Rahul Sharma


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Routes of administration  Oral
Biological half-life  20 hours
CAS ID  458-24-2
ATC code  A08AA02 (WHO)
Molar mass  231.26 g/mol
AHFS/Drugs.com  International Drug Names
Pregnancy category  AU: B2 US: C (Risk not ruled out)
Legal status  AU: S4 (Prescription only) US: Schedule IV

Settlement diet pills fen phen

Fenfluramine (former brand names Pondimin, Ponderax and Adifax), also known as 3-trifluoromethyl-N-ethylamphetamine, is an anorectic that is no longer marketed. In combination with phentermine, it was part of the anti-obesity medication Fen-phen.


Fenfluramine was introduced on the U.S. market in 1973 and withdrawn in 1997. It is the racemic mixture of two enantiomers, dexfenfluramine and levofenfluramine. The drug increases the level of serotonin, a neurotransmitter 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. The result is a feeling of fullness and reduced appetite.

Exposed the hidden dangers of phentermine fenfluramine and fen phen

Withdrawal due to heart disease

The drug was withdrawn from the U.S. market in 1997 after reports of heart valve disease and pulmonary hypertension, including a condition known as cardiac fibrosis. It was subsequently withdrawn from other markets around the world. It was banned in India in 1998.

The distinctive valvular abnormality seen with fenfluramine is a thickening of the leaflet and chordae tendineae. One mechanism used to explain this phenomenon involves heart valve serotonin receptors, which are thought to help regulate growth. Since fenfluramine and its active metabolite norfenfluramine stimulate serotonin receptors, this may have led to the valvular abnormalities found in patients using fenfluramine. In particular norfenfluramine is a potent inhibitor of the re-uptake of 5-HT into nerve terminals. 5-HT2B receptors. Fenfluramine and its active metabolite norfenfluramine affect the 5-HT2B receptors which are plentiful in human cardiac valves. The suggested mechanism by which fenfluramine causes damage is through over or inappropriate stimulation of these receptors leading to inappropriate valve cell division. Supporting this idea is the fact that this valve abnormality has also occurred in patients using other drugs that act on 5-HT2B receptors.

According to a study of 5743 former users conducted by a plaintiff's expert cardiologist, damage to the heart valve continued long after stopping the medication. Of the users tested, 20 percent of women, and 12 percent of men were affected. For all ex-users, there was a sevenfold increase of chances of needing surgery for faulty heart valves caused by the drug.

Other adverse effects and recreational use potential

There have been reports associating fenfluramine with depression, psychosis, exacerbation of pre-existing psychosis (schizophrenia), and sleep disturbances. These effects may be mediated by serotonergic neurotoxicity/depletion of serotonin with chronic administration and/or activation 5-HT2A receptors. In overdose, fenfluramine can result in serotonin syndrome and death. Unlike various other amphetamine derivatives, fenfluramine is reported to be dysphoric, "unpleasantly lethargic", and non-addictive. However, it has been reported to be used recreationally at high doses ranging between 80 and 400 mg, which have been described as producing euphoria, amphetamine-like effects, sedation, and hallucinogenic effects, along with anxiety, nausea, diarrhea, and sometimes panic attacks, as well as depressive symptoms once the drug had worn off. At high doses (e.g., 240 mg, or between 200–600 mg), fenfluramine induces a psychedelic state resembling that produced by lysergic acid diethylamide (LSD). While fenfluramine binds only very weakly to the 5-HT2 receptors, its active metabolite norfenfluramine binds to and activates the 5-HT2B and 5-HT2C receptors with high affinity and the 5-HT2A receptor with moderate affinity; as such, indirect (via induction of serotonin release) and/or direct activation of the 5-HT2A receptor would be expected to be responsible for the psychedelic effects of the drug at sufficient doses.


Prepn: L. G. Beregi et al., FR M1658; eidem, US 3198833 (1963, 1965 both to Sci. Union et Cie Soc. Franc. Recherche Méd.). Prepn of optical isomers: eidem, US 3198834 (1965 to Sci. Union et Cie Soc. Franc. Recherche Med.).


Fenfluramine Wikipedia

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