Why I invested in PMNSee the pre-clinical data compared to the competing anti-amyloid approaches at: https://d1io3yog0oux5.cloudfront.net/_885dce8a29ec04d7e57c9212d4e47761/promisneurosciences/db/1004/8793/pdf/2023+AAIC+PMN310+poster.pdf
PMN310 stands out from the competition in its selectivity. It is highly targeted.
PMN310 showed selective binding to oligomers, not monomers, and strong binding to a toxic oligomerenriched fraction from AD brain
• PMN310 protected against the pathogenic activity of Aβ oligomers in vitro, and preserved memory function in two rodent models of AD
• PMN310 targeting of toxic Aβ oligomers was minimally impacted by monomer competition. Antibodies that were outcompeted by pre-exposure to monomers showed no clinical benefit in phase 2/3 trials while antibodies that were less impacted by monomer competition produced positive clinical data
• PMN310 did not react with plaque or vascular deposits in AD brain, avoiding diversion away from toxic oligomers and suggesting that it may reduce the risk of ARIA observed with plaque-binding antibodies
• The greater selectivity of PMN310 for toxic oligomers may translate into greater clinical benefit and a potentially improved safety profile