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2C-x2C-B, 2C-I, 2C-E +5 more2C-B, 2C-I, 2C-E, LSD, psilocybin, DMT, mescaline, DOI show less
2C-C
4-chloro-2,5-dimethoxyphenethylamine
2C-C (2,5-dimethoxy-4-chlorophenethylamine) is a synthetic psychedelic of the phenethylamine class. It is the chloro structural analog of 2C-B, the most familiar member of the halogenated 2C series. It activates serotonin receptors in the brain, producing perceptual distortion with an unusually quiet, sedating character.
2C-C (2,5-dimethoxy-4-chlorophenethylamine) is a synthetic psychedelic of the phenethylamine class. It is the chloro structural analog of 2C-B, distinguished by lower potency and a quieter, more sedating character.[1] 2C-C is a 5-HT₂A receptor agonist, producing its effects by disrupting normal sensory filtering in the prefrontal cortex.[2]
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2C-x2C-B, 2C-I, 2C-E +5 more2C-B, 2C-I, 2C-E, LSD, psilocybin, DMT, mescaline, DOI show less
Alexander Shulgin first synthesized 2C-C and documented it as entry #22 in PiHKAL (1991).[1] It appeared briefly on research chemical markets in the early 2000s but never caught on — its lower potency and harder synthesis kept it a niche curiosity. It is now scheduled by name in the United States and controlled under class provisions in most developed jurisdictions.
Subjective effects include geometric visual patterns, color enhancement, empathogenic warmth, sedation, and a pervasive calm. The experience is defined by stillness — a gentle, contemplative drift with soft visual overlay rather than the stimulating push typical of most 2C analogs. Slow onset, nausea, and mild body load are common unwanted effects.
2C-C does not produce physical dependence, and no human death has been attributed to it alone — though animal studies found neurotoxic effects and signs of abuse potential at high doses.[2] Combining it with MAOIs or tramadol risks a dangerous serotonin overload — fever, muscle rigidity, altered consciousness — that can be life-threatening. No controlled human study exists; the safety profile rests on animal data and class-level inference.
History[edit]
Discovery
Alexander Shulgin synthesized 2C-C at his private laboratory in Lafayette, California, as part of a systematic study of 4-position substituents on the 2C scaffold. He documented it as entry #22 in PiHKAL: A Chemical Love Story (1991).[1] He noted that handling liquid chlorine — one of two synthesis routes — was considerably less convenient than working with bromine or iodine.[3]
Market History & Scheduling
2C-C appeared on research chemical markets in the early 2000s alongside other 2C analogs but never achieved the uptake of 2C-B or 2C-I — users seeking phenethylamine psychedelia preferred more potent analogs. The United States explicitly scheduled it by name in the Food and Drug Administration Safety and Innovation Act of July 2012. Most other developed jurisdictions control it either by specific listing or through catch-all provisions targeting 2,5-dimethoxyphenethylamine derivatives.
The "2C" designation refers to the two carbon atoms separating the amine nitrogen from the aromatic ring — a naming convention Shulgin applied across the entire series. The trailing "C" denotes chlorine at the 4-position. Among users, 2C-C earned a reputation as the "quiet one" of the halogenated analogs — lower potency and a sedating character kept it a niche curiosity rather than a sought-after psychedelic.
Chemistry[edit]
Structural Class
2C-C belongs to the 2C family of phenethylamine psychedelics, which includes 2C-B, 2C-I, and 2C-F. All share the same molecular backbone — a 2,5-dimethoxyphenethylamine scaffold — with different atoms at the 4-position. In 2C-C, that atom is chlorine.
Within the halogenated series, larger halogens produce stronger serotonin receptor binding — iodine is most potent, then bromine, then chlorine — placing 2C-C at the lower end of potency.[4] Its hydrochloride salt melts at 220–222°C.[3]
Molecular Properties
| Molecular formula | C₁₀H₁₄ClNO₂ |
| Molecular weight | 215.67 g/mol |
Pharmacology[edit]
Mechanism of Action
2C-C activates serotonin receptors in the brain — the same targets responsible for psychedelic effects across all phenethylamine hallucinogens.[5][6] This triggers a chain of excitatory signals in the prefrontal cortex that disrupts normal sensory processing. Rat studies confirm the mechanism directly: blocking those receptors eliminates 2C-C's behavioral effects entirely.[7]
At high doses, 2C-C also activates dopamine reward pathways. Rodent studies found increased activity in the brain's reward center and altered dopamine signaling in the prefrontal cortex.[2] This may account for the preclinical abuse signals seen at elevated doses.
Pharmacokinetics
No human pharmacokinetic study has been published for 2C-C. Based on structural analogy with 2C-B, metabolism likely involves breakdown by liver enzymes and monoamine oxidase.[8]inferred 2C-C has also been identified as a breakdown product of 25C-NBOMe in human liver tissue.[8]
Neuroscience[edit]
Where It Acts
No neuroimaging data exist for 2C-C — the following is inferred from serotonergic psychedelic neuroscience generally. Serotonin receptors concentrate in the prefrontal cortex; when activated, they flood cortical neurons with excitatory signals that disrupt normal sensory filtering.[5][6] This also impairs the thalamus — the brain's sensory gatekeeper — producing the pattern overlay and sensory flooding characteristic of the 2C class.[9]
At high doses, 2C-C additionally recruits dopamine reward pathways. Rodent studies found increased neural activity in the brain's reward center and altered dopamine signaling in the prefrontal cortex.[2] This may explain the preclinical abuse signals found at elevated doses.
