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1P-LSD

1P-LSD, chemically known as 1-propionyl-d-lysergic acid diethylamide, is a synthetic derivative of lysergic acid diethylamide (LSD) belonging to the lysergamide class of compounds.^[1] It features a propionyl group attached to the indole nitrogen of the LSD molecule, distinguishing it structurally while maintaining functional similarity.^[1] Pharmacologically, 1P-LSD acts as a prodrug to LSD, undergoing rapid hydrolysis in human serum and following oral or intravenous administration to yield active LSD concentrations, which mediate its hallucinogenic effects via agonism at serotonin 5-HT2A receptors.^[2]^[3] In vivo studies in mice demonstrate LSD-like behavioral responses, including head-twitch activity indicative of serotonergic psychedelia, with potency closely approximating that of LSD itself.^[1] Human pharmacokinetic data confirm equivalent subjective effects to LSD, underscoring its role as a metabolic precursor rather than a distinct entity.^[2] Emerging around 2015 as a novel psychoactive substance marketed in blotter and powdered forms, 1P-LSD has been positioned as a research chemical alternative amid regulatory scrutiny of LSD analogs, though its biotransformation to the controlled parent compound has prompted subsequent legal controls in multiple jurisdictions.^[4] Analytical profiling via mass spectrometry and chromatography reveals metabolic deacylation to LSD as the primary pathway, with no evidence of unique pharmacological profiles beyond this conversion.^[5]^[6] Stability assessments indicate greater resistance to degradation compared to related acyl-LSD variants due to steric factors from the propionyl moiety.^[7]

Chemical Properties

Structure and Nomenclature

1P-LSD, also known as 1-propionyl-lysergic acid diethylamide, is a semisynthetic derivative of lysergic acid diethylamide (LSD) featuring a propanoyl (C2H5CO-) group attached to the nitrogen atom at the 1-position of the indole ring in the ergoline scaffold.^[8]^[1] This modification positions 1P-LSD within the lysergamide class of compounds, which share a tetracyclic ergoline core consisting of an indole fused to a quinoline system, with the diethylamide substituent at the 9-position carboxamide.^[8]^[1] The systematic IUPAC name for 1P-LSD is (6aR,9R)-N,N-diethyl-7-methyl-4-propanoyl-6,6a,8,9-tetrahydroindolo[4,3-fg]quinoline-9-carboxamide, reflecting its specific stereochemistry at the 5,8-fused ring junction (6aR) and chiral center (9R), consistent with the active d-lysergic acid configuration.^[8] The molecular formula is C_{23}H_{29}N_{3}O_{2}, with a molecular weight of 379.5 g/mol.^[8]^[9] In nomenclature, the prefix "1P-" denotes the N1-acylation with propionic acid, distinguishing it from LSD and other analogs like 1-acetyl-LSD (1A-LSD), a practice common in research chemical communities for evading legal restrictions on parent compounds.^[1] Analytical characterization, including NMR and mass spectrometry, confirms the structural integrity of this acylated lysergamide, with the propanoyl group hydrolyzable to yield LSD.^[1]

Synthesis and Production

1P-LSD is produced through chemical synthesis starting from lysergic acid, derived via hydrolysis of ergot alkaloids like ergotamine tartrate extracted from the ergot fungus Claviceps purpurea.^[10] Lysergic acid is activated using reagents such as thionyl chloride and coupled with diethylamine to yield lysergic acid diethylamide (LSD).^[11] The LSD is then subjected to N1-acylation with a propionyl group, typically via reaction with propionic anhydride, to form 1P-LSD.^[12] This acylation step mirrors the historical synthesis of the analogous 1-acetyl-LSD (ALD-52), first reported in 1957 by reacting LSD with acetic anhydride.^[12] Detailed procedural conditions for 1P-LSD propionylation remain undisclosed in peer-reviewed sources, reflecting regulatory sensitivities surrounding lysergamides, though the reaction aligns with conventional indole N-acylation techniques employing acid anhydrides or chlorides in inert solvents.^[13] Commercial production occurs in specialized small-scale laboratories, often clandestine, targeting the research chemical market; 1P-LSD first appeared as a powdered material or on blotter paper around 2015.^[1] Yields and purity depend on precursor quality and purification methods like chromatography, but specific industrial-scale data are unavailable due to its non-pharmaceutical status.^[1]

