Cedars-sinai Medical Center

University of California

Prometheus Biosciences, Inc.

Prometheus Laboratories Inc.

Hitachi Chemical Company, Ltd.

The Uab Research Foundation

Corixa Corporation

Hitachi Chemical Research Center, Inc.

Dr. Falk Pharma Gmbh

Stephan R Targan

Jerome I Rotter

Kent D Taylor

Huiying Yang

Scott E Plevy

Dermot McGovern

Marla C Dubinsky

Janine M Bilsborough

Jonathan Braun

Dalin Li

Eric A Vasiliauskas

Jeffry Dean Watkins

Christopher L Sutton

Janine Bilsborough

Cindy T Dickerson

Bradley Henkle

Arthur L Beaudet

Phillip R Fleshner

David Q Shih

Patricia McNeeley

Carol J Landers

Ling Mei

Devendra Vora

Kathrin S Michelsen

Dermot P Mcgovern

Hiroo Toyoda

Alda Vidrich

Rafael Rojas

Matthew Reissman

Mary J Barry

Michael J Lodes

Masato Mitsuhashi

Clive N Svendsen

Robert N Barrett

Nancy Ann Hosken

Robert Hershberg

Dhruv Sareen

Raodoh Mohamath

Gil Y Melmed

Michael Workman

Uthra Rajamani

Xiuqing Guo

Charles O Elson

William S Mow

J Monty Watkins

Talin Haritunians

Rebecca Gonsky

Maria T Abreu

Richard L Deem

Philip Fleshner

Kent Taylor

Johnathan Braun

Mark Eggena

Alka Potdar

Richard Deem

Kazuhito Sugimura

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

The present invention relates to the finding that TL1A enhances differentiation of TH17 cells, and enhance IL17 secretion from TH17 cells. In one embodiment, the present invention provides a method of treating an inflammatory disease comprising determining the presence of a TL1A signaling profile, and treating the disease by administering a composition comprising a therapeutically effective dosage of one or more inhibitors of TL1A or TH17 cell differentiation. In another embodiment, the disease is characterized by TH17 differentiation.

Signature of TL1A (TNFSF15) signaling pathway

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

This invention provides methods of diagnosis, predicting and diagnosing susceptibility to, predicting disease progression and treatment of inflammatory bowel disease (IBD), including Crohn's disease and/or subtypes of Crohn's disease (CD) and/or Ulcerative Colitis (UC). In one embodiment, a method of the invention is practiced by determining the presence or absence of the genetic variants NOD2, TLR8, TLR2, CARD8, CARD15 and/or JAK3 to diagnose, predict and diagnose susceptibility and predict disease progression in an individual. In another embodiment, a method of the invention is practiced by determining the presence or absence of anti-Cbir1, anti-OmpC, ASCA, anti-I2 and/or pANCA in an individual. In another embodiment, the invention further associates the presence or absence of the risk variants with the expression of anti-Cbir1, anti-OmpC, ASCA, anti-I2 and/or pANCA for the diagnosis, prediction of susceptibility, prediction of disease progression and/or treatment of IBD, including CD and/or UC.

Diagnosis and treatment of inflammatory bowel disease

The present invention relates to methods of prognosing responsiveness to anti-TNFα therapy by determining the presence or absence of risk factors in the individual. In one embodiment, the risk factors are genetic markers, serological markers and/or clinical phenotypes associated with non-responsiveness to treatment with anti-TNFα therapy in an individual diagnosed with IBD.

Methods of determining responsiveness to anti-TNFα therapy in inflammatory bowel disease

The aspects disclosed herein describe methods of identifying a subject that is non-responsive to anti-TNF therapy. The aspects disclosed herein further provide for a method of selecting a therapy for a subject with Inflammatory Bowel Disease (IBD), and treating the subject with the therapy.

Kit comprising contiguous nucleobases, including position 76, of RS5745994

Described herein are humanized anti-TL1A antibodies and pharmaceutical compositions for the treatment of inflammatory bowel disease (IBD), such as Crohn's Disease (CD) and ulcerative colitis (UC).

Humanized antibodies to TNF-like ligand 1A (TL1A) and uses thereof

Organs-on-chips are microfluidic devices for culturing living cells in micrometer sized chambers in order to model physiological functions of tissues and organs. Engineered patterning and continuous fluid flow in these devices has allowed culturing of intestinal cells bearing physiologically relevant features and sustained exposure to bacteria while maintaining cellular viability, thereby allowing study of inflammatory bowl diseases. However, existing intestinal cells do not possess all physiologically relevant subtypes, do not possess the repertoire of genetic variations, or allow for study of other important cellular actors such as immune cells. Use of iPSC-derived epithelium, including IBD patient-specific cells, allows for superior disease modeling by capturing the multi-faceted nature of the disease.

Systems and methods for growth of intestinal cells in microfluidic devices

Optimized anti-TL1A antibodies

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 the finding that TL1A enhances differentiation of TH17 cells, and enhance IL17 secretion from TL17 cells. In one embodiment, the present invention provides a method of treating an inflammatory disease comprising determining the presence of a TL1A signaling profile, and treating the disease by administering a composition comprising a therapeutically effective dosage of one or more inhibitors of TL1A or TH17 cell differentiation. In another embodiment, the disease is characterized by TH17 differentiation.

The present invention relates to methods of prognosing responsiveness to anti-TNF&#x3b1; therapy by determining the presence or absence of risk factors in the individual. In one embodiment, the risk factors are genetic markers, serological markers and/or clinical phenotypes associated with non-responsiveness to treatment with anti-TNF&#x3b1; therapy in an individual diagnosed with IBD.

Methods of determining responsiveness to anti-TNF&#x3b1; therapy in inflammatory bowel disease

Described herein are methods of diagnosing inflammatory bowel disease, including but not limited to Crohn's Disease (CD), Ulcerative Colitis (UC), and/or Medically Refractive Ulcerative Colitis (MR-UC), using RNA-SET2, TL1A and/or IFN-Y. The methods may comprise treating inflammatory bowel disease by administering a therapeutically effective amount of a therapeutic agent to a subject. Described further herein are processes for patient identification and/or stratification.

Methods of diagnosing inflammatory bowel disease through RNASET2

Growing community of inventors

Santa Monica, CA, United States of America

Stephan R Targan