Substituted cathinones for sale

The emergence of legal substituted cathinones in the research chemicals market was preceded by measures to limit the turnover of classical psychostimulants: amphetamine, methamphetamine, cocaine, MDMA (ecstasy). The response to the prohibitive measures was the introduction on the research chemicals market of designer psychostimulants from another class—piperazines. The emergence of another class, synthetic substituted cathinones, on the illegal market in the mid-to-late-zero years of design psychostimulants can be considered a response to the restriction of piperazine turnover. As in the case of piperazines, new legal research chemicals should be an alternative to the already banned psychostimulants, such as, amphetamine, cocaine, ecstasy, methamphetamine.


It is believed that toxicokinetics and biotransformation processes of substituted cathinones, amphetamines and phenylethylamines are very similar, since there is an obvious proximity of the substances structures. The presence of a keto group somewhat reduces the substituted cathinones permeability through blood-brain barrier. In addition, the keto group can undergo a reduction with the alcohol formation.

As an example of substituted cathinones biotransformation, mephedrone metabolism in male Sprague-Dowley rats, which received a chemical chemical orally at a dose of 30 mg/kg, can be considered. In rodent blood samples, after 30, 60 and 120 min, N-demethylation, hydroxylation, and carboxylation products were detected. For a more detailed idea of ​​the possible ways of mephedrone biotransformation, these works are supplemented by information from other sources. It can be seen that both  unmodified mephedrone molecule and the metabolite after N-demethylation undergo hydroxylation. In the first biotransformation phase, the main role is played by cytochrome P-450 CYP2D6. As with amphetamines, methyl group presence in the a-position of the cathinones ethyl radical makes it difficult to degrade them with the monoamine oxidases participation.


The toxicodynamics of synthetic cathinones basically corresponds to the toxicity mechanisms of the classical psychostimulants: cocaine, amphetamine, methamphetamine, ecstasy. Consequently, substituted cathinones are stimulants, although they are inferior to their phenylisopropylamine analogues in this respect. The lower activity is associated with weak penetration through the BBB (presence of the polar keto group).

The main clinical and narcological manifestations of exposures to substituted cathinones are based on the monoaminergic systems excitation of the brain and the body as a whole. The cause of activation is an increase in the synaptic concentration of dopamine, norepinephrine and serotonin. Neurochemical targets of synthetic substituted cathinones—monoamine transport systems, providing their reuptake (reagent) from the synaptic cleft:

  • dopamine transporter (DAT) system;
  • norepinephrine transporter (NET) system;
  • serotonin transporter (SERT) system;
  • vesicular monoamine transporter (VMAT2).

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Benzedrone (4-MBC)
Benzedrone; 4-MBC [Designer Drug]; 4-Methyl-N-benzylcathinone; AKOS022329826; 2-(Benzylamino)-1-(4-methylphenyl)-1-propanone Oral, insufflation, intravenous, rectal, smoking (±)-1-(4-methylphenyl)-2-(benzylamino)propan-1-one 1225617-75-3 C17H19NO 253.34 g/mol


Dibutylone (bk-DMBDB)
1-(1,3-Benzodioxol-5-yl)-2-(dimethylamino)butan-1-one; β-Keto-dimethylbenzodioxolylbutanamine; bk-DMBDB; Dibutylone Oral, snorting, inhalation (vaporization), injection, rectal 1-(Benzo[d][1,3]dioxol-5-yl)-2-(dimethylamino)butan-1-one 802286-83-5 C13H17NO3 235.28 g·mol−1


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