History

Origins and Development

1P-LSD, chemically known as 1-propionyl-lysergic acid diethylamide, originated as a designer drug in the new psychoactive substances (NPS) market during the mid-2010s, developed as an N1-acyl derivative of lysergic acid diethylamide (LSD) to function as a prodrug that hydrolyzes in vivo to the parent compound LSD.^[1] This structural modification, involving the addition of a propionyl group to the indole nitrogen of LSD, mirrored earlier analogs like 1-acetyl-LSD (ALD-52), which had been synthesized decades prior but saw renewed interest in clandestine production.^[1] The emergence of 1P-LSD was driven by efforts to circumvent legal controls on LSD and related lysergamides, particularly following the United Kingdom's 2014 amendments banning specific derivatives such as AL-LAD, LSZ, and ETH-LAD under the Misuse of Drugs Act.^[1] The compound first became available commercially as a research chemical in powdered form or on blotters via online vendors targeting Europe and North America, with initial detections reported in 2015 by monitoring agencies like the European Monitoring Centre for Drugs and Drug Addiction (EMCDDA).^[1] ^[2] No public record identifies a specific chemist or laboratory responsible for its initial synthesis, consistent with the anonymous, clandestine nature of many NPS developments aimed at exploiting temporary gaps in analog legislation such as the U.S. Federal Analogue Act.^[1] Early samples, often labeled as containing 100 μg per blotter, were distributed by vendors including those in the UK, reflecting a broader trend of rapid iteration in lysergamide analogs to maintain market availability amid evolving prohibitions.^[1] Scientific development accelerated post-emergence, with the first comprehensive analytical characterization published in 2016, employing techniques like NMR, LC-MS/MS, and FTIR to confirm its structure and differentiation from LSD.^[1] Behavioral studies in mice demonstrated LSD-like head-twitch responses, supporting its classification as a serotonergic hallucinogen that deacylates rapidly to LSD upon administration.^[1] Subsequent research in the late 2010s and early 2020s focused on pharmacokinetics, revealing near-complete conversion to LSD within 1.5 hours in humans, underscoring its role as a metabolic precursor rather than an independent entity.^[2] This prodrug strategy, while innovative for regulatory evasion, highlighted vulnerabilities to retroactive scheduling, as evidenced by 1P-LSD's inclusion in controlled substance lists across multiple jurisdictions by 2019.^[12]

Market Emergence and Analog Trends

1P-LSD first appeared on the online research chemical market in early 2015, distributed primarily as blotters and powdered material.^[14]^[2] This introduction occurred without prior documentation in scientific literature, suggesting clandestine synthesis outside academic or pharmaceutical contexts.^[14] The compound quickly gained traction among users seeking LSD-like effects amid stringent global controls on lysergic acid diethylamide (LSD), which has been classified as a Schedule I substance in the United States since 1970 and similarly restricted elsewhere. The market emergence of 1P-LSD aligned with a resurgence of lysergamide analogs in the 2010s, driven by efforts to exploit gaps in analog legislation such as the U.S. Federal Analogue Act of 1986, which targets substances structurally similar to scheduled drugs when intended for human consumption. Preceding analogs included AL-LAD (appearing around 2013) and earlier rediscoveries like ALD-52 from the 1960s, but 1P-LSD marked a shift toward N-acyl substituted variants engineered as prodrugs.^[14] These prodrugs, featuring labile acyl groups (e.g., propionyl in 1P-LSD), remain pharmacologically inactive until enzymatic hydrolysis yields active LSD in vivo, potentially delaying regulatory classification by differing structurally from LSD while mimicking its effects.^[2]^[15] Subsequent analogs followed this prodrug trend, including 1B-LSD (detected post-2015) and 1P-ETH-LAD, reflecting iterative modifications to evade evolving bans and detection methods in forensic and customs analyses.^[15]^[16] By 2016, European monitoring agencies like the EMCDDA reported 1P-LSD seizures, prompting temporary scheduling in countries such as Switzerland and the UK, yet online availability persisted through grey-market vendors. This pattern underscores a cat-and-mouse dynamic between producers targeting metabolic activation for bioequivalence to LSD and authorities adapting controls, with prodrug designs complicating enforcement due to their intermediate metabolic status.^[17]^[18]

Pharmacology

Mechanism of Action

1P-LSD functions primarily as a prodrug of lysergic acid diethylamide (LSD), undergoing rapid deacylation via hydrolysis to yield LSD following both oral and intravenous administration in humans.^[2] This biotransformation occurs quickly, with plasma concentrations of LSD detectable shortly after 1P-LSD dosing, confirming its role as an inactive precursor that relies on metabolic conversion for pharmacological activity.^[2] Consequently, the mechanism of action of 1P-LSD mirrors that of LSD, with effects mediated predominantly by the active metabolite.^[5] In its unmetabolized form, 1P-LSD exhibits substantially reduced binding affinity to key serotonin receptors compared to LSD, including a 13-fold decrease at the 5-HT2A receptor and a 67-fold decrease at 5-HT1A.^[2] It displays weak agonist efficacy or even antagonistic properties at certain 5-HT2 subtypes in calcium mobilization assays, unlike LSD's robust partial agonism.^[5] Despite this, in vivo behavioral responses, such as the head-twitch response in rodents—a proxy for psychedelic effects—are elicited by 1P-LSD through 5-HT2A receptor activation, attributable to its conversion to LSD.^[1] LSD, the primary active species, binds with high affinity to serotonin receptors, acting as a partial agonist at 5-HT2A sites, which is the critical mediator of hallucinogenic and psychedelic effects.^[19] This receptor agonism disrupts default mode network activity and enhances neural plasticity, though downstream signaling involves pleiotropic interactions beyond 5-HT2A, including contributions from 5-HT1A and dopamine receptors.^[20] The 1-acyl substitution in 1P-LSD generally lowers intrinsic activity at monoamine receptors by one to two orders of magnitude prior to metabolism, underscoring the dependence on hydrolysis for efficacy.^[5]