Theoretical Framework
One influential model proposes that serotonergic psychedelics flatten the brain's predictive hierarchy — weakening top-down expectations and allowing more raw sensory input to reach awareness. 2C-C's unusually quiet, sedating character raises the question of whether its lower potency produces a genuinely different pattern of brain activity compared to more stimulating analogs.
- Does 2C-C's sedating character reflect genuinely different network-level effects — such as less disruption of the default mode network — compared to stimulating analogs like 2C-B?
- At what dose does dopaminergic recruitment become significant in humans, and does it alter subjective experience or abuse liability?
- Does 2C-C promote neuroplastic changes at sub-hallucinogenic doses?
Subjective Effects[edit]
2C-C occupies an unusual niche in the 2C family. Where most analogs lean toward stimulation and visual intensity, 2C-C tends toward relaxation and quiet introspection. The experience builds slowly, settling into a contemplative space — soft visual enhancement, mild empathogenic warmth, and a pervasive calm that define the trip from beginning to end.
Relative to 2C-B, the most familiar reference in the halogenated series, 2C-C is less visually intense, less stimulating, and less socially activating. It sits closer to a gentle, reflective psychedelic than a recreational or social one — a distinction that makes set and setting especially important.
Synthesized by Alexander Shulgin and documented as entry #22 in PiHKAL (1991),[3][4] 2C-C has remained among the least explored of the 2C analogs. It never achieved the popularity of 2C-B or 2C-I, partly because synthesizing the chloro derivative is less convenient than bromination or iodination. It is now scheduled in most developed jurisdictions and circulates rarely on research chemical markets.
Subjective effects include geometric visual patterns, color enhancement, sedation, and empathogenic warmth. The experience is defined by an unusual stillness within the 2C family — a gentle, contemplative drift with soft visual overlay rather than energetic push. Slow onset, nausea, and mild body load are common unsought effects.
No physical dependence has been documented, and no human fatality has been attributed solely to 2C-C. Rodent studies reveal neurotoxicity markers and preclinical abuse signals at high doses,[5] complicating the assumption that serotonergic psychedelics carry negligible addiction risk; tolerance develops rapidly with cross-tolerance to other hallucinogens.[6] No controlled human study has been conducted — the safety profile rests entirely on class-level inference and limited animal data.
History[edit]
Discovery
2C-C was first synthesized by Alexander Shulgin at his private laboratory in Lafayette, California, as part of a systematic study of 4-position substituents on the 2,5-dimethoxyphenethylamine scaffold. The compound appears as entry #22 in PiHKAL: A Chemical Love Story (1991),[3] with the synthesis likely dating to the late 1970s or early 1980s. Shulgin described two routes — direct chlorination with liquid chlorine in glacial acetic acid, and halide exchange from 2C-B via cuprous chloride — noting that handling liquid chlorine was considerably less convenient than working with bromine or iodine.[4]
Market History
2C-C appeared on online research chemical markets in the late 1990s and early 2000s alongside the broader wave of 2C analogs entering recreational circulation. It never achieved the uptake of 2C-B or 2C-I — users seeking phenethylamine psychedelia typically preferred the more potent bromo or iodo analogs at lower doses. No clinical trials, therapeutic investigations, or institutional human studies have been conducted; the compound's entire human effects literature consists of Shulgin's self-experiments documented in PiHKAL.
Scheduling
The United States explicitly named 2C-C in the Food and Drug Administration Safety and Innovation Act (FSSIA) of July 2012, which scheduled multiple 2C analogs by name rather than relying solely on the Federal Analogue Act. Most other developed jurisdictions control 2C-C either by specific listing or through catch-all provisions targeting 2,5-dimethoxyphenethylamine derivatives.
The "2C" designation refers to the two carbon atoms separating the amine nitrogen from the aromatic ring — a naming convention Shulgin applied across the entire series. The trailing "C" denotes the chlorine substituent at the 4-position, following the same logic that gives 2C-B its bromine-derived name. Among users, 2C-C's reputation as the "quiet one" of the halogenated 2C analogs reflects both its lower potency and its sedating character — qualities that have kept it a niche curiosity rather than a sought-after psychedelic.
Chemistry[edit]
Structural Class
2C-C belongs to the 2C family of phenethylamine psychedelics, a series built on the 2,5-dimethoxyphenethylamine backbone with variable substituents at the 4-position. In 2C-C, the 4-position substituent is chlorine, placing it alongside 2C-B (bromine), 2C-I (iodine), and 2C-F (fluorine) in the halogenated sub-series.
Within this series, halogen size at the 4-position correlates with receptor affinity and potency: iodo > bromo > chloro > fluoro.[1] Chlorine's smaller atomic radius produces weaker hydrophobic interactions within the 5-HT₂A binding pocket, accounting for 2C-C's position at the lower end of the potency range among halogenated analogs.
Molecular Properties
| Molecular formula | C₁₀H₁₄ClNO₂ |
| Molecular weight | 215.67 g/mol |
The molecule comprises a phenethylamine core with methoxy groups at the 2- and 5-positions and a chlorine atom at the 4-position. The two methoxy groups provide the electron density and steric profile required for 5-HT₂A receptor recognition, while the chloro substituent modulates binding affinity and lipophilicity.
Stereochemistry
2C-C has no chirality center and exists as a single achiral compound. No stereoisomer considerations apply.
Physical Properties
The hydrochloride salt melts at 220–222°C.[4] No published data exist for solubility, pKa, or partition coefficient. The free base is expected to be a liquid or low-melting solid based on analogy with other 2C free bases.
