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1V-LSD
1-pentanoyllysergic acid diethylamide
1V-LSD (1-valeroyl-lysergic acid diethylamide) — also known as Valerie — is a synthetic psychedelic of the lysergamide class. It is a prodrug for LSD, meaning the body converts it into LSD after ingestion.[1] Once converted, it activates serotonin receptors in the brain, producing the visual and cognitive shifts characteristic of classical psychedelics.[2]
1V-LSD (1-valeroyl-lysergic acid diethylamide) — also known as Valerie — is a synthetic psychedelic of the lysergamide class. It is a prodrug for LSD, converting to its parent compound after ingestion.[1] Once converted, 1V-LSD acts through LSD's 5-HT₂A receptor agonism, disrupting the brain's default filtering of sensory and cognitive input.[2]
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1V-LSD appeared on research chemical markets around 2020–2021 as the fifth in a series of closely related LSD derivatives.[3] Each compound in the series was created after Germany banned the previous one, making 1V-LSD a direct product of regulatory evasion. Germany scheduled 1V-LSD in March 2023; in most other countries it remains unscheduled but may still be illegal under structural analog laws.
Subjective effects include geometric visual patterns, color enhancement, time alteration, thought acceleration, and ego dissolution. The experience mirrors LSD — a long-arc, all-encompassing shift in perception and emotion with a characteristic electric body feel. Thought loops, anxious fixation, and difficulty sleeping through the extended tail are common unwanted effects.
1V-LSD produces no physical dependence, and LSD — its active metabolite — has no established lethal dose in humans.[4] The primary risk is psychological: high doses can trigger acute panic or psychotic breakdown, and the danger scales with dose and personal vulnerability.[2] Only one peer-reviewed study exists for this compound specifically; everything else is inferred from LSD class data.[3]
History[edit]
Discovery
LSD was synthesized in 1938, and its psychedelic effects were discovered accidentally in 1943.[4] The first N1-acyl derivative, ALD-52, was made in the 1950s and found to produce similar effects — later explained by its conversion to LSD in the body.[5]
The N1-Acyl Lysergamide Series
Starting in the mid-2010s, a succession of LSD derivatives entered the research chemical market, each extending the chemical chain by one carbon: ALD-52 → 1P-LSD → 1B-LSD → 1V-LSD → 1H-LSD.[3][6][5] Each new compound appeared after Germany banned the previous one.[3]
Market Appearance
1V-LSD entered the market around 2020–2021 and was formally characterized in 2022.[3] It was subsequently detected on blotter products in Japan.[7] Germany scheduled it in March 2023; most other jurisdictions have not specifically banned it.
The name "1V-LSD" follows the systematic convention for this compound family — "V" for valeroyl, the C5 acyl chain. The compound acquired the street name "Valerie" in research chemical circles.[3]
Chemistry[edit]
Structure
1V-LSD is a lysergamide — a chemical family built on the ergoline ring system, the same scaffold underlying LSD. It is derived from LSD by attaching a five-carbon (valeroyl) group to the molecule's indole nitrogen, making it the C5 member of the N1-acyl LSD series.[3]
This modification removes direct receptor activity, converting it into a functionally inert precursor that the body must hydrolyze to release LSD.[1]
| Molecular formula | C₂₅H₃₃N₃O₂ |
| Molecular weight | 407.5 g/mol |
Pharmacology[edit]
Mechanism of Action
1V-LSD is a prodrug for LSD. Attaching the valeroyl group blocks direct receptor activity — the compound is functionally inert until liver and blood enzymes cleave that group and release LSD.[1] No direct binding data exist for 1V-LSD itself; the prodrug model rests on converging evidence from related derivatives.[3]
After oral administration of the closely related 1P-LSD, only LSD was detected in blood and urine — the parent compound was absent.[8] The enzymes responsible for conversion include liver cytochrome P450s and plasma carboxylesterases.[9] Once LSD is released, blocking serotonin receptors completely eliminates the psychedelic experience.[2]
Pharmacokinetics
No human pharmacokinetic data exist for 1V-LSD itself.[3] Following conversion, LSD's pharmacokinetics apply: oral bioavailability of approximately 80%, peak blood levels at 1–2.5 hours, and a half-life of roughly 2.7–6.4 hours at standard doses.[10][8] People with a slow-metabolizing variant of the CYP2D6 liver enzyme experience approximately 75% higher overall LSD exposure and a longer experience.[11]
Neuroscience[edit]
Where It Acts
No neuroimaging data exist for 1V-LSD. As a prodrug for LSD, its brain effects are inferred from LSD research. LSD disrupts the default mode network — the brain system underlying self-focused thought — and this disruption correlates with ego dissolution.citation needed
Why It Matters
LSD also opens the brain's sensory filters, flooding the cortex with signals normally suppressed, producing the visual intensification and sensory overload characteristic of the experience.citation needed It can also promote structural changes in brain connections, including direct binding to a growth-promoting receptor with roughly 1,000 times the affinity of conventional antidepressants.[12]
Whether 1V-LSD itself crosses into the brain or requires peripheral conversion first remains unknown. The CYP2D6 genetic variant that causes 75% higher LSD exposure[11] predicts stronger and longer brain effects, but this has not been tested with neuroimaging. No neuroimaging data exist for any N1-acyl LSD derivative.
