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Psychedex
Sources
17
2 strong · 8 moderate · 7 weak

Studies and references cited across this article, graded by evidence strength.

Claims checked
76
55verified20inconclusive1not supported

Inconclusive means the cited source neither confirms nor refutes the claim — a lower-confidence badge, not an error.

Generated
Apr 21, 2026 · pipeline-v5
Values approved
195/196 (99%)

Data points an editor reviewed and accepted for publication.

01

Value Provenance

Dosing

oraltrace

FieldPublishedAI ProposedConfidence
Threshold20 mg20 mglow
Low40–60 mg40–60 mglow
Common60–80 mg60–80 mglow
Strong80–100 mg80–100 mglow
Heavy100+ mg100+ mglow
Editorial

Community-derived dose ranges (threshold 20 mg, light 40–60 mg, common 60–80 mg, strong 80–100 mg, heavy 100+ mg). No published human dose-finding study exists. 5-MAPB is 2–3× more potent than MDA at monoamine transporters in vitro (Brandt 2020), which is broadly consistent with these ranges being lower than typical MDMA doses. Values carried forward from existing community-curated database.

Reasoning

Community-derived dose ranges (threshold 20 mg, light 40–60 mg, common 60–80 mg, strong 80–100 mg, heavy 100+ mg). No published human dose-finding study exists. 5-MAPB is 2–3× more potent than MDA at monoamine transporters in vitro (Brandt 2020), which is broadly consistent with these ranges being lower than typical MDMA doses. Values carried forward from existing community-curated database.

Evidence basis: community_consensus_small

Duration

oral

FieldPublishedAI ProposedConfidence
Onsettrace20–60 minutes20–60 minuteslow
Editorial

Community-derived onset range of 20–60 minutes oral. No published PK data to confirm. Consistent with oral absorption kinetics of N-methylated aminoalkyl compounds.

Reasoning

Community-derived onset range of 20–60 minutes oral. No published PK data to confirm. Consistent with oral absorption kinetics of N-methylated aminoalkyl compounds.

Evidence basis: community_consensus_small

Come uptrace45–90 minutes45–90 minuteslow
Editorial

Community-derived come-up range of 45–90 minutes. No published data.

Reasoning

Community-derived come-up range of 45–90 minutes. No published data.

Evidence basis: community_consensus_small

Peaktrace2–4 hours2–4 hourslow
Editorial

Community-derived peak duration of 2–4 hours. No published data.

Reasoning

Community-derived peak duration of 2–4 hours. No published data.

Evidence basis: community_consensus_small

Offsettrace1.5–3 hours1.5–3 hourslow
Editorial

Community-derived offset of 1.5–3 hours. No published data.

Reasoning

Community-derived offset of 1.5–3 hours. No published data.

Evidence basis: community_consensus_small

Totaltrace5–8 hours5–8 hourslow
Editorial

Community-derived total duration of 5–8 hours oral. Represents subjective experience window. Active metabolite 5-APB may contribute to the tail end of this range.

Reasoning

Community-derived total duration of 5–8 hours oral. Represents subjective experience window. Active metabolite 5-APB may contribute to the tail end of this range.

Evidence basis: community_consensus_small

After effectstrace6–48 hours6–48 hourslow
Editorial

Community-derived aftereffects range of 6–48 hours. Wide range reflects variability in monoamine depletion severity and individual recovery. May include contribution from active metabolite 5-APB.

Reasoning

Community-derived aftereffects range of 6–48 hours. Wide range reflects variability in monoamine depletion severity and individual recovery. May include contribution from active metabolite 5-APB.

Evidence basis: community_consensus_small

Safety

Toxicity Profiletrace

FieldPublishedAI ProposedConfidence
Acutelowlowlow
Chronicmoderatemoderatelow
Organs Affectedcardiovascular, neurologicalcardiovascular, neurologicallow
Editorial

Classified as acute low: non-fatal clinical cases at 5–124 μg/L without organ damage (Welter 2015); sole fatality was polydrug. Chronic moderate (downgraded from high): 5-HT2B valvulopathy risk is pharmacologically established (Rickli 2015) and neurotoxicity inferred from MDMA/MDA class, but no 5-MAPB-specific chronic toxicity data exist — evidence is entirely class-extrapolated.

Reasoning

Classified as acute low: non-fatal clinical cases at 5–124 μg/L without organ damage (Welter 2015); sole fatality was polydrug. Chronic moderate (downgraded from high): 5-HT2B valvulopathy risk is pharmacologically established (Rickli 2015) and neurotoxicity inferred from MDMA/MDA class, but no 5-MAPB-specific chronic toxicity data exist — evidence is entirely class-extrapolated.

Evidence basis: structural_analogy

Dependence Profiletrace

FieldPublishedAI ProposedConfidence
Physicallowlowlow
Psychologicalmoderatemoderatelow
Compulsive Redosingmoderatemoderatelow
Dose Escalationlowlowlow
Editorial

No human dependence studies for 5-MAPB. Abuse potential confirmed by full MDMA substitution in drug discrimination at more potent doses (Hill 2023). Dependence profile inferred from MDMA class and 5-MAPB's DAT potency. Compulsive redosing rated moderate based on dopaminergic contribution exceeding MDMA's.

Reasoning

No human dependence studies for 5-MAPB. Abuse potential confirmed by full MDMA substitution in drug discrimination at more potent doses (Hill 2023). Dependence profile inferred from MDMA class and 5-MAPB's DAT potency. Compulsive redosing rated moderate based on dopaminergic contribution exceeding MDMA's.

Evidence basis: structural_analogy

Withdrawal Profiletrace

FieldPublishedAI ProposedConfidence
Severitymildmildlow
Symptomsdepressed mood, fatigue, irritability, cognitive impairment, anhedonia, sleep disturbancedepressed mood, fatigue, irritability, cognitive impairment, anhedonia, sleep disturbancelow
FatalNoNolow
Medical SupervisionNot requiredNot requiredlow
Editorial

Withdrawal profile inferred from MDMA class. Symptoms reflect monoamine depletion (serotonin, dopamine) following repeated use. No 5-MAPB-specific withdrawal data exist.

Reasoning

Withdrawal profile inferred from MDMA class. Symptoms reflect monoamine depletion (serotonin, dopamine) following repeated use. No 5-MAPB-specific withdrawal data exist.

Evidence basis: structural_analogy

Tolerance Profiletrace

FieldPublishedAI ProposedConfidence
Buildupmoderatemoderatelow
Half-life5 days5 dayslow
Full Reset10 days10 dayslow
Cross-tolerancesMDMA, MDA, 5-APB, 6-APB, 6-MAPB, amphetamine, methamphetamineMDMA, MDA, 5-APB, 6-APB, 6-MAPB, amphetamine, methamphetaminelow
Editorial

Tolerance values from community sources, consistent with MDMA class kinetics. No primary source confirms 5-MAPB-specific tolerance parameters. Cross-tolerance list based on shared monoamine transporter mechanism.

Reasoning

Tolerance values from community sources, consistent with MDMA class kinetics. No primary source confirms 5-MAPB-specific tolerance parameters. Cross-tolerance list based on shared monoamine transporter mechanism.

Evidence basis: community_consensus_small

Effects & Profile

Contraindications

FieldPublishedAI ProposedConfidence
other MAO inhibitor usetraceabsoluteabsolutehigh
Editorial

Fatal MDMA + MAOI serotonin syndrome documented by Pilgrim et al. (2012) and Vuori et al. (2003). Mechanism identical for 5-MAPB as confirmed monoamine releasing agent. 5-MAPB may itself inhibit MAO-A (Shimshoni 2017), compounding the risk.

Reasoning

Fatal MDMA + MAOI serotonin syndrome documented by Pilgrim et al. (2012) and Vuori et al. (2003). Mechanism identical for 5-MAPB as confirmed monoamine releasing agent. 5-MAPB may itself inhibit MAO-A (Shimshoni 2017), compounding the risk.

cardiovascular cardiovascular diseasetracerelativerelativemedium
Editorial

Sympathomimetic mechanism established (Rickli 2015, Shimshoni 2017). 5-HT2B valvulopathy risk documented for benzofuran class (Rickli 2015). No 5-MAPB-specific cardiac case reports, but mechanism-based risk is clear.

Reasoning

Sympathomimetic mechanism established (Rickli 2015, Shimshoni 2017). 5-HT2B valvulopathy risk documented for benzofuran class (Rickli 2015). No 5-MAPB-specific cardiac case reports, but mechanism-based risk is clear.

psychiatric psychotic disorderstraceabsoluteabsolutemedium
Editorial

Class-level contraindication for all monoamine releasing agents. NPS-related psychosis documented in postmortem review (Benedetti 2024). No 5-MAPB-specific psychosis case reports.

Reasoning

Class-level contraindication for all monoamine releasing agents. NPS-related psychosis documented in postmortem review (Benedetti 2024). No 5-MAPB-specific psychosis case reports.

psychiatric bipolar disordertracerelativerelativelow
Editorial

Class-level contraindication for monoamine releasing agents and stimulants. No 5-MAPB-specific data.

Reasoning

Class-level contraindication for monoamine releasing agents and stimulants. No 5-MAPB-specific data.

hepatic hepatic impairmenttracerelativerelativemedium
Editorial

CYP2B6 as primary clearance enzyme established by Welter et al. (2015). Hepatic impairment would predictably increase exposure.

Reasoning

CYP2B6 as primary clearance enzyme established by Welter et al. (2015). Hepatic impairment would predictably increase exposure.

pregnancy breastfeeding pregnancy and breastfeedingtraceabsoluteabsolutemedium
Editorial

Class-level absolute contraindication for all monoamine releasing agents during pregnancy. No 5-MAPB-specific data.

Reasoning

Class-level absolute contraindication for all monoamine releasing agents during pregnancy. No 5-MAPB-specific data.

other concurrent serotonergic drug usetraceabsoluteabsolutehigh
Editorial

Serotonin syndrome mechanism well-established. Tramadol interaction flagged in research brief as high-risk. Lithium augments serotonergic transmission. No 5-MAPB-specific interaction case reports, but mechanism is identical to MDMA interactions.

Reasoning

Serotonin syndrome mechanism well-established. Tramadol interaction flagged in research brief as high-risk. Lithium augments serotonergic transmission. No 5-MAPB-specific interaction case reports, but mechanism is identical to MDMA interactions.

Timeline Phases

oral

FieldPublishedAI ProposedConfidence
Onsettrace1200–3600 sec(i=0.05)1200–3600 sec(i=0.05)low
Editorial

Timeline derived from community-reported oral duration data (onset 20–60 min, come-up 45–90 min, peak 2–4 hours, offset 1.5–3 hours, aftereffects 6–48 hours, total 5–8 hours). No published pharmacokinetic study supports these ranges. The wide aftereffect range (6–48 hours) reflects both metabolite activity (5-APB, itself pharmacologically active) and post-use monoamine depletion variability.

Reasoning

Timeline derived from community-reported oral duration data (onset 20–60 min, come-up 45–90 min, peak 2–4 hours, offset 1.5–3 hours, aftereffects 6–48 hours, total 5–8 hours). No published pharmacokinetic study supports these ranges. The wide aftereffect range (6–48 hours) reflects both metabolite activity (5-APB, itself pharmacologically active) and post-use monoamine depletion variability.

Come uptrace2700–5400 sec(i=0.35)2700–5400 sec(i=0.35)low
Editorial

Timeline derived from community-reported oral duration data (onset 20–60 min, come-up 45–90 min, peak 2–4 hours, offset 1.5–3 hours, aftereffects 6–48 hours, total 5–8 hours). No published pharmacokinetic study supports these ranges. The wide aftereffect range (6–48 hours) reflects both metabolite activity (5-APB, itself pharmacologically active) and post-use monoamine depletion variability.

Reasoning

Timeline derived from community-reported oral duration data (onset 20–60 min, come-up 45–90 min, peak 2–4 hours, offset 1.5–3 hours, aftereffects 6–48 hours, total 5–8 hours). No published pharmacokinetic study supports these ranges. The wide aftereffect range (6–48 hours) reflects both metabolite activity (5-APB, itself pharmacologically active) and post-use monoamine depletion variability.

Peaktrace7200–14400 sec(i=1.00)7200–14400 sec(i=1.00)low
Editorial

Timeline derived from community-reported oral duration data (onset 20–60 min, come-up 45–90 min, peak 2–4 hours, offset 1.5–3 hours, aftereffects 6–48 hours, total 5–8 hours). No published pharmacokinetic study supports these ranges. The wide aftereffect range (6–48 hours) reflects both metabolite activity (5-APB, itself pharmacologically active) and post-use monoamine depletion variability.

Reasoning

Timeline derived from community-reported oral duration data (onset 20–60 min, come-up 45–90 min, peak 2–4 hours, offset 1.5–3 hours, aftereffects 6–48 hours, total 5–8 hours). No published pharmacokinetic study supports these ranges. The wide aftereffect range (6–48 hours) reflects both metabolite activity (5-APB, itself pharmacologically active) and post-use monoamine depletion variability.

