And Sodium Oxybate
And Sodium Oxybate Uses, Dosage, Side Effects, Food Interaction and all others data.
Sodium oxybate (Xyrem) is a central nervous system depressant used for the treatment of cataplexy and extreme daytime sleepiness (EDS) associated with narcolepsy. It is the sodium salt of gamma hydroxybutyric acid (GHB) which is an endogenous compound and a metabolite of the neurotransmitter GABA. The exact mechanism of action for treating EDS and cataplexy is not known but is is hypothesised that its therapeutic effects are due to GABA(B) effects on noradrenergic, dopaminaergic and thalamocorticol neurons. The drug follows non-linear pharmacokinetics. As it has been associated with misuse/abuse it is strictly controlled and all patients and prescribers must enroll in the sodium oxybate REMs program in order to gain access to the medication.
Sodium oxybate works through an unknown mechanism to treat narcolepsy by inducing sleep within about 5-15 minutes of administration.
| Trade Name | And Sodium Oxybate |
| Generic | Calcium oxybate + magnesium oxybate + potassium oxybate + sodium oxybate |
| Type | Oral |
| Therapeutic Class | |
| Manufacturer | |
| Available Country | United States |
| Last Updated: | September 19, 2023 at 7:00 am |
Uses
Sodium oxybate is a central nervous system depressant used to treat cataplexy and excessive daytime sleepiness (EDS) associated with narcolepsy.
For the treatment of cataplexy and excessive daytime sleepiness (EDS) associated with narcolepsy.
And Sodium Oxybate is also used to associated treatment for these conditions: Cataplexy, Excessive Daytime Sleepiness
How And Sodium Oxybate works
The exact mechanism of action is unknown. It is the sodium salt of the endogenous compound gamma hydroxybutyrate which is a metabolite of the GABA neurotransmitter and it's thought that it's therapeutic effects are mediated via GABA B actions at noradrenergic, dopaminergic and thalamocortical neurons.
Toxicity
Symptoms of overdose may include; depressed consciousness that may fluctuate rapidly between a confusional, agitated combative state with ataxia and coma, emesis, diaphoresis, headache and impaired psychomotor skills. Depth of coma varies with the amount ingested and myoclonus and tonic-clonic seizures have been reported. Oral LD50 of 9690mg/kg in rats .
Volume of Distribution
Vd of 37.7-67.7
Elimination Route
Absolute bioavailability is approximately 88%. Tmax of 30.7-51.9min .
Half Life
0.5 to 1 hour.
Clearance
Total clearance of 895-1361mL/min .
Elimination Route
The major metabolite is carbon dioxide which is cleared by expiration, less then 5% appears as the unchanged drug in the urine within 6-8 hours after dosing.
Innovators Monograph
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