generation run 2026-04-20
68 min completedmodel pipeline-v5plan not recordedrun/2f51e7ee…Selection
Verification
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The model's own caveats
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Reproduce
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- 29 source keys (listed under Sources)
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- not recorded — template version, prompt hash and git SHA are written from 2026-09 onward
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- none — agent transcripts are persisted from 2026-09 onward
23 searches — query, source, results, what was kept and why
| # | source | query | seen | kept | rationale |
|---|---|---|---|---|---|
| 1 | OpenAlex | 2C-B 4-bromo-2,5-dimethoxyphenethylamine psychedelic - citations sorted | 10 | 4 | Most cited landmark papers on 2C-B pharmacology |
| 2 | ClinicalTrials.gov | 2C-B psychedelic | 1 | 1 | Only registered clinical trial for 2C-B |
| 3 | Web | Alexander Shulgin 2C-B synthesis discovery 1974 PIHKAL history | 10 | 2 | Historical context and discovery narrative |
| 4 | PubMed | Papaseit Farre 2C-B observational pharmacological effects | 2 | 1 | First published human observational pharmacology study of 2C-B |
| 5 | Web/DEA | 2C-B Schedule I DEA legal status US UK Germany Australia | 10 | 2 | Legal status across major jurisdictions |
| 6 | PubChem | 2C-B compound lookup | 1 | 1 | Primary chemical identity verification |
| 7 | ClinicalTrials.gov | NCT05523401 study details | 1 | — | Only registered clinical trial for 2C-B |
| 8 | PubMed | 4-bromo-2,5-dimethoxyphenethylamine pharmacokinetics metabolism | 7 | 5 | Primary pharmacokinetic sources |
| 9 | PubMed | 2C-B 4-bromo-2,5-dimethoxyphenethylamine pharmacology receptor binding | 3 | 3 | Key receptor pharmacology papers |
| 10 | PubMed | Mallaroni 2C-B psilocybin subjective experience assessment | 1 | 1 | First controlled clinical study of 2C-B; primary human PK and PD data |
| 11 | Web | NCT05523401 2C-B Basel Holze Liechti published results 2024 2025 | 10 | 1 | First controlled study comparing 2C-B to psilocybin |
| 12 | DEA/DOJ | 2C-B Schedule I DEA scheduling history | 1 | — | Authoritative US/international scheduling history |
| 13 | PubMed/PMC | Papaseit 2018 2C-B observational study pharmacokinetics | 1 | 1 | Primary human PK data from observational study |
| 14 | PubMed | phenylalkylamine hallucinogen head twitch 2C-B behavioral pharmacology | 2 | 1 | In vivo 5-HT2A agonism data for 2C-B; hallucinogenic potency benchmark |
| 15 | Erowid | PIHKAL 2C-B entry Shulgin dose duration synthesis | 1 | 1 | Primary source for Shulgin's characterization and synthesis description |
| 16 | PubMed | NBOMe receptor interaction profiles 2C drugs binding | 1 | 1 | Contains binding affinity data for 2C-B across multiple receptor types |
| 17 | PubMed | 4-bromo-2,5-dimethoxyphenethylamine 5-HT2A antagonist agonist Xenopus oocyte | 1 | 1 | Key paper on complex 5-HT2A pharmacology of 2C-B |
| 18 | PubMed | Gonzalez Torrens Farre 2C-B emotions novel psychoactive drug 2015 | 1 | 1 | Characterization of 2C-B as stimulant/hallucinogen/entactogen/empathogen |
| 19 | PubMed/OpenAlex | Papaseit 2018 2C-B referenced works | 5 | — | Citation graph exploration |
| 20 | Web/EUDA | 2C-B EMCDDA European drug report prevalence seizures 2022 2023 | 10 | 1 | Primary EU-level epidemiology and prevalence data |
| 21 | PubMed | 2C-B case report poisoning emergency department | 1 | 1 | Drug testing/detection context for harm reduction |
| 22 | Multiple | Seed data verification against published sources | — | — | Quality control and data validation |
| 23 | Web | 2C-B Canada legal status controlled substances scheduling | 10 | 1 | Canadian legal scheduling information |
101 claims by section — every cited sentence, checked against its source
safety28 · 15 ok
Claim in safety — inconclusiveinconclusiveworking →
Claim in safety — inconclusiveinconclusiveworking →
Claim in safety — inconclusiveinconclusiveworking →