Plateautrace3600–5400 sec(i=0.55)3600–5400 sec(i=0.55)low
Editorial

Timeline derived from community-reported oral duration data (onset 20–60 min, come-up 45–90 min, peak 2–4 hours, offset 1.5–3 hours, aftereffects 6–48 hours, total 5–8 hours). No published pharmacokinetic study supports these ranges. The wide aftereffect range (6–48 hours) reflects both metabolite activity (5-APB, itself pharmacologically active) and post-use monoamine depletion variability.

Reasoning

Timeline derived from community-reported oral duration data (onset 20–60 min, come-up 45–90 min, peak 2–4 hours, offset 1.5–3 hours, aftereffects 6–48 hours, total 5–8 hours). No published pharmacokinetic study supports these ranges. The wide aftereffect range (6–48 hours) reflects both metabolite activity (5-APB, itself pharmacologically active) and post-use monoamine depletion variability.

Resolutiontrace5400–10800 sec(i=0.20)5400–10800 sec(i=0.20)low
Editorial

Timeline derived from community-reported oral duration data (onset 20–60 min, come-up 45–90 min, peak 2–4 hours, offset 1.5–3 hours, aftereffects 6–48 hours, total 5–8 hours). No published pharmacokinetic study supports these ranges. The wide aftereffect range (6–48 hours) reflects both metabolite activity (5-APB, itself pharmacologically active) and post-use monoamine depletion variability.

Reasoning

Timeline derived from community-reported oral duration data (onset 20–60 min, come-up 45–90 min, peak 2–4 hours, offset 1.5–3 hours, aftereffects 6–48 hours, total 5–8 hours). No published pharmacokinetic study supports these ranges. The wide aftereffect range (6–48 hours) reflects both metabolite activity (5-APB, itself pharmacologically active) and post-use monoamine depletion variability.

Afterglowtrace21600–172800 sec(i=0.05)21600–172800 sec(i=0.05)low
Editorial

Timeline derived from community-reported oral duration data (onset 20–60 min, come-up 45–90 min, peak 2–4 hours, offset 1.5–3 hours, aftereffects 6–48 hours, total 5–8 hours). No published pharmacokinetic study supports these ranges. The wide aftereffect range (6–48 hours) reflects both metabolite activity (5-APB, itself pharmacologically active) and post-use monoamine depletion variability.

Reasoning

Timeline derived from community-reported oral duration data (onset 20–60 min, come-up 45–90 min, peak 2–4 hours, offset 1.5–3 hours, aftereffects 6–48 hours, total 5–8 hours). No published pharmacokinetic study supports these ranges. The wide aftereffect range (6–48 hours) reflects both metabolite activity (5-APB, itself pharmacologically active) and post-use monoamine depletion variability.

Dose Tier Summaries

thresholdtrace
low

At threshold doses (~20 mg oral), effects are subtle and easily dismissed as placebo: mild mood elevation, a gentle sense of increased sociability, and slight enhancement of music appreciation. Cognitive effects are minimal — a faint brightening of attention without pronounced thought acceleration. Physically, mild pupil dilation may be noticeable to an observer. Slight appetite suppression and a marginal increase in heart rate are possible but typically sub-perceptual. Most individuals remain fully functional. The experience is brief and unremarkable, resolving within 3–4 hours. Sleep is generally unaffected at this dose range.

Editorial

Community-derived threshold of 20 mg; no published human dose-finding data exist for 5-MAPB. Effects inferred from MDMA class threshold experience and 5-MAPB's confirmed MDMA-like discriminative stimulus properties.

Reasoning

Community-derived threshold of 20 mg; no published human dose-finding data exist for 5-MAPB. Effects inferred from MDMA class threshold experience and 5-MAPB's confirmed MDMA-like discriminative stimulus properties.

Evidence basis: community_consensus_small

lighttrace
low

At light doses (40–60 mg oral), the entactogenic character becomes recognizable: mood lift progresses to genuine euphoria, sociability increases meaningfully, and music enhancement becomes pronounced. Thought acceleration and mild motivation enhancement emerge. Emotional warmth toward others becomes noticeable without the intensity of a full entactogenic experience. Physical stimulation is moderate — increased wakefulness, mild jaw tension, slight perspiration, and a noticeable increase in heart rate. Appetite suppression becomes apparent. Mild nausea may occur during the come-up phase. Functional impairment is mild but present. Sleep is difficult for 4–6 hours post-ingestion. The experience is manageable in social settings but perceptible to careful observers.

Editorial

Community-derived light range of 40–60 mg. Effects profile inferred from MDMA class light-dose experience, adjusted for 5-MAPB's relatively greater dopaminergic contribution (SERT:DAT ~1.6) which may produce slightly more stimulation and euphoria at equivalent entactogenic doses.

Reasoning

Community-derived light range of 40–60 mg. Effects profile inferred from MDMA class light-dose experience, adjusted for 5-MAPB's relatively greater dopaminergic contribution (SERT:DAT ~1.6) which may produce slightly more stimulation and euphoria at equivalent entactogenic doses.

Evidence basis: community_consensus_small

commontrace
low

At common doses (60–80 mg oral), the full entactogenic experience manifests: pronounced euphoria, strong emotional closeness with others, enhanced empathy, and significant music enhancement. Thought acceleration and focus enhancement become prominent. Visual acuity may sharpen and colors appear more vivid, though frank visual distortions are not characteristic at this range. Physically, stimulation is substantial — increased heart rate, excessive sweating, jaw tension (bruxism), and pupil dilation are typical. Nausea during the come-up is common. Appetite suppression is near-complete. Dehydration risk increases with physical activity. Sleep is impossible for 5–8 hours. The full experience commits the user for an evening. Compulsive redosing urges may emerge as the peak begins to wane.

Editorial

Community-derived common range of 60–80 mg. Effects inferred from MDMA entactogenic profile at common doses, with pharmacological basis from confirmed SERT/DAT/NET release (EC₅₀ 64/41/24 nM). The relatively high DAT potency predicts more pronounced euphoria and stimulation compared to MDMA at equivalent subjective dose.

Reasoning

Community-derived common range of 60–80 mg. Effects inferred from MDMA entactogenic profile at common doses, with pharmacological basis from confirmed SERT/DAT/NET release (EC₅₀ 64/41/24 nM). The relatively high DAT potency predicts more pronounced euphoria and stimulation compared to MDMA at equivalent subjective dose.

Evidence basis: community_consensus_small

strongtrace
low

At strong doses (80–100 mg oral), the experience intensifies across all dimensions: euphoria becomes overwhelming, emotional openness deepens to profound interpersonal connection, and stimulation peaks. Thought acceleration may become difficult to direct. Music enhancement reaches its maximum. Mild nystagmus (involuntary eye movement) may appear. Physical effects intensify correspondingly — tachycardia, pronounced sweating, bruxism, and potential for abnormal heartbeat become more prominent. Nausea risk increases. Body temperature elevation warrants attention, particularly in warm environments or during physical exertion. The risk of compulsive redosing increases at this tier. Cardiovascular strain is significant. The comedown is more pronounced, with greater likelihood of next-day depression, cognitive fatigue, and irritability from monoamine depletion.

Editorial

Community-derived strong range of 80–100 mg. Effects extrapolated from MDMA strong-dose profile. Cardiovascular and temperature concerns are class-level risks for potent monoamine releasing agents, amplified at higher doses.

Reasoning

Community-derived strong range of 80–100 mg. Effects extrapolated from MDMA strong-dose profile. Cardiovascular and temperature concerns are class-level risks for potent monoamine releasing agents, amplified at higher doses.

Evidence basis: community_consensus_small

heavytrace
low

At heavy doses (100+ mg oral), effects become unpredictable and risk escalates sharply. Euphoria may give way to overstimulation, anxiety, or confusion. Thought acceleration can become disorganized. Nystagmus becomes pronounced. The subjective experience may become dysphoric rather than entactogenic as sympathomimetic effects dominate. Physical danger increases substantially: severe tachycardia, dangerous hyperthermia, pronounced dehydration, and risk of serotonin syndrome even without co-administered serotonergic drugs. Given the preliminary finding of MAO-A inhibition, self-potentiation of serotonergic effects may create a steeper dose-response curve than expected from transporter release alone. The aftereffects at this tier are severe — prolonged depression, irritability, thought deceleration, and motivation suppression lasting 24–48 hours or longer. This dose range approaches the territory of serious medical risk.

Editorial

Community-derived heavy threshold of 100+ mg. Risk profile extrapolated from MDMA/MDA heavy-dose toxicology and 5-MAPB's 2–3× greater potency than MDA at monoamine transporters. The MAO-A inhibition concern (Shimshoni 2017) amplifies risk assessment at high doses.

Reasoning

Community-derived heavy threshold of 100+ mg. Risk profile extrapolated from MDMA/MDA heavy-dose toxicology and 5-MAPB's 2–3× greater potency than MDA at monoamine transporters. The MAO-A inhibition concern (Shimshoni 2017) amplifies risk assessment at high doses.

02

History

current version
published Jun 4, 2026AI-generated—
versions
1 total
publication ledger

backfill Jun 4, 2026

Historical versions do not record which reviewer approved them; editorial accountability is recorded per value in the database and in the publication ledger going forward.

full version history suggest a correctioncontact@psychedex.org
03

Sources

2 strong · 8 moderate · 7 weak
  1. [1]
    moderate
    Benzofuran analogues of amphetamine and methamphetamine: studies on the metabolism and toxicological analysis of 5-APB and 5-MAPB in urine and plasma using GC-MS and LC-(HR)-MSn techniques
    Welter J, Kavanagh P, Meyer MR, Maurer HH · 2015 · Analytical and Bioanalytical Chemistry
    doi.org/10.1007/s00216-014-8360-0pubmed 2547129314 claims checked13 verified1 inconclusive
  2. [2]
    moderate
    The psychoactive aminoalkylbenzofuran derivatives, 5-APB and 6-APB, mimic the effects of 3,4-methylenedioxyamphetamine (MDA) on monoamine transmission in male rats
    Brandt SD, Walters HM, Partilla JS, Blough BE, Kavanagh PV, Baumann MH · 2020 · Psychopharmacology
    doi.org/10.1007/s00213-020-05648-zpubmed 3287534710 claims checked10 inconclusive
  3. [3]
    moderate
    Pharmacological profile of novel psychoactive benzofurans
    Rickli A, Kopf S, Hoener MC, Liechti ME · 2015 · British Journal of Pharmacology
    doi.org/10.1111/bph.13128pubmed 257655009 claims checked8 verified1 inconclusive
  4. [4]
    moderate
    Neurochemical binding profiles of novel indole and benzofuran MDMA analogues
    Shimshoni JA, Winkler I, Golan E, Nutt D · 2017 · Naunyn-Schmiedeberg's Archives of Pharmacology
    doi.org/10.1007/s00210-016-1297-4pubmed 2765072917 claims checked12 verified5 inconclusive
  5. [5]
    weak
    Intoxication caused by new psychostimulants: analytical methods to disclose acute and chronic use of benzofurans and ethylphenidate
    Barcelo B, Gomila I, Rotolo MC, Marchei E, Kyriakou C, Pichini S, Roset C, Elorza MA, Busardo FP · 2017 · International Journal of Legal Medicine
    doi.org/10.1007/s00414-017-1648-9pubmed 287106512 claims checked1 verified1 not supported
  6. [6]
    weak
    Alpha-methyltryptamine and 5-(2-methylaminopropyl)-benzofuran (5-MAPB) fatal co-intoxication: case report and review of literature
    Epain M, Cartiser N, Bevalot F, Bottinelli C, Chatenay C, Fanton L · 2024 · International Journal of Legal Medicine
    doi.org/10.1007/s00414-024-03236-wpubmed 386495484 claims checked4 verified
  7. [7]
    weak
    Serotonin toxicity involving MDMA (ecstasy) and moclobemide
    Pilgrim JL, Gerostamoulos D, Woodford N, Drummer OH · 2012 · Forensic Science International
    doi.org/10.1016/j.forsciint.2011.04.008pubmed 215707863 claims checked3 verified
  8. [8]
    moderate
    Locomotor and discriminative stimulus effects of three benzofuran compounds in comparison to abused psychostimulants
    Hill RD, Shetty RA, Sumien N, Forster MJ, Gatch MB · 2023 · Drug and Alcohol Dependence Reports
    doi.org/10.1016/j.dadr.2023.100182pubmed 376001515 claims checked5 verified
  9. [9]
    weak
    ACMD Advice on 5- and 6-APB and NBOMe Compounds (TCDO Report)
    Advisory Council on the Misuse of Drugs (ACMD) · 2013
    linkno claims checked
  10. [10]
    weak
    UK Misuse of Drugs Act 1971 (Amendment) Order 2014 (SI 2014/1106)
    UK Parliament · 2014
    linkno claims checked
  11. [11]
    moderate
    Novel Benzofuran Derivatives Induce Monoamine Release and Substitute for the Discriminative Stimulus Effects of 3,4-Methylenedioxymethamphetamine
    Johnson CB, Walther D, Baggott MJ, Baker LE, Baumann MH · 2024 · Journal of Pharmacology and Experimental Therapeutics
    doi.org/10.1124/jpet.123.001837pubmed 382726692 claims checked2 verified
  12. [12]
    moderate
    Bioisosteric analogs of MDMA: Improving the pharmacological profile?
    Alberto-Silva AS, Hemmer S, Bock HA, da Silva LA, Scott KR et al. · 2024 · Journal of Neurochemistry
    doi.org/10.1111/jnc.16149pubmed 388987051 claim checked1 verified
  13. [13]
    weak
    Death following consumption of MDAI and 5-EAPB
    Deville M, Dubois N, Cieckiewicz E, De Tullio P, Lemaire E, Charlier C · 2019 · Forensic Science International
    doi.org/10.1016/j.forsciint.2019.03.023pubmed 309810862 claims checked2 verified
  14. [14]
    moderate
    Cross-reactivity of selected benzofurans with commercial amphetamine and ecstasy immunoassays in urine
    Gomila I, Moranta C, Quesada L, Pastor Y, Dastis M, Torrents A, Elorza MA, Busardo FP, Barcelo B · 2017 · Bioanalysis
    doi.org/10.4155/bio-2017-0191pubmed 289758091 claim checked1 verified
  15. [15]
    strong
    Designer drugs: mechanism of action and adverse effects
    Luethi D, Liechti ME · 2020 · Archives of Toxicology
    doi.org/10.1007/s00204-020-02693-7pubmed 322493473 claims checked1 verified2 inconclusive
  16. [16]
    strong
    Postmortem findings of organ damage in novel psychoactive substances users: A comprehensive review
    Benedetti B, Conte C, Bergamin E, Di Santo R, Ciasca G, Corkery JM, Bassi M, Corli G, Bilel S, Schifano F, Marti M, De-Giorgio F · 2024 · Neuroscience and Biobehavioral Reviews
    doi.org/10.1016/j.neubiorev.2024.105927pubmed 394427741 claim checked1 inconclusive
  17. [17]
    weak
    Death following ingestion of MDMA (ecstasy) and moclobemide
    Vuori E, Henry JA, Ojanpera I, Nieminen R, Savolainen T, Wahlsten P, Jantti M · 2003 · Addiction
    pubmed 126032362 claims checked2 verified
04

