Cytokinetics at Jefferies Conference: Aficamten’s Market Expansion

On Wednesday, 04 June 2025, Cytokinetics Inc (NASDAQ:CYTK) presented at the Jefferies Global Healthcare Conference 2025, outlining a strategic vision centered on its lead drug candidate, aficamten. The company emphasized the drug’s potential in treating hypertrophic cardiomyopathy (HCM), while addressing regulatory hurdles and market opportunities. Despite challenges such as the FDA’s REMS requirement, Cytokinetics remains optimistic about expanding its market reach.

Key Takeaways

• Cytokinetics is focusing on aficamten for treating obstructive and non-obstructive HCM, aiming to capture a largely untapped market.
• The FDA’s request for a REMS program has led to a PDUFA extension, but the company plans to make this process less burdensome for physicians.
• Aficamten’s peak sales potential is estimated at $4 billion, with further growth expected from non-obstructive HCM treatment.
• Regulatory reviews are underway in the U.S., China, and Europe, with expected approvals in 2024 and 2025.
• The company is investing in its go-to-market strategy, emphasizing a broader reach beyond existing cardiology centers.

Financial Results

• Aficamten’s peak sales potential in obstructive HCM is projected to reach at least $4 billion.
• Bristol Myers Squibb anticipates similar sales for mavacamten, highlighting competitive market dynamics.
• Cytokinetics sees additional upside in non-obstructive HCM, potentially boosting aficamten’s market share.

Operational Updates

• Aficamten’s New Drug Application is under FDA review, with a decision expected in late 2024.
• Regulatory approvals are also anticipated in China and Europe, with timelines set for 2024 and 2025, respectively.
• Enrollment for the Acacia trial in non-obstructive HCM is complete, with data expected in early 2026.
• The MAPLE study has met its primary efficacy endpoint, with results to be published in 2024.

Future Outlook

• Cytokinetics plans to expand the HCM treatment market by targeting community cardiologists.
• The company is building a specialized cardiology franchise in North America and Europe, leveraging its myosin modulator portfolio.
• A streamlined REMS program and higher dosing efficacy are key to differentiating aficamten.
• The MAPLE study data will support aficamten’s launch and market positioning.

Q&A Highlights

• The REMS requirement led to a 90-day PDUFA extension; Cytokinetics aims to simplify the process for physicians.
• The company focuses on newly diagnosed patients, rather than switching those on mavacamten, to expand the market.
• A successful Acacia study could further propel market expansion and aficamten’s adoption.
• Confidence in the dosing regimen used in the Acacia trial suggests positive outcomes.

Cytokinetics’ comprehensive approach to aficamten’s market entry underscores its commitment to innovation and growth. For more details, refer to the full conference call transcript below.

Full transcript - Jefferies Global Healthcare Conference 2025:

Akash Shuari, Pharma and Biotech Analyst, Jefferies: Alright. Good morning, everyone. I appreciate, you all joining us in, beautiful Times Square. My name is Akash Shuari.

I’m a pharma and biotech analyst here at Jefferies. I have the pleasure of hosting the Cytokinetics management team and the happy belated birthday to Robert. Robert, why don’t I hand it off to you for some brief intro remarks and then we’ll get started.

Robert, Cytokinetics: Thank you, and thanks for inviting us to participate in the conference. Good to see everybody. Very exciting times at Cytokinetics. We’ve got an application pending review with FDA and also with China and EMA. Expectations are that we’ll be in a position to go to market with aficamtan for the potential treatment of O HCM, pending FDA and China approval this year, and in Europe, EMA approval next year.

This is based on the results of SEQUOIA HCM, which are presented and published, and with many subsequent publications, we think, build a strong case for aficamtan, as could be a meaningful opportunity for patients with OHCM. So aficampton is a cardiac myosin inhibitor. It’s also been the subject of a study called MAPLE, which is not going to be part of the initial labeling. But we have top lined the MAPLE results. We indicated by press release that the study met its primary efficacy endpoint.

We didn’t include any data in that press release, but we do expect that that data could be presented and published later this year and provide some wind in the sails for potential aficamtan as we go to market. So those are two studies, SEQUOIA and MAPLE, in patients with obstructive HCM, which we think represents about half of hypertrophic cardiomyopathy, the other half being non obstructive HCM. And there’s a study called Acacia that we recently announced completed patient enrollment, accelerated and over enrolled, and we expect to see those data first part of twenty twenty six. And therefore, this is further evidence of the way we roll at Cytokinetics with ample clinical research providing, we hope, support for the use of aficamtan for patients with hypertrophic cardiomyopathy. Aficamtan represents the first of three legs of a three legged stool, the other two being omecamtiv and CK586, also myosin modulators, one an activator, one an inhibitor, the former for potential treatment of heart failure with reduced ejection fraction, the latter heart failure with preserved ejection fraction.

