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Etizolam

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4 sources

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🔗 MergedComparePsychonautWikiTripSitPharmacologyDrugCentral

Collated from PsychonautWiki, TripSit, Pharmacology, DrugCentral. Where sources differ (e.g. dosing), Compare shows them side by side.

Sections
DepressantThienodiazepinesBenzodiazepineResearch-chemicalHabit-formingPW

Also known as Etizolam, Etilaam, Etizest, Depas, etiz, sedekopan, etizola, inxity, zoly, lamet, towaPW

Fatal overdose may occur when thienodiazepines are combined with other depressants such as opiates, benzodiazepines, barbiturates, gabapentinoids, alcohol or other GABAergic substances.[1] It is strongly discouraged to combine these substances, particularly in common to heavy doses.PW

Addiction potentialPW
highly addictive with a high potential for abuse
ToxicityPW
low toxicity; potentially lethal when mixed with depressants like alcohol or opioids
TolerancePW
full tolerance within a couple of days of continuous use; baseline after 7 - 14 days
Cross-tolerancePW
benzodiazepine, thienodiazepine

Oral

Route dataPsychonautWiki

Dose
WeakerStronger
ThresholdLightCommonStrongHeavy
0.2 mg0.5–1 mg1–2 mg2–5 mg5 mg+
06.25 mg
LightCommonStrongHeavy
Duration
ShorterLonger
Onset15–30 minutes
Come-up30–60 minutes
Peak2–3 hours
Offset1.5–2.5 hours
Total5–7 hours
After-effects6–24 hours
OnsetCome-upPeakOffset

🧬 Receptor activityDC

TargetActionAffinitySource
GABA-A receptor alpha-1/beta-2/gamma-2 (GABRA1)—8.1 EC50DRUGCENTRAL
GABA-A receptor alpha-2/beta-3/gamma-2 (GABRG2)——DRUGCENTRAL
GABA-A receptor alpha-3/beta-3/gamma-2 (GABRG2)——DRUGCENTRAL
GABA-A receptor alpha-5/beta-3/gamma-2 (GABRG2)——DRUGCENTRAL
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Mechanism of actionPH

Etizolam is selectively a full agonist at GABA-A receptors to increase GABAergic transmission and enhance GABA-induced Cl- currents. It is reported to bind to the benzodiazepine binding site which is located across the interface between the alpha and gamma subunits. Benzodiazapines are reported to only bind to receptors that contain gamma 2 and alpha 1/2/3/5 subunits. Alpha-1-containing receptors mediate the sedative effects of etizolam whereas alpha-2 and alpha-3 subunit-containing receptors mediate the anxiolytic effect. Etizolam shows high potency and affinity towards GABA-A receptor with alpha 1 beta 2 gamma 2S subunit combination. By binding to the regulatory site of the receptor, etizolam potentiates GABA transmission by facilitating the opening of GABA-induced chloride channels. Etizolam is a specific antagonist at PAFR. It inhibits PAF-induced platelet aggregation by inhibiting PAF binding to the receptors located on the surface of platelets with an IC50 of 22nM.

PharmacodynamicsPH

Etizolam is a CNS depressant with anxiolytic, anticonvulsant, sedative-hypnotic and muscle relaxant effects. It acts on the benzodiazepine site of the GABA-A receptor as an agonist to increase inhibitory GABAergic transmission throughout the central nervous system. Studies indicate that etizolam mediates its pharmacological actions with 6 to 10 times more potency than that of diazepam. Clinical human studies performed in Italy showed clinical effectiveness of etizolam in relieving symptoms in patients with generalized anxiety disorders with depressive symptoms. Etizolam also mediates imipramine-like neuropharmacological and behavioral effects, as well as minor effects on cognitive functioning. It is shown to substitute the actions of a short-acting barbiturate, pentobarbitol, in a drug discrimination study. Etizolam is an antagonist at platelet-activating-factor (PAF) receptor and attenuates the recurrence of chronic subdural hematoma after neurosurgery in clinical studies. It is shown to inhibit PAF-induced bronchoconstriction and hypotension.

Pharmacokinetics

Half-lifePH

The average elimination half life of etizolam following a single oral dose of 0.5mg is 3.4 hours but may be increased up to 17 hours depending on the rate of metabolism. The main metabolite α-hydroxyetizolam displays a longer elimination half life of 8.2 hours.

AbsorptionPH

Etizolam is well absorbed from the intestines with a biological bioavailability of 93% following oral administration. After a single oral dosing of 0.5mg etizolam, it takes approximately 0.9 hours to reach the peak plasma concentration of 8.3 ng/mL.
In a rat study, the amounts of etizolam excreted was 30% in urine was 70% in feces, while the values in a mouse study were 40% in urine and 60% in feces.
Apparent distribution volume was 0.9 ± 0.2 L/kg following a single oral doing of 0.5mg etizolam.

MetabolismPH

Biotransformation of etizolam is extensive and involves hydroxylation and conjugation. The main metabolite formed via 1'-hydroxylation is α-hydroxyetizolam which retains pharmacological activity comparable to that of the parent drug, indicating that the action of metabolites may contribute to the clinical effects of etizolam. CYP3A4 is predicted to be the main CYP enzyme responsible for mediating etizolam metabolism. CYP2C18 and CYP2C19 are also involved in the metabolic pathways.
Etizolam has known human metabolites that include 7-(2-chlorophenyl)-4-ethyl-13-methyl-3-thia-1,8,11,12-tetrazatricyclo[8.3.0.02,6]trideca-2(6),4,7,10,12-pentaen-9-ol and alpha-Hydroxyetizolam.

Plan when to take Etizolam — see where onset, peak and comedown land on the clock

Fact-sheets from PsychonautWiki. Harm-reduction reference only — not medical advice.