6-APB
6-(2-aminopropyl)benzofuran
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6-APB (6-(2-aminopropyl)benzofuran) — also known as Benzofury — is a synthetic empathogen of the phenethylamine class. It is a close structural analog of MDA, distinguished by longer duration and a more psychedelic character. 6-APB is a non-selective monoamine releasing agent, producing its effects by elevating serotonin, dopamine, and norepinephrine while directly activating serotonin receptors.[1]
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MDMA, MDA, 5-APB +2 moreMDMA, MDA, 5-APB, serotonin releasing agents, dopaminergic stimulants show less
6-APB appeared on the European recreational market around 2010–2011, sold as a legal alternative to MDMA under the trade name "Benzofury." Pharmacological characterization followed in 2013–2015, establishing its receptor profile and confirming mechanistic parallels to MDMA.[2][1] The compound is now controlled in the United Kingdom and Germany, though it remains unscheduled in several other jurisdictions.
Subjective effects include empathy enhancement, euphoria, emotional openness, color enhancement, and stimulation. The experience occupies a middle ground between MDMA and MDA — a sustained entactogenic warmth layered with mild psychedelic coloring that unfolds gradually and holds its plateau longer than either comparator. Nausea during onset, bruxism, and an extended comedown are common unsought effects.
No physical dependence data exist for 6-APB, and the lethal dose is unknown in any species. The defining long-term concern is cardiac: 6-APB potently activates 5-HT₂B receptors, the same mechanism by which fenfluramine caused heart valve damage.[1][3][4] No clinical trials, human pharmacokinetic studies, or cardiac imaging data have been published — the current understanding rests entirely on in vitro pharmacology and a single case report.[5]
History[edit]
Discovery
6-APB belongs to a series of benzofuran amphetamine analogs explored as potential entactogens during the 1990s and 2000s. The identity of the original synthesizer and the precise date of first synthesis are undocumented in the published literature.citation needed The compound does not appear in Alexander Shulgin's PiHKAL.citation needed
Emergence and scientific characterization
6-APB entered the European recreational drug market around 2010–2011, marketed as "Benzofury" and sold as a legal alternative to MDMA.citation needed The first peer-reviewed case report appeared in 2013, documenting acute psychosis in a patient who had consumed 6-APB alongside cannabis and a synthetic cannabinoid.[5] Iversen et al. published the first systematic pharmacological screening that same year,[2] followed by Rickli et al.'s comprehensive in vitro profiling in 2015[1] — these two studies remain the primary pharmacological references for the compound.
Regulatory response
The United Kingdom temporarily controlled 6-APB from June 2013,[6] then permanently classified all benzofuran derivatives as Class B substances in June 2014.[7] Germany subsequently listed 6-APB in Annex II of the Betäubungsmittelgesetz.[8]
The name "6-APB" derives from the compound's structure: the "6" denotes attachment at the 6-position of the benzofuran ring, while "APB" abbreviates aminopropylbenzofuran. The trade name "Benzofury" — a portmanteau of benzofuran and fury — was coined for the UK legal high market and became the compound's most recognized street name. 6-APB is often discussed alongside its positional isomer 5-APB and the broader family of benzofuran entactogens, collectively positioned as legal MDMA alternatives during the early 2010s novel psychoactive substance wave.
Chemistry[edit]
Structural class
6-APB (1-(1-benzofuran-6-yl)propan-2-amine) is a substituted benzofuran built on the amphetamine scaffold. Where MDA carries a 3,4-methylenedioxy group on its phenyl ring, 6-APB replaces it with a benzofuran ring fused at the 6-position — a swap that preserves entactogenic activity while altering receptor selectivity and duration.[1] 6-APB is a positional isomer of 5-APB, which carries the aminopropyl chain at the 5-position instead.
