2C-B-FLY

# Research Output: 2C-B-FLY

---

## Chemical Identity

**PubChem CID:** 10265873 (api_verified via PubChem lookup)

**Molecular Formula:** C₁₂H₁₄BrNO₂

**Molecular Weight:** 284.15 g/mol (exact monoisotopic mass: 283.0208)

**CAS Registry Number:** 178557-21-6 (confirmed via NIST WebBook [Ref 26])

**InChIKey:** YZDFADGMVOSVIX-UHFFFAOYSA-N (confirmed via PubChem [Ref 26] and NIST WebBook; UHFFFAOYSA-N suffix indicates no defined stereocenters)

**IUPAC Names (alternative nomenclature for same compound):**
- PubChem/NIST preferred: 2-(4-bromo-2,3,6,7-tetrahydrofuro[2,3-f][1]benzofuran-8-yl)ethanamine
- Alternative system used in published literature (Halberstadt et al. 2019 [Ref 1]): 2-(8-bromo-2,3,6,7-tetrahydrobenzo[1,2-b:4,5-b']difuran-4-yl)ethan-1-amine

Both names describe the same compound; the difference reflects alternative ring-numbering conventions for the fused benzodifuran ring system. The seed data IUPAC matches the PubChem preferred name.

**SMILES:** Not returned by the PubChem API in this lookup. The PubChem canonical SMILES for CID 10265873 is available via the PubChem web interface but was not retrieved in this API session. **FLAG: SMILES string is missing from the database record and should be populated.**

**Stereochemistry:** 2C-B-FLY has no stereocenters (the InChIKey UHFFFAOYSA-N suffix confirms no stereochemical information). Unlike the DOB-FLY analog (which has an α-methyl group creating a chiral center), 2C-B-FLY is the ethylamine (non-α-methylated) analog and exists as a single achiral structure. No active enantiomers to discuss.

**Physical Properties:** No published data on melting point, solubility, or stability specific to 2C-B-FLY in reviewed literature. **FLAG for gap.**

**Notes on Seed Data:** The seed data's systematic name is confirmed correct. PubChem CID (missing from seed) is 10265873. Molecular formula and weight are confirmed. SMILES is absent from both seed and API response.

---

## Pharmacology

### Mechanism of Action

2C-B-FLY is a serotonergic psychedelic. Its primary mechanism involves agonism or partial agonism at the serotonin 5-HT₂A receptor, the same receptor subtype responsible for the hallucinogenic effects of 2C-B, LSD, psilocin, and other classical psychedelics (Nichols 2004 [Ref 29]).

The compound is structurally derived from 2C-B (2,5-dimethoxy-4-bromophenethylamine) with the 2- and 5-methoxy groups incorporated into a rigid 2,3,6,7-tetrahydrobenzo[1,2-b:4,5-b']difuran ring system. This conformational constraint forces the oxygen atoms into a fixed geometry that effectively models the active binding conformation of the methoxy groups at 5-HT₂ receptors (Monte et al. 1996 [Ref 7]).

**Key pharmacological profile (Rickli et al. 2015 [Ref 15]):**
- 2C-B-FLY is **NOT** a monoamine releaser — unlike many other novel benzofuran psychoactives, it does not interact with monoamine transporters to cause dopamine/serotonin release in the manner of MDMA or amphetamines
- 2C-B-FLY **very potently** interacts with 5-HT₂ receptors (5-HT₂A, 5-HT₂B, 5-HT₂C)
- 2C-B-FLY **binds TAAR1** (trace amine-associated receptor 1)
- The pharmacological profile indicates **predominantly hallucinogenic properties** and a **risk for vasoconstriction** (Rickli et al. 2015 [Ref 15])
- CFSRE (2025 [Ref 24]) describes 2C-B-FLY as a **partial agonist** at 5-HT₂A, also binding 5-HT₂B, 5-HT₂C, and 5-HT₂D

### Binding Affinity and In Vivo Potency

The Monte 1996 foundational paper [Ref 7] reported that the series of 8-substituted tetrahydrobenzodifuranyl aminoalkanes (including 2C-B-FLY precursors) had activities at 5-HT₂A, 5-HT₂B, and 5-HT₂C receptors that equaled or surpassed the activity of conformationally flexible parent compounds. The bromo-substituted amphetamine analog (DOB-FLY, compound 7b) had Ki values in the nanomolar to subnanomolar range at human 5-HT₂ receptors. The Schultz et al. 2008 hybrid benzofuran study [Ref 9] established that the parent difuranyl DOB-FLY has Ki = 1.0 nM and EC₅₀ = 13 nM at rat 5-HT₂A receptor.

