2C-T-2

4-(ethylthio)-2,5-dimethoxyphenethylamine

Sources

4 strong · 13 moderate · 2 weak

Studies and references cited across this article, graded by evidence strength.

Claims checked

54verified3partial16inconclusive1not supported

Inconclusive means the cited source neither confirms nor refutes the claim — a lower-confidence badge, not an error.

Generated

Apr 26, 2026 · pipeline-v5

Values approved

205/206 (100%)

Data points an editor reviewed and accepted for publication.

Value Provenance

Dosing

insufflatedtrace

Field	Published	AI Proposed	Confidence
Threshold	1 mg	1 mg	low
Low	3–7 mg	3–7 mg	low
Common	7–15 mg	7–15 mg	low
Strong	15–20 mg	15–20 mg	low
Heavy	20+ mg	20+ mg	low
Editorial	No published pharmacokinetic or dosing data exist for insufflated 2C-T-2. All values are derived from community reports. Insufflated doses are characteristically lower than oral for 2C compounds due to bypassing first-pass metabolism. Ranges widened to reflect high uncertainty.
	ReasoningReasoning No published pharmacokinetic or dosing data exist for insufflated 2C-T-2. All values are derived from community reports. Insufflated doses are characteristically lower than oral for 2C compounds due to bypassing first-pass metabolism. Ranges widened to reflect high uncertainty. Evidence basis: community_consensus_small

oraltrace

Field	Published	AI Proposed	Confidence
Threshold	3 mg	3 mg	medium
Low	5–12 mg	5–12 mg	medium
Common	12–20 mg	12–20 mg	medium
Strong	20–25 mg	20–25 mg	medium
Heavy	25+ mg	25+ mg	medium
Editorial	Shulgin's PiHKAL documents 12–25 mg as the oral active range. The threshold (3 mg) and light tier lower bound (5 mg) derive from community reports and are below Shulgin's documented minimum. Common (12–20 mg) and strong (20–25 mg) tiers align with the published PiHKAL data. Existing database values are consistent with these ranges.
	ReasoningReasoning Shulgin's PiHKAL documents 12–25 mg as the oral active range. The threshold (3 mg) and light tier lower bound (5 mg) derive from community reports and are below Shulgin's documented minimum. Common (12–20 mg) and strong (20–25 mg) tiers align with the published PiHKAL data. Existing database values are consistent with these ranges. Evidence basis: community_consensus_large

Duration

oral

Field	Published	AI Proposed	Confidence
Totaltrace	6–8 hours	6–8 hours	medium
Editorial	Shulgin's PiHKAL documents 6–8 hours oral duration. Community reports consistent at 6–10 hours, with the wider range reflecting dose-dependent variation.
	ReasoningReasoning Shulgin's PiHKAL documents 6–8 hours oral duration. Community reports consistent at 6–10 hours, with the wider range reflecting dose-dependent variation. Evidence basis: community_consensus_large
Onsettrace	20–45 minutes	20–45 minutes	medium
Editorial	Community consensus for oral 2C-T-2 onset. Consistent with phenethylamine psychedelic class pharmacokinetics.
	ReasoningReasoning Community consensus for oral 2C-T-2 onset. Consistent with phenethylamine psychedelic class pharmacokinetics. Evidence basis: community_consensus_large
Peaktrace	1.5–3 hours	1.5–3 hours	medium
Editorial	Community reports indicate 1.5–3 hour peak within the 6–8 hour total duration from PiHKAL.
	ReasoningReasoning Community reports indicate 1.5–3 hour peak within the 6–8 hour total duration from PiHKAL. Evidence basis: community_consensus_large
Offsettrace	1–2 hours	1–2 hours	medium
Editorial	Gradual offset consistent with Shulgin's overall 6–8 hour duration.
	ReasoningReasoning Gradual offset consistent with Shulgin's overall 6–8 hour duration. Evidence basis: community_consensus_large
After effectstrace	2–4 hours	2–4 hours	low
Editorial	Community reports of residual stimulation and mood elevation lasting 2–4 hours after primary effects resolve. No published data.
	ReasoningReasoning Community reports of residual stimulation and mood elevation lasting 2–4 hours after primary effects resolve. No published data. Evidence basis: community_consensus_small
Come uptrace	30–60 minutes	30–60 minutes	medium
Editorial	Community consensus. Come-up for 2C-T series is typically gradual over 30–60 minutes.
	ReasoningReasoning Community consensus. Come-up for 2C-T series is typically gradual over 30–60 minutes. Evidence basis: community_consensus_large

insufflated

Field	Published	AI Proposed	Confidence
Onsettrace	1–5 minutes	1–5 minutes	low
Editorial	Community reports of very rapid insufflated onset. No published pharmacokinetic data for this route.
	ReasoningReasoning Community reports of very rapid insufflated onset. No published pharmacokinetic data for this route. Evidence basis: community_consensus_small
Offsettrace	0.5–1 hours	0.5–1 hours	low
Editorial	Faster offset than oral. Community reports only.
	ReasoningReasoning Faster offset than oral. Community reports only. Evidence basis: community_consensus_small
After effectstrace	1–3 hours	1–3 hours	low
Editorial	Shorter aftereffects consistent with shorter total duration. Community reports only.
	ReasoningReasoning Shorter aftereffects consistent with shorter total duration. Community reports only. Evidence basis: community_consensus_small
Come uptrace	5–15 minutes	5–15 minutes	low
Editorial	Compressed come-up via insufflation based on community reports.
	ReasoningReasoning Compressed come-up via insufflation based on community reports. Evidence basis: community_consensus_small
Peaktrace	1–1.5 hours	1–1.5 hours	low
Editorial	Shorter peak than oral, consistent with bypassed first-pass metabolism. Community reports only.
	ReasoningReasoning Shorter peak than oral, consistent with bypassed first-pass metabolism. Community reports only. Evidence basis: community_consensus_small
Totaltrace	3–5 hours	3–5 hours	low
Editorial	Community reports indicate approximately halved total duration compared to oral. No published data.
	ReasoningReasoning Community reports indicate approximately halved total duration compared to oral. No published data. Evidence basis: community_consensus_small

Safety

Toxicity Profiletrace

Field	Published	AI Proposed	Confidence
Acute	low	low	low
Chronic	low	low	low
Organs Affected	cardiovascular, neurological	cardiovascular, neurological	low
Editorial	Classified as low (downgraded from moderate): acute toxicity evidence derives from 2C class-level data (Dean et al. 2013), not 2C-T-2-specific studies. In vitro neurotoxicity (Gil-Martins et al. 2024) at suprapharmacological concentrations. No confirmed 2C-T-2 fatalities. Chronic toxicity unknown — classified as low by structural analogy to other serotonergic psychedelics with no documented organ damage at typical doses.
	ReasoningReasoning Classified as low (downgraded from moderate): acute toxicity evidence derives from 2C class-level data (Dean et al. 2013), not 2C-T-2-specific studies. In vitro neurotoxicity (Gil-Martins et al. 2024) at suprapharmacological concentrations. No confirmed 2C-T-2 fatalities. Chronic toxicity unknown — classified as low by structural analogy to other serotonergic psychedelics with no documented organ damage at typical doses. Evidence basis: published_case_series

Dependence Profiletrace

Field	Published	AI Proposed	Confidence
Physical	none	none	medium
Psychological	negligible	negligible	medium
Compulsive Redosing	negligible	negligible	medium
Dose Escalation	negligible	negligible	medium
Editorial	No 2C-T-2-specific dependence data exist. Classification based on established serotonergic psychedelic class pharmacology: absence of DAT interaction (Luethi et al. 2018), rapid 5-HT2A tolerance, and general psychedelic class characteristics of negligible dependence liability.
	ReasoningReasoning No 2C-T-2-specific dependence data exist. Classification based on established serotonergic psychedelic class pharmacology: absence of DAT interaction (Luethi et al. 2018), rapid 5-HT2A tolerance, and general psychedelic class characteristics of negligible dependence liability. Evidence basis: structural_analogy

Withdrawal Profiletrace

Field	Published	AI Proposed	Confidence
Severity	none	none	medium
Symptoms	—	—	medium
Fatal	No	No	medium
Medical Supervision	Not required	Not required	medium
Editorial	No withdrawal syndrome documented for any serotonergic psychedelic. 2C-T-2 does not produce physiological dependence.
	ReasoningReasoning No withdrawal syndrome documented for any serotonergic psychedelic. 2C-T-2 does not produce physiological dependence. Evidence basis: structural_analogy

Tolerance Profiletrace

Field	Published	AI Proposed	Confidence
Buildup	rapid	rapid	medium
Half-life	3 days	3 days	medium
Full Reset	7 days	7 days	medium
Cross-tolerances	LSD, psilocybin, mescaline, DMT, 2C-B, 2C-E, 2C-T-7, DOx series	LSD, psilocybin, mescaline, DMT, 2C-B, 2C-E, 2C-T-7, DOx series	medium
Editorial	Tolerance mechanism established by de la Fuente Revenga et al. 2022 (DOI in mouse model) and Wallach et al. 2023. Specific timeline values are class-level consensus, not verified for 2C-T-2. Cross-tolerance with other 5-HT2A agonist psychedelics is well-established.
	ReasoningReasoning Tolerance mechanism established by de la Fuente Revenga et al. 2022 (DOI in mouse model) and Wallach et al. 2023. Specific timeline values are class-level consensus, not verified for 2C-T-2. Cross-tolerance with other 5-HT2A agonist psychedelics is well-established. Evidence basis: structural_analogy

Effects & Profile

Contraindications

Field	Published	AI Proposed	Confidence
psychiatric psychotic disorderstrace	absolute	absolute	medium
Editorial	Class-level contraindication for serotonergic psychedelics. No 2C-T-2-specific data, but mechanism (5-HT2A agonism) is established.
	ReasoningReasoning Class-level contraindication for serotonergic psychedelics. No 2C-T-2-specific data, but mechanism (5-HT2A agonism) is established.
psychiatric bipolar disordertrace	relative	relative	medium
Editorial	Class-level contraindication. No 2C-T-2-specific case data.
	ReasoningReasoning Class-level contraindication. No 2C-T-2-specific case data.
other MAO inhibitor therapytrace	absolute	absolute	high
Editorial	Directly supported by Theobald & Maurer 2007 demonstrating MAO-A/B as primary metabolic enzymes for 2C-T-2. Impaired clearance creates potentially lethal serotonin syndrome risk.
	ReasoningReasoning Directly supported by Theobald & Maurer 2007 demonstrating MAO-A/B as primary metabolic enzymes for 2C-T-2. Impaired clearance creates potentially lethal serotonin syndrome risk.
neurological epilepsytrace	relative	relative	medium
Editorial	Dean et al. 2013 documents seizures as a clinical feature of 2C drug intoxication. Pre-existing seizure disorder increases baseline risk.
	ReasoningReasoning Dean et al. 2013 documents seizures as a clinical feature of 2C drug intoxication. Pre-existing seizure disorder increases baseline risk.
other lithium therapytrace	absolute	absolute	medium
Editorial	Class-level contraindication from community consensus. No published case series for 2C-T-2 specifically, but the risk is well-established across the psychedelic class.
	ReasoningReasoning Class-level contraindication from community consensus. No published case series for 2C-T-2 specifically, but the risk is well-established across the psychedelic class.
cardiovascular cardiovascular diseasetrace	relative	relative	medium
Editorial	Dean et al. 2013 documents hypertension and tachycardia as common presentations of 2C drug intoxication. Class-level cardiovascular risk.
	ReasoningReasoning Dean et al. 2013 documents hypertension and tachycardia as common presentations of 2C drug intoxication. Class-level cardiovascular risk.
pregnancy breastfeeding pregnancytrace	absolute	absolute	medium
Editorial	Standard precautionary contraindication. No published reproductive toxicity data for 2C-T-2 or any 2C compound.
	ReasoningReasoning Standard precautionary contraindication. No published reproductive toxicity data for 2C-T-2 or any 2C compound.

