(-)-Epigallocatechin gallate
Catalog No: CFN99569
(-)-Epigallocatechin Gallate is an antioxidant polyphenol flavonoid form green tea, and inhibits the activation of EGFR, HER2 and HER3, with antitumor activity. (-)-Epigallocatechin gallate treatment enduring to cardio protection at mitochondrial level, it has protective effects against βA-induced neuronal apoptosis through scavenging reactive oxygen species, which may be beneficial for the prevention of Alzheimer's disease.
Rocaglaol
Catalog No: CFN99609
Rocaglaol is a potent anticancer drug that induces apoptosis of LNCaP cells through the mitochondrial pathway and its G2/M-phase cell cycle arrest is associated with the down-regulation of Cdc25C and the dephosphorylation of Cdc2. Rocaglaol can reduce tissue inflammation and neuronal cell death by inhibiting NF-kappa B and AP-1 signaling, resulting in significant neuroprotection in animal models of neurodegeneration. Rocaglaol derivatives can prevent or to limit the cardiotoxicity of an antineoplastic agent, in particular to prevent or to limit the apoptosis of cardiomyocytes induced by such agent. Rocaglaol, pyrimidinone and aglaiastatin are potent inhibitors of the growth of K--cells, with IC50 values of 1-10 ng/mL, and induce normal morphology in K--cells at 10-30 ng/mL, they also specifically inhibit protein synthesis.
Isoliensinine
Catalog No: CFN99574
Isoliensinine has anti-cancer, anti-fibrosis, anti-proliferative, antioxidant, and anti-inflammatory activities, it inhibited TNF-alpha and TGF-beta 1; decreased the overexpression of growth factors Platelet-derived growth factor (PDGF)-beta, basic fibroblast growth factor (bFGF), proto-oncogene c-fos, c-myc and hsp70; and activated ROS and p38 MAPK/JNK .
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.