GBL

gamma-butyrolactone

Sources

18 strong · 6 moderate · 12 weak

Studies and references cited across this article, graded by evidence strength.

Values approved

109/109 (100%)

Data points an editor reviewed and accepted for publication.

Value Provenance

Dosing

oraltrace

Field	Published	AI Proposed	Confidence
Threshold	0.3 mL	0.3 mL	medium
Low	0.3–0.9 mL	0.3–0.9 mL	medium
Common	0.9–1.5 mL	0.9–1.5 mL	medium
Strong	1.5–3 mL	1.5–3 mL	medium
Heavy	3+ mL	3+ mL	medium
Editorial	Values from existing DB seed data, consistent with community consensus (PsychonautWiki, Erowid) and clinical literature describing narrow therapeutic window. No published controlled human dose-response study exists for GBL specifically. The dose-response curve is extremely steep — 0.5 mL can separate euphoria from unconsciousness. Estimated lethal dose ~60 mg/kg (~3.75 mL pure GBL for 70 kg person) falls disturbingly close to the heavy threshold. Individual sensitivity varies substantially. Safety-critical: these values assume pure GBL (density 1.12 g/mL).
	ReasoningReasoning Values from existing DB seed data, consistent with community consensus (PsychonautWiki, Erowid) and clinical literature describing narrow therapeutic window. No published controlled human dose-response study exists for GBL specifically. The dose-response curve is extremely steep — 0.5 mL can separate euphoria from unconsciousness. Estimated lethal dose ~60 mg/kg (~3.75 mL pure GBL for 70 kg person) falls disturbingly close to the heavy threshold. Individual sensitivity varies substantially. Safety-critical: these values assume pure GBL (density 1.12 g/mL). Evidence basis: community_consensus_large

Duration

oral

Field	Published	AI Proposed	Confidence
Onsettrace	3–10 minutes	3–10 minutes	medium
Editorial	DB seed value (3–10 min). Consistent with GBL's lipophilicity enabling rapid GI absorption and near-instantaneous blood lactonase conversion to GHB. Faster than oral GHB onset (15–30 min) due to bypassing hepatic first-pass.
	ReasoningReasoning DB seed value (3–10 min). Consistent with GBL's lipophilicity enabling rapid GI absorption and near-instantaneous blood lactonase conversion to GHB. Faster than oral GHB onset (15–30 min) due to bypassing hepatic first-pass. Evidence basis: community_consensus_large
Come uptrace	5–15 minutes	5–15 minutes	medium
Editorial	DB seed value (5–15 min). Consistent with published GHB Tmax of 20–60 minutes post-oral GBL; the come_up occupies the ascending limb of the plasma concentration curve.
	ReasoningReasoning DB seed value (5–15 min). Consistent with published GHB Tmax of 20–60 minutes post-oral GBL; the come_up occupies the ascending limb of the plasma concentration curve. Evidence basis: community_consensus_large
Peaktrace	30–45 minutes	30–45 minutes	medium
Editorial	DB seed value (30–45 min). Consistent with GHB elimination half-life of 20–60 minutes; peak effects correspond to Cmax plateau before rapid clearance begins.
	ReasoningReasoning DB seed value (30–45 min). Consistent with GHB elimination half-life of 20–60 minutes; peak effects correspond to Cmax plateau before rapid clearance begins. Evidence basis: community_consensus_large
Offsettrace	15–30 minutes	15–30 minutes	medium
Editorial	DB seed value (15–30 min). Consistent with rapid GHB elimination (t1/2 20–60 min); the short offset reflects capacity-limited metabolism switching to first-order kinetics at declining concentrations.
	ReasoningReasoning DB seed value (15–30 min). Consistent with rapid GHB elimination (t1/2 20–60 min); the short offset reflects capacity-limited metabolism switching to first-order kinetics at declining concentrations. Evidence basis: community_consensus_large
Totaltrace	1–2 hours	1–2 hours	medium
Editorial	DB seed value (1–2 hours). Consistent with GHB pharmacokinetics (short half-life, rapid clearance). The compressed total duration relative to other depressants is a defining feature of GBL.
	ReasoningReasoning DB seed value (1–2 hours). Consistent with GHB pharmacokinetics (short half-life, rapid clearance). The compressed total duration relative to other depressants is a defining feature of GBL. Evidence basis: community_consensus_large
After effectstrace	1–3 hours	1–3 hours	medium
Editorial	DB seed value (1–3 hours). Residual sedation, mild fatigue, and possible headache persist after subjective effects resolve. Driving impairment advisory extends to at least 3 hours post-use.
	ReasoningReasoning DB seed value (1–3 hours). Residual sedation, mild fatigue, and possible headache persist after subjective effects resolve. Driving impairment advisory extends to at least 3 hours post-use. Evidence basis: community_consensus_large

