generation run 2026-05-09
86 min completedmodel pipeline-v5plan not recordedrun/e1b3873a…Selection
Verification
- record
- seen / partial
- working
The model's own caveats
- structural_inference
- sparse_evidence
- safety_data_unverified
Reproduce
- inputs
- 26 source keys (listed under Sources)
- plan
- not recorded — template version, prompt hash and git SHA are written from 2026-09 onward
- model
- pipeline-v5
- streams
- none — agent transcripts are persisted from 2026-09 onward
23 searches — query, source, results, what was kept and why
| # | source | query | seen | kept | rationale |
|---|---|---|---|---|---|
| 1 | OpenAlex | pyrazolam benzodiazepine designer drug | 10 | 5 | Selected for citation ranking, historical context, and pharmacological scope |
| 2 | PubMed | pyrazolam pharmacology benzodiazepine | 15 | 10 | Selected articles with direct pyrazolam data or closely relevant designer BZD data |
| 3 | PubChem | pyrazolam | 1 | 1 | Used to verify chemical identity data from the brief |
| 4 | ClinicalTrials.gov · absence | pyrazolam | 0 | 0 | Confirms absence of formal clinical trial history |
| 5 | PubMed · absence | pyrazolam synthesis Fryer triazolo benzodiazepine 1980s | 0 | 0 | Will need to find via web search |
| 6 | WebSearch | pyrazolam GABA alpha subunit binding affinity Ki nM IC50 selectivity alpha2 alpha3 anxiolytic | 10 | 2 | GABA receptor pharmacology data |
| 7 | WebSearch | pyrazolam legal status scheduling United States UK EU DEA 2026 | 10 | 3 | Legal status data not available in PubMed; web search necessary |
| 8 | WebSearch | pyrazolam Fryer synthesis 1970s 1980s American Cyanamid triazolo benzodiazepine original patent | 10 | 1 | Critical correction to assumed synthesis history |
| 9 | WebSearch | pyrazolam characterization serum urine Auwarter Moosmann 2013 research chemical | 10 | 1 | Primary characterization study with pharmacokinetic data |
| 10 | PMC / Abouchedid 2018 | — | 1 | 3 | Specific pyrazolam pharmacokinetic and use-pattern data |
| 11 | PubMed | pyrazolam metabolism urine detection | 5 | 2 | Direct pyrazolam metabolism data |
| 12 | Multiple sources | pyrazolam metabolism contradiction | 2 | 3 | Critical data contradiction requiring flagging |
| 13 | WebSearch | pyrazolam case report intoxication poisoning hospital clinical symptoms treatment | 10 | 1 | Only published pyrazolam-specific poisoning case report |
| 14 | WebSearch | pyrazolam Australia Canada legal status scheduled controlled | 10 | 2 | Legal status data |
| 15 | PubChem CID 12562545 | CID 12562545 | 1 | 1 | Chemical identity verification |
| 16 | WebSearch | pyrazolam CAS 39243-02-2 physical properties melting point | 10 | 1 | Physical properties not in academic literature |
| 17 | PubMed | 8-Substituted triazolobenzodiazepines GABA pharmacology Cook Rowlett | 1 | 1 | Directly relevant structural analog pharmacology |
| 18 | Multiple | pyrazolam synthesis history original patent | 5 | 1 | Origin and synthesis history |
| 19 | WebSearch | pyrazolam CAS 39243-02-2 physical properties melting point density | 10 | 1 | Physical property data absent from academic literature |
| 20 | WebSearch | pyrazolam case report intoxication hospital clinical symptoms | 10 | 1 | Only pyrazolam-specific poisoning case report |
| 21 | WebSearch | pyrazolam alpha subunit GABA anxiolytic selectivity alpha2 alpha3 NOT euphoria most anxiolytic designer | 10 | 0 | Community/secondary evidence for subunit selectivity - no primary source found |
| 22 | PubMed | GABA alpha1 sedation alpha2 anxiolytic benzodiazepine subunit selective pharmacology | 5 | 2 | Mechanistic basis for pyrazolam alpha2/3 selectivity interpretation |
| 23 | WebFetch | — | 1 | 4 | UK use pattern and pharmacokinetic data |
79 claims by section — every cited sentence, checked against its source
safety17 · 12 ok
The Magny 2026 poisoning involved co-ingestion with high-concentration ethanolsupported
Vodka solution contained ethanol (330 g/L) and pyrazolam (450 mg/L). s11419-025-00750-3
Flumazenil was administered.supported
Flumazenil administered. s11419-025-00750-3
Seven of 24 patients exposed only to NPS benzodiazepines required ICU admissionpartially supported
Seven cases required ICU admission; responded to flumazenil. 15563650.2018.1510502
