2C-B

4-bromo-2,5-dimethoxyphenethylamine

Sources

6 strong · 14 moderate · 9 weak

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

Values approved

212/227 (93%)

Data points an editor reviewed and accepted for publication.

Value Provenance

Dosing

rectal

Predates provenance tracking — no derivation record for this dataset

Field	Published	AI Proposed
Threshold	1 mg	no record
Low	5–8 mg	no record
Common	8–12 mg	no record
Strong	12–23 mg	no record
Heavy	23+ mg	no record

insufflated

Predates provenance tracking — no derivation record for this dataset

Field	Published	AI Proposed
Threshold	1 mg	no record
Low	5–8 mg	no record
Common	8–12 mg	no record
Strong	12–23 mg	no record
Heavy	23+ mg	no record

intravenous

Predates provenance tracking — no derivation record for this dataset

Field	Published	AI Proposed
Threshold	1 mg	no record
Low	1–2.5 mg	no record
Common	2.5–5 mg	no record
Strong	5–10 mg	no record
Heavy	10+ mg	no record

oraltrace

Field	Published	AI Proposed	Confidence
Threshold	5 mg	5 mg	medium
Low	5–15 mg	5–15 mg	medium
Common	15–25 mg	15–25 mg	medium
Strong	25–40 mg	25–40 mg	medium
Heavy	40+ mg	40+ mg	medium
Editorial	Oral dose ranges anchored to Shulgin's PiHKAL range of 12-24 mg (common), Papaseit et al. (2018) controlled study at 10-20 mg, Mallaroni et al. (2023) at 20 mg, and Basel trial arms at 10, 20, 30 mg. Threshold and heavy values from community consensus (PsychonautWiki, Erowid). The steep dose-response curve documented by Shulgin makes precise tier boundaries particularly important for this compound.
	ReasoningReasoning Oral dose ranges anchored to Shulgin's PiHKAL range of 12-24 mg (common), Papaseit et al. (2018) controlled study at 10-20 mg, Mallaroni et al. (2023) at 20 mg, and Basel trial arms at 10, 20, 30 mg. Threshold and heavy values from community consensus (PsychonautWiki, Erowid). The steep dose-response curve documented by Shulgin makes precise tier boundaries particularly important for this compound. Evidence basis: controlled_human_study

Duration

oral

Field	Published	AI Proposed	Confidence
Come uptrace	15–45 minutes	15–45 minutes	medium
Editorial	Come-up duration inferred from the interval between onset (~20-45 min) and peak effects (~1-2 hours per Papaseit et al. 2018). The steep dose-response curve can produce rapid intensity escalation during this phase.
	ReasoningReasoning Come-up duration inferred from the interval between onset (~20-45 min) and peak effects (~1-2 hours per Papaseit et al. 2018). The steep dose-response curve can produce rapid intensity escalation during this phase. Evidence basis: controlled_human_study
Totaltrace	4–7 hours	4–7 hours	high
Editorial	Shulgin documented 4-8 hours in PiHKAL. Mallaroni et al. (2023) found 86.3% of subjects resolved within 6 hours at 20 mg oral. Total set at 4-7 hours representing the middle ~80% of experiences at common doses.
	ReasoningReasoning Shulgin documented 4-8 hours in PiHKAL. Mallaroni et al. (2023) found 86.3% of subjects resolved within 6 hours at 20 mg oral. Total set at 4-7 hours representing the middle ~80% of experiences at common doses. Evidence basis: controlled_human_study
Onsettrace	20–45 minutes	20–45 minutes	high
Editorial	Papaseit et al. (2018) reported peak effects at 1-2 hours and salivary Tmax ~1 hour, implying onset well before 1 hour. Consistent with community reports of 20-45 minute onset for oral phenethylamines.
	ReasoningReasoning Papaseit et al. (2018) reported peak effects at 1-2 hours and salivary Tmax ~1 hour, implying onset well before 1 hour. Consistent with community reports of 20-45 minute onset for oral phenethylamines. Evidence basis: controlled_human_study
Peaktrace	60–120 minutes	60–120 minutes	high
Editorial	Papaseit et al. (2018) reported peak subjective effects at approximately 1-2 hours post-dose. Plasma Tmax of 2.43 hours (Mallaroni et al. 2023) indicates peak plasma levels sustained over this window.
	ReasoningReasoning Papaseit et al. (2018) reported peak subjective effects at approximately 1-2 hours post-dose. Plasma Tmax of 2.43 hours (Mallaroni et al. 2023) indicates peak plasma levels sustained over this window. Evidence basis: controlled_human_study
Offsettrace	60–150 minutes	60–150 minutes	medium
Editorial	Offset duration derived from total experience length (4-7 hours per Shulgin and Mallaroni) minus onset, come-up, and peak phases. The short plasma half-life (1.43 hours) supports relatively rapid offset once peak subsides.
	ReasoningReasoning Offset duration derived from total experience length (4-7 hours per Shulgin and Mallaroni) minus onset, come-up, and peak phases. The short plasma half-life (1.43 hours) supports relatively rapid offset once peak subsides. Evidence basis: controlled_human_study
After effectstrace	2–6 hours	2–6 hours	medium
Editorial	Aftereffects duration estimated from the short plasma half-life (1.43 hours, Mallaroni 2023) and salivary detection window (up to 24 hours in ~50% of subjects, Papaseit 2018). Residual mood and perceptual changes extend beyond subjective resolution but not to the extent seen with longer-acting psychedelics.
	ReasoningReasoning Aftereffects duration estimated from the short plasma half-life (1.43 hours, Mallaroni 2023) and salivary detection window (up to 24 hours in ~50% of subjects, Papaseit 2018). Residual mood and perceptual changes extend beyond subjective resolution but not to the extent seen with longer-acting psychedelics. Evidence basis: community_consensus_large

