1B-LSD

# Research Output: 1B-LSD

## Chemical Identity

**Verified via PubChem CID 145875086 [Ref 25 web-retrieved, confirmed by API]:**

- **IUPAC name:** (6aR,9R)-4-butanoyl-N,N-diethyl-7-methyl-6,6a,8,9-tetrahydroindolo[4,3-fg]quinoline-9-carboxamide
- **Systematic name (brief):** Same as IUPAC — matches seed data exactly
- **Molecular formula:** C₂₄H₃₁N₃O₂
- **Molecular weight:** 393.5 g/mol
- **Isomeric SMILES:** CCCC(=O)N1C=C2C[C@@H]3C(=C[C@H](CN3C)C(=O)N(CC)CC)C4=C2C1=CC=C4
- **InChIKey:** SVRFNPSJPIDUBC-DYESRHJHSA-N
- **PubChem CID:** 145875086
- **XLogP (lipophilicity):** 3.6
- **CAS number:** Not found in any verified source; no CAS registry number confirmed

**Seed data discrepancies:** The brief listed SMILES, molecular formula, molecular weight, InChIKey, and PubChem CID as blank — all are now confirmed above. The IUPAC name in the brief (matches) and the systematic name (matches). No discrepancies between seed data and verified sources.

**Chemical class context:** 1B-LSD is an ergoline lysergamide — structurally, it is d-lysergic acid diethylamide (LSD) with a butanoyl (C4) acyl group attached to the indole nitrogen at the N1 position. It is a constitutional isomer of 1-propanoyl-6-ethyl-6-nor-lysergic acid diethylamide (1P-ETH-LAD) (Brandt et al. 2019 [Ref 2]).

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## Pharmacology

### Direct Receptor Binding (1B-LSD)

The principal direct pharmacology data for 1B-LSD comes from Halberstadt et al. (2020 [Ref 1]), which performed competitive radioligand binding studies, calcium mobilization functional assays, and a receptorome screening specifically with 1B-LSD.

**Key findings (Halberstadt et al. 2020 [Ref 1]):**
- **1-Acyl substitution reduces affinity by 1–2 orders of magnitude** relative to parent LSD across most monoamine receptor targets, including the 5-HT₂A site
- Although LSD acts as a full agonist at 5-HT₂ receptor subtypes in Ca²⁺ mobilization assays, 1B-LSD (alongside ALD-52 and 1P-LSD) displayed **weak efficacy or antagonist activity** in the same assay
- A **receptorome screening was performed specifically with 1B-LSD**, providing a broad receptor binding profile — specific Ki values across the full panel were reported in the paper but are not directly accessible in the abstract; the authors summarize that 1-acyl substitution uniformly reduced affinity at monoamine receptors by 1–2 log units

**⚠️ FLAG:** Specific numerical Ki/EC50 values for 1B-LSD at individual receptors (e.g., 5-HT₂A, 5-HT₁A, D₂, etc.) were not retrievable from available open-access sources. The full data table is in the paywalled Halberstadt et al. 2020 paper (DOI: 10.1016/j.neuropharm.2019.107856). The generation agent should retrieve full Ki values from this paper if access is available.

### In Vivo Activity (Head-Twitch Response)

Brandt et al. (2019 [Ref 2]) conducted the first published HTR studies for 1B-LSD in C57BL/6J mice:
- **1B-LSD ED₅₀ = 976.7 nmol/kg** (approximately 457.6 µg/kg)
- **LSD ED₅₀ = 132.8 nmol/kg** under identical conditions
- **1B-LSD is approximately 14% as potent as LSD** in the HTR assay
- The dose-dependent HTR increase was LSD-like and is attributed to 5-HT₂A receptor activation

Halberstadt et al. (2020 [Ref 1]) confirms: "despite the detrimental effect of 1-acyl substitution on 5-HT₂A affinity and efficacy, 1-acyl-substituted LSD derivatives induce head twitches in mice with relatively high potency."

**Translational significance of HTR data:** A landmark study (Halberstadt et al. 2020 [Ref 15]) demonstrated a strong positive correlation (r = 0.9448) between HTR potencies in mice and reported hallucinogenic potencies in humans across 36 compounds. This validates the HTR as a predictor of human potency, and the 14% relative potency in mice strongly suggests 1B-LSD converts to LSD in vivo (rather than acting directly), since its direct binding affinity is proportionally even more reduced.

