1B-LSD
1-butanoyl-d-lysergic acid diethylamide
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1B-LSD (1-butanoyl-lysergic acid diethylamide) is a synthetic psychedelic of the lysergamide class. It is a prodrug of LSD — the body converts it to LSD, which is the actual active compound. It activates serotonin receptors in the brain,[1] producing the perceptual and cognitive shifts characteristic of classical psychedelics.
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LSD, psilocybin, mescaline +5 moreLSD, psilocybin, mescaline, DMT, DOI, 1P-LSD, ALD-52, 1CP-LSD show less
It appeared on the research chemical market in August 2016, with no prior record in the scientific literature.[2] It was the fourth in a series of chemically modified LSD derivatives, each designed to exploit gaps in controlled substance scheduling law. It remains unscheduled by name in most countries and circulates in small quantities as blotter or pellets.
Subjective effects include geometric visual patterns, color enhancement, time alteration, thought acceleration, and ego dissolution. The experience is widely reported as indistinguishable from LSD — long, analytically sharp, with a buzzing physical stimulation unlike the sedation typical of other psychedelics. Thought loops, anxious fixation, and difficulty sleeping through the extended offset are common unsought effects.
1B-LSD does not produce physical dependence, and the active compound LSD has no established lethal dose in humans.[3] The primary danger is psychological: acute panic and destabilizing ego dissolution scale with dose[4] and pre-existing anxiety.[5] No clinical studies of 1B-LSD have been conducted — all safety conclusions rest on the LSD evidence base and an unconfirmed prodrug hypothesis.
History[edit]
Discovery
1B-LSD appeared on the research chemical market in August 2016, with no prior history in the scientific literature.[2] Its original synthesizer is unknown. The first scientific characterization was published in 2019 by Brandt and colleagues.[2]
The N1-acyl lysergamide series
It belongs to a series of LSD derivatives, each carrying a different carbon chain attached to the same position on the molecule. The lineage runs from ALD-52 (first synthesized in the 1950s)[6][7] through 1P-LSD[8] to 1B-LSD (2016)[2] and on to 1CP-LSD, which provided the first direct evidence of LSD release in human serum.[9] Each new compound was designed to sit just outside the scheduling laws that had caught its predecessor.
Regulatory response
Germany explicitly controlled 1B-LSD under its novel psychoactive substance law in July 2019,[10] and it falls under the United Kingdom's blanket Psychoactive Substances Act 2016. Most other jurisdictions have not named it directly.
Chemistry[edit]
Structural identity
1B-LSD (1-butanoyl-d-lysergic acid diethylamide) is a synthetic lysergamide — a chemical family built on the ergoline ring system, the same core scaffold as LSD. It is distinguished by a four-carbon butanoyl chain at the indole nitrogen, placing it structurally between 1P-LSD (three-carbon chain) and longer-chain relatives in the same series.[2] Its molecular formula is C₂₄H₃₁N₃O₂ (molecular weight 393.5 g/mol).
The butanoyl chain is also the key to how 1B-LSD works. Enzymes in the blood strip it away after ingestion, releasing LSD as the active compound.[2] This makes 1B-LSD a prodrug — a compound that is itself pharmacologically inactive but converts to an active substance in the body.