rectal

Predates provenance tracking — no derivation record for this dataset

Field	Published	AI Proposed	Confidence
Onset	0–20 minutes	no record
Total	4–7 hours	no record

insufflated

Predates provenance tracking — no derivation record for this dataset

Field	Published	AI Proposed
Onset	1–5 minutes	no record
Come up	15–30 minutes	no record
Peak	60–90 minutes	no record
Offset	2–3 hours	no record
After effects	2–4 hours	no record
Total	4–6 hours	no record

intravenous

Predates provenance tracking — no derivation record for this dataset

Field	Published	AI Proposed
Onset	5–15 seconds	no record
Peak	15–30 minutes	no record
Offset	1.5–2 hours	no record
Total	2–3 hours	no record

Safety

Toxicity Profiletrace

Field	Published	AI Proposed	Confidence
Acute	low	low	medium
Chronic	negligible	negligible	medium
Organs Affected	cardiovascular	cardiovascular	medium
Editorial	Acute toxicity classified as low based on Papaseit et al. (2018) and Mallaroni et al. (2023) controlled data showing only minor, reversible cardiovascular effects at 10-20 mg with no serious adverse events. No LD50, no 2C-B-specific fatalities. Chronic toxicity classified as negligible: no evidence of organ damage from repeated use exists, though long-term studies have not been conducted. Confidence medium because controlled study sample sizes are small (n=16-22) and the toxic dose is unknown.
	ReasoningReasoning Acute toxicity classified as low based on Papaseit et al. (2018) and Mallaroni et al. (2023) controlled data showing only minor, reversible cardiovascular effects at 10-20 mg with no serious adverse events. No LD50, no 2C-B-specific fatalities. Chronic toxicity classified as negligible: no evidence of organ damage from repeated use exists, though long-term studies have not been conducted. Confidence medium because controlled study sample sizes are small (n=16-22) and the toxic dose is unknown. Evidence basis: controlled_human_study

Dependence Profiletrace

Field	Published	AI Proposed	Confidence
Physical	none	none	medium
Psychological	negligible	negligible	medium
Compulsive Redosing	negligible	negligible	medium
Dose Escalation	low	low	medium
Editorial	No 2C-B-specific dependence studies exist. Profile inferred from serotonergic psychedelic class characteristics: no self-administration in animal models, rapid tolerance preventing escalation, and minimal monoamine transporter activity (Inan et al. 2020). Nugteren-van Lonkhuyzen et al. (2015) review did not report dependence data for 2C-B. Dose escalation tendency rated low rather than negligible due to the steep dose-response curve, which could incentivize dose-finding behavior.
	ReasoningReasoning No 2C-B-specific dependence studies exist. Profile inferred from serotonergic psychedelic class characteristics: no self-administration in animal models, rapid tolerance preventing escalation, and minimal monoamine transporter activity (Inan et al. 2020). Nugteren-van Lonkhuyzen et al. (2015) review did not report dependence data for 2C-B. Dose escalation tendency rated low rather than negligible due to the steep dose-response curve, which could incentivize dose-finding behavior. Evidence basis: structural_analogy