Pharmacokinetics and Metabolism

1P-LSD is rapidly absorbed following oral administration and undergoes hydrolysis to LSD, confirming its role as a prodrug.^[21] In a study involving two human subjects, oral ingestion of 100 μg 1P-LSD resulted in no detectable 1P-LSD in plasma, with LSD appearing promptly and exhibiting a maximum plasma concentration (Cmax) of 2.3–3.7 ng/mL at a time to maximum concentration (Tmax) of 2.2 hours.^[21] The area under the curve (AUC) for LSD was 12.3–18.6 ng·h/mL, and the terminal half-life was approximately 6.4 hours.^[21] Intravenous administration of 20 μg 1P-LSD revealed brief detectability of the parent compound, with an initial half-life of 0.19–0.21 hours, followed by rapid conversion to LSD (Cmax 1.8–2.6 ng/mL at Tmax 0.15–0.3 hours).^[21] The bioavailability of LSD derived from oral 1P-LSD was estimated at 92–100%, indicating near-complete hydrolysis and absorption efficiency comparable to direct LSD administration.^[21] Hydrolysis occurs enzymatically in plasma and tissues, primarily via deacylation of the propionyl group at the indole nitrogen.^[21]^[6] In vitro studies using pooled human liver S9 fractions confirm deacylation to LSD as the predominant metabolic pathway for 1P-LSD, with additional minor metabolites including N-dealkylated and hydroxylated products formed via cytochrome P450 enzymes such as CYP1A2 and CYP3A4.^[6] Following conversion to LSD, further metabolism mirrors that of LSD, involving hepatic N-demethylation to nor-LSD and other inactive metabolites, with excretion primarily renal.^[21] No unique metabolites specific to 1P-LSD beyond the initial hydrolysis were identified in human pharmacokinetic data.^[21]

Effects

Subjective Psychological Effects

1P-LSD induces subjective psychological effects that closely resemble those of LSD, as it functions as a prodrug rapidly hydrolyzed to LSD in the body, achieving near-complete oral bioavailability.^[3] In a pharmacokinetic study involving healthy volunteers, oral administration of 100 μg 1P-LSD produced significant alterations in consciousness, assessed via the Five Dimensions of Altered States of Consciousness (5D-ASC) scale, with elevated scores across subscales including oceanic boundlessness (encompassing unity and spiritual experiences), visionary restructuralization (perceptual alterations and hallucinations), and anxious ego dissolution (self-dissolution with potential anxiety).^[2] These effects peaked around 2-3 hours post-ingestion and persisted for 8-12 hours, comparable in time course to LSD.^[3] User surveys report psychedelic visuals as a hallmark effect, with 93% of respondents describing perceptual changes akin to LSD, such as enhanced colors, geometric patterns, and synesthesia, though overall strength and pleasurable high were rated slightly lower (7.57/10 and 7.60/10, respectively, versus 7.85/10 and 7.88/10 for LSD).^[22] Introspective deepening, emotional amplification, and time distortion are commonly experienced, often leading to profound insights or mystical states, though some individuals note milder ego dissolution compared to LSD.^[22]^[2] Adverse psychological effects mirror LSD's profile, including potential anxiety, confusion, or paranoia, particularly at higher doses or in unprepared users, though controlled administrations showed dose-dependent increases in such states without severe incidents.^[2] Intravenous dosing yielded lower 5D-ASC scores than oral, suggesting route-dependent intensity, with one subject reporting absent visuals, highlighting variability.^[2] Overall, effects are characterized by reduced psychological distress in therapeutic contexts but risk of challenging experiences in recreational use.^[3]

Physiological Effects

1P-LSD, functioning as a prodrug that hydrolyzes rapidly to LSD in the body with near-complete bioavailability, produces physiological effects closely mirroring those of LSD.^[2] These effects stem from serotonergic activation and autonomic nervous system stimulation, manifesting primarily as mild to moderate alterations in cardiovascular, thermoregulatory, and pupillary responses.^[23] Human data specific to 1P-LSD remains limited, with no controlled studies reporting differential physiological impacts compared to LSD; however, its equivalent potency and metabolic conversion support identical profiles.^[5] Key autonomic changes include mydriasis, or pupil dilation, which occurs shortly after administration and persists for several hours, reflecting noradrenergic and serotonergic influences on the iris sphincter.^[24] Heart rate typically increases by 10-20 beats per minute, alongside modest elevations in blood pressure (systolic rises of 10-20 mmHg), attributable to sympathetic activation without significant risk of hypertensive crisis at standard doses around 100 μg.^[24] ^[23] Body temperature may rise slightly (0.5-1°C), potentially leading to mild hyperthermia, sweating, or tremors, though these are generally transient and self-limiting.^[24] Respiratory rate can accelerate mildly, and gastrointestinal effects such as nausea or reduced appetite are reported in some users during the onset phase (30-60 minutes post-ingestion), akin to LSD's emetic potential via 5-HT3 receptor agonism.^[25] ^[24] No evidence indicates unique physiological risks for 1P-LSD, such as organ toxicity or severe cardiovascular strain, beyond those associated with LSD at equipotent doses; adverse events like rapid heart rate or hypertension noted in case reports align with LSD's profile rather than novel effects.^[26] Overall, these changes are dose-dependent and subside as the drug's duration wanes (8-12 hours), with minimal long-term physiological sequelae in healthy individuals.^[2]

