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4-Aminobutyric acid (GABA) GABA Receptor agonist

Name: 4-Aminobutyric acid (GABA)
Brand: Selleck Chemicals
SKU: S4700
Rating: 5 (1 reviews)

Cat.No.S4700

4-Aminobutyric acid (4-Aminobutanoic acid, GABA, Gamma-aminobutyric acid, Piperidic acid) is a naturally occurring neurotransmitter with central nervous system (CNS) inhibitory activity.

Chemical Structure

Molecular Weight: 103.12

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Quality Control

Batch: Purity: 98.94%

98.94

Related Targets	Adrenergic Receptor AChR 5-HT Receptor COX Calcium Channel Histamine Receptor Dopamine Receptor TRP Channel Cholinesterase (ChE) GluR
Other GABA Receptor Inhibitors	Dihydromyricetin CGP52432 Oxiracetam Ginkgolide A Pentylenetetrazol Emamectin Benzoate Nefiracetam Piracetam Bemegride 6-Hydroxyflavone (6-HF)

Chemical Information, Storage & Stability

Molecular Weight	103.12	Formula	C₄H₉NO₂	Storage (From the date of receipt)	3 years-20°Cpowder
CAS No.	56-12-2	Download SDF		Storage of Stock Solutions	1 year-80°Cin solvent 1 month-20°Cin solvent
Synonyms	4-Aminobutanoic acid, GABA, Gamma-aminobutyric acid, Piperidic acid			Smiles	C(CC(=O)O)CN

Solubility

In vitro
Batch:

Water : 21 mg/mL

DMSO : Insoluble
(Moisture-contaminated DMSO may reduce solubility. Use fresh, anhydrous DMSO.)

Ethanol : Insoluble

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In vivo
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In vivo Formulation Calculator (Clear solution)

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Method for preparing DMSO master liquid: mg drug pre-dissolved in μL DMSO ( Master liquid concentration mg/mL, Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug. )

Method for preparing in vivo formulation: Take μL DMSO master liquid, next addμL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH₂O, mix and clarify.

Method for preparing in vivo formulation: Take μL DMSO master liquid, next add μL Corn oil, mix and clarify.

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Mechanism of Action

Targets/IC₅₀/Ki	GABA receptor
In vitro	γ-Aminobutyric acid (GABA) functions primarily as an inhibitory neurotransmitter in the mature central nervous system. The addition of this compound 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. It 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, it produces membrane depolarization and Ca2+ influx, leading to the activation of PI3K/Akt-dependent growth and survival pathways.
In vivo	4-Aminobutyric acid (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 anaesthesia. It is neuroprotective in animal models of stroke. This compound 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. In the adult brain, GABA induces a fast inhibition in neurons mainly through the GABAA receptor (GABAAR). It 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 glycaemia, improved metabolic conditions, and maintained close to normal glucose tolerance during a period of 53 d after STZ injections.
References	[1] https://pubmed.ncbi.nlm.nih.gov/17942900/ [2] https://pubmed.ncbi.nlm.nih.gov/21709230/ [3] https://pubmed.ncbi.nlm.nih.gov/20133656/

Clinical Trial Information

(data from https://clinicaltrials.gov, updated on 2024-05-22)

NCT Number	Recruitment	Conditions	Sponsor/Collaborators	Start Date	Phases
NCT06261450	Not yet recruiting	Fragile X Syndrome	Université de Sherbrooke\|Canadian Institutes of Health Research (CIHR)\|Jazz Pharmaceuticals\|Centre de recherche du Centre hospitalier universitaire de Sherbrooke	April 1 2024	Phase 2
NCT06381479	Recruiting	Stress\|Sleep Disorder	National Taiwan Sport University\|Bened Biomedical Co. Ltd.	April 19 2024	Not Applicable
NCT06361368	Not yet recruiting	Insomnia	National Yang Ming University\|Bened Biomedical Co. Ltd.	April 2024	Not Applicable
NCT06057233	Not yet recruiting	Epilepsy Temporal Lobe	University Hospital Grenoble\|Université Grenoble-Alpes\|Institut National de la Santé Et de la Recherche Médicale France	March 2024	--

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