ProMIS Neurosciences Presents Alzheimer’s Advances, PMN 310 Updates, at 2017 AAN Meeting

ProMIS Neurosciences Presents Alzheimer’s Advances, PMN 310 Updates, at 2017 AAN Meeting

Canada’s ProMIS Neurosciences today presented the latest results of its Alzheimer’s disease therapeutic program and discussed its lead candidate drug PMN 310 on the final day of the April 22-28 annual meeting of the American Academy of Neurology in Boston.

The company’s chief development officer, Johanne Kaplan, presented the poster, “Achieving the optimal profile for Alzheimer’s immunotherapy: Rational generation of antibodies specific for toxic Aβ oligomers,” which were written by Dr. Steven Plotkin and his team.

The presentation’s authors predict five distinct targets on toxic pathogenic Aβ oligomers, using the company’s Collective Coordinates platform, which  predicts novel targets known as disease specific epitopes (DSEs). ProMIS also gave an update on its lead product candidate, PMN 310.

“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 (Aβ) — will demonstrate a ‘best in class’ product profile for treatment of AD,” the company’s president and CEO, Dr. Elliot Goldstein, said in a press release. “Indeed, by virtually no binding to Aβ monomer, ProMIS mAb products should allow improved efficacy by avoiding targeting of this abundant, non-toxic form of Aβ. Similarly, by not targeting plaque which is associated with neurovascular edema — a dose-limiting adverse event — we anticipate improved safety and tolerability for our products.”

The monoclonal antibody (mAb) PMN 310 was shown to preserve cognitive function in preclinical studies evaluating short-term memory retention.

In a previous study that led to ProMIS making PMN 310 its lead candidate, the company tested the drug in mice models. Researchers observed that when normal mice were exposed to an object, they would remember it and spend more time exploring a newly introduced object. However, when mice given oligomer lost the ability to discriminate between known and novel objects, they spent equivalent amounts of time exploring both.

These results suggest that giving PMN 310 to mice completely prevented the loss of short-term memory formation caused by toxic molecules.

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