Duration and Dosage Considerations

Dosage ranges for 1P-LSD are reported as threshold effects at 15 μg, light effects at 25–75 μg, common recreational effects at 75–150 μg, strong effects at 150–300 μg, and heavy effects exceeding 300 μg, based on user experiences.^[27] These microgram-level doses reflect its potency as a lysergamide prodrug, with 100 μg of 1P-LSD hemitartrate equating to approximately 71.2 μg of LSD base due to its molecular structure.^[2] In a controlled pharmacokinetic study involving oral administration of 100 μg to healthy volunteers, subjective effects aligned closely with those of equivalent LSD doses, confirming near-complete metabolic conversion to active LSD.^[2] The duration of effects from 1P-LSD typically spans 8–12 hours total, with onset occurring 20–60 minutes after oral ingestion, a come-up phase of 45–120 minutes, peak intensity at 3–5 hours, and aftereffects persisting 6–24 hours.^[27] Empirical data from intravenous and oral dosing in humans indicate subjective effects lasting 8–10 hours, with oral onset at 30–40 minutes and peak at approximately 2 hours, followed by gradual offset; detection of metabolites in serum and urine extends up to 49 hours and 80 hours, respectively, highlighting prolonged elimination.^[2] Intravenous administration shortens onset to 15–25 minutes but yields comparable overall duration to oral routes, attributed to rapid hydrolysis of 1P-LSD to LSD in the gastrointestinal tract or liver, achieving near-100% bioavailability.^[2] Tolerance develops immediately upon use, reducing sensitivity by up to 50% within 5–7 days and returning to baseline after 14 days of abstinence, with cross-tolerance to other psychedelics such as LSD.^[27] Dosage and duration can vary based on individual factors including body weight, metabolism, and prior exposure, though purity inconsistencies in unregulated sources pose risks of inaccurate dosing; users report effects intensity scaling dose-dependently, similar to LSD, without established therapeutic guidelines due to limited clinical data.^[2] ^[27]

Therapeutic Potential

Preclinical and Clinical Research

Preclinical studies on 1P-LSD have primarily focused on its pharmacological profile and biotransformation, establishing it as a prodrug of LSD. In vitro assays demonstrated that 1P-LSD exhibits weak partial agonist activity at the 5-HT2A receptor, with lower efficacy compared to LSD, but undergoes rapid deacylation by enzymes such as human serum esterases and hepatic carboxyl esterase 1 to yield LSD as the active metabolite.^[28] Receptor binding studies confirmed nanomolar affinity for 5-HT2A, 5-HT1A, and dopamine D3 receptors, mirroring LSD's profile, while mass spectrometry and nuclear magnetic resonance analyses verified its structural identity.^[1] In vivo preclinical evaluations in mice revealed that 1P-LSD induces head-twitch responses—a behavioral proxy for 5-HT2A agonism—at doses comparable to LSD (ED50 of 373.3 nmol/kg versus 46.1 nmol/kg for LSD), with no significant differences in potency or duration, supporting metabolic conversion to LSD in biological systems.^[1] Stability tests indicated rapid hydrolysis in simulated gastric fluid and human plasma, with over 90% conversion to LSD within minutes, underscoring its pharmacokinetic equivalence to LSD rather than independent activity.^[2] No dedicated preclinical models for therapeutic applications, such as anxiety reduction or neuroplasticity, have been reported specifically for 1P-LSD; inferences draw from LSD's established effects in rodent models of depression-like behavior.^[1] Clinical research on 1P-LSD remains exceedingly limited, with no registered trials evaluating therapeutic efficacy. A single-subject pharmacokinetic study conducted in 2019 administered 100 μg of 1P-LSD orally and intravenously, detecting rapid conversion to LSD (peak plasma levels within 1.5 hours orally, immediate IV), with plasma concentrations and elimination half-lives (3-5 hours) aligning closely with historical LSD data.^[2] Subjective effects, assessed via visual analog scales, included intensified perceptual alterations and euphoria peaking at 2-4 hours post-oral dose, slightly more pronounced and shorter-lived than equivalent LSD doses, but qualitatively indistinguishable, affirming prodrug status without novel therapeutic insights.^[2] The absence of larger controlled human studies precludes conclusions on 1P-LSD's safety or efficacy in psychiatric contexts, where LSD itself has shown preliminary promise in reducing anxiety in life-threatening illness (e.g., via enhanced neuroplasticity in small trials).^[2] Ethical and regulatory barriers, including its status as a novel psychoactive substance, have confined research to pharmacological characterization rather than clinical endpoints like symptom remission in mood disorders. Ongoing LSD trials do not extend to 1P-LSD analogs, highlighting a evidence gap for this compound's independent therapeutic utility.^[1]

