{"id":998900,"date":"2026-08-29T10:33:08","date_gmt":"2026-08-29T14:33:08","guid":{"rendered":"https:\/\/www.marketnewsdesk.com\/index.php\/cytokinetics-announces-additional-results-from-acacia-hcm-and-maple-hcm-presented-in-late-breaking-clinical-trial-session-at-the-european-society-of-cardiology-esc-congress-2026\/"},"modified":"2026-08-29T10:33:08","modified_gmt":"2026-08-29T14:33:08","slug":"cytokinetics-announces-additional-results-from-acacia-hcm-and-maple-hcm-presented-in-late-breaking-clinical-trial-session-at-the-european-society-of-cardiology-esc-congress-2026","status":"publish","type":"post","link":"https:\/\/www.marketnewsdesk.com\/index.php\/cytokinetics-announces-additional-results-from-acacia-hcm-and-maple-hcm-presented-in-late-breaking-clinical-trial-session-at-the-european-society-of-cardiology-esc-congress-2026\/","title":{"rendered":"Cytokinetics Announces Additional Results from ACACIA-HCM and MAPLE-HCM Presented in Late Breaking Clinical Trial Session at the European Society of Cardiology (ESC) Congress 2026"},"content":{"rendered":"
\n

\n Additional Results from ACACIA-HCM Demonstrate Improvements in\u00a0<\/em>
\n Cardiac Structure and Diastolic Function in Patients with Non-Obstructive HCM<\/em>\n <\/p>\n

\n New Analysis of MAPLE-HCM Finds Aficamten Outperformed Metoprolol Across Pre-Trial Treatment Groups in Patients with Obstructive HCM<\/em>\n <\/p>\n

SOUTH SAN FRANCISCO, Calif., Aug. 29, 2026 (GLOBE NEWSWIRE) — Cytokinetics, Incorporated (Nasdaq: CYTK) today announced that additional results from ACACIA-HCM (A<\/strong>ssessment C<\/strong>omparing A<\/em><\/strong>ficamten<\/em> to Placebo on C<\/strong>ardiac Endpoints I<\/strong>n A<\/strong>dults with Non-Obstructive HCM<\/strong>) and MAPLE-HCM (M<\/em><\/strong>etoprolol<\/em> vs A<\/em><\/strong>ficamten<\/em> in P<\/strong>atients with L<\/strong>VOT Obstruction on E<\/strong>xercise Capacity in HCM<\/strong>) were presented in a Late Breaking Clinical Session at the European Society of Cardiology (ESC) Congress 2026 in Munich, Germany and simultaneously published in Circulation<\/em> and the Journal of the American College of Cardiology: Heart Failure<\/em>, respectively.<\/p>\n

\u201cThe findings from these additional analyses of ACACIA-HCM and MAPLE-HCM elaborate on the primary results from each trial and expand the body of evidence supporting the potential use of aficamten<\/em> across the spectrum of HCM,\u201d said Stephen Heitner, M.D., Cytokinetics\u2019 Chief Medical Officer. \u201cIn particular, the additional results from ACACIA-HCM suggest that the benefits of aficamten<\/em> in non-obstructive HCM extend beyond exercise capacity and symptom burden to also include improvements in wall thickness and diastolic function, pointing to the potential mechanisms by which aficamten<\/em> is effective in these patients. Given the lack of approved therapies for non-obstructive HCM, these findings highlight the potential impact aficamten<\/em> could have on this population independent from relief of left ventricular outflow tract obstruction.\u201d<\/p>\n

\n ACACIA-HCM: Effect of <\/strong>
\n
\n Aficamten<\/em>
\n <\/strong>
\n on Cardiac Structure and Function in Patients with Symptomatic Non-Obstructive HCM<\/strong>\n <\/p>\n

