Serotoninergic anorectic agent, dexfenfluramine acts to increase the serotonin level in extracellular space of the brain causing reduced appetite. This effect promotes its use in obesity treatments. Its ability to, dissolve in lipids provide easier transportation across blood brain barrier.
Scientists developed dexfenfluramine, dextrorotary stereoisomer of fenfluramine to reduce the side effect of fenfluramine, developed in 1960s and marketed as pondimin. Approval of dexfenfluramine by FDA took place in 1976 but its introduction to market took place later in 1995 by Wyeth since fenfluramine had shown to cause hypertension in some people using it to fight obesity. Later withdrawal on September 15, 1997 from US market was due to side effect associated with heart problems.
Dexfenfluramine is a synthetic anti-obesity chemical with molecular weight of 267.7, white crystalline powder, with high solubility saline solution, alcohol and chloroform. Dexfenfluramine has a solubility of 100nm in water. It also acts to decrease the growth hormones such as leptin and insulin but lead to increase in gherlin. Dexfenfluramine is more potent in inhibition of serotonin reuptake than active metabolite nordexfenfluramine. However, it is less potent in acceleration of serotonin release into the synaptic cleft.
Administration of dexfenfluramine is mainly through oral, inhalation routes and lesser extent intravenous infusion in compound called dexfenfluramine hydrochloride (C12H16F3N,HCl)1. Oral administration of compound under the name of ‘redux’ was in capsules enclosing white crystalline powder weighing 15mg. The oral route is favoured due to resistance of dexfenfluramine to acidic media in the stomach. In addition, the hydrophobic nature of the drug is favours diffusion through the gastro intestinal walls. In some cases though rare,