Clofibrate: Difference between revisions

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==Synthesis==
==Synthesis==
[[File:Clofibrate synthesis.svg|thumb||center|700px|Clofibrate synthesis.<ref>http://drugsynthesis.blogspot.co.uk/2012/04/laboratory-synthesis-of-clofibrate.html</ref>]]
[[File:Clofibrate synthesis.png|thumb||center|700px|Clofibrate synthesis.<ref>http://drugsynthesis.blogspot.co.uk/2012/04/laboratory-synthesis-of-clofibrate.html</ref>]]


==References==
==References==

Revision as of 21:56, 23 July 2014

Clofibrate
Clinical data
AHFS/Drugs.comMicromedex Detailed Consumer Information
Pregnancy
category
  • AU: B1
  • US: C (Risk not ruled out)
Routes of
administration
Oral
ATC code
Legal status
Legal status
  • US: Discontinued
Pharmacokinetic data
Protein bindingVariable, 92–97% at therapeutic concentrations
MetabolismHydrolyzed to clofibric acid; hepatic glucuronidation
Elimination half-lifeHighly variable; average 18–22 hours. Prolonged in renal failure
ExcretionRenal, 95 to 99%
Identifiers
CAS Number
PubChem CID
DrugBank
ChemSpider
UNII
KEGG
ChEBI
ChEMBL
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
FormulaC12H15ClO3
Molar mass242.698 g/mol
3D model (JSmol)
Boiling point148 °C (298.4 °F)
  (verify)

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

Clofibrate synthesis.[2]

References

  1. "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.
  2. http://drugsynthesis.blogspot.co.uk/2012/04/laboratory-synthesis-of-clofibrate.html

Template:Lipid modifying agents