Cytokinetics Announces Four Presentations at the American College of Cardiology Annual Scientific Session & Expo
Rhea-AI Summary
Cytokinetics (Nasdaq: CYTK) announced four ACC 2026 presentations on MYQORZO (aficamten) for symptomatic obstructive hypertrophic cardiomyopathy (oHCM), including pooled and subgroup analyses, treatment interruption data, hypertension subgroup results, and ECG‑echocardiography correlations.
Notable facts: regulatory approvals in US, EU, and China; pooled n=371; washout analysis n=182; ECG odds ratios significant (p<0.001).
Positive
- Regulatory approvals in US, EU, and China for MYQORZO
- Pooled efficacy analysis of n=371 showing aficamten superior to metoprolol and placebo
- Washout safety analysis of n=182 showed no increased cardiac adverse events
- ECG improvements: ST changes OR 0.23 and LVH strain OR 0.15 (p<0.001)
Negative
- Aficamten associated with a small mean SBP increase of +3.6 mmHg versus −8.3 mmHg with metoprolol
- Rates of uncontrolled hypertension emerged in 34% (aficamten) vs 25% (metoprolol); p=0.38
News Market Reaction – CYTK
In the Mar 16 session, CYTK gained 1.28%, reflecting a mild positive market reaction.
Data tracked by StockTitan Argus on the day of publication.
Key Figures
Historical Context
| Date | Event | Sentiment | 24h Move | Catalyst |
|---|---|---|---|---|
| Mar 02 | Investor conferences | Neutral | -1.2% | Management scheduled appearances at four March 2026 investor conferences. |
| Feb 24 | Earnings results | Positive | -10.3% | Reported Q4/full-year 2025 results and outlined MYQORZO approvals and 2026 guidance. |
| Feb 17 | EU approval | Positive | +0.5% | European Commission approved MYQORZO tablets for symptomatic obstructive HCM in adults. |
| Feb 12 | Earnings date | Neutral | +1.9% | Company set the date and time for its fourth-quarter 2025 results call. |
| Feb 09 | Grant awards | Positive | +1.6% | Announced communications grants to patient advocacy groups focused on HCM education. |
24h Move is the share-price change in the day after each event; other market factors may also have contributed.
Recent major positive events, including MYQORZO approvals and earnings with strong revenue growth, have sometimes been followed by weak or negative price reactions, while smaller operational updates have more often aligned modestly with the news tone.
Over the last months, Cytokinetics moved from planning events and grants toward full commercial execution. The company reported Q4 and full-year 2025 results with multi-region MYQORZO approvals and detailed its transition to a commercial-stage model on Feb 24. Earlier, the European Commission approved MYQORZO for symptomatic oHCM adults on Feb 17. Operational items like conference participation, earnings timing, and patient community grants produced only modest price reactions, framing today’s ACC data as another step consolidating the MYQORZO profile.
Key Terms
obstructive hypertrophic cardiomyopathy medical
allosteric medical
left ventricular outflow tract (lvot) obstruction medical
valsalva gradient medical
electrocardiographic (ecg) medical
st segment medical
left ventricular hypertrophy (lvh) strain pattern medical
systolic blood pressure (sbp) medical
AI-generated analysis. How Rhea-AI works. Not financial advice.
New Analyses from Three Trials in Obstructive HCM Support Findings from Previously Published Data on MYQORZO™ (aficamten)
SOUTH SAN FRANCISCO, Calif., March 16, 2026 (GLOBE NEWSWIRE) -- Cytokinetics, Incorporated (Nasdaq: CYTK) today announced four presentations related to MYQORZO™ (aficamten) at the American College of Cardiology (ACC) Annual Scientific Session & Expo taking place March 28–30, 2026 in New Orleans, LA. Recently approved for the treatment of adults with symptomatic obstructive hypertrophic cardiomyopathy (oHCM) by the U.S. Food and Drug Administration, European Commission, and the China National Medical Products Administration, MYQORZO is an allosteric and reversible inhibitor of cardiac myosin motor activity. In patients with oHCM, myosin inhibition with MYQORZO reduces cardiac contractility and consequently, left ventricular outflow tract (LVOT) obstruction.
“We are pleased to contribute further evidence that we believe will help physicians and patients with clinical decision making,” said Stephen Heitner, M.D., Senior Vice President, Clinical Research and Development. “The new data can help empower evidence-based choices of therapy for patients living with symptomatic oHCM, showing that aficamten improves exercise capacity, when compared to placebo or the beta blocker, metoprolol, while maintaining its safety profile.”
