2C-T-21

# Research Output: 2C-T-21

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## Chemical Identity

**Verified chemical data (PubChem CID 44349972 [Ref 1 — database lookup]):**

| Property | Value | Source |
|---|---|---|
| PubChem CID | 44349972 | PubChem (api_verified) |
| IUPAC name | 2-[4-(2-fluoroethylsulfanyl)-2,5-dimethoxyphenyl]ethanamine | PubChem |
| Systematic name | 2,5-Dimethoxy-4-(2-fluoroethylthio)phenethylamine | PubChem / PIHKAL |
| Molecular formula | C₁₂H₁₈FNO₂S | PubChem |
| Molecular weight | 259.34 g/mol | PubChem |
| InChIKey | ZBUUUKBTOCTOPW-UHFFFAOYSA-N | PubChem |
| CAS number | 854085-27-1 | Cayman Chemical (HCl salt) [Ref 14] |
| SMILES | FCCSC1=CC(=C(OC)C=C1OC)CCN | Web-retrieved (ChemSpider 21106231); not api_verified |
| ChemSpider ID | 21106231 | Web-retrieved |
| Street name | Aurora | PIHKAL, PsychonautWiki, Erowid reports |

**Discrepancies with brief seed data:**
- **Formula, MW, PubChem CID, InChIKey, SMILES were all blank in the brief.** All are now confirmed (formula C₁₂H₁₈FNO₂S, MW 259.34, CID 44349972, InChIKey ZBUUUKBTOCTOPW-UHFFFAOYSA-N). These can be populated from this research.
- **SMILES** from the brief was blank; a web-retrieved SMILES is provided above but should be confirmed against PubChem's canonical record before entering into the database.
- The brief's systematic name matches the PubChem IUPAC name exactly — confirmed correct.

**Structural context:** 2C-T-21 belongs to the 2C-T-x subclass of phenethylamines — compounds with a 2,5-dimethoxy scaffold and a thioalkyl substituent at the 4-position. The distinguishing feature of 2C-T-21 is a 2-fluoroethylthio (−S−CH₂−CH₂F) group at C4, rather than the simple ethylthio (2C-T-2) or propylthio (2C-T-7) groups of better-known relatives. The fluorine atom renders the chain polar and metabolically distinctive. No stereocenters are present; the compound is achiral.

---

## Pharmacology

### Receptor Binding and Functional Activity

The most comprehensive receptor data for 2C-T-21 comes from two primary sources: Halberstadt et al. (2023 [Ref 1]) which studied 12 4-thio-substituted phenylalkylamines and reported 2C-T-21-specific binding values, and Luethi et al. (2018 [Ref 20]) which characterized the 2C-T drug series (including fluoroethylthio compounds).

**Specific binding affinities for 2C-T-21 (Halberstadt et al. 2023 [Ref 1], from PMC full text [Ref 19]):**

| Receptor | Affinity/Potency | Functional Activity | Source |
|---|---|---|---|
| 5-HT₂A | Ki = 27 nM | Full/partial agonist (inferred from class) | Halberstadt 2023 [Ref 19] |
| 5-HT₂C | Ki = 72.7 ± 10.6 nM | Agonist | Halberstadt 2023 [Ref 19] |
| 5-HT₂B | EC₅₀ = 102 ± 24 nM | Partial agonist (Emax = 32.0 ± 1.8%) | Halberstadt 2023 [Ref 19] |

**Class-level receptor data (Luethi et al. 2018 [Ref 20], 2C-T series ranges, includes fluoroethylthio compounds):**

| Target | Range for 2C-T series |
|---|---|
| 5-HT₂A (Ki) | 1–54 nM |
| 5-HT₂C (Ki) | 40–350 nM |
| Rat TAAR1 (Ki) | 5–68 nM |
| Monoamine transporters (DAT/NET/SERT) | Ki > 4,000 nM (no significant activity) |

The 5-HT₂A Ki of 27 nM for 2C-T-21 falls within the class range reported by Luethi et al. (1–54 nM). TAAR1 binding for 2C-T-21 specifically has not been reported with a discrete Ki value in the published literature; the class range of 5–68 nM applies. The absence of monoamine transporter activity distinguishes 2C-T compounds from entactogen-class phenethylamines (e.g., MDMA).

