1cP-LSD

# Research Output: 1cP-LSD

## Chemical Identity

**Verified via PubChem CID 155884675** (Ref 1 — database lookup):

- **Molecular Formula:** C₂₄H₂₉N₃O₂
- **Molecular Weight:** 391.5 g/mol
- **IUPAC Name:** (6aR,9R)-4-(cyclopropanecarbonyl)-N,N-diethyl-7-methyl-6,6a,8,9-tetrahydroindolo[4,3-fg]quinoline-9-carboxamide
- **InChIKey:** RAFUPYYDHPFASC-DYESRHJHSA-N
- **PubChem CID:** 155884675
- **Chemical Class:** Indole / Indoleamine / Tryptamine / Ergoline / Lysergamide (N1-acylated LSD derivative)

**Seed data discrepancies / gaps:**
- SMILES string: **Not returned by PubChem API.** The brief lists no SMILES; this remains unverified via structured tool. Flag for editorial retrieval directly from PubChem web entry or ChEMBL.
- CAS number: Not identified in any search. No CAS number is registered in accessible databases — likely absent as 1cP-LSD post-dates classic CAS registration workflows for designer compounds.
- IUPAC name in brief **confirmed identical** to PubChem entry.
- Molecular formula and weight confirmed. No discrepancies.

**Physical properties (limited data):**
Brandt et al. (2020 [Ref 1]) note the compound is distributed in blotter and pellet form. No published melting point, aqueous solubility, or formal stability data were found in the literature. Analytical work used methanol solutions; Tusiewicz et al. (2024 [Ref 14]) note that methanol can cause alcoholysis of N1-acyl LSD derivatives (including 1cP-LSD), producing LSD as an artifact — a critical consideration for analytical and harm-reduction contexts. Diethyl ether, tert-butyl methyl ether, dichloromethane, and acetone provide more stable extraction conditions (Tusiewicz et al. 2024 [Ref 14]).

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## Pharmacology

### Receptor Pharmacology

1cP-LSD is a **prodrug of LSD** (d-lysergic acid diethylamide). The N1-cyclopropanecarbonyl substituent at the indole nitrogen renders the compound a weak or inactive 5-HT₂A ligand in its intact form. Brandt et al. (2020 [Ref 1]) confirmed that incubation of 1cP-LSD with human serum at 37°C produces LSD, establishing the prodrug mechanism. This pattern was first described for 1P-ETH-LAD (Brandt et al. 2017 [Ref 16=actually Ref 7, Part III: PMID 28342178]) and definitively demonstrated in humans for 1P-LSD (Grumann et al. 2020 [Ref 5]).

The broader "Return of the Lysergamides" series confirms a class principle: **N1-acylation is detrimental to 5-HT₂A receptor activity, but in-vivo hydrolysis rapidly restores LSD-level activity** (Brandt et al. 2025, 1F-LSD paper [Ref 32]; Brandt et al. 2022 [Ref 9], 1V-LSD). Once hydrolyzed to LSD, the pharmacological profile matches LSD at all receptor targets.

### LSD Receptor Profile (Active Metabolite)
LSD — the active form — binds with nanomolar affinity at:
- **5-HT₂A receptor:** Primary psychedelic target; agonist/partial agonist activating Gq and β-arrestin2 pathways. Crystal structure of LSD bound to 5-HT₂B (Wacker et al. 2017 [Ref 16]) reveals an EL2 "lid" that explains LSD's characteristically slow dissociation kinetics at both 5-HT₂B and 5-HT₂A, contributing to prolonged duration of action. Active-state 5-HT₂A cryo-EM structure with LSD (Kim et al. 2020 [Ref 17]) shows arrestin-biased conformation.
- **5-HT₁A receptor:** Partial agonist. Activity at 5-HT₁A may modulate aspects of the LSD experience, including anxiolytic-like effects (Inserra et al. 2021 [Ref 29]).
- **Dopamine D₁/D₂/D₃/D₄ receptors:** Partial agonist activity documented; ergolines interact broadly with dopaminergic receptors (Ray 2010 [Ref 18]; Nichols 2018 [Ref 30]).
- **5-HT₂C receptor:** Agonist activity documented (Inserra et al. 2021 [Ref 29]).
- **TrkB (BDNF receptor):** Moliner et al. (2023 [Ref 26]) demonstrated LSD directly binds TrkB with ~1,000-fold higher affinity than classical antidepressants; this is mechanistically distinct from 5-HT₂A activation and mediates neuroplastic/antidepressant effects. 5-HT₂A-dependent (head-twitch) and TrkB-dependent (neuroplastic) effects are pharmacologically separable.

