Cytokinetics, Incorporated (NASDAQ:CYTK) Q3 2024 Earnings Call Transcript

Cytokinetics, Incorporated (NASDAQ:CYTK) Q3 2024 Earnings Call Transcript November 6, 2024

Cytokinetics, Incorporated misses on earnings expectations. Reported EPS is $-1.36 EPS, expectations were $-1.27.

Operator: Good afternoon, and welcome to Cytokinetics’ Third Quarter 2024 Conference Call. At this time, I would like to inform you that this call is being recorded. And all participants are in a listen-only mode. At the company’s request, we will open the call to questions after the presentation [Operator Instructions] I will now turn the call over to Diane Weiser, Cytokinetics’ Senior Vice President of Corporate Affairs. Please go ahead.

Diane Weiser: Good afternoon, and thanks for joining us on the call today. Robert Blum, President and Chief Executive Officer, will begin with an overview of the quarter and recent developments; Fady Malik, EVP of R&D, will provide updates related to clinical development program for aficamten; Andrew Callos, EVP and Chief Commercial Officer will address commercial readiness activities for aficamten; Stuart Kupfer, SVP and Chief Medical Officer, will provide updates regarding omecamtiv mecarbil, CK-586 and our earlier stage development pipeline; Sung Lee, EVP and Chief Financial Officer, will provide a financial overview of the third quarter. And finally, Robert will review our corporate development strategies and review expected upcoming milestones.

Please note that portions of the following discussion, including our responses to questions, contain statements that relate to future events and performance rather than historical facts and constitute forward-looking statements. Our actual results might differ materially from those projected in these forward-looking statements. Additional information concerning factors that could cause our actual results to differ materially from those in these forward-looking statements is contained in our SEC filings, including our current report regarding our third quarter 2024 financial results filed on Form 8-K that was furnished to the SEC today. We undertake no obligation to update any forward-looking statements after this call. And now, I will turn the call over to Robert.

Robert Blum: Thank you, Diane, and thanks to all for joining us today. As we communicated just a few weeks ago at our Investor and Analyst Day, we made significant progress across our pipeline in the third quarter. Most importantly, we completed the rolling submission and submitted our new drug application to the FDA for aficamten. This is an exciting milestone for Cytokinetics as well as the physician and patient communities, and it brings us one step closer to hopefully bringing aficamten to patients suffering from obstructive HCM. It reflects a tremendous amount of work from our colleagues for which we’re especially grateful. While we have requested priority review of the submission, our base case is standard review. The next step will be the expected announcement of filing acceptance and assigned PDUFA date.

During Q3, we also supported CORXEL, formerly Ji Xing, in filing the NDA in China for aficamten for obstructive HCM, which we’re pleased to announce today was recently accepted for filing. Meanwhile, our commercial preparations for the potential approval and launch of aficamten in the United States are dialing up according to plan. As Andrew will elaborate, we’re executing pre-launch activities, including recently launching an HCM disease awareness campaign for health care professionals. In addition, we selected third-party external partners to support education, distribution and patient support, altogether forming a bespoke patient experience. And we refined sales territory configurations, as well as sales training and recruiting programs in the United States, while we also concurrently hired our initial geographic and functional team leaders in Europe.

During the quarter, we continued to present and publish additional data from SEQUOIA-HCM, further strengthening the evidence supporting its potential next-in-class safety and efficacy profile. As Fady will elaborate, the additional analyses show that treatment with aficamten is associated with improvements in exercise capacity, gradients, symptoms, biomarkers, cardiac structure and function, as well as favorable cardiac remodeling. Together, these analyses expand in meaningful ways on the overall profile of aficamten and are enabling of the positioning that we foresee for a next-in-class cardiac myosin inhibitor that we believe can expand the category and activate broader adoption. Beyond aficamten, we prepared to start 2 new clinical trials from within our emerging specialty cardiology franchise, COMET-HF, the confirmatory Phase III clinical trial of omecamtiv mecarbil and AMBER-HFpEF, the Phase II clinical trial of CK-586.

As Stuart will share, each of omecamtiv mecarbil and CK-586 offers an opportunity to expand our specialty cardiology franchise by targeting underserved populations at opposite ends of the spectrum of heart failure, those with severely reduced ejection fraction and those with supernormal ejection fraction. Finally, while our specialty cardiology franchise remains our top priority, our research dedicated to novel muscle-directed therapies has continued within our labs in South San Francisco, and our long-standing innovation in muscle biology continues with another promising drug candidate called CK-089, readying to begin a first-in-human study. CK-089 is a fast skeletal muscle troponin activator, which we believe may have potential therapeutic application to a specific type of muscular dystrophy.

You’ll be hearing more about how we have applied lessons learned with prior fast skeletal troponin activators to our next level plans for CK-089, as it will soon begin clinical development in this fourth quarter. Where we stand today at Cytokinetics is a reflection of thoughtful planning, strategic positioning and prudent capital deployment, all in service of realizing the full potential of our muscle biology platform. We are not a company expecting to simply build for the success of a single drug candidate. Instead, we’re focused on building momentum across our pipeline and planning for our future by prosecuting a portfolio of multiple muscle-directed drug candidates designed to address diseases of high unmet need. By doing so, we hope to impact the lives of both patients, as well as return meaningful value to shareholders in enduring ways.

With that, I’ll turn the call over to Fady, please.

Fady Malik: Thanks, Robert. In the third quarter, we presented additional data from SEQUOIA-HCM and FOREST-HCM at 3 medical congresses, the European Society of Cardiology Congress, the Hypertrophic Cardiomyopathy Society Scientific Sessions and the Heart Failure Society of America Annual Scientific Meeting. These prespecified analyses build on the primary results presented and published earlier this year to dig deeper into the profile of aficamten. The depth and volume of these analyses is truly extraordinary with 8 presentations, 5 being late breakers, plus 5 simultaneous publications in leading cardiac journals. Each of these analyses exceeded our best case expectations for aficamten and gives us confidence in the opportunity for aficamten to address the significant unmet need in obstructive HCM.

Key amongst the additional data from SEQUOIA-HCM are findings that show that aficamten may be associated with favorable cardiac remodeling and improvements in several measures of cardiac structure and function. Together, these data show that aficamten appears to change the architecture of the heart and its potential to be disease modifying, something that’s key to changing the trajectory of HCM. Other analyses from SEQUOIA-HCM presented during the quarter showed that treatment with aficamten improved patient symptoms, quality of life and cardiac biomarkers. Furthermore, a responder analysis showed aficamten was associated with broad clinical efficacy as the majority of patients who received aficamten in SEQUOIA-HCM achieved one or more clinically relevant outcome.

