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γ-Aminobutyric acid

Catalog No. T0508 CAS 56-12-2

Synonyms: Gamma-aminobutyric acid, 4-Aminobutyric acid, GABA, 4-Aminobutanoic acid, Piperidic acid

γ-Aminobutyric acid (4-Aminobutyric acid) is the most common inhibitory neurotransmitter in the central nervous system.

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γ-Aminobutyric acid, CAS 56-12-2

Pack Size	Availability	Price/USD
50 mg	In stock	$ 30.00
100 mg	In stock	$ 43.00
200 mg	In stock	$ 58.00
500 mg	In stock	$ 93.00

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Purity: 98%

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Description	γ-Aminobutyric acid (4-Aminobutyric acid) is the most common inhibitory neurotransmitter in the central nervous system.
In vitro	γ-Aminobutyric acid (GABA) functions primarily as an inhibitory neurotransmitter in the mature central nervous system. The addition of GABA into the cell culture medium promoted the proliferation of GABRP-expressing PDAC cells, but not GABRP-negative cells, and GABAA receptor antagonists inhibited this growth-promoting effect by GABA. The HEK293 cells constitutively expressing exogenous GABRP revealed the growth-promoting effect of GABA treatment. GABA treatment in GABRP-positive cells increased intracellular Ca2+ levels and activated the mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/Erk) cascade[1]. GABA exerts antidiabetic effects by acting on both the islet β-cells and immune system. Unlike in adult brain or islet α-cells in which GABA exerts hyperpolarizing effects, in islet β-cells, GABA produces membrane depolarization and Ca2+ influx, leading to the activation of PI3K/Akt-dependent growth and survival pathways[2].
In vivo	GABA is the principal inhibitory neurotransmitter in the adult brain that has a parallel inhibitory role in the immune system. GABAergic medications are used to treat anxiety, alcohol withdrawal, epilepsy, and to induce sedation, and anesthesia. GABA is neuroprotective in animal models of stroke. GABA treatment decreases inflammatory cytokine production in peripheral macrophages. It decreases T cell autoimmunity and the development of inflammatory responses in the nonobese diabetic mouse model of type 1 diabetes[3]. In the adult brain, GABA induces a fast inhibition in neurons mainly through the GABAA receptor (GABAAR). GABA is produced by pancreatic β-cells. GABA released from β-cells can act on GABAAR in the α-cells, causing membrane hyperpolarization and hence suppressing glucagon secretion. GABA-treated mice showed higher circulating insulin, lower glucagon, nearly normal glycemia, improved metabolic conditions, and maintained close to normal glucose tolerance during a period of 53 d after STZ injections[2].
Cell Research	GABRP-positive cell lines, KLM-1 and PK-45P, and GABRP-negative cell lines, PK-59 and KP-1N, are incubated with GABA or GABA receptor agonist Muscimol at serial concentration (0, 1, 10, 100 μmol/L) in appropriate medium supplemented with 1% FBS for 6 days. To inhibit the GABA-mediated pathway, cells are incubated with 250 μmol/L of GABAA receptor antagonist bicuculline methiodide or 1 mmol/L of GABAB receptor antagonist CGP-35348. After 6 days of exposure to either of these drugs, cell viability is measured by MTT assay as described above.(Only for Reference)

Synonyms	Gamma-aminobutyric acid, 4-Aminobutyric acid, GABA, 4-Aminobutanoic acid, Piperidic acid
Molecular Weight	103.12
Formula	C4H9NO2
CAS No.	56-12-2

Storage

Powder: -20°C for 3 years | In solvent: -80°C for 1 year

Solubility Information

H2O: 10 mM

DMSO: Insoluble

References and Literature

1. Takehara A, et al. Cancer Res. 2007, 67(20):9704-12. 2. Soltani N, et al. Proc Natl Acad Sci U S A. 2011, 108(28):11692-7. 3. Bhat R, et al. Proc Natl Acad Sci U S A. 2010, 107(6):2580-5.

Related compound libraries

This product is contained In the following compound libraries：

Anti-Cancer Clinical Compound Library Drug Repurposing Compound Library Membrane Protein-targeted Compound Library Inhibitor Library Microbial Natural Product Library Anti-Cancer Approved Drug Library Anti-Neurodegenerative Disease Compound Library Human Endogenous Metabolite Library Anti-Cancer Drug Library Marine Natural Product Library

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Keywords

γ-Aminobutyric acid 56-12-2 Membrane transporter/Ion channel Metabolism Neuroscience GABA Receptor Endogenous Metabolite metabotropic γ-Aminobutyric acid Receptor Gamma-aminobutyric acid CNS 4-Aminobutyric acid migration ionotropic depolarization γ Aminobutyric acid central nervous system cortex development GAD neuron GABA G-protein chemotaxis 4-Aminobutanoic acid Piperidic acid Gamma-aminobutyric acid Receptor r-Aminobutyric acid inhibit Inhibitor neurotransmitter polyamine γAminobutyric acid inhibitor

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