6-APDB
6-(2-aminopropyl)-2,3-dihydrobenzofuran
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6-APDB (1-(2,3-dihydro-1-benzofuran-6-yl)propan-2-amine) — also known as 4-Desoxy-MDA — is a synthetic empathogen of the substituted benzofuran class. It is a structural analog of MDA with the methylenedioxy oxygen replaced by a methylene bridge. 6-APDB is a triple monoamine releasing agent, producing its effects by reversing serotonin, norepinephrine, and dopamine transporters with preferential serotonergic activity.[1]
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MDMA, MDA, 6-APB +3 moreMDMA, MDA, 6-APB, 5-APB, 5-APDB, methylone show less
Synthesized in 1993 by Nichols and colleagues at Purdue University as part of a search for non-neurotoxic MDA alternatives,[2] the compound remained a laboratory curiosity until the late 2000s when it appeared on European research chemical markets as an MDMA substitute. It is now controlled as Class B in the United Kingdom and subject to analogue legislation in several other jurisdictions.
Subjective effects include empathy enhancement, tactile euphoria, stimulation, and mild perceptual distortion. The experience is MDMA-like in character — emotional warmth and interpersonal openness dominating over stimulation — but builds more slowly and persists longer than its better-known relative.[3] Compulsive redosing urges and a post-experience mood dip from serotonin depletion are common unsought effects.
No physical dependence has been documented, but 6-APDB carries a specific cardiovascular toxicity absent from MDMA: potent 5-HT₂B receptor agonism linked to heart valve damage upon repeated use.[1][4] Unlike acute serotonergic risks shared across entactogens, this valvulopathy hazard is cumulative — damage accrues silently over repeated exposures with no warning symptoms until structural changes are established.[5] No clinical studies have been conducted; the current understanding rests entirely on in vitro pharmacology, animal behavioral data, and structural analogy to MDMA.
History[edit]
Discovery
6-APDB was first synthesized and characterized in 1993 by A.P. Monte, D. Marona-Lewicka, N.V. Cozzi, and D.E. Nichols at Purdue University.[2] The compound — designated "compound 6" in the original paper — emerged from a structure-activity investigation of MDA analogs aimed at separating entactogenic effects from neurotoxicity. By replacing both oxygen atoms of MDA's methylenedioxy ring with a methylene bridge forming a dihydrobenzofuran system, the researchers created what they termed a "nonoxygenated isostere" — structurally related to MDA but theoretically resistant to the oxidative metabolic pathway implicated in serotonergic neurotoxicity.[2]
Research chemical era
6-APDB remained exclusively a laboratory compound for over fifteen years after its synthesis. It entered recreational circulation in the late 2000s to early 2010s as part of the European novel psychoactive substance wave, sold alongside its positional isomer 5-APDB and the unsaturated analogs 5-APB and 6-APB under marketing names including "benzofury".[6] No controlled human studies were conducted during this period — all pharmacological knowledge beyond the 1993 paper derives from in vitro receptor profiling[1] and animal behavioral studies.[3]
Prohibition
Regulatory response was swift. On 10 June 2013, the UK Advisory Council on the Misuse of Drugs placed 6-APDB under a Temporary Class Drug Order alongside the other benzofuran entactogens.[7] Later that year, permanent Class B scheduling using a generic benzofuran definition eliminated the market in the UK.[8] The compound's serotonin₂B agonism and controlled status have excluded it from the entactogen-assisted psychotherapy research pipeline that has advanced MDMA toward clinical approval.[9]
The name "6-APDB" follows systematic research chemical nomenclature: 6 denotes the ring position of the aminopropyl chain on the benzofuran scaffold, AP stands for aminopropyl, and DB for dihydrobenzofuran. The alternate name 4-Desoxy-MDA reflects its conceptual derivation — MDA with the 4-position oxygen removed. In recreational markets, it was rarely sold under its own name, instead appearing as a component of "benzofury" blends or simply as a generic MDMA replacement without specific compound identification.
Chemistry[edit]
Structural class
6-APDB belongs to the phenethylamine, amphetamine, and dihydrobenzofuran chemical classes. It is the saturated (2,3-dihydro) structural analog of 6-APB, and a direct structural analog of MDA in which the methylenedioxy oxygen at the 4-position has been replaced by a methylene bridge, closing the ring into a dihydrobenzofuran system.[2] This relationship is reflected in its alternate name 4-Desoxy-MDA.
