1cP-AL-LAD

# Research Output: 1cP-AL-LAD

---

## Chemical Identity

**PubChem CID:** 162368406 — confirmed via PubChem API [Ref 29]

**IUPAC Name (confirmed):** (6aR,9R)-4-(cyclopropanecarbonyl)-N,N-diethyl-7-prop-2-enyl-6,6a,8,9-tetrahydroindolo[4,3-fg]quinoline-9-carboxamide

An alternate IUPAC representation given in the primary analytical paper (Kavanagh et al. 2023 [Ref 1]): 1-(cyclopropanecarbonyl)-N,N-diethyl-6-(prop-2-en-1-yl)-9,10-didehydroergoline-8β-carboxamide. Both names refer to the same compound; the PubChem form uses the hexahydroindoloquinoline ring numbering.

The systematic name given in the brief seed data — "(6aR,9R)-4-(cyclopropanecarbonyl)-N,N-diethyl-7-prop-2-enyl-6,6a,8,9-tetrahydroindolo[4,3-fg]quinoline-9-carboxamide" — **exactly matches PubChem CID 162368406** [Ref 29]. No discrepancy.

**Molecular Formula:** C26H31N3O2 — confirmed PubChem [Ref 29]
**Molecular Weight:** 417.5 g/mol — confirmed PubChem [Ref 29]
**InChIKey:** VSABTUDYQCMWKE-AUSIDOKSSA-N — confirmed PubChem [Ref 29]
**Isomeric SMILES:** CCN(CC)C(=O)[C@H]1CN([C@@H]2CC3=CN(C4=CC=CC(=C34)C2=C1)C(=O)C5CC5)CC=C — confirmed PubChem REST API [Ref 29]

**CAS Number:** Not found in any consulted source. Not listed in PubChem record.

**Brief seed data gaps confirmed:** The brief listed SMILES, molecular formula, molecular weight, InChIKey, and PubChem CID as absent. All are now confirmed above. No discrepancies detected between seed data systematic name and PubChem.

**Structural relationship:** 1cP-AL-LAD is the N1-cyclopropanoyl (cyclopropanecarbonyl) derivative of AL-LAD (N6-allyl-6-nor-LSD). It differs from AL-LAD by addition of a cyclopropanecarbonyl group at the N1 position of the ergoline ring. It differs from 1cP-LSD by the N6-allyl substituent replacing the N6-methyl of LSD's ergoline core, and from 1P-AL-LAD (the propanoyl analog) by the cyclopropanoyl rather than propanoyl acyl group at N1 [Ref 1].

**Physical properties:** No melting point, solubility, or stability data found in any consulted source. Commercial samples analysed as powder and on blotter paper [Ref 1].

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## Pharmacology

### Direct Pharmacological Data for 1cP-AL-LAD

**No published receptor binding, functional assay, or in vitro pharmacological data specific to 1cP-AL-LAD has been identified.** Tanaka et al. (2023 [Ref 2]) explicitly state: "The metabolic pathways and biological activities of 1cP-AL-LAD and 1cP-MIPLA have not been reported." No head-twitch response (HTR), drug discrimination, or human pharmacokinetic data have been published for 1cP-AL-LAD as of May 2026.

All pharmacological inferences below are **structural analog inferences** and are so labelled.

### Mechanism of Action (Structural Analog Inference)

**⚠️ FLAG — Structural Analog Inference:** The following mechanism is inferred from the class-wide pattern of N1-acyl lysergamides, not from direct experimental data on 1cP-AL-LAD.

N1-acyl substitution on the ergoline ring system dramatically reduces affinity at monoamine receptors by 1–2 orders of magnitude compared to the parent compound. Halberstadt et al. (2020 [Ref 12]) demonstrated this for ALD-52, 1P-LSD, and 1B-LSD: all showed weak efficacy or acted as antagonists in functional Ca²⁺ assays at the 5-HT₂A receptor. High plasma LSD concentrations were detected in rats after 1P-LSD administration, confirming in vivo prodrug conversion [Ref 12].

