ProMIS Neurosciences issues white paper entitled: Critical Insight - Toxic soluble Amyloid beta oligomers ("prions"), not plaque, drive pathogenesis in Alzheimer's disease
TORONTO, Oct. 4, 2016 /CNW/ - ProMIS Neurosciences ("ProMIS" or the "Company"), a company focused on discovery and development of precision treatments for neurodegenerative diseases, today announced it has issued a new scientific white paper entitled: 'Critical Insight - Toxic soluble Amyloid beta oligomers ("prions"), not plaque, drive pathogenesis in Alzheimer's disease'. This is one of a series of commentaries from the ProMIS scientific team offering insight on the Company's emerging product portfolio and Alzheimer's disease (AD) science in the popular press.
"The recent Nature publication1 discussing the results of Biogen's PRIME study, completed in 2015, focused on the role of aducanumab in reducing plaque burden in AD. However, there is now an extensive and growing body of literature supporting that toxic oligomers (prions) of Amyloid beta (A?), and not plaque, seem to be the primary drivers of neurodegeneration and cognitive decline in AD," said Dr. Elliot Goldstein, ProMIS CEO.
Both Biogen's Nature article and a poster on aducanumab's binding properties submitted a year later at the Alzheimer's Association International Conference (AAIC, June 2016), are consistent with the current understanding of AD pathogenesis. The investigators on the aducanumab study indicated that the apparent clinical benefit observed in PRIME could be explained by the binding of aducanumab to oligomeric forms of A?. The authors also state that reductions in toxic A? oligomers, rather than reduction of plaque, may have had a more functionally relevant impact on cognition in the PRIME study.
Commenting on the PRIME study Dr. Johanne Kaplan, ProMIS Chief Development Officer, stated: "The scientific literature and results of prior clinical trials suggest the ideal monoclonal antibody (mAb) therapeutic specifically binds the neurotoxic prion-like strains of A?; with no binding to A? monomers to avoid reduced efficacy due to off-target binding, and no binding to plaque to avoid the edema (brain swelling) associated with disruption of plaque".
ProMIS has identified multiple therapeutic candidates against five A? epitope targets that do not bind monomer (a sixth target is under evaluation). As announced on Sept. 13, 2016, generation of mAbs against the first three epitopes yielded candidates with the desired target profile of selective binding to soluble toxic oligomers from AD brain extracts, with little or no binding to monomers or plaque in AD brain tissue. Analysis of antibodies against the other three epitopes is ongoing.
"When Biogen announced clinical data from the PRIME trial almost two years ago it created a very positive reaction" stated ProMIS Executive Chairman, Eugene Williams. "The data also demonstrated areas where there could be significant improvement over aducanumab. ProMIS is making great progress in developing a mAb product portfolio that delivers those improvements to generate better drugs for AD patients."
________________________1 Sevigny, J et al (2016) The antibody aducanumab reduces A? plaques in Alzheimer's disease. Nature 537: 50-56.
About ProMIS Neurosciences, Inc.
The mission of ProMIS Neurosciences is to discover and develop precision medicine therapeutics for effective treatment of neurodegenerative diseases, in particular Alzheimer's disease and ALS.
ProMIS Neurosciences' proprietary target discovery engine is based on the use of two, complementary techniques. The Company applies its thermodynamic, computational discovery platform—ProMIS™ and Collective Coordinates — to predict novel targets known as Disease Specific Epitopes (DSEs) on the molecular surface of misfolded proteins. Using this unique "precision medicine" approach, ProMIS Neurosciences aims to develop novel antibody therapeutics and specific companion diagnostics for Alzheimer's disease and ALS. The company has also developed two proprietary technologies to specifically identify very low levels of misfolded proteins in a biological sample. In addition, ProMIS Neurosciences owns a portfolio of therapeutic and diagnostic patents relating to misfolded SOD1 in ALS, and currently has a preclinical monoclonal antibody therapeutic against this target.
The TSX has not reviewed and does not accept responsibility for the adequacy or accuracy of this release. This information release may contain certain forward-looking information. Such information involves known and unknown risks, uncertainties and other factors that may cause actual results, performance or achievements to be materially different from those implied by statements herein, and therefore these statements should not be read as guarantees of future performance or results. All forward-looking statements are based on the Company's current beliefs as well as assumptions made by and information currently available to it as well as other factors. Readers are cautioned not to place undue reliance on these forward-looking statements, which speak only as of the date of this press release. Due to risks and uncertainties, including the risks and uncertainties identified by the Company in its public securities filings, actual events may differ materially from current expectations. The Company disclaims any intention or obligation to update or revise any forward-looking statements, whether as a result of new information, future events or otherwise.
For further information please consult the Company's website at: www.promisneurosciences.com
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SOURCE ProMIS Neurosciences Inc.