Selegiline, also known as L-deprenyl, is a substituted phenethylamine, a selective, irreversible inhibitor of Type B monoamine oxidase. Selegiline is available in pill form under many brand names (Eldepryl, Carbex, Atapryl) and is used to reduce symptoms in early-stage Parkinson's disease. Selegiline delays the time point when the L-DOPA (levodopa) treatment becomes necessary from about 11 months to about 18 months after diagnosis, which is beneficial despite not being definitive evidence of neuroprotection. The rationale for adding selegiline to levodopa is to decrease the required dose of levodopa and thus reduce the motor complications of levodopa therapy. Selegiline is also delivered via a transdermal patch (brand name, Emsam) and in this form, Selegiline is used as a treatment for the major depressive disorder. Selegiline (brand name Anipryl) is also used (at extremely high dosages relative to humans) in veterinary medicine to treat the symptoms of Cushing's disease and cognitive dysfunction (Canine Cognitive Dysfunction) in dogs. Side effects of the pill form include, in decreasing order of frequency, nausea, hallucinations, confusion, depression, loss of balance, insomnia, increased involuntary movements, agitation, arrhythmia, slow heart rate, delusions, hypertension, new or increased angina pectoris, and syncope. The main side effects of the patch form for depression included application site reactions, insomnia, diarrhea, and sore throat.

Carbidopa is a competitive inhibitor of aromatic L-amino acid decarboxylase that does not cross the blood-brain barrier, is routinely administered with levodopa (LD) for the treatment of the symptoms of idiopathic Parkinson’s disease (paralysis agitans), postencephalitic parkinsonism, and symptomatic parkinsonism, which may follow injury to the nervous system by carbon monoxide intoxication and/or manganese intoxication. Current evidence indicates that symptoms of Parkinson’s disease are related to depletion of dopamine in the corpus striatum. Administration of dopamine is ineffective in the treatment of Parkinson’s disease apparently because it does not cross the blood-brain barrier. However, levodopa, the metabolic precursor of dopamine, does cross the blood- brain barrier, and presumably is converted to dopamine in the brain. When levodopa is administered orally it is rapidly decarboxylated to dopamine in extracerebral tissues so that only a small portion of a given dose is transported unchanged to the central nervous system. For this reason, large doses of levodopa are required for adequate therapeutic effect and these may often be accompanied by nausea and other adverse reactions, some of which are attributable to dopamine formed in extracerebral tissues. Carbidopa inhibits decarboxylation of peripheral levodopa. Carbidopa has not been demonstrated to have any overt pharmacodynamic actions in the recommended doses.