2C-C
2C-C, also known as 4-chloro-2,5-dimethoxyphenethylamine, is a psychedelic drug of the phenethylamine and 2C families. It is taken orally.
2C-C was first described in the scientific literature by Alice Cheng and Neal Castagnoli in 1984. It was described in greater detail by Alexander Shulgin in his 1991 book PiHKAL. The drug is Schedule I of section 202 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.
Use and effects
In his book PiHKAL, Alexander Shulgin lists 2C-C's dose range as 20 to 40mg orally and its duration as 4 to 8hours. Its onset is described as delayed compared to 2C-B and as being 1.5 to 2hours. In addition to oral administration, a single report of 20mg by intravenous injection was described as overwhelming, with effects peaking after 5minutes and lasting perhaps 15minutes. The effects of 2C-C have been reported to include psychedelic visuals, sensual enhancement, stimulation, sedation, and relaxation, among others. Its stimulating effects are said to be less than those of 2C-B and it is said to be sedating in some ways.Interactions
2C drugs like 2C-C are known to be metabolized by the monoamine oxidase enzymes MAO-A and MAO-B. Monoamine oxidase inhibitors such as phenelzine, tranylcypromine, moclobemide, and selegiline may potentiate the effects of 2C drugs like 2C-C. This may result in overdose and serious toxicity.Pharmacology
Pharmacodynamics
2C-C acts as an agonist of the serotonin 5-HT2 receptors. It also binds to the serotonin 5-HT1A receptor with 15-fold lower affinity than for the serotonin 5-HT2A receptor. The drug shows little or no affinity for the monoamine transporters and shows very weak or negligible monoamine reuptake inhibition. It shows high affinity for the rat trace amine-associated receptor 1, but only weak affinity for the mouse TAAR1.In contrast to many other psychedelics, 2C-C, as well as 2C-P and certain 2C NBOMe analogues, has shown reinforcing effects in rodents. It produces dose-dependent conditioned place preference in mice and self-administration in rats. These findings suggest that 2C-C may have misuse potential. The mechanism by which these effects are produced is unknown. However, 2C-C was found to decrease dopamine transporter expression and to increase DAT phosphorylation in the nucleus accumbens and medial prefrontal cortex similarly to methamphetamine in rodents. 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.
2C-C has also been found to produce neurotoxicity at high doses in rodents, which appears to be mediated via neuroinflammation.