Pharmacology[edit]
Mechanism of action
1B-LSD is a prodrug of LSD. Enzymes in the blood strip away the butanoyl group after ingestion, releasing LSD as the active compound.[2][1] Related N1-acyl derivatives have been confirmed to release LSD in plasma,[9] but this conversion has not been directly verified for 1B-LSD itself — prodrug status is strongly inferred from structural analogy. inferred
LSD as active moiety
Once converted, the pharmacology is that of LSD. LSD activates serotonin receptors on cortical neurons,[3] disrupting the brain's normal filtering of sensory input and producing the psychedelic state. Structural studies reveal why the effects last so long: the receptor folds over the LSD molecule like a lid, trapping it and prolonging receptor activation.[11][12]
Pharmacokinetics
No human pharmacokinetic data exist for 1B-LSD. LSD itself reaches peak blood levels about 1–1.5 hours after oral ingestion[13] and clears with a half-life of roughly 3–5 hours.[14] People with slow CYP2D6 enzyme activity — a liver enzyme that breaks down LSD — experience roughly 75% higher exposure, with prolonged and intensified effects.[15]
Neuroscience[edit]
Where it acts
No neuroimaging studies of 1B-LSD exist — the following is established for LSD and expected to apply after prodrug conversion. LSD activates serotonin receptors on cortical neurons,[3] opening a broader flow of perceptual and associative signals than the brain normally allows. It also disrupts the brain network tied to the sense of self; stronger disruption tracks with the intensity of ego dissolution.[3]
Why it matters
One leading framework proposes that psychedelics weaken the brain's established predictive patterns while amplifying incoming signals — allowing rigid beliefs and emotional patterns to shift. This may explain both the acute experience and lasting effects seen in clinical trials for depression and addiction. LSD also stimulates growth of new neural connections through signaling pathways involving BDNF,[16] and these changes outlast the experience itself.
Whether 1B-LSD crosses the blood-brain barrier intact or is fully converted to LSD in the bloodstream first remains unknown. Individual differences in the enzymes that cleave the butanoyl chain may produce unpredictable variation in effective dose — a source of variability absent with LSD itself. The gap between mouse potency data (1B-LSD at roughly 14% of LSD's potency) and human reports of near-equivalent effects has not been explained.[1]
Subjective Effects[edit]
The 1B-LSD experience is vivid, analytically sharp, and long-lasting — defined by an unusual clarity of thought alongside perceptual intensification. Set and setting shape the outcome dramatically: the same dose can produce serene contemplation or acute distress depending on the user's emotional state and surroundings.[5]
Most users describe the experience as indistinguishable from LSD. Compared to psilocybin, it runs longer and carries more physical stimulation — the body feels buzzed and alert rather than sedated. The cognitive tone tends toward analytical sharpness rather than the introspective warmth typical of tryptamine psychedelics.
Effect Grid
At common doses (75–150 µg oral), the full psychedelic experience emerges: pronounced open- and closed-eye visuals including geometric patterns overlaying surfaces, colour shifting, drifting and morphing of objects, and tracers behind moving objects. Time distortion becomes significant — hours may feel like minutes or vice versa. Thought connectivity increases dramatically, often producing novel associations, personal insights, and a sense of conceptual depth. Emotional intensification is marked; music, art, and interpersonal interactions can feel profoundly meaningful.
Physically, pupil dilation is prominent. Stimulation, jaw tension (trismus), temperature dysregulation, and peripheral vasoconstriction (cold extremities) are common. Nausea is less frequent than with tryptamine psychedelics but may occur during the come-up.
Functional impairment is substantial. The experience demands 8–12 hours of commitment. Sleep is impossible during the active phase and may remain difficult for several hours after resolution.
Modeled from the effect's dose-dependence curve — not per-substance measurements.
