1cP-LSD
1-cyclopropanoyl-lysergic acid diethylamide
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1cP-LSD (1-cyclopropanoyl-lysergic acid diethylamide) is a synthetic psychedelic of the lysergamide class. It is a prodrug of LSD — the body converts it into LSD after ingestion. Once converted, it activates serotonin receptors in the brain, producing the visual and cognitive shifts characteristic of classical psychedelics.
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1cP-LSD appeared on research chemical markets in approximately July 2019, designed for legal sale after 1P-LSD was banned in Germany.[1] It became part of a predictable cycle in which each new lysergamide derivative exploits the gap between market appearance and government scheduling.[2] Germany banned it in July 2021; it remains available in some countries, though legal status varies and continues to change.
Subjective effects include geometric visual patterns, brightened colors, time alteration, thought acceleration, and ego dissolution.[3] The experience is functionally identical to LSD — long, expansive, and analytically outward-directed, shaped profoundly by mindset and surroundings.[4] Thought loops, anxious fixation, and difficulty sleeping through the extended tail are common unsought effects.
1cP-LSD does not produce physical dependence, and rapid tolerance after a single dose makes compulsive redosing self-limiting.[5][6] The primary risk is psychological — high-dose experiences can trigger acute panic or psychosis-like states, with particular danger for anyone with a personal or family history of psychotic illness.[7] No controlled human studies have been conducted, and all pharmacological knowledge rests on confirmed conversion to LSD.[1]
History[edit]
Discovery
1cP-LSD first appeared on the online research chemical market in approximately July 2019.[1] It has no academic synthesis precedent — it was designed for commercial distribution specifically to fill the legal gap left when 1P-LSD was captured by German drug law. Brandt et al. confirmed in 2020 that it converts to LSD in human blood and produces psychedelic behavior in mice at roughly 32% of LSD's potency.[1]
The lysergamide series
1cP-LSD was the sixth compound documented in the "Return of the Lysergamides" series, which tracked N1-acylated LSD derivatives as they appeared on the market.[1] The series includes 1P-LSD (2016),[8] 1B-LSD (2019),[9] 1V-LSD (2022),[10] and 1F-LSD (2025).[11] Each confirmed the same principle: attaching an acyl group to LSD's indole nitrogen blocks direct receptor activity until the body strips it off.
Regulatory succession
Each derivative emerged to fill the legal gap left by the previous ban.[2] When Germany banned 1cP-LSD in July 2021,[12] 1V-LSD was already being marketed as its replacement. Forensic detection in Japanese blotter products confirmed international distribution by late 2019.[13]
The name "1cP-LSD" follows the systematic shorthand used across the N1-acylated series: "1" marks the N1 position, "cP" abbreviates cyclopropanoyl, and "LSD" identifies the parent scaffold. In research chemical communities, 1cP-LSD is discussed informally alongside 1P-LSD and 1V-LSD as "legal acid" — reflecting their shared LSD endpoint rather than any distinct experiential identity of their own.
Chemistry[edit]
Structural class
1cP-LSD is a lysergamide — a chemical family built on a rigid four-ring ergoline skeleton. It differs from LSD by one structural addition: a cyclopropanecarbonyl group attached to the indole nitrogen.[1]
This addition blocks receptor binding, making 1cP-LSD inactive until the body cleaves it off — regenerating LSD.[11][10] The cyclopropane ring introduces slightly different physical properties compared with the straight-chain variants in the same derivative series, though whether this changes its effects has not been studied.[14]
Molecular properties
| Molecular formula | C₂₄H₂₉N₃O₂ |
| Molecular weight | 391.5 g/mol |
Pharmacology[edit]
Mechanism of action
1cP-LSD is a prodrug of LSD. The cyclopropanecarbonyl group at the indole nitrogen blocks receptor binding until serum enzymes strip it off, releasing active LSD.[1] This has been confirmed across the entire N1-acylated series — and in human subjects for 1P-LSD, where oral administration produced only LSD in blood and urine.[15] Once converted, the pharmacological profile is identical to LSD, with serotonin receptor activation driving the psychedelic effects.[16][17]
