that we've had for our recent phase IIs that we've announced over the past couple of years. And the actual elements of the study included about 200 subjects. It was a 2-to-1 active to placebo ratio, looking at the PANSS score at week 6. This particular study trial had a few objectives. One was to rapidly get to data.
We're in a competitive space, and we needed to make sure we could get the type of signal that we're looking for to invest further in this muscarinic category because we have a portfolio of assets. So rapid time to data. We wanted to identify a dose or dosage that separated itself from placebo. We wanted to look at different dosing regimens as well, and then look at safety and tolerability. So a number of the objectives there, as I shared, and overall, we met all the objectives of this particular study. So all the doses that we used, ranging from 20 mg once daily to 30 mg BID, they're all active, but the 20 milligram dose separated itself from the other active doses as well as placebo.
We also see from a dosing regimen that the 20 mg dose is once daily and has no titration associated with it. So very nice profile there on the dose and dosing regimen. In terms of the efficacy, what did we see? We saw placebo-corrected PANSS improvement, about 7.5. A total PANSS improvement of 18.2, with an effect size of 0.61. So overall, very nice competitive profile relative to the muscarinics and really better than any of the antipsychotics that have been approved over the past 20 years. Safety and tolerability was really good across the board.
We did see somnolence and dizziness kind of rise to the top in terms of AEs, but I'd point out that the most common AE in the study was headache, and that was in the placebo group. So I think that overall, we see very nice safety and tolerability profile there. The efficacy that we see not only was strong, but occurred early in the study. We saw separation of the 20 mg dose as early as week one, and it was stat sig at week three, all the way through the end of the study at week six. So overall, the profile of the 20 mg dose was outstanding. It's everything that we wanted to see to move the program into phase III.
So next year we'll be looking at taking a different approach of a trial design in schizophrenia. Very simple approach of one-to-one active to placebo. We'll look at starting a pivotal program around the middle of next year. The efficacy that we saw really was required to invest further in the muscarinic, but the safety, the tolerability, and the dosing regimen really allows you to think about other indications, which we all know is a significant interest for everyone in the muscarinic category. So subsequent to the schizophrenia study, starting next year, we'll look at initiating a program, another indication that we're currently trying to evaluate what the best opportunity is to move forward with the profile that we have. So stay tuned on that.
and also looking at taking the learnings of this study and marrying that with the data that's coming from the other muscarinic agonist that we have, and moving one of those forward into patients next year as well. So that kind of gives you a holistic approach of the entire muscarinic portfolio, starting with the phase II data, which we feel is very positive, anchored around that 20 mg dose and gives you some high-level thoughts on the muscarinic portfolio.
Awesome. So, I mean, one question we get a lot, and I think... I mean, you can take it positive or negative.
Mm-hmm.
In terms of tolerability profile, it looks pretty interesting and clean, but at the same time, there's no dose response as well, from, like, any safety events are not dose-related either. How do you read that? I mean, like, is it normal on your side that you do not see a dose response on tolerability either?
Maybe I'll just take a step back and walk you through our thought process here, because I think it's important to understand just where did we end up in terms of dosing.
Mm-hmm.
You know, I think that if you look at our program, in many ways we feel like we're a first-in-class type of approach here. We didn't have 30 years of clinical development experience that we've seen with xanomeline, which is one element of KarXT that's in the hands of BMS now. We didn't have a PAM ligand like we saw with Cerevel with emraclidine, now in the hands of AbbVie. So in many ways we're starting off here with a more traditional approach, developing a CNS medicine, and oftentimes what you lean on, as bad as they are, you start with animal models.
Right.
With five six eight, we've seen the molecule perform very well in about a dozen different molecule or models of schizophrenia and related disease states. In those animal models of disease, the dose that correlates to the exposure that we saw with the 20 mg dose is the one that most commonly outperforms all others in those animal models. So I think that gave us comfort early on in this program, and it really starting at the early days in the hands of Sosei Heptares, now Nxera. They gave us confidence that this type of exposure that we see with the 20 mg dose was important. If you look at target engagement, we know with the muscarinic class that there is a heart rate effect, and we see that across the board.
In all the doses that we've studied, it's very similar to xanomeline and emraclidine. So we see the target engagement that's responsible for activation of the M4 subtype of the muscarinics. We take those pieces of information, the exposure data from the animal models, the target engagement with the heart rate effects, and we move that into healthy volunteers, and we get a really nice profile across a range of doses, well-tolerated medicine in phase I. We've studied 568 in about a hundred and twenty subjects, a good portion of elderly as well. We pulled out a couple of the doses that we saw worked well in terms of PD effect, target engagement in the SAD study, and we conducted a biomarker study in a multiple ascending dose fashion in phase I. This is the mismatch negativity study.
