5F-PB-22
Viewing r1 — May 11, 2026 — CURRENT
Back to HistoryInteractions, related substances, and reports reflect the current entry and are not shown for historical revisions.
5F-PB-22 — also known as 5F-QUPIC — is a synthetic cannabinoid of the indole-3-carboxylate class. It is a fluorinated structural analog of PB-22, distinguished by extreme CB1 potency.[1] 5F-PB-22 is a full agonist at CB1 cannabinoid receptors, producing its effects by overriding the brain's endocannabinoid signaling without the self-limiting ceiling present in cannabis.
Psychedex is in open beta. We are still fine-tuning the generation and review process. Please double-check sources.
5F-PB-22 appeared on recreational "Spice" markets in 2012–2013 as a structurally novel synthetic cannabinoid — the first to combine an ester bond with a quinoline substructure.[2] Its scaffold was sufficiently distinct from previously controlled compounds to evade existing analog act provisions, prompting rapid scheduling responses worldwide. The compound was permanently placed in United States Schedule I in 2016[3] and is now internationally controlled under the 1971 UN Convention.
Subjective effects include euphoria, sedation, perceptual distortion, and cognitive impairment. The experience resembles an intensified cannabis intoxication compressed into a narrow dose range, where the margin between desired effects and dangerous overdose is razor-thin. Anxiety, paranoia, and acute agitation are characteristic unsought effects.
Dependence liability is moderate at the class level, with cross-tolerance to other cannabinoids.[4] Postmortem blood concentrations in fatal cases overlap substantially with those in surviving individuals[5][6] — tolerance, polydrug use, and individual variation determine whether a given dose is survivable. No controlled human studies have been conducted; the evidence base rests on forensic casework, in vitro pharmacology, and animal data.
History[edit]
Discovery and market emergence
PB-22, the non-fluorinated parent compound, was first identified in herbal blend seizures in Japan between 2012 and 2013. 5F-PB-22, its terminally fluorinated structural analog, followed rapidly onto commercial "Spice" markets — the first synthetic cannabinoid class to combine an ester bond linkage with a quinoline substructure.[2] No academic researcher is credited with its deliberate synthesis; the compound's origin is consistent with clandestine production targeting regulatory gaps.
Regulatory response
The United States Drug Enforcement Administration placed 5F-PB-22 under temporary Schedule I control in January 2014, alongside PB-22, AB-FUBINACA, and ADB-PINACA.[7] Permanent scheduling followed in September 2016,[3] with the United Kingdom, China, and the United Nations enacting controls between 2015 and 2018.[8] The scheduling pace — from first market detection to US temporary placement in under two years — reflected heightened regulatory awareness of the evolving designer drug landscape.
Context of use
5F-PB-22 reached users primarily through herbal blend products sold online and in head shops, and through synthetic cannabinoid-infused paper circulated in prisons.[9] The compound's extreme potency — active in the low-milligram range — made it well-suited for covert application to paper substrates at concentrations sufficient for psychoactive effects from small pieces. In the United States, forensic identification in postmortem cases during 2013 linked 5F-PB-22 to the herbal product marketed as "Psyclone".[5]
The compound circulates under two naming conventions: 5F-PB-22 in Western forensic literature and 5F-QUPIC in Japanese analytical reports, reflecting parallel identification on either side of the Pacific. The brand name "Psyclone" became briefly notorious in 2013 when it was linked to multiple fatalities in the United States.[5] Unlike earlier-generation synthetic cannabinoids such as JWH-018, 5F-PB-22 never acquired widespread street slang — its market lifespan was compressed by rapid scheduling.
Chemistry[edit]
Structural class
5F-PB-22 belongs to the indole-3-carboxylate structural class of synthetic cannabinoids, specifically the quinolinyl ester subgroup. Three modular components define the architecture: an indole core bearing a 3-carboxylate group, esterified to a quinolin-8-yl ring system, with a 5-fluoropentyl chain at the indole nitrogen.
