SOUTH SAN FRANCISCO, CA, Sep. 15, 2009 (Marketwire) --
SOUTH SAN FRANCISCO, CA -- (Marketwire) -- 09/15/09 -- Cytokinetics, Incorporated (NASDAQ: CYTK) announced today that data relating to two Phase IIa clinical trials evaluating omecamtiv mecarbil (formerly CK-1827452), one in stable heart failure patients and one in patients with ischemic cardiomyopathy and angina, were presented in three poster presentations at the 2009 Heart Failure Society of America Annual Meeting in Boston, Massachusetts.
"We are pleased to present these data at the largest annual gathering of heart failure specialists in the United States. Over 5 million people in the United States alone suffer from heart failure, which, despite recent advances in treatment, remains a debilitating disease that increasingly contributes to the medical and economic burdens that are currently the subject of an intense scientific and political debate in our country," stated Andrew A. Wolff, MD, FACC, Cytokinetics' Senior Vice President of Clinical Research and Development and Chief Medical Officer. "Together with our partner, Amgen, we look forward to progressing omecamtiv mecarbil into additional clinical trials, in order to further evaluate this novel drug candidate in patients with a diagnosis of heart failure."
Poster Presentations
A poster titled, "An Analysis of the Response to CK-1827452, a Selective Cardiac Myosin Activator, in Stable Heart Failure Patients Stratified by Baseline Cardiac Function" was presented on Monday, September 14, by Fady Malik, MD, PhD, FACC, Vice President, Biology and Therapeutics, Cytokinetics, Inc., South San Francisco, California. The primary objective of our clinical trial was to evaluate the safety and tolerability of omecamtiv mecarbil administered as an intravenous infusion to stable heart failure patients. This analysis compared the response to omecamtiv mecarbil in the patient sub-group with more severely depressed cardiac function to those with more preserved cardiac function. The authors concluded that patients with reduced stroke volumes ( < 50 mL) at baseline had pharmacodynamic responses to omecamtiv mecarbil that were generally greater than those in patients with greater stroke volumes at baseline, demonstrating pharmacodynamic activity in this more severely affected sub-population of patients from the study. Statistically significant increases in systolic ejection time, stroke volume, cardiac output, fractional shortening, and ejection fraction occurred across the population in a concentration-dependent manner. In addition, the data demonstrated statistically significant correlations between increasing omecamtiv mecarbil plasma concentration and decreases in left ventricular end-systolic volume and left ventricular end-diastolic volume as well as heart rate. The authors concluded that these findings support further study in a larger patient population, and translation of this novel and unique mechanism into higher-risk populations with heart failure.
A poster titlted, "Phase II Safety Study Evaluating the Novel Cardiac Myosin Activator, CK-1827452, in Patients with Ischemic Cardiomyopathy and Angina" was presented on Tuesday, September 15, 2009 by Will Chou, MD, Medical Director, Cytokinetics, Inc., South San Francisco, California. This poster presentation included data from a double-blind, randomized, placebo-controlled Phase IIa clinical trial evaluating the effect of omecamtiv mecarbil on symptom-limited exercise tolerance in heart failure patients with ischemic cardiomyopathy and angina, and included a detailed public disclosure of specific adverse events in the trial. Previously, these data were summarized in a poster presentation at the 2009 Heart Failure Congress of the European Society of Cardiology, held in Nice, France, and at the European Society of Cardiology Congress 2009 held in Barcelona, Spain. The primary safety endpoint of this clinical trial was stopping an exercise treadmill test, performed during double-blind therapy with either omecamtiv mecarbil or placebo, due to angina at a stage earlier than the shorter of two baseline exercise treadmill tests. This endpoint occurred in one patient receiving placebo and in no patients receiving either the lower or higher of two dose levels of omecamtiv mecarbil. The authors concluded that in heart failure patients with ischemic cardiomyopathy and angina, who theoretically could be most vulnerable to the possible deleterious consequences of systolic ejection time prolongation, treatment with omecamtiv mecarbil, at doses producing plasma concentrations previously demonstrated in other trials to increase cardiac function, did not deleteriously affect a broad range of safety assessments in the setting of exercise.