One of the four pre-specified outcomes was a complete hemodynamic response, defined as having a resting LVOT gradient of less than 30 and a Valsalva LVOT gradient of less than 50, which was achieved by two-thirds of patients in SEQUOIA-HCM. These data were complemented by findings from an integrated safety analysis that pulled data from REDWOOD-HCM, SEQUOIA-HCM and FOREST-HCM and reinforced the safety profile of aficamten. Finally, an analysis of open-label data from FOREST-HCM showed that the majority of patients who attempted withdrawal of standard of care medications at the discretion of an investigator were successful with some patients achieving monotherapy, suggesting that the potential for aficamten to be tolerated and effective as monotherapy in patients with oHCM.

This hypothesis is being explored further in the MAPLE-HCM trial, which I’ll address in a moment. Five of the recent publications were recently assembled collectively in the November 5 issue of the Journal of American College of Cardiology, nearly an entire issue devoted to aficamten. As we continue to curate the data from SEQUOIA-HCM, each subsequent analysis elaborates on the primary results from SEQUOIA-HCM to reinforce the effect of aficamten on clinical outcomes, symptom burden, cardiac biomarkers and cardiac structure and function. Together, this large and growing body of evidence paints a clear picture of the relevance of aficamten to clinical practice as a next-in-class cardiac myosin inhibitor and potentially the cardiac myosin inhibitor of choice for both physicians and patients.

All of these clinical work streams also continue to be supported by our medical affairs organization. During the quarter, our field medical teams met with health care professionals, including many HCM KOLs, hospital and IDN leadership and formulary decision-makers to discuss and educate about the results from SEQUOIA-HCM. Now moving to the ongoing clinical trials program for aficamten. We’re pleased to report that during the third quarter, we completed enrollment in MAPLE-HCM. Through the rest of this year, we will continue conducting this important trial, and we expect to share results from MAPLE-HCM in the first half of 2025, ahead of when we hope to launch aficamten commercially. If positive, MAPLE-HCM represents the first potential label expansion opportunity for aficamten with results that may provide the rationale to position it as first-line therapy in practice guidelines.

During the quarter, we also continued enrollment in ACACIA-HCM, the pivotal Phase 3 clinical trial of aficamten in patients with symptomatic non-obstructive HCM. We now have activated over 90 sites in 13 countries, ensuring that the results from ACACIA-HCM will be representative of a broad and diverse study population. Enrollment is brisk, and we expect to continue to activate new sites and enroll patients at existing and new sites through this year and into next year towards our goal of completing enrollment in 2025. Additionally, we continued conduct of CEDAR-HCM, evaluating the pediatric population of patients with symptomatic OHCM as well as an additional Phase 1 study of aficamten in healthy Japanese and Caucasian participants that may support development of aficamten in Japan.

Altogether, I’m proud of the substantial progress we made across the clinical development program for aficamten in the third quarter. Now I’ll turn it over to Andrew.

Andrew Callos: Thanks, Fady. In the third quarter, we continued our commercial readiness activities for the potential approval and launch of aficamten in the U.S. We were pleased to launch HCM Beyond the Heart, an unbranded disease awareness campaign for healthcare professionals. The campaign was borne out of market research and real-world feedback from cardiologists, nurses and patients and highlights the story of five individuals living with HCM to illuminate the multidimensional struggle faced daily by people living with HCM. We are planning to showcase this campaign, at the upcoming AHA Scientific Sessions in Chicago next week, and we plan to launch a similar patient-focused unbranded awareness campaign in first quarter of 2025.

The launch of HCM Beyond the Heart, also marked the first deployment of our omnichannel digital communication strategies, which has successfully validated our investment in planning and set the stage for broader digital engagement to come ahead of and through the time of potential approval and launch in 2025. During the third quarter, we selected third-party external partners for our bespoke patient experience, which we believe is a key element of differentiation for our potential commercial launch. We also made significant progress towards solidifying our promotional launch campaign. Additionally, we advanced our sales force preparations, including finalizing our customer call list and establishing the geographic boundaries, for our planned sales territories.

We have also designed a robust recruiting plan, training curriculum for the approximately 125 to 150 reps we expect to bring on board. While we do not plan to hire sales reps until closer to launch next year, we already have hundreds of qualified candidates in our pipeline prior to going out into the marketplace to recruit. From the payer side, we continued pre-approval information exchange with key payers and made progress in developing our payer value dossier for both U.S. and ex-U.S. payers. Our SEQUOIA team was also active in presenting and publishing research highlighting the unmet need in HCM, the associated cost burden given current treatment and the potential value of aficamten in HCM. Moving on to commercial readiness activities in Europe, our plan is to prioritize major markets and gate hiring and capital deployment alongside regulatory and reimbursement milestones at a country level.

During the third quarter, we designed our distribution model, refined regulatory and labeling strategies, establish country launch sequencing, engage with European key opinion leaders and progress development of HTA dossier while continuing engaging with key HTAs for early scientific advice. We also established our initial go-to-market plan for Germany, which is expected to be the first country where we launch aficamten in Europe. We now have a head of Europe in place and are recruiting for key country leadership in the UK and France, as well as functional leadership roles for European operations, again, alongside gated investment. As we get closer to the potential approval of launch of aficamten, our commercial readiness activities are continuing to ramp up.

Importantly, what we’re building today for aficamten will enable synergies with future potential commercial launches across our specialty cardiology franchise. Shared resources, systems, commercial infrastructure and sales organization will facilitate enhanced efficiencies and effectiveness with each specialty cardiology launch. With that, I will turn the call over to Stuart.

Stuart Kupfer: Thanks, Andrew. I’ll start with CK-586, our next cardiac myosin inhibitor for the potential treatment of a subset of patients with heart failure with preserved ejection fraction or HFpEF, and hypercontractility. During the quarter, we presented the full data from the Phase 1 study of CK-586 at the American College of Clinical Pharmacology, which showed that CK-586 was safe and well tolerated. No serious adverse events were observed and no study stopping criteria were met. The half-life of CK-586 was observed to be between 14 to 17 hours. CK-586 demonstrated dose proportional exposure and a PK/PD relationship for left ventricular ejection fraction that appeared shallow and predictable. At the highest single dose of 600 milligrams, the mean decrease in ejection fraction was less than 5%.

