Setanaxib (GKT137831) effectively inhibits Nox1/4 (Kis=140±40/110±30 nM)[1]. Setanaxib (GKT137831) administration during a 72-hour normoxia or hypoxia exposure reduces HPASMC proliferation under normoxic conditions at 20 μM but does not affect HPAEC proliferation in normoxia. In prevention studies, Setanaxib (GKT137831) reduces proliferation induced by hypoxia in both HPASMCs and HPAECs at concentrations of 5 and 20 μM. Further tests, including PCNA expression or manual cell counting, confirm that Setanaxib (GKT137831) diminishes hypoxia-induced proliferation in pulmonary vascular cells[2].
体内研究
In the latter phase of CCl4 injections, some mice receive daily doses of Setanaxib (GKT137831). CCl4 causes more severe liver fibrosis in SOD1mu mice than in WT mice. However, Setanaxib (GKT137831) treatment lessens liver fibrosis in both SOD1mu and WT mice. Additionally, the elevated α-SMA expression in the livers of SOD1mu mice treated with Setanaxib (GKT137831) is significantly reduced, aligning with levels seen in WT mice treated with the NOX1/4 inhibitor[1].
Setanaxib (GKT137831) administration during a 72-hour normoxia or hypoxia exposure reduces HPASMC proliferation under normoxic conditions at 20 μM but does not affect HPAEC proliferation in normoxia. In prevention studies, Setanaxib (GKT137831) reduces proliferation induced by hypoxia in both HPASMCs and HPAECs at concentrations of 5 and 20 μM. Further tests, including PCNA expression or manual cell counting, confirm that Setanaxib (GKT137831) diminishes hypoxia-induced proliferation in pulmonary vascular cells[2].
搜索