Timeline Phases

oral

Field	Published	AI Proposed	Confidence
Onsettrace	1200–2700 sec(i=0.05)	1200–2700 sec(i=0.05)	medium
Editorial	Oral timeline based on Shulgin's PiHKAL duration of 6\u20138 hours and community reports. Phase breakdowns inferred from class-level phenethylamine psychedelic pharmacology and user experience reports. No controlled pharmacokinetic data exist to anchor onset/peak timing precisely.
	ReasoningReasoning Oral timeline based on Shulgin's PiHKAL duration of 6\u20138 hours and community reports. Phase breakdowns inferred from class-level phenethylamine psychedelic pharmacology and user experience reports. No controlled pharmacokinetic data exist to anchor onset/peak timing precisely. Evidence basis: community_consensus_large
Come uptrace	1800–3600 sec(i=0.30)	1800–3600 sec(i=0.30)	medium
Editorial	Oral timeline based on Shulgin's PiHKAL duration of 6\u20138 hours and community reports. Phase breakdowns inferred from class-level phenethylamine psychedelic pharmacology and user experience reports. No controlled pharmacokinetic data exist to anchor onset/peak timing precisely.
	ReasoningReasoning Oral timeline based on Shulgin's PiHKAL duration of 6\u20138 hours and community reports. Phase breakdowns inferred from class-level phenethylamine psychedelic pharmacology and user experience reports. No controlled pharmacokinetic data exist to anchor onset/peak timing precisely. Evidence basis: community_consensus_large
Peaktrace	5400–10800 sec(i=1.00)	5400–10800 sec(i=1.00)	medium
Editorial	Oral timeline based on Shulgin's PiHKAL duration of 6\u20138 hours and community reports. Phase breakdowns inferred from class-level phenethylamine psychedelic pharmacology and user experience reports. No controlled pharmacokinetic data exist to anchor onset/peak timing precisely.
	ReasoningReasoning Oral timeline based on Shulgin's PiHKAL duration of 6\u20138 hours and community reports. Phase breakdowns inferred from class-level phenethylamine psychedelic pharmacology and user experience reports. No controlled pharmacokinetic data exist to anchor onset/peak timing precisely. Evidence basis: community_consensus_large
Plateautrace	3600–5400 sec(i=0.50)	3600–5400 sec(i=0.50)	medium
Editorial	Oral timeline based on Shulgin's PiHKAL duration of 6\u20138 hours and community reports. Phase breakdowns inferred from class-level phenethylamine psychedelic pharmacology and user experience reports. No controlled pharmacokinetic data exist to anchor onset/peak timing precisely.
	ReasoningReasoning Oral timeline based on Shulgin's PiHKAL duration of 6\u20138 hours and community reports. Phase breakdowns inferred from class-level phenethylamine psychedelic pharmacology and user experience reports. No controlled pharmacokinetic data exist to anchor onset/peak timing precisely. Evidence basis: community_consensus_large
Resolutiontrace	3600–5400 sec(i=0.20)	3600–5400 sec(i=0.20)	medium
Editorial	Oral timeline based on Shulgin's PiHKAL duration of 6\u20138 hours and community reports. Phase breakdowns inferred from class-level phenethylamine psychedelic pharmacology and user experience reports. No controlled pharmacokinetic data exist to anchor onset/peak timing precisely.
	ReasoningReasoning Oral timeline based on Shulgin's PiHKAL duration of 6\u20138 hours and community reports. Phase breakdowns inferred from class-level phenethylamine psychedelic pharmacology and user experience reports. No controlled pharmacokinetic data exist to anchor onset/peak timing precisely. Evidence basis: community_consensus_large
Afterglowtrace	7200–14400 sec(i=0.05)	7200–14400 sec(i=0.05)	medium
Editorial	Oral timeline based on Shulgin's PiHKAL duration of 6\u20138 hours and community reports. Phase breakdowns inferred from class-level phenethylamine psychedelic pharmacology and user experience reports. No controlled pharmacokinetic data exist to anchor onset/peak timing precisely.
	ReasoningReasoning Oral timeline based on Shulgin's PiHKAL duration of 6\u20138 hours and community reports. Phase breakdowns inferred from class-level phenethylamine psychedelic pharmacology and user experience reports. No controlled pharmacokinetic data exist to anchor onset/peak timing precisely. Evidence basis: community_consensus_large

insufflated

Field	Published	AI Proposed	Confidence
Onsettrace	60–300 sec(i=0.05)	60–300 sec(i=0.05)	low
Editorial	No published pharmacokinetic or safety data exist for insufflated 2C-T-2. All timing is derived from community user reports. The faster onset and shorter duration are consistent with bypassing first-pass metabolism via nasal mucosa absorption, a well-established pharmacokinetic principle for this drug class.
	ReasoningReasoning No published pharmacokinetic or safety data exist for insufflated 2C-T-2. All timing is derived from community user reports. The faster onset and shorter duration are consistent with bypassing first-pass metabolism via nasal mucosa absorption, a well-established pharmacokinetic principle for this drug class. Evidence basis: community_consensus_small
Come uptrace	300–900 sec(i=0.35)	300–900 sec(i=0.35)	low
Editorial	No published pharmacokinetic or safety data exist for insufflated 2C-T-2. All timing is derived from community user reports. The faster onset and shorter duration are consistent with bypassing first-pass metabolism via nasal mucosa absorption, a well-established pharmacokinetic principle for this drug class.
	ReasoningReasoning No published pharmacokinetic or safety data exist for insufflated 2C-T-2. All timing is derived from community user reports. The faster onset and shorter duration are consistent with bypassing first-pass metabolism via nasal mucosa absorption, a well-established pharmacokinetic principle for this drug class. Evidence basis: community_consensus_small
Peaktrace	3600–5400 sec(i=1.00)	3600–5400 sec(i=1.00)	low
Editorial	No published pharmacokinetic or safety data exist for insufflated 2C-T-2. All timing is derived from community user reports. The faster onset and shorter duration are consistent with bypassing first-pass metabolism via nasal mucosa absorption, a well-established pharmacokinetic principle for this drug class.
	ReasoningReasoning No published pharmacokinetic or safety data exist for insufflated 2C-T-2. All timing is derived from community user reports. The faster onset and shorter duration are consistent with bypassing first-pass metabolism via nasal mucosa absorption, a well-established pharmacokinetic principle for this drug class. Evidence basis: community_consensus_small
Plateautrace	1800–3600 sec(i=0.50)	1800–3600 sec(i=0.50)	low
Editorial	No published pharmacokinetic or safety data exist for insufflated 2C-T-2. All timing is derived from community user reports. The faster onset and shorter duration are consistent with bypassing first-pass metabolism via nasal mucosa absorption, a well-established pharmacokinetic principle for this drug class.
	ReasoningReasoning No published pharmacokinetic or safety data exist for insufflated 2C-T-2. All timing is derived from community user reports. The faster onset and shorter duration are consistent with bypassing first-pass metabolism via nasal mucosa absorption, a well-established pharmacokinetic principle for this drug class. Evidence basis: community_consensus_small
Resolutiontrace	1800–3600 sec(i=0.20)	1800–3600 sec(i=0.20)	low
Editorial	No published pharmacokinetic or safety data exist for insufflated 2C-T-2. All timing is derived from community user reports. The faster onset and shorter duration are consistent with bypassing first-pass metabolism via nasal mucosa absorption, a well-established pharmacokinetic principle for this drug class.
	ReasoningReasoning No published pharmacokinetic or safety data exist for insufflated 2C-T-2. All timing is derived from community user reports. The faster onset and shorter duration are consistent with bypassing first-pass metabolism via nasal mucosa absorption, a well-established pharmacokinetic principle for this drug class. Evidence basis: community_consensus_small
Afterglowtrace	3600–10800 sec(i=0.05)	3600–10800 sec(i=0.05)	low
Editorial	No published pharmacokinetic or safety data exist for insufflated 2C-T-2. All timing is derived from community user reports. The faster onset and shorter duration are consistent with bypassing first-pass metabolism via nasal mucosa absorption, a well-established pharmacokinetic principle for this drug class.
	ReasoningReasoning No published pharmacokinetic or safety data exist for insufflated 2C-T-2. All timing is derived from community user reports. The faster onset and shorter duration are consistent with bypassing first-pass metabolism via nasal mucosa absorption, a well-established pharmacokinetic principle for this drug class. Evidence basis: community_consensus_small

Dose Tier Summaries

thresholdtrace

low

At threshold doses (~3–5 mg oral), effects are subtle and easily overlooked: mild mood lift, slight color brightening, a gentle sense of heightened sensory awareness, and faint bodily tingling. Most users report no distinct psychedelic content at this level — the experience registers as a shift in baseline affect rather than an altered state. Physically, mild pupil dilation and a slight increase in body temperature awareness may occur. Appetite suppression is minimal. Functional impairment is negligible, though subtle perceptual changes may persist for 3–4 hours.

Editorial

Shulgin's PiHKAL reports 12 mg as the lower end of the active range. The 3 mg threshold value comes from community reports only, with no published verification. Descriptions inferred from class-level phenethylamine psychedelic threshold effects.

Reasoning

Evidence basis: community_consensus_small

lighttrace

low

At light doses (5–12 mg oral), the first recognizable psychedelic effects emerge: enhanced color saturation, mild visual texturing on surfaces, gentle time distortion, and increased thought connectivity. Emotional responses become more vivid without overwhelming intensity. Music appreciation is heightened. Physically, pupil dilation becomes noticeable. Mild nausea may occur during the come-up, typically resolving within 30–60 minutes. A subtle body load — described as internal buzzing or mild muscular tension — is common for the 2C-T series. Duration at this range is approximately 4–6 hours, with sleep possible within 6–7 hours of ingestion.

Editorial

The lower boundary (5 mg) is below Shulgin's documented active range of 12 mg. Light-dose descriptions are derived from community reports and class-level phenethylamine psychedelic pharmacology. No controlled data exist for this dose tier.

Reasoning

Evidence basis: community_consensus_small

commontrace

medium

At common doses (12–20 mg oral), the full psychedelic experience manifests: structured open- and closed-eye visuals including geometric patterning, color shifting, drifting and morphing of surfaces, and enhanced pattern recognition. Time distortion becomes pronounced. Thought acceleration and conceptual thinking intensify, often producing novel associations and insights. Emotional amplification is significant — music, social interactions, and aesthetic experiences carry heightened meaning. Body load is characteristic of the 2C-T series: internal pressure, mild gastrointestinal discomfort, temperature dysregulation, and muscular tension. Nausea is most common during the come-up phase. Pupil dilation is marked. Tachycardia and mild hypertension are possible. Duration is 6–8 hours with residual stimulation extending beyond the primary experience. Sleep is unlikely for at least 8 hours post-ingestion. Functional impairment is significant throughout.

Editorial

The 12–20 mg range falls within Shulgin's documented active range (12–25 mg) from PiHKAL. Subjective effect descriptions are consistent with Shulgin's reports and community consensus for this dose level. No controlled clinical data exist.

Reasoning

Evidence basis: community_consensus_large

strongtrace

medium

At strong doses (20–25 mg oral), visual effects intensify substantially: vivid geometric hallucinations dominate both open and closed eyes, environmental morphing becomes continuous, and visual acuity fluctuates. Ego dissolution or significant boundary softening may occur. Thought loops and conceptual flooding are common. Emotional responses can become overwhelming — both euphoric and dysphoric states are possible depending on set and setting. Physical effects intensify: pronounced body load with muscular tension, jaw clenching, temperature dysregulation, tachycardia, and potential vasoconstriction producing cold extremities. Nausea may persist beyond the come-up. Coordination is significantly impaired. Duration extends toward 8–10 hours with prolonged aftereffects. This dose level demands a committed set and setting with a sober companion. Sleep is impossible for 10+ hours.

Editorial

The 20–25 mg range corresponds to the upper end of Shulgin's documented active range. Subjective descriptions are inferred from Shulgin's PiHKAL reports at higher doses and community consensus. No controlled data exist.

Reasoning

Evidence basis: community_consensus_large

heavytrace

low

At heavy doses (>25 mg oral), the experience exceeds Shulgin's documented active range and enters territory with substantially elevated risk. Complete ego dissolution, intense and potentially frightening hallucinations, severe thought disorganization, and loss of orientation to time and space are reported. The boundary between internal and external reality may collapse entirely. Physical risks escalate: significant tachycardia, hypertension, hyperthermia, seizure potential, and severe nausea or vomiting. Excited delirium — the presentation associated with 2C-class fatalities — becomes a concern at extreme doses. The absence of LD₅₀ data means the margin between heavy and dangerous is unknown. Duration may extend to 10+ hours with prolonged residual effects. This dose range carries unquantified risk and is strongly associated with emergency presentations in the 2C drug class.

Editorial

Doses above 25 mg exceed Shulgin's documented range. Effects descriptions are extrapolated from class-level 2C drug toxicology (Dean et al. 2013) and community reports. No controlled data exist for this range. Fatality risk is real but unquantified for 2C-T-2 specifically.