Pharmacokinetics
No human pharmacokinetic data exist for 1cP-LSD. All timing is inferred from 1P-LSD and LSD reference studies. The 20–60 minute onset delay users commonly report reflects the time needed for hydrolysis before active LSD reaches circulation.[18] Grumann et al. found that oral 1P-LSD in human volunteers produces only LSD in blood and urine, with an LSD half-life of approximately 5.7 hours.[15]
Once LSD is circulating, its kinetics govern the experience: peak plasma concentrations 1.5–2 hours after dosing, effects lasting 6.7–11 hours,[3] oral bioavailability approximately 80%,[19] and a plasma half-life of 2.6–3.6 hours.[20] Individual variation in intensity correlates with CYP2D6 liver enzyme function.[4]
Neuroscience[edit]
Where it acts
As a prodrug of LSD, 1cP-LSD engages the same brain systems documented in LSD neuroimaging research. LSD disrupts the default mode network — the brain's resting-state system for self-referential thought — producing ego dissolution and the dissolution of personal boundaries.[7] It also impairs the brain's normal filtering of sensory input, allowing more raw information through and contributing to visual patterns, synesthesia, and perceptual intensification.[7]
Why it matters
At the whole-brain level, LSD increases global connectivity — a shift from focused, modular processing toward a more interconnected state that scales with subjective intensity.[3] The REBUS model frames this as the brain relaxing its grip on existing beliefs and patterns, allowing sensory experience to arrive more freshly — which accounts for ego dissolution and the quality of heightened novelty that characterizes psychedelic perception.
Beyond acute effects, LSD promotes brain plasticity through a separate pathway. Moliner et al. found that LSD binds a key growth factor receptor about 1,000 times more strongly than classical antidepressants,[21] suggesting it can drive neural growth independent of the psychedelic experience itself.
The rate and completeness of 1cP-LSD's conversion to LSD in humans has not been measured — nor has whether its cyclopropanoyl group produces different hydrolysis kinetics than the propanoyl of 1P-LSD. The cyclopropanecarboxylic acid released during hydrolysis has not been studied for brain activity or toxicity.[1]
Subjective Effects[edit]
The 1cP-LSD experience is, by all available evidence, identical to LSD — a direct consequence of confirmed prodrug conversion.[4] The onset is slightly delayed while the body converts the prodrug, but once active LSD reaches circulation, the experience unfolds identically: expansive, analytical, and outward-directed, with perception and thought both intensifying. Context shapes the outcome profoundly — the same dose in different settings can bring euphoric clarity or deep distress.
Within its chemical family, 1cP-LSD is experientially interchangeable with 1P-LSD and 1V-LSD — all three generate LSD as their active metabolite.[3] Compared to psilocybin, the experience runs longer, feels more stimulating, and tends toward visually complex, analytically oriented states rather than psilocybin's characteristic introspective warmth.
Effect Grid
At common doses (75–150 µg oral), the full psychedelic experience emerges. Pronounced open-eye visuals dominate: geometric patterns overlay surfaces, colour saturation and shifting intensify, objects drift and morph, and tracers follow moving stimuli. Closed-eye visuals become vivid and structured. Time distortion is significant — minutes may feel like hours. Thought connectivity increases dramatically, often producing novel associations and conceptual insights. Emotional amplification is strong; music, art, nature, and interpersonal connection can feel profoundly meaningful.
Physically, jaw tension, temperature dysregulation, peripheral vasoconstriction (cold extremities), stimulation, and difficulty urinating are common. Nausea is less frequent than with tryptamine psychedelics. Pupil dilation is pronounced.
The experience lasts 8–12 hours and demands a clear schedule. Sleep is impossible during the active phase. A ceiling effect for positive drug effects appears near 100 µg, while ego dissolution and anxiety continue to increase above this level.
Modeled from the effect's dose-dependence curve — not per-substance measurements.
