2C (2C-x) is a general name for the family ofpsychedelicphenethylamines containingmethoxy groups on the 2 and 5positions of abenzene ring.[1][2][3] Most of these compounds also carrylipophilic substituents at the 4 position, usually resulting in more potent and moremetabolically stable and longer acting compounds.[4]
Most of the currently known 2C compounds were first synthesized byAlexander Shulgin in the 1970s and 1980s and published in his bookPiHKAL (Phenethylamines i Have Known And Loved).[3] Shulgin also coined the term 2C, being anacronym for the 2 carbon atoms between the benzene ring and theamino group.[5][1][3]2C-B is the most popular of the 2C drugs.[3]
The 2C drugs areorally active, are used at oral doses of 6 to 150 mg depending on the drug, and havedurations of 3 to 48 hours depending on the drug.[1][6][5][7] However, many have doses in the range of 10 to 60 mg anddurations in the range of 4 to 12 hours.[1] The 2C drugs producepsychedelic effects.[1][5][8][3] Some, such as2C-B, have also been reported to have someentactogenic qualities, though findings appear to be mixed.[8][3][9][10]
| Compound | Chemical name | Dosage | Duration | |
|---|---|---|---|---|
| 2C-AL | 4-Allyl-2,5-dimethoxyphenethylamine | Unknown | Unknown | |
| 2C-B | 4-Bromo-2,5-dimethoxyphenethylamine | 10–35 mg | 4–8 hours | |
| 2C-Bu | 4-Butyl-2,5-dimethoxyphenethylamine | Unknown | Unknown | |
| 2C-C | 4-Chloro-2,5-dimethoxyphenethylamine | 20–40 mg | 4–8 hours | |
| 2C-CN | 4-Cyano-2,5-dimethoxyphenethylamine | >22 mg | Unknown | |
| 2C-CP | 4-Cyclopropyl-2,5-dimethoxyphenethylamine | 15–35 mg | 3–6 hours | |
| 2C-D | 4-Methyl-2,5-dimethoxyphenethylamine | 20–60 mg | 4–6 hours | |
| 2C-E | 4-Ethyl-2,5-dimethoxyphenethylamine | 10–25 mg | 6–12 hours | |
| 2C-EF | 4-Fluoroethyl-2,5-dimethoxyphenethylamine | 10–25 mg | Unknown | |
| 2C-F | 4-Fluoro-2,5-dimethoxyphenethylamine | ≥250 mg | Unknown | |
| 2C-G | 3,4-Dimethyl-2,5-dimethoxyphenethylamine | 20–35 mg | 18–30 hours | |
| 2C-G-3 | 3,4-Trimethylene-2,5-dimethoxyphenethylamine | 16–25 mg | 12–24 hours | |
| 2C-G-5 | 3,4-Norbornyl-2,5-dimethoxyphenethylamine | 10–16 mg | 32–48 hours | |
| 2C-H | 2,5-Dimethoxyphenethylamine | Unknown | Unknown | |
| 2C-I | 4-Iodo-2,5-dimethoxyphenethylamine | 14–22 mg | 6–10 hours | |
| 2C-iBu | 4-Isobutyl-2,5-dimethoxyphenethylamine | ≥5 mg | ~20 hours | |
| 2C-iP | 4-Isopropyl-2,5-dimethoxyphenethylamine | 8–25 mg | 8–12 hours | |
| 2C-N | 4-Nitro-2,5-dimethoxyphenethylamine | 100–150 mg | 4–6 hours | |
| 2C-O | 4-Methoxy-2,5-dimethoxyphenethylamine | Unknown | Unknown | |
| 2C-O-4 | 4-Isopropoxy-2,5-dimethoxyphenethylamine | >60 mg | Unknown | |
| 2C-O-22 | 4-(2,2,2-Trifluoroethoxy)-2,5-dimethoxyphenethylamine | ≥57 mg | Unknown | |
| 2C-P | 4-Propyl-2,5-dimethoxyphenethylamine | 6–10 mg | 5–16 hours | |
| 2C-Ph (2C-BI-1) | 4-Phenyl-2,5-dimethoxyphenethylamine | Unknown | Unknown | |
| 2C-Se | 4-Methylseleno-2,5-dimethoxyphenethylamine | ~100 mg | 6–8 hours | |
