Psychedex is in open beta. We are still fine-tuning the generation and review process. Please double-check sources.
LSD, psilocybin, mescaline +3 moreLSD, psilocybin, mescaline, DOM, DOI, DOC show less
DOB
2,5-dimethoxy-4-bromoamphetamine
DOB (2,5-dimethoxy-4-bromoamphetamine) is a synthetic psychedelic of the substituted amphetamine class. It is among the most potent members of the DOx family, which layers psychedelic effects over an amphetamine-like stimulation. It activates serotonin receptors in the brain, producing the visual and cognitive shifts of classical psychedelics.
DOB (2,5-dimethoxy-4-bromoamphetamine) is a synthetic psychedelic of the substituted amphetamine class. It is among the most potent members of the DOx family, distinguished by an ultra-long duration of action. DOB is a partial agonist at 5-HT₂A receptors,[1] producing its effects by disrupting serotonin-mediated sensory filtering and cognitive processing.
Psychedex is in open beta. We are still fine-tuning the generation and review process. Please double-check sources.
LSD, psilocybin, mescaline +3 moreLSD, psilocybin, mescaline, DOM, DOI, DOC show less
Alexander Shulgin first synthesized DOB around 1967 and documented its effects in his landmark volume PIHKAL.[1] Its greatest scientific contribution was as a laboratory tool — radiolabeled forms became standard instruments for mapping serotonin receptor binding sites in the brain.[2] DOB has been federally scheduled in the United States since 1973[3] and remains internationally controlled with no approved medical use.
Subjective effects include geometric visual patterns, color enhancement, thought acceleration, emotional enhancement, and physical stimulation. The experience has a driven, energetic quality — alert and propulsive rather than dreamy or sedating, reflecting its dual nature as both a psychedelic and a stimulant.[4] Muscle tension, vasoconstriction, and an inability to sleep through the full duration are characteristic unsought effects.
DOB does not produce physical dependence,[5] but active doses sit close to toxic ones — one confirmed human fatality exists.[6] The narrow margin is compounded by severe blood vessel constriction at high doses and the impossibility of sleeping through adverse effects. No controlled human studies exist; the evidence base rests on laboratory pharmacology, animal models, and self-report.
History[edit]
Discovery
DOB was first synthesized by Alexander Shulgin around 1967, part of his systematic exploration of the DOx compound family.[1][7] He documented his synthesis and self-experiments in PIHKAL (1991), which remains the primary source of human experiential data on DOB.[1] The DOx family entered the scientific literature the same year when researchers showed that DOM, a close relative, was roughly 100 times more potent than mescaline.[8]
Scientific Contribution
DOB's most significant impact has been as a laboratory tool. Radiolabeled forms became standard instruments for mapping serotonin receptor binding sites in brain tissue.[2][9] In 1988, researchers found that drug potencies at DOB-labeled receptor sites closely predicted human hallucinogenic potencies — helping confirm serotonin receptor activation as the primary driver of psychedelic effects.[2]
Prohibition and Modern Status
DOB was placed in Schedule I in the United States in September 1973,[3] among the earliest phenethylamine hallucinogens to be federally controlled. It was subsequently listed under the UN Convention on Psychotropic Substances and is controlled in most major jurisdictions.[7] No clinical trials have been registered for DOB; scientific use remains limited to receptor pharmacology research.[10]
The WHO assigned DOB the name brolamfetamine in 1986.[7] In practice, the compound is known by its abbreviation DOB — a naming convention shared across the DOx class, where the final letter identifies the 4-position substituent.
Chemistry[edit]
Structural Class
DOB belongs to the DOx family — 4-substituted 2,5-dimethoxyamphetamines. The scaffold is an amphetamine base with methoxy groups at two ring positions and a bromine atom at a third.[11]
The alpha-methyl group distinguishes DOB from its close relative 2C-B and contributes to greater receptor selectivity.[12] Its molecular formula is C₁₁H₁₆BrNO₂ (274.15 g/mol).[7]
Pharmacology[edit]
Mechanism of Action
DOB is a partial agonist at serotonin receptors — the receptor type responsible for hallucinogenic effects.[13] Activating these receptors alters perception, cognition, and mood,[14] and blocking them abolishes DOB's hallucinogenic effects entirely.[15]
In animal studies, DOB produces effects cross-tolerant with LSD while retaining a secondary stimulant character — consistent with its hybrid structure as a psychedelic built on an amphetamine scaffold.[4]
Pharmacokinetics
No published human pharmacokinetic data exist for DOB.[6] Onset after oral dosing ranges from 15 minutes to 3 hours,[1] and metabolic pathways are inferred from studies of 2C-B[16] — large inter-individual variation is expected. inferred
Neuroscience[edit]
Where It Acts
DOB's effects originate in serotonin receptors concentrated on neurons in the prefrontal cortex — the same cellular trigger as other classical psychedelics.[5] Activating these receptors disrupts the brain's default filtering of sensory information, allowing more raw input into conscious awareness and increasing communication between regions that do not normally interact.
As a partial agonist with roughly half the receptor-level activity of serotonin,[13] DOB may produce a quantitatively different pattern of network disruption than higher-efficacy psychedelics — though this has never been directly tested.
