Licochalcone B is an extract from the root of Glycyrrhiza uralensis . Licochalcone B inhibits amyloid β ( 42 ) self-aggregation ( IC 50 =2.16 μM) and disaggregate pre-formed Aβ 42 fibrils, reduce metal-induced Aβ 42 aggregation through chelating metal ionsLicochalcone B inhibits phosphorylation of NF-κB p65 in LPS signaling pathway. Licochalcone B inhibits growth and induces apoptosis of NSCLC cells. Licochalcone B specifically inhibits the NLRP3 inflammasome by disrupting NEK7‐NLRP3 interaction In Vitro Licochalcone B (IC 50 : 2.16 μM) inhibits self-mediated Aβ42 aggregation and disaggregates Aβ42 pre-formed fibrils. Licochalcone B (0-12 μM, 48 h) reduces the ROS generation and protects cells from H 2 O 2 -induced cell death in SH-SY5Y cells. Licochalcone B (10 μM, 1 h) inhibits LPS-induced NF-κB activation in RAW264.7 cells. Licochalcone B (10 μM, 1 h) inhibits the LPS-induced phosphorylation of NF-κB p65 at serine 276, and inhibited the expression of TNFα and MCP-1. Licochalcone B (0-20 μM, 24 or 48 h) inhibits human NSCLC cell growth. MCE has not independently confirmed the accuracy of these methods. They are for reference only. Western Blot AnalysisCell Line: RAW264.7 cells Concentration: 10 µM Incubation Time: 1 h Result: Inhibited the phosphorylation of NF-κB at serine 276 but not at serine 536. In Vivo Licochalcone B (1-25 mg/kg, oral gavage) alleviates oxidative stress of hepatotoxicity in mice induced by CCl 4. MCE has not independently confirmed the accuracy of these methods. They are for reference only. Animal Model: Mice induced by CCl 4Dosage: 1, 5, 25 mg/kg Administration: Oral gavage. Result: Elevated the levels of SOD and GSH, and reduced the GSSG levels. Form:Solid IC50& Target:NLRP3