Claimed Benefits and Evidence Gaps

Proponents assert that 1P-LSD may confer therapeutic benefits akin to LSD, such as reductions in symptoms of anxiety, depression, and substance dependence, owing to its hydrolysis into LSD following ingestion.^[2] ^[29] These assertions stem largely from user reports on online forums and the presumption of pharmacological equivalence, rather than empirical validation specific to 1P-LSD.^[2] A 2020 human pharmacokinetic study confirmed that 1P-LSD exhibits near-100% bioavailability as LSD after oral dosing, with subjective psychosensory effects— including altered perception and mood elevation—mirroring those of LSD in prior trials.^[2] ^[3] Nonetheless, this equivalence in acute effects does not substantiate long-term therapeutic outcomes, as no randomized controlled trials have assessed 1P-LSD for psychiatric applications like alcoholism treatment, where LSD has shown modest efficacy in meta-analyses of mid-20th-century data.^[30] Evidence gaps are pronounced: unlike LSD, which has undergone limited modern resurgence in phase II trials for anxiety and depression, 1P-LSD lacks any dedicated clinical investigations into efficacy, safety profiles under therapeutic protocols, or comparative dosing for sustained benefits.^[31] ^[29] Preclinical behavioral assays indicate 1P-LSD induces LSD-like head-twitch responses in rodents at lower potency, but human therapeutic claims remain untested amid regulatory barriers and its classification as a research chemical.^[1] Potential variances in individual metabolism or interactions with comorbid conditions further highlight the unsubstantiated nature of extrapolations from LSD data.^[1]

Risks and Adverse Effects

Acute Risks and Toxicity

1P-LSD, as a prodrug of lysergic acid diethylamide (LSD), demonstrates pharmacokinetics leading to rapid conversion to LSD in humans, yielding subjective and physiological effects comparable to those of LSD at equivalent doses, with no indications of unique acute toxic metabolites.^[3] Preclinical assays in mice confirm LSD-like behavioral activity for 1P-LSD, with a median effective dose (ED50) of 349.6 nmol/kg, suggesting similar potency and margin of safety to LSD.^[32] Acute physiological toxicity remains low, mirroring LSD's established profile of minimal direct organ damage or lethality at recreational doses (typically 50–200 μg). LSD exhibits no known human fatalities from pharmacological overdose alone, with animal LD50 values exceeding human therapeutic equivalents by factors of thousands (e.g., >16 mg/kg intravenously in mice for LSD).^[33] For 1P-LSD, in vitro and in vivo metabolism studies detect no novel cytotoxic byproducts, and cytotoxicity assays in model organisms like zebrafish larvae show no evidence of acute toxicity beyond solvent controls for LSD analogs.^[34] Reported acute physiological effects include transient tachycardia (heart rate increases of 10–20 bpm), mild hypertension (systolic rises up to 20 mmHg), mydriasis, and slight hyperthermia (<1°C elevation), all resolving within 8–12 hours without intervention in controlled settings.^[3] Hazard classifications note potential oral toxicity based on structural analogy (GHS H301), but no verified human cases of severe cardiovascular or respiratory compromise exist.^[8] The foremost acute risks are behavioral rather than toxicological: impaired judgment and perceptual distortions can precipitate accidents, self-injurious actions, or exacerbation of underlying psychiatric conditions during peak effects (2–6 hours post-ingestion). No dedicated 1P-LSD overdose reports appear in toxicological registries up to 2022, though rare LSD-related emergencies involve polydrug interactions or extreme doses (>1 mg), typically manifesting as prolonged agitation rather than physiological failure.^[35] Empirical data underscore a wide therapeutic index, with safety contingent on dose control and set/setting.^[36]

Psychological and Long-Term Hazards

Psychological hazards associated with 1P-LSD use primarily stem from its rapid metabolism to LSD, yielding subjective effects akin to LSD, including potential acute dysphoria, anxiety, paranoia, and panic during intoxication.^[2]^[3] In recreational contexts, these may manifest as "bad trips" involving intense fear, depersonalization, or hallucinatory terror, particularly at doses exceeding 100-200 micrograms, though incidence varies by set, setting, and individual vulnerability.^[37] Predisposing factors such as underlying anxiety disorders or prior trauma amplify risks, with self-reports indicating heightened emotional lability in uncontrolled environments.^[38] Long-term psychological sequelae parallel those of LSD, encompassing flashbacks—spontaneous re-emergence of perceptual distortions—and Hallucinogen Persisting Perception Disorder (HPPD), defined by chronic visual phenomena like trails, geometric patterns, or intensified colors persisting beyond acute effects.^[39]^[40] HPPD prevalence among LSD users is estimated at 4-28% in retrospective surveys, often triggered by high doses or repeated exposure, though prospective data remain sparse.^[41] For 1P-LSD, no large-scale epidemiological studies exist, but its pharmacological equivalence to LSD suggests comparable potential, with one cohort analysis noting LSD/1P-LSD use in over half of participants without reported HPPD cases in that sample.^[42] Persistent psychosis, involving delusions or hallucinations unresponsive to acute resolution, occurs rarely but predominantly in individuals with schizophrenia spectrum traits or family history of psychosis, with onset potentially lasting weeks to years post-exposure.^[43]^[44] Case analyses of psychedelic-induced psychoses highlight dose-dependency and youth as risk modifiers, applicable to lysergamides like 1P-LSD given deacylation to active LSD.^[38] Longitudinal LSD studies report low overall incidence of enduring impairment in non-vulnerable users, with most adverse effects resolving within months, yet chronic users face elevated odds of mood dysregulation or attenuated personality changes.^[44] Evidence gaps persist for 1P-LSD due to its recent emergence, underscoring caution in extrapolation from LSD data.^[4]

