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Lipase Inhibitor, THL (Tetrahydrolipstatin), is a compound that has been shown to rapidly inactivate lipoprotein lipase (LPL). This agent has been found to bind both subunits of LPL, induce tetramerisation, and cause local conformational changes. The exception to lipase inhibition capacities of THL is phospholipase A2, which is not affected by THL. Mechanistic studies suggest that THL inhibits the thioesterase domain of fatty acid synthase (FAS) and as a result halts cell proliferation and causes cell apoptosis. More detailed experiments show that gradually THL affects the retinoblastoma protein pathway and leads to cell-cycle arrest at G₁/S boundary. Lipase Inhibitor, THL is an inhibitor of pancreatic and gastric lipase, as well as carboxyl ester lipase (CEL) and diacylglycerol lipase-α (DAGLα). Lipase Inhibitor, THL also activates caspase-3.

Orlistat is a digestive lipase inhibitor. It inhibits diacylglycerol lipase α (DAGLα), DAGLβ, α/β-hydrolase domain-containing protein 12 (ABHD12), ABHD16A, and platelet-activating factor acetylhydrolase (PAF-AH; IC₅₀s = 0.06, 0.1, 0.08, 0.03, and 0.05 µM, respectively), as well as pancreatic lipase and hormone-sensitive lipase (IC₅₀s = 0.65 and 2.1 µg/ml, respectively) but does not inhibit fatty acid amide hydrolase (FAAH) or KIAA1363 (IC₅₀s = >100 µM for both). Orlistat decreases ionomycin-induced production of the endocannabinoid 2-arachidonoyl glycerol (2-AG) in N18TG2 murine neuroblastoma cells when used at a concentration of 1 µM. It also inhibits fatty acid synthase (FASN; K_iapp = ~0.1 µM for the human enzyme) and the proliferation of PC3 prostate cancer cells in a concentration-dependent manner. Orlistat (10 mg/kg) decreases serum cholesterol levels and total body weight in a mouse model of obesity induced by a high-fat diet.Formulations containing orlistat have been used in the treatment of adult obesity.