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. Structurally close to MDA, it produces similar entactogenic warmth but lasts longer and carries more psychedelic coloring. It works by releasing serotonin, dopamine, and norepinephrine in the brain and by 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 in European recreational markets around 2010–2011, sold as a legal alternative to MDMA under the name Benzofury. Pharmacologists characterized its receptor profile in 2013–2015, confirming it shared MDMA's release mechanism and carried a specific cardiac risk.[2][1] The United Kingdom classified it as Class B in 2014; it remains unscheduled in several other countries.
Subjective effects include empathy enhancement, euphoria, emotional openness, color brightening, and mild visual distortions. The experience occupies a middle ground between MDMA and MDA — a sustained entactogenic warmth with a slow-building, long-lasting psychedelic overlay. Nausea during onset, bruxism, and a drawn-out comedown are common.
6-APB does not produce physical dependence, and no lethal dose has been established in any species. The defining long-term concern is cardiac: repeated activation of a serotonin receptor on heart valve cells can cause scarring — the same mechanism behind fenfluramine's valve damage.[1][3][4] The evidence base is thin — what is known comes almost entirely from lab studies and a single published case report.[5]
History[edit]
Discovery
6-APB belongs to a family of benzofuran analogs explored as potential entactogens. Its origin is undocumented — the compound does not appear in Shulgin's PiHKAL,citation needed and no primary source records who synthesized it first.citation needed
Emergence and scientific characterization
It appeared in European markets around 2010–2011 as "Benzofury," sold as a legal MDMA alternative.citation needed A 2013 case report documented acute psychosis in a patient who combined it with cannabis and a synthetic cannabinoid.[5] Iversen et al.[2] and Rickli et al.[1] established the compound's pharmacological profile in 2013–2015.
Regulatory response
The United Kingdom temporarily controlled 6-APB in June 2013,[6] then permanently classified all benzofuran derivatives as Class B in June 2014.[7] Germany subsequently listed it in its controlled substances law.[8]
The name "6-APB" reflects its structure: "6" marks the attachment point on the benzofuran ring, and "APB" abbreviates aminopropylbenzofuran. The trade name "Benzofury" — blending 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 isomer 5-APB as part of the benzofuran entactogen family, 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 — an amphetamine-based compound built on a fused bicyclic ring (molecular formula C₁₁H₁₃NO, 175.23 g/mol).
Where MDA carries a methylenedioxy bridge on its ring, 6-APB replaces it with a benzofuran ring at the 6-position — preserving entactogenic activity while altering receptor selectivity and extending duration.[1] It is a positional isomer of 5-APB, which carries the same substituent at the 5-position.
Pharmacology[edit]
Mechanism of action
6-APB forces serotonin, dopamine, and norepinephrine out of nerve terminals through the same transporter-reversal mechanism used by MDMA.[1][9] The serotonin surge drives empathy and emotional warmth; the dopamine component produces stimulation and euphoria. It also directly activates serotonin receptors,[2][1][9] likely accounting for the psychedelic coloring.
5-HT₂B agonism and cardiac risk
6-APB is a full agonist at a serotonin receptor found on heart valve cells.[1][2] Chronic activation causes the valve tissue to thicken and scar — the same mechanism behind the heart valve damage caused by fenfluramine and other drugs.[3][4][10] No heart imaging studies of 6-APB users have been published.
Pharmacokinetics
No controlled human pharmacokinetic studies exist for 6-APB. The compound is broken down by liver enzymes, with the unchanged parent compound appearing as the main urinary marker.[11] One metabolic pathway generates toxic byproducts — blocking it reduces liver cell damage in lab tests.[12]
Neuroscience[edit]
Where it acts
No neuroimaging studies have been conducted with 6-APB. Based on its pharmacological profile, the acute serotonin surge is expected to reduce threat reactivity and heighten social connection — the neural pattern associated with the entactogenic state of empathy and openness.[13][14]
Why it matters
6-APB sits between pure entactogens like MDMA and classical psychedelics like LSD.[1][9] Pure entactogens flood serotonin to produce prosocial warmth; classical psychedelics bind serotonin receptors directly to produce visuals and cognitive shifts. 6-APB does both, producing the hybrid character users describe.
The dopamine component is stronger than in MDMA — animal models show 6-APB fully substitutes for MDMA in behavioral tests.[15] This deeper reward engagement contributes to both the euphoric quality and the compound's abuse potential.
Key unknowns include whether 6-APB has meaningful activity at the serotonin receptor responsible for classical psychedelic effects, whether repeated use damages serotonin-producing nerve terminals as documented for high-dose MDMA, whether chronic exposure causes detectable heart valve thickening, and how the two mirror-image forms of the molecule differ in potency.
Subjective Effects[edit]
6-APB delivers a hybrid experience that blends entactogenic warmth with mild psychedelic coloring. At lower doses, the entactogenic character dominates — empathy, emotional closeness, a gentle stimulant glow. As dose increases, colors deepen, thought patterns shift, and visual distortions appear at the periphery. Set and setting shape the experience substantially.
