2C-B - Revision history

MDElliottMD: home-claude: Erowid dosing (erowid-claude source; URLs verified; em-dash clean)

2026-05-26T16:10:46Z

home-claude: Erowid dosing (erowid-claude source; URLs verified; em-dash clean)

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 | voice  = Commentary
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MDElliottMD: Link legal-status field to the USLegal: namespace

2026-05-22T16:47:32Z

Link legal-status field to the USLegal: namespace

← Older revision		Revision as of 16:47, 22 May 2026
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	\| bioavailability = Not well characterized		\| bioavailability = Not well characterized
	\| pregnancy = Not established		\| pregnancy = Not established
	\| legal = Schedule I (United States)		\| legal = [[USLegal:DEA Schedule I\|Schedule I]] (United States)
	\| mechanism = 5-HT2A partial agonist		\| mechanism = 5-HT2A partial agonist
	\| intro = 2C-B, chemically 4-bromo-2,5-dimethoxyphenethylamine, is a synthetic psychedelic [[:Category:Phenethylamines\|phenethylamine]] first prepared in 1974 by [[Alexander Shulgin]] at his home laboratory in Lafayette, California. It is the founding member of the [[:Category:2C-x series\|2C series]], a family of 2,5-dimethoxy-4-substituted phenethylamines that Shulgin and his collaborators developed as variations on the [[Mescaline\|mescaline]] skeleton. 2C-B occupies a distinctive position in the psychedelic medicine landscape: a compound with a mescaline-class structural lineage, a [[Receptor:5-HT2A\|5-HT2A]] pharmacology shared with the [[:Category:Psychedelics\|classical psychedelics]], and a subjective character that has been described as bridging the [[:Category:Empathogens\|entactogenic]] register of [[MDMA]] and the visionary register of the classical psychedelics. It had a brief legal-sale era in the late 1980s and early 1990s before being placed in [[Schedule I]] of the United States [[Controlled Substances Act]], temporarily in 1994 and permanently in 1995, and in Schedule II of the [[Convention on Psychotropic Substances\|United Nations Convention on Psychotropic Substances]] in 2001.		\| intro = 2C-B, chemically 4-bromo-2,5-dimethoxyphenethylamine, is a synthetic psychedelic [[:Category:Phenethylamines\|phenethylamine]] first prepared in 1974 by [[Alexander Shulgin]] at his home laboratory in Lafayette, California. It is the founding member of the [[:Category:2C-x series\|2C series]], a family of 2,5-dimethoxy-4-substituted phenethylamines that Shulgin and his collaborators developed as variations on the [[Mescaline\|mescaline]] skeleton. 2C-B occupies a distinctive position in the psychedelic medicine landscape: a compound with a mescaline-class structural lineage, a [[Receptor:5-HT2A\|5-HT2A]] pharmacology shared with the [[:Category:Psychedelics\|classical psychedelics]], and a subjective character that has been described as bridging the [[:Category:Empathogens\|entactogenic]] register of [[MDMA]] and the visionary register of the classical psychedelics. It had a brief legal-sale era in the late 1980s and early 1990s before being placed in [[Schedule I]] of the United States [[Controlled Substances Act]], temporarily in 1994 and permanently in 1995, and in Schedule II of the [[Convention on Psychotropic Substances\|United Nations Convention on Psychotropic Substances]] in 2001.

MDElliottMD: Repoint receptor links to the new Receptor: namespace

2026-05-22T03:01:07Z

Repoint receptor links to the new Receptor: namespace

← Older revision		Revision as of 03:01, 22 May 2026
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	\| legal = Schedule I (United States)		\| legal = Schedule I (United States)
	\| mechanism = 5-HT2A partial agonist		\| mechanism = 5-HT2A partial agonist
	\| intro = 2C-B, chemically 4-bromo-2,5-dimethoxyphenethylamine, is a synthetic psychedelic [[:Category:Phenethylamines\|phenethylamine]] first prepared in 1974 by [[Alexander Shulgin]] at his home laboratory in Lafayette, California. It is the founding member of the [[:Category:2C-x series\|2C series]], a family of 2,5-dimethoxy-4-substituted phenethylamines that Shulgin and his collaborators developed as variations on the [[Mescaline\|mescaline]] skeleton. 2C-B occupies a distinctive position in the psychedelic medicine landscape: a compound with a mescaline-class structural lineage, a [[5-HT2A ~~receptor~~\|5-HT2A]] pharmacology shared with the [[:Category:Psychedelics\|classical psychedelics]], and a subjective character that has been described as bridging the [[:Category:Empathogens\|entactogenic]] register of [[MDMA]] and the visionary register of the classical psychedelics. It had a brief legal-sale era in the late 1980s and early 1990s before being placed in [[Schedule I]] of the United States [[Controlled Substances Act]], temporarily in 1994 and permanently in 1995, and in Schedule II of the [[Convention on Psychotropic Substances\|United Nations Convention on Psychotropic Substances]] in 2001.		\| intro = 2C-B, chemically 4-bromo-2,5-dimethoxyphenethylamine, is a synthetic psychedelic [[:Category:Phenethylamines\|phenethylamine]] first prepared in 1974 by [[Alexander Shulgin]] at his home laboratory in Lafayette, California. It is the founding member of the [[:Category:2C-x series\|2C series]], a family of 2,5-dimethoxy-4-substituted phenethylamines that Shulgin and his collaborators developed as variations on the [[Mescaline\|mescaline]] skeleton. 2C-B occupies a distinctive position in the psychedelic medicine landscape: a compound with a mescaline-class structural lineage, a [[Receptor:5-HT2A\|5-HT2A]] pharmacology shared with the [[:Category:Psychedelics\|classical psychedelics]], and a subjective character that has been described as bridging the [[:Category:Empathogens\|entactogenic]] register of [[MDMA]] and the visionary register of the classical psychedelics. It had a brief legal-sale era in the late 1980s and early 1990s before being placed in [[Schedule I]] of the United States [[Controlled Substances Act]], temporarily in 1994 and permanently in 1995, and in Schedule II of the [[Convention on Psychotropic Substances\|United Nations Convention on Psychotropic Substances]] in 2001.

