- In weaning piglets: intestinal GABAergic system (including GABA transporters SLC6A13 and GABA receptor subunits GABA_B2 and GABA_Aβ2). [1]
- In Drosophila: GABA synthetic enzyme Gad1; ionotropic GABA receptors Lcch3 and RdI; metabotropic GABA receptors GABA-B-R1, -2, -3. [2]

γ-Aminobutyric acid (30 μM) depolarizes cortical progenitor cells (E16 cells), causes inward currents in ventricular zone (VZ) cells, and inhibits DNA synthesis at a half-maximum response concentration of 5 μM [3]. Gamma-aminobutyric acid (1–5 μM; 18 h) increases cortical plate (cp) cell motility and inhibits migration, while G protein activation is involved in chemotactic signaling. GAD is expressed by cp neurons. Growth is restricted and cell cycle arrest occurs in the S phase due to the activation of GABA A receptors by γ-aminobutyric acid [5].

- In weaned piglets, dietary supplementation of GABA (20 mg/kg feed for 3 weeks) significantly promoted growth rate in the third week and reduced feed conversion ratio in the second week. It also increased the kidney organ index. [1]
- GABA supplementation inhibited ileal mRNA expression of IL-22, proinflammatory cytokines IL-1 and IL-18, and Muc1; promoted expression of anti-inflammatory cytokines IFN-γ, IL-4, IL-10, TLR6, and MyD88. [1]
- GABA significantly decreased ileal expression of GABA transporter SLC6A13 and GABA receptor subunits GABAB2 and GABA_Aβ2. [1]
- GABA increased levels of most amino acids in the ileal mucosa (e.g., alanine, phenylalanine, tryptophan, proline, serine, threonine, cystine, tyrosine, histidine, ornithine, carnosine) but reduced serum levels of several amino acids (histidine, serine, arginine, alanine, proline, cystine, lysine, methionine, isoleucine, leucine, phenylalanine). [1]
- GABA supplementation modulated the intestinal microbiota: reduced relative abundance of Firmicutes (phylum), Clostridia (class), and Clostridium_sensu_stricto_1 (genus); increased Proteobacteria, Bacteroidetes, Cyanobacteria, Fusobacteria, Actinobacteria, etc. It also increased community richness (observed species, Chao1, ACE) and diversity (Shannon, Simpson, PD whole tree). [1]
- In Drosophila, GABA is produced by cells expressing Gad1, which form specific clusters in the brain. GABA is released by local neurons (LN1 and LN2L) and mACT projection neurons in the antennal lobe. GABA receptors (Lcch3, RdI, GABA-B-R2) are widely expressed in most antennal lobe neurons, including projection neurons and local neurons. [2]

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Mice's ability to sleep can be improved by gamma-aminobutyric acid (33.95, 102.25, 306.75 mg/kg; po; single dose) [6]. ? In rats (DEHP) exposed to di(2-ethylhexyl) phthalate, gamma-aminobutyric acid (1, 2, 4? mg/kg/d; oral; 30 days) decreases anxiety, improves food consumption, and repairs exposure-related damage [7].

Cell Migration Assay[4]
Cell Types: Cortical Plate (cp) Neuronal
Tested Concentrations: 1-5 μM
Incubation Duration: 18 hrs (hours)
Experimental Results: Promotes motility via G protein activation and blocks attractants via GABAA receptor-mediated depolarization induced migration.

- Piglet study: Sixteen healthy weaned piglets (21 days old, Duroc × Landrace × Landrace, average body weight 6.43 kg) were randomly assigned to two groups (n=8 per group). The control group received a basal corn- and soybean meal-based diet; the GABA group received the same diet supplemented with 20 mg/kg GABA. The experiment lasted 3 weeks. Piglets were housed individually at 25±2°C with free access to feed and water. Body weight and feed intake were monitored weekly. After 3 weeks, piglets were sacrificed, and blood, ileum, ileal mucosa, and luminal contents were collected. [1]
- Drosophila study: Adult female flies (5–10 days old) were used. In situ mRNA hybridization was performed on dissected brains using DIG-labeled probes against Gad1, Lcch3, RdI, GABA-B-R1, -R2, -R3. Fluorescent in situ hybridization was combined with GAL4-driven GFP expression to identify cell types. Antibody labeling (anti-GFP, anti-CD8, nc82) and confocal microscopy were used. [2]

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Animal/Disease Models: Pathogen-free (SPF) Bagg albino (Balb/c) mice (18–20 g, 8 weeks old) [6]
Doses: 33.95, 102.25, 306.75 mg/kg single dose; administered at 20 mL/kg; Measured results in hrs (hrs (hours)): more effectively extend sleep time, increase sleep rate, and shorten sleep latency.

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Animal/Disease Models: SD (SD (Sprague-Dawley)) rats induced by DEHP (500 mg/kg) [7]
Doses: 1, 2, 4 mg/kg
Route of Administration: po (oral gavage); combined administration; 30 days
Experimental Results: Treated with DEHP Levels of nitric oxide and nitric oxide synthase are diminished in rats.

