Dopamine releasing agent

[7] The inability to identify selective DRAs has been attributed to the strong phylogenetic similarities between the DAT and NET.

[16] Selective DRAs might have different clinical effects in the treatment of attention deficit hyperactivity disorder (ADHD) than the NDRAs like amphetamines and norepinephrine–dopamine reuptake inhibitors (NDRIs) like methylphenidate that are currently used.

[19] For example, they might have improved therapeutic selectivity by reducing or eliminating the cardiovascular and sympathomimetic side effects of NDRAs.

[21] Amphetamines like dextroamphetamine and dextromethamphetamine are fairly balanced NDRAs but release norepinephrine about 2- to 3-fold more potently than dopamine.

[1][23] A number of potentially more well-balanced NDRAs, including levomethcathinone (l-MC),[15] 3-chloroamphetamine (3-CA; PAL-304),[1][24] 3-chloromethcathinone (3-CMC; clophedrone; PAL-434),[25] and 2-phenylmorpholine (2-PM; PAL-632),[26] are known, and all appear to be roughly equipotent in inducing dopamine versus norepinephrine release.

[30][31][32] There is reportedly some, albeit mixed, in-vitro evidence that the antidepressant and modestly selective DRI amineptine may, in addition to inhibiting the reuptake of dopamine, selectively induce the presynaptic release of dopamine without affecting release of norepinephrine or serotonin.

[33][34][35] However, amineptine is larger than the known small structural size limit of monoamine releasing agents,[3] suggesting that it may not in fact be a DRA.