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2C-P
2,5-dimethoxy-4-propylphenethylamine
2C-P (2,5-dimethoxy-4-propylphenethylamine) is a synthetic psychedelic of the phenethylamine class. It is the most potent and longest-acting member of the 2C series, with an unusually narrow margin between a common and a dangerous dose. It activates serotonin receptors in the brain, producing the visual and cognitive shifts characteristic of classical psychedelics.
2C-P (2,5-dimethoxy-4-propylphenethylamine) is a synthetic psychedelic of the phenethylamine class. It is the most potent and longest-acting member of the 2C series, distinguished by an exceptionally narrow dosing margin. 2C-P is a 5-HT₂A receptor agonist, producing its effects by disrupting serotonin-mediated sensory filtering and cortical processing.
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Alexander Shulgin first synthesized 2C-P and documented it in PiHKAL (1991).[1] It circulated on online research chemical markets through the 2000s before the United States scheduled it in 2012.[2] It remains available on illicit markets, and emergency case reports confirm continued use.[3]
Subjective effects include geometric visual patterns, time alteration, conceptual thinking, euphoria, and ego dissolution. The experience is defined by its length — a slow-building, all-day alteration of perception and cognition demanding more planning and endurance than most psychedelics. Severe body load, prolonged agitation, and overwhelming confusion are characteristic unwanted effects, worsening sharply with small dose increases.
Physical dependence risk is low — rapid tolerance after a single dose limits compulsive use[4][5] — but the steep dose–response curve makes acute overdose a real hazard. The slow onset is the dominant danger: premature redosing can push a session into cardiovascular crisis.[6] Evidence is extremely limited — Shulgin's self-experiments, a handful of emergency case reports, and one rodent study[7] are the entire record.
History[edit]
Discovery
Alexander Shulgin first synthesized 2C-P and published it as entry #35 in PiHKAL (1991), naming it "Selene" after the Greek moon goddess.[1] His self-experiments established an active dose range of 6–10 mg and a duration of 10–16 hours. He also documented 16 mg as a "clear overdose" and "physical disaster" — the most important safety observation in the compound's entire record.[1]
Market appearance and scheduling
After PiHKAL was published, 2C-P began circulating through online research chemical vendors in the 2000s. The United States placed it under Schedule I in 2012 via the synthetic Drug Abuse Prevention Act;[2] Germany followed in 2014, and Canada in 2016.[8] No clinical trials have ever been conducted.
Clinical documentation
Two published reports document 2C-P in clinical settings. A 2015 case series described five young males presenting with serotonin syndrome after recreational use.[6] A 2017 Swiss report described a patient who unknowingly ingested 2C-P sold as 2C-B, yielding the first pharmacokinetic estimate and confirming the adulterant risk of unregulated supply.[3]
Shulgin's name "Selene" — after the Greek moon goddess — reflects his practice of assigning personal names to favored compounds.[1] Even within experienced psychedelic communities, 2C-P carries a cautious reputation — its unforgiving dose–response curve and marathon length invite comparison to DOM, another long-duration psychedelic, though the two belong to different chemical families.
Chemistry[edit]
Structural class
2C-P belongs to the 2C-X family of phenethylamines. Its defining feature is an n-propyl chain at the 4-position of the aromatic ring — longer than the substituents on 2C-B, 2C-I, and 2C-E.
Across the 2C series, larger 4-position substituents correlate with higher receptor affinity and longer duration,[9] which accounts for 2C-P being both the most potent and the longest-acting of the group.
Molecular properties
| Molecular formula | C₁₃H₂₁NO₂ |
| Molecular weight | 223.31 g/mol |
Pharmacology[edit]
Mechanism of action
2C-P activates serotonin receptors in the brain — the same target responsible for psychedelic effects across the entire 2C family.[7][5][10] In rodents, blocking these receptors fully eliminates 2C-P's effects, confirming they are the primary driver.[7] The propyl substituent makes 2C-P bind more strongly and act longer than shorter-chain relatives in the same family.[9]
Secondary targets
Like other 2C compounds, 2C-P may weakly inhibit the enzymes that break down serotonin (monoamine oxidase) at concentrations reached in the body.[11] Whether this is clinically meaningful at recreational doses is unknown, but it creates a theoretical basis for dangerous interactions with other serotonergic drugs. At high doses in rodents, it also altered dopamine signaling in reward-related brain areas.[7]
Pharmacokinetics
The body breaks down 2C-P through multiple liver pathways — including removing methoxy groups and conjugation reactions.[12][13] The best available estimate of half-life is approximately 19 hours, derived from a single emergency case.[3] This explains both the all-day duration and why complications can persist long after the peak.
Neuroscience[edit]
Where it acts
2C-P activates neurons in the prefrontal cortex — the brain's filtering layer for sensory information. When this filtering is disrupted, raw perceptions and emotions break through the brain's usual editing process, producing hallucinations and altered thought patterns. No neuroimaging data exist for 2C-P; these effects are inferred from research on psilocybin and LSD.citation needed
Why it matters
The most useful framework for 2C-P's effects: the brain ordinarily predicts what it is about to perceive, relying on past experience as a shortcut rather than processing everything fresh. 2C-P disrupts this prediction process, giving raw sensory and emotional signals greater access to conscious experience. 2C-P's all-day duration may produce deeper destabilization of these patterns than shorter-acting psychedelics — though this remains speculative.