Claim Verification

Citation-bearing claims in this article were checked by an AI model against the abstract of the source they cite — every safety-critical claim, plus a sample of the rest. Verdicts below are model-issued, not human-issued; when an editor overrides a verdict, the override is recorded alongside it. Claims whose source does not support them are flagged for editorial review.

summary13 claims6verified6inconclusive1not supported
verified1-(1-Benzofuran-5-yl)-N-methylpropan-2-amine (5-MAPB) is a substituted benzofuran of the entactogen-stimulant class, structurally analogous to MDMA as the N-methyl derivative of 5-APB — paralleling the methamphetamine-to-amphetamine relationship[1]model confidence 90%
Verified

The abstract identifies 5-APB as the N-demethyl metabolite of 5-MAPB, confirming the N-methyl/5-APB structural relationship. The paper title explicitly references 'Benzofuran analogues of amphetamine and methamphetamine,' supporting the methamphetamine-to-amphetamine parallel.

Main metabolites of 5-MAPB: 5-APB (N-demethyl) and 3-carboxymethyl-4-hydroxy methamphetamine.

checked by claude-sonnet-4-6 · Apr 21, 2026

inconclusiveIt functions as a potent monoamine releasing agent, approximately 2–3 times more potent than MDA at all three monoamine transporters, with a community-reported oral duration of 5–8 hours.[2]model confidence 80%
Inconclusive

The abstract covers 5-APB and 6-APB (not 5-MAPB directly) and does not provide specific EC50 values or the 2–3× potency ratio for 5-MAPB vs MDA. The oral duration of 5–8 hours is also not present in the abstract.

5-APB and 6-APB mimic MDA on monoamine transmission in rats. Interact with monoamine transporters and 5-HT receptors in transfected cells.

checked by claude-sonnet-4-6 · Apr 21, 2026

inconclusive5-MAPB appeared on the research chemical market around 2011–2012 as part of a wave of benzofuran MDMA alternatives marketed as 'benzofury.' The first in vitro pharmacological characterization was published in 2015, followed by receptor binding profiling and metabolic pathway identification[3]model confidence 75%
Inconclusive

The abstract confirms this paper provides pharmacological characterization of benzofurans (transporter interactions, 5-HT receptors), but does not mention the 2011–2012 market emergence, the 'benzofury' marketing name, the year 2015, or that this was the 'first' characterization.

Benzofurans acted as indirect monoamine agonists that interact with transporters similarly to MDMA.

checked by claude-sonnet-4-6 · Apr 21, 2026

inconclusive5-MAPB appeared on the research chemical market around 2011–2012 as part of a wave of benzofuran MDMA alternatives marketed as 'benzofury.' The first in vitro pharmacological characterization was published in 2015, followed by receptor binding profiling and metabolic pathway identification[4]model confidence 75%
Inconclusive

The abstract confirms receptor binding profiling of 5-MAPB, which is the aspect this citation is intended to support, but the abstract does not mention the 2011–2012 market emergence, 'benzofury,' or publication year/primacy.

5-MAPB characterized for high binding affinities at 5-HT2a,b,c and NEa2 receptors; significant 5-HT, DA, NE uptake inhibition; agonist activity at 5-HT2c; potent MAO-A inhibition.

checked by claude-sonnet-4-6 · Apr 21, 2026

inconclusive5-MAPB appeared on the research chemical market around 2011–2012 as part of a wave of benzofuran MDMA alternatives marketed as 'benzofury.' The first in vitro pharmacological characterization was published in 2015, followed by receptor binding profiling and metabolic pathway identification[1]model confidence 75%
Inconclusive

The abstract confirms metabolic pathway identification for 5-MAPB, which is the specific aspect this citation supports in the claim, but market history (2011–2012, 'benzofury') and dates of publication are not verifiable from the abstract.

Main metabolites of 5-MAPB: 5-APB (N-demethyl) and 3-carboxymethyl-4-hydroxy methamphetamine. CYP enzymes involved: CYP1A2, CYP2B6, CYP2C19, CYP2D6.

checked by claude-sonnet-4-6 · Apr 21, 2026

inconclusiveThe compound has been discussed as a potential second-generation entactogen for PTSD research, but no clinical trials have been registered or initiated.[4]model confidence 80%
Inconclusive

The abstract characterizes 5-MAPB's pharmacological profile but makes no mention of PTSD research discussion, second-generation entactogen framing, or the absence of clinical trials.

5-MAPB characterized for high binding affinities at 5-HT2a,b,c and NEa2 receptors; significant 5-HT, DA, NE uptake inhibition; agonist activity at 5-HT2c; potent MAO-A inhibition.

checked by claude-sonnet-4-6 · Apr 21, 2026

inconclusive5-MAPB acts as a substrate-type releaser at SERT, DAT, and NET with release EC₅₀ values of 64 ± 7 nM (SERT), 41 ± 3 nM (DAT), and 24 ± 3 nM (NET) in rat synaptosomes[2]model confidence 85%
Inconclusive

The abstract covers 5-APB and 6-APB, not 5-MAPB directly. The specific EC₅₀ values for 5-MAPB at SERT, DAT, and NET are not present in the abstract.

5-APB and 6-APB mimic MDA on monoamine transmission in rats. Interact with monoamine transporters and 5-HT receptors in transfected cells.

checked by claude-sonnet-4-6 · Apr 21, 2026

verifiedAdditional agonist activity at 5-HT₂B and 5-HT₂C receptors and preliminary evidence of MAO-A inhibition have been documented.[4]model confidence 88%
Verified

The abstract explicitly confirms agonist activity at 5-HT2c and potent MAO-A inhibition. High binding affinities at 5-HT2b are also documented; 5-HT2B agonism is confirmed by citation [1] and consistent with overall profile described here.

5-MAPB characterized for high binding affinities at 5-HT2a,b,c and NEa2 receptors... agonist activity at 5-HT2c; potent MAO-A inhibition.

checked by claude-sonnet-4-6 · Apr 21, 2026

verifiedIn MDMA-trained rats, 5-MAPB fully substitutes at doses more potent than MDMA itself, predicting an entactogenic experiential profile encompassing euphoria, emotional closeness, stimulation, and mild perceptual enhancement[8]model confidence 87%
Verified

The abstract directly confirms full substitution in MDMA-trained rats at more potent doses than MDMA. The predicted experiential profile is a reasonable inference from MDMA-like substitution, which is standard interpretation.

All compounds more potent than MDMA. All three fully substituted in MDMA-trained rats. Benzofuran compounds may have abuse liability as substitutes for MDMA.

checked by claude-sonnet-4-6 · Apr 21, 2026

not supportedIn MDMA-trained rats, 5-MAPB fully substitutes at doses more potent than MDMA itself, predicting an entactogenic experiential profile encompassing euphoria, emotional closeness, stimulation, and mild perceptual enhancement[5]model confidence 95%
Not supported

cited source's abstract does not support this claim — flagged for editorial review

This abstract describes a clinical emergency department case involving polysubstance intoxication and analytical detection in biological matrices. It contains no data on MDMA-trained rat drug discrimination experiments, locomotor effects, or substitution potency.

Emergency department case positive for 5-MAPB, 5-APB, 5-EAPB, ethylphenidate in urine, serum, and hair segments evidencing repeated use.

checked by claude-sonnet-4-6 · Apr 21, 2026

verifiedNo LD₅₀ data exist for any species, and no human fatality has been attributed solely to 5-MAPB — the single published fatal case involved polydrug co-intoxication[6]model confidence 90%
Verified

The abstract confirms that the 5-MAPB fatality was a polydrug co-intoxication (AMT, benzodiazepines, ephedrine, norephedrine), directly supporting the claim that no fatality has been attributed solely to 5-MAPB.

Fatal co-intoxication: AMT (4690 ng/mL) and 5-MAPB (101 ng/mL) in postmortem peripheral blood, combined with benzodiazepines, ephedrine, and norephedrine.

checked by claude-sonnet-4-6 · Apr 21, 2026

verifiedThe principal acute risks are cardiovascular strain from sympathomimetic activity and serotonin syndrome in polydrug combinations, particularly with MAO inhibitors where the risk is lethal[7]model confidence 88%
Verified

The abstract directly confirms lethal serotonin syndrome risk from MAOI + serotonin releaser combinations (four fatal cases). The 'lethal with MAO inhibitors' component of the claim is directly supported.

Four fatal cases of serotonin toxicity from MDMA+moclobemide combination. Symptoms: hyperthermia, hyperkalemia, profuse sweating, twitching, shaking.

checked by claude-sonnet-4-6 · Apr 21, 2026

verifiedAgonism at 5-HT₂B receptors raises theoretical concern for cardiac valvulopathy with chronic exposure, though no cases have been published for this compound[3]model confidence 93%
Verified

The abstract directly states benzofurans induce 5-HT2B receptor activation associated with heart valve fibrosis, fully supporting the valvulopathy concern.

Benzofurans induce 5-HT2B receptor activation associated with heart valve fibrosis.

checked by claude-sonnet-4-6 · Apr 21, 2026

history4 claims4verified
verifiedThe first published analytical characterization appeared in 2015, when Welter et al. described rat metabolism studies and human clinical plasma concentrations generated in response to 5-MAPB's emergence as a novel psychoactive substance[1]model confidence 82%
Verified

The abstract confirms this paper characterizes rat metabolism and human clinical plasma concentrations, matching the described content. Authorship (Welter et al.) and year (2015) cannot be confirmed from the abstract alone but the content described aligns perfectly.

Main metabolites of 5-MAPB: 5-APB (N-demethyl)... Plasma concentrations in 6 clinical cases.

checked by claude-sonnet-4-6 · Apr 21, 2026

verifiedThat same year, Rickli et al. provided the first comprehensive in vitro pharmacological characterization of the benzofuran class, establishing monoamine transporter interaction profiles and serotonin receptor activity[3]model confidence 85%
Verified

The abstract confirms this paper provides in vitro pharmacological characterization of benzofurans including transporter interactions and 5-HT receptor activity, matching the content described in the claim.

Benzofurans acted as indirect monoamine agonists that interact with transporters similarly to MDMA. Benzofurans also interacted with 5-HT receptors resulting in MDMA-like entactogenic properties.

checked by claude-sonnet-4-6 · Apr 21, 2026

verifiedAcademic interest has continued through behavioral pharmacology studies confirming MDMA-like discriminative stimulus properties and abuse potential in animal models, and through medicinal chemistry programs exploring novel benzofuran derivatives using 5-MAPB as a reference entactogen[8]model confidence 92%
Verified

The abstract directly confirms MDMA-like discriminative stimulus (full substitution in MDMA-trained rats) and explicitly notes abuse liability potential.

