Continued Promise for BAN2401—An Anti-Amyloid β Protofibril Antibody 

  • Alzheimer Disease
  • Dementia

In multiple presentations at the Alzheimer’s Association International Conference in Los Angeles, July 14-18, 2019, data suggest continued promise of BAN2401 (Eisai, Woodcliff Lake, NJ) for treatment of Alzheimer’s disease. 

Because of safety concerns for APOE4 carriers, the phase 2 clinical study of BAN2401 (NCT01767311) had a nontraditional Bayesian study design that left some questions regarding the results of the trial. Analysis was conducted that showed when the data was converted into the more familiar frequency-based statistical analysis, statistical significance of the treatment effect remained. In addition, results estimated for what would have occurred if proportional groups of people who were APOE4 carriers or noncarriers had been studied suggest a larger treatment effect would have occurred. 

A pharmacokinetic study showed that BAN2401 binds amyloid β (Aβ) protofibrils 30 times more strongly than other antibodies to Aβ protofibrils in vitro, suggesting that the primary target of BAN2401 is novel, and thus has continued promise despite the failure of several other amyloid-targeting investigative agents that have failed in clinical trials.

Data from a subgroup of participants in the phase 2 study who consented to have cerebrospinal fluid drawn and analyzed at various timepoints was also presented.  Individuals who received 10mg/kg once or twice per month (n = 23) had reduced phosphorylated tau (p-tau) levels (-13%), neurogranin (-11%) and slower increase in neurofilament light (NfL) levels (-48%) compared to those who received placebo over the 18-month trial period. Biomarker reductions were greater in people who were ApoE4 carriers vs noncarriers.

The new data also shows a positive correlation between clinical cognition endpoints and reduction of amyloid beta in the brain at 12 months and 18 months of treatment. Increased exposure to BAN2401 measured by serum concentrations correlated with larger reductions of amyloid beta in the brain measured by PET imaging.
Taken together these results support continued research into BAN2401 as a potential disease-modifying treatment for AD as well as the role of Aβ protofibrils in the disease process.  

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