Semorinemab Fails to Show Efficacy in Early Alzheimer’s Phase 2 Trial

Semorinemab Fails to Show Efficacy in Early Alzheimer’s Phase 2 Trial
Note: This story was updated Oct. 12, 2020, to note that semorinemab is intended to target phosphorylated and non-phosphorylated forms of tau.  Semorinemab, a monoclonal antibody against tau, failed to significantly alter dementia's progression in people with early Alzheimer's disease (AD) taking part in a Phase 2 clinical trial. The investigational therapy, which is being jointly developed by AC Immune and Genentech (a Roche company), also failed to meet secondary trial goals related to cognition and daily living. "Today’s news is surprising and disappointing, given what we as a field know about Tau and its strong spatiotemporal correlation with both symptoms and pathology in AD," Andrea Pfeifer, PhD, CEO of AC Immune, said in a press release. Among the molecular changes that happen in the brains of people with Alzheimer's is the formation of abnormal "tangles" made of the protein tau. In Alzheimer's, tangles made of tau — particularly phosphorylated tau, which refers to the tau protein with a phosphoryl group attached to it — are thought to drive disease progression. Semorinemab, an antibody that targets phosphorylated and non-phosphorylated forms of tau, was designed to lessen the extent of these tangles in the brain, thereby easing disease progression. The experimental antibody was evaluated in the Genentech-sponsored Phase 2 clinical trial called TAURIEL (NCT03289143), which enrolled 457 people with early (prodromal to mild) Alzheimer's across 97 global sites. For 73 weeks, patient were given either semorinemab (three different doses) or a placebo, administered intravenously (by injection directly into the bloodstream). The trial's main measure of treatment effectiveness was changes in scores on the Clinical Dementia Rating-Sum of Boxes
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