Orlistat (Tetrahydrolipstatin, Xenical, Alli, Ro-18-0647)

Hypolipemic cell permeable and irreversible pancreatic, gastric and carboxylester lipase inhibitor. Anti-obesity and antihypercholesterolemic compound. Antitumor compound by inhibition of the thioesterase domain of fatty acid synthase (FASN). Anti-proliferative. Causes cell cycle arrest at G1 phase. Apoptosis inducer through caspase-3 activation. Sn-1-selective-diacylglycerol lipases alpha (DAGLalpha) inhibitor. Targets serine hydrolases in the nervous system, such as diacylglycerol lipase (DAGL), which is responsible for the conversion of DAG to 2-AG. Partially inhibits the hydrolysis of triglycerides and lowers the absorption of dietary fat, promoting weight loss.\nPromotes the sensitivity to TRAIL in cancer cells by ROS-mediated pathways. \n\nStorage and Stability:\nShort-term Storage: +4 degrees C\nLong-term Storage: -20 degrees C\nStable for at least 2 years after receipt when stored at -20 degrees C.

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SPECIFICATIONS

Catalog Number

045122

Size

50mg

Purity

>98% (HPLC)

References

Product Reference: \n?Interactions of lipoprotein lipase with the active-site inhibitor tetrahydrolipstatin (Orlistat): A. Lookene, et al.; Eur. J. Biochem. 222, 395 (1994)\n?Mode of action of orlistat: R. Guerciolini; Int. J Obes. Relat. Metab. Disord. 2, S12 (1997) (Review)\n?Degree of in vivo inhibition of human gastric and pancreatic lipases by Orlistat (Tetrahydrolipstatin, THL) in the stomach and small intestine: B. Sternby, et al.; Clin. Nutr. 21, 395 (2002)\n?Orlistat is a novel inhibitor of fatty acid synthase with antitumor activity: S.J. Kridel, et al.; Cancer Res. 64, 2070 (2004)\n?The use of orlistat in the treatment of obesity, dyslipidaemia and Type 2 diabetes: R.H. Nelson & J.M. Miles; Expert Opin. Pharmacother. 6, 2483 (2005) (Review)\n?Antitumoral actions of the anti-obesity drug orlistat (XenicalTM) in breast cancer cells: blockade of cell cycle progression, promotion of apoptotic cell death and PEA3-mediated transcriptional repression of Her2/neu (erbB-2) oncogene: J.A. Menendez, et al.; Ann. Oncol. 16, 1253 (2005)\n?Development of the first potent and specific inhibitors of endocannabinoid biosynthesis: T. Bisogno, et al.; Biochim. Biophys. Acta 1761, 205 (2006)\n?Orlistat accelerates gastric emptying and attenuates GIP release in healthy subjects: F.Y. Enc, et al.; Am. J. Physiol. Gastrointest. Liver Physiol. 296, G482 (2008)\n?Fatty acid synthase inhibition with Orlistat promotes apoptosis and reduces cell growth and lymph node metastasis in a mouse melanoma model: M.A. Carvalho, et al.; Int. J. Cancer. 123, 2557 (2008)\n?Antitumor effect of orlistat, a fatty acid synthase inhibitor, is via activation of caspase-3 on human colorectal carcinoma-bearing animal: H.Y. Chuang, et al.; Biomed. Pharmacother. 65, 286 (2011)\n?The anti-obesity drug orlistat promotes sensitivity to TRAIL by two different pathways in hormone-refractory prostate cancer cells: J. Fujiwara, et al.; Int. J. Oncol. (Epub ahead of print) (2012)\n?

Alternative Names

Tetrahydrolipstatin, Xenical, Alli, Ro-18-0647