产品
编 号：F332470
分子式：C20H12O2
分子量：284.31
分子式：C20H12O2
分子量：284.31
产品类型
规格
价格
是否有货
5mg
询价
询价
10mg
询价
询价
25mg
询价
询价
50mg
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询价
结构图
CAS No: 3519-82-2
产品详情
生物活性：
INCA-6 (Triptycene-1,4-quinone) is a cell-permeable NFAT inhibitor. INCA-6 specifically blocks targeting of NFAT(P) substrate to the ?calcineurin (CN) phosphatase site and is an effective inhibitor of CN-NFAT signaling.
体内研究：
INCA-6 (5.0, or 25.0 μM) treatment significantly reduces pathologic neovascularization in oxygen-induced retinopathy (OIR).Animal Model:Rats bearing OIR model
Dosage:2.5, 5.0, or 25.0 μM
Administration:Intravitreal injection on days 14(0) and 14(3)
Result:Decreased the severity of OIR in a dose dependent manner. Significant inhibition was seen at 5.0 and 25.0 μM concentrations.
体外研究：
INCA-6 (5 μM; for 24-hour) prevents?transient outward K+?current (Ito)?downregulation in 3-Hz cells.Pre-treatment of BV-2 cells with INCA-6 (10 μM) significantly inhibits ATP-induced CXCL2 expression in BV-2 cells. INCA-6 also inhibits ATP-induced CXCL2 expression in rat primary microglia.?INCA-6 (5 μM) reduces SERCA2 transcript levels as well as protein expression, in the absence or in the presence of ?thapsigargin (TG).INCA-6 (1.0 and 2.5 μM; 24 hours?) treatment significantly decreases both VEGF and serum-induced human retinal microvascular endothelial cells (HRMEC) proliferation, but does not affect baseline proliferation.
INCA-6 (Triptycene-1,4-quinone) is a cell-permeable NFAT inhibitor. INCA-6 specifically blocks targeting of NFAT(P) substrate to the ?calcineurin (CN) phosphatase site and is an effective inhibitor of CN-NFAT signaling.
体内研究：
INCA-6 (5.0, or 25.0 μM) treatment significantly reduces pathologic neovascularization in oxygen-induced retinopathy (OIR).Animal Model:Rats bearing OIR model
Dosage:2.5, 5.0, or 25.0 μM
Administration:Intravitreal injection on days 14(0) and 14(3)
Result:Decreased the severity of OIR in a dose dependent manner. Significant inhibition was seen at 5.0 and 25.0 μM concentrations.
体外研究：
INCA-6 (5 μM; for 24-hour) prevents?transient outward K+?current (Ito)?downregulation in 3-Hz cells.Pre-treatment of BV-2 cells with INCA-6 (10 μM) significantly inhibits ATP-induced CXCL2 expression in BV-2 cells. INCA-6 also inhibits ATP-induced CXCL2 expression in rat primary microglia.?INCA-6 (5 μM) reduces SERCA2 transcript levels as well as protein expression, in the absence or in the presence of ?thapsigargin (TG).INCA-6 (1.0 and 2.5 μM; 24 hours?) treatment significantly decreases both VEGF and serum-induced human retinal microvascular endothelial cells (HRMEC) proliferation, but does not affect baseline proliferation.
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