Format

Send to

Choose Destination
See comment in PubMed Commons below
IDrugs. 2010 Oct;13(10):723-31.

Preladenant, a novel adenosine A(2A) receptor antagonist for the potential treatment of parkinsonism and other disorders.

Author information

1
University of Connecticut, Behavioral Neuroscience Division, Department of Psychology, 406 Babbidge Road, Unit 1020, Storrs, CT 06269-1020, USA. john.salamone@uconn.edu

Abstract

Adenosine A(2A) receptor antagonists exert antiparkinsonian effects in animal models and several drugs in this class are currently being assessed in clinical trials. Preladenant (SCH-420814) is an adenosine A(2A) receptor antagonist with a high affinity and very high selectivity for adenosine A(2A) receptors, which is being developed by Merck & Co Inc (following its acquisition of Schering-Plough Corp) for the potential treatment of Parkinson's disease. Preclinical studies in rodent and primate models of parkinsonism demonstrated that preladenant can reverse the motor impairments induced by dopamine depletion or antagonism. Phase I and II clinical trials indicated that preladenant was well tolerated. Moreover, preladenant met its major endpoints by reducing OFF time and increasing ON time in l-DOPA-treated patients with Parkinson's disease, without worsening dyskinesias. Therefore, preladenant may have considerable utility for the treatment of Parkinson's disease, as well as the parkinsonian side effects of dopamine D2 receptor antagonists. As research has suggested that adenosine A(2A) receptor antagonists are active in animal models of effort-based decision making, it is possible that preladenant could also be useful for treating energy-related symptoms, such as fatigue, psychomotor retardation and anergia in patients with parkinsonism or depression. At the time of publication, phase III clinical trials were recruiting patients with Parkinson's disease.

PMID:
20878595
[Indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Loading ...
    Support Center