Therefore, if the concentration of T-705-RTP can be increased by inhibiting T-705 metabolic degradation, the antiviral efficacy can be enhanced. COVID-19 has characteristic symptoms caused by SARS-CoV-2. While most cases result in mild symptoms, some progress to viral pneumonia and multi-organ failure. Although the mechanism of COVID-19 pneumonia is still being researched, the SARS-CoV-2 virus, like other viral pneumonia, proliferates in the lung tissue at the early stage of infection, and inflammatory symptoms in the lung appear due to the action of the immune system. As the alveolar disease progresses, respiratory failure develops, and death may follow. It is speculated that the rapid proliferation of virus causes the most alarming acute respiratory distress syndrome in the lungs and the excessive response of the immune system to the virus, causing respiratory failure and subsequent septic shock or multi-organ failure in the later stages of severe COVID-19, known as a cytokine storm. To prevent this serious symptom, it is necessary to prevent the proliferation of SARS-CoV-2 and suppress the immune reaction that causes inflammation. As a drug therapy, it is highly possible that an RNA replication inhibitor such as T-705 alone cannot have an immediate effect because it can stop the multiplication of SARS-CoV-2 but cannot eliminate the existing virus. Therefore, an RNA replication inhibitor requires a combination of immunity, thus, with an unavoidable immune inflammation.