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2C-B
4-bromo-2,5-dimethoxyphenethylamine
2C-B (2,5-dimethoxy-4-bromophenethylamine) — Nexus, Bromo, Venus — is a synthetic psychedelic of the phenethylamine class. It is a close structural relative of mescaline, distinguished by a shorter duration. It activates serotonin receptors in the brain,[1] producing the visual distortion and sensory intensification characteristic of psychedelics, paired with warmth and sociability.
2C-B (2,5-dimethoxy-4-bromophenethylamine) — Nexus, Bromo, Venus — is a synthetic psychedelic of the phenethylamine class. It is a close structural relative of mescaline, distinguished by shorter duration and a steep dose-response curve. 2C-B is a partial agonist at serotonin 5-HT₂A receptors,[1] producing its effects by disrupting sensory filtering while engaging entactogenic warmth.
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Alexander Shulgin synthesized 2C-B in 1974 and documented his synthesis and experience notes in PiHKAL.[2] It circulated in psychotherapy settings and club culture for two decades before US Schedule I placement in 1995. Despite international prohibition, availability has expanded across European drug markets, and a clinical trial comparing it to MDMA and psilocybin has been completed.[3]
Subjective effects include color enhancement, geometric visual patterns, tactile intensification, heightened sociability, and sensory amplification.[4][5] The experience occupies a boundary between psychedelic perception and entactogenic warmth — vivid and pleasurable at lower doses, shifting steeply toward full psychedelic territory with small dose increases. Nausea during onset, anxiety at higher doses, and difficulty sleeping are common unwanted effects.
2C-B does not produce physical dependence, and no fatality has been attributed to it in published literature.[6] The dominant risk is its steep dose-response curve — small dose increases can escalate a manageable experience into overwhelming psychedelic intensity.[2] Most safety knowledge rests on class-level pharmacology and a small number of clinical observations — the evidence base for 2C-B specifically remains thin.[1]
History[edit]
Discovery
Alexander Shulgin synthesized 2C-B in 1974 and tested it in humans the following year.[7]citation needed It was the twentieth entry in his 2C phenethylamine series. He documented his synthesis and experiential notes in PiHKAL (1991), noting an active oral range of 12–24 mg and a steep dose-response curve.[2]
Clinical and Cultural Significance
Shulgin proposed 2C-B for psychedelic-assisted psychotherapy, and it saw limited clinical use in some European settings before widespread scheduling.[1] By the early 1990s it had spread through rave and club culture, often sold as or mixed into MDMA.[7]
Prohibition and Modern Use
The United Kingdom controlled phenethylamines as a class by 1977.[7] The United States placed 2C-B in Schedule I on June 2, 1995,[8] and the United Nations added it to Schedule II in 2001.[7] Despite prohibition, availability has grown — the EUDA reported 944 seizures across 15 EU member states,[9] and a Phase 1 clinical trial comparing 2C-B to MDMA and psilocybin has been completed.[3]
The name "2C-B" follows Shulgin's system: "2C" marks the two-carbon chain between the phenyl ring and the amine, and "B" identifies the 4-bromo substituent. Street names from the 1990s — "Nexus," "Bromo," and "Venus" — reflect its reputation as a sensual, boundary-zone psychedelic distinct from the intensity of LSD or the empathogenic character of MDMA.
Chemistry[edit]
Structural Class
2C-B belongs to the 2C family of substituted phenethylamines, sharing a structural core with mescaline.[2] A bromine atom at the 4-position gives it its name and distinguishes it from related compounds — and from its more potent amphetamine structural analog DOB, which is roughly three times more potent and substantially longer-acting.[10]
2C-B is also the structural parent of the NBOMe series: adding a chemical group to the amine produces 25B-NBOMe, which is far more potent and carries a markedly different safety profile.[11]
Molecular Properties
| Molecular formula | C₁₀H₁₄BrNO₂ |
| Molecular weight | 260.13 g/mol |
Pharmacology[edit]
Mechanism of Action
2C-B activates serotonin receptors — the same receptors responsible for the effects of all classical serotonergic psychedelics.[1][12][5] It acts as a partial activator, not a full one, which may explain why the experience is less overwhelming than some other psychedelics at comparable doses.
Unlike MDMA, 2C-B does not release serotonin into the brain — its warmth and sociability arise through receptor activation rather than a chemical flood.[13][14] It also interacts with dopamine, epinephrine, and histamine receptors,[15] which may shape its distinctive character, though their individual roles remain uncharacterized.
Pharmacokinetics
At 20 mg oral, 2C-B reaches peak blood levels in about 2.4 hours, with a half-life of roughly 1.4 hours.[1][14] The body breaks it down primarily through monoamine oxidase enzymes, producing inactive metabolites that do not contribute to psychedelic effects.[16][3] Animal and human metabolism differ significantly, limiting the usefulness of rodent toxicology data for predicting human effects.[17][16]
Neuroscience[edit]
Where It Acts
No neuroimaging studies of 2C-B have been published. It is expected to engage the same brain circuits as other serotonergic psychedelics — disrupting the default mode network and reducing the brain's filtering of incoming sensory information.citation needed The warmth and sociability it produces, without significant serotonin release,[13] may reflect a specific balance of serotonin receptor activation or contributions from its broader receptor interactions.[15]
Why It Matters
One influential framework proposes that activating serotonin receptors loosens the brain's top-down expectations, letting raw sensory information through with less filtering.citation needed 2C-B fits this pattern: sensory intensification dominates at lower doses, with deeper cognitive disruption emerging steeply at higher ones. Whether 2C-B also triggers the new synapse growth documented for other psychedelics remains untested.citation needed
- Does 2C-B produce the same default mode network disruption observed with psilocybin and LSD? Its shorter duration and partial agonist profile may yield a qualitatively different neural signature.