Scientific Presentations Include:
Evaluation of Aficamten or Beta-Blocker Monotherapy Versus Placebo in Patients with Obstructive Hypertrophic Cardiomyopathy: A Pooled Analysis of SEQUOIA-HCM and MAPLE-HCM (1186-09)
Moderated Poster Presentation, March 30,2026, 11:00 AM-12:00 PM CT, E Hall
P. Christian Schulze, M.D., Ph.D., Chair of the Department of Medicine and Division of Cardiology, Angiology and Intensive Medical Care at the University Hospital Jena
A new analysis based on combined data from SEQUOIA-HCM (Safety, Efficacy, and Quantitative Understanding of Obstruction Impact of Aficamten in HCM) and MAPLE-HCM (Metoprolol vs Aficamten in Patients with LVOT Obstruction on Exercise Capacity in HCM) evaluated aficamten or metoprolol monotherapy versus placebo. Patients (n=371) were pooled into three groups: aficamten as monotherapy, metoprolol as monotherapy, and placebo without background beta-blockers. For patients with symptomatic oHCM, treatment with beta-blocker monotherapy was no different compared to placebo across many clinically relevant outcomes (exercise capacity, symptoms, cardiac biomarkers and Valsalva gradient). Conversely, aficamten as monotherapy was superior to both metoprolol and placebo, consistent with previously published1 findings and supporting the emerging role of aficamten in the treatment of symptomatic oHCM.
Clinical Implications Associated with Temporary Treatment Interruption and Reinitiation of Aficamten Therapy in Obstructive Hypertrophic Cardiomyopathy (906-11)
Oral Presentation, March 29, 2026, 9:30 AM-10:30 AM CT, Hall E
Martin Maron, M.D., Director, Hypertrophic Cardiomyopathy Center, Lahey Hospital & Medical Center; and National Principal Investigator of SEQUOIA-HCM
This new analysis evaluated data from SEQUOIA-HCM and FOREST-HCM (Follow-up, Open-Label, Research Evaluation of Sustained Treatment with Aficamten in HCM) related to the safety of interrupting treatment with aficamten. The analysis, which included 182 participants, evaluated the impact of discontinuing treatment with aficamten for a four-week washout period after assessment of the primary endpoint at 24-weeks as occurred per protocol in SEQUOIA-HCM. Most of these patients subsequently reinitiated treatment in the open-label extension, FOREST-HCM. The analyses showed that washout of aficamten was not associated with increased risk of cardiac adverse events or rebound compared to placebo. One (
Aficamten Versus Metoprolol in Patients with Hypertension and Obstructive Hypertrophic Cardiomyopathy (1395-221)
Poster Presentation, March 28, 2026, 2PM-3PM CT, Hall E
Ahmad Masri, M.D., MS, Director of the Hypertrophic Cardiomyopathy Center at Oregon Health & Science University
A new analysis of MAPLE-HCM evaluated the efficacy and safety of treatment with aficamten vs. metoprolol in patients with hypertension at baseline, which is common in patients with oHCM. In this analysis of 175 patients,
Electrocardiographic Changes and Associations with Echocardiographic Changes in Patients with Symptomatic Obstructive Hypertrophic Cardiomyopathy: Insights from the SEQUOIA-HCM Trial (1514-243)
Poster Presentation, March 29, 2026, 2PM-3PM CT, Hall E
Alberto Foà, M.D., Ph.D., Cardiologist, Brigham and Women's Hospital, Harvard Medical School; Heart Failure and Transplant Unit - IRCCS Azienda Ospedaliero-Universitaria di Bologna
A new analysis of SEQUOIA-HCM examined electrocardiographic (ECG) changes in patients with symptomatic oHCM following 24 weeks of treatment with aficamten or placebo. The results showed that, compared to placebo, aficamten decreased the presence of ST segment changes (adjusted odds ratio 0.23;
About MYQORZO® (aficamten)
MYQORZO® (aficamten) is a cardiac myosin inhibitor approved in the U.S., China and European Union for the treatment of symptomatic obstructive hypertrophic cardiomyopathy (oHCM). In patients with oHCM, myosin inhibition with MYQORZO reduces cardiac contractility and consequently, left ventricular outflow tract (LVOT) obstruction. MYQORZO was engineered to achieve a predictable exposure response, rapid onset of action and reversibility.2
Aficamten is also under clinical investigation in ACACIA-HCM, a Phase 3 trial in patients with non-obstructive HCM (nHCM) and CEDAR-HCM, in a pediatric population with oHCM. Aficamten has not been deemed safe or effective for use in either of these patient populations. In addition, aficamten is being studied in FOREST-HCM, an open-label extension clinical study.
INDICATIONS AND USAGE
MYQORZO is indicated for the treatment of adults with symptomatic oHCM to improve functional capacity and symptoms.
