Redwood Bioscience, Inc.

Biogen Ma Inc.

Intrexon Corporation

Biovation Limited

Merck Patent Gmbh

Tel Aviv University

Polytherics Limited

Proclara Biosciences, Inc.

Cornell University

Dana-Farber-Cancer Institute Inc.

Emory University

Research Corporation Technologies, Inc.

Merck Patent Gesellschaft MIT Beschraenkter Haftung

Micromet Ag

Vasgene Therapeutics, Inc

Francis Joseph Carr

Gordon James Freeman

Timothy David Jones

David Rabuka

Anita Anne Hamilton

Graham Carter

Matthew Baker

Timothy Gareth Jones

Stephen D Gillies

Rafi Ahmed

Robert George Edward Holgate

Paul H Weinreb

Shelia Marie Violette

Yaron R Hadari

Neil H Bander

Diljeet Singh Athwal

Jeannick Cizeau

Glen MacDonald

Beka Solomon

Robert Hofmeister

Nicholas Ronald Glover

Stephen Williams

Kurt R Gehlsen

Richard Fisher

Yair Sapir

Valery Krasnoperov

Koen Hellendoorn

Gal Markel

Joycelyn Entwistle

Tehila Ben-Moshe

James Peter Gregson

Jacob Schachter

Rona Ortenberg

Elizabeth M Mandel-Bausch

Ilana Mandel

Birgit Kohleisen

Patrick Bäuerle

Alemseged Truneh

Michael Tal

Christian Itin

Ulla Lenkkeri-Schütz

Robert George Holgate

Fiona Suzanne Adair

Anja Sibylle Tessarz

Tim West

Denis Georges Bosc

Simon William Keen

Arron Hearn

Nurit Rachamim

Sarit Samira

Ronald Ellis

Polina Rabinovich-Toidman

Rom E Eliaz

Meital Sooliman

Idan Rakover

Gordan J Freeman

Timothy D Jones

James P Greggson

Laura Davies

Alyson Rust

Tim Jones

Ulla Lenkkeri-Schuetz

Laura Clare Perry

Patrick Baeuerle

The present disclosure provides antibodies specific for an epitope present on CD22. The antibodies are useful in various treatment, diagnostic, and monitoring applications, which are also provided.

Antibody specific for CD22 and methods of use thereof

An antibody or antigen-binding portion thereof which binds to PSMA and comprises a heavy chain variable domain comprising the sequence given in SEQ ID NO:33, wherein SEQ ID NO:33 is: EVQLVQSGXE XKKPGASVKV SCKXSGYTFT EYTIHWVXQA XGKGLEWIGN INPNXGGTTY NOKFEDRXTXTVDKSTSTAY MELSSLRSED TAVYYCAAGW NFDYWGOGTT VTVSS wherein: Xis A or P Xis V or L Xis A or T Xis R or K Xis P or H Xis N or Q Xis V or A; and Xis I or L whereby the heavy chain variable domain comprises up to 3 amino acid sequence modification(s) between positions 1-30, 36-49, 67-98 and 105-115 of SEQ ID NO: 33. The invention also provides compounds that include the antibody or antigen-binding portion thereof, such as conjugates, and their use in the treatment or diagnosis of diseases, in particular cancers, particularly prostate cancer.

Antibodies, uses thereof and conjugates thereof

Humanized antibodies and antibody fragments thereof that bind to &#x3b1;v&#x3b2;6 are disclosed. Also disclosed are methods of using these antibodies and antibody fragments to treat or prevent &#x3b1;v&#x3b2;6-mediated diseases such as fibrosis and cancer.

Anti-alpha V beta 6 antibodies and uses thereof

Humanized antibodies and antibody fragments thereof that bind to &#x3b1;v&#x3b2;6 are disclosed. Also disclosed are methods of using these antibodies and antibody fragments to diagnose, treat, and/or prevent &#x3b1;v&#x3b2;6-mediated diseases such as acute tissue injury, fibrosis, and cancer.