Claim in safety — inconclusiveinconclusiveworking →
Claim in safety — inconclusiveinconclusiveworking →
Dean et al. reviewed the 2C drug class broadly and identified at least 5 deaths in the published literature attributed to 2C compoundssupported
At least 5 deaths reported; excited delirium common among fatalities. s13181-013-0295-x
Clinical features in severe 2C-class toxicity include sympathomimetic toxidrome, serotonin toxicity syndrome, or excited delirium, with presentations of hallucinations, agitation, aggression, hypertension, tachycardia, seizures, and hyperthermiasupported
Sympathomimetic and serotonin toxicity presentations. Excited delirium common among fatalities. s13181-013-0295-x
Claim in safety — inconclusiveinconclusiveworking →
2C-B is not detected by standard immunoassay drug screenssupported
These drugs do not reliably trigger a positive result on rapid drug immunoassays. Notes difficulty with laboratory confirmation of 2C drugs. s13181-013-0314-y
Specialized analytical methods are required: Kerrigan et al. developed a validated GC-SIM urine method with a limit of detection of 2–10 ng/mL, and Thomann et al. published an LC-MS/MS plasma methodsupported
GC-MS method for detecting 2C-B and 9 other phenethylamines in urine; LOD 2-10 ng/mL; LOQ 10 ng/mL. pmid:21871155
Specialized analytical methods are required: Kerrigan et al. developed a validated GC-SIM urine method with a limit of detection of 2–10 ng/mL, and Thomann et al. published an LC-MS/MS plasma methodsupported
First human plasma PK study with validated LC-MS/MS method; 30 mg oral dose. j.dmd.2025.100086
Mild open-eye hallucinations occurred in 5 of 16 subjects (31%) at doses of 10–20 mg oral in the Papaseit et al. study; these were not characterized as psychotic phenomenasupported
mild hallucinations (5 subjects) fphar.2018.00206
Psilocybin at 15 mg produced greater dysphoria and ego dissolution than 2C-B at 20 mg in the Mallaroni et al. comparison, suggesting a lower acute psychological risk profile at these doses — though the steep dose-response curve documented by Shulgin means small dose increases could substantially alter this profile.supported
2C-B showed lighter profile; less dysphoria and ego dissolution than psilocybin. cpt.2958
Caudevilla-Gálligo et al. reported lower incapacitation with 2C-B compared to ayahuasca or Salvia divinorum in their survey of recreational users.supported
lower incapacitation than other psychedelics. 0269881111431752
Tolerance to 2C-B's psychedelic effects is expected to develop rapidly (within hours to days) through 5-HT₂A receptor downregulation and internalization — a mechanism demonstrated for the class by Wallach et al., who showed that β-arrestin-biased 5-HT₂A agonists induce receptor downregulation and tachyphylaxissupported
Beta-arrestin-biased ligands block psychedelic effects and induce receptor downregulation and tachyphylaxis. s41467-023-44016-1
Claim in safety — inconclusiveinconclusiveworking →
Tramadol is a weak serotonin reuptake inhibitor and μ-opioid agonist; combined with 5-HT₂A agonists, the serotonergic burden creates a documented pathway to serotonin toxicitysupported
Tramadol is a weak serotonin reuptake inhibitor; combinations with serotonergic drugs can precipitate life-threatening serotonin toxicity. pmid:16051647
Case reports of tramadol-related serotonin syndrome with serotonergic co-administration support this risksupported
Case report: lithium addition precipitated serotonin syndrome in patient on tramadol and amitriptyline. bcr-2017-221383
Case reports of tramadol-related serotonin syndrome with serotonergic co-administration support this risksupported
Case report of tramadol-SSRI serotonin syndrome. Tramadol has serotonergic properties that combine with other serotonergic drugs. ajcr.892264
Claim in safety — inconclusiveinconclusiveworking →
Claim in safety — inconclusiveinconclusiveworking →
