Full Press Release Details
SOUTH SAN FRANCISCO, Calif., Jan. 18, 2024 (GLOBE NEWSWIRE) -- Cytokinetics, Incorporated (Nasdaq: CYTK) today announced an upcoming presentation at CMR 2024 taking place online and in person in London, UK from January 25-27, 2024.
Title: Effect of Aficamten on Structure and Function in Patients with Obstructive Hypertrophic Cardiomyopathy: The FOREST-HCM CMR Sub-study
Presenter: Ahmad Masri, M.D., MS, Director of the Hypertrophic Cardiomyopathy Center at Oregon Health & Science University
Date: January 25, 2024
Session Title: Rapid Fire – Large Clinical Trials and Registries
Session Time: 2:40 – 3:40 PM GMT
Presentation Time: 2:55 – 3:00 PM GMT
Location: Kiosk 6R-TC-04, Cambridge
Cytokinetics is a late-stage, specialty cardiovascular biopharmaceutical company focused on discovering, developing and commercializing first-in-class muscle activators and next-in-class muscle inhibitors as potential treatments for debilitating diseases in which cardiac muscle performance is compromised. As a leader in muscle biology and the mechanics of muscle performance, the company is developing small molecule drug candidates specifically engineered to impact myocardial muscle function and contractility. Cytokinetics is preparing for regulatory interactions for aficamten, its next-in-class cardiac myosin inhibitor, following positive topline results from SEQUOIA-HCM, the pivotal Phase 3 clinical trial in obstructive hypertrophic cardiomyopathy. Aficamten is also currently being evaluated in two ongoing Phase 3 clinical trials: MAPLE-HCM, evaluating aficamten as monotherapy compared to metoprolol as monotherapy in patients with obstructive HCM and ACACIA-HCM, evaluating aficamten in patients with non-obstructive HCM. Cytokinetics is also developing omecamtiv mecarbil, a cardiac muscle activator, in patients with heart failure. Additionally, Cytokinetics is developing CK-136, a cardiac troponin activator for the potential treatment HFrEF and other types of heart failure, such as right ventricular failure, resulting from impaired cardiac contractility, and CK-586, a cardiac myosin inhibitor with a mechanism of action distinct from aficamten for the potential treatment of HFpEF.
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