Medimmune Limited

Ocimum Biosolutions, Inc.

Amgen Inc.

The Brigham and Women's Hospital, Inc.

Brandon Higgs

Meina Liang

Michael Elashoff

Donna Mendrick

Arthur Castle

Mark Porter

Kory Johnson

Lorin Roskos

David Fairman

Marlon Rebelatto

Rajesh Narwal

Paul Robbins

Carlos Chavez

Carina Herl

Min Pak

Hong Lu

Keith Steele

Anmarie Boutrin

Li Shi

Shengyan Hong

Amy Schneider

Jing Li

Raffaella Faggioni

Koustubh Ranade

Yen-Wah Lee

Katie Streicher

Inna Vainshtein

Robert A Gasser, Jr

Bing Wang

Barbara E White

Steven A Greenberg

Chris Morehouse

William Rees

Robert W Georgantas, Iii

Jingjing Chen

Yihong Yao

Michael Orr

Linda Chang

Bahija Jallal

Wei Zhu

Provided herein are methods of treating B7-H1-expressing tumors comprising administering an effective amount of MEDI4736 or an antigen-binding fragment thereof.

Anti-B7-H1 antibodies for treating tumors

The present invention relates to the use of the Chemokine (C&#x2014;C motif) ligand 20 (CCL20) as a biomarker to stratify or identify populations of patients suffering from interleukin-23 (IL23)-mediated diseases (e.g., Crohn's disease) responsive to treatment with an, anti-IL23 antagonist (including, e.g., anti-IL23 antibodies). Levels of CCL20 above or below a predetermined threshold can be used, for example, (i) to determine whether a patient with an IL23-mediated disease or disorder such a Crohn's disease is eligible or non-eligible for treatment with a therapeutic agent, (ii) to determine whether treatment with a certain agent should be commenced, suspended, or modified, (iii) to diagnose whether the IL23-mediated disease is treatable or not treatable with a specific therapeutic agent, or (iv) to predict the outcome of treating the IL23-mediated disease with a specific therapeutic agent. CCL20 can be used in combination with other IL23 pathway biomarkers such as IL22 and/or lipocalin-2 (LCN2).

CCL20 as a predictor of clinical response to IL23-antagonists

The present invention relates to the use of components of the IL23 pathway as biomarkers, e.g., IL22, LCN2 and combinations thereof, to stratify or identify populations of patients suffering from IL23-mediated diseases (e.g., Crohn's disease) responsive to treatment with an anti-IL23 antagonist (including, e.g., anti-IL23 antibodies or antigen-binding fragments thereof). Levels of IL23 pathway biomarkers above or below a predetermined threshold can be used, for example, (i) to determine whether a patient with an IL23-mediated disease or disorder such a Crohn's disease is eligible or non-eligible for treatment with a therapeutic agent (e.g., an ant-IL23 antibody), (ii) to determine whether treatment with a certain agent should be commenced, suspended, or modified, (iii) to diagnose whether the IL23-mediated disease is treatable or not treatable with a specific therapeutic agent, or (iv) to predict the outcome of treating the IL23-mediated disease with a specific therapeutic agent.

Prediction of clinical response to IL23-antagonists using IL23 pathway biomarkers

The disclosure provides methods for treating a subject having a type I IFN-mediated disease or disorder comprising administration of a fixed does of an anti-interferon alpha receptor antibody. The disclosure also provides methods for suppressing a type I interferon (IFN) gene signature (GS) in a subject. In addition, the disclosure provides methods of prognosing or monitoring disease progression in a subject having a type I IFN-mediated disease or disorder, methods of predicting a dosage regimen, methods of identifying a candidate therapeutic agent, methods of identifying a patient as a candidate for a therapeutic agent, and methods of designating a personalized therapy.

Fixed dosage regimens for anti-type I interferon receptor (IFNAR) antibodies

The present invention is based on the elucidation of the global changes in gene expression and the identification of toxicity markers in tissues or cells exposed to a known toxin. The genes may be used as toxicity markers in drug screening and toxicity assays. The invention includes a database of genes characterized by toxin-induced differential expression that is designed for use with microarrays and other solid-phase probes.

Methods for determining hepatotoxins

Primary rat hepatocyte toxicity modeling

The present invention is based on the elucidation of the global changes in gene expression and the identification of toxicity markers in tissues or cells exposed to a known cardiotoxin. The genes may be used as toxicity markers in drug screening and toxicity assays. The invention includes a database of genes characterized by toxin-induced differential expression that is designed for use with microarrays and other solid-phase probes.

Molecular cardiotoxicology modeling

The present invention is based on the elucidation of the global changes in gene expression and the identification of toxicity markers in tissues or cells exposed to a known renal toxin. The genes may be used as toxicity markers in drug screening and toxicity assays. The invention includes a database of genes characterized by toxin-induced differential expression that is designed for use with microarrays and other solid-phase probes.

Methods for determining renal toxins

Molecular toxicology modeling

Growing community of inventors

Gaithersburg, MD, United States of America

Brandon Higgs