generation run 2026-04-26
66 min completedmodel pipeline-v5plan not recordedrun/556be83c…Selection
Verification
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- seen / partial
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The model's own caveats
none raised on this run
Reproduce
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- 31 source keys (listed under Sources)
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- model
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24 searches — query, source, results, what was kept and why
| # | source | query | seen | kept | rationale |
|---|---|---|---|---|---|
| 1 | ClinicalTrials.gov · absence | 1V-LSD lysergamide | 0 | 0 | No trials exist for this compound |
| 2 | PubMed | LSD lysergic acid diethylamide serotonin 5-HT2A receptor binding affinity pharmacology | 15 | 4 | Foundational receptor pharmacology papers relevant to LSD class mechanism |
| 3 | PubMed | LSD lysergic acid diethylamide human pharmacokinetics bioavailability metabolism | 3 | 2 | Grumann 2020 is critical for prodrug evidence in humans; Arikci 2025 for LSD PK |
| 4 | PubMed | 1V-LSD lysergamide novel psychoactive | 1 | 1 | Only published primary research paper specifically on 1V-LSD |
| 5 | PubMed | return of the lysergamides 1P-LSD 1B-LSD ALD-52 analytical characterization | 10 | 8 | Series provides direct SAR context for 1V-LSD |
| 6 | PubChem | 1V-LSD | 1 | 1 | Primary chemical identity verification |
| 7 | PubMed | LSD mouse head twitch response hallucinogen 5-HT2A Halberstadt | 10 | 1 | Key methodology paper for HTR assay used in 1V-LSD study |
| 8 | OpenAlex | 1V-LSD valeroyl lysergamide | 11 | 10 | All relevant to 1V-LSD or lysergamide class pharmacology and forensics |
| 9 | PubMed | 1-valeroyl-LSD pharmacology | 1 | 0 | Duplicate of step 2 |
| 10 | PubMed | LSD Holze 2021 pharmacokinetics subjective effects healthy volunteers | 4 | 4 | Critical LSD PK and dose-response data applicable to 1V-LSD as LSD prodrug |
| 11 | PubMed | PMID 28129538 | 1 | 1 | Foundational structural biology of LSD binding |
| 12 | PubMed | HPPD hallucinogen persisting perception disorder LSD psychedelic | 8 | 5 | HPPD is key psychological risk for LSD class; directly applicable to 1V-LSD |
| 13 | PubMed | LSD Dolder 2017 pharmacokinetics subjective effects | 1 | 1 | Foundational LSD PK characterization |
| 14 | PubMed | PMID 37280397 | 1 | 1 | Novel LSD mechanism of action via TrkB |
| 15 | PubMed | PMID 40283936 | 1 | 1 | Comprehensive LSD safety and clinical research review applicable to 1V-LSD as prodrug |
| 16 | OpenAlex | 1P-LSD propanoyl lysergic acid diethylamide NPS research chemical | 8 | 2 | Key 1P-LSD analytical methods; stability relevant to 1V-LSD prodrug detection |
| 17 | DOI Crossref | 10.1002/dta.3205 | 1 | 1 | Primary 1V-LSD paper DOI verification |
| 18 | OpenAlex | LSD serotonin 5HT2A dopamine binding affinity receptor Ki | 8 | 2 | Comprehensive receptor binding Ki data for LSD applicable to 1V-LSD |
| 19 | PubMed | PMID 36779453 | 1 | 1 | Stability context for N1-acyl LSD forensic analysis |
| 20 | PubMed | PMID 31756337 | 1 | 1 | Critical pharmacological characterization of the entire N1-acyl LSD class including mechanism |
| 21 | WebSearch | 1V-LSD legal status United States Australia Canada United Kingdom | 10 | 0 | Additional legal status verification |
| 22 | PubMed | LSD therapeutic clinical trial anxiety depression addiction | 7 | 2 | Therapeutic context for LSD class pharmacology |
| 23 | PubMed | LSD metabolite OH-LSD urine detection forensic | 1 | 1 | LSD metabolic profile applicable to 1V-LSD as LSD prodrug |
| 24 | WebSearch | 1V-LSD NpSG Germany scheduling ban 2022 2023 | 10 | 2 | Legal status for key jurisdictions |
76 claims by section — every cited sentence, checked against its source
pharmacology20 · 16 ok
