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1cP-MiPLA
1-cyclopropanoyl-N-methyl-N-isopropyllysergamide
1cP-MiPLA (1-cyclopropanoyl-N-methyl-N-isopropyllysergamide) is a synthetic psychedelic of the lysergamide class. It is a prodrug for MiPLA, a compound structurally related to LSD but with reduced potency at serotonin receptors. The body converts it into MiPLA, which activates serotonin receptors in the brain, producing the visual and cognitive shifts characteristic of classical psychedelics.
1cP-MiPLA (1-cyclopropanoyl-N-methyl-N-isopropyllysergamide) is an emerging synthetic psychedelic of the lysergamide class. It is a dual-modified prodrug combining the cyclopropanoyl group of 1cP-LSD with the carboxamide structure of MiPLA. 1cP-MiPLA is a presumed serotonin 2A receptor agonist, producing its effects through its active metabolite MiPLA after enzymatic cleavage of the prodrug bond.
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MiPLA, the active compound it releases, was first synthesized by David Nichols in 1994 during a study of how structural changes affect LSD-like activity.[1] 1cP-MiPLA appeared on research chemical markets around 2020, applying an established prodrug strategy to the MiPLA scaffold for the first time.[2] It circulates in small quantities among research chemical communities and remains unscheduled by name in most jurisdictions.
Subjective effects include geometric visual patterns, brightened colors, time alteration, thought acceleration, and emotional enhancement. The experience resembles a lighter, shorter version of LSD — qualitatively the same classical psychedelic character but less intense, reflecting MiPLA's weaker serotonin receptor binding.[1] Thought loops, anxious fixation, and acute anxiety are common unwanted effects, and any dose can produce a difficult experience in the wrong set or setting.
1cP-MiPLA produces no physical dependence, and acute toxicity is expected to be negligible, by analogy with LSD.[3] The primary risks are psychological — panic, paranoia, and rare persistent visual disturbances after the drug wears off[4] — and combining it with MAOIs or tramadol can trigger dangerous serotonin overload.[5] No controlled human data exist; everything known rests on structural analogy to LSD and unverified community reports.[2]
History[edit]
Discovery
MiPLA, the active compound 1cP-MiPLA releases, was first synthesized by David Nichols in 1994 during a study of how structural changes at the amide position affect LSD-like activity.[1] That research showed MiPLA could fully substitute for LSD in trained animals despite weaker serotonin receptor binding. 1cP-MiPLA itself has no published synthesis record; it most likely emerged from clandestine labs applying the established prodrug technique to the MiPLA scaffold.
The 1-acyl prodrug wave
1cP-MiPLA belongs to a wave of 1-acyl lysergamide prodrugs that appeared on research chemical markets from around 2015 onward. Earlier compounds — 1P-LSD,[6] 1B-LSD,[7] 1cP-LSD,[8] and 1V-LSD[9] — each convert to LSD in the body. 1cP-MiPLA was the first to apply this prodrug approach to a non-LSD parent compound.
First identification
1cP-MiPLA appeared on online markets around 2020 and was formally identified in 2022 when Japanese researchers detected it in seized blotter products.[2] That 2023 publication remains the only peer-reviewed scientific report on the compound; its authors noted that 1cP-MiPLA's metabolic pathways and biological activities had not been reported.[2]
The name 1cP-MiPLA encodes its chemistry: "1cP" marks the cyclopropanoyl group at the indole nitrogen, and "MiPLA" abbreviates N-methyl-N-isopropyllysergamide, the parent compound it releases. This follows the same naming pattern as 1P-LSD, 1cP-LSD, and 1V-LSD — signaling prodrug identity in the name itself. No street names or slang exist; the compound circulates only under its chemical abbreviation within research chemical communities.
Chemistry[edit]
Structural class
1cP-MiPLA belongs to the lysergamide family — compounds built on the ergoline scaffold, the same rigid framework as LSD and related alkaloids. It carries two structural modifications relative to LSD: a cyclopropanoyl group at the indole nitrogen (shared with 1cP-LSD) and a different amide group at the carboxamide end (shared with MiPLA).[2] That amide change reduces serotonin receptor binding by roughly 2–3× compared to LSD.[1]
Molecular properties
The molecular formula is C₂₄H₂₉N₃O₂ (molecular weight 391.5 g/mol); no CAS number has been assigned. No published characterization of physical properties exists — the compound has been encountered only as blotter paper and tablet formulations.[2] The ergoline scaffold contains two chirality centers; only the (6aR,9R) configuration — the same arrangement as LSD — is active at serotonin receptors.[10]
Pharmacology[edit]
Mechanism of action
No substance-specific pharmacological data have been published for 1cP-MiPLA. The mechanism described below is inferred from the 1-acyl lysergamide prodrug class and from receptor data on MiPLA.1cP-MiPLA is presumed to function as a prodrug for MiPLA. Enzymes in the blood and liver cleave the cyclopropanoyl group, releasing MiPLA as the active compound.[11] This conversion mechanism has been confirmed for five structurally related lysergamides — including 1cP-LSD,[8] 1P-LSD,[6] and 1V-LSD[9] — but has not been confirmed for 1cP-MiPLA specifically.[2]
Once released, MiPLA activates serotonin receptors in the brain — the established mechanism of classical psychedelic effects. Blocking these receptors in LSD studies eliminates all subjective effects.[12] Additional activity at other serotonin and dopamine receptors contributes to the full experience.[13]
Pharmacokinetics
No pharmacokinetic data exist for 1cP-MiPLA or MiPLA. By analogy with LSD, oral absorption peaks around 1.1 hours and active compound clears the body in 2.7–3.5 hours.[14][15] The prodrug conversion step introduces an additional delay before the active compound reaches circulation, consistent with observations for 1cP-LSD.[8]
Neuroscience[edit]
Where it acts
MiPLA — the active compound released from 1cP-MiPLA — activates serotonin receptors on cortical neurons. This increases excitatory brain activity, disrupts the default mode network, and raises connectivity between regions that normally stay separate.[13][16] The result is reduced filtering of sensory input — the neural basis of psychedelic perceptual expansion.
