CHICAGO— For the first time, Pfizer, Inc. released promising pre-clinical data on its investigational immunotherapy compound PF-04360365, a humanized anti-amyloid monoclonal antibody being studied for the treatment of Alzheimer's disease (AD). In this study, a single injection of PF-04360365 in genetically engineered mice reduced brain levels of beta amyloid, a protein that accumulates in the brains of those with AD, initiating a cascade of events that lead to brain cell damage and death.[i]a, 1b These data were presented today at the Alzheimer's Association 2008 International Conference on Alzheimer's Disease (ICAD).
Pfizer's PF-04360365 is a highly selective and potent monoclonal antibody that targets the C-terminal end of the beta amyloid 1-40 peptide. This means that PF-04360365 does not bind to the Amyloid Precursor Protein, from which beta amyloid is derived, and which the body needs to function normally. This may be beneficial for the risk/benefit profile of this molecule. In addition, PF-04360365 has been designed to minimize the risk of dangerous inflammation in the brain. This selectivity and design of the molecule suggest the compound may be able to safely remove beta amyloid from the brain, prevent plaque formation - a hallmark of AD - and potentially slow or halt AD disease progression. Two phase I studies of PF-04360365 are currently underway in AD patients.
“We have come a long way in understanding how people with Alzheimer's may react to various forms of immunotherapy,” says Thomas Lanz, Senior Scientist at Pfizer and lead researcher of this PF-04360365 study. “This is an important area of research in the fight against Alzheimer's disease, and it's one the scientific community is optimistic about. We are glad to contribute to the body of knowledge that may one day fulfill the potential of this approach.”
The primary study objective was to determine the effect of PF-04360365 on beta amyloid levels in the brain and blood.
Results from this study demonstrated that treatment with a single injection of PF-04360365 significantly reduced levels of beta amyloid in the brains of mice genetically modified to overproduce amyloid and plaque buildup. In the study, beta amyloid was significantly reduced in the hippocampus, an area of the brain that impacts memory and one of the first areas of the brain to become damaged in those with AD. The compound also increased levels of beta amyloid in the blood up to 100-fold.
“Pfizer is pleased to unveil these promising data on our investigational monoclonal antibody compound as one example of our researchers' commitment and vision to lift the burden of Alzheimer's on patients and those who care for them,” says Liam Ratcliffe, Senior Vice President and Development Head for Pfizer Neurosciences. “Our hope is that this compound as well as others Pfizer is exploring for Alzheimer's may one day be able to slow cognitive decline or even reverse memory loss in the patients caught in the grips of this terrible disease.”
AD is a progressive disorder characterized by the gradual loss of memory and a decline in cognitive ability; changes in behavior; and a loss in ability to carry out daily activities[ii]. It places a tremendous burden on patients, those caring for them, and healthcare systems, costing the U.S. Government more than $148 billion in 2005.[iii] AD remains one of the world's most undiagnosed diseases, with only one-third of the world's approximately 18 million sufferers receiving treatment.[iv]
[i] Hardy J, Selkoe DJ. The Amyloid Hypothesis of Alzheimer's Disease: Progress and Problems on the Road to Therapeutics. Science. 2002;297:353-6.
[ii] Alzheimer's Association. What is Alzheimer's? Accessed at: [iii] Alzheimer's Association. 2008 Alzheimer's Disease Facts and Figures. Available at: [iv] World Health Organization. Alzheimer's Disease: The Brain Killer. Available at: [v] U.S. Census Bureau. An Aging World: 2001. Available at: Pfizer South Africa
Solly Mabotha
Pfizer Public Relations Manager
www.pfizer.com
