1320-61-2O=C([O-])CCCOSJZRECIVHVDYJC-UHFFFAOYSA-M4-hydroxybutyrate is a 4-hydroxy monocarboxylic acid anion resulting from the removal of a proton from the carboxy group of 4-hydroxybutyric acid. It has a role as an intravenous anaesthetic and an anaesthesia adjuvant. It is a 4-hydroxy monocarboxylic acid anion, a short-chain fatty acid anion and a hydroxy fatty acid anion. It is functionally related to a butyrate. It is a conjugate base of a 4-hydroxybutyric acid.
1320-61-2、591-81-1DTXSID10157296CHEBI:16724安全情報は参考情報です。供給元の安全データシート(SDS)、適用法令、専門家による評価に代わるものではありません。
This chemical does not meet GHS hazard criteria for 100% (2 of 2) of all reports.
Not Classified
Aggregated GHS information provided per 2 reports by companies from 1 notifications to the ECHA C&L Inventory.
GHB reaches much higher concentrations in the brain and activates GABAB receptors, which are primarily responsible for its sedative effects. GHB receptors are densely expressed in many areas of the brain, including the cortex and hippocampus, and these are the receptors that GHB displays the highest affinity for. There has been somewhat limited research into the GHB receptor; however, there is evidence that activation of the GHB receptor in some brain areas results in the release of glutamate, the principal excitatory neurotransmitter. Activation of both the GHB receptor and GABA(B) is responsible for the addictive profile of GHB. GHB's effect on dopamine release is biphasic,[19] low concentrations stimulate dopamine release via the GHB receptor.[20] Higher concentrations inhibit dopamine release via GABA(B) receptors as do other GABA(B) agonists such as baclofen and phenibut.[21] After an initial phase of inhibition, dopamine release is then increased via the GHB receptor. This explains the paradoxical mix of sedative and stimulatory properties of GHB, as well as the so-called "rebound" effect, experienced by individuals using GHB as a sleeping agent, wherein they awake suddenly after several hours of GHB-induced deep sleep. That is to say that, over time, the concentration of GHB in the system decreases below the threshold for significant GABAB receptor activation and activates predominantly the GHB receptor, leading to wakefulness.
Route of Elimination: Animal studies indicate that metabolism is the major elimination pathway for sodium oxybate, producing carbon dioxide and water via the tricarboxylic acid (Krebs) cycle and secondarily by beta-oxidation. Succinic acid enters the Krebs cycle where it is metabolized to carbon dioxide and water. Fecal and renal excretion is negligible. 5% renal elimination. Half Life: 30 to 60 minutes
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