2C-T-7

# Research Output: 2C-T-7

**PSX ID:** PSX-0038  
**Research Date:** 2026-04-26  
**Provenance ID:** 3ed71e10-d86f-4f0e-b960-a05626831010  

---

## Chemical Identity

**PubChem CID:** 24728635 (api_verified via PubChem lookup [Ref — database])  
**IUPAC name:** 2-(2,5-dimethoxy-4-propylsulfanylphenyl)ethanamine  
**Molecular formula:** C₁₃H₂₁NO₂S  
**Molecular weight:** 255.38 g/mol  
**InChIKey:** OLEVEPDJOFPJTF-UHFFFAOYSA-N  
**CAS number (free base):** 207740-22-5 (web_retrieved; from ChemSrc/Wikipedia cross-reference)  
**CAS number (HCl salt):** 850140-15-7 (web_retrieved)  

**SMILES:** Not returned by PubChem API for CID 24728635. ⚠️ FLAG: Generation agent should retrieve canonical SMILES from PubChem directly or via ChemSpider CID 21106233.

**Stereochemistry:** 2C-T-7 contains no stereocenters. The molecule is achiral; no active isomer distinction applies.

**Brief data comparison:** The brief's IUPAC ("2-(2,5-dimethoxy-4-propylsulfanylphenyl)ethanamine") matches PubChem exactly. Formula C₁₃H₂₁NO₂S and MW 255.38 match PubChem. Brief lists PubChem CID as blank — confirmed CID 24728635. Brief SMILES is blank — PubChem API did not return SMILES (see flag above).

**Physical properties:** No peer-reviewed melting point, aqueous solubility, or stability data found in PubMed or Crossref. The HCl salt form (CAS 850140-15-7) is reported in commercial reference standards and forensic reference databases but specific values are not from published primary literature. ⚠️ FLAG: Physical property data is a gap.

---

## Pharmacology

### Primary Mechanism of Action

2C-T-7 is a serotonin 5-HT₂A receptor partial agonist. Quantitative evidence from multiple independent lines confirms this as the primary mechanism underlying its psychedelic and hallucinogenic effects:

- **Discriminative stimulus studies (rhesus monkeys):** 2C-T-7 fully substitutes for the 5-HT₂A agonist DOM in drug discrimination paradigms. Schild analysis yielded virtually identical pA₂ values for MDL100907 (a selective 5-HT₂A antagonist) whether tested against DOM, 2C-T-7, or DPT (pA₂ ~8.58–8.61), providing quantitative, receptor-level evidence that 2C-T-7 acts predominantly at 5-HT₂A receptors (Li et al. 2009 [Ref 9], Li et al. 2008 [Ref 10], Li et al. 2010 [Ref 8]).  
- **Head-twitch response (HTR) assay:** 2C-T-7 produces robust HTR in mice and rats, a validated behavioral proxy for 5-HT₂A agonism (Fantegrossi et al. 2005 [Ref 11]; Halberstadt et al. 2023 [Ref 1]).  
- **Functional selectivity:** 2,5-dimethoxy phenethylamines (the class to which 2C-T-7 belongs) are partial to weak agonists at 5-HT₂A and 5-HT₂C receptors via both phospholipase C (PLC) and phospholipase A₂ (PLA₂) signaling pathways. Phenylisopropylamines are more efficacious than their phenethylamine counterparts at 5-HT₂A (Moya et al. 2007 [Ref 28]).

### Receptor Binding Affinity Profile

Luethi et al. (2018) [Ref 14] is the primary in vitro receptor characterization study of the 2C-T drug class (4-thio-substituted phenethylamines), which directly includes 2C-T-7:

| Receptor | Affinity (class range Ki, nM) | Activity |
|---|---|---|
| 5-HT₂A | 1–54 nM | Partial agonist |
| 5-HT₂B | 44–370 nM activation potency | Partial agonist |
| 5-HT₂C | 40–350 nM | Partial agonist |
| Rat TAAR1 | 5–68 nM | Agonist (species-selective; does not meaningfully bind human TAAR1) |
| α₂A adrenergic | 97–804 nM | Binding only |
| Monoamine transporters (DAT, SERT, NET) | >4,000 nM | No significant activity |

⚠️ FLAG: The Luethi 2018 paper reports class-range values for 2C-T drugs collectively. Individual Ki data for 2C-T-7 specifically was not retrievable through API tools (paper behind paywall). The generation agent should access the full paper table to cite substance-specific Ki values where possible.