- How does the dual psychedelic-entactogenic character arise — from a specific balance of serotonin receptor subtypes, from broader receptor interactions, or from an emergent property of the overall pharmacology?
- How does 2C-B's apparent antagonism at serotonin receptors in isolated cell preparations[18] reconcile with its clear serotonin-mediated effects in living animals[10]?
Subjective Effects[edit]
2C-B sits at the boundary between psychedelic and entactogenic experience. Colors sharpen, surfaces ripple, touch intensifies — vivid sensory experience paired with warmth and pleasure.[4][5] The dose-response curve is unusually steep: small increases push the experience steeply into full psychedelic territory. Set and setting exert strong influence across the entire active range.
Compared to psilocybin, the experience brings less dysphoria and less ego dissolution.[14] Compared to MDMA, the perceptual component is far more prominent, and the empathogenic quality weaker than commonly assumed — controlled testing found neither compound produced measurable empathogenic changes on standardized assessment.[14]
Synthesized by Alexander Shulgin in 1974, 2C-B was first tested in humans the following year and documented in PiHKAL as entry #20.[2] It circulated in psychotherapy and club culture for two decades before US Schedule I placement in 1995.[3] Despite international prohibition, availability has expanded across European drug markets, and a Phase 1 clinical trial comparing it to MDMA and psilocybin has been completed.[4]
Subjective effects include color enhancement, geometric visual patterns, tactile enhancement, sociability enhancement, and sensory amplification. The experience occupies a boundary zone between psychedelic perception and entactogenic warmth — vivid sensory intensification paired with pleasure and social openness that shifts steeply toward full psychedelic territory with small dose increases.[5][6] Nausea during onset, anxiety at higher doses, and difficulty sleeping are common unsought effects.
2C-B produces no physical dependence, and no fatality has been attributed specifically to the compound in published literature.[7] The primary risk is the steep dose-response curve: small increments above the active range can escalate a manageable experience into overwhelming psychedelic intensity, making accurate dosing critical.[2] The first controlled human study appeared only in 2018,[1] and the evidence base remains thin — most safety inferences rest on class-level pharmacology and a small number of clinical observations.
History[edit]
Discovery
Alexander Shulgin synthesized 2C-B in 1974 at his private laboratory in Lafayette, California, and tested it in humans the following year.[8]citation needed The compound was the twentieth in his 2C series — phenethylamines built on a 2,5-dimethoxy scaffold — and he considered it pharmacologically distinctive from the outset. He formalized his synthesis and experiential accounts in PiHKAL (1991), entry #20, noting an active oral range of 12–24 mg, a duration of 4–8 hours, and a steep dose-response curve.[2]
Clinical and Cultural Significance
Shulgin proposed 2C-B for psychedelic-assisted psychotherapy, and the compound saw limited therapeutic use in some European clinical settings before comprehensive scheduling.[1] No formal clinical data emerged from this era. By the early 1990s, 2C-B had entered recreational circulation through the rave and club scene, frequently sold as or adulterated into MDMA.[8]
Prohibition and Modern Use
The United Kingdom controlled phenethylamines as a class under the Misuse of Drugs Act by 1977.[8] The United States placed 2C-B in Schedule I on June 2, 1995,[3] and the United Nations added it to Schedule II in 2001.[8] Despite prohibition, availability has expanded — the EUDA reported 944 seizures across 15 EU member states, predominantly in tablet form.[9] The first controlled human pharmacological study appeared in 2018,[1] and a Phase 1 trial comparing 2C-B to MDMA and psilocybin has since been completed.[4]
The name "2C-B" derives from Shulgin's naming convention: "2C" denotes the two-carbon chain between the phenyl ring and the terminal amine, while "B" identifies the 4-bromo substituent. Street names from the 1990s club scene — "Nexus," "Bromo," and "Venus" — reflect its reputation as a sensual, boundary-zone psychedelic distinct from the intensity of LSD or the empathogenic directness of MDMA.
Chemistry[edit]
Structural Class
2C-B belongs to the 2C family of substituted phenethylamines — compounds sharing a 2,5-dimethoxy pattern on the phenyl ring with a two-carbon chain to the terminal amine. The parent scaffold is mescaline, and the 2C series represents systematic exploration of ring substitution patterns on this core structure.[2]
The 4-bromo substituent distinguishes 2C-B from other 2C compounds: 2C-I carries iodine at the same position, 2C-E an ethyl group. The absence of an alpha-methyl group differentiates it from the amphetamine structural analog DOB, which is roughly three times more potent and substantially longer-acting.[10]
2C-B also serves as the structural parent of the NBOMe series. Adding an N-benzyl group to the amine produces 25B-NBOMe, a full serotonin 2A receptor agonist with dramatically greater potency and a markedly different safety profile.[11] Hansen et al. used 2C-B as the base scaffold for a 48-compound N-benzyl series exploring this relationship.[12]
Molecular Properties
| Molecular formula | C₁₀H₁₄BrNO₂ |
| Molecular weight | 260.13 g/mol |
The molecule consists of a phenethylamine backbone with methoxy groups at the 2- and 5-positions and a bromine atom at the 4-position. The bromine contributes significant molecular weight and influences both lipophilicity and receptor binding geometry.[13]
Stereochemistry
2C-B has no chirality center. The phenethylamine scaffold lacks the alpha-methyl group present in amphetamine derivatives, so no enantiomers or stereoisomers of pharmacological relevance exist. This contrasts with DOB, which has R- and S-enantiomers with differing receptor affinities.
