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1cP-AL-LAD
1-cyclopropanoyl-N6-allyl-6-norlysergic acid diethylamide
1cP-AL-LAD is a synthetic psychedelic of the lysergamide class. It is a prodrug of AL-LAD, a close structural relative of LSD. It activates serotonin receptors in the brain, producing the visual and cognitive shifts characteristic of classical psychedelics.
1cP-AL-LAD is an emerging synthetic psychedelic of the lysergamide class. It is a prodrug of AL-LAD, a close structural relative of LSD. AL-LAD is a 5-HT₂A receptor agonist, producing its effects by disrupting the brain's default filtering of sensory and cognitive input.
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AL-LAD, the parent compound, was first synthesized in the 1980s; 1cP-AL-LAD emerged around 2022–2023 by combining structural features of 1cP-LSD[1] and AL-LAD.[2] It was developed to exploit legal gaps created by government bans on earlier analogs. It circulates as blotter paper through online research chemical vendors and remains unscheduled in most jurisdictions.
Subjective effects include geometric visual patterns, brightened colors, time alteration, accelerated thinking, and elevated mood. The experience follows the classical lysergamide arc — visually rich, cognitively expansive, with a light stimulant edge, shaped heavily by mindset and environment. Thought loops, anxious fixation, and difficulty sleeping are common unwanted effects.
1cP-AL-LAD produces no physical dependence, and serotonergic psychedelics carry an extremely high physiological safety margin;[3] rapid tolerance after a single dose makes compulsive use self-limiting.[4] The primary risks are psychological — acute distress, rare persistent visual disturbances, and psychiatric destabilisation, amplified sharply by combinations with MAOIs or lithium. No pharmacological, toxicological, or clinical study of 1cP-AL-LAD exists; its entire profile is inferred from structural analogy.
History[edit]
Discovery
AL-LAD (N6-allyl-6-nor-LSD) was first synthesised in the mid-1980s by Andrew Hoffman and David Nichols, exploring modifications to the LSD scaffold.[5] citation needed It entered the research chemical market in 2013, with studies confirming hallucinogenic potency comparable to LSD.[6]
The N1-acyl prodrug wave
Through the mid-2010s, online vendors sequentially introduced N1-acylated lysergamides — 1P-LSD, 1cP-LSD, and others — exploiting the lag between novel structural analog releases and country-specific bans.[7] Germany's 2021 NpSG revision banned 1cP-LSD and related acyl lysergamides, creating commercial pressure to introduce further variants.[8] 1cP-AL-LAD — merging the cyclopropanoyl group of 1cP-LSD with AL-LAD's allyl scaffold — appeared on vendor sites around 2022–2023.
Scientific characterisation
Two independent forensic studies in 2023 constitute the entire published record. Kavanagh and colleagues characterised the compound's analytical profile and identified 17 impurities in a commercial sample;[9] Tanaka and colleagues identified it in sheet products monitored in Japan.[10] Both noted the complete absence of metabolic or biological activity data. As of May 2026, no pharmacological, toxicological, or clinical study of 1cP-AL-LAD has been published.
The name 1cP-AL-LAD follows the systematic convention used across the N1-acyl lysergamide series: the prefix denotes the acyl group (1cP = 1-cyclopropanoyl at N1), and the base name identifies the parent lysergamide (AL-LAD = N6-allyl-6-nor-LSD). This pattern — shared with 1P-LSD, 1V-LSD, and 1cP-LSD — locates a compound within the prodrug lineage. No street names or informal nomenclature have been documented.
Chemistry[edit]
Structural class
1cP-AL-LAD is a lysergamide — a chemical family built on the ergoline ring system. It combines two structural changes to the LSD scaffold: the N6 methyl group is replaced by an allyl chain, creating the AL-LAD core,[6] and a cyclopropanecarbonyl group is attached at the indole nitrogen — the same prodrug design used in 1cP-LSD.[1] It differs from the closely related 1P-AL-LAD only in that acyl group.[9]
Molecular identity
Its molecular formula is C₂₆H₃₁N₃O₂ (molecular weight 417.5 g/mol).[11] No melting point, solubility, or stability data have been published; commercial samples have been examined as powder and on blotter paper.[9]
Pharmacology[edit]
Mechanism of action
inferred No receptor binding data for 1cP-AL-LAD exist.[10] The cyclopropanoyl group at N1 is expected to be cleaved in the body before the drug reaches the brain — confirmed for 1cP-LSD, where human serum hydrolysis yields LSD,[1] and demonstrated for 1P-AL-LAD converting to AL-LAD in human liver tissue.[2]
This prodrug pattern holds across the entire N1-acyl lysergamide class — the acylated forms show weak or no direct receptor activity, yet produce high blood levels of the active parent compound.[12][13][14][15][16] If hydrolysis occurs as expected, the active compound is AL-LAD — a serotonergic psychedelic acting primarily through serotonin receptors, with secondary effects on dopamine signaling.[17]
Pharmacokinetics
inferred No human pharmacokinetic data exist for 1cP-AL-LAD. By analogy with the only N1-acyl lysergamide studied in a controlled human trial, the body likely converts it nearly completely to AL-LAD before it enters circulation — only the deacylated compound appears in blood and urine.[18] LSD's oral bioavailability is approximately 80%.[19] AL-LAD is then broken down by liver enzymes into hydroxylated and dealkylated metabolites.[20][2]
Neuroscience[edit]
Where it acts
inferred If the expected conversion to AL-LAD occurs, the active compound acts on serotonin receptors concentrated on neurons in the prefrontal cortex, increasing electrical activity and disrupting normal communication between brain regions.[17] Blocking those receptors with ketanserin fully reverses the psychedelic effect of LSD — confirming this is the necessary target, a finding presumed to extend to AL-LAD.[21]
Why it matters
The thalamus normally filters incoming sensory signals before they reach conscious awareness; psychedelics disrupt this gating, allowing more unfiltered information through. citation needed This is thought to explain the intensified perception, pattern recognition, and synesthesia of the psychedelic state.
