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AL-LAD
N6-allyl-6-norlysergic acid diethylamide
AL-LAD (N6-allyl-6-norlysergic acid diethylamide) is a synthetic psychedelic of the lysergamide class. It is a close structural analog of LSD, with slightly lower potency. It activates serotonin receptors in the brain, producing the visual and cognitive shifts characteristic of classical psychedelics.[1]
AL-LAD (N6-allyl-6-norlysergic acid diethylamide) is a semi-synthetic psychedelic of the lysergamide class. It is a close structural analog of LSD, with slightly lower potency and shorter duration. AL-LAD is a 5-HT₂A receptor agonist,[1] producing its effects by disrupting serotonin-mediated sensory and cognitive filtering.
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First synthesized in Japan in 1976[2] and pharmacologically characterized in 1985 alongside other LSD analogs,[3] AL-LAD remained obscure for nearly three decades. It entered the research chemical market in 2013 as a legal alternative to LSD, distributed on blotter paper.[4] It remains unscheduled in most jurisdictions and continues to circulate in small quantities.
Subjective effects include geometric visual patterns, brightened colors, time alteration, thought acceleration, and mood elevation.[5] The experience is often described as a gentler version of LSD — visually rich and stimulating, but with a softer onset and less demanding peak. Thought loops, anxious fixation, and difficulty sleeping are common unwanted effects.
AL-LAD produces no physical dependence, and no lethal dose has been established in any species.[6] The primary risk is psychological — anxiety, panic, or psychosis in predisposed individuals — and tolerance builds so fast that compulsive use is self-limiting.[7] No controlled human studies have been conducted; what is known comes from animal assays, metabolism data, and one user survey.
History[edit]
Discovery
AL-LAD was first synthesized in 1976 by a Japanese research team investigating derivatives of norlysergic acid.[2] Hoffman and Nichols characterized it pharmacologically in 1985, establishing it as an active LSD structural analog alongside ETH-LAD and PRO-LAD.[3]
Research chemical era
The compound remained an academic curiosity for nearly three decades. In 2013 it entered the commercial novel psychoactive substances market, sold as a tartrate salt on blotter paper — marketed as a legal alternative to LSD in jurisdictions where LSD was controlled.[4][8]
Present status
No clinical research program has been established for AL-LAD. Unlike LSD or psilocybin, it has not entered psychiatric clinical trials. It continues to appear in the novel psychoactive supply chain — detected as an impurity in related blotter products as recently as 2023.[9]
The name AL-LAD comes from its structure: AL for the allyl substituent at the N6 nitrogen, and LAD for lysergic acid diethylamide. Alexander and Ann Shulgin documented the compound in TiHKAL: The Continuation (1997), contributing early dosing observations and experiential notes that shaped community knowledge.[10]
Chemistry[edit]
Structural class
AL-LAD belongs to the lysergamide family of ergoline alkaloids — the same structural class as LSD. Its molecular formula is C₂₂H₂₇N₃O.
It differs from LSD by a single substitution at one nitrogen position, which slightly reduces potency and alters the compound's metabolic profile.[3] AL-LAD is also the active metabolite of the prodrug 1P-AL-LAD; the liver removes the prodrug's acyl group to yield AL-LAD as the primary active compound.[11] The allyl substituent introduced by that modification is itself subject to metabolic oxidation in the liver.[12]
Pharmacology[edit]
Mechanism of action
AL-LAD activates serotonin receptors in the brain — specifically the subset most responsible for psychedelic effects. Blocking those receptors in animals abolished AL-LAD's hallucinogenic activity entirely.[1] It is roughly 75% as potent as LSD by this measure.[4] This activation triggers a specific intracellular signaling pathway thought to drive its psychedelic effects.[13]
Secondary targets
As an ergoline, AL-LAD likely also binds dopamine receptors — a secondary binding profile shared across the structural class.[14] Once bound to its primary receptor, the molecule is slow to leave: a protein loop closes over the binding site and traps it inside — a mechanism confirmed in LSD and likely shared by AL-LAD.[15]
Metabolism
AL-LAD is broken down by two liver enzymes, CYP1A2 and CYP3A4, through reactions including hydroxylation of the ergoline ring and removal of the allyl group.[12] The parent compound is not detectable in urine at expected doses, indicating extensive conversion before excretion.[11]
Neuroscience[edit]
Where it acts
AL-LAD's psychedelic effects come from activating serotonin receptors concentrated in the prefrontal cortex.[4] This raises excitability in cortical circuits, disrupting the brain's normal filtering of sensory input. The result is perceptual intensification, loosened cognitive associations, and altered self-awareness.
Why it matters
The leading model of how psychedelics work holds that this receptor activation reduces the brain's reliance on its own internal predictions, letting raw sensory information dominate conscious experience. This explains both the potential for therapeutic insight — rigid thought patterns loosen — and the risk of destabilized reality-testing in vulnerable individuals.
- Does AL-LAD's N6-allyl group alter its neuroplasticity profile compared to LSD?
- Does its shorter reported duration reflect different receptor binding kinetics?
- Is there a ceiling on subjective intensity, possibly due to modulation by secondary serotonin receptors?
Subjective Effects[edit]
AL-LAD produces a psychedelic experience in the classical lysergamide tradition — visual, cognitive, and emotional dimensions emerge together rather than sequentially. The experience has a soft, forgiving character: the onset is gradual, the peak is less forceful than LSD, and the exit is relatively smooth.[5] Set and setting shape the emotional tone throughout.
