Genentech and AC Immune reported the Phase 2 TAURIEL trial evaluating the anti-Tau antibody, semorinemab, in early (prodromal to mild) Alzheimer’s disease (AD), did not meet its primary efficacy endpoint of reducing decline on Clinical Dementia Rating-Sum of Boxes (CDR-SB) compared to placebo. Two secondary endpoints, Alzheimer’s Disease Assessment Scale-Cognitive Subscale 13 (ADAS-Cog13) and Alzheimer’s Disease Cooperative Study Group – Activities of Daily Living Inventory (ADCS-ADL) were also not met.
TAURIEL was a 73-week, double-blind, placebo-controlled trial to determine if semorinemab can slow the rate of clinical decline in early (prodromal to mild) AD. The study followed 457 participants across 97 study centers. Overall, the incidence of adverse events was similar between semorinemab and placebo arms and further analysis of these safety data are currently underway. Analysis of additional data, including biomarkers such as Tau-PET, are ongoing. Genentech plans to present the results from the study at an upcoming medical congress. The second Phase 2 (LAURIET) study of semorinemab, in patients with moderate AD, is ongoing.
AC Immune entered into an exclusive worldwide license agreement and research collaboration with Genentech in 2012 for the research, development and commercialization of semorinemab, for the potential treatment of Alzheimer’s disease and other neurodegenerative diseases.
Semorinemab is an anti-Tau antibody. Tau protein has been largely regarded as a promising target for AD because tau tangles have been typically observed in brains of AD patients. The severity of tau pathology is closely correlated with the progression of cognitive decline of AD patients.
Early (prodromal to mild) Alzheimer’s disease
The prodromal stage of AD is also referred to as mild cognitive impairment (MCI) due to AD, and this is the stage where there are obvious symptoms of brain dysfunction. Not only does the individual have to meet criteria for MCI but also the primary underlying pathophysiology is judged by a clinician to be due to AD.5 This can be verified most accurately if there is biomarker evidence of accumulating AD neuropathology. Even without biomarker evidence, however, an experienced clinician can make the diagnosis of prodromal AD if based on their assessments and evaluations, the likely underlying pathophysiology is thought to be AD.