Alkermes at Goldman Sachs Healthcare: Strategic Moves in Sleep Disorders

On Monday, 09 June 2025, Alkermes Plc (NASDAQ:ALKS) presented at the Goldman Sachs 46th Annual Global Healthcare Conference, outlining its strategic focus on developing innovative treatments for sleep disorders. The company highlighted both promising developments in its orexin portfolio and challenges in navigating competitive landscapes and regulatory pathways.

Key Takeaways

• Alkermes is advancing ALKS 2680, targeting narcolepsy and idiopathic hypersomnia (IH), with promising Phase 1b data.
• The company maintains a strong financial base with its existing commercial portfolio, supporting ongoing research and development.
• Alkermes aims for significant market penetration of ALKS 2680, especially in NT1, with strategic pricing and global expansion plans.
• Phase 2 studies are underway, with results expected to guide future dosing and commercialization strategies.
• The company’s orexin program distinguishes itself by directly targeting the brain’s wakefulness circuitry.

Financial Results

• Top Line Revenue: Alkermes reported a billion-dollar revenue driven by its own medicines, providing a robust financial foundation.
• Commercial Portfolio: Products like VIVITROL, ARISTADA, and LYBALVI contribute to sustained profitability, funding pipeline development.
• EBITDA Guidance: Confidence remains high in meeting the EBITDA guidance for the year.

Operational Updates

• Pipeline Focus: The primary focus is on the REXN portfolio, particularly ALKS 2680, with ongoing Phase 2 studies (Vibrance 1, 2, and 3) involving approximately 300 patients.
• Phase 2 Studies: Vibrance-1 (NT1) results are expected in early Q3, while Vibrance-2 (NT2/IH) explores higher doses. A Data Safety Monitoring Board oversees these studies.
• Sales Force Expansion: The company expanded its sales force to support ARISTADA, enhancing its market reach.

Future Outlook

• ALKS 2680 Strategy: Alkermes plans to launch ALKS 2680 in the US, with potential global commercialization, including Europe and Asia, and is open to partnerships in Japan.
• Pricing Strategy: The company intends to maintain competitive pricing, with the US price serving as a benchmark.
• Market Penetration: Expected deep penetration in NT1 and 30-50% in NT2, contingent on data quality and pricing.
• Combination Therapy: Potential combination with oxybates is under evaluation, with ongoing studies assessing sleep architecture.

Q&A Highlights

• Orexin Agonist Opportunity: Alkermes aims for a label covering NT1, NT2, and IH, positioning ALKS 2680 as a comprehensive treatment.
• Takeda Comparison: Takeda’s drug is seen as incomplete due to twice-daily dosing and limited indications.
• Dosing Flexibility: Emphasis on a range of doses for ALKS 2680, with Phase 2 informing Phase 3 dosing.
• AE Profile: Mild to moderate adverse effects, primarily insomnia and polyuria, with no discontinuations in Phase 1b.
• Visual Disturbances: Monitoring ongoing for doses not used in Phase 2.

For further details, readers are encouraged to refer to the full conference call transcript.

Full transcript - Goldman Sachs 46th Annual Global Healthcare Conference:

Unidentified speaker: Great. Good morning, everyone. Thanks so much for joining us. I’m really pleased to be joined by Richard Pops, chairman and CEO of Alkermes. Thanks so much, Rich, for joining us.

Richard Pops, chairman and CEO, Alkermes: Thanks for having us.

Unidentified speaker: Yeah. Maybe before we jump into your commercial business and your pipeline, I can start with a big picture question here. Alkermes has been undergoing this evolution over the last couple years. Maybe just level set for us. What spurred this change?

Where do you see the company today? And where do you hope to see it in the next five years?

Richard Pops, chairman and CEO, Alkermes: Well, of all, it’s great to be here with you. It’s great to meet you in person for the time, and thanks for doing the work on the company. The company is a super interesting company because it’s never really been the same for any long period of time. It’s evolved from, you know, an early, early focus on on very narrow aspect of of neuroscience into a broader drug delivery company with a lot of deals with big pharmaceutical companies that drove a royalty business, and then taking those royalties and and segueing into a proprietary products business. So today, with a billion dollar top line all driven by our own medicines that we’ve made and marketed ourselves, a few years ago, we just decided that we wanted to keep moving higher and higher up the value chain.