The single post-mortem case (Lehmann et al. 2019) involved pyrazolam (femoral blood 28 µg/L) in a polydrug death attributed to positional asphyxia, with co-detected diclazepam, 3-fluorophenmetrazine, amphetamine, and caffeinesupported
Femoral blood pyrazolam 28 µg/L. Cause of death: positional asphyxia from poly-drug intoxication including designer benzodiazepines and synthetic stimulants. j.forsciint.2019.109959
Bäckberg et al. (2019) identified pyrazolam in clinical NPS benzodiazepine intoxication cases through the Swedish STRIDA projectsupported
Bioanalytical and clinical data on NPS BZD intoxications from the Swedish STRIDA project. Pyrazolam detected in clinical intoxication cases. 15563650.2018.1506130
Høiseth et al. (2016) detected pyrazolam in blood from drugged drivers and criminal offenders in Norway, correlating blood levels with clinical impairment.supported
Blood concentrations of new designer benzodiazepines in drugged drivers and criminal offenders; relates concentrations to clinical impairment. j.forsciint.2016.09.006
Claim in safety — inconclusiveinconclusiveworking →
Claim in safety — inconclusiveinconclusiveworking →
All characterizations derive from benzodiazepine class pharmacology.supported
Review of NPS benzodiazepines; covers PK parameters, metabolic pathways, analytical methods; notes pyrazolam among first commercial NPS BZDs. dta.2211
Claim in safety — inconclusiveinconclusiveworking →
Claim in safety — inconclusiveinconclusiveworking →
A published case report of designer benzodiazepine (bromazolam) detoxification via diazepam substitution and gradual taper provides a template approachsupported
23-year-old woman admitted for detoxification from designer BZD bromazolam. Daily use 6 mg bromazolam converted to 20 mg diazepam. Fixed-dose and symptom-triggered regimen. Tapered without complications. 10550887.2024.2365006
The benzodiazepine class is characterized as having high potential for both physical and psychological dependence.supported
Neurobiological and pharmacologic properties result in high potential for misuse and physical dependence. j.mcna.2021.08.012
Claim in safety — inconclusiveinconclusiveworking →
The Lehmann 2019 fatality involved pyrazolam combined with diclazepam and stimulants.supported
Cause of death: positional asphyxia from poly-drug intoxication including designer benzodiazepines and synthetic stimulants. j.forsciint.2019.109959
However, the Moosmann data suggesting minimal metabolism imply this interaction pathway may be of limited significance for pyrazolam specifically.supported
No detectable metabolites in serum/urine. Excreted largely unchanged. s11419-013-0187-4
Stimulant combinations: Abouchedid et al. (2018) found that 16.1% of pyrazolam-related forum discussions concerned use as a stimulant comedown aidpartially supported
Primary motivations: anxiolysis 53%, sedation/sleep 11%, stimulant withdrawal 10.1%, euphoria 6.1%, functional capacity 8.5%. s13181-018-0659-3
pharmacology14 · 13 ok
It binds at the classical benzodiazepine site located at the α+/γ2− subunit interface, enhancing the inhibitory effect of endogenous GABA by increasing the frequency of chloride ion channel opening without directly gating the channel.supported
In vitro γ-aminobutyric acid A (GABAA) receptor activity and binding interactions at the α+/γ2– interface of 53 prescription and designer benzodiazepines s42004-026-02001-x
This subtype selectivity profile has functional consequences: α1-mediated effects include sedation, amnesia, and ataxia, while α2 and α3 subunits mediate anxiolysis and, to a lesser extent, muscle relaxationsupported
α1 mediates sedation; α2/α3 mediate anxiolysis; α5 associated with cognitive effects. α2/α3-selective PAMs developed as non-sedating anxiolytics. acs.jmedchem.9b01312
Claim in pharmacology — inconclusiveinconclusiveworking →
The α2/α3 selectivity claim rests on three converging lines of evidence: (1) the 2026 in vitro GABA-A receptor study characterizing 53 benzodiazepines at α1β2γ2 assemblies, which found pyrazolam to be equally potent as bromazolam but significantly less efficacious — consistent with partial or subtype-selective engagement at α1; (2) structure-activity data from Golani et al., who demonstrated that the closely related compound SH-TRI-108 (differing from pyrazolam only at the 8-position: 8-ethynyl vs. 8-bromo) exhibited a 25-fold functional potency difference between α1β3γ2 and α2β3γ2 subtypes; and (3) the subjective effects profile reported by users, which consistently identifies pronounced anxiolysis with limited sedation, a pattern mechanistically consistent with α2/α3-preferring compounds.supported