The full receptor promiscuity of LSD across 5-HT₁A, 5-HT₂A, 5-HT₂C, and multiple dopaminergic and adrenergic sites is summarized by Ray (2010 [Ref 18]) and reviewed in Cummins et al. (2025 [Ref 31]).

### Behavioral Pharmacology
Brandt et al. (2020 [Ref 1]) assessed 1cP-LSD in the mouse head-twitch response (HTR) assay — the standard in-vivo proxy for 5-HT₂A-mediated hallucinogen activity:
- **1cP-LSD HTR ED₅₀ = 430.0 nmol/kg** (C57BL/6J mice, IP)
- Comparator compounds in the series: LSD = 132.8 nmol/kg; 1P-LSD = 349.6 nmol/kg; AL-LAD = 174.9 nmol/kg; 1B-LSD = 976.7 nmol/kg; 1V-LSD = 373 nmol/kg
- 1cP-LSD is approximately 32% the potency of LSD in this assay; the reduced HTR potency relative to LSD is consistent with partial hydrolysis kinetics and lower intrinsic 5-HT₂A activity of the intact prodrug form

**Important caveat:** HTR potency in mice does not directly translate to human effective doses. The analogy between mouse HTR and human hallucinogenic effects is an approximation. No human potency data for 1cP-LSD exist.

### Pharmacokinetics

**No direct human PK studies exist for 1cP-LSD.** All available data are by structural analogy to 1P-LSD and from LSD reference studies.

**Prodrug hydrolysis (class mechanism):**
For 1P-LSD, Grumann et al. (2020 [Ref 5]) demonstrated in two human volunteers:
- Oral 1P-LSD 100 μg → only LSD detectable in serum and urine (1P-LSD undetectable orally)
- LSD elimination half-life ≈ 5.7h after oral 1P-LSD
- Bioavailability of LSD after oral 1P-LSD ≈ 100%
- 1P-LSD detectable for ≤4.16h IV (half-life dominated by rapid hydrolysis)
- Subjective effects were comparable to LSD in the literature

By structural analogy, 1cP-LSD is expected to behave similarly: orally administered 1cP-LSD undergoes rapid N1-deacylation to LSD, and the pharmacological experience reflects LSD pharmacokinetics. The cyclopropanoyl group (vs. propanoyl in 1P-LSD) may have marginally different hydrolysis kinetics due to steric and electronic effects, but this has not been measured.

**LSD reference PK (applicable via prodrug):**
- Dolder et al. (2017 [Ref 12]): oral LSD, dose-proportional PK, first-order elimination, half-life in the range of 2.6–3.6h
- Holze et al. (2021 [Ref 19, PMID 33059356]): LSD 25–200 μg, Tmax ≈ 1.5–2h, subjective duration 6.7–11h dose-dependently
- Holze et al. (2021 microdose [Ref not yet cited; PMID 32975835]): LSD half-life 2.7h in microdose PK
- Arikci et al. (2025): oral LSD absolute bioavailability 80%; bioequivalence of base/tartrate formulations

**Metabolism:** LSD is extensively metabolized hepatically. CYP enzymes are involved (CYP2D6 functionality correlated with LSD experience variability per Vizeli et al. 2024 [Ref — PMID 39231959]). Primary metabolites include nor-LSD, O-H-LSD, and trioxylated LSD, though the detailed metabolite profile for 1cP-LSD-derived LSD in humans has not been separately characterized.

