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Brasofensine (NS-2214, BMS-204756) is a phenyltropane that had been under development for the treatment of Parkinson’s and Alzheimer’s disease. Phase II trials 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. In animal models of Parkinson’s disease, brasofensine was effective in stimulating LMA and reversing akinesia.
The isomerization of brasofensine is not between the alpha and beta positions on the 2 position of the tropane ring but rather 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 consigned the name BMS-205912
In PD, symptoms do not begin to manifest until there has been an 80% reduction in dopaminergic neurons, particularly in the substantia nigra brain region.
Diclofensine (Ro 8-4650) was developed by Hoffmann-La Roche in the 1970s in the search for a new antidepressant. It was found that the (S)-isomer was responsible for activity. Is a stimulant drug which acts as a triple monoamine reuptake inhibitor, primarily inhibiting the reuptake of dopamine and norepinephrine, with affinities (Ki) of 16.8 nM, 15.7 nM, and 51 nM for DAT, NET, and SERT (dopamine, norepinephrine and serotonin transporters), respectively. It was found to be an effective antidepressant in human trials, with relatively few side effects, but was ultimately dropped from clinical development, possibly due to concerns about its abuse potential.
25g, 50g, 100g, 500g, 1kg
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