Within the lysergamide family, AL-LAD sits close to LSD but is measurably lighter — similar in character, weaker in peak intensity, with a milder comedown.[5] Compared to psilocybin, it is more stimulating, more visually oriented, and longer-lasting, though no direct comparison study exists.
First synthesized in 1976 in Japan[2] and pharmacologically characterized by Hoffman and Nichols in 1985,[3] AL-LAD remained an obscure research compound for nearly three decades. It entered the novel psychoactive substances market in 2013 as a legal LSD alternative distributed on blotter paper.[4] It remains unscheduled in most jurisdictions and continues to circulate in small quantities among research chemical users.
Subjective effects include geometric visual patterns, color enhancement, time alteration, thought acceleration, and mood elevation. The experience is described as a gentler, less forceful version of the LSD experience — visually rich and cognitively stimulating but with a softer entry and less demanding peak.[5] Thought loops, anxious fixation, and difficulty sleeping are common unsought effects.
AL-LAD produces no physical dependence, and no lethal dose has been established in any species.[6] The primary risk is psychological — acute anxiety, panic, and psychosis precipitation in predisposed individuals — scaling with dose and vulnerability, while rapid tolerance via 5-HT₂A downregulation makes compulsive redosing self-limiting.[7] No controlled human studies have been conducted; the current understanding rests on animal assays, metabolism data, one user survey, and class-level ergoline pharmacology.
History[edit]
Discovery
AL-LAD was first synthesized in 1976 by Tetsukichi Niwaguchi, Yuji Nakahara, and Hisashi Ishii at the National Institute of Hygienic Sciences in Tokyo, as part of a systematic investigation into norlysergic acid amide derivatives.[2] The first pharmacological characterization came in 1985, when Andrew Hoffman and David Nichols demonstrated that AL-LAD possessed LSD-like discriminative stimulus properties in rats, establishing it alongside ETH-LAD and PRO-LAD as active LSD analogs.[3]
Research chemical era
AL-LAD remained an academic curiosity for nearly three decades. It entered the commercial new psychoactive substances market in 2013, distributed as a tartrate salt on blotter paper.[4] Its emergence coincided with a wave of novel lysergamides — including 1P-LSD, ETH-LAD, and LSZ — marketed as legal alternatives to LSD in jurisdictions where the parent compound was controlled.[8]
Present status
No clinical or institutional research program has been established for AL-LAD. Unlike LSD or psilocybin, which have progressed through clinical trials for psychiatric indications, AL-LAD remains a compound of preclinical and forensic-analytical interest. As of 2023, it continues to appear in the NPS supply chain — Kavanagh et al. detected AL-LAD as an impurity in 1cP-AL-LAD blotter samples.[9]
The name AL-LAD derives from its chemical structure: AL for the allyl substituent at the N6 nitrogen and LAD for lysergic acid diethylamide. Alexander and Ann Shulgin documented the compound in TiHKAL: The Continuation (1997), providing qualitative dosing observations and experiential notes that informed subsequent community knowledge.[10]
Chemistry[edit]
Structural class
AL-LAD belongs to the lysergamide family of ergoline alkaloids. Its core structure is 6-norlysergic acid diethylamide — the N6-demethylated form of LSD — with an allyl (prop-2-en-1-yl) group attached at the N6 nitrogen. This single substitution distinguishes AL-LAD from LSD (N6-methyl), ETH-LAD (N6-ethyl), and PRO-LAD (N6-propyl), all characterized as a systematic series by Hoffman and Nichols.[3]
AL-LAD is also the active metabolite of the prodrug 1P-AL-LAD, which undergoes liver-mediated removal of its 1-propanoyl group to yield AL-LAD as the primary active product.[11]
Molecular properties
| Molecular formula | C₂₂H₂₇N₃O |
| Molecular weight | 349.5 g/mol |
The molecule comprises a tetracyclic ergoline ring system fused with an indole moiety, bearing a diethylamide group at C-9 and the N6-allyl substituent. The allyl group introduces a terminal alkene capable of metabolic oxidation.[12]
Stereochemistry
AL-LAD has two chirality centres at C-6a and C-9, with absolute configuration (6aR,9R) — the natural d-lysergic acid configuration shared by all pharmacologically active ergolines, including LSD. It is synthesized and distributed as a single enantiomer.
Physical properties
No published data on melting point, solubility, or thermostability have been identified. As an ergoline compound, AL-LAD is expected to be light-sensitive and subject to degradation upon prolonged UV exposure. The commercial form is a tartrate salt distributed on blotter paper.[4] citation needed
Pharmacology[edit]
Mechanism of action
AL-LAD activates the serotonin 5-HT₂A receptor, the primary target responsible for psychedelic effects. This was confirmed in the mouse head-twitch response assay — a standard behavioral test for hallucinogenic activity — where pretreatment with the selective 5-HT₂A blocker M100907 abolished the response across the lysergamide series.[1]
Brandt et al. measured AL-LAD's potency in the same assay, finding an ED₅₀ of 174.9 nmol/kg compared to 132.8 nmol/kg for LSD — placing AL-LAD at roughly 75% of LSD's potency.[4] The dose-response curve follows an inverted U shape, with peak response at 200 µg/kg.