And if you think about it from the early days when you’re when you’re taking other people’s drugs and improving them, that drives a certain amount of value creation. But the ultimate the zenith of value creation in our business is making brand new molecules, doing new things for patients that haven’t been done before. And we got interested in this area of neuroscience associated with the sleep wake cycle and circadian rhythm a number of years ago. And we had a hunch that it would bear fruit, but, of course, you don’t know until until you do. And the interesting thing scientifically has been the segue from our making technologies that would take other drugs and improve their PK or PD through formulation to everything we do now is based on on our own chemistry and has been for a number of years.

So one of our great technical strengths is in is in our chemistry. And that turns out to be an essential prerequisite to going after the sorexin space is that the molecular design is quite complicated. So it’s been a it’s been a continuous evolution. And coincidentally, and and I don’t think any of us could have predicted the the certain macro environment we’re in right now for big pharma and small pharma with a premium now for new molecules that can command a higher price point without payer control for long periods of time, they’ve never been more valuable. So we’re we’re we’re really pleased with where we’re positioned right now because the commercial business drives substantial and sustained profitability that funds the pipeline, and we see the pipeline growing and expanding over time.

Unidentified speaker: Great. Well, maybe to your point, billion in top line revenue, yet I think the focus very much this year is on your pipeline, on the REXN portfolio that you have here, and you’ve referred to this space before as a new white space for the field. Maybe speak a little bit more about what in particular makes you so interested? What makes you convicted in the orexin opportunity?

Richard Pops, chairman and CEO, Alkermes: The short answer is data because they’re the the promise of the orexins became manifest from a neuroscience perspective fairly recently. Mean, the papers were published in 1999, February, identifying the circuitry in the brain for the time that actually drove wakefulness. There have been all kinds of development work, as you know, on the sleep side in service of having more wakefulness during the day. But now having discovered this bundle of neurons that drives wakefulness in the brain across multiple regions of the brain, the question was, could you replicate the natural ligand, which is a neuropeptide, with a small molecule and drive that wakefulness rather than just helping people sleep better so they’re more awake. So it’s a much more direct intervention with the circuitry that’s relevant.

So we, and I I think Takeda, were really the leaders in this, demonstrating that indeed that that small molecule agents could recapitulate what the neuropeptide does. And now where the where the program stands, I think, between our data and and others’ data is that it’s very clear that these these small molecule agents can drive significant wakefulness in NT one patients. And the the open question right now that I think will make a long way to answering in our phase two data will be what’s the tolerability like of doing so over time in in these patients. And so far, data look very good. So your conviction grows as you get more and more data sets under your belt.

Unidentified speaker: Maybe to that point, before we jump into the phase two and the expectations ahead of those studies, just remind us what you did see in the phase one study here. What can we expect next or this week at the sleep meeting? And maybe help us put that into context compared to these other assets that are out there.

Richard Pops, chairman and CEO, Alkermes: So the secret you could take different approaches to your early clinical work. Ours was informed by the fact that we made the decision that healthy volunteers who are sleep deprived really didn’t serve much predictive purpose at all. And we knew that because we ran a phase zero study where we just ran through the methodology of how we would test an orexin agonist. And in that, we we interrogated whether we kept patients up till 04:00 in the morning, whether that would drive sleep pressure, an outlook as to what you would see in an NT one patient. And we determined no.

So what we did in our program was we went into phase one in healthy volunteers in a single ascending dose format, which is typical, and then moved very quickly into a multiple ascending dose format, which allowed us to to credential multiple doses to allow us to go right to patients. So our one our phase one b study was conducted in patients with NT one, NT two, NIH. And in a very data intensive crossover design, each patient received multiple doses, and we tried to get a sense of the dose response that we received using the hallmark efficacy test, which is this maintenance of wake chromatose. And the data were were were quite clear, and that’s what was so exciting about it. It wasn’t ambiguous.

In a dose dependent fashion, we could see increases in the maintenance of wakefulness test across n t one, n t two, NIH, albeit at slightly higher doses for the NT two and IHs than the NT ones. But we showed that in that study that that ALKS twenty six eighty was highly potent once a day dosing in a dose dependent fashion. That was all the information then we we fed into our our modeling to design phase two. And phase two is what’s what’s underway now. So at at sleep this week in in in Seattle, you won’t see any brand new data from the one b study.

That’s been widely you’ll see some new quanted EEG. You qualifying that as a biomarker, and you’re looking at it in the brains of of of of of patients. And I think you’ll see some panel discussions and and and just more education about the about the orexin pathway. Great.

