Licochalcone A
Catalog No: CFN99575
Licochalcone A is an estrogenic flavanoid extracted from licorice root, showing antimalarial, antileishmanial, anticancer, anti-inflammatory, antibacterial and antiviral activities. It could be a promising strategy in treating osteoporotic weight-bearing bones fractures with defects, and be a useful compound for the development of antibacterial agents for the preservation of foods containing high concentrations of salts and proteases, in which cationic peptides might be less effective.
Licochalcone B
Catalog No: CFN99576
Licochalcone B has antitumor, antimetastatic, cardioprotective, antioxidant, antiapoptotic, and anti-inflammatory effects, it can significantly inhibit LPS-induced phosphorylation at serine 276 and transcriptional activation of NF-KB. Licochalcone B can protect the liver from carbon tetrachloride (CCl4)-induced injury, the protection may be due to inhibition of p38 and NFκB signaling, which subsequently reduces inflammation in the liver.
Licochalcone C
Catalog No: CFN99577
Licochalcone C has cardioprotection effect, via antioxidant, anti-inflammatory, and anti-apoptotic activities; it shows inhibition of bacterial growth and cellular respiration. Licochalcone C exhibits inhibitory activity with cytotoxicity in a rat basophilic leukemia cell line, RBL-2H3. It induces apoptosis via B-cell lymphoma 2 family proteins in T24 cells, it may be a potential adjuvant therapeutic agent for bladder cancer.
Licochalcone E
Catalog No: CFN93297
Licochalcone E is a potential LXRβ agonist, which has chemopreventive, cytotoxic, anti-inflammatory, antimicrobial, antidiabetic effects; it increases the levels of PPARγ expression, at least in part, via the stimulation of Akt signals and functions as a PPARγ partial agonist. Licochalcone E may be used for the treatment of hepatotoxicity, and primarily exhibits its protective role through a PPARγ/NF-κB-mediated pathway. Licochalcone E is also a potential activator of the Nrf2/ARE-dependent pathway and is therapeutically relevant not only to oxidative-stress-related neurodegeneration but also inflammatory responses of microglial cells both in vitro and in vivo.
