Ropinirole: Difference between revisions - Wikipedia


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== Pharmacology ==

Ropinirole acts as a [[Dopamine receptor D2|D<sub>2</sub>]], [[Dopamine receptor D3|D<sub>3</sub>]], and [[Dopamine receptor D4|D<sub>4</sub>]] [[dopamine]] [[receptor (biochemistry)|receptor]] [[agonist]] with highest [[Chemical affinity|affinity]] for D<sub>3</sub>, which are mostly found in the limbic areas.<ref>{{Cite journal|last1=Shill|first1=Holly A.|last2=Stacy|first2=Mark|date=2009|title=Update on ropinirole in the treatment of Parkinson's disease|url=https://pubmed.ncbi.nlm.nih.gov/19557097/|journal=Neuropsychiatric Disease and Treatment|volume=5|pages=33–36|issn=1176-6328|pmc=2695212|pmid=19557097}}</ref> It is weakly active at the [[5-HT2 receptor|5-HT<sub>2</sub>]], and [[alpha-2 adrenergic receptor|α<sub>2</sub>]] receptors and is said to have virtually no affinity for the [[5-HT1 receptor|5-HT<sub>1</sub>]], [[GABA receptor|GABA]], [[muscarinic acetylcholine receptor|mAChRs]], [[alpha-1 adrenergic receptor|α<sub>1</sub>]], and [[Beta adrenergic receptor#.CE.B2 receptors|β-adrenoreceptors]].<ref name="RopPharmacology">{{cite journal | author=Eden, R. J.| title=Preclinical Pharmacology of Ropinirole (SK&F 101468-A) a Novel Dopamine D 2 Agonist| year=1991| journal=Pharmacology Biochemistry and Behavior| volume=38| issue=1| pages=147&ndash;154| doi=10.1016/0091-3057(91)90603-Y | pmid=1673248| s2cid=26842270|display-authors=etal}}</ref>

Ropinirole is metabolized primarily by [[cytochrome P450]] [[CYP1A2]] to form two [[metabolites]]; SK&F-104557 and SK&F-89124, both of which are renally excreted,<ref name="RPL">[http://www.richmondpharmacology.com/downloads/Publications/L3%20MDS%20ESRD%20poster.pdf An open-label, parallel-group, repeat-dose study to investigate the effects of end-stage renal disease and haemodialysis on the pharmacokinetics of ropinirole] | Authors: Debra J. Tompson, Deborah Hewens, Nancy Earl, David Oliveira, Jorg Taubel, Suzanne Swan, Luigi Giorgi | 13th International Congress of Parkinson’s Disease and Movement Disorders, Paris, France, June 7–11, 2009</ref> and at doses higher than clinical, is also metabolized by [[CYP3A4]]. At doses greater than 24&nbsp;mg, [[CYP2D6]] may be inhibited, although this has been tested only [[in vitro]].<ref name=TompsonD/>