1P-LSD
1-propionyllysergic acid diethylamide
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1P-LSD (1-propionyl-lysergic acid diethylamide) is a semi-synthetic psychedelic of the lysergamide class. It is a confirmed prodrug of LSD, pharmacologically inert until converted to LSD in the body.[1][2] 1P-LSD acts as a partial agonist at 5-HT₂A receptors through its active metabolite, disrupting the brain's default filtering of sensory and cognitive input.[3]
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1P-LSD appeared on research chemical markets in early 2015 with no prior description in published literature.[4] It became the first in a series of N1-acylated LSD prodrugs that emerged sequentially as jurisdictions banned each predecessor. It remains unscheduled in several countries but falls under structural analog legislation in others.
Subjective effects include geometric visual patterns, color enhancement, time alteration, thought acceleration, emotional intensification, and ego dissolution.[5] The experience is a slow-building, panoramic alteration of perception and cognition — sustained over many hours, strongly shaped by mindset and environment,[6] with a stimulant-edged body feel distinguishing the lysergamide character from shorter-acting tryptamines. Thought loops, anxious fixation, and difficulty sleeping through the extended tail are common unsought effects.
1P-LSD produces no physical dependence,[3] and rapid tolerance after a single dose — driven by downregulation — makes compulsive redosing self-limiting.[7] The primary risk is psychological — acute anxiety, potential psychosis precipitation in predisposed individuals, and uncommon persistent perceptual changes — scaling with dose and vulnerability.[8] All human data derive from a single two-subject study;[2] the safety profile rests on extrapolation from LSD.
History[edit]
Discovery
The structural template for 1P-LSD was established decades before the compound itself appeared. LSD was first synthesized by Albert Hofmann at Sandoz Laboratories in 1938, and its psychedelic properties were discovered accidentally in 1943. In the 1950s, Sandoz chemists synthesized 1-acetyl-LSD (ALD-52), an N1-acylated structural analog that produced comparable psychedelic effects in humans — creating the prodrug framework from which 1P-LSD and its successors would later emerge.
Emergence on the research chemical market
1P-LSD appeared on online research chemical markets in approximately January 2015, sold as blotter and powder.[4] No academic laboratory has claimed synthesis of the compound, and it had no prior description in the scientific literature — Brandt and colleagues provided the first peer-reviewed documentation of its existence and pharmacological characterization.[4]
Regulation and successor compounds
Jurisdictions moved to control 1P-LSD through existing analog frameworks and novel psychoactive substance legislation. Each ban triggered the appearance of structurally modified successors on the research chemical market: 1B-LSD, 1cP-LSD,[9] 1V-LSD, 1T-LSD, and 1F-LSD[10] — each confirmed as an LSD prodrug through the "Return of the Lysergamides" research series by Brandt and colleagues, establishing the cat-and-mouse dynamic between NPS markets and regulators as a defining case study.
The "1P" prefix denotes the 1-propionyl substitution — a naming convention shared across the N1-acyl lysergamide series (1cP for cyclopropanoyl, 1V for valeroyl, 1B for butanoyl). In research chemical communities, 1P-LSD is widely described as "completely interchangeable" with LSD, a characterization supported by its confirmed complete prodrug conversion. The sequential emergence of each successor compound after its predecessor's scheduling has made this series the most prominent example of iterative analog design in the novel psychoactive substance landscape.
