Argenica Therapeutics Limited announced positive initial preclinical data on ARG- 007's ability to inhibit human recombinant Amyloid-Beta (Abeta) aggregation in a preclinical (in vitro) model of Alzheimer's Disease. Abeta aggregation is thought to be one of the main causes of Alzheimer's Disease, with the Abeta accumulation in senile plaques causing memory loss and confusion. Argenica engaged leading preclinical Contract Research Organisation QPS, based in Austria, to undertake the study.

The aim of the study was to determine the effects of ARG-007 in comparison to controls in inhibiting human recombinant Abeta aggregation using the cell- free Abeta aggregation assay. In this study, three concentrations of ARG-007 were used to determine the drug's efficacy in inhibiting human recombinant Abeta aggregation - 2.5 µM, 7.5 µM and 25 µM. Abeta aggregation was assessed at 4 hours, 10 hours and 16 hours post administration of ARG-007. The results of this study show ARG-007 has a positive effect in inhibiting Abeta aggregation at the 10 hour and 16 hour post administration time points, compared to the vehicle controls.

This in vitro (in petri dish) cell-free Abeta aggregation assay model provides important insights into the pathogenesis of Alzheimer's Disease by simulating the disease in a less complex environment compared to in vivo (in living organism) systems. It provides preliminary information on mechanisms and possible protective roles of ARG-007 in Alzheimer's Disease.