Other therapies go after both forms of amyloid beta, giving PMN310 an important safety edge, ProMIS said. The study involved both human brain cells in a lab and mice.
A key implication of the findings is that researchers should be able to increase doses of PMN310 in clinical trials without harming patients, a possibility that’s unlikely in human studies of other therapies, ProMIS said. Research has shown that increasing doses of other therapies has led to bleeding in the brain.
Their inability to hone in on toxic forms only may be behind the alterations that scientists have seen in treated patients’ brains, researchers suggested. These include brain swelling and bleeding.
“PMN310 was designed to selectively target the toxic, prion-like Aβ [amyloid beta] oligomers, now widely believed to be a root cause of AD [Alzheimer’s disease],” Dr. Elliot Goldstein, the president and chief executive officer of ProMIS Neurosciences, said in a press release. “By not targeting [non-toxic] Aβ 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 aducanumab.
“Confirmation of such an improved safety profile in clinical trials would allow for administration of higher doses to AD patients, thereby leading to greater therapeutic potency of PMN310,” Goldstein added.
The new study compared how PMN310, bapineuzumab and aducanumab bind with amyloid beta.
While bapineuzumab and aducanumab bound with both toxic and non-toxic amyloid beta in the brain, PMN310 bound only with harmful forms of the protein, researchers discovered.
Their findings confirmed the results of studies comparing PMN310 and aducanumab.
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