generation run 2026-05-09
87 min completedmodel pipeline-v5plan not recordedrun/643af2b9…Selection
Verification
- record
- seen / partial
- working
The model's own caveats
15 further caveats recorded as free text — readable on the working page
Reproduce
- inputs
- 30 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
19 searches — query, source, results, what was kept and why
| # | source | query | seen | kept | rationale |
|---|---|---|---|---|---|
| 1 | PubChem | 1B-LSD / 1-butanoyl-LSD | 1 | 1 | 1B-LSD data retrieved for structural analogy comparison. |
| 2 | ModernMind.eu | — | 1 | 4 | — |
| 3 | PubMed | LSD serotonin receptor binding pharmacokinetics human metabolism CYP | 8 | 5 | — |
| 4 | PsychonautWiki · absence | — | 0 | — | — |
| 5 | PubMed | 1BP-LSD lysergamide psychedelic | 10 | 3 | — |
| 6 | PubChem · absence | 1BP-LSD | 0 | 0 | No entry available; proceeded with web search. |
| 7 | WebSearch | 1BP-LSD psychedelic research chemical lysergamide | 10 | 2 | — |
| 8 | PubMed | 1-butanoyl-LSD lysergic acid diethylamide analog | 2 | 2 | — |
| 9 | WebSearch | 1BP-LSD legal status Germany NpSG scheduled 2025 2026 | 10 | 2 | — |
| 10 | PubMed | LSD 5-HT2A receptor binding mechanism crystal structure | 1 | 1 | — |
| 11 | WebSearch | 1S-LSD Germany NpSG ban November 2025 Bundesrat | 10 | 3 | — |
| 12 | PubMed | psychedelic hallucinogen cross-tolerance serotonin receptor downregulation | 1 | 1 | — |
| 13 | WebSearch/WebFetch | 1BP-LSD molecular formula SMILES InChIKey CAS vendor | 1 | 3 | — |
| 14 | OpenAlex | LSD lithium seizures drug interaction challenging experiences psychedelic | 5 | 2 | — |
| 15 | WebSearch | 1BP-LSD boronopropionyl breakdown products LSD 4-hydroxybenzoic acid pinacol boric acid | 1 | 2 | — |
| 16 | Multiple | 1BP-LSD molecular formula cross-reference | 3 | 2 | — |
| 17 | WebSearch | LSD Schedule I DEA 1971 Convention Psychotropic Substances international | 10 | 2 | — |
| 18 | OpenAlex | LSD lithium seizures drug interaction challenging experiences psychedelic | 5 | 1 | — |
| 19 | PubMed | Holze LSD dose-dependent subjective effects acute 2021 | 1 | 1 | — |
68 claims by section — every cited sentence, checked against its source
safety20 · 12 ok
Cross-tolerance: Cross-tolerance exists across the serotonergic psychedelic class: LSD, psilocybin, DMT, mescaline, and other LSD analogspartially supported
Cross-tolerance between DOI and LSD. acschemneuro.2c00170
In silico toxicity predictions for structurally related N1-acyl LSD analogs (ALD-52, 1P-LSD, 1B-LSD, 1V-LSD, 1cP-LSD) predicted oral LD₅₀ values in rats of 49–85 mg/kg (Percepta platform), with low dermal and ocular irritation risk across the class. 1B-LSD — the closest structural analog to 1BP-LSD in the Jurowski et al. assessment — showed a 75% predicted probability of hematotoxicity and variable hERG channel inhibition (IC₅₀) across computational platforms. 1BP-LSD itself was not included in this analysis.supported
Predicted oral LD50 in rats: 49-85 mg/kg (Percepta). 1B-LSD predicted hematotoxicity 75%. Cardiotoxicity: hERG IC50 varies. Low dermal/ocular irritation risk. s00204-025-04255-1
In silico toxicity predictions for structurally related N1-acyl LSD analogs (ALD-52, 1P-LSD, 1B-LSD, 1V-LSD, 1cP-LSD) predicted oral LD₅₀ values in rats of 49–85 mg/kg (Percepta platform), with low dermal and ocular irritation risk across the class. 1B-LSD — the closest structural analog to 1BP-LSD in the Jurowski et al. assessment — showed a 75% predicted probability of hematotoxicity and variable hERG channel inhibition (IC₅₀) across computational platforms. 1BP-LSD itself was not included in this analysis.supported
Predicted oral LD50 in rats: 49-85 mg/kg (Percepta). 1B-LSD predicted hematotoxicity 75%. Cardiotoxicity: hERG IC50 varies. Low dermal/ocular irritation risk. s00204-025-04255-1
