PARGY-LAD
propargyllysergic acid diethylamide
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PARGY-LAD (6-propargyl-6-nor-LSD) is a semi-synthetic psychedelic of the lysergamide class. It is a reduced-potency structural analog of LSD, requiring roughly three to four times the dose for comparable intensity. PARGY-LAD is a presumed 5-HT₂A receptor agonist, producing its effects by disrupting serotonin-mediated sensory filtering in the cortex.[1]
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LSD, psilocybin, mescaline +3 moreLSD, psilocybin, mescaline, DMT, AL-LAD, ETH-LAD show less
Synthesized by Andrew J. Hoffman under David E. Nichols at Purdue University in 1985 as part of a systematic study of LSD analogs,[2] PARGY-LAD received limited human testing by Alexander Shulgin, documented in TiHKAL (1997), but never attracted clinical or pharmaceutical interest.[3] A brief 2014 market appearance was undermined by confirmed sample adulteration, and the compound remains largely unavailable.[4]
Subjective effects include geometric visual patterns, time alteration, conceptual thinking alterations, and ego dissolution. The experience is described as qualitatively LSD-like — a broad perceptual and cognitive shift — but arriving at higher doses and resolving sooner.[3][5] Anxiety, thought loops, and residual stimulation are expected unsought effects based on lysergamide class patterns.
PARGY-LAD produces no physical dependence, and rapid tolerance after a single dose makes compulsive redosing self-limiting.[6] The primary risk is psychological — anxiety, paranoia, and disorientation scaling with dose and predisposition — compounded by the near-impossibility of verifying that material sold as PARGY-LAD is authentic. No receptor binding data, pharmacokinetic studies, or clinical trials exist; the entire human evidence base rests on a single qualitative report.[3]
History[edit]
Discovery
PARGY-LAD was first synthesized in 1985 by Andrew J. Hoffman, working in David E. Nichols's laboratory at Purdue University.[2] The compound was one of several N6-substituted norlysergamides — alongside AL-LAD and ETH-LAD — designed to map how structural modifications at the N6 nitrogen affect psychedelic potency. Alexander Shulgin later tested PARGY-LAD in humans, documenting threshold effects near 160 µg and full psychedelic activity near 500 µg in TiHKAL (1997).[3]
Research chemical market
PARGY-LAD appeared briefly on the grey market in September 2014, offered alongside other novel lysergamides.[4] A sample submitted to Wedinos, a UK drug-checking service, was found to contain AL-LAD and LSZ rather than the labeled compound.[4] The vendor withdrew the product shortly afterward, and most community experience reports from this period cannot be reliably attributed to PARGY-LAD.
Present status
PARGY-LAD has never entered clinical trials, received regulatory assessment, or attracted pharmaceutical interest. It remains one of the least characterized lysergamides to have reached human use, with no formal pharmacological data published beyond the 1985 synthesis paper and Shulgin's qualitative notes.
The name "PARGY-LAD" follows the abbreviation convention used for Nichols-era lysergamide analogs: the N6 substituent prefix (propargyl, shortened to PARGY) appended to LAD (lysergic acid diethylamide). This mirrors AL-LAD (allyl-LAD) and ETH-LAD (ethyl-LAD).
Chemistry[edit]
Structure
PARGY-LAD belongs to the lysergamide family, built on the tetracyclic ergoline ring system shared by LSD and all related compounds. Its defining modification is a propargyl group — a three-carbon chain ending in a carbon–carbon triple bond — attached at the N6 nitrogen of the norlysergic acid diethylamide scaffold.
This places PARGY-LAD in a series of N6-substituted nor-lysergamides that includes AL-LAD (allyl), ETH-LAD (ethyl), and PRO-LAD (propyl). The propargyl group differs from allyl by one degree of unsaturation: a triple bond where allyl has a double bond. This seemingly minor change reduces potency relative to both LSD and AL-LAD.[3]
Molecular properties
| Molecular formula | C₂₂H₂₅N₃O |
| Molecular weight | 347.5 g/mol |
Compared to LSD (C₂₀H₂₅N₃O, 323.4 g/mol), the propargyl substitution adds two carbon atoms and increases molecular weight by approximately 24 g/mol.[7]
Stereochemistry
PARGY-LAD possesses the (6aR,9R) absolute configuration — the same arrangement found in all biologically active d-lysergamides.[7] This configuration is required for binding at psychedelic-relevant receptors; the mirror-image isomer is pharmacologically inactive.[1]
Physical properties
No melting point, solubility, or stability data have been published for PARGY-LAD. By analogy with LSD and related lysergamides, the free base is expected to be sensitive to light, heat, and oxidation. These inferences remain unconfirmed for the compound specifically.
