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Biological: Behavioural genetics · Evolutionary psychology · Neuroanatomy · Neurochemistry · Neuroendocrinology · Neuroscience · Psychoneuroimmunology · Physiological Psychology · Psychopharmacology (Index, Outline)
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Fenfluramine chemical structure | |
| N-ethyl-1-[3-(trifluoromethyl)- phenyl]propan-2-amine IUPAC name | |
| CAS number 458-24-2 |
ATC code A08AA02 |
| PubChem 3337 |
DrugBank APRD00319 |
| Chemical formula | {{{chemical_formula}}} |
| Molecular weight | 231.257 |
| Bioavailability | ? |
| Metabolism | Hepatic |
| Elimination half-life | 20 hours |
| Excretion | Renal |
| Pregnancy category | ? (United States) ? (Australia) |
| Legal status | Unscheduled, Withdrawn from market |
| Routes of administration | Oral |
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 form of dexfenfluramine. It is designed to increase the level of the neurotransmitter serotonin. This depresses the central nervous system, regulating mood and appetite. 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The drug was withdrawn from the U.S. market in 1997 after reports of heart valve disease and pulmonary hypertension, including a condition known as cardiac fibrosis.
The distinctive valvular abnormality seen with fenfluramine is a thickening of the leaflet and chordae tendinae. Roth (2007) 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
- Roth, B Drugs and Valvular Heart Disease. N Engl J Med 2007;356:6 PMID 17202450
External links
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