Clinical data | |
---|---|
Routes of administration | Oral, insufflation, rectal |
Legal status | |
Legal status |
|
Pharmacokinetic data | |
Onset of action | 20–40 min. (Oral) |
Elimination half-life | 2.48 ± 3.20 h [1] |
Duration of action | 4–12 hours depending on route of administration |
Identifiers | |
| |
CAS Number | |
PubChem CID | |
DrugBank | |
ChemSpider | |
UNII | |
KEGG | |
ChEBI | |
ChEMBL | |
CompTox Dashboard ( EPA) | |
ECHA InfoCard | 100.164.088 |
Chemical and physical data | |
Formula | C10H14BrNO2 |
Molar mass | 260.131 g·mol−1 |
3D model ( JSmol) | |
| |
|
2C-B (4-bromo-2,5-dimethoxyphenethylamine) is a synthetic psychedelic drug of the 2C family, mainly used as a recreational drug. [2] The substance was first synthesized by Alexander Shulgin in 1974, and gained an initial reputation for potential psychotherapeutic use, but its use has been limited to mainly recreational use. To date, there is limited scientific information regarding the drug's pharmacokinetics and pharmacological effects in humans. The existing studies primarily classify 2C-B as a stimulant, and hallucinogen, and less commonly as an entactogen, and empathogen. [3]
2C-B, also referred to by a number of slang names, is known to circulate in the illicit market in multiple forms: [4] [5] most commonly as a powder, and less commonly in capsules or pills. For recreational use, the substance is generally consumed orally or nasally. In Shulgin's book PiHKAL, the dosage range is listed as 12–24 mg. [6]
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.[ citation needed] 2C-B was first sold commercially as a purported aphrodisiac [7] under the trade name "Erox", which was manufactured by the German pharmaceutical company Drittewelle. [8] For several years, it was available as tablets in Dutch smart shops under the name "Nexus" and "B-Dub".[ citation needed]
2C-B first became popularized in the United States as a short-lived substitute for the street drug ecstasy (MDMA) when the latter became illegal in 1985. [9] Many 2C-B users are young adults who attend raves. [4] 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 the 2000s. [10]
In 2011, street prices in the United States ranged between $10 and $30 per tablet when purchased in small quantities. [4] Larger retail purchases cost between $200 and $500 per gram. Wholesale purchases of 2C-B would lower the price ($100 to $300 per gram in 2001, $30 to $100 on the darknet in 2020). [7]
The September 1998 issue of Journal of Analytical Toxicology reported that very little data exists about the pharmacological properties, metabolism, and toxicity of 2C-B. The relationship between its use and death are unknown. [7] The common oral recreational dose is around 15–25 mg, [11] at which visual and auditory effects are experienced. Severe adverse reactions are extremely rare, but use of 2C-B was linked to significant brain injury in one case report; the alleged "2C-B" was never actually discovered by testing so the only evidence suggesting 2C-B was the cause was the victim's own words, without taking into consideration that adulteration and impurities are very common in illicit drugs. [12]
Oral | Insufflated | |
---|---|---|
ED50 | 10 mg | 4–6 mg |
Moderate | 15–25 mg | 5–9 mg |
Strong | 26–35 mg | 10–20 mg |
Extremely Intense | >35 mg | >20 mg |
Duration | 4–8 hours | 2–4 hours |
The lethal dosage is unknown. It was reported in PiHKAL, by Alexander Shulgin, that a psychologist had accidentally taken a 100 mg dose orally without apparent harm. [6]
When sold as "Ecstasy", tablets containing 2C-B often contain about 5 mg of the drug, an amount which produces stimulatory effects that mimic the effects of MDMA; in contrast, tablets marketed as 2C-B have larger quantities of the drug (10–20 mg) which cause hallucinogenic effects. [13] Street purity of 2C-B, when tested, has been found to be relatively high. [14] Researchers in Spain found that 2C-B samples in the country doubled between 2006 and 2009, switched from primarily powder form to tablets, and exhibited "low falsification rates". [15] An analysis of street samples in the Netherlands found impurities "in small percentages"; only one of the impurities, the N-acetyl derivative of 2C-B, could be identified, and comprised 1.3% of the sample. The authors suggested that this compound was a by-product of 2C-B synthesis. [13]
Little academic research has been conducted on the effects of 2C-B in humans. The information available is largely anecdotal and limited. Effects are often described as being more easily managed than other psychedelics; [16] [17] it is often compared to a mixture of a serotonergic psychedelic and MDMA. [15] At 5–10 mg, experiments with young chickens have shown it to produce effects similar to a low dosage of amphetamines. [18]
The anecdotal effects of 2C-B that have been reported by users on online discussion forums include: [19] [20] [21]
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 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 route of administration, dose, and other factors. [19]
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. [16] 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.