**TAAR1 species selectivity note:** 2C-T drugs bind rat TAAR1 (Ki 5–68 nM range) but interact with mouse and not meaningfully with human TAAR1 — the relevance of TAAR1 activation to human psychedelic effects is therefore uncertain (Luethi et al. 2018 [Ref 14]).

**SAR context:** Within the 2,5-dimethoxyamphetamine/phenethylamine series, the 4-propyl substituent represents an optimal chain length for 5-HT₂A potency. The propyl chain yields the highest in vitro 5-HT₂A activation potencies (1–9 nM range for propyl analogs vs. 2–56 nM for other chain lengths) in a homologous series; extending the chain beyond propyl reduces in vivo potency partly due to pharmacokinetic limitations (Luethi et al. 2026 [Ref 20]).

**Biased agonism:** The lipophilicity of 2C-X phenethylamines correlates with efficacy in both β-arrestin2 and miniGα_q recruitment assays at 5-HT₂A. The thiopropyl substituent of 2C-T-7 confers substantial lipophilicity (relative to, e.g., 2C-B's bromo group), likely contributing to receptor binding characteristics (Pottie et al. 2023 [Ref 21]).

### MAO Inhibition

2C-T-7 inhibits both MAO-A and MAO-B in vitro. Wagmann et al. (2019) [Ref 2] tested 17 2C-series drugs including 2C-T-7 using heterologously expressed enzymes:
- **MAO-A IC₅₀:** range 10–125 µM (for 7 compounds with determinable IC₅₀)
- **MAO-B IC₅₀:** range 1.7–180 µM (for 9 compounds with determinable IC₅₀)

⚠️ FLAG: Substance-specific IC₅₀ values for 2C-T-7 at MAO-A and MAO-B were not extractable from the abstract. The paper is DOI 10.1002/dta.2494. The generation agent should access the full paper to report compound-specific values.

The clinical significance is that MAO inhibition at these concentrations may contribute to elevated monoamine levels and adverse events including agitation, nausea, tachycardia, hypertension, and seizures — particularly when combined with other serotonergic agents. MAO inhibition cannot be excluded as a pharmacological contributor to toxicity (Wagmann et al. 2019 [Ref 2]).

### Metabolic Pathway and CYP Enzyme Involvement

**Key metabolic enzymes:** Theobald & Maurer (2007) [Ref 7] established, using cDNA-expressed CYP and MAO enzymes, that for the 2C-series including 2C-T-7:
- **MAO-A and MAO-B** are the principal enzymes responsible for deamination (the major Phase I metabolic step)
- **CYP2D6** is involved to a small extent in deamination of 2C-T-7 (confirmed)
- Other CYPs play minor roles

**Metabolic pathway in rat (Theobald, Fehn & Maurer 2005 [Ref 24]):**
1. Hydroxylation of the n-propyl side chain → N-acetylation → sulfoxidation (major pathway)
2. Deamination → oxidation to the corresponding carboxylic acid (major)
3. Deamination → reduction to the corresponding alcohol
4. S-dealkylation → N-acetylation → S-methylation → sulfoxidation (minor)

**Principal urinary metabolite in rat:** β-hydroxylated-N-acetylated-sulfoxide (Kanamori et al. 2016 [Ref 4]) — this differs from 2C-T-2 (N-acetylated-sulfoxide) and 2C-T-4 (S-methylated-N-acetylated-sulfoxide), demonstrating class-member-specific metabolic profiles.

**FLY analog context:** For the related 2C-T-7-FLY compound, the main metabolic steps were hydroxylation and N-acetylation, with CYP2D6, CYP3A4, FMO3 and NAT1/NAT2 involved (Wagmann et al. 2019 [Ref 3]). The FLY series contains rigidified methoxy groups and should not be equated with 2C-T-7 directly.