Pharmacology[edit]
Mechanism of Action
2C-B is a partial agonist at serotonin 5-HT₂A, 5-HT₂B, and 5-HT₂C receptors.[1][6] Its psychedelic effects arise primarily through 5-HT₂A activation, consistent with the mechanism shared by all classical serotonergic psychedelics.[14] In mice, 2C-B produces the head-twitch response — a validated behavioral proxy for hallucinogenic activity — at roughly one-third the potency of its amphetamine structural analog DOB.[10]
Unlike MDMA, 2C-B does not function as a significant monoamine releaser or reuptake inhibitor.[15] This distinction is clinically observable: in a controlled comparison, neither 2C-B nor MDMA produced measurable empathogenic changes on standardized testing, and 2C-B's entactogenic reputation may reflect perceptual warmth rather than the serotonin-flood mechanism behind MDMA's empathogenesis.[16]
Broader receptor screening reveals that 2C-B interacts with dozens of receptor sites beyond the serotonin system — including dopamine, adrenergic, and histamine targets.[17] These secondary interactions may contribute to the compound's distinctive experiential profile, though their individual roles remain uncharacterized.
Pharmacokinetics
At 20 mg oral, 2C-B reaches peak plasma concentration in approximately 2.4 hours with a plasma half-life of 1.43 hours.[16] Salivary measurements at 10–20 mg show an earlier peak at roughly 1 hour, consistent with salivary partitioning preceding full plasma distribution.[1]
The body breaks down 2C-B primarily through MAO-A and MAO-B enzymes, producing inactive metabolites that do not contribute to psychedelic effects.[18][4] A minor metabolic pathway involves CYP2D6.[4] Rats and humans metabolize 2C-B through different pathways — a species gap that limits the usefulness of rodent toxicology data for predicting human effects.[19][18]
Oral bioavailability has not been calculated, no human pharmacokinetic data exist for non-oral routes, and the toxic dose remains unknown.
Neuroscience[edit]
Where It Acts
No neuroimaging studies of 2C-B have been published. As a 5-HT₂A partial agonist, the compound is expected to engage the cortical and thalamic circuits demonstrated for other serotonergic psychedelics — disrupting default mode network integrity, reducing the brain's sensory gating, and increasing the range of neural states available to consciousness.citation needed
2C-B's combined psychedelic-entactogenic character raises the question of whether its neural signature differs from purely serotonergic psychedelics. The entactogenic warmth — sociability and pleasure without significant monoamine release[15] — may reflect a specific balance of 5-HT₂A versus 5-HT₂C activation or contributions from the compound's broad secondary receptor interactions.[17]
Why It Matters
The REBUS model (Relaxed Beliefs Under Psychedelics) proposes that 5-HT₂A agonism loosens the brain's top-down predictions, allowing raw sensory information greater influence on conscious experience.citation needed 2C-B's pattern — pronounced sensory intensification at lower doses, deeper cognitive disruption steeply emerging at higher doses — fits this framework of dose-dependent relaxation of perceptual filtering.
Whether 2C-B promotes structural neuroplasticity — the dendritic growth and new synapse formation demonstrated for other serotonergic psychedelics — remains untested.citation needed As a partial agonist with lower potency than LSD or DMT, it may fall below the threshold for significant neuroplastic effects, or the relationship may prove nonlinear.
- Does 2C-B produce the same pattern of default mode network disruption observed with psilocybin and LSD? Its shorter duration and partial agonist profile may yield a qualitatively different neural signature.
- How does the dual psychedelic-entactogenic character arise — from a specific ratio of 5-HT₂A to 5-HT₂C activation, from broad secondary receptor interactions, or from an emergent property of the overall pharmacological profile?
- How does 2C-B's apparent antagonism at 5-HT₂A receptors in isolated cell preparations[20] reconcile with its clear 5-HT₂A-mediated effects in living animals[10]?
Subjective Effects[edit]
2C-B occupies a boundary zone between psychedelic and entactogenic experience. At lower doses, sensory intensification dominates — colors brighten, surfaces breathe, touch becomes electric — while cognitive architecture remains largely intact. Small dose increases shift the experience steeply toward full psychedelic territory, with geometric visual patterns, thought disruption, and emotional enhancement emerging disproportionately.[5][6] Set and setting exert unusually strong influence across the entire active range.
Compared to psilocybin, 2C-B produces less dysphoria, less ego dissolution, and a shorter experience at equivalent recreational doses, while matching psilocybin's impairment of psychomotor function and spatial memory.[16] Relative to MDMA, the perceptual component is far more prominent; the empathogenic component is weaker than commonly assumed — controlled testing found neither compound produced measurable empathogenic changes on standardized assessment.[16]
Effect Grid
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.
Modeled from the effect's dose-dependence curve — not per-substance measurements.
