AmyP53 restores spontaneous synaptic activity of brain slices (hippocampus) that are destroyed by oligomers of amyloid proteins (Alzheimer's disease Aβ protein). Synaptic activity is recorded in real time by electrophysiology.
To block the formation of amyloid pores in Alzheimer’s and Parkinson’s diseases, our researchers created the AmyP53 molecule, which prevents amyloid protein binding to brain cells.
The design of AmyP53 took into account multiple biochemical, biophysical and pharmacological parameters to avoid the traditional pitfalls in the development of therapeutic solutions.
By targeting a common mechanism directly causing symptoms, AmyP53 is the first therapeutic solution specifically designed to treat two major neurodegenerative diseases: Alzheimer & Parkinson.
AmyP53 is innovative in several ways:
This is a new therapeutic route that has never been exploited until now (brain gangliosides).
It is not toxic in vivo: exceptional tolerance in animals well beyond the therapeutic doses envisaged in humans.
AmyP53 is the only drug candidate active in all forms of Alzheimer’s and Parkinson’s disease, including forms caused by genetic mutations (familial forms).