Smithkline Beecham Corporation

Other

Ai Therapeutics, Inc.

Smithkline Beecham Corporation, Et Al.

Peter R Young

Peter C McDonnell

Dean E McNulty

Jerry Leroy Adams

Timothy Francis Gallagher

James E Strickler

John Richard Heys

David W Green

Mark Robert Hurle

Keith Charles Deen

John C Lee

Kong B Tan

Jonathan Marc Rothberg

Henri Lichenstein

Connie L Erickson-Miller

Sean Landrette

Alemseged Truneh

John Cheung-Lun Lee

Phillip Cohen

Derk J Bergsma

Catherine E Ellis

Jeffrey L Mooney

Yuan Zhu

Stephen Dudley Holmes

George P Livi

Sherin Salaheldin Abdel-Meguid

Conrad Gerald Chapman

Rajeev Aurora

Alexander H Taylor

Lisa A Marshall

Jonathan M Rothberg

Helen Elizabeth Clinkenbeard

Amy K Roshak

Allan R Shatzman

Megan McHale McLaughlin

Sanjay Kumar

Kay Elizabeth Murphy

Michael R Brigham-Burke

George D Rose

Patricia Townsend Cohen

Michael Joseph Browne

Preston Hensley

Stephanie F Guerrera

K B Tan

Janice R Connor

Ian E James

Craig Alan Rosen

Ivo Rogulia Siemens

Tian-Li Yue

Kb Tan

John Emery

Jun Zou

Patricia T W Cohen

Provided are compositions and methods related to the use of apilimod in combination with glutamatergic agents for treating neurological diseases and disorders, and for the treatment of cancer.

Combination therapy with apilimod and glutamatergic agents

TR7 polypeptides and polynucleotides and methods for producing such polypeptides by recombinant techniques are disclosed. Also disclosed are methods for utilizing TR7 polypeptides and polynucleotides in the design of protocols for the treatment of chronic and acute inflammation, arthritis, septicemia, autoimmune diseases (such as inflammatory bowel disease and psoriasis), transplant rejection, graft versus host disease, infection, stroke, ischemia, acute respiratory disease syndrome, restenosis, brain injury, AIDS, bone diseases, cancer (such as lymphoproliferative disorders), atherosclerosis, and Alzheimers disease, among others and diagnostic assays for such conditions.

Tumor necrosis related receptor, TR7

Erythropoietin receptor agonist and antagonist antibodies and their use in enhancing erythropoiesis are disclosed.

Erythropoietin receptor antibodies

IL-1ra beta polypeptides and polynucleotides and methods for producing such polypeptides by recombinant techniques are disclosed. Also disclosed are methods for utilizing IL-1ra beta polypeptides and polynucleotides in the design of protocols for the treatment of chronic and acute inflammation, septicemia, arthritis, inflammatory bowel disease, graft vs. host disease, autoimmunity, stroke, cardiac ischemia, acute respiratory disease syndrome (ARDS), psoriasis, restenosis, traumatic brain injury, AIDS, cachexia, allergy, parasite infection, allergic rhinitis, allergic asthma, atopic dermatitis, allergic inflammatory diseases, and delayed hypersensitivity, among others, and diagnostic assays for such conditions.

Interleukin-1 receptor antagonist beta (IL-1rabeta)

This invention relates to drug binding proteins, to genes encoding same and to assays and methods for screening pharmaceuticals. More specifically, this invention relates to a Cytokine Suppressive Anti-Inflammatory Drug (CSAID) binding protein, to a gene encoding same and to assays and screens useful in the evaluation and characterization of drugs of this pharmacologic class.

Antibodies produced against cytokine suppressive anti-inflammatory drug binding proteins

The present invention relates to tumor necrosis factor receptor (TNF-R) related polypeptides and their ligands, hereinafter referred to as TR1, TR2, TL2 and TL4. The invention relates to methods to identify agonists and antagonists of TR1, TR2, TL2 and TL4.

