The Efficacy of Two Specific Toll-Like Receptor 4 Antagonists (G2013 & M2000) In Clinical Inflammatory Disease

Authors

  • Mahsa Taeb Department of Immunology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran, and Department of Immunology, School of Medicine, Rafsanjan University of Medical Sciences, Rafsanjan, Iran
  • Mehdi Rahmani Department of Immunology, School of Medicine, Rafsanjan University of Medical Sciences, Rafsanjan, Iran
  • Laleh Sharifi Uro-Oncology Research Center, Tehran University of Medical Sciences, Tehran, Iran
  • Abbas Mirshafiey Department of Immunology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran, and Livonian Biotech Millennium Ltd, Riga, LV-1013, Latvia

Keywords:

Toll-like receptor 4, Mannuronic acid, Guluronic acid, M2000, G2013, Inflammation

Abstract

Toll-like receptors (TLRs) are receptors of the innate immune system that detect pathogen- associated molecular patterns and endogenous “danger” molecules. Among the family, the fundamental role of Toll-like receptor 4 (TLR 4) has been underscored in the initiation of pro- inflammatory cellular signaling pathways. Therefore, the appropriate suppression of Toll-like receptor 4 signaling is vital to maintain the balance between autoimmunity and inflammatory responses to avoid detrimental effects caused by the host immune system. This paper reviewed the structure of TLRs and their essential role in inflammation, specifically Toll-like receptor 4, its signaling cascade, and its antagonists. Recently, using two new drugs, M2000 (β-D-Mannuronic acid) and G2013 (α-L-Guluronic acid), the novel Toll-like receptor 4 antagonists are proposed to control inflammatory conditions. Immunosuppressive and anti-inflammatory properties of M2000 and G2013 have been examined in invitro, pre-clinical, and clinical trial studies. Experimental and clinical studies on these drugs revealed TLR4 antagonistic properties with significant efficacy for controlling inflammatory responses and treating autoimmune diseases.

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Published

25-05-2023