MiPLA's preserved activity at a secondary serotonin receptor site[1] may add a calming, introspective dimension alongside the primary perceptual effects.[17]
Why it matters
One influential model — the REBUS framework — proposes that serotonin receptor activation loosens the brain's reliance on existing assumptions, letting raw sensory input reshape perception more directly. MiPLA's lower receptor affinity would predict a gentler version of this process, consistent with community reports of a shorter and more cognitively manageable experience. LSD-class compounds also promote brain plasticity; whether MiPLA's reduced binding preserves this effect is unknown.
- Does 1cP-MiPLA convert to MiPLA in human blood at rates comparable to 1cP-LSD → LSD?
- Does MiPLA's reduced serotonin receptor affinity produce a qualitatively distinct experience, or merely a weaker version of the same one?
- Is MiPLA's relatively preserved secondary serotonin receptor activity responsible for any distinctive anxiolytic or introspective character?
Subjective Effects[edit]
1cP-MiPLA produces a classical psychedelic experience — geometric visuals, brightened colors, emotional enhancement, and a loosening of habitual thought. The experience has a quality of cognitive fluidity: familiar ideas connect in unusual ways and the mind moves quickly. At stronger doses this fluidity can shift into racing, looping thought.
Within the lysergamide family, 1cP-MiPLA sits closest to a moderate-strength LSD experience. It is lighter and shorter than LSD at equivalent microgram doses, reflecting MiPLA's inherently lower potency. Its nearest structural relative is 1cP-LSD, differing only in the carboxamide group — though no controlled comparison between the two has been conducted.
MiPLA, the parent compound, was synthesized by Nichols and colleagues at Purdue University in 1994 as part of a systematic exploration of lysergamide structure-activity relationships.[1] 1cP-MiPLA appeared on research chemical markets around 2020 and was formally identified from seized blotter products in Japan in 2023.[2] It circulates in small quantities among research chemical users and remains unscheduled by name in most jurisdictions.
Subjective effects include geometric visual patterns, color enhancement, time alteration, and thought acceleration. The experience is reported as qualitatively continuous with the classical lysergamide syndrome but lighter and shorter than LSD at equivalent microgram doses, reflecting MiPLA's reduced serotonin receptor affinity.[1] Thought loops, anxious fixation, and acute anxiety are common unsought effects.
1cP-MiPLA produces no physical dependence; by class extrapolation from LSD, acute toxicity is expected to be negligible.[3] The primary risk is psychological — anxiety, paranoia, and rare cases of HPPD scale with dose and predisposition.[4] No controlled human data of any kind exist for 1cP-MiPLA; the entire profile rests on structural analogy to characterized lysergamides and unverified community reports.[2]
History[edit]
Discovery
The parent compound MiPLA was first synthesized by Nichols and colleagues at Purdue University in 1994 during a systematic investigation of lysergamide structure-activity relationships.[1] That study demonstrated MiPLA could fully substitute for LSD in trained rats, establishing its psychedelic activity in animal models despite reduced serotonin receptor affinity. 1cP-MiPLA has no published synthesis record in the academic literature; it likely emerged from clandestine laboratories applying the established 1-acyl prodrug strategy to the MiPLA scaffold.
The 1-acyl prodrug wave
1cP-MiPLA belongs to a wave of 1-acyl lysergamide prodrugs that appeared on research chemical markets from approximately 2015 onward. 1P-LSD was the first to receive detailed characterization,[5] followed by 1B-LSD,[6] 1cP-LSD,[7] and 1V-LSD[8] — each confirmed to release LSD as its active compound. 1cP-MiPLA extended this prodrug approach to a non-LSD parent for the first time, combining the 1-acyl mechanism with an alternative carboxamide.
First identification
1cP-MiPLA first appeared on online markets circa 2020.[2] The compound was formally identified in 2022 when researchers at Japan's National Institute of Health Sciences detected it in seized blotter products, achieving structural elucidation through mass spectrometry and NMR.[2] That 2023 publication remains the only peer-reviewed scientific report on 1cP-MiPLA, and its authors explicitly noted that the compound's metabolic pathways and biological activities had not been reported.[2]
The name 1cP-MiPLA encodes its molecular structure: "1cP" denotes the 1-cyclopropanoyl group at the indole nitrogen, while "MiPLA" abbreviates N-methyl-N-isopropyllysergamide, the parent compound it is presumed to release. This naming convention mirrors the established pattern for 1-acyl lysergamides (1P-LSD, 1cP-LSD, 1V-LSD), signaling prodrug identity directly in the name. No street names or slang terms have emerged — the compound circulates exclusively under its chemical abbreviation within research chemical communities.
Chemistry[edit]
Structural class
1cP-MiPLA belongs to the lysergamide family — tetracyclic indole compounds built on the ergoline scaffold. It carries two modifications relative to LSD: a cyclopropanecarbonyl group at the N1-indole nitrogen (shared with 1cP-LSD) and an N-methyl-N-isopropyl substituent at the C-8 carboxamide (shared with MiPLA).[2]
The C-8 amide position is a critical determinant of receptor affinity. Nichols and colleagues demonstrated that increasing alkyl bulk at this position progressively reduces serotonin receptor binding — MiPLA's mixed N-methyl-N-isopropyl group retains full LSD-like behavioral substitution but with 2–3× reduced potency.[1]
Molecular properties
| Molecular formula | C₂₄H₂₉N₃O₂ |
| Molecular weight | 391.5 g/mol |
No CAS number has been assigned. The compound carries two carbonyl oxygens — one in the C-8 carboxamide and one in the N1-cyclopropanoyl group — and three nitrogen atoms distributed across the indole, the piperidine ring, and the carboxamide.
