Psychedex is in open beta. We are still fine-tuning the generation and review process. Please double-check sources.
+1 more
2C-xLSD, psilocybin, mescaline +4 moreLSD, psilocybin, mescaline, 2C-B, 2C-E, DOI, DMT show less
2C-I
4-iodo-2,5-dimethoxyphenethylamine
2C-I (2,5-dimethoxy-4-iodophenethylamine) is a synthetic psychedelic of the phenethylamine class. It is a close relative of mescaline, distinguished by an iodine atom that sharply increases its potency. It activates serotonin receptors in the brain, producing the visual distortions and perceptual shifts characteristic of classical psychedelics.[1]
2C-I (2,5-dimethoxy-4-iodophenethylamine) is a synthetic psychedelic of the phenethylamine class. It is a halogenated relative of mescaline, distinguished by its iodine substituent and substantially higher potency by weight. 2C-I is a 5-HT₂A receptor agonist, producing its effects by activating serotonin signaling pathways that alter perception and cognition.[1]
Psychedex is in open beta. We are still fine-tuning the generation and review process. Please double-check sources.
+1 more
2C-xLSD, psilocybin, mescaline +4 moreLSD, psilocybin, mescaline, 2C-B, 2C-E, DOI, DMT show less
Alexander Shulgin first synthesized 2C-I in 1977 and documented it in his 1991 book PiHKAL.[2] When 2C-B was placed into Schedule I in 1995, 2C-I emerged as an unscheduled substitute, sold openly through online research chemical vendors.[3] It was permanently scheduled in the United States in 2012 and remains prohibited in most major jurisdictions.
Subjective effects include geometric visual patterns, brightened colors, tactile enhancement, mood elevation, and a persistent physical energy.[2] The experience carries a distinct stimulant character — more physically energizing than tryptamine psychedelics, with vivid colors and a social warmth that places it between 2C-B and mescaline. Jaw tension, nausea, and anxious overstimulation are common unwanted effects.
2C-I does not produce physical dependence,[4] and rapid tolerance limits repeated use;[5] the primary risk is cardiovascular — high blood pressure and vasoconstriction can trigger serious events in predisposed individuals.[6] Combining it with antidepressants or MAOIs dramatically amplifies effects and risks a life-threatening serotonin response. No controlled human studies have been conducted — most knowledge comes from a single case report and class-level analogy.
History[edit]
Discovery
Alexander Shulgin first synthesized 2C-I in 1977 during his systematic exploration of substituted phenethylamines. He documented the compound's synthesis, dosing, and self-experiment reports in PiHKAL: A Chemical Love Story in 1991.[2]
Commercial availability
When the DEA placed 2C-B into Schedule I in 1995, 2C-I emerged as an unscheduled substitute.[3] It was sold openly by Dutch smart shops and online research chemical vendors through the early 2000s. Forensic toxicology confirmed its presence in recreational drug supplies across the United States[6] and Europe.
Prohibition and modern status
The European Union required all member states to ban 2C-I in December 2003.citation needed The United States permanently placed it in Schedule I under the synthetic Drug Abuse Prevention Act of 2012.[7] No clinical trials have been registered for the compound.
The name follows Shulgin's convention: "2C" marks the two-carbon chain between the aromatic ring and the amino group, while "I" indicates the iodine atom at position 4. Among the 2C family, 2C-I was considered more visually active than 2C-C and longer-lasting than 2C-B, though it earned a reputation for an inconsistent dose-response relationship.
Chemistry[edit]
Structural class
2C-I belongs to the 2C family of substituted phenethylamines — compounds built around a phenethylamine backbone with methoxy groups at positions 2 and 5. These methoxy groups are essential for serotonin receptor activity.[8]
The iodine atom at position 4 is the heaviest halogen in the common 2C series, setting 2C-I apart from close relatives like 2C-B (bromine) and 2C-C (chlorine).
Molecular properties
| Molecular formula | C₁₀H₁₄INO₂ |
| Molecular weight | 307.13 g/mol |
2C-I is the direct structural parent of 25I-NBOMe. Adding a single chemical group to 2C-I's nitrogen creates 25I-NBOMe, which is approximately 14 times more potent in animal assays.[1] The two compounds can look identical — a confusion that has contributed to fatalities.
Pharmacology[edit]
Mechanism of action
2C-I activates serotonin receptors in the brain — the receptor type responsible for psychedelic effects. This has been confirmed directly: blocking those receptors completely abolishes 2C-I's behavioral effects in animals.[1][9] The signal runs predominantly through a pathway identified as the key predictor of psychedelic potential in animal models.[5]
2C-I also acts at dopamine, epinephrine, acetylcholine, and other receptor systems.[10][11] Animal discrimination studies show that trained animals recognize its effects as similar to LSD, DMT, and MDMA.[7]
Pharmacokinetics
No human pharmacokinetic data have been published. A rat metabolism study identified several breakdown pathways — including removal of methoxy groups and conjugation reactions that prepare metabolites for urine excretion.[12] The specific liver enzymes responsible are unknown.inferred
Neuroscience[edit]
Where it acts
No brain imaging or electrical recording studies have been conducted with 2C-I. As a serotonin-activating psychedelic, it is expected to engage the prefrontal cortex, disrupt the brain's sensory filtering, and increase communication between normally unconnected brain regionsinferred — effects documented for psilocybin and LSD, but not directly confirmed for 2C-I.
