1P-LSD
1-propionyllysergic acid diethylamide
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1P-LSD (1-propionyl-lysergic acid diethylamide) is a synthetic psychedelic of the lysergamide class. It is a confirmed prodrug of LSD — the body converts it entirely into LSD before it acts.[1][2] Once converted, it activates serotonin receptors in the brain, producing the visual and cognitive shifts characteristic of classical psychedelics.[3]
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1P-LSD first appeared on online drug markets in early 2015 with no prior history in scientific literature.[4] It became the first in a series of structurally modified LSD prodrugs, each appearing after its predecessor was banned. Today it remains unscheduled in some countries and falls under structural analog or blanket-ban laws in others.
Subjective effects include geometric visual patterns, vivid color enhancement, time alteration, thought acceleration, emotional intensification, and ego dissolution.[5] The experience is slow-building and panoramic — lasting many hours, with a stimulant-edged quality that distinguishes it from shorter psychedelics like psilocybin.[6] Thought loops, anxious fixation, and difficulty sleeping through the long tail are common unwanted effects.
1P-LSD does not produce physical dependence, and no death from its direct pharmacological action has been documented.[3] The real risks are psychological — acute panic and potential psychosis in vulnerable individuals — and intensify sharply when combined with serotonin-raising drugs, which can trigger a life-threatening overheating crisis.[7] Human-specific data come from a single two-subject study;[2] most of what is known is extrapolated from LSD research.
History[edit]
Discovery
LSD was first synthesized by Albert Hofmann in 1938, with its psychedelic properties discovered accidentally five years later. In the 1950s, Sandoz chemists made ALD-52 (1-acetyl-LSD) — an N1-acylated structural analog with comparable effects in humans. That compound established the prodrug framework that 1P-LSD and its successors would later follow.
Emergence on the research chemical market
1P-LSD appeared on online drug markets in approximately January 2015, sold as blotter and powder.[4] It had no prior scientific description — Brandt and colleagues provided the first documentation of its existence and pharmacology.[4]
Regulation and successor compounds
As jurisdictions moved to ban 1P-LSD, structurally modified successors appeared in sequence: 1B-LSD, 1cP-LSD,[8] 1V-LSD, 1T-LSD, and 1F-LSD.[9] Each was confirmed as an LSD prodrug through the "Return of the Lysergamides" research series by Brandt and colleagues. The cycle became a defining case study in the cat-and-mouse dynamic between novel psychoactive substance markets and regulators.
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 interchangeable with LSD, supported by its confirmed complete prodrug conversion. The sequential appearance of successor compounds after each ban 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 a lysergamide — the same chemical family as LSD, built on the same tetracyclic ring scaffold.[4] Its molecular formula is C₂₃H₂₉N₃O₂ (molecular weight 379.5 g/mol).
A propionyl group attached at the N1 position is the only structural difference from LSD; liver enzymes remove it in the body, releasing free LSD — making 100 µg of 1P-LSD functionally equivalent to 100 µg of LSD itself.[2]
Pharmacology[edit]
Prodrug mechanism
1P-LSD is pharmacologically inactive as taken. The propionyl group reduces its binding to serotonin receptors by one to two orders of magnitude compared to LSD.[1] Liver enzymes remove it, releasing free LSD — confirmed in human liver tissue[10] and in two human subjects who showed only LSD in their blood and urine, approaching 100% conversion.[2]
Mechanism of action
Once converted, LSD acts as a partial agonist at serotonin receptors in the prefrontal cortex.[3] This disrupts the brain's default filtering of perception and thought, producing the psychedelic state. LSD also engages dopamine receptors,[11] adding a stimulant-like, emotionally expansive quality that distinguishes it from psilocybin.
Pharmacokinetics
All pharmacokinetics are those of LSD after conversion. The half-life following oral 1P-LSD is approximately 6.4 hours.[2] Drugs that slow liver metabolism can raise LSD blood levels — paroxetine, an antidepressant, increased LSD peak concentration by 1.4× and total exposure by 1.5× in a controlled study.[12]
Neuroscience[edit]
Where it acts
Since 1P-LSD converts entirely to LSD, its effects in the brain are LSD's. LSD activates serotonin receptors in the prefrontal cortex, loosening the brain's usual filtering of perception and thought.[3] Dopamine receptor engagement adds a stimulant-like, energizing dimension at higher doses.[11]
Why it matters
One framework proposes that serotonin receptor activation loosens the brain's predictive filtering, letting raw sensory input drive experience more than usual.[13] LSD also promotes new connections between neurons through a separate mechanism.[14] Together, these may explain why a single dose can produce psychological changes lasting weeks.
No direct neuroimaging studies of 1P-LSD exist. Key open questions include whether 1P-LSD crosses into the brain intact — potentially converting to LSD locally — or whether all conversion happens in the liver. Whether the propionylated form itself promotes new neuron connections, or only LSD does, is also unknown. The mechanism behind oral 1P-LSD's apparently higher LSD bioavailability compared to oral LSD[2][15] is unexplained. The precise basis of the approximately 14-day tolerance reset[16] also remains open.