Chemistry[edit]
Structural overview
1P-LSD (1-propionyl-d-lysergic acid diethylamide) is built on the tetracyclic lysergic acid scaffold shared by all lysergamides. It differs from LSD by a single modification: a propionyl group (–COCH₂CH₃) attached to the nitrogen-1 position of the indole ring. This N1-acyl substitution places 1P-LSD in a defined prodrug series alongside ALD-52 (acetyl), 1cP-LSD (cyclopropanoyl), 1V-LSD (valeroyl), and related compounds.[4]
Molecular properties
| Molecular formula | C₂₃H₂₉N₃O₂ |
| Molecular weight | 379.5 g/mol |
The propionyl group adds 56.1 g/mol over LSD (323.4 g/mol), yielding a molar ratio of approximately 1.17:1 — meaning 100 µg of 1P-LSD contains roughly 85 µg of LSD-equivalent mass. In practice, 100 µg oral 1P-LSD hemitartrate produces effects comparable to 100 µg LSD, suggesting functional dose equivalence at this scale.[2]
Stereochemistry
1P-LSD retains the (6aR,9R) absolute configuration of d-lysergic acid diethylamide — the pharmacologically active stereoisomer. The two chirality centers at C-6a and C-9 enforce the spatial arrangement required for serotonin receptor binding.
Physical properties
The hemitartrate salt is typically encountered as a white to off-white crystalline powder and on blotter paper.[4] No peer-reviewed data on melting point, solubility, or photostability specific to 1P-LSD have been published. By analogy with LSD, the compound is expected to degrade under ultraviolet light and oxidative conditions; storage in cool, dark, airtight conditions is standard practice.
Pharmacology[edit]
Prodrug mechanism
1P-LSD does not act directly at serotonin receptors. The propionyl group reduces binding affinity by one to two orders of magnitude compared to LSD.[1] Pharmacological activity requires removal of this group in the liver, releasing free LSD into the bloodstream.
This conversion has been confirmed at three levels: in human liver tissue,[11] in rats,[1] and in two human subjects who showed no detectable 1P-LSD in blood or urine — only LSD, approaching 100% bioavailability.[2]
The prodrug mechanism is shared across an entire structural class: ALD-52, 1cP-LSD,[9] 1B-LSD, 1V-LSD, 1T-LSD, and 1F-LSD[10] all convert to LSD in the body. Longer acyl chains reduce conversion efficiency — 1P-LSD is approximately 27 times more potent than 1-dodecanoyl-LSD in mouse behavioral assays, reflecting slower hydrolysis of bulkier groups.[12]
Mechanism of action
Once liberated, LSD acts as a partial agonist at 5-HT₂A receptors on layer V pyramidal neurons in the prefrontal cortex.[3] This disrupts the brain's default filtering of sensory and cognitive input, producing the characteristic perceptual, cognitive, and emotional shifts of the psychedelic state.
LSD also engages dopamine D₂, 5-HT₁A, and TAAR₁ receptors,[13] adding a stimulant-like dimension and broader emotional range that distinguishes lysergamides from more serotonin-selective psychedelics like psilocybin.
Pharmacokinetics
All downstream pharmacokinetics are those of LSD. Oral 1P-LSD undergoes near-complete first-pass conversion; when administered intravenously, intact 1P-LSD remains detectable for up to 4.16 hours before full conversion.[2] The terminal half-life of LSD following oral 1P-LSD is approximately 6.4 hours.[2]
Drugs that inhibit the liver enzymes responsible for LSD metabolism can alter exposure. In a controlled study, the antidepressant paroxetine increased LSD peak concentration by 1.4× and total exposure by 1.5×.[14]
Behavioral pharmacology
In mice, 1P-LSD induces the head-twitch response — a validated behavioral marker of psychedelic activity — at approximately 38% of LSD's potency (ED₅₀ = 349.6 nmol/kg versus 132.8 nmol/kg for LSD).[4] The reduced potency reflects incomplete prodrug conversion within the brief assay timeframe rather than intrinsic pharmacological differences, since the active metabolite is identical.
Neuroscience[edit]
Where it acts
As a complete prodrug of LSD, 1P-LSD's neural effects are those of LSD. No direct neuroimaging studies of 1P-LSD have been published.
LSD activates 5-HT₂A receptors on cortical pyramidal neurons, disrupting default mode network integrity and reducing thalamocortical gating — allowing normally filtered sensory and associative information to reach consciousness.[3] The result is increased communication between brain regions that do not normally interact and elevated neural signal diversity across cortical networks. At higher doses, LSD modulates dopaminergic signaling through combined D₂, 5-HT₁A, and TAAR₁ activation,[13] adding an energizing, emotionally expansive dimension.