Molecular properties
| Molecular formula | C₁₁H₁₃NO |
| Molecular weight | 175.23 g/mol |
The molecular structure consists of a benzofuran bicyclic ring with a 2-aminopropyl side chain at the 6-position. The furan oxygen introduces an electron-donating heteroatom that modulates the ring's electronic properties relative to MDA's methylenedioxy bridge. Moderate lipophilicity allows adequate penetration into the central nervous system.
Stereochemistry
6-APB contains one chirality center at the alpha carbon of its aminopropyl group, analogous to the stereogenic center in amphetamine and MDMA. The compound is typically encountered as a racemic mixture. No published studies have characterized pharmacological differences between the R- and S-enantiomers — a significant gap, given that enantiomers of structurally related compounds (amphetamine, MDMA) differ substantially in receptor affinity and transporter potency.
Physical properties
No published data on melting point, boiling point, or aqueous solubility exist for 6-APB. The compound is typically sold as the hydrochloride or succinate salt.citation needed
Pharmacology[edit]
Mechanism of action
6-APB functions as a non-selective monoamine releasing agent, forcing serotonin, dopamine, and norepinephrine out of nerve terminals through the same transporter-reversal mechanism used by MDMA.[1] This mechanism was corroborated by Rudin et al. using APB compounds as reference standards in a comparison study.[9] The serotonin release drives entactogenic effects — empathy, emotional openness, and prosocial warmth — while the dopamine component produces stimulation and euphoria.
Beyond monoamine release, 6-APB directly activates 5-HT₂B receptors with high affinity[2] and interacts with additional serotonin receptor subtypes that likely contribute psychedelic-like qualities.[1] Full 5-HT₂ receptor agonism has been confirmed in related benzofuran compounds.[9] Whether 6-APB possesses meaningful 5-HT₂A activity — which would explain its reported visual and cognitive effects — has not been confirmed by direct binding studies.citation needed
5-HT₂B agonism and cardiac risk
6-APB is a full agonist at the 5-HT₂B receptor, independently confirmed by two research groups.[1][2] This receptor, when chronically activated on heart valve cells, drives fibrotic tissue remodeling — the same mechanism by which fenfluramine, pergolide, and other drugs caused heart valve disease.[3][4] Rickli et al. explicitly flagged this risk for benzofuran compounds.[1]
No human heart imaging studies of 6-APB users have been published. The relationship between cumulative exposure and valve damage remains entirely uncharacterized.[10]
Pharmacokinetics
No controlled human pharmacokinetic studies exist for 6-APB. Bioavailability, peak plasma concentration, and half-life are unknown in humans.
The compound is metabolized through several cytochrome P450 enzymes, with the unchanged parent compound representing the primary urinary analyte.[11] Laboratory work has shown that one metabolic pathway produces toxic intermediates, and blocking this pathway reduces liver cell damage in vitro.[12]
Neuroscience[edit]
Where it acts
No direct neuroimaging or neurochemical measurement studies have been conducted with 6-APB. The following mechanisms are inferred from the compound's characterized pharmacological profile.
As a potent serotonin releaser, 6-APB is expected to produce acute serotonin surges across cortical and subcortical regions. The MDMA literature links this pattern to reduced threat reactivity in the amygdala and enhanced prefrontal-amygdala connectivity — neural signatures of the entactogenic state of empathy and emotional openness.[13][14] The dopaminergic component, which drives more pronounced locomotor stimulation than MDMA in animal models,[15] activates the mesolimbic mesolimbic pathway and likely underlies the compound's euphoric and reinforcing qualities.
Why it matters
6-APB sits at an intermediate point on the entactogen-psychedelic spectrum — a continuum defined by the balance between monoamine release (entactogenic pole) and direct serotonin receptor agonism (psychedelic pole).[1][9] Pure entactogens like MDMA drive prosocial effects mainly through serotonin flooding; classical psychedelics like LSD act by directly binding serotonin receptors. 6-APB does both, which accounts for its hybrid experiential character. The dopaminergic potency demonstrated by full substitution for MDMA in drug discrimination assays[15] further engages the reward system, contributing to both the euphoric experience and the compound's abuse potential.