Together, these data demonstrate pharmacologic properties that may enable once-daily fixed dose administration. Because the data from this Phase 1 study were supportive of advancing the Phase 2, we began start-up activities for AMBER-HFpEF, which is the Phase 2 clinical trial of CK-586 in patients with symptomatic HFpEF with ejection fraction of at least 60%, designed to evaluate the safety, tolerability and pharmacodynamic profile of CK-586 compared to placebo. We’re pleased to share that we’re on track to start AMBER-HFpEF before the end of the year. Next, let’s move to omecamtiv mecarbil, our cardiac myosin activator for the potential treatment of a subset of patients with heart failure with severely reduced ejection fraction. During the quarter, we conducted study start-up activities for COMET-HF, the confirmatory Phase 3 clinical trial assessing the efficacy and safety of omecamtiv mecarbil in 1,800 patients with symptomatic heart failure with severely reduced ejection fraction less than 30%.

COMET-HF is designed with pragmatic features to improve efficiency of study conduct and reduce patient burden. We expect to begin this trial during this fourth quarter. Heart failure with reduced ejection fraction or HFrEF, represents about half of the population of heart failure. Drilling down further, estimates point to a large and growing population of patients with high-risk heart failure and severely reduced ejection fraction below 30%. These are patients who have recurrent heart failure events. They may have limiting use of guideline-directed medical therapy due to poor tolerability and have very elevated NT-proBNP consistent with severe heart failure. Despite the use of SGLT2 inhibitors with a large residual risk of cardiovascular events in this subset of patients with HFrEF.

In GALACTIC-HF, this subset of patients with severely reduced ejection fraction experienced a substantially greater treatment benefit with omecamtiv mecarbil. Whereas omecamtiv mecarbil is targeting patients with heart failure and severely reduced ejection fraction, CK-586 is designed to address patients with super abnormal ejection fracture at the opposite end of the spectrum of heart failure. These patients also have high unmet need and despite advances in care with SGLT2 inhibitors have a poor prognosis following heart failure hospitalization. While the pathophysiology of these two heart failure populations is different, medical need for both patient subgroups remains high despite guideline-directed medical therapy with markedly increased risk of cardiovascular mortality and hospitalization for acute decompensated heart failure.

Both omecamtiv mecarbil and CK-586 represent opportunities to expand our specialty cardiology franchise into these populations at either end of the heart failure spectrum. Now looking beyond our specialty cardiology franchise, as Robert mentioned, we’re pleased to be renewing our neuromuscular pipeline with a novel drug candidate arising from our research called CK-089. CK-089 is a fast skeletal muscle troponin activator or FSTA, designed to amplify skeletal muscle response to nerve input, extending time to fatigue and increasing muscle force and power with potential therapeutic application to a specific type of muscular dystrophy. Having completed IND-enabling studies, we expect to start a first-in-human Phase 1 study of CK-089 in healthy subjects soon.

We look forward to sharing more details of our plans to reinvigorate our neuromuscular development activities as informed by prior learnings very soon. What this means is that by the end of this year, we will have one or more drug candidates in each phase of clinical development from Phase 1 to Phase 3, which conveys the richness of our pipeline in muscle-directed therapies. And with that, I will pass it over to Sung.

Sung Lee: Thanks, Stuart. We’re pleased to report our third quarter of 2024 financial results. Starting with the balance sheet. We finished the third quarter of 2024 with approximately $1.3 billion in cash, cash equivalents and investments compared to $1.4 billion at the end of the second quarter of 2024. Cash, cash equivalents and investments declined by approximately $81 million during the third quarter of 2024. Moving on to the income statement. Total revenues in the third quarter of 2024 were $0.5 million compared to $0.4 million for the same period in 2023. R&D expenses in the third quarter of 2024 were $84.6 million compared to $82.5 million for the same period in 2023. The increase was primarily driven by higher personnel-related expenses to progress our pipeline, partially offset by the completion of clinical trials in 2023.

G&A expenses in the third quarter of 2024 were $56.7 million compared to $40.1 million for the same period in 2023. The increase was primarily driven by investments for commercial readiness and personnel-related expenses. Net loss for the second quarter of 2024 was $160.5 million or $1.36 per share basic and diluted compared to a net loss of $129.4 million or $1.35 per share basic and diluted for the same period in 2023. Turning to the financial guidance for 2024. We are reiterating all aspects of our prior guidance, which can be found in our press release. As we head towards the end of 2024, our balance sheet remains an asset and positions us well to prepare for the potential launch of aficamten, advance our earlier and later-stage pipeline and invest in our proven muscle biology platform.

We stand to realize synergies from the commercial and R&D investments as our potential future medicines and development activities can all leverage the infrastructure and capabilities that we are creating today and in the years to follow. We believe these capital allocation priorities can enable us to become a leader in specialty cardiology with multiple medicines, delivering benefit for patients and sustainable growth for investors. With that, I’ll hand it back over to Robert.

Robert Blum: Thank you, Sung. The third quarter indeed was marked by important achievements, continuing a year marked by substantial progress. By this time next year, we expect that our company will look quite different, and we’re building our infrastructure and capabilities to ensure our successes in the years to come. To that end, during the quarter, we further strengthened our executive leadership team with the addition of Brett Pletcher, who joined as EVP, Chief Legal Officer in August. Brett is a seasoned attorney and industry executive with deep experience developing operational reach and capacity and providing practical legal advice, having spent 17 years at Gilead, 13 of those as General Counsel. We’re fortunate to have Brett join our team as we look ahead to the next important chapters for Cytokinetics and increased scope and scale as we mature corporate development.

Cytokinetics is well funded and well positioned for future successes. As we advance towards the potential approval and launch of aficamten in the United States with global launches hopefully to follow, we’re approaching an important inflection point for our company. As we look ahead to that point and beyond, we’re laying the groundwork for our Vision 2030 and sustained growth and enduring future successes as a premier specialty cardiology company. As you’ve heard, this business remains anchored in aficamten for the potential treatment of HCM, followed by omecamtiv mecarbil for the potential treatment of heart failure with severely reduced ejection fraction, and then CK-586 for the potential treatment of heart failure with preserved ejection fraction.

