Dopamine deficiency, caused by a loss of dopamine-producing cells in certain parts of the brain, may be responsible for many of the symptoms of Parkinson's disease. Although it would make sense to give dopamine to help treat Parkinson's, this does not work, since dopamine cannot cross the blood-brain barrier.
- Levodopa -- Levodopa is a precursor of dopamine, which means that the body can use it to make dopamine. Unlike dopamine, levodopa crosses the blood-brain barrier.
- Carbidopa -- Carbidopa delays the conversion of levodopa into dopamine until it reaches the brain, preventing or diminishing some of the side effects that often accompany levodopa therapy. Carbidopa also reduces the amount of levodopa needed for Parkinson's disease treatment.
- Entacapone -- Entacapone inhibits an enzyme (catechol-O-methyltransferase or COMT) that breaks down levodopa before it has a chance to reach the brain. Entacapone increases the level of levodopa in the body and helps it to work longer.
Levodopa is the "real" medication in carbidopa-levodopa-entacapone that treats Parkinson's disease. The other two medications help levodopa work better and longer.
In clinical studies, carbidopa-levodopa-entacapone has been shown to be more effective than just carbidopa-levodopa for Parkinson's treatment. In these studies, people who were experiencing wearing-off fluctuations of their carbidopa-levodopa therapy were given either entacapone or a placebo (a "sugar pill" with no active ingredient) to take with each dose of their carbidopa-levodopa. These studies showed that entacapone helped the carbidopa-levodopa work longer, with shorter "off" periods (when the medication did not work well) and longer "on" periods (when the medication worked well).