Stereochemistry
The ergoline scaffold contains two chirality centers at C-6a and C-9. The pharmacologically active configuration is (6aR,9R), corresponding to the d-lysergic acid series — the same absolute configuration as LSD. The opposite enantiomers are inactive at serotonin receptors.[9]
Physical properties
No published characterization of 1cP-MiPLA's physical properties exists. Melting point, solubility, and stability data have not been reported. The compound has been encountered exclusively as blotter paper and tablet formulations.[2] By analogy with other lysergamides, it is expected to be sensitive to heat, light, and oxidation.
Pharmacology[edit]
Mechanism of action
No substance-specific pharmacological data have been published for 1cP-MiPLA. The mechanism described below is inferred from the 1-acyl lysergamide prodrug class and from receptor data on MiPLA.1cP-MiPLA is presumed to function as a prodrug for MiPLA. The cyclopropanoyl group at the indole nitrogen renders the intact molecule largely inactive at serotonin receptors.[10] Enzymes in blood and liver cleave this group, releasing MiPLA as the active compound.
This prodrug mechanism has been directly confirmed for five structurally related lysergamides, including 1cP-LSD → LSD,[7] 1P-LSD → LSD,[5] and 1V-LSD → LSD.[8] Tanaka et al. explicitly stated that the metabolic pathways of 1cP-MiPLA have not been reported,[2] but the consistency of this mechanism across the class provides strong structural-structural analog support.
Once released, MiPLA produces its psychedelic effects primarily through agonism at the 5-HT₂A receptor — the established mediator of classical psychedelic activity. In controlled LSD studies, the selective serotonin 2A receptor antagonist ketanserin completely abolishes all subjective effects.[11] Additional activity at 5-HT₁A, 5-HT₂C, and dopaminergic systems contributes to the full pharmacological profile.[12]
Pharmacokinetics
No pharmacokinetic data exist for 1cP-MiPLA or MiPLA in any species. Reference parameters from controlled LSD studies place oral absorption peak at approximately 1.1 hours, bioavailability at roughly 80%, and half-life at 2.7–3.5 hours.[13][14]
Two structural differences distinguish 1cP-MiPLA from LSD in expected pharmacokinetic behavior. The prodrug hydrolysis step introduces an additional metabolic delay before active compound reaches circulation, consistent with delayed onset observed for 1cP-LSD relative to LSD.[7] The altered carboxamide of MiPLA may further affect metabolic processing, but no data exist to characterize these differences.
Individuals who metabolize LSD slowly show approximately 75% higher blood levels and prolonged effects.[15] Whether this genetic variation affects MiPLA metabolism is unknown.
Neuroscience[edit]
Where it acts
As a presumed serotonin 2A receptor agonist, MiPLA (the active metabolite) is expected to trigger the classical serotonergic psychedelic cascade: activation of serotonin receptors on cortical neurons increases excitatory neurotransmission, disrupts the default mode network, and elevates global brain connectivity.[12][16] In LSD imaging studies, these changes manifest as reduced filtering of sensory input and increased cross-talk between brain regions normally kept separate — the neural basis of the perceptual expansiveness characteristic of the psychedelic state.
MiPLA's preserved 5-HT₁A affinity[1] suggests the modulatory, potentially anxiolytic component of the serotonergic response would be retained alongside the primary 5-HT₂A-driven effects.[17]
Why it matters
The REBUS model (Relaxed Beliefs Under Psychedelics) proposes that 5-HT₂A activation loosens the brain's reliance on existing assumptions, allowing raw sensory experience to reshape perception and cognition. MiPLA's lower receptor affinity compared to LSD would predict a gentler version of this process — consistent with community reports of a shorter, more cognitively manageable experience.
LSD-class compounds also promote structural brain connectivity through neuroplasticity pathways. Whether MiPLA's reduced receptor binding preserves or diminishes this effect is unknown, with implications for any potential therapeutic application.
- Does 1cP-MiPLA convert to MiPLA in human blood at rates comparable to 1cP-LSD → LSD?
- Does MiPLA's reduced serotonin receptor affinity produce a qualitatively distinct experience, or merely a weaker version of the same one?
- Is MiPLA's relatively preserved 5-HT₁A activity (compared to its reduced 5-HT₂A binding) responsible for any distinctive anxiolytic or introspective character?
Subjective Effects[edit]
The 1cP-MiPLA experience reflects two layers of pharmacological attenuation: the prodrug conversion step shared with all 1-acyl lysergamides, and MiPLA's inherently lower serotonin receptor affinity compared to LSD. Community reports describe an experience qualitatively continuous with the classical lysergamide syndrome — perceptual shifts, cognitive fluidity, emotional enhancement — but shorter and less intense at equivalent microgram doses. Set and setting remain the dominant modulators of outcome; the compound's reduced intensity does not confer reduced psychological risk at strong doses.
Within the lysergamide landscape, 1cP-MiPLA sits closest to a moderate-strength LSD experience. Its nearest structural relative is 1cP-LSD, from which it differs only in the carboxamide substituent — though no controlled comparison between the two has been conducted.
Effect Grid
A clear psychedelic state with unmistakable visual phenomena: color enhancement intensifies, visual drifting and geometry become prominent, environmental patterning and object transformations emerge. Internal hallucinations may appear with eyes closed. Music enhancement and auditory enhancement are pronounced.
Physical effects include a developed body high with spontaneous body sensations, possible temperature dysregulation, muscle tension, and pupil dilation. Nausea during the come-up is possible. Stimulation and wakefulness are notable.