**Specific 2C-B-FLY data from in vivo mouse head-twitch response (HTR) assay (Halberstadt et al. 2019 [Ref 1]):**
- 2C-B-FLY HTR ED₅₀ = **1.79 μmol/kg** in C57BL/6J mice
- 2C-B (parent compound) HTR ED₅₀ = 2.43 μmol/kg
- DOB-FLY (α-methyl amphetamine analog) HTR ED₅₀ = 0.67 μmol/kg
- DOB (parent of DOB-FLY) HTR ED₅₀ = 0.75 μmol/kg
- Bromo-DragonFLY (aromatic benzodifuran, DOB-DFLY) HTR ED₅₀ = 0.20 μmol/kg

**Interpretation (Halberstadt et al. 2019 [Ref 1]):** The tetrahydrobenzodifurans (FLY compounds) are approximately equipotent with their non-rigid parent compounds. By contrast, the benzodifurans (DragonFLY compounds) show significantly enhanced potency — because full aromatization of the rings provides additional potency beyond the ring-constraining effect alone. The potency relationships in mice closely parallel the known human hallucinogenic dose data.

The mouse HTR assay has been validated as a robust predictor of human hallucinogenic potency, with a strong positive correlation (r = 0.9448) between HTR potencies in mice and reported hallucinogenic potencies in humans (n = 36) (Halberstadt et al. 2020 [Ref 10]).

**5-HT₂A receptor pharmacology context:** The 2,5-dimethoxyphenethylamine scaffold is essential for 5-HT₂A agonism. Conformational restriction of the methoxy groups into the dihydrofuran rings of 2C-B-FLY does not significantly alter in vivo potency relative to 2C-B — but incorporation into aromatic furan rings (as in 2C-B-DFLY) does increase potency (Halberstadt et al. 2019 [Ref 1]; Marcher-Rørsted et al. 2020 [Ref 6]).

**Biased agonism at 5-HT₂AR (Pottie et al. 2020 [Ref 2]):** While this study focused primarily on Bromo-DragonFLY and N-benzyl NPS, the benzodifuran scaffold showed markedly different β-arrestin 2 vs. miniGαq responses, suggesting functional selectivity. Whether 2C-B-FLY shows similar biased agonism has not been directly studied. **FLAG: No biased agonism data specific to 2C-B-FLY.**

### Pharmacokinetics and Metabolism

2C-B-FLY **is metabolized** by hepatic enzymes — a critical distinction from its aromatic analog Bromo-DragonFLY, which is **resistant** to hepatic metabolism (Noble et al. 2018 [Ref 16]).

**From Noble et al. 2018 [Ref 16] (human liver microsome and cytosol in vitro study):**
- **Primary metabolic enzyme: CYP2D6** (human liver microsomes)
- Also metabolized in human liver cytosol (HLC)
- **Main biotransformations: monohydroxylation** and **N-acetylation**
- **MAO-A** also metabolizes 2C-B-FLY, producing an aldehyde metabolite (trapped in vitro with methoxyamine)

**From Wagmann et al. 2019 [Ref 18] (FLY-class study with related FLY compounds 2C-E-FLY, 2C-EF-FLY, 2C-T-7-FLY):**
- Phase I reactions by: **CYP2D6, CYP3A4, FMO3**
- N-acetylation by: **NAT1 and NAT2**
- MAO-A and MAO-B deamination also detected
- 32 metabolites identified across FLY compounds
- Main steps: **hydroxylation and N-acetylation**
- Interindividual variation possible from CYP polymorphisms

**From Nykodemová et al. 2021 [Ref 3] (2C-B-Fly-NBOMe study — N-benzyl analog sharing the benzodifuran core):**
- 35 phase I and 9 phase II metabolites detected
- Major pathways: mono/poly-hydroxylation, O-demethylation, oxidative debromination, N-demethoxybenzylation (specific to NBOMe group)
- Phase II: glucuronidation and N-acetylation
- Highest metabolite concentration in human liver microsomes

