Pyrazolam
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Pyrazolam (8-bromo-1-methyl-6-pyridin-2-yl-4H-triazolo-benzodiazepine) is a synthetic depressant of the benzodiazepine class. It is structurally derived from triazolam, distinguished by its unusually selective anxiolytic profile. Pyrazolam is a positive allosteric modulator of the GABA-A, producing its effects by enhancing inhibitory signaling with preferential activity at receptor subtypes that mediate anxiety relief over sedation.[1]
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Synthesized by Leo Sternbach and Armin Walser at Hoffmann-La Roche in the early 1970s, pyrazolam was never advanced into clinical development.[2] It resurfaced in 2012 as one of the first designer benzodiazepines sold online, an event researchers described as marking the beginning of an entire novel psychoactive substance class.[3] It remains federally unscheduled in the United States but is controlled in several European jurisdictions.
Subjective effects include anxiolysis, mild sedation, muscle relaxation, and cognitive slowing.[4] The experience is defined by its narrowness — a clean reduction of anxiety without the euphoria, heavy sedation, or mental fog typical of most benzodiazepines, making it highly sensitive to the user's baseline anxiety level.[5] Residual impairment beyond the perceived effects window, delusions of sobriety, and compulsive redosing are characteristic unsought effects.
Pyrazolam carries high abuse liability and low-to-moderate acute toxicity — the allosteric mechanism limits overdose risk alone, but combining with other depressants eliminates that ceiling.[6] Chronic use produces physical dependence with withdrawal that can include seizures; tolerance develops rapidly with full cross-tolerance to all benzodiazepines.[7] No clinical trials exist — pharmacological understanding rests on a single self-administration study and structural inference.[8]
History[edit]
Discovery
Pyrazolam was synthesized by Leo Sternbach and Armin Walser at Hoffmann-La Roche as part of a systematic exploration of triazolobenzodiazepine structures. The work was documented in US Patent 3,954,728, filed in 1972 and issued in 1976.[2] Despite claims of pharmacological activity, Hoffmann-La Roche never advanced the compound into preclinical development, and it remained a laboratory curiosity for four decades.
Emergence as a designer benzodiazepine
Pyrazolam reappeared around 2012 on online markets selling research chemicals. Moosmann et al. documented this emergence, explicitly noting that pyrazolam's appearance "marked the beginning of designer benzodiazepines being sold as recreational drugs or 'self medication'".[3] Alongside diclazepam and flubromazepam, it formed the first wave of designer benzodiazepines — compounds of moderate potency and established structural lineage.[9] A second wave followed with higher-potency agents like clonazolam and flubromazolam, whose capacity for severe sedation and amnesia at sub-milligram doses shifted regulatory urgency.[9]
Regulatory response
Pyrazolam was reported to the EMCDDA Early Warning System in 2013.[10] National scheduling proceeded unevenly: the United Kingdom classified it as Class C in June 2017,[5] Germany brought it under the NpSG in 2019, while it remains federally unscheduled in the United States as of 2026. This fragmented response typified the regulatory lag that designer benzodiazepines exploited as a class.[11]
The name pyrazolam follows benzodiazepine naming conventions: the -azolam suffix indicates a triazolobenzodiazepine containing a fused triazole ring, shared by triazolam and alprazolam. The pyr- prefix references the pyridine ring at position 6, distinguishing it from its chlorophenyl-bearing relatives. Among research chemical communities, pyrazolam earned a reputation as the functional benzodiazepine — valued not for recreational effects but for its narrow anxiolytic action that left cognition and productivity largely intact, a quality that set it apart from the euphoric and sedating designer benzodiazepines that followed.[5]
Chemistry[edit]
Structural class
Pyrazolam is a triazolobenzodiazepine — a structural family defined by the fusion of a 1,2,4-triazole ring to a 1,4-benzodiazepine scaffold. This motif is shared with clinically established compounds including triazolam, alprazolam, and estazolam. The fused triazole confers greater conformational rigidity and metabolic stability compared to classical 1,4-benzodiazepines like diazepam.