The downstream signaling pathway involves 5-HT₂A coupling to Gq/11 proteins rather than β-arrestin2 recruitment, as demonstrated by Wallach et al.[13] This Gq-dependent pathway is presumed to mediate AL-LAD's psychedelic activity, though direct confirmation for this specific compound has not been published.
No binding affinity data have been published for AL-LAD at any receptor target.
Secondary targets
As an ergoline derivative, AL-LAD likely interacts with multiple receptor systems beyond 5-HT₂A. LSD and structural analogs bind dopamine D₂ receptors with affinity comparable to their serotonin binding,[14] and partial agonism at 5-HT₁A receptors is characteristic of the ergoline class. The related lysergamide LSM-775 showed 5-HT₁A activity strong enough to mask its psychedelic effects in behavioral assays,[15] illustrating how this secondary target can shape the overall experience.
LSD is also a potent 5-HT₂B agonist, a property linked to heart valve damage at high chronic doses in the ergot drug class. Whether AL-LAD shares this binding profile is unknown. safety citation needed
Receptor residence time
Wacker et al. solved the crystal structure of LSD bound to the serotonin 5-HT₂B receptor, revealing that a loop of protein (extracellular loop 2) forms a "lid" over the binding pocket that traps the molecule inside.[16] AL-LAD shares the ergoline scaffold that engages this architecture, suggesting a similar trapping mechanism, but no specific data on AL-LAD's binding duration have been published.
Metabolism
Wagmann et al. investigated AL-LAD's metabolic breakdown using human liver preparations.[12] The primary metabolizing enzymes are CYP1A2 and CYP3A4, with principal reactions including hydroxylation of the ergoline ring and removal of the allyl group. The parent compound was not detectable in rat urine at expected doses, indicating extensive metabolism before excretion.
Additional metabolic data came from studies of the prodrug 1P-AL-LAD, which confirmed AL-LAD as the most abundant metabolite and identified fourteen total metabolites of the combined system.[11]
Neuroscience[edit]
Where it acts
AL-LAD's psychedelic effects are driven by activation of 5-HT₂A receptors concentrated on layer V pyramidal neurons of the prefrontal cortex.[4] This increases glutamate signaling in cortical and thalamic circuits, elevating excitability and disrupting the brain's normal filtering of sensory input.
The result — perceptual intensification, loosened cognitive boundaries, and altered self-awareness — mirrors the network-level changes observed with LSD and psilocybin, including disruption of the default mode network, the brain system most associated with the stable sense of self.
Why it matters
The REBUS (Relaxed Beliefs Under Psychedelics) framework offers the most explanatory model: 5-HT₂A activation reduces the brain's reliance on top-down predictions, allowing raw sensory information greater influence over conscious experience. This accounts for both the therapeutic potential (loosening rigid thought patterns) and the risk profile (destabilizing reality-testing in vulnerable individuals).
Serotonergic psychedelics including LSD also promote structural brain changes — increased dendritic spine density and new synaptic connections — through 5-HT₂A-dependent activation of growth factor pathways. Whether AL-LAD produces comparable neuroplasticity remains untested.
- Does AL-LAD's N6-allyl substitution alter its neuroplasticity profile compared to LSD?
- Does its shorter reported duration reflect different binding kinetics at the 5-HT₂A receptor?
- Is the inverted U-shaped dose-response curve attributable to 5-HT₁A modulation, and does this translate to a ceiling on subjective intensity in humans?
Subjective Effects[edit]
AL-LAD produces a serotonergic psychedelic experience qualitatively consistent with the lysergamide class — visual, cognitive, and affective dimensions emerge together rather than sequentially unlocking at higher doses. Set and setting exert strong influence over the emotional tone and trajectory of the experience. Users describe a gentler arc than LSD: a softer onset, a less demanding peak, and a more forgiving exit, which may reflect AL-LAD's lower receptor potency.
Within the lysergamide family, AL-LAD sits between LSD and lower-potency ergolines. Users in the Coney et al. survey described it as similar in character to LSD but weaker in peak intensity, with a milder comedown.[5] Compared to psilocybin, the ergoline pharmacology predicts a more stimulating, visually-oriented, and longer-lasting profile, though no direct comparison study exists.
Effect Grid
Full psychedelic experience across visual, cognitive, and emotional domains. Visual geometry emerges — geometric patterns overlay surfaces, colour enhancement is pronounced, and visual distortion of spatial relationships becomes apparent. Tracers may follow moving objects. Time distortion is marked, with minutes feeling stretched or compressed unpredictably.
Cognitive effects are prominent: thought connectivity increases, conceptual thinking deepens, and introspective thought loops may develop. Emotional lability is common — euphoria, wonder, anxiety, and vulnerability can cycle rapidly. Set and setting become critical modulators of experience quality at this tier.
Body stimulation is moderate, with pupil dilation, mild nausea possible during come-up, and increased heart rate. Functional impairment is significant — do not drive or operate machinery. Total duration is 7–10 hours with highly variable afterglow (2–18 hours).
Modeled from the effect's dose-dependence curve — not per-substance measurements.
