| Literature DB >> 26711576 |
Tal Hasson1, Sarah Kolitz2, Fadi Towfic3, Daphna Laifenfeld1, Shlomo Bakshi1, Olga Beriozkin1, Maya Shacham-Abramson1, Bracha Timan1, Kevin D Fowler3, Tal Birnberg1, Attila Konya4, Arthur Komlosh1, David Ladkani1, Michael R Hayden1, Benjamin Zeskind3, Iris Grossman5.
Abstract
Glatiramer acetate (Copaxone®; GA) is a non-biological complex drug for multiple sclerosis. GA modulated thousands of genes in genome-wide expression studies conducted in THP-1 cells and mouse splenocytes. Comparing GA with differently-manufactured glatiramoid Polimunol (Synthon) in mice yielded hundreds of differentially expressed probesets, including biologically-relevant genes (e.g. Il18, adj p<9e-6) and pathways. In human monocytes, 700+ probesets differed between Polimunol and GA, enriching for 130+ pathways including response to lipopolysaccharide (adj. p<0.006). Key differences were confirmed by qRT-PCR (splenocytes) or proteomics (THP-1). These studies demonstrate the complexity of GA's mechanisms of action, and may help inform therapeutic equivalence assessment.Entities:
Keywords: Gene expression; Glatiramer acetate; Microarray; Multiple sclerosis; Therapeutic equivalence
Mesh：
Substances：
Year: 2015 PMID： 26711576 DOI： 10.1016/j.jneuroim.2015.11.020
Source DB: PubMed Journal: J Neuroimmunol ISSN： 0165-5728 Impact factor: 3.478