Music enhancement · Auditory enhancement · Geometry · Touch enhancement · Tracers · After-images · Depth perception distortion · Perspective distortion · Holotropic state · Visual melting · Visual morphing · Brightness alteration · Environmental patterning · Light sensitivity · Sound sensitivity · Symmetrical texture repetition · Auditory distortion · Visual processing acceleration · Auditory misinterpretation · Peripheral vision distortion · Proprioceptive distortion · Spatial disorientation · Visual diffraction · Visual haze / noise · Visual acuity enhancement · Peripheral misidentification · Vestibular distortion · Visual magnification · Synesthesia · Ganzfeld effect · Sleep-transition hallucinations · Dreaming enhancement · Olfactory enhancement · Taste enhancement · Tinnitus · Internal hallucinations · Object transformations · Environmental orbism / cubism · Object activation · Visual recursion · External hallucinations · Perspective hallucinations · Auditory hallucinations · Visual scenery slicing · Shadow people · Visual flipping · Gustatory hallucination · Olfactory hallucination
Tracers · After-images · Depth perception distortion · Perspective distortion · Holotropic state · Visual melting · Visual morphing · Brightness alteration · Environmental patterning · Light sensitivity · Sound sensitivity · Symmetrical texture repetition · Auditory distortion · Visual processing acceleration · Auditory misinterpretation · Peripheral vision distortion · Proprioceptive distortion · Spatial disorientation · Visual diffraction · Visual haze / noise · Visual acuity enhancement · Peripheral misidentification · Vestibular distortion · Visual magnification · Synesthesia · Ganzfeld effect · Sleep-transition hallucinations · Dreaming enhancement · Olfactory enhancement · Taste enhancement · Tinnitus · Internal hallucinations · Object transformations · Environmental orbism / cubism · Object activation · Visual recursion · External hallucinations · Perspective hallucinations · Auditory hallucinations · Visual scenery slicing · Shadow people · Visual flipping · Gustatory hallucination · Olfactory hallucination
Wakefulness · Body high · Spontaneous body sensations · Appetite suppression · Insomnia · Laughter fits · Tactile euphoria · Muscle tension · Bodily lightness · Body schema distortion · Dry mouth · Heart rate perception changes · Physical fatigue · Restlessness · Tingling / electric sensations · Vibrations / buzzing · Nausea · Excessive sweating · Sexual arousal enhancement · Breathing alteration · Bruxism · Dehydration sensation · Dizziness · Temperature dysregulation · Increased urination · Abnormal heartbeat · Involuntary body movements · Bodily heaviness · Bodily pressures · Headache · Kundalini-like energy · Muscle relaxation · Nystagmus (eye wobbles) · Trembling · Salivation · Pain enhancement · Sedation · Sexual arousal suppression · Vomiting · Watery eyes · Motor control enhancement · Yawning · Seizure threshold reduction · Bodily dissociation · Tactile hallucination
Appetite suppression · Insomnia · Laughter fits · Tactile euphoria · Muscle tension · Bodily lightness · Body schema distortion · Dry mouth · Heart rate perception changes · Physical fatigue · Restlessness · Tingling / electric sensations · Vibrations / buzzing · Nausea · Excessive sweating · Sexual arousal enhancement · Breathing alteration · Bruxism · Dehydration sensation · Dizziness · Increased urination · Abnormal heartbeat · Involuntary body movements · Bodily heaviness · Bodily pressures · Headache · Kundalini-like energy · Muscle relaxation · Nystagmus (eye wobbles) · Trembling · Salivation · Pain enhancement · Sedation · Sexual arousal suppression · Vomiting · Watery eyes · Motor control enhancement · Yawning · Seizure threshold reduction · Bodily dissociation · Tactile hallucination
Introspection enhancement · Openness enhancement · Thought connectivity · Pattern recognition enhancement · Conceptual thinking · Immersion enhancement · Cognitive euphoria · Thought acceleration · Increased nature relatedness · Multiple thought streams · Creativity enhancement · Analysis enhancement · Humor enhancement · Focus suppression · Information processing enhancement · Memory fragmentation · Memory suppression · Thought disorganization · Thought loops · Cognitive dysphoria · Cognitive fatigue · Cognitive impairment · Confusion · Memory replays · Synchronicity · Language enhancement · Motivation enhancement · Focus enhancement · Information processing suppression · Language suppression · Motivation suppression · Analysis suppression · Thought deceleration · Thought organization · Compulsive redosing urge · Delusions of sobriety · Delusions · Amnesia · Delirium