Why It Matters
Research on psychedelics suggests that activating these receptors loosens the brain's top-down predictions, allowing raw sensory information to flow more freely into awareness. DOB's partial agonism may produce a partial version of this effect. Whether its exceptional duration produces meaningfully different outcomes than shorter psychedelic experiences remains an open question.
DOB's unique pharmacological profile raises several unanswered questions. Does 18–30 hours of sustained receptor activation produce fundamentally different network dynamics than a standard psychedelic experience? Does the amphetamine-derived stimulant component measurably alter the neural signature?
Subjective Effects[edit]
The DOB experience layers classical psychedelic perception over a persistent amphetamine-like stimulation. The result is alert and propulsive — driven and energetic rather than dreamy or introspective. Set and setting exert powerful influence, and the commitment required is exceptional by any standard.
Compared to LSD, DOB shares a similar visual and cognitive character but carries a heavier stimulant body load and roughly double the duration. Relative to its DOx sibling DOM, DOB is more potent by weight with a comparable ultra-long timeline — both occupy the endurance end of psychedelic experience.
Synthesized by Alexander Shulgin circa 1967, DOB was documented extensively in his landmark volume PIHKAL.[2] Its primary scientific legacy is as a radioligand — tritiated and brominated forms became standard tools for mapping serotonin receptor binding sites in the brain.[3] Federally scheduled in the United States since 1973,[4] DOB remains internationally controlled with no approved medical use.
Subjective effects include geometric visual patterns, color enhancement, thought acceleration, emotional enhancement, and physical stimulation. The experience carries a driven, energetic quality — classical psychedelic perception layered over an amphetamine-like body stimulation that distinguishes it from sedating tryptamine psychedelics.[5] Muscle tension, vasoconstriction, and an inability to sleep through the extended duration are characteristic unsought effects.
DOB produces no physical dependence,[6] but active doses sit in close proximity to toxic doses — one confirmed fatality has been documented.[7] The narrow safety margin is compounded by the impossibility of sleeping through adverse effects during the extended duration, and high-dose vasoconstriction poses a distinct cardiovascular risk. No controlled human studies have been published; the evidence base rests on in vitro pharmacology, animal models, self-report, and a single overdose case report.
History[edit]
Discovery
DOB was first synthesized by Alexander Shulgin circa 1967 as part of his systematic exploration of 4-substituted 2,5-dimethoxyamphetamines — a structural family known as the DOx class.[2][8] The parent class had entered the scientific literature the same year with DOM, which Snyder, Faillace, and Hollister demonstrated was roughly 100 times more potent than mescaline.[9] Shulgin documented DOB's synthesis, self-experiments, and pharmacological profile in PIHKAL: A Chemical Love Story (1991), which remains the primary published source of human experiential data on the compound.[2]
Scientific Contribution
DOB's most significant impact has been as a laboratory tool rather than a substance of widespread use. Radiolabeled forms — [³H]DOB and (R)-(−)-[⁷⁷Br]DOB — became standard radioligands for characterizing serotonin 5-HT₂ receptor binding sites in brain tissue.[3][10] In 1988, Peroutka and colleagues showed that drug potencies at DOB-labeled receptor sites correlated strongly with human hallucinogenic potencies (r = 0.89), a finding that helped confirm 5-HT₂A agonism as the primary mechanism of psychedelic action.[3]
Prohibition and Modern Status
DOB was placed in Schedule I of the United States Controlled Substances Act in September 1973,[4] making it among the earliest phenethylamine hallucinogens to be federally scheduled. It was subsequently listed in Schedule I of the UN Convention on Psychotropic Substances and is controlled in most major jurisdictions.[8] No clinical trials have been registered for DOB, and its scientific use remains confined to receptor pharmacology research.[11]
The World Health Organization assigned DOB the International Nonproprietary Name (INN) brolamfetamine in 1986.[8] In practice, the compound is known almost exclusively by its abbreviation DOB — a naming convention shared across the DOx class (DOM, DOI, DOC), where the final letter denotes the 4-position substituent (bromine, in this case).
Chemistry[edit]
Structural Class
DOB belongs to the DOx family — 4-substituted 2,5-dimethoxyamphetamines. The parent scaffold is amphetamine bearing methoxy groups at the 2- and 5-positions of the phenyl ring and a bromine atom at the 4-position. This places DOB at the intersection of two structural lineages: the 2,5-dimethoxyphenethylamine hallucinogens (including 2C-B, its alpha-desmethyl structural analog) and the amphetamine stimulants.
The alpha-methyl group distinguishes DOB from 2C-B and confers both greater receptor selectivity[12] and the metabolic resistance characteristic of amphetamines. The 2,5-dimethoxy substitution pattern is essential: removing either methoxy group modestly reduces receptor binding in vitro but profoundly attenuates hallucinogenic activity in vivo, suggesting the motif plays a mechanistic role beyond simple receptor affinity.[13]
Molecular Properties
| Molecular formula | C₁₁H₁₆BrNO₂ |
| Molecular weight | 274.15 g/mol |
The molecule contains a single chirality center at the alpha-carbon. The aromatic ring bears the bromine substituent at position 4, flanked by methoxy groups at positions 2 and 5. The bromine atom contributes to the compound's lipophilicity and favorable binding interactions within the 5-HT₂A receptor pocket.