Within the benzofuran series, the "6" designates the position of the aminopropyl side chain on the benzofuran ring, distinguishing it from the 5-positional isomer 5-APDB. Both isomers were synthesized and characterized in the same 1993 publication.[2]
Molecular properties
| Molecular formula | C₁₁H₁₅NO |
| Molecular weight | 177.24 g/mol |
The compound has moderate lipophilicity (XLogP 1.7).[10]
Stereochemistry
The α-methyl group on the propylamine side chain creates a chirality center, producing R and S enantiomers. No published data address 6-APDB's stereospecific pharmacology directly. Indirect evidence from structurally related benzofuran derivatives suggests the S-isomer functions as an efficacious triple monoamine releaser at all three transporters, while the R-isomer preferentially releases serotonin with diminished dopaminergic activity.[11] Whether this pattern extends to 6-APDB has not been tested.
Physical properties
No melting point, solubility, or salt-form characterization data have been published in peer-reviewed literature. The compound is available from research chemical suppliers in freebase and hydrochloride salt forms. No stability or degradation pathway studies have been published.
Pharmacology[edit]
Mechanism of action
6-APDB works by entering monoamine neurons through their reuptake transporters and forcing the transporters to run in reverse, flooding the synapse with serotonin, norepinephrine, and dopamine. This substrate-type releasing mechanism is shared with MDMA.[1] The selectivity profile favors serotonin release over norepinephrine and dopamine — the same ordering as MDMA and opposite to methamphetamine, which preferentially releases dopamine.[1]
Beyond transporter reversal, 6-APDB acts at several receptor targets. It partially activates 5-HT₂A receptors, likely contributing to mild perceptual effects and empathogenic qualities. It activates TAAR1 (trace amine-associated receptor 1), which modulates monoamine neuron firing — a feature shared with classical amphetamines.[1]
Critically, 6-APDB is a potent agonist at 5-HT₂B receptors — a property that distinguishes it from MDMA, which does not significantly activate this receptor.[1] Chronic 5-HT₂B activation is the mechanism by which fenfluramine and ergotamine caused cardiac valve fibrosis.[4][12]
In animal behavioral studies, 6-APDB fully substituted for MDMA's discriminative cue in trained rats and produced locomotor stimulation in mice, but did not substitute for methamphetamine, cocaine, or DOM — confirming an MDMA-like rather than classical stimulant or psychedelic profile.[3]
Pharmacokinetics
No human pharmacokinetic studies exist for 6-APDB. Plasma half-life, bioavailability, volume of distribution, and metabolic pathways have not been characterized in humans.
Metabolic data from the structural analog 5-APB provide limited extrapolation: the related compound 5-MAPB is metabolized by liver enzymes including CYP2B6 and CYP2D6.[13] By structural analogy to MDMA, CYP2D6 is likely involved in 6-APDB's metabolism, but this remains inferential.inferred
Community-reported oral data suggest an onset of 30–60 minutes, peak effects at 2–3 hours, and total duration of 6–8 hours.citation needed No pharmacokinetic modeling exists to correlate these subjective timelines with plasma concentrations.
Neuroscience[edit]
Where it acts
6-APDB's entactogenic effects arise from serotonin flooding the amygdala and prefrontal cortex, suppressing threat-response circuitry and facilitating prosocial emotional processing. The dopaminergic component activates the brain's mesolimbic pathway (ventral tegmental area to nucleus accumbens), producing stimulation and euphoria.[3] TAAR1 activation modulates dopamine neuron firing rates, potentially limiting the reinforcing "wanting" quality compared to pure stimulants.[1][14]
Why it matters
The entactogenic state — emotional openness with reduced fear — aligns with the memory reconsolidation framework applied to MDMA therapy: serotonin-mediated fear extinction enables access to aversive memories without the associated threat response.[2][9] The original benzofuran synthesis program was motivated precisely by this therapeutic potential, seeking compounds that could replicate MDMA's prosocial effects without its neurotoxic metabolic pathway.
