GHB

4-hydroxybutanoic acid

Overview

GHB belongs to Depressants.

Key safety note: GHB has one of the steepest dose–response curves of any recreational drug: the gap between an active dose, deep unconsciousness and life-threatening respiratory depression can be under a gram, so a small increase, or redosing before the first dose has peaked, can cause sudden coma.[3][5]
Effects
Subjective effects vary. What a substance feels like depends on dose, individual physiology, mindset, and setting. The points below describe commonly reported effects, not guaranteed, uniform, or desirable outcomes.
  • At low doses: mild euphoria, relaxation, sociability, lowered inhibition and increased libido: effects users often compare to alcohol or MDMA (hence the nickname 'liquid ecstasy').
  • At higher doses: pronounced sedation, dizziness, nausea and loss of coordination, and over a narrow range an abrupt slide into deep sleep or coma from which the person cannot be roused.
  • Onset is fast (roughly 10–30 minutes) and the experience is short (about 1.5–2.5 hours), which tempts redosing before the first dose has worn off: a major cause of accidental overdose.
Dosing & duration
Harm-reduction note: These are commonly cited reference ranges, not a recommendation or a “safe” dose. Potency, purity, body chemistry, tolerance, and drug combinations vary widely. Start low, go slow, wait for full effects before redosing, and never assume an unknown product matches these figures. Missing data is not evidence of safety.

Oral, as a liquid. Recreational doses are swallowed diluted in water. Medical sodium oxybate is an oral solution taken at night.. GHB has one of the steepest dose–response curves of any recreational drug: the difference between a common dose and one causing unconsciousness can be under a gram, and the risk of death rises sharply above roughly 10 g. Street GHB is a liquid of unknown, variable concentration, so 'a capful' or 'a swig' is never a reliable measure: dose by volume with a syringe from a known concentration, wait the full 1.5–2 hours for peak effect before even considering a redose, and never combine it with alcohol or other depressants. The figures below (grams of pure GHB) are reference ranges, NOT a recommendation or a 'safe' dose.

Dose ranges

Threshold

0.5 g

Light

0.5–1 g

Common

1–2.5 g

Strong

2.5–4 g

Heavy

4 g + (risk of death above ~10 g)

Duration

onset

10–30 minutes

total

1.5–2.5 hours

after effects

Possible grogginess, with repeated or daily use, rapid physical dependence and a dangerous withdrawal syndrome

Chemical & Physical Properties
FormulaC4H8O3
Molar mass104.1 g/mol
StateSolid
Melting point48–50 °C
Boiling point180 °C (dec)
DensityNot reported
Vapor pressureNot reported
pKa4.72 at 25 °C
LogP-0.6 (predicted, XLogP3)
SolubilityVery soluble in water, alcohol and ether.
Refractive indexNot reported
Identifiers & Synonyms
CAS591-81-1
CAS (enantiomer)
PubChem CID10413
InChIKeySJZRECIVHVDYJC-UHFFFAOYSA-N
InChIInChI=1S/C4H8O3/c5-3-1-2-4(6)7/h5H,1-3H2,(H,6,7)
SMILESC(CC(=O)O)CO

Synonyms

  • γ-Hydroxybutyric acid
  • 4-Hydroxybutanoic acid
  • Gamma-hydroxybutyrate
  • Sodium oxybate (salt)
  • Xyrem (medical)
  • Liquid ecstasy (misuse)
  • Sodium oxybate
  • Xyrem
  • Gina
Pharmacodynamics & Biochemistry