Auditory enhancement · Music enhancement · Environmental patterning · Visual breathing · Visual morphing · Depth perception distortion · Symmetrical texture repetition · After-images · Tracers · Brightness alteration · Light sensitivity · Perspective distortion · Touch enhancement · Visual diffraction · Peripheral vision distortion · Sound sensitivity · Spatial disorientation · Visual haze / noise · Visual melting · Synesthesia · Visual acuity enhancement · Auditory distortion · Auditory misinterpretation · Peripheral misidentification · Proprioceptive distortion · Vestibular distortion · Visual processing acceleration · Visual magnification · Olfactory enhancement · Taste enhancement · Object transformations · Internal hallucinations · External hallucinations · Object activation · Environmental orbism / cubism · Visual recursion · Auditory hallucinations · Visual scenery slicing · Perspective hallucinations
Visual morphing · Depth perception distortion · Symmetrical texture repetition · After-images · Tracers · Brightness alteration · Light sensitivity · Perspective distortion · Touch enhancement · Visual diffraction · Peripheral vision distortion · Sound sensitivity · Spatial disorientation · Visual haze / noise · Visual melting · Synesthesia · Visual acuity enhancement · Auditory distortion · Auditory misinterpretation · Peripheral misidentification · Proprioceptive distortion · Vestibular distortion · Visual processing acceleration · Visual magnification · Olfactory enhancement · Taste enhancement · Object transformations · Internal hallucinations · External hallucinations · Object activation · Environmental orbism / cubism · Visual recursion · Auditory hallucinations · Visual scenery slicing · Perspective hallucinations
Stimulation · Body high · Bodily lightness · Appetite suppression · Insomnia · Tactile euphoria · Body schema distortion · Muscle tension · Dizziness · Dry mouth · Heart rate perception changes · Laughter fits · Physical fatigue · Restlessness · Tingling / electric sensations · Vibrations / buzzing · Nausea · Excessive sweating · Sexual arousal enhancement · Dehydration sensation · Increased urination · Involuntary body movements · Bodily pressures · Breathing alteration · Headache · Motor control impairment · Trembling · Vasoconstriction · Yawning · Salivation · Bruxism · Nystagmus (eye wobbles) · Motor control enhancement · Seizure threshold reduction
Appetite suppression · Insomnia · Tactile euphoria · Body schema distortion · Muscle tension · Dizziness · Dry mouth · Heart rate perception changes · Laughter fits · Physical fatigue · Restlessness · Tingling / electric sensations · Vibrations / buzzing · Nausea · Excessive sweating · Sexual arousal enhancement · Dehydration sensation · Increased urination · Involuntary body movements · Bodily pressures · Breathing alteration · Headache · Trembling · Vasoconstriction · Yawning · Salivation · Bruxism · Nystagmus (eye wobbles) · Motor control enhancement · Seizure threshold reduction
Aesthetic enhancement · Introspection enhancement · Thought acceleration · Conceptual thinking · Immersion enhancement · Cognitive flexibility · Openness enhancement · Thought connectivity · Creativity enhancement · Increased nature relatedness · Multiple thought streams · Humor enhancement · Memory suppression · Thought loops · Focus enhancement · Analysis enhancement · Cognitive fatigue · Cognitive impairment · Information processing enhancement · Memory fragmentation · Synchronicity · Motivation enhancement · Confusion · Memory replays · Thought disorganization · Language enhancement · Thought organization · Cognitive dysphoria · Language suppression · Delusions
Conceptual thinking · Immersion enhancement · Cognitive flexibility · Openness enhancement · Thought connectivity · Creativity enhancement · Increased nature relatedness · Multiple thought streams · Humor enhancement · Memory suppression · Thought loops · Focus enhancement · Analysis enhancement · Cognitive fatigue · Cognitive impairment · Information processing enhancement · Memory fragmentation · Synchronicity · Motivation enhancement · Confusion · Memory replays · Thought disorganization · Language enhancement · Thought organization · Cognitive dysphoria · Language suppression
Simultaneous emotions · Anxiety · Catharsis · Dysphoria
Disinhibition · Sociability enhancement · Trust enhancement · Communication enhancement · Flow state · Communication suppression · Boundary dissolution · Ego dissolution · Cognitive disconnection · Identity alteration
Flow state · Communication suppression · Boundary dissolution · Ego dissolution · Cognitive disconnection · Identity alteration
Time cessation
Transpersonal visions · Entity contact
Recursive awareness
Timeline
Initial alerts emerge — subtle shifts in visual texture, mild anticipatory arousal, and faint body awareness. Effects are sub-perceptual to barely perceptual.
Progressive intensification of visual and cognitive effects. Colour saturation increases, geometric patterns begin forming, and body load emerges. Mild anxiety or excitement is common during this transitional phase.
Full expression of psychedelic effects across visual, cognitive, and emotional domains. Geometric patterning, time distortion, thought connectivity, and emotional lability reach maximum intensity. Set and setting are the dominant modulators of experience quality.
Gradual reduction in intensity. Visual effects diminish first while cognitive and emotional effects persist. Thought patterns begin linearising.
Residual mood elevation, mild perceptual sensitivity, and a reflective or contemplative state. Duration is highly variable (2–18 hours) across individuals.
⚠ Do not drive or operate heavy machinery for at least 12 hours after ingestion, as residual perceptual and cognitive effects may persist for up to 18 hours.