Visual drifting · Symmetrical texture repetition · Touch enhancement · Environmental patterning · Visual breathing · Auditory enhancement · After-images · Depth perception distortion · Tracers · Brightness alteration · Light sensitivity · Peripheral vision distortion · Perspective distortion · Visual morphing · Auditory distortion · Sound sensitivity · Visual diffraction · Visual haze / noise · Visual melting · Peripheral misidentification · Synesthesia · Visual magnification · Visual acuity enhancement · Auditory misinterpretation · Holotropic state · Proprioceptive distortion · Spatial disorientation · Vestibular distortion · Visual processing acceleration · Olfactory enhancement · Taste enhancement · Flashbacks · Object transformations · Visual recursion · Internal hallucinations · Environmental orbism / cubism · External hallucinations · Object activation · Auditory hallucinations · Visual scenery slicing · Perspective hallucinations · Visual processing suppression · Visual flipping · Persisting hallucinations
Visual breathing · Auditory enhancement · After-images · Depth perception distortion · Tracers · Brightness alteration · Light sensitivity · Peripheral vision distortion · Perspective distortion · Visual morphing · Auditory distortion · Sound sensitivity · Visual diffraction · Visual haze / noise · Visual melting · Peripheral misidentification · Synesthesia · Visual magnification · Visual acuity enhancement · Auditory misinterpretation · Holotropic state · Proprioceptive distortion · Spatial disorientation · Vestibular distortion · Visual processing acceleration · Olfactory enhancement · Taste enhancement · Flashbacks · Object transformations · Visual recursion · Internal hallucinations · Environmental orbism / cubism · External hallucinations · Object activation · Auditory hallucinations · Visual scenery slicing · Perspective hallucinations · Visual processing suppression · Visual flipping · Persisting hallucinations
Stimulation · Spontaneous body sensations · Tactile euphoria · Appetite suppression · Sexual arousal enhancement · Laughter fits · Wakefulness · Tingling / electric sensations · Nausea · Excessive sweating · Dizziness · Dry mouth · Heart rate perception changes · Muscle tension · Nasal congestion · Nystagmus (eye wobbles) · Physical fatigue · Vibrations / buzzing · Abnormal heartbeat · Dehydration sensation · Bodily lightness · Bodily pressures · Insomnia · Restlessness · Trembling · Bruxism · Bodily heaviness · Body schema distortion · Breathing alteration · Headache · Involuntary body movements · Muscle relaxation · Pain suppression · Respiratory stimulation · Vasoconstriction · Vomiting · Motor control enhancement · Tactile hallucination · Bodily dissociation
Appetite suppression · Sexual arousal enhancement · Laughter fits · Wakefulness · Tingling / electric sensations · Nausea · Excessive sweating · Dizziness · Dry mouth · Heart rate perception changes · Muscle tension · Nasal congestion · Nystagmus (eye wobbles) · Physical fatigue · Vibrations / buzzing · Dehydration sensation · Bodily lightness · Bodily pressures · Insomnia · Restlessness · Trembling · Bruxism · Bodily heaviness · Body schema distortion · Breathing alteration · Headache · Involuntary body movements · Muscle relaxation · Pain suppression · Respiratory stimulation · Vasoconstriction · Vomiting · Motor control enhancement · Tactile hallucination · Bodily dissociation
Conceptual thinking · Immersion enhancement · Thought connectivity · Pattern recognition enhancement · Cognitive euphoria · Cognitive flexibility · Introspection enhancement · Creativity enhancement · Humor enhancement · Memory suppression · Thought acceleration · Cognitive impairment · Increased nature relatedness · Multiple thought streams · Analysis enhancement · Cognitive fatigue · Confusion · Focus suppression · Information processing enhancement · Information processing suppression · Memory fragmentation · Synchronicity · Thought disorganization · Thought loops · Focus enhancement · Language enhancement · Motivation enhancement · Analysis suppression · Cognitive dysphoria · Language suppression · Thought deceleration · Thought organization · Compulsive redosing urge · Delusions of sobriety · Memory replays · Delusions · Amnesia
Pattern recognition enhancement · Cognitive euphoria · Cognitive flexibility · Introspection enhancement · Creativity enhancement · Humor enhancement · Memory suppression · Thought acceleration · Cognitive impairment · Increased nature relatedness · Multiple thought streams · Analysis enhancement · Cognitive fatigue · Confusion · Focus suppression · Information processing enhancement · Information processing suppression · Memory fragmentation · Synchronicity · Thought disorganization · Thought loops · Focus enhancement · Language enhancement · Motivation enhancement · Analysis suppression · Cognitive dysphoria · Language suppression · Thought deceleration · Thought organization · Delusions of sobriety · Memory replays · Delusions · Amnesia
Empathy enhancement · Simultaneous emotions · Anxiety · Catharsis · Anxiety suppression · Dysphoria · Anhedonia · Irritability
Anxiety suppression · Dysphoria · Anhedonia · Irritability
Sociability enhancement · Communication enhancement · Derealization · Flow state · Depersonalization · Boundary dissolution · Cognitive disconnection · Ego dissolution · Identity alteration · Telepathic feelings
Depersonalization · Boundary dissolution · Cognitive disconnection · Ego dissolution · Identity alteration · Telepathic feelings
Time cessation
Non-dual awareness · Transpersonal visions · Death-rebirth sequence
Recursive awareness
Timeline
First alerts emerge as subtle mood shift, mild bodily awareness, and faint visual brightening. Easily mistaken for placebo at this stage.
Effects build noticeably: color saturation increases, mild euphoria and stimulation develop, and nausea may occur. The steep dose-response curve means intensity can accelerate rapidly during this phase.
Maximum intensity with full visual enhancement, sensory amplification, and entactogenic warmth. Cardiovascular effects peak (up to +19 mmHg systolic). Salivary Tmax occurs around 1 hour; plasma Tmax at approximately 2.
Sustained effects at reduced intensity. Visual phenomena and mood elevation persist but the acute peak subsides. Cognitive function begins returning.
Gradual return to baseline. Visual effects fade first, followed by mood normalization. The short plasma half-life (1.
Residual mood elevation, mild sensory sensitivity, and reflective mental state. Physical baseline largely restored. Some users report difficulty sleeping if the experience occurred in the evening.
Safety[edit]
- Acute toxicity
- Low
- Chronic toxicity
- Negligible
- Withdrawal
- None
- Tolerance buildup
- rapid
- Tolerance reset
- 14 days
- Physical
- None
- Psychological
- Negligible
- Compulsive redosing
- Negligible
- Dose escalation
- Low
- Cross-tol.
