| Literature DB >> 30480471 |
Arnt V Kristen1,2, Senda Ajroud-Driss3, Isabel Conceição4, Peter Gorevic5, Theodoros Kyriakides6, Laura Obici7.
Abstract
Hereditary transthyretin-mediated amyloidosis is a rapidly progressive, heterogeneous disease caused by the accumulation of misfolded transthyretin protein as amyloid fibrils at multiple sites, and is characterized by peripheral sensorimotor neuropathy, autonomic neuropathy and/or cardiomyopathy. Current treatment options have limited efficacy and often do not prevent disease progression. Patisiran is a novel RNA interference therapeutic that specifically reduces production of both wild-type and mutant transthyretin protein. In Phase II, III and long-term extension studies in patients with hereditary transthyretin-mediated amyloidosis, patisiran has consistently slowed or improved progression of neuropathy. In addition, the Phase III trial demonstrated significant improvements in quality of life measures and indicators of cardiomyopathy. Here, we highlight efficacy and safety data from the patisiran clinical trial programme.Entities:
Keywords: cardiomyopathy; clinical trials; disease-modifying therapy; hATTR amyloidosis; patisiran; polyneuropathy
Year: 2018 PMID: 30480471 DOI: 10.2217/nmt-2018-0033
Source DB: PubMed Journal: Neurodegener Dis Manag ISSN: 1758-2024