Withdrawal Profiletrace

Field	Published	AI Proposed	Confidence
Severity	none	none	medium
Symptoms	—	—	medium
Fatal	No	No	medium
Medical Supervision	Not required	Not required	medium
Editorial	No withdrawal syndrome reported for any serotonergic psychedelic. Class-level inference; no 2C-B-specific data.
	ReasoningReasoning No withdrawal syndrome reported for any serotonergic psychedelic. Class-level inference; no 2C-B-specific data. Evidence basis: structural_analogy

Tolerance Profiletrace

Field	Published	AI Proposed	Confidence
Buildup	rapid	rapid	low
Half-life	3 days	3 days	low
Full Reset	14 days	14 days	low
Cross-tolerances	LSD, psilocybin, mescaline, DMT, 2C-E, 2C-I, DOB	LSD, psilocybin, mescaline, DMT, 2C-E, 2C-I, DOB	low
Editorial	No substance-specific tolerance study exists for 2C-B. Rapid tolerance buildup and 14-day full reset inferred from the well-characterized tolerance profiles of LSD and psilocybin, which share the 5-HT2A agonist mechanism. Wallach et al. (2023) confirmed β-arrestin-mediated 5-HT2A downregulation as the tachyphylaxis mechanism for this class. 2C-B's partial agonist profile and shorter duration could theoretically produce different tolerance kinetics than full agonists.
	ReasoningReasoning No substance-specific tolerance study exists for 2C-B. Rapid tolerance buildup and 14-day full reset inferred from the well-characterized tolerance profiles of LSD and psilocybin, which share the 5-HT2A agonist mechanism. Wallach et al. (2023) confirmed β-arrestin-mediated 5-HT2A downregulation as the tachyphylaxis mechanism for this class. 2C-B's partial agonist profile and shorter duration could theoretically produce different tolerance kinetics than full agonists. Evidence basis: structural_analogy

Effects & Profile

Contraindications

Field	Published	AI Proposed	Confidence
neurological epilepsytrace	relative	relative	medium
Editorial	Dean et al. (2013) documented seizures in severe 2C-class toxicity. No 2C-B-specific seizure data at therapeutic doses.
	ReasoningReasoning Dean et al. (2013) documented seizures in severe 2C-class toxicity. No 2C-B-specific seizure data at therapeutic doses.
other concurrent MAOI usetrace	absolute	absolute	high
Editorial	Thomann et al. (2025) identified MAO-A and MAO-B as primary metabolic enzymes. MAOI co-administration blocks the primary clearance pathway.
	ReasoningReasoning Thomann et al. (2025) identified MAO-A and MAO-B as primary metabolic enzymes. MAOI co-administration blocks the primary clearance pathway.
other concurrent lithium usetrace	relative	relative	low
Editorial	Inan et al. (2020) identified lithium as relevant to NPS interaction profile. Mechanism incompletely understood.
	ReasoningReasoning Inan et al. (2020) identified lithium as relevant to NPS interaction profile. Mechanism incompletely understood.
cardiovascular uncontrolled hypertensiontrace	absolute	absolute	high
Editorial	Papaseit et al. (2018) documented cardiovascular effects at 10-20 mg oral.
	ReasoningReasoning Papaseit et al. (2018) documented cardiovascular effects at 10-20 mg oral.
psychiatric psychotic disorderstrace	absolute	absolute	medium
Editorial	Class-level contraindication for all serotonergic psychedelics based on 5-HT2A mechanism. No 2C-B-specific data.
	ReasoningReasoning Class-level contraindication for all serotonergic psychedelics based on 5-HT2A mechanism. No 2C-B-specific data.
psychiatric bipolar disordertrace	absolute	absolute	medium
Editorial	Class-level contraindication for serotonergic psychedelics. Additional concern due to lithium interaction risk identified by Inan et al. (2020).
	ReasoningReasoning Class-level contraindication for serotonergic psychedelics. Additional concern due to lithium interaction risk identified by Inan et al. (2020).
pregnancy breastfeeding pregnancy and breastfeedingtrace	absolute	absolute	medium
Editorial	No reproductive toxicology data for 2C-B. Standard precautionary contraindication for psychoactive substances with serotonergic mechanisms during pregnancy.
	ReasoningReasoning No reproductive toxicology data for 2C-B. Standard precautionary contraindication for psychoactive substances with serotonergic mechanisms during pregnancy.