Whether 6-APDB produces neurotoxicity to serotonergic terminals remains untested — the "non-neurotoxic" framing from 1993 is a design hypothesis, not a demonstrated finding.[2] The cumulative 5-HT₂B exposure threshold for cardiac valve damage in benzofuran users is entirely unknown. Whether the R and S enantiomers differ in therapeutic ratio — as demonstrated for related benzofurans[11] — remains unexplored.
Subjective Effects[edit]
6-APDB's experiential character is defined by serotonergic dominance: emotional openness, interpersonal warmth, and reduced social anxiety form the core of the experience across the active dose range, with stimulation and mild perceptual shifts as secondary features. At lower doses the experience is gentle and social; higher doses bring stronger perceptual effects and more pronounced physical stimulation. Set and setting exert substantial influence, particularly during the comedown phase where serotonin depletion can amplify pre-existing mood states.
Within the entactogen class, 6-APDB sits between MDMA and MDA — structurally an MDA structural analog with MDMA-like subjective character,[3] but with a slower onset arc and longer total duration that gives the experience a more sustained, less peaking quality than MDMA.citation needed
Effect Grid
At common doses (70–100 mg oral), the full entactogenic experience manifests: pronounced empathy enhancement, emotional openness, tactile euphoria, and a strong sense of interpersonal connection. Music enhancement becomes prominent. Thought acceleration, creativity enhancement, and immersion enhancement are characteristic. Mild perceptual effects may appear — visual haze, subtle tracers, enhanced color saturation — though substantially less intense than classical psychedelics.
Physically, stimulation is marked: increased heart rate, bruxism, pupil dilation, increased sweating, temperature dysregulation, and appetite suppression. Spontaneous body sensations and bodily lightness are commonly reported.
Sleep is impossible for approximately 6–8 hours. The experience demands a committed time window and is incompatible with responsibilities requiring focused cognition.
Modeled from the effect's dose-dependence curve — not per-substance measurements.
Tracers · Visual haze / noise · Dreaming enhancement · Sound sensitivity · Symmetrical texture repetition · Peripheral misidentification · Color alteration · After-images · Environmental patterning · Geometry · Synesthesia · Visual breathing · Visual drifting · External hallucinations · Internal hallucinations
Symmetrical texture repetition · Peripheral misidentification · Color alteration · After-images · Environmental patterning · Geometry · Synesthesia · Visual breathing · Visual drifting · External hallucinations · Internal hallucinations
Pupil dilation · Wakefulness · Appetite suppression · Physical fatigue · Excessive sweating · Tactile euphoria · Spontaneous body sensations · Dry mouth · Heart rate perception changes · Bodily lightness · Bruxism · Dehydration sensation · Insomnia · Muscle tension · Restlessness · Tingling / electric sensations · Sexual arousal enhancement · Headache · Laughter fits · Nausea · Nystagmus (eye wobbles) · Vibrations / buzzing · Dizziness · Motor control impairment · Sexual arousal suppression · Increased urination · Abnormal heartbeat · Brain zaps · Trembling · Motor control enhancement · Vomiting
Physical fatigue · Excessive sweating · Tactile euphoria · Spontaneous body sensations · Dry mouth · Heart rate perception changes · Bodily lightness · Bruxism · Dehydration sensation · Insomnia · Muscle tension · Restlessness · Tingling / electric sensations · Sexual arousal enhancement · Headache · Laughter fits · Nausea · Nystagmus (eye wobbles) · Vibrations / buzzing · Dizziness · Sexual arousal suppression · Increased urination · Abnormal heartbeat · Brain zaps · Trembling · Motor control enhancement · Vomiting
Aesthetic enhancement · Introspection enhancement · Immersion enhancement · Cognitive flexibility · Novelty enhancement · Humor enhancement · Compulsive redosing urge · Creativity enhancement · Thought acceleration · Motivation suppression · Motivation enhancement · Pattern recognition enhancement · Cognitive impairment · Language enhancement · Thought connectivity · Focus enhancement · Increased nature relatedness · Thought deceleration · Confusion · Memory replays
Cognitive flexibility · Novelty enhancement · Humor enhancement · Creativity enhancement · Thought acceleration · Motivation suppression · Motivation enhancement · Pattern recognition enhancement · Cognitive impairment · Language enhancement · Thought connectivity · Focus enhancement · Increased nature relatedness · Thought deceleration · Confusion · Memory replays
Anxiety suppression · Emotional lability · Irritability · Catharsis · Simultaneous emotions · Anhedonia · Anxiety · Dysphoria
Simultaneous emotions · Anhedonia · Anxiety · Dysphoria
Emotional susceptibility · Communication enhancement · Flow state · Craving · Boundary dissolution
Boundary dissolution
Timeline
First alerts appear as subtle mood shift, mild bodily warmth, and faint stimulation. Effects are easily overlooked initially.
