Several studies have confirmed that cytokine storms play a critical role in causing a case to worsen from mild to severe or critical.The current treatment for cytokine storms is limited, so the international medical community is focusing on a specific and effective remedy.Jaktinib hydrochloride is a broad spectrum JAK inhibitor.It can inhibit cytokineinduced immune activation by multiple mechanisms and also slow viral proliferation by inhibiting AAK without causing unacceptable toxicity.Jaktinib hydrochloride has potential for the treatment of patients with coronavirus disease, co ronavirusdisease, cytokines, jaktinib hydrochloride, feasibility. Among all of the challenges for medical professionals, treatment of critical patients has always been the top priority. Studies indicate that a cytokine storm is an important signal that a patients condition had changed from mild to severe or critical and even lifethreatening.In fact, how to suppress that cytokine storm is one of the keys to hopefully curing those critical patients. Suppressing cytokine storms prior to their occurrence or in their early stages has been crucial to reducing the severity of COVID in patients and improving their prognosis.This implies that a medication to suppress cytokine storms would hold promise.Jaktinib hydrochloride is a broad spectrum novel JAK inhibitor that is expected to inhibit cytokine storms in patients with COVID. After entering the lung cells, the virus replicates in large quantities, triggering humoral and cellular immune responses, perhaps systematically.In the ear lystages of infection, the body dep loys a large number of T cells to fight the virus while some patients will have a lower cellular immunity because of over consumption of T cells.Meanwhile, antivirus specific antibodies will also begin to be produced.As the disease Targetmol’s Aniracetam progresses, the destruction of lung cells by the virus increases, and the bodys immune response and leukocyterelated cytokine release further kills and eliminates the virus along with necrotic lung cells.In addition, the excessive increase in inflammatory factors, such as var ious in ter leuk ins, can tr igger a ser ies of cytokine storms.These excessive inflammatory reactions backfire, resulting in injury and causing overwhelming pulmonary inflammation or secondary fibrotic lesions; they can also ultimately lead to respiratory failure or even death in severe cases.At present, one of the direct clinical manifestations of COVID in severe cases is the mult ip le organ damage caused by cytokine storms.Although the virus is the initiating factor, immune overexpression caused by cytokine storms is a direct cause of systematic injury.Forinstance, cl in icalev idence ind ica testhatafter reaching the turning point of cytokine storms, highflow oxygen and invasive ventilation are ineffective, eventu allyresultingintheuseofextr acorporeal membrane oxygenation. One of the direct reasons for this is that patients with COVID have scarce surfactants in the alveoli, impaired lung interstitia, impaired ventilation, and thusly as a consequence of unconvertible ventilation failure, ECMO is the only potential rescue technique.Although the factors that cause COVID to worsen frommi ld to severe or critical are similar, the main problem has to be handled in a quite different manner.Cytokine storms can directly damage the pulmonary capillary mucosa, lead ing to a lveo lar edema and inactivation ofsurf act antproteins, whichc anfurtherinduce inflamma to ry fac to rs todiffuse in the lungs, cause a lveo larstruc tures to damaged and degenera te, and result in pulmonary ventilation dysfunction.