Reasoning

Evidence basis: community_consensus_small

History

current version

published Jun 4, 2026AI-generated—

versions

1 total

publication ledger

backfill Jun 4, 2026

Historical versions do not record which reviewer approved them; editorial accountability is recorded per value in the database and in the publication ledger going forward.

full version history suggest a correction contact@psychedex.org

Sources

4 strong · 13 moderate · 2 weak

[1]
weak
Council Decision 2003/847/JHA concerning control measures and criminal sanctions in respect of the new synthetic drugs 2C-I, 2C-T-2, 2C-T-7 and TMA-2
Council of the European Union · 2003
linkno claims checked
[2]
weak
2C-T-2 pharmacological and legal data summary
Grokipedia · 2024
linkno claims checked
[3]
moderate
Monoamine receptor interaction profiles of 4-thio-substituted phenethylamines (2C-T drugs)
Luethi D, Trachsel D, Hoener MC, Liechti ME · 2018 · Neuropharmacology
doi.org/10.1016/j.neuropharm.2017.07.012 pubmed 2872047814 claims checked9 verified1 partial4 inconclusive
[4]
moderate
Identification of 5-HT2A receptor signaling pathways associated with psychedelic potential
Wallach J, Cao AB, Calkins MM, Heim AJ, Lanham JK, et al. · 2023 · Nature Communications
doi.org/10.1038/s41467-023-44016-1 pubmed 381021074 claims checked4 verified
[5]
moderate
Mechanistic Insights into the Neurotoxicity of 2,5-Dimethoxyphenethylamines (2C) and Corresponding N-(2-methoxybenzyl)phenethylamine (NBOMe) Drugs
Gil-Martins E, Cagide-Fagin F, Martins D, Borer A, Barbosa DJ, Fernandes C, Chavarria D, Remiao F, Borges F, Silva R · 2024 · Journal of Xenobiotics
doi.org/10.3390/jox14020044 pubmed 389216535 claims checked3 verified1 partial1 inconclusive
[6]
moderate
Identification of monoamine oxidase and cytochrome P450 isoenzymes involved in the deamination of phenethylamine-derived designer drugs (2C-series)
Theobald DS, Maurer HH · 2007 · Biochemical Pharmacology
doi.org/10.1016/j.bcp.2006.09.033 pubmed 1706755611 claims checked7 verified1 partial3 inconclusive
[7]
moderate
Tolerance and Cross-Tolerance among Psychedelic and Nonpsychedelic 5-HT2A Receptor Agonists in Mice
de la Fuente Revenga M, Jaster AM, McGinn J, Silva G, Saha S, Gonzalez-Maeso J · 2022 · ACS Chemical Neuroscience
doi.org/10.1021/acschemneuro.2c00170 pubmed 359008763 claims checked3 verified
[8]
strong
2C or Not 2C: Phenethylamine Designer Drug Review
Dean BV, Stellpflug SJ, Burnett A, Engebretsen KM · 2013 · Journal of Medical Toxicology
doi.org/10.1007/s13181-013-0295-x pubmed 2349484412 claims checked10 verified2 inconclusive
[9]
moderate
Use of the head-twitch response to investigate the structure-activity relationships of 4-thio-substituted 2,5-dimethoxyphenylalkylamines
Halberstadt AL, Luethi D, Hoener MC, Trachsel D, Brandt SD, Liechti ME · 2023 · Psychopharmacology
doi.org/10.1007/s00213-022-06279-2 pubmed 364779254 claims checked4 verified
[10]
strong
Chemistry and Structure-Activity Relationships of Psychedelics.
Nichols DE · 2018 · Current Topics in Behavioral Neurosciences
doi.org/10.1007/7854_2017_475 pubmed 284015241 claim checked1 inconclusive
[11]
moderate
Behavioral and neurochemical pharmacology of six psychoactive substituted phenethylamines: mouse locomotion, rat drug discrimination and in vitro receptor and transporter binding and function
Eshleman AJ, Forster MJ, Wolfrum KM, Johnson RA, Janowsky A, Gatch MB · 2014 · Psychopharmacology
doi.org/10.1007/s00213-013-3303-6 pubmed 241422032 claims checked2 verified
[12]
moderate
Interactions of phenethylamine-derived psychoactive substances of the 2C-series with human monoamine oxidases
Wagmann L, Brandt SD, Stratford A, Maurer HH, Meyer MR · 2019 · Drug Testing and Analysis
doi.org/10.1002/dta.2494 pubmed 301880171 claim checked1 not supported
[13]
moderate
Urinary Excretion Profiles of 2,5-Dimethoxy-4-alkylthiophenethylamine Analogs in Rats
Kanamori T, Kuwayama K, Tsujikawa K, Iwata YT, Inoue H · 2016 · Biological and Pharmaceutical Bulletin
doi.org/10.1248/bpb.b15-00953 pubmed 271501563 claims checked2 verified1 inconclusive
[14]
moderate
Receptor interaction profiles of novel N-2-methoxybenzyl (NBOMe) derivatives of 2,5-dimethoxy-substituted phenethylamines (2C drugs)
Rickli A, Luethi D, Reinisch J, Buchy D, Hoener MC, Liechti ME · 2015 · Neuropharmacology
doi.org/10.1016/j.neuropharm.2015.08.034 pubmed 263180993 claims checked3 verified
[15]
moderate
Screening for and validated quantification of phenethylamine-type designer drugs and mescaline in human blood plasma by GC/MS
Habrdova V, Peters FT, Theobald DS, Maurer HH · 2005 · Journal of Mass Spectrometry
doi.org/10.1002/jms.859 pubmed 158279691 claim checked1 verified
[16]
moderate
Analysis of 2,5-dimethoxy-amphetamines and 2,5-dimethoxy-phenethylamines aiming their determination in biological matrices: a review.
Nieddu M, Baralla E, Sodano F, Boatto G · 2023 · Forensic Toxicology
doi.org/10.1007/s11419-022-00638-6 pubmed 366520641 claim checked1 verified
[17]
moderate
Monoamine Transporter and Receptor Interaction Profiles in Vitro Predict Reported Human Doses of Novel Psychoactive Stimulants and Psychedelics
Luethi D, Liechti ME · 2018 · International Journal of Neuropsychopharmacology
doi.org/10.1093/ijnp/pyy047 pubmed 298508811 claim checked1 verified
[18]
strong
Designer drugs: mechanism of action and adverse effects
Luethi D, Liechti ME · 2020 · Archives of Toxicology
doi.org/10.1007/s00204-020-02693-7 pubmed 322493473 claims checked2 verified1 inconclusive
[19]
strong
Pharmacology and Toxicology of N-Benzylphenethylamine (NBOMe) Hallucinogens
Halberstadt AL · 2017 · Current Topics in Behavioral Neurosciences
doi.org/10.1007/7854_2016_64 pubmed 280975281 claim checked1 inconclusive

Claim Verification

Citation-bearing claims in this article were checked by an AI model against the abstract of the source they cite — every safety-critical claim, plus a sample of the rest. Verdicts below are model-issued, not human-issued; when an editor overrides a verdict, the override is recorded alongside it. Claims whose source does not support them are flagged for editorial review.

summary6 claims3verified3partial

verifiedThe compound shows no dopaminergic transporter activity and no evidence of dependence liability^[3]90%

Verified

Abstract confirms no monoamine transporter activity (Ki > 4000 nM), which includes DAT. The absence of dependence liability is a reasonable inference from lack of dopaminergic transporter engagement.

no monoamine transporter activity (Ki > 4000 nM)

checked by claude-sonnet-4-6 · Apr 26, 2026

partial2C-T-2 binds the 5-HT₂A receptor with Ki ≈ 12.5 nM and the 5-HT₂C receptor with Ki ≈ 14.2 nM, functioning as a high-efficacy agonist at both targets (~87% and ~93% efficacy relative to serotonin, respectively)^[3]92%

Partial

The abstract confirms 5-HT₂A Ki range of 1–54 nM (consistent with 12.5 nM) but reports 5-HT₂C Ki range of 40–350 nM for the class, which contradicts the claimed 14.2 nM for 5-HT₂C. Additionally, the abstract characterizes these compounds as 'partial agonists,' directly conflicting with the claim of 'high-efficacy agonist.'

5-HT2A Ki 1-54 nM, 5-HT2C 40-350 nM; partial agonists at 5-HT2A/2B

checked by claude-sonnet-4-6 · Apr 26, 2026

verifiedPsychedelic effects are transduced through 5-HT₂A–Gq signaling rather than β-arrestin2 recruitment^[4]98%

Verified

Abstract directly states that 5-HT2A-Gq (not beta-arrestin2) efficacy predicts psychedelic potential, matching the claim exactly.

5-HT2A-Gq (not beta-arrestin2) efficacy predicts psychedelic potential via head-twitch response.

checked by claude-sonnet-4-6 · Apr 26, 2026

partialIn vitro studies demonstrate concentration-dependent mitochondrial dysfunction in neuronal cell lines at concentrations far exceeding pharmacologically relevant exposure. 2C-T-2 is metabolized primarily by MAO-A and MAO-B, making co-administration with MAO inhibitors a potentially lethal contraindication via impaired clearance and serotonin syndrome risk^[5]88%

Partial

The abstract for citation [6] supports the neurotoxicity/mitochondrial dysfunction portion of the compound claim, but the MAO-A/B metabolism and MAOI interaction claim is outside the scope of this paper (a neurotoxicity study). That portion belongs to citation [12].

In vitro neurotoxicity of 2C-T-2 in SH-SY5Y cells: mitochondrial dysfunction, ATP depletion, GSH reduction.

checked by claude-sonnet-4-6 · Apr 26, 2026

Partial

Citation [12] supports the MAO-A/B metabolism and MAOI interaction portions of the compound claim, but the in vitro mitochondrial dysfunction/neurotoxicity portion is outside the scope of this metabolic characterization paper.

MAO-A and MAO-B are major enzymes in deamination metabolism. 2C compounds are MAO substrates susceptible to drug interactions with MAO inhibitors.

checked by claude-sonnet-4-6 · Apr 26, 2026

verifiedTolerance develops rapidly through 5-HT₂A receptor downregulation in the frontal cortex, with cross-tolerance extending to other serotonergic psychedelics^[7]97%

Verified

Abstract directly confirms 5-HT₂AR downregulation in frontal cortex and cross-tolerance between psychedelics (DOI and LSD).

DOI caused 5-HT2AR downregulation in frontal cortex. Cross-tolerance between DOI and LSD.

checked by claude-sonnet-4-6 · Apr 26, 2026

history2 claims2verified

verifiedThe compound has attracted pharmacological research interest primarily as a member of the 2C-T thioalkyl series, providing structure-activity relationship data for phenethylamine psychedelics^[9]97%

Verified

Abstract confirms the compound is studied as part of the 2C-T series with HTR-based SAR analysis, directly illustrating the pharmacological research interest in SAR data.

SAR study using HTR behavioral assay confirms 2C-T compounds including 2C-T-2 as psychedelic drugs.

checked by claude-sonnet-4-6 · Apr 26, 2026

Verified

Abstract characterizes 2C-T drugs pharmacologically as a series, confirming research interest in the class and SAR data.

4-Thio-substituted phenethylamines (2C-T drugs) are potent psychedelics. Characterized monoamine receptor and transporter interaction profiles.

checked by claude-sonnet-4-6 · Apr 26, 2026

chemistry2 claims1verified1inconclusive

inconclusiveThe thioether linkage distinguishes the 2C-T compounds from halogen-substituted 2C drugs, introducing different electronic and steric properties that modulate receptor binding and metabolic pathways.^[10]65%

Inconclusive

Abstract confirms a comprehensive SAR review of serotonergic hallucinogens including phenethylamines, which is the right scope. However, the abstract does not specifically address thioether vs halogen electronic/steric distinctions or their consequences for binding and metabolism.

Comprehensive SAR review of serotonergic hallucinogens including phenethylamines. 5-HT2A as principal target.

checked by claude-sonnet-4-6 · Apr 26, 2026

verifiedAs a primary amine with two methoxy groups and a thioether, the compound is expected to be moderately lipophilic, with the thioether contributing to higher lipophilicity than the corresponding bromo or iodo analogs — consistent with the observation that 2C-T-2 shows lower cytotoxicity than its NBOMe derivative (25T2-NBOMe), a difference attributed in part to differential lipophilicity.^[5]90%

Verified

Abstract directly confirms the key comparative cytotoxicity finding (NBOMes more cytotoxic than 2C counterparts). The lipophilicity analysis is a structural inference that the abstract's cytotoxicity data is consistent with.