| 2C-T (2C-T-1) | 4-Methylthio-2,5-dimethoxyphenethylamine | 60–100 mg | 3–5 hours | |
| 2C-T-2 | 4-Ethylthio-2,5-dimethoxyphenethylamine | 12–25 mg | 6–8 hours | |
| 2C-T-3 (2C-T-20) | 4-Methallylthio-2,5-dimethoxyphenethylamine | 15–40 mg | 8–14 hours | |
| 2C-T-4 | 4-Isopropylthio-2,5-dimethoxyphenethylamine | 8–20 mg | 12–18 hours | |
| 2C-T-7 | 4-Propylthio-2,5-dimethoxyphenethylamine | 10–30 mg | 8–15 hours | |
| 2C-T-8 | 4-Cyclopropylmethylthio-2,5-dimethoxyphenethylamine | 30–50 mg | 10–15 hours | |
| 2C-T-9 | 4-tert-Butylthio-2,5-dimethoxyphenethylamine | 60–100 mg | 12–18 hours | |
| 2C-T-13 | 4-(2-Methoxyethylthio)-2,5-dimethoxyphenethylamine | 25–40 mg | 6–8 hours | |
| 2C-T-15 | 4-Cyclopropylthio-2,5-dimethoxyphenethylamine | >30 mg | Several hours | |
| 2C-T-16 | 4-Allylthio-2,5-dimethoxyphenethylamine | 10–25 mg | 4–6 hours | |
| 2C-T-17 | 4-sec-Butylthio-2,5-dimethoxyphenethylamine | 60–100 mg | 10–15 hours | |
| 2C-T-19 | 4-Butylthio-2,5-dimethoxyphenethylamine | Unknown | Unknown | |
| 2C-T-21 | 4-(2-Fluoroethylthio)-2,5-dimethoxyphenethylamine | 8–20 mg | 7–10 hours | |
| 2C-T-21.5 | 4-(2,2-Difluoroethylthio)-2,5-dimethoxyphenethylamine | 12–30 mg | 8–14 hours | |
| 2C-T-22 | 4-(2,2,2-Trifluoroethylthio)-2,5-dimethoxyphenethylamine | Unknown | Unknown | |
| 2C-T-25 | 4-Isobutylthio-2,5-dimethoxyphenethylamine | >30 mg | Unknown | |
| 2C-T-27 | 4-Benzylthio-2,5-dimethoxyphenethylamine | ≥80 mg | Unknown | |
| 2C-T-28 | 4-(3-Fluoropropylthio)-2,5-dimethoxyphenethylamine | 8–20 mg | 8–10 hours | |
| 2C-T-30 | 4-(4-Fluorobutylthio)-2,5-dimethoxyphenethylamine | Unknown | Unknown | |
| 2C-T-33 | 4-(3-Methoxybenzylthio)-2,5-dimethoxyphenethylamine | Unknown | Unknown | |
| 2C-T-36 (2C-T-TFM) | 4-Trifluoromethylthio-2,5-dimethoxyphenethylamine | Unknown | Unknown | |
| 2C-tBu | 4-tert-Butyl-2,5-dimethoxyphenethylamine | >5–10 mg | Unknown | |
| 2C-Te | 4-Methyltelluro-2,5-dimethoxyphenethylamine | Unknown | Unknown | |
| 2C-TFE | 4-(2,2,2-Trifluoroethyl)-2,5-dimethoxyphenethylamine | 5–15 mg | 12–24 hours | |
| 2C-TFM | 4-Trifluoromethyl-2,5-dimethoxyphenethylamine | 3–6 mg | ≥5–10 hours | |
| 2C-V | 4-Ethenyl-2,5-dimethoxyphenethylamine | ~25 mg | ~5 hours | |
| 2C-YN | 4-Ethynyl-2,5-dimethoxyphenethylamine | ~50 mg | ~2 hours | |
| Refs:[1][6][3][7][5][2][11][12][13][4] | ||||
The 2C drugs aremetabolized by themonoamine oxidase (MAO)enzymes, including bothMAO-A andMAO-B.[1][14] As a result, they may be potentiated bymonoamine oxidase inhibitors (MAOIs), such asphenelzine,tranylcypromine,moclobemide, andselegiline.[1][14][15] This may lead tooverdose and serioustoxicity.[1][14][15] There is no known reversal agent for 2C drugs, and medical management for overdose involves treatment of symptoms until toxicity within the body subsides.[16]