**Onset delay:** Because 1cP-LSD requires an initial hydrolysis step before generating active LSD, onset may be slightly delayed relative to direct LSD administration. This is consistent with the brief's listed onset of 20–60 minutes.

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## History

**Market emergence:** 1cP-LSD (1-cyclopropanoyl-LSD; 1-cyclopropionyl-LSD) first appeared on the online research chemical market approximately **July 2019**, following regulatory action against 1P-LSD in Germany under the NpSG (Brandt et al. 2020 [Ref 1] describe it as having "recently emerged" at time of writing). Tanaka et al. (2020 [Ref 3]) document forensic detection of 1cP-LSD in paper sheet products collected in Japan from **September 2019 to March 2020**, confirming market presence by late 2019 at the latest.

**Prior publication history:** Before Brandt et al. (2020), 1cP-LSD had no published characterization in the scientific literature. Unlike 1-acetyl-LSD (ALD-52), which was synthesized in the 1950s as part of Hofmann's early ergoline work, 1cP-LSD appears to have been synthesized specifically for the research chemical market — no academic precursor synthesis has been identified. The compound was not listed in the classical psychedelic pharmacology literature.

**"Return of the Lysergamides" context:** Brandt et al. (2020 [Ref 1]) placed 1cP-LSD as Part VI in a series that began with 1P-LSD (Part I, 2016 [Ref 6]). The series documents the sequential emergence of N1-acylated LSD derivatives as research chemicals following scheduling actions.

**Regulatory and market succession:** In Germany, 1cP-LSD became the dominant legally-available lysergamide after 1P-LSD was captured by NpSG regulation in 2019. It was in turn banned under an NpSG amendment effective **July 2021** (web sources [Ref 36]), at which point 1V-LSD was marketed as its successor. This reflects a regulatory "arms race" pattern well-documented for the N1-acyl LSD derivative class (Luethi & Liechti 2020 [Ref 28]; Ponce 2024 [Ref — OpenAlex W4393014559]).

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## Subjective Effects

**No controlled human studies specific to 1cP-LSD exist.** Available information derives from: (a) the LSD literature (applicable via the prodrug mechanism), (b) the veterinary study in dogs (Hernández-Álvarez et al. 2026 [Ref 4]), and (c) community reports (PsychonautWiki [Ref 25]).

### Effects from LSD Research (Applicable via Prodrug Mechanism)

Holze et al. (2021 [Ref 19]) characterized dose-dependent LSD effects at 25–200 μg in a double-blind RCT (n=16):
- Dose-proportional subjective response from 25 μg upward
- **Ceiling effect for "good drug effects"** around 100 μg; ego dissolution and anxiety increase further at 200 μg
- **Duration:** 6.7–11h dose-dependently; subjective duration increases with dose
- **Autonomic effects:** Moderate increases in blood pressure and heart rate
- 5-HT₂A antagonist ketanserin fully blocked LSD effects

Hirschfeld et al. (2023 [Ref 20]) — meta-analysis of LSD dose-response with 5D-ASC/MEQ30 data:
- Sigmoid dose-response with plateau at ~100 μg
- Most strongly modulated domains: perceptual changes, illusory imagination, ego dissolution
- Anxiety and "dread of ego dissolution" showed smaller effect sizes
- Non-pharmacological factors (set, setting, personality) contribute substantially to variability

Subjective domains documented in controlled LSD research include: visual distortions, tracers, color enhancement, synesthesia, internal and external hallucinations; altered body sense; thought acceleration; emotional amplification; ego dissolution; time distortion; mystical-type experiences; enhanced sociability. These closely map the effects taxonomy in the seed data.

### Veterinary Study (1cP-LSD Specific)
Hernández-Álvarez et al. (2026 [Ref 4]) administered 10 μg oral 1cP-LSD (approximately equivalent to a human threshold dose when scaled by body weight) to shelter dogs over 3 weeks. Documented behavioral improvements: increased sociability, calmness, and positive emotional reactivity. Effects persisted 3 weeks after cessation. This study provides the only experimental 1cP-LSD dosing data outside mouse HTR, but the cross-species translation to humans is limited.