Pyrazolam (compound 38) was equally as potent as bromazolam but significantly less efficacious. Positive allosteric modulators show wide variation in potency and efficacy. s42004-026-02001-x
The α2/α3 selectivity claim rests on three converging lines of evidence: (1) the 2026 in vitro GABA-A receptor study characterizing 53 benzodiazepines at α1β2γ2 assemblies, which found pyrazolam to be equally potent as bromazolam but significantly less efficacious — consistent with partial or subtype-selective engagement at α1; (2) structure-activity data from Golani et al., who demonstrated that the closely related compound SH-TRI-108 (differing from pyrazolam only at the 8-position: 8-ethynyl vs. 8-bromo) exhibited a 25-fold functional potency difference between α1β3γ2 and α2β3γ2 subtypes; and (3) the subjective effects profile reported by users, which consistently identifies pronounced anxiolysis with limited sedation, a pattern mechanistically consistent with α2/α3-preferring compounds.supported
SH-TRI-108 (8-ethynyl-1-methyl-6-(pyridin-2-yl) analog of pyrazolam) showed 25-fold functional potency difference between α1 and α2 subtypes. fphar.2021.625233
The sole published human pharmacokinetic data for pyrazolam derive from a self-administration study by Moosmann et al. (2013), in which one of the authors ingested 1 mg orally (two 0.5 mg tablets).supported
Self-administration study (1 mg oral): elimination half-life ~17 hours (vendor claimed 6h). s11419-013-0187-4
The elimination half-life was approximately 17 hourssupported
elimination half-life ~17 hours (vendor claimed 6h) s11419-013-0187-4
The elimination half-life was approximately 17 hourssupported
Half-life ~17h (3x longer than vendor-advertised). s13181-018-0659-3
This value is substantially longer than the 6-hour half-life advertised by vendors at the time of the study — a discrepancy noted explicitly by Abouchedid et al.supported
Half-life ~17h (3x longer than vendor-advertised). s13181-018-0659-3
Pyrazolam remained detectable in serum for more than 50 hours and in urine for up to 6 days following a single 1 mg dose.supported
Detectable in serum >50h, urine up to 6 days. s11419-013-0187-4
Moosmann et al. (2013) detected no metabolites in serum or urine after their 1 mg self-administration, concluding that pyrazolam is excreted largely unchangedsupported
No detectable metabolites in serum/urine. Excreted largely unchanged. s11419-013-0187-4
Pettersson Bergstrand et al. (2018), analyzing urine from real-world intoxication cases, identified a parent glucuronide as the most abundant urinary metabolite, alongside mono-hydroxy metabolites and their glucuronide conjugatessupported
Main urinary metabolites of pyrazolam: parent glucuronide, mono-hydroxy metabolites, mono-hydroxy glucuronides. Parent glucuronide is the most common metabolite without enzymatic hydrolysis. dta.2243
A subsequent in vitro study by the same group (2019), using pooled human liver microsomes, failed to detect UGT1A4- or other UGT-mediated glucuronidation of pyrazolamsupported
Pyrazolam glucuronides were not detected in incubations with individual UGTs or pooled human liver microsomes, suggesting no significant direct glucuronidation. dta.2463
The blood-to-plasma ratio was addressed by Manchester et al. (2022) in a QSAR study of designer benzodiazepines, though the specific numerical value for pyrazolam was not extracted from the available abstract.supported
Blood-to-plasma ratio and QSAR-predicted GABA-A receptor binding affinity for multiple designer BZDs. s11419-022-00616-y
summary11 · 8 ok
Pyrazolam (8-bromo-1-methyl-6-pyridin-2-yl-4H-triazolo-benzodiazepine) is a triazolobenzodiazepine derivative and positive allosteric modulator of the GABA-A receptor, active at oral doses of 0.5–3 mg with a subjective effects duration of 5–8 hourspartially supported
Recreational doses 0.5-4mg. Half-life ~17h (3x longer than vendor-advertised). s13181-018-0659-3
Claim in summary — inconclusiveinconclusiveworking →
