2C-T

# Research Output: 2C-T

**Substance:** 2C-T (2,5-Dimethoxy-4-methylthiophenethylamine)
**PSX ID:** PSX-0035
**Research Date:** 2026-05-11
**Provenance ID:** 2faa0c01-eaa3-4fb6-bbba-9b4066efa1a5

---

## Chemical Identity

**Verified via PubChem CID 12315927 [Ref 10 (PubChem)]:**

| Field | Value |
|---|---|
| IUPAC Name | 2-(2,5-dimethoxy-4-methylsulfanylphenyl)ethanamine |
| Common Name | 2C-T; Tesseract |
| Molecular Formula | C₁₁H₁₇NO₂S |
| Molecular Weight | 227.33 g/mol |
| PubChem CID | 12315927 |
| InChIKey | UPZMYCMLLQTYEM-UHFFFAOYSA-N |
| SMILES | COc1cc(CCN)c(OC)cc1SC |
| Melting Point (HCl salt) | 240–241 °C (from PiHKAL [Ref 10]) |

**Discrepancies with seed data:** The seed data was missing the molecular formula (C₁₁H₁₇NO₂S), molecular weight (227.33), SMILES, InChIKey, and PubChem CID — all now confirmed from PubChem. The IUPAC name in the seed data ("2-(2,5-dimethoxy-4-methylsulfanylphenyl)ethanamine") is accurate and matches PubChem's listing.

**Structural context:** 2C-T is the parent compound of the 2C-T-x series, characterized by a methylthio (–SCH₃) group at the 4-position of the 2,5-dimethoxyphenethylamine scaffold. Chain extension of the thioether (2C-T-2 = ethylthio, 2C-T-7 = n-propylthio) markedly increases potency — 2C-T is the shortest and least potent member of the series (Halberstadt et al. 2023 [Ref 23]).

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## Pharmacology

### Primary Mechanism
2C-T acts as a partial agonist at serotonin 5-HT₂A receptors — the primary mechanism underlying psychedelic effects in the phenethylamine class (Luethi et al. 2018 [Ref 12]; Ray 2010 [Ref 6]).

### Receptor Binding Affinities

**2C-T–specific data** (Halberstadt et al. 2023 [Ref 23]):
- 5-HT₂A binding affinity (Ki): **49 nM**
- Mouse head-twitch response (HTR) ED₅₀: **13.8 µmol/kg** (i.p.)
- HTR is a validated translational model for 5-HT₂A–mediated hallucinogenic activity in humans (r = 0.9448, Halberstadt et al. 2020 [Ref 17])

**2C-T drug class data** — binding range across 2C-T-x compounds (Luethi et al. 2018 [Ref 12]):
- 5-HT₂A Ki: 1–54 nM (2C-T falls at 49 nM, the upper end — least potent member)
- 5-HT₂C Ki: 40–350 nM
- 5-HT₂A activation potency: 1–53 nM
- 5-HT₂B activation EC₅₀: 44–370 nM (partial agonism)
- Rat TAAR1 Ki: 5–68 nM (high affinity; no activity at human TAAR1)
- Monoamine transporters (NET/DAT/SERT): Ki > 4,000 nM (no meaningful interaction)

**Comparative potency within the 2C-T-x series** (Halberstadt et al. 2023 [Ref 23]):
| Compound | Alkylthio Chain | 5-HT₂A Ki (nM) | HTR ED₅₀ (µmol/kg) |
|---|---|---|---|
| 2C-T | Methylthio | 49 | 13.8 |
| 2C-T-2 | Ethylthio | 9 | 1.44 |
| 2C-T-7 | n-Propylthio | 5.3 | 2.12 |
| 2C-T-19 | Butylthio | 6.9 | 3.27 |
| 2C-T-16 | Allylthio | 9.2 | 5.80 |

2C-T is approximately **10-fold less potent** than 2C-T-2 and 2C-T-7 at the 5-HT₂A receptor. Increasing alkylthio chain length from methylthio to ethylthio produces the most significant potency gain (Halberstadt et al. 2023 [Ref 23]).