**Prodrug hypothesis:** By strong structural analogy with both axes of modification:
1. *N1-cyclopropanoyl axis:* Brandt et al. (2020 [Ref 3]) showed that 1cP-LSD (cyclopropanoyl group at N1, methyl at N6) converts to LSD in human serum — confirming the N1-cyclopropanoyl group is hydrolysed in vivo.
2. *N6-allyl axis:* Brandt et al. (2022 [Ref 4]) showed that 1P-AL-LAD (propanoyl at N1, allyl at N6) converts to AL-LAD as the most abundant metabolite in pooled human liver microsomes, with 14 metabolites detected including N1-deacylation as the primary step.

**Conclusion (inferred):** 1cP-AL-LAD is most probably a prodrug for AL-LAD, with the cyclopropanoyl group hydrolysed in vivo to yield AL-LAD. This pattern is consistent across all studied N1-acyl lysergamides including ALD-52, 1P-LSD, 1B-LSD, 1V-LSD, 1cP-LSD, 1P-AL-LAD, 1P-ETH-LAD, 1F-LSD, and 1T-LSD [Refs 3, 4, 6, 7, 14, 15, 35].

### Receptor Pharmacology of AL-LAD (Active Metabolite)

**⚠️ FLAG — No primary peer-reviewed source found for AL-LAD-specific Ki values.** The following values are from secondary sources (web aggregators referencing Nichols group work); they are included for context only and require verification against the primary Nichols/Hoffman publications which could not be retrieved:

- 5-HT₂A (radioligand [³H]ketanserin, rat frontal cortex): Ki ≈ 8.1 nM
- 5-HT₂A (radioligand [¹²⁵I]-R-DOI): Ki ≈ 3.4 nM
- Dopamine D1: K₀.₅ ≈ 189 nM
- Dopamine D2: K₀.₅ ≈ 12.3 nM

For comparison, LSD has 5-HT₂A affinity in the low-nanomolar range and was crystallised in complex with the 5-HT₂B receptor (Wacker et al. 2017 [Ref 11]), establishing that ergolines bind deep in the orthosteric pocket with EL2 "lid" closure causing slow dissociation kinetics [Ref 11]. A Gq-coupled active-state structure of HTR2A with a hallucinogen was also resolved (Kim et al. 2020 [Ref 9]).

AL-LAD's behavioral potency in the mouse HTR assay: ED₅₀ = 174.9 nmol/kg — slightly less potent than LSD (ED₅₀ = 132.8 nmol/kg) (Brandt et al. 2017 [Ref 5]). HTR is a 5-HT₂A-mediated behavior that correlates strongly with human hallucinogenic potency (r = 0.9448; Halberstadt et al. 2020 [Ref 13]).

### Comparative Potency of N1-Acyl Analogs (Prodrug Series, Mouse HTR)

For context on expected potency reduction from N1-acylation:

| Compound | N1 group | N6 group | HTR ED₅₀ (nmol/kg) |
|---|---|---|---|
| LSD | — | methyl | 132.8 |
| AL-LAD | — | allyl | 174.9 |
| 1P-AL-LAD | propanoyl | allyl | 491 |
| 1cP-LSD | cyclopropanoyl | methyl | 430 |
| 1V-LSD | valeroyl | methyl | 373 |
| 1B-LSD | butanoyl | methyl | 976.7 |

Sources: [Refs 3, 4, 5, 14, 15]

1cP-AL-LAD's HTR potency has not been measured. Extrapolating from the AL-LAD baseline (174.9 nmol/kg) and the ~2.8x potency reduction seen for 1P-AL-LAD vs AL-LAD, a rough estimate would place 1cP-AL-LAD in the 400–600 nmol/kg range — but **this is unvalidated speculation and must be labelled as such in any article prose.**

### Receptor Classes

Based on the class profile of serotonergic lysergamides, AL-LAD (the active metabolite) is expected to act at:
- **5-HT₂A** (primary psychedelic target — partial agonist) [Refs 9, 10, 11]
- **5-HT₂C** (agonist, class-wide) [Ref 10]
- **5-HT₁A** (partial agonist, class-wide) [Ref 10]
- **Dopamine D1/D2** (activity documented for LSD class) [Ref 10]

Pharmacological class in brief ("Serotonin receptor ligand, Dopamine receptor ligand, Dopamine receptor agonist, Serotonin 1A receptor partial agonist, Serotonin 2A receptor agonist, Serotonin 2C receptor agonist") is consistent with class expectations. **No direct experimental confirmation for 1cP-AL-LAD or AL-LAD from a verified primary source was retrieved.**

### Metabolism and CYP Enzymes

No direct metabolic data for 1cP-AL-LAD has been published.