	\| history = The compound that became 2C-B emerged from Shulgin's systematic exploration of the structure-activity relationships of mescaline analogs, a program he had begun in the mid-1960s. Shulgin's hypothesis was that modifications to the trimethoxyphenethylamine skeleton might yield compounds active at lower doses than mescaline's, with subjective profiles that varied in characteristic ways with the substituent at the 4-position of the phenyl ring. 2C-B, with bromine at the 4-position, was one of the most striking results. The first published description appeared in 1975 in Psychopharmacology Communications, the short-lived journal that was one of the few outlets willing to publish Shulgin's work in that era.<ref name="shulgin1975">Shulgin AT, Carter MF. Centrally active phenethylamines. Psychopharmacology Communications. 1975;1(1):93-98.</ref>		\| history = The compound that became 2C-B emerged from Shulgin's systematic exploration of the structure-activity relationships of mescaline analogs, a program he had begun in the mid-1960s. Shulgin's hypothesis was that modifications to the trimethoxyphenethylamine skeleton might yield compounds active at lower doses than mescaline's, with subjective profiles that varied in characteristic ways with the substituent at the 4-position of the phenyl ring. 2C-B, with bromine at the 4-position, was one of the most striking results. The first published description appeared in 1975 in Psychopharmacology Communications, the short-lived journal that was one of the few outlets willing to publish Shulgin's work in that era.<ref name="shulgin1975">Shulgin AT, Carter MF. Centrally active phenethylamines. Psychopharmacology Communications. 1975;1(1):93-98.</ref>
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	\| pk_metabolism =		\| pk_metabolism =
	\| pk_elimination =		\| pk_elimination =
	\| pharmacodynamics = 2C-B is a partial agonist at the serotonin 5-HT2A receptor, with additional activity at [[5-HT2C ~~receptor~~\|5-HT2C]] and [[5-HT2B ~~receptor~~\|5-HT2B]] and weak inhibition of [[Monoamine transporter\|monoamine transporters]].<ref name="nichols2016">Nichols DE. Psychedelics. Pharmacological Reviews. 2016;68(2):264-355. PMID 26841800.</ref> The pharmacological profile is intermediate between the classical 5-HT2A psychedelics such as [[LSD]] and psilocybin and the entactogens such as MDMA. The 5-HT2A action is the principal driver of the psychedelic component; the transporter activity may contribute to the entactogenic character at lower doses. Oral 2C-B has an onset of roughly 45 to 75 minutes and a duration of approximately four to eight hours, which is shorter than psilocybin and considerably shorter than LSD. The compound is structurally a phenethylamine in the mescaline lineage rather than a [[:Category:Tryptamines\|tryptamine]]; the 4-bromo substituent on the 2,5-dimethoxyphenethylamine scaffold confers substantially higher 5-HT2A affinity than mescaline's 3,4,5-trimethoxy parent compound, accounting for the dose-potency difference.		\| pharmacodynamics = 2C-B is a partial agonist at the serotonin 5-HT2A receptor, with additional activity at [[Receptor:5-HT2C\|5-HT2C]] and [[Receptor:5-HT2B\|5-HT2B]] and weak inhibition of [[Monoamine transporter\|monoamine transporters]].<ref name="nichols2016">Nichols DE. Psychedelics. Pharmacological Reviews. 2016;68(2):264-355. PMID 26841800.</ref> The pharmacological profile is intermediate between the classical 5-HT2A psychedelics such as [[LSD]] and psilocybin and the entactogens such as MDMA. The 5-HT2A action is the principal driver of the psychedelic component; the transporter activity may contribute to the entactogenic character at lower doses. Oral 2C-B has an onset of roughly 45 to 75 minutes and a duration of approximately four to eight hours, which is shorter than psilocybin and considerably shorter than LSD. The compound is structurally a phenethylamine in the mescaline lineage rather than a [[:Category:Tryptamines\|tryptamine]]; the 4-bromo substituent on the 2,5-dimethoxyphenethylamine scaffold confers substantially higher 5-HT2A affinity than mescaline's 3,4,5-trimethoxy parent compound, accounting for the dose-potency difference.

	{{ShulginsCorner		{{ShulginsCorner

MDElliottMD: Repoint CYP2D6/CYP3A4 links to the new Enzyme: namespace

2026-05-22T02:57:14Z

Repoint CYP2D6/CYP3A4 links to the new Enzyme: namespace

← Older revision		Revision as of 02:57, 22 May 2026
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	* '''Lithium: seizure and severe-reaction risk.''' Lithium combined with psychedelics including 2C-B is associated with a markedly increased risk of seizures and severe adverse reactions; the mechanism is distinct from serotonin syndrome. Avoid combination.		* '''Lithium: seizure and severe-reaction risk.''' Lithium combined with psychedelics including 2C-B is associated with a markedly increased risk of seizures and severe adverse reactions; the mechanism is distinct from serotonin syndrome. Avoid combination.
	* '''Psychostimulants: additive cardiovascular load.''' 2C-B itself produces modest sympathomimetic effects (elevated heart rate, mild blood pressure increase); concurrent psychostimulants compound the cardiovascular burden.		* '''Psychostimulants: additive cardiovascular load.''' 2C-B itself produces modest sympathomimetic effects (elevated heart rate, mild blood pressure increase); concurrent psychostimulants compound the cardiovascular burden.
	* '''CYP interactions: not well characterized.''' Human metabolism of 2C-B has not been comprehensively studied. In vitro work suggests [[~~Pharmacopedia~~:~~Pharmacogenomics sandbox/Enzyme~~ CYP2D6\|CYP2D6]] and [[~~Pharmacopedia~~:~~Pharmacogenomics sandbox/Enzyme~~ CYP3A4\|CYP3A4]] involvement; strong inhibitors of these enzymes may increase 2C-B exposure.		* '''CYP interactions: not well characterized.''' Human metabolism of 2C-B has not been comprehensively studied. In vitro work suggests [[Enzyme:CYP2D6\|CYP2D6]] and [[Enzyme:CYP3A4\|CYP3A4]] involvement; strong inhibitors of these enzymes may increase 2C-B exposure.

	\| pregnancy_details = Not characterized. 2C-B has not been studied in human pregnancy; no preclinical reproductive toxicology data are available in the public literature. The compound's Schedule I status precludes systematic study under conventional regulatory frameworks. Avoid in pregnancy on first-principles grounds.		\| pregnancy_details = Not characterized. 2C-B has not been studied in human pregnancy; no preclinical reproductive toxicology data are available in the public literature. The compound's Schedule I status precludes systematic study under conventional regulatory frameworks. Avoid in pregnancy on first-principles grounds.

MDElliottMD: 2C-B final link addendum (web-claude, consolidated): merge new links onto the citation-corrected page (5-HT2A/2C/2B receptors, monoamine transporter, Schedule I, Controlled Substances Act, Convention on Psychotropic Substances, Medicines Control Council, Ann Shulgin, Empathogens); psychostimulants house-term fix; propagate the lithium clinical correction into the interactions field

2026-05-22T01:40:44Z

2C-B final link addendum (web-claude, consolidated): merge new links onto the citation-corrected page (5-HT2A/2C/2B receptors, monoamine transporter, Schedule I, Controlled Substances Act, Convention on Psychotropic Substances, Medicines Control Council, Ann Shulgin, Empathogens); psychostimulants house-term fix; propagate the lithium clinical correction into the interactions field