### Duration Confirmation
Seed data duration (total 8–12h) is **consistent with** LSD research data (Holze 2021: 6.7–11h) and community reports. The total duration range is conservative and appropriate. The brief's duration values are not contradicted by any published source and are consistent with structural analog data.

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## Safety & Toxicity

### Acute Toxicity
**No published human acute toxicity data exist specifically for 1cP-LSD.** The brief correctly notes: "Inferred from pharmacological class — not sourced from literature. Review recommended."

Jurowski et al. (2026 [Ref 2]) — the only toxicology study specific to 1cP-LSD — used multi-platform **in silico** modeling (ADMETlab 3.0, Percepta, STopTox, ProTox 3.0, VEGA, TEST 5.1.2):
- **Predicted rat LD₅₀ (oral):** 49–85 mg/kg (Percepta platform); other platforms gave varying values
- **Pulmonary toxicity risk predicted at 81%** (1cP-LSD, among highest in the series)
- **Genotoxicity alerts: up to 90% predicted probability** (Percepta) — but OCHEM platform classified all lysergamide analogs as **non-mutagenic**. This is a direct in silico conflict that cannot be resolved without experimental data.
- **hERG channel inhibition** (cardiotoxicity): 1cP-LSD showed lower predicted cardiotoxic risk than 1V-LSD (IC₅₀ = 1.4 μM for 1V-LSD); 1cP-LSD specific IC₅₀ values not extracted in the abstract

**⚠️ FLAG:** All toxicology values for 1cP-LSD come exclusively from computational prediction. No in vitro or in vivo experimental toxicology data have been published. The conflicting genotoxicity signals (Percepta vs. OCHEM) and the elevated pulmonary toxicity prediction are hypotheses requiring experimental validation.

**LSD class toxicity (applicable by analogy):** LSD is regarded as having very low acute toxicity in humans. No confirmed human fatalities from LSD overdose have been documented in the literature. Animal LD₅₀ data for LSD: rats ~46 mg/kg (IV, historical data). The therapeutic index for LSD is considered very wide. LSD does not produce organ damage in standard toxicological evaluations (Inserra et al. 2021 [Ref 29]).

### HPPD
Hallucinogen Persisting Perception Disorder (HPPD) is a known risk with LSD and related compounds. Halpern et al. (2018 [Ref 23]) reviewed HPPD: Type I (brief flashbacks) is more common; Type II (chronic perceptual disturbances) is rarer. Pre-existing anxiety and visual symptoms (floaters, tinnitus) may predict vulnerability. Müller et al. (2022 [Ref 24]) found limited HPPD incidence in controlled LSD research settings, but acknowledged inadequate long-term data.

**No HPPD cases specific to 1cP-LSD have been published.**

### Cardiovascular Effects
LSD in controlled studies produces moderate, dose-dependent increases in heart rate and blood pressure (Holze et al. 2021 [Ref 19]). Vasoconstriction is documented at the receptor level (ergoline activity at adrenergic receptors). These effects are transient and non-dangerous in healthy individuals at typical recreational doses, but are relevant for individuals with cardiovascular pathology.

### Psychological Risks
As an LSD prodrug, 1cP-LSD carries the same psychological risk profile as LSD:
- Acute anxiety and panic reactions, dose-dependent; anxiety increases substantially at >100 μg LSD-equivalent (Holze et al. 2021 [Ref 19])
- "Bad trips" / challenging experiences — psychologically distressing experiences, particularly in adverse set and setting
- Risk of acute psychotic episodes in vulnerable individuals (those with personal or family history of psychosis)
- Ego dissolution at higher doses (>100 μg LSD-equivalent)

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## Harm Reduction

### Testing and Identification
Tusiewicz et al. (2024 [Ref 14]) establish that:
- GC-MS analysis of 1cP-LSD in methanol causes alcoholysis → LSD detected as artifact; correct identification requires non-protic solvents
- UV spectroscopy can be used as supplementary screening tool
- 1cP-LSD and 1cP-MiPLA (a structural isomer) can be differentiated by GC-MS ion ratios; this is critical for accurate identification
- Reagent testing (Ehrlich, Hofmann) will produce positive results for both LSD and N1-acyl derivatives since the indole scaffold is intact; these tests do not differentiate 1cP-LSD from LSD. Confirmatory testing via MS is required for identification

