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    Argenica Therapeutics identifies Alzheimer’s breakthrough from preclinical data

    Biotechnology company Argenica Therapeutics (AGN) has received positive initial preclinical data on ARG-007’s ability to inhibit human recombinant Amyloid-Beta (Abeta) aggregation in a preclinical model of Alzheimer’s Disease.

    The company says Abeta aggregation is thought to be one of the main causes of Alzheimer’s, with Abeta accumulation in senile plaques causing memory loss and confusion.

    Argenica engaged Austrian-based leading preclinical Contract Research Organisation (QPS) to undertake the study, which aimed to determine the effects of ARG-007 in comparison to controls in inhibiting human recombinant Abeta aggregation using the cell-free Abeta aggregation assay.

    This is extremely encouraging data showing the potential new indication for ARG-007″

    In this study, 3 concentrations of ARG-007 were used to determine the drug’s efficacy in inhibiting human recombinant Abeta aggregation including 2.5 micrometres (µm), 7.5µm, and 25µm.

    Abeta aggregation was assessed at 4 hours, 10 hours, and 16 hours after administering ARG-007. Argenica reports 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 times, compared to the vehicle controls.

    At the 16 hour time point, when Abeta had reached maximum aggregation, all 3 concentrations of ARG-007 showed a ‘significant’ reduction in Abeta aggregation compared to the controls, with 25µm showing a greater than 50% reduction.

    The company says this in vitro cell-free Abeta aggregation assay model provides important insights into the pathogenesis of Alzheimer’s by simulating the disease in a less complex environment compared to in vivo systems. Argenica also notes the assay model provides preliminary information on mechanisms and possible protective roles of ARG-007 in Alzheimer’s Disease.

    Commenting on the data, Argenica Therapeutics Managing Director Liz Dallimore said: “This is extremely encouraging data showing the 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.”

    Argenica reports the global Alzheimer’s Disease therapeutics market size was valued at USD$4.04 billion in 2021, and is expected to expand at a compound annual growth rate (CAGR) of 16.2% from 2022 to 2030.

    According to the World Health Organization (WHO), the economic cost burden will range from USD$1.3 trillion to USD$2.8 trillion by 2030. Alzheimer’s Disease accounts for 60% to 70% of all cases of dementia, with government, and non-government organisations investing ‘extensively’ in the development of diagnostics and therapies for the disease as a result of its rising prevalence globally.

    The only approved drug to treat Alzheimer’s is Aducanumab, which targets the Abeta protein, however Argenica notes concerns have been raised regarding its safety.

    Argenica reports it has now further engaged QPS to undertake an in vivo study in 5xFAD mice, a model of familial Alzheimer’s. These aged mice will receive multiple doses of ARG-007 over an extended period of time, with results to assess the effect on Abeta levels and plaques, Tau protein levels, neuroinflammation , and neurodegernation.

    Argenica Therapeutics is a biotechnology company focused on developing novel therapeutics to reduce brain tissue death after a stroke, and improve patient outcomes.

    The company’s lead neuroprotective peptide candidate ARG-007, has been demonstrated to improve outcomes in preclinical stroke models, and is currently in the process of being verified for its safety and toxicity before beginning phase one clinical trials in humans.

    Argenica aims for ARG-007 to be administered by first responders to protect brain tissue against damage during a stroke, with further potential to enhance recovery once a stroke has taken place.

    Harry Mulholland
    Harry Mulholland
    Hailing from the Central Coast region of NSW, Harry is a passionate journalist with a background in print, radio and ESG news. When not bashing away on his keyboard, he can be found brewing a coffee or playing with his dog.