Dexpramipexole, formerly known as KNS-760704 and (R)-Pramipexole, is under development for the treatment of amyotrophic lateral sclerosis (ALS), formerly known as Lou Gehrig’s disease. The drug failed to show efficacy in terms of function or survival in a Phase III study of patients with ALS. Dexpramipexole is a low molecular weight, water-soluble, orally bioavailable, renally excreted compound with linear pharmacokinetics, and has been shown to be well tolerated in human subject testing. KNS-760704 is the enantiomer of pramipexole, and has been shown to improve mitochondrial function and to confer significant cellular protection in neurons under stress. A 2010 Phase II clinical trial involving 102 patients showed a slowing of ALS disease progression.[5] In January 2013, Biogen Idec announced that it was discontinuing its development of dexpramipexole in ALS due to lack of efficacy in a Phase III study.[1] References: Vieira FG, LaDow E, Moreno A, Kidd JD, Levine B, Thompson K, Gill A, Finkbeiner S, Perrin S. Dexpramipexole is ineffective in two models of ALS related neurodegeneration. PLoS One. 2014 Dec 19;9(12):e91608. doi: 10.1371/journal.pone.0091608. eCollection 2014. PubMed PMID: 25526593; PubMed Central PMCID: PMC4272269.

纯度：≥98%

CAS：104632-28-2