Adamowicz & Mulka (2022 [OpenAlex W4283577141]) developed and validated an LC-MS/MS method for detection of 1cP-LSD and related analogs (ALD-52, 1P-LSD, 1B-LSD) in whole blood with LOD 0.01 ng/mL — relevant for forensic and clinical toxicology contexts.

### General Psychedelic Harm Reduction
For 1cP-LSD (acting as LSD prodrug):
- Start at lower doses due to individual variability; the seed data threshold (15 μg) and light (25–75 μg) ranges are appropriate starting points
- Adequate set (mental state) and setting (physical environment) strongly influence outcome (Vizeli et al. 2024 [PMID 39231959])
- Sober sitter recommended for first-time use or high-dose sessions
- Do not redose if effects are delayed — onset delayed relative to direct LSD due to prodrug hydrolysis step (20–60 min); perceived lack of effect should not prompt early redosing
- Avoid combination with tramadol or other serotonergic/seizure-threshold-lowering drugs (see Interactions)
- Avoid in individuals with personal or family history of psychosis or schizophrenia

---

## Tolerance & Dependence

### Tolerance
1cP-LSD is expected to produce rapid tolerance via the LSD mechanism:
- **Mechanism:** Repeated 5-HT₂A agonist exposure → receptor downregulation in frontal cortex (Buckholtz et al. 1990 [Ref 11]) → reduced sensitivity to subsequent doses
- de la Fuente Revenga et al. (2022 [Ref 10]) demonstrated that DOI tolerance in mice develops within 24h of a single dose, with cross-tolerance to LSD; 5-HT₂A downregulation confirmed as mechanism (β-arrestin-2 independent)
- **Clinical expectation:** Tolerance builds rapidly, within 1–3 days of repeated use; return to baseline requires approximately 14 days; consistent with seed data (half-life 6 days, full reset 14 days)
- These values in the seed data are **consistent with** published LSD class data but are extrapolations, not direct 1cP-LSD measurements

### Cross-Tolerance
Cross-tolerance to other serotonergic psychedelics (psilocybin, DMT, mescaline) via shared 5-HT₂A downregulation mechanism is well-established for LSD and extends to the prodrug class by inference.

### Dependence
- **Physical dependence:** None documented for LSD or related lysergamides
- **Psychological dependence:** Considered low; LSD does not produce dopaminergic reinforcement or withdrawal syndrome
- **Abuse potential:** Low; rapid tolerance development limits compulsive use patterns
- Inserra et al. (2021 [Ref 29]) note that psychedelics present limited dependence liability, consistent with seed data characterization

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## Interactions

### Tramadol — **DANGEROUS** (seed data rating confirmed as warranted but not directly evidenced for 1cP-LSD)
Mechanism basis: Tramadol lowers seizure threshold (dose-dependent seizures in rats: Lagard et al. 2016 [Ref 33]) and acts as a serotonin/norepinephrine reuptake inhibitor. LSD-class compounds also lower seizure threshold (listed in effects taxonomy). The combination creates compounded seizure risk and serotonergic burden. Seizures in rats from tramadol are independent of brain serotonin per Lagard et al. (2016 [Ref 33]), though tramadol also increases brain serotonin concentrations, which overlaps with the serotonergic mechanism of LSD.
**⚠️ FLAG:** The "dangerous" severity rating is clinically plausible but is not based on a published human case report or controlled study for 1cP-LSD specifically, nor even for LSD + tramadol directly. This is inferred from each compound's independent mechanisms. The generation agent should note this as class-level inference.

### Cannabis — **UNKNOWN** (seed data rating)
No published data on 1cP-LSD + cannabis combination. Cannabis (CB₁ agonist) and LSD (5-HT₂A agonist) act through distinct receptors; anecdotal reports suggest intensification of psychedelic effects. No controlled interaction studies found.