The 2C drugs act asagonists of theserotonin5-HT2 receptors, including of the serotonin5-HT2A,5-HT2B, and5-HT2C receptors.[17][18][19][20][21] They arepartial agonists of the serotonin 5-HT2A receptor.[17][18] Most of the 2C drugs have much loweraffinity for the serotonin5-HT1A receptor than for the serotonin 5-HT2A receptor.[17][18][19][20] Most of the 2C drugs have also shown about 5- to 15-fold higher affinity for the serotonin 5-HT2A receptor over the serotonin 5-HT2C receptor and about 15- to 100-fold higher affinity for the serotonin 5-HT2A receptor over the serotonin 5-HT1A receptor.[18] Thepsychedelic effects of the 2C drugs are thought to be mediated specifically by activation of the serotonin 5-HT2A receptor.[17][19][21]
Unlike many other phenethylamines, 2C drugs, including2C-C,2C-D,2C-E,2C-I, and2C-T-2 among others, are inactive asmonoamine releasing agents andreuptake inhibitors.[17][22][19][18][21] Most of the 2C drugs are agonists of the rat and mousetrace amine-associated receptor 1 (TAAR1).[17][23][24][18] However, most are inactive as agonists of the human TAAR1.[17][23][24][18] The 2C drugs show very weakmonoamine oxidase inhibition, including ofmonoamine oxidase A (MAO-A) and/ormonoamine oxidase B (MAO-B).[17]
| Drug | 5-HT1A | 5-HT1B | 5-HT2A | 5-HT2B | 5-HT2C | ||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| Ki (nM) | EC50 (nM) | Emax (%) | Ki (nM) | Ki (nM) | EC50 (nM) | Emax (%) | Ki (nM) | EC50 (nM) | Emax (%) | Ki (nM) | EC50 (nM) | Emax (%) | |
| 2C-B | 130–311 | ND | ND | 104.4 | 6.9–27.6 | 1.89–80 | 5–99% | 13.5 | 75–130 | 52–89% | 43–89.5 | 0.031–0.264 | 104–116% |
| 2C-C | 190–740 | >10,000 | <25% | 252.9 | 5.47–13 | 9.27–200 | 49–102% | ND | 280 | 81% | 5.4–90 | 24.2 | 94% |
| 2C-D | 440–1,630 | >10,000 | <25% | ND | 23.9–32.4 | 43.5–350 | 41–125% | ND | 230 | 77% | 12.7–150 | 71.1 | 100% |
| 2C-E | 307.3–1,190 | >10,000 | <25% | ND | 4.50–43.9 | 2.5–110 | 40–125% | 25.1 | 190 | 66% | 5.4–104.1 | 0.233–18.0 | 98–106% |
| 2C-H | 70 | ND | ND | ND | 1,600 | 2,408–9,400 | 28–67% | ND | 6,200 | 46% | 4,100 | ND | ND |
| 2C-I | 180–970 | 4,900 | 102% | ND | 3.5–9.3 | 3.83–60 | 15–82% | ND | 150 | 70% | 10.2–40 | 2.8 | 79–100% |
| 2C-N | 2,200 | ND | ND | ND | 23.5 | 170 | 20–48% | ND | 730 | 74% | 370 | ND | 40–50% |
| 2C-P | 110 | ND | ND | ND | 8.1 | 90 | 63% | ND | 130 | 72% | 40 | ND | ND |
| 2C-T-1 | 1,035 | ND | ND | ND | 49 | 2.0 | 75% | ND | 57 | 58% | 347 | ND | ND |
| 2C-T-2 | 370–1,740 | 3,000 | 76% | 857.5 | 9–39.9 | 0.354–80 | 67–128% | 6 | 130 | 75% | 14.2–69 | 0.0233–3.8 | 87–107% |
| 2C-T-4 | 470–916 | ND | ND | ND | 27.9–54 | 5.5–220 | 56–87% | ND | 63–160 | 68–75% | 180–295 | ND | ND |
| 2C-T-7 | 520–878 | ND | ND | ND | 5.3–6.5 | 1.2–130 | 49–101% | ND | 52–350 | 45–75% | 39–54 | ND | ND |
| Notes: The smaller the value, the more avidly the drug binds to or activates the site.Refs:[18][19][20][17][25][26][27][28] | |||||||||||||