Auditory enhancement · Depth perception distortion · Tracers · Geometry · Visual breathing · Symmetrical texture repetition · Touch enhancement · Perspective distortion · After-images · Brightness alteration · Environmental patterning · Light sensitivity · Sound sensitivity · Visual morphing · Ganzfeld effect · Sleep-transition hallucinations · Auditory distortion · Visual melting · Auditory misinterpretation · Dreaming suppression · Peripheral vision distortion · Proprioceptive distortion · Spatial disorientation · Visual diffraction · Visual haze / noise · Synesthesia · Visual acuity enhancement · Peripheral misidentification · Vestibular distortion · Visual magnification · Visual processing acceleration · Olfactory enhancement · Taste enhancement · Flashbacks · Object transformations · Visual recursion · Internal hallucinations · Object activation · Visual scenery slicing · External hallucinations · Environmental orbism / cubism · Perspective hallucinations · Auditory hallucinations · Visual flipping · Shadow people · Persisting hallucinations
Visual breathing · Symmetrical texture repetition · Touch enhancement · Perspective distortion · After-images · Brightness alteration · Environmental patterning · Light sensitivity · Sound sensitivity · Visual morphing · Ganzfeld effect · Sleep-transition hallucinations · Auditory distortion · Visual melting · Auditory misinterpretation · Dreaming suppression · Peripheral vision distortion · Proprioceptive distortion · Spatial disorientation · Visual diffraction · Visual haze / noise · Synesthesia · Visual acuity enhancement · Peripheral misidentification · Vestibular distortion · Visual magnification · Visual processing acceleration · Olfactory enhancement · Taste enhancement · Flashbacks · Object transformations · Visual recursion · Internal hallucinations · Object activation · Visual scenery slicing · External hallucinations · Environmental orbism / cubism · Perspective hallucinations · Auditory hallucinations · Visual flipping · Shadow people · Persisting hallucinations
Stimulation · Spontaneous body sensations · Appetite suppression · Insomnia · Body high · Heart rate perception changes · Physical fatigue · Muscle tension · Bodily lightness · Body schema distortion · Breathing alteration · Laughter fits · Restlessness · Tactile euphoria · Temperature dysregulation · Tingling / electric sensations · Vibrations / buzzing · Nausea · Abnormal heartbeat · Excessive sweating · Sexual arousal enhancement · Bodily heaviness · Bodily pressures · Dehydration sensation · Dizziness · Dry mouth · Kundalini-like energy · Nystagmus (eye wobbles) · Increased urination · Involuntary body movements · Bruxism · Headache · Pain enhancement · Respiratory stimulation · Trembling · Salivation · Diarrhea · Sexual arousal suppression · Watery eyes · Motor control enhancement · Yawning · Vomiting · Seizure threshold reduction · Bodily dissociation · Tactile hallucination · Phantom limb sensations
Insomnia · Body high · Heart rate perception changes · Physical fatigue · Muscle tension · Bodily lightness · Body schema distortion · Breathing alteration · Laughter fits · Restlessness · Tactile euphoria · Tingling / electric sensations · Vibrations / buzzing · Nausea · Abnormal heartbeat · Excessive sweating · Sexual arousal enhancement · Bodily heaviness · Bodily pressures · Dehydration sensation · Dizziness · Dry mouth · Kundalini-like energy · Nystagmus (eye wobbles) · Increased urination · Involuntary body movements · Bruxism · Headache · Pain enhancement · Respiratory stimulation · Trembling · Salivation · Diarrhea · Sexual arousal suppression · Watery eyes · Motor control enhancement · Yawning · Vomiting · Seizure threshold reduction · Bodily dissociation · Tactile hallucination · Phantom limb sensations
Aesthetic enhancement · Introspection enhancement · Openness enhancement · Thought connectivity · Multiple thought streams · Immersion enhancement · Cognitive euphoria · Thought acceleration · Cognitive flexibility · Increased nature relatedness · Creativity enhancement · Memory suppression · Thought disorganization · Thought loops · Cognitive fatigue · Cognitive impairment · Confusion · Synchronicity · Humor enhancement · Analysis enhancement · Cognitive dysphoria · Focus suppression · Information processing enhancement · Information processing suppression · Memory fragmentation · Memory replays · Focus enhancement · Language enhancement · Motivation enhancement · Language suppression · Motivation suppression · Memory enhancement · Delusions of sobriety · Delusions · Amnesia · Delirium