Entactogenic effects build progressively: empathy enhancement, emotional warmth, and tactile sensitivity increase. Stimulation, pupil dilation, and jaw tension become noticeable.
Maximum entactogenic intensity: pronounced empathy enhancement, tactile euphoria, music enhancement, and emotional openness. Stimulation, bruxism, sweating, and temperature dysregulation are at their strongest.
Gradual decline in entactogenic and stimulant effects. Cognitive fatigue and emotional flatness replace euphoria. Residual stimulation persists, maintaining wakefulness.
Residual mood effects ranging from gentle warmth to low mood and irritability, depending on dose and individual neurobiology. Appetite returns gradually. Cognitive performance may remain subtly impaired.
Safety[edit]
- Acute toxicity
- Low
- Chronic toxicity
- Moderate
- Withdrawal
- None
- Tolerance buildup
- moderate
- Tolerance reset
- 75 days
- Physical
- Negligible
- Psychological
- Low
- Compulsive redosing
- Moderate
- Dose escalation
- Low
- Cross-tol.
- MDMA · MDA · 6-APB
Toxicity
No lethal dose has been established for 6-APDB in any species, and no case reports of 6-APDB-specific overdose or fatality exist in the indexed literature.
Cardiovascular toxicity
6-APDB is a confirmed serotonin₂B receptor agonist.[1] Chronic activation of this receptor causes heart valve fibrosis and pulmonary arterial hypertension — the same mechanism that led to fenfluramine's withdrawal from the market.[4][12] This risk applies specifically to repeated or frequent use and is not shared with MDMA. The cumulative exposure threshold required to produce detectable valve damage from benzofuran entactogens is unknown.
The mechanism involves activation of growth-promoting signaling in valve tissue cells, leading to fibrotic thickening.[15] 5-HT₂B agonism remains a critical safety liability in pharmaceutical development.[16]
Serotonin toxicity
As a potent serotonin releaser, 6-APDB carries significant risk of serotonin syndrome when combined with other serotonergic agents. Features include agitation, involuntary muscle jerking, overheating, rapid heart rate, and tremor. Life-threatening complications include body temperature exceeding 41°C, muscle breakdown, and organ failure.safety citation needed
Neurotoxicity
The original synthesis aimed to produce non-neurotoxic entactogens by modifying the methylenedioxy ring oxygens implicated in MDA/MDMA's toxic metabolic pathway.[2] No studies have directly tested whether 6-APDB actually avoids serotonergic terminal damage. The "non-neurotoxic" framing remains a design hypothesis, not a confirmed finding.
Acute intoxication
The closest published clinical data come from the structural analog 6-APB: a case of acute psychosis with agitation and paranoia was documented following recreational use combined with cannabis.[17] Intoxication reports for the benzofuran class consistently involve multiple substances, complicating attribution of specific effects to individual compounds.[5]
Psychological risks
Acute psychosis has been documented for the structural analog 6-APB.[17] Compulsive redosing is reported as a feature of 6-APDB use, increasing acute toxicity risk through cumulative dose escalation.
Comedown effects include depressed mood, cognitive fatigue, and irritability — consistent with post-release serotonin depletion observed across the entactogen class.citation needed No published data address long-term psychiatric effects specific to 6-APDB.
Tolerance & dependence
No published studies characterize tolerance or dependence for 6-APDB specifically. As a serotonin releasing agent, tolerance develops through downregulation and transporter desensitization following repeated exposure — the same mechanism observed with MDMA.[5] Cross-tolerance with MDMA and other entactogens is expected.
Community estimates suggest tolerance half-life of approximately 25 days and full reset at 2.5 months.citation needed These values are unverified.
6-APDB's MDMA-like discriminative stimulus profile suggests MDMA-like abuse potential.[3] Benzofurans' greater potency than MDMA may increase risk for reinforcement-related adverse outcomes.[18]
Drug interactions
The most critical interactions arise from 6-APDB's potent serotonin-releasing activity.