### Functional Pharmacology
2C-T and its congeners act as **partial agonists** at 5-HT₂A and 5-HT₂B receptors (Luethi et al. 2018 [Ref 12]). The benzylthio subclass (not applicable to 2C-T) shows minimal 5-HT₂B activation (EC₅₀ > 3,000 nM). No relevant monoamine transporter activity distinguishes 2C-T-class compounds from stimulant phenethylamines (Luethi et al. 2018 [Ref 12]).

### MAO Interactions
**FLAG for editorial review — pharmacological class "MAOI" in seed data:**
The seed data classifies 2C-T as a "Monoamine oxidase inhibitor." The published evidence partially supports but significantly qualifies this:

- Jacob & Shulgin (1981 [Ref 1]) demonstrated that 4-thiomescaline and related thiophenethylamines **serve as substrates for bovine plasma MAO in vitro**, but found **no correlation** between MAO substrate activity and psychotomimetic potency.
- Wagmann et al. (2019 [Ref 13]) tested 17 2C-series compounds for human MAO-A and MAO-B inhibition in vitro: 13/17 showed MAO-A inhibition and 11/17 showed MAO-B inhibition, with IC₅₀ values of 10–125 µM for MAO-A. **2C-T itself was not individually reported** but the class shows weak-to-moderate in vitro MAO inhibitory activity.
- Selective MAO-A inhibition has been attributed primarily to **2C-T-7** and **4-MTA** (4-methylthioamphetamine) — compounds with longer n-propyl or methyl thio chains on amphetamine backbones — in the published drug harm literature (web-retrieved source).
- **The "MAOI" classification should be qualified**: 2C-T and its congeners are MAO substrates with weak in vitro MAO inhibitory activity, but they are not pharmacologically equivalent to prescription MAOIs (phenelzine, selegiline). The MAOI interaction risk is relevant primarily as a metabolic consideration: MAOIs can potentiate 2C-T effects by slowing its oxidative deamination (Rached et al. 2026 [Ref 19]).

**Recommendation:** Reclassify as "MAO substrate / weak MAO inhibitor" rather than "MAOI" as the primary pharmacological classification. The interaction risk with prescription MAOIs is real and should appear in the Interactions section.

### TAAR1 Activity
2C-T-class compounds show high affinity for rat TAAR1 (Ki range 5–68 nM) but do not interact with human TAAR1 (Luethi et al. 2018 [Ref 12]). The pharmacological significance of TAAR1 affinity in rodents without human TAAR1 activity is unclear and should not be emphasized in human-facing content.

### Pharmacokinetics
No published pharmacokinetic studies for 2C-T in humans or animals were found. The following is inferred from structural analogy:

- **Route:** Oral (primary); no published data on inhalation, insufflation, or parenteral routes
- **Onset:** 30–45 minutes (consistent with intestinal absorption of oral phenethylamines; supported by user reports [Ref 14, Ref 10])
- **Tmax:** ~1–2 hours (inferred from 2C-B Tmax ~1h from Papaseit et al. 2018 [Ref 20])
- **Metabolism:** Presumed via oxidative deamination by MAO-A/MAO-B, with possible CYP450 involvement; no published metabolite studies for 2C-T
- **Half-life:** Not published for 2C-T specifically

⚠️ **FLAG:** No human PK data for 2C-T. All pharmacokinetic inferences are class-level extrapolations from 2C-B data.

---

## History

### Discovery and Synthesis
2C-T was synthesized by **Alexander Shulgin** (assisted by Philip Jacob based on the sulfur analogues series). The compound first appeared in the published literature as part of the thiophenethylamine series: Jacob and Shulgin published three foundational papers on "Sulfur analogues of psychotomimetic agents" in *Journal of Medicinal Chemistry* (1981 [Ref 1], 1983 [Ref 2], 1984 [Ref 3]), establishing the structure-activity relationships for 4-alkylthio substituted phenethylamines and amphetamines. Web sources cite an initial description of 2C-T in **1976**, though the specific 1976 publication was not located in PubMed — it may be a conference abstract or informal communication predating the 1981 paper.

