Abstract: Fibroblast growth factor receptor (FGFR) extracellular domain (ECD) acidic region muteins that have been engineered to exhibit decreased tissue binding by increasing the number of acidic amino acid residues within the D1-D2 linker region are provided. Polynucleotides encoding FGFR ECD acidic region muteins are also provided. Methods of making FGFR ECD acidic region muteins, and methods of using such molecules to treat proliferative disorders, including cancers, disorders of angiogenesis, and macular degeneration, are also provided.

Abstract: The present invention relates to novel, soluble, recombinant variants RANKL (Receptor Activator of Nuclear Factor—?B Ligand) proteins, which may be expressed solubly in E. coli, variants that act as RANKL antagonists, and methods for generating the same.

Abstract: The present invention relates to novel, soluble, recombinant RANKL (Receptor Activator of Nuclear Factor—?B Ligand) variant proteins which may be expressed solubly in E. coli, variants that have substantially reduced binding to OPG, variants that act as RANKL antagonists, and methods for generating the same.

Abstract: Disclosed is a newly identified secreted molecule, identified herein as “monocyte, granulocyte, and dendritic cell colony stimulating factor” (MGD-CSF), the polypeptide sequence, and polynucleotides encoding the polypeptide sequence. Also provided is a procedure for producing the polypeptide by recombinant techniques employing, for example, vectors and host cells. Additionally, procedures are described to modify the disclosed novel molecules of the invention to prepare fusion molecules. Also disclosed are methods for using the polypeptides and active fragments thereof for treatment of a variety of diseases, including, for example, cancer, autoimmune and inflammatory diseases, infectious diseases, and recurrent pregnancy loss.

Abstract: The present invention relates to therapeutic uses of ErbB ligands, including betacellulin. The therapeutic uses include methods of using ErbB ligand family compounds alone, or in conjunction with other agents, for reducing blood glucose levels, treating Type I and Type II diabetes, obesity, muscle wasting diseases, and cardiotoxicity.

Abstract: Variant antibodies and Fc fusion proteins with reduced immunogenicity are described. In particular, the variants of antibodies and Fc fusion proteins have reduced ability to bind one or more human class II MHC molecules are described.

Abstract: The invention relates to variants of BMP-2 with improved properties and methods for their use.

Abstract: The present invention relates to novel erythropoietin protein variants with altered immunogenicity.

Abstract: The invention relates to variants of BMP-7 with improved properties and methods for their use.

Abstract: The present invention relates to novel apolipoprotein A-I proteins with altered immunogenicity.

Abstract: The present invention relates to non-naturally occurring variant Tumor Necrosis Factor Super Family member proteins with reduced immunogenicity. More specifically, the present invention relates to variant BAFF, RANKL, TRAIL, CD40L and APRIL proteins with reduced immunogenicity.

Abstract: The present invention relates to non-naturally occurring variant C1q Super Family member proteins with reduced immunogenicity. More specifically, the present invention relates to variant adiponectin and CTRP1 proteins with reduced immunogenicity.

Abstract: The invention relates to methods for modulating the side effects, including immunogenicity, of a protein therapeutic via derivatization with a protein protecting group using reversible or labile linkages.

Abstract: The present invention relates to variant ciliary neurotrophic factor (CNTF) proteins that possess neuroprotective and/or weight loss activity and reduced immunogenicty. In particular, variants of CNTF with reduced ability to bind one or more human class 11 MHC molecules are described.

Abstract: The invention relates to interferon variants with improved properties and methods for their use.

Abstract: Methods for determining whether a biological macromolecule binds to a compound are disclosed. The methods include: a) obtaining a Fourier-Transform Infrared spectrum of a solution which contains a biological macromolecule and obtaining a Fourier-Transform Infrared spectrum of a solution which includes a compound; b) obtaining a Fourier-Transform Infrared spectrum of a solution which contains the biological macromolecule and compound of step a); c) subtracting the Fourier-Transform Infrared spectrum of the biological macromolecule of step a) and the Fourier-Transform Infrared spectrum of the compound of step a) from the Fourier-Transform spectrum of step b) to determine a subtracted index; and d) determining that the compound of step a) binds to the biological macromolecule of step a) when the subtracted index of step c) is not equal to zero.