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Argenica Therapeutics Limited (ASX: AGN) (“Argenica” or the “Company”), a biotechnology company developing novel therapeutics to reduce brain tissue death after brain injury, is pleased to announce 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.1
Highlights:
- Preclinical data has shown ARG-007 significantly inhibited the aggregation of human recombinant Amyloid-Beta (Abeta) in a cell-free Abeta aggregation assay model.
- 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.
- At 16 hours following ARG-007 administration, a 25 µM dose of ARG-007 reduced Abeta aggregation by more than 50% compared to vehicle controls.
- Argenica will now progress to animal studies to further confirm the efficacy of ARG-007 in Alzheimer’s Disease and will update the market as milestones are meet.
- The global Alzheimer's therapeutics market size was valued at USD4.04 billion in 2021 and is expected to expand at a compound annual growth rate (CAGR) of 16.2% from 2022 to 2030.
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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