- LSD · psilo · mesc
Toxicity
No lethal dose has been established for 2C-B in any species, and no fatality has been specifically attributed to the compound in published literature.[6]
Acute Toxicity
At controlled oral doses of 10–20 mg, blood pressure rises up to +19 mmHg systolic and +13 mmHg diastolic, and heart rate increases up to +13 bpm.[1] These effects are notably milder than those seen with MDMA.[14] No serious adverse events occurred in any published controlled study.[1][14]
Class-Level Toxicity
At least 5 deaths have been attributed to the broader 2C drug class, with most involving 2C-E and other compounds rather than 2C-B specifically.[6] Severe toxicity from 2C-class drugs can present as agitation, hallucinations, dangerously high blood pressure, rapid heart rate, seizures, overheating, and muscle breakdown.[6][11]
Analytical Detection
2C-B is not detected by standard drug screens.[19] Identifying it requires specialized laboratory testing,[20][3] meaning clinicians may not recognize it as the cause of a presentation without targeted analysis.
Psychological Risks
In controlled settings, mild hallucinations occurred in roughly one-third of participants at 10–20 mg oral.[1] Psilocybin at 15 mg produced greater dysphoria and ego dissolution than 2C-B at 20 mg,[14] suggesting lower acute psychological risk at these doses — though the steep dose-response curve[2] means small dose increases could substantially alter this profile.
No published data exist on 2C-B-specific risks of persisting perceptual changes or psychiatric destabilization. As a serotonin receptor agonist, class-level risks apply: individuals with personal or family history of psychotic spectrum disorders or bipolar disorder face elevated risk.safety citation needed
Tolerance and Dependence
Tolerance is expected to develop rapidly through serotonin downregulation, consistent with other serotonergic psychedelics.[12] Cross-tolerance with LSD, psilocybin, and mescaline is expected but unconfirmed for 2C-B specifically.
Physical dependence does not develop with serotonergic psychedelics. Psychological dependence potential is negligible — these substances have low reinforcing properties and do not support habitual use in animal models.[21]
Drug Interactions
Serotonergic Agents
Tramadol combines serotonin reuptake inhibitor with 2C-B's serotonin receptor activation, creating a documented pathway to serotonin syndrome — a potentially life-threatening overheating and seizure response.[22][23][24]
SSRIs and SNRIs taken chronically may reduce 2C-B's effects through receptor downregulation. Acute combination adds serotonergic burden. Strong CYP2D6 inhibitors such as paroxetine and fluoxetine could affect a minor metabolic pathway, though clinical significance is uncertain.[13][3]
MAO Inhibitors
Monoamine oxidase enzymes are the primary pathway by which the body clears 2C-B.[3] Any MAO inhibitor — including antidepressants such as phenelzine, tranylcypromine, and moclobemide, and selective inhibitors such as selegiline — could dramatically increase 2C-B exposure to dangerous levels.safety citation needed
Other Interactions
Lithium may lower seizure threshold when combined with serotonergic psychedelics.[13] No 2C-B-specific data exist.
MDMA combined with 2C-B ("Nexus-flipping") adds serotonergic and cardiovascular burden.[2][4] No controlled study of this combination has been published.
Cannabis has no published interaction data. Synergistic or unpredictable effects are possible but uncharacterized.
Contraindications
7 knownNo 2C-B-specific contraindication studies exist. The following are inferred from pharmacology and class characteristics.
Heart conditions: The dose-dependent blood pressure and heart rate increases[1] pose added risk for individuals with uncontrolled cardiovascular disease. Absolute contraindication.
Psychotic spectrum disorders, bipolar disorder: Class-level risk of triggering psychotic or manic episodes in predisposed individuals.safety citation needed Absolute contraindication.
MAO inhibitor use: The primary metabolic enzymes are MAO-A and MAO-B.[3] Concurrent MAOI use could dramatically increase plasma exposure. Absolute contraindication.
Lithium use: Incompletely understood interaction with possible seizure risk.[13] Relative contraindication.
Seizure disorders: Seizures are documented in severe 2C-class toxicity.[6] Relative contraindication.
Pregnancy and breastfeeding: No reproductive data exist. Contraindicated as precaution.safety citation needed
Harm Reduction[edit]
Forms & Identification
The steep dose-response curve makes accurate identification and dosing unusually consequential. A 5 mg difference can shift the experience from gentle sensory enhancement to overwhelming psychedelia. Pressed tablets vary widely in content[4] — the dose per tablet is unpredictable without testing.
2C-B is sometimes sold as or confused with MDMA. Its NBOMe derivatives — particularly 25B-NBOMe — carry a substantially different safety profile at far lower active doses.[11] Reagent testing can distinguish 2C-B from many substitutes but cannot confirm dose.
Guidelines
- Test every batch with a reagent kit before use. Testing identifies the substance but not the dose.
- Start with a low dose and wait at least 2.5 hours before considering redosing — peak effects can arrive later than expected.
- Weigh powder doses with a milligram-precision scale. Eyeballing is dangerous given the steep dose-response curve.
- For pressed tablets of unknown provenance, start with half or less.
- Eat lightly 2–3 hours before dosing. An empty stomach accelerates onset; a full stomach can delay and then intensify effects unpredictably.
- Have water available. Mild dehydration can amplify discomfort.
- Prepare the environment in advance — lighting, temperature, music, comfort items.
- Keep a familiar, calming space accessible for retreat if the experience becomes overwhelming.
Set & Setting
Set and setting exert unusually strong influence across the entire dose range. The warmth of lower doses can shift to anxiety and perceptual overload in unfamiliar or chaotic environments. A comfortable, familiar space with trusted company provides the strongest foundation.
First experiences benefit from a sober, experienced sitter who can provide grounding if unexpected intensity arises. Daytime or early evening use allows the relatively short duration to resolve before sleep is needed.
Aftercare & integration. Most people return to baseline within 6–8 hours, but subtle perceptual shifts and emotional processing can continue for a day or two. Sleep may come easily given the short duration, though residual stimulation can delay it.
