2C-I
Pharmaceutical compound
From Wikipedia, the free encyclopedia
2C-I, also known as 4-iodo-2,5-dimethoxyphenethylamine, is a psychedelic drug of the phenethylamine and 2C families.[1][3][2][4] It is taken orally.[1][2]
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| Other names | 4-Iodo-2,5-dimethoxyphenethylamine; 2,5-Dimethoxy-4-iodophenethylamine; 25I; Cimbi-88; 2C-DOI |
| Routes of administration | Oral[1][2] |
| Drug class | Serotonin 5-HT2 receptor agonist; Serotonin 5-HT2A receptor agonist; Serotonergic psychedelic; Hallucinogen |
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| Pharmacokinetic data | |
| Onset of action | ≤40 minutes[1] |
| Duration of action | 6–10 hours[1][2] |
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| ECHA InfoCard | 100.217.507 |
| Chemical and physical data | |
| Formula | C10H14INO2 |
| Molar mass | 307.131 g·mol−1 |
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| Melting point | 246 °C (475 °F) |
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2C-I was first synthesized and described by Alexander Shulgin in 1977[5][6] and was described in further detail in his 1991 book PiHKAL (Phenethylamines I Have Known and Loved).[1] The drug is used recreationally. 2C-I is sometimes confused with other related psychedelic drugs such as 25I-NBOMe (NBOMe-2C-I), nicknamed "Smiles" and "N-bomb" in the media.[7][8][9]
Use and effects
In his book PiHKAL (Phenethylamines I Have Known and Loved), Alexander Shulgin lists 2C-I's dose as 14 to 22 mg orally and its duration as 6 to 10 hours.[1][2] Its onset is within 40 minutes and peak effects occur after about 2 hours.[1] In addition to oral administration, 2C-I may also be insufflated.[10] The effects of 2C-I have been reported to include color enhancement, psychedelic visuals, emotional enhancement, limited insights, increased energy, enhanced conversation and honesty, improved mood, and sensual immersion.[1] The sensual effects of 2C-I were described as different from and possibly less than those of 2C-B.[1]
Interactions
2C-I is metabolized by the monoamine oxidase (MAO) enzymes MAO-A and MAO-B.[2][11] Monoamine oxidase inhibitors (MAOIs) such as phenelzine, tranylcypromine, moclobemide, and selegiline may potentiate the effects of 2C-I.[2][11][12] This may result in overdose and serious toxicity.[12][2]
Pharmacology
Pharmacodynamics
| Target | Affinity (Ki, nM) |
|---|---|
| 5-HT1A | 107–970 (Ki) 4,900 (EC50) 102% (Emax) |
| 5-HT1B | 56 |
| 5-HT1D | 40 |
| 5-HT1E | 131 |
| 5-HT1F | ND |
| 5-HT2A | 3.5–9.3 (Ki) 1.48–513 (EC50) 17–93% (Emax) |
| 5-HT2B | 9.3 (Ki) 19.1–150 (EC50) 70–101% (Emax) |
| 5-HT2C | 9.3–40 (Ki) 0.46–537 (EC50) 44–107% (Emax) |
| 5-HT3 | >10,000 |
| 5-HT4 | ND |
| 5-HT5A | >10,000 |
| 5-HT6 | ND |
| 5-HT7 | 1,316 |
| α1A | 5,100–>10,000 |
| α1B | >10,000 |
| α1D | >10,000 |
| α2A | 70–305 |
| α2B | 608 |
| α2C | 315 |
| β1 | 4,512 |
| β2 | >10,000 |
| β3 | ND |
| D1 | 13,000 |
| D2 | 1,013–2,700 |
| D3 | 989–5,000 |
| D4 | 2,788 |
| D5 | >10,000 |
| H1 | 6,100 |
| H2 | >10,000 |
| H3 | >10,000 |
| M1 | >10,000 |
| M2 | 1,429 |
| M3 | 950 |
| M4 | 1,129 |
| M5 | 2,151 |
| I1 | ND |
| σ1 | >10,000 |
| σ2 | 5,470 |
| MOR | 2,522 |
| DOR | ND |
| KOR | >10,000 |
| TAAR1 | 3,300 (Ki) (mouse) 120 (Ki) (rat) 2,400 (EC50) (mouse) 190 (EC50) (rat) >10,000 (EC50) (human) 51% (Emax) (mouse) 50% (Emax) (rat) |
| SERT | 950–4,900 (Ki) 5,600–13,000 (IC50) IA (EC50) |
| NET | 15,000 (Ki) 22,000 (IC50) IA (EC50) |
| DAT | >30,000 (Ki) 126,000 (IC50) IA (EC50) |
| MAO-A | 125,000 (IC50) |
| MAO-B | 55,000 (IC50) |
| Notes: The smaller the value, the more avidly the drug binds to the site. All proteins are human unless otherwise specified. Refs: [13][14][15][16][17][18] [19][20][21][22][23][24] | |
2C-I acts as a serotonin receptor agonist. It produces psychedelic effects via serotonin 5-HT2A receptor activation.
It is inactive as a monoamine releasing agent and shows negligible activity as a monoamine reuptake inhibitor.[15][14]
2C-I is a highly potent anti-inflammatory drug similarly to various other serotonergic psychedelics.[22] However, 2C-I showed the highest anti-inflammatory potency of any other assessed drug in a large series in one study.[22] It was more potent than (R)-DOI in terms of anti-inflammatory activity.[22]
Chemistry
History
2C-I was first described in the scientific literature by Alexander Shulgin and colleagues in 1977.[5][6] Its properties and effects in humans were described by Shulgin in 1978.[5] The drug was subsequently described in greater detail by Shulgin in his 1991 book PiHKAL (Phenethylamines I Have Known and Loved).[1] In the early 2000s, 2C-I was sold in Dutch smart shops as a recreational drug after the related drug 2C-B was banned.[27]
Society and culture
Legal status
Australia
2C-I is a schedule 9 prohibited substance in Australia under the Poisons Standard (October 2015).[28] A schedule 9 drug is outlined in the Poisons Act 1964 as "Substances 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 the CEO".[29]
Canada
As of October 31, 2016, 2C-I is a controlled substance (Schedule III) in Canada.[30]
European Union
In December 2003, the European Council issued a binding order compelling all European Union member states to ban 2C-I within three months.[31]
Finland
Illegal: scheduled in the "government decree on substances, preparations and plants considered to be narcotic drugs".[32]
Sweden
Sveriges riksdag added 2C-I to schedule I ("substances, plant materials and fungi which normally do not have medical use") as a narcotic on March 16, 2004, published by the Medical Products Agency in their regulation LVFS 2004:3.[33]
United Kingdom
In the United Kingdom,2C-I is controlled as a Class A substance.[31]
United States
As of July 9, 2012, in the United States 2C-I is a Schedule I substance under the Synthetic Drug Abuse Prevention Act of 2012, making possession, distribution and manufacture illegal.[31] A previous bill, introduced in March 2011, that would have done the same passed the House of Representatives, but was not passed by the Senate.[34]