Cytokinetics, Incorporated (NASDAQ: CYTK) announced today that three abstracts summarizing non-clinical data regarding its smooth muscle contractility program were presented at the 2009 Scientific Sessions of the American Heart Association in Orlando, Florida.
"Our smooth muscle contractility program leverages our expertise in the contractile apparatus of muscle systems, which has generated clinical stage drug candidates in both our cardiac and skeletal muscle programs," stated David J. Morgans, PhD Cytokinetics' Executive Vice President of Preclinical Research and Development. "We are pleased to share these three presentations relating to our novel mechanism approach for modulation of smooth muscle contractility. We believe that these data demonstrate the potential of smooth muscle myosin inhibitors for the treatment of patients with diseases that may cause significant morbidity, such as refractory systemic hypertension and pulmonary arterial hypertension."
Oral Presentations
An oral presentation titled "Inhibition of Smooth Muscle Myosin, a Novel Anti-Hypertensive Strategy" was presented on Monday, November 16, 2009 by Fady Malik, MD, PhD, FACC, Vice President, Biology and Therapeutics, Cytokinetics, Inc., South San Francisco, California. This presentation summarized non-clinical research evaluating smooth muscle myosin inhibitors in models of hypertension. The authors concluded that smooth muscle myosin inhibition reduced vascular resistance and lowered blood pressure in a canine model of hypertension. In addition, the pattern of regional vasodilation is different for a specific smooth muscle myosin inhibitor, CK-2018448, as compared to the calcium channel blocker, amlodipine. For CK-2018448, blood flow to the kidney increased without change in blood flow to the limb. In contrast, for amlodipine, the largest increases in blood flow were found in the limb. The authors concluded that the smooth muscle myosin inhibitor and the calcium channel blocker elicited different patterns of regional vasodilation. In addition, the renal vasodilation induced by smooth muscle myosin inhibition could have salutary effects in conditions accompanied by renal insufficiency such as hypertension, acute heart failure, and acute renal failure due to an interruption of adequate blood flow to the kidney.