Merck known as MSD outside the United States and Canada, announced today presentations at the upcoming Alzheimer’s Association International Conference (AAIC) being held in Vancouver, British Columbia, Canada on July 14-19, 2012.
At the conference, Merck scientists are scheduled to present results from multiple preclinical and clinical studies investigating the safety and efficacy of ß-amyloid precursor protein site cleaving enzyme (BACE) inhibitors, including MK-8931, the company’s lead compound currently being investigated as a potential treatment for Alzheimer’s disease.
“The prevalence of Alzheimer’s disease is growing rapidly due to the aging population, creating an unsustainable burden on patients, caregivers and the economy,” said Darryle D. Schoepp, Ph.D., senior vice president and head of Neuroscience and Ophthalmology franchise, Merck Research Laboratories. “Merck is committed to discovering and developing novel medicines to treat neurodegenerative brain diseases, such as Alzheimer’s and dementia, and is focused on rapidly advancing its BACE inhibitor program.”
Select Merck presentations at AAIC include:
July 15, 2012
P1-221: Safety and pharmacokinetics of the novel BACE inhibitor MK-8931 in healthy subjects following single and multiple dose administration.
P1-225: A study to evaluate the pharmacokinetics and pharmacodynamics of single and multiple oral doses of the novel BACE inhibitor MK-8931 in Japanese subjects.
P1-229:Population pharmacokinetic modeling of the novel BACE inhibitor MK-8931 following single and multiple dose administration in healthy subjects.
July 18, 2012
P4-196: The novel BACE inhibitor MK-8931 dramatically lowers CSF Abeta peptides in healthy subjects following single and multiple dose administration.
Earlier this year, Merck disclosed the results of a two part randomized, double-blind, placebo-controlled single dose study evaluating the safety and tolerability of MK-8931 in 40 healthy adults 18 to 45 years of age. Single doses of MK-8931 were associated with marked reductions in amyloid beta peptide concentration levels with a mean reduction from baseline of up to 92 percent. MK-8931 was generally well tolerated in these healthy subjects with no serious adverse events and no study discontinuations. Adverse events were generally mild to moderate in intensity and transient in duration and included headache (57 percent and 50 percent), nasal congestion (23 percent and 30 percent) and dizziness (20 percent and 40 percent, for MK-8931 and placebo respectively).
The amyloid hypothesis predicts that abnormal accumulation of amyloid-ß peptide is a central event in the progression of Alzheimer’s disease. The enzyme BACE is a key enzyme in the initiation of synthesis of amyloid ß peptide. Inhibition of BACE is therefore believed to provide a promising means for therapeutic intervention in Alzheimer’s disease.
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