And in that particular cohort of subjects, we saw a nice effect across five, 10 and 20, with the 20 mg dose producing effect size of 0.7, which for all of you that follow effect sizes, you know that 0.7 is pretty robust there. So our feeling moving into the phase II trial was the 20 mg dose is gonna be a very important dose for us, and we did anchor around that. This is a very acute, severe patient population that we're studying in phase II. They require hospitalization, so it was important to offer, at the lowest dose studied, one that we thought would work.
Mm-hmm.
So we start there, and then when we think about the other doses, we're interested in safety and tolerability of multiples. We know at the end of the day, in schizophrenia and really in psychiatry, safety and tolerability wins the day if you have efficacy along with that. So we're interested in exploring those higher doses and seeing if we're leaving any efficacy on the table. We did that study, and that's the phase II. It was an ambitious one. If you think about what we studied, we looked at different dosing regimens. Some arms had titration, some arms did not. Looked at once a day BID. So there's a lot of different things, a lot of different questions that we're trying to address in this single study, again, to rapidly get to data.... So that takes us to the dose response.
It is what it is. We would say that all doses are active. The 20 mg dose outperformed the other doses. It's a nonlinear dose response that is very familiar in this space. I think if you go look at the antipsychotics that were approved over the past 20 years, I would say two-thirds to three-quarters of them had a nonlinear dose response. Contemporary examples, you can look at Latuda or Caplyta. So I think that we're used to seeing that being a neuroscience company. We've seen that in some of the preclinical models that we've tested with NBI-568. It's difficult to explain. We may not ever know why, but where we end up at the end of the day is a very nice dose in the 20 mg with a very competitive profile.
Got it.
Sometime over the coming month, I think we're going to be able to disclose more of the preclinical and also phase I data that Kyle just shared. Because a lot of the questions have really come back to confidence around the 20 mg dose. We do have a lot of confidence from the preclinical information that Kyle just highlighted, as well as the biomarker study with the phase I subjects. We look forward to sharing that information because we are quite confident in what we saw in the 20 mg dose.
Got it. So, I mean, like, of course, like, we saw a couple of major deals. So obviously, Bristol bought Karuna, and then AbbVie bought Cerevel. And they both talked about, more so AbbVie, about longer acting. So, I mean, granted, right now you are probably a few years behind the leaders, but given yours is a once-daily formulation, a single drug versus what Karuna is doing, is that something with the longer acting or injectable kind of formulation, you can actually bridge that gap? How-- Yeah.
Yeah, I think from a long-acting injectable perspective, we certainly see value there. I mean, that's one of the cornerstones of one of our follow-on VMAT2 inhibitors to differentiate and offer patients a different type of option to INGREZZA, which we find quite challenging to make a long-acting injectable. And we certainly have seen companies from the antipsychotic space do well there. I think where we start with NBI-568 is first and foremost, getting the schizophrenia trial up and running for phase III. That's where the competition is right now. We need to make sure that we execute and perform well there.
The next piece is moving into a different indication, because we think we've got a really interesting novel profile in NBI-568 that differentiates us quite nicely from the other muscarinic programs, in particular, KarXT. And we would like to get that second indication up and running as quickly as possible. I think where we go from there is, you know, we could look at alternative formulations at that point. But I do want to point out, one of the things that differentiates us over the work that we see from BMS and AbbVie now is that we have a portfolio of agonists. So it's not just about, you know, what indication, what formulation, but it's also about what compound for us. And all those different elements are part of our conversation that we're having internally here at Neurocrine now.
Got it. Got it, and then maybe, like... So basically, horses for the courses kind of approach is, is fair? Like, different indications and different molecules, could that be the case?
It's certainly something that we've talked about, obviously, given some of the challenges that the industry faces now with things like the IRA-
Right
... and things like that. I think it makes sense for us to think about what we wanna do, more in parallel, or put the different types of interest that we have from an indication perspective in, into different molecules. That being said, you know, we have five six eight that has fantastic data.
Mm-hmm.
And we really do wanna put our foot down on the gas here and move that forward as quickly as we can, and see what we can do to explore other indications, starting with the molecule that we have right now.
I mean, the safety profile lends itself to testing-
Right
Well beyond schizophrenia. And as Kyle said at the onset, that was one of the major goals, to be able to see what the safety and tolerability profile was for NBI-568. And then also the additional work that we did with the elderly in the phase I really positions NBI-568 in a unique way to be able to take it into a variety of different indications quite quickly.
