Merck (NYSE: MRK), known as MSD outside the United States and Canada, announced it has started a Phase II/III clinical trial designed to evaluate the safety and efficacy of MK-8931 versus placebo in patients with mild-to-moderate Alzheimer's disease. MK-8931 is Merck's novel investigational oral β-amyloid precursor protein site-cleaving enzyme (BACE) inhibitor, and is the first with this mechanism to advance to this stage of clinical research. The global, multi-center study, called EPOCH, is designed to initially evaluate the safety of MK-8931 in a cohort of 200 patients prior to advancing into a larger Phase III study.
"Merck is committed to advancing the understanding and treatment of Alzheimer's disease," said Darryle D. Schoepp, Ph.D., senior vice president and head of Neuroscience and Ophthalmology, Merck Research Laboratories. "As the global health and financial burden of Alzheimer's disease grows, innovative research is critically needed, and we need to accelerate this research wherever possible. This new study is an important step in our overall strategy to understand the potential of the BACE inhibitor mechanism and MK-8931, our lead compound, in multiple stages of Alzheimer's disease."
About the EPOCH study
EPOCH is a 78-week, randomized, placebo-controlled, parallel-group, double-blind Phase II/III clinical trial to evaluate the efficacy and safety of one of three oral doses of MK-8931 (12, 40 or 60 mg) administered daily versus placebo. The study is anticipated to eventually enroll up to 1,700 patients in the main Phase III cohort. The primary efficacy outcomes of the study are the change from baseline in Alzheimer's Disease Assessment Scale Cognitive Subscale (ADAS-Cog) score and the change from baseline in the Alzheimer's Disease Cooperative Study – Activities of Daily Living (ADCS-ADL) score.
For more information about the EPOCH study, please visit
or call 1-855-55-EPOCH (37624).
About BACE Inhibition and MK-8931
The amyloid hypothesis asserts that the formation of amyloid peptides that lead to amyloid plaque deposits in the brain is the underlying cause of Alzheimer's disease. BACE is believed to be a key enzyme in the production of amyloid β peptide. Evidence suggests that inhibiting BACE decreases the production of amyloid β peptide and may therefore reduce amyloid plaque formation and modify disease progression.