Advertisement
The negative results were largely driven by an unusually large placeboresponse in the subgroup of monotherapy subjects. In the subgroup of subjectsreceiving cholinesterase inhibitors, the change in ADAS-cog favored treatmentover placebo, although this difference was not statistically significant.Similarly, in this subgroup, numeric improvements were seen in all of the foursecondary endpoints, which included the Mini-Mental State Exam, theAlzheimer's Disease Cooperative Study -- Activities of Daily Living, theClinician Interview-Based Impression of Change with Caregiver Input and theNeuropsychiatric Inventory.
Advertisement
"Based on this information, I believe that further development of thiscompound merits consideration," said Pierre N. Tariot, M.D., Professor ofResearch Psychiatry, Director of the Memory Disorders Center of the BannerAlzheimer's Institute in Phoenix, and chairman of the study's data and safetymonitoring board.
"While we are disappointed that the trial did not meet the primaryendpoint, we are encouraged by the favorable trend seen in the subgroup ofsubjects receiving cholinesterase inhibitors," said Stephen R. Murray, M.D.,Ph.D., Chief Medical Officer. "Clearly there is a significant need for newoptions for the treatment of Alzheimer's disease, and we believe that theeffects of MEM 1003 seen in this study warrant further investigation."
Subjects participating in the study were randomized at enrollment into oneof three treatment groups -- 30 mg of MEM 1003 twice a day, 90 mg of MEM 1003twice a day or placebo twice a day. During the double-blind treatment segmentof the study, subjects received MEM 1003 or placebo for a period of 12 weeks,which was followed by a four-week single-blind placebo treatment. Secondarymeasures assessed changes in activities of daily living, behavior and globalfunction.
MEM 1003 was generally well-tolerated in the trial. The rates oftreatment-emergent adverse events were similar in all arms of the trial.There were seven treatment-emergent serious adverse events (SAEs) in fivesubjects, including two deaths. Four of the subjects were in the 30 mg dosegroup and the fifth subject was in the 90 mg dose group. None of the SAEswere deemed to be treatment-related by the investigators.
The Company expects to report top-line results from its Phase 2a clinicaltrial of MEM 3454, its lead nicotinic alpha-7 agonist, in Alzheimer's diseaseby the middle of the fourth quarter.
About MEM 1003
MEM 1003 is a neuronal L-type calcium channel modulator that MemoryPharmaceuticals is developing for the treatment of Alzheimer's disease. Byblocking L-type calcium channels, MEM 1003 may regulate the flow of calciumand reestablish normal levels of calcium, which may help treat and prevent theonset of Alzheimer's disease.
Conference Call and Webcast Information
Memory Pharmaceuticals will hold a conference call on Monday, October 15,2007, at 9:00 a.m. EDT to discuss the top-line data from the trial. Theconference call will also be broadcast live from the "Investors" section ofthe Company's website. Memory Pharmaceuticals' senior management will host theconference call. Investors and other interested parties may access the callas fo