ProMIS Neurosciences’ PMN310 antibody demonstrates significant cognitive benefit in a mouse model of Alzheimer’s disease
Transgenic mouse model reflects latest scientific understanding of disease – toxic oligomers of amyloid create cognitive deficit
Excerpt from the Press Release:
ORONTO, Ontario and CAMBRIDGE, Mass., March 02, 2022 (GLOBE NEWSWIRE) — ProMIS Neurosciences, Inc. (TSX: PMN) (OTCQB: ARFXF), a biotechnology company focused on the discovery and development of antibody therapeutics targeting misfolded proteins such as toxic oligomers, announced today that PMN310, its lead antibody therapeutic candidate for Alzheimer’s disease (AD), showed a significant cognitive benefit in a widely recognized animal model of AD.
The APP/L mouse is a “transgenic” model of AD in which human amyloid-beta oligomers lead to cognitive deficits. In this model, treatment with PMN310 which selectively targets toxic oligomers of amyloid-beta preserved memory using the water maze readout, to the extent that the PMN310 treated mice were indistinguishable from “non-transgenic” control mice.
“This model closely aligns with the most current understanding of the biology of Alzheimer’s disease, that small clumps of misfolded amyloid-beta (toxic oligomers) are the most pathogenic species1”, stated Dr. Neil Cashman, ProMIS Chief Scientific Officer. “In our opinion, studies in transgenic mouse models that focus on plaque removal or monomer depletion are not representative of human disease. Indeed, drug candidates that showed plaque reduction in animal models were disappointing in the clinic, and targeting amyloid monomers which worked in these models, universally failed in clinical trials.”
This positive result builds on earlier in vivo data for PMN310. We have previously published2 on the protective activity of PMN310 in a novel object recognition model where toxic oligomers of amyloid-beta are injected in the brain of mice to create a memory deficit. In this model, co-injection of PMN310 prevented the loss of memory caused by toxic oligomers.
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