ETH-LAD
N⁶-ethyl-6-norlysergic acid diethylamide
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ETH-LAD (N⁶-ethyl-6-norlysergic acid diethylamide) is a semi-synthetic psychedelic of the lysergamide class. It is the N⁶-ethyl structural analog of LSD, with roughly twice the potency per microgram.[1] ETH-LAD is a presumed 5-HT₂A receptor agonist, producing its effects by disrupting serotonergic filtering of sensory and cognitive input.[2][3]
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First synthesized in 1976 by Niwaguchi and colleagues,[4] ETH-LAD was pharmacologically characterized by Hoffman and Nichols in 1985 as one of the most potent lysergamides tested.[1] The compound remained a laboratory curiosity until it appeared on novel psychoactive substance markets in the 2010s.[5] It is unscheduled in most jurisdictions, though explicitly controlled in the United Kingdom, Germany, and Switzerland.
Subjective effects include mild geometric visual patterns, tactile enhancement, cognitive clarity, and emotional warmth.[6] The experience is characterized by a gentler, less psychologically demanding quality than LSD — lucidity and warmth in place of the overwhelming perceptual flood typical of higher-dose lysergamide experiences. Nausea, muscle tension, and unpredictable body load at higher doses are common unsought effects.
ETH-LAD produces no physical dependence; rapid tolerance after a single dose makes compulsive redosing self-limiting.[2][7] The primary risk is psychological — acute anxiety and panic reactions that scale with dose and predisposition, compounded by an anecdotally unpredictable dose-response curve at higher ranges. No controlled studies, clinical trials, or toxicity data have been published; the current understanding rests on a single 1985 animal study, Shulgin's self-reports, and community experience.
History[edit]
Discovery
ETH-LAD was first synthesized in 1976 by Niwaguchi, Nakahara, and Ishii as part of a series investigating amide derivatives of norlysergic acid.[4] The compound received no pharmacological evaluation until Hoffman and Nichols at Purdue University published a systematic study of N⁶-alkyl norlysergamides in 1985.[1] Their work established that ETH-LAD and the closely related AL-LAD were 1.6–2.3× more potent than LSD in rat drug discrimination assays — the most potent compounds in the series.
Human documentation
Alexander Shulgin published the first account of ETH-LAD's effects in humans in TiHKAL: The Continuation (1997).[6] He described it as gentler and less aggressive than LSD, with maintained cognitive clarity, warmth, appetite enhancement, and diuretic properties — features unusual among lysergamides. He also flagged concerning potency degradation in stored solutions, even under optimal conditions.
Novel psychoactive substance era
ETH-LAD became commercially available as a research chemical in the 2010s, part of a wave that included AL-LAD and LSZ.[8] Brandt et al. provided the first comprehensive analytical characterization in 2017, noting that the compound's market presence had outpaced forensic identification capabilities.[5] Global Drug Survey data from 2016 documented significant user populations in the United Kingdom and United States, with users rating LSD analogues as producing weaker effects and lower perceived risk of harm than LSD itself.[9]
The name ETH-LAD derives from the N⁶-ethyl substitution on the Lysergic Acid Diethylamide scaffold — a systematic naming convention shared by other lysergamide analogs like AL-LAD (N⁶-allyl) and PRO-LAD (N⁶-propyl). The compound occupies a minor but persistent niche among psychedelic research chemical communities, valued for its reported cognitive clarity and gentler character, though its reputation for batch-to-batch inconsistency and storage instability has limited wider adoption.
Chemistry[edit]
Structural class
ETH-LAD belongs to the lysergamide family, sharing the tetracyclic ergoline ring system found in LSD, AL-LAD, 1P-LSD, and all semi-synthetic lysergamides. The sole structural difference from LSD is at the N⁶ position of the ergoline nitrogen: where LSD carries a methyl group, ETH-LAD carries an ethyl group. The diethylamide group at position 9, responsible for psychedelic activity, is unchanged.
