National Research Council of Canada

Alethia Biotherapeutics Inc.

Adc Therapeutics Sa

University of Pittsburgh

Gilead Sciences, Inc.

Other

UniversitÈ Laval

Cephalon, Inc.

Me Therapeutics Inc.

Daiichi Sankyo Company, Limited

The Royal Institution for the Advancement of Learning / Mcgill University

Traian Sulea

Maureen D O'Connor-McCourt

Jason Baardsnes

Gilles Bernard Tremblay

Mario Filion

John C Zwaagstra

Maria L Jaramillo

Danica Stanimirovic

Anna N Moraitis

Kristin Kemmerich

Bernard Massie

Mehdi Arbabi-Ghahroudi

Yves Durocher

Renald Gilbert

Myriam Banville

Bruno Gaillet

Ilia Alexandre Tikhomirov

Arsalan S Haqqani

Rénald Gilbert

Anne E G Lenferink

Catherine Collins

Suzanne Grothe

Andrew Peterson Hinck

Michel Gilbert

Adam Clarke

Matthew Pollard

Jamshid Tanha

Salim Dhanji

Matthew Stuible

Philippe A Tessier

Maria Moreno

Anne Marcil

Enrico O Purisima

Balu Chakravarthy

Kevin Henry

Maureen D O'Connor

Gregory Hussack

Pnina Brodt

Kenneth Harder

David Wilson

Umberto Banderali

Marzia Martina

Nazanin Larijani Rohani

Christopher R Corbeil

John Priatel

Maurizio Acchione

Mélanie Tardif

Jennifer Stratton

Jason Baarsdness

Stanimirovic Danica

Kemmerich Kristin

Massie Bernard

Gilbert Rénald

Maureen D O'Connor-Mccourt

Maureen D O'CONNOR-Mccourt

Recombinant transforming growth factor (TGF)-β monomers modified to inhibit dimerization and block TGF-β signaling are described. The recombinant TGF-β monomers lack the ability to bind and recruit TGF-β type I receptor (TβRI), but retain the capacity to bind the high affinity TGF-β type II receptor (TβRII), and in some instances, include mutations that increase their affinity for TβRII. Nucleic acid molecules and vectors encoding the recombinant TGF-β monomers are also described. Isolated cells, such as T cells, can be re-programmed with a TGF-β monomer-encoding nucleic acid or vector to secrete the monomer. Use of the recombinant TGF-β monomers and/or cells producing the recombinant TGF-β monomers, to inhibit TGF-β signaling, such as to treat disorders associated with aberrant TGF-β signaling, are also described.

Engineered TGF-beta monomers and their use for inhibiting TGF-beta signaling

The present application discloses methods of making anti-G-CSF antibodies, anti-G-CSF antibodies, methods of screening the activity of anti-G-CSF antibodies, pharmaceutical compositions of anti-G-CSF antibodies, kits containing anti-G-CSF antibodies, and methods of using anti-G-CSF antibodies to treat a disease.

Anti-G-CSF antibodies and uses thereof

The present invention is directed to anti-Her2 antibodies and fragments thereof, compositions, and uses thereof. The antibodies and fragments thereof bind to Her2-expressing cells in a pH-dependent manner, with low affinity at the physiological pH typical of normal cells and tissues, and with high affinity at the slightly acidic pH characteristic to solid tumors. Furthermore, the antibodies inhibit the growth of tumor spheroids at a level comparable to that of the benchmark anti-Her2 antibody Herceptin at acidic pH, whereas these effects were significantly reduced at physiological pH. This pH selectivity of cellular growth inhibition is maintained upon antibody conjugation to cytotoxic drugs. The invention also includes methods of treating solid tumors, methods of detecting solid tumors, and methods of pH-dependent capturing of the Her-2 ectodomain.

Antibody variants with pH-dependent antigen binding for selective targeting of solid tumors

The present invention relates, in general, to polypeptides capable of binding and neutralizing transforming growth factor beta (TGF-beta) ligands, and uses of these polypeptides for treating disorders related to TGF-beta expression or activation (e.g. cancer and fibrotic diseases), and methods of making such molecules.

TGF-β-receptor ectodomain fusion molecules and uses thereof

Herein described are antibodies to epidermal growth factor receptor (EGER) having an EGER binding affinity that is sufficient to kill disease cells presenting EGFR at high density, but is insufficient for binding to normal cells. A therapeutic effect is thus achieved while avoiding adverse events that result from unintended binding to normal cells.

