Bicuculline methochloride  (Synonyms: (+)-Bicuculline methochloride; d-Bicuculline methochloride)

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

IC50: 3 μM (GABA_A)^[3]

Bicuculline methochloride (1 μM and 3 μM) attains the maximal response of GABA. Bicuculline methochloride 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 methochloride (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.

Bicuculline methochloride (1.25-3 mg/kg; s.c.) 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 methochloride (1.5-3.2 mg/kg; s.c.) 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 methochloride 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.

417.84

C₂₁H₂₀ClNO₆

38641-83-7

C[N+]([C@](C1=C2C=C3C(OCO3)=C1)([H])[C@@](O4)([H])C(C=CC5=C6OCO5)=C6C4=O)(CC2)C.[Cl-]

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]