Detail:

        2C-B or 2,5-dimethoxy-4-bromophenethylamine is a psychedelic drug of the 2C family. It was first synthesized by Alexander Shulgin in 1974. In Shulgin's book PiHKAL, the dosage range is listed as 12–24 mg. 2C-B is sold as a white powder sometimes pressed in tablets or gel caps and is also referred to by a number of other names. The drug is usually taken orally, but can also be insufflated or vaporized.

History:

        2C-B was synthesized from 2,5-dimethoxybenzaldehyde by Alexander Shulgin in 1974. It first saw use among the psychiatric community as an aid during therapy. It was considered one of the best drugs for this purpose because of its short duration, relative absence of side effects, and comparably mild nature. Shortly after becoming popular in the medical community, it became popular recreationally. 2C-B was first sold commercially as an aphrodisiac under the trade name "Erox", which was manufactured by the German pharmaceutical company Drittewelle. For several years, it was available as tablets in Dutch smart shops under the name "Nexus".

Patterns of use:

        2C-B first became popularized in the United States as a short-lived legal substitute for the street drug Ecstasy when MDMA became illegal in 1985. Many 2C-B users are young adults who attend raves. Though 2C-B is still used in the rave subculture, commonly mistaken for and/or sold as Ecstasy, its intentional use has become more common. In recent years, 2C-B has emerged as the drug of choice for club drug users in Colombia.

        Street prices range between $10 and $30 per tablet in the United States in 2011 when bought in small quantities. Larger retail purchases cost between $200 and $500 per gram. Wholesale purchases of 2C-B can lower the price ($100 to $300 per gram in 2001.

Duration:

        When orally consumed, 2C-B has a much longer delay before the onset of effects than when it is insufflated. Oral ingestion generally takes roughly 45–75 minutes for the effects to be felt, plateau lasts 2–4 hours, and coming down lasts 1–2 hours. Rectal administration ("boofing") onset varies from 5–20 minutes. Insufflated onset takes 1–10 minutes for effects to be felt. The duration can last from 4 to 12 hours depending on ROA, dose, and other factors.

        With insufflation the effects are more abrupt and intense but have a significantly shorter duration, while oral usage results in a milder, longer experience. When insufflated, the onset happens very rapidly, usually reaching the peak at about 20–40 minutes and plateauing for 2–3 hours. 2C-B is also considered one of the most painful drugs to insufflate, with users reporting intense nasal burning lasting as long as 30 minutes. The sudden intensity of the experience combined with the pain can often start the experience with a negative imprint and nausea is also increased with insufflation, compounding the issue.

Pharmacology:

          Unlike most hallucinogens, 2C-B has been shown to be a low efficacy serotonin 5-HT2A receptor partial agonist or even full antagonist. This suggests that the 5-HT2C receptor is primarily responsible for mediating the effects experienced by users of 2C-B, although functional antagonism of 5-HT2A or activation of the 5-HT2A-coupled phospholipase D pathway may also play a role. The rank order of 5-HT2A receptor antagonist potency for this family of drugs is 2C-I > 2C-B > 2C-D > 2C-H.

        Research suggests that 2C-B increases dopamine levels in the brains of rats, which may contribute to its psychoactivity.

        2C-B has been shown to be metabolized by liver hepatocytes resulting in deamination and demethylation that produces several products. Oxidative deamination results in the 2-(4-bromo-2,5-dimethoxyphenyl)-ethanol (BDMPE) and 4-bromo-2,5-dimethoxyphenylacetic acid (BDMPAA) metabolites. Additionally, 4-bromo-2,5-dimethoxybenzoic acid (BDMBA) can be produced also by oxidative deamination. Further metabolism of BDMPE and BDMPAA may occur by demethylation. Alternatively, the later metabolites can be generated by demethylation of 2C-B followed by oxidative deamination.

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