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N-Methyl-1-1-(1,3-benzodioxol-5-yl)-butanamine (MBDB): It's Properties and Possible Risks (2000)

N-Methyl-1-1-(1,3-benzodioxol-5-yl)-butanamine (MBDB): It's Properties and Possible Risks (2000)

  1. Jatelka
    Addiction Biology (2000) 5, 269-282

    Aerts, Mallerat and Rigter

    Abstract
    MBDB (N-methyl-1 -(1,3-benzodioxol -5-yl)-2-aminobutane) is the a -ethyl homologue of MDMA (3,4-methylenedioxy-N-methylamphetamine). MBDB is metabolized and excreted similarly to MDMA: presumably, the major ity of oral MBDB is excreted in ur ine unmetabolized. The main metabolic routes in man are thought to be O-dealkylation and subsequent methylation, sulphation and glucuronidation of the newly formed hydroxy groups. The major acute neuropharmacological effects of MBDB in the rat are an increase in serotonin release in the brain and an inhibition of serotonin and noradrenaline re-uptake. These effects compare well with those of MDMA, although the latter is more potent. MBDB may also slightly increase dopamine release and inhibit dopamine re-uptake, but to a lesser extent than MDMA. This is important, as dopamine release has been implicated in the reinforcing qualities of substances such as cocaine and amphetamine. The neuroendocrine effects of MBDB resemble those of MDMA. Both substances increase plasma ACTH, corticosterone, prolactin and renin. The neurophysiological effects of MBDB are character ized by a decrease in electrical activity throughout the brain, most notably in the alpha2 and delta frequency bands. In contrast, hallucinogens increase the activity in the alpha1 band, especially in the corpus striatum. In drug discrimination tests in the rat, MBDB, like MDMA, can be distinguished clearly from both stimulants and hallucinogens. The class of substances to which MBDB belongs may be named entactogens. MBDB dose-dependently increases locomotor activity and decreases exploratory behaviour in the rat and causes distress vocalization and wing extension in the newly hatched chicken. The rewarding properties of MBDB appear to be smaller than those of MDMA, as suggested by a 2.5 times weaker potency in the conditioned place preference test in rats. The main subjective effects of MBDB in man are a pleasant state of introspection, with greatly facilitated interpersonal communication and a pronounced sense of empathy and compassion between subjects. In this respect, MBDB again resembles MDMA. However, there are also differences. MBDB has a slower and more gentle onset of action than MDMA, produces less euphoria and has less stimulant properties. The few toxicological data available suggest that MBDB may cause serotonergic deficits in the brain, although the potency of MBDB to cause this neurotoxic effect is smaller than that of MDMA. Severe acute reactions in man as have been reported for MDMA have not been published for MBDB. The dependence potential of MBDB appears to be small, probably even smaller than that of MDMA. MBDB has been available at least since 1994 but its position on the synthetic drugs market is marginal. Subjective reports indicate that MBDB is less popular among users than MDMA. The reason may be that MBDB produces less euphor ia than MDMA. Another possible explanation is that MBDB largely lacks the stimulant proper ties of MDMA. We calculated a margin of safety with a method similar to one used in the risk assessment of pharmaceuticals. The results suggest that MBDB is three times less likely to cause serotonergic brain deficits than MDMA. However, it should be noted that for both substances the margin of safety is less than one, indicating that the risk of neurotoxicity is not negligible. In animals, serotonergic brain deficits after exposure to MDMA have been linked to the degeneration of serotonergic nerve terminals.