Safety

Toxicity Profiletrace

Field	Published	AI Proposed	Confidence
Acute	high	high	high
Chronic	moderate	moderate	high
Organs Affected	CNS, respiratory, cardiovascular	CNS, respiratory, cardiovascular	high
Editorial	Work-notes upgrade acute toxicity from seed 'moderate' to 'high' based on narrow therapeutic window and confirmed fatalities (Dargan 2009, Lenz 2008). Chronic remains 'moderate' per work-notes (medium confidence — long-term data sparse). Organs: CNS (primary), respiratory (depression), cardiovascular (bradycardia/asystole). Supported by Schep et al. 2012 systematic review and Dufayet et al. 2023.
	ReasoningReasoning Work-notes upgrade acute toxicity from seed 'moderate' to 'high' based on narrow therapeutic window and confirmed fatalities (Dargan 2009, Lenz 2008). Chronic remains 'moderate' per work-notes (medium confidence — long-term data sparse). Organs: CNS (primary), respiratory (depression), cardiovascular (bradycardia/asystole). Supported by Schep et al. 2012 systematic review and Dufayet et al. 2023. Evidence basis: published_case_series

Dependence Profiletrace

Field	Published	AI Proposed	Confidence
Physical	high	high	high
Psychological	high	high	high
Compulsive Redosing	high	high	high
Dose Escalation	moderate	moderate	high
Editorial	Work-notes specify physical=high, psychological=high, compulsive redosing=high, dose escalation=moderate. Supported by Wojtowicz et al. 2008 systematic review (57 withdrawal episodes), Schep et al. 2012, Kamal et al. 2016. Reinforcement mechanism from VTA disinhibition model consistent with Van Nieuwenhuijzen et al. 2014 Fos mapping.
	ReasoningReasoning Work-notes specify physical=high, psychological=high, compulsive redosing=high, dose escalation=moderate. Supported by Wojtowicz et al. 2008 systematic review (57 withdrawal episodes), Schep et al. 2012, Kamal et al. 2016. Reinforcement mechanism from VTA disinhibition model consistent with Van Nieuwenhuijzen et al. 2014 Fos mapping. Evidence basis: systematic_review

Withdrawal Profiletrace

Field	Published	AI Proposed	Confidence
Severity	life_threatening	life_threatening	high
Symptoms	tremor, hallucinations (auditory and visual), tachycardia, insomnia, anxiety, agitation, hypertension, diaphoresis, confusion, disorientation, delusions, paranoia, seizures, rhabdomyolysis	tremor, hallucinations (auditory and visual), tachycardia, insomnia, anxiety, agitation, hypertension, diaphoresis, confusion, disorientation, delusions, paranoia, seizures, rhabdomyolysis	high
Fatal	Yes	Yes	high
Medical Supervision	Required	Required	high
Editorial	Wojtowicz et al. 2008 systematic review (n=57 episodes): tremor 67%, hallucinations 63%, tachycardia 63%, insomnia 58%, seizures 7%, rhabdomyolysis 7%. Onset 6–24 hours after last dose. Duration days to 21 days in severe cases. Death reported. Benzodiazepines provide incomplete efficacy; baclofen and barbiturates may be needed.
	ReasoningReasoning Wojtowicz et al. 2008 systematic review (n=57 episodes): tremor 67%, hallucinations 63%, tachycardia 63%, insomnia 58%, seizures 7%, rhabdomyolysis 7%. Onset 6–24 hours after last dose. Duration days to 21 days in severe cases. Death reported. Benzodiazepines provide incomplete efficacy; baclofen and barbiturates may be needed. Evidence basis: systematic_review

Tolerance Profiletrace

Field	Published	AI Proposed	Confidence
Buildup	rapid	rapid	medium
Half-life	—	—	medium
Full Reset	10.5 days	10.5 days	medium
Cross-tolerances	GHB, 1,4-butanediol	GHB, 1,4-butanediol	medium
Editorial	Work-notes: buildup rapid (well-documented), reset ~10.5 days (community-sourced, not confirmed by controlled study). Cross-tolerances with GHB and 1,4-BD confirmed by Towiwat et al. 2013. Mechanism from Kamal et al. 2016 (multi-system neuroadaptation). Confidence medium because reset period lacks primary source verification.
	ReasoningReasoning Work-notes: buildup rapid (well-documented), reset ~10.5 days (community-sourced, not confirmed by controlled study). Cross-tolerances with GHB and 1,4-BD confirmed by Towiwat et al. 2013. Mechanism from Kamal et al. 2016 (multi-system neuroadaptation). Confidence medium because reset period lacks primary source verification. Evidence basis: community_consensus_large