Serotonergic psychedelics also promote rapid growth of new connections between neurons.[22] Whether AL-LAD retains the same neuroplastic potency is unknown — its allyl group alters binding geometry at the receptor, and downstream signaling may differ from LSD.
- Does 1cP-AL-LAD actually convert to AL-LAD in humans? Direct confirmation — measuring AL-LAD in the blood after oral 1cP-AL-LAD — has never been performed.
- Does the allyl group change what happens after receptor binding? Different substituents can bias the receptor toward different downstream pathways, potentially making the experience subtly different from LSD.
- What is the therapeutic index? No toxicity data exist. The margin between an active dose and a dangerous one is entirely undefined for this compound.
Subjective Effects[edit]
The 1cP-AL-LAD experience is expected to follow the classical lysergamide arc — a long, gradual build into a visually rich, cognitively expansive state with a light stimulant character running through it. Geometric patterns emerge across surfaces while time stretches and thinking opens up. The experience bends sharply toward mindset and environment.[23]
Compared to psilocybin, the experience is more outwardly engaged and analytically toned, with stronger visual geometry and less introspective weight. Compared to LSD, no controlled comparison exists for 1cP-AL-LAD specifically; individual variation across lysergamides is substantial.
1cP-AL-LAD appeared on online vendor sites around 2022–2023, combining the cyclopropanoyl prodrug group of 1cP-LSD[1] with the allyl scaffold of AL-LAD.[2] Two independent forensic studies in 2023 provided its first analytical characterisation — neither reported any biological activity data.[3][4] It circulates primarily as blotter paper through online research chemical vendors, unscheduled in most jurisdictions.
Subjective effects include geometric visual patterns, color enhancement, time alteration, thought acceleration, and mood elevation. The experience is expected to follow the classical lysergamide template — an outwardly engaged, analytically toned alteration of perception with prominent visual geometry and a light stimulant edge, shaped heavily by mindset and environment. Thought loops, anxious fixation, and difficulty sleeping are common unsought effects.
1cP-AL-LAD produces no physical dependence; rapid tolerance after a single dose makes compulsive redosing self-limiting,[5] and the serotonergic psychedelic class carries an extremely high physiological safety margin.[6] The primary risks are psychological — acute distress scaling with dose and predisposition, rare persistent visual disturbances, and psychiatric destabilisation in vulnerable individuals. No pharmacological, toxicological, or clinical study has been conducted on 1cP-AL-LAD; its entire profile is inferred from structural analogy.
History[edit]
Discovery
The parent compound AL-LAD (N6-allyl-6-nor-LSD) was first synthesised in the mid-1980s at Purdue University by Andrew Hoffman and David Nichols, as part of a systematic exploration of structure-activity relationships at the N6 position of the ergoline ring.[7] citation needed AL-LAD entered the novel psychoactive substance market in 2013 in both powder and blotter form, with mouse studies confirming hallucinogenic potency broadly comparable to LSD.[8]
The N1-acyl prodrug wave
Through the mid-2010s, NPS vendors sequentially introduced N1-acylated lysergamides — 1P-LSD, 1cP-LSD, 1V-LSD, and others — to exploit the gap between the pace of novel structural analog introduction and substance-specific scheduling.[9] Germany's 2021 NpSG revision banned 1cP-LSD and structurally related acyl lysergamides, creating commercial pressure to introduce further analogs.[10] 1cP-AL-LAD — merging the cyclopropanoyl group of 1cP-LSD with the allyl scaffold of AL-LAD — appeared on online vendor sites around 2022–2023.
Scientific characterisation
No scientific literature on 1cP-AL-LAD predates 2023. Two independent forensic studies constitute the entire published record: Kavanagh and colleagues characterised the compound's analytical profile and identified 17 impurities in a commercial sample,[3] while Tanaka and colleagues reported its identification in sheet products monitored in Japan.[4] Both groups noted the complete absence of metabolic or biological activity data. As of May 2026, no pharmacological, toxicological, or clinical study of 1cP-AL-LAD has been published.
The name 1cP-AL-LAD follows the systematic naming convention used across the N1-acyl lysergamide series: the prefix denotes the acyl group (1cP = 1-cyclopropanoyl at the N1 position), and the base name identifies the parent lysergamide (AL-LAD = N6-allyl-6-nor-LSD). This pattern — shared with 1P-LSD, 1V-LSD, and 1cP-LSD — functions as shorthand within the research chemical community for locating a compound within the prodrug lineage. No street names or informal nomenclature have been documented.
Chemistry[edit]
Structural class
1cP-AL-LAD belongs to the lysergamide family — ergoline-derived compounds sharing a tetracyclic core with an amide group at C-8. It sits at the intersection of two structural modifications applied to the LSD scaffold:
- N6-allyl substitution: The methyl group on LSD's N6 nitrogen is replaced by an allyl (prop-2-en-1-yl) chain, producing the AL-LAD scaffold.[8]
- N1-cyclopropanoyl addition: A cyclopropanecarbonyl group is attached at the indole nitrogen (N1), following the same prodrug design used in 1cP-LSD.[1]
1cP-AL-LAD differs from 1P-AL-LAD only in the N1 acyl group: cyclopropanecarbonyl versus propanoyl.[3]
Molecular identity
| Molecular formula | C₂₆H₃₁N₃O₂ |
| Molecular weight | 417.5 g/mol |
The molecule consists of the tetracyclic ergoline ring system bearing a diethylcarboxamide at C-8β, an allyl group on N6, and a cyclopropanecarbonyl group on the indole nitrogen. Two carbonyl groups are present: the C-8 amide and the N1 acyl linkage.[11]
Stereochemistry
1cP-AL-LAD retains the (6aR,9R) configuration — the natural ergoline stereochemistry shared by LSD and all pharmacologically active lysergamides.[11] The 9,10-double bond in the D ring is preserved, maintaining the planarity across the C/D junction essential for serotonin receptor binding.
Physical properties
No melting point, solubility, or stability data have been published. Commercial samples have been analysed as powder and on blotter paper.[3] Like other lysergamides, the free base is expected to be sensitive to light, heat, and oxidation.