Hoffman and Nichols demonstrated that short-to-intermediate N⁶-alkyl chains (ethyl, allyl) optimize potency, while longer chains progressively reduce it.[1] The acylated derivative 1-propionyl ETH-LAD (1P-ETH-LAD) functions as a prodrug, undergoing hydrolysis to ETH-LAD in human serum,[5] mirroring the established 1P-LSD → LSD conversion.[10]
Molecular properties
| Molecular formula | C₂₁H₂₇N₃O |
| Molecular weight | 337.5 g/mol |
The molecular formula reflects one additional CH₂ unit compared to LSD (C₂₀H₂₅N₃O, 323.4 g/mol), corresponding to the methyl-to-ethyl substitution at N⁶.
Stereochemistry
ETH-LAD has two stereogenic centers at positions 6a and 9 of the ergoline ring. The biologically active form is the (6aR,9R) configuration, matching the d-lysergic acid scaffold shared by all active lysergamides. The mirror-image (6aS,9S) isomers are pharmacologically inactive.
Stability and identification
Shulgin noted that ETH-LAD in solution showed potency degradation over months, even under dark, frozen, and anaerobic conditions[6] — suggesting lower stability than LSD itself. Brandt et al. provided GC-MS, HPLC, ¹H-NMR, and GC solid-state IR data for forensic identification[5] but did not characterize bulk physical properties.
A constitutional isomer, N-ethyl-N-isopropyllysergamide (EIPLA), shares identical molecular formula and mass but produces distinct mass spectral fragmentation.[11] The two cannot be distinguished by standard colorimetric reagent tests; definitive identification requires GC-MS, HPLC, or NMR.
Pharmacology[edit]
Mechanism of action
ETH-LAD's primary mechanism is agonism at the serotonin 5-HT₂A receptor, particularly on pyramidal neurons in cortical layer V.[2][3] The necessity of 5-HT₂A activation for the psychedelic response has been confirmed across the lysergamide class: the selective antagonist ketanserin fully blocks the subjective effects of LSD in humans,[12] and M100907 abolishes the behavioral signature of related analogs including 1P-LSD[13] and AL-LAD.[8]
ETH-LAD is predicted to share LSD's unusually slow dissociation from the 5-HT₂A receptor. Crystallographic work has shown that an extracellular loop closes over LSD once bound, trapping the molecule and extending receptor occupancy.[14] This mechanism likely accounts for the prolonged duration of action common to the lysergamide class.
By structural analogy with LSD, the broader receptor profile is expected to include partial agonism at 5-HT₁A, 5-HT₂C, and dopamine D₂ receptors.[15][2] No ETH-LAD-specific binding data have been published.
Pharmacokinetics
No human pharmacokinetic data exist for ETH-LAD. All parameters are inferred from LSD, which shows dose-proportional kinetics with a plasma half-life of approximately 2.4 hours and subjective effects lasting 6.7–11 hours depending on dose.[12][16] Time to peak plasma concentration is approximately 2 hours, consistent with survey data for LSD analogues collectively.[9]
ETH-LAD's reported duration of 8–12 hours orally[6] aligns with these reference values. The gap between the short plasma half-life and prolonged subjective duration reflects the slow receptor dissociation kinetics described above.[14]
Metabolism
Wagmann et al. established ETH-LAD's metabolic fate using human liver preparations.[17] The primary metabolizing enzymes are CYP1A2 and CYP3A4, with predominant biotransformations including N-dealkylation and hydroxylation. Parent compound and metabolites were undetectable in rat urine at expected recreational doses — meaning standard urine drug screening would be unlikely to confirm ETH-LAD use.