← Older revision		Revision as of 01:40, 22 May 2026
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	\| legal = Schedule I (United States)		\| legal = Schedule I (United States)
	\| mechanism = 5-HT2A partial agonist		\| mechanism = 5-HT2A partial agonist
	\| intro = 2C-B, chemically 4-bromo-2,5-dimethoxyphenethylamine, is a synthetic psychedelic [[:Category:Phenethylamines\|phenethylamine]] first prepared in 1974 by [[Alexander Shulgin]] at his home laboratory in Lafayette, California. It is the founding member of the [[:Category:2C-x series\|2C series]], a family of 2,5-dimethoxy-4-substituted phenethylamines that Shulgin and his collaborators developed as variations on the [[Mescaline\|mescaline]] skeleton. 2C-B occupies a distinctive position in the psychedelic medicine landscape: a compound with a mescaline-class structural lineage, a 5-HT2A pharmacology shared with the [[:Category:Psychedelics\|classical psychedelics]], and a subjective character that has been described as bridging the entactogenic register of [[MDMA]] and the visionary register of the classical psychedelics. It had a brief legal-sale era in the late 1980s and early 1990s before being placed in Schedule I of the United States Controlled Substances Act, temporarily in 1994 and permanently in 1995, and in Schedule II of the United Nations Convention on Psychotropic Substances in 2001.		\| intro = 2C-B, chemically 4-bromo-2,5-dimethoxyphenethylamine, is a synthetic psychedelic [[:Category:Phenethylamines\|phenethylamine]] first prepared in 1974 by [[Alexander Shulgin]] at his home laboratory in Lafayette, California. It is the founding member of the [[:Category:2C-x series\|2C series]], a family of 2,5-dimethoxy-4-substituted phenethylamines that Shulgin and his collaborators developed as variations on the [[Mescaline\|mescaline]] skeleton. 2C-B occupies a distinctive position in the psychedelic medicine landscape: a compound with a mescaline-class structural lineage, a [[5-HT2A receptor\|5-HT2A]] pharmacology shared with the [[:Category:Psychedelics\|classical psychedelics]], and a subjective character that has been described as bridging the [[:Category:Empathogens\|entactogenic]] register of [[MDMA]] and the visionary register of the classical psychedelics. It had a brief legal-sale era in the late 1980s and early 1990s before being placed in [[Schedule I]] of the United States [[Controlled Substances Act]], temporarily in 1994 and permanently in 1995, and in Schedule II of the [[Convention on Psychotropic Substances\|United Nations Convention on Psychotropic Substances]] in 2001.

	\| history = The compound that became 2C-B emerged from Shulgin's systematic exploration of the structure-activity relationships of mescaline analogs, a program he had begun in the mid-1960s. Shulgin's hypothesis was that modifications to the trimethoxyphenethylamine skeleton might yield compounds active at lower doses than mescaline's, with subjective profiles that varied in characteristic ways with the substituent at the 4-position of the phenyl ring. 2C-B, with bromine at the 4-position, was one of the most striking results. The first published description appeared in 1975 in Psychopharmacology Communications, the short-lived journal that was one of the few outlets willing to publish Shulgin's work in that era.<ref name="shulgin1975">Shulgin AT, Carter MF. Centrally active phenethylamines. Psychopharmacology Communications. 1975;1(1):93-98.</ref>		\| history = The compound that became 2C-B emerged from Shulgin's systematic exploration of the structure-activity relationships of mescaline analogs, a program he had begun in the mid-1960s. Shulgin's hypothesis was that modifications to the trimethoxyphenethylamine skeleton might yield compounds active at lower doses than mescaline's, with subjective profiles that varied in characteristic ways with the substituent at the 4-position of the phenyl ring. 2C-B, with bromine at the 4-position, was one of the most striking results. The first published description appeared in 1975 in Psychopharmacology Communications, the short-lived journal that was one of the few outlets willing to publish Shulgin's work in that era.<ref name="shulgin1975">Shulgin AT, Carter MF. Centrally active phenethylamines. Psychopharmacology Communications. 1975;1(1):93-98.</ref>

	The compound entered psychotherapeutic underground practice in the late 1970s, where it gained a reputation as a potential adjunct to psychotherapy.<ref name="papaseit2018"/> Interest grew particularly after MDMA was placed in Schedule I, on an emergency basis in 1985 and permanently in 1988,<ref name="blok2020">Blok G. [From Adam to ecstacy; legal use of MDMA in the 1970s and 1980s]. Tijdschrift voor Psychiatrie. 2020;62(8):702-706. PMID 32816299.</ref> removing that medicine from the limited circle of therapists who had been using it adjunctively. 2C-B remained legal in the United States until 1994<ref name="fr1994"/> and, for a window of years, in much of Europe. [citation needed] During that period it was used by some therapists as an MDMA-adjacent option for couples and individual work. [citation needed] It was sold commercially as an aphrodisiac under the brand name Nexus<ref name="papaseit2018"/> and, in some accounts, the name Eroxan, with commercial sale dated to the late 1980s. [citation needed] As Nexus, 2C-B became particularly identified with South Africa, where it had a brief and conspicuous run as a legally sold aphrodisiac in the early 1990s before the South African Medicines Control Council scheduled it. [citation needed]		The compound entered psychotherapeutic underground practice in the late 1970s, where it gained a reputation as a potential adjunct to psychotherapy.<ref name="papaseit2018"/> Interest grew particularly after MDMA was placed in Schedule I, on an emergency basis in 1985 and permanently in 1988,<ref name="blok2020">Blok G. [From Adam to ecstacy; legal use of MDMA in the 1970s and 1980s]. Tijdschrift voor Psychiatrie. 2020;62(8):702-706. PMID 32816299.</ref> removing that medicine from the limited circle of therapists who had been using it adjunctively. 2C-B remained legal in the United States until 1994<ref name="fr1994"/> and, for a window of years, in much of Europe. [citation needed] During that period it was used by some therapists as an MDMA-adjacent option for couples and individual work. [citation needed] It was sold commercially as an aphrodisiac under the brand name Nexus<ref name="papaseit2018"/> and, in some accounts, the name Eroxan, with commercial sale dated to the late 1980s. [citation needed] As Nexus, 2C-B became particularly identified with South Africa, where it had a brief and conspicuous run as a legally sold aphrodisiac in the early 1990s before the South African [[Medicines Control Council]] scheduled it. [citation needed]

	{{ShulginsCorner		{{ShulginsCorner
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	}}		}}

	The full account of the synthesis, qualitative effects, and dose range was published in 1991 in Shulgin and Shulgin's [[PiHKAL]]: A Chemical Love Story, the first half of which is autobiographical and the second half of which is a methodical catalog of 179 phenethylamines that Shulgin and his collaborators synthesized and self-tested. The book included full experimental procedures and was published as a deliberate political act: Shulgin held a [[Drug Enforcement Administration]] analytical license to possess and study scheduled compounds, and chose to make the chemistry public knowledge in the conviction that the information should not be the property of governments. In 1994 a DEA inspection of his laboratory ended with Shulgin surrendering that license, an episode Ann Shulgin recounts in the opening chapter of the companion volume TiHKAL.<ref name="tihkal-invasion">Shulgin A, Shulgin A. TIHKAL: The Continuation. Berkeley, CA: Transform Press; 1997. Chapter 1, "Invasion".</ref>		The full account of the synthesis, qualitative effects, and dose range was published in 1991 in Shulgin and [[Ann Shulgin\|Shulgin]]'s [[PiHKAL]]: A Chemical Love Story, the first half of which is autobiographical and the second half of which is a methodical catalog of 179 phenethylamines that Shulgin and his collaborators synthesized and self-tested. The book included full experimental procedures and was published as a deliberate political act: Shulgin held a [[Drug Enforcement Administration]] analytical license to possess and study scheduled compounds, and chose to make the chemistry public knowledge in the conviction that the information should not be the property of governments. In 1994 a DEA inspection of his laboratory ended with Shulgin surrendering that license, an episode Ann Shulgin recounts in the opening chapter of the companion volume TiHKAL.<ref name="tihkal-invasion">Shulgin A, Shulgin A. TIHKAL: The Continuation. Berkeley, CA: Transform Press; 1997. Chapter 1, "Invasion".</ref>