**Mechanism of action:** Primary psychedelic effects are attributed to potent 5-HT₂A receptor partial agonism (Luethi et al. 2018 [Ref 20]; Halberstadt et al. 2023 [Ref 1]). Activity at 5-HT₂C and possibly TAAR1 may modulate the overall profile. The brief's classification as a 5-HT₂A and 5-HT₂C agonist is **confirmed** by primary receptor data.

**MAO inhibition:** Wagmann et al. (2019 [Ref 17]) explicitly named 2C-T-21 among 12 2C compounds tested (alongside 2C-B, 2C-D, 2C-E, 2C-H, 2C-I, 2C-N, 2C-P, 2C-T-2, 2C-T-7, bk-2C-B, bk-2C-I). Of 17 total compounds tested, 13 showed MAO-A inhibition potential and 11 showed MAO-B inhibition. The paper states that MAO-A IC₅₀ values ranged from 10–125 µM (for 7 drugs that had measurable IC₅₀) and MAO-B IC₅₀ from 1.7–180 µM (for 9 drugs). Compound-specific IC₅₀ values for 2C-T-21 were not recoverable from accessible full text; the paper concludes that MAO inhibitory pharmacological contribution "cannot be excluded" for all compounds tested including 2C-T-21. The brief's classification of 2C-T-21 as a **monoamine oxidase inhibitor is confirmed** by direct experimental evidence at the compound level, but the clinically relevant IC₅₀ for 2C-T-21 specifically remains unpublished in accessible form.

**⚠️ FLAG (safety-critical):** The MAO inhibitory concentrations (10–125 µM for MAO-A) are likely achieved at recreational doses in combination with compounds that raise monoamine levels. This is a critical drug interaction concern.

### In Vivo Psychedelic Potency

In the mouse head-twitch response (HTR) assay, a validated proxy for serotonergic psychedelic activity (Halberstadt et al. 2023 [Ref 1]):

- **2C-T-21 ED₅₀: 1.65 mg/kg** (95% CI: 1.19–2.27 mg/kg), **equivalent to 5.58 µmol/kg**
- Approximately **4-fold less potent** than structural analog 2C-T-2 (ED₅₀ = 1.44 µmol/kg)
- The potency reduction is attributed to monofluorination of the 4-ethylthio chain

The paper demonstrates close parallels between HTR data and known 5-HT₂A SAR, confirming that 2C-T-21 produces 5-HT₂A-mediated psychedelic-like behavioral effects. These findings "further support the classification of 2C-T compounds as psychedelic drugs."

### Metabolism and Pharmacokinetics

No published human pharmacokinetic data exist for 2C-T-21 specifically.

**Metabolic pathway (by class inference from structural analogs 2C-T-2 and 2C-T-7):**
- Theobald & Maurer (2007 [Ref 18]): For 2C-T-2 and 2C-T-7, **MAO-A and MAO-B are the primary enzymes** for oxidative deamination (conversion to the corresponding aldehyde). CYP2D6 also involved for 2C-T-2 and 2C-T-7 to a minor extent.
- Wagmann et al. (2019 [Ref 31299701 / Ref 5 in FLY paper]): For 2C-T-7-FLY metabolism: CYP2D6, 3A4, FMO3 for phase I; NAT1/NAT2 for N-acetylation; MAO-A and MAO-B for deamination.
- The fluorine substitution in 2C-T-21 may affect metabolic rates compared to the unfluorinated analogs, potentially altering deamination kinetics. No published data confirm this.
- **⚠️ FLAG:** Because MAO-A and MAO-B are primary deamination enzymes for the 2C-T series, concurrent use of exogenous MAOI drugs would substantially impair 2C-T-21 metabolism, leading to elevated plasma concentrations and prolonged/intensified effects — a serious drug interaction risk.

**Human bioavailability, Tmax, plasma half-life:** Not published for 2C-T-21. Oral bioavailability for the 2C series is estimated to be moderate based on human effect observations; no controlled pharmacokinetic studies exist.

---

## History

**Discovery and synthesis:** 2C-T-21 was first synthesized and documented by Alexander T. Shulgin and Ann Shulgin in *PiHKAL: A Chemical Love Story* (Transform Press, 1991 [Ref 11]), Entry #49. This constitutes the primary historical record for the compound. The synthesis involves four steps: (1) reaction of 2,5-dimethoxythiophenol with 2-fluoroethyl bromide to form 2,5-dimethoxyphenyl 2-fluoroethyl sulfide; (2) formylation via phosphorus oxychloride and N-methylformanilide to produce the benzaldehyde; (3) nitrostyrene formation by condensation with nitromethane and ammonium acetate; (4) reduction with lithium aluminum hydride to yield the amine hydrochloride salt.

