Brasofensine

Brasofensine (NS-2214, BMS-204756) is a phenyltropane that had been under development by Bristol-Myers Squibb for the treatment of Parkinson's and Alzheimer's diseases.
In animal models of Parkinson's disease, brasofensine was effective in stimulating LMA and reversing akinesia. Phase II trials in humans were conducted in 1996 and brasofensine was shown to be both effective and well tolerated at a dose of 4 mg; however, development was stopped after "in vivo" cis-anti isomerization of the 2α-methyloxime group was reported. 
The isomerization of brasofensine did not involve epimerization at 2-position of the tropane ring, but rather involved the "E"/"Z"-isomerization of the imine (i.e. "methyl-aldoxime"). It was believed that this process occurs "in vivo", although it cannot be ruled out as a possibility that some isomerization also occurs prior to ingestion. The ("Z")-isomer has been assinged the name BMS-205912.
In Parkison's disease, symptoms do not begin to manifest until there has been an 80% reduction in dopaminergic neurons, particularly in the substantia nigra brain region.
Metabolism and distribution.
Brasofensine is not particularly stable and is readily metabolized. It was studied in humans in doses ranging from 2-50 mg. Because metabolism in rats is much greater than in humans, the amount of metabolites detected in their urine (and feces) was also much greater than for humans, who excrete more of the product intact. In radiolabeling studies using 14C, most (~90%) of the 14C was detected in the urine of humans, whereas for rats as much as 80% of the 14C was in their feces.
It is well known that a Schiff base is more stable than a regular imine. Imine formation is a reversible process, and in the study by Zhu "et al"., none of the aldehyde was recovered/detected by GC-MS. Instead, the breakdown products were "N"-demethyl metabolites.