Subjective Effects[edit]
The 1V-LSD experience follows the LSD template — a slow-building, all-encompassing shift in perception, cognition, and emotion with high sensitivity to context and setting. Onset may be slightly more gradual than LSD directly, plausibly reflecting the hydrolysis step, though this has not been confirmed.[3]
Compared to psilocybin, the experience is longer, more stimulating, and more visually structured at equivalent subjective intensity. Relative to LSD administered directly, no qualitative differences have been established — the prodrug model predicts pharmacological equivalence once conversion is complete.[8]
1V-LSD appeared on the research chemical market around 2020–2021 as the fifth in a homologous series of N1-acyl LSD derivatives.[3] Each compound in the series emerged after its predecessor was banned in Germany, making 1V-LSD a product of iterative regulatory evasion. Germany scheduled the compound in March 2023; in most other jurisdictions it remains in a legal grey area, subject to structural analog legislation.
Subjective effects include geometric visual patterns, color enhancement, time alteration, thought acceleration, and ego dissolution. The experience mirrors LSD — a slow-building, all-encompassing alteration of perception, cognition, and emotion, with a characteristic somatic electricity that distinguishes the lysergamide body feel from tryptamine sedation. Thought loops, anxious fixation, and difficulty sleeping through the extended tail are common unsought effects.
1V-LSD produces no physical dependence, and LSD — its active metabolite — has no established lethal dose in humans.[4] The primary risk is psychological: high doses can trigger acute panic and psychotic decompensation in predisposed individuals, with intensity scaling by dose and vulnerability to setting.[2] Only one peer-reviewed study exists specifically for this compound; all safety characterizations rest on LSD class data and structural analogy.[3]
History[edit]
Discovery
LSD was synthesized by Albert Hofmann at Sandoz Laboratories in 1938; its psychedelic properties emerged during accidental self-exposure on April 19, 1943.[4] The first N1-acyl derivative, ALD-52 (1-acetyl-LSD), was synthesized at Sandoz in the 1950s by Stoll and coworkers.[5] ALD-52 produced psychedelic effects similar to LSD — an observation later explained by prodrug hydrolysis rather than direct receptor activity.
The N1-Acyl Lysergamide Series
Starting in the mid-2010s, a succession of N1-acyl LSD derivatives entered the online research chemical market, each extending the acyl chain by one carbon: ALD-52 (C2) → 1P-LSD (C3) → 1B-LSD (C4) → 1V-LSD (C5) → 1H-LSD (C6) → 1DD-LSD (C12).[3][6][5] Each new compound appeared after Germany's NpSG scheduled its predecessor, with vendors pivoting to the next unscheduled homolog. The series was systematically characterized in the "Return of the Lysergamides" publications by Brandt, Kavanagh, Halberstadt, and collaborators.[7][8][9][10][3]
Market Appearance
1V-LSD entered the market around 2020–2021 and was analytically characterized in 2022 as Part VII of that series.[3] The compound was subsequently detected in blotter products in Japan, marking the first identification of multi-position-modified LSD analogs in Japanese drug markets.[11] A validated forensic detection method was developed, though no positive specimens were found among 325 urine samples tested.[12]
The name "1V-LSD" follows the systematic convention for N1-acyl LSD derivatives, where the prefix denotes the acyl chain — "V" for valeroyl (pentanoyl, C5). The compound acquired the street name "Valerie" within the research chemical community.[3]
Chemistry[edit]
Structure
1V-LSD belongs to the lysergamide family — ergoline alkaloids built on the tetracyclic indole-fused quinoline ring system of lysergic acid. The compound is derived from LSD by attaching a pentanoyl (valeroyl, C₅H₉O) group to the N1 indole nitrogen, making it the C5 member of the N1-acyl LSD series.[3]
The molecule retains the diethylamide group at C9 and the N6-methyl group characteristic of active d-lysergamides. Its (6aR,9R) configuration corresponds to the dextrorotatory series — the biologically active form. The l-lysergamide epimer is pharmacologically inactive; epimerization under basic or thermal conditions is a known degradation pathway.citation needed
| Molecular formula | C₂₅H₃₃N₃O₂ |
| Molecular weight | 407.5 g/mol |
Stability and Handling
No published data on melting point, solubility, or crystalline form exist for 1V-LSD. By analogy with related N1-acyl derivatives, the compound is susceptible to hydrolysis under acidic conditions and in alcoholic solvents.[13][14] The pentanoyl group may offer greater steric protection of the N1-acyl bond than the shorter acetyl group of ALD-52.[14]
Methanol extraction causes artifact conversion of N1-acyl LSD derivatives to LSD, complicating forensic identification.[14] No academic synthesis paper has been published; the compound is presumed to be synthesized from d-LSD via acylation with valeric anhydride or valeryl chloride.
Structure-Activity Relationships
1V-LSD sits in a homologous series where each derivative extends the N1-acyl chain by one carbon. Across the series, N1-acylation reduces receptor affinity by 1–2 orders of magnitude relative to LSD, converting each compound from an active psychedelic to a functionally inert precursor that requires hydrolysis to liberate LSD.[1] The longer the acyl chain, the greater the steric bulk shielding the N1 position — a factor that may influence both hydrolysis rate and chemical stability.