At high doses in rodents, 2C-P also altered dopamine signaling and triggered brain inflammation in the striatum.[7] Whether this occurs in humans at recreational doses is unknown.
- Does 2C-P promote structural neuroplasticity via the signaling pathways demonstrated for other serotonergic psychedelics?
- What drives the dopaminergic effects at high doses — direct receptor activity or indirect modulation through serotonin-dopamine interactions?
- Does prolonged receptor engagement produce qualitatively different patterns of brain reorganization compared to shorter-acting compounds?
Subjective Effects[edit]
The experience is defined by its length above all else. The altered state builds slowly and then holds for the better part of a waking day — a commitment that shapes everything: planning, environment, physical endurance, and psychological readiness all carry more weight than with most psychedelics.
Compared to 2C-B, 2C-P is roughly 3–4 times more potent by weight and several times longer in duration. In its marathon character it resembles DOM more than any other common psychedelic — a long, demanding session rather than a contained evening experience.
First synthesized by Alexander Shulgin and documented in PiHKAL (1991), 2C-P was explored through self-experiments that established its active dose range and steep dose–response curve.[1] The compound circulated on online research chemical markets through the 2000s before scheduling in the United States, Germany, and Canada. It remains available on illicit markets, with emergency case reports confirming continued use despite prohibition.[2]
Subjective effects include geometric visual patterns, time alteration, conceptual thinking, euphoria, and ego dissolution. The experience is defined by its marathon quality — a slow-building, all-day alteration of perception and cognition that demands more preparation and endurance than most psychedelics. Severe body load, prolonged agitation, and overwhelming confusion at doses only slightly above the common range are characteristic unsought effects.
Physical dependence liability is low — rapid tolerance after a single dose limits compulsive use[3][4] — but acute toxicity risk is elevated by the steep dose–response curve. At 16 mg, only 60% above the upper common dose, Shulgin documented a "physical disaster";[1] the slow onset invites premature redosing that can push a session into cardiovascular emergency.[5] No clinical trials have been conducted — the evidence base rests on Shulgin's self-experiments, a handful of emergency case reports, and one rodent study.[6]
History[edit]
Discovery
Alexander Shulgin first synthesized 2C-P and documented it as entry #35 in PiHKAL (1991), assigning the compound the personal name "Selene".[1] Self-experiments established oral activity at 6–10 mg with a duration of 10–16 hours, making it among the most potent and longest-acting compounds in the 2C series. Critically, Shulgin flagged 16 mg as a "clear overdose" and "physical disaster" — an observation that remains the single most important primary safety datum for this compound.[1]
Market appearance and scheduling
Following ''PiHKAL'''s publication, 2C-P entered circulation through online research chemical vendors operating through the 2000s and early 2010s. Regulatory response came in waves: the United States placed 2C-P under Schedule I in 2012 via the synthetic Drug Abuse Prevention Act,[7] Germany scheduled it in 2014, and Canada added it to Schedule III in 2016.[8] No clinical trials or formal pharmacological characterization has ever been conducted.
Clinical documentation
Published clinical evidence is limited to two reports. A 2015 case series described five males aged 17–21 presenting with serotonergic toxicity after recreational use.[5] A 2017 Swiss case report documented a patient who ingested 2C-P sold as 2C-B, providing the first pharmacokinetic estimate and exposing the adulterant risk inherent to unregulated markets.[2] Both post-date US scheduling, confirming continued availability despite prohibition.
Shulgin's name "Selene" — after the Greek moon goddess — reflects his practice of assigning personal names to favored compounds.[1] Among the 2C series, 2C-P's reputation centers on its unforgiving dose–response relationship and marathon duration, earning a cautious regard even within experienced psychedelic communities. It is sometimes compared to DOM for its extended timeline and potency-per-milligram, though the two belong to different structural subclasses.
Chemistry[edit]
Structural class
2C-P belongs to the 2C-X family of phenethylamines, built on a 2,5-dimethoxyphenethylamine scaffold with an n-propyl chain at the 4-position of the aromatic ring. This propyl group is longer and more lipophilic than substituents on shorter-chain relatives like 2C-B (4-bromo), 2C-I (4-iodo), and 2C-E (4-ethyl). Across the 2C series, increasing the size and lipophilicity of the 4-substituent correlates with higher receptor affinity and longer duration[9] — the propyl chain is one of the longest alkyl groups Shulgin explored, accounting for 2C-P's exceptional potency and extended action.
Molecular properties
| Molecular formula | C₁₃H₂₁NO₂ |
| Molecular weight | 223.31 g/mol |
The molecule consists of a phenethylamine backbone with methoxy groups at positions 2 and 5 and a straight-chain propyl group at position 4. The free base is an amine; the hydrochloride salt is the form most commonly encountered in forensic and analytical contexts.
Stereochemistry
2C-P is achiral — the phenethylamine backbone lacks a stereocenter at the α-carbon, unlike amphetamine-class compounds where the α-methyl group introduces chirality. No stereoisomeric considerations apply.