This franchise design is intentional with common features across these patient populations and the prescribers that treat them, including a limited distribution model, few or ineffective available therapies, and high unmet patient need. Each of these underscore potential for higher return on investment and provide us the ability to realize R&D and commercial synergies. To achieve these objectives, we’re committed to investing wisely and maintaining a strong financial foundation to enable both forward motion as well as velocity. Looking back at the quarter, I’m proud of the tremendous progress we’ve made towards achieving our vision. Now, I’ll recap our upcoming milestones. For aficamten, we expect to continue advancing our go-to-market strategies and prepare to launch aficamten in the United States in 2025, of course, subject to FDA approval.

We expect to submit an MAA to the EMA in Q4 2024 and coordinate with CORXEL to support the planned launch of aficamten in China in 2025, pending approval. We expect to complete conduct of MAPLE-HCM and share results in the first half of 2025. We expect to continue enrollment in ACACIA-HCM through 2024 with objective to complete enrollment in 2025. And we expect to continue enrollment in CEDAR-HCM, the Phase I as well as the Phase I study of aficamten in Japanese and Caucasian participants. And for omecamtiv mecarbil, we expect to start COMET-HF, the confirmatory Phase III clinical trial in this Q4 2024. For CK-586, we expect to start AMBER-HFpEF, the Phase II clinical trial also in this Q4 2024. And for earlier clinical development, preclinical development and ongoing research, we expect to initiate clinical development of CK-089 by starting a Phase I study in healthy volunteers in this fourth quarter and we expect to continue ongoing preclinical development and research activities directed to additional muscle biology-focused programs through this year.

Operator, with that, we can now please open the call up to questions.

Operator: Thank you. [Operator Instructions] And our first question will come from Akash Tewari from Jefferies. Your line is open.

Q&A Session

Unidentified Analyst: Hi. Thank you for taking my question. This is Phoebe [ph] on for Akash. Looking at the SEQUOIA data, it seems like the largest magnitude of LVF reductions were seen in hypercontractile patients with LVEF greater than 75. If you had a mechanism that could show gradient relief benefits without affecting LVF, first, would it be considered and would be clinically useful for patients with severe hypercontractility? And second, would you still expect to see a benefit on pVO2? Thank you.

Robert Blum: Thank you. I’ll ask Fady to respond to that, please.

Fady Malik: Yeah. I think the underlying point that you made is that this is a disease of hypercontractility. And in some cases and in most cases, it leads to obstruction as well. Having an ejection fraction of 80% is just not normal. It’s not normal even in people that have that don’t have hypertrophic cardiomyopathy. And so we think one of the targets in treating this disease is to both reduce the contractility to more normal levels so that the tissue remodeling, the myofibral dray, the cardiac wall stresses can all begin to decline as well as to reduce the gradient. And so I don’t know if just treating obstruction by itself is sufficient. You can do that with septal reduction therapy, for instance, and that does result in substantial improvement in patient symptoms.

But often, they go on to develop non-obstructive HCM and issues over time as their disease progresses. So I don’t believe that just treating but not decreasing the hypercontractility is potentially a therapeutic benefit.

Operator: Thank you. Our next question will come from Tess Romero from JPMorgan. Your line is open.

Robert Blum: Good afternoon, Tess.

Tess Romero: Good afternoon, Robert and team. Hope you’re all well. Thanks for taking the question. So on the Phase III MAPLE-HCM trial in patients with symptomatic OHCM, how confident are you in a positive trial here? And specifically, could you walk us through the magnitude of change for aficamten over metaprolol you need to hit a p-value that is significant? And relatedly, what can you tell us on how the patients that enrolled dried with your expectations?

Robert Blum : Good questions. Obviously, as we approach the readout of MAPLE-HCM expected next year, we believe that this study will play an important role in consideration and adoption of aficamten, hopefully also in line with evolving guidelines. And the study, MAPLE-HCM was specifically designed, if anything, perhaps as would be accelerating what would otherwise be potentially a Phase IV study and could enable label expansion. I’ll ask Fady to speak to how we design the study and how we feel about the patients that were enrolled.

Fady Malik : Yes. Hi, Tess, I think this has been a study that has been very highly welcomed by the investigator community is answering an important question for them. In terms of enrolling patients, we’ve done very well, I think, in enrolling patients who meet the target, have meaningful symptoms, have meaningful reduction in their exercise capacity and whom initiating treatment with aficamten or metoprolol, we’ll be able to assess, which — what is the magnitude of benefit for each of those therapies and how they compare. So we think for several reasons that aficamten has already shown benefit on top of beta blockers. And so these are patients that — who were symptomatic and given beta blockers had inadequate treatment or inadequate response to treatment and subsequently responded to aficamten.

In the SEQUOIA, we had patients on aficamten not on beta blockers. We had beta blocker patients, not on any other therapy. And I think that gave us a window into what we expect to see here, which I think is the results will be consistent with the hypothesis of this trial. I’m not going to speculate really on what is meaningful or how big of a change we’re looking for. We have powered the trial somewhat conservatively with looking at a delta peak VO2 of about 2 with decent power to show anything down to probably 1.5 in terms of change in peak VO2, which covers the region where SEQUOIA was positive as well. So I think we’re adequately powered, and we look forward to the results.

Tess Romero : Great. Thanks so much for taking our question.

Fady Malik : Thanks, Tess.

Robert Blum : Thank you.

Operator: Thank you. And our next question will come from Salim Syed from Mizuho. Your line is open.

Robert Blum : Hello, Salim.

Salim Syed : Hey, Robert. Thanks for the color and the question. I guess one for me on MAPLE as well. Assuming you guys actually get the result you want here, could you just maybe give us your thoughts on getting those results published and into treatment guidelines? Like how often does the committee meet and when that could potentially happen? Could it happen prior to the supplementary approval? Thank you.

Robert Blum : Yes. So obviously, we can’t commit for what others will be doing, but the guidelines are updated in a continuous way and regularly, not just once a year. And as you’ve seen already in this year, we’ve been aggressive about ensuring that data go quickly from presentation to publication. I think we’ve had a quite uncommon number of presentations and publications this year, underscoring how closely we’re working with the academic community to make sure these data get properly peer reviewed and published for consideration. So that won’t change next year.

Q – Salim Syed: Could you — you think you can get it done prior to the actual approval? Because I think the threshold is publication, correct?

Robert Blum: Well, for consideration of guidelines you’re saying?

Q – Salim Syed: Yes. Yes, correct. Yes.

Robert Blum: I would think that, that makes a big difference. And it’s certainly our goal to get it published as soon as possible next year. I don’t think we should be ahead of even having the data committing to whether that would be ahead of potential approval. But knowing that this is our objective, I think you should assume we’ll continue to be very aggressive.