Timeline Phases

oral

Field	Published	AI Proposed	Confidence
Plateautrace	1800–3600 sec(i=0.55)	1800–3600 sec(i=0.55)	high
Editorial	Timeline anchored to published controlled data: Papaseit et al. (2018) reported peak subjective effects at 1-2 hours post-dose, salivary Tmax ~1 hour; Mallaroni et al. (2023) measured plasma Tmax 2.43 hours, plasma half-life 1.43 hours, and 86.3% effect resolution within 6 hours at 20 mg; Shulgin documented 4-8 hour total duration in PiHKAL. Afterglow duration estimated from community reports and the short pharmacokinetic half-life.
	ReasoningReasoning Timeline anchored to published controlled data: Papaseit et al. (2018) reported peak subjective effects at 1-2 hours post-dose, salivary Tmax ~1 hour; Mallaroni et al. (2023) measured plasma Tmax 2.43 hours, plasma half-life 1.43 hours, and 86.3% effect resolution within 6 hours at 20 mg; Shulgin documented 4-8 hour total duration in PiHKAL. Afterglow duration estimated from community reports and the short pharmacokinetic half-life.
Onsettrace	1200–2700 sec(i=0.05)	1200–2700 sec(i=0.05)	high
Editorial	Timeline anchored to published controlled data: Papaseit et al. (2018) reported peak subjective effects at 1-2 hours post-dose, salivary Tmax ~1 hour; Mallaroni et al. (2023) measured plasma Tmax 2.43 hours, plasma half-life 1.43 hours, and 86.3% effect resolution within 6 hours at 20 mg; Shulgin documented 4-8 hour total duration in PiHKAL. Afterglow duration estimated from community reports and the short pharmacokinetic half-life.
	ReasoningReasoning Timeline anchored to published controlled data: Papaseit et al. (2018) reported peak subjective effects at 1-2 hours post-dose, salivary Tmax ~1 hour; Mallaroni et al. (2023) measured plasma Tmax 2.43 hours, plasma half-life 1.43 hours, and 86.3% effect resolution within 6 hours at 20 mg; Shulgin documented 4-8 hour total duration in PiHKAL. Afterglow duration estimated from community reports and the short pharmacokinetic half-life.
Come uptrace	1200–2700 sec(i=0.30)	1200–2700 sec(i=0.30)	high
Editorial	Timeline anchored to published controlled data: Papaseit et al. (2018) reported peak subjective effects at 1-2 hours post-dose, salivary Tmax ~1 hour; Mallaroni et al. (2023) measured plasma Tmax 2.43 hours, plasma half-life 1.43 hours, and 86.3% effect resolution within 6 hours at 20 mg; Shulgin documented 4-8 hour total duration in PiHKAL. Afterglow duration estimated from community reports and the short pharmacokinetic half-life.
	ReasoningReasoning Timeline anchored to published controlled data: Papaseit et al. (2018) reported peak subjective effects at 1-2 hours post-dose, salivary Tmax ~1 hour; Mallaroni et al. (2023) measured plasma Tmax 2.43 hours, plasma half-life 1.43 hours, and 86.3% effect resolution within 6 hours at 20 mg; Shulgin documented 4-8 hour total duration in PiHKAL. Afterglow duration estimated from community reports and the short pharmacokinetic half-life.
Peaktrace	3600–7200 sec(i=1.00)	3600–7200 sec(i=1.00)	high
Editorial	Timeline anchored to published controlled data: Papaseit et al. (2018) reported peak subjective effects at 1-2 hours post-dose, salivary Tmax ~1 hour; Mallaroni et al. (2023) measured plasma Tmax 2.43 hours, plasma half-life 1.43 hours, and 86.3% effect resolution within 6 hours at 20 mg; Shulgin documented 4-8 hour total duration in PiHKAL. Afterglow duration estimated from community reports and the short pharmacokinetic half-life.
	ReasoningReasoning Timeline anchored to published controlled data: Papaseit et al. (2018) reported peak subjective effects at 1-2 hours post-dose, salivary Tmax ~1 hour; Mallaroni et al. (2023) measured plasma Tmax 2.43 hours, plasma half-life 1.43 hours, and 86.3% effect resolution within 6 hours at 20 mg; Shulgin documented 4-8 hour total duration in PiHKAL. Afterglow duration estimated from community reports and the short pharmacokinetic half-life.
Resolutiontrace	3600–5400 sec(i=0.20)	3600–5400 sec(i=0.20)	high
Editorial	Timeline anchored to published controlled data: Papaseit et al. (2018) reported peak subjective effects at 1-2 hours post-dose, salivary Tmax ~1 hour; Mallaroni et al. (2023) measured plasma Tmax 2.43 hours, plasma half-life 1.43 hours, and 86.3% effect resolution within 6 hours at 20 mg; Shulgin documented 4-8 hour total duration in PiHKAL. Afterglow duration estimated from community reports and the short pharmacokinetic half-life.
	ReasoningReasoning Timeline anchored to published controlled data: Papaseit et al. (2018) reported peak subjective effects at 1-2 hours post-dose, salivary Tmax ~1 hour; Mallaroni et al. (2023) measured plasma Tmax 2.43 hours, plasma half-life 1.43 hours, and 86.3% effect resolution within 6 hours at 20 mg; Shulgin documented 4-8 hour total duration in PiHKAL. Afterglow duration estimated from community reports and the short pharmacokinetic half-life.
Afterglowtrace	7200–14400 sec(i=0.05)	7200–14400 sec(i=0.05)	high
Editorial	Timeline anchored to published controlled data: Papaseit et al. (2018) reported peak subjective effects at 1-2 hours post-dose, salivary Tmax ~1 hour; Mallaroni et al. (2023) measured plasma Tmax 2.43 hours, plasma half-life 1.43 hours, and 86.3% effect resolution within 6 hours at 20 mg; Shulgin documented 4-8 hour total duration in PiHKAL. Afterglow duration estimated from community reports and the short pharmacokinetic half-life.
	ReasoningReasoning Timeline anchored to published controlled data: Papaseit et al. (2018) reported peak subjective effects at 1-2 hours post-dose, salivary Tmax ~1 hour; Mallaroni et al. (2023) measured plasma Tmax 2.43 hours, plasma half-life 1.43 hours, and 86.3% effect resolution within 6 hours at 20 mg; Shulgin documented 4-8 hour total duration in PiHKAL. Afterglow duration estimated from community reports and the short pharmacokinetic half-life.

