Fenfluramine
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| Fenfluramine
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| Systematic (IUPAC) name | |
| N-ethyl-1-[3-(trifluoromethyl)- phenyl]propan-2-amine | |
| Identifiers | |
| CAS number | |
| ATC code | A08 |
| PubChem | |
| DrugBank | |
| Chemical data | |
| Formula | C12H16F3N |
| Mol. mass | 231.257 |
| Pharmacokinetic data | |
| Bioavailability | ? |
| Metabolism | Hepatic |
| Half life | 20 hours |
| Excretion | Renal |
| Therapeutic considerations | |
| Pregnancy cat. |
? (United States) |
| Legal status |
Schedule IV, Withdrawn from market |
| Routes | Oral |
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Fenfluramine is a drug that was part of the Fen-Phen anti-obesity medication (the other drug being phentermine). Also known as Pondimin, fenfluramine was introduced on the U.S. market in 1973. It is the racemic mixture of two enantiomers, dexfenfluramine and levofenfluramine. It is designed to increase the level of the neurotransmitter serotonin, a chemical that regulates mood, appetite and other functions. Fenfluramine causes the release of serotonin by disrupting vesicular storage of the neurotransmitter, and reversing serotonin transporter function.[1] The end result is a feeling of fullness and loss of appetite.
The drug was withdrawn from the U.S. market in 1997 after reports of heart valve disease and pulmonary hypertension, including a condition known as cardiac fibrosis. After the US withdrawal of fenfluramine, it was also withdrawn from other markets around the world.
The distinctive valvular abnormality seen with fenfluramine is a thickening of the leaflet and chordae tendinae. Roth[2] suggested a mechanism by which fenfluramine damaged the valves. Heart valves also have serotonin receptors, which regulate their growth. He reported that fenfluramine and its active metabolite norfenfluramine stimulated the serotonin receptors 5-hydroxytryptamine (5-HT). In particular norfenfluramine is a potent agonist (stimulant) of 5-HT2B receptors. These receptors are plentiful in human cardiac valves and appear to be essential for normal cardiac development. Roth suggested that the mechanism by which fenfluramine causes damage is through inappropriately stimulating the valve cells to divide. This valve damage is found in other drugs that act on 5-HT2B receptors.
References
- ↑ Nestler, Eric J. "Molecular Neuropharmacology: A Foundation for Clinical Neuroscience" McGraw-Hill, 2001.
- ↑ Roth, B Drugs and Valvular Heart Disease. N Engl J Med 2007;356:6 PMID 17202450
External links
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Antiobesity preparations (A08) | |
|---|---|
| Centrally acting | Phentermine - Fenfluramine - Amfepramone - Dexfenfluramine - Mazindol - Cathine - Clobenzorex - Sibutramine - Rimonabant - Taranabant |
| Peripherally acting | Orlistat |
Acknowledgement and Attribution Regarding Sources of Content
Some of the initial content on this page may be incorporated in part from copyleft sources in the public domain including wikis such as Wikipedia and AskDrWiki. Drug information for patients came from the The National Library of Medicine. Infectious disease information may have come from the Centers for Disease Control (CDC). Differential Diagnoses are drawn from clinicians as well as an amalgamation of 3 sources: 1.The Disease Database; 2. Kahan, Scott, Smith, Ellen G. In A Page: Signs and Symptoms. Malden, Massachusetts: Blackwell Publishing, 2004:3; 3. Sailer, Christian, Wasner, Susanne. Differential Diagnosis Pocket. Hermosa Beach, CA: Borm Bruckmeir Publishing LLC, 2002:7 .