IMPORTANT SAFETY INFORMATION
| WARNING: RISK OF HEART FAILURE MYQORZO reduces left ventricular ejection fraction (LVEF) and can cause heart failure due to systolic dysfunction. Echocardiogram assessments are required prior to and during treatment with MYQORZO to monitor for systolic dysfunction. Initiation of MYQORZO in patients with LVEF < Because of the risk of heart failure due to systolic dysfunction, MYQORZO is available only through a restricted program under a Risk Evaluation and Mitigation Strategy (REMS) called the MYQORZO REMS Program. |
CONTRAINDICATIONS
MYQORZO is contraindicated with concomitant use of rifampin.
WARNING AND PRECAUTIONS
Heart Failure
MYQORZO reduces cardiac contractility, which can reduce LVEF and cause heart failure.
Patients who experience a serious intercurrent illness (eg, serious infection) or arrhythmia (eg, new or uncontrolled atrial fibrillation) may be at greater risk of developing systolic dysfunction and heart failure.
Assess patients’ clinical status and LVEF prior to and during treatment and adjust the MYQORZO dose accordingly. New or worsening arrhythmia, dyspnea, chest pain, fatigue, leg edema, or elevations in N-terminal pro-B-type natriuretic peptide may be signs and symptoms of heart failure.
Initiation of MYQORZO in patients with LVEF <
MYQORZO REMS Program
MYQORZO is available only through a restricted program called the MYQORZO REMS Program, because of the risk of heart failure due to systolic dysfunction.
Notable requirements of the MYQORZO REMS Program include:
- Prescribers must be certified by enrolling in the MYQORZO REMS Program
- Patients must enroll in the MYQORZO REMS Program and comply with ongoing monitoring requirements
- Pharmacies must be certified by enrolling in the MYQORZO REMS Program and must only dispense to patients who are authorized to receive MYQORZO
- Wholesalers and distributors must only distribute to certified pharmacies
Further information is available at www.MYQORZOREMS.com, or at 1-844-285-7367.
Cytochrome P450 Interactions Leading to Heart Failure or Loss of Effectiveness
MYQORZO is metabolized primarily by CYP2C9, and to a lesser extent by CYP3A, CYP2D6, and CYP2C19 enzymes. Initiation of medications that inhibit multiple P450 pathways of MYQORZO elimination (eg, fluconazole, voriconazole, or fluvoxamine) or strong CYP2C9 inhibitors, and discontinuation of moderate-to-strong CYP3A inducers may lead to increased blood concentrations of aficamten and increase the risk of heart failure due to systolic dysfunction. Conversely, initiation of medications that induce P450 pathways of MYQORZO (eg, rifampin, moderate-to-strong CYP3A inducers) may lead to decreased blood concentrations of aficamten and potential loss of effectiveness. Assess LVEF 2 to 8 weeks after initiation of such inhibitors or after discontinuation of such inducers and adjust the dose of MYQORZO accordingly.
Advise patients of the potential for drug interactions. Advise patients to inform their healthcare provider of all concomitant medications prior to and during MYQORZO treatment.
ADVERSE REACTIONS
Hypertension (
Please see full Prescribing Information, including Boxed WARNING and Medication Guide.
About Hypertrophic Cardiomyopathy
Hypertrophic cardiomyopathy (HCM) is a disease in which the heart muscle becomes abnormally thick. HCM can be obstructive, when thickened muscle blocks blood flow, or non-obstructive, when blood flow is not blocked but heart function is still affected. In obstructive HCM, the thickening of cardiac muscle leads to the inside of the left ventricle becoming smaller, stiffer and less able to relax and fill with blood. Ultimately, HCM limits the heart’s pumping function, leading to reduced exercise capacity and a variety of symptoms.
HCM is the most common monogenic inherited cardiovascular disorder, with well over 300,000 patients diagnosed in the U.S.3 However, there are an estimated 400,000-800,000 additional patients who remain undiagnosed.4,5,6 Approximately half of patients with HCM have obstructive HCM (oHCM) and half have non-obstructive HCM (nHCM).3
People with HCM are at high risk of also developing cardiovascular complications including atrial fibrillation, stroke and mitral valve disease.7 People with HCM are at risk for potentially fatal ventricular arrhythmias and it is one of the leading causes of sudden cardiac death in younger people or athletes.8 A subset of patients with HCM are at high risk of progressive disease leading to dilated cardiomyopathy and heart failure necessitating cardiac transplantation.
About Cytokinetics
Cytokinetics is a specialty cardiovascular biopharmaceutical company, building on its over 25 years of pioneering scientific innovations in muscle biology, and advancing a pipeline of potential new medicines for patients suffering from diseases of cardiac muscle dysfunction. Cytokinetics’ MYQORZO™ (aficamten) is a cardiac myosin inhibitor approved in the U.S., Europe and China for the treatment of adults with symptomatic obstructive hypertrophic cardiomyopathy (oHCM). Aficamten is also being studied for the potential treatment of non-obstructive HCM. Cytokinetics is also developing omecamtiv mecarbil, an investigational cardiac myosin activator for the potential treatment of patients with heart failure with severely reduced ejection fraction and ulacamten, an investigational cardiac myosin inhibitor for the potential treatment of heart failure with preserved ejection fraction, while continuing pre-clinical research and development in muscle biology.