Unlike most psychedelics, 2C-B has been shown to be a low efficacy human serotonin 5-HT2A and 5-HT2C receptor partial agonist. [25] This suggests that activation of the 5-HT2A-coupled phospholipase D pathway [25] or functional antagonism of 5-HT2A may also play a role. The rank order of 5-HT2A receptor antagonist potency for this family of drugs in Xenopus is 2C-I > 2C-B > 2C-D > 2C-H. [26]
Research suggests that 2C-B increases dopamine levels in the brains of rats, which may contribute to its psychoactivity. [27]
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 also be produced 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. [23]
There is species differentiation in the metabolism of 2C-B. Mice hepatocytes produce 4-bromo-2,5-dimethoxy-phenol (BDMP), a previously unknown metabolite. Meanwhile, human, monkey and rabbit hepatocytes produce 2-(4-bromo-2-hydroxy-5-methoxyphenyl)-ethanol (B-2-HMPE), but dog, rat and mouse hepatocytes do not. [23] 2C-B also reduces aggressive responses in drugged rats. [28]
Analogues and derivatives of 2C-B:
25-N:
Other:
A variety of N-substituted derivatives of 2C-B have been tested, including N-methyl-2CB, N,N-dimethyl-2CB, N-ethyl-2CB and N-benzyl-2CB. Most simple alkyl derivatives were considerably less potent than 2C-B, with N-ethyl-2CB for instance having a 40 times lower affinity for the 5-HT2A receptor. The N- benzyl derivative however was found to have higher binding affinity than 2C-B itself, with N-(4-bromobenzyl)-2CB binding even more tightly. [33] This initial research did not include functional assays of activity, but later led to the development of potent substituted N-benzyl derivatives such as 25B-NBOMe, [34] and 25B-NBOH.
2C-B was used as entheogen by the Sangoma, Nyanga, and Amagqirha people in place of their traditional plants; they refer to the chemical as Ubulawu Nomathotholo, which roughly translates to "Medicine of the Singing Ancestors". [35] [36] [37]
Exposing compounds to the reagents gives a colour change which is indicative of the compound under test.
Marquis | Mecke | Mandelin | Liebermann | Froehde | Robadope |
---|---|---|---|---|---|
Yellow to green | Yellow to olive brownish | green | Yellow to black | Yellow to green | Slow pink |
Ehrlich | Hofmann | Simon's | Scott | Folin | |
No reaction | No reaction | No reaction | No reaction | (Light) purple |
The UN Commission on Narcotic Drugs added 2C-B to Schedule II of the Convention on Psychotropic Substances in March 2001. [38]
2C-B is a scheduled drug in most jurisdictions. [39] The following is a partial list of territories where the substance has been scheduled.
2C-B is controlled under the List 1, as well as similar substances like 2C-I or 2C-T-2. [40]
2C-B is controlled in Australia and on the list of substances subject to import and export controls (Appendix B). It was placed on Schedule One of the Drugs Misuse and Trafficking Act when it first came to notice in 1994, when in a showcase legal battle chemist R. Simpson was charged with manufacturing the substance in Sydney. Alexander Shulgin came to Australia to testify on behalf of the defense, to no avail.
2C-B is not specifically listed in the Australia Poisons Standard (October 2015), however similar drugs such as 2C-T-2 and 2C-I are making 2C-B fall under the Australian analogue act. [41]
In Belgium, 2C-B is a controlled substance making production, distribution, and possession illegal.
In Brazil, 2C-B is a controlled substance making production, distribution, and possession illegal.
In Canada, 2C-B is classified under Controlled Drugs and Substances Act as Schedule III as "4-bromo-2,5-dimethoxybenzeneethanamine and any salt, isomer or salt of isomer thereof". [42]
2C-B has been rescheduled (Schedule III), in a new amendment, taking effect on October 31, 2016. This is to include the other 2C-x analogues. [43]
In August 2007, 2C-B, along with many other psychologically active substances, [44] was added to Ley 20.000, known as the Ley de Drogas .
Possession of more than 200 mg of 2C-B is punishable with a two years jail sentence. [45] Smaller amount is punishable by a fine. The 200 mg threshold is merely a guideline which the court can reconsider depending on circumstances.
In Denmark, 2C-B is listed as a category B drug. [46]
In Estonia, 2C-B is classified as Schedule I.
In Germany, 2C-B is controlled in the Betäubungsmittelgesetz (BtMG) Anlage I as "Bromdimethoxyphenethylamin" (BDMPEA).