MAO inhibitors: Since MAO-A and MAO-B are the primary metabolic enzymes for 2C-B, concurrent use of monoamine oxidase inhibitors — including irreversible inhibitors (phenelzine, tranylcypromine), reversible inhibitors (moclobemide), and selective MAO-B inhibitors (selegiline) — would be expected to substantially increase 2C-B plasma exposure, potentially to dangerous levelssupported
MAO-A, MAO-B, cytosolic enzymes, and CYP2D6 identified as key metabolic enzymes. j.dmd.2025.100086
Claim in safety — inconclusiveinconclusiveworking →
Claim in safety — not_supportednot supportedworking →
Cardiovascular disease, uncontrolled hypertension, arrhythmia: Dose-dependent increases in blood pressure and heart rate at recreational doses represent added cardiovascular burden in individuals with compromised cardiac functionsupported
n=16 recreational users, oral 10-15-20mg. Increased BP/HR. fphar.2018.00206
Concurrent MAOI use: MAO-A and MAO-B are the primary metabolic enzymes for 2C-Bsupported
MAO-A, MAO-B, cytosolic enzymes, and CYP2D6 identified as key metabolic enzymes. j.dmd.2025.100086
Claim in safety — inconclusiveinconclusiveworking →
Claim in safety — inconclusiveinconclusiveworking →
pharmacology18 · 10 ok
Claim in pharmacology — not_supportednot supportedworking →
Claim in pharmacology — inconclusiveinconclusiveworking →
The psychedelic effects are mediated primarily through 5-HT₂A-Gq signaling rather than β-arrestin2 recruitment, consistent with the signaling pathway model established by Wallach et al. for psychedelic-potential prediction.supported
5-HT2A-Gq (not beta-arrestin2) efficacy predicts psychedelic potential via head-twitch response magnitude in mice. s41467-023-44016-1
In vivo confirmation of 5-HT₂A agonism comes from head-twitch response (HTR) studies in C57BL/6J mice, where 2C-B produced an ED₅₀ of 2.43 μmol/kg — a validated behavioral proxy for hallucinogenic activity in humanssupported
2C-B ED50=2.43 μmol/kg for head-twitch response in C57BL/6J mice; confirms in vivo 5-HT2A agonism. j.neuropharm.2018.10.037
This potency is approximately three-fold lower than DOB (ED₅₀ = 0.75 μmol/kg), consistent with the established potency-reducing effect of removing the alpha-methyl group from phenethylamine psychedelics.supported
2C-B ED50=2.43 μmol/kg for head-twitch response in C57BL/6J mice. DOB (alpha-methyl analog) ED50=0.75 μmol/kg for comparison. j.neuropharm.2018.10.037
Villalobos et al. demonstrated that in Xenopus laevis oocytes expressing rat 5-HT₂A receptors, 2C-B acts as a functional antagonist, blocking 5-HT-induced currents, while maintaining partial agonist activity at 5-HT₂Csupported
2C-B acts as 5-HT2A antagonist (blocking 5-HT-induced currents) but partial agonist at 5-HT2C in Xenopus oocytes. pmid:15006903
This divergence likely reflects differences between heterologous expression systems and intact neural circuits: the robust in vivo HTR data confirm functionally relevant 5-HT₂A agonism in living animals.supported
2C-B ED50=2.43 μmol/kg for head-twitch response in C57BL/6J mice; confirms in vivo 5-HT2A agonism. j.neuropharm.2018.10.037
Claim in pharmacology — inconclusiveinconclusiveworking →
Claim in pharmacology — inconclusiveinconclusiveworking →
Ray profiled 2C-B alongside 24 other psychedelics at 51 receptor sites in the NIMH Psychoactive Drug Screening Program, demonstrating that phenylalkylamines are "not as selective as generally believed, interacting with 42 of 49 broadly assayed sites"supported
Receptor affinity pharmacology of 25 psychedelic drugs at 51 receptors, transporters, and ion channels (NIMH-PDSP). Phenylalkylamines interact with 42 of 49 sites tested. journal.pone.0009019
Claim in pharmacology — inconclusiveinconclusiveworking →
Claim in pharmacology — inconclusiveinconclusiveworking →
Metabolism proceeds primarily through MAO-A and MAO-B-mediated oxidative deamination, producing 4-bromo-2,5-dimethoxyphenylacetic acid (BDMPAA) as the major urinary metabolite (73% of human urinary output), with 4-bromo-2-hydroxy-5-methoxyphenylacetic acid (B-2-HMPAA) accounting for 13%supported
Human urine metabolite profile: 4-bromo-2,5-dimethoxyphenylacetic acid (73%), 4-bromo-2-hydroxy-5-methoxyphenylacetic acid (13%). MAO identified as key metabolic enzyme. j.1556-4029.2012.02289.x