Stereochemistry
The R-(−) enantiomer is the pharmacologically active form, binding with approximately four-fold higher affinity at 5-HT₂A than the racemic mixture.[1][12] Electrophysiological studies confirmed the potency rank order: (−)-DOB > DOM > (+)-DOB.[14] This R-stereopreference is consistent across phenethylamine hallucinogens and is notably the opposite enantioselectivity from MDMA and other entactogens, where the S-(+) isomer is more active.[13]
Physical Properties
| Melting point (freebase) | 63–65 °C |
| Melting point (hydrochloride salt) | 207–208 °C |
| Appearance | White to off-white solid |
Physical property data derive from encyclopedia entries.[8] No published solubility or stability data have been identified in the primary literature.
Pharmacology[edit]
Mechanism of Action
DOB is a partial agonist at serotonin 5-HT₂A receptors — the primary target responsible for its hallucinogenic effects.[1] Activation of this receptor triggers intracellular signaling cascades that alter perception, cognition, and mood.[15] The behavioral hallmarks of DOB's hallucinogenic action are abolished by selective 5-HT₂A antagonists, confirming receptor-level mediation.[16]
In animal models, DOB produces predominantly LSD-like effects with a secondary amphetamine-like component — cross-tolerant with LSD while retaining a partial stimulant pharmacological signature.[5] This dual character reflects DOB's hybrid structural ancestry: a psychedelic phenethylamine built on an amphetamine scaffold.
Pharmacokinetics
No published human pharmacokinetic data exist for DOB.[7] What is known derives from a single overdose case report, structural analog inference, and self-report documentation.[2]
Onset after oral administration ranges from 15 minutes to 3 hours. The overdose case report documents hallucination onset at approximately 15 minutes;[7] Shulgin reports onset latency up to 3 hours at lower doses.[2] Total duration runs 18–30 hours — significantly longer than most psychedelics including LSD and a defining characteristic of DOx compounds.
No direct metabolism studies have been published for DOB. Metabolic pathway inference relies on studies of 2C-B, its alpha-desmethyl analog.[17] Expected metabolic routes include oxidative deamination, O-demethylation, and further oxidation. Large inter-individual variation was observed between human donors in these analog studies. inferred
Neuroscience[edit]
Where It Acts
DOB's hallucinogenic effects are driven by 5-HT₂A receptors concentrated on layer V pyramidal neurons in the prefrontal cortex — the same cellular trigger activated by other serotonergic psychedelics.[6] Activation of these receptors disrupts the default mode network, loosens the brain's sensory filtering at the thalamus, and increases communication between brain regions that do not normally interact.
As a partial agonist with roughly half the receptor-level efficacy of serotonin,[1] DOB may produce a quantitatively different pattern of network disruption than higher-efficacy psychedelics — though this has never been tested directly.
Why It Matters
The REBUS model (Relaxed Beliefs Under Psychedelics) proposes that 5-HT₂A activation loosens the brain's top-down predictions, allowing raw sensory information to flow more freely into conscious awareness. DOB's partial agonist profile may produce a partial version of this effect.
Separately, 5-HT₂A agonists are established psychoplastogens — compounds that promote structural brain changes including new dendritic connections.[6] Whether DOB's extended duration and partial agonism produce comparable neuroplastic effects to other psychedelics remains unknown.
DOB's unique pharmacological profile raises several unanswered questions. Does 18–30 hours of sustained 5-HT₂A occupancy produce fundamentally different network dynamics than a standard psychedelic experience? Does the amphetamine-derived stimulant component measurably alter the neural signature?
Subjective Effects[edit]
The DOB experience is defined by two pharmacological forces acting in concert: classical psychedelic perception driven by 5-HT₂A activation, and a persistent amphetamine-like stimulation running underneath. This gives the experience a driven, energetic quality — alert and propulsive rather than dreamy or sedating. Set and setting exert powerful influence across the dose range, and the extraordinarily long commitment makes preparation and environment critically important.
Compared to LSD, DOB shares a similar visual and cognitive character but carries a heavier stimulant body load and roughly double the duration. Relative to its DOx class sibling DOM, DOB is more potent by weight with a comparable ultra-long timeline — both occupy the endurance end of phenethylamine psychedelia.
Effect Grid
At common doses (0.75–1.75 mg oral), the full psychedelic experience develops: pronounced open-eye visuals including geometric overlays, color shifting, object morphing, and tracers. Closed-eye imagery becomes vivid and complex. Synesthesia may occur. Thought connectivity increases substantially, producing novel associations, introspective depth, and time distortion. Emotional amplification is significant — responses to music, art, and interpersonal interactions can feel profoundly meaningful.
Physically, stimulation is prominent: tachycardia, mild hypertension, jaw tension, temperature dysregulation, and peripheral vasoconstriction (cold extremities). Nausea is possible during the come-up. Body load is moderate and sustained.
The experience lasts 18–24 hours with no possibility of sleep during the active phase. This is a full-day commitment requiring advance planning for food, hydration, and a safe setting.
Modeled from the effect's dose-dependence curve — not per-substance measurements.