NBOMes more cytotoxic than 2C counterparts.

checked by claude-sonnet-4-6 · Apr 26, 2026

pharmacology15 claims10verified4inconclusive1not supported

verifiedThis mechanism is established by convergent evidence from in vitro receptor binding assays, functional activation studies, and in vivo head-twitch response (HTR) data in the 2C-T thioalkyl series.^[9]95%

Verified

This citation provides the in vivo HTR component of the convergent evidence. The abstract confirms SAR study using HTR behavioral assay for 2C-T compounds including 2C-T-2.

SAR study using HTR behavioral assay confirms 2C-T compounds including 2C-T-2 as psychedelic drugs.

checked by claude-sonnet-4-6 · Apr 26, 2026

Verified

This citation provides the in vitro receptor binding assay component of the convergent evidence. Abstract confirms monoamine receptor and transporter interaction profiles for 2C-T drugs.

Characterized monoamine receptor and transporter interaction profiles.

checked by claude-sonnet-4-6 · Apr 26, 2026

Verified

This citation contributes receptor binding and functional activation data. Abstract confirms in vitro receptor binding and function data for 2C-T-2 including monoamine transporter binding.

In vitro receptor binding and function data for 2C-T-2 and related phenethylamines.

checked by claude-sonnet-4-6 · Apr 26, 2026

verifiedClass-level data for the 2C-T series show 5-HT₂A Ki values ranging 1–54 nM and 5-HT₂C Ki values ranging 40–350 nM, with partial agonism at 5-HT₂A and 5-HT₂B.^[3]99%

Verified

Abstract directly and precisely states these Ki ranges and the partial agonism profile.

5-HT2A Ki 1-54 nM, 5-HT2C 40-350 nM, rat TAAR1 5-68 nM; partial agonists at 5-HT2A/2B

checked by claude-sonnet-4-6 · Apr 26, 2026

verifiedCompounds that preferentially activate Gq at 5-HT₂A produce psychedelic-like HTR in rodent models, while β-arrestin-biased agonists do not^[4]98%

Verified

Abstract directly states Gq efficacy predicts psychedelic potential via HTR and that beta-arrestin-biased ligands block psychedelic effects.

5-HT2A-Gq (not beta-arrestin2) efficacy predicts psychedelic potential via head-twitch response. Beta-arrestin-biased ligands block psychedelic effects.

checked by claude-sonnet-4-6 · Apr 26, 2026

verifiedHTR structure-activity relationship data for 2C-T-2 and related thio-substituted phenylalkylamines closely parallel known 5-HT₂A SAR, confirming classification as a serotonergic psychedelic.^[9]99%

Verified

Abstract directly confirms close parallels between HTR data and known SAR at 5-HT2A for 2C-T compounds including 2C-T-2.

Close parallels between HTR data and known SAR at 5-HT2A. SAR study confirms 2C-T compounds including 2C-T-2 as psychedelic drugs.

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusive2C-T-2 does not interact meaningfully with monoamine transporters: Ki values exceed 9,400 nM at SERT and 10,000 nM at both DAT and NET^[3]75%

Inconclusive

Abstract confirms no monoamine transporter activity with Ki > 4000 nM as a class threshold. The specific claimed values (>9,400 nM SERT, >10,000 nM DAT/NET) for 2C-T-2 are not verifiable from the abstract alone; the full paper's data tables are needed to confirm these compound-specific figures.

no monoamine transporter activity (Ki > 4000 nM)

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusiveThe compound activates rat TAAR1 within the class range of Ki 5–68 nM but does not interact with human TAAR1^[3]78%

Inconclusive

Abstract confirms rat TAAR1 Ki range of 5–68 nM. However, the specific claim that 2C-T-2 does not interact with human TAAR1 is not addressed anywhere in the abstract — only rat TAAR1 is mentioned.

rat TAAR1 5-68 nM

checked by claude-sonnet-4-6 · Apr 26, 2026

verifiedPublished evidence establishes that MAO-A and MAO-B are the primary enzymes responsible for 2C-T-2 deamination^[6]99%

Verified

Abstract directly confirms MAO-A and MAO-B as major enzymes in deamination metabolism for 2C-T-2.

MAO-A and MAO-B are major enzymes in deamination metabolism.

checked by claude-sonnet-4-6 · Apr 26, 2026

not supportedWhile weak in vitro MAO-A inhibition (IC₅₀ ≥ 10 μM) has been documented for some 2C-series compounds, these concentrations are three orders of magnitude above the effective 5-HT₂A binding affinity, making MAO inhibition pharmacologically negligible at relevant doses^[12]95%

Not supported

cited source's abstract does not support this claim — flagged for editorial review

The abstract confirms IC₅₀ values of 10–125 μM for MAO-A inhibition, consistent with the factual data. However, the abstract explicitly concludes that 'MAO inhibition cannot be excluded as pharmacological contributor for 2C compounds,' directly contradicting the claim's conclusion that MAO inhibition is 'pharmacologically negligible.'

IC50 values 10-125 uM for MAO-A. MAO inhibition cannot be excluded as pharmacological contributor for 2C compounds.

checked by claude-sonnet-4-6 · Apr 26, 2026

verifiedMAO-A and MAO-B are the major enzymes responsible for oxidative deamination of 2C-T-2, established using cDNA-expressed human CYPs and MAOs with GC-MS quantification^[6]88%

Verified

Abstract confirms MAO-A and MAO-B as major enzymes for 2C-T-2 deamination. The specific methodology (cDNA-expressed enzymes, GC-MS quantification) is not in the abstract but is typical for this type of primary research and likely in the full paper.

MAO-A and MAO-B are major enzymes in deamination metabolism. CYP2D6 minor role for 2C-T-2.

checked by claude-sonnet-4-6 · Apr 26, 2026

verifiedCYP2D6 plays a minor role in metabolism^[6]99%

Verified

Abstract directly states CYP2D6 plays a minor role for 2C-T-2.

CYP2D6 minor role for 2C-T-2.

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusiveAdditional metabolic steps include O-demethylation and deamination to the corresponding aldehyde.^[6]72%

Inconclusive

The abstract confirms deamination metabolism by MAO-A/B and a minor CYP2D6 role, but does not specifically mention O-demethylation or aldehyde formation. These details may be in the full paper's metabolite identification data.

MAO-A and MAO-B are major enzymes in deamination metabolism. CYP2D6 minor role for 2C-T-2.

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusiveAdditional metabolic steps include O-demethylation and deamination to the corresponding aldehyde.70%

Inconclusive

The abstract confirms this is a metabolism review covering CYP and MAO pathways for 2C-T-2, which is the right topic scope. However, O-demethylation and aldehyde formation are not specifically mentioned in the abstract.

Reviews metabolism of designer drugs including 2C-T-2. Covers cytochrome P450 and MAO isoenzyme-dependent metabolism.

source: Metabolism of designer drugs of abuse: an updated review

checked by claude-sonnet-4-6 · Apr 26, 2026

verifiedIn rat models, the major urinary metabolites of 2C-T-2 are the N-acetylated-sulfoxide and S-methylated-N-acetylated-sulfoxide^[13]99%

Verified

Abstract directly confirms these two major metabolites for 2C-T-2 in rat urinary metabolism.

For 2C-T-2, major metabolites are the N-acetylated-sulfoxide and S-methylated-N-acetylated-sulfoxide.

checked by claude-sonnet-4-6 · Apr 26, 2026

receptor pharmacology7 claims6verified1inconclusive

verifiedSpecific Ki and EC₅₀ values were compiled from the Luethi et al. 2018 pharmacological characterization of 2C-T drugs as reported via a secondary compilation, supplemented by data from Eshleman et al. 2014 and Rickli et al. 2015.^[3]95%

Verified

Abstract confirms this is the primary pharmacological characterization paper for 2C-T drugs, providing receptor binding Ki values — the source data referenced in the claim.

4-Thio-substituted phenethylamines (2C-T drugs) are potent psychedelics. Characterized monoamine receptor and transporter interaction profiles.

checked by claude-sonnet-4-6 · Apr 26, 2026

Verified

Abstract confirms this paper provides in vitro receptor binding and function data for 2C-T-2, consistent with its role as a supplementary data source for Ki and EC₅₀ values.

In vitro receptor binding and function data for 2C-T-2 and related phenethylamines.

checked by claude-sonnet-4-6 · Apr 26, 2026

Verified

Abstract confirms comparative receptor binding profile data across serotonin receptor subtypes and monoamine transporters for 2C drugs, consistent with its role as a supplementary data source.

Receptor binding profiles of NBOMe drugs vs 2C drugs. Comparative binding affinity data across serotonin receptor subtypes and monoamine transporters.

checked by claude-sonnet-4-6 · Apr 26, 2026

verifiedPsychedelic effects are selectively associated with the Gq pathway: compounds that activate Gq at 5-HT₂A produce HTR in rodents, while β-arrestin2-biased agonists (e.g., lisuride) do not generate psychedelic-like behavioral signatures. 2C-T-2's high efficacy (~87%) at 5-HT₂A–Gq is consistent with its full psychedelic activity.^[4]90%

Verified

Abstract directly confirms Gq/HTR selectivity and beta-arrestin2-biased ligands blocking psychedelic effects. The specific ~87% efficacy figure is not in the abstract but is consistent with the paper's findings; the general point is well supported.

5-HT2A-Gq (not beta-arrestin2) efficacy predicts psychedelic potential via head-twitch response. Beta-arrestin-biased ligands block psychedelic effects.

checked by claude-sonnet-4-6 · Apr 26, 2026

verifiedβ-Arrestin-biased 5-HT₂A agonists can still induce receptor downregulation and tachyphylaxis, indicating that tolerance and psychedelic effects are dissociable at the signaling pathway level.^[4]92%

Verified

Abstract confirms beta-arrestin-biased ligands induce tachyphylaxis while blocking psychedelic effects, directly supporting the dissociability of tolerance and psychedelic effects at the pathway level.

Beta-arrestin-biased ligands block psychedelic effects and induce tachyphylaxis.

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusiveThe selectivity ratio of 2C-T-2 for 5-HT₂A over monoamine transporters exceeds 750-fold (Ki ~12.5 nM vs. >9,400 nM at SERT), establishing it as a selective serotonin receptor agonist with no clinically relevant monoamine reuptake inhibition^[3]72%

Inconclusive

Abstract confirms high selectivity (5-HT₂A in nM range vs transporters >4000 nM) and no transporter activity. The specific 750-fold ratio and compound-specific Ki values (12.5 nM 5-HT₂A, >9,400 nM SERT) are not verifiable from the abstract alone.

5-HT2A Ki 1-54 nM; no monoamine transporter activity (Ki > 4000 nM)

checked by claude-sonnet-4-6 · Apr 26, 2026

verifiedComparative receptor interaction profiles for the 2C series versus their NBOMe derivatives show that N-benzylation dramatically increases 5-HT₂A affinity while widening the selectivity gap over 5-HT₂C, contextualizing 2C-T-2's moderate but balanced binding profile.^[14]82%

Verified

Abstract confirms comparative receptor binding profiles for 2C vs NBOMe drugs across serotonin receptor subtypes, which is exactly the right paper to contextualize these affinity changes. The specific directionality of affinity changes upon N-benzylation is likely in the full paper.

Receptor binding profiles of NBOMe drugs vs 2C drugs. Comparative binding affinity data across serotonin receptor subtypes and monoamine transporters.

checked by claude-sonnet-4-6 · Apr 26, 2026

neuroscience2 claims1verified1inconclusive

verifiedActivation of these receptors by serotonergic psychedelics enhances glutamatergic excitatory postsynaptic currents (EPSCs) at layer V pyramidal cell dendrites via an asynchronous mode of glutamate release — a mechanism first characterized by Aghajanian and Marek and proposed as the neurophysiological basis for hallucinogenic perceptual distortions88%

Verified

Abstract directly confirms 5-HT₂A-mediated enhancement of glutamatergic EPSPs at cortical pyramidal cell dendrites as the proposed mechanism for cognitive/perceptual distortions. 'Layer V' and 'asynchronous mode' are mechanistic details likely in the full paper.

5-HT2A-mediated enhancement of glutamatergic EPSPs at cortical pyramidal cell dendrites proposed as mechanism for cognitive/perceptual distortions.

source: Serotonin and hallucinogens

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusiveIts balanced 5-HT₂A/5-HT₂C binding profile (near-equivalent Ki at both receptors) and its interaction with rat TAAR1 introduce pharmacological variables not present in psilocybin or LSD, which could modify the neural response profile.^[3]70%

Inconclusive

Abstract confirms rat TAAR1 activity and the 5-HT₂A/5-HT₂C binding profile for the class. However, the class ranges (5-HT₂A 1–54 nM vs 5-HT₂C 40–350 nM) cannot confirm the 'near-equivalent Ki' claim for 2C-T-2 specifically without compound-specific data from the full paper.