Subjective Effects[edit]
The 1P-LSD experience is wide-spectrum and sustained — perception, thought, emotion, and body awareness shift together over many hours. It builds slowly, holds long, and resolves gradually. Set and setting shape its character profoundly; the substance provides the conditions, but what emerges varies widely.[6]
Compared to psilocybin, 1P-LSD lasts substantially longer at equivalent intensity and carries a stimulant-edged, energized quality.[5][17] Where psilocybin tends toward introspection, 1P-LSD feels more expansive. Its active metabolite engages dopamine alongside serotonin — that broader receptor profile accounts for the distinction.
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 exist. As a complete prodrug of LSD, its toxicological profile is LSD's — a substance with an extremely high therapeutic index and no documented deaths from direct pharmacological action.[3]
Heart and circulation
LSD produces modest, dose-dependent increases in heart rate and blood pressure. At 100 µg, these effects are moderate and comparable to psilocybin.[17] They are clinically relevant primarily for those with pre-existing heart conditions.[18]
Chronic toxicity
No chronic toxicity data exist for 1P-LSD. Over seven decades of LSD use have produced no evidence of organ damage at psychoactive doses.
Psychological Risks
Acute anxiety and panic occur with dose-dependent frequency. Anxiety and ego dissolution scores were significantly higher at 200 µg than at 100 µg LSD.[5] Pre-existing anxiety increases vulnerability, but dose is the primary predictor.[6]
LSD can trigger psychotic episodes in predisposed individuals, with documented cases of schizophrenia-like symptoms.[19] Personal or family history of psychosis, schizophrenia, or bipolar disorder is an absolute contraindication.
Persistent visual disturbances after use — visual haze / noise, trailing, geometric overlays — are a recognized but uncommon condition.[20] The cause is not fully understood but may involve changes to inhibitory neurons from serotonin receptor stimulation.[21]
Tolerance & Dependence
1P-LSD is not addictive: no physical dependence develops, no withdrawal occurs, and psychological dependence is uncommon.[3][22] Tolerance builds rapidly after a single dose and extends to all serotonergic psychedelics including psilocybin and mescaline.[16] Full sensitivity commonly returns after approximately 14 days of abstinence.citation needed
Drug Interactions
Serotonergic interactions
The most serious risk is serotonin toxicity — a potentially life-threatening condition involving dangerous fever, muscle rigidity, and unstable heart rate — when 1P-LSD is combined with drugs that strongly raise serotonin levels. Tramadol and MAOIs are the highest-risk agents and both combinations are contraindicated.[23][24][7]
SSRIs/SNRIs carry lower serotonin syndrome risk, but certain SSRIs raise LSD plasma levels — paroxetine increased peak concentration 1.4× and total exposure 1.5×.[12] In a controlled study, paroxetine pretreatment reduced anxiety and nausea without diminishing pleasant effects.[12] Risk is not zero at high doses of both agents.[7]
Other interactions
MDMA co-administration increases LSD plasma levels and prolongs effects, with more cardiovascular strain than either substance alone.[25]
Cannabis: No controlled data exist. Community reports suggest it may intensify the 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 it.safety citation needed
Contraindications
Absolute contraindications:
- Personal or family history of psychotic disorders (schizophrenia, schizoaffective disorder) — LSD can precipitate acute psychosis[19]
- Bipolar disorder — risk of manic episode precipitationsafety citation needed
- Concurrent MAOI use — serotonin toxicity risk[7]
- Concurrent tramadol use — serotonin toxicity risk[23]
Relative contraindications:
- Uncontrolled high blood pressure or significant heart disease[18]
- Liver impairment — may alter LSD exposure from prodrug conversion[10]
- Pregnancy and breastfeeding — no safety data existsafety citation needed
- Concurrent lithium therapy — seizure risk from community reportssafety citation needed
- Epilepsy or seizure disorders — theoretical lowered seizure thresholdsafety citation needed
Harm Reduction[edit]
Forms & Identification
1P-LSD is most commonly found on blotter paper or as a white to off-white powder. N1-acyl lysergamides are visually indistinguishable from each other and from LSD itself. Ehrlich's reagent confirms an indole is present (purple color change) but cannot differentiate 1P-LSD from LSD or its analogs. A drug checking service is the only reliable method for precise identification.
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 assessing 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, with 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. A familiar, physically safe space with a calm retreat area reduces difficult reactions. A trusted, sober companion is strongly recommended — especially at higher doses or for first-time use.
Avoid use during periods of emotional lability, unresolved anxiety, or high external stress. These are documented predictors of difficult experiences and do not 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.
Experiences 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 like meditation. Distressing perceptual changes, anxiety, or depersonalization persisting beyond a few days warrant consultation with a mental health professional.
Recovery & Support
While 1P-LSD does not produce physical dependence, patterns of repeated use to escape difficult emotions 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 threatens 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, rapid heart rate — after combining substances.
Immediate steps
- Move to a quiet, low-stimulation environment
- Speak calmly, use the person's name, and remind them they have taken a drug and it will end
- Do not restrain 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 analog and blanket-ban legislation in several countries despite rarely being specifically named in controlled substances schedules.
| 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.[26] |
| United Kingdom | Illegal | Covered by the Psychoactive Substances Act 2016; production, supply, and possession with intent to supply are prohibited.[26] |
| 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.[26] |
| Canada | Not specifically scheduled | Not listed under the Controlled Drugs and Substances Act. Analog considerations may apply.[26] |
| Australia | Prohibited | Classified as a controlled substance under federal scheduling.[26] |
references
- [1] ^abHalberstadt 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] ^abcdBrandt 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
- [5] ^abcHolze 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