Thought connectivity · Multiple thought streams · Immersion enhancement · Cognitive euphoria · Thought acceleration · Cognitive flexibility · Increased nature relatedness · Creativity enhancement · Memory suppression · Thought disorganization · Thought loops · Cognitive fatigue · Cognitive impairment · Confusion · Synchronicity · Humor enhancement · Analysis enhancement · Cognitive dysphoria · Focus suppression · Information processing enhancement · Information processing suppression · Memory fragmentation · Memory replays · Focus enhancement · Language enhancement · Motivation enhancement · Language suppression · Motivation suppression · Memory enhancement · Delusions · Amnesia · Delirium
Euphoria · Simultaneous emotions · Anxiety · Catharsis · Dysphoria · Irritability
Dysphoria · Irritability
Social connection · Trust enhancement · Ego inflation · Automaticity · Flow state · Sociability enhancement · Communication enhancement · Communication suppression · Compulsive behavior reduction · Sociability suppression · Social disconnection · Identity alteration · Boundary dissolution · Cognitive disconnection · Ego dissolution · Telepathic feelings
Flow state · Sociability enhancement · Communication enhancement · Communication suppression · Compulsive behavior reduction · Sociability suppression · Social disconnection · Identity alteration · Boundary dissolution · Cognitive disconnection · Ego dissolution · Telepathic feelings
Time cessation
Non-dual awareness · Transpersonal memory access · Voidness · Death-rebirth sequence · Entity contact · Cessation · Near-death experience
Entity contact · Cessation · Near-death experience
Lucid dreaming enhancement · Lucidity enhancement · Mindfulness enhancement · Recursive awareness
Timeline
First alerts emerge as subtle mood shifts, mild stimulation, and a faint sense of perceptual sharpening. The prodrug deacylation step may contribute to variability in onset timing.
Effects build progressively: colours brighten, surfaces begin to drift, and thought patterns become more fluid. Mild nausea and body load may accompany the ascent. Anxiety about the intensifying experience is common.
Maximum intensity: pronounced visual distortions, geometric patterning, time distortion, thought connectivity, and emotional amplification. Ego dissolution may occur at higher doses. The dominant perceptual shift is a sense of fluid, interconnected awareness.
Effects gradually recede in waves rather than linearly. Visual intensity diminishes, cognitive clarity returns, and emotional tone often shifts toward reflective warmth. Residual stimulation and mild visual activity may persist.
Residual mood elevation, enhanced pattern recognition, and mild perceptual sensitivity may persist for hours to a full day. Sleep quality may be reduced on the night following use.
⚠ Do not drive or operate heavy machinery until after a full night of sleep following the experience.
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
Acute toxicity
No human fatalities from 1B-LSD have been reported. Computational modeling has estimated a rat oral lethal dose, with predictions suggesting blood toxicity risk among the highest in the N1-acyl series — but these are unvalidated computer predictions only.[17] safety citation needed The active compound LSD has no established lethal dose in humans.[3]
Cardiovascular effects
LSD produces mild-to-moderate increases in heart rate and blood pressure with no abnormal heart rhythm signal identified in controlled studies.[18] No 1B-LSD-specific cardiovascular data exist.
Poisoning and overdose
A documented cluster of poisonings occurred when users accidentally inhaled white powder sold as cocaine — symptoms included perceptual disturbances, rapid heart rate, and agitation, with no fatalities.[19] This illustrates contamination risk rather than the danger of intentional lysergamide use.
Psychological risks
At doses equivalent to 200 µg LSD and above, acute panic and ego dissolution become the primary limiting effects.[4] Pre-existing anxiety and emotional state at the time of use are strong predictors of a difficult experience.[5]
Persistent visual disturbances after the experience ends — geometry, after-images, halos, and trailing effects — are documented with LSD-class substances.[20] This condition, known as Hallucinogen Persisting Perception Disorder (HPPD), can last months to years; adolescent onset has been documented.[21] No 1B-LSD-specific cases have been reported.