Shulgin's authoritative description of 2C-T appears in **PiHKAL: A Chemical Love Story** (Transform Press, 1991 [Ref 11]), Entry #39, which provides synthesis, dosage, duration, and personal accounts. In his commentary, Shulgin noted that 2C-T was prepared "alongside ALEPH-1" (the amphetamine analogue DOT/ALEPH-1) but that its full pharmacological evaluation came several years later. He characterized 2C-T as having "relatively low potency" but observed that "higher 2C-T's proved to be a treasure house" — a prescient remark given the subsequent recreational distribution of 2C-T-2, 2C-T-4, and 2C-T-7 (Shulgin & Shulgin 1991 [Ref 11]).

### Nomenclature
The "2C" prefix denotes the **two-carbon** chain between the phenyl ring and the amino group (distinguishing phenethylamines from amphetamines). "T" indicates **thio** (sulfur) at the 4-position. The naming convention was Shulgin's systematic classification for his 2,5-dimethoxyphenethylamine series.

### Market and Cultural Context
2C-T has **very limited presence** on the recreational drug market compared to its congeners. Unlike 2C-T-2 and 2C-T-7 — which experienced significant recreational distribution in the late 1990s–2000s and were associated with fatalities — 2C-T itself remained largely within psychonaut research communities due to its lower potency and shorter duration relative to the longer-chain analogues (Dean et al. 2013 [Ref 5]; Baumeister et al. 2015 [Ref 21]).

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## Subjective Effects

### Published Human Data
The only published human psychopharmacological data for 2C-T is from **Shulgin's PiHKAL** (1991 [Ref 11]), which documents four personal experience accounts at doses of 60 mg, 75 mg (two subjects), and 100/125 mg. No controlled human studies of 2C-T have been conducted.

### PiHKAL Accounts (Shulgin et al. 1991 [Ref 11])
- **60 mg:** Enhanced poetic thought described as "easy and natural." Subject noted potential as an MDMA substitute ("opens things up but doesn't get in the way").
- **75 mg (first account):** Rapid onset within 15 minutes. Tactile sensitivity and warm feelings. No visual component reported. Subject achieved deep sleep with vivid dreams and felt refreshed the following day.
- **75 mg (second account):** Described as "thin and fragile plus two." Emotional detachment characterized as "a hooded cloak brought down over my head." Minimal psychedelic character.
- **100–125 mg:** Psychedelic properties present but without strong visuals. Some emotional distance from effects. Verbal communication easy. Physical stomach discomfort noted at higher doses.

### User Report Data (Erowid [Ref 14])
An Erowid experience report (85 mg oral) describes:
- Onset by T+40 min, peak approximately T+1h10min, baseline approximately T+5h00
- Minimal open-eye visuals (mild color saturation)
- Gentle but persistent stomach pressure (body load)
- "More on the stoning side" — sedative rather than stimulating character
- Cannabis co-administration markedly enhanced visual effects
- Enhanced photosensitivity (light sensitivity)
- Good sleep and well-being the following day
- Described as "mostly harmless" and "the Cinderella of the 2C-T-x's" — suggesting relative lack of intensity compared to congeners

### Effect Profile Synthesis
The convergent picture from PiHKAL and user reports describes 2C-T as:
- **Less visual** than 2C-T-2 and 2C-T-7 (consistent with its lower 5-HT₂A binding affinity)
- **More tactile** component at common doses
- **Brief duration** (3–5h, shorter than most psychedelics)
- **Stomach discomfort** is a consistent body load
- **Low recreational demand** — its limited market presence reflects user consensus that it is less rewarding than longer-chain congeners