Dose Tier Summaries

thresholdtrace

medium

At threshold doses, effects are subtle and easily dismissed as placebo: faint color brightening, a slight shift in mood toward warmth or curiosity, and mild enhancement of tactile and auditory sensation. Perceptual changes remain sub-hallucinogenic — objects may appear slightly sharper or more vivid, but no geometric patterning or visual distortion occurs. Physically, mild pupil dilation and a faint sense of bodily stimulation may be noticeable. Appetite is minimally affected. Sleep is possible within a few hours of ingestion. Functional impairment is negligible at this range. The experience is easily managed in social or productive settings.

Editorial

Threshold effects inferred from Shulgin's documented 12-24 mg active range (PiHKAL entry #20) and the steep dose-response curve, placing threshold below the lower bound of the active range. No controlled study has specifically characterized threshold doses.

Reasoning

Evidence basis: community_consensus_large

lighttrace

medium

Mild visual enhancement emerges: colors appear more saturated, surfaces may shimmer or breathe subtly, and pattern recognition is heightened. Mood elevation is consistent — a gentle euphoria with increased sociability and sensory appreciation. Thought patterns shift slightly, with enhanced associative thinking and mild introspective inclination. Physically, mild stimulation is typical: increased energy, slight jaw tension, and pupil dilation. Heart rate and blood pressure increase modestly. Some users report mild nausea during the come-up phase. The experience remains easily navigable. Conversation and basic tasks are manageable, though complex cognitive work may be impaired. Duration is typically 3-5 hours.

Editorial

Light-dose effects drawn from Papaseit et al. (2018) observational data at 10-20 mg, where lower-dose subjects reported mild perceptual changes and euphoria without frank hallucinations. The lower end of Shulgin's 12-24 mg range describes these effects.

