Exebryl-1 is a unique small molecule compound designed and developed with over 9-years of pre-clinical research at ProteoTech Inc (Kirkland, WA). Using 2 different APP transgenic mouse models (i.e. Swedish and London mutation, Tg2576 mice), Exebryl-1 was analyzed for reduction of brain beta-amyloid protein (Aß) and memory improvement by Morris water maze testing and probe trials. Blood brain penetration was examined with radiolabeled Exebryl-1 in Sprague Dawley rats. Effects of Exebryl-1 on secretase modulation in APP-overexpressing cell lines, and the effects of Exebryl-1 on tau protein aggregation in vitro, was also examined. Exebryl-1 caused a marked reduction in Aß formation and accumulation in transgenic mouse brain following oral administration. Exebryl-1 was effective at all stages of the disease, even in older APP transgenic animals that posessed a high Aß brain load. Morris water maze testing and probe trials demonstrated marked improvements in hippocampus-dependent memory following Exebryl-1 treatment. Data also demonstrated that Exebryl-1 effectively reduced soluble and insoluble forms of Aß 40 and 42 in APP transgenic mouse brain, as well as causing a marked increase in CSF Aß (believed to be due to effective Aß clearance from brain). Following a single oral dose in rats, Exebryl-1 penetrates the blood-brain-barrier within 30 minutes, reaching peak levels at 4 hours. Exebryl-1 also reduced Aß generation, by serving as a modulator of beta- and alpha-secretase, most likely by binding to the Aß region within APP. In vitro evidence also suggested that Exebryl-1 effectively reduces tau protein aggregation in a dose-dependent manner. These studies suggest that Exebryl-1 may be effective at lowering Aß, plaque and tangle load in Alzheimer's disease (AD) patients. Exebryl-1 is believed to represent a new disease-modifying small molecule for the treatment of AD and related disorders.
No takes yet. Share an insight, caveat, or question.
Snow et al. (2009) studied this question.