.GAMMA.-AMINOBUTYRIC ACID

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

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

2,5-Dimethyl-N-Phenyl-3H-diazaphophol-4-imine is a quinonoid tautomer of GABAA and GABAB agonist progabide. According to quantum mechanical calculations, a quinonoid form is predominant in polar solvents, while aromatic tautomer is prevalent in apolar solvents. Progabide is a prodrug of gamma-aminobutyric acid and was investigated for the treatment of epilepsy, Parkinson's disease, schizophrenia, clinical depression, anxiety disorder, and other diseases. Progabide was marketed in France by Sanofi Aventis under tradename Gabrene for use in monotherapy and also as adjunctive therapy for generalized tonic-clonic, myoclonic, partial seizures, and for Lennox‐Gastaut syndrome, in both children and adults.

Originator

Approval Year

Targets

Primary Target	Pharmacology	Condition	Potency
GABA-A receptor; anion channel 203	Agonist 2,752		200.0 nM [Ki]
GABA-A receptor; anion channel 203	Agonist 2,752		40.0 µM [Ki]

Conditions

Condition	Modality	Highest Phase	Product
Type 1 diabetes mellitus 18	Primary	Phase II 1,147	Unknown
Stress 12	Primary	Phase I 438	Unknown
Partial Seizures 4	Preventing	Not Provided 511	THERAPENTIN-90
Vascular diseases of the brain 4	Primary	Approved 8,583	Gammalon
Atherosclerosis of cerebral arteries 4	Primary	Approved 8,583	Gammalon
Chronic cerebrovascular insufficiency 4	Primary	Approved 8,583	Gammalon

C_max

Value	Dose	Co-administered	Analyte	Population
688.53 ng/mL	2 g single, oral		.GAMMA.-AMINOBUTYRIC ACID plasma	Homo sapiens
767.77 ng/mL	2 g 3 times / day steady-state, oral		.GAMMA.-AMINOBUTYRIC ACID plasma	Homo sapiens

AUC

Value	Dose	Co-administered	Analyte	Population
932.91 ng × h/mL	2 g single, oral		.GAMMA.-AMINOBUTYRIC ACID plasma	Homo sapiens
1078.11 ng × h/mL	2 g 3 times / day steady-state, oral		.GAMMA.-AMINOBUTYRIC ACID plasma	Homo sapiens

T_1/2

Value	Dose	Co-administered	Analyte	Population
5.08 h	2 g single, oral		.GAMMA.-AMINOBUTYRIC ACID plasma	Homo sapiens
5.24 h	2 g 3 times / day steady-state, oral		.GAMMA.-AMINOBUTYRIC ACID plasma	Homo sapiens

PubMed

Show entries

Title	Date	PubMed
gamma-Aminobutyric acid in brain: its formation from glutamic acid.	1950 Nov	14794689
[Potential therapeutic activity of GABA-mimetic drugs in neuropsychiatry].	1979	45343
Biphasic effect of direct GABA mimetic drugs on haloperidol-induced catalepsy [proceedings].	1979 Nov	574045
Effect of the new gamma-aminobutyric acid agonist SL 76 002 on striatal acetylcholine: relation to neuroleptic-induced extrapyramidal alterations.	1980	6105775
Pharmacology of the GABAergic system: effects of progabide, a GABA receptor agonist.	1984	6089242

Showing 1 to 5 of 9 entries

Previous1 2Next

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.