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| Other names | 2,5-Dimethoxy-4-chlorophenethylamine; 4-Chloro-2,5-dimethoxyphenethylamine |
| Routes of administration | Oral[1] |
| Drug class | Serotonin5-HT2 receptoragonist;Serotonergic psychedelic;Hallucinogen |
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| Pharmacokinetic data | |
| Onset of action | 1.5–2 hours[1] |
| Duration of action | 4–8 hours[1] |
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| CompTox Dashboard(EPA) | |
| ECHA InfoCard | 100.218.153 |
| Chemical and physical data | |
| Formula | C10H14ClNO2 |
| Molar mass | 215.68 g·mol−1 |
| 3D model (JSmol) | |
| Melting point | 220 to 221 °C (428 to 430 °F) (hydrochloride) |
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2C-C, also known as4-chloro-2,5-dimethoxyphenethylamine, is apsychedelic drug of thephenethylamine and2C families.[1] It is takenorally.[1]
2C-C was first described in thescientific literature by Alice Cheng and Neal Castagnoli in 1984.[2] It was described in greater detail byAlexander Shulgin in his 1991 bookPiHKAL (Phenethylamines I Have Known and Loved).[1] The drug isSchedule I of section 202(c) of theControlled Substances Act in theUnited States, signed into law as of July 2012 under theFood and Drug Administration Safety and Innovation Act.[3]
In his bookPiHKAL (Phenethylamines I Have Known and Loved),Alexander Shulgin lists 2C-C's dose range as 20 to 40 mgorally and itsduration as 4 to 8 hours.[1] Itsonset is described as delayed compared to2C-B and as being 1.5 to 2 hours.[1] In addition to oral administration, a single report of 20 mg byintravenous injection was described as overwhelming, with effects peaking after 5 minutes and lasting perhaps 15 minutes.[1] The effects of 2C-C have been reported to includepsychedelic visuals, sensual enhancement,stimulation,sedation, andrelaxation, among others.[1] Its stimulating effects are said to be less than those of 2C-B and it is said to be sedating in some ways.[1]
2C drugs like 2C-C are known to bemetabolized by themonoamine oxidase (MAO)enzymesMAO-A andMAO-B.[4][5]Monoamine oxidase inhibitors (MAOIs) such asphenelzine,tranylcypromine,moclobemide, andselegiline may potentiate the effects of 2C drugs like 2C-C.[4][5][6] This may result inoverdose and serioustoxicity.[6][4]
| Target | Affinity (Ki, nM) |
|---|---|
| 5-HT1A | 190–740 (Ki) >10,000 (EC50Tooltip half-maximal effective concentration) <25% (EmaxTooltip maximal efficacy) |
| 5-HT1B | ND |
| 5-HT1D | ND |
| 5-HT1E | ND |
| 5-HT1F | ND |
| 5-HT2A | 5.47–13 (Ki) 9.27–200 (EC50) 49–102% (Emax) |
| 5-HT2B | ND (Ki) 280 (EC50) 81% (Emax) |
| 5-HT2C | 5.4–90 (Ki) 24.2 (EC50) 94% (Emax) |
| 5-HT3 | ND |
| 5-HT4 | ND |
| 5-HT5A | ND |
| 5-HT6 | ND |
| 5-HT7 | ND |
| α1A | 13,000 |
| α1B,α1D | ND |
| α2A | 530 |
| α2B,α2C | ND |
| β1–β3 | ND |
| D1 | 13,000 |
| D2 | 2,100 |
| D3 | 17,000 |
| D4 | ND |
| D5 | ND |
| H1 | 14,000 |
| H2–H4 | ND |
| M1–M5 | ND |
| I1 | ND |
| σ1,σ2 | ND |
| TAAR1Tooltip Trace amine-associated receptor 1 | 4,100 (Ki) (mouse) 110 (Ki) (rat) 2,300 (EC50) (mouse) 340 (EC50) (rat) >10,000 (EC50) (human) 57% (Emax) (mouse) 51% (Emax) (rat) |
| SERTTooltip Serotonin transporter | 24,000 (Ki) 72,000–74,000 (IC50Tooltip half-maximal inhibitory concentration) >100,000 (EC50) (rat) |
| NETTooltip Norepinephrine transporter | >30,000 (Ki) 63,000–93,000 (IC50) 100,000 (EC50) (rat) |
| DATTooltip Dopamine transporter | >30,000 (Ki) 305,000 (IC50) >100,000 (EC50) (rat) |
| 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:[7][8][9][10][11][12][13][14] | |
2C-C acts as anagonist of theserotonin5-HT2 receptors.[15][9] It also binds to the serotonin5-HT1A receptor with 15-fold loweraffinity than for the serotonin5-HT2A receptor.[15][9] The drug shows little or no affinity for themonoamine transporters (MATs) and shows very weak or negligiblemonoamine reuptake inhibition.[9][16] It shows high affinity for the rattrace amine-associated receptor 1 (TAAR1), but only weak affinity for the mouse TAAR1.[15][9]
In contrast to many other psychedelics, 2C-C, as well as2C-P and certain 2CNBOMeanalogues, has shownreinforcing effects in rodents.[15][16] It producesdose-dependentconditioned place preference (CPP) in mice andself-administration in rats.[15][16] These findings suggest that 2C-C may havemisuse potential.[15][16] Themechanism by which these effects are produced is unknown.[16] However, 2C-C was found to decreasedopamine transporter (DAT)expression and to increase DATphosphorylation in thenucleus accumbens andmedial prefrontal cortex (mPFC) similarly tomethamphetamine in rodents.[15][16] Decreased DAT expression may result in reduceddopaminereuptake, while DAT phosphorylation is associated with dopaminereverse transport andefflux, in turn increasingextracellular dopamine levels.[15][16]
2C-C has also been found to produceneurotoxicity at high doses in rodents, which appears to be mediated vianeuroinflammation.[16]
Thechemical synthesis of 2C-C has been described.[1]
Analogues of 2C-C include2C-B,2C-I,DOC, and25C-NBOMe, among others.[1][17]
2C-C was first described in thescientific literature by Alice Cheng and Neal Castagnoli in 1984.[2] It was described in greater detail, including its properties and effects in humans, byAlexander Shulgin in his 1991 bookPiHKAL (Phenethylamines I Have Known and Loved).[1]
As of October 2015 2C-C is a controlled substance in China.[18]
As of October 31, 2016; 2C-C is a controlled substance (Schedule III) in Canada.[19]
Scheduled in the "government decree on psychoactive substances banned from the consumer market".[20]
2C-C is anAnlage I controlled drug.
Sveriges riksdags health ministryStatens folkhälsoinstitut classified 2C-C as "health hazard" under the actLagen om förbud mot vissa hälsofarliga varor (translatedAct on the Prohibition of Certain Goods Dangerous to Health) as of Mar 1, 2005, in their regulation SFS 2005:26 listed as 2,5-dimetoxi-4-klorfenetylamin (2C-C), making it illegal to sell or possess.[21]
As of July 9, 2012, in theUnited States 2C-C is aSchedule I substance under theFood and Drug Administration Safety and Innovation Act of 2012, making possession, distribution and manufacture illegal.[22]