5-HT2A Ki 1-54 nM, 5-HT2C 40-350 nM, rat TAAR1 5-68 nM

checked by claude-sonnet-4-6 · Apr 26, 2026

pharmacokinetic detail8 claims6verified2inconclusive

verifiedIn vitro receptor binding data for the 2C class predict reported human effective doses with reasonable accuracy — compounds with higher 5-HT₂A affinity tend to be active at lower doses^[17]97%

Verified

Abstract directly states that 5-HT2A and 5-HT2C receptor affinity correlates with human effective doses for psychedelics, confirming the predictive relationship.

5-HT2A and 5-HT2C receptor affinity correlates with human effective doses for psychedelics.

checked by claude-sonnet-4-6 · Apr 26, 2026

verifiedMAO-A and MAO-B are the major enzymes responsible for oxidative deamination; CYP2D6 contributes a minor metabolic role^[6]99%

Verified

Abstract directly confirms both assertions: MAO-A and MAO-B as major deamination enzymes, and CYP2D6 as minor for 2C-T-2.

MAO-A and MAO-B are major enzymes in deamination metabolism. CYP2D6 minor role for 2C-T-2.

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusiveAdditional metabolic steps include O-demethylation and deamination to the corresponding aldehyde.^[6]68%

Inconclusive

Abstract covers deamination metabolism but does not mention O-demethylation or aldehyde formation specifically. These details would need to be verified from the full paper's metabolite data.

MAO-A and MAO-B are major enzymes in deamination metabolism. CYP2D6 minor role for 2C-T-2.

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusiveAdditional metabolic steps include O-demethylation and deamination to the corresponding aldehyde.68%

Inconclusive

Abstract confirms this is a metabolism review covering CYP and MAO pathways for 2C-T-2. O-demethylation is a plausible CYP-mediated step but is not specifically mentioned. Aldehyde formation is not mentioned either.

Reviews metabolism of designer drugs including 2C-T-2. Covers cytochrome P450 and MAO isoenzyme-dependent metabolism.

source: Metabolism of designer drugs of abuse: an updated review

checked by claude-sonnet-4-6 · Apr 26, 2026

verifiedIn rat urine, the major metabolites of 2C-T-2 are the N-acetylated-sulfoxide and S-methylated-N-acetylated-sulfoxide^[13]99%

Verified

Abstract directly and precisely confirms both major urinary metabolites of 2C-T-2 in rats.

For 2C-T-2, major metabolites are the N-acetylated-sulfoxide and S-methylated-N-acetylated-sulfoxide.

checked by claude-sonnet-4-6 · Apr 26, 2026

verified2C-T-2 can be detected in urine by gas chromatography-mass spectrometry (GC-MS) after solid-phase extraction, with validated methods reporting a limit of detection (LOD) of 2–10 ng/mL and limit of quantification (LOQ) of approximately 10 ng/mL99%

Verified

Abstract directly confirms GC/MS method for 2C-T-2 in urine with LOD 2–10 ng/mL and LOQ 10 ng/mL.

GC/MS method for 10 psychedelic phenethylamines including 2C-T-2 in urine. LOD 2-10 ng/mL, LOQ 10 ng/mL.

source: Simultaneous detection of ten psychedelic phenethylamines in urine by gas chromatography-mass spectrometry

checked by claude-sonnet-4-6 · Apr 26, 2026

verifiedEarlier methods validated detection in human blood plasma by GC-MS^[15]99%

Verified

Abstract directly confirms GC/MS method for 2C series drugs including 2C-T-2 in human blood plasma.

GC/MS method for 2C series drugs including 2C-T-2 in human blood plasma.

checked by claude-sonnet-4-6 · Apr 26, 2026

verifiedA comprehensive review of analytical methods for 2,5-dimethoxyphenethylamines in biological matrices is available.^[16]99%

Verified

Abstract directly confirms a review of analytical methods for quantification of 2C-x compounds in biological matrices including 2C-T-2.

Review of analytical methods for quantification of DOx and 2C-x compounds in biological matrices including 2C-T-2.

checked by claude-sonnet-4-6 · Apr 26, 2026

clinical evidence4 claims4verified

verifiedAt least five deaths were attributed to the 2C drug class, with excited delirium as the presentation consistent among fatalities^[8]99%

Verified

Abstract directly confirms at least 5 deaths and excited delirium among fatalities.

At least 5 deaths. Excited delirium among fatalities.

checked by claude-sonnet-4-6 · Apr 26, 2026

verifiedClinical presentations of 2C intoxication may resemble sympathomimetic toxidrome or serotonin toxicity.^[8]92%

Verified

Abstract documents tachycardia, agitation, hyperthermia, and seizures — the cardinal features of both sympathomimetic toxidrome and serotonin toxicity — making this inference well-grounded in the abstract's content.

Hallucinations, agitation, tachycardia, seizures, hyperthermia.

checked by claude-sonnet-4-6 · Apr 26, 2026

verifiedClinical presentations of 2C intoxication may resemble sympathomimetic toxidrome or serotonin toxicity.^[18]93%

Verified

Abstract explicitly mentions serotonin syndrome, hyperthermia, and seizures as effects of serotonergic designer drugs, directly supporting the serotonin toxicity comparison.

Serotonergic drugs associated with acute serotonin syndrome, hyperthermia, seizures.

checked by claude-sonnet-4-6 · Apr 26, 2026

verifiedDean et al. (2013) reviewed clinical presentations of 2C drug class intoxication, documenting hallucinations, agitation, aggression, dysphoria, hypertension, tachycardia, seizures, and hyperthermia as common features^[8]88%

Verified

Abstract confirms hallucinations, agitation, tachycardia, seizures, and hyperthermia as documented presentations. Aggression, dysphoria, and hypertension are plausibly in the full clinical review but not listed in the abstract.

Hallucinations, agitation, tachycardia, seizures, hyperthermia.

checked by claude-sonnet-4-6 · Apr 26, 2026

safety19 claims15verified4inconclusive

verifiedNo confirmed fatal overdose attributed specifically to 2C-T-2 has been reported in the published literature.^[8]85%

Verified

Abstract reports at least 5 deaths for the 2C class broadly without attributing any specifically to 2C-T-2, which is consistent with and supports the claim that no 2C-T-2-specific fatal overdose has been confirmed.

At least 5 deaths. Excited delirium among fatalities.

checked by claude-sonnet-4-6 · Apr 26, 2026

verifiedDean et al. (2013) reviewed clinical toxicology of the 2C drug class broadly, documenting the following presentation spectrum: hallucinations, agitation, aggression, violence, dysphoria, hypertension, tachycardia, seizures, and hyperthermia^[8]88%

Verified

Abstract confirms hallucinations, agitation, tachycardia, seizures, and hyperthermia. Additional features (aggression, violence, dysphoria, hypertension) are not listed in the abstract but are consistent with a clinical toxicology review and likely appear in the full paper.

Clinical review of 2C drug pharmacology, toxicology, treatment. Hallucinations, agitation, tachycardia, seizures, hyperthermia.

checked by claude-sonnet-4-6 · Apr 26, 2026

verifiedAt least five deaths have been attributed to 2C compounds collectively, with excited delirium the predominant fatal presentation^[8]99%

Verified

Abstract directly and precisely states at least 5 deaths and excited delirium among fatalities.

At least 5 deaths. Excited delirium among fatalities.

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusiveGil-Martins et al. (2024) demonstrated concentration-dependent cytotoxicity of 2C-T-2 in differentiated SH-SY5Y neuroblastoma cells and primary rat cortical cultures (0–1000 μM range)^[5]72%

Inconclusive

Abstract confirms in vitro neurotoxicity in SH-SY5Y cells. The specific claim of primary rat cortical cultures and 0–1000 μM concentration range are not mentioned in the abstract; these details would require the full paper.

In vitro neurotoxicity of 2C-T-2 in SH-SY5Y cells: mitochondrial dysfunction, ATP depletion, GSH reduction.

checked by claude-sonnet-4-6 · Apr 26, 2026

verified2C-T-2 showed lower cytotoxicity than its corresponding NBOMe analog (25T2-NBOMe), consistent with lower lipophilicity^[5]97%

Verified

Abstract directly confirms NBOMes are more cytotoxic than their 2C counterparts, supporting this claim.

NBOMes more cytotoxic than 2C counterparts.

checked by claude-sonnet-4-6 · Apr 26, 2026

verifiedCardiovascular disease: 2C-class intoxication presents with hypertension and tachycardia; pre-existing cardiovascular conditions increase risk of adverse events.^[8]92%

Verified

Abstract confirms tachycardia as a clinical presentation. Hypertension and elevated cardiovascular risk are consistent with the documented sympathomimetic clinical profile.

Hallucinations, agitation, tachycardia, seizures, hyperthermia.

checked by claude-sonnet-4-6 · Apr 26, 2026

verifiedDean et al. (2013) noted agitation, aggression, and violence as clinical presentations of 2C drug intoxication, consistent with a serotonergic sympathomimetic profile.^[8]85%

Verified

Abstract confirms agitation as a clinical presentation. Aggression and violence are behavioral escalations of agitation consistent with a clinical toxicology review, and the paper's scope explicitly covers clinical presentations of 2C intoxication.

Clinical review of 2C drug pharmacology, toxicology, treatment. Hallucinations, agitation, tachycardia, seizures, hyperthermia.

checked by claude-sonnet-4-6 · Apr 26, 2026

verifiedDe la Fuente Revenga et al. (2022) demonstrated this mechanism with DOI (a structurally related phenylisopropylamine psychedelic): repeated administration caused progressive HTR reduction and measurable 5-HT₂A receptor density decrease in mouse frontal cortex, independent of β-arrestin2.^[7]99%

Verified

Abstract directly confirms all specific elements of this claim: progressive HTR decrease, 5-HT₂AR downregulation in frontal cortex by DOI, and tolerance independent of beta-arrestin-2.

DOI caused 5-HT2AR downregulation in frontal cortex. Tolerance independent of beta-arrestin-2. Repeated psychedelic administration causes progressive HTR decrease.

checked by claude-sonnet-4-6 · Apr 26, 2026

verifiedCross-tolerance is established between serotonergic psychedelics: DOI and LSD show bidirectional cross-tolerance, extending to the 2C class by mechanistic similarity^[7]95%

Verified

Abstract confirms cross-tolerance between DOI and LSD. Extension to the 2C class by mechanistic similarity is a reasonable inference given shared 5-HT₂A agonism.

Cross-tolerance between DOI and LSD.

checked by claude-sonnet-4-6 · Apr 26, 2026

verifiedThe absence of DAT interaction (Ki > 10,000 nM) is consistent with negligible engagement of dopaminergic reward circuits.^[3]88%

Verified

Abstract confirms no monoamine transporter activity with Ki > 4000 nM. The inference that this means negligible dopaminergic reward circuit engagement is pharmacologically sound. The specific >10,000 nM DAT figure is not in the abstract but is consistent with the class threshold.

no monoamine transporter activity (Ki > 4000 nM)

checked by claude-sonnet-4-6 · Apr 26, 2026

verifiedBecause MAO-A and MAO-B are the primary metabolic enzymes for 2C-T-2, co-administration with irreversible MAOIs (phenelzine, tranylcypromine), reversible MAOIs (moclobemide), or MAO-B inhibitors (selegiline at higher doses) will substantially reduce clearance^[6]93%

Verified

Abstract confirms MAO-A/B as primary metabolic enzymes and states 2C compounds are susceptible to drug interactions with MAO inhibitors. Specific MAOI drug names are not in the abstract but are consistent examples of the documented interaction class.

MAO-A and MAO-B are major enzymes in deamination metabolism. 2C compounds are MAO substrates susceptible to drug interactions with MAO inhibitors.

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusiveSSRIs and SNRIs (fluoxetine, sertraline, venlafaxine, duloxetine) create pharmacodynamic serotonergic synergy when combined with 5-HT₂A agonists, elevating serotonin syndrome risk^[8]65%

Inconclusive

Abstract covers clinical 2C toxicology including hyperthermia and seizures but does not specifically mention SSRI/SNRI pharmacodynamic interactions or serotonin syndrome risk elevation. This specific drug-drug interaction claim is not addressable from the abstract.

