generation run 2026-04-26
58 min completedmodel pipeline-v5plan not recordedrun/df59fdc9…Selection
Verification
- record
- seen / partial
- working
The model's own caveats
none raised on this run
Reproduce
- inputs
- 37 source keys (listed under Sources)
- plan
- not recorded — template version, prompt hash and git SHA are written from 2026-09 onward
- model
- pipeline-v5
- streams
- none — agent transcripts are persisted from 2026-09 onward
23 searches — query, source, results, what was kept and why
| # | source | query | seen | kept | rationale |
|---|---|---|---|---|---|
| 1 | PubMed | 1P-LSD prodrug LSD metabolism human serum hydrolysis | 1 | 1 | Key analog PK data for extrapolation to 1cP-LSD |
| 2 | PubMed | LSD subjective effects psychedelic altered states consciousness 5D-ASC human study | 6 | 3 | Directly relevant to subjective effects section via LSD prodrug mechanism |
| 3 | PubMed | return lysergamides Brandt Halberstadt new psychoactive substance analytical | 7 | 7 | Complete series provides context for 1cP-LSD potency comparisons |
| 4 | PubChem | 1cP-LSD | 1 | 1 | Primary compound record for 1cP-LSD |
| 5 | PubMed (via PMID fetch) | PMID 28129538 | 1 | 1 | Key structural paper for LSD receptor binding mechanism |
| 6 | ClinicalTrials.gov · absence | 1cP-LSD lysergamide psychedelic | 0 | 0 | No trials exist |
| 7 | PubMed | LSD crystal structure 5-HT2A receptor Wacker ergoline binding | 1 | 1 | Structural basis for LSD/lysergamide 5-HT2A binding relevant to mechanism |
| 8 | OpenAlex | 1cP-LSD lysergamide designer drug new psychoactive substance | 14 | 7 | All directly relevant to 1cP-LSD characterization, detection, or use |
| 9 | PubMed | 1cP-LSD 1-cyclopropionyl-LSD lysergamide | 4 | 4 | All directly about 1cP-LSD |
| 10 | PubMed | lysergic acid diethylamide LSD pharmacokinetics human half-life metabolism | 8 | 4 | LSD PK reference data applicable via prodrug mechanism |
| 11 | PubMed | LSD tolerance cross-tolerance tryptamine serotonin receptor downregulation | 2 | 2 | Mechanism basis for 1cP-LSD tolerance via LSD class |
| 12 | Web search | 1cP-LSD Germany banned July 2021 NpSG UK Psychoactive Substances Act scheduling history | 10 | 3 | Primary legal status information for major jurisdictions |
| 13 | PsychonautWiki | — | 1 | 1 | Community consensus dose/duration data; confirms seed data values |
| 14 | PubMed | tramadol seizure serotonin mechanism serotonin syndrome opioid | 2 | 2 | Mechanistic basis for tramadol-psychedelic dangerous interaction warning |
| 15 | OpenAlex | LSD lysergic acid diethylamide receptor binding affinity Ki serotonin dopamine | 8 | 3 | Pharmacology and interaction data |
| 16 | PubMed PMID fetch | Multiple PMIDs: 39624022 (1F-LSD), 8726753 (Bonson SSRI-LSD), 30883864 (Holze LSD formulation), 28342178 (ETH-LAD) | 4 | 4 | Pharmacology mechanism and interactions |
| 17 | PubMed | LSD adverse effects HPPD hallucinogen persisting perception disorder | 8 | 3 | HPPD risk documentation relevant to 1cP-LSD via LSD prodrug |
| 18 | PubMed | Dolder LSD pharmacodynamics autonomic subjective healthy volunteers controlled | 3 | 2 | Dose-response and autonomic effects directly applicable via prodrug mechanism |
| 19 | ClinicalTrials.gov · absence | 1cP-LSD lysergamide psychedelic | 0 | 0 | Confirms absence of clinical trial data |
| 20 | Web search | 1cP-LSD first appeared research chemical market 2019 history synthesis discovery | 10 | 1 | History section - market appearance date |
| 21 | Multiple · absence | Cross-referencing seed data against published sources | 0 | 0 | Quality assurance cross-reference |
