Oxidopamine, also known as 6-hydroxydopamine (6-OHDA) or 2,4,5-trihydroxyphenethylamine, is a synthetic monoaminergic neurotoxin used by researchers to selectively destroy dopaminergic and noradrenergic neurons in the brain.

[1] The toxin oxidopamine is an antagonist of the neurotransmitter dopamine, and is commonly used for making experimental animal models in Parkinson's disease.

Parkinson disease leads to degeneration of dopaminergic midbrain neurons resulting in dopamine depletion.

ROS generation is also increased by oxidopamine via inhibition of complex I and IV of the electron transport chain.

[citation needed] Oxidopamine was long ago characterized and synthesized, starting from 2,4,5-trimethoxy and 2,4,5-tribenzyloxybenzaldehyde respectively, by Harley-Mason and Lee and Dickson.

In consequence of the general low yields and the relatively involved procedures, it is wished to report an alternate scheme for the synthesis of this pharmacon.

Within the neuron, oxidopamine is oxidized by monoamine oxidase producing the toxic products hydrogen peroxide (H2O2), catecholamine quinones and reactive oxygen species (ROS).

[8] In order to induce Parkinsonism in animals, around 70% of the dopaminergic neurons in the substantia nigra of the brain must be destroyed, and this is often achieved either with oxidopamine or another neurotoxin MPTP.

However, recent research suggests that 6-OHDA modifies proteins via cysteine modification, implying an additional cause of neuronal cell death.

[9] Oxidopamine is administered via an injection and causes an increase of outflow, and a decrease for intraocular pressure (IOP), lasting for a few days up to two weeks.

The most common adverse effects caused by injections are hyperemia, subconjunctival hemorrhage, transient mydriasis, chemosis, lid edema, and ptosis (which may last for a few weeks).