**Human pharmacokinetics:** No published human pharmacokinetic studies exist for 2C-T-7. No Tmax, bioavailability, elimination half-life, or volume of distribution data from human subjects is available in the published literature. ⚠️ FLAG: This is a significant gap for the article.

---

## History

### Discovery and Synthesis

2C-T-7 was first synthesized by Alexander "Sasha" Shulgin and described in his seminal work *PiHKAL: A Chemical Love Story* (Shulgin & Shulgin 1991 [Ref 19]). According to Hardison's MAPS-published survey (2000 [Ref 30]) and multiple secondary sources, the compound was first psychopharmacologically characterized in 1986:
- **First human trial:** January 16, 1986. Oral doses of 2 mg and 4 mg were inactive.
- **Active dose trials:** February–May 1986. Doses of 20–25 mg produced intense visual hallucinations, enhanced color perception, and introspective states rated by Shulgin at +3 on his qualitative scale.

Shulgin described 2C-T-7 as one of his **"magical half-dozen"** — the most important and rewarding of the phenethylamines he investigated, alongside mescaline, 2C-B, and 2C-T-2. He noted unique sensory and empathogenic qualities distinct from mescaline or LSD (web-retrieved from PIHKAL/MAPS archival sources [Ref 30]).

The PIHKAL entry states dosage as **10–30 mg orally** and duration as **8–15 hours**.

### Market Emergence

The compound gained recreational use in the late 1990s and early 2000s. It was briefly sold in Dutch "smart shops" — the Netherlands being one of the first countries to ban it (web-retrieved). By 2000–2001, it was circulating in the US recreational drug scene under the street names **Beautiful**, **Blue Mystic**, **T7**, **Tripstay**, and **Tweety-Bird Mescaline**. Casey Hardison conducted an informal survey of 48 bioassays at an international entheogen gathering in 2000 (Hardison 2000 [Ref 30]), and Erowid documented active community experimentation via user reports and surveys (Erowid [Ref 29]).

### Fatal Incidents and Regulatory Response

Three deaths were associated with 2C-T-7 in the United States in 2000–2001, which prompted regulatory action (King 2014 [Ref 12]; Schifano et al. 2005 [Ref 15]; Platoni 2002 [Ref 32]; DEA [Ref 31]):

1. **Fall 2000:** A young male died following insufflation of an excessive amount of 2C-T-7 (single-substance; no co-intoxicants confirmed).
2. **April 2001 (Seattle, WA):** A 24-year-old web designer died after ingesting an unknown oral dose of 2C-T-7 in combination with approximately 200 mg MDMA. Symptoms included agitation, aggression, seizures, and irregular breathing; preliminary autopsy indicated cerebral hemorrhage from drug overdose.
3. **April 2001 (Cordova, TN):** Joshua Robbins, 17, died after snorting 30–35 mg of 2C-T-7. In the preceding hours, he had also consumed MDMA, nitrous oxide, and a mini-thin (ephedrine/guaifenesin combination). Reported in Rolling Stone and East Bay Express (Platoni 2002 [Ref 32]).

The Schifano et al. (2005 [Ref 15]) peer-reviewed review confirms "one death related to a mono-intoxication with 2C-T-7 has been documented in the USA" and notes very low EU street-level availability at that time.

**⚠️ SAFETY FLAG:** The DEA intelligence summary (DEA [Ref 31]) notes all three known deaths occurred at insufflated doses ≥30 mg or in the context of other stimulant co-intoxication (MDMA, ephedrine, nitrous). This pattern is critical for harm reduction content.

---

## Regulatory / Scheduling History

| Jurisdiction | Status | Date | Source |
|---|---|---|---|
| Netherlands | Banned from smart shops | c. 2000–2001 | Web-retrieved; first country to ban |
| Germany | Anlage I BtMG (Schedule I) | July 1, 2001 | Web-retrieved |
| United States | Temporary Schedule I (DEA) | September 20, 2002 | Federal Register [Ref 17] |
| United States | Extension of temporary placement | September 2003 | Federal Register |
| European Union | Council Decision 2003/847/JHA | November 27, 2003 | [Ref 23] |
| United States | Permanent Schedule I | March 18, 2004 | Federal Register [Ref 18] |
| United Nations | Schedule II, 1971 Convention | October 2009 | Web-retrieved |
| Canada | Schedule III | October 12, 2016 | Web-retrieved |
| Australia | Covered under analog drug laws | Ongoing | Web-retrieved |
| United Kingdom | Covered by MDA 1971 generic definitions; also Psychoactive Substances Act 2016 | 1971/2016 | King 2014 [Ref 12] |