| 22 | PubMed | Multiple PMIDs: Holze 2021 dose-dependent LSD, Holze 2021 microdose, Vizeli 2024, Schmid 2018, Arikci 2025 | 5 | 5 | Core LSD pharmacology reference set applicable by prodrug analogy |
| 23 | All sources combined | 1cP-LSD compound identity, pharmacology, history, legal status, safety | 45 | 1 | Complete data extraction for research output |
79 claims by section — every cited sentence, checked against its source
safety23 · 17 ok
Severe cardiovascular disease: Relative contraindication. LSD produces dose-dependent hypertension and tachycardia.supported
Moderate increases in BP/HR. s41386-020-00883-6
Adolescence: Relative contraindication. Developing brains may be more vulnerable to HPPD and other perceptual disturbances.supported
Case report of HPPD in adolescent. Illustrates HPPD risk in younger users. pb.4525
Jurowski et al. conducted the only toxicological assessment — a multi-platform in silico modeling study (ADMETlab 3.0, Percepta, STopTox, ProTox 3.0, VEGA, TEST 5.1.2) — yielding the following computational predictions:supported
Multi-platform in silico toxicity prediction for five LSD analogs including 1cP-LSD. s00204-025-04255-1
Claim in safety — inconclusiveinconclusiveworking →
Claim in safety — inconclusiveinconclusiveworking →
LSD produces moderate, dose-dependent increases in heart rate and blood pressuresupported
Moderate increases in BP/HR. s41386-020-00883-6
Acute anxiety and panic: Dose-dependent; anxiety increases substantially at doses exceeding 100 µg LSD-equivalent, with ego dissolution and "dread of ego dissolution" becoming prominent at 200 µg.supported
Ceiling for good effects at 100ug; ego dissolution and anxiety increase at 200ug. s41386-020-00883-6
Acute anxiety and panic: Dose-dependent; anxiety increases substantially at doses exceeding 100 µg LSD-equivalent, with ego dissolution and "dread of ego dissolution" becoming prominent at 200 µg.supported
Meta-analysis of LSD dose-response using 5D-ASC/MEQ30 data. Sigmoid increase with plateau at ~100ug. Most strongly modulated: perceptual changes, illusory imagination, ego dissolution. s41386-023-01588-2
Challenging experiences: Psychologically distressing episodes occur with significant frequency, particularly in adverse set and setting or at high doses. Non-pharmacological factors — personality, psychological state, and environment — contribute substantially to outcome variability.supported
CYP2D6 functionality correlated with anxiety response. Openness to Experience predicts mystical effects. Previous hallucinogen use negatively predicts altered consciousness. s41398-024-03074-9
Claim in safety — inconclusiveinconclusiveworking →
HPPD: Hallucinogen Persisting Perception Disorder is a recognized risk with LSD-class compounds. Halpern et al. classified HPPD into Type I (brief, benign flashbacks) and Type II (chronic perceptual disturbances). Müller et al. found limited HPPD incidence in controlled LSD research settings but acknowledged inadequate long-term follow-up data. Pre-existing anxiety and visual symptoms may predict vulnerability. No HPPD cases specific to 1cP-LSD have been published. Mori-Kreiner et al. documented an HPPD case in a 16-year-old, highlighting adolescent vulnerability to LSD-class compounds.supported
Review of HPPD. Two types: Type I (brief flashbacks), Type II (chronic). Pre-existing anxiety and visual symptoms may predict vulnerability. 7854_2016_457
HPPD: Hallucinogen Persisting Perception Disorder is a recognized risk with LSD-class compounds. Halpern et al. classified HPPD into Type I (brief, benign flashbacks) and Type II (chronic perceptual disturbances). Müller et al. found limited HPPD incidence in controlled LSD research settings but acknowledged inadequate long-term follow-up data. Pre-existing anxiety and visual symptoms may predict vulnerability. No HPPD cases specific to 1cP-LSD have been published. Mori-Kreiner et al. documented an HPPD case in a 16-year-old, highlighting adolescent vulnerability to LSD-class compounds.supported