The ester bond is the defining structural feature, distinguishing PB-22-type compounds from the amide-linked and ketone-linked cannabinoid classes (e.g., JWH-series, AM-series). This bond is susceptible to hydrolysis by carboxylesterases — a property that governs the compound's metabolic fate and limits its duration of action.[10]
The parent compound PB-22 (QUPIC) lacks the terminal fluorine; 5F-PB-22 differs only by a fluorine atom at the 5-position of the N-pentyl chain. Ten positional isomers exist, incorporating quinolinyl and isoquinolinyl substitution variants, not all of which are scheduled under current legislation.[11]
Molecular properties
| Molecular formula | C₂₃H₂₁FN₂O₂ |
| Molecular weight | 376.4 g/mol |
The 5-fluoropentyl chain provides a terminal carbon–fluorine bond that modulates lipophilicity and receptor binding relative to the non-fluorinated parent. The compound is highly lipophilic (logP 5.80–6.74),[6] which promotes efficient brain penetration but makes parent compound detection in urine unreliable at standard testing thresholds.
Stereochemistry
5F-PB-22 contains no chirality centers and exists as a single achiral species. No stereoisomeric considerations apply to its pharmacological activity. Crystal structure has been determined by X-ray diffraction.[12]
Pharmacology[edit]
Mechanism of action
5F-PB-22 is a full agonist at both CB1 and CB2 cannabinoid receptors, with particularly strong activity at CB1.[1] Full agonism means the compound drives maximal receptor activation — unlike THC in cannabis, which is a partial agonist with a built-in ceiling on its effects. This distinction is central to the compound's risk profile: there is no pharmacological brake on receptor stimulation as dose increases.
CB1 dependence of all pharmacological effects has been confirmed by two convergent lines of evidence: the CB1 blocker AM251 abolishes the compound's activity entirely, and no effects are observed in mice lacking CB1 receptors.[1] The compound also activates CB2 receptors, though with approximately four-fold lower potency.[13]
As a potent full CB1 agonist, 5F-PB-22 may engage additional targets shared across the synthetic cannabinoid class, including orphan receptors GPR55 and GPR18, PPARs, and TRPV1 channels.[14] No published data directly characterize 5F-PB-22 activity at any of these non-cannabinoid targets.
Dopamine and reward
In animal studies, 5F-PB-22 significantly increased dopamine release in the nucleus accumbens shell — the brain region most closely associated with reward and compulsive drug-seeking — but not in other dopamine-rich areas.[1] This selective pattern is a pharmacological signature of abuse liability and was completely abolished by CB1 blockade, confirming the effect is mediated through cannabinoid receptors.
Pharmacokinetics
No human pharmacokinetic study has been published for 5F-PB-22. Key parameters — oral bioavailability, plasma half-life, time to peak concentration, and protein binding — remain uncharacterized.
The compound's high lipophilicity (logP 5.80–6.74) predicts extensive tissue distribution and efficient brain penetration.[6] Parent compound is functionally absent from urine in routine drug testing because its lipophilicity exceeds the threshold for reliable urinary detection.
Metabolism
The primary metabolic pathway is rapid ester hydrolysis by carboxylesterase 1 (CES1) in the liver.[10] This hydrolysis produces the 3-carboxyindole metabolite, which is the major urinary marker used in forensic detection (urinary concentrations 8.25–880 ng/mL).[15] Additional metabolic routes include chain hydroxylation, omega-oxidation, oxidative defluorination, and glucuronide conjugation.[2][16]
When alcohol is present, liver enzymes catalyze a transesterification reaction converting 5F-PB-22 to its ethyl ester — a unique metabolite confirmed in both laboratory studies[17] and postmortem blood at 0.4 μg/L.[18] The ethyl ester has reduced receptor activity compared to the parent compound but serves as a forensic marker of concurrent alcohol and synthetic cannabinoid consumption.
Hydroxylated metabolites of structurally related synthetic cannabinoids retain full activity at CB1 and CB2 receptors, though with reduced potency.[19] Active metabolites may therefore contribute to both the duration and toxicity of 5F-PB-22 in vivo.
Neuroscience[edit]
Where it acts
5F-PB-22 acts through CB1 receptors concentrated on nerve terminals in the hippocampus, basal ganglia, cerebellum, and prefrontal cortex — regions governing memory, movement, coordination, and decision-making. Activation suppresses neurotransmitter release at these synapses, disrupting the balance between excitatory and inhibitory signaling that underlies normal cognition and motor control.
The compound selectively stimulates dopamine release in the nucleus accumbens shell via the ventral tegmental area pathway[1] — the brain's core reward circuit. This selective activation maps onto the "wanting" component of addiction: the compulsive motivation to seek the drug, distinct from the hedonic pleasure of taking it.
Why it matters
The endocannabinoid system normally operates through on-demand release of partial agonists (anandamide and 2-AG) that fine-tune neural signaling. 5F-PB-22 overrides this calibration with supraphysiological full agonism, flooding a system designed for delicate self-regulation. The absence of CBD — which in cannabis provides a counterbalancing brake on CB1 activation[20] — removes an additional regulatory mechanism.
