Editing 2C-B (section)

===Pharmacokinetics===
With 30{{nbsp}}mg 2C-B by [[oral administration]], its [[Cmax (pharmacology)|peak]] concentrations (mean ± SD) were 5.4 ± 1.7{{nbsp}}ng/mL and its [[Tmax (pharmacology)|time to peak]] concentrations were 2.3 ± 1.0{{nbsp}}hours.<ref name="ThomannRudinKraus2025" />

2C-B has been shown to be [[drug metabolism|metabolized]] by [[liver]] [[hepatocytes]], resulting in [[deamination]] and [[demethylation]] that produces several [[metabolite|product]]s. [[Oxidative deamination]] results in the 2-(4-bromo-2,5-dimethoxyphenyl)ethanol (BDMPE) and 4-bromo-2,5-dimethoxyphenylacetic acid (BDMPAA) metabolites. Additionally, 4-bromo-2,5-dimethoxybenzoic acid (BDMBA) can be produced 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.<ref name="CarmoHengstlerdeBoer2005" /> Deamination of 2C-B is mediated by the [[monoamine oxidase]] (MAO) [[enzyme]]s [[MAO-A]] and [[MAO-B]].<ref name="DeanStellpflugBurnett2013" /><ref name="TheobaldMaurer2007" /><ref name="ThomannRudinKraus2025" />

There is species differentiation in the metabolism of 2C-B. Mice hepatocytes produce 4-bromo-2,5-dimethoxyphenol (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.<ref name="CarmoHengstlerdeBoer2005" />

2C-B's metabolites BDMPAA and 4-bromo-2-hydroxy-5-methoxyphenylacetic acid (B-2-HMPAA) in humans occur at peak concentrations 280-fold and 17-fold higher than those of 2C-B with [[oral administration]] of 2C-B, respectively.<ref name="ThomannRudinKraus2025" />

The [[elimination half-life]] of 2C-B in humans is 1.2 to 2.5{{nbsp}}hours.<ref name="PapaseitFarréPérez-Mañá2018" /><ref name="ThomannRudinKraus2025" />