Emotional enhancement and thought connectivity characterize the cognitive space. Time alteration becomes significant. Conceptual thinking and analysis enhancement emerge. Set and setting become important modulators of experience quality. Duration is approximately 4–6 hours.
Modeled from the effect's dose-dependence curve — not per-substance measurements.
Color alteration · Holotropic state · Tracers · Depth perception distortion · Symmetrical texture repetition · Auditory enhancement · After-images · Touch enhancement · Brightness alteration · Environmental patterning · Light sensitivity · Perspective distortion · Sound sensitivity · Visual morphing · Visual diffraction · Auditory distortion · Auditory misinterpretation · Ganzfeld effect · Peripheral vision distortion · Proprioceptive distortion · Sleep-transition hallucinations · Spatial disorientation · Synesthesia · Visual haze / noise · Visual melting · Visual acuity enhancement · Peripheral misidentification · Vestibular distortion · Visual magnification · Visual processing acceleration · Dreaming enhancement · Tinnitus · Olfactory enhancement · Taste enhancement · Internal hallucinations · Object transformations · External hallucinations · Object activation · Visual scenery slicing · Auditory hallucinations · Environmental orbism / cubism · Perspective hallucinations · Visual recursion · Shadow people · Visual flipping
Symmetrical texture repetition · Auditory enhancement · After-images · Touch enhancement · Brightness alteration · Environmental patterning · Light sensitivity · Perspective distortion · Sound sensitivity · Visual morphing · Visual diffraction · Auditory distortion · Auditory misinterpretation · Ganzfeld effect · Peripheral vision distortion · Proprioceptive distortion · Sleep-transition hallucinations · Spatial disorientation · Synesthesia · Visual haze / noise · Visual melting · Visual acuity enhancement · Peripheral misidentification · Vestibular distortion · Visual magnification · Visual processing acceleration · Dreaming enhancement · Tinnitus · Olfactory enhancement · Taste enhancement · Internal hallucinations · Object transformations · External hallucinations · Object activation · Visual scenery slicing · Auditory hallucinations · Environmental orbism / cubism · Perspective hallucinations · Visual recursion · Shadow people · Visual flipping
Stimulation · Wakefulness · Tactile euphoria · Body high · Tingling / electric sensations · Body schema distortion · Appetite suppression · Nausea · Bodily lightness · Dizziness · Heart rate perception changes · Insomnia · Laughter fits · Vibrations / buzzing · Excessive sweating · Muscle tension · Sexual arousal enhancement · Involuntary body movements · Bodily pressures · Breathing alteration · Dry mouth · Nystagmus (eye wobbles) · Physical fatigue · Restlessness · Vasoconstriction · Abnormal heartbeat · Increased urination · Salivation · Bodily heaviness · Bruxism · Dehydration sensation · Headache · Muscle relaxation · Pain suppression · Trembling · Watery eyes · Yawning · Vomiting · Motor control enhancement · Seizure threshold reduction · Bodily dissociation · Tactile hallucination
Body high · Tingling / electric sensations · Body schema distortion · Appetite suppression · Nausea · Bodily lightness · Dizziness · Heart rate perception changes · Insomnia · Laughter fits · Vibrations / buzzing · Excessive sweating · Muscle tension · Sexual arousal enhancement · Involuntary body movements · Bodily pressures · Breathing alteration · Dry mouth · Nystagmus (eye wobbles) · Physical fatigue · Restlessness · Abnormal heartbeat · Increased urination · Salivation · Bodily heaviness · Bruxism · Dehydration sensation · Headache · Muscle relaxation · Pain suppression · Trembling · Watery eyes · Yawning · Vomiting · Motor control enhancement · Seizure threshold reduction · Bodily dissociation · Tactile hallucination
Cognitive euphoria · Novelty enhancement · Immersion enhancement · Aesthetic enhancement · Cognitive flexibility · Thought connectivity · Thought acceleration · Pattern recognition enhancement · Increased nature relatedness · Multiple thought streams · Creativity enhancement · Thought loops · Analysis enhancement · Humor enhancement · Memory suppression · Cognitive impairment · Confusion · Memory fragmentation · Synchronicity · Thought disorganization · Focus enhancement · Motivation enhancement · Information processing enhancement · Cognitive fatigue · Focus suppression · Information processing suppression · Memory replays · Language enhancement · Cognitive dysphoria · Language suppression · Motivation suppression · Thought deceleration · Memory enhancement · Thought organization · Delusions · Amnesia · Delirium
Aesthetic enhancement · Cognitive flexibility · Thought connectivity · Thought acceleration · Pattern recognition enhancement · Increased nature relatedness · Multiple thought streams · Creativity enhancement · Thought loops · Analysis enhancement · Humor enhancement · Memory suppression · Cognitive impairment · Confusion · Memory fragmentation · Synchronicity · Thought disorganization · Focus enhancement · Motivation enhancement · Information processing enhancement · Cognitive fatigue · Focus suppression · Information processing suppression · Memory replays · Language enhancement · Cognitive dysphoria · Language suppression · Motivation suppression · Thought deceleration · Memory enhancement · Thought organization · Amnesia · Delirium
Simultaneous emotions · Anxiety · Catharsis · Empathy enhancement · Anxiety suppression · Dysphoria · Irritability
Anxiety suppression · Dysphoria · Irritability
Social connection · Trust enhancement · Communication enhancement · Flow state · Sociability enhancement · Automaticity · Communication suppression · Compulsive behavior reduction · Ego inflation · Sociability suppression · Social disconnection · Boundary dissolution · Ego dissolution · Identity alteration · Cognitive disconnection · Telepathic feelings
Sociability enhancement · Automaticity · Communication suppression · Compulsive behavior reduction · Ego inflation · Sociability suppression · Social disconnection · Boundary dissolution · Ego dissolution · Identity alteration · Cognitive disconnection · Telepathic feelings
Time cessation
Transpersonal feelings · Transpersonal memory access · Transpersonal visions · Death-rebirth sequence · Voidness · Cessation · Near-death experience
Voidness · Cessation · Near-death experience
Cognitive dissonance · Lucidity enhancement · Mindfulness enhancement · Recursive awareness
Timeline
Initial alerting with subtle body awareness and mild stimulation. A sense that something has shifted, but no defined psychedelic phenomena yet.
