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Argenica Therapeutics’ novel therapeutic being developed to reduce brain tissue death after stroke has also been shown to prevent the uptake and aggregation of the key neurodegenerative protein linked to both Parkinson’s and Alzheimer’s diseases, further reinforcing its potential to treat a range of neurological issues.

The ARG-007 treatment is moving to Phase 2 clinical trials after demonstrated successes in treating brain issues, including reducing tissue death by up to 70 per cent after a stroke and significantly reducing damage caused by traumatic injuries.

And preclinical data published this week in the Biomedicines journal has now shown ARG-007 reducing the cellular uptake of alpha-synuclein protein, known as the ‘Parkinson’s Protein’, aggregates by 84 per cent, with the inhibitory effect increasing up to 90 per cent with further doses.

It was an enormous leap forward for treatment of Parkinson’s when researchers discovered a new tool that can reveal abnormal alpha-synuclein, one of the insoluble protein deposits proving to be a common element of major age-related neurodegenerative disorders, and Argenica Managing Director Dr Liz Dallimore said the data released today was extremely encouraging.

If you also consider it with our Abeta data previously announced, it is even more exciting and encouraging. The scientific community now understands that neurodegenerative diseases are extremely complex, however the aggregation and accumulation of several proteins in the brain appear to be an important contributor,” Dr Dallimore said.

“The ability of a therapy such as ARG-007 to work on a number of these protein aggregates is very important from a scientific perspective, and we look forward to progressing preclinical studies in this area further,” she added.

Forward plan

A decision on Phase 2 trials backed by the Australian Stroke Foundation and the Australasian Stroke Trials Network is expected by mid-September, and Argenica will continue to progress ARG-007’s efficacy on Alzheimer’s, with data from a mouse model expected early next year.

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