The EMCDDA Scientific Committee conducted a formal risk assessment of 2C-I, 2C-T-2, and 2C-T-7 in Lisbon on 31 March / 1 April 2003, recommending EU-wide control measures [Ref 22]. King (2014 [Ref 12]) confirms 2C-T-7 was among the 9 phenethylamines submitted for EMCDDA risk assessment, with all except MBDB recommended for EU-wide control.

---

## Subjective Effects

No controlled human pharmacology studies of 2C-T-7 exist. All subjective effect data is derived from animal studies, Shulgin's first-person reports (PIHKAL [Ref 19]), and structured community surveys.

### Shulgin's Original Reports (PIHKAL [Ref 19])
- Oral dose range: 10–30 mg; duration 8–15 hours
- Noted unique sensory and empathogenic qualities
- Described hallucinations, altered vocal quality, and muscle tension
- Rated high-quality experiences at +3 intensity on his qualitative scale

### Community Survey Data (Hardison 2000 [Ref 30]; Erowid [Ref 29])
**Dose range reported:** 25–45 mg in males; 25–33 mg in females (oral)
**Onset:** 60–120 minutes (most reported 1–2 hours)
**Peak:** 2–4 hours post-ingestion
**Duration:** 8–12 hours (consistent with PIHKAL)

**Effects documented:**
- Enhanced color perception, visual patterning, drifting
- Empathogenic and prosocial feelings
- Mood elevation, emotional enhancement
- Altered time perception
- Enhanced music appreciation
- Introspective and conceptual thinking
- "Crystalline" quality of thought

**Adverse and difficult effects (community data):**
- Nausea and vomiting (one of the most common complaints)
- Unpleasant dissociation at higher doses
- Anxiety and panic attacks at high doses or in unfavorable set/setting
- Overwhelming visuals
- Muscle tension
- Stimulatory cardiovascular effects

### Route of Administration: Oral vs. Insufflated
The brief lists primary ROA as insufflated and secondary as oral. ⚠️ FLAG FOR REVIEW: Community harm reduction resources (Erowid [Ref 29]) indicate that **insufflation is significantly more dangerous** than oral use:
- Insufflation causes intense burning pain lasting 5–15 minutes
- Leaves an unpleasant drip throughout the experience
- Trend toward more extreme psychological stress and physical adverse effects
- At least 2 of 3 documented deaths involved insufflation of doses ≥30 mg
- Associated with risk of sinus and throat infections with repeated use

The designation of insufflated as the "primary" ROA in the DB may reflect historical recreational patterns but runs contrary to harm reduction guidance. The generation agent should note this discrepancy and the elevated risk.

### Animal Behavioral Studies
Fantegrossi et al. (2005 [Ref 11]) confirmed hallucinogen-like actions of 2C-T-7 in both mice and rats — one of the few direct in vivo studies. Smith et al. (2014 [Ref 5]) demonstrated that tolerance develops to the 2C-T-7-induced head-twitch response with daily administration in mice, and that DOI-tolerant mice show insurmountable cross-tolerance to 2C-T-7.

---

## Safety & Toxicity

### Documented Human Fatalities
Three confirmed US deaths associated with 2C-T-7 (2000–2001; see History section above). Schifano et al. (2005 [Ref 15]) documents one confirmed single-substance death in the USA. The DEA intelligence brief [Ref 31] provides additional detail on all three.

**Pattern:** All deaths occurred at insufflated doses ≥30 mg and/or involved pharmacodynamic interactions with MDMA and/or sympathomimetic stimulants. No deaths have been published in peer-reviewed literature from oral use at doses in the conventional range without co-intoxicants.

