INDEPENDENT ANALYSIS OF SOLANEZUMAB PROVIDES EVIDENCE THAT COMPOUND MAY REMOVE AMYLOID FROM BRAIN IN ALZHEIMER'S DISEASE
INDEPENDENT ANALYSIS OF SOLANEZUMAB PROVIDES EVIDENCE THAT COMPOUND MAY REMOVE
AMYLOID FROM BRAIN IN ALZHEIMER'S DISEASE
Results cause for "cautious" optimism in scientific community
MONACO, October 29, 2012 – The Clinical Trials in Alzheimer's Disease (CTAD) 2012 conference featured findings from an independent analysis of Phase III clinical trial data on the compound solanezumab showing effects on levels of amyloid in blood. The findings reported the second part of an independent raw data analysis of Eli Lilly's solanezumab studies as reported by Rachelle Doody, MD, PhD Baylor School of Medicine's Effie Marie Cain Chair in Alzheimer's Disease Research. The analysis was executed under her leadership as chair of Alzheimer's Disease Cooperative Study (ADCS) Data and Publications Committee.
The results support continued interest in amyloid as a therapeutic target in AD research. Beta amyloid is a measurable biomarker thought to contribute to the cognitive decline in people with AD. In her summary of the findings Dr. Doody said, "The beta amyloid biomarker results in the trial support the small, yet significant cognitive benefit, especially for the Alzheimer's disease patients. We think that the benefit is related to the removal of soluble amyloid from the brain and into the blood."
There were no changes noted in other AD biomarkers such as tau, phosphorylated tau, hippocampal volume, whole brain volume, or amyloid accumulation measured by PET imaging. The solanezumab analysis was presented at CTAD in Monaco this week. The analysis involved a closer examination of pooled data from the Eli Lilly Expedition clinical trials. A total of 2,052 patients were randomized to receive either a 400 mg dose of Solanezumab IV or a placebo. Earlier this month at the
American Neurological Association in Boston, Dr. Doody reported that the Expedition trial data showed positive results on cognition in the pre-specified sub analyses of mild patients that was more pronounced in the pooled analyses when the two mild-moderate studies were combined. CTAD conference organizers offered perspective on the additional solanezumab data. Jacques Touchon, MD, PhD from Montpelier University Hospital in Toulouse, France said, "The findings are cause for
cautious optimism in the drive to develop and design of future AD trials." Michael Weiner, MD from the University of California, San Francisco and Principal Investigator in the landmark Alzheimer's Disease Neuroimaging Initiative (ADNI) said, " It shows that research like solanezumab bolsters the need for large biomarker trials like ADNI to move as quickly as possible to the earliest identifiable stages of the disease."
The researchers said the findings in these studies will help set the course for Alzheimer's disease secondary prevention trials that are due to start in 2013. Those trials will focus on people who have biomarker evidence of Alzheimer's disease but have yet to show any symptoms. Researchers are hopeful that targeting patients earlier may result in more effective treatments.
Alzheimer's is a progressive and ultimately fatal neurodegenerative disease that today affects more than 35 million individuals, robbing them of their memory, independence, and ability to think and understand. By 2050, the number of people with AD is expected to exceed 115 million worldwide if nothing is done to slow or prevent the disease.
CTAD embraces the organizing committee mandate to maintain CTAD's unique role in AD research: To provide a
substantive, clinical research-oriented conference and an annual opportunity for the world's preeminent clinical
researchers to engage in both formal and informal exchanges of views. CTAD's ongoing commitment to providing a
relatively intimate forum has resulted in the conference's reputation for facilitating and fostering international
collaboration in AD clinical research matters. More information is available at www.ctad.fr/.
Genevieve Matthews, 858-699-9187
Virginia Bader, 703-508-6927