It resurfaced in 2012 as one of the earliest designer benzodiazepines sold through online research chemical vendors, an event that Moosmann et al. described as marking "the beginning of designer benzodiazepines being sold as recreational drugs or self-medication"supported
Documents that pyrazolam appeared on internet shops selling research chemicals in 2012, marking the beginning of designer BZDs sold as recreational drugs. jms.3279
Claim in summary — inconclusiveinconclusiveworking →
Pyrazolam acts at the classical benzodiazepine binding site at the α+/γ2− interface of GABA-A receptorssupported
In vitro γ-aminobutyric acid A (GABAA) receptor activity and binding interactions at the α+/γ2– interface of 53 prescription and designer benzodiazepines s42004-026-02001-x
Structure-activity studies of closely related 8-substituted triazolobenzodiazepines demonstrate that modifications at the 8-position modulate α1 subunit engagement, providing a mechanistic basis for pyrazolam's anxiolytic-selective profilesupported
SH-TRI-108 showed 25-fold functional potency difference between α1 and α2 subtypes. 8-position substitution affects α1 C-loop binding. fphar.2021.625233
As a GABA-A positive allosteric modulator, the compound carries the class-wide risk profile of respiratory depression when combined with other CNS depressants — the single published fatality involving pyrazolam was a polydrug death attributed to positional asphyxiasupported
Cause of death: positional asphyxia from poly-drug intoxication including designer benzodiazepines and synthetic stimulants. j.forsciint.2019.109959
Claim in summary — inconclusiveinconclusiveworking →
The pharmacokinetic profile remains incompletely characterized: a single self-administration study established an elimination half-life of approximately 17 hours, but the metabolic fate of pyrazolam is the subject of an unresolved three-way contradiction in the published literature.supported
Self-administration study (1 mg oral): elimination half-life ~17 hours (vendor claimed 6h). No detectable metabolites in serum/urine. Excreted largely unchanged. s11419-013-0187-4
The pharmacokinetic profile remains incompletely characterized: a single self-administration study established an elimination half-life of approximately 17 hours, but the metabolic fate of pyrazolam is the subject of an unresolved three-way contradiction in the published literature.supported
Main urinary metabolites of pyrazolam: parent glucuronide, mono-hydroxy metabolites, mono-hydroxy glucuronides. Parent glucuronide is the most common metabolite without enzymatic hydrolysis. dta.2243
The pharmacokinetic profile remains incompletely characterized: a single self-administration study established an elimination half-life of approximately 17 hours, but the metabolic fate of pyrazolam is the subject of an unresolved three-way contradiction in the published literature.supported
Pyrazolam glucuronides were not detected in incubations with individual UGTs or pooled human liver microsomes, suggesting no significant direct glucuronidation. dta.2463
pharmacokinetic-detail9 · 7 ok
These values derive from a single self-administration study (n = 1, dose = 1 mg oral)supported
Self-administration study (1 mg oral): elimination half-life ~17 hours (vendor claimed 6h). s11419-013-0187-4
Femoral blood concentration was 28 µg/L (28 ng/mL) in a polydrug death involving pyrazolam, diclazepam, 3-fluorophenmetrazine, amphetamine, and caffeinesupported
Femoral blood pyrazolam 28 µg/L. Higher concentrations in tissues than blood. Cause of death: positional asphyxia from poly-drug intoxication including designer benzodiazepines and synthetic stimulants. j.forsciint.2019.109959
Claim in pharmacokinetic-detail — inconclusiveinconclusiveworking →
Claim in pharmacokinetic-detail — inconclusiveinconclusiveworking →
Vendors advertised a half-life of approximately 6 hours at the time pyrazolam entered the market — roughly three times shorter than the measured valuesupported
Half-life ~17h (3x longer than vendor-advertised). s13181-018-0659-3
The authors concluded that pyrazolam is excreted largely in unchanged form.supported
Excreted largely unchanged. s11419-013-0187-4
