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Genentech, Inc.

Sugen Incorporated

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University of California

New York University

Yissum Research Development Company of the Hebrew University of Jerusalem Ltd.

Genetech, Inc.

Bio-signal Corporation Ltd.

Boehringer Mannheim Gmbh

Lead Discovery Center Gmbh

Eberhard-karls-universität Tübingen Universitätsklinikum

Icrf Patents Limited

Max-flanck-gesellschaft Zuer For{overscore (d)}erung Der

Agency for Science, Technology and Research

Axel Ullrich

Robert M Hudziak

H Michael Shepard

Brian M Fendly

Aviv Gazit

László Örfi

Alex Levitzki

Birgit Millauer

Reiner Lammers

Klaus Peter Hirth

Pjotr Knyazev

Wolfgang Vogel

Istvan Szekely

Laura Kay Shawver

Elaina Mann

Johannes Bange

Janis Haimichael

Joseph Schlessinger

Mikhail L Gishizky

Jan M Sap

Donna Pruess Schwartz

Werner Risau

Tamas Bajor

Niels Peter Mo Slashedller

Cornelia Lechner

Niels Peter Moller

Peng Cho Tang

James M Lee

György Kéri

Alane M Gray

Gyorgi Keri

István Szabadkai

Klaus Seedorf

Naohito Aoki

Thomas Ciossek

Miriam Fuchs

Yixiang Zhang

Irmingard Sures

Karin Bach Moller

Jennie Powell Mather

Howard M Goodman

William J Rutter

Dennis J Slamon

John Shine

Thomas J Dull

Raymond Pictet

Robert Torka

Frauke Hildegard Alves

Heimo Riedel

Fairooz F Kabbinavar

Karin Bach Mo Slashedller

Oliver Nayler

Alexei Kharitonenkov

John Chirgwin

Zhengjun Chen

Andreas Gschwind

Stefan Hart

Michael Derek Waterfield

Uwe Koch

Hong Yang Wang

Jan Eickhoff

Janakiraman Ramachandran

Carsten Schultz-Fademrecht

Bert Klebl

Kurt W Naujoks

Axel Choidas

Ilse Bartke

Edmund Hoppe

Esther Zwick-Wallasch

Arjun Singh

Henrik Daub

Laura K Shawyer

Edward Htun-Van Der Horst

Norbert Prezel

Alexander Wolf

J Schlessinger

Gunter Kostka

Luitgard Seedorf

Axel Obermeier

Frank Bohmer

Sylvia-Annette Bohmer

Han Kiat Ho

Alexei Igorevich Kharitonenkov

Hans-U Haring

Yeong Woong Kim

Norbert Prenzel

Hans-Jurgen Berger

Mathias Falcenberg

John R Bell

Hans-Jörg Bühring

Charles Cant

Frauke Hildegard Elisabeth Alves

Tatjana Knyazeva

Naohita Aoki

Niels Peter M&oslash;ller

Yuri Cheburkin

Zhengiun Chen

Irman Gard Sures

Kéri György

Peter Vajkoczy

The present invention is related to compound capable of modulating the activity and/or expression of the protein kinase GRK5, thereby enhancing the expression and/or release of insulin. The invention is further related to methods of identifying said compounds for the treatment of diseases of the carbohydrate metabolism. The invention is further related to methods of treatment of diseases of the carbohydrate metabolism, particularly diabetes mellitus type 2.

Method for treatment of diabetes by a small molecule inhibitor for GRK5

Novel compounds which are inhibitors of receptor tyrosine kinases of the AXL receptor family are described herein. These compounds are suitable for the treatment or prevention of disorders associated with, accompanied by or caused by hyperfunction of a receptor of the AXL family. The compounds are suitable for the treatment of hyperproliferative disorders, such as cancer, particularly cancer metastases.

Quinoline derivatives as AXL kinase inhibitors

The present invention relates to quinolinyloxyphenylsulfonamides and stereoisomeric forms, solvates, hydrates and/or pharmaceutically acceptable salts of these quinolinyloxyphenylsulfonamide compounds as well as pharmaceutical compositions containing at least one of these compounds together with at least one pharmaceutically acceptable carrier, excipient and/or diluent. Said quinolinyloxyphenylsulfonamides are useful for prophylaxsis, treatment and/or after-treatment of hyperproliferative disorders, such as cancer, tumors and particularly cancer metastases.