Effects & Profile

Contraindications

Field	Published	AI Proposed	Confidence
other Concurrent ketamine or dissociative usetrace	absolute	absolute	high
Editorial	Work-notes list as absolute contraindication with high confidence. Supported by Schep et al. 2012 and DB interaction data (ketamine, PCP, MXE all classified lethal).
	ReasoningReasoning Work-notes list as absolute contraindication with high confidence. Supported by Schep et al. 2012 and DB interaction data (ketamine, PCP, MXE all classified lethal).
other Concurrent alcohol usetrace	absolute	absolute	high
Editorial	Work-notes list as absolute contraindication with high confidence. Supported by Galicia et al. 2019 (ED outcomes data), Thai et al. 2006 (human GHB-ethanol interaction), and Schep et al. 2012 systematic review.
	ReasoningReasoning Work-notes list as absolute contraindication with high confidence. Supported by Galicia et al. 2019 (ED outcomes data), Thai et al. 2006 (human GHB-ethanol interaction), and Schep et al. 2012 systematic review.
other Concurrent opioid usetrace	absolute	absolute	high
Editorial	Work-notes list as absolute contraindication with high confidence. Supported by Schep et al. 2012 and Dufayet et al. 2023. All opioids in the DB interaction table are classified lethal.
	ReasoningReasoning Work-notes list as absolute contraindication with high confidence. Supported by Schep et al. 2012 and Dufayet et al. 2023. All opioids in the DB interaction table are classified lethal.
other Concurrent CNS depressant medicationstrace	absolute	absolute	high
Editorial	Work-notes list as absolute contraindication with high confidence. Baclofen is listed lethal in DB interactions; benzodiazepines and other sedatives carry established additive CNS depression risk per Schep et al. 2012 and Ghio et al. 2014.
	ReasoningReasoning Work-notes list as absolute contraindication with high confidence. Baclofen is listed lethal in DB interactions; benzodiazepines and other sedatives carry established additive CNS depression risk per Schep et al. 2012 and Ghio et al. 2014.
respiratory Respiratory conditionstrace	relative	relative	medium
Editorial	Work-notes list as relative contraindication with medium confidence. Respiratory depression is well-documented in GBL/GHB clinical literature; the contraindication for respiratory conditions is a standard pharmacological inference.
	ReasoningReasoning Work-notes list as relative contraindication with medium confidence. Respiratory depression is well-documented in GBL/GHB clinical literature; the contraindication for respiratory conditions is a standard pharmacological inference.
cardiovascular Cardiac conduction disorderstrace	relative	relative	medium
Editorial	Work-notes list as relative contraindication with medium confidence. Bradycardia documented in clinical literature; Dargan et al. 2009 reported asystole as cause of death in first UK GBL fatality.
	ReasoningReasoning Work-notes list as relative contraindication with medium confidence. Bradycardia documented in clinical literature; Dargan et al. 2009 reported asystole as cause of death in first UK GBL fatality.
neurological History of seizurestrace	relative	relative	medium
Editorial	Work-notes list as relative contraindication with medium confidence. Seizure rate of 7% in withdrawal from Wojtowicz et al. 2008 systematic review (n=57 episodes).
	ReasoningReasoning Work-notes list as relative contraindication with medium confidence. Seizure rate of 7% in withdrawal from Wojtowicz et al. 2008 systematic review (n=57 episodes).
psychiatric History of substance dependencetrace	relative	relative	medium
Editorial	Work-notes list as relative contraindication with medium confidence. High reinforcement documented in clinical literature; dependence develops faster than alcohol or benzodiazepines per Schep et al. 2012.
	ReasoningReasoning Work-notes list as relative contraindication with medium confidence. High reinforcement documented in clinical literature; dependence develops faster than alcohol or benzodiazepines per Schep et al. 2012.
pregnancy breastfeeding Pregnancy and breastfeedingtrace	relative	relative	low
Editorial	Work-notes list as relative contraindication with low confidence. No human data available; classification is entirely precautionary.
	ReasoningReasoning Work-notes list as relative contraindication with low confidence. No human data available; classification is entirely precautionary.