Pharmacology[edit]
Mechanism of action
inferred No receptor binding or behavioural pharmacology data specific to 1cP-AL-LAD exist.[4] All mechanistic claims are inferred from structural analogs.
1cP-AL-LAD is most probably a prodrug for AL-LAD. The cyclopropanoyl group at N1 is expected to be cleaved in the body before the drug reaches the brain — a pattern confirmed for the closely related compound 1cP-LSD, where human serum hydrolysis yields LSD.[1] The same deacylation has been demonstrated for 1P-AL-LAD converting to AL-LAD in human liver microsomes.[2]
This prodrug pattern holds across the entire N1-acyl lysergamide class. The acylated forms show weak or no direct activity at serotonin receptors, yet administration produces high blood levels of the deacylated parent compound — confirming that the body converts them before they act.[12] The pattern extends to 1V-LSD,[13] 1B-LSD,[14] 1P-ETH-LAD,[15] and 1F-LSD/1T-LSD.[16]
If the expected hydrolysis occurs, the active compound is AL-LAD — a serotonergic psychedelic acting primarily through 5-HT₂A receptors, with secondary activity at 5-HT₂C, 5-HT₁A, and dopamine D1/D2 receptors.[17]
Pharmacokinetics
inferred No human pharmacokinetic data exist for 1cP-AL-LAD. The following is assembled from analog data.
Absorption
By analogy with 1P-LSD — the only N1-acyl lysergamide studied in a controlled human trial — oral administration likely results in near-complete conversion to the active form before it reaches general circulation. When volunteers took 100 µg oral 1P-LSD, only LSD was detectable in blood and urine; no intact 1P-LSD was found.[18] LSD itself has an oral bioavailability of approximately 80%.[19]
Metabolism and elimination
The primary metabolic step is expected to be removal of the cyclopropanoyl group, yielding AL-LAD. AL-LAD then undergoes further processing through liver enzymes, producing hydroxylated and dealkylated metabolites.[20] A study of the closely related 1P-AL-LAD identified 14 metabolites in human liver microsomes.[2]
The half-life of LSD derived from oral 1P-LSD is approximately 6.4 hours.[18] A comparable half-life is expected for AL-LAD derived from 1cP-AL-LAD, though this has not been measured.
Neuroscience[edit]
Where it acts
inferred No neuroimaging or electrophysiology data specific to 1cP-AL-LAD or AL-LAD exist. As a presumed serotonin 2A receptor agonist, AL-LAD is expected to act on serotonin receptors concentrated on pyramidal neurons in the prefrontal cortex, triggering cascades that increase excitability and disrupt normal communication between cortical regions.[17] The selective 5-HT₂A blocker ketanserin fully reverses LSD-type psychedelic effects, confirming this receptor as the necessary target — a finding presumed to extend to AL-LAD.[21]
Serotonergic psychedelics also disrupt the thalamus's role as a sensory gatekeeper, allowing a wider stream of unfiltered information to reach cortical areas. This is thought to underlie the perceptual intensification, pattern recognition, and synesthesia characteristic of the psychedelic state. citation needed
Why it matters
The Relaxed Beliefs Under Psychedelics (REBUS) model proposes that psychedelics reduce the brain's reliance on established assumptions, allowing raw sensory data to surface with less top-down filtering. For a lysergamide like AL-LAD, this predicts the characteristic loosening of perceptual certainty, conceptual fluidity, and heightened sensitivity to environment. citation needed
Serotonergic psychedelics also promote structural brain changes — rapid growth of new dendritic connections in cortical neurons via BDNF-TrkB-mTOR signalling pathways.[22] Whether AL-LAD retains full neuroplastic potency is unknown; its allyl group alters binding geometry at the receptor, and downstream signalling may differ from LSD.
- Does 1cP-AL-LAD actually convert to AL-LAD in humans? The evidence from related compounds is strong, but direct confirmation — measuring plasma AL-LAD after oral 1cP-AL-LAD — has never been performed.
- Does the allyl group change what happens after receptor binding? Different substituents can bias the receptor toward different intracellular pathways, potentially producing a subtly different experiential and neuroplastic profile compared to LSD.
- What is the therapeutic index? No toxicity data of any kind exist. The margin between an active dose and a dangerous one remains entirely undefined for this specific compound.
Subjective Effects[edit]
The 1cP-AL-LAD experience, mediated through its presumed active metabolite AL-LAD, is expected to follow the classical lysergamide arc: a gradual build into a long, visually rich, cognitively expansive state. The prodrug conversion step may contribute to a somewhat slower onset than LSD itself, though this has not been formally compared. Set and setting exert outsized influence — the same dose can produce profoundly different outcomes depending on mindset, physical environment, and social context.[23]
Compared to psilocybin, the lysergamide class generally produces a more outwardly engaged, analytically toned experience with more prominent visual geometry and stronger stimulant character. Compared to LSD, no controlled comparison data exist for 1cP-AL-LAD specifically, and individual variability across lysergamides is substantial.
Effect Grid
Full psychedelic experience — prominent visual drifting, geometric patterning, colour enhancement, and tracers dominate the visual field. Auditory enhancement and music enhancement are marked. Internal hallucinations may emerge, particularly with eyes closed.
Thought acceleration and conceptual thinking are pronounced. Emotional enhancement amplifies both positive and challenging feelings. Introspective depth increases substantially. Time alteration makes minutes feel stretched or compressed unpredictably.
Body load includes muscle tension, possible nausea during come-up, pupil dilation, and moderate stimulation. Appetite suppression is near-total. Set and setting become critical determinants of experience quality. Sleep is impossible for 8+ hours. Commercial samples may contain active impurities (AL-LAD, 1P-AL-LAD) that modestly alter the experience profile.
Modeled from the effect's dose-dependence curve — not per-substance measurements.
