包装 | 价格(元) |
10mM (in 1mL DMSO) | 电议 |
2mg | 电议 |
5mg | 电议 |
10mg | 电议 |
50mg | 电议 |
Cell lines | Monolayers of HPAECs and HPASMCs, Pulmonary artery endothelial cells |
Preparation method | Soluble in DMSO. General tips for obtaining a higher concentration: Please warm the tube at 37 ℃ for 10 minutes and/or shake it in the ultrasonic bath for a while. Stock solution can be stored below -20℃ for several months. |
Reacting condition | 0.1–20 μM, 24 hours |
Applications | GKT137831 (5 μM, 20 μM) attenuated hypoxia-induced HPAECs and HPASMCs proliferation. GKT137831 (20 μM) attenuated hypoxia-induced H2O2 generation in HPAECs and HPASMCs. During the entire 72-hour hypoxia exposure, GKT137831 administration during the last 24 hours attenuated hypoxia-induced reductions in HPAEC and HPASMC PPARγ expression. |
Animal models | C57Bl/6 mice exposed to normoxic or hypoxic conditions for 3 weeks, wild-type (WT) and SOD1G37R mutant C57BL/6J mice, Diabetic apolipoprotein E-deficient mice |
Dosage form | Oral gavage, 30 or 60 mg/kg/d, daily for 10 days |
Application | GKT137831 (30 or 60 mg/kg/d) attenuated chronic hypoxia-induced right ventricular hypertrophy, pulmonary vascular remodeling, increases in vessel wall thickness, and proliferation. GKT137831 attenuated hypoxia-induced reductions in PPARγ and increased in TGF-β1 expression. In WT and SOD1mut mice, GKT137831 (60 mg/kg, intragastric (IG) injection) blocked liver fibrosis and downregulated markers of oxidative stress, inflammation, and fibrosis. In diabetic apolipoprotein E-deficient mice, GKT137831 (60 mg/kg/d, p.o.) attenuated diabetes mellitus-accelerated atherosclerosis. |
Other notes | Please test the solubility of all compounds indoor, and the actual solubility may slightly differ with the theoretical value. This is caused by an experimental system error and it is normal. |
产品描述 | Ki: 140 nM and 110 nM GKT137831 is a specific dual NADPH oxidase Nox1/Nox4 inhibitor, respectively[1]. Both Nox1 and Nox4 expressed in vascular smooth muscle cells (VSMCs) are targeted to discreet intracellular locations, are differentially regulated in response to growth factors and vascular injury, and are activated by distinct mechanis In vitro: GKT137831 lowers hypoxia-induced H(2)O(2) release, cell proliferation, and TGF-β1 expression and attenuated reductions in PPARγ in HPAECs and HPASMCs. [2] GKT137831 also is a blockade of oxidative stress in response to hyperglycemia in human aortic endothelial cells. [3] In vivo: In WT and SOD1mut mice, GKT137831 (60 mg/kg i.g.) prevents liver fibrosis and downregulates markers of oxidative stress, inflammation, and fibrosis. [1] In mouse model of chronic hypoxia exposure, GKT137831 (60 mg/kg/d p.o.) attenuates lung PPARγ and TGF-β1 expression of chronic hypoxia–induced right ventricular hypertrophy, vascular remodeling, lung cell proliferation, and hypoxic alterations [2]. GKT137831 (60 mg/kg/d p.o.) also attenuates diabetes mellitus-stimulated atherosclerosis in diabetic apolipoprotein E-deficient mice. [3] Furtermore, GKT137831 prevents the increase of oxidative stress in angII-infused c-hNox4Tg mice, abolishes Akt-mTOR and NF-κB signaling pathway and lowers cardiac remodeling. [4] Clinical trial: Clinical study has been conducted. References: |