CELLADON ANNOUNCES SUCCESSFUL PRECLINICAL TRIALS IN CONGESTIVE HEART FAILURE

La Jolla, CA- June 2, 2005- Celladon Corporation announced today that its collaborators presented successful results of heart failure trials conducted in large animal models. Drs. Roger J. Hajjar, M.D. and David Kaye, MD, Ph.D. presented data on treatment of advanced heart failure in preclinical models using Celladon's therapeutic agents targeting the Sarcoplasmic Reticulum ATPase2a (SERCA2a) pump. The SERCA2a pump is a central control point for progression of heart failure, and treatments targeting this pathway essentially reversed the deterioration in cardiac function in experimental models. Furthermore, the therapeutic agents were delivered using delivery methodologies easily translated into clinical procedures for human heart failure, which are similar to how coronary angioplasty is performed.

Dr. Kaye presented data from an ovine model of pacing induced heart failure. The pacing model induces moderate to severe heart failure, with animals that have left ventricular ejection fractions of around 25%, which is typical in humans of the NYHA Class III group of heart failure patients. Animals treated with the SERCA2a gene restored left ventricular ejection fractions to normal levels. Other hemodynamic parameters mirrored the effects on ejection fraction. The agents were delivered using a novel device developed by V-Kardia, a cardiovascular device company of The Baker Heart Research Institute, the largest and leading cardiovascular research institute in Australia.

Dr. Hajjar presented data from a porcine model of mitral regurgitation induced heart failure. The porcine model generates a progressive heart failure model similar to Class III patients. Animals treated with the SERCA2a gene induced not only short term improvement but by using adeno-associated vectors (AAV) targeted to the heart, Dr Hajjar also showed that there was long-term improvement in ventricular function indices following gene transfer of SERCA2a.

"Celladon's therapeutic candidate targets the SERCA2a pathway, an important regulator of myocardial contractility. Malfunction in this pathway is associated with progressive heart failure," said Krisztina Zsebo, Ph.D., President of Celladon Corporation. "These large animal studies by Celladon's collaborators, indicate that AAV agents targeting this pathway can reverse the progression of congestive heart failure. Gene delivery may provide a new approach to unlocking the therapeutic potential of this pathway, whereas previous traditional small molecule attempts have not been successful. These results will pave the way for the first clinical trial of gene therapy for heart failure using AAV vectors." Celladon plans to initiate human trials with this agent in 2006.

Congestive heart failure (CHF) is a serious condition in which the heart loses its ability to pump blood efficiently. According to the National Heart, Lung and Blood Institute, about 5 million people in the United States alone have heart failure, and another 550,000 new cases are diagnosed each year. CHF contributes to or causes about 300,000 deaths annually. The disease is most common in people aged 65 or older, women and African Americans.