Geometry · Visual breathing · Depth perception distortion · Perspective distortion · Brightness alteration · Environmental patterning · Visual morphing · Symmetrical texture repetition · After-images · Visual diffraction · Music enhancement · Dreaming suppression · Light sensitivity · Peripheral vision distortion · Sound sensitivity · Spatial disorientation · Visual melting · Holotropic state · Touch enhancement · Auditory enhancement · Auditory distortion · Auditory misinterpretation · Peripheral misidentification · Proprioceptive distortion · Visual haze / noise · Synesthesia · Visual acuity enhancement · Vestibular distortion · Visual processing acceleration · Flashbacks · Tinnitus · Object transformations · External hallucinations · Internal hallucinations · Environmental orbism / cubism · Object activation · Perspective hallucinations · Visual recursion · Auditory hallucinations · Persisting hallucinations
Brightness alteration · Environmental patterning · Visual morphing · Symmetrical texture repetition · After-images · Visual diffraction · Music enhancement · Dreaming suppression · Light sensitivity · Peripheral vision distortion · Sound sensitivity · Spatial disorientation · Visual melting · Holotropic state · Touch enhancement · Auditory enhancement · Auditory distortion · Auditory misinterpretation · Peripheral misidentification · Proprioceptive distortion · Visual haze / noise · Synesthesia · Visual acuity enhancement · Vestibular distortion · Visual processing acceleration · Flashbacks · Tinnitus · Object transformations · External hallucinations · Internal hallucinations · Environmental orbism / cubism · Object activation · Perspective hallucinations · Visual recursion · Auditory hallucinations · Persisting hallucinations
Wakefulness · Appetite suppression · Restlessness · Dry mouth · Insomnia · Spontaneous body sensations · Muscle tension · Nausea · Dehydration sensation · Excessive sweating · Body high · Heart rate perception changes · Body schema distortion · Bodily pressures · Motor control impairment · Physical fatigue · Tingling / electric sensations · Abnormal heartbeat · Bruxism · Bodily lightness · Breathing alteration · Dizziness · Headache · Respiratory stimulation · Tactile euphoria · Trembling · Vibrations / buzzing · Involuntary body movements · Increased urination · Diarrhea · Nystagmus (eye wobbles) · Sexual arousal enhancement · Salivation · Vomiting · Tactile hallucination
Dry mouth · Insomnia · Spontaneous body sensations · Muscle tension · Nausea · Dehydration sensation · Excessive sweating · Body high · Heart rate perception changes · Body schema distortion · Bodily pressures · Physical fatigue · Tingling / electric sensations · Abnormal heartbeat · Bruxism · Bodily lightness · Breathing alteration · Dizziness · Headache · Respiratory stimulation · Tactile euphoria · Trembling · Vibrations / buzzing · Involuntary body movements · Increased urination · Diarrhea · Nystagmus (eye wobbles) · Sexual arousal enhancement · Salivation · Vomiting · Tactile hallucination
Immersion enhancement · Novelty enhancement · Conceptual thinking · Cognitive euphoria · Aesthetic enhancement · Introspection enhancement · Multiple thought streams · Openness enhancement · Analysis suppression · Memory suppression · Thought loops · Cognitive fatigue · Cognitive flexibility · Cognitive impairment · Confusion · Increased nature relatedness · Thought disorganization · Creativity enhancement · Language suppression · Cognitive dysphoria · Focus suppression · Information processing suppression · Memory fragmentation · Motivation enhancement · Synchronicity · Analysis enhancement · Humor enhancement · Delusions of sobriety · Memory replays · Focus enhancement · Information processing enhancement · Compulsive redosing urge · Language enhancement · Delusions
Cognitive euphoria · Aesthetic enhancement · Introspection enhancement · Multiple thought streams · Openness enhancement · Analysis suppression · Memory suppression · Thought loops · Cognitive fatigue · Cognitive flexibility · Cognitive impairment · Confusion · Increased nature relatedness · Thought disorganization · Creativity enhancement · Language suppression · Cognitive dysphoria · Focus suppression · Information processing suppression · Memory fragmentation · Motivation enhancement · Synchronicity · Analysis enhancement · Humor enhancement · Memory replays · Focus enhancement · Information processing enhancement · Compulsive redosing urge · Language enhancement · Delusions
Euphoria · Simultaneous emotions · Empathy enhancement · Dysphoria · Irritability · Catharsis
Irritability · Catharsis
Depersonalization · Disinhibition · Social connection · Sociability enhancement · Ego inflation · Sociability suppression · Trust enhancement · Communication enhancement · Flow state · Boundary dissolution · Cognitive disconnection · Identity alteration · Ego dissolution · Telepathic feelings
Ego inflation · Sociability suppression · Trust enhancement · Communication enhancement · Flow state · Boundary dissolution · Cognitive disconnection · Identity alteration · Ego dissolution · Telepathic feelings
Time cessation
Transpersonal visions · Death-rebirth sequence · Entity contact · Voidness · Cessation
Cessation
Timeline
First alerts emerge as a subtle body awareness, mild stimulation, and slight perceptual brightening. Onset latency is highly variable — 15 minutes at high doses, up to 90 minutes at common doses.
Gradual intensification of visual and cognitive effects. Nausea may occur during this phase. Stimulation becomes more pronounced.
