Anavex Life Sciences Corp (AVXL)

[crescentmotor]

Even within that subgroup {ABCLEAR3], there is no established amyloid or tau biomarker effect.

Blarcamesine's MOA is designed to enhance autophagy, a process upstream from conventional pathologies that later result in aggregated ß-amyloid or fibrillary tangles. So far as I have seen, amyloid or tau biomarker readings were primarily used for patient selection baseline criteria to establish the existence of AD. Can you show me where changes in the baseline amyloid or tau readings were prespecified as clinical trial primary outcomes in AVXL's 2b/III trial? I only remember them being cited as "other endpoints". I'm not sure changes in these biomarkers are even related to Blarcamesine's MOA in patients benefitting from treatment because Blarcamesine would not be expected to reverse prior damage; however, the placebo group readings would be expected to increase with the passage of time.