By analogy from 1P-AL-LAD (Brandt et al. 2022 [Ref 4]):
- Primary step: N1-deacylation → AL-LAD (most abundant metabolite)
- Secondary reactions: hydroxylation of the core lysergamide ring or the N6-allyl group, dihydrodiol formation, N-dealkylation, dehydrogenation, and combinations thereof (14 total metabolites)

For AL-LAD (Wagmann et al. 2019 [Ref 6]):
- Metabolism via human liver S9 fraction primarily by **CYP1A2 and CYP3A4** (N-dealkylation and hydroxylation)

For 1P-LSD in humans (Grumann et al. 2020 [Ref 22]):
- Oral administration: only LSD detected in serum/urine (complete prodrug conversion)
- LSD terminal elimination half-life: ~6.4 h
- Bioavailability of LSD from oral 1P-LSD: ~100%

For LSD itself (Arikci et al. 2025 [Ref 23]):
- Absolute oral bioavailability: 80%
- All oral formulations bioequivalent

**⚠️ FLAG:** No human pharmacokinetic data for 1cP-AL-LAD. All metabolic data extrapolated from structural analogs.

---

## History

### AL-LAD (Parent Compound)

AL-LAD (N6-allyl-6-nor-lysergic acid diethylamide) was first synthesised by Japanese researchers around 1976 (citation not retrieved — historical claim from secondary sources only). It was subsequently characterised by Hoffman and Nichols at Purdue University circa 1984–1985 as part of a systematic SAR study of N6-substituted lysergamides including ETH-LAD and PRO-LAD. Pfaff, Huang, Marona-Lewicka, Oberlender, and Nichols published a review covering this work in the NIDA Research Monograph 146 ("Lysergamides revisited", 1994 [Ref 21]).

**⚠️ FLAG:** The original Hoffman & Nichols ~1985 primary paper could not be retrieved via PubMed searches. The 1994 NIDA monograph chapter (Pfaff et al. [Ref 21]) was confirmed to exist (PMID 8742794) but returned an empty abstract. Editorial should verify primary historical source.

AL-LAD appeared on the NPS ("research chemical") market in 2013 in both powdered and blotter form (Brandt et al. 2017 [Ref 5]).

### 1cP-AL-LAD Specifically

**No pre-2023 scientific literature found on 1cP-AL-LAD.** The compound appears to have emerged as a commercial research chemical in 2022–2023, following the regulatory pressure that removed 1cP-LSD from several European markets through the 2021 German NpSG revision [Ref 33].

Two independent forensic papers published in 2023 mark the first scientific documentation of 1cP-AL-LAD:

1. Kavanagh et al. (Drug Testing and Analysis, 2023 [Ref 1]): Described the analytical profile of 1cP-AL-LAD obtained from an online vendor, including HPLC-ESI-QTOF-MS impurity profiling. This appears to be the first comprehensive analytical publication for the compound. Kavanagh et al. also detected 1cP-AL-LAD on commercial "blotters" sold online for recreational use.

2. Tanaka et al. (Forensic Toxicology, 2023 [Ref 2]): First report of 1cP-AL-LAD identified in sheet products seized or monitored in Japan. Identified by GC-MS, LC-PDA-MS, LC-Q-TOF-MS, and NMR. This appears to be the first forensic identification in an Asian jurisdiction.

Both papers explicitly note the absence of published metabolic pathway or biological activity data for 1cP-AL-LAD.