Pharmacology[edit]
Mechanism of Action
2C-C acts as an agonist at serotonin 5-HT₂A and 5-HT₂C receptors — the same targets responsible for psychedelic effects across all phenethylamine hallucinogens. Binding at 5-HT₂A triggers a signaling cascade that increases excitatory neurotransmitter release onto prefrontal cortex neurons, disrupting the brain's normal sensory processing and producing perceptual distortion.[7][8]
The psychedelic response depends specifically on one branch of the 5-HT₂A signaling pathway (Gq-coupled) rather than another (β-arrestin2), a distinction confirmed through behavioral studies in mice.[9] In rats, 2C-C produces characteristic 5-HT₂A-mediated behaviors — wet dog shakes and back muscle contractions — completely blocked by the selective 5-HT₂A antagonist M100907, providing direct proof that its effects are 5-HT₂A-dependent.[2]
Beyond serotonin, high-dose 2C-C also activates the brain's dopamine mesolimbic pathway. Rodent studies found increased neural activity in the nucleus accumbens and altered dopamine receptor expression in both the nucleus accumbens and prefrontal cortex.[5] This dopaminergic recruitment may contribute to the compound's preclinical abuse signals and any stimulant-like properties at higher doses.
Pharmacokinetics
No human pharmacokinetic study has been published for 2C-C. All parameters below are inferred from structural analogy with 2C-B and class pharmacology.
Oral administration is the primary route, with onset at 20–45 minutes and full effects at approximately 1.5–2 hours.[4][10] Total duration runs 4–8 hours, with a 2–3 hour peak.[4][10] Intravenous administration of 20 mg produced overwhelming effects peaking within approximately 5 minutes, consistent with bypassing first-pass metabolism.[4]
Metabolism has not been directly studied. Based on structural analogy with 2C-B, primary routes likely include breakdown by liver enzymes and monoamine oxidase.[11]inferred 2C-C has also been identified as a metabolite of 25C-NBOMe through N-dealkylation in human liver microsomes.[11]
Key pharmacokinetic parameters — peak blood levels, half-life, oral bioavailability, and protein binding — remain entirely uncharacterized in humans.
Neuroscience[edit]
Where It Acts
No direct neuroimaging or electrophysiology data exist for 2C-C. The following is inferred from class-level neuroscience of serotonin 2A receptor agonist psychedelics.
5-HT₂A receptors concentrate on neurons in the prefrontal cortex. When activated, they increase excitatory signaling that disrupts normal cortical processing — the cellular trigger for perceptual distortion across all phenethylamine psychedelics.[7][8] This cortical disruption also impairs the thalamus's ability to filter sensory input, producing the sensory flooding and pattern overlay characteristic of the 2C class.[12]
At high doses, 2C-C additionally recruits the dopamine mesolimbic pathway. Rodent studies found increased neural activation in the nucleus accumbens and altered dopamine signaling in the prefrontal cortex[5] — a finding that may explain preclinical indicators of abuse potential.
Theoretical Framework
The REBUS (Relaxed Beliefs Under Psychedelics) model proposes that 5-HT₂A agonists flatten the brain's predictive processing hierarchy, weakening top-down expectations and allowing more bottom-up sensory information to reach awareness. 2C-C's reportedly quiet, sedating character — unusual for the 2C class — raises the question of whether its lower potency or unique receptor interactions produce a distinct pattern of brain activity compared to more stimulating analogs.
5-HT₂A agonists are also known to promote structural brain changes (dendritic growth, new synaptic connections) through downstream signaling cascades. Whether 2C-C shares these neuroplastic properties is unknown but expected given its confirmed 5-HT₂A activity.
- Does 2C-C's sedating character reflect genuinely different network-level effects — such as less disruption of the default mode network — compared to stimulating analogs like 2C-B?
- At what dose does dopaminergic recruitment become significant in humans, and does it alter subjective experience or abuse liability?
- Does 2C-C promote neuroplastic changes at sub-hallucinogenic doses?
Subjective Effects[edit]
2C-C occupies an unusual niche within the 2C family: where most analogs push toward stimulation and visual intensity, 2C-C trends toward relaxation and gentle introspection. The experience builds slowly — up to two hours to full effects — and settles into a contemplative space with soft visual enhancement, mild empathogenic warmth, and a pervasive calm. Set and setting strongly modulate the experience, as with all serotonergic psychedelics, but the compound's intrinsic character consistently favors stillness over energy.
Relative to 2C-B, the most familiar reference point in the halogenated series, 2C-C is less visually intense, less stimulating, and less socially activating at comparable effect levels. It sits closer to a quiet, reflective psychedelic than a recreational or social one.
Effect Grid
At common doses (30–50 mg oral), the full psychedelic experience develops. Visual phenomena become pronounced — color saturation intensifies, geometric patterns overlay surfaces, mild drifting and morphing of objects occurs, and closed-eye visuals emerge as complex imagery. Auditory enhancement adds depth to music. Cognitive effects include enhanced introspection, novel thought connectivity, and mild time distortion. Emotional tone is warm and introspective — 2C-C produces mild empathogenic warmth without the stimulant drive of 2C-B.
Physically, the experience is characterized by relaxation rather than stimulation. Pupil dilation is marked. Mild nausea during come-up resolves by peak. Heart rate and blood pressure elevation are expected but typically mild at this range. Body load is generally light.
Sleep is impossible during the 2–3 hour peak. Total experience commitment is 5–8 hours. The slow come-up (up to 2 hours) requires patience — redosing before full onset is a common error.
Modeled from the effect's dose-dependence curve — not per-substance measurements.
