CA77.1 (oral gavage; 10 mg/kg; single dose) exhibits brain penetration with favorable pharmacokinetics. Its Cmax, AUClast, Tmax, and T1/2 are 3534 ng/g, 8338 h*ng/g, 1 hour, and 1.89 hours, respectively^[1].

CA77.1 (oral gavage; 30 mg/kg; 6 months) normalizes the locomotor hyperactivity of PS19 mice to control levels and decreases the levels and number of neurons with pathogenic tau conformations in the hippocampus, amygdala, and piriform cortex. Additionally, the elevated number of microglial cells and the presence of large Iba1-positive cells with rod-like dystrophic morphology in vehicle-treated PS19 mice are reduced following CA77.1 treatment^[1].

CA77.1 (0-30 µM; 16 hours) activates CMA in NIH 3T3 cells, which stably express the KFERQ-PS-Dendra reporter, in a dose- and time-dependent manner. CMA activity is measured by the average number of fluorescent puncta per cell^[1].

CA77.1 (20 µM; 6 hours) does not affect LC3-II expression or autophagic flux in NIH 3T3 cells^[1].