So you begin to understand how we’re thinking about building a business off of our longstanding pioneering innovation in this pharmacology. These are three potential new medicines all directed to the same customer segment, and where we think we can build an enduring and sustainable business around a specialty cardiology franchise model, both in North America and Europe. I’m joined today by our Chief Commercial Officer, Andrew Kalos, as well as Dan Jacoby, who leads cardiovascular clinical research. And we’re looking forward to a good conversation about plans and progress and prospects.

Akash Shuari, Pharma and Biotech Analyst, Jefferies: Perfect. And I always do enjoy our conversations. Robert, why don’t we start? Cytokinetics, scientifically, you guys run the way that you design trials, way that you think about amplifying certain signals with AFI, I think it’s been impressive. I think the three month PDUFA delay, that seems out of character for a company that’s been on the ball with its development program on Aficamtiv before.

But the sense I get is you guys took a calculated risk and, you know, whether it paid off or not, it a, doesn’t mean that your confidence on Afacanthan getting approved has changed at all. And then b, help us understand why, you know, your team did take that calculated risk to not submit a REMS and the initial interactions with the FDA.

Robert, Cytokinetics: Yes, of course. So, aficamtin follows behind a drug called mavacamten that was invented in our laboratories, licensed to a company called MyoKardia. BMS bought MyoKardia, and now aficamten is coming in as may open up further opportunity for patients. When the BMS application was ultimately approved, in reading the summary basis of approval, it was clear that FDA mandated a REMS program. And even with submission of a REMS, there was a PDUFA extension in order to seek approval for mavacamten, now called KAMZIOS.

We had three meetings with FDA before we submitted our NDA. In all three meetings, we discussed safety, tolerability, and risk mitigation, risk management. And attending those meetings with FDA were representatives of the Drug Review Division, but also the Division of Risk Management that oversees the REMS programs. And in those meetings, we discussed, asked, and answered questions about the potential for a REMS, and it was deemed reasonable based on minuteed meetings with FDA that we could submit without a REMS, and we chose to do that. The FDA indicated to us that that would be something that would be subject to review post NDA submission and filing.

FDA accepted our submission for filing without a REMS, and they certainly didn’t mandate a REMS. So we thought that was a good risk to take, and we incorporated into labeling that which would be enabling of risk mitigation, risk management. Upon acceptance of the NDA and further review, FDA determined that a REMS should be required and asked us to submit one. We were ready to do that. We knew that that was a possibility.

We basically took language around risk mitigation that had been submitted in the draft labeling. We moved it into a REMS, and we promptly submitted that REMS. Upon its receipt, FDA accepted it and said, this constitutes a major amendment, and therefore a ninety day extension, which is their prerogative. But we think that we did right by this application, because if anything, socializing this risk mitigation underscores differentiation that even as may be within a REMS, we think ultimately will serve our interests as we hopefully will seek approval and gain approval of aficamtan, and it may be approved with a differentiated risk mitigation even within a REMS. So we think all this speaks to the same upside as could occur with a differentiated positioning if aficamtin is ultimately approved, albeit unfortunately now with a ninety day extension.

Akash Shuari, Pharma and Biotech Analyst, Jefferies: Makes sense. Now, I know there’s we’re gonna speculate, but sometimes we have to. This is the way I kinda see it. I am very confident you’re gonna have less echoes. I’m very confident you’re gonna be able to get patients to an optimal dose more quickly because frankly, you’ve shown that in all of your studies.

When I think about no REMs or or REMs and I I to me, it’s not the titration. I think it’s more of a theoretical question on durability and echo monitoring there. And here’s you know, it’s funny. You and I have talked about this with, you know, some of your competitors and it’s like you you one of the things you mentioned is the FDA doesn’t just look at the mean or the median. They look at the entire range of exposures with DDIs, etcetera, etcetera.

And, you know, one of the concerns we’ve had with Camsius, and this is a theoretical one, is you can have different levels of drug accumulation for a subset of these patients, and if you can have that accumulation, you can induce, you know, you know, some a systolic dysfunction. That’s a theoretical concern that Bristol answered with more data. You have the forest data you submitted here, but you don’t have a lot of real world evidence at this point. Right? When I think about what led to one REMS or no you know, a REMS or no REMS, is it fair to think maybe we should be thinking about the durability and that theoretical concern rather than anything with the initial titration?

