• Abinit Saha, Ashish Ranjan Sharma, Manojit Bhattacharya, Garima Sharma, Sang-Soo Lee, and Chiranjib Chakraborty.
• Department of Biotechnology, School of Life Science and Biotechnology, Adamas University, Kolkata, West Bengal, India.
• Arch. Med. Res. 2020 Aug 1; 51 (6): 595-597.

AbstractPresently, we need more therapeutic molecules for this COVID-19 outbreak. The severity and mortality of the disease is associated with a high level of release of cytokine in the patients which is known as CRS (cytokine release syndrome) or cytokine storm syndrome. IL-6 is a type of pro-inflammatory cytokine which release in the severe COVID-19 patients. This cytokine initiates CRS the JAK-STAT or MAPK/NF-κB-IL-6 pathway. Tocilizumab, a humanized monoclonal antibody, is designed to bind both mIL-6R (membrane bound receptor for IL-6) and sIL-6R (soluble receptor for IL-6) and inhibit the JAK-STAT or MAPK/NF-κB-IL-6 signaling pathway. It finally stops the cytokine storm syndrome. However, we need to understand that how tocilizumab is bound with mIL-6R or sIL-6R. Similarly, we also need to understand more about the real molecular mechanism of activity of tocilizumab.Copyright © 2020 IMSS. Published by Elsevier Inc. All rights reserved.

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