For additional information about Cytokinetics, visit www.cytokinetics.com and follow us on X, LinkedIn, Facebook and YouTube.
Forward-Looking Statements
This press release contains forward-looking statements for purposes of the Private Securities Litigation Reform Act of 1995 (the “Act”). Cytokinetics disclaims any intent or obligation to update these forward-looking statements and claims the protection of the Act's safe harbor for forward-looking statements. Examples of such statements include, but are not limited to, statements, express or implied, related to Cytokinetics’ research and development activities; clinical trial initiation, design, enrollment, conduct, progress, continuation, completion, timing and results; regulatory submissions, review processes, approval timing and outcomes, including with respect to supplemental applications and approvals in jurisdictions outside the United States; the scope, expansion, modification, durability or continuation of labeling and promotional claims; commercial readiness, launch timing, market access and reimbursement; anticipated patient, prescriber and payer adoption; expectations regarding market opportunity, growth and market share; pipeline development and expansion into additional indications or geographies; access to and use of capital; and Cytokinetics’ business strategy, objectives and future plans. Such statements are based on management's current expectations and assumptions; however, actual results may differ materially due to various risks and uncertainties, including, but not limited to, uncertainties inherent in drug development and commercialization; the timing, conduct and outcomes of clinical trials; regulatory review and approval processes in the United States and other jurisdictions; differences in regulatory requirements, labeling, market access or promotional restrictions across jurisdictions; the ability to obtain, expand, maintain or continue desired labeling, promotional claims or commercial positioning for approved products; potential legal, intellectual property or regulatory constraints affecting commercialization and marketing claims; patient and prescriber acceptance of MYQORZO as compared to alternative therapies; the availability and terms of reimbursement from commercial and government payers; manufacturing, supply and distribution risks; competition; and the availability of sufficient capital to execute Cytokinetics’ business plans. These forward-looking statements speak only as of the date they are made, and Cytokinetics undertakes no obligation to subsequently update any such statement, except as required by law. For further information regarding these and other risks related to Cytokinetics’ business, investors should consult Cytokinetics’ filings with the Securities and Exchange Commission (the “SEC”).
CYTOKINETICS® and the CYTOKINETICS C-shaped logo are registered trademarks of Cytokinetics in the U.S. and certain other countries.
MYQORZOTM is a trademark of Cytokinetics in the U.S., and a registered trademark in the European Union.
Contact:
Cytokinetics
Diane Weiser
Senior Vice President, Corporate Affairs
(415) 290-7757
References
- Maron, MS, et al. Aficamten for Symptomatic Obstructive Hypertrophic Cardiomyopathy. N Engl J Med. doi:10.1056/NEJMoa2401424
- Hartman JJ, Hwee DT, Roebrt-Paganin J, et al. Aficamten is a small-molecule cardiac myosin inhibitor designed to treat hypertrophic cardiomyopathy. Nat Cardiovasc Res. 2024;3(8) :1003-1016. doi:10.1038/s44161-024-00505-0
- Butzner M, et al. Epidemiology of Hypertrophic Cardiomyopathy in the United States From 2016 to 2023. JACC Adv. 2026. 2026;5(2):102552. doi:10.1016/j.jacadv.2025.102552
- CVrg: Heart Failure 2020-2029, p 44; Maron et al. 2013 doi:10.1016/S0140-6736(12)60397-3; Maron et al 2018 10.1056/NEJMra1710575
- Symphony Health 2016-2021 Patient Claims Data DoF;
- Maron MS, Hellawell JL, Lucove JC, Farzaneh-Far R, Olivotto I. Occurrence of Clinically Diagnosed Hypertrophic Cardiomyopathy in the United States. Am J Cardiol. 2016; 15;117(10):1651-1654.
- Gersh, B.J., Maron, B.J., Bonow, R.O., Dearani, J.A., Fifer, M.A., Link, M.S., et al. 2011 ACCF/AHA guidelines for the diagnosis and treatment of hypertrophic cardiomyopathy. A report of the American College of Cardiology Foundation/American Heart Association Task Force on practice guidelines. Journal of the American College of Cardiology and Circulation, 58, e212-260.
- Hong Y, Su WW, Li X. Risk factors of sudden cardiac death in hypertrophic cardiomyopathy. Current Opinion in Cardiology. 2022 Jan 1;37(1):15-21