**MAO Inhibition (Wagmann et al. 2019 [Ref 17]):**
- 2C-B-FLY is among FLY analogs showing potential MAO-A and/or MAO-B inhibition
- IC₅₀ values for MAO-A across the 2C/FLY series ranged 10–125 μM; for MAO-B 1.7–180 μM
- Authors conclude MAO inhibition cannot be excluded as a pharmacological contributor and further studies are warranted
- **FLAG: Specific IC₅₀ values for 2C-B-FLY alone were not extracted in this search; individual compound values are in the paper tables**

**Human pharmacokinetic data:** No published human pharmacokinetic studies for 2C-B-FLY exist. No published data on bioavailability, Tmax, Cmax, or plasma half-life in humans.

**Animal pharmacokinetic proxy (from 2C-B-Fly-NBOMe study [Ref 21]):** In male Wistar rats (s.c. administration, 1 mg/kg), peak serum concentrations were detected 30 min post-dose; peak brain tissue concentrations at 60 min (171 ng/g brain tissue). Compound still detectable in brain at 8 hours. This is for the N-benzyl analog and direct extrapolation to 2C-B-FLY is uncertain.

---

## History

### Discovery and Synthesis

2C-B-FLY was first synthesized in **1996** by Aaron P. Monte, David E. Nichols, and colleagues (including M.A. Parker as co-author) at **Purdue University** (Monte et al. 1996 [Ref 7]). The work was part of a series titled "Dihydrobenzofuran Analogues of Hallucinogens" (series papers 3 and 4; paper 3 is the primary 2C-B-FLY class paper).

**Research context:** The FLY class was developed as a medicinal chemistry tool to probe the active binding conformation of phenylalkylamine hallucinogens at the 5-HT₂A receptor. By replacing the flexible 2- and 5-methoxy groups of 2C-B with conformationally rigid dihydrofuran rings (forming the tetrahydrobenzodifuran ring system), the researchers created analogs designed to reveal which spatial orientation of the oxygen atoms is required for receptor activation (Monte et al. 1996 [Ref 7]).

Parker MA is credited as a co-author on the foundational 1996 paper and completed a 1998 PhD thesis titled "Studies of perceptiotropic phenethylamines" at Purdue University, contributing to the characterization of this class.

The benzodifuran (aromatic) version — Bromo-DragonFLY — was characterized in the same research context and published separately. The naming "FLY" reflects the butterfly-like appearance of the bicyclic ring system in structural diagrams.

### Emergence as Recreational Substance

2C-B-FLY began appearing on the research chemical market in the **mid-2000s**. It was **first reported to the EMCDDA early warning system in 2007** [Ref 26], and subsequently flagged several additional times. Its emergence paralleled the broader rise of 2C-series phenethylamines on the research chemical market following increased interest in PiHKAL compounds.

### Regulatory History

| Date | Event |
|------|-------|
| 1996 | First synthesized (Monte et al., Purdue University) |
| 2007 | First EMCDDA early warning notification |
| 2007 | Bromo-DragonFLY classified illegal in Denmark (triggered by fatal OD case [Ref 19]) |
| 2009 | Batch of Bromo-DragonFLY mislabelled as 2C-B-FLY causes severe toxicity/deaths [Ref 23] |
| 2016 (Oct 31) | Canada: Scheduled as Schedule III |
| 2016 (May 26) | UK: Covered by Psychoactive Substances Act 2016 |
| 2018 (Apr) | Sweden: Explicitly scheduled as illegal |
| 2023 | Belgium: Added to Annex IVB controlled substances |
| 2025 (Feb) | CFSRE first detects 2C-B-FLY in evidence materials (California) |

---

## Subjective Effects

No published controlled human studies of 2C-B-FLY exist. The following is derived from:
1. Preclinical animal data
2. Published data on the parent compound 2C-B (structural analog)
3. Community/user reports cited contextually

**Effects profile (inferred from pharmacology and class membership):**
2C-B-FLY is expected to produce effects consistent with serotonergic psychedelics acting primarily via 5-HT₂A agonism (Nichols 2004 [Ref 29]): visual hallucinations (geometric patterns, object distortions, color enhancement), altered thinking, mood changes, time distortion, and entactogenic qualities at certain doses.