2C-B is schedule I (tabella I). [47]
In Japan, 2C-B was scheduled in 1998. It was previously marketed as "Performax".
In Luxembourg, 2C-B is a prohibited substance since 2001. [48]
In the Netherlands, 2C-B was scheduled on July 9, 1997.
In the Netherlands, 2C-B became a list I substance of the Opium Law despite no health incidents occurring. Following the ban, other phenethylamines were sold in place of 2C-B until the Netherlands became the first country in the world to ban 2C-I, 2C-T-2 and 2C-T-7 alongside 2C-B.
In Norway, 2C-B was classified as Schedule II on March 22, 2004, listed as 4-bromo-2,5-dimethoxyphenethylamine. [49]
2C-B is schedule I (I-P group) in Poland.
Banned as a narcotic drug with a criminal penalty for possession of at least 10 mg. [50]
In Spain, 2C-B was added to Category 2 prohibited substances in 2002.
2C-B is currently classified as Schedule I in Sweden.
2C-B was first classified as "health hazard" under the act Lagen om förbud mot vissa hälsofarliga varor (Act on the Prohibition of Certain Goods Dangerous to Health) as of April 1, 1999, under SFS 1999:58 [51] that made it illegal to sell or possess. Then it became schedule I as of June 1, 2002, published in LVFS 2002:4 [52] but mislabeled "2-CB" in the document. However, this was corrected in a new document, LVFS 2009:22 [53] effective December 9, 2009.
In Switzerland, 2C-B is listed in Anhang D of the DetMV and is illegal to possess. [54]
All drugs in the 2C family are Class A under the Misuse of Drugs Act which means they are illegal to produce, supply or possess. Possession carries a maximum sentence of seven years imprisonment while supply is punishable by life imprisonment and an unlimited fine. [55]
In the United States, 2C-B is classified as CSA Schedule I Section (d) Subsection (3) 4-Bromo-2,5-dimethoxyphenethylamine.
In the United States, a notice of proposed rulemaking published on December 20, 1994, in the Federal Register and after a review of relevant data, the Deputy Administrator of the Drug Enforcement Administration (DEA) proposed to place 4- bromo- 2,5-DMPEA into Schedule I, making 2C-B illegal in the United States. [56] This became permanent law on July 2, 1995. [57]
Clinical data | |
---|---|
Routes of administration | Oral, insufflation, rectal |
Legal status | |
Legal status |
|
Pharmacokinetic data | |
Onset of action | 20–40 min. (Oral) |
Elimination half-life | 2.48 ± 3.20 h [1] |
Duration of action | 4–12 hours depending on route of administration |
Identifiers | |
| |
CAS Number | |
PubChem CID | |
DrugBank | |
ChemSpider | |
UNII | |
KEGG | |
ChEBI | |
ChEMBL | |
CompTox Dashboard ( EPA) | |
ECHA InfoCard | 100.164.088 |
Chemical and physical data | |
Formula | C10H14BrNO2 |
Molar mass | 260.131 g·mol−1 |
3D model ( JSmol) | |
| |
|
2C-B (4-bromo-2,5-dimethoxyphenethylamine) is a synthetic psychedelic drug of the 2C family, mainly used as a recreational drug. [2] The substance was first synthesized by Alexander Shulgin in 1974, and gained an initial reputation for potential psychotherapeutic use, but its use has been limited to mainly recreational use. To date, there is limited scientific information regarding the drug's pharmacokinetics and pharmacological effects in humans. The existing studies primarily classify 2C-B as a stimulant, and hallucinogen, and less commonly as an entactogen, and empathogen. [3]
2C-B, also referred to by a number of slang names, is known to circulate in the illicit market in multiple forms: [4] [5] most commonly as a powder, and less commonly in capsules or pills. For recreational use, the substance is generally consumed orally or nasally. In Shulgin's book PiHKAL, the dosage range is listed as 12–24 mg. [6]
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.[ citation needed] 2C-B was first sold commercially as a purported aphrodisiac [7] under the trade name "Erox", which was manufactured by the German pharmaceutical company Drittewelle. [8] For several years, it was available as tablets in Dutch smart shops under the name "Nexus" and "B-Dub".[ citation needed]
2C-B first became popularized in the United States as a short-lived substitute for the street drug ecstasy (MDMA) when the latter became illegal in 1985. [9] Many 2C-B users are young adults who attend raves. [4] 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 the 2000s. [10]
In 2011, street prices in the United States ranged between $10 and $30 per tablet when purchased in small quantities. [4] Larger retail purchases cost between $200 and $500 per gram. Wholesale purchases of 2C-B would lower the price ($100 to $300 per gram in 2001, $30 to $100 on the darknet in 2020). [7]
