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Clofibrate
Clinical data
AHFS/Drugs.com	Micromedex Detailed Consumer Information
Pregnancy; category	AU: B1; ;
Routes of; administration	By mouth
ATC code	C10AB01 (WHO) ;
Legal status
Legal status	US: Discontinued;
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%
Identifiers
	IUPAC name ethyl 2-(4-chlorophenoxy)-2-methylpropanoate;
CAS Number	637-07-0 ;
PubChem CID	2796;
IUPHAR/BPS	2667;
DrugBank	DB00636 ;
ChemSpider	2694 ;
UNII	HPN91K7FU3;
KEGG	D00279 ;
ChEBI	CHEBI:3750 ;
ChEMBL	ChEMBL565 ;
CompTox Dashboard (EPA)	DTXSID3020336 ;
ECHA InfoCard	100.010.253
Chemical and physical data
Formula	C12H15ClO3
Molar mass	242.70 g·mol−1
3D model (JSmol)	Interactive image;
Boiling point	148 °C (298 °F)
	SMILES Clc1ccc(OC(C(=O)OCC)(C)C)cc1;
	InChI InChI=1S/C12H15ClO3/c1-4-15-11(14)12(2,3)16-10-7-5-9(13)6-8-10/h5-8H,4H2,1-3H3 ; Key:KNHUKKLJHYUCFP-UHFFFAOYSA-N ;
	(verify)

Clofibrate (trade name Atromid-S) is a lipid-lowering agent used for controlling the high cholesterol and triacylglyceride level in the blood. It belongs to the class of fibrates. 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.

It was patented in 1958 by Imperial Chemical Industries and approved for medical use in 1963.^[1] Clofibrate was discontinued in 2002 due to adverse effects.

Complications and controversies

It can induce SIADH, syndrome of inappropriate secretion of antidiuretic hormone ADH (vasopressin). Clofibrate can also result in formation of cholesterol stones in the gallbladder.

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".^[2]

References

^ Fischer J, Ganellin CR (2006). Analogue-based Drug Discovery. John Wiley & Sons. p. 474. ISBN 9783527607495.
^ "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. doi:10.1016/s0140-6736(84)90595-6. PMID 6147641. S2CID 2473318.

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[Fis2006-1] Fischer J, Ganellin CR (2006). Analogue-based Drug Discovery. John Wiley & Sons. p. 474. ISBN 9783527607495.

[2] "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. doi:10.1016/s0140-6736(84)90595-6. PMID 6147641. S2CID 2473318.

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