Full psychedelic effects plateau at maximum intensity: vivid visual distortions, profound cognitive alteration, emotional amplification, and prominent stimulation. The peak is sustained for many hours — significantly longer than LSD or psilocybin peaks.
Effects remain clearly present but begin a very gradual decline from peak intensity. Visual phenomena soften, cognitive effects shift toward reflective processing, and physical stimulation persists. This extended plateau is a defining feature of DOx pharmacology.
Progressive return toward baseline over several hours. Residual visual enhancement and mild cognitive alteration persist. Physical stimulation diminishes.
Residual mood elevation or fatigue, subtle perceptual sensitivity, and cognitive processing of the experience. May last through the following day. Physical exhaustion from the extended duration is common.
Safety[edit]
- Acute toxicity
- Critical
- Chronic toxicity
- Low
- Withdrawal
- None
- Tolerance buildup
- rapid
- Tolerance reset
- 8.5 days
- Physical
- None
- Psychological
- Negligible
- Compulsive redosing
- Negligible
- Dose escalation
- Negligible
- Cross-tol.
- LSD · psilo · mesc
Toxicity
Acute Toxicity
No lethal dose has been established for DOB in any species. The only human toxicity data come from a single case report in which two men co-ingested an unknown quantity of DOB sold as a designer drug.[6] The heavier individual (113 kg) survived; the lighter (65 kg) developed convulsions and metabolic acidosis and died on day 6.[6]
Case authors estimate an effective dose of approximately 2 mg for an 80 kg person, placing active doses (1–3 mg) in close proximity to the toxic dose — an extremely narrow safety margin.[6] Standard urine drug screens do not detect DOB; targeted laboratory analysis is required.[6]
Vasoconstriction
High-dose DOB constricts blood vessels — a class property of DOx compounds.[17] The related compound Bromo-DragonFLY has caused fatal arterial spasm and limb tissue death through this mechanism.[18] No data quantify DOB's specific dose-response relationship for this effect. safety citation needed
Analytical Detection
DOB can be identified by specialized mass spectrometry with characteristic product ions.[19] Standard amphetamine immunoassays return negative results[6] — clinicians must be specifically informed of suspected DOx ingestion to request appropriate testing.
Psychological Risks
DOB shares the class-wide psychological risks of serotonergic psychedelics: acute anxiety, panic, paranoia, thought disorganization, and transient psychotic symptoms — risks that scale with dose and inadequate preparation.[5]
The exceptionally long duration (18–30 hours) compounds these risks: psychological distress extends far beyond a normal waking period, and sleep is impossible during active effects. No published data address persistent perceptual changes or psychosis precipitation specifically from DOB; by class inference, individuals with personal or family history of psychotic disorders face elevated risk.
Tolerance & Dependence
DOB produces rapid tolerance to its hallucinogenic effects after even a single dose — the body downregulates the relevant serotonin receptors.[5] Cross-tolerance develops with other serotonergic psychedelics including LSD and psilocybin. Chronic SSRI use can significantly weaken or abolish DOB's effects.[20]
Serotonergic psychedelics as a class are not habit-forming and do not produce compulsive use or withdrawal.[5] No evidence for physical dependence on DOB exists.
Drug Interactions
Serotonergic Agents
Combining DOB with serotonin-releasing drugs (e.g., tramadol, MDMA) or serotonin reuptake inhibitors raises theoretical risk of dangerous serotonin excess — a potentially life-threatening overheating and seizure response. Tramadol is classified as dangerous when combined with DOB, based on pharmacological inference. inferred Chronic SSRI/SNRI use may significantly attenuate or abolish DOB's effects.[20]
MAO Inhibitors
MAOIs slow the breakdown of amphetamine-type compounds, potentially increasing DOB exposure. Combined with DOB's serotonergic activity, this poses significant theoretical risk of serotonin excess and dangerous blood pressure elevation. inferred
Cannabis
No published interaction data exist for DOB and cannabis. Molecular-level crosstalk between cannabinoid and serotonin receptors has been documented, and cannabis could theoretically modulate the DOB experience in unpredictable ways. citation needed
Contraindications
7 knownNo DOB-specific contraindication studies exist. The following are inferred from DOB's pharmacological class:
- Psychotic disorders (personal or family history): serotonin receptor agonism may trigger or worsen psychotic episodes. Absolute contraindication by class consensus.[5]
- Bipolar disorder: Risk of manic episode.
- Heart and vascular disease: stimulant effects (rapid heartbeat, elevated blood pressure) and vasoconstriction pose direct risk. Particularly dangerous in peripheral vascular disease.
- Lithium: lithium combined with serotonergic psychedelics is associated with unpredictable and potentially dangerous intensification. Absolute contraindication.
- MAOIs: Risk of dangerous blood pressure elevation and serotonin excess.
- Pregnancy and breastfeeding: No safety data exist. Contraindicated by precautionary principle.
- Seizure disorders: Convulsions documented in the fatal overdose case.[6]
Harm Reduction[edit]
Forms & Identification
DOB is active at very low doses (1–3 mg), meaning accurate identification and measurement are critically important — small errors in quantity can mean the difference between an active dose and a dangerous one. Standard drug screening panels do not detect DOB,[6] making reagent testing the primary verification tool.
The extreme potency means DOB may appear on blotter paper, where it can be mistaken for LSD — a confusion made more dangerous by radically different dosing and duration profiles.