No direct receptor binding or biotransformation data have been published for 1V-LSD itself; the prodrug hypothesis rests on converging evidence from structurally related N1-acyl LSD derivatives.supported
Analytical characterization via MS, GC, LC, NMR, GC-sIR, Raman spectroscopy. HTR ED50 = 373 nmol/kg (~1/3 potency of LSD). Likely prodrug for LSD via hydrolysis. dta.3205
N1-acyl substitution reduces monoamine receptor affinity by 1–2 orders of magnitude relative to LSD and converts the compound from a 5-HT₂A partial agonist to a weak partial agonist or functional antagonist in calcium flux assayssupported
1-acyl substitution reduces monoamine receptor affinity by 1-2 orders of magnitude. ALD-52, 1P-LSD, 1B-LSD show weak efficacy or act as antagonists at 5-HT2A in Ca2+ assays. j.neuropharm.2019.107856
In vitro hydrolysis: Incubation of 1CP-LSD with human serum produces LSD. N1-deacylation is the primary metabolic reaction for 1P-AL-LAD in pooled human liver microsomes. Temperature-dependent hydrolysis of ALD-52 and 1P-LSD to LSD occurs in serum at room temperature.supported
1CP-LSD incubated with human serum -> LSD formation (in vitro prodrug evidence). dta.2789
In vitro hydrolysis: Incubation of 1CP-LSD with human serum produces LSD. N1-deacylation is the primary metabolic reaction for 1P-AL-LAD in pooled human liver microsomes. Temperature-dependent hydrolysis of ALD-52 and 1P-LSD to LSD occurs in serum at room temperature.supported
1P-AL-LAD metabolized to AL-LAD in human liver microsomes (pHLM). N1-deacylation primary metabolic reaction. dta.3281
Claim in pharmacology — inconclusiveinconclusiveworking →
In vitro hydrolysis: Incubation of 1CP-LSD with human serum produces LSD. N1-deacylation is the primary metabolic reaction for 1P-AL-LAD in pooled human liver microsomes. Temperature-dependent hydrolysis of ALD-52 and 1P-LSD to LSD occurs in serum at room temperature.supported
Temperature-dependent hydrolysis of 1P-LSD to LSD (up to 21% in serum at RT). j.jpba.2019.05.062
In vivo human evidence: After oral or intravenous administration of 100 µg 1P-LSD to two human volunteers, only LSD was detected in serum and urine — not 1P-LSD itself — with LSD t½ ≈ 5.7–6.4 h; bioavailability of LSD from oral 1P-LSD was "close to 100%".supported
1P-LSD oral ingestion: only LSD detected in serum/urine (not parent 1P-LSD). LSD t1/2 ≈ 5.7h. 1P-LSD bioavailability of LSD close to 100% via oral prodrug. dta.2821
In vivo animal evidence: High LSD plasma levels were detected in rats after 1P-LSD administration. Both 1F-LSD and 1T-LSD hydrolyzed to LSD after in vivo administration to mice.supported
High LSD plasma levels after 1P-LSD in rats confirms prodrug status. j.neuropharm.2019.107856
In vivo animal evidence: High LSD plasma levels were detected in rats after 1P-LSD administration. Both 1F-LSD and 1T-LSD hydrolyzed to LSD after in vivo administration to mice.supported
1F-LSD and 1T-LSD both serve as prodrugs. N1-acylated LSD derivatives hydrolyzed to LSD in vivo. dta.3829
Claim in pharmacology — inconclusiveinconclusiveworking →
1V-LSD was tested in C57BL/6J mice using the head-twitch response (HTR) assay — a 5-HT₂A-mediated behavior validated as a predictive proxy for hallucinogenic potency in humans (r = 0.9448 across 41 compounds).supported
Strong correlation (r=0.9448) between HTR potency in mice and hallucinogenic potency in humans across 41 compounds. j.neuropharm.2019.107933
1V-LSD induced a dose-dependent HTR with an ED₅₀ of 373 nmol/kg (approximately 152 µg/kg), roughly one-third the potency of LSD (ED₅₀ = 132.8 nmol/kg) under identical conditionssupported
HTR ED50 = 373 nmol/kg (~1/3 potency of LSD). dta.3205
The decreased potency relative to LSD likely reflects incomplete hydrolysis efficiency rather than direct 5-HT₂A activity.supported