Timeline Phases

oral

Field	Published	AI Proposed	Confidence
Onsettrace	180–600 sec(i=0.20)	180–600 sec(i=0.20)	medium
Editorial	Work-notes specify oral timeline: onset 3–10 min, come_up 5–15 min, peak 30–45 min, offset 15–30 min, afterglow 1–3 hours. Intensity weights from notes: 0.2, 0.6, 1.0, 0.4, 0.15. Consistent with published GHB PK (Tmax 20–60 min, t1/2 20–60 min) and DB seed duration data. Driving advisory verbatim from work-notes.
	ReasoningReasoning Work-notes specify oral timeline: onset 3–10 min, come_up 5–15 min, peak 30–45 min, offset 15–30 min, afterglow 1–3 hours. Intensity weights from notes: 0.2, 0.6, 1.0, 0.4, 0.15. Consistent with published GHB PK (Tmax 20–60 min, t1/2 20–60 min) and DB seed duration data. Driving advisory verbatim from work-notes. Evidence basis: community_consensus_large
Come uptrace	300–900 sec(i=0.60)	300–900 sec(i=0.60)	medium
Editorial	Work-notes specify oral timeline: onset 3–10 min, come_up 5–15 min, peak 30–45 min, offset 15–30 min, afterglow 1–3 hours. Intensity weights from notes: 0.2, 0.6, 1.0, 0.4, 0.15. Consistent with published GHB PK (Tmax 20–60 min, t1/2 20–60 min) and DB seed duration data. Driving advisory verbatim from work-notes.
	ReasoningReasoning Work-notes specify oral timeline: onset 3–10 min, come_up 5–15 min, peak 30–45 min, offset 15–30 min, afterglow 1–3 hours. Intensity weights from notes: 0.2, 0.6, 1.0, 0.4, 0.15. Consistent with published GHB PK (Tmax 20–60 min, t1/2 20–60 min) and DB seed duration data. Driving advisory verbatim from work-notes. Evidence basis: community_consensus_large
Peaktrace	1800–2700 sec(i=1.00)	1800–2700 sec(i=1.00)	medium
Editorial	Work-notes specify oral timeline: onset 3–10 min, come_up 5–15 min, peak 30–45 min, offset 15–30 min, afterglow 1–3 hours. Intensity weights from notes: 0.2, 0.6, 1.0, 0.4, 0.15. Consistent with published GHB PK (Tmax 20–60 min, t1/2 20–60 min) and DB seed duration data. Driving advisory verbatim from work-notes.
	ReasoningReasoning Work-notes specify oral timeline: onset 3–10 min, come_up 5–15 min, peak 30–45 min, offset 15–30 min, afterglow 1–3 hours. Intensity weights from notes: 0.2, 0.6, 1.0, 0.4, 0.15. Consistent with published GHB PK (Tmax 20–60 min, t1/2 20–60 min) and DB seed duration data. Driving advisory verbatim from work-notes. Evidence basis: community_consensus_large
Resolutiontrace	900–1800 sec(i=0.40)	900–1800 sec(i=0.40)	medium
Editorial	Work-notes specify oral timeline: onset 3–10 min, come_up 5–15 min, peak 30–45 min, offset 15–30 min, afterglow 1–3 hours. Intensity weights from notes: 0.2, 0.6, 1.0, 0.4, 0.15. Consistent with published GHB PK (Tmax 20–60 min, t1/2 20–60 min) and DB seed duration data. Driving advisory verbatim from work-notes.
	ReasoningReasoning Work-notes specify oral timeline: onset 3–10 min, come_up 5–15 min, peak 30–45 min, offset 15–30 min, afterglow 1–3 hours. Intensity weights from notes: 0.2, 0.6, 1.0, 0.4, 0.15. Consistent with published GHB PK (Tmax 20–60 min, t1/2 20–60 min) and DB seed duration data. Driving advisory verbatim from work-notes. Evidence basis: community_consensus_large
Afterglowtrace	3600–10800 sec(i=0.15)	3600–10800 sec(i=0.15)	medium
Editorial	Work-notes specify oral timeline: onset 3–10 min, come_up 5–15 min, peak 30–45 min, offset 15–30 min, afterglow 1–3 hours. Intensity weights from notes: 0.2, 0.6, 1.0, 0.4, 0.15. Consistent with published GHB PK (Tmax 20–60 min, t1/2 20–60 min) and DB seed duration data. Driving advisory verbatim from work-notes.
	ReasoningReasoning Work-notes specify oral timeline: onset 3–10 min, come_up 5–15 min, peak 30–45 min, offset 15–30 min, afterglow 1–3 hours. Intensity weights from notes: 0.2, 0.6, 1.0, 0.4, 0.15. Consistent with published GHB PK (Tmax 20–60 min, t1/2 20–60 min) and DB seed duration data. Driving advisory verbatim from work-notes. Evidence basis: community_consensus_large