Method of identifying agonist and antagonists for tumor necrosis related receptors TR1 and TR2

The IL-1H4 polypeptides and polynucleotides and methods for producing such polypeptides by recombinant techniques are disclosed. Also disclosed are methods for utilizing IL-1H4 polypeptides and polynucleotides in therapy, and diagnostic assays for such.

Interleukin-1 homologue, IL-1H4

TR6 polypeptides and polynucleotides and methods for producing such polypeptides by recombinant techniques are disclosed. Also disclosed are methods for utilizing TR6 polypeptides and polynucleotides in the design of protocols for the treatment of chronic and acute inflammation, arthritis, septicemia, autoimmune diseases (e.g. inflammatory bowel disease, psoriasis), transplant rejection, graft vs. host disease, infection, stroke, ischemia, acute respiratory disease syndrome, restenosis, brain injury, AIDS, Bone diseases, cancer, atheroschlerosis, and Alzheimers disease, among others and diagnostic assays for such conditions.

Tumor necrosis factor related receptor, TR6

The present invention relates to tumor necrosis factor receptor (TNF-R) related polypeptide and its ligand, hereinafter referred to as TR1 and TL3. The invention relates to methods to identify agonists and antagonists of TR1 and TL3.

Method of identifying agonists and antagonists for tumor necrosis related receptor TR1

Human PPP1R5 polypeptides and DNA (RNA) encoding such PPP1R5 and a procedure for producing such polypeptides by recombinant techniques is disclosed. Also disclosed are methods for utilizing such PPP1R5, or compounds which inhibit or stimulate PPP1R5 for dysfunctions or diseases which involve resistance to the action of insulin on glycogen synthesis are also disclosed. Agonist and antagonists of these PPP1R5 proteins and methods of their use are also disclosed. Also disclosed are diagnostic assays for detecting diseases related to mutations in the nucleic acid sequences and altered concentrations of the polypeptides. Also disclosed are diagnostic assays for detecting mutations in the polynucleotides encoding the PPP1R5 and for detecting altered levels of the polypeptide in a host.

Protein phosphatase 1 binding protein, R5

EF-7 polypeptides and polynucleotides and methods for producing such polypeptides by recombinant techniques are disclosed. Also disclosed are methods for utilizing EF-7 polypeptides and polynucleotides in therapy, and diagnostic assays for such.

Cytokine family member EF-7

CSBP/p38 is a MAP kinase that is activated in response to stress, endotoxin, interleukin 1 and tumor necrosis factor. Using a catalytically inactive mutant (D168A) of human CSBP2 as the bait in a yeast two-hybrid screen, a kinase has been cloned which shares &tilde;70% amino acid identity to MAPKAP kinase-2, and thus was designated MAPKAP kinase-3. The binding of CSBP to MAPKAP kinase 3 was confirmed in vitro by the precipitation of epitope-tagged CSBP1, CSBP2 and CSBP2(D168A) and endogenous CSBP from mammalian cells by a bacterially-expressed GST-MAPKAP kinase-3 fusion protein and in vivo by co-precipitation of the epitope-tagged proteins co-expressed in HeLa cells. MAPKAP kinase-3 was phosphorylated by both CSBP1 and CSBP2, and was then able to phosphorylate HSP27 in vitro. Treatment of HeLa cells with sorbitol or TNF resulted in activation of CSBP and MAPKAP kinase-3 and activation of MAPKAP kinase-3 could be blocked by preincubation of cells with 4-(4-Fluorophenyl)-2-(4-methylsulfinylphenyl)-5-4-pyridyl)-1H-imidazole, a specific inhibitor of CSBP kinase activity. These data suggest that MAPKAP kinase-3 is activated by stress and cytokines and is a novel substrate of CSBP both in vitro and in vivo. The use of MAPKAP kinase-3 in screens for the identification of pharmaceutically active compounds is disclosed.

Methods of the identification of pharmaceutically active compounds

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Lawrenceville, NJ, United States of America

Peter R Young