	The United States Drug Enforcement Administration placed 2C-B in Schedule I on a temporary, emergency basis in January 1994,<ref name="fr1994">Drug Enforcement Administration. Schedules of Controlled Substances: Temporary Placement of 4-Bromo-2,5-dimethoxyphenethylamine Into Schedule I. Final Rule. Federal Register. 1994 Jan 6;59:671.</ref> and made the placement permanent in 1995.<ref name="fr1995">Drug Enforcement Administration. Schedules of Controlled Substances; Placement of 4-Bromo-2,5-Dimethoxyphenethylamine Into Schedule I. Final Rule. Federal Register. 1995 Jun 2;60:28718.</ref> The United Nations Convention on Psychotropic Substances added it to Schedule II in 2001.<ref name="papaseit2018"/> Most other jurisdictions scheduled the compound on similar timelines. For roughly a decade after the US scheduling, 2C-B circulated as a clandestine product in European and South American party scenes, often sold as MDMA or under one of the brand names that survived the legal sale era. In the 2010s and 2020s a small body of formal clinical research has emerged: an observational study at the Universitat Autònoma de Barcelona reported the acute pharmacology of oral 2C-B in experienced users,<ref name="papaseit2018">Papaseit E, Farré M, Pérez-Mañá C, Torrens M, et al. Acute Pharmacological Effects of 2C-B in Humans: An Observational Study. Frontiers in Pharmacology. 2018;9:206. PMID 29593537.</ref> and groups at Maastricht University and the University of Basel have begun controlled comparisons of 2C-B with [[Psilocybin\|psilocybin]] and MDMA.		The United States Drug Enforcement Administration placed 2C-B in Schedule I on a temporary, emergency basis in January 1994,<ref name="fr1994">Drug Enforcement Administration. Schedules of Controlled Substances: Temporary Placement of 4-Bromo-2,5-dimethoxyphenethylamine Into Schedule I. Final Rule. Federal Register. 1994 Jan 6;59:671.</ref> and made the placement permanent in 1995.<ref name="fr1995">Drug Enforcement Administration. Schedules of Controlled Substances; Placement of 4-Bromo-2,5-Dimethoxyphenethylamine Into Schedule I. Final Rule. Federal Register. 1995 Jun 2;60:28718.</ref> The United Nations Convention on Psychotropic Substances added it to Schedule II in 2001.<ref name="papaseit2018"/> Most other jurisdictions scheduled the compound on similar timelines. For roughly a decade after the US scheduling, 2C-B circulated as a clandestine product in European and South American party scenes, often sold as MDMA or under one of the brand names that survived the legal sale era. In the 2010s and 2020s a small body of formal clinical research has emerged: an observational study at the Universitat Autònoma de Barcelona reported the acute pharmacology of oral 2C-B in experienced users,<ref name="papaseit2018">Papaseit E, Farré M, Pérez-Mañá C, Torrens M, et al. Acute Pharmacological Effects of 2C-B in Humans: An Observational Study. Frontiers in Pharmacology. 2018;9:206. PMID 29593537.</ref> and groups at Maastricht University and the University of Basel have begun controlled comparisons of 2C-B with [[Psilocybin\|psilocybin]] and MDMA.
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	<titration slug="harm-reduction" author="MDElliottMD" title="Harm reduction considerations">		<titration slug="harm-reduction" author="MDElliottMD" title="Harm reduction considerations">
	2C-B is a Schedule I controlled substance in the United States with no approved medical use and no legal supply chain that guarantees product identity or purity; in modern markets it is frequently misrepresented as MDMA or substituted with other compounds, including the structurally similar but pharmacologically distinct [[DOB]]. Onset after oral administration is typically 45-75 minutes; the long onset combined with the steep dose-response curve drives a common harm pattern in which inexperienced users redose during the onset window and overshoot the intended dose. Combinations with serotonergic medicines ([[:Category:Selective Serotonin Reuptake Inhibitors (SSRIs)\|SSRIs]], [[:Category:Serotonin–Norepinephrine Reuptake Inhibitors (SNRIs)\|SNRIs]], [[:Category:Monoamine Oxidase Inhibitors (MAOIs)\|MAOIs]], [[Tramadol\|tramadol]], [[Dextromethorphan\|dextromethorphan]]) carry [[Serotonin syndrome\|serotonin syndrome]] risk and should be avoided. [[Lithium]] is a separate concern: combined with psychedelics it is associated with a markedly increased risk of seizures and severe adverse reactions, and should likewise be avoided. Combinations with ~~stimulants~~ increase cardiovascular load. The general harm-reduction principles for psychedelic experiences (set, setting, sober companion, advance arrangement of supportive contacts) apply to 2C-B as they do to other 5-HT2A agonists.		2C-B is a Schedule I controlled substance in the United States with no approved medical use and no legal supply chain that guarantees product identity or purity; in modern markets it is frequently misrepresented as MDMA or substituted with other compounds, including the structurally similar but pharmacologically distinct [[DOB]]. Onset after oral administration is typically 45-75 minutes; the long onset combined with the steep dose-response curve drives a common harm pattern in which inexperienced users redose during the onset window and overshoot the intended dose. Combinations with serotonergic medicines ([[:Category:Selective Serotonin Reuptake Inhibitors (SSRIs)\|SSRIs]], [[:Category:Serotonin–Norepinephrine Reuptake Inhibitors (SNRIs)\|SNRIs]], [[:Category:Monoamine Oxidase Inhibitors (MAOIs)\|MAOIs]], [[Tramadol\|tramadol]], [[Dextromethorphan\|dextromethorphan]]) carry [[Serotonin syndrome\|serotonin syndrome]] risk and should be avoided. [[Lithium]] is a separate concern: combined with psychedelics it is associated with a markedly increased risk of seizures and severe adverse reactions, and should likewise be avoided. Combinations with [[:Category:Psychostimulants\|psychostimulants]] increase cardiovascular load. The general harm-reduction principles for psychedelic experiences (set, setting, sober companion, advance arrangement of supportive contacts) apply to 2C-B as they do to other 5-HT2A agonists.
	</titration>		</titration>