Tolerance and dependence
Tolerance develops almost immediately after a single dose. Serotonin receptors in the frontal cortex reduce in number within 24 hours,[22] and this cross-tolerance extends to all serotonergic psychedelics.[22] Community data point to a tolerance half-life of about 6 days, with full reset in roughly 14 days.[23]
Psychedelics do not produce physical dependence or addiction.[3] Rapid tolerance limits compulsive redosing — the same dose taken the next day produces markedly diminished effects. Substance use disorder reports linked to LSD have appeared in pharmacovigilance databases, though their interpretation is methodologically limited.[24]
Drug interactions
Serotonergic combinations
Combining 1B-LSD with tramadol — which both blocks serotonin reuptake and acts on opioid receptors — creates a dangerous risk of serotonin syndrome.[25][26] safety citation needed Serotonin toxicity means muscle rigidity, high fever, rapid heart rate, and seizures — a potentially life-threatening state that requires emergency care.
CYP2D6 inhibitors
Several common drugs — including fluoxetine, paroxetine, bupropion, and haloperidol — block CYP2D6, the liver enzyme that breaks down LSD.[15] This raises LSD blood levels by roughly 1.4–1.5 times,[27] producing a stronger and longer experience than expected.
SSRIs and antidepressants
Paroxetine increased LSD blood levels while simultaneously reducing anxiety and nausea — higher drug exposure, lower distress.[27] Long-term SSRI use may separately reduce psychedelic effects by lowering serotonin receptor density over time.
Lithium
Lithium combined with LSD-class psychedelics is associated with increased seizure risk in anecdotal reports. safety citation needed No controlled study has confirmed this, but the consistency of reports warrants treating it as a potentially dangerous combination.
Cannabis
Cannabis is anecdotally reported to intensify psychedelic effects, particularly during the offset phase. No controlled study exists. citation needed
Contraindications
Personal or family history of psychotic disorders and concurrent lithium use are absolute contraindications. Relative contraindications include bipolar disorder, seizure disorders, pregnancy, tramadol use, and CYP2D6 poor metabolizer status — which substantially increases LSD exposure and may cause unexpectedly prolonged and intense effects.[15] No 1B-LSD-specific contraindication data exist; all are inferred from the LSD evidence base.
Harm Reduction[edit]
Forms & Identification
1B-LSD is distributed exclusively on blotter paper or as small pellets.[23] Visual inspection cannot confirm identity or dose — all N1-acylated LSD derivatives look identical to each other and to LSD itself.
Reagent testing narrows the field but cannot distinguish between members of this series. Quantitative analysis through a drug-checking service is the only reliable method to confirm identity and dose.
Guidelines
- Test every sample with a reagent kit before use. Send samples to a drug-checking service when available.
- Start with a low dose and wait at least 2–3 hours before considering the experience has fully developed — prodrug conversion may slow onset.
- Eat lightly several hours beforehand. Stay hydrated throughout.
- Clear all obligations for the day and the following morning. Residual effects can impair sleep.
- Keep the environment calm. Have water, blankets, familiar music, and a quiet space available.
- Avoid redosing. Tolerance develops almost immediately — a second dose within 24 hours produces markedly reduced effects and extends the experience without proportional benefit.
- Wait a minimum of 14 days between experiences to allow full tolerance reset.
Set & Setting
The psychological environment matters as much as the dose. Pre-existing anxiety, unresolved emotional distress, and unfamiliar or chaotic surroundings are the strongest predictors of difficult experiences.[5]
Choose a safe, comfortable, and familiar location. Begin only when in a stable emotional state. A trusted, sober companion — a sitter — substantially reduces the risk of panic-driven behavior during the extended experience window.
Aftercare & integration. The days following a psychedelic experience often bring lingering emotional sensitivity, altered perspective, and disrupted sleep. These aftereffects are normal and typically resolve within a week.
Journaling or discussing the experience with a trusted person can help process unusual or difficult material. If distressing thoughts, visual disturbances, or depersonalization persist beyond two weeks, consult a mental health professional experienced with psychedelic integration. Allow insights to settle naturally rather than forcing interpretation.
Recovery & Support
Psychedelics do not produce physical dependence, but patterns of repeated use to escape distress or avoid processing difficult emotions warrant attention. If psychedelic use is interfering with daily functioning, relationships, or mental health stability, professional support is appropriate.