Color alteration · Environmental patterning · Tracers · Visual breathing · Visual drifting · Brightness alteration · Depth perception distortion · Light sensitivity · Perspective distortion · Sound sensitivity · Symmetrical texture repetition · Visual morphing · After-images · Auditory distortion · Peripheral vision distortion · Spatial disorientation · Visual diffraction · Visual haze / noise · Auditory misinterpretation · Ganzfeld effect · Holotropic state · Peripheral misidentification · Proprioceptive distortion · Synesthesia · Touch enhancement · Visual melting · Visual acuity enhancement · Dreaming enhancement · Vestibular distortion · Visual magnification · Visual processing acceleration · Taste enhancement · Flashbacks · Object transformations · Internal hallucinations · Object activation · Visual recursion · Environmental orbism / cubism · External hallucinations · Perspective hallucinations · Visual flipping · Auditory hallucinations · Visual scenery slicing · Persisting hallucinations
Visual drifting · Brightness alteration · Depth perception distortion · Light sensitivity · Perspective distortion · Sound sensitivity · Symmetrical texture repetition · Visual morphing · After-images · Auditory distortion · Peripheral vision distortion · Spatial disorientation · Visual diffraction · Visual haze / noise · Auditory misinterpretation · Ganzfeld effect · Holotropic state · Peripheral misidentification · Proprioceptive distortion · Synesthesia · Touch enhancement · Visual melting · Visual acuity enhancement · Dreaming enhancement · Vestibular distortion · Visual magnification · Visual processing acceleration · Taste enhancement · Flashbacks · Object transformations · Internal hallucinations · Object activation · Visual recursion · Environmental orbism / cubism · External hallucinations · Perspective hallucinations · Visual flipping · Auditory hallucinations · Visual scenery slicing · Persisting hallucinations
Body high · Insomnia · Spontaneous body sensations · Wakefulness · Appetite suppression · Bodily lightness · Heart rate perception changes · Laughter fits · Dry mouth · Dizziness · Body schema distortion · Nausea · Physical fatigue · Restlessness · Tactile euphoria · Tingling / electric sensations · Vibrations / buzzing · Bodily pressures · Excessive sweating · Headache · Muscle tension · Temperature dysregulation · Dehydration sensation · Breathing alteration · Bruxism · Involuntary body movements · Nystagmus (eye wobbles) · Respiratory stimulation · Sexual arousal enhancement · Sexual arousal suppression · Trembling · Vomiting · Bodily dissociation · Tactile hallucination
Wakefulness · Appetite suppression · Bodily lightness · Heart rate perception changes · Laughter fits · Dry mouth · Dizziness · Body schema distortion · Nausea · Physical fatigue · Restlessness · Tactile euphoria · Tingling / electric sensations · Vibrations / buzzing · Bodily pressures · Excessive sweating · Headache · Muscle tension · Dehydration sensation · Breathing alteration · Bruxism · Involuntary body movements · Nystagmus (eye wobbles) · Respiratory stimulation · Sexual arousal enhancement · Sexual arousal suppression · Trembling · Vomiting · Bodily dissociation · Tactile hallucination
Cognitive euphoria · Immersion enhancement · Increased nature relatedness · Introspection enhancement · Novelty enhancement · Openness enhancement · Pattern recognition enhancement · Thought acceleration · Thought connectivity · Creativity enhancement · Multiple thought streams · Humor enhancement · Analysis enhancement · Cognitive impairment · Synchronicity · Thought loops · Focus enhancement · Information processing enhancement · Motivation enhancement · Analysis suppression · Cognitive fatigue · Confusion · Focus suppression · Information processing suppression · Memory fragmentation · Memory replays · Memory suppression · Thought disorganization · Language enhancement · Cognitive dysphoria · Language suppression · Compulsive redosing urge · Delusions of sobriety · Delusions
Introspection enhancement · Novelty enhancement · Openness enhancement · Pattern recognition enhancement · Thought acceleration · Thought connectivity · Creativity enhancement · Multiple thought streams · Humor enhancement · Analysis enhancement · Cognitive impairment · Synchronicity · Thought loops · Focus enhancement · Information processing enhancement · Motivation enhancement · Analysis suppression · Cognitive fatigue · Confusion · Focus suppression · Information processing suppression · Memory fragmentation · Memory replays · Memory suppression · Thought disorganization · Language enhancement · Cognitive dysphoria · Language suppression · Delusions of sobriety · Delusions
Simultaneous emotions · Empathy enhancement · Anxiety · Catharsis · Anxiety suppression · Dysphoria · Irritability · Mania
Catharsis · Anxiety suppression · Dysphoria · Irritability
Communication enhancement · Flow state · Sociability enhancement · Depersonalization · Disinhibition · Communication suppression · Ego inflation · Sociability suppression · Social disconnection · Boundary dissolution · Cognitive disconnection · Ego dissolution · Identity alteration · Telepathic feelings
Disinhibition · Communication suppression · Ego inflation · Sociability suppression · Social disconnection · Boundary dissolution · Cognitive disconnection · Ego dissolution · Identity alteration · Telepathic feelings
Time cessation
Entity contact · Transpersonal memory access · Transpersonal visions · Cessation · Death-rebirth sequence · Near-death experience · Voidness
Death-rebirth sequence · Near-death experience · Voidness
Mindfulness enhancement · Recursive awareness
Timeline
Initial alerting — subtle body awareness, mild stimulation, possible yawning. Prodrug hydrolysis is occurring; onset may feel slower and less distinct than LSD.
Progressive intensification — visual field begins to shift, colours brighten, body high develops. Nausea and anticipatory anxiety are most common during this phase.
Full expression of psychedelic effects — visual geometry, colour enhancement, thought acceleration, emotional amplification. Ego dissolution possible at high doses. Set and setting maximally influential.
Gradual diminution — visual effects recede first, cognitive effects and emotional processing linger. Physical stimulation wanes. Appetite may begin to return.
Residual cognitive openness and mild visual aftereffects possible. Physical fatigue develops. Sleep may remain difficult for several hours.
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
inferred No toxicity data exist for 1cP-AL-LAD — no lethal dose, no therapeutic index, no organ damage assessment.safety citation needed
Acute toxicity
Serotonergic psychedelics carry an extremely high physiological safety margin. No human death has been attributed solely to direct LSD toxicity in the clinical literature — psychological risks dominate over organ damage at recreational doses.[3] This class-level assessment is presumed to extend to 1cP-AL-LAD, but no substance-specific confirmation exists.