Physical properties
No systematic characterization of 2C-P's physical properties has been published. Melting point, solubility, and stability data are absent from peer-reviewed sources. Seized samples have been described as white powder.[5]
Pharmacology[edit]
Mechanism of action
2C-P acts primarily as an agonist at serotonin 5-HT₂A receptors, the molecular target responsible for psychedelic effects across the phenethylamine class. Rodent studies confirm this assignment: 2C-P produces head-twitch responses characteristic of 5-HT₂A activation, and the selective antagonist M100907 fully blocks these effects.[6][4][10]
The 2,5-dimethoxy scaffold is essential for activity — removing either methoxy group substantially reduces psychedelic effects even when receptor binding is only modestly changed.[11] The 4-propyl group increases lipophilicity, and across the 2C series, larger 4-position substituents progressively enhance receptor affinity.[9]
No published study has measured specific binding strength or potency values for 2C-P at any receptor. Class-level data indicate strong 5-HT₂A affinity with partial agonist characteristics.[9]
Secondary targets
5-HT₂C receptors represent the primary secondary target, with lower affinity than 5-HT₂A across the 2C class.[9] Related phenethylamines show weak activity at TAAR1 (TAAR1).[9][12] Activity at monoamine transporters is minimal or absent.[9][12]
2C-P was among 17 2C-series compounds tested for monoamine oxidase (MAO) inhibition; across the panel, most compounds inhibited both MAO-A and MAO-B at micromolar concentrations.[13] Whether this MAO inhibition is clinically relevant at recreational doses is uncertain but cannot be excluded.
At high doses in rodents, 2C-P altered dopamine receptor expression and DAT activity in reward-related brain regions.[6] These dopaminergic effects were dose-dependent and absent at lower doses, suggesting they are secondary or toxicity-associated rather than part of the primary psychedelic mechanism.
Pharmacokinetics
No formal pharmacokinetic study exists for 2C-P. The best available estimate of half-life is approximately 19 hours, derived from two blood samples in a single emergency case.[2] This aligns with the prolonged subjective duration but represents a rough approximation, not a validated population parameter.
Plasma concentrations reached approximately 20 µg/L in one sampled intoxication case; urine was positive in all five patients in the earliest case series.[5]
The body processes 2C-P through multiple metabolic pathways including demethylation of the methoxy groups, deamination, acetylation, and conjugation reactions.[14][15] These pathways were characterized by mass spectrometry analysis of urine, confirming analytical detectability at common doses.[14] The specific liver enzymes involved have not been studied directly for 2C-P, though related 2C compounds suggest involvement of common drug-metabolizing enzymes.inferred
Neuroscience[edit]
Where it acts
As a serotonin 2A receptor agonist, 2C-P is expected to act on layer V pyramidal neurons in the prefrontal cortex, increasing cortical excitability and disrupting the brain's normal filtering of sensory information. No neuroimaging or electrophysiological data have been published for 2C-P specifically — neural effects are inferred from the broader psychedelic literature on compounds like psilocybin and LSD.citation needed
At high doses in rodents, 2C-P altered dopamine signaling in the nucleus accumbens and prefrontal cortex,[6] suggesting engagement of reward circuitry beyond the typical serotonergic psychedelic profile. Microglial activation observed in the striatum at these doses points to possible neuroinflammatory processes.[6]
Why it matters
The relaxed beliefs under psychedelics (REBUS) model offers the most relevant framework: 5-HT₂A agonism loosens the brain's reliance on prior expectations, allowing raw sensory and emotional signals greater access to conscious experience. 2C-P's prolonged duration — potentially an entire waking day of altered cortical dynamics — may produce deeper destabilization of established belief patterns than shorter-acting psychedelics, though this remains speculative. Whether 2C-P promotes structural brain changes (neuroplasticity) as demonstrated for other psychedelics has not been tested.
- Does 2C-P promote structural neuroplasticity via the signaling pathways demonstrated for other serotonergic psychedelics?
- What drives the dopaminergic engagement at high doses — direct receptor activity or indirect modulation through serotonin-dopamine interactions?
- Does the prolonged receptor occupancy produce qualitatively different patterns of brain reorganization compared to shorter-acting compounds?
Subjective Effects[edit]
2C-P's experiential character is shaped more by its duration and dose sensitivity than by any single perceptual quality. The altered state unfolds over the timescale of a waking day, not an evening — the slow onset and extended commitment demand a level of planning unusual among psychedelics. Set and setting carry proportionally greater weight because environmental and psychological conditions inevitably shift during a session this long, and small dose miscalculations produce disproportionately intense responses.
Compared to 2C-B, the most familiar 2C compound, 2C-P is roughly 3–4 times more potent by weight and several times longer in duration. The experiential texture is closer to DOM in its marathon quality than to the contained, manageable arc of a 2C-B session.
Effect Grid
At common doses (6–10 mg oral), the full psychedelic experience develops: pronounced open and closed-eye visuals including geometric patterning, color shifting, drifting and morphing of surfaces, and tracers. Time distortion becomes significant. Conceptual thinking intensifies, producing novel associations, introspective depth, and emotional amplification. Euphoria is typical. At the upper end of this range, ego dissolution and boundary loss become possible.
Physically, moderate stimulation, body load, pupil dilation, and temperature dysregulation are expected. Tachycardia and mild hypertension are common serotonergic effects. Nausea may occur during the prolonged come-up.
The 1–3 hour onset and 10–16 hour total duration require commitment to an entire day. Sleep is impossible for most of the experience. Do not redose during the long come-up — the steep dose-response curve makes small increases disproportionately intense.
Modeled from the effect's dose-dependence curve — not per-substance measurements.
