Bicuculline methobromide  (Synonyms: (+)-Bicuculline methobromide)

Bicuculline methobromide is a selective GABAA Receptor antagonist with an IC₅₀ value of 3 μM. Bicuculline methobromide induces clonic tonic convulsions in mammals and can also be used to block Ca²⁺ activated potassium channels. Bicuculline methobromide can be used in studies of epilepsy and other related psychiatric disorders^[1][2].

Bicuculline methobromide (1 μM and 3 μM) attains the maximal response of GABA. Bicuculline methobromide appears to shift the dose–response curves of GABA in parallel to the right without decreasing GABA maximal response, suggesting that it is a competitive antagonist at human α₁β₂γ_2L GABA_A receptors expressed in Xenopus oocytes^[3].
Bicuculline methobromide (1-100 μM; 2 min; applied as outside-out patches) potently blocks both Apamin (HY-P0256)-sensitive small-conductance calcium-activated potassium channels (SK2) currents and Apamin-insensitive SK1 currents in Xenopus oocytes^[4].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Note:
Please do not refer to only one article to determine the experimental conditions. It is recommended to determine the optimal experimental conditions (animal strain, age, dosage, frequency and cycle, detection time and indicators, etc.) through preliminary experiments before the formal experiment.

Bicuculline methobromide (subcutaneous injection, 1.25-3 mg/kg) can cause clonus-tonic convulsions in a dose-dependent manner in mice and these convulsions are enhanced by injection of the μ-opioid agonist morphine^[1].
Bicuculline methobromide (subcutaneous injection, 1.5-3.2 mg/kg) induces male Swiss S mice generalized seizures with a CD₅₀ (convulsant dose) of 2.2 mg/kg for clonus and CD₅₀ of 2.4 mg/kg for tonus. Seizures induced by Bicuculline at the dose of 3.2 mg/kg can be blocked by pretreatment (i.p.) with the NMDA antagonists MK-801, CPP and CGS 19755^[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

462.29

C₂₁H₂₀BrNO₆

66016-70-4

C[N+]1([C@](C2=C(CC1)C=C3C(OCO3)=C2)([H])[C@@]4([H])C5=C(C6=C(OCO6)C=C5)C(O4)=O)C.[Br-]

Room temperature in continental US; may vary elsewhere.

Please store the product under the recommended conditions in the Certificate of Analysis.

• [1]. Y Yajima, et al. Effects of differential modulation of mu-, delta- and kappa-opioid systems on bicuculline-induced convulsions in the mouse. Brain Res. 2000 Apr 17;862(1-2):120-6.  [Content Brief]

  [2]. W A Turski, et al. Excitatory amino acid antagonists protect mice against seizures induced by bicuculline. Brain Res. 1990 Apr 23;514(1):131-4.  [Content Brief]

  [3]. Huang SH, et al. Bilobalide, a sesquiterpene trilactone from Ginkgo biloba, is an antagonist at recombinant alpha1beta2gamma2L GABA(A) receptors. Eur J Pharmacol. 2003;464(1):1-8.  [Content Brief]

  [4]. Khawaled R, et al. Bicuculline block of small-conductance calcium-activated potassium channels. Pflugers Arch. 1999 Aug;438(3):314-21.  [Content Brief]