Geometry · Visual breathing · Tracers · Auditory enhancement · Brightness alteration · Light sensitivity · Touch enhancement · Auditory distortion · After-images · Depth perception distortion · Environmental patterning · Peripheral vision distortion · Perspective distortion · Sound sensitivity · Symmetrical texture repetition · Visual diffraction · Visual haze / noise · Visual morphing · Visual acuity enhancement · Auditory misinterpretation · Proprioceptive distortion · Spatial disorientation · Visual melting · Dreaming enhancement · Synesthesia · Vestibular distortion · Visual magnification · Olfactory enhancement · Taste enhancement · Visual processing acceleration · Internal hallucinations · Object transformations · External hallucinations · Object activation · Visual recursion · Auditory hallucinations · Environmental orbism / cubism
Brightness alteration · Light sensitivity · Touch enhancement · Auditory distortion · After-images · Depth perception distortion · Environmental patterning · Peripheral vision distortion · Perspective distortion · Sound sensitivity · Symmetrical texture repetition · Visual diffraction · Visual haze / noise · Visual morphing · Visual acuity enhancement · Auditory misinterpretation · Proprioceptive distortion · Spatial disorientation · Visual melting · Dreaming enhancement · Synesthesia · Vestibular distortion · Visual magnification · Olfactory enhancement · Taste enhancement · Visual processing acceleration · Internal hallucinations · Object transformations · External hallucinations · Object activation · Visual recursion · Auditory hallucinations · Environmental orbism / cubism
Stimulation · Nausea · Appetite suppression · Body high · Heart rate perception changes · Tingling / electric sensations · Muscle tension · Wakefulness · Dehydration sensation · Dizziness · Dry mouth · Insomnia · Physical fatigue · Tactile euphoria · Excessive sweating · Sexual arousal enhancement · Laughter fits · Restlessness · Vasoconstriction · Vibrations / buzzing · Abnormal heartbeat · Bruxism · Bodily heaviness · Bodily lightness · Bodily pressures · Body schema distortion · Breathing alteration · Headache · Nystagmus (eye wobbles) · Sedation · Trembling · Involuntary body movements · Vomiting · Motor control enhancement · Tactile hallucination
Body high · Heart rate perception changes · Tingling / electric sensations · Muscle tension · Wakefulness · Dehydration sensation · Dizziness · Dry mouth · Insomnia · Physical fatigue · Tactile euphoria · Excessive sweating · Sexual arousal enhancement · Laughter fits · Restlessness · Vibrations / buzzing · Abnormal heartbeat · Bruxism · Bodily heaviness · Bodily lightness · Bodily pressures · Body schema distortion · Breathing alteration · Headache · Nystagmus (eye wobbles) · Sedation · Trembling · Involuntary body movements · Vomiting · Motor control enhancement · Tactile hallucination
Conceptual thinking · Immersion enhancement · Thought connectivity · Cognitive euphoria · Cognitive flexibility · Introspection enhancement · Openness enhancement · Humor enhancement · Memory suppression · Thought acceleration · Creativity enhancement · Increased nature relatedness · Multiple thought streams · Analysis enhancement · Cognitive fatigue · Cognitive impairment · Confusion · Focus suppression · Information processing suppression · Memory replays · Thought loops · Cognitive dysphoria · Language suppression · Memory fragmentation · Motivation suppression · Synchronicity · Thought disorganization
Cognitive flexibility · Introspection enhancement · Openness enhancement · Humor enhancement · Memory suppression · Thought acceleration · Creativity enhancement · Increased nature relatedness · Multiple thought streams · Analysis enhancement · Cognitive fatigue · Cognitive impairment · Confusion · Focus suppression · Information processing suppression · Memory replays · Thought loops · Cognitive dysphoria · Language suppression · Memory fragmentation · Motivation suppression · Synchronicity · Thought disorganization
Simultaneous emotions · Empathy enhancement · Anxiety · Catharsis · Anxiety suppression · Dysphoria · Irritability
Anxiety suppression · Dysphoria · Irritability
Disinhibition · Trust enhancement · Communication enhancement · Communication suppression · Depersonalization · Flow state · Boundary dissolution · Identity alteration · Ego dissolution
Depersonalization · Flow state · Boundary dissolution · Identity alteration · Ego dissolution
Time cessation
Recursive awareness
Timeline
First alerts appear 20–45 minutes after ingestion — subtle mood shift, faint bodily awareness, possible mild stomach sensation. Effects are easily overlooked at this stage.
A notably slow come-up distinguishes 2C-C from faster 2C analogs. Effects build gradually over 45–90 minutes with emerging color enhancement, gentle body warmth, and mild cognitive shift. Patience is required — premature redosing is a common error.
Full effects plateau for 2–3 hours. Visual phenomena, introspective cognition, and emotional warmth reach maximum intensity. The character is relaxed rather than stimulating — described as "a very intense form of relaxation" at common doses.
Effects gradually diminish over 1–3 hours. Visual phenomena fade first, followed by cognitive and emotional return toward baseline. Physical relaxation may persist.
Residual mood elevation, mild perceptual sensitivity, and physical relaxation may persist for 2–6 hours after primary effects resolve. Cognitive function returns to near-baseline but subtle shifts in emotional tone may continue.
⚠ Do not drive or operate machinery until the following day, as residual perceptual sensitivity and impaired reaction time may persist beyond subjective awareness of effects.
Safety[edit]
- Acute toxicity
- Low
- Chronic toxicity
- Moderate
- Withdrawal
- None
- Tolerance buildup
- rapid
- Tolerance reset
- 14 days
- Physical
- None
- Psychological
- Low
- Compulsive redosing
- Negligible
- Dose escalation
- Negligible
- Cross-tol.