In vitro incubation of pyrazolam with pooled human liver microsomes expressing UDP-glucuronosyltransferases (UGTs) failed to produce detectable glucuronide conjugates, including via UGT1A4 — the enzyme most commonly responsible for N-glucuronidation of benzodiazepinessupported
Pyrazolam glucuronides were not detected in incubations with individual UGTs or pooled human liver microsomes, suggesting no significant direct glucuronidation. Metabolism of related DBZDs primarily via UGT1A4. dta.2463
In the 2026 acute poisoning case reported by Magny et al., plasma pyrazolam concentration was 500 ng/mL at 5 hours post-ingestion, declining to 270 ng/mL at 72 hourssupported
Plasma pyrazolam 500 ng/mL at 5h post-ingestion, decreasing to 270 ng/mL at 72h. s11419-025-00750-3
Confirmatory identification requires LC-MS/MS or LC-HRMSsupported
LC-HRMS method for 28 NPS BZDs in urine. Pyrazolam detected in patient urine samples. j.clinms.2018.08.004
clinical-evidence6 · 6 ok
The sole controlled human exposure data derive from the Moosmann et al. (2013) self-administration study, in which a single investigator ingested 1 mg orally and provided serial blood and urine samples for pharmacokinetic analysissupported
Self-administration study (1 mg oral): elimination half-life ~17 hours (vendor claimed 6h). No detectable metabolites in serum/urine. s11419-013-0187-4
Abouchedid et al. (2018) analyzed online forum posts to characterize availability, cost, and user motivations for pyrazolam use in the UK, identifying anxiolysis as the primary self-reported motivation (53% of coded posts) and documenting recreational dose ranges of 0.5–4 mg.supported
Recreational doses 0.5-4mg. Primary motivations: anxiolysis 53%, sedation/sleep 11%, stimulant withdrawal 10.1%, euphoria 6.1%, functional capacity 8.5%. s13181-018-0659-3
Høiseth et al. (2016) detected pyrazolam in blood samples from drugged drivers and criminal offenders in Norway, correlating blood concentrations with clinical impairment.supported
Blood concentrations of new designer benzodiazepines in drugged drivers and criminal offenders; relates concentrations to clinical impairment. j.forsciint.2016.09.006
The compound has never been approved as a pharmaceutical product in any jurisdiction and has never entered formal clinical development.supported
Review of NPS benzodiazepines; notes pyrazolam among first commercial NPS BZDs. dta.2211
The compound has never been approved as a pharmaceutical product in any jurisdiction and has never entered formal clinical development.supported
Pyrazolam among first designer BZDs online alongside diclazepam and flubromazepam. wps.20236
Bäckberg et al. (2019) identified pyrazolam in clinical intoxication cases through the Swedish STRIDA project, providing emergency department presentation data.supported
Bioanalytical and clinical data on NPS BZD intoxications from the Swedish STRIDA project. Pyrazolam detected in clinical intoxication cases. 15563650.2018.1506130
comparative-pharmacology5 · 3 ok
Pyrazolam requires doses in the 0.75–3 mg range for comparable subjective intensity, and the qualitative character differs — users consistently describe pyrazolam's effects as more "functional" and less cognitively impairing at anxiolytic-equivalent doses.partially supported
Recreational doses 0.5-4mg. Primary motivations: anxiolysis 53%, sedation/sleep 11%, stimulant withdrawal 10.1%, euphoria 6.1%, functional capacity 8.5%. s13181-018-0659-3
Claim in comparative-pharmacology — inconclusiveinconclusiveworking →
In the 2026 α1β2γ2 GABA-A receptor assay, pyrazolam demonstrated potency equivalent to bromazolam but significantly lower efficacysupported
Pyrazolam (compound 38) was equally as potent as bromazolam but significantly less efficacious. s42004-026-02001-x
Claim in comparative-pharmacology — inconclusiveinconclusiveworking →
Pyrazolam's metabolic fate remains unresolved, but the Moosmann data suggesting minimal hepatic metabolism would, if confirmed, represent a clinically meaningful departure from the metabolic profile of its closest structural relativesupported
No detectable metabolites in serum/urine. Excreted largely unchanged. s11419-013-0187-4
history5 · 3 ok