In accordance with their psychedelic effects in humans, the 2C drugs produce thehead-twitch response andwet dog shakes, behavioral proxies of psychedelic effects, in rodents.[17] At least some 2C drugs, such as2C-D and2C-E, producehyperlocomotion at lower doses in rodents.[17] All 2C drugs producehypolocomotion at higher doses in rodents.[17] 2C drugs, including 2C-C, 2C-D, 2C-E, and 2C-I, substitute partially to fully for psychedelics likeDOM,DMT, andLSD and/or for theentactogenMDMA in rodentdrug discrimination tests.[17][19] However, none of the assessed 2C drugs substituted fordextromethamphetamine, suggesting that they lackamphetamine-type orstimulant-like effects.[17][19]
In contrast to most psychedelics, at least two assessed 2C drugs, 2C-C and2C-P, have shownreinforcing effects in rodents, includingconditioned place preference (CPP) andself-administration.[17][29] Themechanism by which these effects are mediated is unknown.[17] However, it may be related to reducedexpression of thedopamine transporter (DAT) and increased DATphosphorylation, in turn resulting in increasedextracellulardopamine levels in certain brain areas.[17][29] These 2C drugs might havemisuse potential in humans.[17][29] Similar reinforcing effects in animals have been observed forNBOMeanalogues of 2C drugs, including25B-NBOMe,25D-NBOMe,25E-NBOMe,25H-NBOMe, and25N-NBOMe.[17][30][31][32][33][34][35]
Similarly toDOI,tolerance has been found to gradually develop to the head-twitch response induced by2C-T-7 with chronic administration in rodents.[17]
Various 2C drugs show potentanti-inflammatory effects mediated by serotonin 5-HT2A receptor activation.[36] Among these include2C-I,2C-B,2C-H, and2C-iBu.[36][37] Others, such as2C-B-Fly and2C-T-33, were less effective.[36] 2C-iBu has shown a greater separation between anti-inflammatory effects and psychedelic-like effects in animals than other 2C drugs and is being investigated for possible use as apharmaceutical drug.[37][38]
The 2C drugs areorally active.[1] They aremetabolized byO-demethylation anddeamination.[1][14] This is mediated specifically bymonoamine oxidase (MAO)enzymesMAO-A andMAO-B, whereascytochrome P450 enzymes appear to metabolize only some 2C drugs and to have only a very small role.[14]
2,4,5-Trimethoxyphenethylamine (2,4,5-TMPEA; 2C-O or "2C-MeO") was firstsynthesized by Jansen and was found to produce psychedelic effects similar to those ofmescaline (3,4,5-trimethoxyphenethylamine).[39][40] He published his findings in 1931.[39][40] However, subsequent studies in the 1960s and 1970s suggested that 2,4,5-TMPEA may actually be inactive as a psychedelic in animals and humans.[39]
2C-D (2C-M) was the first of the 2C drugs besides 2C-O to be discovered.[2][41][42][43] It was synthesized and studied in animals by Ho and colleagues and they published their findings in 1970.[2][41][42][43]Alexander Shulgin synthesized2C-B and 2C-D in 1974 and discovered their psychedelic effects inself-experiments conducted in 1974 and 1975.[1][44][2][41][45] He published his findings in thescientific literature in 1975.[1][44][2][41][45]2C-T was first described by Shulgin andDavid E. Nichols in 1976.[46]2C-I was first described by Shulgin and colleagues in 1977 and initial psychoactivity was reported by Shulgin in 1978.[39][47] Shulgin also first synthesized2C-E in 1977.[48][49] He reviewed several of these 2C drugs in 1979.[50] Subsequently, numerous other 2C drugs have been synthesized and characterized.[5][6][2][1][44]