- 2C-B · 2C-I · 2C-E
Toxicity
Acute Toxicity
No lethal dose has been established for 2C-C in any species, and no human death has been attributed solely to the compound. The one fatality where 2C-C was detected involved 25C-NBOMe poisoning — 2C-C appeared only as a trace metabolite of the actual toxic agent.[10]
Class-level acute risks for 2C compounds include agitation, hallucinations, high blood pressure, rapid heart rate, seizures, and dangerously elevated body temperature.[11] At least five deaths have been reported across the broader 2C class — primarily involving 2C-E and 2C-T-7.[11]
Cardiovascular Effects
5-HT₂A activation constricts blood vessels and stimulates the heart — elevated blood pressure and heart rate are expected. This cardiovascular stress is confirmed for 2C-B at standard doses;[12] 2C-C is expected to produce similar effects, possibly at higher absolute doses given its lower potency.
Dangerous blood pressure elevation and heart rhythm disturbances have been documented across the 2C and NBOMe classes.[13]
Neurotoxicity (Preclinical)
Rodent studies at high doses found impaired movement and coordination, memory deficits, brain inflammation in the striatum, and altered dopamine signaling.[2] The doses involved are not specified in the published data, and extrapolation to human-relevant amounts requires caution. safety citation needed
Detection Limitations
Standard drug screens do not detect 2C compounds, creating a risk of unrecognized intoxication in emergency settings.[14] Specialized laboratory testing is required for confirmation.[15]
Psychological Risks
No study quantifies psychological adverse event rates for 2C-C specifically. Class-level risks for serotonergic psychedelics include acute anxiety, panic, paranoia, dysphoria, and confusion — with risk scaling with dose and personal vulnerability.[11]
Other possible risks include persistent visual disturbances after use (no 2C-C-specific data), psychosis precipitation in people with personal or family history of psychotic disorders, and depersonalization or derealization that is usually transient. 2C-C's milder, sedating profile may carry lower acute distress risk than more stimulating analogs, though this remains unverified.
Tolerance and Dependence
Tolerance builds within 24 hours of a single dose, through serotonin downregulation in the brain.[16] Cross-tolerance extends to other phenethylamine hallucinogens and to tryptamine psychedelics, with phenethylamines developing tolerance more rapidly than tryptamines.[17] Repeated use at intervals shorter than roughly 7–14 days produces diminishing effects.
No physical dependence or withdrawal has been documented for 2C-C. However, rodent studies found dose-dependent signs of abuse potential — preclinical indicators that challenge the conventional "non-addictive" characterization of serotonergic psychedelics.[2][13]
Drug Interactions
Serotonergic Combinations
Tramadol (dangerous): tramadol raises serotonin levels; combined with 2C-C's serotonin receptor activation, the risk of serotonin syndrome rises substantially — a potentially life-threatening state involving dangerous body temperature elevation, muscle rigidity, and altered mental state.[18] safety citation needed
MAOIs (dangerous): Monoamine oxidase inhibitors block the primary breakdown pathway for phenethylamines, dramatically amplifying and prolonging effects while simultaneously elevating serotonin syndrome risk through multiple converging mechanisms. safety citation needed
SSRIs/SNRIs: Long-term use typically reduces psychedelic effects through receptor downregulation. Acute high-dose combinations may increase serotonin syndrome risk.
Stimulant Combinations
Stimulants compound the cardiovascular stress of 2C-C — elevated blood pressure and heart rate add together with each substance. The dopaminergic activity demonstrated at high doses[2] may further compound with dopaminergic stimulants.
Cannabis
No published interaction data exist. Cannabis may unpredictably enhance psychological distress or psychotic-like experiences.
Lithium
Lithium combined with serotonergic psychedelics has been associated with seizure risk in community reports. No controlled data exist for this interaction with any 2C compound. safety citation needed
Contraindications
8 knownAbsolute
- Concurrent MAOI use: Dangerous potentiation and serotonin syndrome risk.
- Personal history of psychotic disorders: All 5-HT₂A agonists carry risk of psychosis precipitation.
- Concurrent lithium use: Seizure risk.
Relative
- Heart conditions: High blood pressure, coronary artery disease, or irregular heart rhythm increase cardiac event risk under sympathomimetic load.
- Family history of psychotic disorders: Elevated risk of psychosis precipitation.
- Bipolar disorder: Risk of manic episode.
- Liver impairment: Presumed liver metabolism; impaired clearance could prolong or intensify effects.
- Pregnancy and breastfeeding: No safety data exist.
- Concurrent tramadol use: Serotonin syndrome risk.
Harm Reduction[edit]
Forms & Identification
2C-C most commonly circulates as a white to off-white powder sold as the hydrochloride salt. Because 2C compounds are visually indistinguishable from each other in powder form, reagent testing is essential — not to confirm identity with certainty, but to rule out dangerous substitutions such as NBOMe compounds, which are active at far lower doses and carry significantly higher risk.
A milligram-precision scale (0.001g) is non-negotiable for powder dosing. The difference between a threshold and a strong dose spans only 15–20 mg — an amount invisible to the naked eye.
Guidelines
- Always reagent-test material before use and weigh doses with a milligram-precision scale.
- Start with the lower end of the dose range, especially with untested material or no prior 2C-C experience.
- Allow a minimum of two hours before considering whether effects have fully developed — 2C-C's onset is slower than most 2C analogs.
- Have a sober, trusted person present who knows what was taken and when.
- Eat a light meal 2–3 hours beforehand to reduce nausea; avoid heavy food immediately before dosing.
