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Intestinal Pharmacomanometry as a Guide to Antidepressant Therapy
Published in Fuad Lechin, Bertha van der Dijs, Neurochemistry and Clinical Disorders: Circuitry of Some Psychiatric and Psychosomatic Syndromes, 2020
Fuad Lechin, Bertha van der Dijs, Francisco Gomez, Luis Arocha, Emilio Acosta, Alex E. Lechin
The different responses to FENF, a serotonin releasing agent, seem to involve this neurotransmitter in both groups of depressive disorders found in this study. On the other hand, the finding that high-IT patients responded to treatment with FENF and IMI, whereas the low-IT patients responded to CMI, seems paradoxical since both FENF and CMI supposedly increase serotonin neurotransmission. The therapeutic effects of FENF could be more related to its ability to induce brain serotonin depletion than to the early increase of this neurotransmitter at synaptic level. In this respect, it would be interesting to investigate the changes in CSF-5HIAA levels in FENF in-treatment patients.
Current Trends in Performance- and Image-Enhancing Substance Use Among Gym Goers, Exercisers, and Athletes
Published in Ornella Corazza, Andres Roman-Urrestarazu, Handbook of Novel Psychoactive Substances, 2018
Neha P. Ainsworth, Jake Shelley, Andrea Petróczi
For example, fenfluramine acts primarily as a serotonin-releasing agent by disrupting serotonin storage vesicles and inhibiting serotonin uptake (Baumann, Ayestas, Dersch, Partilla, & Rothman, 2000). The resulting increase in serotonin levels appears to have an appetite suppressing effect. However, cardiac-valve abnormalities are a common side effect of fenfluramine, and the drug was withdrawn in the United States in 1997 following the finding that about 30% developed valve abnormalities (Docherty, 2008). This side effect appears to be linked to the serotonin-mimetic effect of fenfluramine (Roth, 2007).
Current and future pharmacotherapy options for drug-resistant epilepsy
Published in Expert Opinion on Pharmacotherapy, 2022
Fenfluramine (3-trifluoromethyl-N-ethylamphetamine) was initially launched as an appetite suppressant in the 1970s but it was subsequently withdrawn from the market because of the increased risk of valvular heart disease as a side effect [57]. Orphan designation was granted by the EMA for fenfluramine for the treatment of Dravet syndrome in 2013. Currently, fenfluramine is only indicated for Dravet syndrome but studies are currently ongoing for LGS. It is a serotonin-releasing agent with its major active metabolite (norfenfluramine) binding to and activating 5-hydroxytryptamine receptors 2B and 2C with high affinity and 2A with moderate affinity [58]. Evidence from two RCTs in patients with Dravet Syndrome has demonstrated that adjunctive fenfluramine decreased convulsive motor seizures relative to placebo and was generally well tolerated [59,60]. Fenfluramine was also found to improve quality of life in children taking it compared to placebo [60]. As already alluded to, fenfluramine has been trialed in children with LGS in a pilot study, demonstrating more than a 50% reduction in convulsive seizures in most patients [61]. The most common serious adverse event was status epilepticus resulting in hospital admission [59–61] but most adverse events were otherwise minor and included reduced appetite, somnolence, weight loss and fatigue. Large multicenter international studies of fenfluramine in LGS are pending.
Current and emerging drug therapies for the treatment of depression in adults with epilepsy
Published in Expert Opinion on Pharmacotherapy, 2019
Fenfluramine is a substituted amphetamine, acting primarily as a serotonin releasing agent with less effect on the release of noradrenaline and dopamine, which are primarily mediated by its metabolite Norfenfluramine. It was first approved in the US in the 1970s and later marketed for obesity [34]. It was withdrawn in 1997 after reports of cardiac effects (valve disease and fibrosis) and pulmonary hypertension [35]. The use of Fenfluramine in epilepsy was first reported in the 1980s. More recently, Fenfluramine has been investigated in Dravet syndrome showing a significant reduction in focal motor seizures [36]. Fenfluramine is currently under Phase III development by Zogenix (ZX008). Three double-blind, randomized, placebo-controlled studies for the adjunctive treatment in Dravet syndrome are being conducted and a long-term, open-label extension is planned [37]. The mechanism of action suggests an antidepressant effect but evidence is not available. The safety profile suggests potential limitations in terms of long-term tolerability but this is under review.
An update on the pharmacological management of pain in patients with multiple sclerosis
Published in Expert Opinion on Pharmacotherapy, 2020
Clara G. Chisari, Eleonora Sgarlata, Sebastiano Arena, Emanuele D’Amico, Simona Toscano, Francesco Patti
Carbamazepine is a sodium channel blocker that binds to voltage-gated sodium channels in their inactive conformation, preventing repetitive and sustained firing of an action potential. Carbamazepine works also as a serotonin releasing agent and a serotonin reuptake inhibitor [58].