Key unknowns include whether 6-APB has functionally significant 5-HT₂A activity (which would confirm the mechanism behind its psychedelic qualities), whether repeated use produces the serotonergic nerve terminal damage documented for MDMA at high doses, and whether chronic exposure causes detectable heart valve thickening. The pharmacological differences between its R- and S-enantiomers are entirely unexplored.
Subjective Effects[edit]
6-APB delivers a hybrid experience that draws from both entactogenic and psychedelic pharmacology. At lower doses, the entactogenic character dominates — warmth, emotional closeness, and a gentle stimulant glow. As dose increases, psychedelic coloring emerges: color saturation deepens, thought patterns shift, and mild visual distortions enter the periphery. Set and setting shape the experience substantially, and the extended timeline means the environment chosen at the outset anchors a longer commitment than comparable substances.
The closest experiential comparators are MDA and, to a lesser extent, MDMA. 6-APB is consistently described as more psychedelic and longer-lasting than MDMA, with a gentler stimulant push and a slower, more sustained intensity curve that unfolds gradually rather than cresting sharply.
Effect Grid
At common doses (60–90 mg oral), the full entactogenic-psychedelic profile emerges. Empathy enhancement becomes pronounced — emotional openness, feelings of closeness and connection, and enhanced capacity for introspection. Euphoria is robust. The psychedelic component manifests as mild visual distortions: enhanced color saturation, surface texturing, gentle drifting and morphing of objects. Music appreciation deepens substantially. Thought patterns become more associative and fluid.
Physically, stimulation is moderate to strong: elevated heart rate, noticeable jaw clenching, body temperature increase, and significant pupil dilation. Nausea during the come-up is reported by some users. The total experience duration extends to 7–10 hours, considerably longer than MDMA, with residual stimulation and emotional sensitivity persisting beyond the primary effects.
Modeled from the effect's dose-dependence curve — not per-substance measurements.
Visual haze / noise · Color enhancement · Sound sensitivity · Tracers · Auditory distortion · Brightness alteration · Color alteration · Dreaming enhancement · Dreaming suppression · Geometry · Olfactory enhancement · Visual processing acceleration · Symmetrical texture repetition · After-images · Depth perception distortion · Environmental patterning · Peripheral vision distortion · Perspective distortion · Proprioceptive distortion · Spatial disorientation · Synesthesia · Tinnitus · Visual breathing · Visual diffraction · Visual drifting · Taste enhancement · Visual acuity enhancement · Peripheral misidentification · Auditory misinterpretation · Vestibular distortion · Visual magnification · Visual melting · Visual morphing · Flashbacks · Internal hallucinations · Object transformations · Auditory hallucinations · External hallucinations · Object activation · Perspective hallucinations · Persisting hallucinations · Visual flipping · Visual recursion
Auditory distortion · Brightness alteration · Color alteration · Dreaming enhancement · Dreaming suppression · Geometry · Olfactory enhancement · Visual processing acceleration · Symmetrical texture repetition · After-images · Depth perception distortion · Environmental patterning · Peripheral vision distortion · Perspective distortion · Proprioceptive distortion · Spatial disorientation · Synesthesia · Tinnitus · Visual breathing · Visual diffraction · Visual drifting · Taste enhancement · Visual acuity enhancement · Peripheral misidentification · Auditory misinterpretation · Vestibular distortion · Visual magnification · Visual melting · Visual morphing · Flashbacks · Internal hallucinations · Object transformations · Auditory hallucinations · External hallucinations · Object activation · Perspective hallucinations · Persisting hallucinations · Visual flipping · Visual recursion