Prodrug relationship
1-Propionyl ETH-LAD (1P-ETH-LAD) undergoes hydrolysis to ETH-LAD when incubated with human serum, with ETH-LAD remaining detectable at 24 hours.[5] This supports 1P-ETH-LAD functioning as a prodrug, mirroring the established 1P-LSD → LSD conversion.[10]
Neuroscience[edit]
Where it acts
No direct neuroimaging data have been published for ETH-LAD. By class inference, the compound is expected to disrupt thalamocortical gating by activating 5-HT₂A receptors on layer V pyramidal neurons in the prefrontal cortex.[2][3] This reduces the thalamus's filtering function, allowing a broader stream of sensory and associative information to reach conscious processing — the proposed cellular basis for the perceptual intensification and novel associations characteristic of the psychedelic state.
LSD produces dissolution of the default mode network, increased global functional connectivity, elevated neural entropy, and decreased alpha power.[18] ETH-LAD would be expected to produce qualitatively similar changes, though the degree and regional distribution remain uncharacterized.
Why it matters
The REBUS model proposes that psychedelics relax the brain's confidence in its own prior assumptions, allowing raw sensory signals to override habitual patterns of interpretation.[18] This framework accounts for the visual distortions, pattern recognition enhancement, and conceptual loosening reported with ETH-LAD and other lysergamides. Serotonergic psychedelics also promote structural neuroplasticity through signaling cascades downstream of 5-HT₂A activation[2] — whether ETH-LAD's higher behavioral potency translates to enhanced plasticity induction is unknown.
- Does the N⁶-ethyl substitution alter how long ETH-LAD remains bound at the 5-HT₂A receptor compared to LSD, and does this explain qualitative differences in the experience?
- What neural correlates underlie the reported milder visual profile and enhanced tactile and cognitive character compared to LSD?
- Does ETH-LAD promote neuroplasticity to a comparable degree as LSD at equivalent doses?
Subjective Effects[edit]
ETH-LAD produces an experience frequently described as gentler and less psychologically demanding than LSD at comparable effect levels.[6] The qualitative emphasis falls on tactile richness, cognitive lucidity, and emotional warmth rather than dramatic visual hallucinations. At lower doses, the experience is remarkably clear-headed; at higher doses, anecdotal reports describe a sharply nonlinear escalation in body load and unpredictability that distinguishes the dose-response curve from LSD's more gradual climb. As with all serotonergic psychedelics, set and setting profoundly shape the character and trajectory of the experience.
Compared to LSD, ETH-LAD occupies a position of similar duration but reportedly milder visual intensity and reduced psychological pressure at equivalent subjective levels.[9] Shulgin noted appetite enhancement and diuretic effects[6] — properties unusual among lysergamides, which typically suppress hunger.
Effect Grid
At common doses (~60–100 µg oral), the full psychedelic experience emerges: pronounced visual effects including visual drifting, environmental patterning, color shifting, and enhanced closed-eye imagery. Introspection enhancement and thought connectivity increase substantially. Emotional responses deepen — music, nature, and interpersonal interactions take on heightened significance. Cognitive euphoria and a sense of warmth and humor are characteristic.
Physically, stimulation is moderate. Increased appetite and diuretic effects are commonly reported. Some users note mild nausea or muscle tension, though the body load is generally described as manageable at this range. The experience lasts 8–10 hours; sleep is unlikely for at least 8 hours after ingestion.
Modeled from the effect's dose-dependence curve — not per-substance measurements.