Cardiovascular effects
LSD at 100–200 µg produces moderate, self-limiting increases in heart rate and blood pressure.[24][25] Similar effects are expected for any compound that releases AL-LAD in the body, but have not been measured for 1cP-AL-LAD.safety citation needed
Impurity exposure
One commercial sample contained 17 impurities, including confirmed AL-LAD and 1P-AL-LAD plus 15 additional compounds identified only by mass spectral data.[9] Unintended exposure to pharmacologically active impurities is a real risk specific to the unregulated supply chain.
Psychological risks
In a nationally representative sample of psychedelic users (N = 613), 40.9% reported a challenging or distressing experience, and functional impairment lasting more than one day occurred in 8.9%.[23] Key risk factors include negative mindset, disagreeable environment, and higher-than-intended dose.[23]
Some people develop ongoing visual disturbances — geometry, trailing, halos — that persist after the drug experience ends.[26][27] Psychedelics can also trigger psychotic episodes in people with a personal or family history of psychotic disorders; lithium co-use was identified as the top medication risk factor for severe outcomes.[23]
Tolerance and dependence
Tolerance
Tolerance develops almost immediately after a single dose. In rat studies, serotonin receptor binding in the cortex decreased significantly within three days of repeated dosing and recovered within four days of stopping.[4] Cross-tolerance extends across serotonergic psychedelics — LSD, psilocybin, mescaline, and structural analogs — reflecting the shared serotonin receptor mechanism.
Community consensus places full tolerance reset at approximately 14 days.safety citation needed
Dependence
Serotonergic psychedelics have negligible physical dependence liability and do not support compulsive self-administration in animal models.[28] Rapid tolerance inherently discourages repeated use. No withdrawal has been described for the lysergamide class.
Drug Interactions
Serotonergic combinations
Combining 1cP-AL-LAD with drugs that raise serotonin levels poses a risk of serotonin overload — a dangerous state involving high fever, muscle rigidity, and seizures. Tramadol blocks serotonin reuptake[29] and has produced marked serotonin syndrome in overdose;[30] combined with a serotonin receptor activator, it creates a mechanistically dangerous interaction.safety citation needed
MAOIs block the breakdown of serotonin; combining them with a serotonin receptor activator dramatically amplifies toxicity risk. No specific data exist for this combination with 1cP-AL-LAD.
Lithium
Co-use of lithium with psychedelics is associated with seizure risk and amplified, unpredictable effects. Lithium was identified as the top medication risk factor for severe adverse psychedelic outcomes.[23]
Cannabis
The interaction between cannabis and psychedelics is poorly characterized. CBD may reduce the psychedelic effect,[31] but the clinical significance is unknown. THC may increase anxiety and confusion.
Pharmacological reversal
Ketanserin — a drug that blocks serotonin receptors — reverses LSD-induced psychedelic effects when given after the drug.[21] This reversal is expected to extend to 1cP-AL-LAD and may serve as an emergency intervention. Benzodiazepines are used for acute anxiety management.
Contraindications
8 knowninferred No contraindication data specific to 1cP-AL-LAD exist. The following are class-level inferences for serotonergic psychedelics:
Absolute contraindications:
- Personal history of psychotic disorders (schizophrenia spectrum, bipolar disorder with psychotic features)
- Concurrent lithium use — associated with seizures and dangerously amplified effects[23]
- Concurrent MAOI therapy — serotonin toxicity risk
Relative contraindications:
- Personal or family history of HPPD[26]
- Serious heart conditions — moderate stimulant effects expected[24]
- Concurrent serotonergic medications (SSRIs, SNRIs, tramadol) — attenuated or unpredictable effects; serotonin toxicity risk with tramadol[29]
- Pregnancy or breastfeeding — no safety data exist
- Unstable psychiatric conditions — risk of destabilisation
safety citation needed
Harm Reduction[edit]
Forms & Identification
1cP-AL-LAD circulates almost exclusively as blotter paper. Ehrlich's reagent confirms the presence of an indole compound — it reacts to the ergoline core shared by all lysergamides. It cannot distinguish 1cP-AL-LAD from LSD, AL-LAD, or other lysergamides.
One commercial sample contained 17 impurities including other active lysergamides.[9] A positive Ehrlich test confirms a lysergamide is present — not which one, and not that it is pure.
Guidelines
- Test the material. An Ehrlich reagent test confirms the presence of an indole compound. It does not confirm identity or purity.
- Start low. With no clinical data defining the dose-response curve, begin at the lower end of reported ranges and wait at least two hours before assessing whether the dose is sufficient.
- Have a sitter. A sober, trusted person present provides a safety anchor, especially at higher doses or first experiences.
- Prepare the body. Eat a light meal a few hours before. Stay hydrated. Avoid caffeine and other stimulants.
- Prepare the mind. Set an intention. Avoid tripping during periods of acute emotional distress, grief, or anxiety.
- Clear the schedule. The experience lasts many hours with residual effects beyond that. Plan for a full day with no obligations and allow a rest day after.
- Avoid redosing. Tolerance develops immediately. A second dose within hours produces diminished effects and extends duration without proportional intensification.
Set & Setting
The lysergamide experience is shaped heavily by mindset and environment.[23] A comfortable, familiar space with trusted company substantially reduces the probability of a distressing experience. Novel or stimulating environments amplify both positive and negative directions of the experience.
The prodrug conversion step may produce a slower onset than LSD. Patience during the come-up reduces the risk of redosing too early.
Aftercare & integration. The hours and days following a lysergamide experience are a window for processing what surfaced. Write down impressions, emotions, and imagery while memory is fresh — even fragments are useful. Avoid making major life decisions in the first 48 hours.
If the experience was challenging or distressing, talk it through with a trusted person or a therapist experienced in psychedelic integration — this can prevent distress from consolidating. Seek professional attention if persistent anxiety, depersonalisation, or visual disturbances last more than a few days.