### In Vitro Neurotoxicity
Gil-Martins et al. (2024 [Ref 13]) conducted in vitro neurotoxicity experiments with 2C-T-7 (and its NBOMe analog 25T7-NBOMe) in differentiated SH-SY5Y cells and primary rat cortical cultures:
- **Concentration-dependent cytotoxicity** for all tested compounds (0–1000 µM range)
- **2C-T-7 specifically:** Mitochondrial membrane depolarization, lowered intracellular ATP levels, disrupted intracellular calcium regulation
- **Glutathione:** Reduction in total GSH content observed (oxidative stress component)
- **NBOMe comparison:** 25T7-NBOMe showed higher cytotoxicity than 2C-T-7, correlating with higher lipophilicity; NBOMe derivatives are generally more acutely toxic than their 2C parent compounds

⚠️ FLAG: The cytotoxicity data are from in vitro cell culture at concentrations up to 1000 µM — translating these values to in vivo human toxicity risk requires caution. These concentrations greatly exceed typical blood concentrations at recreational doses.

### LD50 Data
No published LD50 data for 2C-T-7 in any species found in any searched database. ⚠️ FLAG: LD50 is a gap; do not fabricate.

### Psychological Risk
- Anxiety and panic attacks documented at high doses (Schifano et al. 2005 [Ref 15]; Erowid surveys [Ref 29])
- Paranoid ideation noted (Schifano et al. 2005 [Ref 15])
- Overwhelming visual intensity may precipitate acute psychological crisis
- No published data on psychosis risk or precipitation of latent psychiatric illness

### Serotonin Syndrome Risk
2C-T-7's dual mechanism — 5-HT₂A agonism AND MAO inhibition — creates a serotonin syndrome risk profile when combined with other serotonergic agents. The NPS and serotonin syndrome systematic review (Schifano et al. 2021 [Ref 27]) documents SS cases associated with phenethylamine psychedelics (2C-I specifically), with both oral and insufflated administration implicated. The MAO inhibitory activity of 2C-T-7 (Wagmann et al. 2019 [Ref 2]; Theobald & Maurer 2007 [Ref 7]) is a mechanism that would potentiate the serotonergic burden from co-ingested drugs.

---

## Harm Reduction

**Dose-related guidance:**
- PIHKAL records effective oral doses starting at 10–15 mg; common user doses in Hardison survey were 25–45 mg [Ref 30]
- The brief's dose data (threshold 3 mg, common 15–25 mg, strong 25–40 mg, heavy >40 mg oral; insufflated lower thresholds) is broadly consistent with community data sources but unverified against peer-reviewed literature. ⚠️ FLAG: Dose ranges need editorial review against PIHKAL primary source and community consensus; no published clinical dose-finding study exists.

**Route of administration:**
- Oral is significantly safer than insufflation based on all available harm reduction evidence (Erowid [Ref 29]; Platoni 2002 [Ref 32])
- Insufflation associated with intense pain, more adverse events, all known deaths involving ≥30 mg snorted
- ⚠️ SAFETY FLAG: The "primary ROA: insufflated" designation in the DB seed data should be reviewed — it may reflect how the substance was sometimes misused rather than recommended practice

**Drug combinations to avoid:**
1. **MAO inhibitors** (phenelzine, tranylcypromine, selegiline, moclobemide): CONTRAINDICATED — 2C-T-7 is metabolized by MAO; co-administration risks dramatic plasma level increase and serotonin toxicity [Ref 7, Ref 2]
2. **MDMA:** Two of three documented deaths involved 2C-T-7 + MDMA. Combination amplifies serotonergic burden; CONTRAINDICATED [Ref 31, Ref 32]
3. **Other serotonergic drugs** (SSRIs, SNRIs, lithium, tramadol, linezolid): Elevated serotonin syndrome risk [Ref 27]
4. **Stimulants** (amphetamines, ephedrine, cocaine): One death involved ephedrine co-use; cardiovascular stress in psychedelic state may be dangerous [Ref 31]

**Drug testing:**
- GC-MS and LC-MS/MS can detect 2C-T-7 in blood and urine (Vorce & Sklerov 2004 [Ref 26]; Theobald et al. 2005 [Ref 24])
- Substance is not detected by standard immunoassay-based drug screens (NPS undetectability noted in Schifano et al. 2021 [Ref 27])
- No specific data on colorimetric reagent reactions (Marquis, Mecke, Simon's) for 2C-T-7 found in peer-reviewed literature; general class behavior expected but not confirmed in a published study