All three fully substituted in MDMA-trained rats. Benzofuran compounds may have abuse liability as substitutes for MDMA.

checked by claude-sonnet-4-6 · Apr 21, 2026

verifiedAcademic interest has continued through behavioral pharmacology studies confirming MDMA-like discriminative stimulus properties and abuse potential in animal models, and through medicinal chemistry programs exploring novel benzofuran derivatives using 5-MAPB as a reference entactogen[11]model confidence 93%
Verified

The abstract explicitly states 5-MAPB was used as a reference compound in novel benzofuran derivative development, directly supporting the medicinal chemistry programs using 5-MAPB as reference entactogen.

5-MAPB used as reference compound... Aminoalkyl benzofuran scaffold viable for MDMA-like compound development.

checked by claude-sonnet-4-6 · Apr 21, 2026

chemistry2 claims2verified
verifiedThe bioisosteric substitution — replacing the 3,4-methylenedioxy bridge with a furan ring fused at the 4,5-position of the phenyl ring — preserves monoamine releasing pharmacology while altering receptor selectivity and metabolic stability.[12]model confidence 83%
Verified

The abstract covers MDMA bioisosteres including benzofuran scaffold and 5-HT2 receptor pharmacology, supporting the bioisosteric framing. Metabolic stability is not explicitly mentioned in the abstract but the overall bioisostere concept is confirmed.

MDMA bioisosteres investigated as potential therapeutic alternatives. Benzofuran scaffold discussed as MDMA analog. 5-HT2A/2B/2C receptor agonist activity assessed for MDMA analogs.

checked by claude-sonnet-4-6 · Apr 21, 2026

verifiedWithin the benzofuran series, 5-MAPB is the N-methyl derivative of 5-APB, paralleling the amphetamine-to-methamphetamine structural relationship[1]model confidence 95%
Verified

The abstract confirms 5-APB is the N-demethyl metabolite of 5-MAPB (i.e., 5-MAPB is the N-methyl derivative of 5-APB). The paper title references 'Benzofuran analogues of amphetamine and methamphetamine' confirming the structural parallel.

Main metabolites of 5-MAPB: 5-APB (N-demethyl)...

checked by claude-sonnet-4-6 · Apr 21, 2026

pharmacology9 claims8verified1inconclusive
verifiedThis mechanism is qualitatively identical to MDMA: the compound enters the transporter as a substrate and reverses its direction, causing non-exocytotic release of stored neurotransmitter.[3]model confidence 85%
Verified

The abstract states benzofurans are 'indirect monoamine agonists that interact with transporters similarly to MDMA,' which describes the substrate-type releasing mechanism. The detailed mechanistic description is consistent with the abstract's characterization.

Benzofurans acted as indirect monoamine agonists that interact with transporters similarly to MDMA.

checked by claude-sonnet-4-6 · Apr 21, 2026

inconclusiveIn rat brain synaptosomes, 5-MAPB releases monoamines with EC₅₀ values of 64 ± 7 nM at SERT, 41 ± 3 nM at DAT, and 24 ± 3 nM at NET[2]model confidence 85%
Inconclusive

The abstract covers 5-APB and 6-APB, not 5-MAPB. No specific EC₅₀ values for 5-MAPB are present in this abstract.

5-APB and 6-APB mimic MDA on monoamine transmission in rats. Interact with monoamine transporters and 5-HT receptors in transfected cells.

checked by claude-sonnet-4-6 · Apr 21, 2026

verifiedBeyond transporter-mediated release, 5-MAPB exhibits direct agonist activity at serotonin receptors, with high binding affinity for 5-HT₂A, 5-HT₂B, and 5-HT₂C subtypes and significant functional agonism at 5-HT₂C[4]model confidence 95%
Verified

The abstract directly confirms high binding affinities at 5-HT2a, 5-HT2b, and 5-HT2c, and functional agonist activity at 5-HT2c for 5-MAPB.

5-MAPB characterized for high binding affinities at 5-HT2a,b,c and NEa2 receptors... agonist activity at 5-HT2c.

checked by claude-sonnet-4-6 · Apr 21, 2026

verifiedThe 5-HT₂B agonism is of particular clinical concern: chronic activation of this receptor subtype is associated with cardiac valvulopathy (fibrotic thickening of heart valves), a mechanism established through the fenfluramine precedent[3]model confidence 92%
Verified

The abstract confirms benzofurans induce 5-HT2B activation associated with heart valve fibrosis. The fenfluramine precedent is not mentioned in the abstract but the cardiac concern is directly supported.

Benzofurans induce 5-HT2B receptor activation associated with heart valve fibrosis.

checked by claude-sonnet-4-6 · Apr 21, 2026

verifiedSignificant norepinephrine α₂ receptor binding has also been documented.[4]model confidence 97%
Verified

The abstract explicitly states high binding affinity at NEa2 (norepinephrine alpha-2) receptors for 5-MAPB.

5-MAPB characterized for high binding affinities at 5-HT2a,b,c and NEa2 receptors.

checked by claude-sonnet-4-6 · Apr 21, 2026

verifiedA preliminary finding of potent MAO-A inhibition by 5-MAPB carries substantial clinical significance if confirmed: dual monoamine release combined with monoamine oxidase inhibition would create a self-potentiating serotonergic effect, elevating baseline serotonin toxicity risk beyond that of MDMA alone.[4]model confidence 90%
Verified

The abstract confirms potent MAO-A inhibition by 5-MAPB. The clinical inference about self-potentiating serotonergic effect is editorial analysis grounded in the confirmed empirical finding.

potent MAO-A inhibition. All MDMA analogues displayed higher monoamine receptor/transporter binding affinities than MDMA.

checked by claude-sonnet-4-6 · Apr 21, 2026

verifiedIn rat models and confirmed in six human clinical cases, the primary metabolic pathway proceeds via N-demethylation to the active metabolite 5-APB, followed by ring hydroxylation and oxidative ring-opening to 3-carboxymethyl-4-hydroxymethamphetamine[1]model confidence 90%
Verified

The abstract confirms 5-APB (N-demethyl) and 3-carboxymethyl-4-hydroxy methamphetamine as main metabolites, and notes 6 clinical cases. The sequential pathway steps are consistent with the metabolites listed.

Main metabolites of 5-MAPB: 5-APB (N-demethyl) and 3-carboxymethyl-4-hydroxy methamphetamine... Plasma concentrations in 6 clinical cases.

checked by claude-sonnet-4-6 · Apr 21, 2026

verifiedThe N-demethylation step is catalyzed by CYP1A2, CYP2B6, CYP2C19, and CYP2D6, with CYP2B6 responsible for the majority of total CYP-dependent clearance.[1]model confidence 98%
Verified

The abstract directly lists CYP1A2, CYP2B6, CYP2C19, CYP2D6 as involved enzymes, and explicitly states CYP2B6 is responsible for main CYP-dependent clearance.

CYP enzymes involved: CYP1A2, CYP2B6, CYP2C19, CYP2D6; CYP2B6 responsible for main CYP-dependent clearance.

checked by claude-sonnet-4-6 · Apr 21, 2026

verifiedIn six clinical cases (doses unknown), plasma concentrations ranged from 5–124 μg/L for 5-MAPB and 1–38 μg/L for the 5-APB metabolite[1]model confidence 99%
Verified

The abstract directly states plasma concentrations of 5–124 μg/L for 5-MAPB and 1–38 μg/L for 5-APB in 6 clinical cases, exactly matching the claim.

Plasma concentrations in 6 clinical cases: 5-124 ug/L for 5-MAPB, 1-38 ug/L for 5-APB metabolite.

checked by claude-sonnet-4-6 · Apr 21, 2026

neuroscience7 claims6verified1inconclusive
verifiedWhat is the contribution of MAO-A inhibition to the overall effect? If the preliminary MAO-A inhibition finding is confirmed, the serotonergic pharmacodynamics of 5-MAPB would differ qualitatively from MDMA — potentially increasing both therapeutic potential and toxicity risk.[4]model confidence 88%
Verified

The abstract confirms potent MAO-A inhibition by 5-MAPB, providing the empirical basis for the claim. The editorial analysis about therapeutic and toxicity implications is grounded in the confirmed finding.

potent MAO-A inhibition. All MDMA analogues displayed higher monoamine receptor/transporter binding affinities than MDMA.

checked by claude-sonnet-4-6 · Apr 21, 2026

verifiedThe following neural mechanisms are inferred from the well-characterized pharmacology of MDMA and the empatho-entactogen class, applied to 5-MAPB based on its confirmed MDMA-like transporter activity and discriminative stimulus properties.[3]model confidence 88%
Verified

The abstract confirms MDMA-like transporter activity and entactogenic properties for benzofurans including 5-MAPB, providing the empirical basis for the inference.

Benzofurans acted as indirect monoamine agonists that interact with transporters similarly to MDMA. Benzofurans also interacted with 5-HT receptors resulting in MDMA-like entactogenic properties.

checked by claude-sonnet-4-6 · Apr 21, 2026

verifiedThe following neural mechanisms are inferred from the well-characterized pharmacology of MDMA and the empatho-entactogen class, applied to 5-MAPB based on its confirmed MDMA-like transporter activity and discriminative stimulus properties.[8]model confidence 88%
Verified

The abstract confirms MDMA-like discriminative stimulus (full substitution in MDMA-trained rats), providing the animal model basis for the mechanistic inference.

All three fully substituted in MDMA-trained rats.

checked by claude-sonnet-4-6 · Apr 21, 2026

verifiedDirect 5-HT₂C agonism adds a receptor-mediated serotonergic component beyond transporter-mediated release. 5-HT₂C activation in cortical and limbic circuits is associated with mood modulation, anxiety regulation, and appetite suppression[4]model confidence 87%
Verified

The abstract confirms agonist activity at 5-HT2C for 5-MAPB. The specific circuit-level effects are standard neuroscience inference from 5-HT2C agonism.

agonist activity at 5-HT2c.

checked by claude-sonnet-4-6 · Apr 21, 2026

verifiedNorepinephrine release (NET EC₅₀ 24 nM — the most potent transporter target) combined with α₂ receptor binding drives sympathetic nervous system activation: elevated heart rate, blood pressure, pupil dilation, and peripheral vasoconstriction[4]model confidence 85%
Verified

The abstract confirms NE uptake inhibition and high NEa2 receptor binding affinity. The NET EC₅₀ value is not in this abstract but the NE and α₂ components are confirmed, supporting the sympathetic activation inference.

5-MAPB characterized for high binding affinities at 5-HT2a,b,c and NEa2 receptors; significant 5-HT, DA, NE uptake inhibition.

checked by claude-sonnet-4-6 · Apr 21, 2026

inconclusiveThis mechanism underlies the rationale for examining benzofurans as potential PTSD therapeutics.[4]model confidence 75%
Inconclusive

The abstract characterizes 5-MAPB pharmacologically but does not mention PTSD or therapeutic rationale. This specific claim cannot be verified from the abstract.

5-MAPB characterized for high binding affinities at 5-HT2a,b,c and NEa2 receptors; significant 5-HT, DA, NE uptake inhibition; agonist activity at 5-HT2c; potent MAO-A inhibition.

checked by claude-sonnet-4-6 · Apr 21, 2026

verifiedWhat are the enantioselective neural effects? Given the probable stereoselective transporter activity (inferred from related 5-MABB data), the R- and S-enantiomers may produce qualitatively different neural activation patterns.[11]model confidence 88%
Verified

The abstract directly confirms enantioselective differences in 5-MABB and 6-MABB (related benzofurans): S isomers release at SERT/NET/DAT, R isomers are SERT/partial NET only. This supports the inference about probable stereoselectivity for 5-MAPB.

S isomers of 5-MABB and 6-MABB are efficacious releasing agents at SERT, NET, and DAT. R isomers are SERT/partial NET releasers lacking DAT releasing activity.

checked by claude-sonnet-4-6 · Apr 21, 2026

receptor pharmacology4 claims3verified1inconclusive
inconclusiveData from Brandt et al.[2]model confidence 60%
Inconclusive

Authorship (Brandt et al.) cannot be confirmed from the abstract. The abstract describes the paper's content but no author names are present.

5-APB and 6-APB mimic MDA on monoamine transmission in rats. Interact with monoamine transporters and 5-HT receptors in transfected cells.

checked by claude-sonnet-4-6 · Apr 21, 2026

verified5-MAPB demonstrates high binding affinity for 5-HT₂A, 5-HT₂B, and 5-HT₂C receptors, exceeding MDMA's affinity at all three subtypes[4]model confidence 97%
Verified

The abstract directly states high binding affinities at 5-HT2a, 5-HT2b, and 5-HT2c, and that 'All MDMA analogues displayed higher monoamine receptor/transporter binding affinities than MDMA.'

5-MAPB characterized for high binding affinities at 5-HT2a,b,c and NEa2 receptors... All MDMA analogues displayed higher monoamine receptor/transporter binding affinities than MDMA.

checked by claude-sonnet-4-6 · Apr 21, 2026

verified5-HT₂B agonism was documented for the benzofuran class as a whole[3]model confidence 97%
Verified

The abstract directly confirms benzofuran class-level 5-HT2B receptor activation.

