Home Neuronal Signaling GABA Receptor agonist 4-Aminobutyric acid (GABA)

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4-Aminobutyric acid (GABA) GABA Receptor agonist

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.
4-Aminobutyric acid (GABA) GABA Receptor agonist Chemical Structure

Chemical Structure

Molecular Weight: 103.12

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Quality Control

Batch: Purity: 98.94%
98.94

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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Chemical Information, Storage & Stability

Molecular Weight 103.12 Formula

C4H9NO2

 Storage (From the date of receipt)
CAS No. 56-12-2 Download SDF Storage of Stock Solutions

Synonyms 4-Aminobutanoic acid, GABA, Gamma-aminobutyric acid, Piperidic acid SMILES C(CC(=O)O)CN

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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 anesthesia. 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 glycemia, improved metabolic conditions, and maintained close to normal glucose tolerance during a period of 53 d after STZ injections.
References

Clinical Trial Information

(data from https://clinicaltrials.gov, updated on 2025-07-30)

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT04062890 WITHDRAWN
Hyperinsulinism; Insulin Resistance; Insulin Sensitivity; Glucose Intolerance; Hypertension
University of Arizona
 2030-04-15 PHASE2
NCT03328455 NOT_YET_RECRUITING
Healthy Aging
University of Nevada, Reno
 2027-12-01
NCT07457736 RECRUITING
Healthy Adult Participants
Yale University
 2026-01-28 EARLY_PHASE1
NCT07549490 NOT_YET_RECRUITING
Acute Pain
National Center for Complementary and Integrative Health (NCCIH)
 2026-09-09
NCT06852469 RECRUITING
Stress Disorders, Post-Traumatic
VA Office of Research and Development
 2025-07-01 PHASE4
NCT04144439 RECRUITING
Epilepsy
Sherief Abd-Elsalam
 2018-07-01 PHASE4

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