Pharmacology[edit]
Mechanism of Action
1V-LSD functions as a prodrug for LSD. N1-acyl substitution eliminates direct receptor activity, converting the compound to a functionally inert precursor that must be hydrolyzed in the body to release LSD.[1] No direct binding or biotransformation data have been published for 1V-LSD itself; the prodrug hypothesis rests on converging evidence from structurally related derivatives.[3]
The evidence for prodrug conversion across the N1-acyl class is strong. Incubation of 1CP-LSD with human serum produces LSD.[10] After oral administration of 100 µg 1P-LSD to two volunteers, only LSD was detected in blood and urine — not 1P-LSD itself — with LSD bioavailability "close to 100%".[15] Similar conversion has been confirmed for 1F-LSD and 1T-LSD in mice.[16] The enzymes responsible include liver cytochrome P450s and plasma carboxylesterases,[17] though the specific enzymes that hydrolyze 1V-LSD have not been identified.
In the mouse head-twitch response assay — a 5-HT₂A-mediated behavior validated as a predictor of hallucinogenic potency in humans[18] — 1V-LSD showed an ED₅₀ of 373 nmol/kg, roughly one-third the potency of LSD (ED₅₀ = 132.8 nmol/kg).[3] The reduced potency likely reflects incomplete hydrolysis rather than direct receptor activity.[3]
Once liberated, LSD acts primarily as a partial agonist at the 5-HT₂A receptor. The 5-HT₂A antagonist ketanserin completely blocks all subjective LSD effects at 40 mg,[2] confirming that this receptor is both necessary and sufficient for the psychedelic experience.
Pharmacokinetics
No human or animal pharmacokinetic data have been published for 1V-LSD itself.[3] Following prodrug conversion, LSD pharmacokinetics apply.
LSD oral bioavailability is approximately 80%, with base and tartrate formulations performing equivalently.[19] Peak plasma levels are reached 1–2.5 hours after ingestion. Half-life ranges from approximately 2.7 hours at microdoses to 5.7–6.4 hours at 100 µg,[15] and extends up to 11.6 hours in individuals who are slow CYP2D6 metabolizers.[20] Slow metabolizers experience approximately 75% higher overall LSD exposure and prolonged subjective effects.[20]
The primary urinary metabolite of LSD is 2-oxo-3-hydroxy-LSD.[21] LSD is detectable in urine for approximately 80 hours after a 100 µg dose. By analogy with 1P-LSD — where the parent compound was detectable in serum for only about 4 hours post-dose[15] — 1V-LSD itself is expected to have a short plasma half-life, with LSD as the principal circulating active species.
Neuroscience[edit]
Where It Acts
No direct neuroimaging data exist for 1V-LSD. As a prodrug for LSD, its neural effects are inferred from LSD research. LSD disrupts the default mode network (DMN) — the brain system underlying self-referential thought — and reduced DMN connectivity correlates directly with the experience of ego dissolution.citation needed Simultaneously, LSD opens thalamocortical gating, the brain's sensory filter, flooding the cortex with information normally suppressed and producing the visual intensification and sensory overload characteristic of the experience.citation needed
LSD also increases global functional connectivity: brain regions that normally communicate weakly begin exchanging information freely, accompanied by increased neural entropy — greater randomness in neural signaling that maps to loosened conceptual boundaries and novel associations.citation needed
Why It Matters
The REBUS (Relaxed Beliefs Under Psychedelics) model offers the most comprehensive framework: LSD relaxes the brain's confidence in its existing models of reality, allowing raw sensory data to override established expectations.citation needed This accounts for visual distortions, ego dissolution, and emotional lability across dose ranges.
LSD also promotes structural neuroplasticity through two independent pathways — classical 5-HT₂A signaling that drives dendritic growth, and direct binding to the TrkB receptor with approximately 1,000-fold higher affinity than conventional antidepressants.[22] Whether 1V-LSD drives neuroplasticity at the same magnitude depends on the completeness of prodrug conversion.
Whether 1V-LSD itself crosses the blood-brain barrier or requires peripheral hydrolysis before entering the brain remains unknown — the answer would affect onset timing and potentially the neuroplasticity profile.
Subjective Effects[edit]
The 1V-LSD experience is shaped as much by psychological preparation and physical environment as by pharmacology. As a prodrug for LSD, its subjective character is that of its parent — a long-arc serotonergic state with high sensitivity to mindset, social context, and sensory input. Onset may be slightly more gradual than LSD administered directly, plausibly reflecting the hydrolysis step, though this has not been confirmed in controlled settings.[3] The experience shifts qualitatively across the dose range: low doses sharpen sensory detail and elevate mood, moderate doses restructure visual and cognitive fields, and high doses dissolve the boundary between self and environment.
Compared to psilocybin, the experience is longer, more stimulating, and more visually structured at equivalent subjective intensity. Relative to LSD administered directly, no qualitative differences have been established — the prodrug hypothesis predicts pharmacological equivalence once hydrolysis is complete.[15]
Effect Grid
At common doses, the full psychedelic experience manifests: pronounced open- and closed-eye visuals including geometric patterning overlaying surfaces, colour shifting, drifting and morphing of objects, and tracers behind moving objects. Time distortion becomes significant — minutes may feel like hours. Thought acceleration and thought connectivity increase dramatically, often producing novel conceptual associations. Emotional intensification is marked; music, nature, and social interactions can feel profoundly meaningful. Ego dissolution begins to emerge at the upper end of this range.