Dose Tier Summaries

thresholdtrace

medium

Barely perceptible effects emerge — a mild relaxation settles across the body, accompanied by a subtle mood lift that may go unnoticed without deliberate attention. Most users report minimal subjective change at this level. Physical effects are negligible: perhaps a faint warmth or slight loosening of muscle tension. No significant cognitive impairment, motor control loss, or sedation. The threshold range carries a specific caution: GBL's dose-response curve is exceptionally steep, and individual sensitivity varies substantially. Effects can increase unpredictably with even fractional volume increases above this range.

Editorial

Work-notes outline threshold as barely perceptible with mild relaxation and subtle mood lift. Expanded with substance-specific steep dose-response warning from research output and prose. No controlled human dose-response study exists for GBL specifically.

Reasoning

Evidence basis: community_consensus_large

lighttrace

medium

Noticeable cognitive euphoria emerges alongside mild stimulation and a distinct anxiolysis. Sociability enhancement becomes apparent — conversation flows more easily, and social warmth increases. Some users describe an empathogenic quality with heightened tactile sensitivity. Muscle relaxation begins, producing a pleasant bodily looseness. Mild disinhibition is present but manageable. Physical effects remain subtle, with no significant motor control impairment or nausea at this level. Cognitive impairment is minimal. Most users retain functional capacity, though judgment may be subtly affected by the disinhibition. Duration of commitment is short — effects resolve within approximately 1.5 hours.

Editorial

Work-notes describe noticeable euphoria, mild stimulation, anxiolysis, sociability, empathogenic warmth, tactile sensitivity, and minimal cognitive impairment. Consistent with published low-dose GHB effects (Bosch & Seifritz 2016; Schep et al. 2012).

Reasoning

Evidence basis: community_consensus_large

commontrace

medium

Full cognitive euphoria dominates the experience, with pronounced disinhibition and sociability enhancement. Sexual arousal enhancement and empathogenic warmth — tactile sensitivity, prosocial openness, emotional closeness — reach their peak expression. Music enhancement is frequently reported. Motor control impairment becomes noticeable as ataxia. Nausea may occur. Memory suppression (anterograde amnesia) is possible even at this range. The compulsive redosing urge typically emerges here, driven by the short duration and desire to sustain euphoria. Cognitive impairment is moderate. Judgment is meaningfully affected by the combination of disinhibition and analysis suppression. The steep dose-response curve means the upper end of this range borders on strong effects — a difference of 0.5 mL can shift the experience substantially.

Editorial

Work-notes describe full euphoria, pronounced disinhibition, sociability, sexual arousal, empathogenic effects, motor control decline, amnesia, compulsive redosing urge, and nausea. Consistent with published moderate-dose GHB effects and the narrow therapeutic window emphasis throughout clinical literature.

Reasoning

Evidence basis: community_consensus_large

strongtrace

medium

Sedation becomes the dominant effect, overriding the stimulant and euphoric qualities seen at lower doses. Cognitive impairment is significant — confusion, spatial disorientation, and thought deceleration are common. Amnesia is likely, with substantial gaps in memory formation. Motor control impairment is pronounced (frank ataxia), making walking difficult and coordination unreliable. Nausea and vomiting may occur. Respiratory depression begins at this range, though it is not typically life-threatening in isolation at the lower end. Risk of loss of consciousness increases substantially toward the upper end. The transition from strong to heavy effects can occur abruptly. Functional capacity is severely compromised; the user should not be alone.

Editorial

Work-notes describe dominant sedation, significant cognitive impairment, pronounced motor control impairment, amnesia, nausea/vomiting, and onset of respiratory depression. Risk of unconsciousness emphasized. Consistent with high-dose clinical presentations in Schep et al. 2012 and Dargan et al. 2009.