Journaling or conversation within 24–48 hours captures insights while they remain vivid. If the experience surfaced difficult emotions, speaking with a therapist trained in psychedelic integration can help. Persistent anxiety, depersonalization, or perceptual disturbances lasting beyond a few days warrant professional consultation.
Recovery & Support
Compulsive 2C-B use is rare — rapid tolerance development and the self-limiting pharmacology of serotonergic psychedelics work against habitual patterns. If use has become a way of avoiding difficult emotions or responsibilities, the pattern deserves attention regardless of the low physiological dependence profile.
Psychedelic-informed therapists and integration circles can help process recurring patterns of use. MAPS integration resources and the Fireside Project (62-FIRESIDE) offer support for psychedelic-related concerns. If substance use is affecting daily functioning, relationships, or wellbeing, SAMHSA's National Helpline (1-800-662-4357) is free, confidential, and available 24/7.
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Most difficult 2C-B experiences involve anxiety, confusion, or uncomfortable sensory intensity — distressing but not medically dangerous at typical doses. Recognizing when a situation crosses from uncomfortable to dangerous is critical.
Seek emergency help immediately if:
- Chest pain, irregular heartbeat, or difficulty breathing
- Seizure activity or loss of consciousness
- Body temperature feels dangerously high (skin hot and dry to the touch)
- Self-harm behavior or complete disconnection from reality
- Symptoms of serotonin syndrome: muscle rigidity, rapid heart rate, agitation, and overheating — especially if other serotonergic substances were taken
While waiting for help:
- Call emergency services. State the substance (2C-B), estimated dose, and time of ingestion.
- Place an unconscious person in the recovery position (on their side, airway clear).
- Keep the person cool if overheating — remove excess clothing, apply cool water.
- Do not restrain a conscious person unless there is immediate danger of self-harm.
- Do not induce vomiting.
Good Samaritan laws in many jurisdictions protect people who call for help during a drug emergency. No reversal agent exists for 2C-B — emergency treatment is supportive.
Legal Status[edit]
International Legal Framework
2C-B is prohibited internationally under Schedule II of the United Nations Convention on Psychotropic Substances, added in 2001,[7] and is controlled in all major jurisdictions. Despite comprehensive prohibition, availability has grown — the EUDA reported 944 seizures across 15 EU member states, predominantly in tablet form.[9]
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| United States | Schedule I (Controlled Substances Act) | Placed June 2, 1995. First encountered by DEA in 1979; clandestine laboratories seized in California (1986), Arizona (1992), California (1994)[8] |
| United Kingdom | Class A / Schedule 1 (Misuse of Drugs Act 1971) | Phenethylamines controlled as a class by 1977[7] |
| Canada | Schedule III (CDSA) | 2016 amendment broadened to all 2C-phenethylamine derivatives and analogs, including NBOMe variants[25] |
| Germany | BtMG Anlage I | Controlled since approximately 1998–1999[7] |
| Australia | Schedule 9 (Prohibited Substance) | Controlled since approximately 1998–1999[7] |
| United Nations | Schedule II (Convention on Psychotropic Substances) | Added in 2001[7] |
| France, Japan, Sweden | Controlled substances | Controlled since approximately 1998–1999[7] |
Legal status changes frequently and varies by jurisdiction. This information is not legal advice.
Analog Act Considerations
In the United States, 2C-B is specifically scheduled, making the Federal Analogue Act unnecessary for prosecution. Canada's 2016 amendment is notable: by scheduling all 2C-phenethylamine derivatives and their analogs — including NBOMe variants — it preemptively covered novel structural modifications to the 2C scaffold.[25]
Safety[edit]
- Acute toxicity
- Low
- Chronic toxicity
- Negligible
- Withdrawal
- None
- Tolerance buildup
- rapid
- Tolerance reset
- 14 days
- Physical
- None
- Psychological
- Negligible
- Compulsive redosing
- Negligible
- Dose escalation
- Low
- Cross-tol.
- LSD · psilo · mesc
Toxicity
No lethal dose has been established for 2C-B in any species, and no fatality has been specifically attributed to the compound in published literature.[7]
Acute Toxicity
At controlled oral doses of 10–20 mg, cardiovascular effects are modest: blood pressure increases up to +19 mmHg systolic and +13 mmHg diastolic, with heart rate increases up to +13 bpm.[1] These effects are appreciably lesser than those observed with MDMA.[16] No serious adverse events occurred in any published controlled study.[1][16]
Class-Level Toxicity
At least 5 deaths have been attributed to the broader 2C drug class, with the majority involving 2C-E and other 2C compounds rather than 2C-B specifically.[7] Severe toxicity from 2C-class drugs can present as agitation, hallucinations, dangerously high blood pressure, rapid heart rate, seizures, overheating, and muscle breakdown.[7][11]
Analytical Detection
2C-B is not detected by standard drug screens.[21] Specialized laboratory methods are required for identification,[22][4] meaning clinicians may not identify 2C-B as the cause of a presentation without targeted testing.
Psychological Risks
In controlled settings, mild open-eye hallucinations occurred in roughly one-third of participants at 10–20 mg oral.[1] Psilocybin at 15 mg produced greater dysphoria and ego dissolution than 2C-B at 20 mg,[16] suggesting lower acute psychological risk at these doses. However, the steep dose-response curve[2] means small dose increases could substantially alter this profile.
No published data exist on 2C-B-specific risk of persisting perceptual changes, psychosis precipitation, or psychiatric destabilization. As a serotonin 2A receptor agonist, class-level risks apply: individuals with personal or family history of psychotic spectrum disorders or bipolar disorder face elevated risk.safety citation needed Recreational users have reported lower incapacitation with 2C-B compared to ayahuasca or Salvia divinorum.[5]
Tolerance and Dependence
No substance-specific tolerance or dependence data exist for 2C-B. Tolerance is expected to develop rapidly through 5-HT₂A downregulation, consistent with the serotonergic psychedelic class.[14] Cross-tolerance with other serotonergic psychedelics (LSD, psilocybin, mescaline) is expected but unconfirmed for 2C-B specifically.