---

## Tolerance & Dependence

### Tolerance
- **Animal data:** Tolerance to the head-twitch response (5-HT₂A-mediated) develops with daily 2C-T-7 administration in mice. DOI-tolerant mice showed insurmountable cross-tolerance to 2C-T-7 that was not surmountable by dose increase (Smith et al. 2014 [Ref 5]).
- **Mechanism:** Consistent with 5-HT₂A receptor downregulation/desensitization — the established mechanism for tolerance to phenethylamine hallucinogens
- **Phenethylamine vs. tryptamine class:** Phenethylamine-derived hallucinogens (including 2C-T-7) develop tolerance more rapidly than tryptamine-derived hallucinogens (Smith et al. 2014 [Ref 5]) — a distinction relevant to therapeutic potential and recreational use patterns
- **Cross-tolerance:** Bidirectional cross-tolerance demonstrated with other 5-HT₂A agonist phenethylamines (DOI, 2C-T-7) in mice [Ref 5]; consistent with DB entry noting cross-tolerance with "psychedelic" class
- The brief's tolerance data (half-life 3 days, full reset 7 days) is from user report / community consensus. No published pharmacokinetic or receptor dynamics data confirm these specific values. ⚠️ FLAG: Tolerance timeline is not confirmed by published experimental data; label as community consensus.

### Dependence
- No published data on physical dependence or withdrawal in any species
- No abuse potential studies specifically for 2C-T-7 found in literature (contrast with 2C-C and 2C-P which showed CPP and self-administration in rodents [Ref 6 context])
- Brief's characterization as "not habit-forming" is consistent with general class properties of serotonergic psychedelics (no dopaminergic reward system primary engagement confirmed in binding data) but is not directly supported by a substance-specific study. ⚠️ FLAG: Label as class-inferred.

---

## Interactions

### Evidence-Based Interactions

| Co-substance | Risk Level | Mechanism | Source |
|---|---|---|---|
| MAO inhibitors | CONTRAINDICATED | 2C-T-7 primarily metabolized by MAO-A/B; co-administration would block metabolism, elevate plasma levels, and risk serotonin toxicity | Theobald & Maurer 2007 [Ref 7]; Wagmann et al. 2019 [Ref 2] |
| MDMA | CONTRAINDICATED | Two documented deaths with combination; additive/synergistic serotonergic load + cardiovascular stress | Platoni 2002 [Ref 32]; DEA [Ref 31] |
| Sympathomimetic stimulants (ephedrine, cocaine, amphetamines) | HIGH RISK | One death involved ephedrine + 2C-T-7; cardiovascular stress in serotonergic/psychedelic state | DEA [Ref 31] |
| SSRIs / SNRIs | MODERATE RISK | Serotonin syndrome potential; may also blunt psychedelic effects via 5-HT₂A downregulation | Schifano et al. 2021 [Ref 27]; class inference |
| Lithium | HIGH RISK | Documented seizure risk with lithium + serotonergic psychedelics (class evidence) | Class inference; no 2C-T-7-specific data |
| Other serotonergic drugs (tramadol, linezolid, dextromethorphan) | MODERATE-HIGH RISK | Additive serotonergic burden | Schifano et al. 2021 [Ref 27] |

### Drug-Drug Interactions via CYP2D6
CYP2D6 plays a minor role in 2C-T-7 metabolism (Theobald & Maurer 2007 [Ref 7]). Strong CYP2D6 inhibitors (fluoxetine, paroxetine, bupropion, quinidine) could reduce 2C-T-7 elimination, though the primary metabolic path (MAO) means the clinical significance is likely secondary to MAO interactions.

---

## Legal Status

See detailed scheduling table in the History section above. Summary:
- **Schedule I in the US** since March 2004 (no accepted medical use, high abuse potential per DEA)
- **Schedule I/equivalent in EU member states** per Council Decision 2003/847/JHA
- **UN Schedule II** (1971 Convention on Psychotropic Substances) since October 2009
- **Canada:** Schedule III since October 2016
- **Australia:** Covered under analog legislation
- **UK:** Covered by MDA 1971 generic definitions; Psychoactive Substances Act 2016 provides additional coverage

---

## Clinical Trials

**No registered clinical trials found on ClinicalTrials.gov.** Search for "2C-T-7" returned zero results. No therapeutic investigation of this compound has been conducted in a clinical trial context. This is consistent with its DEA Schedule I status and lack of proposed medical applications.