Results from a pre-specified exploratory analysis of ACACIA-HCM, the Phase 3 clinical trial of aficamten <\/em>in patients with symptomatic non-obstructive hypertrophic cardiomyopathy (nHCM), were presented in a Late Breaking Clinical Trial Session and simultaneously published in Circulation<\/em><\/a>.1<\/sup><\/p>\n

As previously reported, the primary results from ACACIA-HCM showed that treatment with aficamten<\/em> was associated with significant improvements from baseline to Week 36 compared to placebo in both Kansas City Cardiomyopathy Questionnaire Clinical Summary Score (KCCQ-CSS) and maximal exercise performance (pVO2<\/sub>). This analysis showed that treatment with aficamten<\/em> also demonstrated improvements in measures of cardiac structure and diastolic function at the time of the primary analysis (36 weeks) and at end of treatment (EOT) (up to 72 weeks; median time to end of treatment = 49 weeks).<\/p>\n

At Week 36 and at EOT, aficamten<\/em> significantly improved measures of diastolic function including peak E velocity (p=0.001 and p=0.034, respectively) and septal e\u2019 velocity (p<0.001 for both), suggesting improvement in myocardial relaxation and enhanced early diastolic filling. Septal E\/e\u2019 showed a trend towards improvement at Week 36 (p=0.07), and a statistically significant improvement at EOT (p<0.001). Similarly, left atrial volume index (LAVI) showed a trend toward stabilization at Week 36 (p=0.06) and a statistically significant improvement with longer treatment exposure at EOT (p=0.022). These results in patients with nHCM show that aficamten<\/em> improves diastolic function independent of reducing left ventricular outflow tract (LVOT) obstruction, providing support for the importance of diastolic function as the potential underlying mechanism for the improvements in functional capacity and symptom relief in this population.<\/p>\n

\n Aficamten<\/em> was associated with a modest but statistically significant (p<0.001) reduction in systolic function as measured by left ventricular ejection fraction (LVEF) which remained within normal range at EOT. Left ventricular wall thickness decreased by 0.2 cm at EOT (p<0.001) while left ventricular end-systolic and end-diastolic left ventricular volumes increased (p<0.001).<\/p>\n

\n MAPLE-HCM: <\/strong>
\n
\n Aficamten<\/em>
\n <\/strong>
\n vs. <\/strong>
\n
\n Metoprolol<\/em>
\n <\/strong>
\n in Obstructive HCM According to Pre-Trial Treatment <\/strong>\n <\/p>\n

Results of a post-hoc analysis from MAPLE-HCM, the Phase 3 clinical trial of aficamten<\/em> compared to metoprolol<\/em> in patients (n=175) with symptomatic obstructive HCM (oHCM), were presented in a Late Breaking Clinical Trial Session and simultaneously published in the Journal of the American College of Cardiology: Heart Failure<\/em>.<\/a>2<\/sup><\/p>\n

As previously reported, the primary results of MAPLE-HCM demonstrated superiority of aficamten<\/em> to metoprolol<\/em> on pVO2<\/sub> (change from baseline to Week 24, least squares mean (LSM) treatment difference (SE), +2.3 (0.39) mL\/kg\/min, p<0.001). This post-hoc analysis evaluated the effect of treatment with aficamten <\/em>or metoprolol<\/em> on the primary endpoint and key secondary endpoints according to pre-trial medical therapy.<\/p>\n

At screening, 123 patients were taking a beta blocker while 52 patients were not taking a beta blocker. Of the 52 patients not taking a beta blocker at screening, 22 patients had received no standard of care therapy for at least 12 months before screening. Prior to randomization, all patients underwent a two-week washout period of standard of care therapy.<\/p>\n

Independent of pre-trial medical therapy, aficamten<\/em> demonstrated a consistent treatment effect across multiple efficacy endpoints compared with metoprolol<\/em>. Aficamten<\/em> improved pVO2<\/sub> compared with metoprolol<\/em> for patients not previously taking beta blockers (LSM difference +3.1 mL\/kg\/min, p<0.001), as well as for patients previously taking beta blockers (LSM difference +1.9 mL\/kg\/min, p<0.001) with no difference between groups in the improvement (interaction p = 0.133).<\/p>\n