Pupil dilation · Body high · Spontaneous body sensations · Excessive sweating · Dry mouth · Bruxism · Appetite suppression · Insomnia · Tactile euphoria · Tingling / electric sensations · Dehydration sensation · Laughter fits · Muscle tension · Physical fatigue · Vibrations / buzzing · Sexual arousal enhancement · Bodily lightness · Headache · Heart rate perception changes · Nausea · Nystagmus (eye wobbles) · Restlessness · Brain zaps · Abnormal heartbeat · Breathing alteration · Dizziness · Motor control impairment · Muscle relaxation · Pain suppression · Respiratory stimulation · Trembling · Yawning · Sexual arousal suppression · Bodily pressures · Body schema distortion · Involuntary body movements · Nasal congestion · Salivation · Watery eyes · Increased urination · Vomiting · Motor control enhancement · Seizure threshold reduction · Tactile hallucination
Excessive sweating · Dry mouth · Bruxism · Appetite suppression · Insomnia · Tactile euphoria · Tingling / electric sensations · Dehydration sensation · Laughter fits · Muscle tension · Physical fatigue · Vibrations / buzzing · Sexual arousal enhancement · Bodily lightness · Headache · Heart rate perception changes · Nausea · Nystagmus (eye wobbles) · Restlessness · Brain zaps · Breathing alteration · Dizziness · Motor control impairment · Muscle relaxation · Pain suppression · Respiratory stimulation · Trembling · Yawning · Sexual arousal suppression · Bodily pressures · Body schema distortion · Involuntary body movements · Nasal congestion · Salivation · Watery eyes · Increased urination · Vomiting · Motor control enhancement · Seizure threshold reduction · Tactile hallucination
Openness enhancement · Cognitive fatigue · Novelty enhancement · Immersion enhancement · Humor enhancement · Thought acceleration · Creativity enhancement · Motivation enhancement · Memory suppression · Cognitive flexibility · Cognitive impairment · Suggestibility enhancement · Thought connectivity · Focus enhancement · Language enhancement · Motivation suppression · Thought disorganization · Pattern recognition enhancement · Analysis suppression · Conceptual thinking · Confusion · Focus suppression · Increased nature relatedness · Information processing suppression · Memory fragmentation · Memory replays · Analysis enhancement · Information processing enhancement · Thought deceleration · Cognitive dysphoria · Multiple thought streams · Synchronicity · Thought loops · Thought organization · Language suppression · Delusions
Immersion enhancement · Humor enhancement · Thought acceleration · Creativity enhancement · Motivation enhancement · Memory suppression · Cognitive flexibility · Cognitive impairment · Thought connectivity · Focus enhancement · Language enhancement · Motivation suppression · Thought disorganization · Pattern recognition enhancement · Analysis suppression · Conceptual thinking · Confusion · Focus suppression · Increased nature relatedness · Information processing suppression · Memory fragmentation · Memory replays · Analysis enhancement · Information processing enhancement · Thought deceleration · Cognitive dysphoria · Multiple thought streams · Synchronicity · Thought loops · Thought organization · Language suppression · Delusions
Anxiety suppression · Catharsis · Irritability · Anhedonia · Anxiety · Emotional lability · Simultaneous emotions · Dysphoria · Mania · Suicidal ideation
Anhedonia · Anxiety · Emotional lability · Simultaneous emotions · Dysphoria · Suicidal ideation
Sociability enhancement · Emotional susceptibility · Communication enhancement · Craving · Flow state · Derealization · Automaticity · Compulsive behavior reduction · Depersonalization · Ego inflation · Boundary dissolution · Ego dissolution · Identity alteration · Telepathic feelings
Flow state · Derealization · Automaticity · Compulsive behavior reduction · Depersonalization · Ego inflation · Boundary dissolution · Ego dissolution · Identity alteration · Telepathic feelings
Non-dual awareness · Transpersonal visions
Cognitive dissonance · Recursive awareness
Timeline
First alerts appear as a subtle shift in mood and faint body warmth. Mild restlessness or anticipatory energy may be noticeable.