Molecular structure
| Molecular formula | C₁₆H₁₂BrN₅ |
| Molecular weight | 354.20 g/mol |
The compound is a fused tricyclic system: a benzene ring, a seven-membered 1,4-diazepine ring, and a 1,2,4-triazole ring.[12] A bromine atom at the 8-position influences electronic density and receptor binding. A methyl group on the triazole ring and a pyridine ring at position 6 complete the substitution pattern, distributing five nitrogen atoms across the triazole, diazepine, and pendant pyridine.
Pyrazolam differs from triazolam at two positions: an 8-bromo substituent replaces the 8-chloro group, and a 2-pyridyl ring at position 6 replaces the 2-chlorophenyl ring. These modifications alter both receptor subtype selectivity and metabolic fate.
Stereochemistry
Pyrazolam lacks a chirality center and exists as a single achiral species.
Physical properties
| Melting point | 253–255 °C |
| Density | 1.6 ± 0.1 g/cm³ |
| Boiling point (predicted) | 544.4 ± 60.0 °C at 760 mmHg |
The high melting point reflects strong intermolecular interactions in the crystalline solid, consistent with its planar aromatic system and nitrogen-mediated hydrogen bonding.[12] No published data exist on aqueous solubility or partition coefficient. Pyrazolam is commercially available as pellets (typically 0.5–1 mg per unit) and as bulk powder.[9]
Pharmacology[edit]
Mechanism of action
Pyrazolam enhances the activity of GABA, the brain's primary inhibitory neurotransmitter. It binds at the benzodiazepine site on the GABA-A, increasing the frequency of chloride channel opening when GABA is present — amplifying the brain's own inhibitory signals without directly activating the receptor.[1]
The distinguishing feature of pyrazolam is its apparent preference for GABA-A receptor subtypes containing α2 and α3 subunits over those containing α1 subunits. This matters because α1 subtypes drive sedation and amnesia, while α2 and α3 subtypes mediate anxiety relief and muscle relaxation.[13][14] The result is a compound that reduces anxiety with comparatively little sedative or amnestic burden at low-to-moderate doses.
Direct binding data confirming this selectivity have not been published. The claim rests on converging indirect evidence: in vitro studies showing lower efficacy at α1-containing receptors compared to equally potent compounds like bromazolam,[1] structure-activity data from closely related compounds demonstrating that 8-position modifications strongly influence α1 engagement,[14] and the consistent pattern of user reports describing anxiolysis without heavy sedation.[5]
Pharmacokinetics
The only published human pharmacokinetic data come from a single self-administration study in which one researcher ingested 1 mg orally.[8]
The half-life was approximately 17 hours — substantially longer than the 6-hour figure marketed by vendors at the time.[8][5] The mismatch between the 17-hour half-life and the 5–8 hour subjective effects window reflects a standard pharmacokinetic principle: perceived effects cease when blood levels fall below the effective threshold, well before the drug is fully eliminated. The compound remained detectable in blood for over 50 hours and in urine for up to 6 days following a single dose.[8]
How pyrazolam is broken down in the body remains unresolved. The original self-administration study detected no metabolites, concluding the drug is excreted unchanged.[8] A later study analyzing real-world intoxication samples found glucuronide metabolites.[15] A third study using liver tissue in the laboratory failed to reproduce that glucuronidation.[16] This three-way contradiction has not been resolved.
No data exist for oral bioavailability, protein binding, or volume of distribution.
Neuroscience[edit]
Where it acts
No neuroimaging or electrophysiology studies have been conducted with pyrazolam. Based on established GABA-A neuroscience, its α2/α3-preferring profile shapes which brain networks are most affected.
α2-containing receptors concentrated in the amygdala and hippocampus mediate the anxiolytic core — dampening fear responses without the broad cortical depression that α1-dominant compounds produce.[13] α3-containing receptors in the brainstem modulate arousal and muscle tone. At higher doses, the selectivity gradient narrows as more receptor subtypes become occupied, producing the sedation and cognitive impairment characteristic of the benzodiazepine class.
