| Attributes | Values |
|---|
| rdf:type
| |
| http://linked.open...gbank/description
| - Gamma Hydroxybutyric Acid, commonly abbreviated GHB, is a therapeutic drug which is illegal in multiple countries. It is currently regulated in the US and sold by Jazz Pharmaceuticals under the name Xyrem. However, it is important to note that GHB is a designated Orphan drug (in 1985). Today Xyrem is a Schedule III drug; however GHB remains a Schedule I drug and the illicit use of Xyrem falls under penalties of Schedule I. GHB is a naturally occurring substance found in the central nervous system, wine, beef, small citrus fruits and almost all other living creatures in small amounts. It is used illegally under the street names Juice, Liquid Ecstasy or simply G, either as an intoxicant, or as a date rape drug. Xyrem is a central nervous system depressant that reduces excessive daytime sleepiness and cataplexy in patients with narcolepsy. (en)
|
| http://linked.open...y/drugbank/dosage
| |
| http://linked.open...gy/drugbank/group
| - approved (en)
- illicit (en)
|
| http://linked.open...drugbank/halfLife
| |
| http://linked.open...ugbank/indication
| - Used as a general anesthetic, to treat conditions such as insomnia, clinical depression, narcolepsy, and alcoholism, and to improve athletic performance. (en)
|
| sameAs
| |
| Title
| - Gamma Hydroxybutyric Acid (en)
|
| adms:identifier
| |
| http://linked.open...mechanismOfAction
| - 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. (en)
|
| http://linked.open...drugbank/packager
| |
| http://linked.open...y/drugbank/patent
| |
| http://linked.open...outeOfElimination
| - 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. (en)
|
| http://linked.open.../drugbank/synonym
| - 4-Hydroxybutyric acid (en)
- 4-hydroxybutanoate (en)
- 4-hydroxybutanoic acid (en)
- GHB (en)
- gamma-Hydroxybutyric acid (en)
- 3-carboxypropoxy acid (en)
- 4-hydroxy-butyric acid (en)
- gamma-Hydroxybutyrate (en)
- oxy-n-butyric acid (en)
- γ-Hydroxybutyric acid (en)
|
| http://linked.open...drugbank/toxicity
| - At higher doses, GHB may induce nausea, dizziness, drowsiness, agitation, visual disturbances, depressed breathing, amnesia, unconsciousness, and death. (en)
|
| http://linked.open...umeOfDistribution
| |
| http://linked.open...ynthesisReference
| - Joseph Klosa, "Production of nonhygroscopic salts of 4-hydroxybutyric acid." U.S. Patent US4393236, issued March, 1963. (en)
|
| http://linked.open...ugbank/IUPAC-Name
| |
| http://linked.open...gy/drugbank/InChI
| |
| http://linked.open...Molecular-Formula
| |
| http://linked.open.../Molecular-Weight
| |
| http://linked.open...noisotopic-Weight
| |
| http://linked.open...y/drugbank/SMILES
| |
| http://linked.open.../Water-Solubility
| |
| http://linked.open...ogy/drugbank/logP
| |
| http://linked.open...ogy/drugbank/logS
| |
| http://linked.open...nd-Acceptor-Count
| |
| http://linked.open...-Bond-Donor-Count
| |
| http://linked.open...drugbank/InChIKey
| |
| http://linked.open...urface-Area--PSA-
| |
| http://linked.open...nk/Polarizability
| |
| http://linked.open...bank/Refractivity
| |
| http://linked.open...atable-Bond-Count
| |
| http://linked.open.../affectedOrganism
| - Humans and other mammals (en)
|
| http://linked.open...casRegistryNumber
| |
| http://linked.open...rugbank/clearance
| - * apparent oral cl=9.1 mL/min/kg [healthy adults receiving a single oral dose of 25 mg/kg] * 4.5 mL/min/kg [cirrhotic patients without ascites receiving a single oral dose of 25 mg/kg] * 4.1 mL/min/kg [cirrhotic patients with ascites receiving a single oral dose of 25 mg/kg] (en)
|
| http://linked.open...gbank/containedIn
| |
| http://linked.open...k/Bioavailability
| |
| http://linked.open...bank/Ghose-Filter
| |
| http://linked.open...nk/MDDR-Like-Rule
| |
| http://linked.open...k/Number-of-Rings
| |
| http://linked.open...siological-Charge
| |
| http://linked.open...bank/Rule-of-Five
| |
| http://linked.open...tional-IUPAC-Name
| |
| http://linked.open...strongest-acidic-
| |
| http://linked.open...-strongest-basic-
| |
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