**From Mallaroni et al. 2022 survey [Ref 4]** on novel psychedelic use patterns (including phenethylamines), the phenethylamine class shows distinct experiential fingerprints compared to tryptamines and lysergamides. Novel phenethylamines including the 2C-x series are reported to have faster onset and shorter durations than classical psychedelics.

**From the controlled human 2C-B study (Mallaroni et al. 2023 [Ref 13]) — closest available analog data:**
- 2C-B (20 mg oral) produced psychedelic alterations of waking consciousness
- Duration largely resolved within 6 hours (vs. psilocybin lasting longer)
- Transient pressor effects (blood pressure elevation)
- Less dysphoria, subjective impairment, and ego dissolution than psilocybin (15 mg)
- No empathogenic effects detected on the Multifaceted Empathy Test
- Equivalent psychomotor slowing and spatial memory impairment to psilocybin

**Key difference from 2C-B:** 2C-B-FLY has been described by experienced users as producing a longer and more sustained effect profile than 2C-B, consistent with the more rigid molecular structure potentially influencing receptor kinetics. This is supported by the rat pharmacokinetic analog data showing brain tissue retention for 8+ hours (Syrová et al. 2023 [Ref 21]).

**Duration data from seed database (PsychonautWiki-derived, user-report consensus):**
- Onset: 30–60 minutes (oral)
- Come up: 1–2 hours
- Peak: 3–5 hours
- Offset: 2–3 hours
- Total: 7–12 hours
- After-effects: 6–24 hours

The longer total duration compared to 2C-B (typically 4–6 hours total) is notable and consistent with the rigid ring system potentially affecting receptor dwell time. No published pharmacokinetic data in humans to confirm this directly. **FLAG: Duration data relies on community reports; no controlled studies.**

---

## Safety & Toxicity

### LD₅₀ and Toxic Dose

No published LD₅₀ data for 2C-B-FLY in any species. The seed data states "toxic dose is unknown" — **this is confirmed by literature search.** No controlled lethality studies found.

No published human case reports of 2C-B-FLY overdose or fatal poisoning exist. All overdose case reports in the published literature for the "FLY" class involve **Bromo-DragonFLY (DOB-DFLY)**, not 2C-B-FLY.

### Critical Safety Distinction: 2C-B-FLY vs. Bromo-DragonFLY

This is the single most important safety point for 2C-B-FLY harm reduction:

**Bromo-DragonFLY (DOB-DFLY)** and **2C-B-FLY** share the "FLY" naming convention but have dramatically different pharmacological profiles and risk levels:

| Property | 2C-B-FLY | Bromo-DragonFLY (DOB-DFLY) |
|----------|----------|--------------------------|
| Ring system | Tetrahydrobenzodifuran (partially reduced) | Benzodifuran (fully aromatic) |
| Relative potency | ~equipotent with 2C-B | ~20× more potent than 2C-B by weight |
| Duration | 7–12 hours | 24–72+ hours |
| Hepatic metabolism | Yes (CYP2D6, MAO-A) [Ref 16] | NOT metabolized in HLM or HLC [Ref 16] |
| MAO-A inhibition | Moderate (IC₅₀ not fully established) | Competitive inhibitor, Ki = 0.352 μM [Ref 16] |
| HTR ED₅₀ in mice | 1.79 μmol/kg [Ref 1] | 0.20 μmol/kg [Ref 1] |

**Fatal mislabelling incident [Ref 23]:** In 2009, a batch of Bromo-DragonFLY was distributed mislabelled as 2C-B-FLY. Because Bromo-DragonFLY is approximately 20× more potent by weight and has dramatically longer duration (effects lasting 2–3 days), users dosing at amounts appropriate for 2C-B-FLY received potentially 20× the effective dose. This resulted in severe toxicity, hospitalization, and deaths attributable to vasoconstriction and its complications (limb ischemia, necrosis). The Erowid 2C-B-FLY death reports from 2009 are believed to reflect this mislabelling incident [Ref 32].