Why it matters
Pyrazolam functions as an unintentional test of the anxioselective hypothesis — the long-pursued idea that anxiety relief can be pharmacologically separated from sedation, amnesia, and abuse potential through subtype-selective GABA-A modulation.[13] No deliberately designed α2/α3-selective anxiolytic has reached clinical approval. Yet pyrazolam's widespread unregulated use provides indirect human evidence that the dissociation works: users consistently report pronounced anxiolysis with limited sedation and euphoria.[5]
The critical missing experiment is direct measurement of pyrazolam's binding affinity and functional potency at each GABA-A receptor subtype — the entire selectivity claim rests on inference. Whether the α2/α3 preference slows the rate of tolerance development compared to non-selective benzodiazepines is unknown but clinically significant.[7]
Subjective Effects[edit]
Pyrazolam's experiential character is defined as much by what it lacks as by what it produces. The anxiolytic effect is described as clean — a reduction of baseline anxiety without accompanying euphoria, heavy sedation, or cognitive fog.[5][4] This narrow effect window makes the experience highly sensitive to pre-existing anxiety: individuals with elevated baseline anxiety report pronounced relief, while those without may notice comparatively little change. At higher doses, sedation, muscle relaxation, and cognitive slowing emerge as the selectivity gradient narrows.
Among designer benzodiazepines, pyrazolam is most often compared to diclazepam for its functional, low-profile character, though diclazepam carries a longer half-life and somewhat greater sedative component. The contrast with clonazolam is stark: where clonazolam produces marked sedation, amnesia, and euphoria at sub-milligram doses, pyrazolam at comparable anxiolytic doses leaves cognitive and motor function largely intact.[9]
Effect Grid
At 0.75–1.5 mg, pyrazolam produces clear, sustained anxiety suppression — the primary therapeutic-equivalent range. Anxiolysis is the dominant effect: worry, anticipatory anxiety, and social apprehension are substantially reduced. Mild thought deceleration and analysis suppression emerge, particularly at the upper end of the range.
Sedation becomes noticeable but remains mild. Muscle relaxation is present and perceptible. Motor control is slightly reduced at 1.5 mg but largely preserved at 0.75 mg. Some users report mild physical fatigue. Emotional suppression becomes apparent — emotional reactivity is dampened.
Cognitive function remains substantially preserved at the lower end; mild cognitive impairment emerges at the upper end. Amnesia risk is low but nonzero. The 17-hour half-life means residual drug persists long after subjective effects fade — avoid redosing within 8 hours.
Modeled from the effect's dose-dependence curve — not per-substance measurements.
Dizziness · Body high · Nystagmus (eye wobbles) · Breathing alteration · Nausea suppression · Nausea
Nausea suppression · Nausea
Information processing suppression · Cognitive fatigue · Analysis suppression · Thought deceleration · Motivation suppression · Cognitive euphoria · Memory fragmentation · Language suppression · Thought disorganization · Compulsive redosing urge · Confusion · Amnesia
Thought deceleration · Motivation suppression · Cognitive euphoria · Memory fragmentation · Language suppression · Thought disorganization · Confusion · Amnesia
Timeline
Initial absorption begins. A subtle easing of baseline anxiety may emerge in the final minutes of this phase, though many users report no perceptible change until the come-up.
Anxiolysis intensifies to its full character. Mild muscle relaxation begins. The effect is experienced as a steady quieting of anxious thought rather than a sudden shift.
Maximum anxiety suppression. Sedation and muscle relaxation hold at a stable plateau. At common doses, cognitive function remains largely preserved — the peak is notable for its functional clarity relative to other benzodiazepines.
Anxiolysis and sedation gradually diminish. Effects fade below the threshold of subjective awareness over several hours. Some users do not notice the offset clearly due to the gradual taper.
No positive afterglow in the psychedelic sense. Residual pharmacological activity persists due to the 17-hour elimination half-life — subtle psychomotor impairment is possible without subjective awareness.
⚠ Do not drive or operate machinery for at least 24 hours after the last dose.
Safety[edit]
- Acute toxicity
- Low
- Chronic toxicity
- Low
- Withdrawal
- Severe
- Tolerance buildup
- rapid
- Tolerance reset
- 10.5 days
- Physical
- High
- Psychological
- High
- Compulsive redosing
- Moderate
- Dose escalation
- High
- Cross-tol.
- benzodiazepines · zolpidem · zaleplon
Toxicity
Acute toxicity
No LD50 data exist for pyrazolam in any species, and no therapeutic index has been calculated. As a GABA-A positive allosteric modulator, pyrazolam shares the class-wide ceiling effect: the allosteric mechanism limits maximal chloride channel enhancement, making death from pyrazolam alone unlikely in otherwise healthy individuals.