Why it matters
The REBUS model (Relaxed Beliefs Under Psychedelics) proposes that 5-HT₂A agonism relaxes the brain's high-level predictions, allowing raw sensory input to drive perception more than usual — accounting for vivid imagery, loosened associations, and ego dissolution.[15]
Separately, LSD promotes structural neuroplasticity — increased dendritic branching and new synaptic connections — through direct binding to TrkB receptors, a mechanism independent of 5-HT₂A activation.[16] This dual action — acute perceptual disruption via serotonin receptors and sustained structural rewiring via TrkB — may explain how a single dose produces psychological changes lasting weeks to months.
Key unresolved questions include whether 1P-LSD crosses the blood-brain barrier intact and undergoes local conversion in neural tissue, or whether all conversion is peripheral — a distinction that could affect onset timing and regional receptor exposure. It also remains unknown whether the propionylated form itself binds TrkB receptors directly, or only after conversion to LSD.
Subjective Effects[edit]
The 1P-LSD experience is one of sustained, wide-spectrum alteration — perception, thought, emotion, and body awareness shift in concert over many hours. At lower doses, effects center on visual acuity enhancement, color saturation, and a gentle loosening of habitual thought patterns. Higher doses bring geometric patterning, profound time alteration, and dose-dependent ego dissolution.[5] Set and setting strongly modulate the qualitative character of the experience; dose remains the primary predictor of intensity.[6]
Compared to psilocybin, 1P-LSD produces a substantially longer experience at equivalent intensity, with greater sustained stimulation and a more gradual resolution.[5][18] The broader receptor profile of its active metabolite — engaging dopaminergic and adrenergic pathways alongside serotonin — lends the experience a stimulant-edged, emotionally expansive quality distinct from the more introspective tryptamine character.
Effect Grid
At common doses (75–150 µg oral), the full psychedelic experience emerges. Visual effects are pronounced — geometric patterns overlay surfaces, colors shift and saturate intensely, objects exhibit drifting and morphing, and tracers follow moving objects. Closed-eye visuals become vivid and complex. Time distortion is significant, with minutes feeling stretched or compressed. Thought connectivity increases dramatically, often producing novel associations, insights, and occasional thought loops. Emotional responses intensify markedly — music, art, and interpersonal interactions can feel profoundly meaningful.
Physically, pupil dilation is prominent. Stimulation and wakefulness are sustained throughout. Jaw tension, temperature dysregulation, and peripheral vasoconstriction (cold extremities) are common. Nausea is possible but less frequent than with tryptamine psychedelics. Appetite is suppressed.
Functional impairment is substantial — operating machinery, driving, or managing complex responsibilities is not possible. The experience requires a full-day commitment: 8–12 hours of primary effects plus residual stimulation. Sleep is impossible during active effects.
Modeled from the effect's dose-dependence curve — not per-substance measurements.
