ChEBI: The hydrochloride salt of fenfluramine. It binds to the serotonin reuptake pump, causing inhbition of serotonin uptake and release of serotonin. The resulting increased levels of serotonin lead to greater serotonin receptor activation which in turn lead to
enhancement of serotoninergic transmission in the centres of feeding behavior located in the hypothalamus. This suppresses the appetite for carbohydrates. Fenfluramine hydrochloride was used for treatment of diabetes and obesity. It was withdrawn worldwide
after reports of heart valve disease and pulmonary hypertension.
Fenfluramine hydrochloride, (±)N-ethyl- -methyl-m-(trifluoromethyl)phenethylamine hydrochloride (Pondimin), isunique in this group of drugs, in that it tends to produce sedationrather than excitation. Effects are said to be mediatedprincipally by central serotoninergic, rather than central noradrenergic,mechanisms. In large doses in experimental animals,the drug is a serotonin neurotoxin.It was withdrawnfrom human use after reports of heart valve damage and pulmonaryhypertension. From its structure, more apolar or hydrophobiccharacter than amphetamine, tropism for serotoninergicneurons would be expected. Likewise, thestructure suggests an indirect mechanism. If an indirectmechanism were operative, then all postsynaptic 5-HT receptors could be activated. Evidence from several studies indicatesthat the 5-HT1B and the 5-HT2C receptors are mostresponsible for the satiety effects of 5-HT. 5-HT may alsoinfluence the type of food selected (e.g., lower-fat food intake).The(+) isomer, dexfenfluramine (Redux), has agreater tropism for 5-HT systems than the racemic mixture.It, too, was withdrawn because of toxicity.
Poison by ingestion, intravenous, and intraperitoneal routes. Human systemic effects by ingestion: mydriasis, change in motor activity, nausea. An experimental teratogen. Other experimental reproductive effects. When heated to decomposition it emits very toxic fumes of F-, NOx, and HCl