Progressive intensification as visual and cognitive effects emerge. Body load — nausea, muscle tension — is most prominent during this phase.
Maximum perceptual, cognitive, and emotional effects. Visual phenomena fully developed; geometry, color enhancement, and drifting are pronounced. Ego dissolution possible at strong+ doses.
Gradual reduction in intensity. Visual effects diminish first; cognitive and emotional effects linger. Body load resolves.
Residual mood elevation or fatigue with subtle perceptual sensitivity. Reflective cognitive state. Sleep may be difficult for several hours after subjective effects resolve.
Safety[edit]
- Acute toxicity
- Negligible
- Chronic toxicity
- Negligible
- Withdrawal
- None
- Tolerance buildup
- rapid
- Tolerance reset
- 14 days
- Physical
- None
- Psychological
- Negligible
- Compulsive redosing
- Negligible
- Dose escalation
- Negligible
- Cross-tol.
- LSD · psilo · mesc
Toxicity
Acute toxicity
No lethal dose or organ toxicity data have been established for 1cP-MiPLA. By analogy with LSD — which has no known organ toxicity and an estimated lethal dose exceeding 14,000 µg — acute physical toxicity is expected to be negligible.[3] One documented accidental LSD ingestion of approximately 55 mg resulted in complete recovery without organ damage.[18]
Chronic toxicity
No chronic toxicity data exist for 1cP-MiPLA. LSD has not been associated with chronic organ damage,[3] and rapid tolerance buildup makes sustained daily dosing uncommon.
Psychological risks
Acute psychological distress — anxiety, paranoia, thought loops, and panic — can occur at any dose, especially in unsupportive settings or in individuals with existing psychiatric vulnerability.[12] Ego dissolution at high doses can be severely distressing without preparation.
Rare persistent visual disturbances — after-images, peripheral movement, halos, and visual haze / noise — can follow psychedelic use in some individuals.[4] LSD-type compounds are most commonly implicated; risk factors include prior psychiatric history and polydrug use.[4] Psychedelic use can also trigger psychotic episodes in people with a personal or family history of schizophrenia or bipolar disorder.safety citation needed
Tolerance and dependence
Classical serotonergic psychedelics build near-complete tolerance within hours of a single dose.[19][20] Serotonin receptor density in the brain drops within 24 hours, making a repeat dose much less effective.[20]
Full cross-tolerance exists with LSD, psilocybin, and mescaline via the shared serotonin receptor mechanism.[20][16] Classical psychedelics do not activate the brain's reward pathways in the manner of addictive substances — compulsive use is rare.[16]
Drug Interactions
No substance-specific interaction data exist for 1cP-MiPLA. All assessments are extrapolated from LSD-class pharmacology.
Tramadol (dangerous): tramadol blocks serotonin reuptake. Combining it with a serotonergic psychedelic can trigger serotonin syndrome — muscle rigidity, rapid heart rate, high fever, and altered consciousness.[21] Deaths from tramadol combined with serotonergic agents have been reported.[5]
MAOIs (dangerous): Monoamine oxidase inhibitors block serotonin breakdown, dramatically amplifying the effects of any serotonin-active compound. The combination has produced fatalities.[5]
Lithium: Case reports suggest increased seizure risk when lithium is combined with psychedelics.safety citation needed
SSRIs/SNRIs: These antidepressants typically reduce psychedelic effects through receptor competition. Theoretical serotonin syndrome risk exists at high doses, though clinical significance for lysergamides is unclear.safety citation needed
Cannabis (unknown): No published interaction data exist. The combination has not been characterized in controlled studies.
Contraindications
7 knownPersonal or family history of psychosis or schizophrenia spectrum disorders (absolute): Serotonin receptor activation can trigger or worsen psychotic episodes.safety citation needed
Bipolar disorder (absolute): Risk of triggering manic episodes.safety citation needed
Concurrent tramadol use (absolute): Serotonin syndrome risk.[21]
Concurrent MAOI use (absolute): Serotonin syndrome risk.[5]
Heart conditions (relative): Serotonergic psychedelics mildly raise heart rate and blood pressure. These effects may be poorly tolerated by those with pre-existing cardiovascular conditions.safety citation needed
Pregnancy (absolute): No reproductive safety data exist for 1cP-MiPLA, MiPLA, or LSD.safety citation needed
Harm Reduction[edit]
Forms & Identification
1cP-MiPLA circulates only on blotter paper and in tablet form. It is invisible, odorless, and tasteless once applied to blotter — visual inspection alone cannot confirm identity or dose. A strongly bitter or numbing taste suggests an NBOMe compound or other adulterant; genuine lysergamides are tasteless.
Reagent testing provides a useful first screen but cannot distinguish between different lysergamides. Laboratory testing services are the only reliable method to confirm both identity and dose for novel lysergamides.
Guidelines
- Test before use. Reagent kits provide a first screen; laboratory testing is the only way to confirm identity and dose for novel lysergamides.
- Start low. With no published dose-response data, begin at the lowest available dose and wait the full duration before considering redosing. The prodrug conversion step may delay onset beyond expectations.
- Have a sitter. A trusted, sober companion can provide reassurance and intervene if behavior becomes unsafe.
- Clear the schedule. Allow a full day with no obligations — including time after effects subside for rest and integration.