Pattern recognition enhancement · Conceptual thinking · Immersion enhancement · Cognitive euphoria · Thought acceleration · Increased nature relatedness · Multiple thought streams · Creativity enhancement · Analysis enhancement · Humor enhancement · Focus suppression · Information processing enhancement · Memory fragmentation · Memory suppression · Thought disorganization · Thought loops · Cognitive dysphoria · Cognitive fatigue · Cognitive impairment · Confusion · Memory replays · Synchronicity · Language enhancement · Motivation enhancement · Focus enhancement · Information processing suppression · Language suppression · Motivation suppression · Analysis suppression · Thought deceleration · Thought organization · Delusions of sobriety · Delusions · Amnesia · Delirium
Empathy enhancement · Simultaneous emotions · Anxiety · Catharsis · Dysphoria · Anxiety suppression · Anhedonia · Emotional suppression · Irritability · Mania
Catharsis · Dysphoria · Anxiety suppression · Anhedonia · Emotional suppression · Irritability
Social connection · Trust enhancement · Flow state · Communication enhancement · Sociability enhancement · Automaticity · Depersonalization · Communication suppression · Sociability suppression · Social disconnection · Ego inflation · Compulsive behavior reduction · Self-control enhancement · Craving · Boundary dissolution · Identity alteration · Ego dissolution · Cognitive disconnection · Telepathic feelings
Sociability enhancement · Automaticity · Depersonalization · Communication suppression · Sociability suppression · Social disconnection · Ego inflation · Compulsive behavior reduction · Self-control enhancement · Craving · Boundary dissolution · Identity alteration · Ego dissolution · Cognitive disconnection · Telepathic feelings
Time cessation
Non-dual awareness · Cessation · Death-rebirth sequence · Entity contact · Voidness · Transpersonal memory access · Near-death experience
Voidness · Transpersonal memory access · Near-death experience
Lucid dreaming enhancement · Recursive awareness
Timeline
First alerts emerge as subtle mood shifts, mild body awareness, and a faint sense that perception is beginning to change. The prodrug hydrolysis step may extend onset relative to direct LSD.
Effects build steadily: visual brightening, colour saturation, mild geometric patterning, increasing thought fluidity, and rising body stimulation. Mild anxiety or anticipatory tension is common during this phase.
Maximum intensity across all domains. Vivid geometric visuals, pronounced time distortion, emotional amplification, thought acceleration, and at higher doses, ego dissolution. Autonomic effects (elevated heart rate, blood pressure, pupil dilation) are at their strongest.
Intensity gradually recedes from peak. Visual effects soften but persist; cognitive and emotional effects remain present though less overwhelming. A sense of clarity or insight often emerges during this phase.
Perceptual effects fade to traces — mild visual drift, lingering colour enhancement. Cognitive normalcy returns progressively. Emotional sensitivity remains elevated.
Residual mood elevation, enhanced emotional openness, mild perceptual sensitivity, and reflective cognitive state. Sleep quality may be affected on the night following use. Long-lasting positive mood shifts documented up to 12 months in controlled LSD research.
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
No experimental toxicity data exist for 1cP-LSD. The only assessment is a computational study that produced conflicting results — including up to 90% predicted genotoxicity on one platform while another classified all lysergamides as non-mutagenic.[22]
By analogy with LSD, acute toxicity at typical doses is presumed very low. LSD has no confirmed human fatalities from overdose, and lethal doses in animals are orders of magnitude above the active dose range.[7]
Cardiovascular effects
LSD produces moderate, dose-dependent increases in heart rate and blood pressure.[3] These effects are temporary and clinically insignificant in healthy people, but carry relevance for anyone with pre-existing heart conditions.
Psychological risks
Anxiety and panic increase substantially at higher doses, with ego dissolution and the dread of losing one's sense of self becoming prominent at higher amounts.[3][23] Mindset, psychological state, and environment strongly shape whether the experience turns distressing.[4] Psychosis precipitation is a well-documented risk for people with a personal or family history of psychotic disorders.[7]
Visual disturbances that persist long after the drug clears — ranging from brief benign flashbacks to chronic perceptual changes (Hallucinogen Persisting Perception Disorder, or HPPD)[24] — are a recognized risk with LSD-class compounds. Pre-existing anxiety and visual symptoms increase vulnerability.[24] One published case documents this in a 16-year-old,[25] highlighting adolescent vulnerability.