Tracers · Visual breathing · Holotropic state · Sleep-transition hallucinations · Depth perception distortion · After-images · Music enhancement · Symmetrical texture repetition · Brightness alteration · Environmental patterning · Light sensitivity · Perspective distortion · Visual morphing · Touch enhancement · Auditory enhancement · Peripheral vision distortion · Sound sensitivity · Spatial disorientation · Visual diffraction · Visual haze / noise · Visual melting · Ganzfeld effect · Auditory distortion · Auditory misinterpretation · Dreaming enhancement · Peripheral misidentification · Proprioceptive distortion · Synesthesia · Vestibular distortion · Visual acuity enhancement · Visual magnification · Olfactory enhancement · Taste enhancement · Visual processing acceleration · Tinnitus · Flashbacks · Object transformations · External hallucinations · Visual scenery slicing · Internal hallucinations · Environmental orbism / cubism · Object activation · Perspective hallucinations · Visual recursion · Auditory hallucinations · Visual flipping · Persisting hallucinations
Depth perception distortion · After-images · Music enhancement · Symmetrical texture repetition · Brightness alteration · Environmental patterning · Light sensitivity · Perspective distortion · Visual morphing · Touch enhancement · Auditory enhancement · Peripheral vision distortion · Sound sensitivity · Spatial disorientation · Visual diffraction · Visual haze / noise · Visual melting · Ganzfeld effect · Auditory distortion · Auditory misinterpretation · Dreaming enhancement · Peripheral misidentification · Proprioceptive distortion · Synesthesia · Vestibular distortion · Visual acuity enhancement · Visual magnification · Olfactory enhancement · Taste enhancement · Visual processing acceleration · Tinnitus · Flashbacks · Object transformations · External hallucinations · Visual scenery slicing · Internal hallucinations · Environmental orbism / cubism · Object activation · Perspective hallucinations · Visual recursion · Auditory hallucinations · Visual flipping · Persisting hallucinations
Wakefulness · Body high · Stimulation · Spontaneous body sensations · Insomnia · Appetite suppression · Bodily heaviness · Heart rate perception changes · Physical fatigue · Tingling / electric sensations · Vibrations / buzzing · Bodily pressures · Dehydration sensation · Dizziness · Dry mouth · Excessive sweating · Motor control impairment · Muscle tension · Restlessness · Tactile euphoria · Sexual arousal enhancement · Body schema distortion · Breathing alteration · Headache · Laughter fits · Bruxism · Diarrhea · Involuntary body movements · Pain suppression · Respiratory stimulation · Trembling · Vomiting · Abnormal heartbeat · Nystagmus (eye wobbles) · Salivation · Watery eyes · Bodily dissociation · Tactile hallucination
Spontaneous body sensations · Insomnia · Appetite suppression · Bodily heaviness · Heart rate perception changes · Physical fatigue · Tingling / electric sensations · Vibrations / buzzing · Bodily pressures · Dehydration sensation · Dizziness · Dry mouth · Excessive sweating · Muscle tension · Restlessness · Tactile euphoria · Sexual arousal enhancement · Body schema distortion · Breathing alteration · Headache · Laughter fits · Bruxism · Diarrhea · Involuntary body movements · Pain suppression · Respiratory stimulation · Trembling · Vomiting · Abnormal heartbeat · Nystagmus (eye wobbles) · Salivation · Watery eyes · Bodily dissociation · Tactile hallucination
Multiple thought streams · Novelty enhancement · Thought loops · Immersion enhancement · Aesthetic enhancement · Cognitive impairment · Increased nature relatedness · Openness enhancement · Thought connectivity · Thought acceleration · Cognitive euphoria · Cognitive flexibility · Creativity enhancement · Confusion · Focus suppression · Synchronicity · Thought disorganization · Cognitive dysphoria · Memory suppression · Cognitive fatigue · Analysis enhancement · Humor enhancement · Information processing suppression · Memory fragmentation · Information processing enhancement · Motivation enhancement · Language suppression · Memory replays · Focus enhancement · Language enhancement · Delusions · Amnesia · Delirium
Immersion enhancement · Aesthetic enhancement · Cognitive impairment · Increased nature relatedness · Openness enhancement · Thought connectivity · Thought acceleration · Cognitive euphoria · Cognitive flexibility · Creativity enhancement · Confusion · Focus suppression · Synchronicity · Thought disorganization · Cognitive dysphoria · Memory suppression · Cognitive fatigue · Analysis enhancement · Humor enhancement · Information processing suppression · Memory fragmentation · Information processing enhancement · Motivation enhancement · Language suppression · Memory replays · Focus enhancement · Language enhancement · Amnesia · Delirium
Euphoria · Simultaneous emotions · Dysphoria · Empathy enhancement · Catharsis · Irritability
Catharsis · Irritability
Communication suppression · Sociability suppression · Social connection · Social disconnection · Trust enhancement · Communication enhancement · Flow state · Sociability enhancement · Ego inflation · Boundary dissolution · Identity alteration · Cognitive disconnection · Ego dissolution · Telepathic feelings
Trust enhancement · Communication enhancement · Flow state · Sociability enhancement · Ego inflation · Boundary dissolution · Identity alteration · Cognitive disconnection · Ego dissolution · Telepathic feelings
Time cessation
Entity contact · Non-dual awareness · Death-rebirth sequence · Transpersonal memory access · Voidness · Cessation
Voidness · Cessation
Lucidity enhancement · Recursive awareness
Timeline
First alerts emerge gradually: mild mood shift, faint visual brightening, subtle body awareness. The slow onset is characteristic of 2C phenethylamines and a primary risk factor — do not redose during this window.