The invention relates to polypeptides that comprise a portion of filamentous bacteriophage gene 3 protein (g3p) sufficient to bind to and/or disaggregate amyloid, e.g., the N1-N2 portion of g3p and mutants and fragments thereof, wherein that g3p amino acid sequence has been modified through amino acid substitution to be substantially less immunogenic than the corresponding wild-type g3p amino acid sequence when used in vivo. The polypeptides of the invention retain their ability bind to and/or disaggregate amyloid. The invention relates furthermore to the use of these variant g3p-polypeptides in the treatment and/or prevention of diseases associated with misfolding or aggregation of amyloid.

Polypeptides comprising a modified bacteriophage g3p amino acid sequence with reduced immunogenicity

Methods of treatment to suppress an immune response are provided. The method comprises administering to a subject in need of treatment a naked blocking antibody that binds selectively iNKT cells in an amount effective to suppress the subject's iNKT cell function. Compositions comprising, an isolated, humanized antibody that binds selectively iNKT cells are also provided.

Humanized antibodies to iNKT

Novel antibodies, methods and compositions for treatment of a disease which is susceptible to amelioration by the blocking of APP cleavage.

Methods and compositions with immune therapy for treatment of dementia

exotoxin A or 'PE' is a 66 kD, highly potent, cytotoxic protein secreted by the bacterium. Various forms of PE have been coupled to other proteins, such as antibodies, to generate therapeutically useful cytotoxin conjugates that selectively target cells of a desired phenotype (such as tumor cells). In the present invention, peptides spanning the sequence of an approximately 38 kD form ofexotoxin A protein were analyzed for the presence of immunogenic CD4+ T cell epitopes. Six immunogenic T cell epitopes were identified. Residues were identified within each epitope for introduction of targeted amino acid substitutions to reduce or prevent immunogenic T-cell responses in PE molecules which may be administered to a heterologous host.

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exotoxin A or 'PE' is a 66 kD, highly potent, cytotoxic protein secreted by the bacterium. Various forms of PE have been coupled to other proteins, such as antibodies, to generate therapeutically useful cytotoxin conjugates that selectively target cells of a desired phenotype (such as tumor cells). In the present invention, peptides spanning the sequence of an approximately 38kD form ofexotoxin A protein were analyzed for the presence of immunogenic CD4+ T cell epitopes. Six immunogenic T cell epitopes were identified. Residues were identified within each epitope for introduction of targeted amino acid substitutions to reduce or prevent immunogenic T-cell responses in PE molecules which may be administered to a heterologous host.

A target protein is rendered less immunogenic to a given species by (a) determining at least part of the amino acid sequence of the target protein; (b) identifying in the amino acid sequence one or more potential epitopes for T-cells ('T-cell epitopes') of the given species; and (c) modifying the amino acid sequence to eliminate at least one of the T-cell epitopes identified in step (b) to reduce the immunogenicity of the protein when exposed to the immune system of the given species.

De-immunized streptokinase

Protein, or parts of proteins, may be rendered non-immunogenic, or less immunogenic, to a given species by identifying in their amino acid sequences one or more potential epitopes for T-cells of the given species and modifying the amino acid sequence to eliminate at least one of the T-cell epitopes. This eliminates or reduces the immunogenicity of the protein when exposed to the immune system of the given species. Monoclonal antibodies and other immunoglobulin-like molecules can particularly benefit from being de-immunised in this way: for example, mouse-derived immunoglobulins can be de-immunised for human therapeutic use.

Method for rendering streptokinase less immunogenic to a human

This invention provides methods of protein/polypeptide screening based on the provision of libraries of individual proteins/polypeptides, which in turn can be screened for a number of activities, including cell binding and biological activity. Methods for recovering genes encoding such proteins/polypeptides are also provided.

Methods for protein screening

Growing community of inventors

Aberdeen, United Kingdom

Francis Joseph Carr