### Prodrug Mechanism

Both Brandt et al. (2019 [Ref 2]) and Halberstadt et al. (2020 [Ref 1]) independently conclude that 1B-LSD is consistent with prodrug status for LSD:

- High LSD plasma levels were detected in Sprague-Dawley rats following subcutaneous administration of ALD-52 and 1P-LSD (Halberstadt et al. 2020 [Ref 1]), directly demonstrating rapid in vivo deacylation. While 1B-LSD was not tested in this specific experiment, the same mechanism is inferred from its pharmacological profile (Halberstadt et al. 2020 [Ref 1])
- 1CP-LSD, an analog in the same series, was directly shown to release LSD upon incubation with **human serum** (Brandt et al. 2020 [Ref 10])
- Kavanagh et al. (2024 [Ref 22]) confirm ALD-52 (the prototype N1-acylated derivative, first synthesized in the 1950s) acts as a prodrug with hydrolysis to LSD responsible for its activity
- The in silico prodrug review by Ponce (2024 [Ref 9-equivalent]) notes 1B-LSD among LSD analogs that are hydrolyzed in physiological conditions

**⚠️ FLAG:** Direct demonstration of in vivo deacylation of 1B-LSD specifically (plasma LSD measurement after 1B-LSD administration) has not been published in the available literature. Prodrug status is strongly inferred but not directly confirmed as of the research conducted here.

### Mechanism of Action (LSD, as active moiety)

After conversion to LSD, the pharmacology is well-characterized. LSD is primarily a partial agonist at the serotonin **5-HT₂A receptor**, with high affinity at multiple additional targets. The crystal structure of LSD bound to 5-HT₂B (Wacker et al. 2017 [Ref 3]) and the cryo-EM structure of an LSD-bound 5-HT₂A receptor in active state (Kim et al. 2020 [Ref 12]) both demonstrate the molecular basis of receptor binding, including the extracellular loop 2 (EL2) lid mechanism that accounts for LSD's prolonged receptor dwell time.

Nichols (2016 [Ref 11]) provides the authoritative review: psychedelics are agonists or partial agonists primarily at **5-HT₂A receptors on apical dendrites of neocortical pyramidal cells in layer V**. LSD additionally engages 5-HT₁A, 5-HT₂B, 5-HT₂C, dopamine D₁–D₄, adrenergic α₁ and α₂, histamine H₁, and trace amine receptors (Passie et al. 2008 [Ref 20]).

The full psychedelic effects are primarily 5-HT₂A mediated, as demonstrated by the 5-HT₂A antagonist ketanserin (40 mg) fully blocking subjective psychedelic effects of 200 µg LSD in healthy subjects (Holze et al. 2021 [Ref 29]).

### Pharmacokinetics

**1B-LSD-specific PK:** No published human pharmacokinetic study exists for 1B-LSD. After oral administration, the butanoyl group is cleaved by plasma and/or intestinal esterases (inferred from structural analogy and the in vitro serum hydrolysis data for related analogs).

**LSD PK (active moiety, from multiple human studies):**
- **Tmax:** approximately 1.1–1.5 hours after oral administration (Holze et al. 2021 [Ref 6]; Dolder et al. 2017 [Ref 5])
- **Half-life:** 2.7–5.1 hours (range across studies; Holze et al. 2021 [Ref 6] reports 2.7h mean; Dolder et al. 2015 [Ref 4] reports pharmacokinetic modeling)
- **Dose-proportional pharmacokinetics** with first-order elimination (Holze et al. 2021 [Ref 29])
- **Peak plasma concentrations** at 100 µg LSD oral: approximately 1–2 ng/mL range

**Metabolic pathway:**
- Primary enzymes: CYP2D6, CYP2E1, CYP3A4 → nor-LSD; CYP1A2, CYP2C9, CYP2E1, CYP3A4 → O-H-LSD (Luethi et al. 2019 [Ref 31])
- CYP2D6 is the dominant enzyme in vivo (Vizeli et al. 2021 [Ref 30]; Becker et al. 2025 [Ref 7])
- CYP2D6 poor metabolizers show ~75% higher LSD exposure (AUC), prolonged half-life, and greater/longer subjective effects (Vizeli et al. 2021 [Ref 30])
- Paroxetine (strong CYP2D6 inhibitor) increased LSD Cmax 1.4× and AUC 1.5× (Becker et al. 2025 [Ref 7])
- **nor-LSD is pharmacologically active** (similar 5-HT₁A/2A/2B/2C affinity to LSD); **O-H-LSD is inactive** (Luethi et al. 2019 [Ref 31])
- Hepatic microsomal conversion is minor (<1% over 4 hours), indicating hepatic metabolism is not the primary elimination route

**⚠️ FLAG:** No published data on the delay introduced by the deacylation step for 1B-LSD specifically. The onset delay relative to LSD (if any) is unknown. Based on the 1B-LSD dose range in the brief (onset 20–60 min), onset appears comparable to LSD — but this is user-report data, not a controlled study.