The September 1998 issue of Journal of Analytical Toxicology reported that very little data exists about the pharmacological properties, metabolism, and toxicity of 2C-B. The relationship between its use and death are unknown. [7] The common oral recreational dose is around 15–25 mg, [11] at which visual and auditory effects are experienced. Severe adverse reactions are extremely rare, but use of 2C-B was linked to significant brain injury in one case report; the alleged "2C-B" was never actually discovered by testing so the only evidence suggesting 2C-B was the cause was the victim's own words, without taking into consideration that adulteration and impurities are very common in illicit drugs. [12]
Oral | Insufflated | |
---|---|---|
ED50 | 10 mg | 4–6 mg |
Moderate | 15–25 mg | 5–9 mg |
Strong | 26–35 mg | 10–20 mg |
Extremely Intense | >35 mg | >20 mg |
Duration | 4–8 hours | 2–4 hours |
The lethal dosage is unknown. It was reported in PiHKAL, by Alexander Shulgin, that a psychologist had accidentally taken a 100 mg dose orally without apparent harm. [6]
When sold as "Ecstasy", tablets containing 2C-B often contain about 5 mg of the drug, an amount which produces stimulatory effects that mimic the effects of MDMA; in contrast, tablets marketed as 2C-B have larger quantities of the drug (10–20 mg) which cause hallucinogenic effects. [13] Street purity of 2C-B, when tested, has been found to be relatively high. [14] Researchers in Spain found that 2C-B samples in the country doubled between 2006 and 2009, switched from primarily powder form to tablets, and exhibited "low falsification rates". [15] An analysis of street samples in the Netherlands found impurities "in small percentages"; only one of the impurities, the N-acetyl derivative of 2C-B, could be identified, and comprised 1.3% of the sample. The authors suggested that this compound was a by-product of 2C-B synthesis. [13]
Little academic research has been conducted on the effects of 2C-B in humans. The information available is largely anecdotal and limited. Effects are often described as being more easily managed than other psychedelics; [16] [17] it is often compared to a mixture of a serotonergic psychedelic and MDMA. [15] At 5–10 mg, experiments with young chickens have shown it to produce effects similar to a low dosage of amphetamines. [18]
The anecdotal effects of 2C-B that have been reported by users on online discussion forums include: [19] [20] [21]
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 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 route of administration, dose, and other factors. [19]
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. [16] 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.
Unlike most psychedelics, 2C-B has been shown to be a low efficacy human serotonin 5-HT2A and 5-HT2C receptor partial agonist. [25] This suggests that activation of the 5-HT2A-coupled phospholipase D pathway [25] or functional antagonism of 5-HT2A may also play a role. The rank order of 5-HT2A receptor antagonist potency for this family of drugs in Xenopus is 2C-I > 2C-B > 2C-D > 2C-H. [26]
Research suggests that 2C-B increases dopamine levels in the brains of rats, which may contribute to its psychoactivity. [27]
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 also be produced 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. [23]
There is species differentiation in the metabolism of 2C-B. Mice hepatocytes produce 4-bromo-2,5-dimethoxy-phenol (BDMP), a previously unknown metabolite. Meanwhile, human, monkey and rabbit hepatocytes produce 2-(4-bromo-2-hydroxy-5-methoxyphenyl)-ethanol (B-2-HMPE), but dog, rat and mouse hepatocytes do not. [23] 2C-B also reduces aggressive responses in drugged rats. [28]
Analogues and derivatives of 2C-B:
25-N:
Other:
A variety of N-substituted derivatives of 2C-B have been tested, including N-methyl-2CB, N,N-dimethyl-2CB, N-ethyl-2CB and N-benzyl-2CB. Most simple alkyl derivatives were considerably less potent than 2C-B, with N-ethyl-2CB for instance having a 40 times lower affinity for the 5-HT2A receptor. The N- benzyl derivative however was found to have higher binding affinity than 2C-B itself, with N-(4-bromobenzyl)-2CB binding even more tightly. [33] This initial research did not include functional assays of activity, but later led to the development of potent substituted N-benzyl derivatives such as 25B-NBOMe, [34] and 25B-NBOH.
2C-B was used as entheogen by the Sangoma, Nyanga, and Amagqirha people in place of their traditional plants; they refer to the chemical as Ubulawu Nomathotholo, which roughly translates to "Medicine of the Singing Ancestors". [35] [36] [37]
Exposing compounds to the reagents gives a colour change which is indicative of the compound under test.
