{"id":1018675,"date":"2026-11-09T07:49:35","date_gmt":"2026-11-09T12:49:35","guid":{"rendered":"https:\/\/www.marketnewsdesk.com\/index.php\/cytokinetics-announces-additional-data-related-to-aficamten-presented-at-the-hypertrophic-cardiomyopathy-medical-society-hcms-scientific-sessions-held-in-collaboration-with-the-american-heart-associ\/"},"modified":"2026-11-09T07:49:35","modified_gmt":"2026-11-09T12:49:35","slug":"cytokinetics-announces-additional-data-related-to-aficamten-presented-at-the-hypertrophic-cardiomyopathy-medical-society-hcms-scientific-sessions-held-in-collaboration-with-the-american-heart-associ","status":"publish","type":"post","link":"https:\/\/www.marketnewsdesk.com\/index.php\/cytokinetics-announces-additional-data-related-to-aficamten-presented-at-the-hypertrophic-cardiomyopathy-medical-society-hcms-scientific-sessions-held-in-collaboration-with-the-american-heart-associ\/","title":{"rendered":"Cytokinetics Announces Additional Data Related to Aficamten Presented at the Hypertrophic Cardiomyopathy Medical Society (HCMS) Scientific Sessions Held in Collaboration with the American Heart Association Scientific Sessions 2026"},"content":{"rendered":"
\n

\n New Analyses Across Obstructive and Non-obstructive HCM Expand Clinical Evidence for Aficamten<\/em>\n <\/p>\n

SOUTH SAN FRANCISCO, Calif., Nov. 09, 2026 (GLOBE NEWSWIRE) — Cytokinetics, Incorporated (Nasdaq: CYTK) today announced that new data related to\u00a0aficamten<\/em> were presented at the Hypertrophic Cardiomyopathy Medical Society (HCMS) Scientific Sessions held in collaboration with the American Heart Association Scientific Sessions 2026 in Chicago, IL including two late-breaking oral abstracts with additional data from ACACIA-HCM, and one poster presentation with new data from FOREST-HCM.<\/p>\n

\u201cThe new data further enrich the growing body of clinical evidence establishing aficamten<\/em> as a potentially paradigm-shifting therapy across the spectrum of hypertrophic cardiomyopathy,\u201d said Stephen Heitner, M.D., Cytokinetics\u2019 Chief Medical Officer. \u201cThe advanced imaging data provide crucial insights into favorable cardiac remodeling, showing that aficamten<\/em> may reduce key structural markers of the disease. Concurrently, additional data highlights meaningful improvements in self-reported measures of symptom burden and quality of life. Together, these data deepen our understanding of the biological effects of MYQORZO\u00ae<\/sup> and associated potential clinical benefit.\u201d<\/p>\n

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

New data from the pre-specified cardiac magnetic resonance (CMR) imaging sub-study of ACACIA-HCM characterized the effects of aficamten<\/em> on cardiac structure in patients with non-obstructive hypertrophic cardiomyopathy (nHCM). After 36 weeks of treatment, aficamten<\/em> was associated with favorable cardiac remodeling in patients with symptomatic nHCM. Patients treated with aficamten<\/em> experienced statistically significant (p<0.001) reductions in left ventricular mass index (LVMI) and left ventricular wall thickness compared to placebo (Figure 1).<\/p>\n

\n Figure 1: Changes Associated with Favorable Cardiac Remodeling<\/strong>\n <\/p>\n

\n \n <\/p>\n

The reduction in LVMI was driven by a decrease in myocardial cellular mass, with no significant changes observed in measures of extracellular matrix or myocardial fibrosis. Furthermore, these structural improvements correlated with significant decreases in N-terminal pro-B-type natriuretic peptide (NT-proBNP) and high-sensitivity troponin I, established biomarkers of cardiac wall stress and myocardial injury, respectively. This analysis is evidence that the beneficial structural remodeling occurring is somewhat independent from relief of obstruction, and as a direct effect of aficamten<\/em> on the myocardium.<\/p>\n

\n ACACIA-HCM: Effect of <\/strong>
\n
\n Aficamten<\/em>
\n <\/strong>
\n on Patient-Reported Health Status in nHCM<\/strong>\n <\/p>\n

New analyses from ACACIA-HCM evaluated the long-term impact of aficamten<\/em> on patient-reported health status utilizing the Kansas City Cardiomyopathy Questionnaire Overall Summary Score (KCCQ-OSS), a broader measure of patient experience than the primary endpoint measure of KCCQ Clinical Summary Score (KCCQ-CSS). The data showed that aficamten<\/em> improved patient-reported health status in patients with nHCM, with treatment effects observed across symptoms, physical limitations, quality of life and social function. At Week 36, patients receiving aficamten<\/em> showed a 4.0-point greater improvement in KCCQ-OSS relative to placebo, and using the clinically accepted thresholds, more patients experienced improvements (33.7% vs. 22.5% respectively) and fewer experienced deterioration (7.4% vs. 13.3% respectively). Authors also demonstrated that there appears to be a greater between-group difference with increasing time, through to Week 72 (Figure 2). Importantly, following treatment withdrawal, these effects declined within four weeks, with no differences remaining at the end of the study.<\/p>\n

\n Figure 2: Change in KCCQ-OSS<\/strong>\n <\/p>\n

\n \n <\/p>\n

\n FOREST-HCM:<\/strong>
\n Left Ventricular Systolic Dysfunction in Long-Term <\/strong>
\n
\n Aficamten<\/em>
\n <\/strong>
\n Therapy for oHCM<\/strong>\n <\/p>\n

Published in Journal of Cardiac Failure<\/em>, long-term data from FOREST-HCM, the open-label extension study of aficamten<\/em>, further expands the clinical evidence of the sustained safety and tolerability profile of aficamten<\/em> in patients with oHCM.1<\/sup><\/p>\n

This analysis showed that among 410 patients with oHCM, 12 (2.9%) developed a left ventricular ejection fraction (LVEF) <50% and none with LVEF <40%, representing 2.1 events per 100 patient-years. There were no heart failure hospitalizations or deaths associated with systolic dysfunction and the episodes were transient, asymptomatic, and rapidly reversible after dose reduction or temporary interruption. Lastly, the investigators demonstrated that borderline LVEF (\u226550% to <55%) was clinically benign and did not require dose adjustment or intervention.<\/p>\n

\n About MYQORZO<\/strong>
\n
\n \u00ae<\/strong>
\n <\/sup>
\n (<\/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, United Kingdom and Canada 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 studied in ACACIA-HCM, a completed Phase 3 clinical trial of aficamten<\/em> in patients with nHCM. 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