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	\| pk_metabolism =		\| pk_metabolism =
	\| pk_elimination =		\| pk_elimination =
	\| pharmacodynamics = 2C-B is a partial agonist at the serotonin 5-HT2A receptor, with additional activity at 5-HT2C and 5-HT2B and weak inhibition of monoamine transporters.<ref name="nichols2016">Nichols DE. Psychedelics. Pharmacological Reviews. 2016;68(2):264-355. PMID 26841800.</ref> The pharmacological profile is intermediate between the classical 5-HT2A psychedelics such as [[LSD]] and psilocybin and the entactogens such as MDMA. The 5-HT2A action is the principal driver of the psychedelic component; the transporter activity may contribute to the entactogenic character at lower doses. Oral 2C-B has an onset of roughly 45 to 75 minutes and a duration of approximately four to eight hours, which is shorter than psilocybin and considerably shorter than LSD. The compound is structurally a phenethylamine in the mescaline lineage rather than a [[:Category:Tryptamines\|tryptamine]]; the 4-bromo substituent on the 2,5-dimethoxyphenethylamine scaffold confers substantially higher 5-HT2A affinity than mescaline's 3,4,5-trimethoxy parent compound, accounting for the dose-potency difference.		\| pharmacodynamics = 2C-B is a partial agonist at the serotonin 5-HT2A receptor, with additional activity at [[5-HT2C receptor\|5-HT2C]] and [[5-HT2B receptor\|5-HT2B]] and weak inhibition of [[Monoamine transporter\|monoamine transporters]].<ref name="nichols2016">Nichols DE. Psychedelics. Pharmacological Reviews. 2016;68(2):264-355. PMID 26841800.</ref> The pharmacological profile is intermediate between the classical 5-HT2A psychedelics such as [[LSD]] and psilocybin and the entactogens such as MDMA. The 5-HT2A action is the principal driver of the psychedelic component; the transporter activity may contribute to the entactogenic character at lower doses. Oral 2C-B has an onset of roughly 45 to 75 minutes and a duration of approximately four to eight hours, which is shorter than psilocybin and considerably shorter than LSD. The compound is structurally a phenethylamine in the mescaline lineage rather than a [[:Category:Tryptamines\|tryptamine]]; the 4-bromo substituent on the 2,5-dimethoxyphenethylamine scaffold confers substantially higher 5-HT2A affinity than mescaline's 3,4,5-trimethoxy parent compound, accounting for the dose-potency difference.

	{{ShulginsCorner		{{ShulginsCorner
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	Key interaction concerns for 2C-B specifically:		Key interaction concerns for 2C-B specifically:

	* '''Serotonergic medicines: serotonin syndrome risk.''' Concurrent use of SSRIs, SNRIs, MAOIs, tramadol~~, lithium~~, dextromethorphan, or other strongly serotonergic agents carries serotonin syndrome risk and should be avoided. MAOI co-administration is particularly dangerous.		* '''Serotonergic medicines: serotonin syndrome risk.''' Concurrent use of SSRIs, SNRIs, MAOIs, tramadol, dextromethorphan, or other strongly serotonergic agents carries serotonin syndrome risk and should be avoided. MAOI co-administration is particularly dangerous.
	* '''~~Stimulants~~: additive cardiovascular load.''' 2C-B itself produces modest sympathomimetic effects (elevated heart rate, mild blood pressure increase); concurrent ~~stimulants~~ compound the cardiovascular burden.		* '''Lithium: seizure and severe-reaction risk.''' Lithium combined with psychedelics including 2C-B is associated with a markedly increased risk of seizures and severe adverse reactions; the mechanism is distinct from serotonin syndrome. Avoid combination.
			* '''Psychostimulants: additive cardiovascular load.''' 2C-B itself produces modest sympathomimetic effects (elevated heart rate, mild blood pressure increase); concurrent psychostimulants compound the cardiovascular burden.
	* '''CYP interactions: not well characterized.''' Human metabolism of 2C-B has not been comprehensively studied. In vitro work suggests [[Pharmacopedia:Pharmacogenomics sandbox/Enzyme CYP2D6\|CYP2D6]] and [[Pharmacopedia:Pharmacogenomics sandbox/Enzyme CYP3A4\|CYP3A4]] involvement; strong inhibitors of these enzymes may increase 2C-B exposure.		* '''CYP interactions: not well characterized.''' Human metabolism of 2C-B has not been comprehensively studied. In vitro work suggests [[Pharmacopedia:Pharmacogenomics sandbox/Enzyme CYP2D6\|CYP2D6]] and [[Pharmacopedia:Pharmacogenomics sandbox/Enzyme CYP3A4\|CYP3A4]] involvement; strong inhibitors of these enzymes may increase 2C-B exposure.

MDElliottMD: 2C-B harm-reduction: clinical correction (pharmacist-claude) - lithium moved out of the serotonin-syndrome list into its own sentence (lithium + psychedelic risk is seizures/severe reactions, not serotonin syndrome)

2026-05-22T00:09:48Z

2C-B harm-reduction: clinical correction (pharmacist-claude) - lithium moved out of the serotonin-syndrome list into its own sentence (lithium + psychedelic risk is seizures/severe reactions, not serotonin syndrome)

← Older revision		Revision as of 00:09, 22 May 2026
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	<titration slug="harm-reduction" author="MDElliottMD" title="Harm reduction considerations">		<titration slug="harm-reduction" author="MDElliottMD" title="Harm reduction considerations">
	2C-B is a Schedule I controlled substance in the United States with no approved medical use and no legal supply chain that guarantees product identity or purity; in modern markets it is frequently misrepresented as MDMA or substituted with other compounds, including the structurally similar but pharmacologically distinct [[DOB]]. Onset after oral administration is typically 45-75 minutes; the long onset combined with the steep dose-response curve drives a common harm pattern in which inexperienced users redose during the onset window and overshoot the intended dose. Combinations with serotonergic medicines ([[:Category:Selective Serotonin Reuptake Inhibitors (SSRIs)\|SSRIs]], [[:Category:Serotonin–Norepinephrine Reuptake Inhibitors (SNRIs)\|SNRIs]], [[:Category:Monoamine Oxidase Inhibitors (MAOIs)\|MAOIs]], [[Tramadol\|tramadol~~]], [[Lithium\|lithium~~]], [[Dextromethorphan\|dextromethorphan]]) carry [[Serotonin syndrome\|serotonin syndrome]] risk and should be avoided~~; combinations~~ with stimulants increase cardiovascular load. The general harm-reduction principles for psychedelic experiences (set, setting, sober companion, advance arrangement of supportive contacts) apply to 2C-B as they do to other 5-HT2A agonists.		2C-B is a Schedule I controlled substance in the United States with no approved medical use and no legal supply chain that guarantees product identity or purity; in modern markets it is frequently misrepresented as MDMA or substituted with other compounds, including the structurally similar but pharmacologically distinct [[DOB]]. Onset after oral administration is typically 45-75 minutes; the long onset combined with the steep dose-response curve drives a common harm pattern in which inexperienced users redose during the onset window and overshoot the intended dose. Combinations with serotonergic medicines ([[:Category:Selective Serotonin Reuptake Inhibitors (SSRIs)\|SSRIs]], [[:Category:Serotonin–Norepinephrine Reuptake Inhibitors (SNRIs)\|SNRIs]], [[:Category:Monoamine Oxidase Inhibitors (MAOIs)\|MAOIs]], [[Tramadol\|tramadol]], [[Dextromethorphan\|dextromethorphan]]) carry [[Serotonin syndrome\|serotonin syndrome]] risk and should be avoided. [[Lithium]] is a separate concern: combined with psychedelics it is associated with a markedly increased risk of seizures and severe adverse reactions, and should likewise be avoided. Combinations with stimulants increase cardiovascular load. The general harm-reduction principles for psychedelic experiences (set, setting, sober companion, advance arrangement of supportive contacts) apply to 2C-B as they do to other 5-HT2A agonists.
	</titration>		</titration>