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 lethal dose has been established for AL-LAD in any species, and no human fatalities have been attributed to the compound.[6]
Heart and circulation
AL-LAD produces mild, short-lived increases in heart rate and blood pressure during the experience. A separate concern applies to the broader ergoline class: long-term activation of certain serotonin receptors by ergot-derived drugs has been associated with heart valve damage. Whether AL-LAD shares this binding profile is unknown; at typical infrequent patterns of use, this risk is considered minimal. safety citation needed
Seizure threshold
Activating these serotonin receptors can increase cortical excitability. No AL-LAD-specific seizure data have been published, and no case reports have been identified. safety citation needed
Psychological risks
The primary risks of AL-LAD are psychological. Acute anxiety, panic, paranoia, and persecutory thoughts are the most common adverse outcomes — emergency presentations following LSD use are predominantly for psychological distress rather than physical toxicity.[16]
In people with a personal or family history of psychotic disorders, serotonergic psychedelics can trigger or worsen psychotic episodes.[17] Rarely, use also leaves behind persistent visual disturbances after the experience ends — a condition called HPPD. Pre-existing anxiety disorders and prior perceptual abnormalities are risk factors.[18]
Tolerance and dependence
Tolerance
Tolerance develops rapidly — after a single dose, the serotonin receptors responsible for psychedelic effects reduce in density in the frontal cortex.[7] This tolerance is shared across all classical psychedelics, including LSD, psilocybin, and mescaline.
Community estimates place the tolerance half-life at around 6 days and full reset at 14 days. These figures come from self-report, not controlled study. citation needed
Dependence
AL-LAD does not produce physical dependence or addiction. Hallucinogens do not activate the brain's mesolimbic pathway and do not produce compulsive drug-seeking, dose escalation, or withdrawal.[6]
Drug Interactions
Serotonergic interactions
Tramadol — combining AL-LAD with tramadol raises the risk of serotonin syndrome — a dangerous condition involving overheating, muscle rigidity, and seizures caused by serotonin overload. Tramadol blocks serotonin reuptake while AL-LAD directly activates serotonin receptors, compounding the effect.[19] Tramadol also independently lowers the seizure threshold.
MAOIs — monoamine oxidase inhibitors prevent the body from breaking down serotonin. Combining them with AL-LAD dramatically amplifies serotonin activity and can cause serotonin syndrome. safety citation needed
SSRIs/SNRIs — serotonin reuptake inhibitors may weaken psychedelic effects while simultaneously raising serotonin syndrome risk. The net outcome is unpredictable. safety citation needed
Receptor-level antagonism
Antipsychotics — these medications block the same serotonin and dopamine receptors that AL-LAD activates. Combined use would be expected to block or substantially reduce AL-LAD's effects.
Seizure-related interactions
Lithium — combining lithium with serotonergic psychedelics is associated with increased seizure risk. safety citation needed
Cannabis
Cannabis alters the psychedelic experience in a dose-dependent way.[20] The direction and magnitude of the effect cannot be reliably predicted from available evidence.
Contraindications
8 knownThe following are based on class-level evidence for serotonergic psychedelics. No AL-LAD-specific contraindication data exist.
Absolute:
- Personal or family history of psychotic spectrum disorders (schizophrenia, schizoaffective disorder) — can precipitate or worsen psychotic episodes[17]
- Concurrent lithium use — seizure risk safety citation needed
Relative:
- Heart conditions — transient increases in heart rate and blood pressure
- Concurrent tramadol use — serotonin syndrome risk[19]
- Concurrent MAOI use — serotonin syndrome risk safety citation needed
- Pre-existing anxiety or mood disorders — increased risk of acute distress; may be a risk factor for HPPD[18]
- Pregnancy — no safety data exist safety citation needed
Harm Reduction[edit]
Forms & Identification
AL-LAD circulates almost exclusively as a tartrate salt on blotter paper.[4] Blotter-distributed lysergamides are visually indistinguishable from one another. Ehrlich's reagent confirms the presence of an ergoline structure but cannot distinguish AL-LAD from LSD, ETH-LAD, 1P-LSD, or other lysergamides.
Quantitative analysis — such as liquid chromatography — is required for definitive identification. Drug checking services that offer these methods provide the highest confidence.
Guidelines
- Test all blotter material with Ehrlich's reagent to confirm indole presence before use
- Start with a low dose and wait the full onset period before considering redosing — tolerance begins immediately and a second dose will have diminished effect
- Choose a safe, comfortable environment with no obligations for the full duration plus several hours of recovery
- Keep a sober, trusted companion present, especially at higher doses or during first experiences
- Prepare water, light food, and comfort items in advance
- Avoid combining with other substances, particularly cannabis during the peak
- Clear the following day of commitments to allow rest and integration
Set & Setting
The psychological character of the AL-LAD experience is highly sensitive to environment and mental state. A familiar, comfortable space with controllable lighting, sound, and temperature reduces the likelihood of anxious escalation.
Starting in a positive, rested state — without unresolved emotional distress — provides a more stable foundation. A trusted, sober companion who can offer calm reassurance is the single most effective risk reduction measure for psychedelic use.
Aftercare & integration. The days following a psychedelic experience often involve continued processing of material that surfaced during the session. Journaling thoughts, emotions, and imagery within 24 hours helps preserve insights that otherwise fade.
Physical recovery is straightforward: adequate sleep, hydration, and nutrition. Avoid making major life decisions in the immediate aftermath. If the experience brought up distressing material, talking with a trusted person or a therapist experienced in psychedelic integration can help. Seek professional support if perceptual disturbances, persistent anxiety, or depersonalization continue beyond a few days.