Recovery & Support
Lysergamides carry negligible physical dependence risk, and compulsive use patterns are rare due to rapid tolerance. Psychological difficulty following psychedelic use — persistent anxiety, identity confusion, or difficulty reintegrating the experience — can occur and warrants support.
Resources for psychedelic-specific support include the Fireside Project (call or text 62-FIRESIDE) and MAPS integration resources. If visual disturbances persist beyond two weeks, consult a clinician familiar with HPPD.
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Most difficult psychedelic experiences are psychologically distressing but not medically dangerous. The distinction matters:
Recognising an emergency:
- Expressed intent to harm self or others
- Complete dissociation from reality with inability to respond to voice or touch
- Seizure activity
- Signs of serotonin syndrome (rigid muscles, rapid heart rate, high temperature, agitation) — particularly if other serotonergic substances were taken
Immediate steps:
- 1. Move the person to a calm, quiet environment if safe to do so
- 2. Speak in a slow, reassuring voice — remind them who they are, where they are, and that the effects are temporary
- 3. Do not restrain unless there is immediate danger of self-harm
- 4. If symptoms suggest serotonin toxicity, seizure, or loss of consciousness, call emergency services immediately
- 5. Place an unconscious person in the recovery position
What to tell the dispatcher: Name the substance (1cP-AL-LAD, a lysergamide psychedelic), estimated dose, time of ingestion, and current symptoms. Good Samaritan laws in many jurisdictions protect people who call for help during a drug-related emergency.
Legal Status[edit]
As of May 2026, 1cP-AL-LAD occupies a legal grey area in most jurisdictions — not specifically named in most controlled substance schedules but potentially captured by generic structural analog or NPS legislation.[7]
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| United States | Not explicitly scheduled | Not listed under the Controlled Substances Act. The Federal Analogue Act may apply if intended for human consumption, though prosecution of novel lysergamides under the FAA is rare and legally complex.safety citation needed |
| United Kingdom | Controlled (Psychoactive Substances Act 2016) | Blanket prohibition on psychoactive substances. Supply, import, and export are criminal offences; simple possession is not criminalised under the PSA.citation needed |
| Germany | Prohibited (NpSG) | The 2021 NpSG revision banned 1cP-LSD and structurally related acyl-substituted lysergamides using family-based generic scheduling. Acquisition, possession, and sale are prohibited.[8] |
| Canada | Not explicitly scheduled | Not listed under the Controlled Drugs and Substances Act. Analogue provisions may theoretically apply but no specific guidance or prosecution precedent found.citation needed |
| Australia | Not specifically listed | Not found in TGA schedules or state drug laws. May be captured under analogue provisions in some states.citation needed |
| EU (other) | Variable | Several member states with generic NPS legislation likely cover 1cP-AL-LAD. No comprehensive jurisdiction-by-jurisdiction review performed.[32] |
Analog and prodrug considerations
1cP-AL-LAD's legal status is further complicated by its prodrug nature. If hydrolysis yields AL-LAD — an analog of LSD — some jurisdictions may argue functional equivalence to a scheduled substance. The sequential introduction of N1-acyl lysergamides specifically exploits the gap between generic structural scheduling and substance-specific laws.[7][28]
Legal status changes frequently and varies by jurisdiction. This information reflects available data as of May 2026 and is not legal advice. Verify the current law in the relevant jurisdiction before acting on this information.
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
inferred No toxicity data — lethal dose, therapeutic index, or organ damage assessments — have been published for 1cP-AL-LAD. The toxic dose is unknown.safety citation needed
Acute toxicity
The serotonergic psychedelic class carries an extremely high physiological safety margin. No human death has been attributed solely to the direct toxicity of LSD in the clinical literature, and psychological risks predominate over organ damage at recreational doses.[6] This class-level assessment is presumed to extend to 1cP-AL-LAD, but no substance-specific confirmation exists.
Cardiovascular effects
LSD at 100–200 µg produces moderate, self-limiting increases in heart rate and blood pressure.[24][25] Similar effects are expected for any compound that releases AL-LAD in the body, but have not been measured for 1cP-AL-LAD.safety citation needed
Impurity exposure
Analytical profiling of a commercial sample identified 17 impurities, including confirmed AL-LAD and 1P-AL-LAD plus 15 additional compounds identified only by mass spectral data.[3] Unintended exposure to active impurities is a safety concern specific to the unregulated supply chain.
Psychological risks
In a nationally representative US sample of psychedelic users (N = 613), 40.9% reported at least one challenging or distressing experience. Functional impairment lasting more than one day occurred in 8.9%, and 2.6% sought professional help.[23] Key risk factors included negative mindset, disagreeable environment, lack of psychological support, and dose exceeding the intended level.[23]
Hallucinogen persisting perception disorder (HPPD) — ongoing visual disturbances such as geometry, trailing, and halos after psychedelic use — is a documented rare adverse outcome.[26][27] No HPPD cases have been reported for 1cP-AL-LAD specifically.
Psychedelics can trigger or worsen psychotic symptoms in individuals with a personal or family history of psychotic disorders. Lithium co-use was identified as the top medication risk factor for severe adverse outcomes.[23]
Tolerance and dependence
Tolerance
Tolerance develops almost immediately after a single dose, driven by 5-HT₂A downregulation. In rat studies, cortical serotonin receptor binding decreased significantly within three days of repeated dosing and recovered within four days of stopping.[5] Community consensus places full tolerance reset at approximately 14 days.safety citation needed
Cross-tolerance extends across the serotonergic psychedelic class — LSD, psilocybin, mescaline, and structural analogs — reflecting the shared 5-HT₂A mechanism.
Dependence
Serotonergic psychedelics have negligible physical dependence liability and do not support compulsive self-administration in animal models.[28] Rapid tolerance inherently discourages repeated use. No withdrawal has been described for the lysergamide class.
