Anticonvulsant agent that is an allosteric antagonist at the NR2B subunit of the NMDA glutamate receptor; also has γ-aminobutyric acid (GABAA) receptor agonist properties.
Journal of medicinal chemistry, 51(6), 1534-1545 (2008-03-04)
The antiepileptic effect of felbamate (FBM) is ascribable to gating modification of NMDA receptors. Using site-directed mutagenesis and electrophysiological studies, we found that single-point mutations of four pairs of homologous residues in the external vestibule of the receptor pore, namely
The Journal of pharmacology and experimental therapeutics, 280(3), 1383-1391 (1997-03-01)
Felbamate and meprobamate are structurally related propanediol dicarbamates that possess distinct pharmacological profiles. Felbamate is a minimally sedative, broad-spectrum anticonvulsant, whereas meprobamate is a strong sedative-anxiolytic agent. Previously, we reported that felbamate potentiates gamma-aminobutyric acid(A) (GABA(A)) receptor Cl- currents and
Critical reviews in neurobiology, 12(3), 205-222 (1998-12-10)
Felbamate was launched in 1993 in the U.S. as a "new generation" antiepileptic drug (AED) with a unique mechanism of action. It proved efficacious in patients refractory to other AEDs and was particularly beneficial in children suffering from Lennox-Gastaut syndrome
Felbamate (FBM) is a potent nonsedative anticonvulsant whose clinical effect is chiefly related to gating modification (and thus use-dependent inhibition) rather than pore block of N-methyl-D-aspartate (NMDA) channels at pH 7.4. Using whole-cell recording in rat hippocampal neurons, we examined
The Western journal of medicine, 161(3), 309-314 (1994-09-01)
For the first time in 15 years, new antiepileptic medications are available for the treatment of patients with seizure disorders. These drugs have demonstrated efficacy in animal models of epilepsy and in controlled clinical trials. Felbamate was licensed in 1993
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