Sophoflavescenol is a prenylated flavonol, which shows great inhibitory activity with IC 50 of 0.013 μM against Phosphodiesterase 5 (PDE5) , and also inhibits RLAR, HRAR, AGE, BACE1 , AChE and BChE with IC 50 s of 0.30 µM, 0.17 µM, 17.89 µg/mL, 10.98 µM,
Storage Temp
Store at 2-8°C,Protected from light,Desiccated
Shipped In
Wet ice
Product Description
Sophoflavescenol is a prenylated flavonol, which shows great inhibitory activity with IC 50 of 0.013 μM against Phosphodiesterase 5 (PDE5) , and also inhibits RLAR, HRAR, AGE, BACE1 , AChE and BChE with IC 50 s of 0.30 µM, 0.17 µM, 17.89 µg/mL, 10.98 µM, 8.37 µM and 8.21 µM, respectively.
In Vitro
Sophoflavescenol shows cytotoxicity against human leukaemia (HL-60), Lewis lung carcinoma (LLC), and human lung adenocarcinoma epithelial (A549) cells. Sophoflavescenol exerts notable anti-inflammatory activity by inhibiting nitric oxide generation and tert-butylhydroperoxide-induced ROS generation rather than inhibiting nuclear factor kappa B activation in RAW 264.7 cells. Sophoflavescenol exhibits remarkable inhibition of RLAR activity with an IC 50 value of 0.30 µM, compared with 0.07 µM for epalrestat, a well known ARI. Sophoflavescenol also shows potent inhibitory activity with an IC 50 value of 0.17 µM, comparable to epalrestat (0.15 µM) in the HRAR assay. In the AGE assay, sophoflavescenol (IC 50 17.89 µg/mL) is a more potent inhibitor of AGE formation than aminoguanidine (IC 50 81.05 µg/mL). Sophoflavescenol exerts both potent AChE and BChE inhibitory effects with respective IC 50 values of 8.37 and 8.21 µM. Sophoflavescenol also exhibits good BACE1 inhibition in a dose-dependent manner with an IC 50 value of 10.98 µM. Sophoflavescenol is a mixed inhibitor (K i =0.005 μM) against cGMP PDE5. Sophoflavescenol shows greatest selectivity toward PDE5, 31.5- and 196.2-fold over PDE3 and PDE4, respectively. MCE has not independently confirmed the accuracy of these methods. They are for reference only.
In Vivo
Sophoflavescenol exerts potent in vivo antitumor activity by tumor growth inhibition in the LLC tumor model as well as apoptotic activity by caspase-3 activation in HL-60 cells . MCE has not independently confirmed the accuracy of these methods. They are for reference only.
