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Platform Technology to Address Inflammatory and Degenerative Diseases

Artielle’s novel, differentiated mechanism targets the CD74 receptor on monocytes and blocks the action of macrophage migration inhibitory factor (MIF). This action reduces the chemotactic gradient attracting inflammatory cells to the site of injury and, further, promotes cell death (apoptosis) of these destructive inflammatory mediators. In addition, in neurodegenerative animal models, Artielle’s biologic molecules act directly on the CD74 receptor which is upregulated on microglial cells.

The platform is based on molecules derived from a portion of the MHC II molecule (specifically the α1 and β1 portion) tethered to a peptide (MOG or other peptides in the case of MS) that conveys both disease specificity and conformational stability to the molecules. The targeting of CD74 is strongly correlated with efficacy in animal models and provides a biomarker for activity in the clinic.

On a cellular level, mechanistic studies have shown that Artielle’s lead clinical candidate (RTL1000) and related molecules:

  • Bind to CD74 and downregulate the action of the cytokine MIF (macrophage migration inhibitory factor),
  • Reduce expression of the adhesion molecule ICAM-1,
  • Reverse T-cell infiltration into the CNS, and
  • Switch the cytokine expression from a pro-inflammatory to an anti-inflammatory signature.

In multiple in vivo models of MS, specifically the mouse model of EAE (experimental autoimmune encephalomyelitis), Artielle’s lead molecule, RTL1000, has been shown consistently to:

  • Reverse the signs and symptoms of disease,
  • Produce efficacy lasting greater than one month following a single dose of the drug, and
  • Repair and regenerate myelin and axonal tissue.