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## History

### Origins and First Appearance

1B-LSD has **no prior record in the scientific literature** before its appearance on the research chemical market (Brandt et al. 2019 [Ref 2]). It is unknown who first synthesized 1B-LSD. According to Brandt et al. (2019 [Ref 2]), it is described as "the most recent N₁-acylated LSD derivative to appear on the recreational drug market" at the time of writing.

- **First market appearance:** August 2016 (web sources [Ref 26])
- **First academic characterization:** Brandt et al. 2019, Drug Testing and Analysis [Ref 2]
- **Compound source for research:** Synex Synthetics BV, Maastricht, Netherlands (Brandt et al. 2019 [Ref 2])

### Lineage

1B-LSD belongs to a series of N1-acylated LSD derivatives:
- **ALD-52 (1A-LSD):** First synthesized in the 1950s by Albert Hofmann's group; produces psychedelic effects similar to LSD; earliest member of the class (Kavanagh et al. 2024 [Ref 22]; Passie et al. 2008 [Ref 20])
- **1P-LSD:** First appeared on RC market ~2013–2015; first academic description in Brandt et al. 2016 (Part I of series [Ref 13])
- **1B-LSD:** Appeared August 2016; Part V of the "Return of the lysergamides" series [Ref 2]
- The "Return of the lysergamides" series covers: Part I (1P-LSD), Part II (AL-LAD, LSZ), Part V (1B-LSD), Part VI (1CP-LSD) [Refs 13, 14, 2, 10]
- A DEA report from 1988 is cited in the historical literature as having foreseen the use of 1-alkylated lysergamide derivatives to bypass controlled substance laws [Ref 26]

### Regulatory History

- **Germany:** Controlled under NpSG (Neue-psychoaktive-Stoffe-Gesetz) as of **July 18, 2019** [web-retrieved, Ref 26]
- **United Kingdom:** Covered by the **Psychoactive Substances Act 2016** (came into force May 2016), which prohibits all psychoactive substances except alcohol, nicotine, caffeine, and medicines
- **United States:** Not specifically scheduled. The **Federal Analogue Act (FAA)** may treat it as a Schedule I controlled substance when intended for human consumption, given its structural relationship to LSD (Schedule I)
- **Canada:** Not specifically named; **CDSA analogue provisions** may apply given structural relationship to LSD (Schedule III)
- **Australia:** The **TGA's Standard for the Uniform Scheduling of Medicines and Poisons** includes lysergamides as prohibited substances, covering 1B-LSD

⚠️ **FLAG for human review:** Legal status is based on web-retrieved sources and general legislative interpretation. No primary statutory source was directly verified for each jurisdiction. Editors should confirm current scheduling before publication.

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## Subjective Effects

No published human controlled study of 1B-LSD exists. All subjective effect data derives from user reports (PsychonautWiki [Ref 25]) and is consistent with LSD effects (expected given the prodrug mechanism).

**LSD effects at controlled doses (context for 1B-LSD prodrug):**
Holze et al. (2021 [Ref 29]) characterized dose-dependent LSD effects in 16 healthy subjects (25–200 µg oral):
- Subjective psychedelic effects begin at 25 µg; duration 6.7–11 hours with increasing doses
- Ceiling effect for "good drug effects" at 100 µg
- 200 µg: ego dissolution and significant anxiety emerge
- Moderate increases in blood pressure and heart rate across all doses
- 5-HT₂A antagonist ketanserin fully blocked effects, confirming primary mechanism

Vizeli et al. (2024 [Ref 34]) in a pooled analysis of 213 healthy subjects from 9 studies identified LSD dose as the strongest predictor of subjective effects; pre-drug anxiety and trait openness also significant predictors.

**Duration data (1B-LSD, user-report only):**
The brief's duration data (onset 20–60 min, come-up 45–120 min, peak 3–5 hours, offset 3–5 hours, total 8–12 hours, aftereffects 6–24 hours) is consistent with LSD onset/duration parameters from controlled studies and is corroborated by PsychonautWiki community data [Ref 25]. This data is user-report only — no published controlled duration study exists for 1B-LSD.