Q – Salim Syed: Okay. Got it. Thank you so much.

Operator: Thank you. Our next question will come from Roanna Ruiz from Leerink Partners. Your line is open.

Robert Blum: Good afternoon.

Q – Unidentified Analyst: Hi. Good afternoon. This is [indiscernible] on for Roanna. Thanks for taking our questions. Maybe first on MAPLE, maybe asked a different way. I guess, looking ahead to the results for afi relative to metoprolol next year, I guess, what could the peak VO2 improvement with afi look like in this study relative to what you saw in SEQUOIA previously? And then I guess, like what’s the outlook on the time line of possible guideline adoption for using afi in earlier lines of therapy if the MAPLE data are positive?

Robert Blum: I feel like we might have just answered that, but maybe I’ll turn to Fady and see if there’s anything more he might want to add.

Fady Malik: Yes. I mean I just will reiterate in SEQUOIA, we had 1.74 ml per kilo per minute improvement in patients not on beta blockers. That effect was modestly bigger. So we’re kind of in that range of peak VO2 improvement. Prior publications of metoprolol use in HCM showed that metoprolol doesn’t increase peak VO2. And so you can guess that if we’re in the same ballpark, we might see something in that range. This is a smaller study than SEQUOIA was. We’re treating patients whom are slightly less symptomatic because we wanted to sort of expand the aperture to naive patients and newer patients. So — the exact effect size is a little tricky to handicap, but I don’t think the exact effect size is really what’s important. What’s important is that there is a meaningfully different and better effect of aficamten to improve exercise function and symptoms than metoprolol does in these patients, and that should guide its use in therapy.

As to the guidelines, I mean, we’ll present this. We’ll get it published, I think, fairly rapidly. The guideline committees, they don’t publish their meeting schedules. They don’t publish their timing of updating guidelines, but they are aware that this is a fast-moving field and that they do need to be timely and sort of considering the evidence and revising their guidelines. So leave it at that.

Q – Unidentified Analyst: Got it. And then maybe if I may, could you comment about how you’re thinking about the European launch dynamics for Ai if it’s approved? And I guess, any learning’s that you could apply based on what you’re seeing from the competitor launch throughout Europe? Thank you.

Robert Blum: So we’re really just taking one question for analysts right now, but I suspect you’ll get to your question answered as we go through what looks to be a very long list of folks who want to ask questions. We’ll come back to that. Operator, if we can move to the next one, please.

Operator: Thank you. Our next question comes from Jason Zemansky from BofA. Your line is open.

Robert Blum: Hey, Jason.

Cameron Bozdog: Hey, good afternoon. This is Cameron Bozdog on for Jason. Congrats on the quarter. And thanks for taking our question. So in terms of leveraging aficamten profile to warrant a potential pricing premium, I guess, what factors are likely to be critical here? Is it going to be efficacy, safety, the administrative profile? Or I guess, in other words, do you think less frequent LVEF reductions below 50% in SEQUOIA versus EXPLORER is enough to warrant a pricing premium? Or would you need to see the safety benefit reflected in the monitoring protocols or the label to establish a basis for a premium here? Thank you.

Robert Blum: So first off, your question is kind of presupposing that there’ll be a pricing premium, and we haven’t spoken to that. But instead, we’ve referred to pricing within a relative same ZIP code. But maybe I’ll ask Andrew to comment, if you will, on what we believe is ultimately going to translate to wider adoption for a next-in-class therapeutic in this category.

Andrew Callos: Yeah. So I think Robert answered the pricing, and I’m assuming you’re asking about US pricing where we have the ability to set the price. But in the US, we’ll be in the proximity of what the established price for the market is. In terms of uptake of payers based on price, we’re certainly going to be working and have already been with commercial payers. We’re working on medical exception for Medicare payers. I think we addressed IRA challenges, which is an industry challenge, not unique to us and that’s how we’ll get access that we believe will be within parity of competition. So we’ve really been taking that out of the equation and focusing on educating, promoting and uptake as well as supporting patients.

Robert Blum: So the market research we’ve done underscores the importance of risk mitigation and ultimately, how that can translate to hopefully more physicians prescribing a cardiac myosin inhibitor for more patients. And we do hope that if approved, aficamten could be accompanied by a risk mitigation profile that fits with next-in-class objectives.

Operator: Thank you. Our next question will come from Sean McCutcheon from Raymond James. Your line is open.

Robert Blum: Hey, Sean.

Sean McCutcheon: Hey, guys. Thanks for taking the question. On CK-586, can you speak to the lessons that you took from the EMBARK results? How are the target patients in — and were meaningfully similar or different in your estimation from EMBARK? And what pharmacologic properties do you view as the most valuable provided the mechanism proves out in the sub-segment of HFpEF patients? Thanks.

Robert Blum: Sure. So that’s a good question for Stuart, maybe to pick up on and Fady, if he wants to add anything.

Stuart Kupfer: Sure. Thanks for the question. So first of all, we’re very encouraged with the potential benefit in this population with CK-586 in large part from the data we observed in nondestructive HCM with aficamten. And similar results were observed with mavacamten and nondestructive HCM in terms of the pharmacodynamic improvement, symptomatic improvement. But the EMBARK data do inform and encourage a potential benefit of CK-586 in this population of HFpEF patients with hypercontractility. Now, we are enriching a population, of course, with an ejection fraction of at least 60%. We have a lot to learn in terms of the potential dosing range that maybe effective and safe and tolerable. And so, this first inpatient study will help us characterize the pharmacodynamic benefits.

We’ll be measuring cardiac biomarkers such as NT-proBNP, cardiac troponin and as well, of course, of evaluating ejection fraction. And what we observed, I think, very favorably in our Phase 1 studies is very shallow exposure response profile with respect to only small incremental decreases of ejection fraction with increasing doses of CK-586. So, I’m not going to go into a lot of speculation about comparing study designs or the data from EMBARK, but the data we’ve accumulated so far are very encouraging with CK-586 as well as aficamten in non-obstructive HCM. And so we’re quite optimistic and look forward to this Phase 2 trial.

Robert Blum: The EMBARK study was not a large study, and therefore, there’s still a lot to be learned from testing a cardiac myosin inhibitor in a larger, longer study. So our goal will be to do a proper development program for CK-586 to inform CK-586. Operator, next question please.