Yeah, that's what we found in our work as well. Like, all the previous orthosteric approaches, safety was the biggest challenge more than that, because you said, no one really went as far as there. So let's move on from muscarinics. So I want to talk a little bit about your DAAO inhibitor-
Mm-hmm
... because I think you, we are expecting data this quarter. So this is more of a cognition mechanism at this point. So, talk to us about, I mean, how do you think about the riskiness of this drug at this point? And what have you seen so far, which gives you confidence that you could see something interesting here?
Sure. So, luvadaxistat is our DAAO inhibitor. This is the D-amino acid oxidase inhibitor. And, basically, this is a really creative way to block the metabolism of D-serine in vivo. And D-serine is an important amino acid that acts as a co-agonist of an NMDA receptor. And the hypothesis in cognition is that the NMDA receptor is more or less in an active state, and you really want to try to increase the activity of the NMDA receptor using what the body naturally uses. So what we've seen thus far for luvadaxistat is we start with the phase two trial that was directed towards the negative symptoms of schizophrenia. This is something that was started by our collaborator, Takeda.
And, the primary endpoint in this phase two trial was a negative symptom scale, with the part of the PANSS. And then, the secondaries were what we call the BACS and the SCoRS. The BACS is the Brief Assessment of Cognition in Schizophrenia, and the SCoRS is the Schizophrenia Cognition Rating Scale. So the study read out not long after we executed our partnership with Takeda, and unfortunately, we didn't meet the primary endpoint. But what was really interesting about the outcome of the study is both of the cognition endpoints, the BACS and the SCoRS, did hit statistical significance. So we found that to be really interesting.
We didn't know what to make of it, so we took the data and we shared it with all the key opinion leaders in the space, and they were very enthusiastic about the results. In fact, what we heard from them is that they'd never seen a trial in the cognitive impairment associated with schizophrenia or the negative symptoms, where both of these scales were positive. So they encouraged us to move forward and look at a basically replicate phase two trial, where we moved the secondary endpoints to the BACS and the SCoRS, elevated them into the primary area. So we took their advice, and we are running a replicate study now, and we put the BACS, the Brief Assessment of Cognition scale, into the primary endpoint position and the SCoRS in the secondary.
We'll be seeing the results of that study this month. You know, in terms of the magnitude effect that we saw in that initial phase two trial, both the BACS and the SCoRS moved at about two points. I think if we could replicate something like that in this phase two study, we would view that as a win. All that being said, you know, cognitive impairment associated with schizophrenia has been a very, very challenging area. It's about as high risk as you could get, in my view. And there's not a lot of known about clinical development in this space because there's a number of companies that have worked here. I think we're moving into this with eyes wide open.
We tried to run the best study we could to make it as similar to the initial phase two study as we could, and we'll see results here shortly.
Are you enriching the trial with patients who have cognitive impairment?
We try to just replicate the phase two trial-
Got it.
with the negative symptoms.
Got it.
Same entry, exclusion, inclusion criterion.
Got it. Very helpful. So last two topics I want to touch, Crinecerfont, your smallest product in INGREZZA as well. So let's just talk a little bit about crinecerfont, and your pre-launch activities. I mean, as you are getting ready there.
Sounds good. Matt, you wanna take this?
Yeah. So, it's interesting with Kevin's retirement. We talked a lot about this yesterday. The company was actually founded on CRF, and it's cool to sit here today thinking about we have a medicine utilizing, you know, a CRF mechanism to help patients with congenital adrenal hyperplasia. I think it's quite cool, and personally speaking, you know, just thankful for the company, being able to invest for thirty years behind a mechanism, not giving up, finding a way to help patients with a, with a therapy. So what is CAH? It's a congenital disorder that essentially disallows people from being able to produce cortisol. And without cortisol, patients die. So, back in the nineteen sixties, hydrocortisone was developed, and patients are given super high levels of hydrocortisone to be able to control their disease.
So it's quite interesting to be at a spot in time. Do you wanna talk about pre-launch activities?
Yeah. So, we've got our approved dates, as Kyle mentioned, at the end of December here. And, ahead of that, we have hired the sales force. It's a small, rare disease sales force that's in place, and what they're working on right now is primarily disease state education. We have a campaign called What the CAH you can find online. And they're also developing the relationships with the endocrinology community, who we'll be detailing. So this is all in a compliant fashion. We can't detail the product until when and if it's approved by the FDA, but, those pre-launch activities are ongoing, so we can ensure that we have a really good launch in the beginning of next year.