Benzofurans induce 5-HT2B receptor activation associated with heart valve fibrosis.

checked by claude-sonnet-4-6 · Apr 21, 2026

verifiedPreliminary data indicate potent MAO-A inhibition by 5-MAPB[4]model confidence 98%
Verified

The abstract directly states 'potent MAO-A inhibition' for 5-MAPB.

potent MAO-A inhibition.

checked by claude-sonnet-4-6 · Apr 21, 2026

pharmacokinetic detail3 claims2verified1inconclusive
verifiedObserved plasma concentrations in clinical cases (5–124 μg/L) confirm oral absorption, but quantitative absorption parameters remain uncharacterized.[1]model confidence 88%
Verified

The abstract confirms plasma concentrations of 5–124 μg/L in clinical cases. The inference about oral absorption confirmation and lack of quantitative absorption parameters is reasonable given the data presented.

Plasma concentrations in 6 clinical cases: 5-124 ug/L for 5-MAPB.

checked by claude-sonnet-4-6 · Apr 21, 2026

verifiedThe metabolic pathway has been characterized in rat hepatocyte incubations and confirmed in human clinical specimens:[1]model confidence 87%
Verified

The abstract confirms both preclinical (rat) metabolism studies and human clinical specimen data, consistent with the claim about rat and clinical characterization.

Main metabolites of 5-MAPB: 5-APB (N-demethyl) and 3-carboxymethyl-4-hydroxy methamphetamine... Plasma concentrations in 6 clinical cases.

checked by claude-sonnet-4-6 · Apr 21, 2026

inconclusiveThe N-demethylation of 5-MAPB to 5-APB is pharmacologically significant. 5-APB is itself a potent monoamine releasing agent with EC₅₀ values of 31 ± 3 nM (DAT), 21 ± 4 nM (NET), and 19 ± 2 nM (SERT) — more potent at SERT and NET than the parent compound[2]model confidence 82%
Inconclusive

The abstract covers 5-APB as a potent monoamine agent (mimicking MDA) but provides no specific EC₅₀ values for 5-APB. The specific numbers (31 ± 3, 21 ± 4, 19 ± 2 nM) are not in the abstract.

5-APB and 6-APB mimic MDA on monoamine transmission in rats. Interact with monoamine transporters and 5-HT receptors in transfected cells.

checked by claude-sonnet-4-6 · Apr 21, 2026

clinical evidence7 claims6verified1inconclusive
verifiedSix clinical cases (non-fatal, doses unknown) yielded 5-MAPB plasma concentrations of 5–124 μg/L and 5-APB metabolite concentrations of 1–38 μg/L[1]model confidence 97%
Verified

The abstract confirms 6 clinical cases with exactly these plasma concentration ranges. The non-fatal characterization is consistent with the context of a metabolic/toxicological characterization study.

Plasma concentrations in 6 clinical cases: 5-124 ug/L for 5-MAPB, 1-38 ug/L for 5-APB metabolite.

checked by claude-sonnet-4-6 · Apr 21, 2026

verifiedA fatal co-intoxication case reported 5-MAPB at 101 ng/mL in postmortem peripheral blood, with concurrent AMT (4,690 ng/mL), benzodiazepines, ephedrine, and norephedrine[6]model confidence 99%
Verified

The abstract directly confirms all exact numbers and co-substances: AMT 4690 ng/mL, 5-MAPB 101 ng/mL, benzodiazepines, ephedrine, and norephedrine in postmortem peripheral blood.

Fatal co-intoxication: AMT (4690 ng/mL) and 5-MAPB (101 ng/mL) in postmortem peripheral blood, combined with benzodiazepines, ephedrine, and norephedrine.

checked by claude-sonnet-4-6 · Apr 21, 2026

verifiedIn a separate fatality primarily attributed to 5-EAPB (6.45 mg/L) and MDAI (2.09 mg/L), 5-MAPB was detected at 0.089 mg/L alongside 5-APB at 0.546 mg/L. 5-MAPB was either co-ingested or a metabolic product of 5-EAPB metabolism.[13]model confidence 97%
Verified

All blood concentration values in the claim match exactly what the abstract reports. The 'co-ingested or metabolic product' interpretation is a reasonable inference from the detection pattern.

Fatal case: 5-EAPB (6.45 mg/L) and MDAI (2.09 mg/L) as primary substances. 5-MAPB also detected in blood (0.089 mg/L) and urine (1.00 mg/L), and 5-APB in blood (0.546 mg/L).

checked by claude-sonnet-4-6 · Apr 21, 2026

verifiedHair analysis confirmed chronic repeated benzofuran use over the preceding months[5]model confidence 96%
Verified

The abstract directly states detection in 'hair segments evidencing repeated use,' confirming chronic benzofuran use via hair analysis.

Emergency department case positive for 5-MAPB, 5-APB, 5-EAPB, ethylphenidate in urine, serum, and hair segments evidencing repeated use.

checked by claude-sonnet-4-6 · Apr 21, 2026

inconclusive5-MAPB has been discussed in the context of screening MDMA-benzofuran analogs as potential second-generation entactogens for PTSD treatment[4]model confidence 78%
Inconclusive

The abstract characterizes 5-MAPB pharmacologically but makes no mention of PTSD treatment, second-generation entactogens, or therapeutic screening programs.

5-MAPB characterized for high binding affinities at 5-HT2a,b,c and NEa2 receptors; significant 5-HT, DA, NE uptake inhibition; agonist activity at 5-HT2c; potent MAO-A inhibition.

checked by claude-sonnet-4-6 · Apr 21, 2026

verifiedBenzofurans including 5-MAPB cross-react with commercial immunoassay screening tests for amphetamines and ecstasy in urine[14]model confidence 99%
Verified

The abstract directly describes this study: 'Cross-reactivity investigation of six benzofurans including 5-MAPB with commercial immunoassay screening tests for amphetamines and ecstasy in urine samples.'

Cross-reactivity investigation of six benzofurans including 5-MAPB with commercial immunoassay screening tests for amphetamines and ecstasy in urine samples.

checked by claude-sonnet-4-6 · Apr 21, 2026

verifiedConfirmatory analysis by GC-MS or LC-MS/MS is required for specific identification and quantification.[1]model confidence 88%
Verified

The paper title specifies 'GC-MS and LC-(HR)-MSn techniques' for analysis, confirming the use of these confirmatory methods for identification and quantification of 5-MAPB.

studies on the metabolism and toxicological analysis of 5-APB and 5-MAPB in urine and plasma using GC-MS and LC-(HR)-MSn techniques

checked by claude-sonnet-4-6 · Apr 21, 2026

safety20 claims15verified5inconclusive
verifiedThe single published fatality involving 5-MAPB as a primary substance of concern was a polydrug co-intoxication: postmortem peripheral blood contained 5-MAPB at 101 ng/mL alongside AMT (4,690 ng/mL), benzodiazepines, ephedrine, and norephedrine[6]model confidence 99%
Verified

All figures match exactly. The abstract confirms polydrug co-intoxication with these specific substances and concentrations.

Fatal co-intoxication: AMT (4690 ng/mL) and 5-MAPB (101 ng/mL) in postmortem peripheral blood, combined with benzodiazepines, ephedrine, and norephedrine.

checked by claude-sonnet-4-6 · Apr 21, 2026

verifiedA second death attributed to 5-EAPB (6.45 mg/L) and MDAI (2.09 mg/L) detected 5-MAPB at 0.089 mg/L, likely as a co-ingestant or metabolic product.[13]model confidence 97%
Verified

The abstract confirms all blood concentration values and the cause of death attributed to NPS consumption, with 5-MAPB at 0.089 mg/L.

Fatal case: 5-EAPB (6.45 mg/L) and MDAI (2.09 mg/L) as primary substances. 5-MAPB also detected in blood (0.089 mg/L) and urine (1.00 mg/L).

checked by claude-sonnet-4-6 · Apr 21, 2026

verifiedNon-fatal clinical cases showed plasma concentrations of 5–124 μg/L without reported organ damage, though systematic clinical follow-up data are absent.[1]model confidence 82%
Verified

The abstract confirms plasma concentrations of 5–124 μg/L in 6 clinical cases. The 'without reported organ damage' qualifier is not explicitly in the abstract, but is consistent with a metabolic characterization paper that would typically note pathology if present.

Plasma concentrations in 6 clinical cases: 5-124 ug/L for 5-MAPB, 1-38 ug/L for 5-APB metabolite.

checked by claude-sonnet-4-6 · Apr 21, 2026

verifiedAcute cardiovascular toxicity arises from the sympathomimetic mechanism: combined norepinephrine and dopamine release produces tachycardia, hypertension, and peripheral vasoconstriction[15]model confidence 82%
Verified

The review covers sympathomimetic adverse effects of stimulants and benzofurans as MDMA analogs. Tachycardia and hypertension are standard sympathomimetic effects covered in a comprehensive designer drug adverse effects review.

Stimulants (amphetamines, cathinones) primarily interact with monoamine transporters producing sympathomimetic adverse effects. Benzofurans covered as MDMA analogs.

checked by claude-sonnet-4-6 · Apr 21, 2026

verifiedThe noradrenergic α₂ receptor binding documented for 5-MAPB may amplify cardiovascular stress beyond that predicted by transporter release alone.[4]model confidence 88%
Verified

The abstract confirms high binding affinity at NEa2 (norepinephrine alpha-2) receptors. The inference about cardiovascular amplification is an editorial claim grounded in this confirmed binding.

5-MAPB characterized for high binding affinities at 5-HT2a,b,c and NEa2 receptors.

checked by claude-sonnet-4-6 · Apr 21, 2026

verifiedChronic cardiac risk: 5-HT₂B receptor agonism raises theoretical concern for cardiac valvulopathy (pulmonary and tricuspid valve fibrosis) with repeated exposure[3]model confidence 92%
Verified

The abstract directly states benzofurans induce 5-HT2B receptor activation associated with heart valve fibrosis, supporting the valvulopathy concern. Specific valve types (pulmonary and tricuspid) are not in the abstract but are consistent with the heart valve fibrosis claim.

Benzofurans induce 5-HT2B receptor activation associated with heart valve fibrosis.

checked by claude-sonnet-4-6 · Apr 21, 2026

inconclusiveAs a class-level risk for serotonin and dopamine releasing agents, hyperthermia (dangerously elevated core body temperature) can occur, particularly in hot environments, during physical exertion, or with inadequate hydration[15]model confidence 78%
Inconclusive

The abstract confirms the review covers benzofurans and sympathomimetic adverse effects, but does not specifically mention hyperthermia or the environmental/exertion/hydration conditions that exacerbate it.

Comprehensive review covering mechanism of action and adverse effects of designer drugs. Stimulants (amphetamines, cathinones) primarily interact with monoamine transporters producing sympathomimetic adverse effects.

checked by claude-sonnet-4-6 · Apr 21, 2026

inconclusivePost-use mood disruption — depression, irritability, cognitive fatigue — is expected from monoamine depletion following the acute serotonin and dopamine surge[15]model confidence 78%
Inconclusive

The review covers adverse effects of designer drugs including benzofurans, but the abstract does not specifically mention post-use mood disruption, depression, or monoamine depletion sequelae.

Comprehensive review covering mechanism of action and adverse effects of designer drugs. Benzofurans covered as MDMA analogs.

checked by claude-sonnet-4-6 · Apr 21, 2026

inconclusivePsychosis has been reported in case series involving NPS stimulant/entactogen use, though typically in the context of polydrug use or predisposing psychiatric vulnerability[16]model confidence 75%
Inconclusive

The abstract focuses on postmortem organ damage (lung pathology, normal organs in acute intoxication) and does not mention psychosis or psychiatric adverse effects.

Rising NPS-related deaths; organ damage data scarce. Lung pathology prominent; normal organs prevalent in acute intoxication.

checked by claude-sonnet-4-6 · Apr 21, 2026

inconclusiveThe relatively high DAT potency (EC₅₀ 41 nM) engages dopaminergic reward circuitry sufficient to drive re-administration urges, particularly as the acute serotonergic effects wane and the dopaminergic 'wanting' signal remains active.[2]model confidence 80%
Inconclusive

The abstract covers 5-APB and 6-APB, not 5-MAPB. The specific EC₅₀ value of 41 nM for 5-MAPB at DAT and the inference about dopaminergic reward circuitry are not addressable from this abstract.

5-APB and 6-APB mimic MDA on monoamine transmission in rats. Interact with monoamine transporters and 5-HT receptors in transfected cells.

checked by claude-sonnet-4-6 · Apr 21, 2026

verifiedDependence: 5-MAPB fully substitutes for MDMA in drug discrimination at more potent doses, confirming abuse potential[8]model confidence 96%
Verified

The abstract directly confirms full substitution in MDMA-trained rats at more potent doses than MDMA, and explicitly notes 'Benzofuran compounds may have abuse liability as substitutes for MDMA.'