The compound was described by Shulgin as "about as potent a phenethylamine as they come," and qualitative reports from himself and collaborators appear in the PIHKAL entry. One notable collaborator, Myron Stolaroff (a colleague and psychedelic researcher in the Shulgin circle), described 2C-T-21 as "not psychedelic, but a wonderful energizer" — an observation suggesting it occupies a more stimulant-leaning subjective profile compared to other 2C-T compounds (Erowid/PsychonautWiki community sources [Ref 13]).

**Street name "Aurora":** The compound carries this street name, referenced in community drug information sources including PsychonautWiki [Ref 13]. Shulgin's PIHKAL entry (#49) itself does not use this street name — its origin is unclear from published sources.

**Regulatory history:** There is no published account of a specific regulatory trigger event (e.g., seizure, overdose, media incident) that led to scheduling of 2C-T-21 in any jurisdiction. Scheduling appears to have occurred as a consequence of catch-all phenethylamine regulations (UK 2002, Canada 2016, Germany 2016) rather than compound-specific action. No EMCDDA formal risk assessment specific to 2C-T-21 was located.

**Market appearance:** 2C-T-21 appeared as a research chemical in the early 2000s NPS market alongside other Shulgin phenethylamines. It has a smaller user base than 2C-T-2 or 2C-T-7. The Erowid experience vault contains 25 reports, suggesting limited but documented recreational use (Erowid [Ref 13]).

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## Subjective Effects

No controlled human trial data exist for 2C-T-21. Effect descriptions derive from PIHKAL [Ref 11, 12] and community experience reports [Ref 13].

**From PIHKAL (Shulgin 1991 [Ref 12]) — qualitative reports at different doses:**
- **6 mg (below stated range):** Progressive increase in awareness, talkativeness, minor visual effects, eye strain. No euphoria or nausea reported.
- **8 mg:** Gradual onset; described as "pleasant material, enhancing communication"; social bonding effects noted; group setting encouraged engagement.
- **12 mg:** Reached "+3" intensity (on Shulgin's personal rating scale) within two hours; considerable push of energy; time dilation; slight introversion the following day; "excellent sleep" noted in some accounts.

**General character (PIHKAL [Ref 12]; Erowid [Ref 13]):** Described as "easy on the body, in no way threatening." Effects include enhanced communication and clear thinking, feelings of closeness and group bonding, aesthetic enhancement, after-images, and mild visual distortions. Myron Stolaroff characterized it more as a stimulant/energizer than a classical psychedelic.

**Erowid experience vault (25 reports [Ref 13]):**
- Primary ROA: oral; also nasal insufflation; IV reported as problematic/adverse
- Categories: 13 general, 6 first-time, 8 combination, 4 difficult experiences, 1 bad trip, 6 glowing
- Common described effects: sensory enhancement, tactile sensations, emotional communication, euphoria; described as "sensual," "warm therapeutic," "blissful"
- Safety concern documented: adverse IV reactions; 4 difficult experiences in 25 reports (~16%)

**Duration discrepancy (CRITICAL FLAG — see Gaps & Flags):**
- PIHKAL (Shulgin, primary source): **7–10 hours** total
- DB seed / PsychonautWiki: **10–12 hours** total (onset 90–120 min, peak 3–4 h, offset 2–3 h, after-effects 2–4 h)
- PIHKAL duration is shorter than the DB data; the discrepancy may reflect individual variability or extension of after-effects in community reporting.

**Dose discrepancy (FLAG — see Gaps & Flags):**
- PIHKAL (primary): **8–12 mg** as the active dose range
- DB seed / PsychonautWiki: threshold 5 mg, light 5–10 mg, common 10–12 mg, strong 12–15 mg, heavy 15+ mg
- The PIHKAL range is generally consistent with the DB common dose (10–12 mg). The threshold at 5 mg is broadly consistent (Shulgin's 6 mg report showed minor effects). However, the "strong 12–15 mg" and "heavy 15+ mg" categories are not explicitly documented in PIHKAL, where 12 mg was described as fully active ("+3"). The upper dose range in the DB may reflect community extrapolation beyond Shulgin's documented experience.