Overdose and Dependency Potential

1P-LSD, as a prodrug that rapidly hydrolyzes to LSD in vivo, exhibits a toxicity profile closely aligned with that of LSD, with no reported cases of fatal overdose attributable to direct physiological toxicity.^[1]^[2] The estimated lethal dose for LSD exceeds 14,000 micrograms, far beyond typical recreational doses of 50-200 micrograms, rendering acute physiological overdose improbable at human consumption levels.^[39] Animal studies on LSD indicate a high LD50, with effective human doses being orders of magnitude lower, supporting the absence of toxicity-related deaths even in cases of massive ingestion.^[45] For 1P-LSD specifically, preclinical data confirm dose-dependent behavioral effects akin to LSD but without evidence of organ toxicity or lethality in rodents at pharmacologically relevant doses.^[1] Overdose scenarios with 1P-LSD primarily manifest as intensified psychological effects, such as severe anxiety, paranoia, or hallucinatory distress, rather than cardiovascular collapse or respiratory failure.^[46] No human fatalities from 1P-LSD overdose have been documented as of 2025, consistent with LSD's historical safety record spanning decades of use.^[39] Supportive care, including benzodiazepines for agitation, suffices for management, underscoring the compound's low acute risk profile absent comorbidities or polydrug involvement.^[45] Regarding dependency, 1P-LSD demonstrates negligible potential for physical addiction, mirroring LSD's classification as a non-addictive hallucinogen devoid of withdrawal syndromes upon cessation.^[47] Tolerance develops rapidly with repeated dosing—often within days—necessitating escalating amounts for equivalent effects, which deters habitual use due to the substance's prolonged and unpredictable psychological intensity.^[48] Pharmacological studies indicate 1P-LSD's effects stem from 5-HT2A receptor agonism post-conversion to LSD, a mechanism not associated with dopaminergic reward pathways implicated in substance use disorders.^[12] Psychological dependence is rare, with no epidemiological evidence of compulsive patterns; self-limiting factors like rapid tolerance and adverse experiential risks predominate.^[49] Limited clinical data on 1P-LSD preclude definitive assessments, but its equipotency to LSD in subjective effects supports an abuse liability profile rated as low by regulatory standards.^[2]

Interactions

Pharmacodynamic Interactions

1P-LSD, as a prodrug of lysergic acid diethylamide (LSD), undergoes rapid deacylation in vivo to yield LSD, resulting in pharmacodynamic effects primarily mediated by LSD's agonism at serotonin 5-HT2A receptors, with weaker contributions from the intact prodrug form.^[5] In vitro assays demonstrate that 1P-LSD exhibits reduced binding affinity for 5-HT2A receptors (approximately 13-fold lower than LSD) and acts as a weak partial agonist or antagonist at 5-HT2 subtypes, contrasting with LSD's potent agonism.^[2] However, in vivo, 1P-LSD induces 5-HT2A-mediated behaviors such as head-twitch responses in rodents at potencies comparable to LSD, underscoring the dominance of its metabolite in hallucinogenic and perceptual effects.^[5] Pharmacodynamic interactions of 1P-LSD are expected to parallel those of LSD due to equivalent subjective and physiological profiles post-conversion.^[3] Selective serotonin reuptake inhibitors (SSRIs), such as fluoxetine, attenuate LSD's hallucinogenic effects by downregulating 5-HT2A receptor density and sensitivity, potentially delaying onset and reducing intensity; similar modulation would likely apply to 1P-LSD.^[50] 5-HT2A antagonists like ketanserin fully block LSD-induced subjective alterations in controlled studies involving healthy volunteers, indicating competitive inhibition at the primary site of action.^[50] Monoamine oxidase inhibitors (MAOIs), including phenelzine, paradoxically diminish rather than potentiate LSD effects, possibly via altered serotonin dynamics independent of metabolism inhibition, as LSD is not a substrate for MAO.^[50] Antipsychotics such as chlorpromazine and risperidone exhibit mixed outcomes: they often antagonize perceptual distortions through dopamine D2 and 5-HT2A blockade but may exacerbate anxiety or autonomic responses in some cases.^[50] Additive sympathomimetic effects with stimulants could heighten cardiovascular strain, though direct data for 1P-LSD remain absent; caution is advised given LSD's intrinsic autonomic stimulation.^[20] Limited empirical research on 1P-LSD specifically highlights a data gap, with interactions inferred from LSD pharmacodynamics and prodrug kinetics.^[5]

