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| KAI Pharmaceuticals Initiates Phase I/II Clinical Trial for Treatment of Reperfusion Injury |
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September 28, 2004 Lead drug candidate KAI-9803 receives ‘Fast Track’ designation from the FDA South San Francisco, CA — September 28, 2004 – KAI Pharmaceuticals Inc., announced today that it has initiated a phase I/II clinical trial of KAI-9803, a protein kinase C (PKC) inhibitor designed to reduce reperfusion injury as an adjunct to current treatments of acute myocardial infarction, or heart attack. KAI-9803 is the first drug candidate designed to inhibit the specific PKC enzyme responsible for reperfusion injury. The FDA has granted ‘Fast Track’ designation to KAI-9803 for this indication. Dr. Daria Mochly-Rosen, founder and chief scientific officer of KAI Pharmaceuticals and the George D. Smith Professor of Translational Medicine at Stanford University, and her research team at Stanford have solved specificity issues associated with modulating PKC isozymes, a family of eleven closely related enzymes that participate in a number of different biological processes implicated in disease. By developing selective inhibitors and activators for PKC isozymes, KAI is able to target a specific isozyme of interest without affecting biological processes regulated by other PKC isozymes. “Expanding on the discoveries from Dr. Mochly-Rosen’s lab at Stanford, KAI has developed a portfolio of the first truly selective inhibitors and activators for PKC isozymes, representing an important breakthrough in enzyme-targeted drug discovery and a unique opportunity for therapeutic development,” said John Walker, acting CEO of KAI Pharmaceuticals. “We are excited to advance KAI-9803 into clinical development for an indication clearly recognized as an unmet medical need.” KAI-9803 targets a specific PKC isozyme, delta-PKC, which has been found to activate a cascade of events causing cell injury and death during reperfusion injury. Reperfusion injury occurs when myocardial and endothelial cells undergo necrosis and apoptosis after the reintroduction of blood flow to the ischemic areas following heart attack. Apoptosis is the process whereby cells autodestruct after exposure to certain noxious stimuli. Selective inhibition of the delta-PKC isozyme by KAI-9803 prevents damage to the mitochondria and inhibits both necrosis and apoptosis during reperfusion injury. In preclinical studies, treatment with KAI-9803 resulted in a 70 percent reduction in infarct size, an improvement in heart function, restoration of intracellular energy generation, and protection of myocardial and endothelial cells. “Researchers at Stanford and KAI Pharmaceuticals have redefined our understanding of the science behind reperfusion injury, and we hope that KAI-9803 will redefine the way reperfusion injury is treated,” added Walker. The Phase I/II clinical trial, identified as DELTA MI, will assess the safety and efficacy of KAI-9803 for injection in patients undergoing urgent angioplasty (with or without stent placement) for acute myocardial infarction. This randomized, double-blinded, placebo-controlled clinical study will evaluate increasing doses of KAI-9803. Outcome measures will include clinical endpoints such as heart failure and death, as well as surrogate measures of infarct size, myocardial function, and myocardial perfusion. Performed in collaboration with the Duke Clinical Research Institute, this trial will enroll approximately 150 patients at 30 clinical sites.
About KAI Pharmaceuticals |