Unidentified speaker: So your phase two study is Vibrance one expected to read out early three q’s, so coming coming soon. Maybe you can help frame expectations for what we what we what you would like to see from that study as it relates to MWT, cataplexy rates, the tolerability, as you mentioned, is going to be top of mind there. We’d love to hear your thoughts.

Richard Pops, chairman and CEO, Alkermes: I just think it’s it’s it’s such an exciting moment now because this is this is why we develop new drugs is to get new datasets like this. So when I think about it in the aggregate between vibrance one, two, and three, we’ll have circa 300 patients of new information about orexin two receptor agonism in a whole range of patients in making contributions to ones that were made before, which is this whole range of doses rather than just a single dose that that might be efficacious. So for Vibrance one, Vibrance one is the NT one patient population. It’s a much more monodispersed patient population, so we expect data very similar to what we saw in one b. That is at the doses we’ve chosen, which are four, six, and eight milligram, we expect to to essentially bracket the the the doses that we might end up using in phase three.

Of course, we won’t know this till we look at the data, but but the expectation is that we’ve we’ve created a range of doses then that gives us the ability to to model then for phase three what the what the more precise doses are. So the goal was at the lower dose to have activity, but really, really excellent tolerability. At the highest dose, maybe have maxed out what we see and have more side effects, and define what the edges of those parameters look like to model for phase for phase three. Vibrinance two, I think, will be even more interesting in in a way because it’s a much more variable disease. And there’s no predecessor data of efficacy of a orexin two receptor agonist in NT two because the Takeda study was not successful.

So we have a a higher range of doses, ten, fourteen, and eighteen, in that in that patient population. And when we get those data, then we’ll have to get a sense of of of how important the variable doses are because the disease is much more variable in that case as well as with IH. So I think in the aggregate, this will be the real major contribution of of a of once a day dosing, a range of doses, and a range of diagnoses, looking at a six to eight week double blind period, looking at really fully elaborating tolerability profile, and and and and I think incrementing the field in a significant way.

Unidentified speaker: And then when you think about your n t two, so for Vibrance or sorry, MT one, for Vibrance one, when you think about MWT, I mean, you’re seeing with Takeda’s asset, you can get pretty close to forty minutes on MWT. Do you think that’s necessary? What is the appropriate maybe, threshold that you’d like to see across your doses?

Richard Pops, chairman and CEO, Alkermes: For me, the most important thing is not the absolute number. It’s dose response. Because if you have dose response, you can essentially dial up the duration, and different patients will have different clinical presentations and also different desires. So in a forty minute MWT, I think the important thing to understand about the test itself is that it’s actually a little more complicated than people often realize. The MWT is run over eight hours.

So it’s actually a forty minute test conducted every two hours over eight hours. So the number that you see is an average of that delta from baseline across four different tests over an eight hour period. So it doesn’t tell you much about the shape of the curve. It doesn’t tell you about the the a lot of stuff is buried in that number. The biggest drugs in the field right now move an MWT latency for NT one patients, which might be under five minutes, and move it into the low teens at best.

And as you said, the orexins can almost max out the test. Yeah. Whether you you you can max it out early for the few tests and or all the way and keep people up all night. So I think that what I wanna see in our phase two is what we saw in the one b, which is dose proportionality pushing the MWT to limits that no one’s seen before with oxybate. And we know from patients that this is not just the only measure.

The MWT has the virtue of being a number. You can do stats on it. It’s it’s objective. It tells you nothing about the quality of the wakefulness that patient and I think in the fullness of time, this will be the the virtue of these of this category. Because what we hear from patients in the Takeda study and our study is it’s the quality of the wakefulness compared to being on a stimulant or or or other ways of driving wakefulness per se.

So if this is indeed the natural circuitry in the in the brain that drives overall wakefulness, that applies to cognition and to vigilance and to mood and all kinds of other domains that we’re actually gonna learn more about in these studies as well.

Unidentified speaker: Got it. Maybe one point there. Just remind us what measures you are looking at within these Vibrant studies to be able to detect the quality of wakefulness or

Richard Pops, chairman and CEO, Alkermes: these

Unidentified speaker: other domains, cognition, mood.