- Stay hydrated but do not overdrink — moderate sipping is sufficient.
- Keep the environment comfortable, quiet, and controllable. Have blankets, water, and calming music accessible.
- Do not drive, operate machinery, or make important decisions during the experience.
Set & Setting
2C-C's slow onset — up to two hours before full effects — demands patience. Premature redosing because "nothing is happening" is the most common dosing error with this compound and can result in an unexpectedly intense experience.
Choose a calm, familiar environment with trusted company. The sedating character makes a comfortable space to sit or lie down more important than an activity-rich setting.
Aftercare & integration. The sedating character of 2C-C often leaves users feeling physically drained rather than mentally overstimulated. Prioritize sleep, light nutrition, and gentle activity in the 24 hours following. Avoid stimulants, alcohol, and other psychoactives during this window.
If the experience raised difficult emotions or unexpected psychological material, write about it within a day or two while memories are fresh. Talking with a trusted friend or therapist experienced with psychedelic integration can help. Persistent anxiety, depersonalization, or visual disturbances lasting more than a few days warrant professional consultation.
Recovery & Support
2C-C does not produce physical dependence, but any pattern of psychedelic use that becomes compulsive, escapist, or interferes with daily functioning deserves attention. If use is escalating in frequency or serving as avoidance, peer support communities and psychedelic-informed therapists can help. Organizations such as the Fireside Project (62-FIRESIDE / 623-473-7433) offer free, confidential support for people processing difficult psychedelic experiences.
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Recognizing an emergency: Most uncomfortable experiences — anxiety, nausea, mild confusion — are distressing but not dangerous. Seek immediate help if any of the following occur: seizure, loss of consciousness, chest pain, body temperature hot to the touch, self-harm behavior, or complete disconnection from reality with inability to respond to voice.
Immediate steps:
- Call emergency services if any red-flag symptoms appear.
- Keep the person in a safe, quiet space. Do not restrain them unless there is immediate danger of self-harm.
- If unconscious but breathing, place in the recovery position (on their side).
- Do not induce vomiting.
- Monitor breathing and body temperature while waiting for help.
What to tell the dispatcher: Name the substance (2C-C, a synthetic psychedelic), estimated amount taken, time of ingestion, and current symptoms. Good Samaritan laws in many jurisdictions protect people who call for help during a drug-related emergency.
Legal Status[edit]
2C-C is controlled in most developed jurisdictions, either by specific name or through structural class provisions targeting 2,5-dimethoxyphenethylamine derivatives; it is not scheduled under the United Nations 1971 Convention on Psychotropic Substances.
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| United States | Schedule I (Controlled Substances Act) | Explicitly named in the Food and Drug Administration Safety and Innovation Act (FSSIA), July 2012. Federal Analogue Act may also apply to earlier periods. |
| United Kingdom | Class A (Misuse of Drugs Act 1971) | Controlled under catch-all provisions covering 2,5-dimethoxyphenethylamine derivatives, amended 2002. |
| Canada | Schedule III (CDSA) | Catch-all provision for 2C-phenethylamines, Schedule III item 35.[19] |
| Sweden | Health hazard classification | Controlled under the Act on Prohibition of Certain Goods Dangerous to Health since March 1, 2005. |
| China | Controlled substance | Included in government decree on psychoactive substances, October 2015. |
| Australia | Likely Schedule 9 (Prohibited Substance) | Not individually confirmed; likely falls under same class provisions as 2C-I. citation needed |
Analog Law Considerations
Prior to the 2012 FSSIA, prosecution in the United States could be pursued under the Federal Analogue Act, which treats substances "substantially similar" to a Schedule I compound as equivalent when intended for human consumption. 2C-C's structural similarity to 2C-B (scheduled in 1995) provided a basis for such prosecution.
Legal status changes frequently and varies by jurisdiction. This page is not legal advice.
Safety[edit]
- Acute toxicity
- Low
- Chronic toxicity
- Moderate
- Withdrawal
- None
- Tolerance buildup
- rapid
- Tolerance reset
- 14 days
- Physical
- None
- Psychological
- Low
- Compulsive redosing
- Negligible
- Dose escalation
- Negligible
- Cross-tol.
- 2C-B · 2C-I · 2C-E
Toxicity
Acute Toxicity
No lethal dose has been determined for 2C-C in any species, and no human death has been attributed solely to the compound. The only case identifying 2C-C in a fatality involved 25C-NBOMe poisoning, where 2C-C was detected at trace concentrations as a metabolite of the primary toxic agent.[13]
Class-level acute toxicity for 2C compounds includes agitation, hallucinations, aggression, high blood pressure, rapid heart rate, seizures, and dangerously elevated body temperature.[14] At least five deaths have been reported across the broader 2C class — primarily involving 2C-E and 2C-T-7 — with excited delirium as a consistent finding among fatalities.[14]
Cardiovascular Effects
Blood pressure and heart rate elevation are expected from 5-HT₂A-mediated vasoconstriction and adrenergic activation. Published data for 2C-B confirmed increased blood pressure and heart rate at standard doses.[15] 2C-C is expected to produce similar cardiovascular stress, though potentially at higher absolute doses given its lower potency. Gil-Martins et al. reviewed cardiovascular complications across the 2C and NBOMe classes, including dangerous blood pressure elevation and heart rhythm disturbances.[16]
Neurotoxicity (Preclinical)
Rodent studies at high doses documented neurotoxic effects including impaired movement and coordination, memory deficits across multiple tests, brain inflammation (microglial activation) in the striatum, and altered dopamine signaling.[5] The specific doses producing these effects are not available from published data, and extrapolation to human-relevant doses requires caution. safety citation needed
Detection Limitations
Standard drug screens do not detect 2C compounds, creating a risk of unrecognized intoxication in emergency settings.[17] Specialized laboratory testing (LC-MS/MS) is required for confirmation.[18]
Psychological Risks
No study quantifies psychological adverse event rates for 2C-C specifically. Class-level risks for 5-HT₂A agonist psychedelics include:
- Acute psychological distress: anxiety, panic, paranoia, dysphoria, and confusion, with risk scaling with dose and vulnerability. Agitation, aggression, and dysphoria appear among 2C class intoxication presentations.[14]
- Hallucinogen persisting perception disorder (HPPD): Persistent visual disturbances following use. No 2C-C-specific data exist.