Effects build steadily over 1. 5–3 hours. Visual enhancement, color saturation, and body load increase progressively.
Maximum intensity sustained for 3–5 hours. Full visual distortion, time dilation, conceptual thinking, emotional amplification, and potential ego dissolution. Physical effects (tachycardia, stimulation, body load) are most pronounced.
Intensity diminishes gradually but remains clearly psychedelic. Visuals soften, cognitive effects shift toward reflective processing. Physical stimulation and body load persist.
Slow return toward baseline over 2–4 hours. Residual visual enhancement, emotional sensitivity, and mild stimulation persist. Appetite may begin returning.
Residual mood changes, mild perceptual sensitivity, and cognitive openness may persist for 8–24 hours following resolution. Fatigue is common given the extended experience duration. Sleep quality may be disrupted on the first night.
Safety[edit]
- Acute toxicity
- Moderate
- Chronic toxicity
- Low
- Withdrawal
- None
- Tolerance buildup
- rapid
- Tolerance reset
- 14 days
- Physical
- None
- Psychological
- Low
- Compulsive redosing
- Negligible
- Dose escalation
- Negligible
- Cross-tol.
- LSD · psilo · mesc
Toxicity
Acute toxicity
No lethal dose has been established for 2C-P in any species, and no human death has been attributed to the compound alone. Clinical presentations include dilated pupils, severe agitation, confusion, visual hallucinations, rapid heart rate, and elevated blood pressure.[6] All documented cases resolved with supportive care.
2C-P exhibits a steep dose–response curve. Shulgin documented 16 mg oral — only 60% above the upper common dose of 10 mg — as a "clear overdose" and "physical disaster".[1] Small increases in dose produce disproportionately intense and potentially dangerous effects.
Cardiovascular effects
Rapid heart rate and elevated blood pressure appear in every published case.[3][6] Severe cases may involve vasoconstriction and dangerously elevated body temperature.[14] The prolonged duration means this cardiovascular stress can persist for 10–20 hours — far longer than with most other psychedelics.
Neurotoxicity (animal data)
High-dose 2C-P in rodents caused brain inflammation in the striatum, impaired movement and balance, and damaged memory and learning.[7] These effects were dose-dependent and did not occur at lower doses. Whether they translate to humans at recreational doses is unknown.
Psychological risks
2C-P's combination of high potency, steep dose–response curve, long duration, and slow onset creates elevated risk for prolonged distressing experiences. Severe agitation, confusion, and frightening hallucinations are documented above the common dose range.[3][6]
The slow onset is a particular hazard. Taking more because "nothing is happening" — premature redosing — can turn a manageable experience into an overwhelming one. Ego dissolution, thought loops, and delusions can be intensely distressing when sustained over many hours.
Tolerance and dependence
Tolerance develops rapidly after a single dose — serotonin receptors downregulate, blocking further psychedelic effects.[4][5] This cross-tolerance extends to LSD, psilocybin, mescaline, and other 2C compounds.[5][4]
Physical dependence risk is low — no withdrawal has been documented for any 2C compound. However, rodent studies show reinforcing properties atypical for classical psychedelics, possibly related to dopaminergic effects at high doses.[7]
Drug Interactions
The primary danger is combining 2C-P with any substance that raises serotonin — this can trigger dangerous overheating, muscle rigidity, and seizures. 2C-P both activates serotonin receptors directly and may inhibit the enzymes that clear serotonin,[11] making MAOIs the highest-risk combination and tramadol also dangerous.safety citation needed
SSRIs and SNRIs may reduce psychedelic effects while adding to serotonergic load;safety citation needed lithium combined with serotonergic psychedelics carries risk of seizures.safety citation needed Cannabis lacks specific interaction data for 2C-P but may amplify or unpredictably modify effects — any potentiation is elevated risk given the steep dose–response curve.
Contraindications
7 knownContraindication data specific to 2C-P do not exist. The following are inferred from its pharmacological classinferred:
- Psychotic disorders or family history of psychosis: Activating serotonin receptors may trigger or worsen psychotic episodes.
- Bipolar disorder: Risk of manic or mixed episode precipitation.
- Heart conditions: Rapid heart rate and elevated blood pressure are consistently reported.
- Seizure disorders: Serotonergic excess may lower seizure threshold; related 2C compounds have produced seizures.[15]
- Liver impairment: Extensive liver metabolism suggests altered clearance.
- Pregnancy and breastfeeding: No reproductive toxicity data exist.
- Concurrent serotonergic medication: See Drug Interactions above.
Harm Reduction[edit]
Forms & Identification
2C-P has been sold as, or confused with, 2C-B[3] — a compound active at 15–25 mg, where a 2C-B-sized dose of 2C-P constitutes a severe overdose. 2C-P is visually indistinguishable from other white-powder phenethylamines. Test every sample with reagent kits; quantitative analysis provides stronger assurance.
Guidelines
- Test every sample with reagent kits and, if possible, quantitative analysis. 2C-P is visually indistinguishable from other white-powder phenethylamines.
- Weigh precisely. Use a milligram-precision scale (0.001 g). The difference between a common and dangerous dose is less than 10 mg.
- Start at the lower end of the active range. Individual sensitivity varies, and 2C-P's steep dose–response curve punishes overestimation.
- Do not redose. The onset takes 1–3 hours. Premature redosing is the most common path to overdose with this compound.
- Clear your schedule for 24 hours. The experience may last up to 20 hours, and residual effects can persist beyond that.