Guidelines
- Test all material with appropriate reagent kits before use
- Weigh doses with a milligram-precision scale — volumetric dosing in solution is safer for compounds active at this level
- Begin with the lowest reported active dose and do not redose — onset can take up to 3 hours, and impatient redosing has been a documented source of overdose
- Clear the full following day of all obligations — the experience will last 18–30 hours with residual effects beyond that
- Have a sitter present for the entire duration
- Prepare food, water, and electrolytes in advance — appetite will be suppressed but hydration and nutrition matter over this timeframe
- Avoid all other serotonergic substances for at least 24 hours before and after
Set & Setting
DOB's duration demands preparation beyond what most psychedelic experiences require. Environment must be stable, safe, and comfortable for an extended period — food, water, temperature control, and access to outdoor space should be arranged in advance.
A trusted sitter is strongly recommended, ideally prepared to be present for the full duration or to rotate with another sitter. There is no early exit: sleep is impossible during active effects, and the compound must run its course.
Aftercare & integration. An 18–30 hour psychedelic experience places exceptional demands on the body and mind. In the first 24 hours after effects subside, prioritize sleep, gentle nutrition, and hydration. Physical recovery may take an additional day beyond the acute experience.
The extended duration can produce unusually rich or disorienting psychological material. Journaling within the first few days, before memories consolidate into narrative, can help preserve insights and process difficult moments. If distressing experiences persist beyond a few days — intrusive thoughts, mood instability, or perceptual disturbances — seek professional support from a therapist familiar with psychedelic experiences.
Recovery & Support
DOB does not produce physical dependence or withdrawal, and compulsive use patterns are rare with serotonergic psychedelics. However, repeated use of high-potency, long-duration psychedelics can reflect broader patterns of psychological avoidance or risk-seeking behavior worth examining.
If psychedelic use is causing problems in daily life, or if difficult experiences have left lasting psychological effects, the Fireside Project (62-FIRESIDE / 623-473-7433), MAPS integration List, and local psychedelic integration circles offer support. Professional mental health support is advisable for any persistent distress following psychedelic use.
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Recognizing an emergency: Uncomfortable anxiety and body stimulation are common at active doses. Seek immediate medical help if any of the following occur: loss of consciousness, convulsions, severe chest pain, numbness or color change in extremities (a sign of dangerous vasoconstriction), inability to communicate, or persistent vomiting preventing hydration.
Immediate steps:
- 1. Call emergency services
- 2. Place an unconscious person in the recovery position
- 3. Do not attempt to restrain someone who is agitated unless they are in immediate physical danger
- 4. Do not induce vomiting
- 5. Keep the person cool — stimulant effects can elevate body temperature
- 6. Stay with the person until help arrives
What to tell the dispatcher: Name the substance (DOB, a synthetic psychedelic amphetamine), estimated dose if known, time of ingestion, and current symptoms. Standard drug tests will not detect DOB — communicate this to medical personnel. Good Samaritan laws in many jurisdictions protect people who call for help during a drug emergency.
Legal Status[edit]
DOB is internationally controlled with no approved medical use in any jurisdiction, listed under the UN Convention on Psychotropic Substances.[7]
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| United States | Schedule I (Controlled Substances Act) | Effective September 21, 1973 (38 FR 26447). Among earliest scheduled phenethylamine hallucinogens.[3] |
| United Kingdom | Class A (Misuse of Drugs Act 1971) | Explicitly named as 4-bromo-2,5-dimethoxy-α-methylphenethylamine.[21] |
| Canada | Schedule I (Controlled Drugs and Substances Act) | Specifically listed.[7] |
| Australia | Schedule 9 (Poisons Standard) | Prohibited substance.[7] |
| International | Schedule I (UN Convention on Psychotropic Substances) | Globally controlled.[7] |
Legal status changes frequently and varies by jurisdiction. This information is not legal advice.
Safety[edit]
- Acute toxicity
- Critical
- Chronic toxicity
- Low
- Withdrawal
- None
- Tolerance buildup
- rapid
- Tolerance reset
- 8.5 days
- Physical
- None
- Psychological
- Negligible
- Compulsive redosing
- Negligible
- Dose escalation
- Negligible
- Cross-tol.
- LSD · psilo · mesc
Toxicity
Acute Toxicity
No lethal dose has been established for DOB in any species, and no controlled toxicology studies have been published. The sole human toxicity data come from a single confirmed overdose case report in which two men co-ingested an unknown quantity of DOB sold as an "LSD-like" designer drug.[7]
Both experienced intense hallucinations within 15 minutes, followed by vomiting and loss of consciousness. The heavier individual (113 kg) survived; the lighter individual (65 kg) developed convulsions and metabolic acidosis and died on day 6.[7]
The case authors estimate an effective dose of approximately 2 mg for an 80 kg person, placing active doses (1–3 mg) in close proximity to the toxic dose — an extremely narrow safety margin.[7] Standard urine drug screens do not detect DOB; targeted laboratory analysis is required for identification.