Richard Pops, chairman and CEO, Alkermes: So in the tier that you’ll see at the primary analysis of the primary endpoint at six weeks, so the top line you’ll see, that will be the classic MWT and then the the FBORTH sleepiness scale and the cataplexy rates as captured by the patients on diaries. That triad is is the classic. Beneath that and the FDA recognizes those. FDA does not recognize the PROs, and we indicate, I think, are gonna do a lot of work to try to validate some of these in the in the context of this disease. So we’ll be looking at a at a whole range of of of PROs that you’ll see in a secondary set of analyses later in the year.

But we’ll be looking at at nothing is bespoke. These are off the shelf measures that have been used in other studies. Got it.

Unidentified speaker: And then as you think about the AE profile that you would be comfortable with and that physicians have have spoken to you about being comfortable with, maybe talk to us about that, particularly in the context of what you did see in the phase 1b.

Richard Pops, chairman and CEO, Alkermes: What’s remarkable about the about the class as a whole so far is that given the how potent these molecules are and how profoundly they’re affecting key circuitry in the brain, I think categorically you’d say that the side effect profile has a mild to moderate and transient and quite advantageous at this point. We know from our data and others that the the hallmark AEs that that that appear are insomnia and polyuria, which is this urinary urgency. That those based on the Decatur eight week phase two data appear primarily in the week and then and then diminished as patients get used to being on this this new therapy. Tend to be dose dependent and transient, mild to moderate. Our dataset will provide even more information because we’ll be able to push the dose higher and see what we run into as as we push the dose higher.

It may just be the same things with more frequency and severity. It may new things may emerge. We’ll see when when we unblind. But we have a we have a data safety monitoring board that’s looking at unblinded data through all our studies. And so, obviously, we we we keep rolling with with a green light on those.

So I’m hopeful that the the way that the class will emerge will there be you know, all drugs have side effects, but they won’t be as described, mild to moderate, transient, and not leading to patient discontinuations and counterbalanced by the quality of the wakefulness that patients are experiencing, which is, you know, perhaps different than they’ve ever had before.

Unidentified speaker: So just to confirm, no discontinuations in your phase one b from these AEs?

Richard Pops, chairman and CEO, Alkermes: No. Correct. Okay. No.

Unidentified speaker: And if they stayed mild, moderate, transient,

Richard Pops, chairman and CEO, Alkermes: do you anticipate look at Sandy and Blair. Thumbs up. Okay. Good.

Unidentified speaker: Do you anticipate that would impact uptake in a in a commercial setting if if it was truly just mild, moderate, and transient?

Richard Pops, chairman and CEO, Alkermes: Well, think about what patients are enduring right now with stimulants and and oxidates and and not getting the efficacy that they they they want. So, absolutely, I think that’s I I I fully expect these drugs to have side effects. I fully expect them to be dose dependent, and I fully expect them to have efficacy that has not been seen before. But that’s why you do the phase two to make sure you can you can confirm that. But there’s so much excitement in the in the community.

Reason I’m gonna leave here this evening, fly to Seattle to go to the free conferences. We’ll meet with all the patient groups on narcolepsy, NIH, as well as the KOLs. And if you compare it to a year ago in in in Houston and a year and a half ago to almost to to Brazil, the field has moved from talking a lot about oxybates and and sleep apnea machines to pharynx. Yeah. And it’s because more and more sites are using them in clinical trials even on a blinded basis and getting hands on experience with their patients and what they’re doing.

Unidentified speaker: How concerning are the visual disturbances?

Richard Pops, chairman and CEO, Alkermes: Well, right now, there’s no there’s not enough data to make a a clear statement because we had one occurrence in our n t two population and one occurrence in our n t in our IH population at doses we’re not testing in phase two. But that doesn’t mean we’re we’re we’re sanguine about it. And the point is it there’s a very logical case as to why some type of of pupillary or ocular thing could be an on target effect of a a neorexin two receptor agonist as you as you raise the dose. So in phase two, what we’re doing is in contrast to one b where we had no baseline ophthalmic understanding people could have had glaucoma or or intraocular pressure changes. We didn’t know.

But in one b, all patients have a baseline ophthalmic exam. And to the extent they have any AE, they’ll be worked up in in in a in correct way to try to understand if there’s any basis for it. But we’re blinded, so we won’t know until we we unblind, but I think it’s a really important question.

Unidentified speaker: And then maybe just quick quickly touching on on NT two here and IH, you’ve spoken about the patient population is much more heterogeneous than than NT one gives you the confidence that you’ll be able to actually detect out a signal from these populations since the patient baseline characteristics may be so different?