Pharmacology[edit]
Mechanism of action
No direct receptor binding or functional assay data have been published for PARGY-LAD. All mechanistic understanding is inferred from its structural membership in the lysergamide class.
As a lysergamide retaining the ergoline core and the diethylcarboxamide group, PARGY-LAD is presumed to act primarily through 5-HT₂A receptors on cortical neurons.[1] Activation of these receptors triggers intracellular signaling cascades that disrupt normal sensory filtering and produce the characteristic psychedelic state.[8] This mechanism has been confirmed for LSD through receptor-blocking experiments and structural biology.[9][8]
Secondary targets — inferred from lysergamide class pharmacology — likely include serotonin 5-HT₁A, dopamine D₂, and adrenergic receptors.[10][11] A comprehensive profiling of 41 classical psychedelics across 318 receptors showed that lysergamides as a class engage nearly every serotonin, dopamine, and adrenergic receptor subtype.[10] PARGY-LAD's specific affinities at these targets are unknown. The compound does not act through monoamine reuptake inhibitor, distinguishing it pharmacologically from stimulants.[12]
Pharmacokinetics
No human pharmacokinetic data exist for PARGY-LAD. Absorption, distribution, metabolism, and elimination parameters are entirely uncharacterized.
For class reference, oral LSD reaches peak plasma levels at approximately 1.5–4 hours, with subjective effects lasting 8–12 hours — far longer than the 3.6-hour half-life would predict.[13] This discrepancy is attributed to LSD becoming physically trapped within the serotonin receptor, where a protein loop closes over it and slows dissociation.[9]
PARGY-LAD's shorter reported duration (6–8 hours) may reflect weaker trapping by this mechanism, reduced receptor binding, or faster metabolic clearance — but no data confirm any of these explanations. Metabolic studies of the related compounds AL-LAD and ETH-LAD identified liver enzymes CYP1A2 and CYP3A4 as primary metabolizers.[14] PARGY-LAD is expected to follow a similar pathway, but no specific metabolites have been identified.
Neuroscience[edit]
Where it acts
No neuroimaging or electrophysiology data have been collected for PARGY-LAD. Based on its presumed 5-HT₂A agonism, the compound is expected to act on deep-layer neurons of the prefrontal cortex — the same cellular targets activated by LSD.[1]
In LSD studies, this activation dissolves the normal boundaries between brain networks, increases global connectivity, and elevates neural entropy — changes thought to underlie ego dissolution, sensory intensification, and novel pattern perception.
Why it matters
Serotonergic psychedelics promote structural changes in neurons — increased branching and new synaptic connections — through growth factor signaling pathways.citation needed Recent work has shown that structural modifications at N6 can dissociate a lysergamide's hallucinogenic potency from its ability to promote these neuroplastic changes,[15] raising the question of whether PARGY-LAD's reduced potency correlates with altered neuroplasticity.
The leading theoretical framework — the relaxed beliefs under psychedelics (REBUS) model — proposes that 5-HT₂A activation loosens the brain's established predictions, allowing raw sensory input greater influence over conscious experience.citation needed If PARGY-LAD achieves meaningful receptor occupancy at active doses, this model predicts a qualitatively similar but attenuated effect compared to LSD.
- Does PARGY-LAD achieve sufficient receptor occupancy at human-active doses (275–500 µg) to produce the same pattern of network-level brain changes seen with LSD, or does its reduced potency yield qualitatively different neural effects?
- Does the propargyl modification alter which intracellular signaling pathways are activated at 5-HT₂A, potentially changing the balance between hallucinogenic and neuroplasticity-promoting effects?
- Is the shorter duration attributable to faster receptor dissociation, weaker lid trapping, or distinct metabolic clearance?
Subjective Effects[edit]
PARGY-LAD's experiential character is inferred almost entirely from lysergamide class membership and a single qualitative report by Alexander Shulgin. The experience is expected to unfold as a broad alteration of perception, cognition, and emotion — qualitatively LSD-like but requiring substantially higher doses to reach full expression. As with all serotonergic psychedelics, set and setting exert powerful influence over the direction and emotional tone of the experience; the higher dosing threshold introduces additional uncertainty, since small measurement errors represent a larger absolute microgram difference than with LSD.
