National Institute of Health and Medical Research

Université De Caen Basse Normandie

Université De Caen Normandie

Katholieke Universiteit Leuven

Université Paul Sabatier (Toulouse III)

University College London

Centre Hospitalier Universitaire De Toulouse

Centre Hospitalier Regional Universitaire De Caen

Paion Deutschland Gmbh

Centre Hospitalier Unviersitaire De Caen

Inserm

Denis Vivien

Jerome Parcq

Bart Vanhaesebroeck

Paul Declerck

Typhaine Anquetil

Marie-Pierre Gratacap

Karl-Uwe Petersen

Simon De Meyer

Marina Rubio

Romain Solinhac

Tine Wyseure

Nick Geukens

Vincent Larrue

Jean Darcourt

Richard Macrez

Aude Jaffre

Ann Gils

Bernard Payrastre

Fabian Docagne

Gaëtan Chicanne

Jérôme Parcq

Ischemic conditions are a leading cause of death for both men and women. Ischemia, a condition characterized by reduced blood flow and oxygen to an organ. Re-establishment of blood flow, or reperfusion, and re-oxygenation of the affected area following an ischemic episode is critical to limit irreversible damage. However, reperfusion also associates potentially damaging consequences. For instance, increased vascular permeability is an important contributor to edema and tissue damage following ischemic events. Here the inventors shows that genetic inhibition of PI3K-C2β reduces cerebral infarction in two ischemia/reperfusion (I/R) models and improves neurological outcome. The genetic inhibition stabilizes the blood-brain barrier (BBB) after ischemic stroke and reduces inflammation. Accordingly, the present invention relates to a method for the preservation of vascular endothelial cell barrier integrity in a patient in need thereof comprising administering to the subject a therapeutically effective amount of a PI3KC2β inhibitor.

Use of PI3KC2B inhibitors for the preservation of vascular endothelial cell barrier integrity

Disclosed herein is a bispecific inhibitor for use in treating thrombotic disorders, such as acute thrombotic disorders like stroke and thromboembolism. The bispecific inhibitor is based on monoclonal antibodies targeting TAFI and PAI-1, and shows efficacy in the presence or the absence of plasminogen activators such as tissue-type plasminogen activator (tPA).

Dual targeting of TAFI and PAI-1

The present invention relates to an anti-NMDA antibody or fragment or derivative thereof which is effective in inhibiting the deleterious effects of tissue-type plasminogen activator (t-PA) mediated by N-methyl-D-aspartate (NMDA) receptors and to medical uses, in particular for the treatment of neurological or neurodegenerative disorders, e.g. multiple sclerosis.

Antibody useful in neurological or neurodegenerative disorders

The present invention relates to mutated tissue plasminogen activators, and their use for treating thrombotic diseases.

Mutated tissue plasminogen activators and uses thereof

Growing community of inventors

Caen, France

Denis Vivien