The single published fatality involving pyrazolam was a polydrug death attributed to positional asphyxia, with co-detected diclazepam, 3-fluorophenmetrazine, amphetamine, and caffeine.[6] The cause of death was not attributed to pyrazolam in isolation.
A published poisoning case involved co-ingestion of pyrazolam with high-concentration ethanol; flumazenil was administered.[17] Pyrazolam has been identified in clinical intoxication cases through the Swedish STRIDA project[18] and in blood samples from impaired drivers and criminal offenders in Norway.[19]
The primary acute risk is polydrug toxicity. Co-administration with opioids, alcohol, barbiturates, GHB, or other depressants eliminates the safety ceiling that protects against benzodiazepine-only overdose. Both the published fatality and the published poisoning case involved polydrug contexts.
Chronic toxicity
No substance-specific chronic toxicity data exist. Class-level evidence associates long-term benzodiazepine use with cognitive impairment — particularly affecting memory and reaction time — and increased fall risk in elderly populations. No organ-specific toxicity has been reported for pyrazolam.
Psychological risks
Amnesia and blackout: Dose-dependent memory loss is a class effect of benzodiazepines. Pyrazolam's reduced α1 engagement may attenuate amnesia at lower doses, but amnesia becomes probable at strong and heavy doses.[9]
Delusions of sobriety: Users may subjectively underestimate their impairment while demonstrating measurable deficits in coordination and judgment.
Disinhibition: Reduced prefrontal inhibitory control can produce impulsivity, aggression, or risk-taking — amplified by concurrent alcohol use.
Compulsive redosing: Some users report difficulty stopping once started, consistent with benzodiazepine reinforcement mechanisms, though pyrazolam is described as less reinforcing than high-euphoria compounds such as clonazolam.[4]
Rebound anxiety: Following cessation, anxiety exceeding baseline levels may occur as receptor balance is restored, driving repeated self-administration and contributing to the dependence cycle.
Drug-facilitated crime: Pyrazolam's rapid onset, amnestic potential at higher doses, and limited detectability on standard immunoassay panels place it in the moderate risk category among designer benzodiazepines.[20]
Tolerance and dependence
Tolerance develops rapidly with continuous use — typically within days to weeks — through downregulation.[7] Tolerance to sedative effects emerges early, while anxiolytic tolerance develops more slowly and may be incomplete. Full cross-tolerance exists with all benzodiazepines and other GABA-A modulators including barbiturates and alcohol.[7]
Physical dependence follows sustained use, with severity proportional to dose, duration, and individual vulnerability. Withdrawal symptoms include rebound effect anxiety, insomnia, tremor, sweating, irritability, and — in severe cases — seizures. Given pyrazolam's 17-hour half-life, withdrawal onset is expected 24–48 hours after the last dose, with a more protracted course than short-acting benzodiazepines.[8]
Psychological dependence is driven by the reinforcing reduction of anxiety — users who self-medicate anxiety disorders may develop strong conditioned associations between pyrazolam and relief.[21] A published case of designer benzodiazepine detoxification via diazepam substitution and gradual taper provides a template clinical approach.[22]
Drug interactions
CNS depressant potentiation (dangerous to potentially fatal): Co-administration with alcohol, opioids, other benzodiazepines, barbiturates, GHB/GBL, or gabapentinoids produces additive or synergistic depression of consciousness and breathing.[7] The opioid-benzodiazepine combination is particularly hazardous: opioids suppress breathing directly while benzodiazepines reduce the compensatory arousal response, a synergy responsible for the majority of benzodiazepine-involved overdose deaths.
The published fatality involved pyrazolam combined with Diclazepam and stimulants.[6] The published poisoning involved co-ingestion with high-concentration ethanol.[17]
Stimulant combinations: Use as a stimulant comedown aid was reported in 16.1% of pyrazolam-related forum discussions.[5] While less acutely dangerous than depressant combinations, this pattern creates a reinforcing cycle that may escalate both stimulant and benzodiazepine use.
Contraindications
Respiratory insufficiency (absolute): Pre-existing breathing impairment (COPD, sleep apnea, neuromuscular respiratory weakness) increases vulnerability to GABA-A-mediated respiratory depression.