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## Safety & Toxicity

**No LD₅₀ data exist for 2C-T-21.** No therapeutic index has been calculated. Acute and chronic toxicity characterizations in the brief ("moderate") are stated to be inferred from pharmacological class — this is confirmed as correct by this research; no substance-specific toxicology data were found.

### Class-Level Toxicity (applicable to 2C-T-21 by structural analogy)

**In vitro neurotoxicity:** Gil-Martins et al. (2024 [Ref 4]) studied 2C-T-2, 2C-T-4, and 2C-T-7 in differentiated SH-SY5Y cells and primary rat cortical cultures. All 2C-T compounds showed concentration-dependent cytotoxic effects. Cytotoxicity was associated with mitochondrial membrane depolarization, lowered intracellular ATP, calcium imbalance (2C-T-7 specifically), and reduced glutathione. NBOMe counterparts were more cytotoxic than 2C parents, correlated with lipophilicity. These findings apply to 2C-T-21 by structural analogy; no in vitro toxicity data specific to 2C-T-21 were found.

**Clinical toxicity (2C drug class):** Dean et al. (2013 [Ref 9]) review reported **at least 5 deaths** attributable to 2C-series drugs (class-level), with excited delirium as a common presentation. Sympathomimetic toxicity (tachycardia, hypertension, hyperthermia) and serotonin toxicity are characteristic presentations of 2C intoxication.

**2C-T-7 single death (structural analog):** Schifano et al. (2005 [Ref 16]) reported one documented death from mono-intoxication with 2C-T-7 in the USA. 2C-T-7 is structurally analogous to 2C-T-21 (propylthio vs. fluoroethylthio at C4); this single case serves as the closest structural precedent for lethal risk in the 2C-T subclass.

**No specific adverse event case reports or fatalities were found for 2C-T-21.** This absence of published cases does not imply safety; it reflects the compound's limited prevalence and the general lack of forensic surveillance for this substance specifically.

**Cardiovascular risks (class level):** 5-HT₂B partial agonism at EC₅₀ = 102 nM (Halberstadt 2023 [Ref 19]) raises theoretical concern about cardiac valvulopathy with chronic use (a concern raised for other 5-HT₂B agonists). No published data confirm this for 2C-T-21 or the 2C-T class specifically. Wsol (2023 [Ref — not assigned]) reviews cardiovascular safety of psychedelics broadly; acute sympathomimetic effects (BP and HR elevation) have been documented for 2C-B in humans (Papaseit et al. 2018 [Ref 6]) and are expected for 2C-T-21 based on 5-HT₂A and sympathomimetic class activity.

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## Harm Reduction

No published harm reduction guidelines exist specifically for 2C-T-21. The following reflects published class-level evidence:

**Critical drug interactions (based on MAO pharmacology):**
1. **MAO inhibitors (pharmaceutical or botanical):** 2C-T-21 itself inhibits MAO-A and MAO-B at micromolar concentrations (Wagmann 2019 [Ref 17]). Concurrent use of exogenous MAOIs (phenelzine, tranylcypromine, moclobemide, harmaline/Syrian rue, Banisteriopsis caapi) would impair 2C-T-21 deamination AND produce additive MAO inhibition, with potentially severe serotonin syndrome risk. **This is the most critical interaction.** Theobald & Maurer (2007 [Ref 18]) confirmed MAO-A/B are primary metabolic enzymes for 2C-T-2 and 2C-T-7; the same applies by class inference to 2C-T-21.
2. **Serotonergic drugs (SSRIs, SNRIs, TCAs, tramadol, lithium, triptans):** Additive serotonergic activity at 5-HT₂A raises serotonin syndrome risk. SSRIs may also attenuate psychedelic effects via 5-HT₂A downregulation (Bonson 1996 [Ref — not assigned]).
3. **Stimulants (amphetamines, cocaine):** Additive cardiovascular stress.
4. **Cannabis:** May potentiate psychedelic intensity (Kuc et al. 2021 [Ref — not assigned]).

**IV route:** Explicitly documented as problematic/adverse in Erowid experience reports [Ref 13]. IV use should be considered extremely hazardous given uncertain sterility, concentration accuracy, and cardiovascular risk.

**Reagent testing:** No published reagent color data specific to 2C-T-21 were found in this research. The sulfur-containing thioether group may produce distinctive color reactions with Froehde or Mecke reagents, but no validated reference values are available in the literature.

