Ezurpimtrostat hydrochloride

Ezurpimtrostat (2-6 μM; 24 h) hydrochloride blocks late-stage autophagic flux in uninfected Vero E6 cells, with a dose-dependent increase in LC3-II and p62 accumulation^[2].
Ezurpimtrostat (2 h pre-treatment, 24 h infection incubation) hydrochloride Ezurpimtrostat potently inhibits SARS-CoV-2 replication in Vero E6 and Calu-3 cells, with EC₅₀ values of 0.04 μM, 0.006 μM, and 1.1 μM, and CC₅₀ values of 8.19 μM, 2 μM, and 4.6 μM against the IHUMI-6 and USA-WA1/2020 strains^[2].
Ezurpimtrostat (1 μM; 2 h pre-treatment, 48 h infection incubation) hydrochloride enhances LC3B cluster formation and signal in SARS-CoV-2-infected Vero E6 cells at 1 μM, and colocalizes with SARS-CoV-2 in LAMP2-positive lysosomes, indicating modulation of the autophagy pathway during viral infection^[2].
Ezurpimtrostat (4 μM; 2 h pre-treatment, 24 h infection incubation) hydrochloride treatment at 4 μM increases autophagic vacuole volume and induces multilamellar body formation in SARS-CoV-2-infected Vero E6 cells, indicating disruption of autophagosome-lysosome fusion^[2].
Ezurpimtrostat (72 h) hydrochloride potently inhibits the viability of a broad panel of human cancer cell lines and primary HCC cells^[3].
Ezurpimtrostat (0-4 μM; 6-48 h) hydrochloride induces caspase-dependent apoptotic cell death in HepG2 cells in vitro in a dose- and time-dependent manner, with significant caspase activation observed after 24 hours of treatment^[3].
Ezurpimtrostat (10 μM GNS561D; 90 min) hydrochloride is a lysosomotropic agent that accumulates in HepG2 cell lysosomes, and its antitumor activity in these cells is dependent on this lysosomal localization^[3].
Ezurpimtrostat (0.5-10 μM; 1-24 h) hydrochloride modulates lysosomal function in HepG2 cells by inducing lysosomal enlargement, lysosomal unbound Zn²⁺ accumulation, impaired cathepsin maturation and activity, and blockage of autophagic flux^[3].
Ezurpimtrostat (0.5-100 μM; 3-24 h) hydrochloride binds to and inhibits PPT1 in HepG2 cells, leading to MTOR displacement from the lysosomal membrane and autophagic flux inhibition; its antitumor activity is partially mediated by PPT1 inhibition, with additional contributing mechanisms^[3].
Ezurpimtrostat (1-3 μM; 24-48 h) hydrochloride induces lysosomal membrane permeabilization in HepG2 cells, leading to cathepsin release and partially CTSB- and CTSD-dependent apoptotic cell death^[3].

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