Why it matters
The leading model of psychedelic action proposes that serotonin receptor activation loosens the brain's established assumptions about reality, giving raw sensory input greater influence over perception. This predicts that 2C-I would produce the characteristic visual disruption, cognitive flexibility, and emotional shifts seen with other psychedelics. Whether it also triggers growth of new neural connections — as documented for some psychedelics — is untested.inferred
Several questions remain entirely unaddressed for 2C-I: whether it promotes neural connection growth at recreational doses, how receptor binding duration relates to the 6–10 hour subjective experience, and whether the iodine substituent — the heaviest in the 2C series — produces distinctive brain effects beyond those explained by its size and fat-solubility.
Subjective Effects[edit]
2C-I produces an experience shaped by two forces: serotonergic visuals and a persistent physical energy that runs throughout. The stimulant component is more prominent than in tryptamine psychedelics — colors are vivid, mood lifts, and the body stays active. Set and setting strongly shape the character of the experience; the same dose can yield relaxed sociability or anxious overstimulation.
Relative to 2C-B, 2C-I produces a similar visual and empathogenic profile but lasts longer and responds less predictably to dose changes. Compared to mescaline, the character is similar — the same phenethylamine warmth and visual emphasis — but 2C-I reaches that territory at substantially less weight.
First synthesized by Alexander Shulgin in 1977 and documented in his 1991 book PiHKAL,[2] 2C-I was one of dozens of phenethylamines he designed and self-tested. After 2C-B was placed in Schedule I in 1995, 2C-I emerged as an unscheduled alternative sold through online research chemical vendors. It was permanently scheduled in the United States in 2012 and remains prohibited in most major jurisdictions.
Subjective effects include geometric visual patterns, color enhancement, tactile enhancement, and mood elevation. The experience carries a distinctly stimulating phenethylamine body feel — more physically energizing than tryptamine psychedelics, with vivid color saturation and a social warmth that positions it between 2C-B and mescaline.[2] Jaw tension, nausea, and anxious overstimulation are common unsought effects.
2C-I produces no physical dependence,[3] and rapid tolerance through downregulation limits compulsive use.[4] The primary acute risk is cardiovascular — hypertension and vasoconstriction can precipitate serious events in predisposed individuals.[5][6] No controlled human studies have been conducted; the evidence base rests on a single case report, one animal metabolism study,[7] and pharmacological class analogy.
History[edit]
Discovery
Alexander Shulgin first synthesized 2C-I in 1977 during his systematic exploration of substituted phenethylamines. He published the compound's synthesis, self-experiment reports, and dose-ranging data in PiHKAL: A Chemical Love Story in 1991,[2] documenting an oral dose range of 14–22 mg producing psychedelic effects lasting 6–10 hours.
Commercial availability
When the DEA placed 2C-B into Schedule I in 1995, 2C-I emerged as an unscheduled substitute — part of a recurring pattern in which scheduling one compound drives adoption of structurally related analogs.[8] Through the early 2000s it was sold openly by Dutch smart shops and online research chemical vendors, and forensic toxicology cases confirmed its presence in recreational drug supplies across the United States[5] and Europe.
Prohibition and modern status
The European Union issued a binding order in December 2003 requiring all member states to ban 2C-I within three months.citation needed In the United States, 2C-I was permanently placed in Schedule I under the synthetic Drug Abuse Prevention Act of 2012.[9] No clinical trials have been registered for the compound — a consequence of its restricted legal status and limited institutional interest relative to psychedelics such as psilocybin and LSD.
The name follows Shulgin's naming convention: "2C" denotes the two-carbon chain between the phenyl ring and the amino group (the phenethylamine backbone), while "I" indicates the iodine atom at position 4. Among the 2C family, 2C-I occupied a middle position in user perception — considered more visually active than 2C-C and longer-lasting than 2C-B, though with a less predictable dose-response relationship that earned it a reputation for inconsistency.
Chemistry[edit]
Structural class
2C-I belongs to the 2C family of substituted phenethylamines — compounds sharing a 2,5-dimethoxy substitution pattern on a phenethylamine backbone. The two methoxy groups are essential for serotonin receptor activity; research has shown this motif drives in vivo potency, though removing either group causes only modest reduction in receptor binding.[10]
What distinguishes 2C-I within the series is an iodine atom at the 4-position of the aromatic ring — the largest and heaviest halogen substituent among common 2C compounds (compare 2C-B with bromine, 2C-C with chlorine). The iodine contributes substantial molecular weight and increased lipophilicity relative to lighter halogen analogs.
Molecular properties
| Molecular formula | C₁₀H₁₄INO₂ |
| Molecular weight | 307.13 g/mol |
The molecule consists of a benzene ring bearing methoxy groups at positions 2 and 5, an iodine atom at position 4, and an unsubstituted ethylamine side chain. The iodine alone accounts for 126.9 g/mol of the total molecular weight.