Robert, Cytokinetics: Yes, but and I’m going to ask Andrew and Dan to weigh in. I think ultimately what will drive commercial adoption is how comfortable are physicians who aren’t prescribing mavacamten to be activated to now prescribe aficamten. And that’s where our strategy is rooted. And I do think making that experience a more positive one for physicians and patients is enabling of us to move beyond the roughly 600 physicians who are accounting for about 80% of the mavacamten prescriptions today. And this is where Andrew and his team have done a lot of market research.

They’ve got good strategy. Dan can speak about how that’s bolstered by data we’re seeing from now hundreds of patients in the FORCE study that are out beyond one year. And maybe I’ll ask them to comment on these things.

Andrew Kalos, Chief Commercial Officer, Cytokinetics: I can start. So I think Robert covered kind of this concentration of the current market around centers of excellence where the vast majority of patients are treated today. For the market to expand the need for a broader set of cardiologists to treat patients especially in the community will be critical for really to move out of this kind of linear growth phase to a high growth phase. When we look at differentiation based on Sequoia that certainly I think will bode well based on our research that preference share will shift towards Aficampton. When you look at that as well as a differentiated REMS and when you add on Maple to show that standard of care is not, you know, inferior relative to aficamtan that should unlock more community prescribers who feel like beta blockers are good enough for for some patients.

So that’s I guess that without getting too deep into our strategy, that’s really how we’re thinking about aficamtan and three to six months into our launch assuming we get approved at the end of this year based on this revised PDUFA, that’s when our non obstructive trial reads out, Acacia, which certainly should expand the market and give even further propulsion if that’s a positive study. I’ll turn it to Dan for maybe additional comment.

Dan Jacoby, Cardiovascular Clinical Research Lead, Cytokinetics: Sure, yeah. I really appreciated what you said Akash in terms of your sort of interpretation that we should have fewer echoes and we should be able to get target dose more rapidly. And I think that is reflected in the data from both our phase three study and from forest HCM which used a real world approach to titration. So remember these studies were conducted with site based echocardiography. So the echocardiologist at the site interprets the echo and the dose titration occurs that day.

Which is exactly how it will work in the real world. And in fact in forest, the investigator themselves can look at the echo and look at the patient and make a determination. And that’s exactly how clinical care will work. And we see in that setting rapid improvement in symptoms, biomarkers, gradient. And that improvement is sustained over the extended period of time.

We have over two fifty patients that are out over a year

Andrew Kalos, Chief Commercial Officer, Cytokinetics: Right.

Dan Jacoby, Cardiovascular Clinical Research Lead, Cytokinetics: At our last data cut. And we’re increasingly trying to get this data out for people so they can digest anticipate hopefully bringing some more data into the into play in the coming months or so. And it will reflect, I think, again, what we’ve been seeing all along that confirms your impression.

Akash Shuari, Pharma and Biotech Analyst, Jefferies: Got it. Now, you know, sometimes you’ll hear, I know from the agency and it’s definitive and they’re very clear like, Hey, this is how we think about a certain drug. This is how we not think about a certain drug. But then, when we look at the Bristol experience, they had real world data, they submitted that to the FDA, they made an argument, and then they went away from the quarterly echo monitoring. I can’t help but think, but if there’s a theoretical concern about, you know, drug accumulation over a longer period of time, and you guys have one of the things we’ve noted is meaningfully less PK variability than a lot of your competitor compounds and there is this kind of consistent and exposure that we see with aficamtin.

Why can’t Cytokinetics, let’s say a year, with real world experience and you have more real world data, go back to the FDA and either argue, hey, I think it’s prudent for us to now go into a twelve month echo monitoring paradigm or potentially remove the REMS entirely? Are those avenues that the company could explore here?

Robert, Cytokinetics: Yes. Although I don’t know that it’ll happen as rapidly as maybe you’re alluding. FDA tends to be more relaxing of REMS programs after several years, more than after several months. But, yeah, and as I think you and I have discussed in the past, I don’t think we’d be even talking about a REMS based on our data alone. But based on the category and the mechanism of action, I think it is our expectation that a REMS is going to be a fact of life, at least for a while.

