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2C-C

Pharmaceutical compound From Wikipedia, the free encyclopedia

2C-C
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2C-C is a psychedelic drug of the 2C family. It was first synthesized by Alexander Shulgin, sometimes used as an entheogen. In his book PiHKAL (Phenethylamines i Have Known And Loved), Shulgin lists the dosage range as 20–40 mg. 2C-C is usually taken orally, but may also be insufflated.[1] 2C-C is schedule I of section 202(c) of the Controlled Substances Act in the United States, signed into law as of July, 2012 under the Food and Drug Administration Safety and Innovation Act.[2]

Quick Facts Clinical data, Other names ...

Not much information is known about the toxicity of 2C-C.

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Effects

Over the approximate dose range 20–40 mg, visual effects last approximately 4 to 8 hours.[1]

Interactions

2C drugs like 2C-C are known to be metabolized by the monoamine oxidase (MAO) enzymes MAO-A and MAO-B.[3][4] Monoamine oxidase inhibitors (MAOIs) such as phenelzine, tranylcypromine, moclobemide, and selegiline may potentiate the effects of 2C drugs like 2C-C.[3][4][5] This may result in overdose and serious toxicity.[5][3]

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Pharmacology

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More information Target, Affinity (Ki, nM) ...

2C-C acts as an agonist of the serotonin 5-HT2 receptors.[14][8] It also binds to the serotonin 5-HT1A receptor with 15-fold lower affinity than for the serotonin 5-HT2A receptor.[14][8] The drug shows little or no affinity for the monoamine transporters (MATs) and shows very weak or negligible monoamine reuptake inhibition.[8][15] It shows high affinity for the rat trace amine-associated receptor 1 (TAAR1), but only weak affinity for the mouse TAAR1.[14][8]

In contrast to many other psychedelics, 2C-C, as well as 2C-P and certain 2C NBOMe analogues, has shown reinforcing effects in rodents.[14][15] It produces dose-dependent conditioned place preference (CPP) in mice and self-administration in rats.[14][15] These findings suggest that 2C-C may have misuse potential.[14][15] The mechanism by which these effects are produced is unknown.[15] However, 2C-C was found to decrease dopamine transporter (DAT) expression and to increase DAT phosphorylation in the nucleus accumbens and medial prefrontal cortex (mPFC) similarly to methamphetamine in rodents.[14][15] Decreased DAT expression may result in reduced dopamine reuptake, while DAT phosphorylation is associated with dopamine reverse transport and efflux, in turn increasing extracellular dopamine levels.[14][15]

2C-C has also been found to produce neurotoxicity at high doses in rodents, which appears to be mediated via neuroinflammation.[15]

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Chemistry

Analogues and derivatives

Analogues and derivatives of 2C-C:

25C-NB*:

N-(2C)-fentanyl:

  • N-(2C-C)-fentanyl[16]

Society and culture

China

As of October 2015 2C-C is a controlled substance in China.[17]

Canada

As of October 31, 2016; 2C-C is a controlled substance (Schedule III) in Canada.[18]

Germany

2C-C is an Anlage I controlled drug.

Sweden

Sveriges riksdags health ministry Statens folkhälsoinstitut classified 2C-C 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 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.[19]

United States

As of July 9, 2012, in the United States 2C-C is a Schedule I substance under the Food and Drug Administration Safety and Innovation Act of 2012, making possession, distribution and manufacture illegal.[20]

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See also

References

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