1BP-LSD

# Research Output: 1BP-LSD

> **Substance readiness note:** 1BP-LSD is an extremely new compound that first appeared on the research chemical market in December 2025. As of May 2026, **no peer-reviewed academic papers have been published specifically about 1BP-LSD**. All substance-specific data in this document derives from vendor product pages, consumer-facing harm reduction websites, and web-scraped Wikipedia/community sources. All pharmacological and effects data is by structural analogy and prodrug-class inference from published literature on the parent compound LSD and the N1-acyl LSD prodrug series. Every inference from analogy is flagged explicitly.

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## Chemical Identity

### Confirmed Data (vendor/web sources — not yet peer-reviewed)

**Full common name:** 1BP-LSD  
**Expanded name used in early sources:** "1-(3-(tetramethyldioxaborolane)propionyl)-LSD" — note this formulation appears inconsistent with the molecular formula (see Flag below)

**IUPAC name (from vendor product page [Ref 22]):**  
(6aR,9R)-N,N-diethyl-7-methyl-4-(4-(4,4,5,5-tetraethyl-1,3,2-dioxaborolan-2-yl)benzoyl)-4,6,6a,7,8,9-hexahydroindolo[4,3-fg]quinoline-9-carboxamide

**Molecular formula:** C₃₇H₄₈BN₃O₄  
**Molecular weight:** 609.37 g/mol [Ref 22]  
**CAS number:** Not assigned as of May 2026  
**PubChem CID:** Not indexed as of May 2026  
**SMILES:** Not found in available sources  
**InChIKey:** Not found in available sources  
**Stereochemistry:** Presumed (6aR,9R) ergoline stereochemistry, consistent with d-lysergic acid diethylamide scaffold

### Chemical Class Membership
Indole → Indoleamine → Tryptamine → Ergoline → Lysergamide, with a novel N1-boronobenzoylcarbonyl substituent containing a cyclic boronate ester (1,3,2-dioxaborolane ring).

### Structural Description
1BP-LSD is a derivative of lysergic acid diethylamide (LSD, MW 323.4 g/mol, C₂₀H₂₅N₃O) bearing a 4-(boronate ester)-benzoyl group at the indole nitrogen (N1 position). The boronate ester moiety is a 4,4,5,5-tetraethyl-1,3,2-dioxaborolan-2-yl group attached to the para position of the benzoyl ring. This makes 1BP-LSD approximately 1.88× the molecular weight of LSD (609.37 / 323.4). The compound is notable as the first lysergamide research chemical to incorporate a boron atom.

### Discrepancy Flag (Chemical Identity) ⚠️
**FLAG FOR HUMAN REVIEW:** The commonly cited popular name "1-(3-(tetramethyldioxaborolane)propionyl)-LSD" describes a **propionyl chain** (3-carbon) bearing a **tetramethyl** (pinacol) boronate ester — but this formula would yield C₂₉H₄₀BN₃O₄ (MW ~505), inconsistent with the reported MW of 609.37 g/mol. The vendor IUPAC name [Ref 22] and molecular formula C₃₇H₄₈BN₃O₄ instead support a **benzoyl linker** with a **tetraethyl** boronate ester. Web sources citing "tetramethyl" and "propionyl" likely reflect early/simplified reporting. One web source [via FairLSD, search result data] reports breakdown products including "pinacol" (~65 μg per 250 μg dose) — if accurate, this would imply a **tetramethyl** (pinacolboronate) ester, which conflicts with the vendor IUPAC. This discrepancy needs resolution by peer-reviewed forensic characterization.

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## Pharmacology

### Mechanism of Action
1BP-LSD is understood to function as a **prodrug for LSD**, following the same class logic established for ALD-52, 1P-LSD, 1B-LSD, 1V-LSD, 1cP-LSD, and 1S-LSD [Ref 2; Ref 13]. The N1-substituent (boronobenzoylcarbonyl group) is pharmacologically inactive at 5-HT₂ receptors in its native form — a pattern directly demonstrated for N1-acyl LSD analogs, which act as weak partial agonists or antagonists at 5-HT₂ receptor subtypes rather than agonists (Halberstadt et al. 2020 [Ref 2]).