Effects build steadily over 60–120 minutes — longer than typical MDMA onset. Empathogenic warmth, increasing sociability, and early sensory enhancement develop. Nausea is most likely during this phase.
Full entactogenic-psychedelic expression: pronounced empathy, euphoria, emotional openness, mild visual distortions, and enhanced sensory appreciation. Stimulation and jaw tension are at maximum.
Intensity gradually diminishes from peak. Entactogenic warmth persists while visual and stimulant effects begin to recede. Introspective clarity often emerges during this phase.
A gradual return toward baseline over 1. 5–2. 5 hours.
Residual mood elevation, emotional openness, or conversely fatigue and low mood may persist for 6–24 hours. Some users report a serotonergic 'comedown' with depressed mood in the days following use.
⚠ Do not drive or operate machinery until after a full night of sleep following the experience.
Safety[edit]
- Acute toxicity
- Moderate
- Chronic toxicity
- Moderate
- Withdrawal
- Mild
- Tolerance buildup
- moderate
- Tolerance reset
- 49 days
- Physical
- Low
- Psychological
- Moderate
- Compulsive redosing
- Low
- Dose escalation
- Low
- Cross-tol.
- MDMA · MDA · 5-APB
Toxicity
Acute toxicity
No lethal dose data exist for 6-APB in any species, and no controlled dose-escalation studies have been conducted. As a serotonergic monoamine releaser, the compound carries class-level acute risks: serotonin syndrome (marked by dangerously high body temperature, muscle rigidity, and altered consciousness), seizures, and dangerous drops in blood sodium.[13] Benzofurans as a class have been identified as serious health risks.[16]
Liver toxicity
Laboratory studies show 6-APB damages liver cells in a concentration-dependent manner, producing oxidative stress, energy depletion, and cell death through both programmed and uncontrolled pathways.[12] Toxic metabolites are generated through liver enzyme activity — blocking these enzymes reduces the damage.[12]
The concentrations tested were far higher than expected human blood levels from recreational doses, making direct extrapolation to real-world liver risk uncertain. Its positional isomer 5-APB is approximately twice as toxic to liver cells across all tested models.
Heart and circulation
The 5-HT2B receptor activation by 6-APB represents a specific long-term cardiovascular concern. Chronic activation of this receptor on heart valve cells drives fibrotic tissue remodeling — the established mechanism behind heart valve disease caused by fenfluramine, pergolide, and other drugs.[3][4][10] Rickli et al. explicitly identified this risk for benzofuran compounds.[1]
No human heart imaging studies of 6-APB users have been published. The dose-response relationship between cumulative exposure and valve damage is entirely unknown.
Psychological risks
The single published case report involving 6-APB documents acute psychosis in a patient who also consumed cannabis and a synthetic cannabinoid, preventing sole attribution to 6-APB.[5] The broader designer drug literature associates serotonergic entactogens with anxiety, paranoia, and psychotic symptoms.[17]
No published data exist on 6-APB-specific risks of persistent perceptual changes, depersonalization, or psychiatric destabilization. Given the compound's probable serotonin receptor agonism, such risks are pharmacologically plausible but unquantified.inferred
Tolerance and dependence
No published studies have characterized tolerance or dependence for 6-APB specifically. Animal studies show 6-APB fully substitutes for MDMA in drug discrimination tests, consistent with abuse potential as an MDMA replacement.[15]
Community-reported tolerance parameters — approximately 3.5 weeks to half-reset and 7 weeks to full reset — are unconfirmed by any pharmacological study and may be borrowed from the MDMA literature.safety citation needed Cross-tolerance with other serotonin releasers is expected based on shared mechanisms but undemonstrated for 6-APB. Physical dependence and withdrawal have not been characterized.inferred
Drug interactions
No substance-specific interaction studies have been published for 6-APB. All assessments derive from its pharmacological class.
