Open Access Articles- Top Results for Benserazide


File:Benserazide ball-and-stick.png
Systematic (IUPAC) name
Clinical data
AHFS/ International Drug Names
Pharmacokinetic data
Excretion Renal and fecal
14919-77-8 7pxY
PubChem CID 2327
ChemSpider 2237 7pxY
UNII B66E5RK36Q 7pxY
KEGG D03082 7pxY
ChEMBL CHEMBL1096979 7pxY
Chemical data
Formula C10H15N3O5
257.243 g/mol
 14pxY (what is this?)  (verify)

Benserazide (also called Serazide or Ro 4-4602) is a peripherally-acting aromatic L-amino acid decarboxylase (AADC) or DOPA decarboxylase inhibitor, which is unable to cross the blood–brain barrier.[1]


It is used in the management of Parkinson's disease in combination with L-DOPA (levodopa) as co-beneldopa (BAN), under the brand names Madopar in the UK and Prolopa in Canada, both made by Roche. Benserazide is not approved for use in the US; carbidopa is used instead for the same purpose. These combinations are also used for the treatment of restless legs syndrome.[2]


Levodopa is a precursor to the neurotransmitter dopamine which is administered to increase its levels in the central nervous system. However, most levodopa is decarboxylated to dopamine before it reaches the brain, and since dopamine is unable to cross the blood–brain barrier, this translates to little therapeutic gain with strong peripheral side effects.

Benserazide inhibits the aforementioned decarboxylation, and since it itself cannot cross the blood–brain barrier, this allows dopamine to build up solely in the brain instead. Adverse effects caused by peripheral dopamine, such as vasoconstriction, nausea, and arrhythmia, are minimized. However, benserazide cannot reduce the centrally-mediated side effects of levodopa, particularly dyskinesia.

Benserazide has little therapeutic effect on its own, and its effect occurs synergically in combination with levodopa.

The enzyme inhibited by Benzerazide, catalyzes many different decarboxylations. The same effect of concentrating the conversion of l-dopa into dopamine to the central nervous system can be achieved with the following decarboxylations being confined to the central nervous system:

Centrally-mediated side effects of higher levels of neuro and trace amine transmitters may worsen in combination with monoamine oxidase inhibitors.


File:Benserazide synthesis.svg
Benserazide synthesis.[3]


  1. Shen H, Kannari K, Yamato H, Arai A, Matsunaga M (March 2003). "Effects of benserazide on L-DOPA-derived extracellular dopamine levels and aromatic L-amino acid decarboxylase activity in the striatum of 6-hydroxydopamine-lesioned rats". The Tohoku journal of experimental medicine 199 (3): 149–59. PMID 12703659. doi:10.1620/tjem.199.149. 
  2. Ryan, Melody; Slevin, John T. (2006). "Restless legs syndrome". American Journal of Health-System Pharmacy. 63 (17): 1599-1612. Retrieved on 2008-02-06.