MRL828

MRL828 (0.1-10 μM; 48 h) potently reduces aggregated tau in tau aggregation-induced CHO T-REx P301L cells with a DC₅₀ of 20 nM, while exerting minimal effects on cell viability. Its pharmacodynamic activity depends on the combined action of the tau-binding domain and the autophagy-targeting domain^[1].
The reduction of aggregated tau induced by MRL828 (1 μM; 24-48 h) in tau aggregation-induced CHO T-REx P301L cells depends on p62 and VPS34, components of the autophagy pathway^[1].
MRL828 (1 μM; 48 h) selectively reduces aggregated and phosphorylated tau species in tau aggregation-induced CHO T-REx MAPT^P301L cells, with the greatest reduction observed in detergent-insoluble tau aggregates^[1].
MRL828 (1 μM; 24-48 h) reduces aggregated tau in tau aggregation-induced CHO T-REx tau^P301L cells via an autophagy-dependent, lysosome-independent mechanism that involves increased secretion levels of oligomerized and phosphorylated tau isoforms^[1].
MRL828 (1 μM, 24-48 h) still reduces tau aggregates in the presence of Bafilomycin A1 (HY-100558, 25 nM) or Hydroxychloroquine (HY-W031727, 15 μM), and does not increase the colocalization of MC1-positive tau puncta with the lysosomal marker LAMP2 at 24 h, indicating that its mechanism of action is independent of lysosomes.^[1]

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.