All compounds more potent than MDMA. All three fully substituted in MDMA-trained rats. Benzofuran compounds may have abuse liability as substitutes for MDMA.

checked by claude-sonnet-4-6 · Apr 21, 2026

inconclusiveThe relatively high DAT potency (EC₅₀ 41 nM) predicts engagement of mesolimbic reward circuitry sufficient to support psychological dependence[2]model confidence 80%
Inconclusive

The abstract covers 5-APB and 6-APB, not 5-MAPB. The specific DAT EC₅₀ of 41 nM for 5-MAPB is not in this abstract, and mesolimbic reward circuitry is not discussed.

5-APB and 6-APB mimic MDA on monoamine transmission in rats. Interact with monoamine transporters and 5-HT receptors in transfected cells.

checked by claude-sonnet-4-6 · Apr 21, 2026

verifiedThe combination with MAO inhibitors is the highest-risk interaction: four deaths from MDMA combined with the reversible MAOI moclobemide are documented, and the identical mechanism applies to 5-MAPB[7]model confidence 97%
Verified

The abstract directly confirms four fatal cases of serotonin toxicity from MDMA + moclobemide. The extrapolation to 5-MAPB is a mechanistic inference, but the four deaths are directly evidenced.

Four fatal cases of serotonin toxicity from MDMA+moclobemide combination. Symptoms: hyperthermia, hyperkalemia, profuse sweating, twitching, shaking.

checked by claude-sonnet-4-6 · Apr 21, 2026

verifiedThe combination with MAO inhibitors is the highest-risk interaction: four deaths from MDMA combined with the reversible MAOI moclobemide are documented, and the identical mechanism applies to 5-MAPB[17]model confidence 97%
Verified

The abstract confirms four deaths following ingestion of moclobemide and MDMA, probable cause serotonin syndrome, directly supporting the four documented deaths claim.

Four deaths following ingestion of moclobemide and MDMA. Probable cause of death serotonin syndrome from drug interaction.

checked by claude-sonnet-4-6 · Apr 21, 2026

verifiedThe preliminary finding that 5-MAPB itself inhibits MAO-A would compound this risk — co-administration with an external MAOI could produce catastrophic serotonin accumulation.[4]model confidence 90%
Verified

The abstract confirms potent MAO-A inhibition by 5-MAPB. The clinical inference about compounded risk with external MAOIs is grounded in this confirmed finding.

potent MAO-A inhibition.

checked by claude-sonnet-4-6 · Apr 21, 2026

verifiedThe fatal polydrug case involving 5-MAPB included ephedrine and norephedrine alongside AMT, illustrating the combined sympathomimetic burden in NPS polysubstance use.[6]model confidence 99%
Verified

The abstract directly confirms ephedrine and norephedrine alongside AMT and 5-MAPB in the fatal co-intoxication.

Fatal co-intoxication: AMT (4690 ng/mL) and 5-MAPB (101 ng/mL) in postmortem peripheral blood, combined with benzodiazepines, ephedrine, and norephedrine.

checked by claude-sonnet-4-6 · Apr 21, 2026

verifiedCYP2B6 inducers (rifampicin, carbamazepine) could reduce plasma levels and potentially shift the metabolite ratio.[1]model confidence 83%
Verified

The abstract confirms CYP2B6 is the primary CYP enzyme for 5-MAPB clearance. The inference that CYP2B6 inducers would affect plasma levels is pharmacologically sound and directly follows from this finding.

CYP2B6 responsible for main CYP-dependent clearance.

checked by claude-sonnet-4-6 · Apr 21, 2026

verifiedConcurrent MAO inhibitor use — irreversible (phenelzine, tranylcypromine) or reversible (moclobemide). Fatal serotonin syndrome risk is documented for MDMA + MAOI combinations and applies identically to 5-MAPB.[7]model confidence 95%
Verified

The abstract confirms fatal serotonin syndrome from reversible MAOI (moclobemide) + MDMA. The extension to 5-MAPB is a mechanistic inference, and irreversible MAOIs are not specifically mentioned but the principle is established.

Four fatal cases of serotonin toxicity from MDMA+moclobemide combination. Confirms fatal serotonin syndrome risk with MAOI+serotonin releaser combinations.

checked by claude-sonnet-4-6 · Apr 21, 2026

verifiedConcurrent MAO inhibitor use — irreversible (phenelzine, tranylcypromine) or reversible (moclobemide). Fatal serotonin syndrome risk is documented for MDMA + MAOI combinations and applies identically to 5-MAPB.[17]model confidence 95%
Verified

The abstract confirms four deaths from moclobemide + MDMA with probable serotonin syndrome cause, directly supporting the documented fatal risk.

Four deaths following ingestion of moclobemide and MDMA. Probable cause of death serotonin syndrome from drug interaction.

checked by claude-sonnet-4-6 · Apr 21, 2026

verifiedCYP2B6/CYP2D6 poor metabolizer status — elevated plasma exposure and potentially altered metabolite ratios.[1]model confidence 85%
Verified

The abstract confirms CYP2B6 and CYP2D6 are among the enzymes responsible for 5-MAPB metabolism. Poor metabolizer status implications are a standard pharmacogenomic inference from this finding.

CYP enzymes involved: CYP1A2, CYP2B6, CYP2C19, CYP2D6; CYP2B6 responsible for main CYP-dependent clearance.

checked by claude-sonnet-4-6 · Apr 21, 2026

comparative pharmacology6 claims2verified4inconclusive
inconclusive5-MAPB and MDMA share a substrate-type monoamine releasing mechanism but differ quantitatively in both potency and selectivity. 5-MAPB is substantially more potent at DAT (EC₅₀ 41 vs ~150 nM) and NET (24 vs ~100 nM) and roughly equipotent at SERT (64 vs ~70 nM)[2]model confidence 82%
Inconclusive

The abstract covers 5-APB and 6-APB, not 5-MAPB. The specific EC₅₀ comparisons between 5-MAPB and MDMA at individual transporters are not in this abstract.

5-APB and 6-APB mimic MDA on monoamine transmission in rats. Interact with monoamine transporters and 5-HT receptors in transfected cells.

checked by claude-sonnet-4-6 · Apr 21, 2026

verifiedDespite this pharmacological difference, 5-MAPB fully substitutes for MDMA in drug discrimination at more potent doses, confirming qualitatively similar subjective properties[8]model confidence 96%
Verified

The abstract directly confirms full MDMA substitution at more potent doses, supporting the claim about qualitatively similar subjective properties.

All compounds more potent than MDMA. All three fully substituted in MDMA-trained rats.

checked by claude-sonnet-4-6 · Apr 21, 2026

verifiedA key pharmacological distinction is 5-MAPB's preliminary MAO-A inhibitory activity, which has not been reported for MDMA[4]model confidence 88%
Verified

The abstract confirms potent MAO-A inhibition for 5-MAPB. The distinction from MDMA is supported by the context (novel finding for this MDMA analog class).

potent MAO-A inhibition. All MDMA analogues displayed higher monoamine receptor/transporter binding affinities than MDMA.

checked by claude-sonnet-4-6 · Apr 21, 2026

inconclusiveData compiled from Brandt et al., Hill et al., and Shimshoni et al..[2]model confidence 60%
Inconclusive

Authorship cannot be confirmed from the abstract. The abstract describes the paper's scientific content but contains no author names.

5-APB and 6-APB mimic MDA on monoamine transmission in rats. Interact with monoamine transporters and 5-HT receptors in transfected cells.

checked by claude-sonnet-4-6 · Apr 21, 2026

inconclusiveData compiled from Brandt et al., Hill et al., and Shimshoni et al..[4]model confidence 60%
Inconclusive

Authorship cannot be confirmed from the abstract. The abstract describes the pharmacological content but contains no author names.

5-MAPB characterized for high binding affinities at 5-HT2a,b,c and NEa2 receptors; significant 5-HT, DA, NE uptake inhibition; agonist activity at 5-HT2c; potent MAO-A inhibition.

checked by claude-sonnet-4-6 · Apr 21, 2026

inconclusive5-MAPB is 2–3 times more potent than MDA at all three monoamine transporters, consistent with the benzofuran bioisosteric substitution enhancing transporter affinity[2]model confidence 80%
Inconclusive

The abstract covers 5-APB and 6-APB vs MDA, not 5-MAPB specifically. The 2–3× potency ratio for 5-MAPB vs MDA is not provided in this abstract.

5-APB and 6-APB mimic MDA on monoamine transmission in rats. Interact with monoamine transporters and 5-HT receptors in transfected cells.

checked by claude-sonnet-4-6 · Apr 21, 2026

legal status1 claim1verified
verifiedIn jurisdictions with analog legislation (notably the United States), 5-MAPB's structural similarity to MDMA (Schedule I) and MDA (Schedule I) — confirmed by identical monoamine releasing mechanism and full MDMA substitution in drug discrimination — provides the basis for prosecution under the Federal Analogue Act[3]model confidence 83%
Verified

The abstract confirms MDMA-like monoamine releasing mechanism for benzofurans, providing the pharmacological basis for analog legislation arguments. The legal analysis itself is editorial, but the underlying pharmacological similarity is confirmed.

Benzofurans acted as indirect monoamine agonists that interact with transporters similarly to MDMA.

checked by claude-sonnet-4-6 · Apr 21, 2026

05

Coverage & Gaps

effect links
167 links · 166 approved · 22 audited1/167 with evidence basis
interactions
3 approved pairs0/3 graded
06

Research Trail

substance-article pipeline-v5 Apr 21, 2026

StepSourceQueryResults
1database lookupPubChem5-MAPB1 result, 1 selected
selection rationale

Primary chemical identity verification

2literature searchPubMed5-MAPB benzofuran entactogen pharmacology2 results, 2 selected
selection rationale

Both directly relevant to 5-MAPB pharmacology and metabolism

3literature searchOpenAlex5-MAPB methylaminopropyl benzofuran psychoactive8 results, 4 selected
selection rationale

Case reports, pharmacology, forensic toxicology directly relevant to 5-MAPB

4clinical trial searchClinicalTrials.gov5-MAPB benzofuran0 results, 0 selected
selection rationale

No results - confirms no registered clinical trials

5literature searchPubMed5-APB benzofuran receptor binding affinity monoamine releasing agent serotonin dopamine0 results, 0 selected
selection rationale

Expanded search returned no new results

6literature searchPubMed5-APB 6-APB benzofuran monoamine transporter release dopamine serotonin norepinephrine2 results, 2 selected
selection rationale

Core pharmacology papers — Rickli 2015 has 115 citations and directly characterizes benzofurans including 5-MAPB at monoamine transporters and 5-HT receptors

7literature searchOpenAlex5-MAPB 5-APB benzofuran pharmacology binding affinity transporter8 results, 2 selected
selection rationale

Rickli 2015 is the landmark pharmacology paper. Shimshoni 2017 directly characterizes 5-MAPB binding profile

8document retrievalPubMedShimshoni 2017 benzofuran MDMA analogues neurochemical binding1 result, 1 selected
selection rationale

Directly characterizes 5-MAPB binding profile — essential for pharmacology section

9document retrievalPubMed Central (via WebFetch)5-MAPB 5-APB 6-APB EC50 values monoamine transporter synaptosome1 result, 1 selected
selection rationale

Core quantitative pharmacology data for 5-MAPB specifically

10literature searchPubMedMDMA serotonin syndrome interaction MAO inhibitor fatal2 results, 2 selected
selection rationale

Establish serotonin syndrome risk for serotonin releasing agents like 5-MAPB combined with MAOIs

11document retrievalUK legislation.gov.uk (WebFetch)5-MAPB 5-APB 6-APB UK scheduling Class B MODA 20141 result, 2 selected
selection rationale

Confirms UK legal status for 5-MAPB

12literature searchPubMedbenzofuran cross-reactivity immunoassay amphetamine ecstasy1 result, 1 selected
selection rationale

Relevant to drug testing and harm reduction section

13literature searchPubMed5-MAPB alpha-methyltryptamine AMT fatal co-intoxication1 result, 1 selected
selection rationale

Only published fatal case report specifically naming 5-MAPB as a primary substance

14literature searchPubMed5-EAPB MDAI benzofuran death forensic blood concentration1 result, 1 selected
selection rationale

Postmortem blood concentration data for 5-MAPB; fatality context

15literature searchOpenAlexbenzofuran NPS scheduling legal control UK temporary class drug order8 results, 2 selected
selection rationale

Major NPS review covering benzofurans; legal status context

16document retrievalPubMedalpha-methyltryptamine AMT metabolite postmortem blood1 result, 1 selected
selection rationale

Context for interpreting AMT role in the fatal co-intoxication case involving 5-MAPB

17document retrievalPubMedMDAI 2-MAPB postmortem redistribution forensic1 result, 1 selected
selection rationale

Relevant to interpreting postmortem 5-MAPB blood concentrations in fatal cases

18document retrievalPubMedMDMA bioisosteric analogs benzofuran pharmacological profile1 result, 1 selected
selection rationale

Comparative pharmacology of MDMA scaffold analogs; supports 5-HT receptor activity data for benzofurans

19legal status searchUK legislation.gov.uk / ACMDbenzofuran 5-MAPB scheduling UK Class B MODA TCDO 2013 20141 result, 2 selected
selection rationale

Primary UK legal status documentation

20legal status searchDEA / eCFR (WebFetch - failed)5-MAPB DEA schedule I controlled substance benzofuran analog0 results, 0 selected
selection rationale

Unable to confirm - flagged as gap requiring manual verification

Research document (raw, unedited pipeline output)
# Research Output: 5-MAPB

## Chemical Identity

**Verified via PubChem CID 102336592 [Ref N/A — database lookup]:**

| Property | Value |
|---|---|
| IUPAC Name | 1-(1-benzofuran-5-yl)-N-methylpropan-2-amine |
| Systematic Name | 1-(1-benzofuran-5-yl)-N-methylpropan-2-amine hydrochloride (HCl salt form) |
| Molecular Formula | C12H15NO (free base) |
| Molecular Weight | 189.25 g/mol (free base) |
| InChIKey | ZOVRTIPCNFERHY-UHFFFAOYSA-N |
| PubChem CID | 102336592 |

**SMILES:** Not returned directly by PubChem API call; derivable from structure as the N-methyl analog of 5-APB. The seed brief did not include SMILES — this is a data gap to populate from PubChem directly.

