Five Prime Therapeutics, Inc.

University of California

Xenogen Corporation

Hongbing Zhang

Lewis T Williams

Stephen Kohl Doberstein

Diane Hollenbaugh

Kevin Hestir

Ernestine A Lee

Justin Wong

Minmin Qin

Ali Sadra

Elizabeth Bosch

Ge Wu

Duojia Pan

Gerald M Rubin

Pamela R Contag

Anthony Purchio

Amy Holt

Yan Wang

Loriane Masuoka

The invention provides FGFR fusion proteins, methods of making them, and methods of using them to treat proliferative disorders, including cancers and disorders of angiogenesis. The FGFR fusion molecules can be made in CHO cells and may comprise deletion mutations in the extracellular domains of the FGFRs which improve their stability. These fusion proteins inhibit the growth and viability of cancer cells in vitro and in vivo. The combination of the relatively high affinity of these receptors for their ligand FGFs and the demonstrated ability of these decoy receptors to inhibit tumor growth is an indication of the clinical value of the compositions and methods provided herein.

Methods of treating disease with FGFR1 fusion proteins

FGFR2 fusion proteins comprising C-terminal deletion mutants of FGFR2-IIIC

Polynucleotides encoding FGFR1-IIIc ECD fusion proteins

Pharmaceutical polypeptide compositions promote the survival of cardiac cells, recruit cardiac cells to the cardiac area, stimulate the differentiation of cardiac cells, stimulate the proliferation of cardiac cells, and promote the activity of cardiac cells, thereby treating cardiac conditions. Methods of providing these compositions to the cardiac area include catheterization and direct injection. In preferred embodiments, the compositions comprise one of more of the following growth factors: EGF, bFGF, cardiotrophin-1, thrombin, PDGF-BB, amphiregulin, epiregulin, HB-EGF, TGFalpha, betacellulin, heregulin alpha, NRG-1-beta1-HRG-beta1, FGF 9.

Compositions comprising FGF-9 and betacellulin and methods for treating cardiac conditions

FGFR3-IIIc fusion proteins

The invention provides methods and compositions relating to Kuz involvement in angiogenesis. In various embodiments, the invention provides methods for modulating angiogenesis by specifically modulating the activity of Kuz in a vertebrate animal predetermined to have a pathogenic angiogenesis; methods for modulating angiogenesis by specifically modulating the activity of Kuz in a vertebrate animal and subsequently detecting a resultant angiogenic modulation in the animal; methods for specifically detecting Kuz activity in a vertebrate animal predetermined to have a pathogenic angiogenesis; methods for specifically detecting a pathogenic angiogenesis in a vertebrate animal having a predetermined Kuz activity; and methods for identifying a modulator of angiogenesis by (a) contacting an angiogenic assay system comprising a predetermined amount of Kuz with a candidate agent, under conditions whereby but for the presence of the agent, the system provides a reference angiogenesis; and (b) detecting an agent-biased angiogenesis of the system.

Modulating angiogenesis

The present invention relates to novel transcription control elements derived from a mouse eosinophil peroxidase gene. Such transcription control elements may comprise isolated polynucleotides, expression cassettes, vectors, recombinant cells, and transgenic animals, as described herein.

Isolation and identification of transcription control elements associated with mouse eosinophil peroxidase expression

The present invention relates to novel transcription control elements derived from a mouse eosinophil peroxidase gene. The novel transcription control elements described in the disclosure may comprise isolated polynucleotides, expression cassettes, vectors, recombinant cells, and transgenic animals.

Transgenic mice comprising transcription control elements associated with mouse eosinophil peroxidase expression

Growing community of inventors

Albany, CA, United States of America

Hongbing Zhang