Vytorin: Difference between revisions
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===<b>Ezetimibe</b>=== | ===<b>Ezetimibe</b>=== | ||
When administered, the drug is inactive until it is absorbed. Upon absorption ezetimibe is conjugated to active phenolic glucuronide where it is metabolized within the small intestine and liver. <ref>https://www.accessdata.fda.gov/drugsatfda_docs/label/2008/021445s019lbl.pdf</ref> Ezetimibe limits the internalization of cholesterol by the small intestine. Cholesterol is absorbed into cells with NPC1L1 through clathrin/AP2-mediated endocytosis. AP2 is a multimeric protein that works on the cell membrane to facilitate endocytosis. Ezetimibe inhibits the absorption of cholesterol by blocking the internalization of NPC1L1. <ref>https://www.ncbi.nlm.nih.gov/pubmed/18522832</ref> | When administered, the drug is inactive until it is absorbed. Upon absorption, ezetimibe is conjugated to active phenolic glucuronide where it is metabolized within the small intestine and liver. <ref>https://www.accessdata.fda.gov/drugsatfda_docs/label/2008/021445s019lbl.pdf</ref> Ezetimibe limits the internalization of cholesterol by the small intestine. Cholesterol is absorbed into cells with NPC1L1 through clathrin/AP2-mediated endocytosis. AP2 is a multimeric protein that works on the cell membrane to facilitate endocytosis. Ezetimibe inhibits the absorption of cholesterol by blocking the internalization of NPC1L1. <ref>https://www.ncbi.nlm.nih.gov/pubmed/18522832</ref> | ||
===<b>Simvastatin</b>=== | ===<b>Simvastatin</b>=== | ||
When the drug is administered it is initially inactive. It must be hydrolyzed in order to become active. Once hydrolyzed, simvastatin reduces the amount of mevalonic acid in the blood by competing for HMG-CoA reductase with HMG-CoA. To produce cholesterol, Acetyl CoA is converted into HMG-CoA, which is then converted into mevalonate. Mevalonate is then converted into isopentenyl pyrophosphate (IPP), IPP is converted into squalene, and then finally squalene is converted into cholesterol. Simvastatin reduces the conversion of HMG-CoA to mevalonate, therefore lowering cholesterol levels. Simvastatin targets <scene name='75/757901/Hmg-coa_reductase_w_simvastin/1'>HMG-CoA reductase</scene> which is the enzyme responsible for said conversion. With the synthesis of cholesterol being divided into five major steps, this inability to convert targets only the second step in cholesterol synthesis.<ref>http://www.merck.com/product/usa/pi_circulars/v/vytorin/vytorin_pi.pdf</ref> | When the drug is administered, it is initially inactive. It must be hydrolyzed in order to become active. Once hydrolyzed, simvastatin reduces the amount of mevalonic acid in the blood by competing for HMG-CoA reductase with HMG-CoA. To produce cholesterol, Acetyl CoA is converted into HMG-CoA, which is then converted into mevalonate. Mevalonate is then converted into isopentenyl pyrophosphate (IPP), IPP is converted into squalene, and then finally squalene is converted into cholesterol. Simvastatin reduces the conversion of HMG-CoA to mevalonate, therefore lowering cholesterol levels. Simvastatin targets <scene name='75/757901/Hmg-coa_reductase_w_simvastin/1'>HMG-CoA reductase</scene> which is the enzyme responsible for said conversion. With the synthesis of cholesterol being divided into five major steps, this inability to convert targets only the second step in cholesterol synthesis.<ref>http://www.merck.com/product/usa/pi_circulars/v/vytorin/vytorin_pi.pdf</ref> | ||
