Clofibrate: Difference between revisions
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==Overview== | |||
'''Clofibrate''' (tradename '''Atromid-S''') is an [[organic compound]]. It is marketed as a [[fibrate]]. It is a lipid-lowering agent used for controlling the high cholesterol and [[triacylglyceride]] level in the blood. It increases [[lipoprotein lipase]] activity to promote the conversion of [[VLDL]] to [[LDL]], and hence reduce the level of VLDL. It can increase the level of [[High Density Lipoprotein|HDL]] as well. | '''Clofibrate''' (tradename '''Atromid-S''') is an [[organic compound]]. It is marketed as a [[fibrate]]. It is a lipid-lowering agent used for controlling the high cholesterol and [[triacylglyceride]] level in the blood. It increases [[lipoprotein lipase]] activity to promote the conversion of [[VLDL]] to [[LDL]], and hence reduce the level of VLDL. It can increase the level of [[High Density Lipoprotein|HDL]] as well. | ||
Latest revision as of 21:56, 23 July 2014
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| AHFS/Drugs.com | Micromedex Detailed Consumer Information |
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| Routes of administration | Oral |
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| Pharmacokinetic data | |
| Protein binding | Variable, 92–97% at therapeutic concentrations |
| Metabolism | Hydrolyzed to clofibric acid; hepatic glucuronidation |
| Elimination half-life | Highly variable; average 18–22 hours. Prolonged in renal failure |
| Excretion | Renal, 95 to 99% |
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| E number | {{#property:P628}} |
| ECHA InfoCard | {{#property:P2566}}Lua error in Module:EditAtWikidata at line 36: attempt to index field 'wikibase' (a nil value). |
| Chemical and physical data | |
| Formula | C12H15ClO3 |
| Molar mass | 242.698 g/mol |
| 3D model (JSmol) | |
| Boiling point | 148 °C (298.4 °F) |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Clofibrate (tradename Atromid-S) is an organic compound. It is marketed as a fibrate. It is a lipid-lowering agent used for controlling the high cholesterol and triacylglyceride level in the blood. It increases lipoprotein lipase activity to promote the conversion of VLDL to LDL, and hence reduce the level of VLDL. It can increase the level of HDL as well.
Complications and controversies
It can induce SIADH, syndrome of inappropriate secretion of antidiuretic hormone ADH (vasopressin).
The World Health Organization Cooperative Trial on Primary Prevention of Ischaemic Heart Disease using clofibrate to lower serum cholesterol observed excess mortality in the clofibrate-treated group despite successful cholesterol lowering (47% more deaths during treatment with clofibrate and 5% after treatment with clofibrate) than the non-treated high cholesterol group. These deaths were due to a wide variety of causes other than heart disease, and remain "unexplained".[1]
Clofibrate was discontinued in 2002 due to adverse affects.
Synthesis
References
- ↑ "WHO cooperative trial on primary prevention of ischaemic heart disease with clofibrate to lower serum cholesterol: final mortality follow-up. Report of the Committee of Principal Investigators". Lancet. 2 (8403): 600–4. September 1984. PMID 6147641.
- ↑ http://drugsynthesis.blogspot.co.uk/2012/04/laboratory-synthesis-of-clofibrate.html