And the feedback we've been getting so far has been quite strong. I mean, these patients have had no other therapeutic option for sixty or seventy years. So a lot of the commentary that we've been getting back from clinicians is, you know, "I don't know which patient would benefit from this." But when you look at the clinical results, our KOLs believe that 80% of patients with CAH could benefit from a medicine like this. Because a large majority of patients are being seen by a local endocrinologist, who maybe only will see one to two CAH patients in their entire career. So a lot of the activities are continued education around CAH.
Maybe. Why is there going to be a better hope for being able to control androgens, and then at the same time, be able to reduce the hydrocortisone that the patients are being exposed to for their entire lives? So quite a motivated bunch at this point, I'd say, from the patient community, and a lot of education with the clinicians.
... Yeah, we have done a survey. It's a shameless plug, if you want to look at that survey. Kidding. So let's just talk about INGREZZA as well. Thank you for this, Matt. So, I mean-
I think we do have to appreciate we're four minutes left, and INGREZZA is the last.
So, uh-
Yeah, that's, you know, at the beginning of the conversation, you know, today, and as Kyle laid out the foundation for the company, to be at a $2.25-$2.3 billion dollar guide on INGREZZA, to be in the midst of a position to be able to launch a medicine like crinecerfont, which is a blockbuster, you know, it's quite fortunate. But all the investment that we've been able to make over the years to build the pipeline, to get the pre-clinical engine up and running, has all come on the heels of INGREZZA. It's a really high-margin product. We've shown significant growth over the last, you know, seven years, and-
Right
We're on track to do over $400 million of revenue growth this year. It really is the anchor and positions us for a lot of future success. And, as Kyle said, from a market perspective, eight in ten patients with tardive dyskinesia are not being treated today with a VMAT2 inhibitor. So when you ask, "Okay, what's the opportunity that's left?" The market is quite attractive.
Well, and with 14 more years of exclusivity, too.
Right. Awesome, so one last-
So I had to jam in, you know, the commentary around INGREZZA, because a lot of our time is spent, and energy is spent ensuring that the growth continues for INGREZZA. And it's not always perfect. It looks easy from the outside-
Right
... looking in. It has taken a lot of, lot of effort, and just proud of what the team has been able to accomplish over the last seven years in developing the market.
No, I followed the company since it was expected to be a $500 million drug.
Now in one quarter-
Right
We see that.
So one last question to you, Kyle. Fast-forward one year, September of two thousand and twenty-five. I hope you are coming here. I'll be here. If I ask you the question, like, what would make you look back at the year and say, "It was a great year for us?
If I think about what I'm looking forward to towards the end of this year, all the way through the end of 2025, that's kind of where I start, because that's moving into this year, well, that's where I've got my mindset at right now. I think where you start is continued INGREZZA growth. That's something that Matt laid out the importance of that for the organization. It really is the foundation of everything we do, from the pipeline to investing in even crinecerfont as a commercial product. It all comes from continued INGREZZA growth. The next piece would be approvals from crinecerfont and PDUFA dates later this year, and then a very successful launch of crinecerfont in early 2025. That's the second leg of revenue growth for us, the revenue diversification that we think is key for our long-term success.
Then we've got to execute on the start of at least two registrational programs in psychiatry. We talked about NBI-568. That's gonna be a big lift for us next year, making sure that we're doing whatever we need to do to properly resource that study and execute that optimally as we look to kick off multiple phase III trials there. Then we're not done there. We have NBI-845, which we didn't talk about here, but this is our program for MDD that had some outstanding phase II data in depression in Q2 this year. That's another registrational quality program. We haven't had that many registrational phase III trials ongoing at the same time at Neurocrine in all of my time, almost twenty-five years at Neurocrine.
So we need to make sure we keep our eye on execution there, operational excellence, so we do well in those studies. We also have other data readouts that are coming between now and the next year. We have another depression program, NBI-770. This is our NR2B NAM that will read out next year. We have valbenazine studies that will read out next year in ATS, in the dyskinesia associated with cerebral palsy. So some other high-profile types of studies that we'll see data from. We'll be advancing the molecules that we have in phase I now, which range from a follow-on VMAT2 inhibitor to INGREZZA, to other muscarinics.
So these are all things I'll be very excited to give you updates on this time next year, and hopefully Todd will get us a hotel room here, so we don't have to get up so early in the morning.
Thank you.
Hope is not a strategy.
Appreciate the time here.
Thank you.
Thank you.
On that high note, thank you very much.