Tolerance and dependence
Tolerance develops rapidly — a single dose produces measurable loss of sensitivity within 24 hours through serotonin downregulation.[5][6] Full sensitivity returns in approximately 14 days. Physical dependence does not develop, and no withdrawal has been documented.[7]
Psychological dependence liability is considered low. Rapid tolerance makes dose escalation self-limiting, and LSD-class compounds do not produce the reinforcing patterns that drive compulsive use.[7]
Drug interactions
Serotonergic combinations
Tramadol lowers seizure threshold and raises brain serotonin levels, compounding both risks when combined with LSD-class compounds, which also lower seizure threshold and activate serotonin receptors.[26] inferred Chronic SSRI and SNRI use reduces LSD's psychedelic effects through compensatory receptor changes.[27]
MDMA combined with LSD significantly raises LSD blood levels and duration, and adds cardiovascular strain.[28]
Seizure-threshold interactions
Lithium combined with LSD-class compounds is widely reported as dangerous, with seizure risk. safety citation needed
Pharmacological antagonism
Ketanserin — a serotonin receptor blocker — fully reverses LSD effects when administered before or during the experience.[3]
Cannabis
No published data exist on the 1cP-LSD–cannabis combination. Community reports suggest intensification of psychedelic effects, but no controlled studies have been conducted.
Contraindications
Contraindications are inferred from LSD pharmacology. No 1cP-LSD-specific data have been published.
- Psychotic disorders and family history of psychosis: Absolute contraindication. LSD-class compounds can trigger acute psychosis and may unmask latent illness.[7]
- Bipolar disorder: Relative contraindication. Risk of manic episode. citation needed
- Lithium or seizure-threshold-lowering medications: Absolute contraindication pending further evidence. safety citation needed
- Severe cardiovascular disease: Relative contraindication. LSD raises blood pressure and heart rate.[3]
- Pregnancy: Absolute contraindication. No reproductive toxicity data exist. citation needed
- Adolescence: Relative contraindication. Developing brains may be more vulnerable to lasting perceptual disturbances.[25]
Harm Reduction[edit]
Forms & Identification
1cP-LSD circulates primarily on blotter paper and in pellet form.[1] Standard reagent kits and many laboratory methods cannot distinguish it from LSD — methanol-based preparations cause the prodrug to break down into LSD, producing a false identification.[29] An Ehrlich reagent test confirming an indole compound is present is a minimum first step, but cannot differentiate 1cP-LSD from LSD or other lysergamides.
Blotter dosing is more consistent than pellet form, but neither format guarantees accurate amounts. Start with a fraction of any stated dose to calibrate individual response.
Guidelines
- Test all material with an Ehrlich reagent at minimum. A purple/violet reaction confirms an indole is present.
- Start with a low dose and allow at least 90 minutes before considering the experience fully developed — the hydrolysis step delays onset.
- Arrange a sober sitter — someone who remains unimpaired and available throughout the experience.
- Eat a light meal 2–3 hours before. Avoid caffeine and stimulants on the day.
- Prepare the space: comfortable temperature, accessible water, calming music, minimal hazards.
- Clear the full day and the following morning. Sleep disruption through the tail is common.
- Keep a benzodiazepine on hand if available — it can reduce acute anxiety without fully terminating the experience.
- Do not redose during the experience. Tolerance forms within hours of the first dose, making redosing unpredictable rather than proportional.
Set & Setting
The LSD experience is among the most context-sensitive of any psychoactive substance.[4] Mindset, expectations, and emotional baseline — and the physical and social environment — are the strongest non-pharmacological predictors of whether an experience turns expansive or distressing.
A familiar environment, trusted companions, and at least 12 hours free of obligations provides the strongest foundation. Anxiety, grief, or unresolved interpersonal conflict substantially raise the likelihood of a difficult experience.
Aftercare & integration. The period following an LSD-class experience often brings residual emotional openness and cognitive flexibility lasting hours to days. This window is valuable for reflection but also a period of vulnerability.
Allow at least one full day of low-demand time after the experience. Sleep may be disrupted the first night — this is normal and resolves without intervention. Journaling or voice-recording reflections within 24 hours captures material that fades quickly.
If the experience was challenging, talking it through with a trusted person or integration-trained therapist can prevent unprocessed material from becoming lasting distress. Persistent anxiety, depersonalization, or visual disturbances lasting more than two weeks warrant professional evaluation.
Recovery & Support
LSD-class compounds carry low physical dependence liability, but patterns of frequent use can develop — particularly when experiences are used to avoid underlying psychological difficulties rather than explore them.