With that said, I think the street is over indexing on REMS here because ultimately I think the marketplace is adapting to the existence of a REMS. And workflows and echo capacity are adapting. There’s administrative burden to be sure, but these are patients who didn’t have drugs before. Now they do. And they’re benefiting greatly.

The adherence and compliance, even with the REMS, is quite high. And I think the use of these drugs is underscoring that physicians, their staff, pharmacists and patients have developed the work streams. It’s incumbent upon us within the existing work streams to make it simpler, to make it more convenient, to give more flexibility. And that’s where I think and Andrew should comment that’s where I think being new to market, we can design something that’s more bespoke and custom that should be welcomed by potential customers.

Andrew Kalos, Chief Commercial Officer, Cytokinetics: Yeah, I think Robert covered it well. It really is around differentiation and patient experience, distribution, the entire continuum of prescribing to a patient getting a prescription and making that less onerous, less administrative for an office staff as well as a pharmacy. And that’s how we kind of look at the market. It is a specialty market. It is a market where to gain to get more community engagement and involvement that is going to be required so that their administrative burden, if you will, is relieved relative to what they’re perceiving today and which is limiting the number of prescribers in the CMI category.

Got

Akash Shuari, Pharma and Biotech Analyst, Jefferies: it. Now, maybe second, this is an angle that I you know, we think about REMS and the echos. But one of the angles we’ve always thought about is just straight up efficacy. I mean, read the MA review. Why did they go with a modified REMS?

Because sixty five percent of the patients on chemsios are on two point five and five mg. You know, my team, we’ve worked on this. My suspicion is the PVOT benefit in that lower dose cohort is about one. I mean, we’re we’re that’s I know it’s not published. You kind of have to back into it.

But I have a pretty strong suspicion there’s a meaningful amount of Camzios patients that aren’t actually getting a huge clinical benefit. The way I almost see Camzios is it’s a great drug for patients who need a low dose, thin out the wall. But if you need higher levels of exposure, if you have more impeded exercise gradients, that’s where I think aficamtin could really differentiate. You guys haven’t per se talked about the switch population in your studies. But I know, Dan, you also have some interesting perspectives as a practicing physician.

What percent of Camzius patients do you think would be very receptive to switch onto aficamtin and the clinical profile they have?

Dan Jacoby, Cardiovascular Clinical Research Lead, Cytokinetics: It’s great guess I’ll yeah. I guess sorry. I’ll take this. You know, I we talked last night a little bit about this. You know, I hate to put a number on it.

We obviously, you know, do think that there’s some patients out there may have, I guess, be undertreated on a certain level. And I guess those patients may be candidates for switching. I think my personal experience with this is that you do get patients who just don’t want to deal with the hassle of potential interruption, have an interruption before, don’t want to take the risk of trying to get up to ten or fifteen milligrams, are happy with having reduced symptoms but not necessarily no symptoms. And it’s that kind of patient who if there’s an option that seems to be maybe a little bit easier to use, maybe a little bit safer at higher doses perhaps, that that patient may be interested to kind of investigate that with their physician. So there will be people who will bring that forward.

But as a team, we’re not pursuing that. And Andrew can speak to that specifically as a commercial strategy. But that isn’t a point of an angle for us that we’re particularly going after per se.

Andrew Kalos, Chief Commercial Officer, Cytokinetics: We don’t have that data. That’s not in our trial. We’re going to be pursuing new patients. Over 80% of the market in OHCM should be available in The U. S.

When we launch, if we get approved at the end of the year. So to Dan’s point, that will be really a physician patient dialogue if that switch were to occur, but it’s not going to be driven from a strategy point of view.

Akash Shuari, Pharma and Biotech Analyst, Jefferies: Understood. By the way, I will say from my own our own work, I think about 30% of patients you can do that on LEVF. Let’s say you have a baseline LEVF of 80. You can’t get, you know, reduction with the PK variability chemisias. So that’s at least us.

I don’t know. You don’t have to bless a number.

Robert, Cytokinetics: Akash, you’ve known us to be conservative in the way we think about these things. And I do think that represents upside. I also understand the Street looks to switches as maybe an early biomarker for commercial traction. We anticipate some switches. It’s not strategy.

And there’s at least one key opinion leader who’s on record publicly for saying he expects to switch twothree of his patients, that he’s one of the highest volume mavacamten riders. We do foresee that there will be switches. But to Andrew’s point

Akash Shuari, Pharma and Biotech Analyst, Jefferies: It’s not your strat.