In cell cultures, 5F-PB-22 at biologically relevant concentrations doubled neuronal differentiation and neurite outgrowth through a CB1-dependent mechanism.[21] This raises concern for developing brains, where endocannabinoid signaling guides the wiring of neural circuits during critical periods of prenatal and early postnatal development.
Does rapid ester hydrolysis limit how much intact 5F-PB-22 actually reaches the brain? The gap between extreme potency in the test tube and moderate potency in animal models suggests rapid metabolic breakdown, but the relative contributions of parent compound versus active metabolites to human effects and toxicity remain unknown.
Subjective Effects[edit]
The 5F-PB-22 experience is cannabis-like in character — sedation, euphoria, perceptual softening, cognitive slowing — but compressed into a far narrower dose range with a steeper escalation curve. Full CB1 agonism, without the partial-agonist ceiling of THC or the moderating influence of CBD, means there is no pharmacological brake: effects intensify proportionally with dose until toxicity intervenes. Tolerance state, individual sensitivity, and batch-to-batch variability in herbal blend products all modulate the experience unpredictably.
Relative to JWH-018 and other earlier-generation synthetic cannabinoids, users familiar with those compounds should expect qualitatively similar effects at substantially lower doses. The margin between a desired experience and a medical emergency is markedly reduced — a distinction that defines the risk profile of potent full agonists across the synthetic cannabinoid class.
Effect Grid
Clear cannabis-like intoxication with full CB1 agonist intensity. Euphoria is pronounced, accompanied by sedation and cognitive slowing. Thought deceleration and analysis suppression become obvious. Immersion enhancement may deepen engagement with media or music. Perceptual shifts include color enhancement, music enhancement, and mild vestibular distortion.
Physically, motor control impairment is noticeable — coordination and reaction time are reduced. Bodily heaviness is prominent. Appetite enhancement is reliable. Heart rate elevation (abnormal heartbeat) may become perceptible. Spontaneous body sensations and dehydration sensation are common.
Anxiety and paranoia are possible, especially in naive users, unfamiliar settings, or at the upper end of this range. The compressed margin between desired effects and toxicity makes careful dosing essential.
Modeled from the effect's dose-dependence curve — not per-substance measurements.
Perspective distortion · Proprioceptive distortion · Sound sensitivity · Vestibular distortion · Visual acuity suppression · Visual haze / noise · Taste enhancement · Light sensitivity · Color enhancement · Visual breathing · Visual drifting · Visual processing suppression · Auditory hallucinations · External hallucinations
Visual acuity suppression · Visual haze / noise · Taste enhancement · Light sensitivity · Color enhancement · Visual breathing · Visual drifting · Visual processing suppression · Auditory hallucinations · External hallucinations
Dizziness · Heart rate perception changes · Muscle relaxation · Physical fatigue · Appetite enhancement · Bodily heaviness · Headache · Laughter fits · Nausea · Pain suppression · Restlessness · Spontaneous body sensations · Tactile euphoria · Bodily pressures · Body schema distortion · Constipation · Excessive sweating · Nausea suppression · Tingling / electric sensations · Trembling · Vibrations / buzzing · Vomiting · Breathing alteration · Pupil dilation · Involuntary body movements · Nystagmus (eye wobbles) · Stimulation · Bodily dissociation · Tactile hallucination
Appetite enhancement · Bodily heaviness · Headache · Laughter fits · Nausea · Pain suppression · Restlessness · Spontaneous body sensations · Tactile euphoria · Bodily pressures · Body schema distortion · Constipation · Excessive sweating · Nausea suppression · Tingling / electric sensations · Trembling · Vibrations / buzzing · Vomiting · Breathing alteration · Pupil dilation · Involuntary body movements · Nystagmus (eye wobbles) · Stimulation · Bodily dissociation · Tactile hallucination
Confusion · Focus suppression · Information processing suppression · Memory fragmentation · Thought disorganization · Analysis suppression · Motivation suppression · Thought deceleration · Thought loops · Aesthetic enhancement · Cognitive dysphoria · Cognitive euphoria · Delusions of sobriety · Immersion enhancement · Introspection enhancement · Language suppression · Novelty enhancement · Openness enhancement · Suggestibility enhancement · Creativity enhancement · Humor enhancement · Conceptual thinking · Multiple thought streams · Pattern recognition enhancement · Thought connectivity · Amnesia · Delirium · Delusions
Memory fragmentation · Thought disorganization · Analysis suppression · Motivation suppression · Thought deceleration · Thought loops · Aesthetic enhancement · Cognitive dysphoria · Cognitive euphoria · Immersion enhancement · Introspection enhancement · Language suppression · Novelty enhancement · Openness enhancement · Suggestibility enhancement · Creativity enhancement · Humor enhancement · Conceptual thinking · Multiple thought streams · Pattern recognition enhancement · Thought connectivity · Amnesia · Delirium · Delusions
Emotional enhancement · Emotional lability · Irritability · Simultaneous emotions · Anxiety suppression
Anxiety suppression
Disinhibition · Emotional susceptibility · Social connection · Flow state · Sociability enhancement · Communication enhancement · Cognitive disconnection
Sociability enhancement · Communication enhancement · Cognitive disconnection
Timeline
Onset timing is unpredictable via oral route. First effects emerge gradually — subtle mood shift and mild body awareness. Gastrointestinal absorption and first-pass CES1 metabolism introduce variability.