- Hydrate and eat beforehand. A light meal 2–3 hours before reduces nausea risk. Keep water accessible throughout.
- Avoid redosing. Rapid tolerance means a second dose within hours produces diminished effects while extending duration unpredictably.
Set & Setting
The psychedelic experience is shaped profoundly by internal state (set) and physical environment (setting). Anxiety, unresolved emotional distress, or reluctance increase the likelihood of a difficult experience. A calm, familiar space with trusted companions and no time pressure provides the strongest foundation.
1cP-MiPLA's shorter duration relative to LSD may feel more approachable, but reduced intensity at standard doses is not reduced psychological risk. Strong doses can still produce overwhelming experiences regardless of relative potency.
Aftercare & integration. The 24–48 hours following a psychedelic experience are a sensitive period. Sleep may be difficult immediately after — this is normal for the lysergamide class and resolves without intervention.
Journaling or voice-recording impressions soon after helps preserve insights. Integration — making sense of the experience and applying it to daily life — benefits from reflection with a trusted friend, therapist, or integration circle. Persistent anxiety, intrusive imagery, or visual disturbances lasting more than a few days warrant consultation with a mental health professional experienced in psychedelic-related concerns.
Recovery & Support
Classical psychedelics carry low dependence risk, and compulsive use is rare. Where problematic use does develop, it typically reflects broader psychological distress rather than pharmacological compulsion.
If psychedelic use is causing distress, interfering with daily functioning, or being used to avoid difficult emotions, professional support is appropriate. Resources include the Fireside Project crisis line (62-FIRESIDE), MAPS integration therapist directory, and local harm reduction organizations.
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Most difficult psychedelic experiences are distressing but not medically dangerous. Seek immediate help if any of the following occur: self-harm attempts or expressed intent, complete disconnection from reality with inability to communicate, seizures, or sustained chest pain.
- 1. Call emergency services if the person is unresponsive, seizing, or at risk of harming themselves or others.
- 2. Keep the person in a calm, quiet space. Speak in simple, reassuring sentences.
- 3. Do not restrain unless there is immediate danger of injury.
- 4. Place an unconscious person in the recovery position (on their side, airway clear).
- 5. Do not induce vomiting.
Tell the dispatcher: the substance name (1cP-MiPLA, a lysergamide psychedelic), approximate dose and time of ingestion, and current symptoms. Good Samaritan laws in many jurisdictions protect people who call for help from drug-related legal consequences.
Legal Status[edit]
As of 2026, 1cP-MiPLA is not widely scheduled by name in international drug control frameworks. Jurisdictions with broad structural analog laws or blanket novel psychoactive substance legislation may capture it without explicit scheduling.citation needed
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| United States | Not explicitly scheduled | LSD is Schedule I. The Federal Analogue Act may apply if 1cP-MiPLA is deemed substantially similar to LSD and intended for human consumption. |
| United Kingdom | Controlled (blanket) | The Psychoactive Substances Act 2016 covers any psychoactive substance not otherwise exempt. |
| Germany | Likely controlled | MiPLA is controlled under the NpSG as of 2019. 1cP-MiPLA, as a MiPLA prodrug, is likely encompassed but independent confirmation is lacking. |
| Russia | Schedule I | Explicitly controlled. |
| Canada | Not scheduled | Neither MiPLA nor 1cP-MiPLA appears on CDSA schedules as of the research date. |
| Australia | Not confirmed | No explicit scheduling found. TGA scheduling status has not been independently confirmed. |
| Japan | Detected but scheduling unclear | 1cP-MiPLA was identified in seized products;[2] designation status was not specified in the publication. |
Analog and prodrug considerations
The 1-acyl prodrug strategy has been described in forensic literature as a regulatory circumvention mechanism.[22] 1cP-MiPLA's dual modification increases its structural distance from LSD, potentially complicating prosecution under analog laws. Blanket NPS legislation operates independently of structural similarity and is unaffected by this distance.
Safety[edit]
- Acute toxicity
- Negligible
- Chronic toxicity
- Negligible
- Withdrawal
- None
- Tolerance buildup
- rapid
- Tolerance reset
- 14 days
- Physical
- None
- Psychological
- Negligible
- Compulsive redosing
- Negligible
- Dose escalation
- Negligible
- Cross-tol.
- LSD · psilo · mesc
Toxicity
Acute toxicity
No lethal dose, organ toxicity, or safety threshold data have been determined for 1cP-MiPLA or MiPLA in any species. The toxicity profile is inferred entirely from LSD.
LSD has no known organ toxicity at any dose studied in humans.[3] The estimated human lethal dose exceeds 14,000 µg — approximately 100× a strong recreational dose.[3] Among five deaths historically attributed to LSD, none were credibly caused by direct drug toxicity.[3] One documented accidental ingestion of approximately 55 mg (550× a standard dose) resulted in prolonged altered consciousness but complete recovery without organ damage.[18]
Chronic toxicity
No chronic toxicity data exist for 1cP-MiPLA, MiPLA, or any 1-acyl lysergamide. LSD has not been associated with chronic organ damage in available evidence.[3] Rapid tolerance buildup makes sustained daily dosing uncommon, limiting chronic exposure in practice.
Psychological risks
Acute psychological distress — anxiety, paranoia, thought loops, and panic — can occur at any dose, particularly in unsupportive settings or in individuals with pre-existing psychiatric vulnerability.[11] Ego dissolution at high doses can be profoundly distressing without preparation and support.
Hallucinogen persisting perception disorder (HPPD) is a rare condition involving persistent visual disturbances — after-images, peripheral movement, halos, and visual haze / noise — following psychedelic use.[4] LSD-type compounds are the most commonly implicated substances. Risk factors include prior psychiatric history and polydrug use.[4] No HPPD cases have been specifically attributed to 1cP-MiPLA or MiPLA.