Claim in pharmacology — inconclusiveinconclusiveworking →
Neither metabolite activates the 5-HT₂A receptor, confirming that the parent compound is solely responsible for psychedelic effectssupported
Metabolites BDMPAA and B-2-HMPAA do not activate serotonin 2A receptor. j.dmd.2025.100086
CYP2D6 contributes a minor metabolic pathway.partially supported
MAO-A, MAO-B, cytosolic enzymes, and CYP2D6 identified as key metabolic enzymes. j.dmd.2025.100086
Claim in pharmacology — inconclusiveinconclusiveworking →
A significant species difference exists in metabolic routing: O-demethylation followed by N-acetylation is the major pathway in rats but only a minor fraction in human urinesupported
Human urine metabolite profile: 4-bromo-2,5-dimethoxyphenylacetic acid (73%)... MAO identified as key metabolic enzyme. Species differences from rat. j.1556-4029.2012.02289.x
summary12 · 6 ok
Claim in summary — inconclusiveinconclusiveworking →
Claim in summary — inconclusiveinconclusiveworking →
Claim in summary — inconclusiveinconclusiveworking →
Claim in summary — not_supportednot supportedworking →
2C-B acts as a partial agonist at serotonin 5-HT₂A, 5-HT₂B, and 5-HT₂C receptors, with in vivo 5-HT₂A agonism confirmed by a head-twitch response ED₅₀ of 2.43 μmol/kg in mice — approximately three-fold less potent than its alpha-methylated analog DOBsupported
2C-B ED50=2.43 μmol/kg for head-twitch response in C57BL/6J mice; confirms in vivo 5-HT2A agonism. DOB (alpha-methyl analog) ED50=0.75 μmol/kg for comparison. j.neuropharm.2018.10.037
Metabolism proceeds primarily through MAO-A/MAO-B-mediated oxidative deamination to inactive metabolites, with CYP2D6 as a minor pathway; plasma half-life is 1.43 hours at 20 mg oral.partially supported
2C-B: Tmax 2.43h, t1/2 1.43h. cpt.2958
Metabolism proceeds primarily through MAO-A/MAO-B-mediated oxidative deamination to inactive metabolites, with CYP2D6 as a minor pathway; plasma half-life is 1.43 hours at 20 mg oral.partially supported
MAO-A, MAO-B, cytosolic enzymes, and CYP2D6 identified as key metabolic enzymes. Metabolites BDMPAA and B-2-HMPAA do not activate serotonin 2A receptor. First human plasma PK study with validated LC-MS/MS method; 30 mg oral dose. j.dmd.2025.100086
The subjective experience spans visual intensification, color enhancement, and sensory amplification alongside entactogenic qualities — pleasure and sociability comparable to mdma — that scale steeply with dose into full psychedelic territorysupported
psychedelic + entactogen profile; lower incapacitation than other psychedelics. 0269881111431752
The subjective experience spans visual intensification, color enhancement, and sensory amplification alongside entactogenic qualities — pleasure and sociability comparable to mdma — that scale steeply with dose into full psychedelic territorysupported
2C-B classified as stimulant, hallucinogen, entactogen and/or empathogen. 643878
Claim in summary — inconclusiveinconclusiveworking →
Claim in summary — inconclusiveinconclusiveworking →
Tolerance develops rapidly through 5-HT₂A receptor downregulation, consistent with the serotonergic psychedelic class, though no substance-specific study confirms thissupported
Beta-arrestin-biased ligands block psychedelic effects and induce receptor downregulation and tachyphylaxis. s41467-023-44016-1
pharmacokinetic-detail10 · 10 ok
Mallaroni et al. measured plasma concentrations in 22 healthy subjects following 20 mg oral administration in a double-blind, placebo-controlled design:supported
First double-blind placebo-controlled comparison of 2C-B (20mg) vs psilocybin (15mg) in 22 healthy subjects. cpt.2958
Papaseit et al. measured oral fluid concentrations in 16 subjects at doses of 10–20 mg (mean 15.94 mg):supported
n=16 recreational users, oral 10-15-20mg. fphar.2018.00206
Thomann et al. conducted the first validated LC-MS/MS pharmacokinetic and metabolite analysis using plasma from subjects who received 30 mg oral 2C-B, identifying BDMPAA and B-2-HMPAA as the primary plasma metabolitessupported