- Arrange a sitter — ideally someone experienced with long-duration psychedelics who can provide calm reassurance over many hours.
- Stay hydrated and eat lightly before and during the experience. A session this long depletes physical resources.
Set & Setting
The 10–20 hour duration means the experience will outlast most environments' comfort and most sitters' stamina. Plan for a full waking day — a private, comfortable space with access to food, water, and a place to lie down. A trusted sitter able to sustain support over many hours is strongly recommended.
Psychological preparation matters more here than with shorter psychedelics. Unresolved anxiety or unstable mood compounds over a session this long. Begin from a rested, calm, well-nourished baseline. Avoid public settings or any commitment within 24 hours.
Aftercare & integration. A 10–20 hour psychedelic experience is physically and psychologically exhausting. Sleep first — allow a full night's rest before trying to process the experience. Eat and rehydrate.
In the days following, journaling or talking with a trusted person helps organize what may have been a disorienting or emotionally dense session. Persistent anxiety, mood changes, or intrusive visual phenomena lasting more than two weeks warrant professional consultation. Integration-focused therapists familiar with psychedelic experiences can be found through directories such as the Psychedelic Support Network.
Recovery & Support
2C-P carries low physical dependence risk, and compulsive use is self-limiting — rapid tolerance blocks repeated effects. Psychological patterns of use — seeking the psychedelic state as escape or coping mechanism — are the more relevant concern.
If use is becoming a pattern rather than a choice, support resources include the SAMHSA National Helpline (1-800-662-4357), Fireside Project (62-FIRESIDE), and local peer support groups. Professional help is especially appropriate if psychedelic use is occurring alongside untreated mental health conditions.
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Recognizing an emergency: Uncomfortable body load and anxiety are common and do not alone constitute an emergency. Seek immediate help for: chest pain, seizures, loss of consciousness, inability to communicate, sustained body temperature that feels dangerously elevated through clothing, or self-harm behavior.
Immediate steps:
- 1. Call emergency services if any of the above signs are present.
- 2. Place the person in the recovery position if unconscious but breathing.
- 3. Keep them in a cool, quiet environment. Remove excess clothing if overheating.
- 4. Do not restrain unless there is immediate danger of self-harm.
- 5. Do not induce vomiting.
What to tell the dispatcher: Name the substance (2C-P, a synthetic psychedelic), the estimated dose if known, when it was taken, and current symptoms. Good Samaritan laws in many jurisdictions protect people who call for help during drug emergencies.
Clinical note: Emergency treatment is supportive. The estimated half-life of ~19 hours[3] necessitates extended observation. Benzodiazepines are standard for agitation; serotonin antagonists may be considered for serotonergic toxicity features.
Legal Status[edit]
2C-P is controlled in multiple jurisdictions, primarily through specific scheduling of 2C-class phenethylamines or under broader structural analog legislation. No jurisdiction has approved it for medical or research use.
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| United States | Schedule I (Controlled Substances Act) | Placed under Schedule I via the Synthetic Drug Abuse Prevention Act of 2012; DEA drug code 7524[2] |
| United Kingdom | Class A (Misuse of Drugs Act 1971) | Controlled under the phenethylamine catch-all clausecitation needed |
| Germany | Anlage I (BtMG) | Scheduled December 13, 2014citation needed |
| Canada | Schedule III (CDSA) | Added via order amending Schedule III, effective May 2016[8] |
| Australia | Likely Schedule 9 (Prohibited Substance) | Not confirmed from primary regulatory source; likely captured by catch-all or specific listingcitation needed |
| Netherlands | Status uncertain | Not clearly scheduled at time of research; novel psychoactive substance legislation may applycitation needed |
Analog act considerations
In jurisdictions with analog legislation, 2C-P's structural similarity to other scheduled phenethylamines may provide an additional basis for prosecution, independent of specific scheduling. In the United States, 2C-P is explicitly listed under Schedule I, making analog provisions unnecessary.
Legal status changes frequently and varies by jurisdiction. This table reflects scheduling known at time of publication and is not legal advice.
Safety[edit]
- Acute toxicity
- Moderate
- Chronic toxicity
- Low
- Withdrawal
- None
- Tolerance buildup
- rapid
- Tolerance reset
- 14 days
- Physical
- None
- Psychological
- Low
- Compulsive redosing
- Negligible
- Dose escalation
- Negligible
- Cross-tol.
- LSD · psilo · mesc
Toxicity
Acute toxicity
No lethal dose has been established for 2C-P in any species, and no human death has been attributed solely to this compound in the published literature.
2C-P exhibits a steep dose–response curve. Shulgin documented 16 mg oral — only 60% above the upper common dose of 10 mg — as a "clear overdose" and "physical disaster".[1] Small increases in dose produce disproportionately intense and potentially dangerous effects.
Clinical presentations in published cases include dilated pupils, severe agitation, confusion, visual hallucinations, rapid heart rate, and elevated blood pressure.[5] One case involved substance misidentification — the patient believed he was consuming 2C-B.[2] All documented cases resolved with supportive care.
Cardiovascular effects
Rapid heart rate and elevated blood pressure appear in every published 2C-P case.[2][5] Severe cases may involve vasoconstriction and dangerously elevated body temperature.[16] The prolonged duration means cardiovascular stress may persist for 10–20 hours — far longer than with most other serotonergic psychedelics.
