Anti-adipogenic

(-)-Gallocatechin gallate
Catalog No: CFN99571

(-)-Gallocatechin gallate has cancer-preventive activities, it can precipitate cholesterol, decreasee osteoclastogenesis at 20 microM.
Ginkgolide C
Catalog No: CFN99639

Ginkgolide C is a potent inhibitor of collagen-stimulated platelet aggregation, it may increase intracellular cAMP and cGMP production and MMP-9 activity, inhibit intracellular Ca(2+) mobilization and TXA(2) production. Ginkgolide C has anti-adipogenic and ameliorating Alzheimer disease effects; it also can increase△LVP significantly,enhances the myocardial systolic and diastolic function of rats,but has no significant effect on HR while it shows inotropic activity.
Ginsenoside F2
Catalog No: CFN99755

Ginsenoside F2, an autophagic initiater, which has anti-cancer, and anti-obesity activities. Ginsenoside F2 inhibited the growth and invasion of cancer, and activated the intrinsic apoptotic pathway and mitochondrial dysfunction. Ginsenoside F2 suppresses hair cell apoptosis and premature entry to catagen more effectively than finasteride, it decreases the expression of TGF-β2 and SCAP proteins, the factors in the SCAP pathway could be targets for hair loss prevention drugs.
6-Gingerol
Catalog No: CFN99931

6-Gingerol possesses anti-adipogenic, anti-tumorigenic, anti-invasive, antioxidant, anti-inflammatory, and pro-apoptotic activities, it stimulates apoptosis through upregulation of NAG-1 and G1 cell cycle arrest through downregulation of cyclin D1, multiple mechanisms appear to be involved in 6-gingerol action, including protein degradation as well as β-catenin, PKCε, and GSK-3β pathways. 6-Gingerol can effectively suppress adipogenesis and that it exerts its role mainly through the significant down-regulation of PPARγ and C/EBPα and subsequently inhibits FAS and aP2 expression, also inhibit differentiation in 3T3-L1 cells by attenuating the Akt/GSK3β pathway.
Ginsenoside Rh1
Catalog No: CFN99970

Ginsenoside Rh1 has anti-obesity, anti-inflammatory, antiallergic, and anti-tumor activities, it may improve glucocorticoid efficacy in hormone-dependent diseases. It inhibits MAPK and PI3K/Akt signaling pathways and downstream transcription factors such as NF-κB and AP-1, which play an important role in MMP gene expressions; it also inhibits IFN-gamma-induced JAK/STAT and ERK signaling pathways and downstream transcription factors, and thereby iNOS gene expression.