Tramadol: Classified as lethal. Tramadol inhibits the SERT in addition to its opioid effects.[19] Combined with 6-APDB's serotonin release, this creates extreme serotonin syndrome risk. Tramadol also lowers seizure threshold independently. A death from tramadol combined with multiple serotonergic drugs has been documented.[20]
MDMA: Combining two potent serotonin releasers creates stacked serotonergic load with dramatically elevated risk of serotonin syndrome, overheating, and cardiovascular toxicity.[21]
MAOIs: Combination with monoamine oxidase inhibitors — irreversible (phenelzine, tranylcypromine) or reversible (moclobemide) — produces extreme serotonin elevation with potentially fatal outcome. This is an absolute contraindication.
SSRIs/SNRIs: SSRIs block the serotonin transporter through which 6-APDB releases serotonin, creating a pharmacological conflict that may both blunt effects and paradoxically elevate serotonin syndrome risk.[21]
Intoxication reports for benzofuran compounds consistently involve multiple substances, with high risk of severe adverse effects and death.[5]
Contraindications
Cardiovascular conditions: Pre-existing heart valve disease and pulmonary arterial hypertension are absolute contraindications given 6-APDB's confirmed 5-HT₂B agonism.[1] The compound adds direct pharmacological insult to structurally compromised valve tissue.[15]
Psychiatric conditions: Personal or family history of psychotic disorders is a relative contraindication, supported by the 6-APB psychosis case.[17]
Concurrent medications: MAOIs, SSRIs, SNRIs, tramadol, triptans, lithium, and linezolid are contraindicated due to serotonin syndrome risk.
Liver impairment: If 6-APDB is metabolized through liver enzymes — inferred from analogy to MDMA and 5-APB data[13] — impaired liver function could produce elevated blood levels and prolonged effects.inferred
Harm Reduction[edit]
Forms & Identification
6-APDB circulates primarily as a white to off-white powder or pressed tablets, often without specific compound identification — it was historically sold as part of "benzofury" blends or generic MDMA replacements. The critical testing concern is distinguishing 6-APDB from its unsaturated structural analog 6-APB and from substances with substantially different dose ranges.
Reagent testing can confirm the presence of a benzofuran compound but cannot reliably distinguish between positional isomers (5-APDB vs 6-APDB) or saturated vs unsaturated variants (6-APDB vs 6-APB). Quantitative analysis (GC-MS or similar) is the only reliable identification method. Given the compound's rarity in current markets, any substance sold as 6-APDB warrants particular skepticism about identity and purity.
Guidelines
- Test substance identity before use — reagent kits at minimum, laboratory analysis if accessible
- Start with a low dose and wait at least 90 minutes before considering redosing due to slow onset
- Plan for 6–8 hours of effects plus comedown — ensure no time-critical obligations
- Keep hydrated but avoid overhydration — moderate sipping rather than large volumes
- Avoid frequent use: 5-HT₂B-mediated cardiac risk is cumulative and proportional to total exposure
- Space sessions by at least one month to allow serotonin system recovery
- Have a trusted person present who is aware of what was taken and approximate timing
- Eat a light meal 2–3 hours before; an empty stomach speeds onset but a full stomach may blunt it unpredictably
Set & Setting
The slow onset (30–60 minutes to first effects) creates a window where premature redosing is common — users expecting MDMA-speed onset may assume the dose was insufficient. The extended duration (6–8 hours) means planning for a longer session than typical MDMA use.
A calm, comfortable environment with trusted company supports the entactogenic experience. The compound's empathogenic character responds well to social settings but can amplify existing emotional states during the comedown phase — having a settled, positive headspace at the outset reduces the risk of difficult emotional processing as serotonin levels drop.
Aftercare & integration. The serotonin depletion following 6-APDB use typically produces a mood dip 1–3 days after the experience. This is neurochemical, not psychological — serotonin stores take time to rebuild. Supporting recovery:
- Prioritize sleep in the 48 hours following use
- Eat nutrient-dense foods; tryptophan-rich foods (eggs, turkey, nuts) support serotonin synthesis
- Avoid other serotonergic substances during the recovery window
- Light exercise can improve mood but avoid intense physical exertion while depleted
- If emotional insights arose during the experience, journaling within 24–48 hours helps consolidate them before they fade
If low mood persists beyond 5–7 days, or if pre-existing depression is significantly worsened, seek professional support.
