AMZ30

AMZ30 is selective protein phosphatase methylesterase-1(PME-1) inhibitor with IC₅₀s of 600 nM and 3.5 µM in human cell lysates and in HEK 293T cells, respectively. AMZ30 shows >100-fold selectivity relative to other serine hydrolases. AMZ30 reduces the demethylated form of PP2A in living cells. AMZ30 attenuates muscle cell differentiation. AMZ30 increases the resistance of U87MG and U251MG glioblastoma cells to t-BHP-induced oxidative stress. AMZ30can be used for the study of glioblastoma^[1][2][3]. In Vitro:AMZ30 (50 μM, 24 h) treatment of C2C12 cells significantly inhibits the expression of muscle cell differentiation markers myosin heavy chain (MyHC) and myogenin during differentiation, while moderately but significantly increasing the level of the PP2A catalytic subunit^[1].
AMZ30 (10-40 μM, 24 h) treatment of C2C12 cells transfected with the AP-1 reporter gene significantly reduces AP-1 reporter gene activity^[1].
AMZ30 (50 μM, 24 h) mediates inhibition of Ppme1 and attenuates MAP kinase signaling in C2C12 cells^[1].
AMZ30 (20 μM, 1 h pretreatment) increases the resistance of U87MG and U251MG glioblastoma cells to t-BHP-induced oxidative stress^[2].
AMZ30 (20 μM, 1 h pretreatment) abolishes the sensitizing effect of PME-1 overexpression in U87MG cells and eliminates the increased sensitivity of U251MG shGFP cells to t-BHP-induced oxidative stress^[2].
AMZ30 (20 μM, 1 h) significantly reduces the demethylated form of PP2A and increases the methylated form in HEK 293T cells stably overexpressing PME-1^[3].