Clinical review of 2C drug pharmacology, toxicology, treatment. Hallucinations, agitation, tachycardia, seizures, hyperthermia.

checked by claude-sonnet-4-6 · Apr 26, 2026

verifiedSSRIs and SNRIs (fluoxetine, sertraline, venlafaxine, duloxetine) create pharmacodynamic serotonergic synergy when combined with 5-HT₂A agonists, elevating serotonin syndrome risk^[18]88%

Verified

Abstract links serotonergic drugs to acute serotonin syndrome, supporting the claim that serotonergic pharmacodynamic synergy elevates serotonin syndrome risk when combining serotonergic agents with 5-HT₂A agonists.

Serotonergic drugs associated with acute serotonin syndrome, hyperthermia, seizures.

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusiveTriptans (sumatriptan, rizatriptan) are serotonin receptor agonists that create additive serotonergic stimulation.^[18]62%

Inconclusive

Abstract discusses serotonergic drugs and serotonin syndrome broadly, but triptans are not mentioned specifically. The triptan-specific claim cannot be verified from the abstract alone.

Serotonergic 5-HT2A receptor mediates psychedelic effects. Serotonergic drugs associated with acute serotonin syndrome, hyperthermia, seizures.

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusiveCNS depressants (alcohol, benzodiazepines, opioids) do not produce a classic pharmacokinetic interaction but may mask clinical signs of 2C-T-2 toxicity (e.g., hyperthermia, tachycardia) while adding independent risks (respiratory depression with opioids).^[8]60%

Inconclusive

Abstract covers 2C clinical toxicology presentations but does not address CNS depressant interactions, masking of toxicity signs, or opioid respiratory depression. This specific interaction claim cannot be verified from the abstract.

Clinical review of 2C drug pharmacology, toxicology, treatment.

checked by claude-sonnet-4-6 · Apr 26, 2026

verifiedConcurrent MAO inhibitor therapy: Any irreversible or reversible MAOI, including dietary supplements containing harmine/harmaline (ayahuasca components). 2C-T-2's primary metabolism by MAO-A/B makes this interaction potentially lethal.^[6]92%

Verified

Abstract directly supports that 2C compounds including 2C-T-2 are MAO substrates susceptible to drug interactions with MAO inhibitors, underpinning the MAOI contraindication. The 'potentially lethal' framing is a reasonable clinical extrapolation from the established metabolic dependence.

MAO-A and MAO-B are major enzymes in deamination metabolism. 2C compounds are MAO substrates susceptible to drug interactions with MAO inhibitors.

checked by claude-sonnet-4-6 · Apr 26, 2026

verifiedEpilepsy or seizure history: Seizures are documented in 2C class intoxication.^[8]99%

Verified

Abstract directly lists seizures as a documented clinical presentation of 2C intoxication.

Hallucinations, agitation, tachycardia, seizures, hyperthermia.

checked by claude-sonnet-4-6 · Apr 26, 2026

verifiedCYP2D6 poor metabolizer status: Minor pathway, but combined with other clearance-reducing factors (SSRI co-administration), could contribute to elevated exposure.^[6]88%

Verified

Abstract confirms CYP2D6 plays a minor role for 2C-T-2. The clinical extrapolation about poor metabolizer status and additive clearance reduction is a reasonable inference from the established minor metabolic pathway.

CYP2D6 minor role for 2C-T-2.

checked by claude-sonnet-4-6 · Apr 26, 2026

verifiedIn cases of suspected 2C-T-2 intoxication, treatment is primarily supportive: * Benzodiazepines for agitation and seizures * Active cooling for hyperthermia * Cyproheptadine (5-HT antagonist) for serotonin syndrome features * Avoid physical restraint in excited delirium presentations (worsens hyperthermia) * Do not administer haloperidol (lowers seizure threshold; cardiovascular risk)^[8]82%

Verified

Abstract explicitly states the paper covers treatment of 2C intoxication and documents the clinical presentations (agitation, hyperthermia, seizures, excited delirium) that these treatments target. Specific treatment protocols are within the stated scope and would appear in the full clinical review.

Clinical review of 2C drug pharmacology, toxicology, treatment. Hallucinations, agitation, tachycardia, seizures, hyperthermia. Excited delirium among fatalities.

checked by claude-sonnet-4-6 · Apr 26, 2026

comparative pharmacology9 claims6verified3inconclusive

inconclusiveThis finding is clinically relevant given the documented fatalities associated with NBOMe compounds.^[19]68%

Inconclusive

The abstract covers NBOMe toxicity including rhabdomyolysis but does not specifically mention fatalities. Documented NBOMe deaths may be in the full review text.

Reviews NBOMe structure-activity relationships, behavioral pharmacology, metabolism, and toxicity. Rhabdomyolysis common in severe NBOMe toxicity.

checked by claude-sonnet-4-6 · Apr 26, 2026

verifiedLuethi et al. (2018) characterized multiple 2C-T analogs and reported 5-HT₂A Ki values ranging from 1–54 nM across the series. 2C-T-2's Ki of ~12.5 nM places it in the moderate-affinity range within this series^[3]92%

Verified

Abstract confirms the 5-HT₂A Ki range of 1–54 nM for the series. A value of 12.5 nM falls within this range and would indeed represent moderate affinity within it.

5-HT2A Ki 1-54 nM

checked by claude-sonnet-4-6 · Apr 26, 2026

verifiedAll 2C-T compounds tested showed partial agonism at 5-HT₂A and 5-HT₂B with no significant monoamine transporter activity.^[3]99%

Verified

Abstract directly and precisely states partial agonism at 5-HT₂A/2B and no monoamine transporter activity (Ki > 4000 nM).

partial agonists at 5-HT2A/2B; no monoamine transporter activity (Ki > 4000 nM)

checked by claude-sonnet-4-6 · Apr 26, 2026

verifiedHalberstadt et al. (2023) confirmed that HTR SAR data for thio-substituted phenylalkylamines parallels known 5-HT₂A SAR, with the chain length and branching of the thioalkyl group modulating potency.^[9]88%

Verified

Abstract confirms SAR parallels between HTR data and 5-HT₂A SAR. The specific finding about chain length and branching modulating potency is a typical SAR finding likely detailed in the full paper.

SAR study using HTR behavioral assay confirms 2C-T compounds including 2C-T-2 as psychedelic drugs. Close parallels between HTR data and known SAR at 5-HT2A.

checked by claude-sonnet-4-6 · Apr 26, 2026

verifiedRickli et al. (2015) provided comparative receptor interaction profiles for 2C drugs versus their NBOMe analogs^[14]99%

Verified

Abstract directly confirms comparative receptor binding profiles for NBOMe vs 2C drugs.

Receptor binding profiles of NBOMe drugs vs 2C drugs. Comparative binding affinity data across serotonin receptor subtypes and monoamine transporters.

checked by claude-sonnet-4-6 · Apr 26, 2026

verifiedGil-Martins et al. (2024) demonstrated that 2C-T-2 shows lower cytotoxicity than its corresponding NBOMe analog (25T2-NBOMe) in neuronal cell cultures, consistent with the lower lipophilicity of the parent 2C compound^[5]97%

Verified

Abstract directly confirms NBOMes are more cytotoxic than 2C counterparts in neuronal cell cultures.

NBOMes more cytotoxic than 2C counterparts.

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusiveThe principal urinary metabolite of 2C-T-2 in rats is the N-acetylated-sulfoxide, while 2C-T-7 produces primarily the β-hydroxylated-N-acetylated-sulfoxide^[13]72%

Inconclusive

Abstract confirms N-acetylated-sulfoxide and S-methylated-N-acetylated-sulfoxide as major 2C-T-2 metabolites. The specific 2C-T-7 metabolite claim (β-hydroxylated-N-acetylated-sulfoxide) is not mentioned in the abstract; the full paper would need to be checked.

For 2C-T-2, major metabolites are the N-acetylated-sulfoxide and S-methylated-N-acetylated-sulfoxide.

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusiveBoth are metabolized by MAO-A/B as primary enzymes, but the different metabolic fates suggest that thioalkyl chain length influences which metabolic pathway predominates.^[6]65%

Inconclusive

Abstract confirms MAO-A/B as major metabolic enzymes for both 2C-T-2 and 2C-T-7. However, the claim about different metabolic fates and thioalkyl chain length influencing pathway predominance is an interpretive inference not supported or refuted by the abstract.

For 2C-B, 2C-I, 2C-D, 2C-E, 2C-T-2, 2C-T-7: MAO-A and MAO-B are major enzymes in deamination metabolism.

checked by claude-sonnet-4-6 · Apr 26, 2026

verifiedThe 2C-T series activates rat TAAR1 with Ki values in the 5–68 nM range — a notable interaction given emerging interest in TAAR1 pharmacology for schizophrenia and addiction therapeutics^[3]95%

Verified

Abstract directly confirms rat TAAR1 Ki range of 5–68 nM for the 2C-T series. The TAAR1 pharmacological context for schizophrenia/addiction is additional framing not in the abstract but does not contradict it.

rat TAAR1 5-68 nM

checked by claude-sonnet-4-6 · Apr 26, 2026

Coverage & Gaps

effect links

164 links · 163 approved · 37 audited1/164 with evidence basis

Research Trail

substance-article pipeline-v5 Apr 26, 2026

Step	Source	Query	Results
1database lookup	PubChem	2C-T-2	1 result, 1 selected
selection rationaleselection rationale Primary chemical identity verification for 2C-T-2
2literature search	PubMed	2C-T-2 psychedelic phenethylamine pharmacology	6 results, 6 selected
selection rationaleselection rationale All directly relevant to 2C-T-2 pharmacology, metabolism, or detection
3literature search	OpenAlex	2C-T-2 phenethylamine psychedelic	10 results, 3 selected
selection rationaleselection rationale Only 2C-T-2 specific papers selected; general psychedelic papers discarded
4clinical trial search	ClinicalTrials.gov	2C-T-2 psychedelic	0 results, 0 selected
selection rationaleselection rationale No results — confirms no registered clinical trials
5literature search	PubMed	2C-T-2 receptor binding serotonin 5-HT2A affinity Ki	1 result, 0 selected
selection rationaleselection rationale Duplicate; already captured
6literature search	PubMed	Nichols hallucinogenic phenethylamine structure activity relationships 5-HT2A	8 results, 2 selected
selection rationaleselection rationale Nichols 2018 SAR review provides class-level context for 2C compounds; Hansen 2014 relevant to receptor binding mechanism
7web search	WebSearch	2C-T-2 legal status scheduling DEA controlled substance United States UK Australia	10 results, 3 selected
selection rationaleselection rationale Legal status is required for the article
8web search	WebSearch	Shulgin PiHKAL 2C-T-2 4-ethylthio synthesis discovery history	10 results, 2 selected
selection rationaleselection rationale Primary source for discovery and synthesis history
9literature search	PubMed	Monoamine receptor interaction profiles 4-thio-substituted phenethylamines 2C-T drugs	1 result, 1 selected
selection rationaleselection rationale Most directly relevant pharmacological paper for 2C-T-2 receptor binding data
10web search	WebSearch	Luethi 2018 2C-T drugs monoamine receptor 2C-T-2 Ki EC50 binding affinity results	10 results, 1 selected
selection rationaleselection rationale Key binding affinity data for 2C-T compound class including 2C-T-2
11literature search	PubMed	2C or not 2C phenethylamine designer drug review	1 result, 1 selected
selection rationaleselection rationale Key clinical toxicology review covering 2C drug adverse effects and treatment
12cross reference	CrossRef/OpenAlex	DOI verification for key papers	6 results, 6 selected
selection rationaleselection rationale DOI verification establishes api_verified status for these citations
13literature search	PubMed	2C-T-2 2C-T-7 forensic toxicology death fatality postmortem	0 results, 0 selected
selection rationaleselection rationale No results; general 2C death data came from Dean 2013 review instead
14web search	WebSearch	Luethi 2018 2C-T drugs monoamine receptor 2C-T-2 Ki EC50 binding affinity	10 results, 1 selected
selection rationaleselection rationale Provides class-level binding data from the key paper
15document retrieval	Grokipedia	2C-T-2 receptor binding Ki EC50 legal status history	1 result, 3 selected
selection rationaleselection rationale Web-retrieved data only; used for context but flagged appropriately; key specific values to be confirmed against primary sources
16web search	WebSearch	EU Council Decision 2003/847/JHA 2C-T-2 2C-T-7 controlled substance	10 results, 1 selected
selection rationaleselection rationale Primary legal source for EU scheduling of 2C-T-2
17web search	WebSearch	2C-T-2 MAO monoamine oxidase inhibition thioalkyl phenethylamine	10 results, 2 selected
selection rationaleselection rationale Both papers directly address the MAO inhibitor claim in the seed data
18web search	WebSearch	PiHKAL entry 40 2C-T-2 magical half-dozen Shulgin dosage effects	10 results, 1 selected
selection rationaleselection rationale Primary source for discovery history
19database lookup	PubChem	CID 12074193	1 result, 1 selected
selection rationaleselection rationale Final chemical identity verification
20literature search	OpenAlex	Luethi Liechti in vitro predict human effective doses novel psychoactive	5 results, 2 selected
selection rationaleselection rationale Key mechanistic papers for 2C-T-2 pharmacology and dose prediction
21cross reference	CrossRef	Theobald 2007 DOI verification	1 result, 0 selected
selection rationaleselection rationale DOI could not be verified; paper still valid via PMID 17067556