Symmetrical texture repetition · Environmental patterning · Music enhancement · Brightness alteration · Visual breathing · Visual morphing · Depth perception distortion · Visual diffraction · After-images · Auditory enhancement · Light sensitivity · Perspective distortion · Sound sensitivity · Visual haze / noise · Holotropic state · Auditory distortion · Peripheral vision distortion · Spatial disorientation · Touch enhancement · Visual melting · Visual acuity enhancement · Synesthesia · Auditory misinterpretation · Peripheral misidentification · Proprioceptive distortion · Vestibular distortion · Visual processing acceleration · Visual acuity suppression · Touch suppression · Flashbacks · Object transformations · Internal hallucinations · Visual recursion · External hallucinations · Object activation · Environmental orbism / cubism · Visual scenery slicing · Auditory hallucinations · Perspective hallucinations · Gustatory hallucination · Olfactory hallucination · Persisting hallucinations
Visual breathing · Visual morphing · Depth perception distortion · Visual diffraction · After-images · Auditory enhancement · Light sensitivity · Perspective distortion · Sound sensitivity · Visual haze / noise · Holotropic state · Auditory distortion · Peripheral vision distortion · Spatial disorientation · Touch enhancement · Visual melting · Visual acuity enhancement · Synesthesia · Auditory misinterpretation · Peripheral misidentification · Proprioceptive distortion · Vestibular distortion · Visual processing acceleration · Visual acuity suppression · Touch suppression · Flashbacks · Object transformations · Internal hallucinations · Visual recursion · External hallucinations · Object activation · Environmental orbism / cubism · Visual scenery slicing · Auditory hallucinations · Perspective hallucinations · Gustatory hallucination · Olfactory hallucination · Persisting hallucinations
Wakefulness · Body high · Insomnia · Spontaneous body sensations · Appetite suppression · Muscle tension · Tingling / electric sensations · Temperature dysregulation · Bodily heaviness · Dry mouth · Heart rate perception changes · Laughter fits · Physical fatigue · Restlessness · Vibrations / buzzing · Bodily pressures · Nausea · Dehydration sensation · Excessive sweating · Body schema distortion · Headache · Breathing alteration · Dizziness · Motor control impairment · Tactile euphoria · Trembling · Yawning · Involuntary body movements · Nystagmus (eye wobbles) · Increased urination · Watery eyes · Bruxism · Motor control enhancement · Vomiting · Seizure threshold reduction · Bodily dissociation
Spontaneous body sensations · Appetite suppression · Muscle tension · Tingling / electric sensations · Bodily heaviness · Dry mouth · Heart rate perception changes · Laughter fits · Physical fatigue · Restlessness · Vibrations / buzzing · Bodily pressures · Nausea · Dehydration sensation · Excessive sweating · Body schema distortion · Headache · Breathing alteration · Dizziness · Motor control impairment · Tactile euphoria · Trembling · Yawning · Involuntary body movements · Nystagmus (eye wobbles) · Increased urination · Watery eyes · Bruxism · Motor control enhancement · Vomiting · Seizure threshold reduction · Bodily dissociation
Thought connectivity · Aesthetic enhancement · Openness enhancement · Thought acceleration · Cognitive euphoria · Introspection enhancement · Multiple thought streams · Immersion enhancement · Cognitive flexibility · Creativity enhancement · Cognitive fatigue · Increased nature relatedness · Humor enhancement · Memory suppression · Confusion · Thought loops · Analysis enhancement · Analysis suppression · Cognitive impairment · Focus suppression · Information processing suppression · Memory fragmentation · Synchronicity · Thought disorganization · Information processing enhancement · Language suppression · Thought organization · Focus enhancement · Cognitive dysphoria · Amnesia
Thought acceleration · Cognitive euphoria · Introspection enhancement · Multiple thought streams · Immersion enhancement · Cognitive flexibility · Creativity enhancement · Cognitive fatigue · Increased nature relatedness · Humor enhancement · Memory suppression · Confusion · Thought loops · Analysis enhancement · Analysis suppression · Cognitive impairment · Focus suppression · Information processing suppression · Memory fragmentation · Synchronicity · Thought disorganization · Information processing enhancement · Language suppression · Thought organization · Focus enhancement · Cognitive dysphoria
Anxiety · Empathy enhancement · Catharsis · Dysphoria
Trust enhancement · Communication enhancement · Flow state · Sociability enhancement · Communication suppression · Depersonalization · Social disconnection · Boundary dissolution · Cognitive disconnection · Ego dissolution · Identity alteration
Communication suppression · Depersonalization · Social disconnection · Boundary dissolution · Cognitive disconnection · Ego dissolution · Identity alteration
Time cessation
Transpersonal visions · Entity contact
Recursive awareness
Timeline
First alerts emerge as a subtle shift in perception — mild brightening of colors, gentle body awareness, and a faint cognitive sharpening. Easily dismissed as placebo at this stage.