Reasoning

Evidence basis: community_consensus_large

heavytrace

medium

Deep sedation progressing to unconsciousness defines this range. The user may become unrousable. Respiratory depression is clinically significant — breathing rate and depth decrease, and airway compromise becomes a real possibility, especially if vomiting occurs during unconsciousness. Bradycardia and hypothermia are reported at these doses. Vomiting with aspiration risk is a primary mechanism of GBL-related fatalities. Myoclonus or seizure-like activity may occur. Coma is possible. This dose range is life-threatening. The estimated lethal dose (~60 mg/kg, approximately 3.75 mL pure GBL for a 70 kg person) falls disturbingly close to or within this range. No antidote exists; emergency management is purely supportive. Any person at this dose level requires immediate medical attention.

Editorial

Work-notes describe deep sedation to unconsciousness, respiratory depression, aspiration risk, bradycardia, hypothermia, and coma. Lethal dose proximity emphasized. Consistent with fatal case reports (Dargan et al. 2009, Lenz et al. 2008) and Dufayet et al. 2023 lethal dose estimate.

Reasoning

Evidence basis: published_case_series

History

current version

published Oct 2, 2026system—

versions

2 total · since previous: +0 / −0 citations

publication ledger

publish Oct 2, 2026 · by agent-psx

backfill Jun 4, 2026

Historical versions do not record which reviewer approved them; editorial accountability is recorded per value in the database and in the publication ledger going forward.

full version history suggest a correction contact@psychedex.org

Sources

18 strong · 6 moderate · 12 weak

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strong
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[29]
strong
Acute toxicity and withdrawal syndromes related to γ-hydroxybutyrate (GHB) and its analogues γ-butyrolactone (GBL) and 1,4-butanediol (1,4-BD)
Wood DM, Brailsford AD, Dargan PI · 2011 · Drug Testing and Analysis
doi.org/10.1002/dta.292 pubmed 21548140no claims checked
[30]
strong
Comparative study of equimolar doses of gamma-hydroxybutyrate (GHB), 1,4-butanediol (1,4-BD) and gamma-butyrolactone (GBL) on catalepsy after acute and chronic administration
Towiwat P, Phattanarudee S, Maher TJ · 2013 · Food and Chemical Toxicology
doi.org/10.1016/j.fct.2012.10.009 pubmed 23104245no claims checked
[31]
moderate
Gamma-butyrolactone (GBL) dependence and withdrawal
Bell J, Collins R · 2011 · Addiction
doi.org/10.1111/j.1360-0443.2010.03145.x pubmed 20925687no claims checked
[32]
moderate
Improving GHB withdrawal with baclofen: study protocol for a feasibility study for a randomised controlled trial
Lingford-Hughes A, Patel Y, Bowden-Jones O, et al. · 2016 · Trials
pubmed 27677382no claims checked
[33]
moderate
Clinical relevance of ethanol coingestion in patients with GHB/GBL intoxication
Galicia M, Dargan PI, Dines AM, et al. · 2019 · Toxicology Letters
doi.org/10.1016/j.toxlet.2019.07.001 pubmed 31301370no claims checked
[34]
strong
Gamma-hydroxybutyrate and ethanol effects and interactions in humans
Thai D, Dyer JE, Benowitz NL, Haller CA · 2006 · Journal of Clinical Psychopharmacology
pubmed 16974199no claims checked
[35]
weak
Intoxications due to ingestion of gamma-butyrolactone: organ distribution of gamma-hydroxybutyric acid and gamma-butyrolactone
Lenz D, Rothschild MA, Kröner L · 2008 · Therapeutic Drug Monitoring
doi.org/10.1097/ftd.0b013e3181898c2e pubmed 18824955no claims checked
[36]
strong
Effects of monocarboxylate transporter inhibition on the oral toxicokinetics/toxicodynamics of GHB and GBL
Morse BL, Morris ME · 2013 · Journal of Pharmacology and Experimental Therapeutics
doi.org/10.1124/jpet.112.202796 pubmed 23392755no claims checked

Claim Verification

No claim verification has run for this version.

Coverage & Gaps

effect links

79 links · 79 approved · 0 audited0/79 with evidence basis

interactions

44 approved pairs0/44 graded

GBL

Value Provenance

Dosing

oraltrace →

Duration

oral

Safety

Toxicity Profiletrace →

Dependence Profiletrace →

Withdrawal Profiletrace →

Tolerance Profiletrace →

Effects & Profile

Contraindications

Timeline Phases

oral

Dose Tier Summaries

History

Sources

Claim Verification

Coverage & Gaps

oraltrace

Toxicity Profiletrace

Dependence Profiletrace

Withdrawal Profiletrace

Tolerance Profiletrace