Resources include the Fireside Project (62-FIRESIDE / 623-473-7433), MAPS integration therapist directory, and local psychedelic harm reduction organizations. For general substance use support, SAMHSA's helpline (1-800-662-4357) provides free, confidential referrals.
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Recognizing an emergency
Most difficult psychedelic experiences are distressing but not medically dangerous. Seek immediate help if the person expresses intent to harm themselves or others, loses all contact with reality and cannot be verbally redirected, experiences chest pain or seizure, or shows signs of serotonin syndrome (rigid muscles, high fever, tachycardia) after combining with other serotonergic drugs.
Immediate steps
- 1. Call emergency services if any red flag above is present.
- 2. Move the person to a quiet, low-stimulation environment.
- 3. Speak in calm, simple sentences. Reassure them that the effects are temporary and time-limited.
- 4. Do not physically restrain unless there is immediate danger of self-harm.
- 5. Do not leave them alone.
What to tell the dispatcher
State the substance name (1B-LSD), estimated dose, time of ingestion, and current symptoms. Good Samaritan laws in many jurisdictions protect callers who report a drug-related emergency from prosecution.
Legal Status[edit]
1B-LSD is not scheduled by name under most national controlled substance laws. Its structural relationship to LSD — universally controlled — places it within structural analog or blanket psychoactive substance frameworks in many countries. Germany has explicitly controlled it under novel psychoactive substance legislation since 2019.[10]
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| Germany | Controlled (NpSG) | Prohibited under Neue-psychoaktive-Stoffe-Gesetz since July 18, 2019; production, import to market, trading, and administration prohibited; possession not penalized under NpSG[10] |
| United Kingdom | Illegal (Psychoactive Substances Act 2016) | All psychoactive substances prohibited unless specifically exempted (alcohol, nicotine, caffeine, medicines); no medical exemption for 1B-LSD |
| United States | Unscheduled; Federal Analogue Act applies | Not listed in CSA schedules; as an LSD analog intended for human consumption, treated as Schedule I under the Federal Analogue Act |
| Canada | Unscheduled; analog provisions may apply | Not specifically named in CDSA; structural relationship to LSD (Schedule III) invokes potential analog classification |
| Australia | Prohibited | Lysergamides broadly covered under TGA Standard for the Uniform Scheduling of Medicines and Poisons |
citation needed
Legal status changes frequently. This information is based on web-retrieved sources and general legislative interpretation. Confirm current scheduling against official statutory documents before relying on this information.
references
- [1] ^abcHalberstadt AL, Chatha M, Klein AK, McCorvy JD, Meyer MR, Wagmann L, Stratford A, Brandt SD (2020) Pharmacological and biotransformation studies of 1-acyl-substituted derivatives of d-lysergic acid diethylamide (LSD) — Neuropharmacology doi:10.1016/j.neuropharm.2019.107856
- [2]
- [3]
- [4] ^abHolze F, Vizeli P, Müller F, Ley L, Duerig R, Varghese N, Zizzari P, Liechti ME (2021) Acute dose-dependent effects of lysergic acid diethylamide in a double-blind placebo-controlled study in healthy subjects — Neuropsychopharmacology doi:10.1038/s41386-020-00883-6
- [5] ^abcdVizeli P, Studerus E, Holze F, Schmid Y, Dolder PC, Ley L, Straumann I, Becker AM, Müller F, Arikci D, Liechti ME (2024) Pharmacological and non-pharmacological predictors of the LSD experience in healthy participants — Translational Psychiatry doi:10.1038/s41398-024-03074-9
- [6] ^Kavanagh PV, Westphal F, Pulver B, Elliott S, Stratford A (2024) Analytical and behavioral characterization of 1-dodecanoyl-LSD (1DD-LSD) — Drug Testing and Analysis doi:10.1002/dta.3691