Effects build steadily: visual enhancement becomes unmistakable, emotional tone shifts, and mild physical stimulation develops. Nausea may appear transiently. The characteristic warmth and gentle quality become apparent.
Maximum visual, cognitive, and emotional intensity. Visual drifting, environmental patterning, and enhanced closed-eye imagery are prominent. Cognitive clarity is typically maintained.
Intensity diminishes gradually from peak levels. Visual effects soften, emotional depth remains, and a reflective, contemplative quality predominates. Physical body load, if present, begins to ease.
Residual visual enhancement and mood elevation taper. Cognitive function returns toward baseline. The warm, allowing character may persist as effects fade.
Subtle mood elevation and perceptual freshness may persist for hours to a day. Shulgin described a clean aftermath with no reported next-day effects. Some residual impairment is possible.
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
No LD₅₀ data, controlled toxicity studies, case reports of organ damage, or fatalities have been published for ETH-LAD. The compound is presumed to share the extremely high therapeutic index characteristic of the lysergamide class — for reference, LSD's estimated lethal dose in rats is thousands of times the active human dosecitation needed — but this remains unverified.
Heart and circulation
LSD-class compounds produce mild, transient increases in heart rate and blood pressure.[12][19] No ETH-LAD-specific cardiovascular data exist, but effects are expected to be clinically insignificant in healthy individuals at typical doses.
Temperature dysregulation
Anecdotal reports describe ETH-LAD as producing more pronounced temperature fluctuations than LSD, particularly at higher doses.citation needed No published data confirm or refute this.
Body load
Community reports describe ETH-LAD as having a heavier physical body load than LSD at high doses — more pronounced nausea, muscle tension, and general discomfort — with particular note of an unpredictable dose-response curve.citation needed These reports have not been verified in any published study.
Psychological risks
- Acute anxiety and panic: Dose-dependent, worsened by unfavorable set and setting. Can escalate to severe distress at high doses.
- Psychosis precipitation: serotonergic psychedelics can trigger or worsen psychotic episodes in individuals with a personal or family history of psychotic disorders.[2]
- Hallucinogen Persisting Perception Disorder (HPPD): A recognized class risk. Survey data suggest visual symptoms (visual haze / noise, trailing, halos) occur in over 30% of naturalistic psychedelic users, though persistent and distressing cases are rare.citation needed No ETH-LAD-specific cases have been reported.
Tolerance and dependence
ETH-LAD is not considered habit-forming. Classical psychedelics generally do not produce dependence or addiction.[2] Rapid tolerance develops through 5-HT₂A downregulation within 24 hours of a single dose.[7] Tolerance half-life is approximately 6 days, with full reset at approximately 14 days.inferred
Complete cross-tolerance exists between serotonergic psychedelics acting at the 5-HT₂A receptor. ETH-LAD would be expected to show full cross-tolerance with LSD and partial cross-tolerance with psilocybin and other 5-HT₂A agonists.[7] No physical dependence, withdrawal, or dose escalation has been documented for ETH-LAD or the lysergamide class.
Drug interactions
No ETH-LAD-specific interaction data have been published. All assessments are based on class-level pharmacology.
Serotonergic combinations
Combining ETH-LAD with serotonin-elevating agents creates theoretical risk of serotonin syndrome — a potentially life-threatening condition involving dangerously high body temperature, muscle rigidity, and altered mental status.