The commercial emergence of 1cP-AL-LAD follows the documented pattern of NPS vendors sequentially introducing novel N1-acyl lysergamides (1P-LSD → 1B-LSD → 1V-LSD → 1cP-LSD → 1D-LSD → 1T-LSD → 1cP-AL-LAD etc.) to exploit jurisdictional scheduling gaps [Refs 8, 30].

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## Subjective Effects

**No controlled human studies of 1cP-AL-LAD have been published.** All subjective effect characterisations are extrapolated from class-level data.

### Expected Effects (Structural Analog Inference)

**⚠️ FLAG — No human study data for 1cP-AL-LAD or AL-LAD subjective effects found in peer-reviewed literature.**

By structural analogy as a presumed prodrug for AL-LAD, effects are expected to broadly resemble LSD, with subtle character differences historically attributed to AL-LAD. Community-sourced data from PsychonautWiki [Ref 20] describes the following subjective effects (no primary citations provided by that source):

**Perception:** Geometry, visual drifting, colour enhancement, tracers, after-images, auditory hallucinations, synesthesia
**Cognition:** Conceptual thinking, creativity enhancement, thought acceleration, thought loops
**Feeling:** Euphoria, emotional enhancement, anxiety (dose-dependent)
**Body:** Stimulation, pupil dilation, muscle tension, nausea (especially at higher doses)
**Self:** Ego dissolution (at high doses), boundary dissolution

### Duration (Seed Data)

Dose/duration data from the brief seed data:
- Onset: 20–60 minutes (oral)
- Come-up: 30–60 minutes (oral)
- Peak: 2.5–5 hours (oral)
- Offset: 2–3 hours (oral)
- Aftereffects: 2–18 hours (oral)
- Total: 7–10 hours (oral)

This duration profile matches that of LSD (mean 8.2h in controlled study, Ley et al. 2023 [Ref 26]) and is consistent with an AL-LAD-type prodrug. PsychonautWiki [Ref 20] confirms total duration 7–10 hours. **No controlled study data available for verification.**

### Dose Ranges (Seed Data)

From the brief seed data (oral):
- Threshold: 20 µg
- Light: 50–100 µg
- Common: 100–225 µg
- Strong: 225–350 µg
- Heavy: 350+ µg

PsychonautWiki [Ref 20] confirms identical ranges. These are substantially higher than LSD doses (typical active dose 75–150 µg), consistent with an N1-acyl prodrug with ~3x lower molar potency than its parent. By comparison, 1P-LSD doses in controlled human study were 100 µg (Grumann et al. 2020 [Ref 22]).

**⚠️ FLAG — Dose ranges not verified against a controlled human study. All dose data is community consensus with no primary source.**

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## Safety & Toxicity

### Acute Toxicity

**No toxicity data (LD50, therapeutic index, organ toxicity) published for 1cP-AL-LAD.** The brief states acute toxicity as "negligible" and chronic toxicity as "negligible" with toxic dose "unknown." These assertions cannot be verified from published sources and should be flagged as class-level inference.

By class analogy: LSD has extremely high safety margin in preclinical models; no human LSD fatalities from direct pharmacological toxicity have been documented in the clinical literature. The psychedelic class is generally considered physiologically low-risk at recreational doses, with psychological risks predominating over physiological ones (Luethi & Liechti 2020 [Ref 30]).

### Cardiovascular Effects

LSD at 100–200 µg in controlled human studies produces moderate cardiovascular effects: increased heart rate and blood pressure (Holze et al. 2022 [Ref 24]; Ley et al. 2023 [Ref 26]). These effects are expected to apply to 1cP-AL-LAD by class inference but have not been measured directly.

### Psychological Risks

**Challenging/Distressing Experiences:** Simonsson et al. (2023 [Ref 27]) found in a US nationally representative sample of psychedelic users (N=613) that 40.9% had experienced challenging/difficult/distressing effects. 8.9% experienced functional impairment lasting more than one day. 2.6% sought medical, psychiatric, or psychological assistance. Key risk factors: co-use of lithium or mood stabilisers, negative mindset, dose too large, no psychological support, major life event prior to use.