Stuart Kupfer: No. We have — I just want to add — I’m sorry, Robert, that we — this is a placebo-controlled trial. And so, it’s going to be a much more rigorous assessment of the cardiac myosin inhibitor in this population with HFpEF and hypercontract as opposed to EMBARK.

Robert Blum: Yes. Thank you, Stuart.

Operator: Thank you. Our next question will come from Paul Choi from Goldman Sachs. Your line is open.

Robert Blum: Good afternoon, Paul.

Paul Choi: Good afternoon, Robert and team. Thank you for taking our question. I just want to return to the subject of MAPLE and with regard to any sort of clinical efficacy bar that has been potentially discussed with payers as they think about potential guideline changes there. And have they provided any feedback to you or any sort of physician community commentary on just sort of what would be considered clinically meaningful here versus metaprofile as to drive guideline changes here? Thank you very much.

Robert Blum: Yes. So I’ll ask Andrew to comment, but I think it would be premature for us to be talking about MAPLE with payers before we have data from MAPLE and before we have even an approval potentially based on SEQUOIA. But we are gathering insights into how payers think about these things in a general sense. So maybe, Andrew, if you could comment, please?

Andrew Callos: Certainly, yes. So as Robert had mentioned, our focus right now with payers is based on SEQUOIA. Strategically, we’re discussing options in terms of how you then start to work MAPLE into payer conversations as well as value arguments, both in the US as well as Europe. The value for MAPLE from a physician point of view really does two things. It expands physician population. There is a subset of physicians who are more apathetic to treating with new agents and are okay with beta blockers as is because they don’t really have experience with CMI. So when you show a head-to-head relative to what they’re using today, that certainly releases additional physicians. So it expands the market. And then when you look at preference share, when you have a secondary study that has within the range of similar results is what we’re expecting, then that is a validation for that primary study, which then further enhances share.

So it should work with — for guidelines, it should work with market expansion and it should help with share preference and certainly going to help with value arguments in the US and in Europe. But we’re not talking to payers at the moment about MAPLE.

Paul Choi: Okay, great. Thank you.

Robert Blum: Thank you.

Operator: Thank you. Our next question comes from Jason Butler from Citizens JMP. Your line is open.

Robert Blum: Good morning, Jason.

Jason Butler: Hi, Robert. Thanks for taking the question. Just a quick one on 089. You guys have a long history with this class. Can you just, at a high level, just tell us how 089 differs from the prior candidates? Thanks.

Robert Blum: Yeah. So 089 comes from a very different chemical scaffold, and for which I’ll ask Fady to comment in a moment. But please understand that we’ve applied learnings to our interest as it relates to 089 and in particular, you’ll hear more about how we’re developing it going forward, underscoring that we’re not going to be pursuing the development of 089 in ALS, but rather in a muscular dystrophy and in fact, a rare form of disease where we think it may play a potential role. Fady, do you want to comment on how it may differ from prior fast skeletal compounds?

Fady Malik: Yeah. I mean, CK-089 is a third molecule, and we view each iteration have come to a molecule that is more potent, has better pharmaceutical properties, it’s a challenging target, and we think 089 maximizes the efficacy that we can pull out of this mechanism of action, at least in preclinical models and is better suited in terms of its physical properties for doing dosing and dose ranging and so forth, so still early days. We have some very interesting and promising preclinical data, and we’ll be looking to see if we can translate that going forward into the clinic.

Robert Blum: The world has evolved quite a bit around skeletal muscle since we were advancing two prior compounds. And we’re borrowing from those learnings, too, in terms of how we think about skeletal muscle force, power, endurance, fatigue and muscle function. And we do believe that CK-089 has an opportunity to establish a position where some others have been building value for shareholders. And again, you’ll hear more about our plans as we roll forward into Phase I and hopefully beyond.

Jason Butler: Thank you.

Robert Blum: Thank you.

Operator: Thank you. Our next question comes from Charles Duncan from Cantor Fitzgerald. Your line is open.

Unidentified Analyst: Hi team. This is Asiya [ph] on for Charles. Thank you for taking our question. So we just have one for omecamtiv mecarbil. As you near initiation for COMET-HF, what is your view on its competitive position within the heart failure market, specifically as other treatments for heart failure with reduced ejection fraction continue to develop?

Robert Blum: Thank you an excellent question. I think it warrants being answered by both, Fady and Stuart, as well as Andrew may have a perspective on that, and I’ll ask our team to comment, starting with Fady, please.

Fady Malik: Well, sure. I think in the population that we plan to study omecamtiv mecarbil in people with severely reduced ejection fraction and really severe heart failure, there are a few new options. Many of the drugs that are developed lower blood pressure. They can be challenging to use in these patients because they impact kidney function. And they don’t address the core element of why these patients are so symptomatic at this point in their disease process, which is their cardiac function has deteriorated substantially and is now severely reduced. So, I think omecamtiv has sort of a unique place in terms of being used in this area, and it’s conceptually easy to understand, why it would benefit these patients, to explain to patients why you would use it.

And so I think the enthusiasm that we have been met with as we announced the initiation of this trial rather than announced the intent to conduct COMET in the heart failure community has been quite large. I’m get e-mails weekly, frankly, from investigators that are interested in participating. We’re grateful that we’re continuing to develop omecamtiv mecarbil because it really fills an unmet need for them in terms of what do they do next when the sort of foundational treatments for heart failure are not working.

Robert Blum: Stuart, anything to add from the clinical perspective, before we ask Andrew to comment commercially?

Stuart Kupfer: Just add that Fady said, these patients are running out of options. And if you look at the profile of risk in this population, there is a marked inflection point at the threshold of 30% ejection fraction. The risk of mortality and acute decompensated heart failure goes up dramatically, ejection fraction less than 30%. And as Fady was mentioning, these patients are running out of options. They really don’t have options withdrawing that guideline direct medical therapy and heading towards end-stage heart failure. And again, what we observed in GALACTIC-HF is that this was a population not only with the highest risk of major heart failure events and mortality, this is a population in which omecamtiv mecarbil benefit the most. And so there’s sort of an alignment of the stars here, and we think this is a population that could truly benefit from omecamtiv mecarbil.

Robert Blum: Thank you, Stuart. Andrew?

Andrew Callos: Sure. From a market positioning point of view, so there’s a couple of considerations. One, when we look at kind of future competitive environment, as well as what’s on the market today and the guideline-directed medical therapy kind of quad therapy, our expectation will be completely generic at that point. We also look at what is in the pipeline. So we’re pretty confident in terms of very clear positioning for omecamtiv mecarbil, especially when you consider the clinical arguments that were just described. This patient population also has challenges with hypotension or renal dysfunction or hyperkalemia, where we’re expecting omecamtiv will continue to show a neutral effect on those side effects that are associated with guideline-directed therapy.

