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Names | |
---|---|
IUPAC name
4-Aminohex-5-ynoic acid
| |
Other names
| |
Identifiers | |
3D model (
JSmol)
|
|
ChEMBL | |
ChemSpider | |
ECHA InfoCard | 100.165.059 |
EC Number |
|
PubChem
CID
|
|
UNII | |
CompTox Dashboard (
EPA)
|
|
| |
| |
Properties | |
C6H9NO2 | |
Molar mass | 127.143 g·mol−1 |
Hazards | |
GHS labelling: [2] | |
![]() | |
Warning | |
H315, H319, H335 | |
P261, P264, P264+P265, P271, P280, P302+P352, P304+P340, P305+P351+P338, P319, P321, P332+P317, P337+P317, P362+P364, P403+P233, P405, P501 | |
Except where otherwise noted, data are given for materials in their
standard state (at 25 °C [77 °F], 100 kPa).
|
γ-Acetylenic GABA, also known as 4-aminohex-5-ynoic acid is a potent and irreversible inhibitor of GABA-T. [3]
Like other GABA-T inhibitors, γ-acetylenic GABA causes GABA levels in the brain to be elevated. This is due to 4-aminobutyrate transaminase being the enzyme that converts γ-aminobutyric acid to L-glutamate. Inhibiting the enzyme stops this conversion from happening.
Continuous administration of γ-acetylenic GABA on rats during four days was able to reduce or completely stop seizures that were induced by amygdala overstimulation. [4]
A study has showed that γ-acetylenic GABA could reduce tardive dyskinesia symptoms. This result mostly happened in subjects receiving higher doses. [5]
![]() | |
Names | |
---|---|
IUPAC name
4-Aminohex-5-ynoic acid
| |
Other names
| |
Identifiers | |
3D model (
JSmol)
|
|
ChEMBL | |
ChemSpider | |
ECHA InfoCard | 100.165.059 |
EC Number |
|
PubChem
CID
|
|
UNII | |
CompTox Dashboard (
EPA)
|
|
| |
| |
Properties | |
C6H9NO2 | |
Molar mass | 127.143 g·mol−1 |
Hazards | |
GHS labelling: [2] | |
![]() | |
Warning | |
H315, H319, H335 | |
P261, P264, P264+P265, P271, P280, P302+P352, P304+P340, P305+P351+P338, P319, P321, P332+P317, P337+P317, P362+P364, P403+P233, P405, P501 | |
Except where otherwise noted, data are given for materials in their
standard state (at 25 °C [77 °F], 100 kPa).
|
γ-Acetylenic GABA, also known as 4-aminohex-5-ynoic acid is a potent and irreversible inhibitor of GABA-T. [3]
Like other GABA-T inhibitors, γ-acetylenic GABA causes GABA levels in the brain to be elevated. This is due to 4-aminobutyrate transaminase being the enzyme that converts γ-aminobutyric acid to L-glutamate. Inhibiting the enzyme stops this conversion from happening.
Continuous administration of γ-acetylenic GABA on rats during four days was able to reduce or completely stop seizures that were induced by amygdala overstimulation. [4]
A study has showed that γ-acetylenic GABA could reduce tardive dyskinesia symptoms. This result mostly happened in subjects receiving higher doses. [5]