Recovery & Support
AL-LAD does not produce physical dependence or withdrawal. Any pattern of repeated psychedelic use that interferes with daily functioning, relationships, or wellbeing warrants honest self-assessment.
Support resources include psychedelic integration therapists, peer support communities such as the Fireside Project (62-FIRESIDE / 623-473-7433), and general mental health services. Persistent visual disturbances following psychedelic use (HPPD) are rare but may require specialized clinical attention if symptoms continue.
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Most difficult psychedelic experiences are psychologically distressing but not medically dangerous. The distinction matters.
Uncomfortable but manageable: anxiety, confusion, thought loops, nausea, desire for the experience to end. These respond to reassurance, environment change, and time.
Requires immediate help:
- Expressions of intent to harm self or others
- Complete disconnection from reality with inability to recognize surroundings or people
- Seizure activity
- Chest pain or severely irregular heartbeat
- Loss of consciousness
Immediate steps:
- 1. Stay with the person and speak calmly — do not restrain unless there is immediate danger of self-harm
- 2. Move to a quiet, low-stimulation environment if possible
- 3. Call emergency services if any red flag above is present
- 4. Do not induce vomiting
What to tell the dispatcher: the substance (AL-LAD, or "a lysergamide psychedelic similar to LSD"), estimated dose, time of ingestion, and current symptoms. Good Samaritan laws in many jurisdictions protect people who call for help during a drug emergency.
Legal Status[edit]
AL-LAD is not scheduled under the UN Convention on Psychotropic Substances, but its legal classification varies significantly by country.[21]
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| United States | Unscheduled (federal) | Not specifically listed under the Controlled Substances Act. The Federal Analogue Act (21 U.S.C. § 813) may apply if AL-LAD is intended for human consumption, given its structural and pharmacological similarity to Schedule I LSD. |
| United Kingdom | Class A (Misuse of Drugs Act 1971) | Specifically named and controlled as a Class A substance effective 7 January 2015. |
| Sweden | Schedule I (Narcotics Control Act) | Controlled effective 26 January 2016. |
| Canada | Uncontrolled | Not listed as a controlled substance under the Controlled Drugs and Substances Act as of 2025. |
| France | Controlled substance | Listed as illegal. |
| Denmark | Controlled substance | Listed as illegal. |
| Switzerland | Controlled substance | Listed as illegal. |
| Latvia | Possibly controlled | May be covered by LSD structural analog provisions enacted June 2015. |
| Australia | Restricted | Prohibited under import/export provisions; state-level scheduling may apply. |
| International (UN) | Not scheduled | Not listed under the UN Convention on Psychotropic Substances. |
Legal status for novel psychoactive substances changes frequently. The information above reflects available data as of 2025 and is not legal advice. Verify current local law before acting on this information.
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 lethal dose has been established for AL-LAD in any species, and no human fatalities have been attributed to the compound. The serotonergic psychedelic class is considered physiologically safe at recreational doses, with no established lethal dose in humans.[6]
Heart and circulation
Serotonergic psychedelics produce mild, transient increases in heart rate and blood pressure during acute effects. No AL-LAD-specific cardiovascular data exist.
A separate concern applies to the ergoline class: chronic activation of serotonin₂B receptors by ergot-derived drugs is associated with heart valve damage. Whether AL-LAD shares LSD's 5-HT₂B binding profile is unknown; at typical patterns of infrequent use, this risk is considered minimal. safety citation needed
Seizure threshold
5-HT₂A activation can increase cortical excitability. No AL-LAD-specific seizure data have been published, and no case reports of seizures have been identified. safety citation needed
Psychological risks
The primary risks of AL-LAD are psychological. Acute distress — anxiety, panic, paranoia, and persecutory thoughts — is the most common adverse outcome of serotonergic psychedelic use. Kopra et al. found that emergency treatment following LSD use was predominantly for psychological distress rather than physiological toxicity.[17]
Serotonergic psychedelics can precipitate or worsen psychotic episodes in individuals with personal or family history of psychotic spectrum disorders.[18]
Hallucinogen persisting perception disorder (HPPD) is a rare outcome involving persistent visual disturbances after psychedelic use. Risk factors include pre-existing anxiety disorders and prior perceptual abnormalities.[19] Leistenschneider et al. identified impaired visual memory and executive function in HPPD patients.[20] No AL-LAD-specific HPPD cases have been reported.
Tolerance and dependence
Tolerance
Tolerance develops rapidly after a single dose via 5-HT₂A downregulation in the frontal cortex.[7] Cross-tolerance occurs with all serotonergic psychedelics acting through 5-HT₂A — including LSD, psilocybin, and mescaline.
Community estimates place the tolerance half-life at approximately 6 days and full reset at 14 days, though these values derive from self-report rather than controlled study. citation needed
Dependence
AL-LAD does not produce physical dependence or addiction. Hallucinogens as a class do not engage the brain's mesolimbic pathway as a primary mechanism and do not produce compulsive drug-seeking, dose escalation, or withdrawal.[6]
Drug Interactions
Serotonergic interactions
Tramadol — combining AL-LAD with tramadol carries risk of serotonin syndrome. Tramadol inhibits serotonin reuptake while AL-LAD directly activates serotonin receptors, creating additive serotonergic excess.[21] Tramadol also lowers the seizure threshold.