Drug Interactions
Serotonergic combinations
Combining 1cP-AL-LAD with drugs that increase serotonin levels poses a theoretical risk of serotonin syndrome. Tramadol blocks serotonin reuptake[29] and has produced marked serotonin toxicity in overdose.[30] Combined with a 5-HT₂A agonist, tramadol creates a mechanistically plausible dangerous interaction; no case report exists for this combination with 1cP-AL-LAD or AL-LAD.safety citation needed
MAOIs present a dangerous interaction by the same mechanism — blocking serotonin breakdown while directly activating serotonin receptors amplifies toxicity risk. No specific data exist for this combination with 1cP-AL-LAD.
Lithium
Co-use of lithium with psychedelics is associated with seizure risk and amplified, unpredictable effects. Lithium was identified as the top medication risk factor for severe adverse psychedelic outcomes.[23]
Cannabis
The interaction between cannabis and psychedelics is poorly characterised. CBD has been identified as a negative allosteric modulator of 5-HT₂A,[31] which could theoretically modulate effects, but clinical significance is unknown. THC may increase anxiety and confusion.
Pharmacological reversal
The 5-HT₂A blocker ketanserin reverses LSD-induced psychedelic effects when given after the drug.[21] This reversal is expected to apply to 1cP-AL-LAD by class analogy and may serve as an emergency intervention. Benzodiazepines are used for acute anxiety management.
Contraindications
8 knowninferred No contraindication data specific to 1cP-AL-LAD exist. The following are class-level inferences for serotonergic psychedelics:
Absolute contraindications:
- Personal history of psychotic disorders (schizophrenia spectrum, bipolar disorder with psychotic features)
- Concurrent lithium use — associated with seizures and dangerously amplified effects[23]
- Concurrent MAOI therapy — serotonin toxicity risk
Relative contraindications:
- Personal or family history of HPPD[26]
- Serious heart conditions — moderate stimulant effects expected[24]
- Concurrent serotonergic medications (SSRIs, SNRIs, tramadol) — attenuated or unpredictable effects; serotonin toxicity risk with tramadol[29]
- Pregnancy or breastfeeding — no safety data exist
- Unstable psychiatric conditions — risk of destabilisation
safety citation needed
Harm Reduction[edit]
Forms & Identification
For lysergamides distributed as blotter paper, standard reagent testing provides limited but useful information. Ehrlich's reagent indicates the presence of an indole-containing compound — a necessary but not sufficient confirmation, since it reacts to the ergoline core shared by all lysergamides. It cannot distinguish 1cP-AL-LAD from LSD, AL-LAD, 1P-LSD, or other lysergamides.
Analytical profiling of one commercial sample identified 17 impurities including other active lysergamides.[3] A positive Ehrlich test confirms you have a lysergamide — not which one, and not that it is pure.
Guidelines
- Test your material. An Ehrlich reagent test confirms the presence of an indole compound. It does not confirm identity or purity.
- Start low. With no clinical data to define the dose-response curve, begin at the lower end of reported ranges and wait at least two hours before considering whether the dose is sufficient.
- Have a sitter. A sober, trusted person present during the experience provides a safety anchor, especially at higher doses or first experiences.
- Prepare your body. Eat a light meal a few hours before. Stay hydrated. Avoid caffeine and other stimulants.
- Prepare your mind. Set an intention. Avoid tripping during periods of acute emotional distress, grief, or anxiety.
- Clear your schedule. The experience lasts many hours with residual effects beyond that. Plan for a full day with no obligations and allow a rest day after.
- Avoid redosing. Tolerance develops immediately. A second dose within hours produces diminished effects and extends duration without proportional intensification.
Set & Setting
The lysergamide experience is shaped heavily by mindset and environment.[23] A comfortable, familiar physical space with trusted company substantially reduces the probability of a distressing experience. Novel or stimulating environments amplify both positive and negative directions of the experience. The prodrug conversion step may produce a slower onset than LSD — patience during the come-up reduces the risk of redosing too early.
Aftercare & integration. The hours and days following a lysergamide experience are a window for processing what surfaced. Write down impressions, emotions, and imagery while memory is fresh — even fragments are useful. Avoid making major life decisions in the first 48 hours; the sense of clarity and insight benefits from sober reflection.
If the experience was challenging or distressing, talking through it with a trusted person or a therapist experienced in psychedelic integration can prevent distress from consolidating. Persistent anxiety, depersonalisation, or visual disturbances lasting more than a few days warrant professional attention.
Recovery & Support
Lysergamides carry negligible physical dependence risk, and compulsive use patterns are rare due to rapid tolerance. However, psychological difficulty following psychedelic use — including persistent anxiety, identity confusion, or difficulty reintegrating the experience — can occur and warrants support.
Resources for psychedelic-specific support include the Fireside Project (call or text 62-FIRESIDE) and MAPS integration resources. For broader mental health concerns, a therapist familiar with psychedelic experiences can provide context-appropriate care. If visual disturbances persist beyond two weeks, consult a clinician familiar with HPPD.
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Most difficult psychedelic experiences are psychologically distressing but not medically dangerous. The distinction matters:
Recognising an emergency:
- Expressed intent to harm self or others
- Complete dissociation from reality with inability to respond to voice or touch
- Seizure activity
- Signs of serotonin syndrome (rigid muscles, rapid heart rate, high temperature, agitation) — particularly if other serotonergic substances were taken
Immediate steps:
- 1. Move the person to a calm, quiet environment if safe to do so
- 2. Speak in a slow, reassuring voice — remind them who they are, where they are, and that the effects are temporary
- 3. Do not restrain unless there is immediate danger of self-harm
- 4. If symptoms suggest serotonin toxicity, seizure, or loss of consciousness, call emergency services immediately
- 5. Place an unconscious person in the recovery position
What to tell the dispatcher: Name the substance (1cP-AL-LAD, a lysergamide psychedelic), estimated dose, time of ingestion, and current symptoms. Good Samaritan laws in many jurisdictions protect people who call for help during a drug-related emergency.