HTR ED50 = 373 nmol/kg (~1/3 potency of LSD). Likely prodrug for LSD via hydrolysis. dta.3205
Claim in pharmacology — inconclusiveinconclusiveworking →
Oral bioavailability: 80%; base and tartrate formulations are bioequivalentsupported
LSD oral bioavailability confirmed at 80%. All oral formulations bioequivalent. cpt.3726
Half-life: 2.7 h at microdoses; ~5.7–6.4 h at 100 µg; up to 11.6 h in CYP2D6 poor metabolizerssupported
LSD t1/2 ≈ 5.7h. dta.2821
Claim in pharmacology — inconclusiveinconclusiveworking →
Primary metabolizing enzyme: CYP2D6; poor metabolizers exhibit ~75% higher LSD AUC and prolonged subjective effectssupported
CYP2D6 poor metabolizers had ~75% higher LSD AUC and longer half-lives; greater alterations of mind and longer subjective effects. CYP1A2, CYP2C9, CYP2C19, CYP2B6 had no effect. s41598-021-90343-y
Primary urinary metabolite: 2-oxo-3-hydroxy-LSD (OH-LSD); additional metabolites include nor-LSD, nor-iso-LSD, trioxylated-LSD, and 13/14-hydroxy-LSD glucuronidessupported
OH-LSD (2-oxo-3-hydroxy-LSD) main urine metabolite; nor-LSD, nor-iso-LSD, trioxylated-LSD, 13/14-OH-LSD glucuronides also detected. s1570-0232(01)00494-9
By analogy with 1P-LSD — where the parent compound was detectable in serum for only 4.16 h and in urine for 2.7 h post-dose — 1V-LSD itself is expected to have a short plasma half-life, with LSD as the principal detected active species.supported
1P-LSD oral ingestion: only LSD detected in serum/urine (not parent 1P-LSD). dta.2821
safety17 · 11 ok
No well-documented human fatalities from LSD alone have been reported in the published literaturesupported
Physiologically well tolerated; psychological reactions controllable in supervised settings. j.1755-5949.2008.00059.x
Claim in safety — inconclusiveinconclusiveworking →
An intoxication case involving 1P-LSD was investigated analytically, finding 0.51 ng/mL LSD in urine and 3.4 ng/mL in serum, with 1P-LSD undetected — consistent with complete prodrug conversion.supported
Applied to intoxication case: only LSD detected in urine/serum after oral 1P-LSD ingestion. j.jpba.2019.05.062
Claim in safety — inconclusiveinconclusiveworking →
Claim in safety — inconclusiveinconclusiveworking →
Acute anxiety and distress: In controlled settings, 200 µg LSD produced significant anxiety in healthy volunteerssupported
Greater ego dissolution and anxiety at 200µg. s41386-020-00883-6
Good drug effects plateau at 100 µg while ego dissolution and anxiety continue to increase with dosesupported
Ceiling for good effects at 100µg, greater ego dissolution and anxiety at 200µg. s41386-020-00883-6
Hallucinogen persisting perception disorder (HPPD): A rare complication characterized by re-emergence of perceptual symptoms after drug cessation, without impaired reality testingsupported
HPPD: rare disorder of enduring perceptual symptoms without impaired reality control after psychedelic use. s41598-024-82216-x
Hallucinogen persisting perception disorder (HPPD): A rare complication characterized by re-emergence of perceptual symptoms after drug cessation, without impaired reality testingsupported
39.7% of hallucinogen users reported Type I HPPD symptoms; 4.3% Type II. 02791072.2023.2287081
LSD is the most frequently implicated substance in HPPD case reportssupported
LSD most common hallucinogen causing HPPD. cureus.46262
Prevalence estimates vary widely: up to 39.7% for mild Type I symptoms (brief perceptual disturbances) in one self-report survey, and 4.3% for Type II HPPD with functional impairmentsupported
39.7% of hallucinogen users reported Type I HPPD symptoms; 4.3% Type II. 02791072.2023.2287081
Treatment options include benzodiazepines (clonazepam) or lamotrigine; antipsychotics are generally ineffective.supported
Lamotrigine improved symptoms when antipsychotics failed. cureus.46262
Claim in safety — inconclusiveinconclusiveworking →