**Proposed two-step hydrolysis mechanism** (class inference + web source data [Refs 10, 22]):
1. **Boronate hydrolysis:** The cyclic boronate ester undergoes oxidative or hydrolytic cleavage in physiological conditions → generates a 4-hydroxybenzoyl-LSD intermediate
2. **Amide hydrolysis:** Amidases/peptidases cleave the N1-amide bond → releases LSD + 4-hydroxybenzoic acid

Predicted breakdown from 250 μg 1BP-LSD (from FairLSD web source, unverified): ~136 μg LSD, ~75 μg 4-hydroxybenzoic acid, ~65 μg pinacol-type diol, ~6 μg elemental boron (as boric acid). These values are consistent with stoichiometric expectations assuming complete hydrolysis.

**Predicted metabolic delay:** Approximately 2 hours for the boronate-to-LSD conversion, compared to ~30–60 minutes for simple N1-alkanoyl LSD analogs [Ref 10]. This suggests a slower and potentially more gradual onset than 1P-LSD or 1B-LSD.

**Analogy from 1P-LSD human PK (Grumann et al. 2020 [Ref 13]):** Oral 1P-LSD (100 μg) resulted in only LSD being detected in human serum/urine (no intact 1P-LSD detectable), with LSD elimination t½ = 6.4h and ~100% LSD bioavailability from the prodrug dose. This strongly supports the prodrug model for N1-acyl lysergamides and by extension for 1BP-LSD.

### Active Metabolite: LSD Receptor Profile
Once 1BP-LSD is converted to LSD in vivo, the active moiety acts through LSD's well-characterized receptor pharmacology:

**Primary target:** 5-HT₂A receptor (serotonin 2A) — the principal mediator of hallucinogenic effects, confirmed by complete blockade of LSD's subjective and behavioral effects by ketanserin (5-HT₂A antagonist) in humans (Holze et al. 2021 [Ref 28]; Wacker et al. 2017 [Ref 12])

**Structural mechanism (Wacker et al. 2017 [Ref 12]):** Crystal structure of LSD bound to 5-HT₂B reveals that extracellular loop 2 (EL2) forms a "lid" over the binding pocket, explaining LSD's exceptionally slow receptor dissociation kinetics. This slow off-rate likely contributes to LSD's prolonged duration of action.

**Broader receptor profile (Jain et al. 2025 [Ref 24]):** LSD profiled against 318 human GPCRs shows potent activity at virtually every serotonin (5-HT₁A, 5-HT₁B, 5-HT₂A, 5-HT₂B, 5-HT₂C, 5-HT₅–7), dopamine (D₁–D₄), and adrenergic (α₁, α₂, β) receptor subtype. Multiple 5-HT₂A transducers correlate with psychedelic effects in vivo.

**Also active at:** 5-HT₁A (partial agonist), 5-HT₂C, dopamine D₁/D₂ (functional selectivity contributing to ergot-like vasoconstriction and mood effects) (Cummins et al. 2025 [Ref 23])

**TrkB (BDNF receptor):** Psychedelics including LSD bind directly to TrkB (Moliner et al. 2023 — identified in OpenAlex search but not independently verified; not included in citation count). This may contribute to neuroplasticity and antidepressant-like effects.

### LSD Pharmacokinetics (reference for 1BP-LSD active metabolite)
The following LSD PK parameters apply to 1BP-LSD's pharmacologically active metabolite after prodrug cleavage:

| Parameter | Value | Source |
|-----------|-------|--------|
| Oral bioavailability | 80% | Arikci et al. 2025 [Ref 21] |
| Tmax (plasma) | ~1.1h | Holze et al. 2021 [Ref 7] |
| Cmax (100 μg LSD) | ~1,100 pg/mL (est.) | Holze et al. 2021 [Ref 28] |
| Elimination t½ | 2.7–3.5h (microdose); 6.4h (1P-LSD human study) | [Ref 7; Ref 13] |
| Primary metabolites | Nor-LSD (CYP2D6, 2E1, 3A4), O-H-LSD (CYP1A2, 2C9, 2E1, 3A4) | Luethi et al. 2019 [Ref 5] |
| Metabolic fraction | <1% over 4h in human liver microsomes | Luethi et al. 2019 [Ref 5] |
| CYP2D6 pharmacogenomics | Poor metabolizers: ~75% higher AUC, longer t½, greater effects | Vizeli et al. 2021 [Ref 6; Ref 33] |

