Hundreds of people from more than 30 countries descended on the Keystone Resort in Colorado in late June 2019 to discuss healthcare advancements aimed to ease the global burden of neurodegenerative diseases.
It was the annual Keystone Symposium on Neurodegenerative Diseases where everyone from researchers, tech CEOs and healthcare specialists gathered to oversee the latest in technical and conceptual advances that are expected will provide new therapeutic opportunities. The conference has been a premier event for nearly 50 years.
It’s an issue on the minds of many at the event. According to the World Health Organization, up to one billion individuals suffer from neurological disorders worldwide, with over 100 million affected by neurodegenerative diseases like Alzheimer's disease , Parkinson's disease, ALS and other deadly neurodegenerative disorders.
(Image via Keystone Symposium on Neurodegenerative Diseases.)
Front and centre this year was biotech Company ProMIS Neurosciences Inc. (TSX:PMN, OTCQB:ARFXF, Forum) . Operating at the development stage, PMN is focused on discovering and developing antibody therapeutics selectively targeting toxic oligomer proteins that are believed to be behind the development and progression of neurodegenerative diseases. These diseases include Alzheimer’s, amyotrophic lateral sclerosis (ALS) and Parkinson’s disease (PD). ProMIS is a distinct player in this field because its platform is engineered to target toxic proteins exclusively and may be able to be administered in higher doses than competing treatments. Isolating these specific targets, known as Disease Specific Epitopes, on the molecular surface of misfolded proteins requires this unique precision approach. Its lead antibody candidate, PMN310 is being developed to target and treat Alzheimer’s and the Company is also developing novel selective antibody therapeutics for ALS and PD.
ProMIS’ Chief Development Officer Dr. Johanne Kaplan presented data showing that PMN310 possesses superior selectivity for amyloid beta toxic oligomers (AßOs) and improved therapeutic potential compared with other Aß-directed antibodies.
Dr. Kaplan stated that researchers from all over the world attended Keystone to share perspective and discuss future therapy directions.
“There was genuine optimism and a sense of momentum around therapy development efforts for neurodegenerative diseases. There was a general consensus for the need to selectively target the propagating forms of toxic proteins in pursuit of disease modifying therapies: Our data on PMN310 were very well received.”
Dr. Kaplan’s poster, “Selective targeting of HHQK conformational epitope in amyloid-beta oligomer species by PMN310, a monoclonal antibody rationally designed for greater therapeutic potency in Alzheimer’s disease,” presented data indicating that PMN310 possesses:
- Superior selectivity for toxic AßOs in Alzheimer’s brain samples
- Ability to neutralize the neurotoxicity and propagation (spreading) of AßOs
- Potential to safely administer high doses of PMN310 (reduced risk of brain edema) and achieve greater therapeutic potency compared with other Aß-directed antibodies.
Dr. Kaplan added further context for investors that evidence shows that these AßOs - not amyloid plaque as commonly believed - are the key targets for Alzheimer's disease therapy.
“The current therapeutic gap lies in how to effectively neutralize the toxic oligomer without wasting antibody on non-toxic forms of the protein. We're pleased our data will help inform discussions regarding future directions among the world's most accomplished researchers. Our data demonstrate the unique ability of the ProMIS discovery platform to generate antibodies that bind the toxic species of amyloid beta while preserving healthy forms of the protein. Humanized PMN310 is currently in advanced preclinical development.”
For a deeper look into Dr. Kaplan’s story and her perspective on research highlights from the conference, download Episode 8 of the podcast Saving Minds, available on Apple Podcasts and Spotify.
promisneurosciences.com
FULL DISCLOSURE: This is a paid article produced by Stockhouse Publishing.