Physical dependence does not develop with serotonergic psychedelics. Psychological dependence potential is negligible — serotonergic psychedelics have low reinforcing properties and do not support self-administration in animal models.[23]
Drug Interactions
Serotonergic Agents
Tramadol: Combines serotonin reuptake inhibitor with 2C-B's 5-HT₂A agonism, creating a documented pathway to serotonin syndrome.[24][25][26] No 2C-B-specific case has been published, but the mechanism is well-established.
SSRIs/SNRIs: Chronic SSRI use may attenuate 2C-B's effects through 5-HT₂A downregulation. Acute combination adds serotonergic burden. Strong CYP2D6 inhibitors (paroxetine, fluoxetine) could theoretically affect a minor metabolic pathway, though clinical significance is uncertain.[15][4]
MAO Inhibitors
MAO-A and MAO-B are the primary enzymes that break down 2C-B.[4] Any monoamine oxidase inhibitor — including pharmaceutical antidepressants (phenelzine, tranylcypromine, moclobemide) and selective MAO-B inhibitors (selegiline) — could substantially increase 2C-B exposure to dangerous levels.safety citation needed
Other Interactions
Lithium: The lithium–psychedelic interaction is poorly understood but may involve seizure threshold effects.[15] Anecdotal reports describe increased seizure risk with serotonergic psychedelics. No 2C-B-specific data exist.
MDMA: Combined use ("Nexus-flipping") produces additive serotonergic and cardiovascular burden.[2][5] No controlled study of the combination has been published.
Cannabis: No published data exist. Synergistic or unpredictable effects are possible but uncharacterized.
Contraindications
7 knownNo 2C-B-specific contraindication studies exist. The following are inferred from pharmacology and class characteristics.
Heart conditions: Dose-dependent blood pressure and heart rate increases[1] pose added risk for individuals with uncontrolled cardiovascular disease. Absolute contraindication.
Psychotic spectrum disorders, bipolar disorder: Class-level risk of precipitating psychotic or manic episodes in predisposed individuals.safety citation needed Absolute contraindication.
MAO inhibitor use: Primary metabolic enzymes are MAO-A and MAO-B.[4] Concurrent MAOI use could dramatically increase plasma exposure. Absolute contraindication.
Lithium use: Incompletely understood interaction with possible seizure risk.[15] Relative contraindication.
Seizure disorders: Seizures documented in severe 2C-class toxicity.[7] Relative contraindication.
Pregnancy and breastfeeding: No reproductive data exist. Contraindicated as precaution.safety citation needed
Harm Reduction[edit]
Forms & Identification
The steep dose-response curve that defines 2C-B makes accurate identification and dosing unusually consequential. A difference of 5 mg can shift the experience from gentle sensory enhancement to overwhelming psychedelia. Pressed tablets vary widely in content — the shift from powder to tablets documented in European drug markets[5] means dosage per tablet is unpredictable without testing.
2C-B is sometimes sold as or confused with MDMA, and its NBOMe derivatives (particularly 25B-NBOMe) carry a substantially different safety profile at far lower active doses.[11] Reagent testing can distinguish 2C-B from MDMA and many substitutes, but cannot confirm dose — quantitative testing or known-source material is the only reliable path to dose certainty.
Guidelines
- Test every batch with a reagent kit before use. Testing identifies the substance but not the dose.
- Start with a low dose and wait at least 2.5 hours before considering redosing — peak effects can arrive later than expected.
- Weigh powder doses with a milligram-precision scale. Eyeballing is dangerous given the steep dose-response curve.
- For pressed tablets of unknown provenance, start with half or less.
- Eat lightly 2–3 hours before dosing. An empty stomach accelerates onset; a full stomach can delay and then intensify effects unpredictably.
- Have water available. Mild dehydration can amplify discomfort.
- Prepare the environment in advance — lighting, temperature, music, comfort items.
- Keep a familiar, calming space accessible for retreat if the experience becomes overwhelming.
Set & Setting
Set and setting exert unusually strong influence on 2C-B experiences across the entire dose range. The entactogenic warmth at lower doses can shift toward anxiety and perceptual overload in unfamiliar or chaotic environments. A comfortable, familiar space with trusted company provides the strongest foundation.
First experiences benefit from a sitter — someone sober and experienced who can provide grounding if the steep dose-response curve produces unexpected intensity. Daytime or early evening use allows the relatively short duration to resolve before sleep becomes necessary.
Aftercare & integration. The relatively short duration of 2C-B means most people feel baseline within 6–8 hours, but subtle perceptual shifts and emotional processing can continue for a day or two. Allow time for rest after the experience — sleep may come easily given the short duration, but some residual stimulation can delay it.
Journaling or conversation within 24–48 hours captures insights while they remain vivid. If the experience surfaced difficult emotions or memories, speaking with a trusted friend or a therapist trained in psychedelic integration can help contextualize the material. Persistent anxiety, depersonalization, or perceptual disturbances lasting beyond a few days warrant professional consultation.
Recovery & Support
Compulsive 2C-B use is rare — the rapid tolerance development and self-limiting pharmacology characteristic of serotonergic psychedelics work against habitual patterns. If use has become a way of avoiding difficult emotions or responsibilities, the pattern deserves attention regardless of the substance's low physiological dependence profile.