Concurrent depressant use (absolute): Active use of opioids, barbiturates, alcohol, GHB, or other benzodiazepines constitutes an absolute contraindication due to synergistic respiratory depression risk.
History of benzodiazepine dependence (relative): Prior benzodiazepine use disorder significantly increases risk of relapse. Cross-tolerance means prior dependence on any GABAergic agent increases risk.
Liver impairment (relative): Although pyrazolam's metabolic fate is uncertain, any liver processing could be impaired in liver disease, prolonging exposure.inferred
Pregnancy (absolute): Benzodiazepines carry risk of birth defects (particularly first-trimester exposure) and neonatal withdrawal with late-pregnancy exposure.inferred
Myasthenia gravis (absolute): Benzodiazepine-mediated muscle relaxation and respiratory depression can precipitate crisis.
Harm Reduction[edit]
Forms & Identification
Pyrazolam's active dose range begins below 1 mg, placing it in territory where minor measurement errors produce meaningful differences in effect intensity. Powder form demands a milligram-precision scale — volumetric estimation is unreliable at this scale. Pressed pellets offer more consistent dosing but remain unregulated products with no quality guarantee.
Designer benzodiazepines are not reliably distinguished from one another by appearance alone. Products sold as pyrazolam may contain other compounds, and counterfeit pharmaceutical tablets containing designer benzodiazepines have been documented.[9] Standard benzodiazepine immunoassay panels may not detect pyrazolam, and reagent test kits do not differentiate between benzodiazepine analogs — laboratory analysis is the only definitive identification method.
Guidelines
- Start with the lowest available dose to assess individual sensitivity before considering any increase
- Weigh powder doses with a milligram-precision scale — never estimate by eye
- Set a firm dose limit before taking the first dose; benzodiazepine-induced impairment erodes the judgment needed to stop redosing
- Allow at least 90 minutes before considering whether to redose — onset can be delayed
- Do not combine with alcohol, opioids, GHB, or any other depressant
- Avoid frequent or consecutive-day use; physical dependence can develop within days to weeks of regular use
- Inform a trusted person of the substance, dose, and timing
- Keep a written record of dose and time — memory suppression may prevent accurate recall
Set & Setting
Pyrazolam's anxiolytic-dominant profile means the subjective experience is strongly shaped by baseline anxiety level. Users without significant anxiety may perceive little effect and be tempted to redose — a pattern that increases the risk of overshooting into sedation and amnesia. A familiar, low-stress environment reduces the temptation to chase an effect that may simply not be perceptible without anxiety to relieve.
The 17-hour half-life means the compound remains pharmacologically active well beyond the 5–8 hour window of perceived effects. Planning should account for next-day impairment, particularly regarding driving, operating machinery, or making important decisions.
Aftercare & integration. Residual effects from pyrazolam's 17-hour half-life may include subtle cognitive slowing, reduced reaction time, and emotional suppression for 24–48 hours after the perceived effects resolve. Tasks requiring sharp judgment or fast reflexes should be avoided during this period.
Users who take pyrazolam to manage anxiety should examine whether the underlying anxiety has a treatable cause. Benzodiazepine self-medication masks symptoms without addressing their source, and the rebound effect anxiety that follows each use can create a cycle that worsens the original problem. Evidence-based treatment through a healthcare provider is substantially safer and more effective than self-administration of unregulated compounds.
Recovery & Support
Benzodiazepine dependence requires careful, medically supervised withdrawal. Abrupt cessation after regular use risks seizures, which can be life-threatening. The standard clinical approach is substitution with a long-acting benzodiazepine such as diazepam, followed by a gradual taper over weeks to months.[22]
Anyone experiencing escalating use, inability to skip days, or withdrawal symptoms between doses should seek medical support. The Benzodiazepine Information Coalition (benzoinfo.com) and SAMHSA's helpline (1-800-662-4357) provide resources and referrals. Recovery from benzodiazepine dependence is achievable but benefits from professional guidance — the withdrawal process is physiologically complex and should not be self-managed.
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Recognizing an emergency: The line between uncomfortable and dangerous crosses when breathing becomes slow or shallow, skin or lips develop a blue tint, the person cannot be roused by voice or physical stimulation, or vomiting occurs while semiconscious.