- Tramadol: Overlapping serotonergic load plus seizure threshold lowering. Classified as dangerous by class reasoning.safety citation needed
- MAOIs: Dramatically increase serotonergic load. Risk of serotonin syndrome is substantially elevated.safety citation needed
- SSRIs/SNRIs: chronic use may blunt psychedelic effects through receptor downregulation. Acute interaction dynamics are poorly characterized for lysergamides.inferred
Lithium
Combined use of lithium with LSD has been linked to seizures.safety citation needed This applies to ETH-LAD by class inference.
Cannabis
Cannabis can unpredictably intensify psychedelic effects, increase anxiety, and heighten dissociative elements. No ETH-LAD-specific data exist.
CYP-mediated interactions
ETH-LAD is metabolized by CYP1A2 and CYP3A4.[17] Strong inhibitors of these enzymes (e.g., fluvoxamine for CYP1A2; ketoconazole, ritonavir, grapefruit juice for CYP3A4) could theoretically increase ETH-LAD levels. No clinical data exist to quantify this risk.
Contraindications
All contraindications are inferred from lysergamide class evidence. No ETH-LAD-specific data exist.
- Personal or family history of psychotic disorders: Absolute contraindication. Serotonergic psychedelics can trigger acute psychotic episodes in predisposed individuals.[2]
- Bipolar disorder: Absolute contraindication. Risk of triggering manic episodes.
- Seizure disorders: Relative contraindication. Lysergamides may lower the seizure threshold.safety citation needed
- Heart conditions: Relative contraindication. Transient increases in heart rate and blood pressure may pose risk.[12]
- Concurrent lithium therapy: Absolute contraindication. Associated with seizures and severe adverse events.safety citation needed
- Concurrent MAOI therapy: Absolute contraindication. Risk of serotonin syndrome.
- Pregnancy: Absolute contraindication. No reproductive safety data exist; ergoline derivatives have uterotonic properties.safety citation needed
Harm Reduction[edit]
Forms & Identification
ETH-LAD is typically distributed on blotter paper or as a liquid solution, formats identical to LSD. Because these forms are visually indistinguishable from LSD, other lysergamides, and potentially dangerous compounds like NBOMe series substances, reagent testing alone cannot confirm identity — Ehrlich reagent produces a positive reaction with all indole-containing compounds, including ETH-LAD's constitutional isomer EIPLA.[11]
Shulgin documented potency degradation in stored solutions even under ideal conditions,[6] which means batch-to-batch consistency may vary significantly. When reagent results confirm an indole is present, this rules out NBOMe-class substitutions but cannot distinguish between lysergamides. Quantitative analysis (GC-MS, HPLC) is the only definitive identification method.[5]
Guidelines
- Test every batch. Ehrlich reagent confirms an indole compound; a negative result rules out dangerous substitutions. Definitive identification requires laboratory analysis.
- Start low. ETH-LAD is more potent per microgram than LSD, and the dose-response curve is reportedly less predictable at higher ranges. First experiences should begin at the low end of the active range.
- Allow for full duration. Clear 12+ hours with no responsibilities. Sleep may be difficult for several hours after primary effects resolve.
- Eat lightly beforehand. A light meal 2–3 hours before reduces nausea risk without an empty stomach.
- Avoid redosing. Rapid tolerance onset means additional doses within hours are unlikely to deepen the experience and may increase body load and duration unpredictably.
- Prepare for body load. Keep water, comfortable clothing, and temperature regulation options available — blankets and access to fresh air.
- Have a sober sitter — especially for first experiences or higher doses. The sitter should know what the person took, when, and how much.
Set & Setting
As with all serotonergic psychedelics, the mental state brought to the experience (set) and the physical and social environment (setting) profoundly shape the outcome. ETH-LAD's reputation for gentleness may lead to underestimation of its psychological intensity, particularly at higher doses where the dose-response curve becomes unpredictable.
A familiar, comfortable environment with minimal obligations for the full duration is strongly recommended. The presence of a sober, trusted companion who can provide reassurance during difficult moments substantially reduces the risk of panic escalation.
Aftercare & integration. The days following an ETH-LAD experience may include residual emotional sensitivity, altered sleep patterns, and a lingering sense of cognitive openness. These are typical and usually resolve within 48–72 hours.