Serotonergic potentiation
Combining 6-APB with other serotonergic agents — including MDMA, SSRIs, SNRIs, or triptans — increases the risk of serotonin syndrome.[13][18] Combination with monoamine oxidase inhibitors (MAOIs) presents extreme serotonin toxicity risk and should be treated as potentially lethal.safety citation needed
Tramadol
Tramadol blocks serotonin reuptake and lowers the seizure threshold, presenting a theoretical risk of serotonin toxicity and seizures when combined with 6-APB.safety citation needed
Metabolic interactions
Drugs that inhibit the liver enzymes involved in 6-APB metabolism (including fluoxetine, paroxetine, ketoconazole, ritonavir, and grapefruit juice) could raise 6-APB blood levels.[11][12]
Polydrug combinations
The published case report illustrates severe psychiatric consequences from combining 6-APB with synthetic cannabinoids.[5] A fatal case involving the 5-APB isomer combined with 3-MMC and alcohol demonstrates the lethal potential of benzofuran-stimulant-alcohol combinations.[19]
Contraindications
No contraindications have been established from clinical data specific to 6-APB. The following are derived from its pharmacological profile.
Cardiac conditions
The 5-HT2B agonism profile makes use inadvisable for anyone with pre-existing heart valve disease or conditions requiring cardiac monitoring. Existing valve abnormalities increase vulnerability to further fibrotic damage.[3][10]
Psychiatric conditions
Personal or family history of psychotic disorders constitutes a relative contraindication, consistent with other serotonergic entactogens and probable psychedelic-active compounds.[5]
Liver impairment
The metabolic activation of 6-APB to toxic intermediates[12] warrants caution in anyone with pre-existing liver disease.
Concurrent serotonergic medication
MAOIs, SSRIs, SNRIs, and other serotonin-modulating medications are contraindicated due to serotonin syndrome risk.[13]
Harm Reduction[edit]
Forms & Identification
6-APB circulates as powder, pellets, and capsules, most commonly as the hydrochloride or succinate salt. The succinate salt is notably less potent by weight than the hydrochloride — the same milligram dose of each delivers different amounts of active compound, making salt form identification essential for accurate dosing.
Reagent testing confirms the presence of a benzofuran compound but cannot distinguish 6-APB from its isomers (5-APB, 4-APB) or verify purity. Quantitative analysis through an energy control or drug checking service provides the most reliable identification.
Guidelines
- Test every batch with reagent kits and, where possible, quantitative drug checking services
- Identify the salt form (hydrochloride vs. succinate) before calculating dose — potency per milligram differs significantly
- Use a precision milligram scale; volumetric dosing is unreliable with pressed pellets
- Start with a low dose and wait at least 2 hours before considering a supplement — the come-up is notably slower than MDMA
- Arrange the setting in advance: comfortable temperature, water access, quiet space available for retreat
- Have a sober companion present, especially at higher doses or first experiences
- Eat a light meal 2–3 hours before; avoid alcohol and caffeine
- Plan for the full duration — do not schedule obligations for at least 12 hours
- Space uses widely (minimum 4–6 weeks) given the serotonergic depletion mechanism and unknown cardiac accumulation risk
Set & Setting
The extended duration of 6-APB — substantially longer than MDMA — means that environment and psychological state at the outset shape a much longer commitment. A comfortable, familiar setting with trusted companions reduces the probability of anxiety during the prolonged plateau.
The gradual come-up can tempt redosing before effects have fully developed. Patience during onset prevents accidental overdose from stacking doses.
Aftercare & integration. The serotonin depletion following 6-APB use can produce a period of low mood, fatigue, and irritability in the days afterward. Prioritize sleep, nutrition (foods rich in tryptophan support serotonin recovery), and light physical activity. Avoid other serotonergic substances during recovery.
