Anti-hyperlipidemic

Ficusin A
Catalog No: CFN99817

Ficusin has antioxidant, antilipidemic and antidiabetic effects, it can lower the levels of fasting blood glucose, plasma insulin, body weight gain in HFD-STZ induced diabetic rats, and can significantly enhance the PPARγ expression and improve the translocation and activation of GLUT4 in the adipose tissue, suggests that ficusin improves the insulin sensitivity on adipose tissue and it can be used for the treatment of obesity related type 2 diabetes mellitusl.
Swertiamarin
Catalog No: CFN99818

Swertiamarin possesses anti-hyperglycemic, anti-hyperlipidemic, anti-diabetic activity and enhances β cell regeneration which causes reversal of diabetes. Swertiamarin also possesses significant wound healing, anti-inflammatory, antioxidant, hepatoprotective, peripheral and central antinociceptive properties. Swertiamarin inhibits the development of arthritis by modulating NF-κB/IκB and JAK2/STAT3 signaling, it acts as an anti-rheumatic agent.
Cholic acid
Catalog No: CFN99796

Cholic acid is a major primary bile acid produced in the liver and usually conjugated with glycine or taurine. It facilitates fat absorption and cholesterol excretion. It prevents hepatic TG accumulation, VLDL secretion, and elevated serum TG in mouse models of hypertriglyceridemia;at the molecular level, CA decreases hepatic expression of SREBP-1c and its lipogenic target genes.
Hyodeoxycholic acid
Catalog No: CFN99797

Hyodeoxycholic acid is a secondary bile acid formed in the small intestine by the gut flora, and acts as a TGR5 (GPCR19) agonist, with an EC50 of 31.6 µM in CHO cells. Hyodeoxycholic acid has hypolipidemic effect through regulation of FXR activation, it is a candidate for antiatherosclerotic drug, by significantly increasing the expression of genes involved in cholesterol efflux, such as Abca1, Abcg1,and Apoe,in a macrophage cell line.
Tectorigenin
Catalog No: CFN99920

Tectorigenin has hepatoprotective, antifibrotic, anti-leukemia, antioxidant, and anti-inflammatory activities, it could sensitize paclitaxel-resistant human ovarian cancer cells through inactivation of the Akt/IKK/IκB/NFκB signaling pathway, and promise a new intervention to chemosensitize paclitaxel-induced cytotoxicity in ovarian cancer.