Physically, stimulation is moderate to strong. Jaw tension (trismus), temperature dysregulation, peripheral vasoconstriction producing cold extremities, and difficulty urinating are common. Nausea is less frequent than with tryptamine psychedelics but can occur during the come-up.
Sleep is impossible for 8–10 hours. This is a full-day commitment requiring a cleared schedule and a safe, comfortable environment.
Modeled from the effect's dose-dependence curve — not per-substance measurements.
Auditory enhancement · Visual drifting · Music enhancement · Environmental patterning · Visual breathing · Symmetrical texture repetition · Tracers · Perspective distortion · Depth perception distortion · Brightness alteration · Light sensitivity · Peripheral vision distortion · Sound sensitivity · Visual morphing · Auditory distortion · Touch enhancement · After-images · Proprioceptive distortion · Spatial disorientation · Vestibular distortion · Visual diffraction · Visual melting · Visual acuity enhancement · Synesthesia · Auditory misinterpretation · Ganzfeld effect · Peripheral misidentification · Sleep-transition hallucinations · Visual haze / noise · Visual processing acceleration · Dreaming suppression · Visual magnification · Olfactory enhancement · Taste enhancement · Flashbacks · Object transformations · Internal hallucinations · Object activation · Visual recursion · Auditory hallucinations · External hallucinations · Environmental orbism / cubism · Perspective hallucinations · Visual scenery slicing · Visual flipping · Persisting hallucinations · Shadow people · Visual processing suppression
Visual breathing · Symmetrical texture repetition · Tracers · Perspective distortion · Depth perception distortion · Brightness alteration · Light sensitivity · Peripheral vision distortion · Sound sensitivity · Visual morphing · Auditory distortion · Touch enhancement · After-images · Proprioceptive distortion · Spatial disorientation · Vestibular distortion · Visual diffraction · Visual melting · Visual acuity enhancement · Synesthesia · Auditory misinterpretation · Ganzfeld effect · Peripheral misidentification · Sleep-transition hallucinations · Visual haze / noise · Visual processing acceleration · Dreaming suppression · Visual magnification · Olfactory enhancement · Taste enhancement · Flashbacks · Object transformations · Internal hallucinations · Object activation · Visual recursion · Auditory hallucinations · External hallucinations · Environmental orbism / cubism · Perspective hallucinations · Visual scenery slicing · Visual flipping · Persisting hallucinations · Shadow people · Visual processing suppression
Stimulation · Spontaneous body sensations · Body high · Insomnia · Muscle tension · Heart rate perception changes · Appetite suppression · Excessive sweating · Bodily lightness · Body schema distortion · Laughter fits · Physical fatigue · Restlessness · Tactile euphoria · Tingling / electric sensations · Vibrations / buzzing · Nausea · Sexual arousal enhancement · Breathing alteration · Dizziness · Dry mouth · Temperature dysregulation · Abnormal heartbeat · Involuntary body movements · Bodily pressures · Dehydration sensation · Headache · Nystagmus (eye wobbles) · Trembling · Salivation · Increased urination · Bruxism · Pain suppression · Respiratory stimulation · Sexual arousal suppression · Watery eyes · Yawning · Vomiting · Motor control enhancement · Seizure threshold reduction · Bodily dissociation · Tactile hallucination
Insomnia · Muscle tension · Heart rate perception changes · Appetite suppression · Excessive sweating · Bodily lightness · Body schema distortion · Laughter fits · Physical fatigue · Restlessness · Tactile euphoria · Tingling / electric sensations · Vibrations / buzzing · Nausea · Sexual arousal enhancement · Breathing alteration · Dizziness · Dry mouth · Abnormal heartbeat · Involuntary body movements · Bodily pressures · Dehydration sensation · Headache · Nystagmus (eye wobbles) · Trembling · Salivation · Increased urination · Bruxism · Pain suppression · Respiratory stimulation · Sexual arousal suppression · Watery eyes · Yawning · Vomiting · Motor control enhancement · Seizure threshold reduction · Bodily dissociation · Tactile hallucination
Cognitive flexibility · Introspection enhancement · Openness enhancement · Thought connectivity · Immersion enhancement · Cognitive euphoria · Multiple thought streams · Thought acceleration · Pattern recognition enhancement · Focus suppression · Increased nature relatedness · Creativity enhancement · Memory suppression · Thought loops · Memory replays · Humor enhancement · Analysis enhancement · Thought disorganization · Cognitive fatigue · Cognitive impairment · Confusion · Information processing enhancement · Memory fragmentation · Synchronicity · Focus enhancement · Language enhancement · Cognitive dysphoria · Information processing suppression · Motivation suppression · Motivation enhancement · Analysis suppression · Memory enhancement · Thought organization · Delusions · Amnesia · Delirium
Thought connectivity · Immersion enhancement · Cognitive euphoria · Multiple thought streams · Thought acceleration · Pattern recognition enhancement · Focus suppression · Increased nature relatedness · Creativity enhancement · Memory suppression · Thought loops · Memory replays · Humor enhancement · Analysis enhancement · Thought disorganization · Cognitive fatigue · Cognitive impairment · Confusion · Information processing enhancement · Memory fragmentation · Synchronicity · Focus enhancement · Language enhancement · Cognitive dysphoria · Information processing suppression · Motivation suppression · Motivation enhancement · Analysis suppression · Memory enhancement · Thought organization · Amnesia · Delirium
Euphoria · Simultaneous emotions · Catharsis · Empathy enhancement · Dysphoria · Irritability · Anxiety suppression · Anhedonia · Emotional suppression
Dysphoria · Irritability · Anxiety suppression · Anhedonia · Emotional suppression
Social connection · Trust enhancement · Sociability enhancement · Communication enhancement · Flow state · Ego inflation · Automaticity · Communication suppression · Compulsive behavior reduction · Sociability suppression · Social disconnection · Self-control enhancement · Boundary dissolution · Identity alteration · Ego dissolution · Cognitive disconnection · Telepathic feelings
Flow state · Ego inflation · Automaticity · Communication suppression · Compulsive behavior reduction · Sociability suppression · Social disconnection · Self-control enhancement · Boundary dissolution · Identity alteration · Ego dissolution · Cognitive disconnection · Telepathic feelings
Time cessation
Non-dual awareness · Transpersonal memory access · Death-rebirth sequence · Entity contact · Voidness
Voidness
Anticipatory response · Mindfulness enhancement · Lucidity enhancement · Lucid dreaming enhancement · Recursive awareness
Recursive awareness
Timeline
First alerts emerge as a subtle shift in sensory texture — colours may appear slightly brighter, a faint body buzz develops. The prodrug hydrolysis step may contribute to slightly variable onset timing.