Claim in safety — inconclusiveinconclusiveworking →
Claim in safety — inconclusiveinconclusiveworking →
A meta-analysis of psychedelic RCTs found no association between psychedelics and higher all-cause discontinuation.supported
Not associated with higher all-cause discontinuation. j.euroneuro.2025.09.011
CYP2D6 inhibitors: Fluoxetine, paroxetine, and bupropion may increase LSD exposure following 1V-LSD prodrug conversion by inhibiting the primary metabolic clearance pathway.supported
CYP2D6 poor metabolizers had ~75% higher LSD AUC and longer half-lives. CYP1A2, CYP2C9, CYP2C19, CYP2B6 had no effect. s41598-021-90343-y
history9 · 7 ok
LSD was synthesized by Albert Hofmann at Sandoz Laboratories in Basel, Switzerland, in 1938; its psychedelic properties were discovered accidentally during self-experimentation on April 19, 1943supported
Synthesized 1938, psychoactive effects discovered 1943. j.1755-5949.2008.00059.x
Claim in history — not_supportednot supportedworking →
Each compound extended the acyl chain by one or more carbons: ALD-52 (C2 acetyl) → 1P-LSD (C3 propanoyl) → 1B-LSD (C4 butanoyl) → 1V-LSD (C5 pentanoyl) → 1H-LSD (C6 hexanoyl) → 1DD-LSD (C12 dodecanoyl)supported
1H-LSD HTR ED50 = 192.4 µg/kg (387 nmol/kg), roughly equipotent to ALD-52. N1-acyl LSD derivative anticipated to be hydrolyzed to LSD in vivo. dta.3767
Each compound extended the acyl chain by one or more carbons: ALD-52 (C2 acetyl) → 1P-LSD (C3 propanoyl) → 1B-LSD (C4 butanoyl) → 1V-LSD (C5 pentanoyl) → 1H-LSD (C6 hexanoyl) → 1DD-LSD (C12 dodecanoyl)supported
1DD-LSD HTR ED50 = 2.17 mg/kg (27-fold less potent than LSD). N1-acyl homolog series. dta.3691
The compounds were systematically characterized in the "Return of the Lysergamides" publication series by Brandt, Kavanagh, Halberstadt, and collaborators: Part II covered AL-LAD and LSZ, Part IV LSM-775, Part V 1B-LSD, Part VI 1CP-LSD, and Part VII — the subject of this article — 1V-LSD.supported
Return of the lysergamides. Part IV: Analytical and pharmacological characterization of lysergic acid morpholide (LSM-775) dta.2222
The compounds were systematically characterized in the "Return of the Lysergamides" publication series by Brandt, Kavanagh, Halberstadt, and collaborators: Part II covered AL-LAD and LSZ, Part IV LSM-775, Part V 1B-LSD, Part VI 1CP-LSD, and Part VII — the subject of this article — 1V-LSD.supported
Return of the lysergamides. Part V: Analytical and behavioural characterization of 1-butanoyl-d-lysergic acid diethylamide (1B-LSD) dta.2613
The compounds were systematically characterized in the "Return of the Lysergamides" publication series by Brandt, Kavanagh, Halberstadt, and collaborators: Part II covered AL-LAD and LSZ, Part IV LSM-775, Part V 1B-LSD, Part VI 1CP-LSD, and Part VII — the subject of this article — 1V-LSD.supported
Return of the lysergamides. Part VII: Analytical and behavioural characterization of 1-valeroyl-d-lysergic acid diethylamide (1V-LSD) dta.3205
Claim in history — inconclusiveinconclusiveworking →
A validated forensic LC-MS/MS method for 1V-LSD detection in urine (LOD 0.1 ng/mL) was subsequently developed, though no positive urine specimens were found among 325 samples tested.supported
LC-MS/MS method validated for LSD, OH-LSD, and 9 LSD analogs including 1V-LSD in urine. LOD 0.1 ng/mL. No LSD analogs detected in 325 urine specimens tested. 1556-4029.15572
summary8 · 6 ok
Claim in summary — inconclusiveinconclusiveworking →
1V-LSD first appeared on the online research chemical market around 2020–2021 and was analytically and pharmacologically characterized by Brandt et al. in 2022 as Part VII of the "Return of the Lysergamides" seriessupported
Return of the lysergamides. Part VII: Analytical and behavioural characterization of 1-valeroyl-d-lysergic acid diethylamide (1V-LSD) dta.3205