Claim in safety — inconclusiveinconclusiveworking →
Claim in safety — inconclusiveinconclusiveworking →
LSD-precipitated psychosis typically resolves within hours to days of drug clearance but may be prolonged in vulnerable individuals.supported
Distinguishes acute effects (anxiety, confusion, paranoia), subacute effects (HPPD, prolonged psychosis), and chronic effects. Reviews pre-existing vulnerability factors. 02698811211069100
Claim in safety — inconclusiveinconclusiveworking →
Claim in safety — inconclusiveinconclusiveworking →
Treatment options include clonidine, clonazepam, and levetiracetam; risperidone is specifically contraindicated as it worsens symptoms.supported
Clonidine, clonazepam, levetiracetam show substantial reduction. Risperidone worsens HPPD symptoms. hrp.0000000000000439
Psychiatric destabilization: LSD-class psychedelics carry a risk of triggering latent psychiatric conditions, particularly schizophrenia-spectrum disorders, in individuals with genetic vulnerabilitysupported
Distinguishes subacute effects (HPPD, prolonged psychosis), and chronic effects. Reviews pre-existing vulnerability factors. 02698811211069100
Tolerance: Rapid pharmacodynamic tolerance develops via 5-HT₂A receptor downregulation in the frontal cortex after even a single administrationpartially supported
Repeated psychedelic administration induces rapid tolerance via 5-HT2AR downregulation. acschemneuro.2c00170
Claim in safety — not_supportednot supportedworking →
Cross-tolerance with non-psychedelic 5-HT₂A agonists (such as lisuride) does not occur, implicating a psychedelic-specific mechanism beyond simple 5-HT₂A agonism.supported
Non-psychedelic 5-HT2AR agonists do not induce tolerance. Mechanism is beta-arrestin-2 independent. acschemneuro.2c00170
Claim in safety — inconclusiveinconclusiveworking →
Pharmacokinetic interactions: MDMA co-administration increases LSD plasma levels (both Cmax and AUC), prolongs subjective effects, and produces greater blood pressure and heart rate elevations — a pharmacokinetic interaction whereby MDMA inhibits LSD metabolism.supported
MDMA co-administration with LSD increases LSD Cmax, AUC, and prolongs elimination half-life. Combined use increases blood pressure, heart rate, pupil size more than LSD alone. s41386-023-01609-0
Antipsychotics block psychedelic effects via 5-HT₂A antagonism; risperidone specifically worsens HPPD symptoms.partially supported
Risperidone worsens HPPD symptoms. hrp.0000000000000439
Personal or family history of psychosis, schizophrenia, or schizoaffective disorder: LSD-class psychedelics can precipitate acute psychotic episodes and may trigger the onset of chronic psychotic illness in genetically predisposed individuals.supported
Distinguishes acute effects (anxiety, confusion, paranoia), subacute effects (HPPD, prolonged psychosis), and chronic effects. Reviews pre-existing vulnerability factors. 02698811211069100
Claim in safety — inconclusiveinconclusiveworking →
Claim in safety — inconclusiveinconclusiveworking →
Cardiovascular disease: LSD produces moderate tachycardia and hypertension; individuals with pre-existing cardiovascular conditions face elevated risk.partially supported
Weak autonomic stimulation. No complications in controlled medical settings. npp.2017.86
pharmacology13 · 12 ok
Halberstadt et al. demonstrated that N1-acyl LSD derivatives (ALD-52, 1P-LSD, 1B-LSD) are weak partial agonists or antagonists at 5-HT₂A receptors in their intact form and require in vivo deacylation to liberate LSD as the active moietysupported