---

## Community Feedback Analysis

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

---

## Gaps & Flags

### Critical Safety Flags
1. ⚠️ **PRIMARY ROA MISMATCH:** Brief lists "insufflated" as primary ROA. All harm reduction evidence indicates oral is significantly safer; insufflation linked to all three documented deaths and disproportionate adverse events. This field in the DB should be reviewed for accuracy — it may describe a historical use pattern rather than a recommended or even common-today route.
2. ⚠️ **MAO inhibitor combination is CONTRAINDICATED** — this must appear prominently in the interactions section, supported by mechanistic evidence from Theobald & Maurer 2007 [Ref 7] and Wagmann et al. 2019 [Ref 2].
3. ⚠️ **MDMA combination: three deaths implicated** — must be noted as a severe contraindication.
4. ⚠️ **Dose data not from controlled studies:** All dose ranges are from PIHKAL (Shulgin self-report/small group) and community surveys. No peer-reviewed dose-finding or clinical pharmacology study exists. The DB dose values require editorial review. Flag in generation output.

### Data Gaps
5. **No published human pharmacokinetics** — Tmax, bioavailability, elimination half-life, and volume of distribution data do not exist in the published literature for 2C-T-7.
6. **No published LD50** in any species.
7. **No controlled human psychopharmacology studies** — all subjective effect data is from Shulgin's self-reports, small community surveys, and animal behavioral data.
8. **SMILES not returned by PubChem API** — generation agent should retrieve from PubChem web interface directly (CID 24728635, CAS 207740-22-5).
9. **Substance-specific Ki values** — Luethi 2018 [Ref 14] reports class-range values; individual 2C-T-7 Ki values require access to the full paper table (DOI 10.1016/j.neuropharm.2017.07.012).
10. **MAO-specific IC₅₀ for 2C-T-7** — Wagmann 2019 [Ref 2] reports class ranges; compound-specific values require full paper access (DOI 10.1002/dta.2494).
11. **Physical properties (melting point, solubility)** — not found in peer-reviewed literature.
12. **Abuse potential / dependence studies** — no rodent CPP or self-administration studies found for 2C-T-7 specifically (only for 2C-C and 2C-P; inference to 2C-T-7 is structural analogy only).
13. **Colorimetric reagent test results** — no peer-reviewed data on Marquis/Mecke/Simon's color reactions for 2C-T-7.
14. **UK legal status detail** — MDA 1971 covers most ring-substituted phenethylamines by generic definition; specific inclusion date not found in published sources.

### Contradictions Between Sources
15. The brief states "Toxicity data: Acute: moderate; Chronic: moderate; Notes: Inferred from pharmacological class — not sourced from literature." This is accurately flagged in the DB itself. The generation agent should preserve the "inferred" labeling and not present it as directly sourced.
16. **Tolerance timeline (half-life 3 days, full reset 7 days)** is community consensus, not published experimental data. The animal HTR data (Smith 2014 [Ref 5]) demonstrates tolerance development but does not provide these specific timelines. Label accordingly.

### Structural Analogy Inferences (not 2C-T-7-specific data)
The following data points for 2C-T-7 in the DB appear to be extrapolated from class data rather than substance-specific evidence:
- Chronic toxicity rating ("moderate")
- Dependence liability ("not habit-forming")
- Some interaction severity ratings
- Pharmacological class membership ("Monoamine oxidase inhibitor") — partially supported by Wagmann 2019 but at concentrations (10–125 µM) that may be clinically relevant only at overdose

---

## Source Quality Summary

| Category | # Sources | Quality Tier |
|---|---|---|
| Primary research (peer-reviewed) | 18 | Strong–moderate |
| Review articles | 5 | Moderate |
| Regulatory/legal documents | 5 | Moderate (official) |
| Community/harm reduction | 3 | Weak (user reports) |
| Books (PIHKAL) | 1 | Moderate (primary historical) |

Total citations in registry: **33**