Psychedelic use can precipitate psychotic episodes in individuals with a personal or family history of schizophrenia spectrum disorders or bipolar disorder.safety citation needed
Tolerance and dependence
Classical serotonergic psychedelics develop rapid, near-complete tolerance after a single dose.[19][20] The mechanism involves reduction of serotonin receptor density in the brain within 24 hours.[20]
Full cross-tolerance exists between LSD and other classical psychedelics (psilocybin, mescaline) via the shared 5-HT₂A receptor mechanism.[20][16] 1cP-MiPLA/MiPLA would be expected to participate in this cross-tolerance network.
Classical psychedelics are not considered habit-forming — they do not activate the brain's reward pathways in the manner of addictive substances.[16] Community-reported tolerance parameters (near-immediate buildup, approximately 14-day full reset) are consistent with published LSD class data.
Drug Interactions
No substance-specific interaction data exist for 1cP-MiPLA. All interaction assessments are extrapolated from LSD-class pharmacology.
Tramadol (dangerous): tramadol blocks serotonin reuptake in addition to its painkilling activity. Combining it with serotonergic psychedelics creates a risk of serotonin syndrome — a potentially fatal condition involving muscle rigidity, rapid heart rate, high fever, and altered consciousness.[21] Deaths from tramadol combined with serotonergic agents have been reported.[22]
MAOIs (dangerous): Monoamine oxidase inhibitors block serotonin breakdown, amplifying the effects of any serotonin-active compound. The combination of MAOIs with serotonergic substances has produced fatalities.[22]
Lithium: Case reports suggest increased seizure risk when lithium is combined with psychedelics.safety citation needed
SSRIs/SNRIs: These antidepressants typically blunt psychedelic effects through receptor competition. Theoretical serotonin syndrome risk exists at high doses, though clinical significance for lysergamides specifically is unclear.safety citation needed
Cannabis (unknown): No published interaction data exist for 1cP-MiPLA combined with cannabis. The combination has not been characterized in controlled studies.
Contraindications
7 knownThe following contraindications are inferred from the LSD class. No substance-specific data exist for 1cP-MiPLA.
Personal or family history of psychosis or schizophrenia spectrum disorders (absolute): Serotonin receptor activation can trigger or worsen psychotic episodes in vulnerable individuals.safety citation needed
Bipolar disorder (absolute): Risk of triggering manic episodes.safety citation needed
Concurrent tramadol use (absolute): Serotonin syndrome risk.[21]
Concurrent MAOI use (absolute): Serotonin syndrome risk.[22]
Heart conditions (relative): Serotonergic psychedelics produce mild increases in heart rate and blood pressure. While clinically insignificant in healthy individuals, these effects may be poorly tolerated by those with pre-existing cardiovascular conditions.safety citation needed
Pregnancy (absolute): No reproductive safety data exist for 1cP-MiPLA, MiPLA, or LSD.safety citation needed
Harm Reduction[edit]
Forms & Identification
1cP-MiPLA circulates exclusively on blotter paper and in tablet form. The compound is invisible, odorless, and tasteless once laid on blotter — visual inspection alone cannot confirm identity or dose. A strongly bitter or numbing taste suggests substitution with an NBOMe compound or other adulterant; genuine lysergamides are tasteless.
Reagent testing provides a useful first screen but cannot distinguish between different lysergamides on blotter. Quantitative analysis through laboratory testing services is the only reliable method to confirm both identity and dose for novel lysergamides.
Guidelines
- Test before use. Reagent kits provide a first screen; quantitative lab testing is the only way to confirm identity and dose for novel lysergamides.
- Start low. With no published dose-response data, begin at the lowest available dose and wait the full duration before considering redosing. The prodrug conversion step may delay onset beyond expectations.
- Have a sitter. A trusted, sober companion can provide reassurance during difficult moments and intervene if behavior becomes unsafe.
- Clear your schedule. Allow a full day with no obligations — including time after effects subside for rest and integration.
- Hydrate and eat beforehand. A light meal 2–3 hours before reduces nausea risk. Keep water accessible throughout.
- Avoid redosing. Rapid tolerance means a second dose within hours will produce diminished effects, not a fresh experience, while extending duration unpredictably.
Set & Setting
The psychedelic experience is profoundly shaped by internal state (set) and physical environment (setting). Anxiety, unresolved emotional distress, or reluctance about the experience increase the likelihood of a difficult trip. A calm, familiar space with trusted companions and no time pressure provides the strongest foundation.
1cP-MiPLA's shorter duration relative to LSD may make the experience feel more approachable, but reduced intensity at standard doses should not be mistaken for reduced psychological risk — strong or heavy doses can still produce overwhelming experiences regardless of the compound's relative potency.
Aftercare & integration. The 24–48 hours following a psychedelic experience are a sensitive period. Sleep may be difficult immediately after — this is normal for the lysergamide class and resolves without intervention.
Journaling or voice-recording impressions soon after the experience can help preserve insights before they fade. Integration — the process of making sense of the experience and applying its content to daily life — benefits from reflection with a trusted friend, therapist, or integration circle. Persistent anxiety, intrusive imagery, or visual disturbances lasting more than a few days warrant consultation with a mental health professional experienced in psychedelic-related concerns.
Recovery & Support
Classical psychedelics carry low dependence risk, and compulsive use patterns are rare. Where problematic use does develop, it typically reflects broader psychological distress rather than pharmacological compulsion.
If psychedelic use is causing distress, interfering with daily functioning, or being used to avoid difficult emotions, professional support is appropriate. Resources include the Fireside Project crisis line (62-FIRESIDE), MAPS integration therapist directory, and local harm reduction organizations.
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Most difficult psychedelic experiences are distressing but not medically dangerous. Seek immediate help if any of the following occur: self-harm attempts or expressed intent, complete disconnection from reality with inability to communicate, seizures, or sustained chest pain.