Richard Pops, chairman and CEO, Alkermes: The primary reason we believe that it’s the 1b study where we’ve done it already. And in that study, it’s important to know the patients in any way. I suppose there’s a way of running that one b study where you could have hand selected certain n t two or h patients that look more like n t one patients, I. E, with small low sleep latencies. We didn’t.

We took all comers, and we saw a a reliable dose response at at at these higher doses. So our modeling would turn out to be quite correct in where we thought the doses would have to go. So in in the n t two group, the MWT, recognizing it’s a forty minute test, let’s just to make the numbers simple, let’s say that in n t ones, your average baseline is five minutes. You have a thirty five minute dynamic range then to play with. Let’s say in your n t two population, let’s say the baseline average was twenty five minutes, then, of course, you only have fifteen minutes to deal with.

And the twenty five minutes probably doesn’t represent a central tendency. It’s probably just an amalgam of somebody’s got five, somebody’s got 30, so it’s a much more heterogeneous population. So that’s that’s why we love the phase two design. We’ll just look at the data and see what it tells us. But because we can drive wake if if this circuitry in the brain is driving wakefulness, n t one, think of as a knockout model.

You knock out all those neurons. What’s the what’s the phenotype? This this you know, basically, you’re you’re you’re you’re fighting Venus loop all the time. But the QEEG data from healthy volunteers as well as the data from the n t two NIH has suggested that, call it even supraphysiologic doses, administer, hit this this receptor and drive the circuitry, they’ll drive more wakefulness. And so I I think our our belief is if you see a strong signal in NT one, you should see a signal in NT two, and you should see a signal in IH, and go beyond that.

Maybe then you should see signals in patients with other psychiatric and neuro neurological disorders.

Unidentified speaker: Great. Maybe one last question here for your phase two studies. They all embed, you know, kind of a post dosing, or I guess a post, the six or eight week dosing regimen where the patient can modify their dose. Maybe speak to us about the importance of that, what you hope to learn from it, and how it’ll help inform your phase three.

Richard Pops, chairman and CEO, Alkermes: This is also new knowledge that predecessors haven’t been able to do because without a range of doses to play with, you can’t ask this question. So what are we doing? We have a double we have a double blind period, six week in the NT one, eight week in the NT two NIH, where patients stay in their dosing lane. So they’re randomized to one of three doses or placebo. They stay in that lane for that that that fixed period of time, double blind.

The primary assessment is at the end of that double blind period. Then all patients go, if they wanna continue, they they they move to the middle dose. That’d be six milligrams in the n t one, fourteen in the n t two. And they stay on that dose, and they know they’re on that dose for a two week period. And then for the subsequent five weeks, they get to choose.

Do they wanna go up or down? And that’ll help answer the question about whether or not, you know, maxing out the MWT is the is always the greatest thing to do, or do people have different individual preferences? That’ll be additional information to help us select doses for phase three.

Unidentified speaker: And then maybe if we can switch to the commercial opportunity or how you see this market evolving. You know, I think the company has put out numbers in terms of the prevalence for NT1, NT2, IH patients, and it’s quite large yet a fraction of those patients, only a fraction are treated. So how and where do you see an orexin agonist fitting into this landscape, across all three indications?

Richard Pops, chairman and CEO, Alkermes: And this answer is is is informed by more and more conversations we’re having with with with physicians, and we’ll do more of it this week at at this lead meeting. So I think the the common response we’re hearing is that there’ll be a very deep penetration in n t one because it’s a disease modifying therapy. You’re you’re you’re replacing the deficient neurotransmitter effectively. And the quality so far of the data that we’ve seen is is is sufficiently advanced over what precedes it and the tolerability profile of the things we’ve talked about. And because the clinical presentation of the n t one patient is pretty consistent.

NT two, you hear ranges thirty to fifty percent of patients might be targets for venorexant. Why is that? It’s not that it it it it’s necessary that you’re not driving efficacy in those patients, but these will be expensive drugs. And for many NT two patients with fairly light model modest disease, they might do well just with generic myasthenia or something like that. So they won’t need all of things that an orexin two receptor agonist might bring with it.

But I think that that will really depend on the data we need to see for the n t two in IHs. I know, originally, you you may recall, we weren’t gonna develop twenty six eighty in IH, keeping it only in the narcolepsy indication. But after we got the one b data, we we met with a lot of the thought leaders in NIH, which has overwhelming response. There’s a huge unmet need. There’s a paucity of drugs.