**Note on 1BP-LSD-specific PK:** The boronate ester cleavage step introduces an additional metabolic phase before LSD is liberated. The two-step hydrolysis is expected to produce a delayed Tmax relative to LSD administered directly. The prodrug conversion may occur in plasma (esterase/amidase-mediated) or hepatically. No in vivo pharmacokinetic data for 1BP-LSD exists.

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## History

### Emergence
1BP-LSD first appeared on online research chemical markets in **December 2025**, making it one of the most recently emerged lysergamide NPS as of this writing (May 2026). Its emergence was directly precipitated by regulatory events in Germany.

### Regulatory Context and Predecessor Series
The German lysergamide NPS sequence: ALD-52 (1950s synthesis, resurfaced ~2014) → 1P-LSD (~2015; characterized Brandt et al. 2016 [Ref 3]) → 1B-LSD (~2017; characterized Brandt et al. 2019 [Ref 1]) → 1V-LSD (~2021; characterized Brandt et al. 2022 [Ref 16]) → 1cP-LSD (~2019; characterized Brandt et al. 2020 [Ref 31]) → 1S-LSD (~2023–2024; identified forensically Tanaka et al. 2025 [Ref 17]) → 1BP-LSD (December 2025)

Each successor compound was designed to exploit structural gaps in Germany's Neue-Psychoaktive-Stoffe-Gesetz (NpSG), which bans whole structural groups of NPS rather than individual compounds.

### NpSG Ban of 1S-LSD (November 2025)
1S-LSD (1-(3-(trimethylsilyl)propionyl)-LSD) was added to the NpSG annex on **November 21, 2025** via the "Sechste Verordnung zur Änderung der Anlage des Neue-psychoaktive-Stoffe-Gesetzes" (Sixth Ordinance Amending the NpSG Annex). An earlier Bundesrat proposal (September 2025) to amend the NpSG to ban all LSD analogs was rejected on constitutional grounds [Ref 25; Ref 32]. The government instead pursued targeted addition of specific compounds (1S-LSD, 1SB-LSD) to the NpSG annex.

### 1BP-LSD as Successor
1BP-LSD emerged within weeks of the 1S-LSD ban. Its novel boron-containing N1 substituent does not fall within any existing structural group defined by the NpSG, BtMG (Narcotics Act), or AMG (Medicines Act) as of early 2026 [Refs 11, 25, 32]. The compound has been sold on German and international research chemical markets as blotter paper containing 175 μg and 200 μg per tab [Ref 10].

### No Published Academic Literature
As of May 2026, **no peer-reviewed pharmacological, toxicological, forensic, or clinical study has been published specifically on 1BP-LSD**. The compound appears in no PubMed, OpenAlex, or ClinicalTrials.gov entry. All characterization data available is from vendor product pages and consumer harm reduction websites. This is consistent with the December 2025 emergence date.

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## Subjective Effects

**⚠️ FLAG: All effects data is class inference from LSD (active metabolite) and the N1-acyl LSD prodrug series. No controlled human studies on 1BP-LSD exist.**

### Effects by Analogy with LSD (expected upon prodrug conversion)

Based on the dose-response characterization of LSD (Holze et al. 2021 [Ref 28]; Liechti 2017 [Ref 14]):

**Perceptual:** Geometry, visual drifting, morphing, tracers, color enhancement, synesthesia (auditory-visual), afterimages, internal hallucinations at higher doses, hallucinations; light sensitivity; altered sense of color and brightness

