Revalesio drug alters Alzheimer's progression in animal model
Revalesio's investigational therapeutic RNS60 prevented memory loss and improved learning in mouse models, according to new data the company presented at the Alzheimer's Association International Conference Wednesday.
The experimental drug, which contains charge-stabilized nanostructures, acts in a broad-based manner to change the responsiveness of cells to stress. Revalesio scientists, working with scientists at Rush University Medical Center in Chicago, found that RNS60 increases the response of critical genes associated with neuronal plasticity in the PI3k/pAKT pathway. These plasticity genes, used as a target by other drug developers, play a key role in healthy neurotransmitter and synaptic function.
While Alzheimer's is widely believed to be caused by the accumulation of amyloid-beta plaque--the protein clusters in the brain that characterize the disease--many therapies that have targeted the amyloid beta and neurofibrillary tangles have been unsuccessful. Scientists have recognized that inflammation could be a major contributing factor to disease progression.
"We have a large and expanding data set on RNS60's ability to reduce inflammation, and these findings are a significant advancement in our understanding of how RNS60 may be a treatment for neuro-degenerative diseases," Dr. Richard Watson, Revalesio's chief science officer, said in a statement.
In mouse and cellular models, RNS60 prevented amyloid-beta-induced cell death and tau-neurofibrillary tangles, the company reported. In previous preclinical models, RNS60 has been effective at staving off symptoms of Alzheimer's while leaving no evidence of toxicity behind.
RNS60 has successfully completed Phase I safety studies and is advancing into Phase II clinical trials. The Tacoma, WA-based company is seeking partners for development and commercialization of RNS60.
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