### Duration Data
| Parameter | PiHKAL [Ref 11] | PsychonautWiki [Ref 15] | Erowid report [Ref 14] |
|---|---|---|---|
| Onset | Not specified | 30–45 min | ~40 min |
| Peak | Not specified | 30–115 min | ~1h10min |
| Total duration | 3–5 hours | 3–6 hours | ~5 hours |
| After-effects | Not noted | 1–2 hours | Good sleep/well-being |

**Note on seed data dose range:** Seed data lists a **threshold of 20 mg** not found in PiHKAL (which gives 60–100 mg as the full range). The 20 mg threshold and light-dose tier (40–60 mg) appear in PsychonautWiki, representing community consensus extrapolated from the 2C-T-x class rather than direct experimental evidence for 2C-T. These values are plausible (structural analogy, lower potency vs. congeners) but are labeled **community consensus** in the seed data, which is appropriate.

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## Safety & Toxicity

### Substance-Specific Toxicity
No LD₅₀ data for 2C-T was found in the published literature. No case reports of adverse events, overdose, or fatalities attributable specifically to 2C-T were identified in PubMed searches.

### Class-Level Toxicity (2C Drug Class)
The 2C drug class (including 2C-T congeners) has been associated with:
- Hallucinations, agitation, aggression, and violence
- Sympathomimetic toxidrome: hypertension, tachycardia, hyperthermia, diaphoresis, mydriasis
- Serotonin toxicity presentation
- Excited delirium (most consistent feature in 2C-related fatalities)
- Seizures
- At least **5 deaths** reported in the published literature across the 2C class (Dean et al. 2013 [Ref 5])

Deaths attributed to 2C drugs most commonly involve **2C-T-7** and **2C-T-2** (the higher-potency congeners), often in combination with MDMA or other serotonergic agents. No specific 2C-T fatalities were found in the literature.

### 5-HT₂B Concern
Partial agonism at 5-HT₂B receptors is documented for the 2C-T drug class (Luethi et al. 2018 [Ref 12]). Prolonged 5-HT₂B stimulation has been associated with cardiac valvulopathy in the context of long-term MDMA use and some diet drugs; however, given 2C-T's rare use and low likelihood of chronic repeated dosing, this risk is theoretical at present.

### Seed Data Flag
The seed data states: *"no negative health effects attributed to trying this drug"*. This is consistent with the limited published evidence for 2C-T itself, but should be qualified — class-level risks (see above) exist at higher doses and particularly in combination with MAOIs or other serotonergic drugs.

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## Harm Reduction

### Dosing Caution
2C-T's relatively low potency (5-HT₂A Ki = 49 nM; ~10× less potent than 2C-T-2) means that dose escalation to achieve effects comparable to higher-chain congeners carries risks if users are familiar with 2C-T-2 or 2C-T-7 dosing. The active dose range (60–100+ mg) is substantially higher than most psychedelics, making milligram-precision dosing important.

### Drug Testing
2C-T is a **thiophenethylamine**. Standard reagent tests used for phenethylamines:
- Marquis reagent: 2C-series compounds typically show a color reaction (yellow/orange for mescaline-like compounds); specific reaction for 2C-T not documented
- No published reagent testing color reactions for 2C-T specifically were found

### Contraindications
Based on class-level pharmacology and general psychedelic contraindications:
- **MAOIs:** Combination with prescription MAOIs is potentially dangerous; MAOIs inhibit the oxidative deamination that metabolizes 2C-T, significantly prolonging and intensifying effects; serotonin syndrome risk (Rached et al. 2026 [Ref 19]; Inan et al. 2020 [Ref 9])
- **Serotonergic drugs:** SSRIs, SNRIs, lithium — risk of serotonin syndrome and pharmacodynamic interference
- **History of psychosis, bipolar disorder, schizophrenia:** No specific data for 2C-T; general psychedelic contraindication applies
- **Cardiovascular disease:** 5-HT₂A/₂B agonism produces sympathomimetic effects; caution in hypertension and arrhythmia

### Emergency Response
Standard psychedelic emergency management applies: benzodiazepines for agitation/seizures; antipsychotics (particularly 5-HT₂A antagonists such as olanzapine or quetiapine) for psychosis; aggressive cooling for hyperthermia. No specific 2C-T emergency protocols published.

