FCPR03

Research use only, not for human use.

FCPR03 is a selective inhibitor of phosphodiesterase 4 (PDE4) with IC50s of 31 nM, 47 nM, and 60 nM for PDE4B1, PDE4D7, and PDE4 catalytic domain, respectively.

FCPR03 is a selective inhibitor of phosphodiesterase 4 (PDE4) with IC50s of 31 nM, 47 nM, and 60 nM for PDE4B1, PDE4D7, and PDE4 catalytic domain, respectively. FCPR03 has neuroprotective, anti-inflammatory, and antidepressant-like effects.(In Vitro):FCPR03 displays at least 2100-fold selectivity over other PDEs (PDE1-3 and PDE5-11). In HT-22 cells, FCPR03 (5, 10, and 20 μM) increases cell viability under the oxygen-glucose deprivation (OGD) induced condition in a dose-dependent manner. FCPR03 (20 μM) increases the levels of phosphorylated AKT, GSK-3β, and β-catenin. FCPR03 (20 μM) protects against OGD-induced cellular apoptosis in both HT-22 cells and cortical neurons. The levels of mitochondrial membrane potential (MMP) and ROS are restored by FCPR03. FCPR03 (10 μM) shows significant protective effects.(In Vivo):In adult male Sprague-Dawley rats following cerebral ischemia-reperfusion, FCPR03 increases the levels of phosphorylated AKT, GSK3β and β-catenin within the ischemic penumbra. In rats following MCAO, FCPR03 (1.25, 2.5, 5 mg/kg; i.p.) reduces the infarct volume and improves neurobehavioral outcomes.

FCPR03 (5-20 μM; 30 hours; HT-22 cells) treatment increases cell viability (oxygen-glucose deprivation (OGD)-induced) in a dose-dependent manner, and 10 μM FCPR03 shows significant protective effects.FCPR03 (20 μM; 30 hours; HT-22 cells) treatment protects against OGD-induced cellular apoptosis in both HT-22 cells and cortical neurons. The levels of mitochondrial membrane potential (MMP) and ROS are also restored by FCPR03.FCPR03 (20 μM; 30 hours; HT-22 cells) treatment increases the levels of phosphorylated AKT, glycogen synthase kinase-3β (GSK3β), and β-catenin.Cell Viability Assay Cell Line:HT-22 cells Concentration:5 μM, 10 μM, 20 μM Incubation Time:30 hours Result:Increased cell viability in a dose-dependent manner.Apoptosis Analysis Cell Line:HT-22 cells Concentration:20 μM Incubation Time:30 hours Result:Reversed the effects of OGD and decreased the ratio of apoptotic cells.Western Blot Analysis Cell Line:HT-22 cells Concentration:20 μM Incubation Time:30 hours Result:Increased the levels of phosphorylated AKT, glycogen synthase kinase-3β (GSK3β), and β-catenin.

FCPR03 (1.25-5 mg/kg; intraperitoneal injection; once; adult male Sprague-Dawley rats) treatment reduces the infarct volume and improves neurobehavioral outcomes in rats following MCAO. FCPR03 increases the levels of phosphorylated AKT, GSK3β and β-catenin within the ischemic penumbra of rats following cerebral ischemia-reperfusion. Animal Model:Adult male Sprague-Dawley rats (250-280 g) induced middle cerebral artery occlusion (MCAO) Dosage:1.25 mg/kg, 2.5 mg/kg, 5 mg/kg Administration:Intraperitoneal injection; onceResult:Reduced the infarct volume and improved neurobehavioral outcomes in rats following MCAO.

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Angiogenesis

PDE

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1917347-65-9

299.31

C15H19F2NO3

>98% (HPLC)

In Vitro:?DMSO : 100 mg/mL (334.10 mM)

O=C(NC(C)C)C1=CC=C(OC(F)F)C(OCC2CC2)=C1

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(-20℃)

With Ice Pack

≥ 2 years