These patients need something. So it’s, know, it really makes sense to extend to that as well. So I think it’ll be driven by the quality of the data, but I think that that it starts with NT one and then ripples out from there.

Unidentified speaker: And when you think about these markets, is there a scenario where orexin, t to point NT1, you you see deep penetration there? Is that cannibalization of the existing drugs, or are you essentially growing the market? Because so many of these patients are not being treated right now.

Richard Pops, chairman and CEO, Alkermes: Yeah. That’s a critical question. I think a lot of investors haven’t looked at it carefully enough. Because some will say to us, what fraction of the oxybate market will you take? It’s important to understand that oxybates are not the modal way of treating this disease.

Of the eighty thousand patients who are treated for narcolepsy in the country, about sixteen thousand get oxybates. And a lot more of them have tried have tried oxybates and and and decided not to use oxybates. Oxybates were very difficult to be on for a sustained period of time. But for the patients who found their way to them and and used them, they like them, and they they’re gonna continue to use them. I I think many of them will.

So most of the market is underserved. And I think that when those 16,000 patients drive a couple billion dollar market so I think about the universe. You’ve got 64,000 patients who aren’t getting everything that they that they need. And I think that’s why I think the numbers get so exciting from a financial point of view if you think about having a disease modifying therapy in this in this category.

Unidentified speaker: Disease modifying. So do you see scope for combination use with other agents, or is this truly somebody will will opt for an orexin agonist as monotherapy?

Richard Pops, chairman and CEO, Alkermes: To be determined. I think that in n t one, it will become, it should become frontline monotherapy. But then the question, you know, whether the oxybate. And I think that remains to be seen. In our phase two study, we are we are gonna explore using polysomnography in the double blind period, what the quality of the sleep architecture looks like for somebody who’s on an efficacious dose of an orexin two receptor agonist.

That’s new information. We don’t know that. One school of thought says if we drive meaningful wakeful minutes for twelve hours of the day, you should sleep better, should consolidate sleep better. That’s hypothesis. The other hypothesis is that for the patients who really like what the oxybates do, I.

E. Really guarantee you go to sleep at night and and defragment your sleep in a way, that there there’ll still be a place for those. And I think both both are possible.

Unidentified speaker: Got it. And then as you think about the commercial opportunities, we mentioned IH has relatively fewer offer options compared to NT1 or NT2. Would it make sense to focus your marketing efforts towards specifically IH? I mean, you’ve done this with VIVITROL as you think about alcohol dependence versus opioid dependence. Is that a strategy you would look at?

Richard Pops, chairman and CEO, Alkermes: I don’t think you need to. I think the core of the bull’s eye is gonna be NT1. It’s the most it’s the most explicit demonstration of of of the disease and the huge unmet need. And I think as clinicians see that this agent can be used in their NT1 patients, it will naturally flow into into these other diseases of of hypersalamones. That’s why I think it’s so important to to try to get a a label that accommodates all three because the differential diagnosis in the real world is quite complicated.

People don’t run NWTs in the in in the real world. And in fact, they don’t put people in the sleep lab in the real world. The reimbursement just people are treated based on the clinical symptoms as they present. And the clinical symptoms between NT two, IH, and even NT one sometimes can be almost indistinguishable. I mean, the hallmark distinction between NT two and NT one is cataplexy.

But what we’ve learned is that cataplexy can be explicit where you you lose muscle tone with high emotion to being very subtle and not even detected necessarily by the patient. So that n t one patient may look just like an n t two patient and vice versa sometimes because we have n t two patients with sleep latencies under five minutes. And then IH, the differential between NT two and IH, we’re finding in our clinical trial, sites will say we have NT two patients who enroll. They come in to qualify the patient. Patient has IH and vice versa.

Because the the distinction on that differential diagnosis is the presence or absence of a certain number of these sleep onset REM periods, which you can only really detect via EEG in in a in a sleep lab. So that isn’t happening in real world. People are showing up with a clinical presentation, excessive daytime sleepiness, the doctors have to make the call. So if if you have a drug that’s only indicated for one where the payer says we have to prove that it has it’s much easier if we can just sort of run the gamut and say NT1, NT2, IH range of doses. Go for it.

Got it.