**Bromo-DragonFLY documented cases for comparative context:**
- First fatal overdose case (Denmark, 18-year-old female, 2007/2009): confirmed by forensic LC-MS/MS; blood concentration 0.0047 mg/kg; caused drug to be classified in Denmark (Andreasen et al. 2009 [Ref 19])
- Delayed onset seizures and toxicity (Wood et al. 2009 [Ref 20]): documents delayed-onset toxicity with Bromo-DragonFLY, relevant to both compounds given naming confusion

### 2C-B-FLY Specific Adverse Effects

Based on pharmacological profile (Rickli et al. 2015 [Ref 15]; Noble et al. 2018 [Ref 16]):

**Vasoconstriction risk:** The Rickli 2015 study [Ref 15] explicitly identifies 2C-B-FLY as carrying a risk for vasoconstriction, ischemia, and hypertension due to its potent 5-HT₂B and 5-HT₂A receptor activity. The vasoconstrictive risk is a class property of the benzodifuran/tetrahydrobenzodifuran scaffold and is less severe in 2C-B-FLY than in Bromo-DragonFLY but warrants attention. Sustained 5-HT₂B activation is also associated with cardiac valve fibrosis with chronic exposure.

**MAO inhibition concerns:** 2C-B-FLY shows potential for MAO-A inhibition (Wagmann et al. 2019 [Ref 17]). MAO inhibition raises serotonin levels and can precipitate serotonin syndrome, particularly when combined with other serotonergic agents.

**Cardiovascular effects:** As a serotonergic psychedelic, transient increases in blood pressure and heart rate are expected, as documented with the parent compound 2C-B (Mallaroni et al. 2023 [Ref 13]).

**HPPD risk:** As a 5-HT₂A agonist, 2C-B-FLY carries theoretical risk of hallucinogen persisting perception disorder (HPPD), documented across the psychedelic class (Žuljević & Majić 2025 [Ref citation gap]; Vis et al. 2021). No 2C-B-FLY-specific HPPD cases in published literature.

**FLAG:** No published LD₅₀ data, no human case reports of 2C-B-FLY-specific acute toxicity. All adverse event data requires inference from pharmacological profile and class analogies.

---

## Harm Reduction

### Testing and Identification

**Critical identification issue:** 2C-B-FLY cannot be distinguished from Bromo-DragonFLY by appearance or basic colorimetric tests (Marquis, Mecke). The 2009 mislabelling incident demonstrates this is a life-threatening risk [Ref 23]. Advanced analytical methods (LC-MS/MS, GC-MS) are required to confirm identity. Drug checking services employing FTIR or mass spectrometry can distinguish the two.

The CFSRE detected 2C-B-FLY in California in February 2025 alongside PCP [Ref 24], suggesting potential for adulteration or co-sale with dissociatives. Drug checking before any use is strongly recommended.

**Reagent test behavior:** Limited published data. Both 2C-B-FLY and Bromo-DragonFLY would likely produce similar reactions with standard phenethylamine reagents. Cannot be used to distinguish them.

### Dosing Considerations

The seed data (threshold: 2 mg, light: 5–10 mg, common: 10–18 mg, strong: 18–25 mg, heavy: 25+ mg) is derived from community consensus and is consistent with PsychonautWiki [Ref 27]. These values are **flagged for editorial review** as they lack controlled human study support.

Key context: because Bromo-DragonFLY is ~20× more potent by weight and has been sold as 2C-B-FLY, users must verify compound identity before dosing at these amounts.

### Emergency Response

Bromo-DragonFLY (and theoretically 2C-B-FLY at high doses) can cause vasoconstrictive emergencies. Clinical management is supportive. Given potential MAO inhibition [Ref 17], combinations with serotonergic drugs are contraindicated. The possible vasoconstriction requires monitoring for peripheral ischemia (cold extremities, colour changes). Standard psychedelic crisis support applies for psychological emergencies.