**HPPD:** Hallucinogen Persisting Perception Disorder is a documented rare adverse outcome of 5-HT₂A agonist psychedelic use, attributed to imbalance of inhibitory-excitatory activity in visual processing (Litjens et al. 2014 [Ref 17]; Halpern & Pope 2003 [Ref 28]). Most commonly reported after LSD use. No case reports for 1cP-AL-LAD specifically.

**Psychiatric Decompensation:** Psychedelics can trigger or exacerbate psychotic symptoms in individuals with personal or family history of psychotic disorders (Omidian & Omidian 2025 [PMID 40283936]).

### Case Reports

**No adverse event case reports or overdose reports for 1cP-AL-LAD found in the literature.** Tanaka et al. 2023 [Ref 2] notes the compound in forensic context (Japan) without clinical outcome data.

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## Harm Reduction

### Testing and Identification

1cP-AL-LAD can be identified analytically by GC-MS, LC-PDA-MS, LC-Q-TOF-MS, and NMR spectroscopy (Kavanagh et al. 2023 [Ref 1]; Tanaka et al. 2023 [Ref 2]). Commercial samples may contain impurities including AL-LAD itself and 1P-AL-LAD (confirmed as actual impurities by reference standards); 15 additional impurities tentatively identified by mass spectral data alone [Ref 1].

Indole-containing ergolines react with the Ehrlich reagent (p-dimethylaminobenzaldehyde), producing a purple/violet colour — standard field test for the ergoline class. This does not differentiate 1cP-AL-LAD from LSD, AL-LAD, 1P-AL-LAD, or other indole-containing substances.

### Contraindications

**⚠️ FLAG — Safety-critical. No published contraindications specific to 1cP-AL-LAD found. The following are class-level inferences:**

- Personal or family history of psychotic disorders (schizophrenia, bipolar with psychotic features)
- Personal history of HPPD
- Serious cardiovascular conditions
- Pregnancy or breastfeeding (no data)
- Concurrent serotonergic medications (SSRIs, MAOIs, SNRIs, tramadol)

### Set and Setting

Simonsson et al. 2023 [Ref 27] identified key modifiable risk factors for adverse outcomes: negative mindset, disagreeable physical environment, no psychological support. These findings apply broadly to the psychedelic class.

### Emergency Response

5-HT₂A antagonists (e.g., ketanserin) can reverse LSD-induced psychedelic effects when administered after the drug (Becker et al. 2023 [Ref 25]). This may apply by class analogy to 1cP-AL-LAD. Benzodiazepines are commonly used in clinical settings for acute psychedelic anxiety management (class-level practice).

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## Tolerance & Dependence

### Tolerance

Tolerance to LSD and serotonergic psychedelics develops almost immediately after a dose, mediated primarily by 5-HT₂A receptor downregulation (Buckholtz et al. 1990 [Ref 19]). Receptor binding decreases are evident within 3 days of repeated dosing and reverse within 4 days of cessation (PMID 1969270 [Ref 19]).

The brief seed data states: "Buildup: almost immediately after ingestion; Half-life: 6 days; Full reset: 14 days; Cross-tolerances: psychedelic." These values are consistent with the published literature on LSD-class tolerance.

**⚠️ FLAG — Tolerance half-life of 6 days and full reset of 14 days are not verified against a published primary source for 1cP-AL-LAD or AL-LAD specifically. These appear to be community consensus values for the psychedelic class broadly.**

### Dependence and Abuse Potential

Serotonergic psychedelics including LSD are considered to have negligible physical dependence liability and do not support self-administration in animal models (Henningfield et al. 2023 [Ref 31]). The brief's characterisation of 1cP-AL-LAD as "not habit-forming" is consistent with class pharmacology. Rapid development of tolerance discourages frequent use patterns.

No specific dependence liability studies exist for 1cP-AL-LAD.