Journaling or discussing the experience with a trusted person helps process novel insights or emotionally charged material. If disturbing thoughts, persistent anxiety, or perceptual disturbances continue beyond a week, consultation with a mental health professional experienced with psychedelic experiences is advisable. Integration circles and psychedelic-informed therapists are available in many regions.
Recovery & Support
While ETH-LAD does not produce physical dependence, some individuals develop patterns of frequent psychedelic use that interfere with daily functioning. If psychedelic experiences are being used as a coping mechanism for underlying distress, or if use is escalating despite negative consequences, professional support is appropriate.
Resources include the Fireside Project (psychedelic peer support line), MAPS integration therapist directory, and local mental health services. Harm reduction organizations can provide confidential guidance without judgment.
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Recognizing an emergency
Most difficult psychedelic experiences are uncomfortable but not medically dangerous. Seek immediate help if:
- The person expresses intent to harm themselves or others
- Complete disconnection from reality with inability to communicate
- Seizure activity
- Severe chest pain or sustained tachycardia
- Dangerously high body temperature (skin hot to the touch, confusion, lack of sweating)
Immediate steps
- 1. Call emergency services if any of the above signs are present.
- 2. Move the person to a quiet, safe environment.
- 3. Speak calmly and reassuringly. Do not restrain unless there is immediate danger of self-harm.
- 4. Do not attempt to argue with or talk down altered perceptions — validate their distress while keeping them safe.
- 5. If the person is unconscious, place them in the recovery position.
What to tell the dispatcher
State the substance name (ETH-LAD, a lysergamide psychedelic), the estimated dose, the time of ingestion, and the symptoms observed. Good Samaritan laws in many jurisdictions protect people who call for help during a drug-related emergency.
Legal Status[edit]
ETH-LAD is not scheduled under the 1971 United Nations Convention on Psychotropic Substances, leaving regulation to individual nations. Several jurisdictions have enacted specific controls, while others rely on structural analog provisions. The global legal landscape remains fragmented.
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| United Kingdom | Class A (Misuse of Drugs Act 1971) | Controlled via Statutory Instrument 2014 No. 3271, effective January 7, 2015. Scheduled alongside AL-LAD, ALD-52, PRO-LAD, and LSZ. Maximum penalties: life imprisonment for supply; 7 years for possession.[20] |
| Germany | Controlled (NpSG) | Controlled under the Neue-psychoaktive-Stoffe-Gesetz, effective July 18, 2019. Production, import for market placement, administration to another person, and trading are punishable. Possession is not specifically penalized under NpSG.[21] |
| Switzerland | Controlled (Verzeichnis E) | Scheduled under the Betäubungsmittelgesetz, List E, effective December 1, 2015.[22] |
| United States | Not specifically scheduled | Not listed under the Controlled Substances Act. The Federal Analogue Act (21 U.S.C. § 813) likely applies when intended for human consumption, treating it as Schedule I due to structural and pharmacological similarity to LSD. |
| Canada | Not controlled | Not a controlled substance under the Controlled Drugs and Substances Act as of 2025. |
| Australia | Not specifically scheduled | No specific scheduling information found. Likely falls under analogue provisions of relevant drug legislation.citation needed |
references
- [1] ^abcdHoffman 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
- [2]
- [3] ^abcCummins BR, Billac GB, Nichols DE, Nichols CD (2025) 5-HT2A receptors: Pharmacology and functional selectivity — Pharmacological Reviews doi:10.1016/j.pharmr.2025.100059
- [4] ^abNiwaguchi T, Nakahara Y, Ishii H (1976) Studies on lysergic acid diethylamide and related compounds. IV. Syntheses of various amide derivatives of norlysergic acid and related compounds — Yakugaku Zasshi (Journal of the Pharmaceutical Society of Japan) PMID:987200
- [5]
- [6]