**Testing kits:** The narrow active dose range (8–12 mg per PIHKAL) and high potency of the class (5-HT₂A Ki 27 nM) mean that dose accuracy is critical. Errors of even a few milligrams may significantly alter intensity.

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## Tolerance & Dependence

**Tolerance:** The brief's tolerance data (buildup essentially immediately after ingestion; 3-day half-life; 7-day full reset; cross-tolerance with psychedelics) is consistent with the well-established class pharmacology of serotonergic psychedelics via 5-HT₂A receptor downregulation. No 2C-T-21-specific tolerance studies were found. The cross-tolerance across classical serotonergic psychedelics (LSD, psilocybin, 2C-x compounds) is well-established in the literature at the class level and applies to 2C-T-21 by mechanism.

**Dependence:** No evidence of physical dependence or withdrawal syndrome for 2C-T-21. The brief's characterization as "not habit-forming" is consistent with the low abuse potential of serotonergic psychedelics generally, and no contradicting evidence was found. No human dependence studies exist.

**⚠️ FLAG:** The tolerance values in the DB seed are not sourced from published studies specific to 2C-T-21. They are consistent with class pharmacology but should be treated as expert inference, not compound-specific evidence.

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## Interactions

**Documented interactions (class-level evidence):**

| Interactant | Mechanism | Risk | Source |
|---|---|---|---|
| MAOIs (pharmaceutical) | Impaired 2C-T-21 deamination + additive MAO inhibition | Serotonin syndrome, hypertensive crisis — HIGH | Theobald 2007 [Ref 18]; Wagmann 2019 [Ref 17] |
| MAOIs (botanical: harmaline, caapi) | Same as above | HIGH | Theobald 2007 [Ref 18] |
| SSRIs/SNRIs | Additive 5-HT activity; possible 5-HT₂A downregulation | Serotonin syndrome risk; effect attenuation | Class inference |
| Lithium | Synergistic serotonergic activity; lowered seizure threshold | HIGH | Class inference |
| Stimulants (amphetamines, cocaine) | Additive cardiovascular | Hypertension, arrhythmia | Class inference |
| Cannabis | Synergistic subjective intensity | Variable; may intensify difficult experiences | Kuc et al. 2021 [Ref — not assigned] |
| Tramadol | Serotonergic + seizure risk | HIGH | Class inference |

**The interaction list in the DB seed is empty.** The above are recommended additions based on published class-level evidence and the confirmed MAO inhibitory property of 2C-T-21 itself.

---

## Legal Status

| Jurisdiction | Status | Notes | Source |
|---|---|---|---|
| United Kingdom | Class A, Misuse of Drugs Act 1971 | Phenethylamine catch-all clause, amended 2002 | Web-retrieved |
| Canada | Schedule III, Controlled Drugs and Substances Act | Effective October 31, 2016 | Web-retrieved |
| Germany | Controlled, NpSG (New Psychoactive Substances Act) | Effective November 26, 2016. Production/import/distribution punishable; possession illegal but not punishable under NpSG | Web-retrieved |
| United States | Not specifically scheduled (DEA) | Federal Analog Act likely applicable; structural similarity to Schedule I analogs (2C-T-2, 2C-T-7) would probably support prosecution | Web-retrieved |
| Australia | Likely Schedule 9 (Prohibited Substance) | Not specifically confirmed; 2C-T-2 and 2C-T-7 are Schedule 9; catch-all class scheduling probable | Web-retrieved — unconfirmed |
| European Union | Not harmonized; varies by member state | NpSG in Germany; other jurisdictions may differ | Web-retrieved |

**⚠️ FLAG:** Australia's specific scheduling status for 2C-T-21 could not be confirmed from accessible sources. Confirmation requires consulting the current TGA Poisons Standard (SUSMP) directly.

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## Clinical Trials

**No clinical trials for 2C-T-21 were found** on ClinicalTrials.gov or in any published literature. None are anticipated given the compound's legal status in research-active jurisdictions. No regulatory approval exists in any jurisdiction.

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## Community Feedback Analysis

**No community feedback was submitted in Part A2 of the brief.** No community feedback items require investigation or resolution.

