A Phase 2 trial involving an investigational monoclonal antibody drug, semorinemab, targeting the tau protein, reduced cognitive decline among adults with mild-to-moderate nervous-system-health disease by about 44%, Swiss biotech AC Immune announced Tuesday.
Findings from the placebo-controlled study Lauriet stemmed from 272 adults with mild-to-moderate Alzheimer’s disease across 43 study sites worldwide. Results indicated the drug, developed by Genentech (member of the Roche Group) resulted in a “statistically significant reduction in cognitive decline” by 43.6% at week 49, however the drug failed to slow the rate of functional decline or meet other efficacy endpoints. The drug was suggested to be safe and well-tolerated, without unanticipated safety signals, according to a company release posted Tuesday.
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The tau protein is one several factors believed to contribute to Alzheimer’s disease when it aggregates into toxic tangles, which can damage cells and kill neurons. The antibody drug semorinemab works by targeting a portion of the tau protein, binding to tau and slowing the spread between neurons, the company said.
“The top line results of the Lauriet Phase 2 clinical trial of semorinemab are remarkable in that it is the first time we have seen a therapeutic effect by a monoclonal anti-Tau antibody therapy,” Prof. Andrea Pfeifer, CEO of AC Immune SA, said in part in the release.
“Nevertheless, despite these interesting results, we are still cautious about what this may mean for patients as there was not an impact on the rate of functional decline or other efficacy endpoints,” Pfeifer said.
The CEO raised hopes for the drug moving forward, as the trial was “relatively short” and Alzheimer’s is a slow-moving disease, adding in part: “…the data from the open-label extension may be important in elucidating the potential of semorinemab in this patient population.”
Genentech said the open-label study portion will proceed as planned, and results will be submitted to appear at the Clinical Trials on Alzheimer’s Disease conference in November, according to AC Immune.
Following the controversial FDA approval of Biogen’s Aduhelm (aducanumab) in June, the first Alzheimer’s drug in nearly two decades, which was said to reduce plaques of another protein in the brain, called amyloid beta, neurologist Douglas Scharre, explained that Aduhelm works by clearing toxic amyloid proteins from brain tissue, though patients with late stage Alzheimer’s disease are unlikely to benefit.
Scharre, director of the division of Cognitive Neurology at Ohio State Wexner Medical Center, and clinical investigator on Biogen’s studies, previously told FOX News that amyloid is “a key initiating constituent” for Alzheimer’s disease, but is only the beginning. He compared the toxic amyloid protein buildup to a boulder rolling down a hill: if we can remove the boulder, perhaps we can prevent an avalanche, which underscores the idea of removing amyloid from the brain early.
“The true help with Alzheimer’s I think is going to come when we have five or six of these treatments [like mitigating for the tau protein, reducing chronic inflammation, keeping brain cells healthier and addressing metabolic issues] that we can all focus on these individuals, and then we will see real, significant impact on the devastation of this disease,” Scharre previously said after the FDA approval.