There’s a strong health economic argument as well. And then with little treatment options, we’re expecting kind of premium pricing as well as the fact that this will lay on top of our existing specialty cardiovascular franchise, our field force, our headquarter-based employees, so very little add from a cost basis as well. So a really clear economic argument, really clear business case, really clear clinical argument as well as looking at the future competitive set from a positioning point of view. And that’s why we’re moving forward with omecamtiv from a commercial point of view.

Unidentified Analyst: That makes the last…

Robert Blum: Sure. I just want to comment. I’m really pleased that we’re hearing from more investors and equity research analysts about our strategy for omecamtiv mecarbil and people are doing their work on this. I’ll suggest that I think it’s an opportunity to realize the kind of synergies we’ve been talking about around our specialty cardiology model, and it would be a mistake to believe that we’re targeting a population for which there are good alternatives because they are really not. And we do believe we have a positioning as well as a profile for omecamtiv mecarbil, if positive in this confirmatory study that can translate into a meaningful opportunity. So looking forward to updating you more and more on that. Operator, next question, please.

Operator: Thank you. Our next question will come from Srikripa Devarakonda from Truist Securities. Your line is open.

Robert Blum: Good afternoon.

Srikripa Devarakonda: Good afternoon, Robert and team. Thank you so much for taking my questions. I have a question on MAPLE as well. I think, Fady, you talked about getting imaging data in MAPLE that might suggest a difference in cardiac remodeling. I was wondering if six months — you think six months is enough to demonstrate the difference. I think you had mentioned that it’s the start of showing the difference. And do you think long-term data from FOREST would add to that? Or would you need to show longer data from MAPLE?

Fady Malik: Well, let me put it differently, a little bit differently. Already with SEQUOIA, for instance, we’ve presented data at six months, you start to see changes in terms of reduction of LV mass and left atrial size that reflect positive changes in cardiac structure. So six months is enough. Those changes may increase over time, which means you need longer follow-up. But I think what we’ll see, and I hope we’ll see with MAPLE is that with beta blockers, you don’t see any of those changes over six months. So the process doesn’t even start. It doesn’t — it doesn’t get underway. There’s not really any mechanistic reason to believe that you will see it in those patients. And so if you haven’t started in six months, there’s no reason to believe that somehow much longer treatment with that particular modality is going to lead to the same sort of changes that we’ll demonstrate over time with aficamten.

Srikripa Devarakonda: Got it. So I think the point I was trying to get to is, would this help from a reimbursement perspective that this is not just the exercise capacity, but also the cardiac remodeling that you see at six months?

Robert Blum: Andrew, do you want to take that? I mean, I know from a physician perspective, and we just had — frankly, had a call on this morning with our steering committee. They’re all interested in how to demonstrate that early — earlier use of this mechanism of action may change the course of people’s disease progression. And so there’s really strong interest in the physician community of that question. And it’s difficult to show and likely payers may feel differently. It’s hard to know, but I think it’s an important question to ultimately answer.

Andrew Callos: Yeah. Kripa, thanks for the question. I think ultimately, the more data that we can add to arguments for payers, MAPLE certainly starts to add to that argument. SEQUOIA clearly adds to that argument, having outcomes data. So right now, we’re focused on linking peak VO2 to outcomes, secondaries like New York Heart Class and KCCQ, they all resonate very well with payers. This added to that certainly should help that argument. So we haven’t broached the subject with payers yet. But again, I think additional evidence is always helpful.

Srikripa Devarakonda: Got it. Thank you so much.

Andrew Callos: Thank you.

Operator: Thank you. Our next question comes from Mayank Mamtani from B. Riley Securities. Your line is open.

Robert Blum: Good afternoon.

Mayank Mamtani: Hi. Good afternoon team. Congrats on a strong third quarter and thanks for taking my questions. So for the CK-586 HFpEF Phase 2 trial, 12-week treatment period, what would be your expectation for functional improvement given what you’ve seen in the nHCM patients in REDWOOD? And are you able to quantify beyond, obviously, the proBNP information you’ll get? Or should we just wait for the MYK-224 AURORA study data early next year to understand what good looks like in a placebo-controlled manner? And also thinking how this stacks up relative to the GLP-1 drugs being increasingly used in FpEF? Thanks for taking my question.

Robert Blum: Let me start. I’ll ask Stuart to comment. But I think just I’ll make the point that in our nHCM study in REDWOOD, the nHCM cohort, that was 10 weeks of treatment and that seemed adequate to see meaningful biomarker signals and some symptom improvement. So I think that here, we have a similar chance of seeing that in these patients. This is more of a dose-finding trial. By the time we got to the non-obstructive HCM cohort in REDWOOD, we already had a pretty good sense of doses. But I think, again, the duration of this trial should allow for us to get a sense of how this drug impacts patients’ symptoms and other measures of cardiac function and structure. As to the use of GLP-1, Stuart, do you want to comment on how we’re thinking about that in this population?

Stuart Kupfer: I’m sorry I didn’t quite get the question you said.

Robert Blum: I guess Mayank was asking in how GLP-1s are now being used in HFpEF, how are we incorporating the change in therapy in our consideration of our plans going forward?

Stuart Kupfer: Well, the way we think about this is that these are different mechanisms of action. And there has been — there is some evidence of some benefit for GLP-1 receptor agonist in HFpEF. It’s not completely clear at this point, how much is related to weight reduction or some other potential mechanism. But I think the point is that this population is one that’s high risk of adverse cardiovascular outcomes. And what we’ve seen in — certainly in patients with HFrEf is that addition of new mechanism of action that address different pathways result in incremental risk reduction for adverse heart failure outcomes. And so we anticipate the same with the mechanism of action for CK-586 cardiac myosin inhibition, again, analogous to what we’ve seen so far in patients with non-obstructive HCM. So there’s no reason why these mechanisms shouldn’t be complementary. So we don’t see them as competitive, but add to.

Robert Blum : I think there’s a lot to be appreciated about the spectrum or continuum of heart failure from severely reduced EF to supernormal EF. And I do believe the way we’re positioning is different. One shouldn’t think that all drugs are going to be equally across that spectrum, including GLP-1s.

