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- Atack, J.R. et al. (1999) Neuropsychopharmacology 20, 255.
Alomone Labs Flumazenil inhibits specific binding of Flunitrazepam to rat brain GABA(A) receptors.Percent inhibition of specific binding of 1 nM [3H] Flunitrazepam to membranes from whole rat brain (except cerebellum) was plotted against concentrations of Flumazenil (#F-145), (green circles) and of Diazepam (assay standard, black squares) and used to calculate IC50 and Ki values for Flumazenil (IC50 ≈ 7.35 nM, and Ki ≈ 5.99 nM).
- Atack, J.R. et al. (1999) Neuropsychopharmacology 20, 255.
- Hood, S.D. et al. (2014) Br. J. Clin. Pharmacol. 77, 285.
- Rodrigo, C. (1995) Anesth. Prog. 42, 121.
Flumazenil is an imidobenzodiazepine derivative, also called Ro 15-1788, which acts as a specific benzodiazepine antagonist. It binds with high affinity to the benzodiazepine binding site of GABA(A) receptors. It reduces in a dose-dependent manner the effects of benzodiazepines by competitively displacing benzodiazepines from the receptors. Flumazenil has the ability to reverses the effects caused by benzodiazepines such as sedation, amnesia, hypotonia and anxiolysis1,2.
Oral administration of flumazenil is rapidly absorbed but is metabolized by the liver and has a high hepatic clearance from first pass metabolism. This metabolism limits the oral bioavailability to about 16%. Therefore, the drug is administrated intravenously. Its clinical effects can be seen for only 30-60 min after administration. Most of the drug is metabolized into inactive metabolites. Only 0.2% is excreted unchanged in the urine2,3.
Several recent studies have shown that patients given flumazenil showed significant reduction in benzodiazepine withdrawal symptoms, reduced craving, increased completion of withdrawal and reduced post detoxification relapse rates2.
Flumazenil (#F-145) is a highly pure, synthetic, and biologically active compound.