GHB (γ-hydroxybutyrate) is a short-chain fatty acid that occurs naturally in the brain as a minor metabolite of the inhibitory neurotransmitter GABA. As a drug it is a central-nervous-system depressant used medically (as the sodium salt, sodium oxybate) and recreationally, and its defining pharmacological feature is an unusually steep dose–response curve. Its depressant effects are mediated mainly by agonism at GABA-B receptors, but only at the relatively high (millimolar) concentrations reached with recreational and therapeutic doses. At lower concentrations GHB also binds high-affinity, GHB-specific receptors that modulate dopamine and glutamate release. This dual action is thought to underlie its biphasic profile: mild stimulation, euphoria and disinhibition at low doses giving way to sedation, then anaesthesia and coma as the dose rises. Because GHB is active in the millimolar range rather than binding a receptor with nanomolar affinity, there is no meaningful nanomolar binding table for it. Its pharmacology is described functionally (GABA-B agonism plus GHB-receptor binding) rather than by a Ki profile. GHB is absorbed and eliminated rapidly: it is broken down via succinic semialdehyde into the TCA cycle to carbon dioxide and water, giving a short half-life of roughly 30–60 minutes. This fast clearance combined with the steep dose–response is why the margin between a recreational dose, deep unconsciousness and respiratory depression is dangerously narrow. The industrial precursors GBL (γ-butyrolactone) and 1,4-butanediol are converted to GHB in the body and produce the same effects and risks.

Biological targets

  • GABA-B
Pharmacokinetics
BioavailabilityOral ≈25% (capacity-limited, nonlinear)
Tmax≈20–45 min
Half-life≈0.3–1 h (short, dose-dependent)
VdNot reported
Protein bindingNot reported
MetabolismOxidised via succinic semialdehyde into the TCA cycle to CO₂ and water. Capacity-limited (saturable) kinetics
Excretion<5% renal unchanged
Toxicology & Safety
Harm-reduction note: Toxicity and risk depend on dose, route, purity, combinations, setting, and individual health factors. Missing harms should never be interpreted as evidence of safety.

Not reported

GHB has one of the steepest dose–response curves of any recreational drug: the gap between an active dose, deep unconsciousness and life-threatening respiratory depression can be under a gram, so a small increase, or redosing before the first dose has peaked, can cause sudden coma. The danger is greatly amplified by alcohol and other CNS depressants, which is the most common factor in GHB deaths. Because street GHB is a liquid of unknown, variable concentration, 'a capful' or 'a swig' is never a reliable dose and accurate measurement is essential. Regular use causes rapid physical dependence and a severe, potentially life-threatening withdrawal syndrome (resembling delirium tremens) that needs medical management. GHB and its precursors GBL and 1,4-butanediol are also among the drugs most associated with drug-facilitated sexual assault.[3][5]

Legal Status
Legal note: Legal status can change over time and may vary by country, region, formulation, analogue status, prescription context, and enforcement practice. Always confirm with current official sources before relying on this section.
Interactions & Contraindications

Drug interactions

Alcohol, Benzodiazepines, Opioids Profound, potentially fatal respiratory depression and coma, including with sedating antihistamines: the commonest factor in GHB deaths.[3][5]
Stimulants (amphetamines, cocaine) Can mask GHB's sedation, encouraging over-consumption and hiding the signs of overdose.[5]
GHB precursors (GBL, 1,4-butanediol) GBL and 1,4-butanediol convert to GHB in the body, so taking them together stacks the same effect and risk.[3]

Contraindications

Combining with alcohol or other CNS depressants concurrent alcohol or other CNS depressants.[3][5]
Succinic semialdehyde dehydrogenase deficiency impaired GHB metabolism.[3]
Respiratory disease or sleep apnoea severe respiratory compromise or untreated obstructive sleep apnoea.[5]
Cardiovascular disease, hypertension or arrhythmia with sodium oxybate, caution with the high sodium load in heart failure or hypertension.[2]
Usage & Context
  • Medically, the sodium salt (sodium oxybate, Xyrem/Xywav) is a prescription treatment for narcolepsy with cataplexy, dispensed under tight controls.
  • Recreationally, GHB ('G', 'liquid ecstasy') is used in clubs and parties and in the chemsex scene for its euphoric, disinhibiting and pro-sexual effects. The precursors GBL and 1,4-butanediol are frequently used interchangeably with it.
  • It is one of the drugs most associated with drug-facilitated sexual assault, being roughly colourless, nearly odourless, fast-acting and short-lived.
Sources & Evidence

Further Information