Pyrazolam resurfaced in approximately 2012 when it appeared for sale through online vendors marketing "research chemicals." Moosmann et al. documented this emergence in a 2013 publication on flubromazepam, explicitly noting: "The appearance of pyrazolam in Internet shops selling 'research chemicals' in 2012 marked the beginning of designer benzodiazepines being sold as recreational drugs or 'self medication'"supported
Documents that pyrazolam appeared on internet shops selling research chemicals in 2012, marking the beginning of designer BZDs sold as recreational drugs. jms.3279
Pyrazolam, diclazepam, and flubromazepam constituted the first wave of designer benzodiazepines available onlinesupported
Pyrazolam among first designer BZDs online alongside diclazepam and flubromazepam. wps.20236
Claim in history — inconclusiveinconclusiveworking →
Claim in history — inconclusiveinconclusiveworking →
The United Kingdom classified pyrazolam as a Class C, Schedule 2 substance under the Misuse of Drugs Act 1971 in June 2017, alongside diclazepam, flubromazepam, and etizolamsupported
Classified Class C, Schedule 2 since June 2017 in UK. s13181-018-0659-3
neuroscience5 · 4 ok
Claim in neuroscience — inconclusiveinconclusiveworking →
Pyrazolam represents a de facto probe of the anxioselective hypothesis — the proposition that anxiolysis can be pharmacologically separated from sedation, amnesia, and abuse liability through subtype-selective GABA-A modulationsupported
α2/α3-selective PAMs developed as non-sedating anxiolytics. acs.jmedchem.9b01312
Pyrazolam, as an unintentionally subtype-preferring compound used extensively in non-clinical settings, provides indirect human evidence for the validity of the concept — users consistently report the predicted dissociation of anxiolysis from sedation and euphoria.supported
Primary motivations: anxiolysis 53%, sedation/sleep 11%, euphoria 6.1%. s13181-018-0659-3
Metabolic pathway resolution: Does pyrazolam undergo glucuronidation in vivo, and if so, by which UGT isoform? The three-way contradiction in the published literature requires resolution — ideally through a controlled human pharmacokinetic study with modern analytical sensitivity.supported
No detectable metabolites in serum/urine. Excreted largely unchanged. s11419-013-0187-4
Metabolic pathway resolution: Does pyrazolam undergo glucuronidation in vivo, and if so, by which UGT isoform? The three-way contradiction in the published literature requires resolution — ideally through a controlled human pharmacokinetic study with modern analytical sensitivity.supported
Main urinary metabolites of pyrazolam: parent glucuronide, mono-hydroxy metabolites, mono-hydroxy glucuronides. dta.2243
receptor-pharmacology5 · 4 ok
The binding site is located at the interface between the α and γ2 subunits (α+/γ2− interface).supported
In vitro γ-aminobutyric acid A (GABAA) receptor activity and binding interactions at the α+/γ2– interface of 53 prescription and designer benzodiazepines s42004-026-02001-x
The most informative in vitro data come from a 2026 study that characterized 53 prescription and designer benzodiazepines in a standardized α1β2γ2 GABA-A receptor assaysupported
In vitro GABA-A receptor activity assay of 53 benzodiazepines. s42004-026-02001-x
Golani et al. (2021) systematically studied 8-substituted triazolobenzodiazepine analogs sharing pyrazolam's core scaffoldsupported
8-substituted analogs of triazolam (same scaffold as pyrazolam) evaluated for GABA-A subtype selectivity. fphar.2021.625233
A compound with low α1 efficacy and preserved α2/α3 activity would be predicted to produce anxiolysis with attenuated sedation, amnesia, and euphoria — precisely the profile that users and analysts consistently attribute to pyrazolam.supported
Primary motivations: anxiolysis 53%, sedation/sleep 11%, stimulant withdrawal 10.1%, euphoria 6.1%, functional capacity 8.5%. s13181-018-0659-3
Claim in receptor-pharmacology — inconclusiveinconclusiveworking →
chemistry1 · 0 ok
Claim in chemistry — inconclusiveinconclusiveworking →
effects-overview1 · 1 ok
The anxiolytic effect is described as "clean" or "pure" — a reduction of baseline anxiety without the accompanying euphoria, heavy sedation, or cognitive fog associated with non-selective benzodiazepines such as alprazolam or clonazolamsupported
Primary motivations: anxiolysis 53%, sedation/sleep 11%, stimulant withdrawal 10.1%, euphoria 6.1%, functional capacity 8.5%. s13181-018-0659-3