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## Tolerance & Dependence

### Tolerance
No substance-specific tolerance data for 2C-T was found. Inferred from class:
- Rapid **tachyphylaxis** (functional tolerance) to 5-HT₂A–mediated effects is well-established for the serotonergic hallucinogen class via receptor downregulation and desensitization
- Seed data (cross-tolerance to "psychedelic" class, half-life 3 days, full reset 7 days) is consistent with general psychedelic tolerance pharmacology
- Cross-tolerance with other 5-HT₂A agonists (LSD, psilocybin, mescaline) is expected

### Dependence
- No published evidence of physical dependence or withdrawal syndrome for 2C-T
- Serotonergic hallucinogens as a class show **low dependence liability** in preclinical and clinical literature; 2C-T's low recreational market presence further limits dependence risk
- Seed data characterization ("not habit-forming") is consistent with class pharmacology

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## Interactions

### MAOI Combinations
**HIGH RISK — FLAG for safety review**
Prescription MAOIs (phenelzine, tranylcypromine, moclobemide, selegiline) combined with 2C-T: MAO enzymes are the primary degradative pathway for phenethylamines; MAO inhibition prolongs exposure and potentiates serotonergic/sympathomimetic effects. Cases of serotonin toxicity and agitation with MAOI + 2C-B have been documented (Rached et al. 2026 [Ref 19]). This combination should be considered a serious contraindication.

### Serotonergic Combinations (SSRIs, SNRIs, 5-HT₂A modulators)
SSRIs may blunt psychedelic effects via 5-HT₂A downregulation or through serotonin syndrome risk at higher doses. SNRIs carry similar considerations. No 2C-T–specific data published (Inan et al. 2020 [Ref 9]).

### Stimulants
Additive sympathomimetic effects (hypertension, tachycardia, hyperthermia). Combination with MDMA documented in 2C-T-7 fatalities (Dean et al. 2013 [Ref 5]).

### Cannabis
Cannabis co-administration appeared to substantially enhance visual effects in the user report (Erowid [Ref 14]). No published pharmacological mechanism identified beyond additive CNS effects.

### Lithium
Case reports of seizures with lithium + hallucinogens (LSD/psilocybin class); contraindicated on class grounds; no 2C-T–specific data.

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## Legal Status

### United States
2C-T's scheduling status in the United States is **ambiguous**. The parent compound (2,5-dimethoxy-4-methylthiophenethylamine / "2C-T") was **not found as an explicitly named Schedule I controlled substance** in eCFR searches. However:
- Several 2C-T congeners are explicitly Schedule I: **2C-T-2** (4-ethylthio), **2C-T-4** (4-isopropylthio), and **2C-T-7** (4-n-propylthio) were all permanently placed in Schedule I — 2C-T-7 via the Federal Register in March 2004 [Ref 16].
- The **Federal Analog Act (21 U.S.C. § 813)** may classify 2C-T as a Schedule I-equivalent substance for purposes of prosecution, given its structural and pharmacological similarity to scheduled 2C-T congeners.

⚠️ **FLAG:** The US scheduling status of 2C-T parent compound (methylthio) requires confirmation against the full current eCFR 21 CFR §1308.11. eCFR access was blocked during research.

### United Kingdom
2C-T is a **Class A** controlled substance under the Misuse of Drugs Act 1971 via the phenethylamine catch-all clause. Possession, production, and supply carry the most severe penalties.

### Canada
2C-T is listed under **Schedule III** of the Controlled Drugs and Substances Act, effective October 31, 2016.

### Australia
Likely a **Schedule 9** (Prohibited Substance) under the Therapeutic Goods (Poisons Standard) given the scheduling of the 2C class, though explicit documentation for 2C-T specifically was not retrieved.