Fady Malik : Yes. Remember, GLP-1s are applied in obese people. Not everybody with HFpEF is obese. So there are clearly segments of the HFpEF population that are not going to be helped by GLP-1s just, because they’re not going to need or it would be adverse to give them a lot of weight loss. And patients with high ejection fraction, likewise, we will try to avoid people with metabolic syndrome and obesity as a means of carving out a phenotype that we think is responsive to this mechanism of action.

Robert Blum : Thank you. Operator, next question, please.

Operator: Thank you. Our next question will come from Yasmeen Rahimi from Piper Sandler. Your line is open.

Robert Blum : Good afternoon.

Yasmeen Rahimi : Good afternoon. Hi, Robert. It’s so wonderful. This is the first call in two years that we did not bring up the word in the Q&A of REMS. So it’s nice to see nor am I going to ask a question on that. Okay. So I’m going to — I feel pretty good about not talking about that anymore. But would love to continue the dialogue on MAPLE. I think ultimately, what maybe we need your help on is to understand what is the size of the obstructive market that failed beta blocker or even gets worse on beta blocker? And what kind of cost analysis could you potentially put together to kind of make the argument of down the line of aficamten being positioned as first line. But maybe to the extent you could educate us on the size of the market if MAPLE showed superiority? Would greatly appreciate, and I’ll jump back into the queue.

Robert Blum : Thank you. Andrew, you’ve done some good work around market segmentation. Do you want to tackle that?

Andrew Callos : Sure. Good question. So from a beta blocker point of view, at least in our — this is not from claims data or a large data source from market research. We do know that about 25% of patients experience contraindication to beta blocker, at least what over 100 or so physicians told us and maybe about 80% to 90% have unwanted side effects. So certainly, it’s not an agent that patients love to take from what we’ve heard. When we look at those that fail beta blockers and kind of the value argument, I think our overall — it’s hard to create a value argument around a low-cost generic. I think the value argument has to get elevated to a higher level, things like KCCQ, New York Heart class, what actually does change outcomes as does peak VO2 change outcomes — hard outcomes, outcomes like hospitalization, death, et cetera.

If you have a lower New York Heart class or a better peak VO2, then certainly you have better outcomes, avoiding septal reduction therapy or surgery, the associated comorbidities of — associated with HCM. So these are the kinds of value arguments that we really look at making. I don’t think that a failure of a beta blocker will really help from that regard. I think where it does help, as I alluded to earlier, it creates additional evidence. It creates evidence against what a standard of care is for many physicians and gets them to rethink potentially therapy. So it opens up the market. It’s not a larger population, obviously, it’s still OHCM, but it is a larger market opportunity and therefore, larger market penetration.

Yasmeen Rahimi: Thank you, Andrew.

Robert Blum: I think a lot of the questions we’re getting today relate to MAPLE, and I assume that means that a lot of the analysts are refining their models to understand what MAPLE could mean in terms of opening the market to yet broader adoption. And I appreciate that while I’ll underscore, and as Andrew is pointing out, it’s the body of evidence that I think creates a tipping point around which cardiologists activated perhaps outside of centers of excellence may ultimately feel more comfortable prescribing aficamten if approved. We think that’s going to make a big difference. So it contributes to velocity of commercial launch. It contributes to what will be the expansion of the category beyond where it’s currently perhaps entrenched in centers of excellence.

We’ve talked about the concentration of prescribers, and we do believe that MAPLE can make a meaningful difference in terms of adding to the evidence to support the use of cardiac myosin inhibitors. And that’s where I think it will enable better diffusion of this innovation broader into the marketplace. Operator, next question, please.

Operator: Thank you. Our next question comes from Rohan Mathur from Oppenheimer. Your line is open.

Robert Blum: Good afternoon.

Rohan Mathur: Good afternoon. This is Rohan on for Leland Gershell. Thanks for the update and taking my question. On aficamten, just as you think about implications from the ongoing launch of the cardiac myosin inhibitor, what sort of steps of the commercial process would you expect incumbent therapy maybe catalyze in terms of growing market awareness and helping an uptake in eventual payer coverage once aficamten is potentially available? Thank you.

Robert Blum: Yes. So we’ve done a lot of work around what a next-in-class opportunity can mean for category expansion, broader penetration, activating cardiologists who might not be currently yet prescribing a cardiac myosin inhibitor. We think it has a lot to do with things that we’ve been talking about in terms of next-in-class profile. It’s not just about safety and efficacy. It’s about ease of use and convenience. It’s about the patient experience. And maybe, Andrew, you can talk a bit more about these things.

Andrew Callos: Sure. So really, when you’re the second agent, I think we can — a disease that has a new therapy that hasn’t had a targeted therapy. So we’re doing our own disease awareness campaign. We rolled out a disease aware campaign in HCPs not long ago and with patients in early Q1 I think many of us in the US have seen direct-to-consumer TV advertising for the category. There’s broader disease awareness now. There’s patient organizations. So all these things create awareness by payers. They see these things out in the marketplace by physicians. It gets patients into physician offices talking about maybe additional treatment options. So the increased awareness certainly should have an increased market opportunity for us where we’re not fighting awareness of disease. We’re educating more on aficamten and the unique properties as well as the areas of differentiation.

Rohan Mathur: Thank you.

Robert Blum: Thanks for the question.

Operator: Thank you. And I am showing no further questions from our phone lines. I’d now like to turn the conference back over to President and CEO, Robert Blum, for any closing remarks.

Robert Blum: Thank you. I want to thank all the participants on our call today for your continued support and interest in Cytokinetics. Obviously, a lot to cover today. We’ve had a very busy year. Q3 was a good quarter in terms of progress against our goals. If you haven’t already, I would encourage you to listen in on the investor event that’s archived on our website. We went into some great detail around our strategies, not just as it relates to aficamten and OHCM, but also nHCM and how that creates a through line to our specialty cardiology franchise anchored with both omecamtiv and CK-586. And what you heard today speaks to not just progress around those programs, but also in research and earlier development and how that’s all enveloped in a company that’s being prudent with regard to capital investment deployment and efficiencies that could create commercial synergies.

As I mentioned, our goal is not simply to launch aficamten next year, but to do so in a way that’s differentiated and could be enabling of us to set the table for the franchise that we’ve been talking about. I want to again thank everybody for your interest in what we’re doing, your attention on this call. We look forward to keeping you up to date through the remainder of the year. And with that, operator, we can conclude the call, please.

Operator: Thank you. This concludes today’s conference call. Thank you for your participation. You may now disconnect.