Zymogenetics, Inc.

Cedars-sinai Medical Center

Prometheus Biosciences, Inc.

Other

Bristol-myers Squibb Compnay

Ludwig Institute for Cancer Research Limited

National Jewish Medical Research Center

National Jewish Medical and Research Center

Dr. Falk Pharma Gmbh

Janine M Bilsborough

Yue Yao

Anthony W Siadak

Shirley A Rene

Stephan R Targan

Eric Chadwick

Jane A Gross

Zeren Gao

Steven D Levin

Dalin Li

Dermot P Mcgovern

Sherri L Mudri

James William West

Stephen R Jaspers

Rolf E Kuestner

Cameron Brandt

David Q Shih

Scott R Presnell

Jeffry Dean Watkins

Pierre Van Der Bruggen

Thierry Boon

Donald Y Leung

Steven K Burkhead

Frederick J Ramsdell

Cindy T Dickerson

Bradley Henkle

Erwin Schultz

Laurens Kruidenier

Mahyar Sabripour

Alka Potdar

Donald Y M Leung

Christophe Panichelli

Eric M Chadwick

Shirley Rene

Edward D Howard

Aaron C Haran

Elin Florkiewicz

Donald YM Leung

Described herein are methods and systems for identifying subjects suitable for treatment with an inhibitor of CD30L activity or expression, such as an anti-CD30L antibody. Methods and systems disclosed herein identify subjects suitable for treatment based on a presence of a genotype that is indicative of a disease or condition in the subject for which an inhibitor of CD30L is a suitable treatment. Exemplary conditions include both Crohns disease and primary sclerosing cholangitis. Compositions used to detect the genotypes described herein, and methods of using them are also provided.

Methods and systems for selection and treatment of patients with inflammatory diseases

Disclosed herein are methods, kits and compositions for treating an inflammatory disease. These methods. kits and compositions may be particularly useful for subjects carrying a risk genotype and/or expressing a transcriptomic risk signature that is indicative of severe inflammatory disease phenotypes for which existing treatment options are limited.

Methods of treating refractory inflammatory disease using transcriptomic and genetic risk signatures

Provided are methods, systems, and kits for selecting a patient for treatment with a therapeutic agent based on a presence of a genotype associated with a positive therapeutic response to the therapeutic agent. The therapeutic agent, in some embodiments, is an inhibitor of TL1A activity or expression, such as for example, an anti-TL1A antibody.

Methods of selecting, based on polymorphisms, an inflammatory bowel disease subject for treatment with an anti-TL1A antibody

The invention relates to methods of treating fibrosis and inflammatory bowel disease. In one embodiment, the present invention treats gut inflammation by administering a therapeutically effective dosage of TL1A inhibitors and/or DR3 inhibitors to an individual. In another embodiment, the present invention provides a method of reversing tissue fibrosis in an individual by inhibiting TL1A-DR3 signaling function.

Mitigation and reversal of intestinal fibrosis and inflammation by inhibition of TL1A function

The present invention relates to methods of treating patients suffering from Contact dermatitis, Drug induced delayed type cutaneous allergic reactions, Toxic epidermal necrolysis, Cutaneous T cell Lymphoma, Bullous pemphigoid, Alopecia aereata, Vitiligo, Acne Rosacea, Prurigo nodularis, Scleroderma, Herpes simplex virus, or combination by administering an IL-31RA antagonist.

Methods of treating prurigo nodularis using anti-IL-31RA antibody compositions

Treatment and reversal of fibrosis and inflammation by inhibition of the TL1A-DR3 signaling pathway

Methods of treating skin disorders using anti-IL-31RA antibodies

Novel compositions derived from antigen-binding sites of immunoglobulins having affinity for IL-31 are provided. The compositions exhibit immunological binding properties of antibody molecules capable of binding specifically to a human IL-31. CDR regions derived from same or different immunoglobulin moieties are provided. Also provided are single chain polypeptides wherein Vand Vdomains are attached. The sFv molecules can include ancillary polypeptide moieties which can be bioactive, or which provide a site of attachment for other useful moieties. The compositions are useful in specific binding assays, affinity purification schemes, drug or toxin targeting, imaging, and genetic or immunological therapeutics for inflammatory diseases. The invention thus provides novel polypeptides, the DNAs encoding those polypeptides, expression cassettes comprising those DNAs, and methods of inducing the production of the polypeptides. The invention further provides the amino acid sequences of the variable regions of the monoclonal antibodies and use of these monoclonal antibody or antibody fragment in conjunction with an human IgG4 Fc molecule.

Use of IL-31 monoclonal antibodies for treating pruritus

Described herein are methods and pharmaceutical compositions for the treatment of inflammatory bowel disease (IBD), Crohn's Disease (CD), ulcerative colitis (UC) and medically refractive-ulcerative colitis (MR-UC). In particular, disclosed are anti-TL1A antibodies useful for the treatment of IBD.

Neutralizing anti-TL1A monoclonal antibodies

The present invention relates to methods of treating pruritic diseases, including but not limited to Contact dermatitis, Atopic Dermatitis, Drug induced delayed type cutaneous allergic reactions, Toxic epidermal necrolysis, Cutaneous T cell Lymphoma, Bullous pemphigoid, Alopecia wereata, Vitiligo, Acne Rosacea, Prurigo nodularis, Scleroderma, Herpes simplex virus, or combination thereof by administering IL-31 monoclonal antibodies. The invention provides the hybridomas that generate the monoclonal antibodies and the amino acid sequences of the variable regions of the monoclonal antibodies and chimeric antibodies comprising the amino acid sequences of the light and heavy chain variable regions.

Use of IL-31 monoclonal antibodies for reducing pruritus

The present invention relates to methods of treating pruritic diseases, including but not limited to Contact dermatitis, Atopic Dermatitis, Drug induced delayed type cutaneous allergic reactions, Toxic epidermal necrolysis, Cutaneous T cell Lymphoma, Bullous pemphigoid, Alopecia wereata, Vitiligo, Acne Rosacea, Prurigo nodularis, Scleroderma, Herpes simplex virus, or combination thereof by administering IL-31 monoclonal antibodies. The invention further provides the hybridomas that generate the monoclonal antibodies.

Methods of treating atopic dermatitis with IL-31 monoclonal antibodies

The present invention provides a newly identified B7 receptor, zB7R1 that functions as lymphocyte inhibitory receptor, which is a PD-1-like molecule and is expressed on T cells. The present invention also provides the discovery of zB7R1's ability to bind to CD155. Methods and compositions for modulating zB7R1-mediated negative signaling and interfering with the interaction of its counter-receptor for therapeutic, diagnostic and research purposes are also provided.

Method of treating CD155 expressing cancers

Use of antagonists to IL-31 are used to treat inflammation and pain by inhibiting, preventing, reducing, minimizing, limiting or minimizing stimulation in neuronal tissues. Such antagonists include antibodies and fragments, derivative, or variants thereof. Symptoms such as pain, tingle, sensitization, tickle associated with neuropathies are ameliorated.

Use of IL-31 monoclonal antibodies for treating neuronal inflammation

Use of antagonists to IL-31Ra and OSMRb are used to treat inflammation and pain by inhibiting, preventing, reducing, minimizing, limiting or minimizing stimulation in neuronal tissues. Such antagonists include soluble receptors, antibodies and fragments, derivative, or variants thereof. Symptoms such as pain, tingle, sensitization, tickle associated with neuropathies are ameliorated.

Use of IL-31RA monoclonal antibodies for treating neuronal inflammation

Growing community of inventors

Simi Valley, CA, United States of America

Janine M Bilsborough