βk-2C-B is a designer drug, more specifically it is the beta keto analogue of the controlled substance 2C-B (2,5-dimethoxy-4-bromophenethylamine) which was first synthesized by Alexander Shulgin.

[1] Although a synthesis of the compound had previously been described,[2] in the years after its emergence on the market, papers reporting analytical characterizations of the substance appeared.

Then a Delépine reaction is employed to convert the alkyl halide to a primary amine, affording βk-2C-B as a mixed hydrochloride/hydrobromide salt.

While imine formation is favored in slightly acidic environments, there has been experimental evidence that the intramolecular reaction proceeds readily for βk-2C-B at neutral pH.

When imine formation is present to full extent between two βk-2C-B molecules, a purple pyrazine dimer is formed.

The dimer can be converted back to βk-2C-B by imine hydrolysis: a process where acid catalysis is possible, but not an absolute requirement.

For example, the α-chloro ketones are known to express some level of toxicity, while others were not only found safe, but even some of their analogues have been applied in medicine.

Other routes of entry such as insufflation are generally not recommended by users because, similarly to 2C-B, βk-2C-B will irritate the mucous membrane that lines the nasal cavity.

There are numerous reports of users experiencing intense pain in the nasal region and the excretion of purple colored mucus following insufflation of βk-2C-B, with the latter suggesting a lower bioavailability for this route of administration as compared to ingestion.

These reports express that βk-2C-B has a commencement of action of 20 to 70 minutes and that a significant psychological effect is observed with a total duration of 8 to 12 hours.

Despite being seen as a relatively safe compound within the dosage range listed above, there has been a report of a healthy 25-year-old male user who had cardiac arrest following a dose of 140 mg.

Attending the chemical structure of βk-2C-B, various possible interactions can take place between the compound and target receptors in the body.

Four distinct SARs are proposed for βk-2C-B: Like other substituted cathinones of the phenethylamine family, βk-2C-B is suggested to show affinity for different subtypes of serotonin 5-HT2 receptor.

In an assay measuring β-arrestin2 recruitment to the 5-HT2A receptor, the registered EC50 and efficacy (in comparison to LSD) for βk-2C-B are reported to be 905 nM and 40.8%, respectively.

In general, compounds of the 2C family have been shown to be metabolized by liver hepatocytes, resulting in deamination and demethylation.

Oxidative deamination is common, and substitutes of dimethoxybenzoic acid can be produced following this route of biotransformation.

This because the amine neurotransmitters norepinephrine, epinephrine, serotonin and dopamine all show biotransformation pathways where monoamine oxidase is principally responsible for degradation.

This form of cross-tolerance is extremely common and well-described for compounds sharing similar mechanisms of action as psychedelic phenethylamine derivatives do.