Neurotoxicity (animal data)
High-dose 2C-P in rodents produced brain inflammation in the striatum, impaired movement and balance, and damaged performance on memory and learning tasks.[6] These effects were accompanied by changes in dopamine receptor expression and transporter activity. All neurotoxic effects were dose-dependent and occurred only at high doses. Whether these findings translate to humans at recreational doses is unknown.
Psychological risks
2C-P's combination of high potency, steep dose–response curve, long duration, and delayed onset creates elevated risk for prolonged distressing experiences. At doses above the common range, severe agitation, confusion, and frightening hallucinations are documented.[2][5]
The slow onset increases the risk of premature redosing — taking more because "nothing is happening" — which given the steep dose–response curve can transform a manageable experience into an overwhelming one. Ego dissolution, delusions, and thought loops can be intensely distressing when unexpected or prolonged over many hours.
No data exist on HPPD (HPPD) following 2C-P use. The prolonged receptor engagement suggests theoretical risk, but clinical rarity of HPPD across all psychedelics and absence of 2C-P-specific reports prevent quantification.inferred
Tolerance and dependence
Tolerance to 2C-P's psychedelic effects develops rapidly after a single dose, driven by downregulation of 5-HT₂A receptors in the brain.[3][4] Cross-tolerance extends to all serotonergic psychedelics: LSD, psilocybin, mescaline, and other 2C compounds.[4][3]
Physical dependence liability is low — no withdrawal has been documented for any 2C-class compound. However, rodent studies complicate the picture: dose-dependent conditioned place preference in mice and increased self-administration in rats suggest reinforcing properties atypical for classical psychedelics.[6] These findings may relate to dopaminergic effects at high doses and suggest that 2C-P's dependence profile may not be identical to the broader psychedelic class.
Drug Interactions
The primary interaction risk is serotonin toxicity when 2C-P is combined with other serotonergic agents. 2C-P contributes through direct 5-HT₂A agonism and possible monoamine oxidase inhibition.[13]
Tramadol is flagged as a dangerous combination. Tramadol's serotonin and norepinephrine reuptake inhibitor, combined with 2C-P's receptor agonism and possible MAO inhibition, creates a plausible pathway to serotonin syndrome.safety citation needed
SSRIs and SNRIs may blunt or block psychedelic effects through chronic receptor adaptation while simultaneously increasing serotonin syndrome risk through additive serotonergic load. Lithium combined with serotonergic psychedelics carries risk of seizures and serotonin toxicity.safety citation needed
MAOIs present a dual risk: 2C-P itself exhibits MAO inhibition in laboratory testing,[13] and external MAO inhibitors would further amplify serotonergic activity, substantially increasing serotonin syndrome risk.
Cannabis interaction data do not exist for 2C-P. Cannabis may amplify or unpredictably modify psychedelic effects. Given 2C-P's long duration and steep dose–response curve, any potentiation carries elevated risk.
Contraindications
7 knownContraindication data specific to 2C-P do not exist. The following are inferred from its pharmacological classinferred:
- Psychotic disorders or family history of psychosis: 5-HT₂A agonism may trigger or worsen psychotic episodes.
- Bipolar disorder: Risk of manic or mixed episode precipitation.
- Heart conditions: Rapid heart rate and elevated blood pressure are consistently reported; individuals with pre-existing cardiac conditions face elevated risk.
- Seizure disorders: Serotonergic excess may lower seizure threshold; related 2C compounds have produced seizures in case reports.[17]
- Liver impairment: Extensive liver metabolism suggests altered clearance in hepatic dysfunction, though no specific data exist.
- Pregnancy and breastfeeding: No reproductive toxicity data exist; 5-HT₂A agonism during fetal development is a theoretical concern.
- Concurrent serotonergic medication: See Drug Interactions above.
Harm Reduction[edit]
Forms & Identification
2C-P's extreme potency — active at single-digit milligrams — means even small measurement errors can produce dangerous outcomes. Standard volumetric dosing practices and milligram-precision scales (±1 mg) are essential; eyeballing or "bumping" from a bag is reckless with this compound. The substance has been sold as, or confused with, 2C-B[2] — a compound active at 15–25 mg, where a 2C-B-sized dose of 2C-P would constitute a severe overdose.
Guidelines
- Test every sample with reagent kits and, if possible, quantitative analysis. 2C-P is visually indistinguishable from other white-powder phenethylamines.
- Weigh precisely. Use a milligram-precision scale (0.001 g). The difference between a common and dangerous dose is less than 10 mg.
- Start at the lower end of the active range. Individual sensitivity varies, and 2C-P's steep dose–response curve punishes overestimation.
- Do not redose. The onset takes 1–3 hours. Premature redosing is the most common path to overdose with this compound.
- Clear your schedule for 24 hours. The experience may last up to 20 hours, and residual effects can persist beyond that.
- Arrange a sitter — ideally someone experienced with long-duration psychedelics who can provide calm reassurance over many hours.
- Stay hydrated and eat lightly before and during the experience. A session this long depletes physical resources.
Set & Setting
The 10–20 hour duration means the experience will outlast most indoor environments' comfort and most sitters' stamina. Plan for a full waking day: secure a private, comfortable space with access to food, water, and a place to lie down. A trusted sitter who can rotate shifts or hand off to another person is strongly recommended.
Psychological preparation matters more with 2C-P than with shorter psychedelics. Unresolved anxiety or unstable mood states have more time to compound over a marathon session. Begin from a rested, calm, well-nourished baseline. Avoid public settings, social obligations, or any commitment within 24 hours.
