Results of Lilly’s Solanezumab trial confirm the “real” beta-Amyloid hypothesis
EXPEDITION 3 was the third pivotal trial failure for Lilly’s Solanezumab
- All three trials failed for the same reason: the product binds monomer
The most recent beta-Amyloid science demonstrates that the primary form of beta-Amyloid that kills neurons and causes Alzheimer’s is the
prion (or toxic oligomer), not beta-Amyloid monomer, and not plaque.
- Biogen’s Aducanumab demonstrated efficacy in a phase 2 trial because it does not bind monomer, but was associated with brain swelling because it binds plaque
- ProMIS portfolio does not bind monomer, or plaque, and can be personalized using a companion diagnostic
- The “updated” Aß hypothesis, suggests that Aducanumab will have a therapeutic window, but ProMIS products will be more effective
ProMIS optimal product profile is based on selective targeting of prions: clear differentiation from competitive products
Gene Williams 617.460.0978 eugene.williams@promisneurosciences.com
Elliot Goldstein 415.341.5783 elliot.goldstein@promisneurosciences.com
FULL DISCLOSURE: ProMis Neurosciences Inc. is a paid client of Stockhouse Publishing.