MDElliottMD: 2C-B: link the remaining serotonergic-list terms (SNRIs, lithium, dextromethorphan) per pharmacist-claude verification; all 6 now linked

2026-05-21T23:33:22Z

2C-B: link the remaining serotonergic-list terms (SNRIs, lithium, dextromethorphan) per pharmacist-claude verification; all 6 now linked

← Older revision		Revision as of 23:33, 21 May 2026
Line 51:		Line 51:

	<titration slug="harm-reduction" author="MDElliottMD" title="Harm reduction considerations">		<titration slug="harm-reduction" author="MDElliottMD" title="Harm reduction considerations">
	2C-B is a Schedule I controlled substance in the United States with no approved medical use and no legal supply chain that guarantees product identity or purity; in modern markets it is frequently misrepresented as MDMA or substituted with other compounds, including the structurally similar but pharmacologically distinct [[DOB]]. Onset after oral administration is typically 45-75 minutes; the long onset combined with the steep dose-response curve drives a common harm pattern in which inexperienced users redose during the onset window and overshoot the intended dose. Combinations with serotonergic medicines ([[:Category:Selective Serotonin Reuptake Inhibitors (SSRIs)\|SSRIs]], SNRIs, [[:Category:Monoamine Oxidase Inhibitors (MAOIs)\|MAOIs]], [[Tramadol\|tramadol]], lithium, dextromethorphan) carry [[Serotonin syndrome\|serotonin syndrome]] risk and should be avoided; combinations with stimulants increase cardiovascular load. The general harm-reduction principles for psychedelic experiences (set, setting, sober companion, advance arrangement of supportive contacts) apply to 2C-B as they do to other 5-HT2A agonists.		2C-B is a Schedule I controlled substance in the United States with no approved medical use and no legal supply chain that guarantees product identity or purity; in modern markets it is frequently misrepresented as MDMA or substituted with other compounds, including the structurally similar but pharmacologically distinct [[DOB]]. Onset after oral administration is typically 45-75 minutes; the long onset combined with the steep dose-response curve drives a common harm pattern in which inexperienced users redose during the onset window and overshoot the intended dose. Combinations with serotonergic medicines ([[:Category:Selective Serotonin Reuptake Inhibitors (SSRIs)\|SSRIs]], [[:Category:Serotonin–Norepinephrine Reuptake Inhibitors (SNRIs)\|SNRIs]], [[:Category:Monoamine Oxidase Inhibitors (MAOIs)\|MAOIs]], [[Tramadol\|tramadol]], [[Lithium\|lithium]], [[Dextromethorphan\|dextromethorphan]]) carry [[Serotonin syndrome\|serotonin syndrome]] risk and should be avoided; combinations with stimulants increase cardiovascular load. The general harm-reduction principles for psychedelic experiences (set, setting, sober companion, advance arrangement of supportive contacts) apply to 2C-B as they do to other 5-HT2A agonists.
	</titration>		</titration>

MDElliottMD: Internal-linking pass on 2C-B (web-claude addendum, corrected): ~18 first-occurrence links across intro/history/pharmacodynamics/dosing/interactions; redlinks for Alexander Shulgin, DEA, Serotonin syndrome per the amended linking rule

2026-05-21T23:31:27Z

Internal-linking pass on 2C-B (web-claude addendum, corrected): ~18 first-occurrence links across intro/history/pharmacodynamics/dosing/interactions; redlinks for Alexander Shulgin, DEA, Serotonin syndrome per the amended linking rule

← Older revision		Revision as of 23:31, 21 May 2026
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	\| legal = Schedule I (United States)		\| legal = Schedule I (United States)
	\| mechanism = 5-HT2A partial agonist		\| mechanism = 5-HT2A partial agonist
	\| intro = 2C-B, chemically 4-bromo-2,5-dimethoxyphenethylamine, is a synthetic psychedelic phenethylamine first prepared in 1974 by Alexander Shulgin at his home laboratory in Lafayette, California. It is the founding member of the 2C series, a family of 2,5-dimethoxy-4-substituted phenethylamines that Shulgin and his collaborators developed as variations on the mescaline skeleton. 2C-B occupies a distinctive position in the psychedelic medicine landscape: a compound with a mescaline-class structural lineage, a 5-HT2A pharmacology shared with the classical psychedelics, and a subjective character that has been described as bridging the entactogenic register of MDMA and the visionary register of the classical psychedelics. It had a brief legal-sale era in the late 1980s and early 1990s before being placed in Schedule I of the United States Controlled Substances Act, temporarily in 1994 and permanently in 1995, and in Schedule II of the United Nations Convention on Psychotropic Substances in 2001.		\| intro = 2C-B, chemically 4-bromo-2,5-dimethoxyphenethylamine, is a synthetic psychedelic [[:Category:Phenethylamines\|phenethylamine]] first prepared in 1974 by [[Alexander Shulgin]] at his home laboratory in Lafayette, California. It is the founding member of the [[:Category:2C-x series\|2C series]], a family of 2,5-dimethoxy-4-substituted phenethylamines that Shulgin and his collaborators developed as variations on the [[Mescaline\|mescaline]] skeleton. 2C-B occupies a distinctive position in the psychedelic medicine landscape: a compound with a mescaline-class structural lineage, a 5-HT2A pharmacology shared with the [[:Category:Psychedelics\|classical psychedelics]], and a subjective character that has been described as bridging the entactogenic register of [[MDMA]] and the visionary register of the classical psychedelics. It had a brief legal-sale era in the late 1980s and early 1990s before being placed in Schedule I of the United States Controlled Substances Act, temporarily in 1994 and permanently in 1995, and in Schedule II of the United Nations Convention on Psychotropic Substances in 2001.