Similarly, compared to metoprolol<\/em>, aficamten<\/em> significantly improved key secondary endpoints independent of pre-trial treatment, including KCCQ-CSS and New York Heart Association (NYHA) Functional Class, Valsalva left ventricular outflow tract gradient (LVOT-G) and NT-proBNP.<\/p>\n

There were no differences in the safety profile of aficamten<\/em>, including the rates of serious adverse events, between pre-trial treatment groups.<\/p>\n

\n About ACACIA-HCM<\/strong>\n <\/p>\n

ACACIA-HCM was a Phase 3, multi-center, randomized, double-blind, placebo-controlled clinical trial designed to evaluate the effect of aficamten <\/em>compared to placebo in patients with symptomatic non-obstructive hypertrophic cardiomyopathy (nHCM). The dual primary endpoint was the change in Kansas City Cardiomyopathy Questionnaire (KCCQ) Clinical Summary Score\u00a0and change in maximal exercise performance (peak VO2<\/sub>) from baseline to Week 36.<\/p>\n

Secondary endpoints included the proportion of participants with \u22651 class improvement in NYHA functional class, and changes in the composite z-score of two cardiopulmonary exercise testing (CPET) parameters of sub-maximal exercise performance (VE\/VCO2 <\/sub>and pVO2<\/sub>), NT-proBNP, and left atrial volume index (LAVI) from baseline to Week 36. After 36 weeks of treatment, participants continued treatment with aficamten<\/em> or placebo for up to 72 weeks to evaluate additional secondary and exploration analyses including the time to first cardiovascular event. The trial (outside Japan) concluded when at least 200 patients completed 52 weeks of treatment.<\/p>\n

ACACIA-HCM randomized and treated 517 participants (outside Japan) on a 1:1 basis with aficamten<\/em> or placebo. Randomization was stratified by persistent atrial fibrillation and presence of intracavitary obstruction. At screening, participants enrolled in ACACIA-HCM were required to have resting left ventricular outflow tract gradient (LVOT-G) <30 mmHg and post-Valsalva LVOT-G <50 mmHg in addition to left ventricular ejection fraction (LVEF) \u226560%, respiratory exchange ratio (RER) \u22651.00 and peak VO2<\/sub> \u226490% predicted, NT-proBNP \u2265300 pg\/mL or \u2265900 pg\/mL if atrial fibrillation or atrial flutter were present at screening, NYHA functional class II or III and KCCQ Clinical Summary Score \u226485.<\/p>\n

Each patient received up to four escalating doses of aficamten <\/em>or placebo based on echocardiographic guidance. Participants who received aficamten<\/em> began with 5 mg dosed once daily. At weeks 2, 4 and 6 participants received an echocardiogram to determine if they would be up-titrated to escalating doses of 10, 15 or 20 mg. Dose escalation occurred only if a participant had an LVEF \u226560%. Participants who did not meet escalation criteria continued the same dose or were down-titrated if their LVEF was <50%.<\/p>\n

\n About MAPLE-HCM<\/strong>\n <\/p>\n

MAPLE-HCM was a Phase 3, multi-center, randomized, double-blind active-comparator clinical trial of aficamten<\/em> compared to metoprolol<\/em> in patients with symptomatic obstructive HCM (oHCM). The primary endpoint was the change in peak oxygen uptake (pVO2<\/sub>) from baseline to Week 24 measured by cardiopulmonary exercise testing (CPET). Secondary endpoints include the change from baseline to Week 24 in Kansas City Cardiomyopathy Questionnaire (KCCQ) score, the proportion of patients with \u22651 class improvement in New York Heart Association (NYHA) functional class, and changes in left ventricular mass index (LVMI), left atrial volume index (LAVI), post-Valsalva left ventricular outflow tract gradient (LVOT-G) and NT-proBNP.<\/p>\n