Vasoconstriction
High-dose DOB produces significant vasoconstriction, a class property of DOx compounds.[18] The mechanistically related compound Bromo-DragonFLY has been associated with fatal arterial spasm and limb tissue death.[19] The likely mechanism involves serotonin receptor activation on blood vessel walls. No data quantify DOB's specific dose-response relationship for this effect. safety citation needed
Analytical Detection
DOB can be identified by specialized mass spectrometry with characteristic product ions.[20] Standard amphetamine immunoassays return negative results[7] — clinicians must be specifically informed of suspected DOx ingestion to request appropriate testing.
Psychological Risks
As a potent serotonin 2A receptor agonist, DOB shares the class-wide psychological risks of serotonergic psychedelics: acute anxiety, panic, paranoia, thought disorganization, and transient psychotic symptoms — risks that scale with dose and inadequate preparation.[6]
The exceptionally long duration (18–30 hours) compounds these risks by extending any psychological distress far beyond a normal waking period. Sleep is impossible during active effects, eliminating the usual escape valve.
No published data address the incidence of persistent perceptual changes (HPPD) or psychosis precipitation specifically from DOB. By class inference, individuals with personal or family history of psychotic disorders face elevated risk.
Tolerance & Dependence
DOB produces rapid tolerance to its hallucinogenic effects after even a single dose, driven by the body's downregulation of 5-HT₂A receptors.[6] Cross-tolerance develops with other serotonergic psychedelics including LSD and psilocybin.
Chronic SSRI use reduces 5-HT₂A receptor density and can significantly weaken or abolish DOB's psychedelic effects.[21]
Serotonergic psychedelics as a class are not habit-forming and do not produce compulsive use or withdrawal.[6] No evidence for physical dependence on DOB exists.
Drug Interactions
Serotonergic Agents
Combining DOB with serotonin-releasing drugs (e.g., tramadol, MDMA) or serotonin reuptake inhibitors carries theoretical risk of dangerous serotonin excess. Tramadol is classified as dangerous in community databases when combined with DOB, based on pharmacological inference. inferred
Chronic SSRI/SNRI use may significantly attenuate or abolish DOB's psychedelic effects.[21] Acute co-administration raises theoretical serotonin syndrome concerns, though no published case reports exist for DOB specifically.
MAO Inhibitors
MAOIs slow the breakdown of amphetamine-type compounds, potentially increasing DOB exposure. Combined with DOB's serotonergic activity, MAOI co-administration poses significant theoretical risk of serotonin excess and dangerous blood pressure elevation. inferred
Cannabis
No published interaction data exist for DOB and cannabis. Molecular-level crosstalk between cannabinoid and serotonin receptors has been documented, and cannabis could theoretically modulate the DOB experience in unpredictable ways. citation needed
Contraindications
7 knownNo DOB-specific contraindication studies exist. The following are inferred from DOB's pharmacological class:
- Psychotic disorders (personal or family history): 5-HT₂A agonism may trigger or worsen psychotic episodes. Absolute contraindication by class consensus.[6]
- Bipolar disorder: Risk of manic episode.
- Heart and vascular disease: stimulant effects (rapid heartbeat, elevated blood pressure) and blood vessel constriction pose direct risk. Particularly dangerous in peripheral vascular disease.
- Lithium: lithium combined with serotonergic psychedelics is associated with unpredictable and potentially dangerous intensification. Absolute contraindication.
- MAOIs: Risk of dangerous blood pressure elevation and serotonin excess.
- Pregnancy and breastfeeding: No safety data exist. Contraindicated by precautionary principle.
- Seizure disorders: Convulsions documented in the fatal overdose case.[7]
Harm Reduction[edit]
Forms & Identification
DOB is active at very low doses (1–3 mg), which means accurate identification and measurement are critically important — small errors in quantity can mean the difference between an active dose and a dangerous one. Because DOB is not detected by standard drug screening panels,[7] reagent testing is the primary available tool for users to verify they have the correct substance.
The extreme potency also means DOB may be encountered on blotter paper, where it can be mistaken for LSD — a confusion compounded by radically different dosing and duration profiles.
Guidelines
- Test all material with appropriate reagent kits before use
- Weigh doses with a milligram-precision scale — volumetric dosing in solution is safer for compounds active at this level
- Begin with the lowest reported active dose and do not redose — onset can take up to 3 hours, and impatient redosing has been a documented source of overdose
- Clear the full following day of all obligations — the experience will last 18–30 hours with residual effects beyond that
- Have a sitter present for the entire duration
- Prepare food, water, and electrolytes in advance — appetite will be suppressed but hydration and nutrition matter over this timeframe
- Avoid all other serotonergic substances for at least 24 hours before and after
Set & Setting
DOB's 18–30 hour duration demands a level of preparation beyond what most psychedelic experiences require. The full day-and-night commitment means that environment must be stable, safe, and comfortable for an extended period. Food, water, temperature control, and access to outdoor space should be arranged in advance.
A trusted sitter is strongly recommended — ideally someone prepared to be present for the entire duration, or to rotate with another sitter. Mental preparation should account for the impossibility of sleeping through difficult phases: there is no exit until the compound clears.
Aftercare & integration. An 18–30 hour psychedelic experience places exceptional demands on the body and mind. In the first 24 hours after effects subside, prioritize sleep, gentle nutrition, and hydration. Physical recovery may take an additional day beyond the acute experience.