---

## Interactions

### Tramadol: Dangerous

**Mechanism:** Tramadol inhibits the serotonin transporter (SERT) in human SERT-transfected HEK293 cells (Baldo 2018 [Ref 16]). Combined with 1cP-AL-LAD (presumed 5-HT₂A agonist and serotonin-releasing activity via AL-LAD), this creates risk of serotonergic excess / serotonin syndrome — characterised by altered mental status, autonomic instability, and neuromuscular hyperactivity. The FDA issued a Drug Safety Communication in March 2016 concerning the serotonin toxicity risk of the opioid class [Ref 16].

Bianconi et al. (2022 [Ref PMID 34287102, unlisted in registry]) documented marked and prolonged serotonin toxicity in a tramadol-poisoned patient. The tramadol + serotonergic psychedelic combination is considered dangerous.

**⚠️ FLAG — Interaction severity is inferred from class-level mechanism. No specific case reports of tramadol + 1cP-AL-LAD or tramadol + AL-LAD serotonin syndrome found in the literature.**

### Cannabis: Unknown

The interaction between cannabis/cannabinoids and 5-HT₂A agonists is not well-characterised. Cannabidiol (CBD) has been identified as a negative allosteric modulator of 5-HT₂A (Billard et al. 2025 [PMID 39761844]), which could theoretically modulate 1cP-AL-LAD's effects, but clinical significance is unknown. THC and psychedelics are commonly co-used, and the interaction is unpredictable and may increase anxiety or confusion. "Unknown" severity classification in seed data is appropriate given the absence of controlled data.

### Other Clinically Relevant Interactions (Class-Level Inference, ⚠️ FLAG)

- **MAOIs:** Theoretically dangerous — MAO inhibition combined with serotonergic agonism increases serotonin toxicity risk. No specific data.
- **Lithium:** Co-use associated with seizure risk and amplified/unpredictable psychedelic effects (Simonsson et al. 2023 [Ref 27] identified lithium as top risk factor for adverse outcomes).
- **Ketanserin:** Can reverse LSD-type psychedelic effects (Becker et al. 2023 [Ref 25]) — potential emergency reversal agent by class analogy.

---

## Legal Status

**⚠️ FLAG — Legal status data derived primarily from web sources, not primary legal texts. Should be verified before publication.**

### United States
1cP-AL-LAD is **not explicitly listed** under the Controlled Substances Act. As a lysergamide with structural similarity to LSD (Schedule I), it may fall under the Federal Analogue Act (FAA) if intended for human consumption. However, the FAA is notoriously difficult to prosecute for novel compounds and does not constitute a clear per se scheduling. [Ref: web search, unverifiable]

### United Kingdom
The **Psychoactive Substances Act 2016** prohibits all substances capable of producing a psychoactive effect (with exemptions for alcohol, nicotine, caffeine, and medicines). 1cP-AL-LAD is covered under this blanket prohibition. Possession is not criminalised but supply, import, and export are criminal offences [Ref 33 context].

### Germany
The **NpSG (Neue-Psychoaktive-Stoffe-Gesetz)** 2021 revision, which banned 1cP-LSD and related acyl-substituted lysergamides, also covered 1cP-AL-LAD [Ref 33]. Germany's NpSG uses family-based generic scheduling. Acquisition, possession, and sale are prohibited.

### Canada
1cP-AL-LAD is **not explicitly scheduled** under Canada's Controlled Drugs and Substances Act as of the time of research (May 2026). Its status as an analogue of LSD may theoretically be invoked, but no specific guidance found.

### Australia
Not specifically listed under the Therapeutic Goods Administration schedules or state drug laws found in searches. As with Canada, may theoretically be covered under analogue provisions. No specific data found.

### EU (Other Jurisdictions)
The broad UK and German precedents suggest several EU member states with generic NPS legislation likely cover 1cP-AL-LAD. However, no jurisdiction-by-jurisdiction review was performed.

---

## Clinical Trials

**No clinical trials for 1cP-AL-LAD or AL-LAD found on ClinicalTrials.gov.** A search returned zero results for "AL-LAD lysergamide psychedelic."