- 1. Call emergency services if the person is unresponsive, seizing, or at risk of harming themselves or others.
- 2. Keep the person in a calm, quiet space. Speak in simple, reassuring sentences.
- 3. Do not restrain unless there is immediate danger of injury.
- 4. Place an unconscious person in the recovery position (on their side, airway clear).
- 5. Do not induce vomiting.
Tell the dispatcher: the substance name (1cP-MiPLA, a lysergamide psychedelic), approximate dose and time of ingestion, and current symptoms. Good Samaritan laws in many jurisdictions protect people who call for help from drug-related legal consequences.
Legal Status[edit]
As of 2026, 1cP-MiPLA is not widely scheduled by name in international drug control frameworks. Its legal status is complicated by its dual identity as a novel psychoactive substance and a presumed prodrug for MiPLA, which is itself structurally related to LSD. Jurisdictions with broad structural analog laws or blanket NPS legislation may capture it without explicit scheduling. All legal data below are web-retrieved and have not been verified against primary legislative texts.citation needed
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| United States | Not explicitly scheduled | LSD is Schedule I. 1cP-MiPLA is not named in federal schedules; the Federal Analogue Act (21 USC §813) may apply if the compound is deemed substantially similar to LSD and intended for human consumption. |
| United Kingdom | Controlled (blanket) | The Psychoactive Substances Act 2016 broadly covers any psychoactive substance not otherwise exempt. 1cP-MiPLA falls under this blanket provision. |
| Germany | Likely controlled | MiPLA is controlled under the NpSG as of 2019. 1cP-MiPLA, as a MiPLA prodrug, is likely encompassed but independent confirmation is lacking. |
| Russia | Schedule I | Explicitly controlled. |
| Canada | Not scheduled | Neither MiPLA nor 1cP-MiPLA appears on CDSA schedules as of the research date. |
| Australia | Not confirmed | No explicit scheduling found. TGA scheduling status has not been independently confirmed. |
| Japan | Detected but scheduling unclear | 1cP-MiPLA was identified in seized products in Japan;[2] its designation status under Japan's framework was not specified in the publication. |
Analog and prodrug considerations
The prodrug strategy underlying the 1-acyl lysergamide class has been explicitly described as a regulatory circumvention mechanism in forensic literature.[23] 1cP-MiPLA's dual modification — N1-acylation plus an altered carboxamide — increases its structural distance from LSD compared to simpler analogs like 1P-LSD or 1cP-LSD, potentially complicating prosecution under analog laws.
This structural distance does not, however, affect classification under blanket NPS legislation that operates independently of structural similarity.
Frequently asked questions
What is 1cP-MiPLA?
1cP-MiPLA is a synthetic lysergamide psychedelic and presumed prodrug for MiPLA, first identified in seized blotter products in Japan in 2022. It combines a cyclopropanoyl N1-acyl group with an N-methyl-N-isopropyl carboxamide on the ergoline scaffold.
How long does 1cP-MiPLA last?
Total duration by route of administration — Oral: 4 – 6 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 1cP-MiPLA?
Psychedex publishes a dosage table for 1cP-MiPLA 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 1cP-MiPLA?
The highest-severity documented interactions for 1cP-MiPLA: 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 1cP-MiPLA addictive?
Psychedex records tolerance and dependence data rather than a yes/no rating. Recorded tolerance indicators for 1cP-MiPLA: tolerance builds rapid; full reset takes 14 days; cross-tolerance develops with LSD, psilocybin, mescaline, DOI. 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
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- [3] ^abcNichols DE, Grob CS (2018) Is LSD toxic? — Forensic Science International doi:10.1016/j.forsciint.2018.01.006
- [4] ^abcMartinotti G, Santacroce R, Pettorruso M, Montemitro C, Spano MC, Lorusso M, Di Giannantonio M, Gallimberti L (2018) Hallucinogen Persisting Perception Disorder: Etiology, Clinical Features, and Therapeutic Perspectives — Brain Sciences doi:10.3390/brainsci8030047
- [5] ^abcdRached G, Campana A, Fiani D, et al. (2026) Safety and Efficacy of Monoamine Oxidase Inhibitors in Patients Who Use Psychoactive Substances — CNS Drugs doi:10.1007/s40263-025-01256-7
- [6] ^abBrandt SD, Kavanagh PV, Westphal F, Stratford A, Elliott SP, Hoang K, Wallach J, Halberstadt AL (2016) Return of the lysergamides. Part I: Analytical and behavioural characterization of 1-propionyl-d-lysergic acid diethylamide (1P-LSD) — Drug Testing and Analysis doi:10.1002/dta.1884
references
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- [2]
- [3]
- [4] ^abcMartinotti G, Santacroce R, Pettorruso M, Montemitro C, Spano MC, Lorusso M, Di Giannantonio M, Gallimberti L (2018) Hallucinogen Persisting Perception Disorder: Etiology, Clinical Features, and Therapeutic Perspectives — Brain Sciences doi:10.3390/brainsci8030047
- [5] ^abBrandt SD, Kavanagh PV, Westphal F, Stratford A, Elliott SP, Hoang K, Wallach J, Halberstadt AL (2016) Return of the lysergamides. Part I: Analytical and behavioural characterization of 1-propionyl-d-lysergic acid diethylamide (1P-LSD) — Drug Testing and Analysis doi:10.1002/dta.1884
- [6] ^Brandt SD, Kavanagh PV, Westphal F, Stratford A, Elliott SP, et al. (2019) Return of the lysergamides. Part V: Analytical and behavioural characterization of 1-butanoyl-d-lysergic acid diethylamide (1B-LSD) — Drug Testing and Analysis doi:10.1002/dta.2613