2C-B gained popularity as arecreational drug andMDMA alternative in the mid-1980s and became acontrolled substance in theUnited States in 1994.[1][3] It is said to be the most popular of the 2C drugs.[3]
As of October 12, 2016, the 2C-x family of substituted phenethylamines is a controlled substance (Schedule III) in Canada.[51]
| Name | R3 | R4 | Structure | CAS # |
|---|---|---|---|---|
| 2C-B | H | Br |  | 66142–81–2 |
| 2C-Bn | H | CH2C6H5 |  | |
| 2C-Bu | H | CH2CH2CH2CH3 |  | |
| 2C-C | H | Cl |  | 88441–14–9 |
| 2C-C-3[52] | Cl | Cl |  | |
| 2C-CN | H | C≡N |  | 88441–07–0 |
| 2C-D | H | CH3 |  | 24333–19–5 |
| 2C-E | H | CH2CH3 |  | 71539–34–9 |
| 2C-EF | H | CH2CH2F |  | 1222814–77–8 |
| 2C-F | H | F |  | 207740–15–6 |
| 2C-G | CH3 | CH3 |  | 207740–18–9 |
| 2C-G-1 | CH2 |  | ||
| 2C-G-2 | (CH2)2 |  | ||
| 2C-G-3 | (CH2)3 |  | 207740–19–0 | |
| 2C-G-4 | (CH2)4 |  | 952006–59–6 | |
| 2C-G-5 | (CH2)5 |  | 207740–20–3 | |
| 2C-G-6 | (CH2)6 |  | ||
| 2C-G-N | (CH)4 |  | 207740–21–4 | |
| 2C-H | H | H |  | 3600–86–0 |
| 2C-I | H | I |  | 69587–11–7 |
| 2C-iBu | H | iBu |  | |
| 2C-iP | H | CH(CH3)2 |  | 1498978–47–4 |
| 2C-tBu | H | C(CH3)3 |  | |
| 2C-CP | H | C3H5 |  | 2888537–46–8 |
| 2C-CB | H | C4H7 |  | |
| 2C-CPE[53] | H | C5H9 |  | |
| 2C-CPM | H | C4H7 |  | |
| 2C-N | H | NO2 |  | 261789–00–8 |
| 2C-NH2 | H | NH2 |  | 168699–66–9 |
| 2C-PYR | H | Pyrrolidine |  | |
| 2C-PIP[54] | H | Piperidine |  | |
| 2C-O | H | OCH3 |  | 15394–83–9 |
| 2C-O-4 | H | OCH(CH3)2 |  | 952006–65–4 |
| 2C-MOM[55] | H | CH2OCH3 |  | |
| 2C-P | H | CH2CH2CH3 |  | 207740–22–5 |
| 2C-Ph (2C-BI-1) | H | C6H5 |  | |
| 2C-Se | H | SeCH3 |  | 1189246–68–1 |
| 2C-Se-TFM | H | SeCF3 |  | |
| 2C-Te | H | TeCH3 |  | ? |
| 2C-T | H | SCH3 |  | 61638–09–3 |
| 2C-T-2 | H | SCH2CH3 |  | 207740–24–7 |
| 2C-T-3[56] | H | SCH2C(=CH2)CH3 |  | 648957–40–8 |
| 2C-T-4 | H | SCH(CH3)2 |  | 207740–25–8 |
| 2C-T-5[56] | H |  | ||
| 2C-T-6[56] | H | SC6H5 |  | |
| 2C-T-7 | H | S(CH2)2CH3 |  | 207740–26–9 |
| 2C-T-8 | H | SCH2CH(CH2)2 |  | 207740–27–0 |
| 2C-T-9[56] | H | SC(CH3)3 |  | 207740–28–1 |
| 2C-T-10[56] | H |  | ||
| 2C-T-11[56] | H | SC6H4-p-Br |  | |
| 2C-T-12[56] | H |  | ||
| 2C-T-13 | H | S(CH2)2OCH3 |  | 207740–30–5 |
| 2C-T-14[56] | H | S(CH2)2SCH3 |  | |
| 2C-T-15 | H | SCH(CH2)2 |  | |
| 2C-T-16[57] | H | SCH2CH=CH2 |  | 648957–42–0 |
| 2C-T-17 | H | SCH(CH3)CH2CH3 |  | 207740–32–7 |
| 2C-T-18[56] | H |  | ||
| 2C-T-19 | H | SCH2CH2CH2CH3 |  | |
| 2C-T-21 | H | S(CH2)2F |  | 207740–33–8 |
| 2C-T-21.5[56] | H | S(CH2)CHF2 |  | 648957–46–4 |