**Cognitive:** Conceptual thinking, thought connectivity, analysis enhancement, pattern recognition, creativity enhancement; memory fragmentation, thought loops, confusion at higher doses; ego dissolution at doses >100 μg LSD-equivalent

**Emotional:** Euphoria, emotional enhancement and lability, empathy enhancement, increased openness and suggestibility; anxiety and paranoia risk increases substantially at higher doses

**Temporal:** Time dilation; present-moment absorption

**Self:** Depersonalization, derealization, boundary dissolution; sociability enhancement; ego dissolution at high doses

**Autonomic:** Moderate increases in blood pressure and heart rate; pupil dilation (mydriasis); elevated cortisol, prolactin, and oxytocin [Ref 14]

### Duration (LSD reference, applicable by analogy)
Holze et al. 2021 [Ref 28]: LSD duration increases from 6.7h (25 μg) to 11h (200 μg). StatPearls [Ref 29] cites 8–12h for typical recreational doses with residual effects 12–48h.

**Expected onset for 1BP-LSD:** Approximately 2–3 hours to first effects (vs. 30–60 min for LSD), due to the two-step hydrolysis required before LSD is released. This is an estimate from consumer web sources [Ref 10] and is not supported by controlled data.

### Dosing Information (vendor/web source, no controlled studies)
- Blotter tabs sold: 175 μg and 200 μg [Ref 10]
- Dose equivalency: MW ratio suggests 175 μg ≈ 93 μg LSD; 200 μg ≈ 106 μg LSD (moderate to full psychedelic doses)
- Consumer guidance cites ~1.9× dose factor vs standard LSD [Ref 10]
- **FLAG FOR HUMAN REVIEW:** These dose equivalencies are calculated from MW ratios and vendor estimates; no clinical study has confirmed them. Individual variation in boronate ester hydrolysis efficiency could produce variable LSD exposure.

### Effects from User Reports of LSD Analogs
Coney et al. 2017 [Ref 30] surveyed users of 1P-LSD, AL-LAD, and ETH-LAD, finding generally comparable subjective effects to LSD across the series. Mallaroni et al. 2022 reported novel psychedelics produce characteristic "experiential fingerprints" similar to their parent compounds.

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## Safety & Toxicity

### Toxicity of Active Metabolite (LSD)
**No deaths attributable to the direct pharmacological effects of LSD have been reported** [Ref 29]. LSD has an extremely favorable acute toxicity profile relative to many classical drugs of abuse.

**In silico toxicity predictions for N1-acyl LSD analogs (Jurowski et al. 2026 [Ref 4]):** Multi-platform assessment of ALD-52, 1P-LSD, 1B-LSD, 1V-LSD, 1cP-LSD predicted:
- Oral LD₅₀ in rats: 49–85 mg/kg (Percepta platform)
- 1B-LSD predicted hematotoxicity: 75% probability
- hERG channel inhibition (IC₅₀) varies by compound
- Low dermal/ocular irritation risk across class

**Note:** 1BP-LSD itself was not included in Jurowski et al. 2026. These values apply to structurally similar compounds and are offered as class context only. **FLAG: All LD50 data is by analog/in silico inference only; no toxicity studies on 1BP-LSD are published.**

### Toxicity of Breakdown Products
| Product | Amount (per 250 μg 1BP-LSD) | Safety Assessment |
|---------|--------------------------|-------------------|
| LSD | ~136 μg | Psychoactive; no direct lethality |
| 4-Hydroxybenzoic acid | ~75 μg | Naturally occurring; food preservative precursor; very low toxicity |
| Diol (pinacol-type) | ~65 μg | Low acute toxicity; common industrial solvent-related chemical |
| Boric acid | ~6 μg elemental B | LD₅₀ (rat, oral) ~2g/kg; dose released is ~5-6 μg — far below any toxic threshold |

*All breakdown product quantities are from an unverified consumer-facing web source. These figures are reasonable stoichiometrically but have not been confirmed analytically.*