Psychedelic-informed therapists and integration circles can help process recurring patterns of use. MAPS integration resources and the Fireside Project (62-FIRESIDE) offer support for psychedelic-related concerns. If substance use of any kind is affecting daily functioning, relationships, or wellbeing, broader support through SAMHSA's National Helpline (1-800-662-4357) is free, confidential, and available 24/7.
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Most difficult 2C-B experiences involve anxiety, confusion, or uncomfortable sensory intensity — distressing but not medically dangerous at typical doses. Recognizing when a situation crosses from uncomfortable to dangerous is critical.
Seek emergency help immediately if:
- Chest pain, irregular heartbeat, or difficulty breathing
- Seizure activity or loss of consciousness
- Body temperature feels dangerously high (skin hot and dry to the touch)
- Self-harm behavior or complete disconnection from reality
- Symptoms of serotonin syndrome: muscle rigidity, tachycardia, agitation, and overheating — especially if other serotonergic substances were taken
While waiting for help:
- Call emergency services. State the substance (2C-B), estimated dose, and time of ingestion.
- Place an unconscious person in the recovery position (on their side, airway clear).
- Keep the person cool if overheating — remove excess clothing, apply cool water.
- Do not restrain a conscious person unless there is immediate danger of self-harm.
- Do not induce vomiting.
Good Samaritan laws in many jurisdictions protect people who call for help during a drug emergency. No reversal agent exists for 2C-B — emergency treatment is supportive.
Legal Status[edit]
International Legal Framework
2C-B is controlled internationally under Schedule II of the United Nations Convention on Psychotropic Substances, added in 2001.[8] The compound is prohibited in all major jurisdictions. Despite comprehensive prohibition, availability has increased: the EUDA reported 944 seizures across 15 EU member states, predominantly in tablet form.[9]
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| United States | Schedule I (Controlled Substances Act) | Placed June 2, 1995. First encountered by DEA in 1979; clandestine laboratories seized in California (1986), Arizona (1992), California (1994)[3] |
| United Kingdom | Class A / Schedule 1 (Misuse of Drugs Act 1971) | Phenethylamines controlled as a class by 1977[8] |
| Canada | Schedule III (CDSA) | 2016 amendment broadened to all 2C-phenethylamine derivatives and analogs, including NBOMe variants[27] |
| Germany | BtMG Anlage I | Controlled since approximately 1998–1999[8] |
| Australia | Schedule 9 (Prohibited Substance) | Controlled since approximately 1998–1999[8] |
| United Nations | Schedule II (Convention on Psychotropic Substances) | Added in 2001[8] |
| France, Japan, Sweden | Controlled substances | Controlled since approximately 1998–1999[8] |
Analog Act Considerations
In the United States, 2C-B is specifically scheduled, so the Federal Analogue Act is not required for prosecution. Canada's 2016 amendment is notable for its breadth: by scheduling all 2C-phenethylamine derivatives and their analogs — including NBOMe variants — it preemptively covered novel structural modifications to the 2C scaffold.[27]
Frequently asked questions
How long does 2C-B last?
Total duration by route of administration — Oral: 4 – 7 hours; Rectal: 4 – 7 hours; Insufflated: 4 – 6 hours; Intravenous: 2 – 3 hours. Ranges vary with dose and individual factors; see the duration table for onset, peak, and after-effect phases.
Where can I find dosage information for 2C-B?
Psychedex publishes a dosage table for 2C-B on this page covering these routes of administration: rectal, insufflated, intravenous, oral. Dose values are presented only in that table, always alongside their route of administration.
What are dangerous combinations with 2C-B?
The highest-severity documented interactions for 2C-B: MAOIs (Lethal), Buspirone (Dangerous), Dopamine agonists (Dangerous), GHB, Baclofen (Dangerous), GHB, GBL (Dangerous). See the interactions section for the full list with mechanisms and severity levels.
Is 2C-B addictive?
Psychedex records tolerance and dependence data rather than a yes/no rating. Recorded tolerance indicators for 2C-B: tolerance builds rapid; full reset takes 14 days; cross-tolerance develops with LSD, psilocybin, mescaline, DMT, 2C-E, 2C-I, DOB. See the article's dependence and safety sections for recorded dependence data.
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First-person accounts of subjective effects, timing, and outcomes — submitted for harm reduction.
references
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- [3] ^abcdefgThomann J, Rudin D, Kraus S, Arikci D, Holze F, Liechti ME, Luethi D (2025) Liquid chromatography-tandam mass spectrometry-based pharmacokinetic and metabolic analysis of 4-bromo-2,5-dimethoxyphenethylamine and its metabolites in human plasma — Drug Metabolism and Disposition doi:10.1016/j.dmd.2025.100086
- [4] ^abcdCaudevilla-Galligo F, Riba J, Ventura M, Gonzalez D, Farre M, Barbanoj MJ, Bouso JC (2012) 4-Bromo-2,5-dimethoxyphenethylamine (2C-B): presence in the recreational drug market in Spain, pattern of use and subjective effects — Journal of Psychopharmacology doi:10.1177/0269881111431752
- [5] ^abcGonzalez D, Torrens M, Farre M (2015) Acute Effects of the Novel Psychoactive Drug 2C-B on Emotions — BioMed Research International doi:10.1155/2015/643878
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references
- [1]
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- [4] ^abcdefghThomann J, Rudin D, Kraus S, Arikci D, Holze F, Liechti ME, Luethi D (2025) Liquid chromatography-tandam mass spectrometry-based pharmacokinetic and metabolic analysis of 4-bromo-2,5-dimethoxyphenethylamine and its metabolites in human plasma — Drug Metabolism and Disposition doi:10.1016/j.dmd.2025.100086
- [5]
- [6] ^abcGonzalez D, Torrens M, Farre M (2015) Acute Effects of the Novel Psychoactive Drug 2C-B on Emotions — BioMed Research International doi:10.1155/2015/643878