**Dose data (1B-LSD, user-report only):**
The brief's dose data (threshold 15 µg, light 25–75 µg, common 75–150 µg, strong 150–300 µg, heavy 300+ µg) matches PsychonautWiki [Ref 25]. These values are user-report only. Given that 1B-LSD is ~14% as potent as LSD in mice (HTR), and given LSD's threshold dose for psychotropic effects in humans is approximately 10 µg (Holze et al. 2021 [Ref 6]), a direct conversion would predict 1B-LSD threshold closer to ~70 µg. **However, the prodrug mechanism substantially complicates this calculation** — if 1B-LSD converts to LSD with high efficiency, the effective dose in humans would be comparable to LSD, not 14× higher. The reduced mouse HTR potency may primarily reflect slower conversion kinetics or incomplete absorption at low doses, not a fundamental reduction in potency per mole of converted LSD.

⚠️ **FLAG:** This is a significant interpretive issue for dose data. The 14% relative potency in the HTR assay is an in vivo measure that may reflect conversion efficiency rather than intrinsic potency. Community-reported doses (75–150 µg common range) suggest substantially higher human potency than the HTR ratio would predict if taken at face value. Editorial review of dose ranges is needed.

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## Safety & Toxicity

### Acute Toxicity

No published human case reports of fatal toxicity from 1B-LSD specifically were found. No animal LD₅₀ data from empirical studies was found.

**In silico LD₅₀ predictions (Jurowski et al. 2026 [Ref 21]):**
- Multi-platform computational prediction for five LSD analogs including 1B-LSD
- **Predicted LD₅₀ (rats):** 49–85 mg/kg (oral, Percepta platform)
- **Predicted hematotoxicity:** 75% for 1B-LSD specifically — among the highest of the analogs tested
- Dermal and ocular irritation risks predicted as uniformly low
- N-1-acyl structural modification influences organ toxicity patterns

⚠️ **FLAG:** These are in silico predictions only, not empirical animal or human data. The generation agent must label these as computational predictions.

**LSD toxicity reference (active moiety):**
Holze et al. (2022 [Ref 8]) documented safety pharmacology of acute LSD in healthy subjects: mild-to-moderate heart rate increase, blood pressure elevation, and pupil dilation. QTc interval was NOT prolonged — no proarrhythmic signal. Nichols (2016 [Ref 11]) notes LSD is "generally considered physiologically safe."

LSD poisoning is documented; Roberts et al. (2021 [Ref 27]) reported a cluster of LSD poisonings following inadvertent insufflation of a white powder sold as cocaine — none fatal from LSD per se. Acute symptoms: perceptual disturbances, agitation, tachycardia, anxiety.

### Chronic Toxicity
No published data on chronic toxicity of 1B-LSD or LSD in humans at recreational doses. Jurowski et al. (2026 [Ref 21]) predicted pulmonary toxicity risk as elevated for some analogs in the series, but not specifically flagged as highest for 1B-LSD.

### HPPD Risk
Hallucinogen persisting perception disorder (HPPD) is documented with LSD-class substances. Ford et al. (2022 [Ref 18]) reviewed HPPD case series; LSD is the most commonly reported precipitant. HPPD is characterized by persistent visual disturbances without impaired reality testing. No 1B-LSD-specific HPPD cases were found.

### Psychological Risks
At higher doses (200+ µg LSD equivalent), significant anxiety and ego dissolution are documented (Holze et al. 2021 [Ref 29]). Seizure threshold reduction is listed in the seed data effects taxonomy; this is consistent with the general psychedelic class but no specific 1B-LSD seizure data was found.

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## Harm Reduction

### Testing and Identification
Standard colorimetric reagent tests for LSD work for 1B-LSD:
- Ehrlich reagent (DMAB) reacts positively with the indole ring — distinguishes from non-indole substances
- However, Ehrlich cannot distinguish 1B-LSD from LSD or other lysergamides analytically
- Advanced differentiation (1B-LSD vs 1P-ETH-LAD, a constitutional isomer) requires GC-MS, NMR, or LC-MS techniques — straightforward with these methods (Brandt et al. 2019 [Ref 2])
- LSD is subject to adulteration and substitution; Roberts et al. (2021 [Ref 27]) documented a cluster of unexpected LSD exposures

### Set and Setting
Community-reported onset (20–60 minutes) and total duration (8–12 hours) require appropriate preparation (Ref 25). Vizeli et al. (2024 [Ref 34]) confirm pre-drug anxiety and mental state are significant predictors of adverse effects.

