Unmet medical needs: neurological diseases
Neurovascular and neurodegenerative disorders
Our ambition:
Create major societal impact
🥇🏆Grand Prize i-Lab
Laureate and Grand Prix of the 23rd edition of the prestigious innovation competition “i-Lab”

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About us

Lys Therapeutics, first-in-class biotherapies against neurological diseases

Meet our team

Dr. Thibault HONEGGER, PhD

Co-founder, member of the Strategic Committee

Philippe DUJARDIN

Co-founder, Chief Financial Officer, member of the Strategic Committee

Dr. Manuel BLANC, PhD, MBA

Co-founder, Chief Executive Officer, President of the Strategic Committee

Dr. François FOSSIEZ, PhD

Head of CMC

Dr. Flavie LESEPT, PhD

Project Manager, Preclinical R&D

Pr. Denis VIVIEN, PhD, PU-PH

Head of Science, President of the Scientific Advisory Board

Werner KLINGER

Head of IT and data protection

Dr. Manuel BLANC

PhD, MBA

Co-founder, CEO, President of the Strategic Committee

Dr. Thibault HONEGGER

PhD

Co-founder, member of the Strategic Committee

Philippe DUJARDIN

Co-founder, member of the Strategic Committee

Pr. Denis VIVIEN

PhD, PU-PH

President of the Scientific Advisory Board – acting CSO

Dr. François FOSSIEZ

PhD

Head of CMC

Dr. Flavie LESEPT

PhD

Project Manager, Preclinical R&D

Werner KLINGER

Head of IT and data protection

Scientific Advisory Board

President of the SAB: Pr. Denis Vivien (PhD, PU-PH), France, co-inventor of Glunomab & expert of tPA, head of the Research Institute “Blood and Brain @ Caen-Normandie”

Dr. Richard Macrez (MD, PhD), France, co-inventor of Glunomab, assistant professor and emergency physician, head of Emergency Unit at Caen-Normandie Hospital

Dr. Désiré COLLEN (MD, PhD), Belgium, inventor of rtPA (alteplase) still the most effective drug for thrombolytic therapy of acute myocardial infarction and ischemic stroke

Pr. Diederik DIPPEL (MD, PhD), the Netherlands, neurologist, co-director of the Erasmus University MC Stroke Center

Pr. Yannick BÉJOT (MD, PhD), France, neurologist, head of Neurology at Dijon-Bourgogne hospital

Pr. Joan MONTANER (MD, PhD), Spain, neurologist, head of Neurovascular Research at the Vall d’Hebron Research Institute

Via BB@C Institute: Pr. Martin Dichgans (MD, PhD), Germany, neurologist, Director of the Institute of Stroke and Dementia Research (Medical Center of the University of Munich), head of the World Stroke Organization

Via BB@C Institute: Pr. Eng Lo (MD, PhD), USA, neurologist, Professor of Neurology and Radiology, Harvard Medical School, and Research Staff, Massachusetts General Hospital

Other partners

See all

Science

An outstanding scientific background

Glunomab / Glunozumab®: a monoclonal antibody counteracting the strong toxicity triggered by the interaction
of an endogenous protease, tissue plasminogen activator (tPA) with NMDA receptors (NMDAr)

Glunozumab schema therapeutic activities 03

Glunomab / Glunozumab® monoclonal antibody, a groundbreaking mechanism of action targeting the blood-brain barrier:

In the pathophysiology of neurological diseases such as stroke, multiple sclerosis, Parkinson’s disease as well as many other neurodegenerative disorders, one protease called tissue plasminogen activator (tPA) is triggering off-target toxicity via the binding to NMDA receptors (NMDAr) present on vascular endothelial cells and neurons, leading to its consequent hyperactivation and causing deleterious increase of the permeability of the blood brain barrier, as well as strong neuroinflammation and excitotoxicity.

By blocking the tPA-NMDAr interaction, Glunomab / Glunozumab® counteracts this tPA-dependent strong toxicity, without interfering with physiological NMDAr functioning.

A systemic drug treatment for CNS pathologies:

Target : NMDA receptors (NMDAr) present on vascular endothelial cells (within the blood vessels)
Strong advantage : no need to cross the blood brain barrier (BBB) to act on the central nervous system (CNS)

A very high specificity:

The epitope is only present on NMDA receptors (GluN1 subunit), not on any other proteins, and is fully conserved among species

A fully characterized mechanism of action:

MoA: antagonism of tPA-NMDAr interaction in the blood vessels, leading to restoration of NMDAr physiological functioning (no perturbation of NMDAr).

Therapeutic effects on blood brain barrier permeability and associated neuroinflammation and excitotoxicity