The invention relates to mammal prolactin (PRL) variants having a mutation
or set of mutations within the 14 N-terminal amino acids thereby
preventing the formation of a disulfide bridge between Cys4 and Cys11
and, a sterically hindering mutation or set of mutations within binding
site 2 of PRL. These variants are useful as antagonists of mammal
prolactin receptors (PRLR), more particularly of human prolactin receptor
(hPRLR).