Effects build steadily with increasing visual distortion, rising stimulation, and growing cognitive fluidity. Mild nausea or abdominal discomfort may occur during this phase. Anxiety can spike as intensity accelerates — this is transient.
Maximum intensity sustained for several hours. Visual hallucinations, time distortion, ego dissolution, and emotional intensification are at their strongest. Cognitive patterns shift toward associative, non-linear thinking.
Intensity remains substantial but has clearly receded from the peak. Visual effects persist with reduced immersiveness. Emotional depth and reflective thought continue.
A gradual return toward baseline. Residual visual shimmer and mild thought loosening persist. Physical tension releases.
Subtle mood elevation, enhanced emotional receptivity, and residual cognitive openness may persist for hours to a full day. Sleep quality may be reduced the first night.
⚠ Do not drive or operate heavy machinery until after a full night of sleep following the experience.
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
Acute Toxicity
LSD has extremely low acute toxicity. No well-documented human fatalities from LSD alone have been reported,[4] and the therapeutic index is estimated to be very high.[13] No case reports of 1V-LSD adverse events or overdose have been identified.
Cardiovascular Effects
LSD moderately increases blood pressure and heart rate.[2] As an ergoline alkaloid, it has vasoconstrictive properties, though clinically significant effects at psychoactive doses are rarely reported.[4]
Psychological Risks
At 200 µg, LSD produced significant anxiety even in healthy volunteers in controlled settings.[2] Positive effects plateau around 100 µg while ego dissolution and anxiety continue to increase with dose.[2] Individuals with a personal or family history of psychotic disorders face elevated risk of acute and potentially prolonged psychotic episodes.
Some people experience persistent visual disturbances after the drug clears — patterns, halos, or after-images that return unexpectedly. LSD is the most frequently implicated substance in such reports,[14][15][16] with prevalence ranging from up to 39.7% for brief mild effects to 4.3% for persistent symptoms with functional impairment.[16] Clonazepam or lamotrigine may help; antipsychotics do not.[14]
Tolerance & Dependence
Tolerance develops within hours of a single dose through serotonin downregulation.[4] This tolerance is shared with psilocybin, mescaline, and other serotonergic psychedelics.[4] Full reset takes approximately 14 days.citation needed
No physical dependence has been documented for LSD in humans.[4] Psychological dependence is rare. A meta-analysis of psychedelic clinical trials found no association between psychedelics and higher discontinuation rates.[17]
Drug Interactions
Tramadol: Classified as dangerous.safety citation needed Tramadol combines weak opioid activity with serotonin reuptake inhibitor. Combining it with 1V-LSD raises the risk of serotonin syndrome — a potentially life-threatening overheating and seizure response — and lowers the seizure threshold.
MAOIs: Combining MAOIs with 1V-LSD amplifies and prolongs effects by blocking serotonin breakdown, and raises the risk of serotonin syndrome.
SSRIs/SNRIs: May reduce psychedelic effects through receptor competition. At high SSRI doses combined with serotonergic psychedelics, serotonin syndrome risk increases.
Lithium: Anecdotal reports link LSD + lithium to seizures and cardiac events.safety citation needed This combination is flagged as high-risk in harm reduction literature.
CYP2D6 inhibitors: Fluoxetine, paroxetine, and bupropion may increase LSD exposure following 1V-LSD conversion by slowing the primary metabolic clearance pathway.[11]
Cannabis: The interaction is not well characterized. THC may enhance psychedelic effects through shared signaling pathways.citation needed Practical significance with 1V-LSD is unstudied.
Contraindications
6 knownPsychotic disorders: Personal or family history of schizophrenia, schizoaffective disorder, or other psychotic illness is an absolute contraindication. LSD-class compounds can trigger acute psychotic episodes and may accelerate onset in predisposed individuals.
Bipolar disorder: Relative contraindication. Psychedelics may trigger manic or mixed episodes, particularly in unmedicated individuals.