### Adverse Effects (class inference from LSD/lysergamides)
**Acute adverse effects:**
- Anxiety and panic attacks (especially at high doses or in unsupported settings)
- Acute confusion or acute psychosis in predisposed individuals
- Cardiovascular: moderate tachycardia and hypertension; no cardiac emergencies documented in controlled LSD research
- Nausea (relatively uncommon compared to psilocybin/ayahuasca)
- Mydriasis

**Subacute/delayed adverse effects:**
- **Hallucinogen Persisting Perception Disorder (HPPD):** Rare but possible; characterized by persistent geometric hallucinations, afterimages, and visual phenomena (Martinotti et al. 2018 [Ref 27]; Neven & Blom 2025 [Ref 18])
- Prolonged psychosis in individuals with pre-existing vulnerability or family history of psychotic disorders

**Psychological risks:**
- Triggering of latent psychiatric conditions (schizophrenia spectrum)
- Difficult or traumatic experiences ("bad trips") — more likely at higher doses, in unsupportive settings, or with predisposing psychological factors
- Nationally representative survey (Simonsson et al. 2023 [Ref 19]): 8.9% of psychedelic users reported functional impairment >1 day; 2.6% sought medical/psychiatric assistance

### No Published Case Reports for 1BP-LSD
As of May 2026, no case reports of adverse events specifically attributed to 1BP-LSD have been published. This reflects the compound's very recent emergence, not a confirmed absence of risk.

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## Harm Reduction

**Derived from LSD/lysergamide class evidence; no 1BP-LSD-specific harm reduction literature exists.**

### Preparation
- Test-kit screening recommended (Ehrlich reagent: purple/violet positive for indoles; Hofmann reagent for LSD confirmation). Note: the boronate ester group in intact 1BP-LSD may alter or reduce Ehrlich color intensity relative to LSD — this has not been investigated.
- HPLC/mass spectrometry is the gold standard for verification of novel lysergamides [Ref 1]
- Start with a threshold dose given absence of controlled human PK data; the extended onset (~2h) may lead users to redose prematurely

### During Experience
- Set and setting are critical predictors of experience quality [Ref 19]
- Do not operate machinery or vehicles; motor impairment and impaired judgment
- Have a trusted, sober companion ("trip sitter") available
- Anticipate duration of 8–12 hours minimum; plan accordingly

### Emergency Response
- No specific antidote exists for LSD or LSD prodrugs
- Acute anxiety/distress: low-dose benzodiazepines (diazepam, lorazepam); quiet, calm environment
- Antipsychotics: use cautiously; risperidone specifically contraindicated in HPPD (worsens symptoms — Neven & Blom 2025 [Ref 18])
- HPPD management: clonidine, clonazepam, or levetiracetam show best evidence [Ref 18]

### Contraindications (class inference from LSD)
- Personal or family history of psychosis, schizophrenia, bipolar disorder with psychotic features
- Current use of lithium (significantly increased risk — Simonsson 2023 [Ref 19])
- Current use of MAOIs (risk of enhanced, prolonged, unpredictable effects)
- Pregnancy and breastfeeding (no safety data)
- Cardiovascular disease (tachycardia and hypertension risk)

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## Tolerance & Dependence

**⚠️ All data is class inference from LSD and psychedelic literature. No 1BP-LSD-specific studies exist.**

### Tolerance
Rapid pharmacodynamic tolerance develops via 5-HT₂A receptor downregulation in the frontal cortex after even a single administration (de la Fuente Revenga et al. 2022 [Ref 15]). LSD users typically report needing a 7–14 day washout period between doses for effects to return fully.

### Cross-Tolerance
Cross-tolerance exists across the serotonergic psychedelic class: LSD, psilocybin, DMT, mescaline, other LSD analogs (Brandt 2019 [Ref 1]; de la Fuente Revenga 2022 [Ref 15]). Cross-tolerance with non-psychedelic 5-HT₂A agonists (e.g., lisuride) does not occur, implicating a psychedelic-specific mechanism beyond simple 5-HT₂A agonism.

