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Cytokinetics Announces Preclinical Data for CK-3773274 and CK-3772271 Presented at the AHA Scientific Sessions 2020

New Findings from Studies of Cardiac Myosin Inhibitors in Animal Models of Hypertrophic Cardiomyopathy and Heart Failure with Preserved Ejection Fraction

articleCytokinetics, IncorporatedNovember 16, 20203/company/cytokinetics-inc/news/cytokinetics-announces-preclinical-data-for-ck-3773274-and-ck-3772271-presented-at-the-aha-scientific-sessions-2020
Cytokinetics Announces Preclinical Data for CK-3773274 and CK-3772271 Presented at the AHA Scientific Sessions 2020

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[{"type":"text","content":"New Findings from Studies of Cardiac Myosin Inhibitors in Animal Models of Hypertrophic Cardiomyopathy and Heart Failure with Preserved Ejection Fraction\nSOUTH SAN FRANCISCO, Calif., Nov. 16, 2020 (GLOBE NEWSWIRE) -- Cytokinetics, Incorporated (Nasdaq: CYTK) today announced that preclinical data for CK-3773274 (CK-274) and CK-3772271 (CK-271) were shared in poster presentations at the American Heart Association (AHA) Scientific Sessions 2020. CK-274 reduced contractility and left ventricular outflow tract (LVOT) peak pressure gradient in cats with naturally occurring hypertrophic cardiomyopathy (HCM) and left ventricular outflow tract obstruction (LVOTO). In the Dahl/Salt sensitive rat model of heart failure with preserved ejection fraction (HFpEF), CK-271 attenuated the development of fibrosis and diastolic dysfunction.\n “We’re pleased to share preclinical data that builds on the growing body of evidence for our pipeline of cardiac myosin inhibitors,” said Brad Morgan, Ph.D., Cytokinetics’ Senior Vice President, Research and Non-Clinical Development. “Collectively, these data demonstrate the potential of this mechanism of action to reduce or arrest the development of cardiac hypercontractility in animal models which may support application in patients with diseases of hypercontractility including HCM and HFpEF.” Previous preclinical data has shown that CK-274 produces exposure related effects on cardiac contractility in healthy animals and mouse models of HCM. New preclinical data demonstrated dose-related changes in left ventricular (LV) systolic function and reductions in LVOT peak pressure gradient in cats with naturally occurring HCM and LVOTO due to the A31P mutation in cardiac myosin binding protein C (cMyBP-C). Treatment with CK-274 (1 mg/kg) reduced mean left ventricular (LV) fractional shortening at 6, 24, and 48 hours post-treatment (mean reduction 13.6%, p = 0.03; 15.4%, p = 0.01; 11.6%, p = 0.02, respectively). In addition to lowering the hypercontractility in cats with naturally occurring HCM and LVOTO, CK-274 reduced the left ventricular outflow tract peak pressure gradient in concentration related manner (median pressure gradient at baseline 27.1 mmHg [interquartile range {IQR} 18.3–33.3] vs 24 hours post-drug, 7.3 mmHg [IQR 14.2–19.7], p= 0.01). CK-274 was well tolerated and no changes in heart rate were obser...

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