Studies on the Metabolism and the Detectability of Camfetamine in Rat Urine Using GC-MS and LC-(HR)-MS Techniques

N-methyl-3-phenyl-norbornan-2-amine (camfetamine; CFA) is sold as a so-called "research chemical" via the internet and belongs as an amphetamine-type stimulant (ATS) to the group of new psychoactive substances (NPS). CFA is an analogue of N-ethyl-3-phenyl-norbornan-2amine (fencamfamine; FCF), which was developed in the 1960’s as an appetite suppressant and a stimulant for treating depressive day-time fatigue, or lack of concentration. Both compounds are camphor derivatives with an amphetamine backbone. FCF is scheduled in several countries, e.g. USA and Germany, but CFA is still uncontrolled. DeLucia et al. described FCF as central nervous stimulant and inhibitor of the dopamine reuptake and releaser of dopamine and noradrenalin [1]. Several other publications described its effects on body weight and addiction potential [2-6]. N-Deethyl FCF was the main metabolite described in man and parahydroxy-aryl FCF in equine [7,8]. So far, no scientific information about the mechanism of action or the metabolism of CFA was published. CFA is described in internet forums (www.bluelight.com, www.eve-rave.ch, www.land-der-traeume.de), as a stimulant or a working aid providing increasing vigilance with typical amphetamine-like side effects. Therefore, CFA should be integrated into drug screening methods used in clinical and forensic toxicology. Kavanagh et al. published mass spectral data only of the synthesized standard [9], but metabolism data are needed for urine screening, as most central active drugs are excreted in a more or less completely metabolized form.