### European Union
No EU-wide scheduling found for 2C-T specifically. Individual member states have varying controls; Germany controls related 2C compounds under the Betäubungsmittelgesetz (BtMG).

---

## Clinical Trials

**No clinical trials** for 2C-T were found on ClinicalTrials.gov. No trials are expected given the compound's Schedule I status in the US, very limited recreational use profile, and lack of any proposed therapeutic application.

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## Community Feedback Analysis

**No community feedback submitted** in Part A2 of the brief. All seed data was cross-referenced against primary literature and found to be generally accurate with the following notes:

- **Dosage data:** Matches PsychonautWiki community consensus; threshold (20 mg) and light-dose tier not in PiHKAL but are community-extrapolated and plausible
- **Duration data:** Matches PsychonautWiki; PiHKAL gives slightly narrower (3–5h) vs. seed (3–6h)
- **Characterization ("emerging"):** Appropriate — 2C-T has very limited literature, no human clinical studies, and minimal market presence
- **Pharmacological class "Monoamine oxidase inhibitor":** Partially supported but misleadingly strong — see Flag below

---

## Gaps & Flags

### Safety-Critical Flags

1. ⚠️ **MAO inhibitor classification**: Seed data lists "Monoamine oxidase inhibitor" as a pharmacological class. The published evidence (Jacob & Shulgin 1981 [Ref 1]; Wagmann et al. 2019 [Ref 13]) supports that 2C-T and related compounds are **MAO substrates** with **weak in vitro MAO inhibitory activity** but NOT clinically meaningful MAOIs in the traditional sense. Selective MAO-A inhibition of clinical concern is documented more specifically for 4-MTA and 2C-T-7. The generation agent should consider revising this classification to "MAO substrate / weak MAOI" and adding appropriate interaction warnings.

2. ⚠️ **US legal status**: The parent 2C-T compound (4-methylthio) does not appear in explicit Schedule I listings in eCFR searches. Federal Analog Act may apply. Jurisdictional legal advice should not be inferred from this research. Editorial review recommended before publishing definitive legal status.

3. ⚠️ **No human PK data**: All onset/Tmax/duration values are from user reports and class inference (2C-B data). No published pharmacokinetic study exists for 2C-T.

### Data Gaps

4. **No substance-specific toxicity data**: No LD₅₀, no case reports, no overdose literature for 2C-T specifically. Class-level risk data (from 2C-T-7, 2C-T-2) is the best available proxy.

5. **No clinical studies**: 2C-T has never been studied in any controlled human study. All human effect data derives from PiHKAL (n=4 accounts by Shulgin and associates) and individual user reports (n=1 Erowid report reviewed).

6. **SMILES/CID gap in seed data**: Now resolved — see Chemical Identity section.

7. **First publication date uncertain**: Web sources cite 1976 as the year 2C-T was first described, but the specific 1976 publication was not located in PubMed searches. PiHKAL (1991) is the authoritative documented primary source.

8. **TAAR1 pharmacology**: High rat TAAR1 affinity (Ki ~5–68 nM for 2C-T class) is documented but lacks human TAAR1 activity (Luethi et al. 2018 [Ref 12]). Functional significance in humans is unclear and should not be emphasized without further data.

9. **Street name "Tesseract"**: Confirmed only in PsychonautWiki [Ref 15]; not documented in peer-reviewed sources. Flag as community-reported name.

10. **Dose sensitivity field empty**: No published dose-sensitivity data for 2C-T. This field cannot be populated from available evidence.

### Areas Relying on Structural Analogy

- All pharmacokinetic data (onset, Tmax, metabolism, half-life) is inferred from class-level (2C-B) and structural analogy
- Dependence/withdrawal characterization derives entirely from class inference
- Safety profile relies heavily on 2C-T-x congeners (2C-T-2, 2C-T-7) rather than 2C-T–specific data
- 5-HT₂B cardiac concern is theoretical, extrapolated from other 5-HT₂B agonists