LSD and psilocybin in phase I trials. HPPD characterization. Limited data on flashback frequency in controlled settings. s00213-022-06066-z
HPPD: Hallucinogen Persisting Perception Disorder is a recognized risk with LSD-class compounds. Halpern et al. classified HPPD into Type I (brief, benign flashbacks) and Type II (chronic perceptual disturbances). Müller et al. found limited HPPD incidence in controlled LSD research settings but acknowledged inadequate long-term follow-up data. Pre-existing anxiety and visual symptoms may predict vulnerability. No HPPD cases specific to 1cP-LSD have been published. Mori-Kreiner et al. documented an HPPD case in a 16-year-old, highlighting adolescent vulnerability to LSD-class compounds.supported
Review of HPPD. Two types: Type I (brief flashbacks), Type II (chronic). Pre-existing anxiety and visual symptoms may predict vulnerability. 7854_2016_457
HPPD: Hallucinogen Persisting Perception Disorder is a recognized risk with LSD-class compounds. Halpern et al. classified HPPD into Type I (brief, benign flashbacks) and Type II (chronic perceptual disturbances). Müller et al. found limited HPPD incidence in controlled LSD research settings but acknowledged inadequate long-term follow-up data. Pre-existing anxiety and visual symptoms may predict vulnerability. No HPPD cases specific to 1cP-LSD have been published. Mori-Kreiner et al. documented an HPPD case in a 16-year-old, highlighting adolescent vulnerability to LSD-class compounds.supported
Case report of HPPD in adolescent. Illustrates HPPD risk in younger users; re-experiencing of intoxication perceptions when sober. pb.4525
Tolerance develops rapidly via 5-HT₂A receptor downregulation in the frontal cortex following repeated agonist exposuresupported
5-day LSD administration decreases 5-HT2 binding in cortex. Correlates with behavioral tolerance development. pmid:1969270
De la Fuente Revenga et al. demonstrated that a single dose of the 5-HT₂A agonist DOI produces measurable tolerance within 24 hours, with cross-tolerance to LSD; the mechanism is β-arrestin-2-independent receptor internalization and downregulationsupported
Cross-tolerance between DOI and LSD. 5-HT2A receptor downregulation mediates tolerance. Mechanism independent of beta-arrestin-2. acschemneuro.2c00170
Claim in safety — inconclusiveinconclusiveworking →
Claim in safety — inconclusiveinconclusiveworking →
Tramadol: The combination of tramadol with LSD-class compounds compounds seizure risk through two mechanisms: tramadol dose-dependently lowers seizure threshold and increases brain serotonin concentrations, while LSD-class compounds also lower seizure threshold and act as serotonergic agonists. No human case reports or controlled studies document this specific interaction for 1cP-LSD or LSD directly — the "dangerous" severity rating is a class-level mechanistic inference.supported
Tramadol induces dose-dependent seizures in rats independent of serotonin mechanism. Tramadol-induced early-onset increase in brain serotonin and norepinephrine concentrations. j.taap.2016.09.013
SSRIs and SNRIs: Chronic SSRI administration attenuates LSD subjective effects, likely via compensatory 5-HT₂A receptor downregulationsupported
Chronic SSRI administration attenuates subjective LSD effects, likely via 5-HT2A receptor downregulation. 0893-133x(95)00145-4