Music enhancement · Visual breathing · Tracers · Auditory enhancement · After-images · Depth perception distortion · Perspective distortion · Symmetrical texture repetition · Touch enhancement · Brightness alteration · Environmental patterning · Light sensitivity · Sound sensitivity · Visual morphing · Auditory distortion · Synesthesia · Auditory misinterpretation · Holotropic state · Peripheral misidentification · Peripheral vision distortion · Proprioceptive distortion · Spatial disorientation · Vestibular distortion · Visual diffraction · Visual haze / noise · Visual melting · Visual acuity enhancement · Dreaming suppression · Visual magnification · Visual processing acceleration · Olfactory enhancement · Taste enhancement · Flashbacks · Object transformations · Visual recursion · External hallucinations · Object activation · Internal hallucinations · Auditory hallucinations · Visual scenery slicing · Environmental orbism / cubism · Perspective hallucinations · Visual flipping · Persisting hallucinations
After-images · Depth perception distortion · Perspective distortion · Symmetrical texture repetition · Touch enhancement · Brightness alteration · Environmental patterning · Light sensitivity · Sound sensitivity · Visual morphing · Auditory distortion · Synesthesia · Auditory misinterpretation · Holotropic state · Peripheral misidentification · Peripheral vision distortion · Proprioceptive distortion · Spatial disorientation · Vestibular distortion · Visual diffraction · Visual haze / noise · Visual melting · Visual acuity enhancement · Dreaming suppression · Visual magnification · Visual processing acceleration · Olfactory enhancement · Taste enhancement · Flashbacks · Object transformations · Visual recursion · External hallucinations · Object activation · Internal hallucinations · Auditory hallucinations · Visual scenery slicing · Environmental orbism / cubism · Perspective hallucinations · Visual flipping · Persisting hallucinations
Wakefulness · Spontaneous body sensations · Appetite suppression · Body high · Insomnia · Muscle tension · Heart rate perception changes · Laughter fits · Physical fatigue · Tingling / electric sensations · Sexual arousal enhancement · Nausea · Excessive sweating · Bodily lightness · Body schema distortion · Dizziness · Restlessness · Tactile euphoria · Vibrations / buzzing · Bodily pressures · Breathing alteration · Headache · Increased urination · Abnormal heartbeat · Involuntary body movements · Bodily heaviness · Dry mouth · Nystagmus (eye wobbles) · Trembling · Motor control enhancement · Salivation · Bruxism · Vomiting · Yawning · Seizure threshold reduction · Bodily dissociation · Tactile hallucination
Body high · Insomnia · Muscle tension · Heart rate perception changes · Laughter fits · Physical fatigue · Tingling / electric sensations · Sexual arousal enhancement · Nausea · Excessive sweating · Bodily lightness · Body schema distortion · Dizziness · Restlessness · Tactile euphoria · Vibrations / buzzing · Bodily pressures · Breathing alteration · Headache · Increased urination · Involuntary body movements · Bodily heaviness · Dry mouth · Nystagmus (eye wobbles) · Trembling · Motor control enhancement · Salivation · Bruxism · Vomiting · Yawning · Seizure threshold reduction · Bodily dissociation · Tactile hallucination
Thought acceleration · Aesthetic enhancement · Introspection enhancement · Multiple thought streams · Openness enhancement · Thought connectivity · Immersion enhancement · Cognitive euphoria · Cognitive flexibility · Memory fragmentation · Creativity enhancement · Humor enhancement · Analysis enhancement · Cognitive impairment · Confusion · Increased nature relatedness · Synchronicity · Memory suppression · Thought disorganization · Thought loops · Cognitive fatigue · Focus suppression · Information processing suppression · Memory replays · Focus enhancement · Information processing enhancement · Language enhancement · Motivation enhancement · Analysis suppression · Cognitive dysphoria · Language suppression · Motivation suppression · Memory enhancement · Thought organization · Delusions · Delirium
Multiple thought streams · Openness enhancement · Thought connectivity · Immersion enhancement · Cognitive euphoria · Cognitive flexibility · Memory fragmentation · Creativity enhancement · Humor enhancement · Analysis enhancement · Cognitive impairment · Confusion · Increased nature relatedness · Synchronicity · Memory suppression · Thought disorganization · Thought loops · Cognitive fatigue · Focus suppression · Information processing suppression · Memory replays · Focus enhancement · Information processing enhancement · Language enhancement · Motivation enhancement · Analysis suppression · Cognitive dysphoria · Language suppression · Motivation suppression · Memory enhancement · Thought organization · Delirium
Simultaneous emotions · Anxiety · Catharsis · Empathy enhancement · Anxiety suppression · Dysphoria · Irritability · Mania
Empathy enhancement · Anxiety suppression · Dysphoria · Irritability
Flow state · Sociability enhancement · Trust enhancement · Depersonalization · Communication enhancement · Ego inflation · Communication suppression · Sociability suppression · Social disconnection · Boundary dissolution · Ego dissolution · Identity alteration · Cognitive disconnection · Telepathic feelings
Communication enhancement · Ego inflation · Communication suppression · Sociability suppression · Social disconnection · Boundary dissolution · Ego dissolution · Identity alteration · Cognitive disconnection · Telepathic feelings
Time cessation
Transpersonal visions · Cessation · Death-rebirth sequence · Entity contact · Transpersonal memory access · Voidness · Near-death experience
Transpersonal memory access · Voidness · Near-death experience
Recursive awareness
Timeline
First alerts appear as subtle shifts in sensory processing — faint visual brightening, mild mood lift, or a sense that something has changed. Physical cues include slight pupil dilation and a nascent body buzz. The onset may be slightly delayed compared to direct LSD due to the required prodrug deacylation step.