Metabolites BDMPAA and B-2-HMPAA do not activate serotonin 2A receptor. First human plasma PK study with validated LC-MS/MS method; 30 mg oral dose. j.dmd.2025.100086
This study confirmed MAO-A, MAO-B, and cytosolic enzymes as the primary BDMPAA-forming pathway, with CYP2D6 identified as a minor metabolic contributor.supported
MAO-A, MAO-B, cytosolic enzymes, and CYP2D6 identified as key metabolic enzymes. j.dmd.2025.100086
MAO-mediated oxidative deamination produces an aldehyde intermediate, which is subsequently oxidized by aldehyde dehydrogenase to BDMPAA (4-bromo-2,5-dimethoxyphenylacetic acid), accounting for 73% of human urinary metabolitessupported
Human urine metabolite profile: 4-bromo-2,5-dimethoxyphenylacetic acid (73%)... MAO identified as key metabolic enzyme. j.1556-4029.2012.02289.x
BDMPAA is pharmacologically inactive at 5-HT₂Asupported
Metabolites BDMPAA and B-2-HMPAA do not activate serotonin 2A receptor. j.dmd.2025.100086
The secondary metabolite B-2-HMPAA (4-bromo-2-hydroxy-5-methoxyphenylacetic acid) accounts for 13% of urinary output, with a minor alcohol metabolite (4-bromo-2,5-dimethoxyphenylethyl alcohol) contributing approximately 4.5%.supported
4-bromo-2-hydroxy-5-methoxyphenylacetic acid (13%), alcohol metabolite (4.5%). j.1556-4029.2012.02289.x
These acetamide metabolites are only minor fractions in human urinesupported
Human urine metabolite profile: 4-bromo-2,5-dimethoxyphenylacetic acid (73%), 4-bromo-2-hydroxy-5-methoxyphenylacetic acid (13%), alcohol metabolite (4.5%). Species differences from rat. j.1556-4029.2012.02289.x
Rohanova et al. characterized 2C-B pharmacokinetics in rats following subcutaneous administration:supported
Rat SC disposition; half-life ~1.1 h; volume of distribution 16 L/kg; high brain:serum ratio (max 13.9); rapid BBB penetration; lung retention. j.toxlet.2008.01.017
Since MAO-A and MAO-B are the primary metabolic enzymes, concurrent administration of monoamine oxidase inhibitors would be expected to substantially increase 2C-B systemic exposuresupported
MAO-A, MAO-B, cytosolic enzymes, and CYP2D6 identified as key metabolic enzymes. j.dmd.2025.100086
receptor-pharmacology9 · 5 ok
Claim in receptor-pharmacology — not_supportednot supportedworking →
Hansen et al. used 2C-B as the reference compound for a 48-member N-benzyl phenethylamine series, establishing its binding at 5-HT₂A and 5-HT₂C as the pharmacological foundation for the entire NBOMe drug classsupported
48-compound SAR study using 2C-B as template; 5-HT2A affinity from subnanomolar to micromolar across series. cn400216u
Claim in receptor-pharmacology — inconclusiveinconclusiveworking →
Claim in receptor-pharmacology — inconclusiveinconclusiveworking →
In intact animals, 2C-B produces robust 5-HT₂A-mediated behavioral responses (HTR ED₅₀ = 2.43 μmol/kg)supported
2C-B ED50=2.43 μmol/kg for head-twitch response in C57BL/6J mice; confirms in vivo 5-HT2A agonism. j.neuropharm.2018.10.037
In Xenopus laevis oocytes expressing rat 5-HT₂A receptors, however, Villalobos et al. found 2C-B to act as a functional antagonist, blocking serotonin-induced ion currents, while retaining partial agonist activity at 5-HT₂Csupported
2C-B acts as 5-HT2A antagonist (blocking 5-HT-induced currents) but partial agonist at 5-HT2C in Xenopus oocytes. pmid:15006903
The 5-HT₂A-Gq signaling pathway, rather than β-arrestin2 recruitment, appears to mediate the psychedelic effects, and the oocyte current assay may preferentially detect different downstream signaling events than those responsible for hallucinogenic activity.supported
5-HT2A-Gq (not beta-arrestin2) efficacy predicts psychedelic potential via head-twitch response magnitude in mice. s41467-023-44016-1
Ray's NIMH-PDSP screen demonstrated that 2C-B interacts with 42 of 49 assayed receptor sites, including serotonin, dopamine, adrenergic, and histamine targetssupported
Phenylalkylamines interact with 42 of 49 sites tested. Diversity of receptor interaction underlies qualitative diversity of drug effects. journal.pone.0009019