Structure-activity relationships
2C-I is the direct structural parent of 25I-NBOMe, which adds an N-2-methoxybenzyl group to the amine nitrogen. This modification dramatically increases potency — 25I-NBOMe is approximately 14 times more potent than 2C-I in mouse behavioral assays.[1]
Stereochemistry
2C-I has no chirality center. Unlike the amphetamine-type psychedelics such as DOI — which possess an alpha-methyl group creating a stereogenic carbon — the 2C phenethylamines have an unsubstituted two-carbon side chain. No stereoisomeric considerations apply to its pharmacological activity.
Pharmacology[edit]
Mechanism of action
2C-I activates the serotonin 5-HT₂A receptor, the primary target responsible for its psychedelic effects. The compound signals predominantly through the Gq protein pathway — a signaling route identified as the key predictor of psychedelic potential in animal models.[4]
This mechanism has been confirmed directly: the selective 5-HT₂A blocker M100907 completely abolishes 2C-I's behavioral effects in mice,[1] and the compound stimulates G protein activation in rat brain tissue.[11]
Beyond 5-HT₂A, 2C-I also acts at 5-HT₂C receptors — activity shared by all compounds carrying the 2,5-dimethoxy phenethylamine scaffold.[10] Comprehensive receptor screening of phenethylamine psychedelics has revealed interactions with dozens of additional targets, including adrenergic, dopamine, and acetylcholine receptors.[12][13] The contribution of these secondary targets to the overall experience is not well understood.
Drug discrimination studies confirm that 2C-I produces effects that trained animals recognize as similar to LSD, DMT, and MDMA.[9]
Pharmacokinetics
No human pharmacokinetic data have been published for 2C-I. Bioavailability, time to peak blood levels, plasma half-life, and distribution throughout the body are all unknown in humans.
The only metabolism study, conducted in rats, identified several metabolic pathways: removal of methoxy groups, direct breakdown of the amine portion of the molecule, and conjugation reactions that prepare metabolites for excretion in urine.[7] Most metabolites were excreted in conjugated form, indicating the body processes the compound extensively before elimination.
The specific liver enzymes responsible for metabolizing 2C-I have not been identified. Based on structural similarity to 2C-B, CYP2D6 and CYP1A2 are plausible candidates, but no direct data exist.inferred
Neuroscience[edit]
Where it acts
No neuroimaging or electrophysiology studies have been conducted with 2C-I. As a serotonin 2A receptor agonist, it is expected to engage the same brain systems as other serotonergic psychedelics: activation of neurons in the prefrontal cortex, disruption of the brain's sensory filtering mechanisms, and increased connectivity between brain regions that do not normally communicate directly.inferred These effects have been demonstrated for structurally related compounds including psilocybin, LSD, and mescaline, but direct confirmation for 2C-I is absent.
Why it matters
The dominant theoretical account of psychedelic action — the REBUS model — proposes that 5-HT₂A activation loosens the brain's established assumptions about reality, allowing raw sensory information greater influence over conscious experience. This framework predicts that 2C-I would produce the characteristic perceptual destabilization, cognitive flexibility, and emotional shifts seen with other psychedelics. Whether 2C-I also promotes the structural brain changes (growth of new neural connections) described for other serotonergic psychedelics remains untested.inferred
Several questions remain entirely unaddressed for 2C-I: whether it promotes growth of new neural connections at the doses used recreationally, how its receptor binding duration relates to its 6–10 hour subjective effects, and whether the iodine substituent — the heaviest halogen in the 2C series — confers distinctive brain effects beyond those explained by its size and fat-solubility.
Subjective Effects[edit]
2C-I produces an experience shaped by its combined serotonergic and mild stimulant pharmacology. The stimulant component is more prominent than in tryptamine psychedelics, lending the experience a persistent physical energy and jaw tension throughout. Set and setting exert strong influence on the character of the experience — the same dose can produce euphoric sociability or anxious overstimulation depending on context. Insufflation is reported as intensely painful and remains uncommon.
Relative to 2C-B, 2C-I is described as producing a similar visual and empathogenic profile at comparable doses but with a longer duration and a less predictable dose-response curve. Compared to mescaline, 2C-I is substantially more potent by weight (14–22 mg versus 200–400 mg) but shares the characteristic phenethylamine body feel and visual emphasis of the class.
Effect Grid
At common doses (10–20 mg oral), the full psychedelic experience manifests: pronounced color enhancement and visual patterning on surfaces, geometric closed-eye visuals, object morphing and drifting, and meaningful shifts in thought connectivity. Emotional responses intensify — music, social connection, and aesthetic experience carry amplified significance. Time distortion becomes apparent.
Physically, moderate stimulation, jaw tension, pupil dilation, and occasional nausea are expected. Body temperature regulation may fluctuate. The experience commits the user for 6–8 hours, with sleep difficult during the active phase.
Shulgin's PiHKAL range of 14–22 mg falls largely within this tier and the lower end of the strong tier.
Modeled from the effect's dose-dependence curve — not per-substance measurements.
