TORONTO, April 27, 2017 /CNW/ - ProMIS Neurosciences ("ProMIS" or the "Company", TSE ticker PMN.TO), a company focused on the discovery and development of precision treatments for neurodegenerative diseases, today announced it will present results on its recent Alzheimer's disease (AD) therapeutic developments on Friday, April 28th at the 2017 annual meeting of the American Academy of Neurology (AAN), held in Boston, MA, from April 22-28.
"Based on our results presented at this year's AAN annual meeting we anticipate ProMIS monoclonal antibodies (mAbs), selectively targeting toxic forms of Amyloid beta (Aß), will demonstrate a 'best in class' product profile for treatment of AD," stated Dr. Elliot Goldstein, ProMIS President and CEO. "Indeed, by virtually no binding to Aß monomer, ProMIS mAb products should allow improved efficacy by avoiding targeting of this abundant, non-toxic form of Aß. Similarly, by not targeting plaque which is associated with neurovascular edema ('brain swelling'), a dose limiting adverse event, we anticipate improved safety and tolerability for our products".
The presentation, entitled Achieving the optimal profile for Alzheimer's immunotherapy: Rational generation of antibodies specific for toxic Aß oligomers is a poster authored by Dr. Steven Plotkin (et al.), the Company's Chief Physics Officer and presented by Dr. Johanne Kaplan, ProMIS Chief Development Officer. Using one of the Company's unique, proprietary discovery platforms, Collective Coordinates, the authors predicted five distinct epitopes (targets) on toxic pathogenic Aß oligomers (prion-like forms of Aß). Results of the predictive methodology indicate that these oligomer-specific epitopes are conformationally distinct, in other words shaped differently from the same primary sequences in either Aß monomer or fibrils, the latter representing the main constituent of Aß plaque. The authors conclude that monoclonal antibodies generated by immunizing with the predicted conformational epitopes bind selectively to toxic Aß oligomers, inhibit Aß propagation (spreading) in vitro, bind preferentially to AD brain tissue and cerebrospinal fluid (CSF), show little or no reactivity to plaques in cadaveric AD brain and protect against Aß toxicity in vitro. Furthermore, the Company's lead product, PMN310, was shown to preserve cognitive function in a preclinical animal model evaluating short term memory retention (dual object recognition test).