Recovery & Support
Compulsive redosing and increasing frequency of use are the primary patterns of concern with entactogens. Warning signs include using more often than monthly, difficulty maintaining planned spacing between sessions, or continued use despite noticing diminished effects (tolerance) or worsening comedowns.
The cumulative cardiac risk from 5-HT₂B agonism means that frequency reduction is not just about psychological wellbeing — it carries direct physical health implications that may not produce symptoms until significant damage has occurred.
Support resources include harm reduction organizations, psychedelic integration therapists, and substance use counselors familiar with entactogen patterns. MDMA-specific recovery resources are broadly applicable given the shared pharmacological class.
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Recognizing an emergency:
- Body temperature hot to the touch through clothing
- Rigid or jerking muscles that cannot be voluntarily relaxed
- Seizure activity
- Chest pain or irregular heartbeat
- Confusion progressing to unresponsiveness
- Extreme agitation with paranoia or psychotic behavior
These signs distinguish a medical emergency from ordinary discomfort (mild jaw tension, moderate stimulation, temporary anxiety).
Immediate steps:
- 1. Call emergency services immediately if any red flags above are present
- 2. Move the person to a cool, quiet space
- 3. Remove excess clothing to help cooling if overheating
- 4. Place in recovery position if consciousness is impaired
- 5. Do NOT restrain unless there is immediate danger of self-harm
- 6. Do NOT give additional substances to "counteract" effects
What to tell the dispatcher:
Name the substance (6-APDB / benzofuran entactogen), approximate amount and time taken, and current symptoms. Good Samaritan laws in many jurisdictions protect people who call for help during drug emergencies.
Legal Status[edit]
6-APDB is explicitly controlled in the United Kingdom as a Class B substance and may fall under structural analog provisions in several other jurisdictions. The compound has no recognized medical use in any jurisdiction and is not under active clinical investigation.
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| United Kingdom | Class B (Misuse of Drugs Act 1971) | Controlled since 2013. Temporary Class Drug Order from 10 June 2013,[7] then permanently scheduled as Class B using generic benzofuran definition.[8] Schedule 1. Maximum penalty for supply: 14 years and/or unlimited fine. |
| United States | Not explicitly scheduled | Not listed under the Controlled Substances Act. May be subject to the Federal Analogue Act (21 U.S.C. § 813) as structurally and pharmacologically similar to MDA (Schedule I). Prosecution is case-by-case.citation needed |
| Canada | Status disputed | Cited variously as Schedule I or Schedule III under the Controlled Drugs and Substances Act as an MDA analogue. Requires verification against current schedule listings.safety citation needed |
| Australia | Potentially controlled by analogy | MDA is Schedule 9 (Prohibited Substance). Australia's "substantially similar" analogue provisions may apply.citation needed |
| Germany | Potentially controlled under NpSG | No explicit scheduling confirmed. The New Psychoactive Substances Act (2016) may encompass 6-APDB under broad designer drug provisions.citation needed |
Analogue act considerations
6-APDB's close structural relationship to MDA creates potential legal liability in jurisdictions with structural analogue legislation. The Federal Analogue Act requires both substantial structural similarity and substantially similar pharmacological effects — criteria 6-APDB meets given its MDA-derived scaffold and MDMA-like discriminative stimulus profile.[3] Analogue provisions typically apply only when the substance is intended for human consumption, and prosecutorial application varies.
references
- [1]
- [2]
- [3]
- [4] ^abcRothman RB, Baumann MH (2009) Serotonergic drugs and valvular heart disease — Expert Opinion on Drug Safety doi:10.1517/14740330902931524
- [5] ^abcdLuethi D, Liechti ME (2020) Designer drugs: mechanism of action and adverse effects — Archives of Toxicology doi:10.1007/s00204-020-02693-7
- [6] ^Schifano F, Vento A, Scherbaum N, Guirguis A (2023) Stimulant and hallucinogenic novel psychoactive substances; an update — Expert Review of Clinical Pharmacology doi:10.1080/17512433.2023.2279192