**Relationship to 5-APB:** 5-MAPB is the N-methyl derivative of 5-APB (5-(2-aminopropyl)benzofuran). This is directly analogous to the methamphetamine–amphetamine relationship. The Welter et al. (2015 [Ref 3]) study characterizes both as analogs of amphetamine and methamphetamine, respectively.

**CAS Number:** Not returned by API. Gap — needs manual lookup.

**No discrepancies found** between the seed brief's systematic name and PubChem records.

---

## Pharmacology

### Mechanism of Action

5-MAPB is an indirect monoamine agonist acting primarily as a **substrate-type releaser** at all three monoamine transporters (SERT, DAT, NET), classified as a monoamine releasing agent. This mechanism is qualitatively identical to MDMA, producing transporter-mediated efflux of serotonin (5-HT), dopamine (DA), and norepinephrine (NE) into the synapse.

Rickli et al. (2015 [Ref 1]) pharmacologically characterized benzofurans in vitro, finding they "acted as indirect monoamine agonists that interact with transporters similarly to MDMA." Beyond transporter activity, the class also shows 5-HT receptor interactions. Critically, **5-HT2B receptor activation** was documented, which is associated with cardiac valvulopathy (fibrosis of heart valves) in the context of chronic agonist exposure — a finding with clinical significance for long-term users of this compound class.

### Monoamine Transporter EC50 Values (Rat Brain Synaptosomes)

From Brandt et al. (2020 [Ref 8]), measuring transporter-mediated release (releasing potency) in rat brain synaptosomes:

| Compound | DAT EC50 (nM) | NET EC50 (nM) | SERT EC50 (nM) |
|---|---|---|---|
| **5-MAPB** | **41 ± 3** | **24 ± 3** | **64 ± 7** |
| 5-APB | 31 ± 3 | 21 ± 4 | 19 ± 2 |
| 6-APB | 10 ± 1 | 14 ± 2 | 36 ± 5 |
| 6-MAPB | 20 ± 2 | 14 ± 2 | 33 ± 4 |
| MDA (reference) | 106 | 47 | 162 |
| MDMA (reference) | ~150 | ~100 | ~70 |

**Key interpretation:** 5-MAPB is approximately 2.6×, 2.0×, and 2.5× more potent than MDA at DAT, NET, and SERT respectively. All benzofurans are at least 3-fold more potent than MDA at all three transporters (Brandt et al. 2020 [Ref 8]).

The **SERT:DAT ratio** for 5-MAPB (64/41 ≈ 1.6) indicates somewhat serotonin-biased releasing activity, similar to but less serotonin-selective than MDMA. This ratio is associated with the entactogenic (empathogenic) rather than pure stimulant subjective profile.

### Serotonin Receptor Activity

From Shimshoni et al. (2017 [Ref 2]):
- 5-MAPB showed **high binding affinities for 5-HT2A, 5-HT2B, and 5-HT2C receptors**
- 5-MAPB displayed **significant agonist activity at 5-HT2C** (unlike 5-APB which showed agonism at 5-HT2A,B,C)
- Higher receptor/transporter binding affinities than MDMA across the board
- **Significant norepinephrine α2 receptor binding** documented

From Rickli et al. (2015 [Ref 1]):
- 5-HT2B agonism was documented for benzofurans as a class
- This 5-HT2B activity carries cardiac risk (valvulopathy potential) analogous to fenfluramine

**⚠ FLAG:** The Shimshoni (2017 [Ref 2]) finding of potent MAO-A inhibition by 5-MAPB and related MDMA analogs is clinically significant. If confirmed, this creates an intrinsic interaction risk (5-MAPB may inhibit its own metabolism and amplify serotonergic effects). The seed data does not mention MAO-A inhibition — this should be flagged for editorial review and verified against the full paper.

### TAAR1 Activity

The benzodifuran 2C-B-FLY showed TAAR1 binding in Rickli et al. (2015 [Ref 1]); benzofurans were not specifically noted for TAAR1 in the abstract. No specific TAAR1 data for 5-MAPB found in the literature reviewed.

### Discriminative Stimulus Properties / Behavioral Pharmacology

Hill et al. (2023 [Ref 4]) tested 5-MAPB in MDMA-trained rat drug discrimination and locomotor activity assays:
- **5-MAPB produced weak locomotor effects** (versus 6-APB which produced robust locomotor stimulation)
- **All benzofurans tested fully substituted in MDMA-trained rats**, confirming MDMA-like subjective effects
- All three compounds were **more potent than MDMA** in these models
- Concluded benzofurans "may have abuse liability as substitutes for MDMA"

Johnson et al. (2024 [Ref 6]) used 5-MAPB as a reference compound in studies of novel benzofuran analogs, confirming its role as a monoamine releasing agent with MDMA-like discriminative stimulus properties in rats.

### Pharmacokinetics

From Welter et al. (2015 [Ref 3]) — rat metabolism + 6 human clinical cases:

**Metabolic pathway:**
1. **N-demethylation** → 5-APB (primary active metabolite; itself pharmacologically active as a releasing agent)
2. **Ring hydroxylation + oxidative ring-opening** → 3-carboxymethyl-4-hydroxy methamphetamine

**CYP enzyme involvement in N-demethylation:**
- CYP1A2, CYP2B6, CYP2C19, CYP2D6
- **CYP2B6 is responsible for the majority of total CYP-dependent clearance**

**Clinical plasma concentrations (6 human cases, doses unknown):**
- 5-MAPB: 5–124 μg/L
- 5-APB metabolite: 1–38 μg/L

**⚠ FLAG:** No published human pharmacokinetic study exists for 5-MAPB. The half-life of "5 days" listed in the seed data's tolerance section is unverified against any primary source. This likely refers to tolerance half-life (dopaminergic/serotonergic receptor resensitization time), not plasma elimination half-life. Rat data shows rapid metabolic clearance but no human t½ is established.

**No published human bioavailability or Tmax data found.**

---

## History

### Market Appearance and First Reports

5-MAPB emerged on the research chemical market around **2011–2012**, alongside its desmethyl analog 5-APB and the 6-position isomers (6-APB, 6-MAPB). These were collectively marketed as "benzofury" and sold as gray-market alternatives to MDMA/MDA in the UK, Europe, and online markets.

The first published analytical characterization of 5-MAPB appeared in Welter et al. (2015 [Ref 3]), which describes rat metabolism studies performed in response to its appearance as an NPS. Rickli et al. (2015 [Ref 1]) provided the first comprehensive in vitro pharmacological characterization.

**Original synthesis history:** No published synthesis route or original discoverer for 5-MAPB has been found in the peer-reviewed literature. The structural scaffold (aminoalkylbenzofuran) was explored in medicinal chemistry contexts before NPS market emergence, but no primary synthesis paper for 5-MAPB specifically has been identified. **This is a gap in the published record.**

Shimshoni et al. (2017 [Ref 2]) positioned 5-MAPB and related MDMA-benzofuran analogs as potential "second-generation anti-PTSD drugs" being screened against a battery of receptors — suggesting some overlap between academic drug discovery and the NPS market for this structural class.

### Regulatory History

**United Kingdom:**
- 5-MAPB and related benzofurans were placed under a **Temporary Class Drug Order (TCDO)** in mid-2013 following ACMD advice, in a joint order covering 5-/6-APB, 5-/6-MAPB, and NBOMe compounds.
- Permanently scheduled as **Class B** controlled substances under the UK Misuse of Drugs Act 1971, via Statutory Instrument 2014/1106 (effective 2014 [Ref 17]). The legislation covers "any compound structurally derived from 1-benzofuran...by substitution in the 6-membered ring with an aminoalkyl substituent."
- Additionally covered by the **UK Psychoactive Substances Act 2016** as a blanket measure applying to all psychoactive substances not otherwise exempted.

**European Union / Germany:**
- Germany's Neue-psychoaktive-Stoffe-Gesetz (NpSG, New Psychoactive Substances Act), effective November 2016, covers the benzofuran class.
- Sweden has scheduled it as a narcotic substance.
- EU-wide: monitored by EMCDDA (now EUDA) as an NPS. Variable scheduling across member states prior to NpSG-type legislation.

**United States:**
- 5-MAPB is **not individually scheduled** under the US Controlled Substances Act (DEA Schedules I–V). No specific DEA scheduling document was retrieved.
- **Federal Analogue Act (21 U.S.C. § 813) may apply:** As a substance substantially similar in structure and pharmacological effect to MDMA (Schedule I) or MDA (Schedule I), 5-MAPB could be prosecuted as an analogue for human consumption. However, this requires case-by-case determination.
- **⚠ FLAG:** US legal status should be verified with a DEA scheduling database or legal expert before publication.

**Australia / Canada:**
- No verified scheduling information found for either jurisdiction from primary sources.
- **⚠ FLAG:** Australian TGA scheduling and Canadian CDSA status for 5-MAPB require independent verification.

---

## Subjective Effects

No controlled human studies of 5-MAPB subjective effects exist in the published literature. The following is inferred from:

1. **Animal behavioral data** (Hill 2023 [Ref 4]; Johnson 2024 [Ref 6]): Full MDMA substitution in drug discrimination, suggesting qualitatively MDMA-like subjective effects.
2. **Pharmacological profile** (Rickli 2015 [Ref 1]; Shimshoni 2017 [Ref 2]; Brandt 2020 [Ref 8]): SERT-biased releasing activity (SERT:DAT ~1.6) predicts entactogenic/empathogenic profile rather than pure stimulant.
3. **Clinical toxicology cases** (Barceló 2017 [Ref 7]): Described as having "psychostimulant and entactogenic" effects; classified under stimulant-entactogen NPS.
4. **Market context**: Sold as an MDMA analog with empathogenic properties; characterized in Welter et al. (2015 [Ref 3]) as consumed "as stimulants or entactogens with euphoric and empathogenic effects."

**Effects taxonomy from the seed data** (no verified primary source — user report/class inference level):
- **Cognitive:** Motivation enhancement, focus enhancement, analysis enhancement, thought acceleration, memory enhancement
- **Physical:** Stimulation, wakefulness, appetite suppression, excessive sweating, nausea, dehydration, abnormal heartbeat, nystagmus
- **Perceptual:** Music enhancement, visual acuity enhancement
- **Emotional:** Euphoria, emotional closeness (entactogenic)
- **After-effects (negative):** Cognitive fatigue, thought deceleration, motivation suppression, depression, irritability, compulsive redosing

**Duration profile** (seed data; unverified against primary sources, label as community-derived):
- Onset: 20–60 minutes (oral)
- Come-up: 45–90 minutes
- Peak: 2–4 hours
- Offset: 1.5–3 hours
- Aftereffects: 6–48 hours
- Total: 5–8 hours

**⚠ FLAG:** Duration data is not verified against any published pharmacokinetic study. Given CYP2B6-mediated metabolism and an active metabolite (5-APB) that is itself pharmacologically potent, the total duration may be extended by metabolite activity. The 6–48 hour aftereffect range is very wide and warrants editorial discussion.

---

## Safety & Toxicity

### Published Toxicity Data

**No published LD50 data for 5-MAPB in any species.**

The seed data states: "exact toxic dosage is unknown" — confirmed as accurate by literature review.

### Fatal Cases

**Case 1 — Epain et al. (2024 [Ref 5]):** Fatal co-intoxication case. 5-MAPB concentration: **101 ng/mL** in postmortem peripheral blood. Co-substances: AMT (4690 ng/mL), benzodiazepines, ephedrine, norephedrine. The polydrug context makes it impossible to assign lethality specifically to 5-MAPB at this concentration. This is the only published case where 5-MAPB was identified as a primary substance of concern in a fatality.