Legal Status[edit]
As of May 2026, 1cP-AL-LAD occupies a legal grey area in most jurisdictions. It is not specifically named in the controlled substance schedules of most countries but may be captured by generic structural analog or NPS legislation. The regulatory landscape for N1-acyl lysergamides is evolving rapidly as governments respond to sequential introduction of novel analogs.[9]
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| United States | Not explicitly scheduled | Not listed under the Controlled Substances Act. The Federal Analogue Act may apply if intended for human consumption, though prosecution of novel lysergamides under the FAA is rare and legally complex.safety citation needed |
| United Kingdom | Controlled (Psychoactive Substances Act 2016) | Blanket prohibition on psychoactive substances. Supply, import, and export are criminal offences; simple possession is not criminalised under the PSA.citation needed |
| Germany | Prohibited (NpSG) | The 2021 NpSG revision banned 1cP-LSD and structurally related acyl-substituted lysergamides using family-based generic scheduling. Acquisition, possession, and sale are prohibited.[10] |
| Canada | Not explicitly scheduled | Not listed under the Controlled Drugs and Substances Act. Analogue provisions may theoretically apply but no specific guidance or prosecution precedent found.citation needed |
| Australia | Not specifically listed | Not found in TGA schedules or state drug laws. May be captured under analogue provisions in some states.citation needed |
| EU (other) | Variable | Several member states with generic NPS legislation likely cover 1cP-AL-LAD. No comprehensive jurisdiction-by-jurisdiction review performed.[32] |
Analog and prodrug considerations
1cP-AL-LAD's legal ambiguity is compounded by its prodrug nature. If hydrolysis yields AL-LAD — itself an analog of LSD — some jurisdictions may argue functional equivalence to a scheduled substance. The sequential introduction of N1-acyl lysergamides by NPS vendors specifically exploits the gap between generic structural scheduling and substance-specific scheduling.[9][28]
Frequently asked questions
What is 1cP-AL-LAD?
1cP-AL-LAD is a synthetic lysergamide psychedelic and presumed prodrug for AL-LAD, active in microgram doses by the oral route. It first appeared in forensic literature in 2023; no clinical, pharmacological, or toxicological studies have been published.
How long does 1cP-AL-LAD last?
Total duration by route of administration — Oral: 7 – 10 hours. Ranges vary with dose and individual factors; see the duration table for onset, peak, and after-effect phases.
Where can I find dosage information for 1cP-AL-LAD?
Psychedex publishes a dosage table for 1cP-AL-LAD 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-AL-LAD?
The highest-severity documented interactions for 1cP-AL-LAD: MAOIs (Lethal), Buspirone (Dangerous), DXM (Dangerous), GHB, Baclofen (Dangerous), GHB, GBL (Dangerous). See the interactions section for the full list with mechanisms and severity levels.
Is 1cP-AL-LAD addictive?
Psychedex records tolerance and dependence data rather than a yes/no rating. Recorded tolerance indicators for 1cP-AL-LAD: tolerance builds rapid; full reset takes 14 days; cross-tolerance develops with LSD, psilocybin, mescaline, DMT, other serotonergic psychedelics. 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] ^abcBrandt SD, Kavanagh PV, Westphal F, Stratford A, Odland AU et al. (2020) Return of the lysergamides. Part VI: Analytical and behavioural characterization of 1-cyclopropanoyl-d-lysergic acid diethylamide (1CP-LSD) — Drug Testing and Analysis doi:10.1002/dta.2789
- [2] ^abcBrandt SD, Kavanagh PV, Westphal F, Pulver B, Schwelm HM, Whitelock K, Stratford A, Auwärter V, Halberstadt AL (2022) Analytical profile, in vitro metabolism and behavioral properties of the lysergamide 1P-AL-LAD — Drug Testing and Analysis doi:10.1002/dta.3281
- [3] ^abLuethi D, Liechti ME (2020) Designer drugs: mechanism of action and adverse effects — Archives of Toxicology doi:10.1007/s00204-020-02693-7
- [4] ^abBuckholtz NS, Zhou DF, Freedman DX, Potter WZ (1990) Lysergic acid diethylamide (LSD) administration selectively downregulates serotonin2 receptors in rat brain — Neuropsychopharmacology PMID:1969270
- [5] ^Pfaff RC, Huang X, Marona-Lewicka D, Oberlender R, Nichols DE (1994) Lysergamides revisited — NIDA Research Monograph PMID:8742794
- [6] ^abBrandt SD, Kavanagh PV, Westphal F, Elliott SP, Wallach J, Colestock T, Burrow TE, Chapman SJ, Stratford A, Nichols DE, Halberstadt AL (2017) Return of the lysergamides. Part II: Analytical and behavioural characterization of N6-allyl-6-norlysergic acid diethylamide (AL-LAD) and (2'S,4'S)-lysergic acid 2,4-dimethylazetidide (LSZ) — Drug Testing and Analysis doi:10.1002/dta.1985
references
- [1] ^abcBrandt SD, Kavanagh PV, Westphal F, Stratford A, Odland AU et al. (2020) Return of the lysergamides. Part VI: Analytical and behavioural characterization of 1-cyclopropanoyl-d-lysergic acid diethylamide (1CP-LSD) — Drug Testing and Analysis doi:10.1002/dta.2789
- [2] ^abcBrandt SD, Kavanagh PV, Westphal F, Pulver B, Schwelm HM, Whitelock K, Stratford A, Auwärter V, Halberstadt AL (2022) Analytical profile, in vitro metabolism and behavioral properties of the lysergamide 1P-AL-LAD — Drug Testing and Analysis doi:10.1002/dta.3281
- [3]
- [4] ^abcTanaka R, Kawamura M, Mizutani S, Kikura-Hanajiri R (2023) Identification of LSD analogs, 1cP-AL-LAD, 1cP-MIPLA, 1V-LSD and LSZ in sheet products — Forensic Toxicology doi:10.1007/s11419-023-00661-1
- [5] ^abBuckholtz NS, Zhou DF, Freedman DX, Potter WZ (1990) Lysergic acid diethylamide (LSD) administration selectively downregulates serotonin2 receptors in rat brain — Neuropsychopharmacology PMID:1969270
- [6] ^abLuethi D, Liechti ME (2020) Designer drugs: mechanism of action and adverse effects — Archives of Toxicology doi:10.1007/s00204-020-02693-7