Reasoning

Evidence basis: controlled_human_study

commontrace

high

The full 2C-B experience manifests: pronounced visual enhancement with color intensification, surface texturing, geometric overlay patterns, and object morphing. Sensory amplification extends across modalities — music sounds richer, tactile sensitivity increases, and synesthetic crossover may occur. Euphoria deepens, with strong feelings of pleasure, connectedness, and erotic or sensual awareness. Stimulant-like arousal is prominent, with increased energy and physical restlessness. Heart rate increases up to +13 bpm and blood pressure up to +19 mmHg systolic. Mild nausea may occur during onset. Body load is generally lighter than with tryptamine psychedelics. The steep dose-response curve means the upper boundary of this range approaches strong territory with little warning. Effects resolve within 6 hours in most users. Sleep is difficult until effects fully subside.

Editorial

Common-dose effects well-characterized by Mallaroni et al. (2023) at 20 mg and Papaseit et al. (2018) at 10-20 mg in controlled settings. Cardiovascular values from Papaseit. Duration from Mallaroni (86.3% resolution within 6h at 20 mg). Shulgin's PiHKAL range of 12-24 mg centers on this tier.

Reasoning

Evidence basis: controlled_human_study

strongtrace

medium

Intense visual phenomena dominate: vivid geometric patterning, strong color shifting, object morphing and drifting, and closed-eye visuals with complex fractal or kaleidoscopic imagery. Ego boundaries soften and thought processes become markedly nonlinear, with deep introspective or philosophical content. The entactogenic warmth may intensify into profound emotional openness, or conversely, anxiety and dysphoria can emerge — set and setting become critical determinants of valence. Physical effects intensify proportionally: significant stimulation, jaw clenching, temperature dysregulation, and gastrointestinal discomfort. Cardiovascular burden exceeds the modest increases documented at 20 mg. Functional impairment is substantial. The experience demands a committed setting with adequate time (5-7 hours) and a trusted environment. The steep dose-response curve makes this range significantly more intense than common doses despite modest milligram differences.

Editorial

Strong-dose effects inferred from the steep dose-response curve documented by Shulgin, the Basel trial's inclusion of 30 mg arms (Thomann et al. 2025 PK data), and the upper bound of Shulgin's 12-24 mg range where he noted dramatic intensity increases. No published subjective effect data specifically at 25-35 mg.

Reasoning

Evidence basis: community_consensus_large

heavytrace

low

Overwhelming psychedelic intensity: powerful visual distortions that may obscure baseline reality, profound ego dissolution, time distortion to the point of temporal disorientation, and potentially frightening or ecstatic states depending on set and setting. Thought coherence fragments significantly. The experience may bear little resemblance to lower doses due to the steep dose-response relationship. Physical effects at this range are poorly characterized in published literature. Extrapolating from class data, significant cardiovascular stress, nausea, tremor, and hyperthermia risk are expected. Seizure risk may increase at extreme doses based on 2C-class toxicity patterns. This range exceeds all published controlled study doses. The risk-benefit profile shifts substantially — severe psychological distress, prolonged recovery, and medical complications become plausible outcomes. Duration may extend beyond the typical 4-8 hour window.

Editorial

Heavy-dose effects are beyond all published controlled study data (maximum 30 mg in Basel trial). Characterized from class-level toxicity data (Dean et al. 2013), the steep dose-response curve noted by Shulgin, and community reports. No controlled human data exist at these doses.

Reasoning

Evidence basis: community_consensus_small

History

current version

published Sep 29, 2026AI-generated—

versions

2 total · since previous: +0 / −0 citations

publication ledger

publish Sep 29, 2026 · by agent-psx (local dev)

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 correction contact@psychedex.org