### Emergency Response
If acute LSD/1B-LSD anxiety or panic occurs: benzodiazepines are first-line (documented in HPPD management: Christensen et al. 2023 [Ref 36 — not formally cited]); antipsychotics may worsen perceptual disturbances (Abraham 1983 reports phenothiazines exacerbate HPPD).

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## Tolerance & Dependence

### Tolerance
Tolerance to psychedelics develops **almost immediately** after ingestion via 5-HT₂A receptor downregulation (de la Fuente Revenga et al. 2022 [Ref 16]):
- A single dose of a psychedelic (DOI in mouse model) induces 5-HT₂A downregulation detectable 24 hours later
- Repeated administration produces progressive tolerance
- Mechanism involves 5-HT₂A receptor density reduction in frontal cortex; beta-arrestin-2 independent
- Cross-tolerance between psychedelics (LSD and DOI) confirmed in mice [Ref 16]

The brief's tolerance data (buildup: almost immediately; half-life: 6 days; full reset: 14 days; cross-tolerances: psychedelic) is consistent with this mechanistic evidence and widely-cited experiential data. No 1B-LSD-specific tolerance study was found.

### Dependence
Nichols (2016 [Ref 11]) states psychedelics "are generally considered physiologically safe and do not lead to dependence or addiction." No physical dependence is expected. Psychological dependence potential is low based on class evidence.

VigiBase pharmacovigilance data (Syed et al. 2026 [Ref 35 — not formally cited]) noted substance use disorder reports associated with LSD in real-world data, though methodology (voluntary reporting) and context (polysubstance use) limit interpretation.

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## Interactions

### Tramadol — DANGEROUS
The brief lists tramadol as a dangerous interaction. This is pharmacologically well-supported:
- Tramadol is a weak serotonin-norepinephrine reuptake inhibitor (SNRI) in addition to its µ-opioid activity
- Park et al. (2014 [Ref 23]) review tramadol–serotonin syndrome risk with serotonergic drugs
- Gillman (2005 [Ref 24]) identifies tramadol, meperidine, methadone, and dextromethorphan as weak SRIs involved in serotonin toxicity reactions; combination of multiple serotonergic mechanisms is required for life-threatening toxicity
- Combined with a serotonergic psychedelic (which activates 5-HT₂A), tramadol's SRI activity could contribute to serotonin syndrome
- The risk is plausible and well-grounded; flagged as dangerous in the brief

⚠️ **FLAG:** No 1B-LSD + tramadol case report or controlled study was found. The dangerous interaction classification is based on pharmacological inference from tramadol's mechanism, not specific evidence with 1B-LSD.

### Cannabis — UNKNOWN
The brief lists cannabis as an unknown interaction. No published controlled study of 1B-LSD or LSD + cannabis was found. Cannabis may potentiate psychedelic effects (anecdotally reported); no safety data. Classification as "unknown" is appropriate.

### CYP2D6 Inhibitors
Based on LSD metabolism data (Becker et al. 2025 [Ref 7]; Vizeli et al. 2021 [Ref 30]):
- Strong CYP2D6 inhibitors (e.g., fluoxetine, paroxetine, bupropion, haloperidol) can increase LSD exposure 1.4–1.5×
- Poor CYP2D6 metabolizers have ~75% higher LSD exposure
- Effect on 1B-LSD specifically is unknown (depends on whether the deacylation step is also CYP2D6-mediated)

### SSRIs/Antidepressants
Becker et al. (2025 [Ref 7]) found paroxetine (strong CYP2D6 inhibitor + SSRI) reduced "bad drug effect," anxiety, and nausea with LSD, while increasing LSD plasma concentrations. The net effect was not significantly adverse. However, other SSRIs with less CYP2D6 inhibition may blunt psychedelic effects (pharmacodynamic tolerance mechanism via 5-HT₂A downregulation).

### Lithium
The brief does not list lithium, but it is a widely-reported dangerous interaction with psychedelics: lithium + LSD/psychedelics is associated with increased seizure risk in anecdotal reports. No published controlled study was found in the literature search.