MDMA: Co-administration of MDMA with LSD 100 µg significantly increases LSD Cmax and AUC, prolongs LSD plasma half-life, and produces additive cardiovascular effects (increased blood pressure, heart rate, mydriasis)supported
LSD Cmax and AUC higher when MDMA co-administered. LSD plasma elimination half-life longer with MDMA. Combined use increases BP, HR, pupil size more than LSD alone. s41386-023-01609-0
Ketanserin (5-HT₂A antagonists): Ketanserin fully blocks LSD effects when administered before or during the experiencesupported
Ketanserin blocks all effects. s41386-020-00883-6
Claim in safety — inconclusiveinconclusiveworking →
pharmacology13 · 10 ok
Brandt et al. confirmed prodrug conversion by incubating 1cP-LSD with human serum at 37°C, demonstrating time-dependent formation of LSDsupported
Human serum incubation confirms prodrug metabolism to LSD. dta.2789
Claim in pharmacology — not_supportednot supportedworking →
This hydrolysis mechanism is shared across the N1-acylated LSD derivative class: it was first described for 1P-ETH-LAD and definitively demonstrated in human subjects for 1P-LSD, where oral administration of 100 µg produced detectable serum LSD with no detectable parent compound.supported
Oral 1P-LSD 100ug in two volunteers: only LSD detected in serum/urine. Confirms prodrug mechanism in humans. dta.2821
The class principle — that N1-acylation is detrimental to 5-HT₂A receptor activity but in-vivo hydrolysis rapidly restores LSD-level activity — has been confirmed across the series, including 1V-LSD and 1F-LSDsupported
N1-acyl LSD derivatives act as weak partial agonists at 5-HT2A and prodrugs for LSD. dta.3205
The class principle — that N1-acylation is detrimental to 5-HT₂A receptor activity but in-vivo hydrolysis rapidly restores LSD-level activity — has been confirmed across the series, including 1V-LSD and 1F-LSDsupported
N1-acylation reduces 5-HT2A activity but compounds rapidly hydrolyze in vivo to LSD. 1F-LSD and 1T-LSD produce HTR and hydrolyze to LSD. dta.3829
The behavioral consequence of this prodrug mechanism was demonstrated in the mouse head-twitch response (HTR) assay — the standard in-vivo proxy for 5-HT₂A-mediated hallucinogenic activity. 1cP-LSD produced an HTR ED₅₀ of 430.0 nmol/kg (C57BL/6J mice, IP), compared with 132.8 nmol/kg for LSD — approximately 32% of LSD potency in this assaysupported
Mouse HTR ED50 = 430.0 nmol/kg (cf. 1P-LSD ED50 = 349.6 nmol/kg). dta.2789
For 1P-LSD, Grumann et al. demonstrated in two human volunteers that oral administration of 100 µg yielded only LSD in serum and urine, with an LSD elimination half-life of approximately 5.7 hours and estimated bioavailability approaching 100%supported
Oral 1P-LSD 100ug in two volunteers: only LSD detected in serum/urine. LSD half-life ~5.7h. Bioavailability of LSD after oral 1P-LSD ~100%. dta.2821
LSD reference pharmacokinetics (applicable via prodrug mechanism): oral LSD exhibits dose-proportional pharmacokinetics with first-order elimination, a Tmax of 1.5–2 hours, and subjective duration of 6.7–11 hours dose-dependently at 25–200 µgsupported
LSD 25-200ug: dose-proportional PK, first-order elimination, duration 6.7-11h dose-dependently. s41386-020-00883-6
Claim in pharmacology — inconclusiveinconclusiveworking →
Plasma half-life ranges from 2.6–3.6 hours, with a microdose half-life of 2.7 hourssupported
LSD microdose PK: 5-20ug doses. Mean elimination half-life 2.7h. cpt.2057
Absolute oral bioavailability of LSD is approximately 80%.supported
LSD absolute oral bioavailability 80% (all formulations equivalent). cpt.3726
CYP2D6 functionality correlates with inter-individual variability in LSD experience intensitysupported
CYP2D6 functionality correlated with anxiety response. s41398-024-03074-9
