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Promis Neurosciences Inc. (PMN.V) has designated PMN 310, a monoclonal antibody (mAb), as its first lead product for development in Alzheimer's disease (AD).

"We previously demonstrated that the mAb therapeutic candidates Promis is developing display the optimal target profile of selectively binding prion-like forms of As and inhibiting both their propagation (spreading) and neurotoxicity in laboratory tests (in vitro)," stated Dr. Neil Cashman, Promis chief scientific officer. "We have now achieved a significant development milestone by demonstrating that PMN 310 directly blocks the neurotoxicity of these prion-like forms of (As) in a well-validated mouse model."

The neuroprotective effect of PMN 310 was investigated at a well-recognized contract research organization (CRO) specializing in neurodegenerative diseases. Injection of prion-like forms of As (also called toxic oligomers) into the brains of mice causes a neurological deficit that can be assessed in a memory-behaviour test called novel object recognition. Normal mice exposed to an object remember the familiar object when re-exposed to it and spend more time exploring a newly introduced object. In contrast, oligomer-injected mice lose the ability to discriminate between known and novel objects and spend equivalent amounts of time exploring both. Results obtained in this assay showed that administration of PMN 310 to mice completely prevented the loss of short-term memory formation caused by toxic oligomers.

"The past year has been devoted to characterizing our mAbs with a view to select and prioritize our therapeutic candidates for AD; these compelling in vivo results have led us to declare PMN 310 our first lead product for development in AD," commented Eugene Williams, Promis executive chairman. "Furthermore, the animal model used is particularly relevant to recent scientific developments that toxic prion-like forms of As are the appropriate target for therapy, and, to our knowledge, PMN 310 is the first mAb specifically designed to address this target."