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Lisuride: Wikis


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From Wikipedia, the free encyclopedia

Systematic (IUPAC) name


CAS number 18016-80-3
ATC code G02CB02 N02CA07
PubChem 28864
DrugBank APRD00636
Chemical data
Formula C20H26N4O 
Mol. mass 338.447 g/mol
Pharmacokinetic data
Bioavailability 10-20% for lisuride hydrogenmaleate
Protein binding about 15%
Metabolism Hepatic
Half life 2 hours
Excretion renal and biliary in equal amounts
Therapeutic considerations
Pregnancy cat.  ?
Legal status Prescription only
Routes Oral, subcutaneous, transdermal
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Lisuride (Dopergin, Proclacam, Revanil) is an antiparkinson agent of the iso-ergoline class, chemically related to the dopaminergic ergoline Parkinson's drugs. Lisuride is described as free base (see table on the right) and as hydrogenmaleate salt.

Lisuride is used to lower prolactin and, in low doses, to prevent migraine attacks. The use of lisuride as initial anti-Parkinsonian treatment has been advocated, delaying the need for levodopa until lisuride becomes insufficient for controlling the Parkinsonian disability. Preliminary trials suggest that the dermal application of lisuride may be useful in the treatment of Parkinson's disease. As lisuride is very poorly absorbed when take orally and has a short half-life, continuous transdermal administration offers significant advantages and could make the compound a far more consistent therapeutic. Lisuride is not currently available in the US, as the drug was not a commercial success in comparison with other dopamine receptor agonist anti-parkinsonian compounds. It is still used clinically in a number of countries in the EU and is still commercially available in the UK and China.

Mode of action

Lisuride is a dopamine and serotonin receptor partial agonist. It has a high affinity for the dopamine D2, D3 and D4 receptors, as well as serotonin 5-HT1A[1] and 5-HT2A/C receptors.[2] While lisuride has a similar receptor binding profile to the more well-known and chemically similar ergoloid N,N-diethyl-lysergamide (LSD), it lacks the psychedelic effects of its sister compound.[3]


  1. ^ Marona-Lewicka D, Kurrasch-Orbaugh DM, Selken JR, Cumbay MG, Lisnicchia JG, Nichols DE (October 2002). "Re-evaluation of lisuride pharmacology: 5-hydroxytryptamine1A receptor-mediated behavioral effects overlap its other properties in rats". Psychopharmacology (Berl.) 164 (1): 93–107. doi:10.1007/s00213-002-1141-z. PMID 12373423. 
  2. ^ Egan CT, Herrick-Davis K, Miller K, Glennon RA, Teitler M (April 1998). "Agonist activity of LSD and lisuride at cloned 5HT2A and 5HT2C receptors". Psychopharmacology (Berl.) 136 (4): 409–14. doi:10.1007/s002130050585. PMID 9600588. 
  3. ^ González-Maeso J, Weisstaub NV, Zhou M, Chan P, Ivic L, Ang R, Lira A, Bradley-Moore M, Ge Y, Zhou Q, Sealfon SC, Gingrich JA (February 2007). "Hallucinogens recruit specific cortical 5-HT(2A) receptor-mediated signaling pathways to affect behavior". Neuron 53 (3): 439–52. doi:10.1016/j.neuron.2007.01.008. PMID 17270739. 

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