[3] It was first demonstrated, in 1978, by Conway et al. and possibly others that, while α-methyldopamine caused acute decreases in the levels of neuronal dopamine, in some areas of the brain in excess of 75%, levels returned to baseline within 12 hours, indicating that α-methyldopamine could not be responsible for the toxic effects observed.

[4] However, the story complicates as α-methyldopamine readily oxidizes to the o-quinone and reacts with endogenous antioxidants in the body, such as glutathione (GSH).

It was demonstrated by Miller et al. (1997), that 5-(glutathion-S-yl)-α-methyldopamine and 5-(N-acetylcystein-S-yl)-α-methyldopamine produced similar effects to the parent compound, but did not induce neurotoxicity when injected intracerebroventricularly.

However, the derivative metabolite 2,5-bis-(glutathion-S-yl)-α-methyldopamine (injected at ~1.5 times the usual per-kg MDMA dose) did in fact induce neurotoxicity, providing initial evidence that this metabolite may be the source of neuronal toxicity following the administration of MDA and MDMA, and the subsequent reduction in serotonergic axons.

Analogues of α-methyldopamine include corbadrine (levonordefrin; α-methylnorepinephrine; 3,4,β-trihydroxyamphetamine), dioxifedrine (α-methylepinephrine; 3,4,β-trihydroxy-N-methylamphetamine), and hydroxyamphetamine (norpholedrine; α-methyltyramine; 4-hydroxyamphetamine)