| Bioactivity | FCPR03 is a potent and selective phosphodiesterase 4 (PDE4) inhibitor with IC50 values of 60 nM, 31 nM and 47 nM for PDE4 catalytic domain, PDE4B1 and PDE4D7, respectively. FCPR03 displays at least 2100-fold selectivity over other PDEs (PDE1-3 and PDE5-11). FCPR03 has anti-inflammatory, neuroprotective and antidepressant-like effects[1][2]. | ||||||||||||
| Invitro | 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[1].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[1].FCPR03 (20 μM; 30 hours; HT-22 cells) treatment increases the levels of phosphorylated AKT, glycogen synthase kinase-3β (GSK3β), and β-catenin[1]. Cell Viability Assay[1] Cell Line: | ||||||||||||
| In Vivo | 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[1]. Animal Model: | ||||||||||||
| Name | FCPR03 | ||||||||||||
| CAS | 1917347-65-9 | ||||||||||||
| Formula | C15H19F2NO3 | ||||||||||||
| Molar Mass | 299.31 | ||||||||||||
| Appearance | Solid | ||||||||||||
| Transport | Room temperature in continental US; may vary elsewhere. | ||||||||||||
| Storage |
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| Reference | [1]. Bingtian Xu, et al. FCPR03, a Novel Phosphodiesterase 4 Inhibitor, Alleviates Cerebral ischemia/reperfusion Injury Through Activation of the AKT/GSK3β/ β-catenin Signaling Pathway. Biochem Pharmacol. 2019 May;163:234-249. [2]. Zheng-Qiang Zou, et al. Novel Phosphodiesterase 4 Inhibitor FCPR03 Alleviates Lipopolysaccharide-Induced Neuroinflammation by Regulation of the cAMP/PKA/CREB Signaling Pathway and NF- κ B Inhibition. J Pharmacol Exp Ther. 2017 Jul;362(1):67-77. |