Clinical Chemistry
July 1, 1999
John K. Fallon, Andrew T. Kicman, J. A. Henry et al.
137 citations
After a 40 mg oral dose of racemic MDMA (ecstasy) to eight men, the R-enantiomer reached higher and longer-lasting plasma levels than the S-enantiomer. The R-enantiomer's half-life was 5.8 hours versus 3.6 hours for S-MDMA, and its area under the curve was 2.4 times greater. More R-MDMA was excreted in urine (21.4% of dose) than S-MDMA (9.3%). The demethylated metabolite MDA appeared in smaller amounts, with S-MDA slightly exceeding R-MDA. Mathematical modeling of plasma enantiomer ratios over time suggests that analyzing stereochemical composition could help estimate time since drug intake for forensic purposes.
Drug Testing and Analysis
July 1, 2011
Leslie A. King, Andrew T. Kicman
99 citations
This special issue introduces new psychoactive substances (NPS), formerly called 'designer drugs' or 'legal highs', defined as narcotic or psychotropic drugs not scheduled under UN conventions but posing comparable public health threats. The article traces their evolution from 1980s fentanyl derivatives and MPTP-contaminated α-prodine causing Parkinson's disease, through phenethylamines like MDMA and hallucinogens, to piperazines, cathinones (e.g., mephedrone), synthetic cannabinoids ('Spice'), and diverse recent compounds. Over half of the approximately 170 substances reported to the EMCDDA since 1997 appeared after 2006. Manufacturing shifted from clandestine labs to legitimate chemical suppliers, with internet sales. The authors note that little is known about their harmful properties, and uncontrolled experimentation risks future public health crises.
British Journal of Pharmacology
February 1, 2002
Mary L. Forsling, John K. Fallon, Darshna Shah et al.
77 citations
MDMA and its metabolites can stimulate release of the hormones vasopressin and oxytocin from rat hypothalamic tissue in the laboratory. The metabolite HMMA (4-hydroxy-3-methoxymethamphetamine) was the most potent, increasing basal vasopressin release more than twofold and oxytocin release by about 60% at a concentration of 10 nM. MDMA itself produced smaller increases. The effect on vasopressin release was consistently greater than on oxytocin. These findings suggest that MDMA-induced hyponatraemia (low blood sodium) may result from excessive vasopressin secretion triggered by the drug or its breakdown products.
Annals of the New York Academy of Sciences
June 1, 2002
John K. Fallon, Dhwanil Shah, Andrew T. Kicman et al.
54 citations
MDMA (ecstasy) can cause dangerously low sodium levels by triggering inappropriate secretion of the antidiuretic hormone arginine vasopressin (AVP). In eight healthy men given a low 40 mg dose of MDMA, plasma AVP rose significantly at 1, 2, and 4 hours. A negative correlation between MDMA and AVP at 1 hour suggested a metabolite might drive the increase. Testing MDMA and five of its metabolites on isolated rat hypothalamus tissue showed all compounds increased AVP release, with the major metabolite HMMA being the most potent and DHMA the least. Most compounds also enhanced AVP release in response to potassium stimulation. These in vitro results confirm that MDMA metabolites, not just the parent drug, contribute to AVP secretion.