Full cannabinoid intoxication — euphoria, sedation, cognitive impairment, and perceptual distortion at maximum intensity. Duration and peak timing are poorly characterized for oral administration.
Effects gradually return toward baseline within total 2–3 hour window. Residual sedation and cognitive slowing may persist.
⚠ Do not drive or operate machinery for at least 4 hours after oral ingestion.
Safety[edit]
- Acute toxicity
- High
- Chronic toxicity
- Moderate
- Withdrawal
- Moderate
- Tolerance buildup
- moderate
- Tolerance reset
- 10.5 days
- Physical
- Moderate
- Psychological
- Moderate
- Compulsive redosing
- Moderate
- Dose escalation
- Moderate
- Cross-tol.
- cannabinoids
Toxicity
No lethal dose has been established for 5F-PB-22 in any species.safety citation needed
Acute toxicity
Multiple fatalities have been attributed to 5F-PB-22. In the United States, four postmortem cases reported abrupt sudden death at blood concentrations of 1.1–1.5 ng/mL.[5] A German fatality involved a blood concentration of just 0.37 ng/mL with alcohol co-detected.[22] In the United Kingdom, combined alcohol (311 mg/100 mL) and synthetic cannabinoid toxicity was certified as the cause of death.[23]
Blood concentrations in impaired but surviving individuals (0.10–5.0 ng/mL) overlap substantially with fatal cases (0.37–1.5 ng/mL).[6][5] There is no reliably "safe" blood level — individual tolerance, polydrug use, and postmortem redistribution confound any attempt to define one.
Class-level adverse effects
A systematic review of approximately 4,000 synthetic cannabinoid presentations reports the following class-level profile[24]:
- Common: Rapid heart rate (37–77% of presentations), agitation (16–41%), nausea (13–94%). Most presentations resolve with supportive care within 8 hours.
- Severe: Heart attack, stroke, blood clots, acute kidney injury, seizures, first-episode psychosis, self-harm, severe vomiting, muscle breakdown.
- Rare/critical: Multiple organ failure,[25] bleeding in the brain, bleeding disorders (associated with contaminated products).
Neurodevelopmental risk
CB1-mediated enhancement of neuronal growth at biologically relevant concentrations in cell cultures[21] raises concern for prenatal and early developmental exposure. No human or animal developmental toxicity studies have been published for 5F-PB-22.
Psychological risks
Full CB1 agonism without co-present CBD substantially increases psychosis risk compared to cannabis.[20] Class-level data identify first-episode psychosis, paranoia, and acute agitation as recognized psychiatric complications of synthetic cannabinoid use.[24] The extreme potency of 5F-PB-22 may compress the dose range at which psychotic symptoms emerge.
Anxiety, Paranoia, and delusions are reported in community data for this compound but have not been characterized under controlled conditions.
Tolerance and dependence
No published study has directly measured tolerance development for 5F-PB-22. Class-level cannabinoid pharmacology predicts CB1 receptor downregulation with repeated full agonist exposure, with estimated full tolerance reset at approximately 1.5 weeks.safety citation needed
Physical and psychological dependence have been documented for synthetic cannabinoids as a class. Regular users meeting dependence criteria have been described, and synthetic cannabinoid use has been reported to relieve cannabis withdrawal symptoms — confirming cross-dependence.[4] Withdrawal symptoms include Anxiety, Nausea, insomnia, and irritability.[26]
Tolerance is a critical confounder in interpreting blood concentrations from fatal cases. Blood levels cannot be judged as toxic or lethal without accounting for tolerance from frequent use.[22]
Drug interactions
The most dangerous documented interaction is with alcohol. Three independent lines of evidence establish the risk:
- Additive depression: Both substances depress the central nervous system; co-use produces additive respiratory and cardiovascular suppression.