MAOIs — monoamine oxidase inhibitors prevent serotonin breakdown, creating potential for serotonin syndrome when combined with serotonergic agonists. safety citation needed
SSRIs/SNRIs — serotonin reuptake inhibitors may weaken psychedelic effects while simultaneously introducing serotonin syndrome risk. The net effect is unpredictable. safety citation needed
Receptor-level antagonism
Antipsychotics — first- and second-generation antipsychotics block 5-HT₂A and/or dopamine D₂ receptors. Coadministration would be expected to block or substantially weaken AL-LAD's effects.
Seizure-related interactions
Lithium — the combination of lithium with serotonergic psychedelics is associated with increased seizure risk. safety citation needed
Cannabis
Cannabis modulates the psychedelic experience in a dose-dependent manner.[22] The direction and magnitude of this modulation could not be determined from available evidence.
Contraindications
8 knownThe following are based on class-level evidence for serotonergic psychedelics. No AL-LAD-specific contraindication data exist.
Absolute:
- Personal or family history of psychotic spectrum disorders (schizophrenia, schizoaffective disorder) — can precipitate or worsen psychotic episodes[18]
- Concurrent lithium use — seizure risk safety citation needed
Relative:
- Heart conditions — transient increases in heart rate and blood pressure
- Concurrent tramadol use — serotonin syndrome risk[21]
- Concurrent MAOI use — serotonin syndrome risk safety citation needed
- Pre-existing anxiety or mood disorders — increased risk of acute distress; may be a risk factor for HPPD[19]
- Pregnancy — no safety data exist safety citation needed
Harm Reduction[edit]
Forms & Identification
AL-LAD circulates almost exclusively as a tartrate salt on blotter paper. Because blotter-distributed lysergamides are visually indistinguishable from one another, reagent testing alone cannot confirm identity — Ehrlich's reagent confirms the presence of an indole (ergoline) structure but cannot distinguish AL-LAD from LSD, ETH-LAD, 1P-LSD, or other lysergamides.
Quantitative analysis (such as liquid chromatography) is required for definitive identification. Drug checking services that offer these methods provide the highest confidence.
Guidelines
- Test all blotter material with Ehrlich's reagent to confirm indole presence before use
- Start with a low dose and wait the full onset period before considering redosing — tolerance begins immediately and a second dose will have diminished effect
- Choose a safe, comfortable environment with no obligations for the full duration plus several hours of recovery
- Keep a sober, trusted companion present, especially at higher doses or during first experiences
- Prepare water, light food, and comfort items (blankets, familiar music) in advance
- Avoid combining with other substances, particularly cannabis during the peak
- Clear the following day of commitments to allow rest and integration
Set & Setting
The psychological character of the AL-LAD experience is highly sensitive to environment and mental state. A familiar, comfortable physical space with controllable stimulation (lighting, sound, temperature) reduces the likelihood of anxious escalation.
Beginning in a positive, rested mental state — without unresolved emotional distress — provides a more stable foundation. A trusted, sober companion who can provide calm reassurance without directing the experience is the single most effective risk reduction measure for psychedelic use.
Aftercare & integration. The days following a psychedelic experience often involve continued processing of material that surfaced during the session. Journaling thoughts, emotions, and imagery while they remain fresh — ideally within 24 hours — helps preserve insights that otherwise fade.
Physical recovery is straightforward: adequate sleep, hydration, and nutrition. Avoid making major life decisions in the immediate aftermath. If the experience was difficult or brought up distressing material, talking with a trusted person or a therapist experienced in psychedelic integration can help contextualize it. Seek professional support if distressing perceptual changes, persistent anxiety, or depersonalization continue beyond a few days.
Recovery & Support
AL-LAD does not produce physical dependence or withdrawal. However, any pattern of repeated psychedelic use that interferes with daily functioning, relationships, or wellbeing warrants honest self-assessment.
Support resources include psychedelic integration therapists, peer support communities such as the Fireside Project (62-FIRESIDE / 623-473-7433), and general mental health services. HPPD — persistent visual disturbances following psychedelic use — is rare but may require specialized clinical attention if symptoms persist.
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Most difficult psychedelic experiences are psychologically distressing but not medically dangerous. The distinction matters.
Uncomfortable but manageable: anxiety, confusion, thought loops, nausea, desire for the experience to end. These respond to reassurance, environment change, and time.
Requires immediate help:
- Expressions of intent to harm self or others
- Complete disconnection from reality with inability to recognize surroundings or people
- Seizure activity
- Chest pain or severely irregular heartbeat
- Loss of consciousness
Immediate steps:
- 1. Stay with the person and speak calmly — do not restrain unless there is immediate danger of self-harm
- 2. Move to a quiet, low-stimulation environment if possible
- 3. Call emergency services if any red flag above is present
- 4. Do not induce vomiting
What to tell the dispatcher: the substance (AL-LAD, or "a lysergamide psychedelic similar to LSD"), estimated dose, time of ingestion, and current symptoms. Good Samaritan laws in many jurisdictions protect people who call for help during a drug emergency.
