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Buy 2C-T-2 Cas 207740-24-7

Buy 2C-T-2 Cas 207740-24-7

2C-T-2, also known as 4-ethylthio-2,5-dimethoxyphenethylamine, is a psychedelic drug of the phenethylamine and 2C families.[1][2][3] It is taken orally.[1]

The drug acts as a serotonin 5-HT2 receptor agonist, including of the serotonin 5-HT2A receptor.[4][5][6][7]

2C-T-2 was discovered by Alexander Shulgin in 1981 and was first described in the scientific literature by Myron Stolaroff in 1990.[8][9][10][1]

Use and effects

In his book PiHKAL (Phenethylamines I Have Known and Loved), Alexander Shulgin lists 2C-T-2’s dose as 12 to 25 mg orally and its duration as 6 to 8 hours.[1] Its onset is within 1 hour and peak effects occur after 1 to 2 hours.[1] The effects of 2C-T-2 have been described.[1] Shulgin rated it as one of the “magical half-dozen” most important psychedelic phenethylamines, along with mescaline2C-B2C-T-7, and others.[1]

Toxicity

A potential risk of neurotoxicity from 2C-T-2 use (and 2C chemical series in general) has been shown in serotonergic and dopaminergic neurons, however the assay used concentrations unlikely to translate to recreational use of the compound (>50 μM). This has also been shown to be magnified in serotonergic-containing cells with combined use of 2C series drugs with alcohol, MDMA, and methamphetamine.[11]

Severe ‘intoxication’ on 2C series drugs has been observed as behavior that includes: intense hallucinations, agitation, aggression, violence, dysphoriahypertensiontachycardiaseizures, and hyperthermia.[12]

Interactions

2C-T-2 is metabolized by the monoamine oxidase (MAO) enzymes MAO-A and MAO-B.[12][13] Monoamine oxidase inhibitors (MAOIs) such as phenelzinetranylcyprominemoclobemide, and selegiline may potentiate the effects of 2C-T-2.[12][13][14] This may result in overdose and serious toxicity.[14][12]

Pharmacology

Pharmacodynamics

2C-T-2 activities
Target Affinity (Ki, nM)
5-HT1A 370–1,740 (Ki)
3,000 (EC50Tooltip half-maximal effective concentration)
76% (EmaxTooltip maximal efficacy)
5-HT1B 858
5-HT1D 86
5-HT1E 415
5-HT1F ND
5-HT2A 9–40 (Ki)
0.354–80 (EC50)
67–107% (Emax)
5-HT2B 6–69 (Ki)
130 (EC50)
75% (Emax)
5-HT2C 14–54 (Ki)
0.0233–3.8 (EC50)
87–107% (Emax)
5-HT3 >10,000
5-HT4 ND
5-HT5A >10,000
5-HT6 1,362
5-HT7 969
α1A 17,000
α1B >10,000
α1D ND
α2A 230–730
α2B 982
α2C 166
β1 9,202
β2 1,184
β3 ND
D1 15,000
D2 2,795–5,100
D3 1,835–11,000
D4 >10,000
D5 >10,000
H1H4 >10,000
M1 >10,000
M2 >10,000
M3 692
M4 >10,000
M5 1,502
I1 2,080
σ1 3,870
σ2 >10,000
TAAR1Tooltip Trace amine-associated receptor 1 2,200 (Ki) (mouse)
40 (Ki) (rat)
96 (EC50) (mouse)
4,300 (EC50) (rat)
>10,000 (EC50) (human)
54% (Emax) (mouse)
86% (Emax) (rat)
SERTTooltip Serotonin transporter 13,000 (Ki)
62,000 (IC50Tooltip half-maximal inhibitory concentration)
IA (EC50)
NETTooltip Norepinephrine transporter >30,000 (Ki)
153,000 (IC50)
IA (EC50)
DATTooltip Dopamine transporter >30,000 (Ki)
332,000 (IC50)
IA (EC50)
MAO-ATooltip Monoamine oxidase A ND (IC50)
MAO-BTooltip Monoamine oxidase B ND (IC50)
Notes: The smaller the value, the more avidly the drug binds to the site. All proteins are human unless otherwise specified. Refs: [15][4][5][6][7][16][17]

2C-T-2 acts as a serotonin 5-HT2 receptor agonist, including of the serotonin 5-HT2A and 5-HT2C receptors.[4][5][6][7] The mechanism of action that produces 2C-T-2’s hallucinogenic effects is shown to be most likely a result from action as a serotonin 5-HT2A5-HT2B, and 5-HT2C serotonin receptor agonist,[5] a mechanism of action shared by the psychedelic tryptamines and phenethylamines to varying degrees.[6][18] 2C-T-2 has also shown to be a partial agonist of adrenergic receptors.[19]

Chemistry

Synthesis

The chemical synthesis of 2C-T-2 has been described.[1][2]

Analogues

Analogues of 2C-T-2 include 2C-T (2C-T-1), 2C-T-42C-T-7Aleph-2, and 25T2-NBOMe, among others.[1][2]

History

2C-T-2 was first synthesized by Alexander Shulgin in 1981.[8] He discovered its psychedelic effects that same year.[20] The drug was first described in the scientific literature by Myron Stolaroff in 1990.[9] Subsequently, it was described in greater detail in a 1991 publication by Shulgin and colleagues[10] and in his 1991 book PiHKAL (Phenethylamines I Have Known and Loved).[1] Following this, 2C-T-2 emerged as a novel designer drug in the 1990s.[8]

Society and culture

Argentina

2C-T-2 is also a controlled substance in Argentina as well as 2C-B and 2C-I.[21]

Australia

2C-T-2 is considered a Schedule 9 prohibited substance in Australia under the Poisons Standard (October 2015).[22] A Schedule 9 substance is a substance which may be abused or misused, the manufacture, possession, sale or use of which should be prohibited by law except when required for medical or scientific research, or for analytical, teaching or training purposes with approval of Commonwealth and/or State or Territory Health Authorities.[22]

Canada

As of October 31, 2016, 2C-T-2 is a controlled substance (Schedule III) in Canada.[23]

China

As of October 2015 2C-T-2 is a controlled substance in China.[24]

Finland

2C-T-2 is classified as a narcotic drug in Finland.[25]

Netherlands

The Netherlands became the first country in the world to ban 2C-T-2, and classify it as a hard drug, by law. In April, 1999, 2C-T-2 became a list I drug of the Opium Law.

Sweden

Schedule I in Sweden. 2C-T-2 was first classified as “health hazard” under the act Lagen om förbud mot vissa hälsofarliga varor (translated Act on the Prohibition of Certain Goods Dangerous to Health) as of April 1, 1999, under SFS 1999:58[26] that made it illegal to sell or possess. The Riksdag added 2C-T-2 to Narcotic Drugs Punishments Act under Swedish schedule I (“substances, plant materials and fungi which normally do not have medical use”) as of March 16, 2004, published by Medical Products Agency (MPA) in regulation LVFS 2004:3 listed as 2C-T-2, 2,5-dimetoxi-4-etyltiofenetylamin.[27]

United Kingdom

2C-T-2 and all other compounds featured in PiHKAL are illegal drugs in the United Kingdom.

United States

2C-T-2 is specifically listed as a schedule I substance under SEC. 1152 of S.3187: Food and Drug Administration Safety and Innovation Act of 2012.[28]

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