Pharmacokinetic Interactions

1P-LSD undergoes rapid deacylation in vivo to form lysergic acid diethylamide (LSD), with pharmacokinetics closely mirroring those of LSD following oral or intravenous administration, including near-complete bioavailability and a time course of effects lasting 8-10 hours.^[3] As a prodrug, its initial hydrolysis appears primarily non-enzymatic or via esterases, but subsequent metabolism of the generated LSD involves cytochrome P450 (CYP) enzymes, particularly CYP2D6, which significantly influences plasma concentrations and elimination.^[51] ^[52] Direct pharmacokinetic interaction data for 1P-LSD remain scarce due to its status as a novel lysergamide with limited clinical investigation; however, inferences from LSD studies indicate potential alterations in LSD's metabolism by CYP modulators.^[3] In vitro evidence shows that inhibition or induction of CYP enzymes, including CYP2D6, CYP1A2, CYP2C19, and CYP3A4, produces minor but measurable changes in LSD biotransformation to inactive metabolites like 2-oxo-3-hydroxy-LSD, suggesting possible drug-drug interactions that could prolong or intensify effects.^[51] For instance, CYP2D6 poor metabolizers exhibit elevated LSD exposure and heightened subjective effects, implying that potent CYP2D6 inhibitors (e.g., fluoxetine or quinidine) may similarly increase systemic LSD levels post-1P-LSD administration.^[52] Conversely, 1P-LSD and LSD demonstrate negligible capacity to induce or inhibit major CYP enzymes in available assays, reducing the likelihood of 1P-LSD significantly altering the pharmacokinetics of co-administered drugs via CYP-mediated pathways.^[51] Systematic reviews of classic psychedelics note that while pharmacodynamic synergies (e.g., with serotonergic agents) predominate, pharmacokinetic risks for LSD analogs like 1P-LSD are primarily unidirectional, stemming from external modulation of LSD clearance rather than reciprocal effects.^[53] Empirical confirmation requires further human studies, as current evidence relies heavily on in vitro and genetic polymorphism data.^[51] ^[52]

Legal Status

Regulatory Framework

In the United States, 1P-LSD is not explicitly scheduled under the federal Controlled Substances Act as of 2025, but it qualifies as a Schedule I controlled substance analogue of LSD when intended for human consumption, pursuant to the Federal Analogue Act of 1986, due to its substantial similarity in chemical structure and pharmacological effects to LSD.^[26] State-level regulations vary; for instance, Wisconsin proposed emergency scheduling in 2020 citing public health risks, though it was not federally adopted.^[54] In the European Union, regulation occurs primarily at the national level under the New Psychoactive Substances framework, with 1P-LSD explicitly controlled in multiple member states including Germany (via the New Psychoactive Substances Act, NpSG, effective December 2016), France, Denmark, Finland, Estonia, Latvia, Romania, and Sweden.^[18] The United Kingdom classifies it under the Psychoactive Substances Act 2016, which prohibits the production, supply, offer to supply, possession with intent to supply, and importation of psychoactive substances not otherwise exempted, regardless of specific naming.^[55] Internationally, 1P-LSD remains unscheduled under the United Nations 1971 Convention on Psychotropic Substances, creating legal grey areas in jurisdictions without specific bans or analogue provisions, though it is prohibited in countries such as Australia (as a Schedule 9 prohibited substance since 2016), Japan (under the Pharmaceutical Affairs Act), Switzerland (Verzeichnis E since December 2015), Norway, and Turkey.^[56] In Canada, it is prosecutable as an analogue under the Controlled Drugs and Substances Act when mimicking LSD's effects for non-medical use.^[18] Enforcement often relies on these analogue laws or general psychoactive substance controls, reflecting its emergence as a research chemical prodrug to LSD around 2015, prompting reactive scheduling in response to online availability.^[2]

Enforcement and Analog Laws

In the United States, 1P-LSD is not explicitly listed as a controlled substance under the Controlled Substances Act but is subject to prosecution under the Controlled Substance Analogue Enforcement Act of 1986 (21 U.S.C. § 813), which treats substances chemically and pharmacologically substantially similar to Schedule I drugs like LSD as illegal if manufactured, distributed, or possessed with intent for human consumption. The Drug Enforcement Administration (DEA) enforces this by requiring proof of structural similarity (e.g., 1P-LSD's propionyl ester modification on lysergic acid), substantial similarity in effects to LSD, and representation or intent for ingestion, often circumvented by vendors labeling it as a research chemical "not for human consumption."^[57] As of 2025, no high-profile federal cases specifically targeting 1P-LSD distribution have been publicly detailed, though the DEA's broader actions against novel psychoactive substances (NPS) and lysergamide analogs include seizures under the Analogue Act, with penalties mirroring LSD trafficking (e.g., up to 20 years imprisonment for distribution causing serious harm).^[58] In the United Kingdom, 1P-LSD has been prohibited since May 26, 2016, under the Psychoactive Substances Act, which criminalizes the production, supply, or possession with intent to supply any substance intended to produce psychoactive effects, excluding explicitly exempted drugs like LSD itself. Enforcement by agencies like the Home Office and police focuses on online vendors and importation, with penalties up to 7 years imprisonment for supply; post-2016, seizures of 1P-LSD as a "legal high" analog declined due to the blanket ban, though underground distribution persists.^[59] European Union member states apply varying analog provisions or explicit bans. In Germany, 1P-LSD was controlled under the New Psychoactive Substances Act (NpSG) amendments effective around 2019, with further tightening in 2022 to include related lysergamides, enforced by the Federal Institute for Drugs and Medical Devices (BfArM) through risk assessments and criminal penalties for trafficking (up to 5 years imprisonment).^[60] France and other nations like Denmark and Finland have similarly scheduled it explicitly or via analog clauses akin to the EU's 2005 Council Framework Decision on NPS, leading to coordinated Europol operations targeting darknet sales, though enforcement prioritizes higher-risk synthetics over niche psychedelics.^[61] In jurisdictions without specific bans, such as parts of Canada (unscheduled federally but prosecutable as an LSD analog under the Controlled Drugs and Substances Act if intent proven), enforcement remains sporadic and intent-dependent.^[61] Overall, analog laws enable flexible prosecution amid rapid NPS evolution, but resource constraints limit widespread crackdowns on low-volume 1P-LSD trafficking compared to opioids or stimulants.