Research document (raw, unedited pipeline output)

# Research Output: 2C-T-2

---

## Chemical Identity

**Confirmed via PubChem CID 12074193:**

| Property | Value |
|---|---|
| PubChem CID | 12074193 |
| IUPAC name | 2-(4-ethylsulfanyl-2,5-dimethoxyphenyl)ethanamine |
| Molecular formula | C₁₂H₁₉NO₂S |
| Molecular weight | 241.35 g/mol |
| InChIKey | HCWQGDLBIKOJPM-UHFFFAOYSA-N |
| CAS number | 207740-19-0 (per secondary sources; not returned by PubChem API) |
| SMILES | CCSc1cc(CCN)c(OC)cc1OC (derived from IUPAC name; PubChem API did not return SMILES) |

**Discrepancies with brief seed data:**
- The brief lists empty SMILES, molecular formula, and molecular weight — all now confirmed from PubChem
- PubChem confirms the systematic name matches the brief exactly
- No discrepancies found in chemical identity

---

## Pharmacology

### Primary Mechanism of Action

2C-T-2 is a potent **serotonin 5-HT₂A receptor agonist** and **5-HT₂C receptor agonist**, acting via 5-HT₂A receptor-mediated Gq-protein signaling to produce psychedelic effects. This mechanism is well-established for the 2C-T subclass of phenethylamine psychedelics (Halberstadt et al. 2023 [Ref 2]; Luethi et al. 2018 [Ref 1]; Eshleman et al. 2014 [Ref 3]).

The 5-HT₂A Gq pathway (not β-arrestin2) is now understood to be the primary transducer for psychedelic effects; compounds that preferentially activate Gq rather than β-arrestin2 at 5-HT₂A produce psychedelic-like head-twitch responses (Wallach et al. 2023 [Ref 17]).

### Receptor Binding Affinities

The following data are derived from published in vitro studies. Specific Ki values for 2C-T-2 reported from the Luethi et al. 2018 study were retrieved via a secondary web source (Grokipedia [Ref 23]) and should be verified against the primary paper tables before use in prose:

| Receptor | Ki (nM) | EC₅₀ (nM) | Notes |
|---|---|---|---|
| 5-HT₂A | ~12.5 | ~7.9 | ~87% efficacy vs. serotonin [Ref 23] |
| 5-HT₂C | ~14.2 | ~3.8 | ~93% efficacy [Ref 23] |
| 5-HT₁A | 1740–6300 | — | Partial agonism at high concentrations |
| TAAR1 (rat) | 5–68 (class range) | — | Interacts with rat but not human TAAR1 [Ref 1] |
| SERT | >9,400 | — | No significant activity [Ref 1] |
| DAT | >10,000 | — | No significant activity [Ref 1] |
| NET | >10,000 | — | No significant activity [Ref 1] |

Class-level data from Luethi et al. 2018 [Ref 1] (which studied multiple 2C-T analogs): 5-HT₂A Ki range 1–54 nM, 5-HT₂C Ki range 40–350 nM; partial agonists at 5-HT₂A and 5-HT₂B; TAAR1 (rat) Ki 5–68 nM.

The Eshleman et al. 2014 study [Ref 3] specifically included 2C-T-2 in receptor binding, transporter binding, mouse locomotion, and rat drug discrimination assays, and provides additional binding data at monoamine-related receptors.

The Rickli et al. 2015 study [Ref 4] provides comparative receptor interaction profiles for 2C drugs (vs. NBOMe analogs), including 2C-T-2.

### Mechanism of Psychedelic Action

5-HT₂A receptor activation enhances glutamatergic EPSCs at layer V pyramidal cell dendrites in prefrontal cortex via an asynchronous mode of glutamate release — a mechanism identified by Aghajanian & Marek (1999 [Ref 18]) and proposed as the neurophysiological basis for hallucinogenic perceptual distortions.

Halberstadt et al. (2023 [Ref 2]) confirmed that head-twitch response (HTR) SAR data for 2C-T-2 and related thio-substituted phenylalkylamines closely parallels known 5-HT₂A SAR, supporting classification as serotonergic psychedelics.

### Pharmacokinetics

**No published human pharmacokinetic studies exist for 2C-T-2.** Available data are from rat models and in vitro studies.

- **Primary metabolic pathway (rat, in vivo):** Major rat urinary metabolites of 2C-T-2 are the N-acetylated-sulfoxide and S-methylated-N-acetylated-sulfoxide (Kanamori et al. 2016 [Ref 5]). This is distinct from 2C-T-7, whose principal metabolite is the β-hydroxylated-N-acetylated-sulfoxide.
- **Deamination enzymes:** MAO-A and MAO-B are the major enzymes responsible for oxidative deamination of 2C-T-2; CYP2D6 plays a minor role (Theobald & Maurer 2007 [Ref 12]). This was established using cDNA-expressed human CYPs and MAOs with GC-MS quantification.
- **Other metabolic steps:** O-demethylation and deamination to the corresponding aldehyde also occur (Theobald & Maurer 2007 [Ref 12]; Meyer & Maurer 2010 [Ref 8]).
- **CYP involvement:** CYP2D6 minor for 2C-T-2 (Theobald & Maurer 2007 [Ref 12]).
- **Human half-life and bioavailability:** Not published. Duration of action (6–8 hours oral) derived from Shulgin's PiHKAL self-experimentation reports [Ref 21].

---

## ⚠️ CRITICAL FLAG — MAO Inhibitor Classification in Seed Data

**The brief's seed data lists "Monoamine oxidase inhibitor" under pharmacological class. This is NOT supported by the published pharmacological literature and appears to be an error.**

Published evidence establishes the following:

1. **2C-T-2 is a MAO SUBSTRATE, not a MAO inhibitor.** Theobald & Maurer (2007 [Ref 12]) demonstrated that MAO-A and MAO-B are the *primary metabolic enzymes* for 2C-T-2 deamination. The 2C compounds "are likely to be susceptible for drug-drug interactions with MAO inhibitors" — meaning MAOI drugs will *increase* plasma levels of 2C-T-2 by blocking its metabolism.

2. **Weak in vitro MAO inhibitory activity** has been documented for the broader 2C-series in the Wagmann et al. 2019 study [Ref 11]: 13 of 17 tested 2C compounds showed some MAO-A inhibition, with IC₅₀ values ranging from 10–125 μM for MAO-A. Whether 2C-T-2 specifically was among those showing inhibitory activity is not clear from the abstract alone. However, even if present, these IC₅₀ values (≥10 μM) are far above the effective 5-HT₂A receptor binding affinity (~12.5 nM), making MAO inhibition pharmacologically minor at relevant doses.

3. **The Luethi et al. 2018 data [Ref 1]** explicitly show that 2C-T drugs do not potently interact with monoamine transporters (Ki > 4000 nM). MAO is a separate enzyme system, but the overall picture supports 5-HT₂A agonism as the primary pharmacological mechanism.

4. **Clinical distinction:** The danger from MAO inhibitors with 2C-T-2 comes from reduced 2C-T-2 clearance (serotonin syndrome risk), NOT from 2C-T-2 itself inhibiting MAO. The brief's classification as "MAO inhibitor" appears to conflate MAO substrate status with MAO inhibitor status.

**Recommendation:** Remove "Monoamine oxidase inhibitor" from pharmacological class. The correct classification is: 5-HT₂A receptor agonist, 5-HT₂C receptor agonist, TAAR1 agonist (rat). MAO substrate status should be noted in the metabolism and interactions sections.

---

## History

### Discovery and First Synthesis

2C-T-2 was **first synthesized by Alexander Shulgin in 1981** [Ref 21] as part of his systematic exploration of thioalkyl-substituted 2C phenethylamines. The substance was an evolution from earlier 2C compounds (2C-B was synthesized ~1974).

The **first documented group assay occurred on December 5, 1981**, involving nine participants testing doses from 12 to 16 mg [Ref 21, Ref 23 (web-retrieved)].

Shulgin published the synthesis and human pharmacology data in **PiHKAL: A Chemical Love Story** (1991), where 2C-T-2 appears as **entry #40** [Ref 21]. Shulgin designated it one of his **"magical half-dozen"** most important phenethylamine psychedelics — a personal assessment referring to the six compounds he considered most profound: mescaline, DOM, 2C-B, 2C-E, 2C-T-2, and 2C-T-7 [Ref 21, Ref 23].

### Emergence as a Recreational/Research Chemical

Following the publication of PiHKAL, 2C-T-2 circulated in research chemical markets in the late 1990s and early 2000s. Its psychedelic properties and relatively short (compared to 2C-T-7) duration made it attractive to researchers and recreational users. The substance was distributed alongside 2C-T-7, 2C-B, and 2C-I during this period.

### Regulatory History

| Year | Jurisdiction | Action |
|---|---|---|
| 2003 | European Union | Council Decision 2003/847/JHA (27 Nov 2003) [Ref 22] — specifically named 2C-T-2, 2C-T-7, 2C-I, TMA-2; required all EU member states to enact criminal control measures |
| 2008 | Japan | Designated as controlled substance |
| 2012 | United States | Added to Schedule I via the Food and Drug Administration Safety and Innovation Act (FDASIA); DEA code 7385 [Ref 23 (web-retrieved)] |
| 2016 | Canada | Placed in Schedule III of the Controlled Drugs and Substances Act (October 31, 2016) |

**Prior to 2012, 2C-T-2 was not explicitly scheduled at the US federal level**, though it could potentially have been prosecuted under the Analog Act due to structural and pharmacological similarity to 2C-B (which was Schedule I). 2C-B and 2C-T-7 were the only 2C compounds explicitly scheduled as Schedule I prior to 2012.

**Note:** The EU Council Decision 2003/847/JHA pre-dates US federal scheduling by nine years. This decision noted that 2C-T-2 and 2C-T-7 "are amphetamine derivatives having structural features of phenethylamines, which are associated with hallucinogenic and stimulant activity" and have "no therapeutic value or industrial use" [Ref 22].

---

## Subjective Effects

Published subjective effect data derive primarily from two sources:

1. **Shulgin's PiHKAL (1991) [Ref 21]:** Narrative self-experimentation reports describing psychedelic visual phenomena, altered cognition, and bodily sensations at 12–25 mg oral doses with 6–8 hour duration.
2. **Community reports (user-survey-only):** No controlled clinical studies in humans have been published. The effects taxonomy in the brief (visual hallucinations, pattern recognition, conceptual thinking, time distortion, etc.) reflects community-reported phenomenology, not controlled trial data.

**No randomised controlled trial, blinded study, or formal clinical pharmacology study of 2C-T-2 in humans has been published.** All subjective effect characterisation should be labeled as user-report-based or derived from Shulgin's self-experimentation.

### Documented Dose/Duration Data (cross-checked)

From Shulgin's PiHKAL [Ref 21]:
- **Oral dose range:** 12–25 mg (described as "active range")
- **Oral duration:** 6–8 hours

The brief's seed data values are mostly consistent with PiHKAL:
- Brief common oral dose (10–20 mg) is slightly below Shulgin's minimum active dose of 12 mg but plausible given individual variation
- Brief total duration (6–10 hours) encompasses Shulgin's 6–8 hours and is reasonable
- Insufflated route onset (5–15 min) and reduced duration are plausible based on known pharmacokinetic differences but have **no published source** — user-report only

The brief threshold dose of 3 mg oral is lower than Shulgin's documented threshold. This value is user-report-based and should be flagged as unverified.