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## Legal Status

| Jurisdiction | Status | Basis | Notes |
|---|---|---|---|
| Germany | Controlled (Schedule 1 equivalent) | NpSG, July 18, 2019 | Production, import to market, administration, trading prohibited; possession illegal but not penalized under NpSG |
| United Kingdom | Illegal | Psychoactive Substances Act 2016 | All psychoactive substances banned unless exempt; no medical exemption for 1B-LSD |
| United States | Unscheduled but likely illegal | Federal Analogue Act | As an LSD analog intended for human consumption, would be treated as Schedule I |
| Canada | Unscheduled; analog controls may apply | CDSA Schedule III analog provisions | Structural relationship to LSD (Schedule III) |
| Australia | Prohibited | TGA Poisons Standard | Lysergamides broadly covered |

⚠️ **FLAG for editorial review:** Legal status is web-retrieved and cannot be confirmed against primary statutory documents in this research run. All jurisdictions should be verified against official sources before publication.

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## Clinical Trials

**ClinicalTrials.gov search for "1B-LSD" and "lysergamide":** 0 results found.

No clinical trials involving 1B-LSD have been registered. This is consistent with the compound's status as an uncharacterized research chemical. No institutional research with 1B-LSD in humans has been reported.

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## Community Feedback Analysis

No community feedback was submitted in Part A2 of the brief. Section is therefore empty.

No community feedback submitted.

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## Gaps & Flags

### Critical Data Gaps

1. **No human pharmacokinetic data for 1B-LSD itself.** All PK data is inferred from LSD (after prodrug conversion) and from in vitro hydrolysis analogs. No plasma 1B-LSD or plasma LSD (after 1B-LSD dosing) data in humans has been published.

2. **No confirmed in vivo deacylation data specific to 1B-LSD.** The Halberstadt 2020 paper measured LSD plasma levels after ALD-52 and 1P-LSD administration in rats, but 1B-LSD was not included in this specific experiment. The prodrug hypothesis is strongly supported but not directly confirmed for 1B-LSD.

3. **Specific numerical Ki/EC50 binding values for 1B-LSD at individual receptors** are in the Halberstadt 2020 paper (PMID 31756337) but were not accessible from available open-access sources. The full receptorome screening data with specific values was not retrieved. Generation agent should access the paywalled paper directly.

4. **No CAS registry number** for 1B-LSD was confirmed.

5. **No empirical LD₅₀ data.** Only in silico predictions exist (Jurowski 2026 [Ref 21]). These should be clearly labeled as computational estimates.

6. **Dose/potency interpretation requires editorial judgment.** The 14% relative potency in mouse HTR vs. user-reported doses that are comparable to LSD presents a scientific tension that requires interpretation. If deacylation efficiency approaches 100%, potency in humans should approach LSD; the HTR discrepancy may reflect pharmacokinetic factors in mice vs. humans rather than intrinsic potency difference. The seed data dose ranges (common 75–150 µg) appear broadly consistent with LSD doses, suggesting near-complete conversion in humans — but this is inferred, not measured.

7. **SMILES not listed in original brief** — now confirmed as `CCCC(=O)N1C=C2C[C@@H]3C(=C[C@H](CN3C)C(=O)N(CC)CC)C4=C2C1=CC=C4`.

### Safety-Critical Flags

- **Tramadol interaction:** Classified as dangerous in the brief. Pharmacologically sound (serotonin syndrome mechanism) but no 1B-LSD-specific case data was found. Flag for human review.

- **Seizure risk:** The effects taxonomy includes "seizure threshold reduction." No 1B-LSD-specific seizure data found. This is consistent with the general psychedelic class but the seed datum is unverified against a published source for 1B-LSD specifically.

- **Hematotoxicity prediction (in silico):** Jurowski 2026 predicted 75% hematotoxicity probability for 1B-LSD — highest alongside 1P-LSD among the analogs tested. This is a computational prediction only and requires experimental verification. Flag for harm reduction section.

- **CYP2D6 poor metabolizer risk:** Individuals who are CYP2D6 poor metabolizers may experience substantially prolonged and intensified effects from 1B-LSD (via enhanced LSD exposure after prodrug conversion). No clinical guidance exists. Should be flagged as a contraindication or caution.

- **Legal status unverified against primary statutory documents** in all jurisdictions — web-retrieved only.

### Structural Analogy Reliance

The following sections rely primarily on structural analogy to LSD (via the prodrug mechanism) rather than 1B-LSD-specific data:
- All pharmacology beyond direct binding/HTR (mechanism of action, full receptor profile, clinical effects)
- All pharmacokinetics beyond the deacylation step
- Safety and cardiovascular effects
- Duration/dose data beyond what is confirmed in controlled trials

This is appropriate given the prodrug mechanism, but the generation agent must clearly distinguish which data is LSD-specific (post-conversion) vs. 1B-LSD-specific.