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Details

Stereochemistry ACHIRAL
Molecular Formula C4H9NO2
Molecular Weight 103.1198
Optical Activity NONE
Defined Stereocenters 0 / 0
E/Z Centers 0
Charge 0

SHOW SMILES / InChI
Structure of .GAMMA.-AMINOBUTYRIC ACID

SMILES

NCCCC(O)=O

InChI

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

HIDE SMILES / InChI

Molecular Formula C4H9NO2
Molecular Weight 103.1198
Charge 0
Count
MOL RATIO 1 MOL RATIO (average)
Stereochemistry ACHIRAL
Additional Stereochemistry No
Defined Stereocenters 0 / 0
E/Z Centers 0
Optical Activity NONE

Description

γ-aminobutyric acid (GABA), a naturally occurring substance, which is a product of decarboxylation of the amino acid glutamate mediated by the synthesizing enzyme glutamic acid decarboxylase. GABA is a major inhibitory neurotransmitter of the brain and acts mainly through the GABAA receptor (GABAAR). GABA is locally produced by the pancreatic beta cells. GABAARs are also expressed in various immune cells, including T-cells, peripheral blood mononuclear cells, and are known to exert immune-inhibitory effects. Recently was studied, that GABA has the potential in treatment of Type I Diabetes. Moreover, was shown, that GABA administration could enhance immunity under stress conditions.

Originator

Approval Year

Targets

Primary TargetPharmacologyConditionPotency
200.0 nM [Ki]

Conditions

ConditionModalityTargetsHighest PhaseProduct
Primary
Unknown
Primary
Unknown
Preventing
THERAPENTIN-90
Primary
Gammalon
Primary
Gammalon
Primary
Gammalon

PubMed

Patents

Sample Use Guides

In Vivo Use Guide
Patients will receive the Active GABA (Gamma-Amino Butyric Acid) capsules. Each capsule 250mg. Dosage will be calculated according to body surface area of the child and divided between 2 meals/day. Larger dose taken with larger meal.
Route of Administration: Oral
In Vitro Use Guide
The HEK293 cells constitutively expressing exogenous GABA receptor π subunit (GABRP) revealed the growth-promoting effect of GABA treatment (serial concentrations: 0, 1, 10, 100 μmol/L);for 6 d). GABA treatment stimulated GABRP-positive pancreatic ductal adenocarcinoma (PDAC) cell proliferatio and activated the mitogen-activated protein kinase/extracellular signal–regulated kinase (MAPK/Erk) cascade. These findings imply that GABA and GABRP could play important roles in PDAC development and progression, and that this pathway can be a promising molecular target for the development of new therapeutic strategies for PDAC.
Substance Class Chemical
Record UNII
2ACZ6IPC6I
Record Status Validated (UNII)
Record Version