Aftercare & integration. A 10–20 hour psychedelic experience is physically and psychologically exhausting. Sleep is the first priority — allow a full night's rest before attempting to process the experience. Eat a substantial meal and rehydrate.
In the days following, journaling or discussing the experience with a trusted person can help organize what may have been a disorienting or emotionally dense session. Persistent anxiety, mood changes, or intrusive visual phenomena lasting more than two weeks warrant professional consultation. Integration-focused therapists familiar with psychedelic experiences can be found through directories such as the Psychedelic Support Network.
Recovery & Support
2C-P carries low physical dependence risk, and compulsive use is self-limiting due to rapid tolerance. Psychological patterns of use — seeking the psychedelic state as escape or coping mechanism — are the more relevant concern with any psychedelic.
If use is becoming a pattern rather than a choice, support resources include the SAMHSA National Helpline (1-800-662-4357), Fireside Project (62-FIRESIDE), and local peer support groups. Professional help is especially appropriate if psychedelic use is occurring alongside untreated mental health conditions.
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Recognizing an emergency: Uncomfortable body load and anxiety are common and do not alone constitute an emergency. Seek immediate help for: chest pain, seizures, loss of consciousness, inability to communicate, sustained body temperature that feels dangerously elevated through clothing, or self-harm behavior.
Immediate steps:
- 1. Call emergency services if any of the above signs are present.
- 2. Place the person in the recovery position if unconscious but breathing.
- 3. Keep them in a cool, quiet environment. Remove excess clothing if overheating.
- 4. Do not restrain unless there is immediate danger of self-harm.
- 5. Do not induce vomiting.
What to tell the dispatcher: Name the substance (2C-P, a synthetic psychedelic), the estimated dose if known, when it was taken, and current symptoms. Good Samaritan laws in many jurisdictions protect people who call for help during drug emergencies.
Clinical note: Emergency treatment is supportive. The estimated half-life of ~19 hours[2] necessitates extended observation. Benzodiazepines are standard for agitation; serotonin antagonists may be considered for serotonergic toxicity features.
Legal Status[edit]
2C-P is controlled in multiple jurisdictions, primarily through specific scheduling of 2C-class phenethylamines or under broader structural analog legislation. No jurisdiction has approved 2C-P for medical or research use.
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| United States | Schedule I (Controlled Substances Act) | Placed under Schedule I via the Synthetic Drug Abuse Prevention Act of 2012; DEA drug code 7524[7] |
| United Kingdom | Class A (Misuse of Drugs Act 1971) | Controlled under the phenethylamine catch-all clausecitation needed |
| Germany | Anlage I (BtMG) | Scheduled December 13, 2014citation needed |
| Canada | Schedule III (CDSA) | Added via order amending Schedule III, effective May 2016[8] |
| Australia | Likely Schedule 9 (Prohibited Substance) | Not confirmed from primary regulatory source; likely captured by catch-all or specific listingcitation needed |
| Netherlands | Status uncertain | Not clearly scheduled at time of research; novel psychoactive substance legislation may applycitation needed |
Analog act considerations
In jurisdictions with analog legislation, 2C-P's structural similarity to other controlled phenethylamines may provide an additional basis for prosecution independent of specific scheduling. In the United States, 2C-P is now explicitly listed under Schedule I, making the Federal Analogue Act unnecessary — but analog provisions remain relevant in jurisdictions where 2C-P is not specifically named.
Frequently asked questions
How long does 2C-P last?
Total duration by route of administration — Oral: 10 – 20 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-P?
Psychedex publishes a dosage table for 2C-P 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-P?
The highest-severity documented interactions for 2C-P: 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-P addictive?
Psychedex records tolerance and dependence data rather than a yes/no rating. Recorded tolerance indicators for 2C-P: tolerance builds rapid; full reset takes 14 days; cross-tolerance develops with LSD, psilocybin, mescaline, 2C-B, 2C-E, 2C-I, 2C-D, DOI, DOM. See the article's dependence and safety sections for recorded dependence data.
experience reports
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First-person accounts of subjective effects, timing, and outcomes — submitted for harm reduction.
references
- [1]
- [2]
- [3]
- [4] ^abcBuckholtz NS, Zhou DF, Freedman DX, Potter WZ (1990) Lysergic acid diethylamide (LSD) administration selectively downregulates serotonin2 receptors in rat brain — Neuropsychopharmacology PMID:1969270
- [5] ^abcdde la Fuente Revenga M, Jaster AM, McGinn J, Silva G, Saha S, Gonzalez-Maeso J (2022) Tolerance and Cross-Tolerance among Psychedelic and Nonpsychedelic 5-HT2A Receptor Agonists in Mice — ACS Chemical Neuroscience doi:10.1021/acschemneuro.2c00170
- [6]
references
- [1]
- [2]
- [3] ^abcBuckholtz NS, Zhou DF, Freedman DX, Potter WZ (1990) Lysergic acid diethylamide (LSD) administration selectively downregulates serotonin2 receptors in rat brain — Neuropsychopharmacology PMID:1969270
- [4] ^abcdde la Fuente Revenga M, Jaster AM, McGinn J, Silva G, Saha S, Gonzalez-Maeso J (2022) Tolerance and Cross-Tolerance among Psychedelic and Nonpsychedelic 5-HT2A Receptor Agonists in Mice — ACS Chemical Neuroscience doi:10.1021/acschemneuro.2c00170
- [5]
- [6]