Relative to LSD, PARGY-LAD occupies a position of reduced potency and modestly shorter duration, most closely paralleling AL-LAD in its pharmacological niche.[3][5] Whether the propargyl modification produces qualitative differences beyond potency reduction — altered visual character, different body load, or distinct cognitive texture — remains an open question. The confirmed adulteration of 2014 commercial samples means most available community reports cannot be reliably attributed to PARGY-LAD.[4]
Effect Grid
At 275–500 µg oral, clear psychedelic effects are present. Visual geometry becomes distinct — patterning on surfaces, color alteration, object transformations, and visual drifting are reliably produced. Symmetrical texture repetition and perspective distortion emerge. Internal hallucinations may appear with eyes closed. Music enhancement is pronounced.
Conceptual thinking, introspection enhancement, and thought connectivity become prominent cognitive features. Time alteration is noticeable — minutes may feel stretched or compressed. Novelty enhancement colors the perceptual field. Emotional enhancement can swing between euphoria and anxiety depending on set and setting.
Body load increases: nausea during the come-up, moderate muscle tension, vasoconstriction, and temperature dysregulation are common. Pupil dilation is evident. Appetite suppression is marked. Sleep is difficult for 6+ hours. Shulgin's "full activity" dose of approximately 500 µg falls at the upper boundary of this tier.
Modeled from the effect's dose-dependence curve — not per-substance measurements.
Geometry · Visual breathing · Auditory enhancement · Brightness alteration · Tracers · Perspective distortion · Environmental patterning · Light sensitivity · Sound sensitivity · Visual morphing · Ganzfeld effect · Holotropic state · After-images · Symmetrical texture repetition · Depth perception distortion · Visual diffraction · Auditory misinterpretation · Peripheral vision distortion · Spatial disorientation · Touch enhancement · Synesthesia · Visual acuity enhancement · Proprioceptive distortion · Auditory distortion · Peripheral misidentification · Vestibular distortion · Visual haze / noise · Visual melting · Olfactory enhancement · Visual processing acceleration · Visual magnification · Taste enhancement · Touch suppression · Tinnitus · Flashbacks · Object transformations · Internal hallucinations · Environmental orbism / cubism · External hallucinations · Object activation · Visual recursion · Auditory hallucinations · Perspective hallucinations · Olfactory hallucination · Persisting hallucinations
Tracers · Perspective distortion · Environmental patterning · Light sensitivity · Sound sensitivity · Visual morphing · Ganzfeld effect · Holotropic state · After-images · Symmetrical texture repetition · Depth perception distortion · Visual diffraction · Auditory misinterpretation · Peripheral vision distortion · Spatial disorientation · Touch enhancement · Synesthesia · Visual acuity enhancement · Proprioceptive distortion · Auditory distortion · Peripheral misidentification · Vestibular distortion · Visual haze / noise · Visual melting · Olfactory enhancement · Visual processing acceleration · Visual magnification · Taste enhancement · Touch suppression · Tinnitus · Flashbacks · Object transformations · Internal hallucinations · Environmental orbism / cubism · External hallucinations · Object activation · Visual recursion · Auditory hallucinations · Perspective hallucinations · Olfactory hallucination · Persisting hallucinations
Wakefulness · Spontaneous body sensations · Appetite suppression · Body high · Insomnia · Tingling / electric sensations · Nausea · Muscle tension · Laughter fits · Physical fatigue · Restlessness · Heart rate perception changes · Vibrations / buzzing · Headache · Excessive sweating · Tactile euphoria · Motor control impairment · Dehydration sensation · Bodily lightness · Body schema distortion · Dizziness · Dry mouth · Abnormal heartbeat · Watery eyes · Nystagmus (eye wobbles) · Sexual arousal enhancement · Involuntary body movements · Bodily pressures · Breathing alteration · Trembling · Yawning · Increased urination · Bruxism · Vomiting · Motor control enhancement · Seizure threshold reduction · Bodily dissociation · Tactile hallucination
