D-Deprenyl: Difference between revisions
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{{DISPLAYTITLE:D-Deprenyl}} | |||
== | == Overview == | ||
D-Deprenyl | [[File:D-Deprenyl.svg|thumb|right|Chemical structure of D-Deprenyl]] | ||
'''D-Deprenyl''', also known as '''selegiline''', is a [[monoamine oxidase inhibitor]] (MAOI) that is primarily used in the treatment of [[Parkinson's disease]] and [[major depressive disorder]]. It is a selective inhibitor of [[monoamine oxidase B]] (MAO-B) at lower doses, which makes it useful in increasing [[dopamine]] levels in the brain. | |||
== | == Mechanism of Action == | ||
D-Deprenyl | D-Deprenyl works by inhibiting the activity of the enzyme [[monoamine oxidase B]], which is responsible for the breakdown of [[dopamine]] in the brain. By inhibiting this enzyme, D-Deprenyl increases the availability of dopamine, which is beneficial in conditions like [[Parkinson's disease]] where dopamine levels are reduced. | ||
==Clinical | == Clinical Uses == | ||
D-Deprenyl is primarily used in the management of [[Parkinson's disease]]. It is often used as an adjunct therapy to [[levodopa]]/[[carbidopa]] treatment. In addition to its use in Parkinson's disease, D-Deprenyl is also used in the treatment of [[major depressive disorder]], particularly in patients who do not respond to other treatments. | |||
== | == Side Effects == | ||
Common side effects of D-Deprenyl include [[nausea]], [[dizziness]], [[insomnia]], and [[orthostatic hypotension]]. At higher doses, it can lose its selectivity for MAO-B and inhibit [[monoamine oxidase A]] (MAO-A) as well, which can lead to more severe side effects and dietary restrictions due to the risk of [[hypertensive crisis]]. | |||
* [[ | |||
== Pharmacokinetics == | |||
D-Deprenyl is well absorbed from the gastrointestinal tract and is metabolized in the liver. It has a relatively long half-life, which allows for once-daily dosing in most patients. The metabolites of D-Deprenyl include [[amphetamine]] and [[methamphetamine]], which can contribute to its stimulating effects. | |||
== History == | |||
D-Deprenyl was first synthesized in the 1960s and was initially investigated for its potential as an [[antidepressant]]. Its ability to selectively inhibit MAO-B was discovered later, leading to its use in the treatment of [[Parkinson's disease]]. | |||
== Related Pages == | |||
* [[Monoamine oxidase inhibitor]] | |||
* [[Parkinson's disease]] | * [[Parkinson's disease]] | ||
* [[ | * [[Dopamine]] | ||
* [[Major depressive disorder]] | |||
[[ | |||
[[Category:Monoamine oxidase inhibitors]] | |||
[[Category:Antiparkinsonian agents]] | |||
[[Category:Antidepressants]] | |||
Latest revision as of 03:51, 13 February 2025
Overview[edit]
D-Deprenyl, also known as selegiline, is a monoamine oxidase inhibitor (MAOI) that is primarily used in the treatment of Parkinson's disease and major depressive disorder. It is a selective inhibitor of monoamine oxidase B (MAO-B) at lower doses, which makes it useful in increasing dopamine levels in the brain.
Mechanism of Action[edit]
D-Deprenyl works by inhibiting the activity of the enzyme monoamine oxidase B, which is responsible for the breakdown of dopamine in the brain. By inhibiting this enzyme, D-Deprenyl increases the availability of dopamine, which is beneficial in conditions like Parkinson's disease where dopamine levels are reduced.
Clinical Uses[edit]
D-Deprenyl is primarily used in the management of Parkinson's disease. It is often used as an adjunct therapy to levodopa/carbidopa treatment. In addition to its use in Parkinson's disease, D-Deprenyl is also used in the treatment of major depressive disorder, particularly in patients who do not respond to other treatments.
Side Effects[edit]
Common side effects of D-Deprenyl include nausea, dizziness, insomnia, and orthostatic hypotension. At higher doses, it can lose its selectivity for MAO-B and inhibit monoamine oxidase A (MAO-A) as well, which can lead to more severe side effects and dietary restrictions due to the risk of hypertensive crisis.
Pharmacokinetics[edit]
D-Deprenyl is well absorbed from the gastrointestinal tract and is metabolized in the liver. It has a relatively long half-life, which allows for once-daily dosing in most patients. The metabolites of D-Deprenyl include amphetamine and methamphetamine, which can contribute to its stimulating effects.
History[edit]
D-Deprenyl was first synthesized in the 1960s and was initially investigated for its potential as an antidepressant. Its ability to selectively inhibit MAO-B was discovered later, leading to its use in the treatment of Parkinson's disease.