Visual breathing · Environmental patterning · Music enhancement · Tracers · Brightness alteration · Touch enhancement · Symmetrical texture repetition · After-images · Auditory enhancement · Depth perception distortion · Light sensitivity · Perspective distortion · Sound sensitivity · Visual morphing · Holotropic state · Auditory distortion · Peripheral vision distortion · Visual diffraction · Visual haze / noise · Visual melting · Synesthesia · Auditory misinterpretation · Dreaming enhancement · Ganzfeld effect · Peripheral misidentification · Proprioceptive distortion · Sleep-transition hallucinations · Spatial disorientation · Vestibular distortion · Visual acuity enhancement · Visual magnification · Olfactory enhancement · Taste enhancement · Visual processing acceleration · Tinnitus · Flashbacks · Object transformations · Environmental orbism / cubism · External hallucinations · Object activation · Visual recursion · Visual scenery slicing · Internal hallucinations · Perspective hallucinations · Visual flipping · Auditory hallucinations · Persisting hallucinations · Shadow people
Brightness alteration · Touch enhancement · Symmetrical texture repetition · After-images · Auditory enhancement · Depth perception distortion · Light sensitivity · Perspective distortion · Sound sensitivity · Visual morphing · Holotropic state · Auditory distortion · Peripheral vision distortion · Visual diffraction · Visual haze / noise · Visual melting · Synesthesia · Auditory misinterpretation · Dreaming enhancement · Ganzfeld effect · Peripheral misidentification · Proprioceptive distortion · Sleep-transition hallucinations · Spatial disorientation · Vestibular distortion · Visual acuity enhancement · Visual magnification · Olfactory enhancement · Taste enhancement · Visual processing acceleration · Tinnitus · Flashbacks · Object transformations · Environmental orbism / cubism · External hallucinations · Object activation · Visual recursion · Visual scenery slicing · Internal hallucinations · Perspective hallucinations · Visual flipping · Auditory hallucinations · Persisting hallucinations · Shadow people
Wakefulness · Spontaneous body sensations · Muscle tension · Appetite suppression · Body high · Heart rate perception changes · Insomnia · Temperature dysregulation · Dehydration sensation · Nausea · Sexual arousal enhancement · Dry mouth · Motor control impairment · Physical fatigue · Restlessness · Tactile euphoria · Tingling / electric sensations · Vibrations / buzzing · Bodily pressures · Dizziness · Excessive sweating · Laughter fits · Involuntary body movements · Increased urination · Bodily lightness · Body schema distortion · Breathing alteration · Bruxism · Headache · Trembling · Diarrhea · Nystagmus (eye wobbles) · Respiratory stimulation · Salivation · Vomiting · Watery eyes · Motor control enhancement · Tactile hallucination
Appetite suppression · Body high · Heart rate perception changes · Insomnia · Dehydration sensation · Nausea · Sexual arousal enhancement · Dry mouth · Motor control impairment · Physical fatigue · Restlessness · Tactile euphoria · Tingling / electric sensations · Vibrations / buzzing · Bodily pressures · Dizziness · Excessive sweating · Laughter fits · Involuntary body movements · Increased urination · Bodily lightness · Body schema distortion · Breathing alteration · Bruxism · Headache · Trembling · Diarrhea · Nystagmus (eye wobbles) · Respiratory stimulation · Salivation · Vomiting · Watery eyes · Motor control enhancement · Tactile hallucination
Introspection enhancement · Openness enhancement · Pattern recognition enhancement · Cognitive euphoria · Cognitive flexibility · Cognitive impairment · Conceptual thinking · Multiple thought streams · Thought connectivity · Creativity enhancement · Memory suppression · Cognitive fatigue · Focus suppression · Humor enhancement · Information processing suppression · Memory fragmentation · Synchronicity · Thought acceleration · Thought disorganization · Thought loops · Analysis enhancement · Analysis suppression · Cognitive dysphoria · Compulsive redosing urge · Confusion · Language suppression · Memory replays · Motivation suppression · Focus enhancement · Information processing enhancement · Motivation enhancement · Language enhancement · Delusions
Cognitive euphoria · Cognitive flexibility · Cognitive impairment · Conceptual thinking · Multiple thought streams · Thought connectivity · Creativity enhancement · Memory suppression · Cognitive fatigue · Focus suppression · Humor enhancement · Information processing suppression · Memory fragmentation · Synchronicity · Thought acceleration · Thought disorganization · Thought loops · Analysis enhancement · Analysis suppression · Cognitive dysphoria · Confusion · Language suppression · Memory replays · Motivation suppression · Focus enhancement · Information processing enhancement · Motivation enhancement · Language enhancement · Delusions
Empathy enhancement · Anxiety · Simultaneous emotions · Catharsis · Dysphoria · Anxiety suppression · Irritability
Dysphoria · Anxiety suppression · Irritability
Depersonalization · Disinhibition · Sociability enhancement · Communication enhancement · Communication suppression · Flow state · Automaticity · Craving · Social disconnection · Boundary dissolution · Cognitive disconnection · Ego dissolution · Identity alteration · Telepathic feelings
Communication suppression · Flow state · Automaticity · Craving · Social disconnection · Boundary dissolution · Cognitive disconnection · Ego dissolution · Identity alteration · Telepathic feelings
Time cessation
Non-dual awareness · Transpersonal memory access · Transpersonal visions
Mindfulness enhancement · Recursive awareness
Timeline
First alerts appear as a subtle shift in body awareness and faint brightening of colors. A mild stimulant undertone is common. Easily mistaken for anticipatory excitement.
Effects build progressively — visual enhancement sharpens, body stimulation increases, and mild nausea may appear. Emotional tone begins shifting. The transition can feel abrupt in its final minutes.