Effects build steadily as LSD concentrations rise following hepatic deacylation. Visual distortions emerge — surface breathing, color enhancement, early geometric patterning. Stimulation and emotional activation increase.
Maximum subjective intensity sustained over a broad plateau. Visual phenomena, thought connectivity, emotional amplification, and time distortion are at their fullest. Ego dissolution is possible at common doses and likely at strong doses.
Effects gradually recede in approximate reverse order of onset. Cognitive clarity returns before visual distortions fully resolve. Emotional intensity diminishes but reflective processing continues.
A period of residual mood elevation, reflective thinking, and subtle perceptual enhancement lasting 6–24 hours. Many users report increased openness, emotional sensitivity, and creative fluency. Mild fatigue may follow the sustained stimulation of the active phase.
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 data for 1P-LSD have been published. As a complete prodrug of LSD, its toxicological profile is that of LSD — a substance with an extremely high therapeutic index and no documented deaths from direct pharmacological action under controlled conditions.[3]
Heart and circulation
LSD produces modest, dose-dependent increases in heart rate and blood pressure. At 100 µg, these cardiovascular effects are moderate and comparable to those of psilocybin.[18] They are clinically relevant primarily in individuals with pre-existing heart conditions.[19]
Chronic toxicity
No chronic toxicity data specific to 1P-LSD exist. Given complete conversion to LSD, over seven decades of human use have revealed no evidence of organ damage at psychoactive doses.
Psychological Risks
Acute anxiety and panic reactions occur with dose-dependent frequency. At 200 µg LSD, anxiety and ego dissolution scores were significantly higher than at 100 µg.[5] Pre-existing anxiety and low psychological well-being increase vulnerability, though dose remains the primary predictor.[6]
LSD can precipitate psychotic episodes in individuals predisposed to psychotic disorders, with documented cases of drug-induced psychosis featuring schizophrenia-like symptoms.[20] Personal or family history of psychosis, schizophrenia, or bipolar disorder is an absolute contraindication.
Hallucinogen persisting perception disorder (HPPD) — persistent visual disturbances such as visual haze / noise, trailing, and geometric overlays after use has ceased — is a recognized but uncommon condition. A systematic review spanning 50 years confirmed its existence but found no randomized controlled trials for treatment.[8] The proposed mechanism involves disruption of low-level visual processing, potentially through changes to inhibitory neuron function following 5-HT₂A stimulation.[21]
Tolerance & Dependence
1P-LSD — via LSD — is not addictive: no physical dependence develops, no withdrawal occurs, and psychological dependence is uncommon.[3][22] LSD does not activate the brain's reward circuitry in the manner characteristic of addictive substances.
Tolerance develops rapidly after a single dose through downregulation in the frontal cortex.[7] Cross-tolerance extends to all serotonergic psychedelics acting through 5-HT₂A, including psilocybin and mescaline.[7] Full sensitivity is commonly reported to return after approximately 14 days of abstinence.citation needed
Drug Interactions
Serotonergic interactions
The most significant pharmacological risk is serotonin toxicity — a potentially life-threatening condition involving dangerous fever, autonomic instability, and muscle rigidity — when 1P-LSD is combined with drugs that strongly inhibit serotonin reuptake.