Immediate steps:
- 1. Call emergency services immediately if the person is unresponsive, breathing abnormally, or showing blue discoloration
- 2. Place the person in the recovery position (on their side, head tilted back) to prevent choking if they vomit
- 3. Do not leave an unconscious or heavily sedated person alone
- 4. Do not induce vomiting
- 5. Monitor breathing continuously until help arrives
What to tell the dispatcher: Name the substance (pyrazolam, a designer benzodiazepine), the approximate amount taken, the time of ingestion, any other substances involved, and current symptoms. Good Samaritan laws in many jurisdictions protect people who call for help during a drug emergency.
Reversal agent: Flumazenil is a benzodiazepine antagonist available in hospital settings. It can reverse benzodiazepine effects but carries risk of precipitating seizures in dependent individuals and has a shorter duration of action than pyrazolam — meaning re-sedation can occur after the flumazenil wears off.[17]
Legal Status[edit]
Pyrazolam occupies a fragmented regulatory position internationally. As of 2026, it is specifically controlled in several jurisdictions but remains unscheduled under many national frameworks, including US federal law. Its status reflects the broader regulatory lag that characterizes responses to designer benzodiazepines.
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| United States (federal) | Not specifically scheduled | Not listed under the Controlled Substances Act as of May 2026. Five other designer benzodiazepines (etizolam, clonazolam, diclazepam, flualprazolam, flubromazolam) have been placed in temporary Schedule I. The Federal Analogue Act may apply if pyrazolam is intended for human consumption.citation needed |
| United States (Alabama) | Schedule I | Controlled since March 18, 2014 — one of the earliest state-level scheduling actions for any designer benzodiazepine.citation needed |
| United Kingdom | Class C, Schedule 2 (Misuse of Drugs Act 1971) | Scheduled via the Misuse of Drugs Act 1971 (Amendment) Order 2017, effective June 2017. Classified alongside diclazepam, flubromazepam, and etizolam.[5] |
| Germany | Controlled (NpSG) | Placed under the Neue-psychoaktive-Stoffe-Gesetz since July 18, 2019. Not scheduled under the BtMG (Narcotics Act).citation needed |
| Sweden | Controlled substance | Specifically scheduled. Pyrazolam has been identified in Swedish STRIDA project intoxication cases.[18] |
| Canada | Ambiguous | Not explicitly named in Schedule IV of the Controlled Drugs and Substances Act. Health Canada's position is that the benzodiazepine class definition may capture unnamed analogs, but pyrazolam's precise status has not been adjudicated.safety citation needed |
| Australia | Controlled substance (ODC listing) | Listed by the Office of Drug Control. Specific schedule number and effective date not confirmed.safety citation needed |
Pyrazolam was first reported to the EMCDDA Early Warning System in 2013.[10] Mullin et al. tracked the compound's market trajectory from the pre-Psychoactive Substances Act 2016 period to the present, documenting the effect of UK scheduling on availability and social discourse patterns.[11]
references
- [1] ^abcNot specified in web search results (2026) In vitro γ-aminobutyric acid A (GABAA) receptor activity and binding interactions at the α+/γ2– interface of 53 prescription and designer benzodiazepines — Communications Chemistry (Nature) doi:10.1038/s42004-026-02001-x
- [2]
- [3] ^abMoosmann B, Huppertz LM, Hutter M, Buchwald A, Ferlaino S, Auwärter V (2013) Detection and identification of the designer benzodiazepine flubromazepam and preliminary data on its metabolism and pharmacokinetics — Journal of Mass Spectrometry doi:10.1002/jms.3279
- [4]
- [5] ^abcdefghiAbouchedid R, Gilks T, Dargan PI, Archer JRH, Wood DM (2018) Assessment of the Availability, Cost, and Motivations for Use over Time of the New Psychoactive Substances-Benzodiazepines Diclazepam, Flubromazepam, and Pyrazolam-in the UK — Journal of Medical Toxicology doi:10.1007/s13181-018-0659-3
- [6] ^abcLehmann S, Sczyslo A, Froch-Cortis J, Rothschild MA, Thevis M, Andresen-Streichert H, Mercer-Chalmers-Bender K (2019) Organ distribution of diclazepam, pyrazolam and 3-fluorophenmetrazine — Forensic Science International doi:10.1016/j.forsciint.2019.109959