Sanggenon C

Sanggenon C, a flavonoid, exerts protective effects against cardiac hypertrophy and fibrosis via suppression of the calcineurin/NFAT2 pathway. Sanggenon C inhibits mitochondrial fission to induce apoptosis by blocking the ERK signaling pathway. Sanggenon C inhibits inducible nitric oxide synthase expression in RAW264.7 cells, and TNF-α-stimulated cell adhesion and VCAM-1 expression, by suppressing NF-κB activity. Sanggenon C possesses antioxidant, anti-inflammatory and antitumor activities^[1][2]. IC50 & Target:calcineurin/NFAT2, NF-κB^[1] In Vitro:Sanggenon C (4-12 μM; 24 h) inhibits the proliferation of human gastric cancer (GC) cells and greatly reduces the number of GC cell colonies formed^[2].
Sanggenon C (6-10 μM; 24 h) inhibits cell cycle arrest and apoptosis of GC cells^[2].
Sanggenon C (6-10 μM; 24 h) markedly downregulates the levels of p-ERK^[2].
Sanggenon C (6-10 μM; 24 h) induces mitochondrial dysfunction of GC cells^[2].
In Vivo:Sanggenon C (10, 20 mg/kg/day; Intraperitoneally; for 3 weeks) improves impaired cardiac function following aortic banding (AB). Sanggenon C protects against cardiac hypertrophy^[1].
Sanggenon C (10, 20 mg/kg/day; Intraperitoneally; for 21 days) suppresses the tumor burden in the nude mice bearing tumor xenografts derived from AGS. Sanggenon C downregulates levels of p-ERK expression^[2].