Bavachalcone

Bavachalcone is a potent inducer of apoptosis. Bavachalcone exerts anticancer activity by promoting autophagy and apoptosis in HepG2 cells. Bavachalcone acts as an anti-neuroinflammatory and antidepressant through the NF-κB pathway. Bavachalcone inhibits osteoclasts by interfering with ERK and Akt signaling pathways and the expression of c-Fos and NFATc1. Bavachalcone exhibits a significant inhibitory effect on baculovirus-expressed BACE-1 in vitro^[1][2][3][4]. In Vitro:Bavachalcone (5 μg/mL; 1-48 h) inhibits osteoclasts by interfering with ERK and Akt signaling pathways and the expression of c-Fos and NFATc1^[1].
. Bavachalcone (0-100 μg/mL; 24h) is toxic to HepG2 cells with IC₅₀ of 20 μg/mL^[3]. Bavachalcone (20 μg/mL; 24 h) induces apoptosis in HepG2^[3].
Bavachalcone (0-20 μg/mL; 24 h) induces cell cycle arrest in HepG2 cells^[3].
Bavachalcone (0-20 μg/mL; 24 h) induces autophagy through Akt-mTOR signaling pathway^[3].
Bavachalcone (5-10 μM; 2 h) inhibits the activation of NF-κB pathway in LPS (HY-D1056)-induced BV2 cells, upregulated the expression of A20 and TAX1BP1, and enhanced their interaction^[4]. In Vivo:Bavachalcone (30-60 mg/kg; Intraperitoneal injection; 4 days) exerts anti-neuroinflammatory and anti-depressive effects in LPS (HY-D1056) -induced mouse models^[4].