For context, several LSD clinical trials exist (as comparator class):
- NCT04849013: Serotonin 5-HT2A receptor in mescaline-induced altered states (COMPLETED, Phase 1, Basel)
- NCT05674669: Dose-ranging study of 50–100 µg LSD in healthy volunteers (COMPLETED, Phase 1, Eleusis Therapeutics)
- NCT04227756: Comparative acute effects of LSD, psilocybin, and mescaline (COMPLETED, Phase 1, Basel) [Ref 26]
- NCT03866252: LSD therapy for major depression (COMPLETED, Phase 2, Basel)

No clinical development pathway identified for 1cP-AL-LAD or AL-LAD.

---

## Community Feedback Analysis

No community feedback submitted in Part A2 of the brief.

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## Gaps & Flags

### Critical Gaps (Safety-Relevant)

1. **No direct pharmacological data for 1cP-AL-LAD:** No receptor binding (Ki/EC50), no in vivo HTR data, no human pharmacokinetic study. All pharmacology is structural analog inference. The generation agent must clearly attribute all pharmacological claims to either (a) 1cP-LSD as N1-cyclopropanoyl LSD analog, (b) 1P-AL-LAD as N1-acyl AL-LAD analog, or (c) AL-LAD as the expected active metabolite.

2. **Dose ranges not verified:** The dose ranges (threshold 20 µg through heavy 350+ µg) appear only in community consensus (PsychonautWiki [Ref 20]). No controlled study or published case series confirms these ranges. They are higher than LSD doses as expected for a prodrug but represent community wisdom, not clinical data. **Flag for editorial review.**

3. **Duration data not verified:** Similar status. The 7–10 hour total duration is plausible for an AL-LAD-type compound and consistent with LSD duration data from controlled studies, but no direct measurement exists for 1cP-AL-LAD.

4. **Toxicity values unverifiable:** Brief states "negligible" acute and chronic toxicity, and toxic dose as "unknown." These are class-level inferences not sourced from published experimental data.

5. **Tramadol interaction:** Classified as "dangerous" in seed data. This is mechanistically plausible but not documented by any specific case report for 1cP-AL-LAD + tramadol. The class-level data (Baldo 2018 [Ref 16]) supports the designation but the generation agent should note the absence of substance-specific evidence.

6. **AL-LAD binding Ki values:** The only binding values found (Ki 5-HT₂A 3.4–8.1 nM; D2 12.3 nM; D1 189 nM) come from secondary sources (web aggregators). No verified peer-reviewed primary paper was retrieved with AL-LAD Ki values. These values should not be presented as verified in the article unless the generation agent can access the original Nichols/Hoffman primary publications.

### Secondary Gaps

7. **History gap:** The original Hoffman/Nichols ~1985 paper on AL-LAD drug discrimination could not be retrieved. The earliest peer-reviewed AL-LAD data accessible was from NIDA monograph (Pfaff et al. 1994 [Ref 21], empty abstract) and Brandt et al. 2017 [Ref 5].

8. **Legal status:** All legal status data comes from secondary web sources, not primary legal texts. Should be verified against official government publications.

9. **No CAS number found:** Not in PubChem or any searched source.

10. **Physical properties absent:** No melting point, aqueous solubility, log P, or stability data found for 1cP-AL-LAD.

11. **Impurity concerns:** Kavanagh et al. [Ref 1] found 17 impurities in a commercial sample including confirmed AL-LAD and 1P-AL-LAD. This is potentially safety-relevant (unintended active compound exposure) and merits mention in harm reduction.

12. **Cannabis interaction labelled "unknown":** No mechanism or interaction data found. This label is appropriate; no published data to upgrade this classification.

### Structural Reliance Summary

The following sections of any generated article rely primarily or entirely on structural analogy rather than substance-specific data:
- All pharmacology (receptor binding, mechanism of action)
- All metabolic data (CYP enzymes, metabolite profile)
- All toxicity data (LD50, therapeutic index)
- Subjective effects (other than brief community confirmation of dose/duration)
- Tolerance mechanism and rate
- Most interactions (except tramadol general class support)

These should all be clearly framed in the article as class-level inferences applicable to 1cP-AL-LAD pending substance-specific research.