Gamma-aminobutyric acid (GABA) is rapidly absorbed after oral administration, with peak plasma levels reached within approximately 60 minutes, followed by rapid clearance and undetectable concentrations within 24 hours; exogenous GABA exhibits poor penetration across the blood–brain barrier and is primarily metabolized by GABA transaminase (GABA‑T) in peripheral tissues. In terms of toxicity, GABA demonstrates very low acute toxicity with an oral LD₅₀ of around 12,680 mg/kg in mice, and at physiological or moderate supplemental doses, it is generally safe, while excessive intake may elicit mild adverse effects including drowsiness, dizziness, transient hypotension, gastrointestinal discomfort, and at high doses, potential central nervous system depression, muscle weakness, or respiratory suppression; no significant carcinogenicity has been identified, and adverse reactions are dose‑dependent and mostly reversible upon discontinuation.

Chronically high levels of GABA are associated with at least 5 inborn errors of metabolism including: D-2-Hydroxyglutaric Aciduria, 4-Hydroxybutyric Aciduria/Succinic Semialdehyde Dehydrogenase Deficiency, GABA-Transaminase Deficiency, Homocarnosinosis and Succinic semialdehyde dehydrogenase deficiency.

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119 mouse LD50 intraperitoneal 4950 mg/kg BEHAVIORAL: GENERAL ANESTHETIC; BEHAVIORAL: ALTERED SLEEP TIME (INCLUDING CHANGE IN RIGHTING REFLEX); LUNGS, THORAX, OR RESPIRATION: OTHER CHANGES Archivum Immunologiae et Therapiae Experimentalis., 13(70), 1965 [PMID:14291430]
119 rat LDLo intracrebral 18 mg/kg Biochemical Pharmacology., 14(1901), 1965 [PMID:5880545]
119 cat LD50 intravenous 5 gm/kg Russian Pharmacology and Toxicology, 47(205), 1984
119 mouse LD50 oral 12680 mg/kg Yakugaku Zasshi. Journal of Pharmacy., 85(463), 1965 [PMID:5318985]
119 rat LD50 intravenous >5 gm/kg United States Patent Document., #3380887

[1]. Effects of dietary gamma-aminobutyric acid supplementation on the intestinal functions in weaning piglets. Food Funct. 2019 Jan 22;10(1):366-378.

[2]. Gamma-aminobutyric acid (GABA)-mediated neural connections in the Drosophila antennal lobe. J Comp Neurol. 2009 May 1;514(1):74-91.