ALD-52, 1P-LSD, 1B-LSD have weak efficacy or act as antagonists in Ca2+ assays. High LSD plasma levels detected in rats after 1P-LSD/ALD-52 SC administration, confirming prodrug status. j.neuropharm.2019.107856
The most direct human evidence comes from Grumann et al., who administered oral 1P-LSD (100 µg) to healthy volunteers and detected only LSD in serum and urine — no intact 1P-LSD was measurable — with an LSD elimination half-life of 6.4 hours and approximately 100% LSD bioavailability from the prodrug dose.supported
Oral 1P-LSD (100μg): only LSD detectable in serum/urine; LSD t1/2=6.4h. Bioavailability of LSD from oral 1P-LSD ~100%. dta.2821
This has been definitively established by blocking studies: the selective 5-HT₂A antagonist ketanserin completely abolishes all subjective and behavioral effects of LSD at doses up to 200 µgsupported
Effects fully mediated by 5-HT2A (blocked by ketanserin). s41386-020-00883-6
The structural basis for LSD's exceptionally prolonged receptor engagement was elucidated by Wacker et al., whose crystal structure of LSD bound to 5-HT₂B revealed that extracellular loop 2 (EL2) forms a "lid" over the binding pocket, trapping the ligand and producing slow dissociation kinetics.supported
Crystal structure of LSD in complex with human 5-HT2B. EL2 'lid' mechanism explains LSD's unusually slow binding kinetics at 5-HT2A and 5-HT2B receptors. j.cell.2016.12.033
Jain et al. profiled LSD against 318 human G protein-coupled receptors (GPCRs), demonstrating potent activity at virtually every serotonin subtype (5-HT₁A, 5-HT₁B, 5-HT₂A, 5-HT₂B, 5-HT₂C, 5-HT₅–₇), dopamine receptors (D₁–D₄), and adrenergic receptors (α₁, α₂, β)supported
41 classical psychedelics profiled against 318 human GPCRs. LSD has potent actions at nearly every serotonin, dopamine, and adrenergic receptor. j.neuron.2025.06.012
Claim in pharmacology — inconclusiveinconclusiveworking →
LSD oral bioavailability is 80%, determined by crossover comparison of oral and intravenous administrationsupported
Absolute oral bioavailability of LSD is 80%. cpt.3726
Time to peak plasma concentration (Tmax) is approximately 1.1 hours after direct LSD administration; for 1BP-LSD, Tmax is expected to be substantially delayed (estimated 3–4 hours total) due to the additional prodrug conversion stepsupported
Tmax ~1.1h cpt.2057
The elimination half-life of LSD ranges from 2.7–3.5 hours at microdoses to 6.4 hours in the 1P-LSD human pharmacokinetic study.supported
elimination half-life ~2.7h cpt.2057
The elimination half-life of LSD ranges from 2.7–3.5 hours at microdoses to 6.4 hours in the 1P-LSD human pharmacokinetic study.supported
LSD t1/2=6.4h dta.2821
LSD is metabolized primarily by cytochrome P450 enzymes: CYP2D6 and CYP2E1 produce nor-LSD, while CYP1A2, CYP2C9, CYP2E1, and CYP3A4 generate 2-oxo-3-hydroxy-LSD (O-H-LSD)partially supported
CYP2D6, CYP2E1, CYP3A4 form nor-LSD; CYP1A2, CYP2C9, CYP2E1, CYP3A4 form O-H-LSD. j.bcp.2019.04.013
Less than 1% of LSD is metabolized over 4 hours in human liver microsomes, consistent with the compound's prolonged duration of actionsupported
Minor metabolism (<1% over 4h in human liver microsomes). j.bcp.2019.04.013
CYP2D6 poor metabolizers exhibit approximately 75% higher area under the curve (AUC), longer elimination half-life, and greater subjective effects compared to extensive metabolizers.supported
CYP2D6 poor metabolizers have ~75% higher LSD AUC and longer half-life. Greater subjective effects and longer duration in poor metabolizers. s41598-021-90343-y
history8 · 3 ok
Claim in history — inconclusiveinconclusiveworking →
Claim in history — inconclusiveinconclusiveworking →
Claim in history — inconclusiveinconclusiveworking →
Claim in history — inconclusiveinconclusiveworking →
