2. Membrane Transporter/Ion Channel Neuronal Signaling
  3. GABA Receptor
  4. Gabaculine

Gabaculine is an amino acid neurotoxin and blood-brain barrier-permeable GABA transaminase inhibitor, with an IC50 of 1 μM in beef and Pseudomonas ovalis. Gabaculine elevates endogenous synaptic and brain GABA levels and enhances GABA activity. Gabaculine induces sedation, hypothermia, loss of righting reflex, and prevents convulsions in mice. Gabaculine is applicable to research related to neurological disorders.

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Gabaculine

Gabaculine 화학구조

CAS No. : 59556-18-2

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Gabaculine Related Antibodies

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제품 설명

Gabaculine is an amino acid neurotoxin and blood-brain barrier-permeable GABA transaminase inhibitor, with an IC50 of 1 μM in beef and Pseudomonas ovalis. Gabaculine elevates endogenous synaptic and brain GABA levels and enhances GABA activity. Gabaculine induces sedation, hypothermia, loss of righting reflex, and prevents convulsions in mice. Gabaculine is applicable to research related to neurological disorders[1][2][3].

In Vitro

Gabaculine potently and irreversibly inhibits GABA transaminase in mouse brain in vitro[1].
Gabaculine potently inhibits GABA transaminase from bovine brain, Pseudomonas ovalis and mouse brain in vitro, with an IC50 of 1 μM against the enzyme derived from bovine brain and Pseudomonas ovalis[2].

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

Gabaculine Related Antibodies
In Vivo

Gabaculine (100 mg/kg; intraperitoneal injection; single administration) completely inhibits GABA transaminase in mouse brains within 4 h and increases whole-brain GABA levels by 15- to 20-fold at 20 h post-administration[1].
Gabaculine (intracerebroventricular injection, 0.12-2.0 μg; intraperitoneal injection, 60 mg/kg; single administration) dose-dependently and time-dependently increases GABA levels in the brain of mice, and exerts a preventive effect on convulsions induced by Picrotoxin (HY-101391) and Thiosemicarbazide (HY-Y0032)[2].
Gabaculine (i.p., 10-400 mg/kg) induces loss of righting reflex in male ddY mice at doses ≥200 mg/kg, but produces no antinociceptive effects at doses up to 100 mg/kg and shows no tonic immobility response to tail-clinch noxious stimulation at doses up to 400 mg/kg[3].

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

Animal Model: ddy mice (male, body weight 26-30 g)[2]
Dosage: 0.12-2.0 μg (i.c.v., GABA elevation; picrotoxin-induced convulsions; thiosemicarbazide-induced convulsions); 60 mg/kg (i.p., GABA elevation)
Administration: i.c.v.; i.p.; 3 hours prior to convulsant/electroshock application
Result: Gradually increased brain GABA content starting at 2 hours post-injection, reaching a maximum ~15 times the control level at 18 hours, and remaining elevated at 24 hours (1.0 μg i.c.v.).
Increased brain GABA content with a similar time course to intraventricular 1.0 μg gabaculine (60 mg/kg i.p.).
Produced a dose-dependent elevation in brain GABA content at 3 hours post-injection (0.12, 0.25, 0.5, 1.0, 2.0 μg i.c.v.).
Prevented picrotoxin-induced convulsions with an ED50 of 0.50 μg (95% confidence limits 0.34-0.78) (i.c.v.).
Prevented thiosemicarbazide-induced convulsions with an ED50 of 0.18 μg (95% confidence limits 0.11-0.22) (i.c.v.).
분자량

139.15

화학식

C7H9NO2
CAS No.
SMILES

O=C(C1=CC=CC(C1)N)O
Structure Classification
Initial Source

Streptomyces togocaensis subspecies 1039
선적

Room temperature in continental US; may vary elsewhere.
보관

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

Gabaculine59556-18-2GABA ReceptorGamma-aminobutyric acid Receptorγ-Aminobutyric acid ReceptorconvulsionsGABAPseudomonas ovalismiceblood-brain barrierglutamate decarboxylasepicrotoxinGABA-transaminaseornithine decarboxylasethiosemicarbazideInhibitorinhibitorinhibit

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