Quinolinyloxyphenylsulfonamides

The present invention relates to a pharmaceutical composition comprising as an active agent an inhibitor of HER3 activity, particularly an anti-HER3-antibody. Further, the use of this composition for the diagnosis, prevention or treatment of hyperproliferative diseases, particularly tumor diseases is disclosed.

Inhibitors of her3 activity

The present invention relates to 1-nitrogen-heterocyclic-2-carboxamides and/or pharmaceutically acceptable salts thereof, the use of these derivatives as pharmaceutically active agents, especially for the treatment and/or prevention of Axl receptor tyrosine kinase subfamily induced disorders, including cancer and primary tumor metastases, and pharmaceutical compositions containing at least one of said 1-nitrogen-heterocyclic-2-carboxamide derivatives and/or pharmaceutically acceptable salts thereof.

Pharmaceutically active compounds as Axl inhibitors

The present invention relates to the modulation of transactivation of receptor tyrosine kinases by G protein or G protein-coupled receptor (GPCR) mediated signal transduction in a cell or an organism comprising inhibiting the activity of the metalloprotease TACE/ADAM17 and/or the activity of the receptor tyrosine kinase ligand amphiregulin.

Inhibition of TACE or amphiregulin for the modulation of EGF receptor signal transactivation

The &#x3b2;-subunit of human nerve growth factor (&#x3b2;NGF) is prepared in essentially pure form in commercially useful quantities using recombinant DNA technology. The nucleotide sequence and vectors encoding human &#x3b2;NGF and host cells transformed with the vectors are also provided. The &#x3b2;NGF which the invention provides is useful, for example, in treating nerve damage.

Human nerve growth factor by recombinant technology

The present invention relates to diagnostic and therapeutic methods in the field of malignant disorders. Most particularly, the invention provides methods of determining the invasivity of malignant disorders and methods for reducing the invasivity of malignant disorders including the prevention or treatment of cancer cell invasion.

Diagnosis and prevention of cancer cell invasion

The invention provides method of diagnosing a receptor tyrosine kinase (RTK)-hyperfunction-induced disorder or a genetic predisposition therefor in a mammal. The method comprises determining the presence of a nucleic acid encoding a mutated fibroblast growth factor receptor-4 (FGFR-4) protein in a nucleic acid sample from a mammal. The presence of a nucleic acid encoding a mutated FGFR-4 protein is indicative of an RTK-hyperfunction-induced disorder or a genetic predisposition therefor.

Method of diagnosing an RTK-hyperfunction induced disorder

The present invention relates to the use of ligands for the FLK-1 receptor for the modulation of angiogenesis and vasculogenesis. The invention s based, in part, on the demonstration that Flk-1 tyrosine kinase receptor expression is associated with endothelial cells and the identification of vascular endothelial growth factor (VEGF) as the high affinity ligand of Flk-1. These results indicate a major role for Flk-1 in the signaling system during vasculogenesis and angiogenesis. Engineering of host cells that express Flk-1 and the uses of expressed Flk-1 to evaluate and screen for drugs and analogs of VEGF involved in Flk-1 modulation by either agonist or antagonist activities is described. The invention also relates to the use of FLK-1 ligands, including VEGF agonists and antagonists, in the treatment of disorders, including cancer, by modulating vasculogenesis and angiogenesis.

Cell line comprising vector encoding truncated FLK-1 receptor

The invention provides a method for the therapeutic treatment of a cancer in a mammal wherein (i) the mammal comprises a mutated fibroblast growth factor receptor-4 (FGFR-4) protein, and (ii) the mutated FGFR-4 comprises at least one point mutation in the transmembrane domain of FGFR-4 that substitutes a hydrophilic amino acid for a hydrophobic amino acid. The method comprises administering to the mammal an effective amount of at least one inhibitor of the mutated FGFR-4.

Use of inhibitors for the treatment of RTK-hyperfunction-induced disorders, particularly cancer

The present invention relates to agents and methods for growth-factor receptor activation by modulating the G-protein mediated signal transduction pathway.

EGF receptor transactivation by G-protein-coupled receptors requires metalloproteinase cleavage of proHB-EGF

The present invention relates to the use of Fibroblast-Growth Factor Receptor (FGFR) agonists for the diagnosis, prevention and/or treatment of pathological conditions including, but not limited to hyperproliferative disorders, bone diseases and vascular diseases. Particularly, the use of FGFR-4 agonists, e.g. anti-FGFR-4 antibodies is described. Further, the invention relates to a pharmaceutical composition comprising the agonist as described above and a screening procedure.

Method for screening FGFR-4 agonists

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Munich, Germany

Axel Ullrich