### SSRIs / SNRIs
Chronic SSRI administration attenuates LSD subjective effects, likely via 5-HT₂A receptor downregulation (Bonson et al. 1996 [Ref 27]). This would reduce the effects of 1cP-LSD when used concurrently with SSRIs. Acute SSRI administration may have different effects.

### MDMA
Straumann et al. (2023 [Ref 34]) demonstrated that MDMA co-administration with LSD 100 μg significantly increased LSD Cmax and AUC and prolonged LSD plasma half-life. Combined use increased blood pressure, heart rate, and pupil size more than LSD alone. This interaction would apply to 1cP-LSD via the prodrug mechanism and is relevant for harm reduction.

### Lithium
Not searched specifically, but the LSD + lithium interaction (seizure risk) is widely recognized in the harm reduction literature. No PubMed results were returned for this specific query in this research session. **⚠️ FLAG:** Lithium interaction warrants a separate targeted search for the generation agent.

### Ketanserin / 5-HT₂A antagonists
Ketanserin fully blocks LSD effects when administered before or after LSD (Becker et al. 2023 [PMID 36342343]). This is the pharmacological rescue mechanism if needed. Applicable to 1cP-LSD via prodrug mechanism.

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## Legal Status

**United States:**
LSD is Schedule I under the Controlled Substances Act (21 U.S.C. § 812). 1cP-LSD is not explicitly scheduled. Under the Federal Analogue Act (21 U.S.C. § 813), any substance "substantially similar" to a Schedule I or II controlled substance may be treated as Schedule I when intended for human consumption. Whether 1cP-LSD meets the "substantially similar" standard has not been adjudicated. Enforcement risk applies. No specific regulatory action identified as of 2025.

**United Kingdom:**
Covered under the **Psychoactive Substances Act 2016** (came into force 26 May 2016), which bans the production, supply, and importation of any substance intended to produce a psychoactive effect, with exemptions for alcohol, tobacco, caffeine, and licensed medicines. 1cP-LSD is not a specific Named Drug under the Misuse of Drugs Act 1971, but the PSA 2016 effectively prohibits it.

**Germany:**
1cP-LSD was banned under an amendment to the **Neue-Psychoaktive-Stoffe-Gesetz (NpSG)** that took effect **July 2021** [Ref 36]. The NpSG bans entire structural groups of psychoactive substances rather than individual named compounds, and the amendment was specifically crafted to capture 1cP-LSD and related lysergamide derivatives. This ended the legal sales of 1cP-LSD in Germany; 1V-LSD was marketed as its successor until it was also banned.

**Canada:**
1cP-LSD does not appear on Schedule I–VI of the Canadian Controlled Drugs and Substances Act as of 2025 and is reported as an uncontrolled substance (web sources, 2025). LSD itself is Schedule III in Canada.

**Australia:**
1cP-LSD is not explicitly listed in the Therapeutic Goods Administration (TGA) Standard for Uniform Scheduling of Medicines and Poisons (SUSMP) by name. LSD is Schedule 9 (prohibited substance). Analogue provisions may apply. Status requires jurisdiction-specific legal advice.

**Netherlands / Switzerland / EU:**
Specific scheduling information for 1cP-LSD in these jurisdictions was not found in published sources. Many EU member states have broad NPS legislation that may apply. The EMCDDA monitoring network covers lysergamide NPS as a class.

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## Clinical Trials

**No clinical trials have been registered or published for 1cP-LSD** (ClinicalTrials.gov search returned zero results for "1cP-LSD" or "lysergamide psychedelic" with 1cP-LSD identifiers).

Extensive clinical trial programs exist for LSD (the active metabolite) — including Holze et al. (2023 [Ref 37]) phase II RCT for anxiety. These are not applicable to 1cP-LSD as a distinct investigational compound; their results would apply to the LSD metabolite that 1cP-LSD generates.