The entactogenic and mildly psychedelic character of the experience may surface emotional material worth processing. Journaling or conversation with a trusted person can help integrate insights. If low mood persists beyond a week or emotional disturbance intensifies, consult a mental health professional.
Recovery & Support
Compulsive use patterns with 6-APB are less common than with pure stimulants, but the reinforcing dopaminergic component and entactogenic reward can drive habitual use. If use has become a regular coping mechanism or frequency has escalated despite diminishing returns, professional support can help.
Resources include the SAMHSA National Helpline (1-800-662-4357), local harm reduction organizations, and therapists experienced with substance use. Online communities and peer support forums provide experience reports and practical guidance from people who have navigated similar patterns.
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Recognizing an emergency: Dangerously high body temperature (skin hot to the touch), muscle rigidity or uncontrollable twitching, seizures, confusion progressing to loss of consciousness, or chest pain. An uncomfortable but manageable experience — anxiety, nausea, mild overheating — is distinct from these signs.
Immediate steps:
- 1. Call emergency services if the person is seizing, unresponsive, or has a body temperature that feels dangerous through clothing
- 2. Move them to a cool environment and remove excess clothing
- 3. If conscious, offer small sips of water — do not force fluids
- 4. Place an unconscious but breathing person in the recovery position
- 5. Do not restrain them unless they are in immediate danger of self-harm
What to tell the dispatcher: Name the substance (6-APB or benzofuran), approximate amount and time taken, current symptoms, and any other substances consumed. Good Samaritan laws in many jurisdictions protect callers who report drug emergencies from prosecution.
Legal Status[edit]
6-APB has been controlled in several jurisdictions, primarily in response to its emergence on the novel psychoactive substance market in 2010–2011. Regulatory approaches range from specific substance-level scheduling to broad structural class controls.
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| United Kingdom | Class B (Misuse of Drugs Act 1971) | Temporarily controlled from June 2013 under SI 2013/1294;[6] permanently classified as Class B from June 2014, covering all 1-benzofuran derivatives[7] |
| Germany | BtMG Annex II (tradeable, not prescribable narcotic) | Listed specifically as "1-(Benzofuran-6-yl)propan-2-amin" in the Betäubungsmittelgesetz[8] |
| United States | Not specifically scheduledsafety citation needed | Not listed in DEA schedules; may be prosecutable under the Federal Analogue Act (21 USC § 813) as substantially similar to Schedule I substances (MDA, MDMA) when intended for human consumption |
| Australia | Presumed Schedule 9 (Prohibited Substance)citation needed | Expected to fall under the Poisons Standard based on structural similarity to MDMA-class substances; not confirmed from primary source |
| Canada | Status uncertaincitation needed | CDSA Schedule III covers amphetamines and derivatives; applicability to 6-APB under analogue provisions unclear |
Analog act considerations
6-APB's close structural relationship to the Schedule I substance MDA creates potential legal liability under structural analog provisions even without specific scheduling. The benzofuran-for-methylenedioxy substitution preserves the fundamental pharmacological activity, and behavioral data confirming MDMA substitution in drug discrimination assays[15] provides scientific evidence of pharmacological similarity that could support analogue prosecution.
references
- [1]
- [2] ^abcdIversen L, Gibbons S, Treble R, Setola V, Huang XP, Roth BL (2013) Neurochemical profiles of some novel psychoactive substances — European Journal of Pharmacology doi:10.1016/j.ejphar.2012.12.006
- [3] ^abcdSmith SA, Waggoner AD, de las Fuentes L, Davila-Roman VG (2009) Role of serotoninergic pathways in drug-induced valvular heart disease and diagnostic features by echocardiography — Journal of the American Society of Echocardiography doi:10.1016/j.echo.2009.05.002
- [4] ^abcLam NT, Balachandran K (2015) The mechanobiology of drug-induced cardiac valve disease — Journal of Long-term Effects of Medical Implants PMID:25955005
- [5]
- [6]