N1-acyl substitution reduces monoamine receptor affinity by 1–2 orders of magnitude relative to LSD, converting the compound from an active 5-HT₂A agonist to a functionally inert precursor that requires in vivo hydrolysis to liberate LSDsupported
1-acyl substitution reduces monoamine receptor affinity by 1-2 orders of magnitude. ALD-52, 1P-LSD, 1B-LSD show weak efficacy or act as antagonists at 5-HT2A in Ca2+ assays. High LSD plasma levels after 1P-LSD in rats confirms prodrug status. j.neuropharm.2019.107856
In mice, 1V-LSD produces a dose-dependent head-twitch response (ED₅₀ = 373 nmol/kg), approximately one-third the potency of LSD (ED₅₀ = 132.8 nmol/kg), consistent with incomplete but efficient prodrug conversionsupported
HTR ED50 = 373 nmol/kg (~1/3 potency of LSD). Likely prodrug for LSD via hydrolysis. dta.3205
Following conversion, LSD acts primarily as a 5-HT₂A partial agonist; ketanserin (40 mg) completely blocks all subjective LSD effectssupported
Ketanserin blocked all effects. 5-HT2A primary mediator. s41386-020-00883-6
As a prodrug for LSD, 1V-LSD inherits LSD's negligible acute toxicity profile: no well-documented human fatalities from LSD alone have been reportedsupported
Physiologically well tolerated; psychological reactions controllable in supervised settings. j.1755-5949.2008.00059.x
Claim in summary — inconclusiveinconclusiveworking →
No biotransformation data, human pharmacokinetic parameters, or controlled dose-response studies have been published for 1V-LSD specifically — all safety and efficacy characterizations rest on LSD class inference pending direct investigation.supported
Analytical characterization via MS, GC, LC, NMR, GC-sIR, Raman spectroscopy. HTR ED50 = 373 nmol/kg (~1/3 potency of LSD). Likely prodrug for LSD via hydrolysis. dta.3205
receptor-pharmacology7 · 5 ok
This receptor is the primary mediator of hallucinogenic effects — the selective 5-HT₂A antagonist ketanserin (40 mg oral) completely blocks all subjective LSD effects in healthy volunteerssupported
Ketanserin blocked all effects. 5-HT2A primary mediator. s41386-020-00883-6
N1-acyl substitution itself reduces monoamine receptor affinity by 1–2 orders of magnitude relative to LSDsupported
1-acyl substitution reduces monoamine receptor affinity by 1-2 orders of magnitude. j.neuropharm.2019.107856
Crystallographic analysis of LSD bound to 5-HT₂B reveals a slow-dissociation mechanism mediated by extracellular loop 2 (EL2), which forms a "lid" over the binding pocket; the same mechanism is inferred at 5-HT₂A and may explain the prolonged duration of action.supported
Crystal structure of LSD bound to 5-HT2B receptor. EL2 'lid' mechanism explains slow LSD dissociation from 5-HT2A and 5-HT2B. j.cell.2016.12.033
Claim in receptor-pharmacology — inconclusiveinconclusiveworking →
TrkB-mediated neuroplasticity effects are independent of 5-HT₂A activation, representing a mechanistically distinct pathway.supported
TrkB-mediated neuroplasticity is independent of 5-HT2A; head-twitch (hallucinogenic proxy) is TrkB-independent. s41593-023-01316-5
5-HT₂A–mGluR2 heterodimer: The 5-HT₂A–mGluR2 receptor complex is required for hallucinogen-specific intracellular signaling; mGluR2 activation abolishes hallucinogen-specific downstream responses.supported
5-HT2A-mGluR2 heterodimer forms functional complex in brain cortex. Hallucinogenic drugs trigger unique cellular responses via this complex. mGluR2 activation abolishes hallucinogen-specific signaling. nature06612
Claim in receptor-pharmacology — inconclusiveinconclusiveworking →
comparative-pharmacology5 · 3 ok
Claim in comparative-pharmacology — inconclusiveinconclusiveworking →
Claim in comparative-pharmacology — inconclusiveinconclusiveworking →
ALD-52 potency is stated as roughly equipotent to 1H-LSD (387 nmol/kg).supported
