Cimiracemoside C Inhibitor

Solid. Powder

98.00%

Store at -20 degree C for 3 years powder
-80 degree C for 2 years in solvent

620.8

<1mg/ml refers to the product slightly soluble or insoluble

C35H56O9

[H][C@@]12CC[C@]3([H])[C@]4(CC14CC[C@]1(C)[C@H]4[C@H](C)C[C@H]5O[C@@]4(O[C@@H]5C(C)(C)O)[C@@H](O)[C@@]21C)CC[C@@H](O[C@@H]1OC[C@H](O)[C@H](O)[C@H]1O)C3(C)C

256925-92-5

AMPK

Ze 450 and some of its components (23-epi-26-deoxyactein, protopine and Cimiracemoside C) were investigated in vitro for their effects on AMP-activated protein kinase (AMPK) compared to metformin in HepaRG cells. Ze 450 (given orally (PO) and intraperitonally (IP)), metformin (PO) and controls were given over 7 days to 68 male ob/ob mice. Glucose and insulin concentrations were measured at baseline and during an oral glucose tolerance test (OGTT). Ze 450 and its components activated AMPK to the same extent as metforminutes. In mice, Ze 450 (PO/IP) decreased significantly average daily and cumulative weight gain, average daily food and water intake, while metformin had no effect. In contrast to metformin, PO Ze 450 virtually did not change maximum glucose levels during OGTT, however, prolonged elimination. Ze 450 administered PO and IP decreased significantly post-stimulated insulin, whereas metformin did not. HOMA-IR index of insulin resistance improved significantly after IP and PO Ze 450 and slightly after metforminutes. In summary, the results demonstrate that Ze 450 reduced significantly body weight, plasma glucose, improved glucose metabolism and insulin sensitivity in diabetic ob/ob mice. In vitro experiments suggest that part of the effects may be related to AMPK activation.

PI3K/Akt/mTOR signaling; AMPK