Body high · Insomnia · Tingling / electric sensations · Nausea · Muscle tension · Laughter fits · Physical fatigue · Restlessness · Heart rate perception changes · Vibrations / buzzing · Headache · Excessive sweating · Tactile euphoria · Dehydration sensation · Bodily lightness · Body schema distortion · Dizziness · Dry mouth · Abnormal heartbeat · Watery eyes · Nystagmus (eye wobbles) · Sexual arousal enhancement · Involuntary body movements · Bodily pressures · Breathing alteration · Trembling · Yawning · Increased urination · Bruxism · Vomiting · Motor control enhancement · Seizure threshold reduction · Bodily dissociation · Tactile hallucination
Thought connectivity · Aesthetic enhancement · Cognitive flexibility · Openness enhancement · Immersion enhancement · Thought acceleration · Pattern recognition enhancement · Cognitive euphoria · Creativity enhancement · Thought loops · Increased nature relatedness · Multiple thought streams · Humor enhancement · Memory suppression · Confusion · Analysis enhancement · Cognitive fatigue · Cognitive impairment · Synchronicity · Information processing enhancement · Language suppression · Cognitive dysphoria · Memory fragmentation · Thought disorganization · Focus enhancement · Motivation enhancement
Immersion enhancement · Thought acceleration · Pattern recognition enhancement · Cognitive euphoria · Creativity enhancement · Thought loops · Increased nature relatedness · Multiple thought streams · Humor enhancement · Memory suppression · Confusion · Analysis enhancement · Cognitive fatigue · Cognitive impairment · Synchronicity · Information processing enhancement · Language suppression · Cognitive dysphoria · Memory fragmentation · Thought disorganization · Focus enhancement · Motivation enhancement
Simultaneous emotions · Anxiety · Catharsis · Dysphoria
Disinhibition · Sociability enhancement · Trust enhancement · Communication enhancement · Flow state · Communication suppression · Boundary dissolution · Ego dissolution · Identity alteration · Cognitive disconnection
Flow state · Communication suppression · Boundary dissolution · Ego dissolution · Identity alteration · Cognitive disconnection
Time cessation
Non-dual awareness · Death-rebirth sequence · Entity contact
Recursive awareness
Timeline
First alerts emerge — mild stimulation, possible slight nausea, and a sense of anticipatory awareness. Perceptual changes are subliminal or absent.
Progressive intensification of perceptual changes. Visual drifting, color enhancement, and building body sensations develop. Cognitive shifts become identifiable.
Full psychedelic effects — visual geometry, conceptual thinking, emotional intensification, and maximum perceptual changes. Time alteration is most pronounced.
Gradual reduction in visual and cognitive intensity. Residual perceptual effects persist. Mood often shifts toward reflective or contemplative.
Subtle residual effects — mild mood elevation or fatigue, slight perceptual sensitivity, possible insomnia. Cognitive baseline gradually returns.
⚠ Avoid driving or operating heavy machinery for at least 12 hours after ingestion.
Safety[edit]
- Acute toxicity
- Low
- Chronic toxicity
- Low
- 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
No controlled toxicity data exist for PARGY-LAD. The toxic dose is unknown.safety citation needed
Lysergamides as a class possess wide margins between psychoactive and lethal doses — no human death has been attributed directly to the pharmacological effects of LSD.[1] In silico predictions for structurally distinct N1-acyl lysergamides yielded estimated rat oral LD₅₀ values of 49–85 mg/kg,[16] but these are not directly applicable to PARGY-LAD, which carries a different modification (N6-propargyl rather than N1-acyl).
No case reports of PARGY-LAD-specific adverse events or emergency presentations have been published. The documented adulteration of 2014 commercial samples[4] means any adverse reports from that period cannot be reliably attributed to this compound.
Class-level acute adverse effects include raised blood pressure, rapid heart rate, elevated body temperature, and — rarely — heart rhythm disturbances, most commonly in the context of polydrug use.safety citation needed
Psychological risks
No substance-specific psychological risk data exist. Class-level risks for serotonergic psychedelics include acute panic, severe anxiety, paranoia, thought disorganization, and — in predisposed individuals — triggering of psychotic episodes.[1]
Hallucinogen persisting perception disorder (HPPD) is a rare but genuine condition following hallucinogen use.[17] Risk factors include pre-existing anxiety, prior HPPD episodes, tinnitus, visual disturbances, and concentration difficulties.[18] Prevention and treatment approaches have been reviewed by Doyle et al..[19] The applicability of these findings to PARGY-LAD is assumed but unconfirmed.
