ProMIS Neurosciences Oligomer Selective Antibody Therapeutic for Alzheimer's Disease, PMN310, Shows Potential for Improved Safety Profile in Direct Comparison to Other Amyloid Beta-Directed...

ProMIS Neurosciences Oligomer Selective Antibody Therapeutic for Alzheimer's Disease, PMN310, Shows Potential for Improved Safety Profile in Direct Comparison to Other Amyloid Beta-Directed Antibodies in Clinical Development

Lack of PMN310 binding to amyloid deposits in Alzheimer's brain tissue may eliminate dose-limiting brain swelling seen with BAN2401 and aducanumab

 

TORONTO and CAMBRIDGE, Mass., Aug. 21, 2018 (GLOBE NEWSWIRE) -- ProMIS Neurosciences, Inc. (TSX: PMN; OTCQB: ARFXF), a biotechnology company focused on the discovery and development of antibody therapeutics selectively targeting toxic oligomers implicated in the development of neurodegenerative diseases, today announced that its lead antibody candidate for Alzheimer's disease (AD), PMN310, showed no binding to amyloid beta (AB) plaque in AD brain samples in stark contrast to BAN2401 and aducanumab which both displayed robust AB plaque reactivity. These findings extend the results ProMIS announced in January 2018, showing greater selectivity of PMN310 for AB oligomers compared to aducanumab.  Binding of therapeutic antibodies to AB deposits in brain tissue, in particular blood vessels, is believed to underlie the development of ARIA (amyloid-related imaging abnormalities; brain swelling and microhemorrhages) in treated AD patients.   

Commenting on these results, ProMIS President and CEO, Elliot Goldstein, MD, stated: "PMN310 was designed to selectively target soluble toxic AB oligomers, now widely believed to be a root cause of AD. By not targeting AB plaque, especially in and around blood vessels in the brain, we anticipate PMN310 may not be associated with the dose-limiting brain swelling seen with plaque-binding antibody therapeutics like BAN2401 and aducanumab. Confirmation of such an improved safety profile in clinical trials would allow for administration of higher doses to AD patients, thereby potentially leading to greater therapeutic potency of PMN310."

The binding profile of PMN310 in human AD brain tissues was directly compared to that of BAN2401 and aducanumab in a preclinical study using the technique of immunohistochemistry (IHC). Results of the study showed binding of BAN2401 and aducanumab to AB plaque throughout the brain and in association with blood vessels. Conversely, binding of PMN310 to AB plaque was not observed in any region of the AD brain tissues.