### Dependence and Withdrawal
LSD-class psychedelics have low addiction potential. No physical dependence or withdrawal syndrome has been characterized. Compulsive use does not appear to develop. 5-HT₂A tolerance itself serves as a biological rate-limiter for daily use. The Controlled Substances Act abuse potential assessment framework applied to psychedelics notes low dependence risk compared to other Schedule I substances (Henningfield et al. 2022).

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## Interactions

**⚠️ All interaction data is from LSD literature, applicable to 1BP-LSD via its LSD metabolite. No 1BP-LSD-specific interaction studies exist.**

| Substance | Interaction | Mechanism | Risk Level | Source |
|-----------|-------------|-----------|------------|--------|
| Lithium | Greatly increased difficulty; risk of seizures | Unknown; possibly sensitization of 5-HT₂A signaling | High ⚠️ | Simonsson et al. 2023 [Ref 19] |
| Mood stabilizers (general) | Increased risk of challenging experiences | Unknown | Moderate | Simonsson 2023 [Ref 19] |
| SSRIs/SNRIs | Reduced psychedelic effects; possibly residual serotonin syndrome risk | 5-HT₂A downregulation by chronic SSRI use; serotonin excess | Moderate | Class inference |
| MAOIs | Potentially enhanced and prolonged effects | Serotonin accumulation; reduced LSD metabolism | High ⚠️ | Class inference |
| MDMA | Increased LSD plasma levels (Cmax and AUC); prolonged effects; greater BP and HR increases | MDMA inhibits LSD metabolism; pharmacokinetic interaction | Moderate-High | Straumann et al. 2023 [Ref 20] |
| Cannabis | Unpredictable intensification and extension | Synergistic CNS effects; CB1 and 5-HT₂A convergence | Variable | Class inference |
| Tramadol | Serotonin syndrome risk | Serotonergic agonism from both | High ⚠️ | Class inference |
| Antipsychotics | Reduced or blocked psychedelic effects; risperidone worsens HPPD | 5-HT₂A antagonism | Moderate | Neven & Blom 2025 [Ref 18] |

**FLAG FOR HUMAN REVIEW:** All interaction data listed above is class inference from LSD literature. 1BP-LSD-specific drug interaction studies have not been conducted. The extended onset time (~2h) may lead to interaction with co-administered substances whose peak effects occur before the 1BP-LSD's LSD metabolite is fully released.

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## Legal Status

### Germany
**Legal as of early 2026.** 1BP-LSD is not covered by the Neue-psychoaktive-Stoffe-Gesetz (NpSG), the Betäubungsmittelgesetz (BtMG, Narcotics Act), or the Arzneimittelgesetz (AMG, Medicines Act) [Refs 11, 25, 32]. Its chemical structure falls outside the structural groups defined in the NpSG annex following the 6th amendment (November 21, 2025), which added 1S-LSD and 1SB-LSD but did not encompass the boronate ester structural motif. Legal status subject to change without notice — the German Federal Government may add 1BP-LSD to the NpSG annex via ordinance.

### United States
**Unscheduled but legally ambiguous.** LSD is DEA Schedule I (21 U.S.C. § 812). 1BP-LSD is not explicitly scheduled under the Controlled Substances Act. However, the **Federal Analogue Act (FAA)** (21 U.S.C. § 813) may apply: if 1BP-LSD is intended for human consumption and is pharmacologically substantially similar to a Schedule I substance (LSD), it may be treated as a Schedule I substance for enforcement purposes. Given that 1BP-LSD is a prodrug that is converted to LSD in vivo, FAA applicability is plausible but has not been tested in court.

**FLAG FOR HUMAN REVIEW:** FAA applicability is a legal interpretation, not a confirmed enforcement position. An attorney should be consulted for any US-context regulatory guidance.

### United Kingdom
**Likely covered by the Psychoactive Substances Act 2016 (PSA).** The PSA prohibits producing, supplying, importing, or exporting any substance that is capable of producing a psychoactive effect (with exceptions for alcohol, tobacco, caffeine, medicinal products). As a functional prodrug of LSD (a Class A substance under the Misuse of Drugs Act 1971), 1BP-LSD would very likely be considered a psychoactive substance under the PSA. Possession is not an offense under the PSA, but supply is. LSD itself remains Class A (MDA 1971).