Tolerance and dependence
Tolerance to psychedelic effects develops rapidly after a single dose, driven by downregulation in the cortex.[6] A single administration of a serotonin 2A receptor agonist produces measurable tolerance within 24 hours, with complete cross-tolerance between LSD and other classical psychedelics.[6]
PARGY-LAD is expected to show cross-tolerance with all classical psychedelics (LSD, psilocybin, mescaline, DMT). Community estimates place the tolerance half-life at approximately 6 days and full reset at approximately 14 days.[5]
Lysergamides do not produce physical dependence and are not reinforcing in animal self-administration models. Compulsive use is rare.[1][12]
Drug interactions
Tramadol — dangerous
Tramadol inhibits serotonin reuptake in addition to its opioid activity.[20] Combining this with PARGY-LAD's serotonin receptor activation creates a plausible risk of serotonin syndrome.[21] No case report specific to PARGY-LAD exists, but the interaction mechanism is well-established for serotonergic combinations.safety citation needed
MAOIs — severe risk
Monoamine oxidase inhibitors can raise serotonin to life-threatening levels when combined with any serotonergic agent.[20] The combination of an MAOI with any lysergamide psychedelic poses severe serotonin toxicity risk.safety citation needed
Lithium
Combination of lithium with classical psychedelics has been associated with seizure risk in case reports.safety citation needed
Cannabis — unknown
No data exist on PARGY-LAD combined with cannabis. Cannabis can intensify and prolong psychedelic experiences, sometimes precipitating anxiety or paranoia.
CYP-mediated interactions
Based on the metabolic pathway inferred from AL-LAD and ETH-LAD,[14] strong inhibitors of CYP1A2 (fluvoxamine, ciprofloxacin) or CYP3A4 (ketoconazole, ritonavir) may increase PARGY-LAD levels, while inducers (rifampicin, carbamazepine) may decrease them. These interactions are theoretical. inferred
Contraindications
Absolute contraindications:
- Personal or family history of psychotic spectrum disorders (schizophrenia, schizoaffective disorder, bipolar I with psychotic features): 5-HT₂A activation can trigger psychotic episodes in predisposed individuals[1]
- Concurrent MAOI use: severe serotonin toxicity risk[20]
- Concurrent tramadol use: serotonin toxicity via dual serotonergic mechanism[21]
- Concurrent lithium use: seizure risk documented with classical psychedelicssafety citation needed
Relative contraindications:
- Heart conditions or uncontrolled high blood pressure: lysergamides produce transient vasoconstriction and rapid heart ratesafety citation needed
- Prior HPPD episodes or predisposing factors (anxiety disorders, pre-existing visual disturbances, tinnitus)[18]
- Pregnancy or breastfeeding: no safety data exist for any lysergamide in human pregnancysafety citation needed
- Severe liver impairment: if metabolism proceeds via CYP1A2/CYP3A4 as with structural analogs, impaired liver function may significantly alter clearance[14]
Harm Reduction[edit]
Forms & Identification
PARGY-LAD's most significant identification challenge is that the only tested commercial sample (2014) contained AL-LAD and LSZ, not PARGY-LAD.[4] Standard Ehrlich and Hofmann reagent tests confirm the presence of an indole (lysergamide) but cannot distinguish between individual lysergamides. A positive reagent result does not confirm PARGY-LAD specifically — only laboratory analysis (mass spectrometry or NMR) can verify identity.
Given the compound's extreme rarity and documented history of adulteration, treat any material labeled PARGY-LAD with elevated skepticism. The practical consequence is that users cannot know with confidence what they are taking without analytical verification.
Guidelines
- Test all material with Ehrlich reagent at minimum — a negative result rules out lysergamides entirely
- Start at the low end of reported dose ranges and wait at least two hours before considering redosing
- Have a sober, trusted companion present who understands psychedelic crisis support
- Prepare the physical environment in advance: comfortable seating, controlled lighting, water, light food, and a quiet space to retreat to
- Avoid dosing on an empty stomach to reduce nausea; a light meal 1–2 hours beforehand is preferable
- Clear the schedule for the full day — effects may persist 6–8 hours with additional residual stimulation
Set & Setting
As with all serotonergic psychedelics, environment and mental state powerfully shape the experience. A familiar, comfortable physical space and a stable emotional baseline reduce the likelihood of acute anxiety or panic.