Tramadol potently inhibits the SERT[23] and is the most commonly implicated opioid in serotonin syndrome cases.[24] Concurrent use with serotonergic psychedelics is contraindicated.
MAOIs impair serotonin breakdown and represent an additional serotonin toxicity risk when combined with 5-HT₂A agonists.[25] This combination is contraindicated.
SSRIs/SNRIs interact through two pathways. Chronic SSRI use may reduce psychedelic effects through downstream receptor changes. Certain SSRIs also increase LSD plasma levels — paroxetine raised peak concentration by 1.4× and total exposure by 1.5×.[14] In a controlled study, paroxetine pretreatment did not alter pleasant effects and reduced anxiety and nausea.[14] The serotonin toxicity risk with SSRIs is lower than with MAOIs but not zero, particularly at high doses of both agents.[25]
Other interactions
MDMA co-administration increases LSD plasma levels and prolongs effects, producing more pronounced cardiovascular strain than either substance alone.[26]
Cannabis: No controlled data exist. Community reports suggest cannabis may intensify the psychedelic experience and increase anxiety.safety citation needed
Lithium: An association between lithium and seizures during LSD use is widely reported in harm reduction communities, but no primary peer-reviewed source documents this interaction.safety citation needed
Contraindications
Absolute contraindications:
- Personal or family history of psychotic disorders (schizophrenia, schizoaffective disorder) — LSD can precipitate acute psychosis in predisposed individuals[20]
- Bipolar disorder — risk of manic episode precipitationsafety citation needed
- Concurrent MAOI use — serotonin toxicity risk[25]
- Concurrent tramadol use — serotonin toxicity risk[23]
Relative contraindications:
- Uncontrolled high blood pressure or significant heart disease — LSD produces dose-dependent cardiovascular stimulation[19]
- Liver impairment — 1P-LSD requires liver enzymes for prodrug conversion; impaired function may alter LSD exposure[11]
- Pregnancy and breastfeeding — no safety data existsafety citation needed
- Concurrent lithium therapy — seizure risk from community reportssafety citation needed
- Epilepsy or seizure disorders — lowered seizure threshold is a theoretical concernsafety citation needed
Harm Reduction[edit]
Forms & Identification
1P-LSD is most commonly encountered on blotter paper or as a white to off-white powder. N1-acyl lysergamides are visually and physically indistinguishable from one another and from LSD itself, making reagent testing alone insufficient for precise identification. Ehrlich's reagent confirms the presence of an indole (the lysergamide core) but cannot differentiate 1P-LSD from LSD, ALD-52, 1cP-LSD, or other analogs. Quantitative analysis through a drug checking service is the only reliable method of confirming identity.
Guidelines
- Test all material with Ehrlich's reagent before use — a positive reaction (purple color change) confirms indole presence
- Start with a low dose and allow at least 2–3 hours before considering whether effects have fully developed; onset may be slower than expected due to the prodrug conversion step
- Prepare the environment in advance: comfortable temperature, access to water, calming music, and a space to lie down
- Arrange for a sober sitter, especially at doses above 100 µg or for first-time experiences
- Clear the schedule for the full day — the experience lasts 8–12 hours, followed by residual effects that may impair sleep
- Eat a light meal 2–3 hours beforehand; avoid heavy food close to dosing
- Keep a pen and notebook available for grounding and reflection during the experience
Set & Setting
The duration and intensity of the 1P-LSD experience make environment and mindset critical variables. A physically safe, familiar space with access to a calm retreat area reduces the likelihood of difficult reactions. A trusted, sober companion is strongly recommended, particularly at higher doses or for those without prior psychedelic experience.
Avoid use during periods of emotional lability, unresolved anxiety, or high external stress. These factors are documented predictors of difficult experiences and do not reliably resolve once the substance takes effect.
Aftercare & integration. The days following a psychedelic experience are a window for reflection. Journal thoughts, emotions, and imagery within 24–48 hours to consolidate insights before they fade. Prioritize sleep, hydration, and light nutrition on the first day after use.
