The drug has been tested in Phase 1 and 2 trials for Crohn’s, but human testing stumbled over local side effects to the infused drug formulation. Recently, the company developing the drug came up with an oral preparation and is now trying to resume clinical trials.

Bacher reported first testing CNI-1493 in cell lines overexpressing APP. The compound left APP processing unchanged but, in dose-dependent fashion, reduced levels of secreted oligomers as detected by the A11 antibody (Kayed et al., 2003). Then Bacher and colleagues treated CRND8 mice with the drug for eight weeks between four and six months of age, when this model progresses from moderate to advanced disease (McLaurin Keystone story). Bacher reported seeing a drastic reduction of soluble brain Aβ levels, as well as of plaques in cortex and hippocampus. Bacher showed no data on the Morris water maze but reported that the treated mice performed better on a novel object recognition task. Besides binding to Aβ, the compound also pacifies microglia in the brain, according to Bacher; however, no detailed cytokine analysis was performed to characterize the microglial response in this mouse model further. In this initial study, the scientists did not yet look for changes of Aβ in plasma or effects on CAA. According to Bacher, this data is in press at the Journal of Experimental Medicine.—Gabrielle Strobel.