Unidentified speaker: Maybe following up on that, as you think about what the potential label could look for 02/1980, you’ve now touched on the potential to be used across these three different indications, multiple doses, once daily, what are the puts and takes to being potentially to market behind Takeda?

Richard Pops, chairman and CEO, Alkermes: Well, I think I think Takeda deserves an enormous amount of credit for for being the mover in the field and doing it responsibly and publishing their data and and, you know, just doing it correctly. Their drug is, I think, a proof of the pharmacology, but it’s a it’s an incomplete product because there’s it’s given twice a day in an interesting regimen because it’s given once in the morning and then another dose three hours later, I believe. Three or four hours later. So it’s not a classic BID dose. It’s just it’s it’s it’s given in that way.

And it’s gonna be indicated only for one of these diagnoses, NT1. And so I think it proves the point, but it opens up a huge vulnerability from a commercial perspective for a drug that could be across all the indications with a range of doses given once a day. And hopefully, that’s what that’s that’s what we have. You know, we you know, the admonishment always is you have to wait for the data. You have to see what we have.

There’s always risk in developing small molecule drugs, particularly for the brain. But so far so good, and what’s so exhilarating is that this is why these companies within, you know, the company, we’ve been waiting years to get this dataset to see what it looks like. And I think it’s gonna it’s gonna answer a lot of questions. Maybe

Unidentified speaker: in the last couple minutes, we can touch on your commercial portfolio. But before we do, just quickly, as you think about 2680 and commercializing this, recognizing that you have commercialized your products exclusively in The U. S, is this a strategy you would also look to employ with 02/1980, or would you actually take on global commercialization?

Richard Pops, chairman and CEO, Alkermes: Well, here’s what you don’t do. You don’t launch your drugs at a lower price than in other countries. 2680 for us from a commercial perspective is a breath of fresh air. We in our existing portfolio is largely Medicaid and Medicare where the payers put up enormous barriers to access. Gross to nets are very high.

Restricted formularies, multiple competing drugs. This is a a completely different space. So it’s a space where they come in high prices, disease modifying therapies, more analogous to, you know, some of the biologics than than than traditional CNS small molecule drugs, and we could absolutely develop it for Europe, ourselves, and Asia. I I I can see in Japan partnering for a number of reasons, but I think we’re thinking about this drug on a on a more global basis. By the way, the reason we don’t commercialize VIVITROL or Nibalvi or ARISTADA in Europe was because of this price differential.

Because it it it Europe was just unwilling to pay a price that that was either directly relevant to The US price at all, which is a fair US price. These are not super expensive drugs. And it just didn’t feel like it was either economic or fair to to to do that. And I think that decision was was a good decision.

Unidentified speaker: And just quickly, the Medicaid and Medicare exposure for n t one, n t two, IH patients Low.

Richard Pops, chairman and CEO, Alkermes: Low. This is largely commercial largely commercial. I think we I think we model it, I’m looking to Blair, somewhere around 80% commercial probably.

Unidentified speaker: Got it. And maybe in the last minute and a half that we have here on your commercial portfolio, anything you’d like to share here as you think about the growth trajectory moving forward for these three products? And then what are the puts and takes to achieving your EBITDA guidance for this year?

Richard Pops, chairman and CEO, Alkermes: I I’m I’m really pleased with where we are on the commercial portfolio and and the way we’ve sort of aligned with The Street on where it is and where it will go. So it’s it’s taken away a lot of the volatility quarter to quarter as people we’ve guided clearly to it. We’re in that lane. And there’s just a in this type of environment, to be able to rely on a multiproduct billion dollar top line that’s profitable as a source of capital to fund our business. It’s it’s rare.

And so I think that the I often say that we live in the post apocalyptic world at Alkermes because we we deal with government price controls all the time. We deal with restricted formularies. We deal with high rebates to get on the system. And we can thrive in in those systems. It’s just a different business model than selling very high priced medicines to a very small patient population, which is a lot of biotech.

So I think that that for for Livaldi, it’s still in a really nice growth phase. ARISTADA is a is a is a long acting injectable atypical antipsychotic benefiting from the fact that we’ve expanded our sales force this year. And VIVITROL continues to surprise after, you know, a long time in the market. It it continues to grow largely in that in that alcohol indication.

Unidentified speaker: Great. Well, with that, Rich, thank you so much for joining us. Thank you, everyone.

Richard Pops, chairman and CEO, Alkermes: Thank you. Thanks.

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