Sophoflavescenol

Sophoflavescenol is a prenylated flavonol, which shows great inhibitory activity with IC₅₀ of 0.013 μM against Phosphodiesterase 5 (PDE5), and also inhibits RLAR, HRAR, AGE, BACE1, AChE and BChE with IC₅₀s of 0.30 μM, 0.17 μM, 17.89 μg/mL, 10.98 μM, 8.37 μM and 8.21 μM, respectively. IC50 & Target: IC50: 0.013 μM (PDE5), 0.30 μM (RLAR), 0.17 μM (HRAR), 17.89 μg/mL (AGE), 10.98 μM (BACE1), 8.37 μM (AChE), 8.21 μM (BChE) 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^[1]. Sophoflavescenol exhibits remarkable inhibition of RLAR activity with an IC₅₀ value of 0.30 μM, compared with 0.07 μM for epalrestat, a well known ARI. Sophoflavescenol also shows potent inhibitory activity with an IC₅₀ value of 0.17 μM, comparable to epalrestat (0.15 μM) in the HRAR assay. In the AGE assay, sophoflavescenol (IC₅₀ 17.89 μg/mL) is a more potent inhibitor of AGE formation than aminoguanidine (IC₅₀ 81.05 μg/mL). Sophoflavescenol exerts both potent AChE and BChE inhibitory effects with respective IC₅₀ values of 8.37 and 8.21 μM. Sophoflavescenol also exhibits good BACE1 inhibition in a dose-dependent manner with an IC₅₀ value of 10.98 μM^[2]. 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^[3]. 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^[1].