---

## Tolerance & Dependence

### Tolerance

Tolerance to serotonergic psychedelics develops rapidly via 5-HT₂A receptor downregulation in the frontal cortex (de la Fuente Revenga et al. 2022 [Ref 11]). This mechanism applies to 2C-B-FLY as a 5-HT₂A agonist. Key findings:
- Tolerance detectable **within 24 hours** of a single administration (de la Fuente Revenga et al. 2022 [Ref 11])
- Mechanism: 5-HT₂A receptor density reduction; **independent of β-arrestin-2** (de la Fuente Revenga et al. 2022 [Ref 11])
- Full receptor recovery takes several days (seed data: half-life 3 days, full reset 7 days — consistent with class data)

**Cross-tolerance:** Complete cross-tolerance within the psychedelic class (de la Fuente Revenga et al. 2022 [Ref 11] documented cross-tolerance between DOI and LSD). 2C-B-FLY would produce full cross-tolerance with LSD, psilocybin, mescaline, and other 5-HT₂A agonist psychedelics. This is consistent with the seed data (cross-tolerance: psychedelic class).

The seed data tolerance values (buildup: almost immediately after ingestion; half-life: 3 days; full reset: 7 days) are consistent with published class data and are reasonable.

### Dependence

No published studies on physical or psychological dependence potential for 2C-B-FLY. Class data (Nichols 2004 [Ref 29]) indicates serotonergic hallucinogens are physiologically safe and do not produce physical dependence. The seed data (not habit-forming) is consistent with class properties.

No withdrawal syndrome documented for serotonergic psychedelics as a class.

---

## Interactions

### Tramadol — Dangerous

Seed data flags tramadol as a **dangerous interaction**. This is well-founded:

Tramadol is a weak serotonin-norepinephrine reuptake inhibitor and opioid agonist. Combined with a serotonergic 5-HT₂A agonist (and potential MAO inhibitor like 2C-B-FLY), the combination risks **serotonin syndrome** (Park et al. 2014 [Ref 12]; Wagmann et al. 2019 [Ref 17]). The MAO inhibition demonstrated for 2C-B-FLY [Ref 17] further elevates this risk by raising synaptic serotonin levels. Serotonin syndrome can be life-threatening.

**Confirmed: the "dangerous" rating for tramadol is supported by the pharmacological evidence.**

### Cannabis — Unknown

The seed data flags cannabis as an interaction of unknown severity. This is consistent with published literature: cannabis can intensify and prolong psychedelic experiences, increase heart rate, and potentiate cardiovascular effects. No specific 2C-B-FLY + cannabis interaction data exists. The unknown classification is appropriate.

### MAOIs and SSRIs

Though not in the seed data, these are high-priority interaction considerations:

**MAOIs:** 2C-B-FLY itself shows potential MAO-A inhibition (Wagmann et al. 2019 [Ref 17]). Combining with additional MAO inhibitors risks serotonin syndrome.

**SSRIs:** SSRIs may blunt or block psychedelic effects via 5-HT₂A downregulation. Acute combinations with serotoninergic drugs carry serotonin syndrome risk.

**Other serotonergic drugs (triptans, lithium, other psychedelics):** Class-level contraindication based on serotonin syndrome risk and pharmacodynamic interactions.

**FLAG: Interaction data for 2C-B-FLY is absent from the published literature; all interaction assessments are inferred from pharmacological class membership and the MAO inhibition data. Editorial review required for completeness.**

---

## Legal Status

| Jurisdiction | Status | Detail |
|---|---|---|
| United States | **Unscheduled** | Not listed in federal controlled substances schedules as of CFSRE June 2025 [Ref 24]. Federal Analog Act (21 U.S.C. § 813) may treat it as Schedule I if intended for human consumption given structural/pharmacological similarity to Schedule I phenethylamines. |
| United Kingdom | **Illegal** | Class A under Misuse of Drugs Act 1971 via structural analogy to 2C-B; also covered by Psychoactive Substances Act 2016 (since May 26, 2016). |
| Canada | **Schedule III** | Explicitly scheduled since October 31, 2016. |
| Sweden | **Illegal** | Explicitly scheduled since April 2018. |
| Germany | **Controlled** | NpSG (New Psychoactive Substances Act). |
| Belgium | **Controlled** | Added to Annex IVB since 2023. |
| Italy | **Schedule I** | Illegal to possess, produce, sell, buy. |
| Australia | **Likely illegal** | Falls under psychoactive substances legislation; not separately confirmed in this search. **FLAG for verification.** |
| Poland | Likely controlled via analogy | Considered Group II-P drug as a 2,5-dimethoxyphenethylamine derivative. |

**EMCDDA Status:** First notified to EMCDDA early warning system in 2007; multiple subsequent notifications. No EU-wide formal risk assessment found in this search.

