1 fluorescence by copper was also abolished in copolymers (1:4) of DED-actin and N-ethylmaleimide-actin

2 ng of DED-actin fluorescence was restored in copolymers (1:9) of N-ethylmaleimide-DED-actin with unla

3 eration more efficiently than either FYAK or Copolymer 1 and induced anergy of HLA-DR2-restricted tra

4                                              Copolymer 1 binds promiscuously and very efficiently to

5                                              Copolymer 1 (Cop 1) is a random synthetic amino acid cop

6                                              Copolymer 1 (Cop 1, Copaxone [Teva Marion Partners, Kans

7                              The activity of copolymer 1 (Cop 1, Copaxone, glatiramer acetate) in sup

8                                              Copolymer 1 (Cop 1, poly (Y, E, A, K)) is a random synth

9                                              Copolymer-1 (COP-1) elicits neuroprotective activities i

10                                              Copolymer 1 [Cop1, glatiramer acetate, Copaxone, poly(Y,

11                                              Copolymer 1 (Copaxone), a random amino acid copolymer [p

12 une encephalomyelitis (EAE) in comparison to Copolymer 1 [Copaxone, poly(Y,E,A,K)n].

13                      Glatiramer acetate (GA; copolymer-1, Copaxone) suppresses the induction of exper

14       Treatment with glatiramer acetate (GA, copolymer-1, Copaxone), a drug approved for multiple scl

15 ted by antibodies to glatiramer acetate (GA, Copolymer-1, Copaxone), a therapeutic agent for multiple

16 in, we demonstrate that adoptive transfer of copolymer-1 immune cells to MPTP recipient mice leads to

17                                              Copolymer 1 [poly(Y,E,A,K)] is a random synthetic amino

18  tfb donor to bt acceptor is observed in the copolymer (<1 ps) compared to transfer from TFB to F8BT

19 d VWAK ameliorated EAE more effectively than Copolymer 1, reduced the number of pathological lesions,