Lithium use: Absolute contraindication due to reports of seizures and cardiac events.safety citation needed
Epilepsy: Relative contraindication. Seizure threshold effects from serotonergic psychedelics are pharmacologically plausible but poorly documented.
Pregnancy: Absolute contraindication. No reproductive toxicity data exist for 1V-LSD. The risk-benefit ratio is categorically unfavorable.
Severe cardiovascular disease: Relative contraindication. LSD's stimulant and vasoconstrictive effects pose theoretical risk in individuals with severe high blood pressure, coronary artery disease, or irregular heart rhythms.
Harm Reduction[edit]
Forms & Identification
1V-LSD circulates almost exclusively on blotter paper, though pellets and liquid solutions also appear. The compound is invisible, tasteless, and odorless on blotter, making visual identification impossible. Reagent testing confirms the presence of a lysergamide but cannot distinguish 1V-LSD from LSD or 1P-LSD. Where available, quantitative analysis through a drug checking service is the only reliable way to confirm identity and dose.
Guidelines
- Test every batch with a reagent kit before use
- Start with a low dose and wait at least 2.5 hours before concluding effects are fully developed — the prodrug hydrolysis step may delay onset
- Choose a safe, comfortable environment with no obligations for 12+ hours
- Arrange a sober sitter, especially for first experiences or higher doses
- Eat a light meal 2–3 hours beforehand; avoid heavy food close to dosing
- Clear the following day — residual effects and fatigue are common
- Keep water, fruit, and comfort items accessible
- Avoid combining with other substances, particularly on first use
Set & Setting
The psychedelic state produced by 1V-LSD is highly sensitive to context. Psychological preparation and physical environment shape the experience as powerfully as dose. A calm, familiar space with trusted company is the strongest single protective factor against adverse psychological reactions. First experiences should involve a sober sitter — someone who remains unimpaired throughout and can provide grounding if distress arises.
Aftercare & integration. The days following a psychedelic experience are as important as the experience itself. Sleep may be disrupted the first night; prioritize rest the following day. Physical recovery is straightforward — hydration, nutrition, and light activity.
Insights or difficult emotions encountered during the experience often surface again afterward. Journaling within 24 hours preserves details for later reflection. If distressing symptoms — persistent anxiety, visual disturbances, or difficulty distinguishing thoughts from reality — last more than a few days, seek professional support.
Recovery & Support
Classical psychedelics like 1V-LSD carry low physical dependence liability, but patterns of problematic use can develop — particularly when psychedelics are used to avoid difficult emotions rather than engage with them. If use is interfering with daily functioning, relationships, or mental health, support is available. Psychedelic-informed therapists can address underlying patterns without stigma.
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Most difficult psychedelic experiences — anxiety, confusion, thought loops — are uncomfortable but not medically dangerous. They resolve as the drug wears off. Recognizing the difference between distress and emergency is critical.
Seek immediate medical help if:
- The person talks about harming themselves or others
- They are completely unresponsive or disconnected from reality
- Seizures occur
- Chest pain, severe headache, or loss of consciousness develops
While waiting for help:
- Move the person to a quiet, low-stimulation space
- Speak calmly and simply — remind them they have taken a drug and the effects will end
- Do not restrain unless there is immediate danger of self-harm
- Do not give other substances to "counteract" the experience
What to tell the dispatcher: Name the substance (1V-LSD or LSD prodrug), approximate dose, time of ingestion, and current symptoms. In many jurisdictions, Good Samaritan laws protect people who call for help during a drug-related emergency.
Legal Status[edit]
1V-LSD occupies a legal grey area in most jurisdictions. It is not specifically scheduled in most countries, but its structural relationship to LSD — a universally controlled substance — exposes it to structural analog legislation and blanket psychoactive substance bans. Germany is the sole jurisdiction with a substance-specific legislative history.
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| Germany | Banned under NpSG (March 2023) | An initial amendment in September 2022 targeting 1V-LSD failed due to a punctuation error in the legislative text. A corrected amendment was enacted in March 2023, definitively scheduling the compound.[18] |
| United Kingdom | Prohibited (Psychoactive Substances Act 2016) | The blanket ban covers all substances capable of producing a psychoactive effect, with limited exemptions. 1V-LSD falls within this prohibition.[19] |
| United States | Not specifically scheduled | LSD is Schedule I under the Controlled Substances Act. 1V-LSD is not explicitly listed but may be prosecuted under the Federal Analogue Act (21 U.S.C. § 813), which treats substances substantially similar to Schedule I drugs as Schedule I when intended for human consumption.[19] |
| Canada | Not specifically listed | LSD is Schedule III under the CDSA. 1V-LSD is not individually scheduled; structurally related compounds may be treated analogously.[19] |
| Australia | Likely prohibited as LSD analog | Lysergamide derivatives are broadly controlled. 1V-LSD is likely prohibited as an analog under existing import and scheduling regulations.[19] |
Analog and Prodrug Considerations
The prodrug relationship between 1V-LSD and LSD complicates legal classification. In jurisdictions with analog legislation — notably the US Federal Analogue Act — the case that 1V-LSD is "substantially similar" to LSD is straightforward: it is designed to produce LSD in the body. Analog act prosecutions still require proof of intent for human consumption and are applied case-by-case.