Full psychedelic effects at maximum intensity: pronounced visual patterning, color saturation, object morphing, thought connectivity, and emotional amplification. The stimulant body load is most prominent during this phase. Time distortion is marked.
Intensity gradually moderates while retaining psychedelic character. Visual effects soften. Cognitive clarity returns incrementally.
Effects taper toward baseline. Residual visual enhancement and mild stimulation linger. Appetite begins returning.
A residual period of mild mood elevation, enhanced appreciation for sensory experience, and gentle introspection. Some residual stimulation may persist, and sleep onset can remain difficult for several hours.
⚠ Do not drive or operate machinery for at least 12 hours after ingestion, as residual stimulation and subtle perceptual changes may impair reaction time and judgment.
Safety[edit]
- Acute toxicity
- Low
- Chronic toxicity
- Negligible
- 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 data exist for 2C-I in any species. The only published case describes a woman who developed worsening consciousness, high blood pressure, and vasoconstriction after taking 2C-I alongside cocaine and MDA — ultimately suffering a hemorrhagic stroke.[6] The polydrug context prevents attributing the outcome to 2C-I alone, but the case shows it contributes enough cardiovascular stress to trigger catastrophic events in predisposed individuals.
Cardiovascular effects
High blood pressure, rapid heart rate, and vasoconstriction are documented in the clinical case report[6] and in class-level reviews of 2C drug poisoning.[13][4] The mechanism involves serotonin-driven blood vessel constriction, with possible additional contribution from epinephrine-type receptor activity.[11]
Class-level fatality data
Reviews of the 2C drug class document at least five deaths attributed to 2C drug intoxication.[13] The predominant fatal presentation is excited delirium — severe agitation, seizures, dangerously high body temperature, and sudden death. The related NBOMe compounds carry higher toxicity risk due to greater potency; severe NBOMe poisoning commonly involves muscle breakdown, extreme body temperature, and vasoconstriction.[14]
Psychological risks
No controlled data on psychological risks exist for 2C-I. By analogy with other serotonergic psychedelics, acute risks include panic, severe anxiety, paranoia, depersonalization, and transient psychotic episodes — especially at higher doses, in uncontrolled settings, or in people with pre-existing psychiatric vulnerability.inferred Clinical reports of 2C drug poisoning document agitation, aggression, and dysphoria.[13]
Tolerance and dependence
Tolerance develops rapidly after use. The brain reduces the availability of serotonin receptors after activation,[5] resetting over approximately 8–9 days.inferred 2C-I does not produce physical dependence, and no case of dependence or withdrawal has been documented.[4]
Cross-tolerance is expected with other serotonergic psychedelics — including LSD, psilocybin, and other 2C compounds — through the same downregulation mechanism.inferred
Drug Interactions
The most dangerous interaction is with other serotonergic drugs. Combined with antidepressants (SSRIs, SNRIs), MAOIs, or serotonin-releasing agents, 2C-I creates a cumulative serotonergic load that can produce serotonin syndrome — dangerously high body temperature, muscle rigidity, rapid heart rate, and agitation.
Tramadol is particularly dangerous. It inhibits serotonin reuptake and lowers the seizure threshold, compounding the seizure risk already documented in 2C drug intoxication.[13]inferred
MAOIs — including ayahuasca, Syrian rue, and pharmaceutical MAOIs — prevent serotonin breakdown. Combining them with 2C-I dramatically amplifies both effects and toxicity. No 2C-I-specific data exist, but class-level evidence is unequivocal.inferred
Lithium is contraindicated with serotonergic psychedelics due to reported seizures and prolonged psychotic episodes in combination with other serotonin-activating compounds.inferred
Cannabis interaction with 2C-I has not been characterized. Community reports suggest intensification of psychedelic effects, but no peer-reviewed data exist.
Contraindications
7 knownPre-existing blood vessel or cerebrovascular conditions are a documented contraindication — the hemorrhagic stroke case demonstrates that substance-induced cardiovascular stress can trigger catastrophic outcomes.[6]
Heart conditions — uncontrolled high blood pressure, structural heart disease, or predisposition to irregular heart rhythm — are a contraindication given the documented cardiovascular effects.[13][4]
Personal or family history of psychotic disorders, epilepsy or lowered seizure threshold, and pregnancy or breastfeeding are all contraindications.inferred[13]
Harm Reduction[edit]
Forms & Identification
2C-I typically circulates as a white to off-white powder or in pressed tablets. Visual inspection cannot distinguish it from other 2C compounds, NBOMe derivatives, or other white powders — reliable identification requires reagent testing.
The distinction matters: 25I-NBOMe, derived directly from 2C-I, is active at microgram doses rather than milligram doses. Confusion between the two has contributed to fatalities. Test every batch.
Volumetric dosing with a milligram-precision analytical balance (±1 mg accuracy) is essential. The active dose range is narrow enough that estimating by eye introduces significant overdose risk.
