{"id":1009353,"date":"2026-10-12T16:05:49","date_gmt":"2026-10-12T20:05:49","guid":{"rendered":"https:\/\/www.marketnewsdesk.com\/index.php\/cytokinetics-announces-additional-data-from-acacia-hcm-presented-at-the-hfsa-annual-scientific-meeting-2026\/"},"modified":"2026-10-12T16:05:49","modified_gmt":"2026-10-12T20:05:49","slug":"cytokinetics-announces-additional-data-from-acacia-hcm-presented-at-the-hfsa-annual-scientific-meeting-2026","status":"publish","type":"post","link":"https:\/\/www.marketnewsdesk.com\/index.php\/cytokinetics-announces-additional-data-from-acacia-hcm-presented-at-the-hfsa-annual-scientific-meeting-2026\/","title":{"rendered":"Cytokinetics Announces Additional Data from ACACIA-HCM Presented at the HFSA Annual Scientific Meeting 2026"},"content":{"rendered":"
\n

\n Additional Analyses from ACACIA-HCM Further Characterize Exercise Performance, Treatment Effect, Dose Titration and Safety of Aficamten in Non-Obstructive HCM<\/em>\n <\/p>\n

SOUTH SAN FRANCISCO, Calif., Oct. 12, 2026 (GLOBE NEWSWIRE) — Cytokinetics, Incorporated (Nasdaq: CYTK) today announced that additional data 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>) were presented at the Heart Failure Society of America (HFSA) Annual Scientific Meeting 2026 in Phoenix, AZ.<\/p>\n

\u201cThese additional analyses from ACACIA-HCM add to the body of evidence supporting the overall benefit-risk profile of aficamten<\/em> in patients with nHCM,\u201d said Stephen Heitner, M.D., Cytokinetics\u2019 Chief Medical Officer. \u201cThe current CPET analysis demonstrates significant improvement in a clinically relevant and novel metric of global exercise performance, while additional data provide insights into dose titration and reinforce our confidence in the safety and treatment effect of aficamten<\/em> in nHCM. We plan to submit a supplemental New Drug Application to the FDA this quarter.\u201d<\/p>\n

\n ACACIA-HCM: Effect of <\/strong>
\n
\n Aficamten<\/em>
\n <\/strong>
\n on Comprehensive Exercise Performance <\/strong>\n <\/p>\n

Data from a prespecified analysis of comprehensive exercise performance from ACACIA-HCM were presented in a Late Breaking Clinical Trial Presentation. This analysis examined the effect of aficamten <\/em>on multiple exercise parameters using the novel 2026 Boston Exercise Aggregate Physiologic Response Score (BEAP-RS). The score captures outputs from five individual domains, ranging from submaximal exercise through to recovery, and generates a composite of global exercise performance. At 36 weeks, treatment with aficamten<\/em> significantly improved BEAP-RS compared to placebo (p<0.001), with improvements in individual exercise and recovery measures across all five domains. Improvement in BEAP-RS correlated significantly with improvements in health status measured by both Kansas City Cardiomyopathy Questionnaire Clinical Summary Score (KCCQ-CSS) (p = 0.001) and New York Heart Association (NYHA) Functional Class (p = 0.001), as well as the cardiac biomarker NT-proBNP (p<0.001). This analysis provides a greater understanding of the complete impact of aficamten <\/em>on exercise capacity in patients with non-obstructive HCM (nHCM).<\/p>\n

\n ACACIA-HCM: Global Efficacy Responder Analysis<\/strong>\n <\/p>\n

Data from a responder analysis of ACACIA-HCM evaluating the global efficacy of aficamten<\/em> in patients with symptomatic nHCM were presented in a Late Breaking Clinical Trial Presentation. The results were published in Circulation <\/em>in August 2026.1<\/sup> The analysis assessed clinical improvements across five key domains. At 36 weeks, a greater proportion of patients treated with aficamten<\/em> demonstrated a clinically meaningful response compared to placebo in all five domains, with statistically significant improvements in four domains: relief of limiting symptoms, decrease in left atrial volume index (LAVI), increase in septal e\u2019 velocity and \u226550% reduction in NT-proBNP (all p<0.05). An increase in peak VO2<\/sub> of at least 0.5 mL\/kg\/min was observed in 45% of patients on aficamten<\/em> compared to 37% on placebo (p=0.1). Overall, 53% of patients on aficamten<\/em> demonstrated a clinical response in three or more domains compared to only 13% of patients on placebo (p<0.001). These data place the primary results into clinical context and underscore the opportunity to impact several aspects of disease burden by addressing the underlying pathobiology in patients living with symptomatic nHCM.<\/p>\n

\n ACACIA-HCM: Dose Titration and Safety<\/strong>\n <\/p>\n

Data related to dose titration and the safety profile of aficamten<\/em> in ACACIA-HCM were also presented. At the end of the titration period, 80.7% of patients were on 15 or 20 mg. Dose titration led to predictable, dose-proportional changes in plasma concentration of aficamten<\/em> and reductions in left ventricular ejection fraction (LVEF), which then remained stable from Week 8 through Week 36. LVEF <50% occurred in 27 (10.5%) patients taking aficamten<\/em> and in two (0.8%) patients taking placebo. The only patient characteristics associated with LVEF <50% were lower baseline LVEF and permanent atrial fibrillation. As previously reported, two participants on aficamten<\/em> experienced a serious adverse event (SAE) of heart failure associated with LVEF <50%. Ten additional patients on aficamten<\/em> had SAEs of heart failure not associated with LVEF <50%, for a total of 12 patients (4.7%) compared to three patients (1.2%) on placebo. All heart failure events in patients treated with aficamten<\/em> occurred during dose titration or prior to Week 12, often following a precipitating event such as rapid atrial fibrillation or infection, and responded to typical medical therapy such as diuretics. Overall, these data suggest that, in ACACIA-HCM, titration of aficamten<\/em> to the maximum tolerated dose based on LVEF alone was generally well tolerated in the great majority of patients with nHCM.<\/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.2<\/sup><\/p>\n

\n Aficamten <\/em>was also evaluated in a pivotal Phase 3 clinical trial, ACACIA-HCM, in patients with non-obstructive HCM (nHCM), which met both dual primary endpoints, demonstrating statistically significant improvements in both dual primary endpoints of Kansas City Cardiomyopathy Questionnaire Clinical Summary Score (KCCQ-CSS) and maximal exercise performance (pVO2<\/sub>). Statistically significant improvements compared to placebo were also observed in key secondary endpoints. There were no new safety signals identified. Left ventricular ejection fraction (LVEF) <50% occurred in 10% of participants taking aficamten<\/em> and in 1% of participants taking placebo. Overall, 12 (4.7 %) patients on aficamten<\/em> had serious adverse events of heart failure compared to three patients (1.2%) on placebo.<\/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\n\n
\u00a0<\/td>\n<\/tr>\n
\n WARNING: RISK OF HEART FAILURE<\/strong>\n <\/td>\n<\/tr>\n
\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

\u00a0<\/td>\n<\/tr>\n<\/table>\n

\n CONTRAINDICATIONS\u00a0<\/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