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
Acute Toxicity
LSD has extremely low acute toxicity. No well-documented human fatalities from LSD alone have been reported,[4] and the therapeutic index is estimated to be very high.[23] No published case reports of 1V-LSD adverse events or overdose have been identified.
An intoxication case involving 1P-LSD found LSD in serum and urine with the parent compound undetected, consistent with complete prodrug conversion.[13]
Cardiovascular Effects
LSD moderately increases blood pressure and heart rate.[2] As an ergoline alkaloid, it has vasoconstrictive properties, though clinically significant vasoconstriction at psychoactive doses is rarely reported outside high-dose or combined-drug scenarios.[4]
Psychological Risks
In controlled settings, 200 µg LSD produced significant anxiety in healthy volunteers.[2] Positive effects plateau around 100 µg while ego dissolution and anxiety continue to increase with dose.[2] Uncontrolled settings amplify the risk of adverse reactions.
Hallucinogen persisting perception disorder (HPPD) is a rare condition in which perceptual disturbances re-emerge after the drug has cleared.[24][25] LSD is the most frequently implicated substance in HPPD case reports.[26] Prevalence estimates range from up to 39.7% for brief, mild disturbances to 4.3% for persistent symptoms with functional impairment.[25] Treatment options include clonazepam or lamotrigine; antipsychotics are generally ineffective.[26]
Individuals with personal or family history of psychotic disorders are at elevated risk for acute and potentially prolonged psychotic episodes following exposure to LSD-class compounds. This risk applies to 1V-LSD by class inference.
Tolerance & Dependence
Rapid tolerance develops within hours of a single dose through 5-HT₂A downregulation.[4] Cross-tolerance is well-established among LSD, psilocybin, mescaline, and other serotonergic psychedelics.[4] Full tolerance reset requires approximately 14 days.citation needed
No physical dependence has been documented for LSD in humans.[4] Psychological dependence is rare. A meta-analysis of psychedelic clinical trials found no association between psychedelics and higher discontinuation rates.[27]
Drug Interactions
Tramadol: Classified as dangerous.safety citation needed Tramadol combines weak opioid activity with serotonin reuptake inhibitor. Co-administration with LSD (following 1V-LSD conversion) raises the risk of serotonin syndrome and lowers the seizure threshold.
MAOIs: Risk of serotonin syndrome; may also potentiate and prolong LSD effects by inhibiting serotonin metabolism.
SSRIs/SNRIs: May blunt psychedelic effects through receptor-level competition. At high SSRI doses combined with serotonergic psychedelics, serotonin syndrome risk increases.
Lithium: Anecdotal reports associate LSD + lithium with seizures and cardiac events.safety citation needed The combination is flagged as high-risk in harm reduction literature.
CYP2D6 inhibitors: Fluoxetine, paroxetine, and bupropion may increase LSD exposure following 1V-LSD conversion by inhibiting the primary metabolic clearance pathway.[20]
Cannabis: Interaction not well characterized. Preliminary evidence suggests THC may enhance psychedelic effects through 5-HT₂A signaling modulation.citation needed Practical significance with 1V-LSD is unstudied.
Contraindications
6 knownPsychotic disorders: Personal or family history of schizophrenia, schizoaffective disorder, or other psychotic illness is an absolute contraindication. LSD-class compounds can precipitate acute psychotic episodes and may accelerate onset in predisposed individuals.
Bipolar disorder: Relative contraindication. Psychedelic-induced mood destabilization may trigger manic or mixed episodes, particularly in unmedicated individuals.
Lithium use: Absolute contraindication due to reports of seizures and cardiac events.safety citation needed
Epilepsy: Relative contraindication. Seizure threshold modulation by serotonergic psychedelics is pharmacologically plausible but poorly documented.
Pregnancy: Absolute contraindication. No reproductive toxicity data exist for 1V-LSD. The risk-benefit ratio is categorically unfavorable.
Severe cardiovascular disease: Relative contraindication. LSD's sympathomimetic and vasoconstrictive effects pose theoretical risk in individuals with severe high blood pressure, coronary artery disease, or irregular heart rhythms.
Harm Reduction[edit]
Forms & Identification
1V-LSD circulates almost exclusively on blotter paper, though pellets and liquid solutions also appear. Doses are measured in micrograms — the compound is invisible, tasteless, and odorless on blotter, making visual identification impossible. Reagent testing can confirm the presence of a lysergamide but cannot distinguish 1V-LSD from LSD, 1P-LSD, or other members of the series. Where available, quantitative analysis through a drug checking service is the only reliable way to confirm identity and dose.
Guidelines
- Test every batch with a reagent kit before use
- Start with a low dose and wait at least 2.5 hours before concluding effects are fully developed — the prodrug hydrolysis step may delay onset
- Choose a safe, comfortable environment with no obligations for 12+ hours
- Arrange a sober sitter, especially for first experiences or higher doses
- Eat a light meal 2–3 hours beforehand; avoid heavy food close to dosing
- Clear the following day — residual effects and fatigue are common
- Keep water, fruit, and comfort items accessible
- Avoid combining with other substances, particularly on first use
Set & Setting
The psychedelic state produced by 1V-LSD is highly sensitive to context. Psychological preparation (set) and physical environment (setting) shape the experience as powerfully as dose. A calm, familiar space with trusted company is the strongest single protective factor against adverse psychological reactions. First experiences should involve a sober sitter — someone who remains unimpaired throughout and can provide grounding if distress arises.
