The science behind the company

Systemic Lupus Erythematosus (SLE), the lead indication for Ermium compounds, is a complex autoimmune disease, driven by dysregulations of both arms of the immune system, namely innate immunity, resulting in a major release of type I IFN and other pro-inflammatory cytokines, and adaptive immunity, involving both B and T lymphocytes. In that respect, breakthrough therapeutic innovations for SLE are likely to be achieved with novel drugs modulating both arms of the immune system simultaneously.

Mechanism Of Action And Target

Ermium compounds, NCE to be orally administered, are efficiently and selectively downmodulating the activated immune system through the inhibition of a lysosomal protein leading to the downmodulation of lysosomal function and autophagy process. 

The inhibition of this lysosomal target is acting upstream, thereby impacting downstream both:

  • the innate immune response through the modulation of TLR7/8/9 activation (known to be key in SLE physiopathology) and the subsequent release of type 1 IFN and other pro-inflammatory cytokines
  • the adaptive immune response, leading to the control of the release of auto-antibodies and pro-inflammatory cytokines

Competitive Advantage

Unique advantage to downmodulate different key immune dysregulations present in SLE patients through lysosomal function/autophagy modulation:

  • impacting excessive innate as well as  adaptive immunity
  • With a broad but selective profile of immuno-modulation, as compared to only modulating one single immune signaling pathway

 

Orally administered compounds have a short washout period, so provide a safety advantage when stopping therapy compared to systemically administrated antibodies.

Background

Proprietary Ermium compounds are derived from IT1t, a known CXCR4 antagonist, with immunomodulatory properties relevant for SLE patients. These properties were found subsequently to result from an innovative and well-differentiated mechanism of action (see above), that is independent of CXCR4.