If use has become a habitual coping mechanism, or experiences are producing more distress than insight, a harm reduction-informed therapist or psychedelic integration specialist can help re-evaluate the pattern. Resources include the Fireside Project (62-FIRESIDE / 623-473-7433), MAPS integration list, and local psychedelic societies. For broader substance use concerns, SAMHSA's National Helpline (1-800-662-4357) provides free, confidential treatment referrals.
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Recognizing an emergency: Anxiety, confusion, and perceptual distortions are expected at moderate-to-high doses and do not require medical intervention. Seek immediate help if the person shows signs of self-harm or suicidal thinking, becomes completely unresponsive, has seizures, develops chest pain or dangerously elevated body temperature, or enters uncontrollable panic with risk of dangerous behavior.
Immediate steps:
- 1. Stay with the person. Speak calmly and simply.
- 2. Move to a quiet, low-stimulation environment if possible.
- 3. Remove access to heights, roads, sharp objects, and other hazards.
- 4. Do not physically restrain unless there is immediate danger to life.
- 5. If symptoms escalate or self-harm risk is present, call emergency services.
What to tell the dispatcher: Name the substance (1cP-LSD or "an LSD structural analog"), approximate dose and time taken, and current symptoms. Good Samaritan laws in many jurisdictions protect callers from drug-related prosecution.
Legal Status[edit]
1cP-LSD has no explicit scheduling in most countries but may be captured by structural analog laws, novel psychoactive substance bans, or its confirmed status as a prodrug of the controlled substance LSD. Legal status varies by jurisdiction and is subject to change; the information below reflects best available data as of early 2026.
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| United States | Not explicitly scheduled | LSD is Schedule I (21 U.S.C. § 812). The Federal Analogue Act (21 U.S.C. § 813) may apply to 1cP-LSD as a "substantially similar" substance when intended for human consumption. No specific enforcement action or adjudication identified as of 2025. |
| United Kingdom | Controlled under PSA 2016 | Covered by the Psychoactive Substances Act 2016, which bans production, supply, and import of any substance intended to produce psychoactive effects (with exemptions for alcohol, tobacco, caffeine, and medicines). Not specifically named under the Misuse of Drugs Act 1971. |
| Germany | Banned (NpSG) | Prohibited under an amendment to the Neue-Psychoaktive-Stoffe-Gesetz effective July 2021. The NpSG bans structural groups rather than individual compounds; the 2021 amendment specifically captured 1cP-LSD and related lysergamides.[12] |
| Canada | Not scheduled | Does not appear on Schedules I–VI of the Controlled Drugs and Substances Act as of 2025. LSD is Schedule III. No analog provisions comparable to the US Federal Analogue Act.citation needed |
| Australia | Not explicitly listed | LSD is Schedule 9 (prohibited). 1cP-LSD is not named in the SUSMP. Analogue provisions in state and territory legislation may apply. Status requires jurisdiction-specific legal advice. |
| European Union (other) | Variable | Many EU member states have broad NPS legislation that may capture 1cP-LSD. The EMCDDA monitors lysergamide NPS as a class. Specific scheduling varies by country. |
Analog and prodrug considerations
1cP-LSD's confirmed conversion to LSD creates legal vulnerability under analog legislation.[2] In jurisdictions with analog provisions — notably the United States — the fact that 1cP-LSD becomes a Schedule I substance in the body strengthens the case for "substantial similarity." Germany's structural class approach under the NpSG has proven most effective at capturing sequential lysergamide derivatives.[12]
references
- [1]
- [2] ^abcLuethi D, Liechti ME (2020) Designer drugs: mechanism of action and adverse effects — Archives of Toxicology doi:10.1007/s00204-020-02693-7
- [3]
- [4]
- [5] ^abBuckholtz NS, Zhou DF, Freedman DX, Potter WZ (1990) Lysergic acid diethylamide (LSD) administration selectively downregulates serotonin2 receptors in rat brain — Neuropsychopharmacology PMID:1969270
- [6] ^abde la Fuente Revenga M, Jaster AM, McGinn J, Silva G, Saha S, Gonzalez-Maeso J (2022) Tolerance and Cross-Tolerance among Psychedelic and Nonpsychedelic 5-HT2A Receptor Agonists in Mice — ACS Chemical Neuroscience doi:10.1021/acschemneuro.2c00170