- Psychosis precipitation: Primarily a risk for individuals with personal or family history of psychotic disorders.
- Depersonalization/derealization: Usually transient during acute effects; rarely persistent.
2C-C's reportedly milder, more sedating profile may carry lower acute distress risk compared to more stimulating analogs, though this remains unverified.
Tolerance and Dependence
Tolerance develops rapidly — within 24 hours of a single dose — through downregulation in the brain.[19] Cross-tolerance exists between phenethylamine hallucinogens and extends to tryptamine psychedelics, with phenethylamine compounds developing tolerance more rapidly than tryptamines.[6] Repeated use at intervals shorter than approximately 7–14 days produces diminishing effects.
No physical dependence or withdrawal has been documented for 2C-C or the 2C class. However, rodent studies found dose-dependent conditioned place preference and increased self-administration — preclinical indicators of abuse potential that challenge the conventional "non-addictive" characterization of serotonergic psychedelics.[5] Gil-Martins et al. further examined abuse potential across the 2C and NBOMe classes.[16]
Drug Interactions
Serotonergic Combinations
Tramadol (dangerous): tramadol's serotonin-boosting properties combined with 2C-C's serotonin receptor activation create a substantially elevated risk of serotonin syndrome — a potentially life-threatening condition involving dangerous body temperature elevation, muscle rigidity, and altered mental state.[20] safety citation needed
MAOIs (dangerous): Monoamine oxidase inhibitors block the primary breakdown pathway for phenethylamines, dramatically amplifying and prolonging effects while simultaneously elevating serotonin syndrome risk through multiple converging mechanisms. safety citation needed
SSRIs/SNRIs: Long-term use typically reduces psychedelic effects through receptor downregulation. Acute high-dose combinations may increase serotonin syndrome risk.
Stimulant Combinations
Combined stimulant effects create additive cardiovascular stress — elevated blood pressure and heart rate compound with each substance. The dopaminergic activity demonstrated for 2C-C at high doses[5] may further compound with dopaminergic stimulants.
Cannabis
No published interaction data exist. Cannabis may unpredictably enhance psychological distress or psychotic-like experiences.
Lithium
Lithium combined with serotonergic psychedelics has been associated with seizure risk in community reports. No controlled data exist for this interaction with any 2C compound. safety citation needed
Contraindications
8 knownAbsolute
- Concurrent MAOI use: Dangerous potentiation and serotonin syndrome risk.
- Personal history of psychotic disorders: All 5-HT₂A agonists carry risk of psychosis precipitation.
- Concurrent lithium use: Seizure risk.
Relative
- Heart conditions: High blood pressure, coronary artery disease, or irregular heart rhythm increase cardiac event risk under sympathomimetic load.
- Family history of psychotic disorders: Elevated risk of psychosis precipitation.
- Bipolar disorder: Risk of manic episode.
- Liver impairment: Presumed liver metabolism; impaired clearance could prolong or intensify effects.
- Pregnancy and breastfeeding: No safety data exist.
- Concurrent tramadol use: Serotonin syndrome risk.
Harm Reduction[edit]
Forms & Identification
2C-C most commonly circulates as a white to off-white powder sold as the hydrochloride salt. Because 2C compounds are visually indistinguishable from each other in powder form, reagent testing is essential — not to confirm identity with certainty, but to rule out dangerous substitutions such as NBOMe compounds, which are active at far lower doses and carry significantly higher risk. A milligram-precision scale (0.001g) is non-negotiable for powder dosing, as the difference between a threshold and a strong dose spans only 15–20 mg.
Guidelines
- Always reagent-test material before use and weigh doses with a milligram-precision scale.
- Start with the lower end of the dose range, especially with untested material or no prior 2C-C experience.
- Allow a minimum of two hours before considering whether effects have fully developed — 2C-C's onset is slower than most 2C analogs.
- Have a sober, trusted person present who knows what was taken and when.
- Eat a light meal 2–3 hours beforehand to reduce nausea; avoid heavy food immediately before dosing.
- Stay hydrated but do not overdrink — moderate sipping is sufficient.
- Keep the environment comfortable, quiet, and controllable. Have blankets, water, and calming music accessible.
- Do not drive, operate machinery, or make important decisions during the experience.
Set & Setting
2C-C's slow onset — up to two hours before full effects — demands patience. Premature redosing because "nothing is happening" is the most common dosing error with this compound and can result in an unexpectedly intense experience. Choose a calm, familiar environment with trusted company. The sedating character makes a comfortable space to sit or lie down more important than an activity-rich setting.
Aftercare & integration. The sedating character of 2C-C often leaves users feeling physically drained rather than mentally overstimulated. Prioritize sleep, light nutrition, and gentle activity in the 24 hours following. Avoid stimulants, alcohol, and other psychoactives during this window.
