text: As further discussed, orlistat is a pancreatic and gastric lipase inhibitor. Orlistat is also a potent thioesterase inhibitor and therefore inhibits fatty acid synthase (FAS). Since FAS is essential for tumor cells, for its growth and survival, and is upregulated and overexpressed in variety of tumors, scientists have high expectations for FAS as an oncology drug target. Orlistat inhibits FAS with the same mechanism as it does with pancreatic lipase, that is by binding covalently to the active serine site. 
  This effect of orlistat as a FAS-inhibitor was first identified in a high throughput screening for enzymes with prostate cancer inhibition activity.  However FAS is resistant to many cancer medicines. Orlistat sensitizes these FAS resistance cancer drugs, by inhibiting FAS. There is a low FAS expression in normal tissues so the activity of orlistat on normal cells is limited. 
  Because of the difference in FAS expression between normal cells and cancer cells, orlistat selectively targets tumor cells. Due to this FAS is a potential drug target in cancer therapy.
  Orlistat works locally in the intestines as a lipase inhibitor, and therefore suffers from several limitations in its development as a systemic drug. Its poor bioavailability and solubility are the main reasons to develop a new anticancer analogue to overcome these limitations.