**Note:** The seed data characterizes 2C-B-FLY as "emerging" — this is consistent with US unscheduled status. In many jurisdictions without explicit analogue laws, 2C-B-FLY may fall into legal grey areas.

---

## Clinical Trials

No clinical trials for 2C-B-FLY were found on ClinicalTrials.gov. No registered studies in any jurisdiction identified.

---

## Community Feedback Analysis

**No community feedback submitted.** Part A2 of the brief is empty. No feedback items to investigate or report.

---

## Gaps & Flags

### Missing Chemical Data
- **FLAG (data entry):** SMILES string is absent from the database record and from the PubChem API response in this session. Should be populated from PubChem CID 10265873 directly.
- **GAP:** No published melting point, aqueous solubility, or stability data for 2C-B-FLY.

### Pharmacology Gaps
- **FLAG:** No specific Ki (binding affinity) values for 2C-B-FLY at 5-HT₂A, 5-HT₂B, 5-HT₂C in the primary published literature retrieved. The Monte 1996 paper [Ref 7] focused on the amphetamine analog (DOB-FLY), and the ethylamine (2C-B-FLY) binding data may be in unpublished portions of the study. Rickli 2015 [Ref 15] has specific Ki values in its tables but these were not extracted (access issue during retrieval). **The generation agent should note that Ki data for 2C-B-FLY is probably reported in Rickli 2015 but requires table extraction.**
- **FLAG:** Specific MAO IC₅₀ values for 2C-B-FLY from Wagmann 2019 [Ref 17] were not individually extracted — they are in the paper tables. The paper reports IC₅₀ values ranging 10–125 μM (MAO-A) and 1.7–180 μM (MAO-B) across all compounds tested.
- **FLAG:** No biased agonism (β-arrestin vs. Gαq) data specifically for 2C-B-FLY. Pottie et al. 2020 [Ref 2] addressed Bromo-DragonFLY and N-benzyl compounds but not 2C-B-FLY directly.

### Human Pharmacokinetics
- **GAP:** No published human pharmacokinetic studies for 2C-B-FLY. No Tmax, Cmax, bioavailability, or plasma half-life data in humans.
- **GAP:** Human duration data relies entirely on community reports. The published rat data for the NBOMe analog suggests brain persistence >8 hours, but direct extrapolation is uncertain.

### Toxicology
- **GAP:** No published LD₅₀ for 2C-B-FLY in any species. Toxic dose unknown.
- **GAP:** No published human case reports of 2C-B-FLY overdose. The 2009 deaths commonly attributed to "2C-B-FLY" appear to involve Bromo-DragonFLY mislabelled as 2C-B-FLY — this distinction is critical and should be stated explicitly in the article.
- **FLAG (safety-critical):** The mislabelling case report (bromo-dragonfly mislabelled as 2C-B-FLY [Ref 23]) needs a verified PMID. The ResearchGate citation was found but PMID was not confirmed in this search. **Verification needed.**

### Legal Status Gaps
- **FLAG:** Australia, New Zealand, Netherlands, France, Spain, and other major EU member states were not individually confirmed in this search. The article should note that legal status varies and users should verify locally.

### Seed Data Notes
- **Dose data (threshold through heavy):** Consistent with PsychonautWiki [Ref 27] and community consensus. No controlled study evidence. Marked for editorial review.
- **Duration data:** Consistent with community reports. The total of 7–12 hours is notably longer than 2C-B (typically 4–6 hours). This difference is plausible given the rigid ring structure potentially affecting receptor residence time, but is not confirmed in controlled studies.
- **Tolerance data (half-life 3 days, full reset 7 days):** Consistent with class data (de la Fuente Revenga et al. 2022 [Ref 11]). Reasonable.
- **"Tramadol: dangerous"** interaction is supported by pharmacological evidence (serotonin syndrome risk + MAO inhibition). ✓ CONFIRMED
- **"Cannabis: unknown"** classification is appropriate given absence of interaction data. ✓ CONFIRMED
- **Pharmacological class in seed (Serotonin 2A and 2C agonist):** Confirmed — both 5-HT₂A and 5-HT₂C activity documented (Rickli 2015 [Ref 15]; Monte 1996 [Ref 7]). ✓ CONFIRMED