The series began with ALD-52 (1-acetyl-LSD, originally synthesized by Albert Hofmann in the 1950s, resurfaced on research chemical markets circa 2014) and continued through 1P-LSD (~2015), 1B-LSD (~2017), 1cP-LSD (~2019), 1V-LSD (~2021), and 1S-LSD (~2023–2024)supported
First forensic identification of 1S-LSD in paper sheet products. Confirms presence as designer drug on online market. s11419-025-00718-3
Claim in history — inconclusiveinconclusiveworking →
Forensic identification of 1BP-LSD can be anticipated in the near term, following the established pattern of Brandt et al.'s Return of the Lysergamides series.supported
Comprehensive analytical characterization of 1B-LSD using NMR, mass spectrometry, GC/LC, IR. HTR studies in C57BL/6J mice. dta.2613
Forensic identification of 1BP-LSD can be anticipated in the near term, following the established pattern of Brandt et al.'s Return of the Lysergamides series.supported
Part of the series establishing N1-acyl LSD derivatives as prodrugs. dta.2789
neuroscience6 · 2 ok
Activation of these receptors initiates a cascade of effects across multiple brain systems:supported
LSD induces bliss, synesthesia, depersonalization, mystical experiences via 5-HT2A. npp.2017.86
Claim in neuroscience — inconclusiveinconclusiveworking →
This mechanism underlies the perceptual intensification, synesthesia, and sensory flooding characteristic of the psychedelic state.supported
LSD induces bliss, synesthesia, depersonalization, mystical experiences via 5-HT2A. npp.2017.86
Claim in neuroscience — inconclusiveinconclusiveworking →
Claim in neuroscience — inconclusiveinconclusiveworking →
Claim in neuroscience — inconclusiveinconclusiveworking →
receptor-pharmacology6 · 3 ok
Based on the N1-acyl lysergamide prodrug model — in which the intact prodrug is a weak partial agonist or antagonist at 5-HT₂A and the pharmacologically active species is LSD — the receptor pharmacology of 1BP-LSD is effectively that of its metabolite, LSD.supported
ALD-52, 1P-LSD, 1B-LSD have weak efficacy or act as antagonists in Ca2+ assays. High LSD plasma levels detected in rats after 1P-LSD/ALD-52 SC administration, confirming prodrug status. j.neuropharm.2019.107856
Claim in receptor-pharmacology — inconclusiveinconclusiveworking →
This structural trapping explains LSD's exceptionally slow receptor off-rate — far slower than serotonin or other ergoline ligands — and directly contributes to the compound's prolonged duration of action (8–12 hours at standard doses).supported
EL2 'lid' mechanism explains LSD's unusually slow binding kinetics at 5-HT2A and 5-HT2B receptors. Explains LSD's prolonged receptor occupancy and duration of action. j.cell.2016.12.033
Jain et al. screened LSD against 318 human GPCRs, revealing one of the broadest receptor engagement profiles of any psychedelicsupported
41 classical psychedelics profiled against 318 human GPCRs. LSD has potent actions at nearly every serotonin, dopamine, and adrenergic receptor. j.neuron.2025.06.012
Claim in receptor-pharmacology — inconclusiveinconclusiveworking →
Claim in receptor-pharmacology — inconclusiveinconclusiveworking →
summary4 · 4 ok
As an N1-acyl lysergamide, 1BP-LSD is presumed to undergo two-step hydrolysis — boronate ester cleavage followed by amide bond scission — to liberate LSD as the sole pharmacologically active metabolitesupported
High LSD plasma levels detected in rats after 1P-LSD/ALD-52 SC administration, confirming prodrug status. j.neuropharm.2019.107856
The prodrug model is well-established for this structural class: oral 1P-LSD (100 µg) in humans produced detectable LSD but no intact prodrug in serum or urinesupported
Oral 1P-LSD (100μg): only LSD detectable in serum/urine dta.2821