Robert, Cytokinetics: Over 80% of the market is still available to us, and it’s incumbent upon us not to compete with BMS or mavacamten, but rather to expand the market for the benefit of more patients getting a cardiac myosin inhibitor.

Akash Shuari, Pharma and Biotech Analyst, Jefferies: Male Understood. Now let’s talk about launch cadence and expectations there. Bristol has, you know, kind of the it seems like there’s two buckets, right? If you can get to the community center setting, you can really increase your patient adds. What we’ve seen with Camsios is 5,000, five thousand, five thousand in terms of patient adds in in that kind of community center setting.

So if we’re thinking about obstructive HCM out of the gate, that’s the big pool. That’s the initial pool. And then maybe six months, a year down the line, you’re thinking about more community center. So, Andrew, in terms of investors and expectations on the HCM launch, we’ve been pointing people, it’s not gonna be worse than the Camzius launch, but I would comp it to the Camzius launch as a realistic cadence for the obstructive HCM launch when you’re out of the gate. Is that fair?

Andrew Kalos, Chief Commercial Officer, Cytokinetics: I think that’s reasonable based on the number of patients that are in the centers now that that key variable, There’s a few of them that could certainly drive that up. One is how long does that community engagement take and how broad is that community engagement? The second is how much of an accelerator does Maple provide to that once Maple gets added. And I guess the third would be if acacia is positive and we’re three to six months into launch, there’s likely a halo effect given you would now have three clinical studies with safety efficacy especially in a clinical study in a brand new population. So I think there’s things that could accelerate.

But for a base case, I think the way you’ve outlined it is reasonable.

Akash Shuari, Pharma and Biotech Analyst, Jefferies: Got it. Makes sense. Let’s hit on Acacia because, you know, the more work we’re doing and it sounds like you guys are the same way. This is a meaningful strategic card flip. Because there could be, you know, maybe where the biggest increase in diagnosis is gonna be in the community center setting for non obstructive patients.

You can have something like that. It really does change the profile. Bristol has, you know with their top line press release, it almost sounded like they’re saying, and this is just not the right mechanism in this population. Like, we learned from that. And, you know, it almost felt to me like, okay, maybe there’s a waning of effect.

Maybe, you know, there’s some issue biologically. There’s some type of compensation. But when we talked to Bristol about it, it’s almost like there is a curve separation. It is durable. It was simply not statistically significant.

Can you talk about some of the differences between, you know, the Bristol study and then Acacia when you think about dose titration, when you think about therapeutic window, and then also your confidence in a dose effect manifesting in non obstructive, given that you’ve seen, at least in your clinical data, eighty percent of your patients can get to higher doses?

Robert, Cytokinetics: So I think you’re touching on some key points. So BMS conducted a study called OHDSI in patients with non obstructive HCM, and they recently top lined that the study did not meet its endpoints. And we hope to see these data presented later this year. We’re conducting a study called Acacia. And in Acacia, in contrast to OHDSI, we basically took the same dosing regimen that we had studied in phase two, and we moved it into phase three.

And we added a high dose that wasn’t in phase two, as could be permitting of getting more patients to more exposure for longer. And the Acacia study also returned to some of the same centers. We didn’t introduce any other variables. We also looked at patients as they enrolled and verified that they did in fact have non obstructive HCM by dint of their echos, Dan and his colleagues looking at every echo. So I do think we did what’s more conventional and classical by keeping things more similar, moving from phase two to phase three.

And based on our phase two data, we remain very optimistic about what we should see in phase three. That’s further buoyed by the fact that those phase two patients have rolled into an open label extension. We’re continuing to monitor those patients. They are getting to higher doses. We are seeing consistent effects as we would hope to see also in phase three.

So in some ways we’re conducting a side by side experiment. One is an open label extension, the other is a randomized controlled study. But we remain bullish on prospects for Acacia. I’m going to turn to Dan, maybe to speak to the things that we’re most encouraged by. But I think fundamentally, we believe the design and conduct of Acacia favors why we should remain encouraged by what we hope to see in Acacia.

Dan Jacoby, Cardiovascular Clinical Research Lead, Cytokinetics: Yeah, thanks Robert. I guess I’ll just add a couple of data points to just back up what you’re saying. So in our paper that we published with the thirty six week follow-up in FORCET on non obstructive hypertrophic cardiomyopathy, sixty five percent of the cohort achieved twenty milligram dosing after titration, which is the highest dose of aficamtiv available with another fifteen or seventeen percent achieving fifteen milligrams. So a total of around eighty percent achieving the top two dosing. The safety was phenomenal with only two patients having to have down titrations.

