Investigating the possible benefit of Astegolimab and Efmarodocokin Alfa in treating severe COVID-19 pneumonia
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Reviewed by Dat Tien Nguyen, B.A, ScM.
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Posted on January 23rd, 2023
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Acute respiratory distress syndrome (ARDS) had been associated with severe and lethal COVID-19. The syndrome was characterized with an hyperexpression of the pro-inflammatory IL-33 and a downregulation of the protective IL-22. Thus, a recent study sponsored by Genetech had been conducted to investigate the possibility of using an anti-IL-33 immunoglobulin (Astegolimab) and an IL-22-like particle (Efmarodocokin alfa) to treat patients with severe COVID-19 pneumonia
The phase 2 clinical trial included 410 patients hospitalized with pneumonia associated with COVID-19, which had been verified by PCR, and had a low capillary oxygen saturation level (SpO2 less than or equal to 93%). These patients were randomly assigned into 3 treatment groups. One group was treated with astegolimab, an antibody that can bind to IL-33 and block the interaction with ST2 receptors. The other group was treated with an IL-22 agonist that can act on the lung epithelial tissue to promote regeneration, efmarodocokin alfa. The outcome of both treatment groups were compared with a group of patients treated with placebo. Upon enrolling into the study, the patients were given either an IV infusion of 700 mg astegolimab, 90 μg/kg efmarodocokin alfa, or matching placebos. By the 15th day, if the patients had not been discharged from the hospital, they would be given another dose of 350 mg astegolimab, 90 μg/kg efmarodocokin alfa, or matching placebo. After the 60-day period of surveillance, the study found that the median day each group needed to reach clinical recovery was 11, 10, 10 days for astegolimab, efmarodocokin alfa, and placebo respectively. Thus, the study concluded that both astegolimab and efamrodockin alfa did not result in a higher rate of clinical recovery.
The phase 2 clinical trial included 410 patients hospitalized with pneumonia associated with COVID-19, which had been verified by PCR, and had a low capillary oxygen saturation level (SpO2 less than or equal to 93%). These patients were randomly assigned into 3 treatment groups. One group was treated with astegolimab, an antibody that can bind to IL-33 and block the interaction with ST2 receptors. The other group was treated with an IL-22 agonist that can act on the lung epithelial tissue to promote regeneration, efmarodocokin alfa. The outcome of both treatment groups were compared with a group of patients treated with placebo. Upon enrolling into the study, the patients were given either an IV infusion of 700 mg astegolimab, 90 μg/kg efmarodocokin alfa, or matching placebos. By the 15th day, if the patients had not been discharged from the hospital, they would be given another dose of 350 mg astegolimab, 90 μg/kg efmarodocokin alfa, or matching placebo. After the 60-day period of surveillance, the study found that the median day each group needed to reach clinical recovery was 11, 10, 10 days for astegolimab, efmarodocokin alfa, and placebo respectively. Thus, the study concluded that both astegolimab and efamrodockin alfa did not result in a higher rate of clinical recovery.