	\| history = The compound that became 2C-B emerged from Shulgin's systematic exploration of the structure-activity relationships of mescaline analogs, a program he had begun in the mid-1960s. Shulgin's hypothesis was that modifications to the trimethoxyphenethylamine skeleton might yield compounds active at lower doses than mescaline's, with subjective profiles that varied in characteristic ways with the substituent at the 4-position of the phenyl ring. 2C-B, with bromine at the 4-position, was one of the most striking results. The first published description appeared in 1975 in Psychopharmacology Communications, the short-lived journal that was one of the few outlets willing to publish Shulgin's work in that era.<ref name="shulgin1975">Shulgin AT, Carter MF. Centrally active phenethylamines. Psychopharmacology Communications. 1975;1(1):93-98.</ref>		\| history = The compound that became 2C-B emerged from Shulgin's systematic exploration of the structure-activity relationships of mescaline analogs, a program he had begun in the mid-1960s. Shulgin's hypothesis was that modifications to the trimethoxyphenethylamine skeleton might yield compounds active at lower doses than mescaline's, with subjective profiles that varied in characteristic ways with the substituent at the 4-position of the phenyl ring. 2C-B, with bromine at the 4-position, was one of the most striking results. The first published description appeared in 1975 in Psychopharmacology Communications, the short-lived journal that was one of the few outlets willing to publish Shulgin's work in that era.<ref name="shulgin1975">Shulgin AT, Carter MF. Centrally active phenethylamines. Psychopharmacology Communications. 1975;1(1):93-98.</ref>
Line 30:		Line 30:
	}}		}}

	The full account of the synthesis, qualitative effects, and dose range was published in 1991 in Shulgin and Shulgin's PiHKAL: A Chemical Love Story, the first half of which is autobiographical and the second half of which is a methodical catalog of 179 phenethylamines that Shulgin and his collaborators synthesized and self-tested. The book included full experimental procedures and was published as a deliberate political act: Shulgin held a Drug Enforcement Administration analytical license to possess and study scheduled compounds, and chose to make the chemistry public knowledge in the conviction that the information should not be the property of governments. In 1994 a DEA inspection of his laboratory ended with Shulgin surrendering that license, an episode Ann Shulgin recounts in the opening chapter of the companion volume TiHKAL.<ref name="tihkal-invasion">Shulgin A, Shulgin A. TIHKAL: The Continuation. Berkeley, CA: Transform Press; 1997. Chapter 1, "Invasion".</ref>		The full account of the synthesis, qualitative effects, and dose range was published in 1991 in Shulgin and Shulgin's [[PiHKAL]]: A Chemical Love Story, the first half of which is autobiographical and the second half of which is a methodical catalog of 179 phenethylamines that Shulgin and his collaborators synthesized and self-tested. The book included full experimental procedures and was published as a deliberate political act: Shulgin held a [[Drug Enforcement Administration]] analytical license to possess and study scheduled compounds, and chose to make the chemistry public knowledge in the conviction that the information should not be the property of governments. In 1994 a DEA inspection of his laboratory ended with Shulgin surrendering that license, an episode Ann Shulgin recounts in the opening chapter of the companion volume TiHKAL.<ref name="tihkal-invasion">Shulgin A, Shulgin A. TIHKAL: The Continuation. Berkeley, CA: Transform Press; 1997. Chapter 1, "Invasion".</ref>

	The United States Drug Enforcement Administration placed 2C-B in Schedule I on a temporary, emergency basis in January 1994,<ref name="fr1994">Drug Enforcement Administration. Schedules of Controlled Substances: Temporary Placement of 4-Bromo-2,5-dimethoxyphenethylamine Into Schedule I. Final Rule. Federal Register. 1994 Jan 6;59:671.</ref> and made the placement permanent in 1995.<ref name="fr1995">Drug Enforcement Administration. Schedules of Controlled Substances; Placement of 4-Bromo-2,5-Dimethoxyphenethylamine Into Schedule I. Final Rule. Federal Register. 1995 Jun 2;60:28718.</ref> The United Nations Convention on Psychotropic Substances added it to Schedule II in 2001.<ref name="papaseit2018"/> Most other jurisdictions scheduled the compound on similar timelines. For roughly a decade after the US scheduling, 2C-B circulated as a clandestine product in European and South American party scenes, often sold as MDMA or under one of the brand names that survived the legal sale era. In the 2010s and 2020s a small body of formal clinical research has emerged: an observational study at the Universitat Autònoma de Barcelona reported the acute pharmacology of oral 2C-B in experienced users,<ref name="papaseit2018">Papaseit E, Farré M, Pérez-Mañá C, Torrens M, et al. Acute Pharmacological Effects of 2C-B in Humans: An Observational Study. Frontiers in Pharmacology. 2018;9:206. PMID 29593537.</ref> and groups at Maastricht University and the University of Basel have begun controlled comparisons of 2C-B with psilocybin and MDMA.		The United States Drug Enforcement Administration placed 2C-B in Schedule I on a temporary, emergency basis in January 1994,<ref name="fr1994">Drug Enforcement Administration. Schedules of Controlled Substances: Temporary Placement of 4-Bromo-2,5-dimethoxyphenethylamine Into Schedule I. Final Rule. Federal Register. 1994 Jan 6;59:671.</ref> and made the placement permanent in 1995.<ref name="fr1995">Drug Enforcement Administration. Schedules of Controlled Substances; Placement of 4-Bromo-2,5-Dimethoxyphenethylamine Into Schedule I. Final Rule. Federal Register. 1995 Jun 2;60:28718.</ref> The United Nations Convention on Psychotropic Substances added it to Schedule II in 2001.<ref name="papaseit2018"/> Most other jurisdictions scheduled the compound on similar timelines. For roughly a decade after the US scheduling, 2C-B circulated as a clandestine product in European and South American party scenes, often sold as MDMA or under one of the brand names that survived the legal sale era. In the 2010s and 2020s a small body of formal clinical research has emerged: an observational study at the Universitat Autònoma de Barcelona reported the acute pharmacology of oral 2C-B in experienced users,<ref name="papaseit2018">Papaseit E, Farré M, Pérez-Mañá C, Torrens M, et al. Acute Pharmacological Effects of 2C-B in Humans: An Observational Study. Frontiers in Pharmacology. 2018;9:206. PMID 29593537.</ref> and groups at Maastricht University and the University of Basel have begun controlled comparisons of 2C-B with [[Psilocybin\|psilocybin]] and MDMA.

	2C-B is not licensed as a medicine in any major jurisdiction. Formal clinical investigation is in early stages. Underground therapeutic use continues in the lineage that began with the late-1970s Shulgin circle. The compound's role in the modern psychedelic-medicine landscape is uncertain: its shorter duration and lower dose-response slope make it logistically tractable, but the limited modern clinical data and the absence of major-trial sponsorship have kept it on the margins of the renaissance that has gathered around psilocybin and MDMA.		2C-B is not licensed as a medicine in any major jurisdiction. Formal clinical investigation is in early stages. Underground therapeutic use continues in the lineage that began with the late-1970s Shulgin circle. The compound's role in the modern psychedelic-medicine landscape is uncertain: its shorter duration and lower dose-response slope make it logistically tractable, but the limited modern clinical data and the absence of major-trial sponsorship have kept it on the margins of the renaissance that has gathered around psilocybin and MDMA.
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	<titration slug="harm-reduction" author="MDElliottMD" title="Harm reduction considerations">		<titration slug="harm-reduction" author="MDElliottMD" title="Harm reduction considerations">
	2C-B is a Schedule I controlled substance in the United States with no approved medical use and no legal supply chain that guarantees product identity or purity; in modern markets it is frequently misrepresented as MDMA or substituted with other compounds, including the structurally similar but pharmacologically distinct DOB. Onset after oral administration is typically 45-75 minutes; the long onset combined with the steep dose-response curve drives a common harm pattern in which inexperienced users redose during the onset window and overshoot the intended dose. Combinations with serotonergic medicines (SSRIs, SNRIs, MAOIs, tramadol, lithium, dextromethorphan) carry serotonin syndrome risk and should be avoided; combinations with stimulants increase cardiovascular load. The general harm-reduction principles for psychedelic experiences (set, setting, sober companion, advance arrangement of supportive contacts) apply to 2C-B as they do to other 5-HT2A agonists.		2C-B is a Schedule I controlled substance in the United States with no approved medical use and no legal supply chain that guarantees product identity or purity; in modern markets it is frequently misrepresented as MDMA or substituted with other compounds, including the structurally similar but pharmacologically distinct [[DOB]]. Onset after oral administration is typically 45-75 minutes; the long onset combined with the steep dose-response curve drives a common harm pattern in which inexperienced users redose during the onset window and overshoot the intended dose. Combinations with serotonergic medicines ([[:Category:Selective Serotonin Reuptake Inhibitors (SSRIs)\|SSRIs]], SNRIs, [[:Category:Monoamine Oxidase Inhibitors (MAOIs)\|MAOIs]], [[Tramadol\|tramadol]], lithium, dextromethorphan) carry [[Serotonin syndrome\|serotonin syndrome]] risk and should be avoided; combinations with stimulants increase cardiovascular load. The general harm-reduction principles for psychedelic experiences (set, setting, sober companion, advance arrangement of supportive contacts) apply to 2C-B as they do to other 5-HT2A agonists.
	</titration>		</titration>