The extended duration can produce unusually rich or disorienting psychological material. Journaling within the first few days, before memories consolidate into narrative, can help preserve insights and process difficult moments. If distressing experiences persist beyond a few days — intrusive thoughts, mood instability, or perceptual disturbances — seek professional support from a therapist familiar with psychedelic experiences.
Recovery & Support
DOB does not produce physical dependence or withdrawal, and compulsive use patterns are rare with serotonergic psychedelics. However, repeated use of high-potency, long-duration psychedelics can reflect broader patterns of psychological avoidance or risk-seeking behavior worth examining.
If psychedelic use is causing problems in daily life, or if difficult experiences have left lasting psychological effects, the Fireside Project (62-FIRESIDE / 623-473-7433), MAPS integration List, and local psychedelic integration circles offer support. Professional mental health support is advisable for any persistent distress following psychedelic use.
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Recognizing an emergency: Uncomfortable anxiety and body stimulation are common at active doses. Seek immediate medical help if any of the following occur: loss of consciousness, convulsions, severe chest pain, numbness or color change in extremities (a sign of dangerous vasoconstriction), inability to communicate, or persistent vomiting preventing hydration.
Immediate steps:
- 1. Call emergency services
- 2. Place an unconscious person in the recovery position
- 3. Do not attempt to restrain someone who is agitated unless they are in immediate physical danger
- 4. Do not induce vomiting
- 5. Keep the person cool — stimulant effects can elevate body temperature
- 6. Stay with the person until help arrives
What to tell the dispatcher: Name the substance (DOB, a synthetic psychedelic amphetamine), estimated dose if known, time of ingestion, and current symptoms. Standard drug tests will not detect DOB — communicate this to medical personnel. Good Samaritan laws in many jurisdictions protect people who call for help during a drug emergency.
Legal Status[edit]
DOB is internationally controlled with no approved medical use in any jurisdiction. It was among the earliest phenethylamine hallucinogens to be formally scheduled, placed under international control through the UN Convention on Psychotropic Substances.[8]
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| United States | Schedule I (Controlled Substances Act) | Effective September 21, 1973 (38 FR 26447). Among earliest scheduled phenethylamine hallucinogens.[4] |
| United Kingdom | Class A (Misuse of Drugs Act 1971) | Explicitly named as 4-bromo-2,5-dimethoxy-α-methylphenethylamine.[22] |
| Canada | Schedule I (Controlled Drugs and Substances Act) | Specifically listed.[8] |
| Australia | Schedule 9 (Poisons Standard) | Prohibited substance.[8] |
| International | Schedule I (UN Convention on Psychotropic Substances) | Globally controlled.[8] |
Frequently asked questions
How long does DOB last?
Total duration by route of administration — Oral: 18 – 30 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 DOB?
Psychedex publishes a dosage table for DOB on this page covering these routes of administration: oral. Dose values are presented only in that table, always alongside their route of administration.
What are dangerous combinations with DOB?
The highest-severity documented interactions for DOB: MAOIs (Lethal), 5-HTP, Tryptophan (Dangerous), Alpha-2 adrenergic receptor antagonist (Dangerous), Amphetamines (Dangerous), Antipsychotics (Dangerous). See the interactions section for the full list with mechanisms and severity levels.
Is DOB addictive?
Psychedex records tolerance and dependence data rather than a yes/no rating. Recorded tolerance indicators for DOB: tolerance builds rapid; full reset takes 8.5 days; cross-tolerance develops with LSD, psilocybin, mescaline, DOM, DOI, DOC. See the article's dependence and safety sections for recorded dependence data.
experience reports
No experience reports yet. Be the first to contribute.
First-person accounts of subjective effects, timing, and outcomes — submitted for harm reduction.
references
- [1]
- [2] ^abcPeroutka SJ, Hamik A, Harrington MA, Hoffman AJ, Mathis CA, Pierce PA, Wang SS (1988) (R)-(-)-[77Br]4-bromo-2,5-dimethoxyamphetamine labels a novel 5-hydroxytryptamine binding site in brain membranes. — Molecular Pharmacology PMID:3173334
- [3]
- [4] ^abMartin WR, Vaupel DB, Nozaki M, Bright LD (1978) The identification of LSD-like hallucinogens using the chronic spinal dog. — Drug and Alcohol Dependence PMID:272982
- [5]
- [6]
references
- [1] ^abcdGlennon RA, Bondarev ML, Khorana N, Young R, May JA, Hellberg MR, McLaughlin MA, Sharif NA (2004) Beta-oxygenated analogues of the 5-HT2A serotonin receptor agonist 1-(4-bromo-2,5-dimethoxyphenyl)-2-aminopropane. — Journal of Medicinal Chemistry PMID:15537358
- [2]
- [3] ^abcPeroutka SJ, Hamik A, Harrington MA, Hoffman AJ, Mathis CA, Pierce PA, Wang SS (1988) (R)-(-)-[77Br]4-bromo-2,5-dimethoxyamphetamine labels a novel 5-hydroxytryptamine binding site in brain membranes. — Molecular Pharmacology PMID:3173334
- [4]
- [5] ^abMartin WR, Vaupel DB, Nozaki M, Bright LD (1978) The identification of LSD-like hallucinogens using the chronic spinal dog. — Drug and Alcohol Dependence PMID:272982
- [6]