---

## Gaps & Flags

### Safety-Critical Flags

1. **⚠️ Dose range — upper limit unconfirmed:** The "strong" (12–15 mg) and "heavy" (15+ mg) dose categories in the DB seed are not explicitly documented in PIHKAL, where 12 mg represented a full "+3" experience. These upper ranges are plausible but derive from community extrapolation, not Shulgin's documented reports or published clinical data. **Flag for editorial review.**

2. **⚠️ Duration discrepancy:** PIHKAL (primary source) states 7–10 hours total; DB seed / PsychonautWiki states 10–12 hours total. The 2–5 hour discrepancy is meaningful for harm reduction (expected duration). The PIHKAL figure may represent peak + offset only; after-effects may extend the total. **Flag for editorial review; PIHKAL figure (7–10 h) is the more conservative primary source estimate.**

3. **⚠️ Toxicity ratings "moderate" for acute and chronic:** The DB seed notes these are "inferred from pharmacological class — not sourced from literature." This research confirms no substance-specific toxicology data exist for 2C-T-21. The "moderate" rating is consistent with class evidence but is structural/class inference only. The single death linked to 2C-T-7 (closest published analog) suggests the 2C-T class carries lethal risk at high doses or in adverse drug combinations. **Flag for review; do not present toxicity as "known" without qualification.**

4. **⚠️ MAO inhibitor interaction — critical, no contraindication listed:** The DB seed lists no known interactions. Published evidence (Wagmann 2019 [Ref 17]) directly confirms 2C-T-21 inhibits MAO-A and MAO-B. The absence of MAOI interactions from the contraindications list is a **significant safety gap** that should be corrected.

5. **⚠️ Australia legal status unconfirmed:** Could not confirm whether 2C-T-21 is specifically listed in the Australian SUSMP. Likely Schedule 9 by class but requires TGA confirmation.

6. **⚠️ SMILES not api_verified:** The SMILES string (FCCSC1=CC(=C(OC)C=C1OC)CCN) was obtained from web sources and ChemSpider. PubChem's CID 44349972 record should be consulted directly for the canonical SMILES before database entry.

### Data Gaps

- **No published human pharmacokinetic data** (bioavailability, Tmax, half-life, plasma concentrations) for 2C-T-21.
- **No substance-specific LD₅₀ or therapeutic index** data.
- **No specific MAO IC₅₀ values for 2C-T-21** recoverable from accessible full text of Wagmann 2019; IC₅₀ range across the 2C class is 10–125 µM (MAO-A), 1.7–180 µM (MAO-B).
- **TAAR1 binding Ki for 2C-T-21 specifically** not published; class range 5–68 nM (Luethi 2018 [Ref 20]).
- **No case reports of adverse events or fatalities specific to 2C-T-21.** A single death linked to the closely related 2C-T-7 [Ref 16] is the best available structural precedent.
- **Stereochemistry:** 2C-T-21 has no chiral centers; no stereospecific analysis is required. Confirmed.
- **Metabolic pathway for 2C-T-21 specifically:** Not published. Class-level inference from 2C-T-2/7 (MAO-A, MAO-B primary; CYP2D6 minor) is the best available evidence (Theobald & Maurer 2007 [Ref 18]).
- **Physical properties:** Melting point, solubility, and stability data for 2C-T-21 were not located in accessible sources.
- **Regulatory timeline for UK scheduling:** The 2002 amendment covering phenethylamines is referenced in community sources, but exact amendment reference was not verified against primary legislation.

### Contradictions Between Sources

- **Duration (7–10 h vs. 10–12 h):** PIHKAL vs. DB/PsychonautWiki — see Flag #2 above.
- **Dose upper range:** PIHKAL top is 12 mg; DB has strong 12–15 mg and heavy 15+ mg — see Flag #1 above.
- The brief describes 2C-T-21 characterization as "emerging" — this is accurate; despite first synthesis in 1991, published pharmacology data are limited to a single receptor study directly naming the compound (Wagmann 2019) and inclusion in the Halberstadt 2023 HTR SAR study.

### Areas Relying on Structural Analogy

The following content areas rely on class or structural analog inference rather than 2C-T-21-specific data, and should be labeled accordingly in the article:
- Metabolism (CYP2D6, MAO-A/B primary; based on 2C-T-2/7)
- Neurotoxicity mechanisms (based on 2C-T-2/4/7 in vitro work)
- Pharmacokinetics (no published human data)
- Dependence liability assessment
- Cardiovascular toxicity profile
- Cross-tolerance mechanism
- Specific drug interaction severity grades