ChemicalBook--->CAS DataBase List--->1917347-65-9

1917347-65-9

1917347-65-9 Structure

1917347-65-9 Structure
IdentificationBack Directory
[Name]

FCPR03
[CAS]

1917347-65-9
[Synonyms]

FCPR03
[Molecular Formula]

C15H19F2NO3
[MOL File]

1917347-65-9.mol
[Molecular Weight]

299.31
Chemical PropertiesBack Directory
[Boiling point ]

382.3±42.0 °C(Predicted)
[density ]

1.189±0.06 g/cm3(Predicted)
[storage temp. ]

Store at -20°C
[solubility ]

DMSO : 100 mg/mL (334.10 mM; Need ultrasonic)
[form ]

Solid
[pka]

14.16±0.46(Predicted)
[color ]

White to off-white
Hazard InformationBack Directory
[Uses]

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].
[Biological Activity]

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].
[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:Adult male Sprague-Dawley rats (250-280 g) induced middle cerebral artery occlusion (MCAO)[1]
Dosage:1.25 mg/kg, 2.5 mg/kg, 5 mg/kg
Administration:Intraperitoneal injection; once
Result:Reduced the infarct volume and improved neurobehavioral outcomes in rats following MCAO.
[IC 50]

PDE4 catalytic domain: 60 nM (IC50); PDE4B1: 31 nM (IC50); PDE4D7: 47 nM (IC50)
[storage]

Store at -20°C
[References]

[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.
Spectrum DetailBack Directory
[Spectrum Detail]

FCPR03(1917347-65-9)1HNMR
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