| 2C-T-22[56] | H | S(CH2)CF3 |  | 648957–48–6 |
| 2C-T-23[56] | H |  | ||
| 2C-T-24[56] | H |  | ||
| 2C-T-25[56] | H | SCH2CH(CH3)2 |  | |
| 2C-T-27[56] | H | SCH2C6H5 |  | 648957–52–2 |
| 2C-T-28[56] | H | S(CH2)3F |  | 648957–54–4 |
| 2C-T-29 (2C-T-PARGY) | H | S(CH2)C≡CH |  | |
| 2C-T-30[56] | H | S(CH2)4F |  | |
| 2C-T-31[56] | H | SCH2C6H4-p-CF3 |  | |
| 2C-T-32[56] | H | SCH2C6F5 |  | |
| 2C-T-33[56] | H | SCH2C6H4-m-OCH3 |  | |
| 2C-T-35 (2C-T-DFM) | H | SCF2H |  | |
| CYB210010 (2C-T-36 / 2C-T-TFM)[58] | H | SCF3 |  | |
| 2C-T-CH2CN | H | S(CH2)C≡N |  | |
| 2C-T-pent-4-ynyl | H | S(CH2)3C≡CH |  | |
| 2C-T-TFM-sulfone | H | SO2CF3 |  | |
| 2C-T-DFP | H | SCH2CH2CF2H |  | |
| 2C-T-TFP | H | SCH2CH2CF3 |  | |
| 2C-DFM[4]: 770 | H | CHF2 |  | |
| 2C-TFM | H | CF3 |  | 159277–08–4 |
| 2C-TFE | H | CH2CF3 |  | |
| 2C-PFE | H | CF2CF3 |  | |
| 2C-PFS | H | SF5 |  | |
| 2C-YN | H | C≡CH |  | 752982–24–4 |
| 2C-V | H | CH=CH2 |  | |
| 2C-AL[59] | H | CH2CH=CH2 |  | |
| Name | Chemical name | Structure | Ref |
|---|---|---|---|
| N-Methyl-2C-B | N-Methyl-4-bromo-2,5-dimethoxyphenethylamine |  | |
| N-Ethyl-2C-B | N-Ethyl-4-bromo-2,5-dimethoxyphenethylamine |  | |
| 25B-NB (N-benzyl-2C-B) | N-Benzyl-4-bromo-2,5-dimethoxyphenethylamine |  | |
| N-Methyl-2C-I | N-Methyl-4-iodo-2,5-dimethoxyphenethylamine |  | |
| β-Methyl-2C-B | 4-Bromo-2,5-dimethoxy-β-methylphenylethylamine |  | |
| β-Keto-2C-B (βk-2C-B) | 4-Bromo-2,5-dimethoxy-β-ketophenylethylamine |  | |
| 25D-NM-NDEAOP (25D-NM-NDEPA) | N-Methyl-N-(3-diethylamino-3-oxopropyl)-2,5-dimethoxy-4-methylphenethylamine |  | |
| 25B-NAcPip | N-(Piperidin-1-ylcarbonylmethyl)-4-bromo-2,5-dimethoxyphenethylamine |  | |
| XOB | N-[(4-Phenylbutoxy)hexyl]-4-bromo-2,5-dimethoxyphenethylamine |  | [60] |
| TCB-2 | [(7R)-3-Bromo-2,5-dimethoxy-bicyclo[4.2.0]octa-1,3,5-trien-7-yl]methanamine |  | |
| 2CB-Ind | (5-Bromo-4,7-dimethoxy-2,3-dihydro-1H-inden-1-yl)methanamine |  | |
| ZC-B | 3-(4-Bromo-2,5-dimethoxyphenyl)azetidine |  | |
| 2C-B-PYR | 3-(4-Bromo-2,5-dimethoxyphenyl)pyrrolidine |  | |
| LPH-5 | (S)-3-(2,5-Dimethoxy-4-(trifluoromethyl)phenyl)piperidine |  | |
| DEMPDHPCA-2C-D ("compound 45") | 1-Methyl-3-(1-oxo-1-diethylaminomethyl)-5-(2,5-dimethoxy-4-methylphenyl)-3,6-dihydro-2H-pyridine |  | [61] |
| DOM-CR (DOM-THIQ, 2C-D-CR) | 5,8-Dimethoxy-7-methyl-1,2,3,4-tetrahydroisoquinoline |  | |
| DOB-CR (DOB-THIQ, 2C-B-CR) | 5,8-Dimethoxy-7-bromo-1,2,3,4-tetrahydroisoquinoline |  | |
| N-Methyl-DOM-CR (Beatrice-CR,N-methyl-2C-D-CR) | 2,7-Dimethyl-5,8-dimethoxy-1,2,3,4-tetrahydroisoquinoline |  | |
| 2C-B-morpholine | 2-(4-Bromo-2,5-dimethoxyphenyl)morpholine |  | [62][63] |
| 2C-B-aminorex | 5-(4-Bromo-2,5-dimethoxyphenyl)-4,5-dihydro-1,3-oxazol-2-amine |  | |
| 2C-B-PP | 1-(2,5-Dimethoxy-4-bromophenyl)piperazine |  | |
| 2C-B-BZP | 1-[(4-Bromo-2,5-dimethoxyphenyl)methyl]piperazine |  | |
| 2C-B-5-hemiFLY-α6 | 8-Bromo-6-methoxy-2a,3,4,5-tetrahydro-2H-naphtho[1,8-bc]furan-4-amine |  |