- Unique metabolic interaction: liver enzymes convert 5F-PB-22 into a novel compound (ethyl ester) when alcohol is present.[18][17]
- Fatality data: Fatal cases have involved very high blood alcohol levels.[23][22]
Additive or synergistic central nervous system depression is expected with co-use of opioids, benzodiazepines, and other sedatives based on class pharmacology. Multiple CNS-active substances were co-detected in fatality case series.[22]
Contraindications
No substance-specific contraindication data exist for 5F-PB-22. The following are inferred from CB1 full agonist pharmacology and class-level adverse event data:
- Heart conditions (absolute): Full CB1 agonism produces rapid heart rate and may trigger heart attacks or dangerous rhythm disturbances.[24]inferred
- Psychotic disorders or family history of psychosis (absolute): Full CB1 agonism without CBD substantially elevates psychosis risk.[20]inferred
- Concurrent alcohol use (absolute): Documented fatalities and a unique metabolic interaction establish this as a high-risk combination.[18][23]inferred
- Pregnancy (absolute): In vitro evidence of CB1-mediated effects on neuronal development raises concern.[21]inferred
- Liver impairment (relative): The primary breakdown enzyme (CES1) is hepatic; impaired function could prolong exposure to the parent compound.inferred
- Kidney impairment (relative): Acute kidney injury is reported in class-level synthetic cannabinoid data.[24]inferred
- Seizure disorders (relative): Seizures are reported in synthetic cannabinoid presentations.[24]inferred
Harm Reduction[edit]
Forms & Identification
5F-PB-22 is rarely encountered as a pure substance. It reaches users almost exclusively through herbal blends ("Spice") where the compound has been dissolved in solvent and sprayed onto inert plant material, or infused into paper for use in custodial settings.[9] In both cases, dosing precision is impossible — concentration varies between batches, within a single batch, and even across different areas of the same piece of paper or herbal material.
Standard immunoassay drug tests (urine dip tests for "cannabis") may not detect synthetic cannabinoids. The compound's extreme lipophilicity means parent compound is nearly undetectable in urine; forensic confirmation requires specialized laboratory testing targeting specific metabolites.[15]
Guidelines
- Start with the smallest possible amount — a single shallow inhalation from herbal material, or a portion of infused paper far smaller than what others may suggest.
- Wait at least 15 minutes before considering any additional dose. Full intensity may not be apparent immediately.
- Never use alone. The margin between intoxication and medical emergency is narrow enough that a sober observer who can call for help is a critical safety measure.
- Avoid all alcohol before, during, and after use. The combination has been directly linked to fatalities and creates a unique toxic metabolite in the body.[18]
- Avoid all other sedatives, including opioids and benzodiazepines.
- Do not drive or operate machinery. Blood concentrations associated with impairment overlap with those found in fatal cases.[6]
Set & Setting
The compressed dose-response curve of 5F-PB-22 means that environmental and psychological preparation carry less protective value than they do for substances with wider safety margins. A calm, familiar environment with a sober companion present is the minimum baseline. The rapid onset via inhalation — the most common route — means that acute crises can develop quickly and without warning.
Aftercare & integration. The short duration of 5F-PB-22's acute effects may create a false sense of rapid recovery. Residual cognitive impairment — thought deceleration, impaired short-term memory, and reduced coordination — can persist for hours beyond the subjective experience.
Hydration, light food, and rest in a safe environment support recovery. Avoid driving or demanding cognitive tasks for the remainder of the day. If anxiety, paranoia, or perceptual disturbances persist beyond 24 hours, seek medical evaluation — persistent symptoms may indicate the emergence of a psychiatric episode requiring professional support.
Recovery & Support
Regular synthetic cannabinoid use can produce physical and psychological dependence with a withdrawal that includes anxiety, nausea, insomnia, and irritability.[26] Withdrawal is not life-threatening but may be distressing enough to drive continued use.
Medical support for withdrawal may include benzodiazepines for symptom relief, with some clinicians reporting benefit from quetiapine.[26] Anyone experiencing difficulty stopping synthetic cannabinoid use should consult a healthcare provider or contact a substance use helpline.