Claim in receptor-pharmacology — inconclusiveinconclusiveworking →
comparative-pharmacology6 · 2 ok
The only published direct head-to-head comparison comes from Mallaroni et al., using 2C-B 20 mg vs. psilocybin 15 mg oral in 22 subjects.supported
First double-blind placebo-controlled comparison of 2C-B (20mg) vs psilocybin (15mg) in 22 healthy subjects. cpt.2958
Claim in comparative-pharmacology — inconclusiveinconclusiveworking →
Claim in comparative-pharmacology — inconclusiveinconclusiveworking →
Claim in comparative-pharmacology — inconclusiveinconclusiveworking →
Claim in comparative-pharmacology — inconclusiveinconclusiveworking →
Rickli et al. profiled 2C-B alongside 2c-c, 2C-D, 2c-e, 2c-i, and mescaline in a comprehensive multi-receptor panel with comparison to lsdsupported
In vitro receptor interaction profiles of NBOMe drugs vs 2C drugs (including 2C-B) and LSD. j.neuropharm.2015.08.034
clinical-evidence5 · 2 ok
Claim in clinical-evidence — inconclusiveinconclusiveworking →
The first published human pharmacological study of 2C-B used an observational design with 16 experienced recreational users at doses of 10–20 mg oral.supported
n=16 recreational users, oral 10-15-20mg. fphar.2018.00206
Pharmacokinetic data from the 30 mg arm have been published by Thomann et al., but the primary comparative outcome results — the trial's core objective of head-to-head comparison across three doses of 2C-B against active comparators — have not appeared in peer-reviewed publication as of April 2026supported
First human plasma PK study with validated LC-MS/MS method; 30 mg oral dose. j.dmd.2025.100086
Claim in clinical-evidence — inconclusiveinconclusiveworking →
Claim in clinical-evidence — inconclusiveinconclusiveworking →
neuroscience4 · 2 ok
Claim in neuroscience — inconclusiveinconclusiveworking →
Claim in neuroscience — inconclusiveinconclusiveworking →
The entactogenic component — pleasure and sociability without significant monoamine release — may reflect a distinct balance of 5-HT₂A versus 5-HT₂C activation, or contributions from the broad receptorome interactions documented by Ray.supported
Diversity of receptor interaction underlies qualitative diversity of drug effects. Phenylalkylamines interact with 42 of 49 sites tested. journal.pone.0009019
How does 2C-B's functional antagonism at 5-HT₂A in heterologous expression systems reconcile with its clear 5-HT₂A-mediated behavioral effects in vivo? This preparation-dependent pharmacology remains mechanistically unexplained.supported
2C-B acts as 5-HT2A antagonist (blocking 5-HT-induced currents) but partial agonist at 5-HT2C in Xenopus oocytes. pmid:15006903
chemistry3 · 2 ok
Claim in chemistry — not_supportednot supportedworking →
The absence of an alpha-methyl group on the ethylamine chain differentiates 2C-B from the corresponding amphetamine analog DOB (2,5-dimethoxy-4-bromoamphetamine), which is approximately three-fold more potent and substantially longer-acting.supported
DOB (alpha-methyl analog) ED50=0.75 μmol/kg for comparison. j.neuropharm.2018.10.037
2C-B also serves as the parent compound for the NBOMe series: N-benzylation at the amine produces 25B-NBOMe, a full 5-HT₂A agonist with dramatically increased potency and a substantially different safety profilesupported
Reviews NBOMe structure-activity relationships, behavioral pharmacology, metabolism, and toxicity. 2C-B identified as reference compound for the 2C-X class. 7854_2016_64
effects-overview3 · 1 ok
Claim in effects-overview — inconclusiveinconclusiveworking →
Claim in effects-overview — inconclusiveinconclusiveworking →
Relative to psilocybin, 2C-B produces less dysphoria, less ego dissolution, and shorter duration at comparable recreational doses, while retaining equivalent psychomotor and spatial memory impairmentsupported
2C-B showed lighter profile; less dysphoria and ego dissolution than psilocybin. Similar cognitive impairment. Effects resolved within 6h in 86.3% vs 63.6% for psilocybin. cpt.2958