Claim in pharmacology — inconclusiveinconclusiveworking →
summary9 · 5 ok
Claim in summary — inconclusiveinconclusiveworking →
Brandt et al. characterized it as Part VI of the "Return of the Lysergamides" series, confirming prodrug conversion to LSD in human serum and documenting a mouse head-twitch response ED₅₀ of 430.0 nmol/kg — approximately 32% of LSD potency in this assaysupported
Mouse HTR ED50 = 430.0 nmol/kg (cf. 1P-LSD ED50 = 349.6 nmol/kg). Human serum incubation confirms prodrug metabolism to LSD. dta.2789
Once hydrolyzed, the resulting LSD activates 5-HT₂A receptors (primary psychedelic target) alongside 5-HT₁A, 5-HT₂C, and dopamine D₁–D₄ receptorssupported
Receptor affinity of 25 psychedelic drugs at 51 targets. Diversity of receptor interaction underlies qualitative diversity. LSD receptor profile included. journal.pone.0009019
Claim in summary — inconclusiveinconclusiveworking →
The experience encompasses visual distortions, geometric patterning, ego dissolution, thought acceleration, emotional amplification, and time distortion — domains characterized in controlled LSD studies at 25–200 µgsupported
LSD 25-200ug: dose-proportional PK, first-order elimination, duration 6.7-11h dose-dependently. Ceiling for good effects at 100ug; ego dissolution and anxiety increase at 200ug. s41386-020-00883-6
Set, setting, and individual disposition strongly modulate subjective outcomes.supported
CYP2D6 functionality correlated with anxiety response. Openness to Experience predicts mystical effects. Previous hallucinogen use negatively predicts altered consciousness. s41398-024-03074-9
No controlled toxicity data exist for 1cP-LSD; the sole toxicological assessment is an in silico modeling study yielding conflicting genotoxicity predictions across computational platformssupported
Multi-platform in silico toxicity prediction for five LSD analogs including 1cP-LSD. Genotoxicity alerts for 1cP-LSD (up to 90%). s00204-025-04255-1
Claim in summary — inconclusiveinconclusiveworking →
Claim in summary — inconclusiveinconclusiveworking →
receptor-pharmacology8 · 7 ok
The intact prodrug has weak or negligible direct 5-HT₂A affinity; all receptor interactions described below pertain to the LSD generated by hydrolysis.supported
Human serum incubation confirms prodrug metabolism to LSD. dta.2789
LSD functions as an agonist or partial agonist, activating both Gq-coupled and β-arrestin2 signaling pathwayssupported
Active-state cryo-EM structure of 5-HT2A bound to 25-CN-NBOH plus engineered Gq heterotrimer. X-ray crystal structures with LSD (arrestin-biased). j.cell.2020.08.024
Cryo-EM structural data for LSD at the 5-HT₂A receptor confirm an arrestin-biased active-state conformation.partially supported
X-ray crystal structures with LSD (arrestin-biased) and methiothepin. Active-state cryo-EM structure of 5-HT2A bound to 25-CN-NBOH. j.cell.2020.08.024
The selective 5-HT₂A antagonist ketanserin completely abolishes all subjective effects of LSD when administered before or concurrent with dosing, confirming 5-HT₂A as the necessary receptor for the psychedelic experience.supported
Ketanserin blocks all effects. s41386-020-00883-6
Claim in receptor-pharmacology — inconclusiveinconclusiveworking →
LSD exhibits partial agonist activity at dopamine D₁, D₂, D₃, and D₄ receptors, consistent with its ergoline scaffold and broad interaction with monoaminergic systemssupported
Receptor affinity of 25 psychedelic drugs at 51 targets. LSD receptor profile included. journal.pone.0009019
Moliner et al. demonstrated that LSD binds directly to the TrkB receptor (tropomyosin receptor kinase B) with approximately 1,000-fold higher affinity than classical antidepressantssupported