MAPLE-HCM enrolled 175 patients, randomized on a 1:1 basis to receive aficamten<\/em> or metoprolol <\/em>as monotherapy in a double-blind, double dummy fashion. Randomization was stratified by CPET exercise modality (treadmill or bicycle) and recently diagnosed versus chronic obstructive HCM. At screening, patients enrolled in MAPLE-HCM had a resting LVOT-G \u226530 mmHg and\/or post-Valsalva LVOT-G \u226550 mmHg in addition to left ventricular ejection fraction (LVEF) \u2265 60%, respiratory exchange ratio (RER) \u2265 1.05 and pVO2 <100% predicted, NYHA functional class II or III and a KCCQ Clinical Summary Score (KCCQ-CSS) score \u2265 35 and \u2264 90. Following the initial screening visit, all participants on standard of care (SOC) therapy underwent a washout period of up to 14 days to wean from SOC therapy, followed by an additional 7 days with no SOC therapy prior to the second screening visit. Each patient received up to four escalating doses of aficamten<\/em> or metoprolol<\/em> based on echocardiographic guidance as well as a matching placebo for the alternate therapy.<\/p>\n

\n About MYQORZO\u00ae (<\/strong>
\n
\n aficamten<\/em>
\n <\/strong>
\n )<\/strong>\n <\/p>\n

MYQORZO\u00ae<\/sup> (aficamten<\/em>) is a cardiac myosin inhibitor approved in the U.S., China, European Union and United Kingdom 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.3<\/sup><\/p>\n

\n Aficamten <\/em>is also under clinical investigation in CEDAR-HCM in a pediatric population with oHCM. Safety and efficacy of aficamten<\/em> have not been established in a pediatric patient population. In addition, aficamten<\/em> is being studied in FOREST-HCM, an open-label extension clinical study.<\/p>\n

\n INDICATION <\/strong>\n <\/p>\n

MYQORZO is indicated for the treatment of adults with symptomatic obstructive hypertrophic cardiomyopathy (oHCM) to improve functional capacity and symptoms.<\/p>\n

\n IMPORTANT SAFETY INFORMATION<\/strong>\n <\/p>\n\n\n
\n WARNING: RISK OF HEART FAILURE<\/strong><\/p>\n

MYQORZO reduces left ventricular ejection fraction (LVEF) and can cause heart failure due to systolic dysfunction.<\/strong><\/p>\n

Echocardiogram assessments are required prior to and during treatment with MYQORZO to monitor for systolic dysfunction. Initiation of MYQORZO in patients with LVEF <55% is not recommended. Decrease the dose of MYQORZO if LVEF is <50% and \u226540%. Interrupt the dose of MYQORZO if LVEF <40% or if the patient experiences heart failure symptoms or worsening clinical status due to systolic dysfunction<\/strong>
\n
\n .<\/em>
\n <\/strong><\/p>\n

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.<\/strong>\n <\/td>\n<\/tr>\n<\/table>\n

\n
\n
CONTRAINDICATIONS <\/strong>\n <\/p>\n

MYQORZO is contraindicated with concomitant use of rifampin.<\/p>\n

\n WARNINGS AND PRECAUTIONS<\/strong>\n <\/p>\n

\n Heart Failure<\/strong>\n <\/p>\n

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.<\/p>\n

Assess patients\u2019 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.<\/p>\n

Initiation of MYQORZO in patients with LVEF <55% is not recommended.<\/p>\n

\n MYQORZO REMS Program <\/strong>\n <\/p>\n

MYQORZO is available only through a restricted program called the MYQORZO REMS Program, because of the risk of heart failure due to systolic dysfunction.<\/p>\n

Notable requirements of the MYQORZO REMS Program include:<\/p>\n