For research use only. Not for therapeutic Use.
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].
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].
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].
| Catalog Number | I015018 |
| CAS Number | 1917347-65-9 |
| Synonyms | 3-(cyclopropylmethoxy)-4-(difluoromethoxy)-N-propan-2-ylbenzamide |
| Molecular Formula | C15H19F2NO3 |
| Purity | ≥95% |
| InChI | InChI=1S/C15H19F2NO3/c1-9(2)18-14(19)11-5-6-12(21-15(16)17)13(7-11)20-8-10-3-4-10/h5-7,9-10,15H,3-4,8H2,1-2H3,(H,18,19) |
| InChIKey | DLTIJXDCEGNJEW-UHFFFAOYSA-N |
| SMILES | CC(C)NC(=O)C1=CC(=C(C=C1)OC(F)F)OCC2CC2 |
| 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. |