Legal Status[edit]
AL-LAD is not scheduled under the United Nations Convention on Psychotropic Substances and occupies a varied legal position across national jurisdictions. Several countries have specifically named AL-LAD in controlled substance legislation since 2015, while others rely on structural analog provisions or have not addressed the compound at all.[23]
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| United States | Unscheduled (federal) | Not specifically listed under the Controlled Substances Act. The Federal Analogue Act (21 U.S.C. § 813) may apply if AL-LAD is intended for human consumption, given its structural and pharmacological similarity to Schedule I LSD. |
| United Kingdom | Class A (Misuse of Drugs Act 1971) | Specifically named and controlled as a Class A substance effective 7 January 2015. |
| Sweden | Schedule I (Narcotics Control Act) | Controlled effective 26 January 2016. |
| Canada | Uncontrolled | Not listed as a controlled substance under the Controlled Drugs and Substances Act as of 2025. |
| France | Controlled substance | Listed as illegal. |
| Denmark | Controlled substance | Listed as illegal. |
| Switzerland | Controlled substance | Listed as illegal. |
| Latvia | Possibly controlled | May be covered by LSD structural analog provisions enacted June 2015. |
| Australia | Restricted | Prohibited under import/export provisions; state-level scheduling may apply. |
| International (UN) | Not scheduled | Not listed under the UN Convention on Psychotropic Substances. |
The legal landscape for novel lysergamides continues to evolve. AL-LAD's emergence on the NPS market in 2013[4] preceded its specific scheduling in the UK and Sweden by one to three years, illustrating the reactive nature of NPS scheduling. The prodrug 1P-AL-LAD was developed in part as a response to AL-LAD scheduling, exploiting regulatory gaps around 1-acyl-substituted lysergamide derivatives.[11]
Frequently asked questions
What is AL-LAD?
AL-LAD is a semisynthetic lysergamide psychedelic derived from the ergoline scaffold, first synthesized in 1976 by Niwaguchi, Nakahara, and Ishii. It acts as a 5-HT₂A receptor agonist at approximately 75% of LSD's potency, with a reported oral duration of 7–10 hours.
How long does AL-LAD last?
Total duration by route of administration — Oral: 7 – 10 hours. Ranges vary with dose and individual factors; see the duration table for onset, peak, and after-effect phases.
Where can I find dosage information for AL-LAD?
Psychedex publishes a dosage table for AL-LAD on this page covering these routes of administration: oral. Dose values are presented only in that table, always alongside their route of administration.
What are dangerous combinations with AL-LAD?
The highest-severity documented interactions for AL-LAD: MAOIs (Lethal), Buspirone (Dangerous), DXM (Dangerous), GHB, Baclofen (Dangerous), GHB, GBL (Dangerous). See the interactions section for the full list with mechanisms and severity levels.
Is AL-LAD addictive?
Psychedex records tolerance and dependence data rather than a yes/no rating. Recorded tolerance indicators for AL-LAD: tolerance builds rapid; full reset takes 14 days; cross-tolerance develops with LSD, psilocybin, mescaline, DMT. See the article's dependence and safety sections for recorded dependence data.
experience reports
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First-person accounts of subjective effects, timing, and outcomes — submitted for harm reduction.
references
- [1] ^abBrandt SD, Kavanagh PV, Westphal F, Stratford A, Elliott SP, Hoang K, Wallach J, Halberstadt AL (2016) Return of the lysergamides. Part I: Analytical and behavioural characterization of 1-propionyl-d-lysergic acid diethylamide (1P-LSD) — Drug Testing and Analysis doi:10.1002/dta.1884
- [2] ^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
- [3] ^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
- [4] ^abcdeBrandt SD, Kavanagh PV, Westphal F, Elliott SP, Wallach J, Colestock T, Burrow TE, Chapman SJ, Stratford A, Nichols DE, Halberstadt AL (2017) Return of the lysergamides. Part II: Analytical and behavioural characterization of N6-allyl-6-norlysergic acid diethylamide (AL-LAD) and (2'S,4'S)-lysergic acid 2,4-dimethylazetidide (LSZ) — Drug Testing and Analysis doi:10.1002/dta.1985
- [5] ^abcConey LD, Maier LJ, Ferris JA, Winstock AR, Barratt MJ (2017) Genie in a blotter: A comparative study of LSD and LSD analogues' effects and user profile — Human Psychopharmacology doi:10.1002/hup.2599
- [6]
references
- [1] ^abBrandt SD, Kavanagh PV, Westphal F, Stratford A, Elliott SP, Hoang K, Wallach J, Halberstadt AL (2016) Return of the lysergamides. Part I: Analytical and behavioural characterization of 1-propionyl-d-lysergic acid diethylamide (1P-LSD) — Drug Testing and Analysis doi:10.1002/dta.1884
- [2] ^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
- [3] ^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
- [4] ^abcdefBrandt SD, Kavanagh PV, Westphal F, Elliott SP, Wallach J, Colestock T, Burrow TE, Chapman SJ, Stratford A, Nichols DE, Halberstadt AL (2017) Return of the lysergamides. Part II: Analytical and behavioural characterization of N6-allyl-6-norlysergic acid diethylamide (AL-LAD) and (2'S,4'S)-lysergic acid 2,4-dimethylazetidide (LSZ) — Drug Testing and Analysis doi:10.1002/dta.1985
- [5] ^abConey LD, Maier LJ, Ferris JA, Winstock AR, Barratt MJ (2017) Genie in a blotter: A comparative study of LSD and LSD analogues' effects and user profile — Human Psychopharmacology doi:10.1002/hup.2599
- [6]