A pre-clinical study run by Argenica Therapeutics (ASX:AGN) has shown strong evidence the company’s flagship neuroprotective drug, ARG-007, can inhibit the buildup of a protein linked to Alzheimer's.
Shares were up 23.4% in the second hour of trade on Thursday.
The protein in question is Amyloid-Beta (Abeta), a naturally occurring compound in the human body.
The study so far is preclinical, meaning no humans nor animals have been tested.
An in-vitro sample mimicking the human body was used instead, with Argenica’s lab team reporting the ability of its ARG-007 to slow down amyloid accumulation and aggregation.
Abeta is a naturally occurring protein in the human body which is found in far higher concentrations than usual in the brains of patients with Alzheimer’s.
In patients with Alzheimer’s, however, the body’s creation of Abeta goes haywire.
Too much of the protein is automatically generated by the body and builds up between neurons in the brain, causing confusion and neurodegeneration.
The phenomenon is referred to as amyloid plaques. The plaques are actually made up of ‘protofilaments’ of Abeta, which come together to form almost fibrous deposits, slowing brain function and damaging the hardwiring needed for basic functions.
“At 16 hours following ARG-007 administration, a 25µM dose of ARG-007 reduced Abeta aggregation by more than 50% compared to vehicle controls,” the company wrote on Thursday.
In short: test results suggest ARG-007 stops Abeta protofilaments from clumping together around neurons in the brain.
Argenica is now moving ahead to animal studies with ARG-007. Many mice models of Alzheimer’s exist, given that mice tend to develop the same amyloid plaques as humans.
These animal studies, and rigorous ethics and legal obligations, must be adhered to before human trials can begin in Australia.
The drug is administered intravenously. ARG-007 was developed in part by researchers at the University of Western Australia. Argenica is tight-lipped about the exact make-up of its flagship drug.
The drug was first imagined as a way to protect brain tissue in patients who had experienced a stroke and had bloodflow cut off to brain tissue.
In heart attack patients, massive cardiac arrest can often cause strokes, given the rapid onset of damage caused by a lack of bloodflow to the brain which can happen quicker than it takes for ambulances to arrive.
Now, the latest preclinical study has shown ARG-007’s neuroprotective abilities has potential upside for Alzheimer’s patients.
One to watch.
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