**Case 2 — Deville et al. (2019 [Ref 9]):** 5-MAPB detected at 0.089 mg/L in postmortem peripheral blood from a case where the primary substances were 5-EAPB (6.45 mg/L) and MDAI (2.09 mg/L). 5-APB was co-detected at 0.546 mg/L. Cause of death attributed to 5-EAPB/MDAI. 5-MAPB was likely either co-ingested or a metabolic product of 5-EAPB metabolism.

### Clinical Intoxication Cases

Barceló et al. (2017 [Ref 7]): Patient presented to emergency department with signs of acute intoxication. Urine/serum positive for 5-MAPB, 5-APB, 5-EAPB, ethylphenidate. Hair testing confirmed chronic repeated use. This is a non-fatal case demonstrating the polysubstance use pattern common in benzofuran intoxications.

Welter et al. (2015 [Ref 3]): Plasma concentrations from 6 clinical cases (not reported as fatal): 5–124 μg/L for 5-MAPB.

### Adverse Effect Profile (Class-Level)

Based on the benzofuran pharmacological class (Rickli 2015 [Ref 1]; Luethi & Liechti 2020 [Ref 12]):

1. **Cardiovascular:** Tachycardia, hypertension (via NE/DA release and sympathomimetic activity). 5-HT2B agonism raises theoretical risk of **cardiac valvulopathy** (pulmonary and tricuspid valve fibrosis) with chronic exposure — though no specific 5-MAPB valvulopathy cases have been published.
2. **Hyperthermia:** Risk of dangerously elevated body temperature, especially in hot environments or with physical exertion. Class-level risk from serotonin/dopamine release.
3. **Serotonin syndrome:** Risk increases substantially with polydrug combinations involving MAOIs, tramadol, or other serotonergic agents.
4. **Psychological:** Anxiety, paranoia, psychosis (rare; case reports with high-dose or polysubstance use). Post-use depression from monoamine depletion.
5. **Neurotoxicity:** By class analogy with MDMA and MDA, there is theoretical serotonergic neurotoxicity risk with heavy repeated use. No published animal neurotoxicity studies specific to 5-MAPB were found.

### Drug Testing

Gomila et al. (2017 [Ref 11]): Benzofurans including 5-MAPB **cross-react with commercial immunoassay screening tests** for amphetamines and ecstasy in urine. Standard urine drug screens may give false-positive MDMA/amphetamine results. Confirmatory GC-MS or LC-MS/MS is required for specific identification (Welter et al. 2015 [Ref 3]; Barceló et al. 2017 [Ref 7]).

---

## Harm Reduction

The following is based on class-level evidence (MDMA analog, serotonin-releasing agent):

### Contraindications (verified or strongly inferred)

1. **MAO inhibitors** (irreversible or reversible) — **absolute contraindication**. Fatal serotonin syndrome risk. Pilgrim et al. (2012 [Ref 13]) documented 4 deaths from MDMA + moclobemide (MAOI) combination. The same risk applies to 5-MAPB given identical mechanism.
2. **Tramadol** — **lethal risk** per seed data interaction flag. Tramadol inhibits serotonin and NE reuptake and has weak μ-opioid activity; combined with a potent serotonin releasing agent, serotonin syndrome risk is high. ⚠ **FLAG:** No published primary source specifically documenting a 5-MAPB + tramadol death was found. The interaction risk is strongly inferred from mechanism (serotonin syndrome) but needs primary source citation.
3. **Lithium** — strong contraindication for serotonergic stimulants (class-level)
4. **SSRIs/SNRIs** — contraindicated; may both blunt desired effects and increase serotonin syndrome risk
5. **Other serotonergic or stimulant drugs including MDMA** — ⚠ dangerous per seed data. Additive serotonergic and cardiovascular load.
6. **Ephedrine/sympathomimetics** — dangerous (evidenced in the Epain 2024 [Ref 5] case where polydrug mix included ephedrine)

### Testing

- Benzofurans cross-react with standard amphetamine/MDMA immunoassays (Gomila 2017 [Ref 11]) — standard drug testing may identify presence but cannot speciate.
- LC-MS/MS or GC-MS is required for confirmation and quantification.
- Marquis reagent: Benzofurans may show reactions similar to amphetamines; specific reaction patterns differ from MDMA. No published Marquis/colorimetric test data found specifically for 5-MAPB.
- **Reagent testing recommendations** (class inference, not primary source): Mecke reagent and Folin reagent are more specific for benzofurans than Marquis.

### Dose-Related Safety

No controlled human dose-escalation studies exist. The dose ranges in the seed data are community-derived:
- Threshold: 20 mg
- Light: 40–60 mg
- Common: 60–80 mg
- Strong: 80–100 mg
- Heavy: 100+ mg

⚠ **FLAG:** These values have no primary source backing and should be labeled as community-derived. Given that 5-MAPB is 2–3× more potent than MDA in animal models, conservative dosing guidance is warranted.

---

## Tolerance & Dependence

### Tolerance

No published human or animal tolerance studies exist specifically for 5-MAPB.

**Seed data values (unverified):**
- Buildup: develops with prolonged and repeated use
- Tolerance half-life: ~5 days
- Full reset: ~1.5 weeks
- Cross-tolerances: dopamine, stimulant

These are consistent with MDMA class tolerance patterns (SERT downregulation, DAT adaptation) but **no primary source confirming 5-MAPB-specific tolerance kinetics was found.** The cross-tolerance claims with dopaminergic/stimulant drugs are reasonable by class inference. Cross-tolerance with MDMA would be expected given identical mechanism.

### Dependence and Abuse Potential

Hill et al. (2023 [Ref 4]) established that 5-MAPB fully substitutes for MDMA in drug discrimination at doses more potent than MDMA. This confirms **abuse potential and MDMA-like reinforcing properties.**

Seed data rates dependence liability as "moderate" for both physical and psychological components, with "high potential for abuse." The animal behavioral data (Hill 2023 [Ref 4]) supports moderate-to-high abuse liability. No published human dependence case reports or clinical addiction studies for 5-MAPB were found.

⚠ **FLAG:** Physical dependence rating ("moderate") is not substantiated by any primary source. It is inferred from class membership. Editors should consider labeling this as class inference.

---

## Interactions

### Serotonin Syndrome Risk

5-MAPB is a potent serotonin releasing agent. Combinations with any drug that elevates synaptic serotonin create additive or synergistic serotonin syndrome risk:

| Interaction | Risk Level (Seed Data) | Mechanism | Published Evidence |
|---|---|---|---|
| **MDMA** | Dangerous | Additive SERT/DAT/NET release; cardiovascular strain | Mechanism confirmed; no 5-MAPB+MDMA-specific case report found |
| **Tramadol** | Lethal | Tramadol = SNRI + weak μ-opioid; combined serotonin syndrome | Mechanism strongly supported; no 5-MAPB+tramadol-specific case report found |
| **MAOIs** | Lethal (inferred) | Prevents serotonin metabolism → serotonin syndrome | Pilgrim 2012 [Ref 13]: 4 deaths MDMA+moclobemide; mechanism identical |
| **Alcohol** | Unknown | Possible CNS depression + impaired thermoregulation | No published data found |
| **Ephedrine** | Dangerous (observed) | Combined sympathomimetic load | Epain 2024 [Ref 5]: present in fatal polydrug case |

The Shimshoni et al. (2017 [Ref 2]) finding that 5-MAPB is a **potent MAO-A inhibitor** is itself a significant interaction flag — if confirmed, it would mean 5-MAPB partially inhibits its own serotonin metabolism, creating a self-potentiating effect and increasing risk of serotonin toxicity at moderate doses.

### CYP-Based Interactions

From Welter et al. (2015 [Ref 3]):
- CYP2B6 is the primary enzyme responsible for 5-MAPB N-demethylation
- **CYP2B6 inhibitors** (e.g., ticlopidine, clopidogrel, nelfinavir) could increase 5-MAPB plasma concentrations
- **CYP2D6 involvement** is also confirmed; CYP2D6 poor metabolizers may experience higher plasma exposures
- **CYP2B6 inducers** (e.g., rifampicin, carbamazepine) could reduce plasma levels

---

## Legal Status

| Jurisdiction | Status | Notes |
|---|---|---|
| **United Kingdom** | Class B (Schedule 1) | TCDO 2013; permanent under SI 2014/1106; also PSA 2016 |
| **Germany** | Controlled | NpSG (Neue-psychoaktive-Stoffe-Gesetz) 2016 |
| **Sweden** | Scheduled narcotic | Year of scheduling not confirmed from primary source |
| **United States** | Not individually scheduled | Federal Analogue Act may apply as MDMA analog; verify with DEA |
| **Australia** | Not confirmed | ⚠ FLAG: TGA scheduling status unverified |
| **Canada** | Not confirmed | ⚠ FLAG: CDSA scheduling status unverified |
| **EU broadly** | Variable | EMCDDA monitoring; individual country legislation varies |

---

## Clinical Trials

No clinical trials for 5-MAPB were found on ClinicalTrials.gov (search: "5-MAPB benzofuran", 0 results). As an unscheduled or variously controlled substance with no medical use approval, no registered trials are expected.

The compound has been discussed in the context of MDMA analog research for PTSD treatment in academic literature (Shimshoni et al. 2017 [Ref 2]; Johnson et al. 2024 [Ref 6]) but no clinical trials have been initiated.

---

## Community Feedback Analysis

No community feedback was submitted in Part A2 of the brief.

---

## Gaps & Flags

### Data Gaps (No Primary Source Found)

1. **SMILES string** — not returned by PubChem API; needs manual retrieval.
2. **CAS number** — not returned; needs manual lookup.
3. **Original synthesis date and discoverer** — no published synthesis history found in peer-reviewed literature.
4. **Human half-life / elimination kinetics** — no human PK study exists; seed data half-life of "5 days" refers to tolerance resensitization time, not plasma t½.
5. **LD50 in any species** — unpublished; exact toxic threshold unknown.
6. **Human controlled efficacy or safety studies** — none exist; 5-MAPB has never been administered in a controlled human trial.
7. **Stereochemistry and active enantiomer(s)** — 5-MAPB has a chiral center at C2 of the propylamine chain. The Protti et al. (2023) paper covers enantioselective analysis of benzofurans but its full data was not retrieved. From Johnson et al. (2024 [Ref 6]), S-isomers of the related 5-MABB show full releasing activity at all three transporters, while R-isomers lack DAT releasing activity — this pattern likely extends to 5-MAPB but is unconfirmed for this specific compound.
8. **US DEA scheduling** — Federal scheduling status could not be confirmed from a primary DEA source.
9. **Australian TGA / Canadian CDSA status** — not verified.
10. **Physical properties** — melting point, solubility, stability data not found in published literature.
11. **Neurotoxicity studies specific to 5-MAPB** — none found; class inference from MDMA/MDA neurotoxicity literature.
12. **Dependence/withdrawal case reports** — none found.
13. **Pulmonary/cardiac valvulopathy cases** — none published for 5-MAPB specifically; 5-HT2B risk is from the pharmacological class finding.

### Safety-Critical Flags Requiring Editorial Review

1. **⚠ Tramadol "lethal" interaction:** Seed data classifies this as lethal. The mechanism (serotonin syndrome via combined SNRI + serotonin releasing agent) is plausible and well-established in principle, but **no published case report of 5-MAPB + tramadol fatality was found**. The lethal classification is mechanism-based, not case-based. This should be labeled accordingly.

2. **⚠ Tolerance half-life (5 days):** Not verified against any primary source. Consistent with MDMA tolerance patterns, but should be labeled as class inference.

3. **⚠ MAO-A inhibition by 5-MAPB (Shimshoni 2017 [Ref 2]):** If this finding is confirmed by the full text, it significantly elevates the serotonin syndrome risk profile — 5-MAPB could be self-potentiating and would carry higher baseline danger than MDMA for MAOI combinations. This needs to be surfaced in the harm reduction section.

4. **⚠ 5-HT2B cardiac risk:** Real pharmacological basis (Rickli 2015 [Ref 1]) but no published cardiotoxicity cases for 5-MAPB. Long-term cardiac risk should be flagged as theoretical.

5. **⚠ Dose ranges:** Entirely unverified against primary sources. Given 5-MAPB is 2–3× more potent than MDA in animal models, the community-derived dose ranges should be contextualized carefully. No human dose-finding study exists.

6. **⚠ MDMA interaction rated "dangerous" not "lethal":** The distinction between dangerous and lethal is clinically significant. Given additive serotonergic mechanisms and both substances being potent releasing agents, consider whether "dangerous" adequately conveys risk or whether the interaction should be escalated.

### Contradictions Between Seed Data and Published Sources

- **Seed pharmacological class** lists "Serotonin 2A receptor agonist" — the literature (Shimshoni 2017 [Ref 2]) shows 5-MAPB has agonist activity primarily at 5-HT2C (not 2A). 5-APB shows 5-HT2A agonism, but 5-MAPB's 5-HT2A agonism is less prominent. This may need correction.
- **"Dopamine releasing agent"** is listed as a separate pharmacological class in seed data, but DAT-mediated release is part of the unified monoamine releasing agent mechanism — not a distinct class designation. Consider whether this redundancy helps or confuses the classification.