LSD and psilocin directly bind TrkB (BDNF receptor) with 1000-fold higher affinity than other antidepressants. s41593-023-01316-5
The full receptor binding profile of LSD spans 5-HT₁A, 5-HT₂A, 5-HT₂C, multiple dopaminergic subtypes, and adrenergic receptorssupported
Receptor affinity of 25 psychedelic drugs at 51 targets. LSD receptor profile included. journal.pone.0009019
history7 · 5 ok
Claim in history — inconclusiveinconclusiveworking →
Tanaka et al. documented forensic detection of 1cP-LSD in paper sheet products collected in Japan between September 2019 and March 2020, confirming international market distribution by late 2019.supported
Forensic identification of 1cP-LSD in paper sheet products from Japan (Sept 2019-Mar 2020). yakushi.20-00124
Claim in history — inconclusiveinconclusiveworking →
The series began with 1P-LSD (Part I, 2016) and continued through AL-LAD and LSZ (Part II), ETH-LAD (Part III), LSM-775 (Part IV), 1B-LSD (Part V), and subsequently 1V-LSD (Part VII, 2022) and 1F-LSD (2025)supported
1P-LSD HTR ED50 = 349.6 nmol/kg; LSD ED50 = 132.8 nmol/kg. dta.1884
The series began with 1P-LSD (Part I, 2016) and continued through AL-LAD and LSZ (Part II), ETH-LAD (Part III), LSM-775 (Part IV), 1B-LSD (Part V), and subsequently 1V-LSD (Part VII, 2022) and 1F-LSD (2025)supported
LSM-775 acts as nonselective agonist at 5-HT1A and 5-HT2A. dta.2222
The series began with 1P-LSD (Part I, 2016) and continued through AL-LAD and LSZ (Part II), ETH-LAD (Part III), LSM-775 (Part IV), 1B-LSD (Part V), and subsequently 1V-LSD (Part VII, 2022) and 1F-LSD (2025)supported
1V-LSD HTR ED50 = 373 nmol/kg (~1/3 potency of LSD). dta.3205
The series began with 1P-LSD (Part I, 2016) and continued through AL-LAD and LSZ (Part II), ETH-LAD (Part III), LSM-775 (Part IV), 1B-LSD (Part V), and subsequently 1V-LSD (Part VII, 2022) and 1F-LSD (2025)supported
N1-acylation reduces 5-HT2A activity but compounds rapidly hydrolyze in vivo to LSD. 1F-LSD and 1T-LSD produce HTR and hydrolyze to LSD. dta.3829
chemistry5 · 5 ok
The defining structural modification is the addition of a cyclopropanecarbonyl group at the N1 (indole nitrogen) position, placing it within the N1-acylated LSD derivative series that includes 1P-LSD (N1-propanoyl), 1B-LSD (N1-butanoyl), and 1V-LSD (N1-valeroyl).supported
Primary characterization paper for 1cP-LSD. Detailed analytical characterization including MS, GC, LC, NMR, IR. dta.2789
The N1-acyl modification has well-characterized structure-activity consequences: it reduces direct 5-HT₂A receptor affinity but permits in-vivo hydrolysis back to LSD, functionally converting these derivatives into prodrugssupported
N1-acylation reduces 5-HT2A activity but compounds rapidly hydrolyze in vivo to LSD. dta.3829
The N1-acyl modification has well-characterized structure-activity consequences: it reduces direct 5-HT₂A receptor affinity but permits in-vivo hydrolysis back to LSD, functionally converting these derivatives into prodrugssupported
N1-acyl LSD derivatives act as weak partial agonists at 5-HT2A and prodrugs for LSD. dta.3205
The compound is distributed commercially on blotter paper and in pellet formsupported
Blotter and pellet analysis included. dta.2789
Analytical work has typically used methanol solutions, but Tusiewicz et al. demonstrated that methanol causes alcoholysis of N1-acyl LSD derivatives — including 1cP-LSD — producing LSD as an analytical artifactsupported
Methanol causes alcoholysis artifacts. molecules29235717
neuroscience5 · 2 ok
Claim in neuroscience — inconclusiveinconclusiveworking →
Claim in neuroscience — inconclusiveinconclusiveworking →
