Safety and Efficacy of MEM 1003 Versus Placebo in Patients With Mild to Moderate Alzheimer's Disease
The purpose of this study is to determine in a 12-week treatment study if MEM 1003 is a safe and effective treatment for patients with mild to moderate Alzheimer's disease.
|Study Design:||Allocation: Randomized
Endpoint Classification: Safety/Efficacy Study
Intervention Model: Parallel Assignment
Masking: Double Blind (Subject, Caregiver, Investigator)
Primary Purpose: Treatment
|Official Title:||A Multicenter, Randomized, Double-Blind, Placebo-Controlled Study to Evaluate Safety and Efficacy of MEM 1003 in Patients With Mild to Moderate Alzheimer's Disease|
- Cognitive function [ Time Frame: Change from baseline at wk 12 ] [ Designated as safety issue: No ]
- Other Cognitive Assessments, activities of daily living, functional assessments and safety [ Designated as safety issue: Yes ]
|Study Start Date:||November 2005|
|Study Completion Date:||October 2007|
|Primary Completion Date:||October 2007 (Final data collection date for primary outcome measure)|
Active 30 mg MEM 1003
Drug: MEM 1003
30 mg twice a day
90 mg MEM 1003
Drug: MEM 1003
90 mg MEM 1003 twice a day
Placebo Comparator: C
Placebo for MEM 1003
Drug: Placebo for MEM 1003
Placebo twice a day
Alzheimer's disease is the leading cause of dementia and one of the most common diseases of the aging population. It is a chronic brain disease that involves gradual memory loss, decline in the ability to perform routine tasks, disorientation, difficulty in learning, loss of language skills, impairment of judgment, and personality changes in affected individuals. The neurodegenerative nature of the disease eventually leads to the failure of other organ systems and death.
Perturbations in calcium homeostasis in the central nervous system, such as those associated with Alzheimer's disease and aging as well as stroke and head trauma can result in an increase in intracellular levels of calcium (Ca2+). Increased levels of Ca2+ may lead to cellular dysregulation and cell death. The role of calcium in these neurodegenerative processes led to the hypothesis that controlling calcium levels may be beneficial, particularly where progressive neuronal damage results in cognitive dysfunction and memory loss.
MEM 1003 is the (+)-enantiomer of a dihydropyridine that has been optimized for central nervous system activity. It inhibits L-type Ca2+ channels and within the anticipated human dosing range has more benign cardiovascular effects than other DHP L-Type calcium channel modulators.
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|Study Director:||Stephen Murray, MD, PhD||Memory Pharmaceutical Corp.|