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. At the 16-hour time point, when Abeta had reached maximum aggregation, all three concentrations of ARG-007 showed a large significant reduction in Abeta aggregation compared to the control, with the 25 µM showing a greater than 50% reduction in Abeta aggregation, as shown in the graph below:

Concentration of ARG-007

Figure 1. An assessment of the extent of Abeta aggregation inhibition at Abeta plateau, 16 hours after the administration of ARG-007, at three different concentrations of the drug, 2.5 µM, 7.5 µM and 25 µM. Data are shown as % of vehicle control (VC) and displayed as bar graphs with group means +SEM (n=4 per group). Statistical analysis involved a two-tailed ANOVA followed by Bonferroni’s Multiple comparison Test (post hoc test) compared to VC *p<0.05; **p<0.01; ***p<0.001.

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.

Dr Liz Dallimore, Argenica’s Managing Director, said“This is extremely encouraging data showing a potential new indication for ARG-007. It is well recognised that Abeta aggregation in the brain plays a key role in initiating Alzheimer’s Disease, and therefore a safe therapeutic drug that can reduce Abeta aggregation is a huge opportunity. We look forward to continuing to progress this exciting opportunity into further animal studies.”

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