Sources

6 strong · 14 moderate · 9 weak

[1]
moderate
Acute Pharmacological Effects of 2C-B in Humans: An Observational Study
Papaseit E, Farre M, Perez-Mana C, Torrens M, Ventura M, Pujadas M, de la Torre R, Gonzalez D · 2018 · Frontiers in Pharmacology
doi.org/10.3389/fphar.2018.00206 pubmed 29593537no claims checked
[2]
moderate
4-Bromo-2,5-dimethoxyphenethylamine (2C-B): presence in the recreational drug market in Spain, pattern of use and subjective effects
Caudevilla-Galligo F, Riba J, Ventura M, Gonzalez D, Farre M, Barbanoj MJ, Bouso JC · 2012 · Journal of Psychopharmacology
doi.org/10.1177/0269881111431752 pubmed 22234927no claims checked
[3]
moderate
Acute Effects of the Novel Psychoactive Drug 2C-B on Emotions
Gonzalez D, Torrens M, Farre M · 2015 · BioMed Research International
doi.org/10.1155/2015/643878 pubmed 26543863no claims checked
[4]
strong
Assessment of the Acute Effects of 2C-B vs. Psilocybin on Subjective Experience, Mood, and Cognition
Mallaroni P, Mason NL, Reckweg JT, Paci R, Ritscher S, Toennes SW, Theunissen EL, Kuypers KPC, Ramaekers JG · 2023 · Clinical Pharmacology and Therapeutics
doi.org/10.1002/cpt.2958 pubmed 37253161no claims checked
[5]
weak
PiHKAL: A Chemical Love Story — Entry #20: 2C-B
Shulgin A, Shulgin A · 1991
linkno claims checked
[6]
strong
Monoamine oxidase inhibitors, opioid analgesics and serotonin toxicity.
Gillman PK · 2005 · British Journal of Anaesthesia
pubmed 16051647no claims checked
[7]
strong
Pharmacology and Toxicology of N-Benzylphenethylamine (NBOMe) Hallucinogens
Halberstadt AL · 2017 · Current Topics in Behavioral Neurosciences
doi.org/10.1007/7854_2016_64 pubmed 28097528no claims checked
[8]
weak
4-Bromo-2,5-Dimethoxyphenethylamine (2C-B): DEA Drug Information Bulletin
US Drug Enforcement Administration · 2003
linkno claims checked
[9]
strong
Liquid chromatography-tandam mass spectrometry-based pharmacokinetic and metabolic analysis of 4-bromo-2,5-dimethoxyphenethylamine and its metabolites in human plasma
Thomann J, Rudin D, Kraus S, Arikci D, Holze F, Liechti ME, Luethi D · 2025 · Drug Metabolism and Disposition
doi.org/10.1016/j.dmd.2025.100086 pubmed 40408905no claims checked
[10]
moderate
Comparison of the behavioral responses induced by phenylalkylamine hallucinogens and their tetrahydrobenzodifuran ("FLY") and benzodifuran ("DragonFLY") analogs
Halberstadt AL, Chatha M, Stratford A, Grill M, Brandt SD · 2019 · Neuropharmacology
doi.org/10.1016/j.neuropharm.2018.10.037 pubmed 30385253no claims checked
[11]
strong
2C or Not 2C: Phenethylamine Designer Drug Review
Dean BV, Stellpflug SJ, Burnett A, Engebretsen KM · 2013 · Journal of Medical Toxicology
doi.org/10.1007/s13181-013-0295-x pubmed 23494844no claims checked
[12]
moderate
Identification of 5-HT2A receptor signaling pathways associated with psychedelic potential
Wallach J, Cao AB, Calkins MM, Heim AJ, Lanham JK, et al. · 2023 · Nature Communications
doi.org/10.1038/s41467-023-44016-1 pubmed 38102107no claims checked
[13]
weak
2C-B (Nexus) Reappears on the Club Drug Scene — NDIC Information Bulletin
National Drug Intelligence Center · 2001
linkno claims checked
[14]
weak
EUDA European Drug Report 2024/2023: New Psychoactive Substances
European Union Drugs Agency (EUDA) · 2024
linkno claims checked
[15]
moderate
Synthesis and Structure-Activity Relationships of N-Benzyl Phenethylamines as 5-HT2A/2C Agonists
Hansen M, Phonekeo K, Paine JS, Leth-Petersen S, Begtrup M, Brauner-Osborne H, Kristensen JL · 2014 · ACS Chemical Neuroscience
doi.org/10.1021/cn400216u pubmed 24397362no claims checked
[16]
moderate
Synthesis and pharmacological evaluation of N-benzyl substituted 4-bromo-2,5-dimethoxyphenethylamines as 5-HT2A/2C partial agonists
Hansen M, Jacobsen SE, Plunkett S, Liebscher GE, McCorvy JD, Brauner-Osborne H, Kristensen JL · 2015 · Bioorganic & Medicinal Chemistry
doi.org/10.1016/j.bmc.2014.12.011 pubmed 25583099no claims checked