A trusted, sober companion is particularly advisable given PARGY-LAD's minimal characterization. The lack of reliable dosing data and verified experience reports means even experienced psychedelic users are operating with less information than usual.
Aftercare & integration. The days following a psychedelic experience often carry residual emotional sensitivity and altered perspective. Journaling within 24–48 hours helps preserve insights before they fade. Discuss the experience with a trusted person — a friend, therapist, or integration circle.
If distressing material surfaced during the experience, professional support from a therapist familiar with psychedelic experiences is advisable. Persistent visual disturbances, anxiety, or depersonalization lasting more than a few days warrant clinical attention, as these may indicate early HPPD or related conditions.
Recovery & Support
Classical psychedelics rarely produce compulsive use patterns, and PARGY-LAD's rapid tolerance development makes sustained daily use pharmacologically self-limiting. If psychedelic use has become a pattern of avoidance or is causing functional impairment, peer support organizations such as the Fireside Project (62-FIRESIDE) and MAPS integration resources offer non-judgmental assistance.
For individuals whose psychedelic experiences have triggered or worsened mental health conditions, clinical care from a psychiatrist familiar with substance-induced disorders is the appropriate next step.
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 any of the following occur: self-harm attempts or expressed intent, complete disconnection from reality with inability to communicate, seizures, chest pain, or loss of consciousness.
Immediate steps:
- 1. Move the person to a quiet, safe space with minimal stimulation
- 2. Speak calmly and reassuringly — do not argue with or contradict their experience
- 3. Do not physically restrain unless there is immediate danger of self-harm
- 4. If symptoms are purely psychological (anxiety, confusion, fear), maintain calm presence and wait
- 5. Call emergency services if physical symptoms appear (seizure, chest pain, unresponsiveness) or if psychological distress includes active self-harm risk
What to tell the dispatcher: State the substance name and approximate dose if known, the time of ingestion, and current symptoms. Good Samaritan laws in many jurisdictions protect callers who report drug-related emergencies from prosecution.
Legal Status[edit]
PARGY-LAD is not specifically scheduled by name under international drug control conventions or in most national controlled substance schedules. Its legal status in most jurisdictions derives from structural analog provisions or blanket psychoactive substance legislation, reflecting its structural relationship to LSD.
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| United States | Not explicitly scheduled; subject to Federal Analogue Act | As a structural analog of LSD (Schedule I), PARGY-LAD is treated as Schedule I under 21 U.S.C. § 813 if intended for human consumption. Prosecution requires demonstrating substantially similar structure and pharmacology — both criteria met given the lysergamide scaffold and LSD-like discriminative stimulus properties.[2] |
| United Kingdom | Controlled under Psychoactive Substances Act 2016 | Blanket ban on psychoactive substances except specifically exempt categories (alcohol, tobacco, caffeine, licensed medicines). Production, supply, and possession with intent to supply are criminal offenses. |
| Germany | Controlled under Neue-psychoaktive-Stoffe-Gesetz (NpSG) | Effective July 18, 2019. Production, import, and supply for placement on the market are punishable offenses. |
| Australia | Presumptively Schedule 9 (Prohibited Substance) | May qualify as an LSD structural analog under the Therapeutic Goods Act. Explicit scheduling not confirmed.citation needed |
| Canada | Not explicitly scheduled | Not listed under the Controlled Drugs and Substances Act. May be subject to analog provisions if marketed for human use.citation needed |
| International | Not scheduled | Not listed under UN Convention on Psychotropic Substances schedules. Not named in any international treaty instrument. |
The compound's brief 2014 market appearance predated several of these legislative instruments. The German NpSG (2016) and the UK Psychoactive Substances Act (2016) were partially motivated by the proliferation of novel lysergamides and other novel psychoactive substances during the 2013–2015 period.
references
- [1]
- [2] ^abcHoffman A, Nichols DE (1985) Synthesis and LSD-like discriminative stimulus properties in a series of N(6)-alkyl norlysergic acid N,N-diethylamide derivatives — Journal of Medicinal Chemistry doi:10.1021/jm00147a022
- [3]
- [4]
- [5]
- [6] ^abcde la Fuente Revenga M, Jaster AM, McGinn J, Silva G, Saha S, Gonzalez-Maeso J (2022) Tolerance and Cross-Tolerance among Psychedelic and Nonpsychedelic 5-HT2A Receptor Agonists in Mice — ACS Chemical Neuroscience doi:10.1021/acschemneuro.2c00170