Claim in neuroscience — inconclusiveinconclusiveworking →
Moliner et al. demonstrated that LSD binds TrkB with approximately 1,000-fold higher affinity than classical antidepressants, activating BDNF-dependent plasticity mechanisms independent of the psychedelic experience itself.supported
LSD and psilocin directly bind TrkB (BDNF receptor) with 1000-fold higher affinity than other antidepressants. Antidepressant effects depend on TrkB binding independent of 5-HT2A activation. s41593-023-01316-5
LSD-class compounds promote dendritic arborization and synaptogenesis through both 5-HT₂A-dependent and TrkB-dependent pathwayssupported
Psychedelics promote plasticity by directly binding to BDNF receptor TrkB. Antidepressant effects depend on TrkB binding independent of 5-HT2A activation. LSD head-twitching is 5-HT2A-dependent, TrkB-independent. s41593-023-01316-5
clinical-evidence3 · 3 ok
The only controlled dosing study of 1cP-LSD outside the mouse head-twitch response assay is a veterinary trial by Hernández-Álvarez et al., in which shelter dogs received 10 µg oral 1cP-LSD over three weeks in a randomized blind designsupported
Randomized blind trial in 20 shelter dogs. Low-dose 1cP-LSD (10 ug oral, 3 weeks) plus ethological intervention. vetsci13010096
Holze et al. separately characterized dose-dependent effects in healthy subjects (n = 16) across LSD 25–200 µg in a double-blind placebo-controlled design: subjective effects were dose-proportional, with a ceiling effect for positive drug effects near 100 µg and continuing increases in ego dissolution and anxiety at 200 µgsupported
LSD 25-200ug: dose-proportional PK, first-order elimination, duration 6.7-11h dose-dependently. Ceiling for good effects at 100ug; ego dissolution and anxiety increase at 200ug. s41386-020-00883-6
Holze et al. conducted a phase II randomized, double-blind, placebo-controlled trial of LSD-assisted therapy in patients with anxiety with and without life-threatening illnesssupported
Phase 2 RCT: LSD-assisted therapy for anxiety with or without life-threatening illness. j.biopsych.2022.08.025
comparative-pharmacology3 · 3 ok
Data from Brandt et al. 2020, Brandt et al. 2016, Brandt et al. 2019, Brandt et al. 2022.supported
Primary characterization paper for 1cP-LSD. Mouse HTR ED50 = 430.0 nmol/kg. dta.2789
Data from Brandt et al. 2020, Brandt et al. 2016, Brandt et al. 2019, Brandt et al. 2022.supported
1P-LSD HTR ED50 = 349.6 nmol/kg; LSD ED50 = 132.8 nmol/kg. dta.1884
Data from Brandt et al. 2020, Brandt et al. 2016, Brandt et al. 2019, Brandt et al. 2022.supported
1B-LSD HTR ED50 = 976.7 nmol/kg (~14% potency of LSD). dta.2613
pharmacokinetic-detail3 · 3 ok
In the only human PK study of an N1-acylated LSD prodrug, Grumann et al. administered 1P-LSD (100 µg) to two volunteers by oral and intravenous routes:supported
Oral 1P-LSD 100ug in two volunteers: only LSD detected in serum/urine. Bioavailability of LSD after oral 1P-LSD ~100%. dta.2821
The disparity between plasma half-life (2.6–3.6 h) and subjective duration (up to 11 h) is explained by LSD's prolonged receptor residence time at 5-HT₂A/₂B, where the EL2 "lid" structure traps the ligand in the binding pocketsupported
EL2 lid explains slow dissociation kinetics. LSD conformational selectivity of diethylamide moiety. Slow binding kinetics at 5-HT2B and 5-HT2A. j.cell.2016.12.033
CYP2D6 genotype correlates with inter-individual variability in subjective LSD experience intensity — individuals with higher CYP2D6 functionality may metabolize LSD more rapidly, potentially altering peak exposure.supported
CYP2D6 functionality correlated with anxiety response. s41398-024-03074-9