216450-65-6

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)

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.

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.