Very little data exists on the human pharmacokinetics and pharmacodynamics of<unk>  and many other recently introduced substituted cathinones, aside from post-mortem results in overdose cases. Like amphetamines, synthetic cathinones exert their stimulating and sympathomimetic effects via increasing synaptic concentration of catecholamines such as dopamine, serotonin and norepinephrine. These molecules are able to inhibit monoamine reuptake transporters producing a decreased clearance of the neurotransmitters from the synapse. Furthermore, they may cause release of biogenic amines from intracellular stores. It appears that<unk>  has high preference for the dopamine transporter. Based on the structure and assuming that<unk>  is metabolized similarly to other cathinones, this compound is likely metabolized through N-dealkylation and/or reduction of the carbonyl group followed by N-dealkylation. Synthetic cathinones are generally less able than amphetamines to cross the blood–brain barrier because the beta-keto group causes an increase in polarity. Unlike other synthetic cathinones, pyrrolidine derivatives have a higher ability to cross the blood–brain barrier because the pyrrolidine ring confers a low polarity to these molecules. The studies on the metabolism of synthetic cathinones have shown that they are N-demethylated, the keto group is reduced to hydroxyl and ring alkyl groups are oxidised.
N-Ethylhexedrone
Dichloroacetic acid
Chloroethane
Helothermine
Dotinurad
Acrylamide
Perfluoroisobutene
Dianethole