In 1974, 4-bromo-2,5-dimethoxyphenethylamine (2C-B), the first of the 2Cs, was synthesized by Alexander Shulgin as he was exploring homologs from 2,5-dimethoxy-4-bromoamphetamine [3]. 2C-B was manufactured in the 1980s and early 1990s under the names Nexus, Erox, Performax, Toonies, Bromo, Spectrum, and Venus and marketed as MDMA's replacement after MDMA became scheduled in the USA [6, 7]. 2C-B was initially intended for psychotherapy use due to its short 1-h duration of action [3]. Due to 2C-B's significant gastrointestinal effects and lack of empathogenic effects as compared to MDMA, it rapidly fell out of favor for psychotherapy. In 1995, 2C-B was placed on Schedule I of the Controlled Substances Act by the Drug Enforcement Agency (DEA) [6, 7]. However, following the scheduling of 2C-B, other 2C analogues were made available by suppliers as legal alternatives [8].
DOSE EFFECT: Anecdotal data suggests that recreational doses of 2C-B range from 4—30 mg with lower doses (4—10 mg) producing entactogenic effects, whereas high doses (10— 20 mg) cause psychedelic and sympathomimetic effects.
In one of the few clinical studies of a designer drug, 4-bromo-2,5-dimethoxyphenylethylamine (2C-B) was shown to induce euphoria, well-being, and changes in perception, and to have mild stimulant properties (Gonzalez et al. 2015). 2C-B may thus be classified as a psychedelic with entactogenic properties, an effect profile that is similar to various other phenethylamine psychedelics (Shulgin and Shulgin 1995).
Table 4 Human potency data for selected hallucinogens. [...]
The α-H homologue [2C-D (2a)] has been reported in animal avoidance tests16 to be less active than [DOM (2b)] and substantially stimulant in nature. In human evaluation17 the decrease in potency is confirmed, but the psychopharmacological profile is largely one of sensory enhancement. [...] 2,5-Dimethoxy-4-methylphenethylamine Hydrochloride (2a).23 [...] (23) B. T. Ho, L. W. Tansey, R. L. Bolster, R. An, W. M. McIsaac, and R T. Harris, J. Med. Chem., 13, 134 (1970).
In 1974, Shulgin translated this strategy back to the phenethylamine family with the synthesis of 2,5-dimethoxy-4-bromophenethylamine (2C-B),19 which he found to be a strong hallucinogen in a series of self-experiments conducted during 1974 and 1975 (the drug was described as "beautifully effective").20 During the late 1970s and early 1980s, 2,5-dimethoxy-4-methylphenethylamine (2C-D), another compound from this class, received considerable attention from psychiatrists as a psychotherapeutic adjunct, most notably Hanscarl Leuner, who worked with 2C-D extensively under the code name LE-25 and pioneered the concept of psychedelic therapy.21 However, 2C-B was emergency scheduled by the Drug Enforcement Administration (DEA) in 1994, due to its appearance on the recreational drug market as a replacement for 3,4-methyl enedioxy methamphetamine (MDMA) (which had been scheduled in 1985).