stable in crystalline form, solutions of limited stability
In general, mephedron is described by users as a drug with stimulant and entactogenic effect, similar to MDMA, cocain or amphetamines. The desired effects reported by users include euphoria, general stimulation, enhanced music appreciation, elevated mood, decreased hostility, improved mental function, decreased appetite and mild sexual stimulation.
Intended effects are typically seen within 15–45 min after oral administration. Slower onset can be seen when mephedrone is taken on full stomache. Duration of action is reported aproximatelly 2–3 hours. After nasal insufflation the peak effects is within 30 min.
The most often unwanted effects associated with mephedrone use are sweating, headaches, palpitations, nauzea, cold or blue fingers. Mephedron users also report inability to concentrate, inability to visually focus, memory problems, altered level of consciousness, erratic behaviour, hallucinations and delusions. These symptoms are mostly described after high mephedrone dose, prolonged use or when mephedrone is combined with some other psychoactive substances.
The most common routes of mephedrone administration are oral ingestion and nasal insufflation, however injection administration is also reported. Mephedrone is not suitable for smoking.
The capacity of mephedrone to affect dopamine (DA) and serotonin (5-HT) extracellular concentration has been related to its psychostimulant and entactogenic effects, respectively (Schifano et al., 2011). Mephedrone shares some of the 5-HT-releasing property of MDMA, but it is a more potent releaser of DA than MDMA. Impact of mephedrone on extracellular level of DA is similar to impact of amphetamine and methamphetamine. Mephedrone is also similar to cocaine, with relative DAT versus SERT inhibition potencies. Another aspect of mechanism of action is mephedrone induces the release of DA through the DAT and 5-HT through the SERT. Furthermore, mephedrone has showed very high blood-brain barrier permeability in in vitro model (Baumann et al., 2012; Kehr et al., 2011; Simmler et al., 2013).
Due to the effect of mephedrone on DA-ergic neurotransmission, the addictive potential of mephedrone was assessed. Users themsleves often described craving for the drug, the compulsive urge to redose (Brunt et al., 2011).
Polydrug use is the most risk factor for fatal intoxication. Combination of mephedrone with another drug seems to amplify dopaminergic and serotonergic stimulations in a synergic way and increase probability of death. However, a few mephedrone-related deaths were monitored in Europe. In these cases mephedrone was the only drug detected post-mortem in blood and urine (Sweden, the United Kingdom...).
An acute mephedrone toxicity has similar clinical features of toxicity consistent with an acute sympathomimetic toxidrome (e.g. hypertension, tachycardia, agitation). These findings are same as we can see with other sympathomimetic recreational drugs such as MDMA or cocaine (Wood et al., 2010).
It is published a case report a 19-year-old man with acute myocarditis after the oral ingestion of mephedrone. Researchers suggest it´s direct toxic effect on the myocyte or through immune-mediated mechanisms (Nicholson et al., 2010).
Another case report in the UK describes hyponatremia and altered mental status. The most probable mechanism of action is mephedrone promotes serotonin-mediated ADH release, and that a mephedrone-induced syndrome of inappropriate ADH secretion (Sammler et al., 2010).