Guidelines
- Test every batch with reagent kits before use
- Weigh doses with a milligram-precision scale — never estimate by eye
- Start at the low end of the dose range for unfamiliar batches or first experiences
- Eat lightly 2–3 hours before dosing to reduce nausea during onset
- Stay hydrated but avoid excessive water intake
- Avoid redosing during the first 2 hours — onset can be slow and unpredictable
- Have a sober sitter present, especially at higher doses or in unfamiliar settings
- Plan for the full duration — arrange transportation, clear the schedule, and secure a comfortable space for the entire experience
Set & Setting
2C-I is highly sensitive to context. The same dose can produce relaxed sociability in a familiar environment or anxious overstimulation in a chaotic one.
A calm setting with trusted people substantially reduces psychological risk. First-time users benefit from the presence of a sober, experienced sitter. The experience extends to 6–10 hours — the setting needs to remain accessible and comfortable throughout.
Aftercare & integration. The day after a 2C-I experience often brings mild fatigue and emotional sensitivity. Prioritize sleep, light food, and low-demand activity. Avoid significant decisions during the 24–48 hours following the experience.
For psychologically intense or distressing experiences, writing down what happened while memory is fresh can aid processing. Talking it through with a trusted person — or a therapist experienced with psychedelic integration — helps contextualize difficult material. If distressing thoughts, perceptual changes, or mood disturbances persist beyond a few days, seek professional support.
Recovery & Support
2C-I does not produce physical dependence, and compulsive use patterns are rare due to rapid tolerance. Any pattern of repeated psychedelic use that interferes with daily functioning, relationships, or mental health warrants honest self-assessment.
Support resources include psychedelic-informed therapists, peer support communities such as the Fireside Project (62-FIRESIDE / 623-473-7433), and harm reduction organizations. If psychedelic use is part of a broader pattern of substance use, SAMHSA's National Helpline (1-800-662-4357) provides free referrals to local treatment services.
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Recognizing an emergency: Most 2C-I experiences involve manageable discomfort. Seek immediate help if any of the following occur: chest pain, severe headache with visual changes, seizure, loss of consciousness, body temperature hot to the touch through clothing, or complete disconnection from reality with self-harm risk.
Immediate steps:
- 1. Call emergency services immediately if the person is unresponsive, seizing, or showing signs of stroke (sudden severe headache, one-sided weakness, slurred speech)
- 2. Place an unconscious but breathing person in the recovery position (on their side, airway clear)
- 3. Do not restrain a conscious, agitated person unless they pose immediate danger to themselves or others
- 4. Cool an overheating person with wet cloths and move them to a cool area
- 5. Stay with the person until help arrives
What to tell the dispatcher: Name the substance (2C-I), approximate amount taken, time of ingestion, and current symptoms. Good Samaritan laws in many jurisdictions protect people who call for help during drug emergencies.
Legal Status[edit]
2C-I is a controlled substance in most major jurisdictions — prohibited under Schedule I in the United States since 2012 and banned across the European Union since 2003.[7]
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| United States | Schedule I (Controlled Substances Act) | Permanently scheduled under the Synthetic Drug Abuse Prevention Act of 2012 (Public Law 112-144)[7] |
| European Union | Banned | EU Council binding order, December 2003; mandatory implementation within 3 months for all member states |
| United Kingdom | Class A, Schedule 1 | Controlled under the Misuse of Drugs Act 1971; phenethylamine generic definition applies |
| Canada | Schedule III | Controlled Drugs and Substances Act, effective October 31, 2016 |
| Australia | Schedule 9 (Prohibited) | Poisons Standard (October 2015); prohibited except for approved research |
| Germany | Anlage I (BtMG) | Controlled under the Betäubungsmittelgesetz; consistent with EU-wide ban |
Legal status data for jurisdictions other than the United States is sourced from secondary references and government databases; primary regulatory documents have not been independently verified for this article.citation needed
Legal status changes frequently and varies by jurisdiction. This information is provided for educational purposes only and does not constitute legal advice. Verify current laws in the relevant jurisdiction before acting on this information.
Safety[edit]
- Acute toxicity
- Low
- Chronic toxicity
- Negligible
- 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 data exist for 2C-I in any species, and no controlled toxicity studies have been published. The toxic dose in humans is unknown.
The sole peer-reviewed case report describes a 39-year-old woman who developed rapidly worsening consciousness, high blood pressure, and vasoconstriction after ingesting 2C-I alongside cocaine and MDA.[5] She suffered a hemorrhagic stroke caused by an underlying blood vessel abnormality worsened by substance-induced cardiovascular stress. The polydrug context prevents attributing the outcome to 2C-I alone, but the case demonstrates that 2C-I contributes to cardiovascular strain sufficient to trigger serious events in predisposed individuals.
Cardiovascular effects
High blood pressure, rapid heart rate, and vasoconstriction are documented in both the clinical case report[5] and class-level reviews of 2C drug poisoning.[6][3] The mechanism involves 5-HT₂A-mediated blood vessel constriction with possible additional contribution from adrenergic receptor activity.[13]
Class-level fatality data
Reviews of the 2C drug class have documented at least five deaths attributed to 2C drug intoxication.[6] The predominant fatal presentation is excited delirium — severe agitation, aggression, seizures, dangerously high body temperature, and sudden death.
The related NBOMe compounds (derived from 2C compounds including 2C-I) carry higher toxicity risk due to greater potency and a steeper dose-response curve. Severe NBOMe poisoning commonly involves muscle breakdown linked to seizures, extreme body temperature, and vasoconstriction.[14] While NBOMe toxicity is more severe than that of the parent 2C compounds, the cardiovascular risk mechanisms are shared.
