Abstract: The present disclosure provides in one aspect a construct comprising the R2 region of FGF23. In other embodiments, the construct functions as a FGF23 antagonist by blocking FGF23 binding to ?-Klotho and cell signaling via FGFR activation. In yet other embodiments, the construct prevents FGFR activation. In yet other embodiments, the construct of the present disclosure can be used to treat diseases or disorders related to FGF23 dysregulation and/or overexpression, such as but not limited to phosphate metabolism disorders.

Abstract: The present invention provides moieties that bind to an Ig-like domain, e.g., D4 or D5, of a human receptor tyrosine kinase, e.g., the human Kit RTK or the PDGFR RTK, or the D7 domain of a type V receptor tyrosine kinase wherein the moieties lock the ectodomain of the receptor tyrosine kinase in an inactive state thereby antagonizing the activity of the receptor tyrosine kinase.

Abstract: The present invention provides moieties that bind to the asymmetric contact interface of a receptor tyrosine kinase (RTK), wherein the moieties inhibit ligand induced trans autophosphorylation of the RTK. The present invention also provides methods of treating or preventing an RTK-associated disease and methods for identifying moieties that bind to an asymmetric contact interface of an RTK.

Abstract: The present invention provides moieties that bind to an Ig-like domain, e.g., D4 or D5, of a human receptor tyrosine kinase, e.g., the human Kit RTK or the PDGFR RTK, or the D7 domain of a type V receptor tyrosine kinase wherein the moieties lock the ectodomain of the receptor tyrosine kinase in an inactive state thereby antagonizing the activity of the receptor tyrosine kinase.

Abstract: The invention provides materials, reagents, systems, and methods for identifying agents useful for treating diseases resulting from abnormal (e.g., excessive) FGF receptor signaling. The invention also provides (therapeutic) agents thus identified, and methods of using such agents in treating such diseases. In certain embodiments, the invention relates to the treatment of various craniofacial disorders, or Craniosynostosis, that result from FGFR (e.g. FGFR2) malfunction, such as Crouzon, Apert, Jackson-Weiss, Pfeiffer Syndromes, Crouzon+acanthosis nigricans, Beare-Stevenson cutis gyrata, and non-syndromic craniosynostosis (NS). The methods comprise administering to the individuals a therapeutically effective amount of an inhibitor of the FGFR2c-FRS2 signaling. The inhibitor inhibits signaling by antagonizing FGFR2c-FRS2 interaction, inhibiting the expression and/or subcellular localization of wild-type or mutant FGFR2c and/or FRS2, inhibiting the kinase activity of FGFR2c (e.g.

Abstract: The invention provides materials, reagents, systems, and methods for identifying agents useful for treating diseases resulting from abnormal (e.g., excessive) FGF receptor signaling. The invention also provides (therapeutic) agents thus identified, and methods of using such agents in treating such diseases. In certain embodiments, the invention relates to the treatment of various craniofacial disorders, or Craniosynostosis, that result from FGFR (e.g. FGFR2) malfunction, such as Crouzon, Apert, Jackson-Weiss, Pfeiffer Syndromes, Crouzon+acanthosis nigricans, Beare-Stevenson cutis gyrata, and non-syndromic craniosynostosis (NS). The methods comprise administering to the individuals a therapeutically effective amount of an inhibitor of the FGFR2c-FRS2 signaling. The inhibitor inhibits signaling by antagonizing FGFR2c-FRS2 interaction, inhibiting the expression and/or subcellular localization of wild-type or mutant FGFR2c and/or FRS2, inhibiting the kinase activity of FGFR2c (e.g.

Abstract: The present invention relates generally to a newly identified adaptor protein FRS2 and related products and methods. FRS2 links protein kinases to activating partners in cells. The invention also relates to nucleic acid molecules encoding portions of FRS2, nucleic acid vectors containing FRS2 related nucleic acid molecules, recombinant cells containing such nucleic acid vectors, polypeptides purified from such recombinant cells, antibodies to such polypeptides, and methods of identifying compounds that enhance or block FRS2 interactions with natural binding partners. Also disclosed are methods for diagnosing abnormal conditions in an organism with FRS2 related molecules or compounds.

Abstract: The present invention relates generally to a newly identified adaptor protein FRS2 and related products and methods. FRS2 links protein kinases to activating partners in cells. The invention also relates to nucleic acid molecules encoding portions of FRS2, nucleic acid vectors containing FRS2 related nucleic acid molecules, recombinant cells containing such nucleic acid vectors, polypeptides purified from such recombinant cells, antibodies to such polypeptides, and methods of identifying compounds that enhance or block FRS2 interactions with natural binding partners. Also disclosed are methods for diagnosing abnormal conditions in an organism with FRS2 related molecules or compounds.

Abstract: The present invention relates generally to a newly identified adaptor protein FRS2 and related products and methods. FRS2 links protein kinases to activating partners in cells. The invention also relates to nucleic acid molecules encoding portions of FRS2, nucleic acid vectors containing FRS2 related nucleic acid molecules, recombinant cells containing such nucleic acid vectors, polypeptides purified from such recombinant cells, antibodies to such polypeptides, and methods of identifying compounds that enhance or block FRS2 interactions with natural binding partners. Also disclosed are methods for diagnosing abnormal conditions in an organism with FRS2 related molecules or compounds.

Abstract: The present invention relates to a method of treating in a mammal certain cancers, other cell proliferative diseases, and/or angiogenesis by using a salt or complex of a sulfated saccharide. The invention also relates to the use of mutant heparin binding growth factors that bind to the growth factor receptor, but not to heparin. The invention also provides pharmaceutical compositions for such methods.