GeNeuro SA, a pioneer of new therapies for neurology and autoimmune
disorders, announced that it has initiated its planned Phase IIb
study “CHANGE-MS” (Clinical trial assessing the HERV-W Env ANtagonist GNbAC1 for Efficacy in Multiple Sclerosis)
with its lead antibody GNbAC1 in Relapsing-Remitting Multiple Sclerosis
(RRMS). The study plans to enroll 260 patients in 68 clinical centers
in the European Union and Eastern Europe. Preliminary results are
expected by the end of 2017.
The aim of the Phase IIb study is to demonstrate on RRMS patients the
clinical benefit of GNbAC1 in neutralizing the MSRV-Env protein, which
has been identified as a potential key factor fueling the inflammatory
and neurodegenerative components of MS. Efficacy will be based on
multiple brain magnetic resonance imaging scans, with an initial
endpoint analysis after 6 months followed by a 6-month extension. By
targeting MSRV-Env, GeNeuro aims to bring to patients a safe and
effective treatment for both relapsing-remitting and progressive forms
of the disease without hampering the patient’s immune system.
GeNeuro was created in 2006 by Eclosion, the Geneva life sciences
accelerator, as a spin-off of Institut Mérieux of France. It develops
first-in-class therapies against diseases associated with the expression
of pathogenic proteins of human endogenous retroviral origin (HERV).
GeNeuro’s lead product, GNbAC1, is a therapeutic antibody that targets
MSRV-Env, a protein expressed in Multiple Sclerosis (MS) lesions from an
early stage, which has been shown to be both pro-inflammatory and an
inhibitor of remyelination, the two major drivers of MS progression.
The Multiple Sclerosis associated retrovirus (MSRV) is normally
latent in the genome of individuals, but it can be re-activated by viral
infections and other co-factors to express a pathogenic protein,
MSRV-Env. MSRV-Env provides a missing link between the observation that
viral infections are associated with the onset of the disease and
expression of the pathogenic factor (the MSRV-Env protein), which can
then explain the inflammatory and demyelinating characteristics of MS.
