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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 | Serotonin5-HT2 receptoragonist;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 |
| 3D model (JSmol) | |
| Melting point | 246 °C (475 °F) |
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2C-I, also known as4-iodo-2,5-dimethoxyphenethylamine, is apsychedelic drug of thephenethylamine and2C families.[1][3][2][4] It is takenorally.[1][2]
2C-I was firstsynthesized and described byAlexander Shulgin in 1977[5][6] and was described in further detail in his 1991 bookPiHKAL (Phenethylamines I Have Known and Loved).[1] The drug is usedrecreationally. 2C-I is sometimes confused with other related psychedelic drugs such as25I-NBOMe (NBOMe-2C-I), nicknamed "Smiles" and "N-bomb" in the media.[7][8][9]
According toAlexander Shulgin in his bookPiHKAL (Phenethylamines I Have Known and Loved), 2C-I has a dose range of 14 to 22 mgorally and aduration of 6 to 10 hours.[1][2] Itsonset is within 40 minutes and peak effects occur after about 2 hours.[1] In addition to oral administration, 2C-I may also beinsufflated.[10] The effects of 2C-I have been reported to include color enhancement,psychedelic visuals,emotional enhancement, limitedinsights, increasedenergy, enhanced conversation andhonesty,improved mood, and sensual immersion.[1] The sensual effects of 2C-I were described as different from and possibly less than those of2C-B.[1]
2C-I ismetabolized by themonoamine oxidase (MAO)enzymesMAO-A andMAO-B.[2][11]Monoamine oxidase inhibitors (MAOIs) such asphenelzine,tranylcypromine,moclobemide, andselegiline may potentiate the effects of 2C-I.[2][11][12] This may result inoverdose and serioustoxicity.[12][2]
| Target | Affinity (Ki, nM) |
|---|---|
| 5-HT1A | 107–970 (Ki) 4,900 (EC50Tooltip half-maximal effective concentration) 102% (EmaxTooltip maximal efficacy) |
| 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 |
| TAAR1Tooltip Trace amine-associated receptor 1 | 3,300 (Ki) (mouse) 120 (Ki) (rat) 2,400 (EC50) (mouse) 190 (EC50) (rat) >10,000 (EC50) (human) 51% (Emax) (mouse) 50% (Emax) (rat) |
| SERTTooltip Serotonin transporter | 950–4,900 (Ki) 5,600–13,000 (IC50Tooltip half-maximal inhibitory concentration) IA (EC50) |
| NETTooltip Norepinephrine transporter | 15,000 (Ki) 22,000 (IC50) IA (EC50) |
| DATTooltip Dopamine transporter | >30,000 (Ki) 126,000 (IC50) IA (EC50) |
| MAO-ATooltip Monoamine oxidase A | 125,000 (IC50) |
| MAO-BTooltip Monoamine oxidase 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 aserotonin receptoragonist. It producespsychedelic effects via serotonin5-HT2A receptor activation.
It is inactive as amonoamine releasing agent and shows negligible activity as amonoamine reuptake inhibitor.[15][14]
2C-I is a highly potentanti-inflammatory drug similarly to various otherserotonergic psychedelics.[22] However, 2C-I showed the highest anti-inflammatorypotency 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]
Thechemical synthesis of 2C-I has been described.[1][25]
Analogues of 2C-I include2C-H (2,5-DMPEA),2C-B,2C-C,DOI, and25I-NBOMe, among others.[1][26][3]
2C-I was first described in thescientific literature byAlexander 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 bookPiHKAL (Phenethylamines I Have Known and Loved).[1] In the early 2000s, 2C-I was sold inDutchsmart shops as arecreational drug after the related drug2C-B was banned.[27]
2C-I is a schedule 9 prohibited substance in Australia under thePoisons 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]
As of October 31, 2016, 2C-I is a controlled substance (Schedule III) in Canada.[30]
In December 2003, theEuropean Council issued a binding order compelling allEuropean Union member states to ban 2C-I within three months.[31]
Illegal: scheduled in the "government decree on substances, preparations and plants considered to be narcotic drugs".[32]
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 theMedical Products Agency in their regulation LVFS 2004:3.[33]
In the United Kingdom, 2C-I is controlled as aClass A substance.[31]
As of July 9, 2012, in theUnited States 2C-I is aSchedule I substance under theSynthetic 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]
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