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	\| pk_metabolism =		\| pk_metabolism =
	\| pk_elimination =		\| pk_elimination =
	\| pharmacodynamics = 2C-B is a partial agonist at the serotonin 5-HT2A receptor, with additional activity at 5-HT2C and 5-HT2B and weak inhibition of monoamine transporters.<ref name="nichols2016">Nichols DE. Psychedelics. Pharmacological Reviews. 2016;68(2):264-355. PMID 26841800.</ref> The pharmacological profile is intermediate between the classical 5-HT2A psychedelics such as LSD and psilocybin and the entactogens such as MDMA. The 5-HT2A action is the principal driver of the psychedelic component; the transporter activity may contribute to the entactogenic character at lower doses. Oral 2C-B has an onset of roughly 45 to 75 minutes and a duration of approximately four to eight hours, which is shorter than psilocybin and considerably shorter than LSD. The compound is structurally a phenethylamine in the mescaline lineage rather than a tryptamine; the 4-bromo substituent on the 2,5-dimethoxyphenethylamine scaffold confers substantially higher 5-HT2A affinity than mescaline's 3,4,5-trimethoxy parent compound, accounting for the dose-potency difference.		\| pharmacodynamics = 2C-B is a partial agonist at the serotonin 5-HT2A receptor, with additional activity at 5-HT2C and 5-HT2B and weak inhibition of monoamine transporters.<ref name="nichols2016">Nichols DE. Psychedelics. Pharmacological Reviews. 2016;68(2):264-355. PMID 26841800.</ref> The pharmacological profile is intermediate between the classical 5-HT2A psychedelics such as [[LSD]] and psilocybin and the entactogens such as MDMA. The 5-HT2A action is the principal driver of the psychedelic component; the transporter activity may contribute to the entactogenic character at lower doses. Oral 2C-B has an onset of roughly 45 to 75 minutes and a duration of approximately four to eight hours, which is shorter than psilocybin and considerably shorter than LSD. The compound is structurally a phenethylamine in the mescaline lineage rather than a [[:Category:Tryptamines\|tryptamine]]; the 4-bromo substituent on the 2,5-dimethoxyphenethylamine scaffold confers substantially higher 5-HT2A affinity than mescaline's 3,4,5-trimethoxy parent compound, accounting for the dose-potency difference.

	{{ShulginsCorner		{{ShulginsCorner
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	* '''Serotonergic medicines: serotonin syndrome risk.''' Concurrent use of SSRIs, SNRIs, MAOIs, tramadol, lithium, dextromethorphan, or other strongly serotonergic agents carries serotonin syndrome risk and should be avoided. MAOI co-administration is particularly dangerous.		* '''Serotonergic medicines: serotonin syndrome risk.''' Concurrent use of SSRIs, SNRIs, MAOIs, tramadol, lithium, dextromethorphan, or other strongly serotonergic agents carries serotonin syndrome risk and should be avoided. MAOI co-administration is particularly dangerous.
	* '''Stimulants: additive cardiovascular load.''' 2C-B itself produces modest sympathomimetic effects (elevated heart rate, mild blood pressure increase); concurrent stimulants compound the cardiovascular burden.		* '''Stimulants: additive cardiovascular load.''' 2C-B itself produces modest sympathomimetic effects (elevated heart rate, mild blood pressure increase); concurrent stimulants compound the cardiovascular burden.
	* '''CYP interactions: not well characterized.''' Human metabolism of 2C-B has not been comprehensively studied. In vitro work suggests CYP2D6 and CYP3A4 involvement; strong inhibitors of these enzymes may increase 2C-B exposure.		* '''CYP interactions: not well characterized.''' Human metabolism of 2C-B has not been comprehensively studied. In vitro work suggests [[Pharmacopedia:Pharmacogenomics sandbox/Enzyme CYP2D6\|CYP2D6]] and [[Pharmacopedia:Pharmacogenomics sandbox/Enzyme CYP3A4\|CYP3A4]] involvement; strong inhibitors of these enzymes may increase 2C-B exposure.

	\| pregnancy_details = Not characterized. 2C-B has not been studied in human pregnancy; no preclinical reproductive toxicology data are available in the public literature. The compound's Schedule I status precludes systematic study under conventional regulatory frameworks. Avoid in pregnancy on first-principles grounds.		\| pregnancy_details = Not characterized. 2C-B has not been studied in human pregnancy; no preclinical reproductive toxicology data are available in the public literature. The compound's Schedule I status precludes systematic study under conventional regulatory frameworks. Avoid in pregnancy on first-principles grounds.

MDElliottMD: Populate 2C-B effects field: 60-effect subjective profile (parser-claude handoff), adapted from PsychonautWiki CC BY-SA 4.0, source approved by Mark; all 60 effect slugs verified in pcp_effects

2026-05-21T23:03:41Z

Populate 2C-B effects field: 60-effect subjective profile (parser-claude handoff), adapted from PsychonautWiki CC BY-SA 4.0, source approved by Mark; all 60 effect slugs verified in pcp_effects

@@ Line 62: / Line 62: @@
 | effects           =
 | pk_absorption     =
 | pk_distribution   =

MDElliottMD: Clear leftover JS-test effect fixture from 2C-B effects field; restore to empty (rev 5173 state) pending a sourcing decision on the effects list

2026-05-21T22:58:59Z

Clear leftover JS-test effect fixture from 2C-B effects field; restore to empty (rev 5173 state) pending a sourcing decision on the effects list

← Older revision		Revision as of 22:58, 21 May 2026
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	\| effects =		\| effects =
	~~<effect ref="nausea" author="MDElliottMD"/>~~
	\| pk_absorption =		\| pk_absorption =
	\| pk_distribution =		\| pk_distribution =