Once released, LSD acts primarily through 5-HT₂A receptor agonism — confirmed by complete blockade with ketanserin — to produce the characteristic psychedelic phenomenology: geometric visual effects, thought connectivity, ego dissolution at higher doses, and emotional intensification, with set and setting as principal non-pharmacological modulators.supported
Ego dissolution and anxiety increase above 100μg. Effects fully mediated by 5-HT2A (blocked by ketanserin). s41386-020-00883-6
Rapid tolerance develops via 5-HT₂A receptor downregulation after a single dose, with 7–14 days required for full recovery; physical dependence does not developpartially supported
Repeated psychedelic administration induces rapid tolerance via 5-HT2AR downregulation. acschemneuro.2c00170
comparative-pharmacology3 · 3 ok
Progressively delayed onset: Brandt et al. observed a trend toward decreased head-twitch response (HTR) potency with increasing N1-acyl chain length in mice, suggesting slower or less efficient prodrug conversion. 1BP-LSD, with its two-step hydrolysis requirement, extends this trend further.supported
1V-LSD (1-pentanoyl-LSD) higher homolog of ALD-52, 1P-LSD, 1B-LSD. HTR ED50 = 373 nmol/kg (~1/3 potency of LSD). dta.3205
User surveys of 1P-LSD, AL-LAD, and ETH-LAD found generally comparable subjective effects to LSD across the analog seriessupported
Survey study of LSD analogue (AL-LAD, 1P-LSD, ETH-LAD) self-reported effects and user profiles compared to LSD. hup.2599
Any perceived qualitative differences between analogs likely reflect differences in onset kinetics and absorption rate rather than distinct receptor pharmacology.supported
High LSD plasma levels detected in rats after 1P-LSD/ALD-52 SC administration, confirming prodrug status. j.neuropharm.2019.107856
effects-overview3 · 1 ok
Claim in effects-overview — inconclusiveinconclusiveworking →
Relative to LSD, 1BP-LSD is pharmacologically identical once prodrug conversion is complete — it occupies the same phenomenological space with the same receptor target, duration range, and effect taxonomysupported
High LSD plasma levels detected in rats after 1P-LSD/ALD-52 SC administration, confirming prodrug status. j.neuropharm.2019.107856
Claim in effects-overview — inconclusiveinconclusiveworking →
pharmacokinetic-detail3 · 2 ok
Claim in pharmacokinetic-detail — not_supportednot supportedworking →
The disparity between LSD's relatively short plasma half-life (2.7–6.4 hours) and its prolonged subjective duration (8–12 hours) is explained by the slow receptor dissociation kinetics demonstrated by Wacker et al.supported
EL2 'lid' mechanism explains LSD's unusually slow binding kinetics. Explains LSD's prolonged receptor occupancy and duration of action. j.cell.2016.12.033
Vizeli et al. demonstrated in a pooled analysis that CYP2D6 poor metabolizers exhibit approximately 75% higher LSD area under the curve (AUC), longer elimination half-life, and greater subjective effect intensity compared to extensive metabolizerssupported
CYP2D6 poor metabolizers have ~75% higher LSD AUC and longer half-life. Greater subjective effects and longer duration in poor metabolizers. s41598-021-90343-y
clinical-evidence1 · 1 ok
The most clinically relevant data point for 1BP-LSD's expected in vivo behavior is the human pharmacokinetic study by Grumann et al., in which 1P-LSD (100 µg, oral) was administered to healthy volunteerssupported
Oral 1P-LSD (100μg): only LSD detectable in serum/urine dta.2821
legal-status1 · 1 ok
The Grumann et al. demonstration that N1-acyl LSD prodrugs produce only LSD in human serum provides a pharmacological basis for such arguments, though legal determination of "substantial similarity" under the FAA involves considerations beyond pharmacology.supported
Oral 1P-LSD (100μg): only LSD detectable in serum/urine dta.2821