Stereochemistry | RACEMIC |
Molecular Formula | C12H16F3N |
Molecular Weight | 231.2573 |
Optical Activity | ( + / - ) |
Defined Stereocenters | 0 / 1 |
E/Z Centers | 0 |
Charge | 0 |
SHOW SMILES / InChI
SMILES
CCNC(C)CC1=CC(=CC=C1)C(F)(F)F
InChI
InChIKey=DBGIVFWFUFKIQN-UHFFFAOYSA-N
InChI=1S/C12H16F3N/c1-3-16-9(2)7-10-5-4-6-11(8-10)12(13,14)15/h4-6,8-9,16H,3,7H2,1-2H3
Molecular Formula | C12H16F3N |
Molecular Weight | 231.2573 |
Charge | 0 |
Count |
MOL RATIO
1 MOL RATIO (average) |
Stereochemistry | RACEMIC |
Additional Stereochemistry | No |
Defined Stereocenters | 0 / 1 |
E/Z Centers | 0 |
Optical Activity | ( + / - ) |
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 Fenfluramine was introduced on the U.S. market in 1973 and withdrawn in 1997.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 The drug was withdrawn from the U.S. market in 1997 after reports of heart valve disease and pulmonary hypertension, including a condition known as cardiac fibrosis. It was subsequently withdrawn from other markets around the world. In this small exploratory and retrospective study, remarkably good results were reported on the use of fenfluramine as an add-on medication for controlling seizures in patients with the Dravet syndrome. The side effects were rare and nonserious and did not result in termination of the treatment. It is possible that this drug may have anticonvulsive effects for other severe epilepsy syndromes, especially in those characterized by photosensitive or induced seizures.
CNS Activity
Originator
Approval Year
Doses
AEs
Overview
CYP3A4 | CYP2C9 | CYP2D6 | hERG |
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OverviewOther
Drug as perpetrator
Drug as victim
Tox targets
Sourcing
PubMed
Patents
Sample Use Guides
Rat midbrain slices were used to make intracellular recordings from dopaminergic neurons of the substantia nigra and the ventral tegmental area. Gamma-aminobutyric acid (GABA)-mediated synaptic transmission was assessed from the inhibitory postsynaptic potentials (IPSPs) mediated by GABAA and GABAB receptors. Intracellular recordings from midbrain SNpc and VTA dopaminergic neurons were performed at 33.0 +/- 0.5°C in a recording chamber submerged with aCSF flowing at a rate of 2.5–3 mL•min-1 and continuously oxygenated, on the stage of an upright (inverted) microscope (Axioscope FS, Zeiss, Gottingen, Germany), equipped for infrared video microscopy (Hamamatsu, Tokyo, Japan) in order to allow a direct visualization of the recorded cells. Neurons, selected for their morphology, were identified as dopaminergic by their electrophysiological properties such as the presence of a regular spontaneous firing activity (0.5–4 Hz), a large inward current (Ih) in response to hyperpolarizing voltages and a membrane hyperpolarization due to dopamine (10–30 mmol•L-1) application . The recording electrodes were filled with 2 mol•L-1 KCl and had a tip resistance of 30–80 MW. GABAB synaptic potentials were evoked using a bipolar tungsten stimulating electrode with a tip separation of 300–700 mkm. Representative recordings showing the effect of fenfluramine in reducing the GABAB-mediated IPSP. Such effects were evident at concentrations below 1 mmol•L-1. The amplitude of synaptic potentials was halved by fenfluramine at concentration around 10 mmol•L-1 and was completely blocked by CGP (1 mmol•L-1), a selective GABAB receptor antagonist. Fenfluramine and sibutramine induce a concentration-dependent reduction of the GABAB-mediated inhibitory postsynaptic potentials (IPSPs).