Cafestol
Catalog No: CFN93071
Cafestol has anticarcinogenic, peripheral antinociceptive and anti-inflammatory activities, it inhibits Cyclic-Strain-induced interleukin-8, intercellular adhesion molecule-1, and monocyte chemoattractant protein-1 production in vascular endothelial cells. Cafestol is a novel extracellular signal-regulated kinase inhibitor with AP-1-targeted inhibition of prostaglandin E2 production in lipopolysaccharide-activated macrophages. Cafestol acts as an agonist ligand for both FXR and PXR, and this may contribute to its impact on cholesterol homeostasis. Cafestol has protective effects against the CCl(4)-induced hepatotoxicity, which possibly involve mechanisms related to its ability to block the CYP2E1-mediated CCl(4) bioactivation and free radical scavenging effects. Cafestol has antidiabetic activity, it increases glucose-stimulated insulin secretion in vitro and increases glucose uptake in human skeletal muscle cells.
Cafestol also has a weak inhibitory effect on osteoclastogenesis and promotes osteoblast differentiation.
Caffeic acid
Catalog No: CFN99190
Caffeic acid has antidiabetic, antioxidant, anticarcinogenic, and anti-inflammatory activities, it can suppress ultraviolet B(UVB)-induced COX-2 expression by blocking Fyn kinase activity, inhibits HBV-DNA replication as well as HBsAg production, also reduces serum DHBV level in DHBV-infected duckling model. Caffeic acid may be used as designed novel therapeutic drugs for Parkinson's disease by inhibiting α-synuclein fibrillation.
Cajanin
Catalog No: CFN98419
Cajanin has potential hypolipidemic effects,possibly via up-regulating the ABCA1 protein expression,subsequently resulting in increased macrophage cholesterol efflux and RCT, it can significantly improve basal glucose uptake in HepG2 cells, its improving effect is concentration dependent, it exhibits effects stronger than that of rosiglitazone, which has been used as an antidiabetic drug. Cajanin has strong mitogenic as well as differentiation-promoting effects on osteoblasts that involved subsequent activation of MEK-Erk and Akt pathways.