Antibodies selective for cells presenting EGFR at high density

The present disclosure concerns antibodies specific for the Na v.7 polypeptides which are capable of antagonizing the biological activity of the Na v.7 polypeptide. The anti-Na v.7 antibodies can be used for alleviating the symptoms of pain and/or for treating or alleviating the symptoms of an hyperproliferative disease. The presence disclosure also concerns immunogens and methods for making antibodies, such as the anti-Na v.7 antibodies, comprising a single-domain antibody.

Antibodies and antibody fragments against HNAV1.7 channel and their use in pain and cancer indications

The present invention relates, in general, to polypeptides capable of binding and neutralizing transforming growth factor beta (TGF-β) ligands, and uses of these polypeptides for treating disorders related to TGF-beta expression or activation (e.g. cancer and fibrotic diseases), and methods of making such molecules.

The present invention relates to compounds, compositions, and methods are provided for covalently linking a cargo molecule, such as a therapeutic or a diagnostic agent, to a glycan in the Fab region of an antibody. Also provided are methods of modeling and producing antibodies having de novo Fab glycosylation sites. Also provided are antibody carrier conjugates, methods of using the conjugates.

Antibody glycoconjugates and methods of production and use

The present document describes an antibody or an antigen-binding fragment that bind to serum albumin comprising three complementarity determining regions (CDR1, CDR2 and CDR3), for half-life extension of biologics. The present invention also relates to pharmaceutical compositions, nucleic acid vectors, cells comprising the nucleic acid vectors, and methods of removing molecules from serum.

Serum albumin binding antibodies for tuneable half-life extension of biologics

It is provided an inhibitor of Toll-like Receptor 2 (TLR2) that specifically blocks an interaction between S1009A and Toll-like Receptor 2 (TLR2), and more particularly a humanized antibody against S100A9 protein for inhibiting and treating inflammatory conditions in a human patient. Particularly, this humanized antibody is specific for blocking the interaction between the S100A9 protein and the TLR-2 receptor.

Humanized anti-S100A9 antibody and uses thereof

Recombinant transforming growth factor (TGF)-&#x3b2; monomers modified to inhibit dimerization and block TGF-&#x3b2; signaling are described. The recombinant TGF-&#x3b2; monomers lack the ability to bind and recruit TGF-&#x3b2; type I receptor (T&#x3b2;RI), but retain the capacity to bind the high affinity TGF-&#x3b2; type II receptor (T&#x3b2;RII), and in some instances, include mutations that increase their affinity for T&#x3b2;RII. Nucleic acid molecules and vectors encoding the recombinant TGF-&#x3b2; monomers are also described. Isolated cells, such as T cells, can be re-programmed with a TGF-&#x3b2; monomer-encoding nucleic acid or vector to secrete the monomer. Use of the recombinant TGF-&#x3b2; monomers and/or cells producing the recombinant TGF-&#x3b2; monomers, to inhibit TGF-&#x3b2; signaling, such as to treat disorders associated with aberrant TGF-&#x3b2; signaling, are also described.

Engineered TGF-&#x3b2; monomers and their use for inhibiting TGF-&#x3b2; signaling

The present invention relates, in general, to polypeptides capable of transmigrating the blood-brain barrier, and uses thereof. More specifically, the present invention relates to polypeptides derived by site-directed mutagenesis of an existing antibody fragment and uses thereof, and methods of making such molecules. The polypeptides of the present invention show enhanced blood-brain barrier crossing and brain exposure levels in vitro and in vivo.

Antibody variants transmigrating the blood-brain barrier and uses thereof

The present invention relates to antibodies and fragments thereof derived by humanization of an existing antibody, and methods of making them. The humanized antibodies of the present invention show enhanced binding to the brain endothelial antigen, improved transmigration across the blood-brain barrier, and increased thermal stability relative to the parent non-humanized antibody.

Humanized antibodies transmigrating the blood-brain barrier and uses thereof

Novel antibodies and antigen binding fragments that specifically bind to KAAG1 and which may be used in the treatment, detection and diagnosis of cancer comprising KAAG1-expressing cells are disclosed herein. Cells expressing the antibodies and antigen binding fragments as well as methods of detecting and treating cancer using the antibodies and fragments are also disclosed. Cancer indications which may benefit from such treatment or detection include ovarian cancer, renal cancer, lung cancer, colorectal cancer, breast cancer, brain cancer, and prostate cancer, as well as melanomas.

Antibodies against kidney associated antigen 1 and antigen binding fragments thereof

Herein described are antibodies to epidermal growth factor receptor (EGFR) having an EGFR binding affinity that is sufficient to kill disease cells presenting EGFR at high density, but is insufficient for binding to normal cells. A therapeutic effect is thus achieved while avoiding adverse events that result from unintended binding to normal cells.

Growing community of inventors

Kirkland, Canada

Traian Sulea