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## Community Feedback Analysis

**No community feedback was submitted** (Part A2 of the brief is empty).

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## Gaps & Flags

### Critical Gaps — Safety-Critical

1. **⚠️ No human pharmacokinetic or pharmacodynamic studies for 1cP-LSD.** All dose/duration data are based on structural analogy to LSD (via prodrug) and community reports. No Tmax, Cmax, t½, or bioavailability values have been measured in humans for 1cP-LSD. The generation agent must clearly label all dose/duration claims as based on structural analogy and community consensus, not direct measurement.

2. **⚠️ Toxicity data are exclusively in silico (Jurowski et al. 2026 [Ref 2]).** The LD₅₀ estimate (49–85 mg/kg, rat, predicted), the 81% pulmonary toxicity prediction, and the genotoxicity alerts are computational outputs, not experimental findings. The conflicting genotoxicity signals (Percepta: 90% risk; OCHEM: non-mutagenic) cannot be resolved from published data. All toxicity claims must be explicitly labeled "predicted" or "in silico" with the source cited.

3. **⚠️ Tramadol interaction rated "dangerous" in seed data — not evidenced by a specific case report or controlled study.** The rating is mechanistically plausible (seizure threshold lowering by both compounds; serotonergic burden) but is class-level inference. Flag for editorial review: the generation agent should not present this as a published documented interaction without qualification.

4. **⚠️ Seizure threshold reduction listed in the effects taxonomy** — this is consistent with the LSD pharmacological class but no 1cP-LSD-specific clinical data support it. Label as class inference.

5. **⚠️ Cannabis interaction rated "unknown"** — confirmed as unknown. No evidence found in either direction.

### Data Gaps — Non-Critical

6. **SMILES string not retrieved** from PubChem API. Brief lists no SMILES. This should be fetched directly from PubChem web entry (CID 155884675) for the generation agent's chemical data section.

7. **CAS number not identified.** 1cP-LSD likely has no formal CAS registration as a post-2019 designer compound. Note as absent.

8. **No published melting point, pKa, aqueous solubility, or log P data** for 1cP-LSD in the literature.

9. **Metabolite profile of 1cP-LSD in humans not characterized.** Brandt et al. (2020 [Ref 1]) show LSD formation in serum; the cyclopropanoic acid co-product of hydrolysis has not been studied for bioactivity or toxicity.

10. **Stereochemistry:** 1cP-LSD carries the same (6aR,9R) configuration as d-LSD; no iso-1cP-LSD characterization studies were found. The PubChem IUPAC name confirms (6aR,9R) stereochemistry.

11. **Lithium + LSD interaction** is a widely reported dangerous combination in harm reduction resources but was not retrieved via PubMed in this research session. The generation agent should include a note on lithium as a suspected dangerous interaction pending a dedicated search.

12. **Discovery/synthesis origin:** Multiple web sources give inconsistent dates (2015 or 2019); the earliest confirmed scientific report is Tanaka et al. (September 2019 detection date) and Brandt et al. (2020, submitted ~late 2019). No academic synthesis pathway paper exists. Origin is attributed to research chemical market actors, not academic chemistry labs.

13. **Dose data:** The seed data dose ranges (threshold 15 μg through heavy 300+ μg) are consistent with:
    - PsychonautWiki community consensus [Ref 25]
    - LSD dose-response data (Holze 2021 [Ref 19]: effects from 25 μg onward)
    - No direct contradiction found in any published source
    These values are based on the LSD reference + community reports, not direct titration studies for 1cP-LSD. The generation agent should note this provenance transparently.

14. **Duration data:** Seed data (total 8–12h) is consistent with LSD research (Holze 2021: 6.7–11h). The seed data aftereffects range (6–24h) is plausible given LSD's prolonged effects. No specific contradiction found.

15. **Tolerance seed data (half-life 6 days, full reset 14 days):** These are class-level values inferred from the LSD tolerance literature. The 14-day full reset is consistent with 5-HT₂A receptor resensitization timelines from animal models (de la Fuente Revenga et al. 2022 [Ref 10]; Buckholtz et al. 1990 [Ref 11]). Not directly measured for 1cP-LSD.