Kaempferitrin
Catalog No: CFN98756
Kaempferitrin exerts immunostimulatory, antidepressant-like , antiosteoporotic , cytotoxic and antitumor effects, the general mechanisms include cell cycle arrest in G1 phase and apoptosis via intrinsic pathway in a caspase dependent pathway. Kaempferitrin is an acute lowering effect on blood glucose in diabetic rats and to stimulate the glucose uptake percentile, as efficiently as insulin in muscle from normal rats.
Theaflavine-3,3'-digallate
Catalog No: CFN98598
Theaflavin-3,3'-digallate is a potent AMP-activated protein kinase (AMPK) activator with anti-adiposity activity in adipocytes, suggesting its potential application in functional foods and nutraceuticals for obesity management. Theaflavin-3,3'-digallate is also an inducer of oxidative stress and apoptosis, it has strong antioxidant and antiangiogenic activities, it inhibits the tube formation of endothelial cells via decreased both MMP-2 and MMP-9 activities in vitro. A combination microbicide containing theaflavin-3,3'-digallate and lactic acid can reduce herpes simplex virus (HSV) transmission. Theaflavin-3,3'-digallate may exert its anti-inflammatory and cancer chemopreventive actions by suppressing the activation of NFkappaB through inhibition of IkappaB kinase (IKK) activity. Theaflavin-3,3'-digallate can repress osteoclastogenesis and prevent wear debris-induced osteolysis via suppression of ERK pathway, it is a promising candidate for the treatment of osteoclast-related osteolytic diseases, such as wear debris-induced peri-implant osteolysis (PIO).
Wedelolactone
Catalog No: CFN98857
Wedelolactone is a potent Î2-arrestin-biased G protein-coupled receptor-35 (GPR35) agonist, GPR35 has been shown to be a target of the asthma drugs cromolyn disodium and nedocromil sodium. Wedelolactone has anti-inflammatory, growth inhibitory, anti-cancer, anti-fibrotic, and pro-apoptotic effects. Wedelolactone stimulates ER genomic and non-genomic signalling pathways; it can significantly inhibit the activation of LX-2 cells, the underlying mechanisms of which included inducing Bcl-2 family involved apoptosis, up-regulating phosphorylated status of ERK and JNK expressions, and inhibiting NF-κB mediated activity.