Abstract: Biologically active conjugates are disclosed which are formed by reaction of a thiol moiety of a biologically active molecule with a non-peptidic polymer having an active sulfone moiety. Also disclosed are compounds having the formula R1—X—R2 wherein at least one of R1 and R2 is a biologically active molecule having a reactive thiol moiety which forms a covalent bond with X, a Michael acceptor-activated non-peptidic polymer. Further disclosed are methods of making the conjugates and compounds of the present invention as well as pharmaceutical compositions containing them. In addition, activated polymers suitable for attachment to a variety of molecules and surfaces are disclosed.

Abstract: Compounds are disclosed having the general formula R1-X-R2, wherein R1 and R2 are biologically active groups, at least one of which is polypeptidic. X is a non-peptidic polymeric group. R1 and R2 may be the same or different. Preferred R1 and R2 groups are TNF inhibitors.

Abstract: The present invention provides nucleic acid molecules encoding a 30kDa TNF inhibitor or a fragment thereof having at least one non-native cysteine residue at the N-terminus, C-terminus, residue 14, or residue 15.

Abstract: At least two substantially purified tumor necrosis factor (TNF) inhibitors are disclosed which are glycoproteins that are active against TNF. The isolation of 3O kDa and 40 KDa TNF inhibitor from urine is disclosed. The deglycosylated form of the 3O kDa TNF inhibitor and 40 kDa TNF inhibitor are described as being active against TNF. The 40 kDa TNF inhibitor is active against both TNF alpha a TNF beta. The amino acid sequence of the 30 kDa TNF inhibitor and the 40 kDa TNF inhibitor are disclosed. Methods for isolating the TNF inhibitors from human U937 cell medium and producing the proteins by recombinant-DNA methods are also described.

Abstract: Insulin-like growth factor I and II binding protein have potentiating and inhibiting activities. Cloning vectors and portable DNA sequences are disclosed.