3-Quinuclidinyl benzilate Stats & Data
O=C(OC1CN2CCC1C2)C(O)(c1ccccc1)c1ccccc1FQMCYHXKXFYRJS-UHFFFAOYSA-NPharmacology
DrugBankMechanism of Action
BZ is a glycolate anticholinergic compound related to atropine, scopolamine, and hyoscyamine (others). ... Acting as a competitive inhibitor of acetylcholine at postsynaptic and postjunctional muscarinic receptor sites in smooth muscle, exocrine glands, autonomic ganglia, and the brain, BZ decreases the effective concentration of acetylcholine seen by receptors at these sites. Thus, BZ causes peripheral nervous system (PNS) effects that in general are the opposite of those seen in nerve agent p
Metabolism
Information on the metabolism of BZ in humans is limited, but Benzylic Acid (BA) and 3-Quinuclidinol are the probable main metabolites ... . It has been estimated that 3% of the BZ is excreted as the parent compound.
Effect Profile
Curated + 4 ReportsLow visuals, headspace, and body load
Tolerance & Pharmacokinetics
drugs.wikiTolerance Decay
Robust quantitative data are lacking. Military summaries note that a second exposure 2–4 weeks later can show faster onset and heightened peak effects (“second‑dose effect”). Treat cross‑tolerance estimates as speculative.
Cross-Tolerances
Experience Report Analysis
ErowidDemographics
Gender Distribution
Reports Over Time
Harm Reduction
drugs.wiki- BZ is an extremely potent, long‑acting muscarinic acetylcholine receptor antagonist intended historically as a military incapacitating agent; “sub‑milligram” amounts can cause days‑long delirium, amnesia, ataxia, and severe disorientation. This is not a recreational drug and exposure should be considered a medical risk scenario.
- Onset is delayed (commonly 2–4 hours), which strongly increases the temptation to redose; redosing substantially raises the risk of prolonged incapacitation, heat injury, urinary retention, and hospitalization. Avoid any redosing.
- BZ markedly impairs sweating and heat dissipation (mydriasis, anhidrosis), creating a real risk of hyperthermia even at ambient temperatures; if exposure occurs, remain in a cool environment, remove excess clothing, use passive cooling, and seek medical evaluation for high temperature, agitation, or muscle rigidity.
- Vision is often severely affected (extreme mydriasis, blurred near focus) for 1–3 days or more—do not drive, cycle, swim, or engage in any hazardous activity until vision and cognition are clearly normal.
- Hydration is important but should be supervised; anticholinergics can cause both dry mouth and urinary retention. If unable to void for 6–8 hours with suprapubic discomfort, seek urgent care—catheterization may be required.
- In suspected anticholinergic toxicity, first‑line hospital care is supportive: cooling, IV fluids, electrolyte/CK monitoring, and cautious benzodiazepines for severe agitation. Physostigmine (a tertiary acetylcholinesterase inhibitor) can rapidly reverse delirium in pure anticholinergic toxidrome but must only be administered in a monitored medical setting due to seizure/bradyarrhythmia risk and is contraindicated in TCA co‑ingestion or QRS widening. Do not attempt any antidotes outside a hospital.
- Combining BZ with other anticholinergics (sedating antihistamines like diphenhydramine, TCAs, anticholinergic antipsychotics/antiemetics) markedly increases toxicity (confusion, hyperthermia, ileus, urinary retention). Alcohol, Z‑drugs, and opioids further impair judgement and breathing, compounding injury and aspiration risk. Stimulants may worsen agitation, hyperthermia, and rhabdomyolysis risk.
- Due to dose variability and idiosyncratic responses, “test dosing” is unsafe here: incapacitating IM doses are on the order of 6–8 µg/kg, and Erowid reports that <1 mg orally can cause profound effects for days.
- Tolerance data are limited. Military reports describe “second‑dose effects” 2–4 weeks after an initial exposure with faster onset and heightened peaks; repeated exposure increases unpredictability rather than safety. Cross‑tolerance with other antimuscarinics is plausible but unquantified.
- People with narrow‑angle glaucoma, prostatic hypertrophy/urinary obstruction, ileus, tachyarrhythmias, severe cardiovascular disease, or cognitive disorders, as well as children and older adults, are at elevated risk from anticholinergic toxicity; any suspected exposure warrants professional assessment.
- Mechanistically, BZ binds with very high affinity in the orthosteric pocket of muscarinic receptors; slow dissociation helps explain prolonged central effects even when plasma levels fall.
- Legal/forensic note: BZ is listed in the Chemical Weapons Convention (Schedule 2). Civilian availability is rare; unexpected “BZ” representations are often misidentifications of other anticholinergics.
- If someone seems intoxicated: do not leave them alone; prevent access to heat, water bodies, traffic, or weapons; avoid physical confrontation; call emergency services if there is fever, severe agitation, confusion, chest pain, seizure, inability to urinate, or loss of consciousness.
References
Drugs.wiki References
- Erowid BZ Vault (Main)
- Erowid BZ Effects
- Erowid BZ Basics (Dose, Duration, History)
- Erowid BZ Dosage (IM µg/kg; ID50; second‑dose effects)
- DrugBank article: M2 receptor structure with 3‑quinuclidinyl benzilate antagonist
- PubChem Compound CID 23056 (3‑Quinuclidinyl benzilate)
- Physostigmine vs benzodiazepines in anticholinergic poisoning (Ann Emerg Med 2000)
- Use of physostigmine by toxicologists; lower intubation rates vs other regimens
- StatPearls: Anticholinergic Toxicity (supportive care, benzos first‑line; physostigmine in refractory cases/with caution)
- Binding kinetics of quinuclidinyl benzilate at muscarinic receptors (slow dissociation)
- Rat toxicokinetics of BZ (LC‑MS/MS)
- TripSit: Scopolamine HR & interactions (analogous antimuscarinic cautions)
- Antidepressants antagonize muscarinic receptors (adds anticholinergic burden)