[{"from": "human", "value": "Please give me some details about this molecule. [C][=C][C][=Branch2][Ring2][=C][=C][C][=C][Ring1][=Branch1][C@@H1][C@H1][Branch2][Ring1][Ring1][C][=Branch1][C][=O][N][Ring1][Branch1][C][=C][C][=C][Branch1][Branch1][C][=C][Ring1][=Branch1][F][C][C][C@@H1][Branch1][N][C][=C][C][=C][Branch1][Branch1][C][=C][Ring1][=Branch1][F][O][O]"}, {"from": "gpt", "value": "The molecule is a lipid-lowering compound that inhibits intestinal cholesterol and phytosterol absorption. The discovery and research of this drug began in the early 1990s, after the intravenous administration of radiolabelled ezetimibe in rats revealed that it was being localized within enterocytes of the intestinal villi - this prompted studies investigating the effect of ezetimibe on intestinal cholesterol absorption. Ezetimibe is used as an adjunctive therapy to a healthy diet to lower cholesterol levels in primary hyperlipidemia, mixed hyperlipidemia, homozygous familial hypercholesterolemia (HoFH), and homozygous sitosterolemia (phytosterolemia).  Unlike other classes of cholesterol-reducing compounds including statins and bile acid sequestrants, ezetimibe has a distinct mechanism of action involving the sterol transporter Niemann-Pick C1-Like 1 (NPC1L1), and is unique in that it does not affect the absorption of fat-soluble nutrients such as fat-soluble vitamins, triglycerides, or bile acids. In genetically NPC1L1-deficient mice, a 70% reduction in intestinal cholesterol absorption was seen, and these mice were insensitive to ezetimibe treatment - it was determined based on these findings that NPC1L1 plays an essential role in promoting intestinal cholesterol uptake via an ezetimibe-sensitive pathway. By interfering with the intestinal uptake of cholesterol and phytosterols, ezetimibe reduces the delivery of intestinal cholesterol to the liver."}]