The present invention relates to C-terminal modified Protoxin II peptides that selectively inhibit the Nav1.7 sodium channel； the present invention also relates to pharmaceutical compositions useful for prophylactic or therapeutic treatment of a disorder responsive to the blockade of sodium ion channels, especially Nav1.7 sodium ion channels； the present invention further provides methods of treating a disorder responsive to the blockade of sodium channels, and particularly Nav1.7 sodium channels, in a mammal sulfuring from excess activity of said channels.
