In Alzheimer's disease (AD) a toxin called amyloid β-peptide (Aß) is accumulated in the brain. Reduced Aβ clearance and/or its increased influx into the brain from the circulation via transports may be responsible for Aβ brain accumulations. Receptor for advanced glycation end products (RAGE) is the main transporter for Aβ transport into brain while low-density lipoprotein receptor-related protein (LRP1) is the major transporter for its efflux from brain. RAGE binds Aβ and transport it into brain, and mediates pathophysiological cellular responses as a consequent of Aβ/RAGE interaction. We have shown that compounds which block Aβ/RAGE interaction also blocks the entry of Aβ into the brain, reduce Aβ-related pathology and improve the regulation of cerebral blood flow (CBF) and cognitive decline. All of which should have important therapeutic beneficial effects in AD. During these studies it was suggested that ADME (absorption, distribution, metabolism and elimination) and early toxicology studies were needed. Based on these suggestions studies are proposed for the lead compound (FPS2-BM). These studies will be out-sourced and conducted by Vendors since the laboratory is currently not equipped for these types of studies. However, we have the expertise to interpret the data generated by the Vendors.