If the experience raised difficult emotions or unexpected psychological material, write about it within a day or two while memories are fresh. Talking with a trusted friend or therapist experienced with psychedelic integration can help contextualize challenging experiences. Persistent anxiety, depersonalization, or visual disturbances lasting more than a few days warrant professional consultation.
Recovery & Support
2C-C does not produce physical dependence, but any pattern of psychedelic use that becomes compulsive, escapist, or interferes with daily functioning deserves attention. If use is escalating in frequency or serving as avoidance, peer support communities and psychedelic-informed therapists can help. Organizations such as the Fireside Project (62-FIRESIDE / 623-473-7433) offer free, confidential support for people processing difficult psychedelic experiences.
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Recognizing an emergency: Most uncomfortable experiences — anxiety, nausea, mild confusion — are distressing but not dangerous. Seek immediate help if any of the following occur: seizure, loss of consciousness, chest pain, body temperature hot to the touch, self-harm behavior, or complete disconnection from reality with inability to respond to voice.
Immediate steps:
- Call emergency services if any red-flag symptoms appear.
- Keep the person in a safe, quiet space. Do not restrain them unless there is immediate danger of self-harm.
- If unconscious but breathing, place in the recovery position (on their side).
- Do not induce vomiting.
- Monitor breathing and body temperature while waiting for help.
What to tell the dispatcher: Name the substance (2C-C, a synthetic psychedelic), estimated amount taken, time of ingestion, and current symptoms. Good Samaritan laws in many jurisdictions protect people who call for help during a drug-related emergency.
Legal Status[edit]
2C-C is controlled in most developed jurisdictions, typically captured by specific naming in scheduling legislation or by structural class provisions targeting 2,5-dimethoxyphenethylamine derivatives. It is not scheduled under the United Nations 1971 Convention on Psychotropic Substances, leaving individual nations to determine their approach.
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| United States | Schedule I (Controlled Substances Act) | Explicitly named in the Food and Drug Administration Safety and Innovation Act (FSSIA), July 2012. Federal Analogue Act may also apply to earlier periods. |
| United Kingdom | Class A (Misuse of Drugs Act 1971) | Controlled under catch-all provisions covering 2,5-dimethoxyphenethylamine derivatives, amended 2002. |
| Canada | Schedule III (CDSA) | Catch-all provision for 2C-phenethylamines, Schedule III item 35.[21] |
| Sweden | Health hazard classification | Controlled under the Act on Prohibition of Certain Goods Dangerous to Health since March 1, 2005. |
| China | Controlled substance | Included in government decree on psychoactive substances, October 2015. |
| Australia | Likely Schedule 9 (Prohibited Substance) | Not individually confirmed; likely falls under same class provisions as 2C-I. citation needed |
Analog Law Considerations
Prior to the 2012 FSSIA, prosecution in the United States could be pursued under the Federal Analogue Act, which treats substances "substantially similar" to a Schedule I compound as equivalent when intended for human consumption. 2C-C's structural similarity to 2C-B (scheduled in 1995) provided a basis for such prosecution, though the Act's requirement to prove both structural and pharmacological similarity created legal ambiguity.
Frequently asked questions
What is 2C-C?
2C-C is a synthetic phenethylamine psychedelic of the 2C family, featuring a 4-chloro substituent on the 2,5-dimethoxyphenethylamine scaffold. First synthesized by Alexander Shulgin and documented in PiHKAL (1991), it acts as a 5-HT₂A and 5-HT₂C receptor agonist.
How long does 2C-C last?
Total duration by route of administration — Oral: 4 – 8 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-C?
Psychedex publishes a dosage table for 2C-C 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-C?
The highest-severity documented interactions for 2C-C: 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-C addictive?
Psychedex records tolerance and dependence data rather than a yes/no rating. Recorded tolerance indicators for 2C-C: tolerance builds rapid; full reset takes 14 days; cross-tolerance develops with 2C-B, 2C-I, 2C-E, LSD, psilocybin, DMT, mescaline, DOI. See the article's dependence and safety sections for recorded dependence data.
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First-person accounts of subjective effects, timing, and outcomes — submitted for harm reduction.
references
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- [4] ^Nichols DE (2018) Chemistry and Structure-Activity Relationships of Psychedelics. — Current Topics in Behavioral Neurosciences doi:10.1007/7854_2017_475
- [5] ^abAghajanian GK, Marek GJ (1997) Serotonin induces excitatory postsynaptic potentials in apical dendrites of neocortical pyramidal cells — Neuropharmacology PMID:9225284
- [6] ^abAghajanian GK, Marek GJ (1999) Serotonin, via 5-HT2A receptors, increases EPSCs in layer V pyramidal cells of prefrontal cortex by an asynchronous mode of glutamate release — Brain Research PMID:10216183
references
- [1] ^abNichols DE (2018) Chemistry and Structure-Activity Relationships of Psychedelics. — Current Topics in Behavioral Neurosciences doi:10.1007/7854_2017_475
- [2] ^abElmore JS, Decker AM, Sulima A, Rice KC, Partilla JS, Blough BE, Baumann MH (2018) Comparative neuropharmacology of N-(2-methoxybenzyl)-2,5-dimethoxyphenethylamine (NBOMe) hallucinogens and their 2C counterparts in male rats — Neuropharmacology doi:10.1016/j.neuropharm.2018.02.033
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- [6] ^abSmith DA, Bailey JM, Williams D, Fantegrossi WE (2014) Tolerance and cross-tolerance to head twitch behavior elicited by phenethylamine- and tryptamine-derived hallucinogens in mice. — The Journal of pharmacology and experimental therapeutics doi:10.1124/jpet.114.219337