The closest comparators are MDA and MDMA. 6-APB is consistently more psychedelic and longer-lasting than MDMA, with a gentler stimulant edge and a slower, more sustained intensity curve that builds 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 has been established for 6-APB in any species. As a serotonergic monoamine releaser, the compound carries class-level acute risks: body temperature can rise to dangerous levels, muscles can seize up, and blood sodium can drop suddenly.[13] Benzofurans as a class have been flagged as serious health risks.[16]
Liver toxicity
Lab studies show 6-APB damages liver cells in a concentration-dependent manner, generating toxic metabolites through liver enzyme activity — blocking these enzymes reduces the damage.[12]
The concentrations tested were far above expected recreational blood levels, making the real-world liver risk uncertain. Its isomer 5-APB is approximately twice as toxic to liver cells across all tested models.
Heart and circulation
6-APB activates a serotonin receptor on heart valve cells. With chronic exposure, this causes the valve tissue to thicken and scar — the same mechanism behind the valve disease caused by fenfluramine, pergolide, and other drugs.[3][4][10] Rickli et al. explicitly identified this risk for benzofuran compounds.[1]
No heart imaging studies of 6-APB users have been published. The dose and frequency of exposure required to cause valve damage are entirely unknown.
Psychological risks
The only published case report involving 6-APB documents acute psychosis in a patient who also consumed cannabis and a synthetic cannabinoid,[5] preventing sole attribution to 6-APB. The broader literature links serotonergic entactogens to anxiety, paranoia, and psychotic symptoms.[17]
No published data exist on 6-APB-specific risks of lasting perceptual changes or psychiatric destabilization. Given its probable serotonin receptor activity, such risks are plausible but unquantified.inferred
Tolerance and dependence
No studies have characterized tolerance or dependence for 6-APB. Animal studies show it fully substitutes for MDMA in behavioral tests, consistent with abuse potential.[15]
Community-reported tolerance resets — approximately 3.5 weeks to half-reset, 7 weeks to full reset — are unconfirmed by any pharmacological study.safety citation needed 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 drugs — MDMA, SSRIs, SNRIs, or triptans — raises the risk of serotonin syndrome: dangerous overheating and muscle rigidity.[13][18] Combining it with MAOIs presents extreme toxicity risk and should be treated as potentially lethal.safety citation needed
Tramadol
Tramadol blocks serotonin reuptake and lowers the seizure threshold. Combined with 6-APB, this creates a theoretical risk of both serotonin toxicity and seizures.safety citation needed
Metabolic interactions
Some drugs slow the liver enzymes that break down 6-APB — including fluoxetine, paroxetine, ketoconazole, ritonavir, and grapefruit juice — potentially raising 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 isomer 5-APB 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 derive from its pharmacological profile.
Cardiac conditions
Pre-existing heart valve disease increases vulnerability to further fibrotic damage from the compound's serotonin receptor activation.[3][10]
Psychiatric conditions
Personal or family history of psychotic disorders is a relative contraindication, consistent with other serotonergic entactogens.[5]
Liver impairment
6-APB is metabolized to toxic intermediates,[12] warranting caution in those with pre-existing liver disease.
Concurrent serotonergic medication
MAOIs, SSRIs, SNRIs, and other serotonin-affecting 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 less potent by weight than the hydrochloride — the same milligram dose 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 a 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
6-APB lasts substantially longer than MDMA. The environment and psychological state at the outset anchor a much longer commitment, so a familiar, comfortable setting with trusted companions matters more here than with shorter-acting substances.
The gradual onset can tempt redosing before effects have fully developed. Patience during the come-up prevents accidental overdose from stacking doses.
Aftercare & integration. The serotonin depletion following 6-APB use can produce low mood, fatigue, and irritability in the days afterward. Prioritize sleep, nutrition (tryptophan-rich foods support serotonin recovery), and light physical activity. Avoid other serotonergic substances during recovery.
The entactogenic and mildly psychedelic character may surface emotional material worth processing. Journaling or conversation with a trusted person can help integrate insights. Persistent low mood beyond a week warrants consultation with a mental health professional.
Recovery & Support
Compulsive use patterns with 6-APB are less common than with pure stimulants, but the dopaminergic 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.
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Recognizing an emergency: High body temperature (skin hot to the touch), muscle rigidity or uncontrollable twitching, seizures, confusion progressing to unconsciousness, or chest pain. These are distinct from uncomfortable but manageable symptoms — anxiety, nausea, mild overheating.
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 around 2010–2011.
| 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 similarity to MDA — a Schedule I substance — creates potential legal liability under structural analog provisions even without specific scheduling. Behavioral data confirming substitution for MDMA in animal tests[15] provides scientific evidence of pharmacological similarity that could support prosecution.
Legal status changes frequently and varies by jurisdiction. The information above reflects published sources and may not be current. Verify status with a legal authority in the relevant jurisdiction before acting on this information.
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]