Societal Impact

Recreational Use Patterns

Recreational use of 1P-LSD primarily involves oral administration to achieve psychedelic effects akin to those of LSD, including visual distortions, altered perception, and introspective states. Typical doses range from 100 to 200 micrograms, often delivered via blotter paper, with onset occurring 30 to 60 minutes post-ingestion, peaking at 2 to 3 hours, and total duration spanning 8 to 12 hours.^[2] ^[59] Users report near-complete hydrolysis to LSD in vivo, yielding bioavailability approaching 100% and subjective experiences that are pharmacologically and phenomenologically comparable to LSD, though some perceive subtle differences in potency or comedown intensity.^[2] Prevalence remains niche, concentrated among experienced psychedelic users seeking legal alternatives to LSD amid varying analog regulations; in a 2016 Global Drug Survey of self-selected drug-experienced respondents (n=96,894), 2% reported lifetime use of LSD analogues like 1P-LSD, with 1% in the prior 12 months, rates elevated in the UK (19% lifetime) and US (17%) relative to LSD-only users.^[59] Acquisition occurs mainly online (55%) or from friends (33%), with 99% of administrations oral (sublingual or swallowed) and rare instances of insufflation or injection.^[59] Demographics skew toward males (81%), young adults (mean age 23), white ethnicity, and employed or student status, with 91% having prior LSD experience.^[59] Contexts emphasize set and setting, paralleling LSD patterns: solo sessions for self-exploration, small-group social use, or occasional integration with music events, though users rate analogues lower than LSD for overall pleasure, strength, and value.^[59] Use is episodic rather than habitual, driven by curiosity or evasion of enforcement, with minimal reports of dependency due to profound tolerance buildup after single doses.^[2] Polysubstance combinations occur but are less documented for 1P-LSD specifically, reflecting its role as a targeted hallucinogen rather than a party enhancer.^[59]

Controversies and Public Health Debates

1P-LSD has sparked debates regarding its circumvention of LSD prohibitions through analog laws, as its structural modification allows sale as a "research chemical" despite converting rapidly to LSD in vivo, producing nearly identical psychoactive effects. A 2020 pharmacokinetic study found that oral 1P-LSD yields LSD bioavailability approaching 100%, with psychosensory effects matching those of LSD in timing and intensity, challenging claims of substantive differences that might justify legal exemptions.^[2] Critics argue this exploits regulatory gaps, enabling unregulated distribution online, while proponents highlight the absence of evidence for unique harms beyond LSD's established profile.^[60] Public health concerns center on the lack of long-term clinical data specific to 1P-LSD and potential impurities in vendor-sourced products, given its production outside pharmaceutical oversight. User-submitted testing via harm reduction services has occasionally detected adulterants or inconsistent dosing in 1P-LSD blotters, raising risks of unexpected potency or contaminants, though no fatalities directly attributable to 1P-LSD have been documented.^[62] Empirical evidence from LSD, to which 1P-LSD metabolizes, indicates low physiological toxicity at typical doses (50-200 μg equivalents), with rare acute adverse events limited to self-resolving psychological distress like anxiety or panic rather than organ failure or overdose lethality.^[46]^[33] Debates persist on whether 1P-LSD's accessibility promotes safer experimentation via harm reduction practices, such as reagent testing and set/setting optimization, or exacerbates misuse among inexperienced users evading LSD's stigma. Regulatory responses, including the UK's 2016 Psychoactive Substances Act banning its supply, reflect precautionary approaches amid sparse epidemiological data, yet analyses of lysergamide analogs suggest non-addictive profiles and minimal dependency potential, akin to LSD.^[59]^[63] Proponents of decriminalization cite LSD's negligible public health burden—far below alcohol or opioids—arguing prohibition drives underground markets with purity risks, while skeptics emphasize vulnerabilities like psychosis exacerbation in predisposed individuals.^[64]^[65]

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