Psychological risks
No controlled data on the psychological risk profile of 2C-I exist. By class analogy with serotonergic psychedelics, acute psychological risks include panic reactions, severe anxiety, paranoia, depersonalization, and transient psychotic symptoms — particularly at higher doses, in uncontrolled settings, or in individuals with pre-existing psychiatric vulnerability.inferred
The risk of HPPD (HPPD) has not been assessed for 2C-I specifically. Clinical presentations of 2C drug poisoning include agitation, aggression, and dysphoria.[6]
Tolerance and dependence
Tolerance develops rapidly after use, consistent with the serotonergic psychedelic class. The mechanism involves 5-HT₂A downregulation — the brain reduces receptor availability after activation.[4] Community-reported parameters suggest near-immediate onset of tolerance, with approximately 4 days to half-reset and 8–9 days to full reset.inferred
2C-I does not produce physical dependence. No case of 2C-I dependence or withdrawal has been documented.[3] The rapid tolerance development itself serves as a functional deterrent against compulsive use.
Cross-tolerance is expected with other serotonergic psychedelics — including LSD, psilocybin, mescaline, and other 2C compounds — through the same receptor downregulation mechanism.inferred
Drug Interactions
The most significant interaction risk arises from co-administration with other serotonergic agents. As a 5-HT₂A agonist, 2C-I combined with drugs that increase serotonin levels — including SSRIs, SNRIs, MAOIs, and serotonin-releasing agents — creates cumulative serotonergic load with potential for serotonin syndrome (dangerously high body temperature, muscle rigidity, agitation, rapid heart rate).
Tramadol is a particularly dangerous combination. Tramadol both inhibits serotonin reuptake and lowers the seizure threshold, compounding the seizure risk documented in excited delirium presentations of 2C drug intoxication.[6]inferred
MAOIs (including ayahuasca, Syrian rue, and pharmaceutical MAOIs) prevent serotonin breakdown, dramatically amplifying both the effects and toxicity potential of 5-HT₂A agonists. No 2C-I-specific MAOI interaction data exist, but the class-level evidence is unequivocal.inferred
Lithium is contraindicated with serotonergic psychedelics due to reported seizures and prolonged psychotic episodes in combination with other 5-HT₂A agonists.inferred
Cannabis interaction with 2C-I has not been characterized. Community reports suggest potentiation of psychedelic effects, but no peer-reviewed data exist.
Contraindications
7 knownPre-existing blood vessel or cerebrovascular conditions are a documented contraindication — the clinical case of hemorrhagic stroke following 2C-I co-ingestion demonstrates that substance-induced cardiovascular stress can trigger catastrophic events in predisposed individuals.[5]
Heart conditions — including uncontrolled high blood pressure, structural heart disease, and conditions predisposing to irregular heart rhythm — constitute a contraindication given the documented sympathomimetic effects.[6][3]
Personal or family history of psychotic disorders is a standard contraindication for all serotonergic psychedelics.inferred
Epilepsy or lowered seizure threshold is a relative contraindication, as seizures are documented in severe 2C drug intoxication.[6]
Pregnancy and breastfeeding are absolute contraindications in the absence of any reproductive safety data.inferred
Harm Reduction[edit]
Forms & Identification
The structured data module above shows reagent results and common forms. 2C-I typically circulates as a white to off-white powder or pressed into tablets, and reliable identification requires reagent testing — visual inspection alone cannot distinguish it from other 2C compounds, NBOMe derivatives, or other white powders. The distinction matters: 25I-NBOMe, derived directly from 2C-I, is active at microgram doses rather than milligram doses, and confusion between the two has contributed to fatalities.
Volumetric dosing with an analytical balance (±1 mg accuracy) is essential. The active dose range is narrow enough that estimating powder by eye introduces significant overdose risk.
Guidelines
- Test every batch with reagent kits before use
- Weigh doses with a milligram-precision scale — never estimate by eye
- Start at the low end of the dose range for unfamiliar batches or first experiences
- Eat lightly 2–3 hours before dosing to reduce nausea during onset
- Stay hydrated but avoid excessive water intake
- Avoid redosing during the first 2 hours — onset can be slow and unpredictable
- Have a sober sitter present, especially at higher doses or in unfamiliar settings
- Plan for the full duration — arrange transportation, clear the schedule, and secure a comfortable space for the entire experience
Set & Setting
2C-I is highly sensitive to context. The same dose can produce relaxed sociability in a comfortable environment or anxious overstimulation in a chaotic one. A familiar, calm setting with trusted people present substantially reduces psychological risk.
First-time users benefit from the presence of an experienced, sober sitter who can provide reassurance if anxiety escalates. Because the duration extends to 6–10 hours, the setting should remain accessible and comfortable for the full experience.
Aftercare & integration. The day following a 2C-I experience often brings mild fatigue and emotional sensitivity. Prioritize sleep, light nutrition, and low-demand activity. Avoid making significant decisions during the 24–48 hours after the experience.
For experiences that were psychologically intense or distressing, writing down what happened while it remains fresh can aid processing. Talking through the experience with a trusted person — or a therapist experienced with psychedelic integration — helps contextualize difficult material. If distressing thoughts, perceptual changes, or mood disturbances persist beyond a few days, seek professional support.