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Recognizing an emergency:
- Unresponsiveness or inability to be roused
- Seizures or rigid, jerking movements
- Chest pain or clutching at the chest
- Severe agitation, self-harm, or psychotic behavior (paranoid delusions, loss of contact with surroundings)
- Vomiting while unconscious or semiconscious
Immediate steps:
- 1. Call emergency services immediately. Do not wait to see if symptoms improve.
- 2. Place an unresponsive person in the recovery position (on their side, airway clear).
- 3. Do not restrain a seizing person — clear the area of hard objects and protect the head.
- 4. Do not induce vomiting.
- 5. Stay with the person until help arrives.
What to tell the dispatcher: A synthetic cannabinoid was used (name it if known), how much and when, and what symptoms are present. Good Samaritan laws in many jurisdictions protect people who call for help during a drug emergency.
No reversal agent exists for synthetic cannabinoid overdose. Treatment is supportive care only.
Legal Status[edit]
5F-PB-22 is internationally controlled under the 1971 United Nations Convention on Psychotropic Substances (Schedule II, placed 2018).[8] Most major jurisdictions have enacted specific controls or blanket new psychoactive substance legislation covering this compound. The scheduling response — from first market appearance in 2012–2013 to United States temporary placement in January 2014 — was faster than many preceding synthetic cannabinoid scheduling cycles.
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| United States | Schedule I (Controlled Substances Act) | Temporary placement 10 January 2014;[7] permanent scheduling September 2016[3] |
| United Kingdom | Class B (Misuse of Drugs Act 1971) | December 2016 MDA amendment; also covered under Psychoactive Substances Act 2016 from 26 May 2016 |
| China | Controlled substance | Controlled from October 2015 |
| Canada | Controlled (CDSA) | Covered under quinolinyl indole-carboxylate structural class provisions |
| Australia | Prohibited import | Criminal Code Regulations |
| United Nations | Schedule II (1971 Convention) | Placed 2018[8] |
| Japan | Controlled (specific date unconfirmed) | PB-22 (parent) identified in Japanese herbal blends 2012–2013; scheduling action likely but date not confirmedcitation needed |
| European Union | Varies by member state | No EU-wide specific control; covered under blanket NPS legislation in many member states |
Ten positional isomers of 5F-PB-22 exist (quinolinyl and isoquinolinyl variants), not all of which are explicitly scheduled under current legislation. Analytical differentiation requires specialized mass spectrometry techniques.[11][27]
references
- [1] ^abcdeDe Luca MA, Castelli MP, Loi B, Porcu A, Martorelli M, Miliano C, Kellett K, Davidson C, Stair JL, Schifano F, Di Chiara G (2016) Native CB1 receptor affinity, intrinsic activity and accumbens shell dopamine stimulant properties of third generation SPICE/K2 cannabinoids: BB-22, 5F-PB-22, 5F-AKB-48 and STS-135. — Neuropharmacology doi:10.1016/j.neuropharm.2015.11.017
- [2] ^abcWohlfarth A, Gandhi AS, Pang S, Zhu M, Scheidweiler KB, Huestis MA (2014) Metabolism of synthetic cannabinoids PB-22 and its 5-fluoro analog, 5F-PB-22, by human hepatocyte incubation and high-resolution mass spectrometry. — Analytical and Bioanalytical Chemistry doi:10.1007/s00216-014-7668-0
- [3] ^abcDEA (Drug Enforcement Administration) (2016) Schedules of Controlled Substances: Placement of PB-22, 5F-PB-22, AB-FUBINACA and ADB-PINACA into Schedule I. Final rule. — Federal Register PMID:27632803
- [4] ^abGunderson EW, Haughey HM, Ait-Daoud N, Joshi AS, Hart CL (2012) "Spice" and "K2" herbal highs: a case series and systematic review of the clinical effects and biopsychosocial implications of synthetic cannabinoid use in humans — The American journal on addictions doi:10.1111/j.1521-0391.2012.00240.x
- [5]
- [6] ^abcdeKakehashi H, Shima N, Ishikawa A, Nitta A, Asai R, Wada M, Nakano S, Matsuta S, Sasaki K, Kamata H, Kamata T, Nishioka H, Miki A, Katagi M (2020) Effects of lipophilicity and functional groups of synthetic cannabinoids on their blood concentrations and urinary excretion. — Forensic Science International doi:10.1016/j.forsciint.2019.110106