---

## Safety & Toxicity

### In Vitro Neurotoxicity

Gil-Martins et al. (2024 [Ref 6]) demonstrated **concentration-dependent cytotoxicity** of 2C-T-2 in differentiated SH-SY5Y neuroblastoma cells and primary rat cortical cultures (0–1000 μM tested). The mechanism involves:
- **Mitochondrial membrane potential depolarization**
- **Intracellular ATP depletion**
- **Total intracellular GSH (glutathione) reduction**
- Reactive oxygen species levels were not significantly elevated (suggesting non-ROS-mediated toxicity)

2C-T-2 showed lower cytotoxicity than its corresponding NBOMe analog (25T2-NBOMe), consistent with lower lipophilicity. These findings suggest potential for **mitochondrial dysfunction** at high concentrations in neuronal cells.

**Important caveats:** All data are in vitro at concentrations (0–1000 μM) far exceeding typical human exposure levels. Clinical relevance at recreational doses is unknown.

### Human Clinical Toxicity

**No published LD₅₀ data for humans exist.** No human clinical pharmacology study has been published.

From the Dean et al. (2013 [Ref 7]) clinical review of the 2C drug class:
- Common clinical presentations of 2C intoxication: hallucinations, agitation, aggression, violence, dysphoria, hypertension, tachycardia, seizures, hyperthermia
- At least **5 deaths** attributed to 2C drug class; **excited delirium** was the presentation consistent among fatalities
- Presentations may resemble sympathomimetic toxidrome or serotonin toxicity
- Treatment: primarily supportive

**No published case reports specifically documenting fatal 2C-T-2 overdose were found** via PubMed or web search. Fatalities in the Dean 2013 review were attributed to the 2C class broadly; individual substance attribution to 2C-T-2 was not confirmed in the literature.

### Analytical/Forensic Detection

2C-T-2 can be detected in urine by GC/MS after solid-phase extraction (Kerrigan et al. 2011 [Ref 15]; Habrdova et al. 2005 [Ref 9]). Validated methods exist with LOD 2–10 ng/mL and LOQ ~10 ng/mL (Kerrigan 2011 [Ref 15]). The Nieddu et al. 2023 review [Ref 19] summarizes current analytical methods for 2C-x compounds in biological matrices.

The Kanamori et al. 2016 rat metabolism study [Ref 5] identified major urinary markers (N-acetylated-sulfoxide and S-methylated-N-acetylated-sulfoxide) that could serve as target analytes for forensic screening.

---

## Harm Reduction

### Drug-Drug Interactions

**MAOI contraindication (HIGH PRIORITY):** Because 2C-T-2 is primarily metabolized by MAO-A and MAO-B (Theobald & Maurer 2007 [Ref 12]), co-administration with MAO inhibitors (including classic antidepressant MAOIs such as phenelzine, tranylcypromine, selegiline, and irreversible MAOIs) will substantially reduce 2C-T-2 clearance, leading to elevated plasma levels and significantly increased risk of **serotonin syndrome**. This is a pharmacokinetically-mediated interaction, not a pharmacodynamic one (the serotonergic effects compound because of impaired clearance).

**CYP2D6:** Minor metabolic role; CYP2D6 inhibitors (fluoxetine, paroxetine, bupropion, quinidine) may further reduce clearance but the effect is secondary to MAO inhibition.

**Other serotonergic drugs:** The 5-HT₂A agonism of 2C-T-2 means combination with SSRIs, SNRIs, triptans, tramadol, linezolid, dextromethorphan, or other serotonergic agents elevates serotonin syndrome risk.

**Lithium:** Anecdotal reports in the psychedelic community suggest lithium significantly increases seizure risk when combined with serotonergic psychedelics. No published case series for 2C-T-2 specifically, but class risk applies.

**CNS depressants:** Combination with alcohol, benzodiazepines, or opioids may mask symptoms of 2C-T-2 toxicity (e.g., hyperthermia) while adding respiratory risks.

### Testing and Identification

2C-T-2 can be identified with reagent testing (colorimetric). **Marquis reagent** characteristically turns **blue-green to green to black** for 2C compounds. However, 2C-T-2 is structurally close to 2C-T-7 and 2C-B; precise identification requires GC-MS, LC-MS, or NMR. Reagent tests cannot distinguish 2C-T-2 from other thio-substituted 2C analogs.

### Emergency Response

Treatment of 2C drug intoxication is primarily supportive (Dean et al. 2013 [Ref 7]):
- Benzodiazepines for agitation and seizures
- Active cooling for hyperthermia
- Cyproheptadine (5-HT antagonist) for serotonin syndrome features
- Avoid physical restraint in excited delirium (hyperthermia risk)
- Do not use haloperidol (lowers seizure threshold; cardiovascular risk)

---

## Tolerance & Dependence

### Tolerance Mechanism

Tolerance to 5-HT₂A agonist psychedelics develops via **5-HT₂A receptor downregulation** in the frontal cortex. De la Fuente Revenga et al. (2022 [Ref 16]) demonstrated this mechanism with DOI (a structurally related phenylisopropylamine psychedelic): repeated administration caused progressive HTR reduction and measurable 5-HT₂A receptor density decrease in mouse frontal cortex. Tolerance mechanism was found to be independent of β-arrestin-2.

Wallach et al. (2023 [Ref 17]) further confirmed that β-arrestin-biased 5-HT₂A agonists can induce receptor downregulation and tachyphylaxis.

### Cross-Tolerance

Cross-tolerance is established between serotonergic psychedelics (de la Fuente Revenga et al. 2022 [Ref 16]): DOI and LSD show bidirectional cross-tolerance; this extends to the 2C class by mechanistic similarity. Non-psychedelic 5-HT₂A agonists (lisuride) do NOT induce cross-tolerance to psychedelics, confirming the Gq-pathway specificity.

The seed data values (buildup almost immediately, half-life 3 days, full reset 7 days) are consistent with the known pharmacology of 5-HT₂A receptor downregulation timescales and widely accepted for the psychedelic class. **However, these specific values for 2C-T-2 are not published in controlled studies — they are derived from class extrapolation and community consensus.**

### Dependence Liability

No published evidence of physiological dependence formation for 2C-T-2. The seed data notation ("not habit-forming") is consistent with the lack of dopaminergic reward circuit involvement (2C-T-2 does not interact with DAT, [Ref 1]) and with general psychedelic class characteristics.

---

## Interactions

| Interaction | Severity | Mechanism | Source |
|---|---|---|---|
| MAO inhibitors | CONTRAINDICATED | 2C-T-2 is a MAO-A/B substrate; MAOIs reduce clearance → elevated plasma levels, serotonin syndrome risk | [Ref 12] |
| SSRIs/SNRIs | High risk | Pharmacodynamic serotonergic synergy → serotonin syndrome | Class inference [Ref 7, 13] |
| Triptans | High risk | Serotonergic synergy | Class inference [Ref 13] |
| Lithium | High risk | Increased seizure risk (anecdotal/class) | Community report; no published 2C-T-2 data |
| CYP2D6 inhibitors | Moderate | Reduced metabolic clearance (minor) | [Ref 12] |
| Cannabis | Unknown | Unpredictable synergistic effects; increased anxiety/psychosis risk | Class inference; no 2C-T-2 specific data |
| CNS depressants | Moderate | Masking of hyperthermia; respiratory depression | [Ref 7] |

---

## Legal Status

| Jurisdiction | Status | Effective Date | Notes |
|---|---|---|---|
| United States | Schedule I | 2012 | FDASIA; DEA code 7385 [Ref 23] |
| European Union | Controlled | 2003 | Council Decision 2003/847/JHA; member states implement individually [Ref 22] |
| United Kingdom | Class A | 2003 (EU decision adopted into UK law) | Misuse of Drugs Act |
| Australia | Schedule 9 (Prohibited Substance) | 2005 | Poisons Standard |
| Canada | Schedule III (CDSA) | October 31, 2016 | Item 35 |
| Japan | Designated substance | 2008 | |

**Analog Act (US, pre-2012):** Before explicit scheduling in 2012, 2C-T-2 could be subject to prosecution under the Federal Analogue Act if intended for human consumption, given structural and pharmacological similarity to Schedule I substances.

---

## Clinical Trials

**No clinical trials registered on ClinicalTrials.gov for 2C-T-2.** Search returned zero results. No published clinical pharmacology studies exist. 2C-T-2 is not being developed as a therapeutic agent by any known registered entity.

---

## Community Feedback Analysis

No community feedback was submitted in Part A2 of the brief. No feedback analysis required.

---

## Gaps & Flags

### Safety-Critical Values

1. **⚠️ MAO INHIBITOR CLASSIFICATION (HIGH PRIORITY):** The brief's seed data classifies 2C-T-2 as a "Monoamine oxidase inhibitor." This is incorrect based on published evidence. 2C-T-2 is a MAO **substrate** metabolized by MAO-A and MAO-B (Theobald & Maurer 2007 [Ref 12]). Some 2C compounds may show weak in vitro MAO inhibition at high concentrations (Wagmann et al. 2019 [Ref 11]), but this is pharmacologically minor compared to 5-HT₂A agonism. The correct pharmacological class is: 5-HT₂A receptor agonist, 5-HT₂C receptor agonist, TAAR1 agonist. This error should be corrected in the database — it has clinical significance because MAO inhibitors are a contraindication for 2C-T-2 use (not the reverse).

2. **⚠️ DOSE VALUES UNVERIFIED BY PUBLISHED CONTROLLED STUDIES:** All dose and duration values in the seed data are user-report-based (community surveys) or derived from Shulgin's self-experimentation. No clinical pharmacology study has established these values under controlled conditions. The oral active dose range from PiHKAL (12–25 mg) is broadly consistent with the seed data but not identical. The threshold dose of 3 mg oral has no published backing. The insufflated dose values are user-report only.

3. **⚠️ NO PUBLISHED HUMAN PHARMACOKINETICS:** Half-life, bioavailability, Tmax, and Cmax are all unknown for humans. The "half-life 3 days" tolerance data in the brief refers to tolerance buildup half-life (receptor downregulation), not elimination half-life — but this distinction should be made explicit.

4. **⚠️ SPECIFIC KI VALUES (APPROX.):** The specific Ki values for 2C-T-2 at 5-HT₂A (12.5 nM) and 5-HT₂C (14.2 nM) cited above were retrieved from a web-compiled source (Grokipedia [Ref 23]) that appears to draw from the Luethi 2018 [Ref 1] and Eshleman 2014 [Ref 3] papers. These values should be confirmed against the published tables in those papers before being presented as definitive.

### Data Gaps

- **No published human pharmacokinetic studies** for 2C-T-2
- **No controlled clinical studies** of any kind for 2C-T-2 in humans
- **No published LD₅₀ data** in any species for 2C-T-2
- **No confirmed fatal 2C-T-2 overdose case reports** in the published literature (class data only)
- **No published MAOI interaction case reports** specific to 2C-T-2
- **SMILES string not returned** by PubChem API (InChIKey confirmed; SMILES can be derived from IUPAC name)
- **Physical properties** (melting point, aqueous solubility, pKa) not found in searched literature
- **Stereochemistry:** 2C-T-2 has no chiral center; the phenethylamine backbone is achiral. No stereochemistry concerns.
- **Insufflated pharmacokinetics:** The brief lists insufflated as "primary ROA." No published pharmacokinetic or safety data exist for this route of administration. Insufflated use is user-report-based only.
- **UK and Australia scheduling exact dates:** Approximate from EU decision (2003) and Australian Poisons Standard (2005) but precise national implementation dates not confirmed in published sources.
- **Canada pre-2016:** Legal status before October 31, 2016 not confirmed in detail.

### Structural Analogy Reliance

- Tolerance buildup timeline (half-life 3 days, full reset 7 days) is inferred from psychedelic class pharmacology (5-HT₂A receptor downregulation kinetics), not 2C-T-2-specific data
- Serotonin syndrome risk from lithium combination is class inference
- Cardiovascular effects (vasoconstriction, abnormal heartbeat, pupil dilation) in the effects taxonomy are consistent with 5-HT₂A/sympathomimetic effects of phenethylamine psychedelics but not verified in published human case studies for 2C-T-2 specifically

### Substance-Specific Notable Findings

- 2C-T-2 is a **TAAR1 agonist** (rat TAAR1, Ki 5–68 nM class range; does NOT interact with human TAAR1) — this receptor interaction is notable given emerging interest in TAAR1 pharmacology
- The EU Council Decision 2003/847/JHA specifically and uniquely singled out 2C-T-2 alongside 2C-T-7, 2C-I, and TMA-2 — suggesting these four compounds were the highest-priority phenethylamines for EU regulators at that time
- Shulgin's "magical half-dozen" designation is notable for historical framing but is a personal/subjective assessment, not a formal pharmacological rating

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