Marquis | Mecke | Mandelin | Liebermann | Froehde | Robadope |
---|---|---|---|---|---|
Yellow to green | Yellow to olive brownish | green | Yellow to black | Yellow to green | Slow pink |
Ehrlich | Hofmann | Simon's | Scott | Folin | |
No reaction | No reaction | No reaction | No reaction | (Light) purple |
The UN Commission on Narcotic Drugs added 2C-B to Schedule II of the Convention on Psychotropic Substances in March 2001. [38]
2C-B is a scheduled drug in most jurisdictions. [39] The following is a partial list of territories where the substance has been scheduled.
2C-B is controlled under the List 1, as well as similar substances like 2C-I or 2C-T-2. [40]
2C-B is controlled in Australia and on the list of substances subject to import and export controls (Appendix B). It was placed on Schedule One of the Drugs Misuse and Trafficking Act when it first came to notice in 1994, when in a showcase legal battle chemist R. Simpson was charged with manufacturing the substance in Sydney. Alexander Shulgin came to Australia to testify on behalf of the defense, to no avail.
2C-B is not specifically listed in the Australia Poisons Standard (October 2015), however similar drugs such as 2C-T-2 and 2C-I are making 2C-B fall under the Australian analogue act. [41]
In Belgium, 2C-B is a controlled substance making production, distribution, and possession illegal.
In Brazil, 2C-B is a controlled substance making production, distribution, and possession illegal.
In Canada, 2C-B is classified under Controlled Drugs and Substances Act as Schedule III as "4-bromo-2,5-dimethoxybenzeneethanamine and any salt, isomer or salt of isomer thereof". [42]
2C-B has been rescheduled (Schedule III), in a new amendment, taking effect on October 31, 2016. This is to include the other 2C-x analogues. [43]
In August 2007, 2C-B, along with many other psychologically active substances, [44] was added to Ley 20.000, known as the Ley de Drogas .
Possession of more than 200 mg of 2C-B is punishable with a two years jail sentence. [45] Smaller amount is punishable by a fine. The 200 mg threshold is merely a guideline which the court can reconsider depending on circumstances.
In Denmark, 2C-B is listed as a category B drug. [46]
In Estonia, 2C-B is classified as Schedule I.
In Germany, 2C-B is controlled in the Betäubungsmittelgesetz (BtMG) Anlage I as "Bromdimethoxyphenethylamin" (BDMPEA).
2C-B is schedule I (tabella I). [47]
In Japan, 2C-B was scheduled in 1998. It was previously marketed as "Performax".
In Luxembourg, 2C-B is a prohibited substance since 2001. [48]
In the Netherlands, 2C-B was scheduled on July 9, 1997.
In the Netherlands, 2C-B became a list I substance of the Opium Law despite no health incidents occurring. Following the ban, other phenethylamines were sold in place of 2C-B until the Netherlands became the first country in the world to ban 2C-I, 2C-T-2 and 2C-T-7 alongside 2C-B.
In Norway, 2C-B was classified as Schedule II on March 22, 2004, listed as 4-bromo-2,5-dimethoxyphenethylamine. [49]
2C-B is schedule I (I-P group) in Poland.
Banned as a narcotic drug with a criminal penalty for possession of at least 10 mg. [50]
In Spain, 2C-B was added to Category 2 prohibited substances in 2002.
2C-B is currently classified as Schedule I in Sweden.
2C-B was first classified as "health hazard" under the act Lagen om förbud mot vissa hälsofarliga varor (Act on the Prohibition of Certain Goods Dangerous to Health) as of April 1, 1999, under SFS 1999:58 [51] that made it illegal to sell or possess. Then it became schedule I as of June 1, 2002, published in LVFS 2002:4 [52] but mislabeled "2-CB" in the document. However, this was corrected in a new document, LVFS 2009:22 [53] effective December 9, 2009.
In Switzerland, 2C-B is listed in Anhang D of the DetMV and is illegal to possess. [54]
All drugs in the 2C family are Class A under the Misuse of Drugs Act which means they are illegal to produce, supply or possess. Possession carries a maximum sentence of seven years imprisonment while supply is punishable by life imprisonment and an unlimited fine. [55]
In the United States, 2C-B is classified as CSA Schedule I Section (d) Subsection (3) 4-Bromo-2,5-dimethoxyphenethylamine.
In the United States, a notice of proposed rulemaking published on December 20, 1994, in the Federal Register and after a review of relevant data, the Deputy Administrator of the Drug Enforcement Administration (DEA) proposed to place 4- bromo- 2,5-DMPEA into Schedule I, making 2C-B illegal in the United States. [56] This became permanent law on July 2, 1995. [57]