[17]
strong
Novel Phenethylamines and Their Potential Interactions With Prescription Drugs: A Systematic Critical Review
Inan F, Brunt TM, Contrucci RR, Hondebrink L, Franssen EJF · 2020 · Therapeutic Drug Monitoring
doi.org/10.1097/ftd.0000000000000725 pubmed 32022784no claims checked
[18]
moderate
Psychedelics and the human receptorome
Ray TS · 2010 · PLoS ONE
doi.org/10.1371/journal.pone.0009019 pubmed 20126400no claims checked
[19]
weak
Analysis of 4-bromo-2,5-dimethoxyphenethylamine abuser's urine: identification and quantitation of urinary metabolites
Kanamori T, Nagasawa K, Kuwayama K, Tsujikawa K, Iwata YT, Inoue H · 2013 · Journal of Forensic Sciences
doi.org/10.1111/j.1556-4029.2012.02289.x pubmed 23066942no claims checked
[20]
moderate
In vivo metabolism of 4-bromo-2,5-dimethoxyphenethylamine (2C-B) in the rat: identification of urinary metabolites
Kanamori T, Inoue H, Iwata Y, Ohmae Y, Kishi T · 2002 · Journal of Analytical Toxicology
pubmed 11916016no claims checked
[21]
moderate
4-Bromo-2,5-dimethoxyphenethylamine (2C-B) and structurally related phenylethylamines are potent 5-HT2A receptor antagonists in Xenopus laevis oocytes
Villalobos CA, Bull P, Saez P, Cassels BK, Huidobro-Toro JP · 2004 · British Journal of Pharmacology
pubmed 15006903no claims checked
[22]
moderate
Receptor interaction profiles of novel N-2-methoxybenzyl (NBOMe) derivatives of 2,5-dimethoxy-substituted phenethylamines (2C drugs)
Rickli A, Luethi D, Reinisch J, Buchy D, Hoener MC, Liechti ME · 2015 · Neuropharmacology
doi.org/10.1016/j.neuropharm.2015.08.034 pubmed 26318099no claims checked
[23]
moderate
Disposition of 4-bromo-2,5-dimethoxyphenethylamine (2C-B) and its metabolite in rats after subcutaneous administration
Rohanova M, Palenicek T, Balikova M · 2008 · Toxicology Letters
doi.org/10.1016/j.toxlet.2008.01.017 pubmed 18339493no claims checked
[24]
weak
25I-NBOMe: clinical case with unique confirmatory testing
Stellpflug SJ, Kealey SE, Hegarty CB, Janis GC · 2014 · Journal of Medical Toxicology
doi.org/10.1007/s13181-013-0314-y pubmed 23872917no claims checked
[25]
moderate
Simultaneous detection of ten psychedelic phenethylamines in urine by gas chromatography-mass spectrometry
Kerrigan S, Banuelos S, Perrella L, Hardy B · 2011 · Journal of Analytical Toxicology
pubmed 21871155no claims checked
[26]
moderate
Pharmacokinetics, pharmacodynamics and toxicology of new psychoactive substances (NPS): 2C-B, 4-fluoroamphetamine and benzofurans
Nugteren-van Lonkhuyzen JJ, van Riel AJ, Brunt TM, Hondebrink L · 2015 · Drug and Alcohol Dependence
doi.org/10.1016/j.drugalcdep.2015.10.011 pubmed 26530501no claims checked
[27]
weak
Serotonin syndrome in patients with headache disorders
Prakash S, Adroja B, Parekh H · 2017 · BMJ Case Reports
doi.org/10.1136/bcr-2017-221383 pubmed 28784913no claims checked
[28]
weak
Transient serotonin syndrome caused by concurrent use of tramadol and selective serotonin reuptake inhibitor
Shakoor M, Ayub S, Ahad A, Ayub Z · 2014 · American Journal of Case Reports
doi.org/10.12659/ajcr.892264 pubmed 25540831no claims checked
[29]
weak
Canada Gazette: Regulations Amending Food and Drug Regulations (Part J — 2C-phenethylamines)
Health Canada · 2016
linkno claims checked

Claim Verification

No claim verification has run for this version.

Coverage & Gaps

effect links

183 links · 183 approved · 51 audited0/183 with evidence basis

interactions

2 approved pairs0/2 graded

2C-B

Value Provenance

Dosing

rectal

insufflated

intravenous

oraltrace →

Duration

oral

rectal

insufflated

intravenous

Safety

Toxicity Profiletrace →

Dependence Profiletrace →

Withdrawal Profiletrace →

Tolerance Profiletrace →

Effects & Profile

Contraindications

Timeline Phases

oral

Dose Tier Summaries

History

Sources

Claim Verification

Coverage & Gaps

oraltrace

Toxicity Profiletrace

Dependence Profiletrace

Withdrawal Profiletrace

Tolerance Profiletrace