1H-LSD HTR ED50 = 192.4 µg/kg (387 nmol/kg), roughly equipotent to ALD-52. dta.3767
Long-chain collapse: 1DD-LSD (C12) retains only ~4% of LSD potency, consistent with steric impedance of hydrolysis or reduced bioavailability of the long-chain derivative.supported
1DD-LSD HTR ED50 = 2.17 mg/kg (27-fold less potent than LSD). N1-acyl homolog series; increased lipophilicity may reduce enzymatic hydrolysis efficiency. dta.3691
The only human PK data in the series come from 1P-LSD, where oral bioavailability of the liberated LSD approached 100%supported
1P-LSD bioavailability of LSD close to 100% via oral prodrug. dta.2821
chemistry3 · 3 ok
By analogy with other N1-acyl LSD derivatives, the compound is expected to be susceptible to hydrolysis under acidic conditions and in alcoholic solventssupported
Temperature-dependent hydrolysis of 1P-LSD to LSD (up to 21% in serum at RT). j.jpba.2019.05.062
The compound is derived from d-LSD by acylation of the N1 indole nitrogen with a pentanoyl (valeroyl, C₅H₉O) group, making it the C5 homolog in the series of N1-acylated LSD derivatives.supported
1V-LSD (also known as 1-valeryl-LSD, 1-pentanoyl-LSD, or 'Valerie') is a new N1-acylated LSD derivative. dta.3205
The pentanoyl group may confer greater steric protection of the N1-acyl bond than the shorter acetyl group of ALD-52, and comparable stability to the propanoyl group of 1P-LSD, based on the steric hindrance trend observed across the series.supported
1P-LSD more stable than ALD-52 due to steric hindrance from propanoyl group. 1556-4029.15224
pharmacokinetic-detail3 · 3 ok
In a pooled analysis of 83 participants, CYP2D6 poor metabolizers exhibited approximately 75% higher LSD area under the curve (AUC) and prolonged subjective effects compared to normal metabolizerssupported
CYP2D6 poor metabolizers had ~75% higher LSD AUC and longer half-lives; greater alterations of mind and longer subjective effects. s41598-021-90343-y
For the structurally analogous 1P-LSD, oral administration to two human volunteers produced rapidly detectable serum LSD, with 1P-LSD itself detectable for only 4.16 h in serum and 2.7 h in urine; LSD then followed biphasic elimination with t½ ≈ 5.7–6.4 hsupported
1P-LSD oral ingestion: only LSD detected in serum/urine (not parent 1P-LSD). LSD t1/2 ≈ 5.7h. dta.2821
Bioavailability of LSD from oral 1P-LSD was "close to 100%", suggesting highly efficient prodrug conversion.supported
1P-LSD bioavailability of LSD close to 100% via oral prodrug. dta.2821
neuroscience2 · 2 ok
The second, recently characterized, involves direct binding to the TrkB (BDNF) receptor with approximately 1,000-fold higher affinity than conventional antidepressants; this TrkB-mediated pathway is independent of 5-HT₂A activationsupported
LSD and psilocin bind TrkB ~1,000-fold higher affinity than other antidepressants. TrkB-mediated neuroplasticity is independent of 5-HT2A. s41593-023-01316-5
The psychoplastogen framework predicts that LSD-class compounds may have therapeutic effects that persist beyond the acute pharmacological window, mediated by structural remodeling of neural circuits.supported
LSD and psilocin bind TrkB ~1,000-fold higher affinity than other antidepressants. TrkB-mediated neuroplasticity is independent of 5-HT2A. s41593-023-01316-5
clinical-evidence1 · 1 ok
A living systematic review and meta-analysis of serotonergic psychedelic RCTs found no association between psychedelics and higher all-cause discontinuation, supporting a favorable tolerability profile for the classsupported
30 RCTs (n=1480). Not associated with higher all-cause discontinuation. j.euroneuro.2025.09.011
effects-overview1 · 1 ok
Onset may be slightly more gradual than LSD itself, plausibly reflecting the hydrolysis step, though this has not been confirmed in controlled settings.supported
Likely prodrug for LSD via hydrolysis. dta.3205