And the efficacy demonstrated a fifty six percent reduction in NT proBNP and a 13 plus increase in KCCQ. All of which speaks very strongly to the fact that at least the therapeutic hypothesis that aficampton as a next in class cardiac myosin inhibitor could demonstrate efficacy in hypercontractility, HCM is definitely still intact.

Robert, Cytokinetics: I just want to take a pause there on the KCCQ improvements. So that’s a very large increase in KCCQ. Admittedly, this is open label, so you have to assume there’s gonna be some placebo effect in phase three. But even if you subtract away the expected placebo effect, you’re still talking about one of the largest potential improvements in KCCQ, as it has been measured in cardiology. So if that’s borne out again in phase three, and that’s way higher than what phase three is powered to demonstrate, we should expect a positive outcome.

Akash Shuari, Pharma and Biotech Analyst, Jefferies: I want to hit on two points on that. So A, when you think about the ODYSSEY protocol, there are instances where Bristol could go in almost one mg increments in terms of increases in doses of chemzios. That’s obviously not what you’ve seen in your protocol or even Forrest, which is even more aggressive. Can you talk about the importance of that? And then number two, placebo is important here.

And, you know, it is open label data that you have right now. How concerned are you about more variability or a higher placebo response? I think in our own work, we’re kind of expecting a five point placebo placebo benefit on KCCQ. Is that reasonable, or are there concerns that that variability might be bigger than expected?

Dan Jacoby, Cardiovascular Clinical Research Lead, Cytokinetics: Yeah. Obviously, we don’t have the data, so this is highly speculative. But if you look at the placebo group KCCQ curves from what we see in CMI trials, you tend to see a rise in the placebo response. And then it flattens and maybe even declines a little bit over more exposure. And that’s consistent with what we know about placebo.

There’s initial enthusiasm. And then as you start to realize that things haven’t changed that much, that kind of deteriorates. So I would be surprised if over a thirty six week treatment period we saw a more exuberant placebo response than we saw over twenty four week treatment periods in SEQUOIA or even in EXPLORER. So I think we’re kind of safe. The other factor that we have to consider here is that while the therapeutic hypothesis, as I said, is intact, NHCM is a somewhat different kind of clinical course in some ways than OHCM.

And over thirty six weeks in a non treat or in a population that’s not effectively treated, there could be some deterioration that could occur. And so maybe you’ll see some of that also in the case CQ. Again, highly speculative, but I think reasonable to kind of think about those things.

Akash Shuari, Pharma and Biotech Analyst, Jefferies: Got it. We’re towards the end and I’m gonna stick in my strategic question, which I always do to you, Robert. And you you also play ball, which I appreciate. Question I get the most right now is non obstructive seems to be a really important clinical card flip. I think Maple, that data, to me, is gonna be solid.

You you had restrictions in terms of what you could do from getting in in a in a publication, which I think investors understand. Could there be strategic news? Like if an investor say, there’s no way there’s strategic moves from cytokines ahead of this non obstructive data, why or why is that not the case?

Robert, Cytokinetics: So I trust you’re using the word strategic to maybe allude to M and A.

Akash Shuari, Pharma and Biotech Analyst, Jefferies: Yes. What

Robert, Cytokinetics: I’ll say is we’re being quite strategic about how we’re thinking about OHCM and as could be further benefited by NHCM in terms of how we’re investing in our go to market strategies. But to your point, I do think the NHCM card flip takes on more significance in light of the Odyssey results being negative, the market showing more prevalence and growth in NHCM. With that said, BMS bought MyoKardia for $13,000,000,000 based on expectations that the OHCM opportunity represented, as they said publicly, 4,000,000,000 in peak sales. They’re on track this year to generate over $1,000,000,000 and I think it’s within reach that they’ll get to $4,000,000,000 based on mavacamten in OHCM. And execute well, we think that Aficampton can do at least that, if not north of that, in OHCM.

NHCM represents further upside to that, too. So we like the way we’re situated. And from a strategic standpoint, we’re investing like we mean it with the goal to become meaningful player here commercially in OHCM and hopefully also NHCM.

Akash Shuari, Pharma and Biotech Analyst, Jefferies: The way I interpret that is not necessarily we have to look at it that paradigm. There could be optionality there. I really appreciate it. Robert, thanks so much and to the broader team. And thank you so much for the investors for joining us.

Really enjoyed

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