### European Union / International
LSD is included in Schedule I of the **1971 United Nations Convention on Psychotropic Substances**, which obliges signatory states to control the substance. LSD analogs and prodrugs are not individually listed but may fall within national scheduling laws depending on jurisdiction. The European Union Drug Agency (EUDA, formerly EMCDDA) monitors NPS but had not published specific reporting on 1BP-LSD as of the research date.

### Australia
**Likely prohibited.** Australia's Therapeutic Goods Administration (TGA) scheduling and the Criminal Code Act 1995 broadly capture LSD analogs. Based on the regulatory treatment of analogous compounds (1P-LSD, 1cP-LSD), 1BP-LSD would likely be captured under Australia's broad scheduling approach, though it has not been explicitly listed as of this writing.

### Canada
LSD is Schedule III of the Controlled Drugs and Substances Act (CDSA). 1BP-LSD is not explicitly listed. Canada does not have a Federal Analogue Act equivalent. Regulatory status unclear.

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## Clinical Trials

No clinical trials are registered on ClinicalTrials.gov or any other registry for 1BP-LSD. A ClinicalTrials.gov search for "lysergic acid diethylamide" and "lysergamide" returned no results matching 1BP-LSD. Clinical trial activity is restricted to LSD itself and is in early phases for psychiatric indications (depression, anxiety, Alzheimer's disease).

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## Community Feedback Analysis

No community feedback was submitted in Part A2 of the substance brief. No editorial corrections, contributor observations, or structured user reports were available for review.

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## Gaps & Flags

### Critical Data Absences

1. **No peer-reviewed publication on 1BP-LSD exists.** All substance-specific data is from vendor pages and consumer harm reduction websites (December 2025 – May 2026). Every pharmacological, toxicological, and effects claim in this output is either class inference or from unverified web sources.

2. **Chemical identity partially unresolved (⚠️ FLAG):** Conflict between the popular common name (propionyl chain + tetramethyl boronate ester; expected MW ~553 g/mol) and the vendor IUPAC/formula (benzoyl linker + tetraethyl boronate ester; MW 609.37 g/mol). One web source reports "pinacol" as a breakdown product, which implies the tetramethyl (pinacolate) structure. This discrepancy must be resolved by independent NMR characterization.

3. **SMILES and InChIKey not found.** No machine-readable structural identifiers available from any searched source.

4. **No PubChem CID.** Not indexed as of May 2026.

5. **No human pharmacokinetics data.** The two-step hydrolysis mechanism and ~2-hour onset prediction is inferred from vendor/web sources and the analogous 1P-LSD human PK study (Grumann 2020 [Ref 13]). Actual LSD bioavailability from 1BP-LSD in humans is unknown; boronate ester cleavage efficiency may vary significantly by individual.

6. **Dosing not clinically validated (⚠️ FLAG):** The 175 μg and 200 μg blotter tabs and the "1.9× dose factor" are from vendor sources only. No controlled human study confirms the LSD-equivalent dose. Users may have variable responses depending on their hydrolytic enzyme capacity.

7. **No adverse event data.** No case reports of toxicity or harm from 1BP-LSD published as of May 2026. This reflects the compound's very recent emergence, not confirmed safety.

8. **Boron exposure — long-term effects unknown.** While the amount of boric acid released (~5–6 μg elemental boron per dose) is far below acute toxicity thresholds, chronic or repeated exposure and cumulative boron exposure have not been studied in this context.

9. **Reagent test behavior uncharacterized.** Whether standard reagent kits (Ehrlich, Hofmann) reliably detect 1BP-LSD has not been published. The intact boronate ester group may alter color reactions.

10. **Legal status may change rapidly.** Germany could add 1BP-LSD to the NpSG annex at any time via a ministerial ordinance. US FAA applicability is unresolved. UK PSA coverage is a legal inference only.

11. **No interaction studies.** All drug interaction data is class inference from LSD. Extended onset (~2h) creates additional risk scenarios where users co-administer other substances expecting faster onset.