Some experiences — particularly those involving ego dissolution, intense emotion, or difficult psychological material — benefit from structured integration. This may include conversation with a trusted person, professional psychedelic integration therapy, or contemplative practices such as meditation. If distressing perceptual changes, anxiety, or depersonalization persist beyond a few days, consult a mental health professional.
Recovery & Support
While 1P-LSD does not produce physical dependence, patterns of repeated use to escape difficult emotions or avoid daily life can develop. If psychedelic use is becoming a coping mechanism rather than an occasional experience, honest self-assessment is warranted.
Support resources include psychedelic-informed therapists, peer support communities, and harm reduction organizations such as the Fireside Project (call or text 62-FIRESIDE) and MAPS integration resources. For broader substance use concerns, SAMHSA's National Helpline (1-800-662-4357) provides free referrals.
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Recognizing an emergency
Most difficult psychedelic experiences are distressing but not medically dangerous. Seek immediate help if the person is threatening self-harm or harm to others, has completely lost contact with reality and cannot be redirected, experiences chest pain or seizures, or shows signs of serotonin syndrome (rigid muscles, dangerous fever, tachycardia) after combining substances.
Immediate steps
- Move the person to a quiet, low-stimulation environment
- Speak calmly, use their name, and remind them they have taken a drug and it will end
- Do not restrain them unless there is immediate danger of self-harm
- If unconscious, place in the recovery position
- Call emergency services if symptoms escalate or self-harm risk is present
What to tell the dispatcher
State the substance (1P-LSD or LSD analog), approximate dose, time of ingestion, and current symptoms. Good Samaritan laws in many jurisdictions protect callers from prosecution for drug-related offenses when seeking emergency help.
Legal Status[edit]
1P-LSD occupies a legal gray area in most jurisdictions. As a structural analog of LSD, it falls within the scope of analog and blanket-ban legislation in several countries despite rarely being specifically named in controlled substances schedules. Each scheduling action on one N1-acyl lysergamide has prompted the rapid appearance of a structural successor.
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| United States | Not specifically scheduled | Subject to the Federal Analogue Act (21 U.S.C. § 813) when intended for human consumption, as LSD is Schedule I. Prosecution requires proof of intent for human use.[27] |
| United Kingdom | Illegal | Covered by the Psychoactive Substances Act 2016; production, supply, and possession with intent to supply are prohibited.[27] |
| Germany | Controlled (NpSG) | Added to the Neue-psychoaktive-Stoffe-Gesetz in July 2019. Trade and supply are prohibited; possession for personal use is not criminalized under the NpSG.[27] |
| Canada | Not specifically scheduled | Not listed under the Controlled Drugs and Substances Act. Analog considerations may apply.[27] |
| Australia | Prohibited | Classified as a controlled substance under federal scheduling.[27] |
references
- [1] ^abcHalberstadt AL, Chatha M, Klein AK, McCorvy JD, Meyer MR, Wagmann L, Stratford A, Brandt SD (2020) Pharmacological and biotransformation studies of 1-acyl-substituted derivatives of d-lysergic acid diethylamide (LSD) — Neuropharmacology doi:10.1016/j.neuropharm.2019.107856
- [2]
- [3]
- [4]
- [5] ^abcdHolze F, Ley L, Müller F, Becker AM, Straumann I, Vizeli P, Kuehne SS, Roder MA, Duthaler U, Kolaczynska KE, Varghese N, Eckert A, Liechti ME (2022) Direct comparison of the acute effects of lysergic acid diethylamide and psilocybin in a double-blind placebo-controlled study in healthy subjects — Neuropsychopharmacology doi:10.1038/s41386-022-01297-2
- [6] ^abcVizeli P, Studerus E, Holze F, Schmid Y, Dolder PC, Ley L, Straumann I, Becker AM, Müller F, Arikci D, Liechti ME (2024) Pharmacological and non-pharmacological predictors of the LSD experience in healthy participants — Translational Psychiatry doi:10.1038/s41398-024-03074-9