Gamma-aminobutyric acid (GABA) is a gamma-amino acid formed by introducing an amino substituent at the C-4 position of butyric acid. It has multiple functions, including as a signaling molecule, a human metabolite, a Saccharomyces cerevisiae metabolite, and a neurotransmitter. It is a gamma-amino acid and a monocarboxylic acid, functionally related to butyric acid, and is the conjugate acid of GABA esters. It is the zwitterionic tautomer of GABA. It is the most common inhibitory neurotransmitter in the central nervous system. GABA is a metabolite found or produced in Escherichia coli (K12 strain, MG1655 strain). GABA has also been reported in Angelica sinensis, microgreen algae, and other organisms with relevant data. GABA is a naturally occurring neurotransmitter with central nervous system (CNS) inhibitory activity. Gamma-aminobutyric acid (GABA) is derived from glutamate, the main excitatory neurotransmitter in the brain. It regulates neuronal excitability by binding to GABA-A and GABA-B receptors, leading to ion channel opening, hyperpolarization, and ultimately inhibiting neurotransmission. GABA is an inhibitory neurotransmitter present in the nervous systems of many species. It is the main inhibitory neurotransmitter in the central nervous system of vertebrates. In vertebrates, GABA acts on inhibitory synapses in the brain. GABA exerts its effects by binding to specific transmembrane receptors on the presynaptic and postsynaptic neuronal plasma membranes. This binding leads to the opening of ion channels, allowing negatively charged chloride ions to flow into the cell or positively charged potassium ions to flow out. This typically results in a negative change in transmembrane potential, usually causing hyperpolarization. Known GABA receptors are mainly divided into three classes. These include GABAA and GABAC ionotropic receptors (which are themselves ion channels) and GABAB metabolotropic receptors (which are G protein-coupled receptors that open ion channels via intermediates (G proteins)). Neurons that output GABA are called GABAergic neurons, and they primarily exert inhibitory effects on receptors in vertebrates. Medium-sized spinous cells are typical examples of inhibitory GABAergic cells in the central nervous system. In insects, GABA has excitatory effects, mediating muscle activation at synapses between nerve and muscle cells and stimulating certain glands. Studies have also shown that GABA has excitatory effects in vertebrates, particularly in the developing cerebral cortex. Organisms synthesize GABA from glutamate using L-glutamate decarboxylase and pyridoxal phosphate as cofactors. Notably, this involves the conversion of the primary excitatory neurotransmitter (glutamate) into the primary inhibitory neurotransmitter (γ-aminobutyric acid, GABA). Drugs that act as GABA receptor agonists (called GABA analogs or GABAergic drugs) or increase the amount of GABA available often have relaxing, anti-anxiety, and anticonvulsant effects. Oral administration of 1 to 3 grams of GABA has also been shown to effectively improve IQ in individuals with intellectual disabilities. Numerous experimental and human epilepsy studies have found insufficient GABA levels in cerebrospinal fluid and brain tissue. Benzodiazepines (such as diazepam) are effective for status epilepticus because they act on GABA receptors. The amount of GABA in the brain increases after taking many antiepileptic drugs. Therefore, GABA is clearly an antiepileptic nutrient. GABA metabolism inhibitors may also cause seizures. Spasticity and involuntary movement syndromes, such as Parkinson's disease, Friedreich ataxia, tardive dyskinesia, and Huntington's disease, all show decreased GABA levels in amino acid tests. Trials of oral administration of 2 to 3 grams of GABA have shown its effectiveness in various epileptic and spastic syndromes. Medications that increase GABA levels also help lower high blood pressure. Oral administration of 3 grams of GABA effectively controls blood pressure. GABA levels are decreased in patients with various encephalopathy. GABA can suppress appetite, and GABA levels are also decreased in patients with hypoglycemia. GABA can lower blood sugar in diabetic patients. Chronic brain syndromes may also present with GABA deficiency; GABA has many promising applications in treatment. The level of GABA in cerebrospinal fluid may help diagnose some very serious diseases. Vitamin B6, manganese, taurine, and lysine can increase GABA synthesis and function, while aspartic acid and glutamate may inhibit GABA's effects. GABA is a major inhibitory neurotransmitter in the brain, and along with serotonin and norepinephrine, it is one of several neurotransmitters that appear to be involved in the pathogenesis of anxiety and mood disorders. There are two main subtypes of postsynaptic GABA receptor complexes: the GABA-A receptor complex and the GABA-B receptor complex. Activation of GABA-B receptors leads to neuronal membrane hyperpolarization, thereby inhibiting neurotransmitter release. In addition to the GABA binding site, GABA-A receptors also have binding sites for benzodiazepines, barbiturates, and neurosteroids. GABA-A receptors are coupled to chloride ion channels; receptor activation induces increased chloride ion influx, leading to membrane hyperpolarization and neuronal inhibition. After being released into the synaptic cleft, free GABA that does not bind to GABA-A or GABA-B receptor complexes can be taken up by neurons and glial cells. Four different membrane transport proteins, GAT-1, GAT-2, GAT-3, and BGT-1, have varying distributions in the central nervous system and are believed to mediate the entry of synaptic GABA into neurons and glial cells. GABA-A receptor subtypes regulate neuronal excitability and rapid changes in fear arousal, such as anxiety, panic, and acute stress responses. Drugs that stimulate GABA-A receptors, such as benzodiazepines and barbiturates, exert anti-anxiety and anti-epileptic effects by reducing neuronal excitability through GABA-A-mediated mechanisms, thereby effectively raising the seizure threshold. Evidence supporting the anticonvulsant and anti-anxiety effects of GABA-A receptors includes: GABA-A antagonists can induce seizures in animals; and positron emission tomography (PET) studies have shown reduced GABA-A receptor binding affinity in patients with panic disorder. Some patients with depression have low plasma GABA levels; in fact, plasma GABA levels may be a useful biomarker for mood disorders.
The most common inhibitory neurotransmitter in the central nervous system.
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C4H9NO2

103.1198

103.063

56-12-2

53504-43-1;5959-35-3 (hydrochloride);6610-05-5 (mono-hydrochloride salt);70582-09-1 (calcium salt (2:1))

119

White to off-white solid powder

1.1±0.1 g/cm3

248.0±23.0 °C at 760 mmHg

195-204ºC

103.8±22.6 °C

0.0±1.0 mmHg at 25°C

1.465

-0.64

2

3

3

7

62.7

0

O([H])C(C([H])([H])C([H])([H])C([H])([H])N([H])[H])=O

BTCSSZJGUNDROE-UHFFFAOYSA-N

InChI=1S/C4H9NO2/c5-3-1-2-4(6)7/h1-3,5H2,(H,6,7)

4-aminobutanoic acid

DF468; gamma-aminobutyric acid; GABA; 56-12-2; Piperidic acid; Piperidinic acid; DF 468; Aminalon

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: This product requires protection from light (avoid light exposure) during transportation and storage.

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

H2O : ~50 mg/mL (~484.87 mM)

Solubility in Formulation 1: 100 mg/mL (969.74 mM) in PBS (add these co-solvents sequentially from left to right, and one by one), clear solution; with sonication (<60°C).

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 (Please use freshly prepared in vivo formulations for optimal results.)