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Fenfluramine chemical structure
Fenfluramine

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
Legal status Withdrawn from market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 mixture of two enantiomers, dextrofenfluramine and levofenfluramine. It increases 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.

Withdrawal due to heart disease[]

The drug was withdrawn from the U.S. market in 1997 after reports of heart valve disease,[2][3] and pulmonary hypertension, including a condition known as cardiac fibrosis. After the US withdrawal of fenfluramine, it was also withdrawn from other markets around the world.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 tendineae. Roth suggested a mechanism by which fenfluramine damaged the valves.[4] 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 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[]

  1. Nestler, Eric J. "Molecular Neuropharmacology: A Foundation for Clinical Neuroscience" McGraw-Hill, 2001.
  2. Connolly HM, Crary JL, McGoon MD, et al (1997). Valvular heart disease associated with fenfluramine-phentermine. N. Engl. J. Med. 337 (9): 581–8.
  3. Weissman NJ (2001). Appetite suppressants and valvular heart disease. Am. J. Med. Sci. 321 (4): 285–91.
  4. Roth BL (2007). Drugs and valvular heart disease. N. Engl. J. Med. 356 (1): 6–9.

Further reading[]

  • Welch JT, Lim DS. (2007): "The synthesis and biological activity of pentafluorosulfanyl analogs of fluoxetine, fenfluramine, and norfenfluramine." Bioorg Med Chem. 15(21):6659. PMID 17765553.

External links[]

Template:Antiobesity preparations


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