Aftercare & integration. The days following a psychedelic experience are as important as the experience itself. Sleep may be disrupted the first night; prioritize rest the following day. Physical recovery is straightforward — hydration, nutrition, and light activity.
Insights or difficult emotions encountered during the experience often surface repeatedly afterward. Journaling within 24 hours, while details remain vivid, preserves material for later reflection. Talking with a trusted friend or an integration-focused therapist can help contextualize challenging experiences. If distressing symptoms — persistent anxiety, visual disturbances, or difficulty distinguishing thoughts from reality — last more than a few days, seek professional support.
Recovery & Support
Classical psychedelics like 1V-LSD carry low physical dependence liability, but patterns of problematic use can develop — particularly when psychedelics are used to avoid processing difficult emotions rather than to engage with them. If use is interfering with daily functioning, relationships, or mental health, support is available. Psychedelic-informed therapists can address underlying patterns without stigma, and peer-led integration circles offer structured environments for working through difficult experiences.
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Most difficult psychedelic experiences — anxiety, confusion, thought loops — are uncomfortable but not medically dangerous. They resolve as the drug wears off. Recognizing the difference between distress and emergency is critical.
Seek immediate medical help if:
- The person talks about harming themselves or others
- They are completely unresponsive or disconnected from reality
- Seizures occur
- Chest pain, severe headache, or loss of consciousness develops
While waiting for help:
- Move the person to a quiet, low-stimulation space
- Speak calmly and simply — remind them they have taken a drug and the effects will end
- Do not restrain unless there is immediate danger of self-harm
- Do not give other substances to "counteract" the experience
What to tell the dispatcher: Name the substance (1V-LSD or LSD prodrug), approximate dose, time of ingestion, and current symptoms. In many jurisdictions, Good Samaritan laws protect people who call for help during a drug-related emergency.
Legal Status[edit]
1V-LSD occupies a legal grey area in most jurisdictions. It is not specifically scheduled in most countries, but its structural relationship to LSD — a universally controlled substance — exposes it to structural analog legislation and blanket psychoactive substance bans. Germany is the sole jurisdiction with a substance-specific legislative history.
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| Germany | Banned under NpSG (March 2023) | An initial amendment in September 2022 targeting 1V-LSD failed due to a punctuation error in the legislative text. A corrected amendment was enacted in March 2023, definitively scheduling the compound.[28] |
| United Kingdom | Prohibited (Psychoactive Substances Act 2016) | The blanket ban covers all substances capable of producing a psychoactive effect, with limited exemptions. 1V-LSD falls within this prohibition.[29] |
| United States | Not specifically scheduled | LSD is Schedule I under the Controlled Substances Act. 1V-LSD is not explicitly listed but may be prosecuted under the Federal Analogue Act (21 U.S.C. § 813), which treats substances substantially similar to Schedule I drugs as Schedule I when intended for human consumption.[29] |
| Canada | Not specifically listed | LSD is Schedule III under the CDSA. 1V-LSD is not individually scheduled; structurally related compounds may be treated analogously.[29] |
| Australia | Likely prohibited as LSD analog | Lysergamide derivatives are broadly controlled. 1V-LSD is likely prohibited as an analog under existing import and scheduling regulations.[29] |
Analog and Prodrug Considerations
The prodrug relationship between 1V-LSD and LSD complicates legal classification. In jurisdictions with analog legislation — notably the US Federal Analogue Act — the argument that 1V-LSD is "substantially similar" to LSD in both structure and pharmacological effect is straightforward: the compound is designed to produce LSD in the body. However, analog act prosecutions require proof of intent for human consumption and are applied case-by-case.
The German legislative history illustrates the regulatory challenge posed by structurally iterative designer drug development. Each scheduling action prompted a market pivot to the next unscheduled homolog in the series.
Frequently asked questions
What is 1V-LSD?
1V-LSD is a synthetic N1-acyl lysergamide that functions as a prodrug for LSD, first appearing on research-chemical markets around 2020–2021. It requires in vivo hydrolysis of its pentanoyl group to liberate LSD, producing equivalent serotonergic psychedelic effects at microgram doses.
How long does 1V-LSD last?
Total duration by route of administration — Oral: 8 – 12 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 1V-LSD?
Psychedex publishes a dosage table for 1V-LSD 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 1V-LSD?
The highest-severity documented interactions for 1V-LSD: 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 1V-LSD addictive?
Psychedex records tolerance and dependence data rather than a yes/no rating. Recorded tolerance indicators for 1V-LSD: tolerance builds rapid; full reset takes 14 days; cross-tolerance develops with LSD, psilocybin, mescaline, DMT, 2C-B. 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] ^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]
- [5] ^abKavanagh 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
- [6] ^Brandt SD, Kavanagh PV, Gare S, Stratford A, Halberstadt AL (2024) Analytical and behavioral characterization of 1-hexanoyl-LSD (1H-LSD) — Drug Testing and Analysis doi:10.1002/dta.3767
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]
- [5] ^abKavanagh 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
- [6] ^Brandt SD, Kavanagh PV, Gare S, Stratford A, Halberstadt AL (2024) Analytical and behavioral characterization of 1-hexanoyl-LSD (1H-LSD) — Drug Testing and Analysis doi:10.1002/dta.3767