Recovery & Support
2C-I does not produce physical dependence, and compulsive use patterns are rare due to rapid tolerance. However, any pattern of repeated psychedelic use that interferes with daily functioning, relationships, or mental health warrants honest self-assessment.
Support resources include psychedelic-informed therapists, peer support communities such as the Fireside Project (62-FIRESIDE / 623-473-7433), and harm reduction organizations. If psychedelic use is part of a broader pattern of substance use, SAMHSA's National Helpline (1-800-662-4357) provides free referrals to local treatment services.
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Recognizing an emergency: Most 2C-I experiences involve manageable discomfort. Seek immediate help if any of the following occur: chest pain, severe headache with visual changes, seizure, loss of consciousness, body temperature hot to the touch through clothing, or complete disconnection from reality with self-harm risk.
Immediate steps:
- 1. Call emergency services immediately if the person is unresponsive, seizing, or showing signs of stroke (sudden severe headache, one-sided weakness, slurred speech)
- 2. Place an unconscious but breathing person in the recovery position (on their side, airway clear)
- 3. Do not restrain a conscious, agitated person unless they pose immediate danger to themselves or others
- 4. Cool an overheating person with wet cloths and move them to a cool area
- 5. Stay with the person until help arrives
What to tell the dispatcher: Name the substance (2C-I), approximate amount taken, time of ingestion, and current symptoms. Good Samaritan laws in many jurisdictions protect people who call for help during drug emergencies.
Legal Status[edit]
2C-I is a controlled substance in most major jurisdictions. Its prohibition followed the broader regulatory response to novel psychoactive substances in the 2000s, with the European Union acting first in 2003 and the United States following with permanent scheduling in 2012. No jurisdiction currently permits 2C-I for medical use outside of specifically approved research exemptions.
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| United States | Schedule I (Controlled Substances Act) | Permanently scheduled under the Synthetic Drug Abuse Prevention Act of 2012 (Public Law 112-144)[9] |
| European Union | Banned | EU Council binding order, December 2003; mandatory implementation within 3 months for all member states |
| United Kingdom | Class A, Schedule 1 | Controlled under the Misuse of Drugs Act 1971; phenethylamine generic definition applies |
| Canada | Schedule III | Controlled Drugs and Substances Act, effective October 31, 2016 |
| Australia | Schedule 9 (Prohibited) | Poisons Standard (October 2015); prohibited except for approved research |
| Germany | Anlage I (BtMG) | Controlled under the Betäubungsmittelgesetz; consistent with EU-wide ban |
Legal status data for jurisdictions other than the United States is sourced from secondary references and government databases; primary regulatory documents have not been independently verified for this article.citation needed
Frequently asked questions
How long does 2C-I last?
Total duration by route of administration — Oral: 6 – 10 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-I?
Psychedex publishes a dosage table for 2C-I 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 2C-I?
The highest-severity documented interactions for 2C-I: 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-I addictive?
Psychedex records tolerance and dependence data rather than a yes/no rating. Recorded tolerance indicators for 2C-I: tolerance builds rapid; full reset takes 8.5 days; cross-tolerance develops with LSD, psilocybin, mescaline, 2C-B, 2C-E, DOI, DMT. 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] ^abcHalberstadt AL, Geyer MA (2014) Effects of the hallucinogen 2,5-dimethoxy-4-iodophenethylamine (2C-I) and superpotent N-benzyl derivatives on the head twitch response — Neuropharmacology doi:10.1016/j.neuropharm.2013.08.025
- [2]
- [3] ^abBaumeister D, Tojo LM, Tracy DK (2015) Legal highs: staying on top of the flood of novel psychoactive substances — Therapeutic Advances in Psychopharmacology doi:10.1177/2045125314559539
- [4] ^abcdGil-Martins E, Barbosa DJ, Borges F, Remiao F, Silva R (2025) Toxicodynamic insights of 2C and NBOMe drugs - Is there abuse potential? — Toxicology Reports doi:10.1016/j.toxrep.2025.101890
- [5] ^abcWallach J, Cao AB, Calkins MM, Heim AJ, Lanham JK, et al. (2023) Identification of 5-HT2A receptor signaling pathways associated with psychedelic potential — Nature Communications doi:10.1038/s41467-023-44016-1
- [6]
references
- [1] ^abcHalberstadt AL, Geyer MA (2014) Effects of the hallucinogen 2,5-dimethoxy-4-iodophenethylamine (2C-I) and superpotent N-benzyl derivatives on the head twitch response — Neuropharmacology doi:10.1016/j.neuropharm.2013.08.025
- [2]
- [3] ^abcdGil-Martins E, Barbosa DJ, Borges F, Remiao F, Silva R (2025) Toxicodynamic insights of 2C and NBOMe drugs - Is there abuse potential? — Toxicology Reports doi:10.1016/j.toxrep.2025.101890
- [4] ^abcWallach J, Cao AB, Calkins MM, Heim AJ, Lanham JK, et al. (2023) Identification of 5-HT2A receptor signaling pathways associated with psychedelic potential — Nature Communications doi:10.1038/s41467-023-44016-1
- [5]
- [6]