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10.3390/ph15010019

http://scihub22266oqcxt.onion/10.3390/ph15010019
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35056076!8778965!35056076
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suck abstract from ncbi


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pmid35056076      Pharmaceuticals+(Basel) 2021 ; 15 (1): ä
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  • Clinical Management of COVID-19 in Cancer Patients with the STAT3 Inhibitor Silibinin #MMPMID35056076
  • Bosch-Barrera J; Roque A; Teixidor E; Carmona-Garcia MC; Arbusa A; Brunet J; Martin-Castillo B; Cuyas E; Verdura S; Menendez JA
  • Pharmaceuticals (Basel) 2021[Dec]; 15 (1): ä PMID35056076show ga
  • COVID-19 pathophysiology is caused by a cascade of respiratory and multiorgan failures arising, at least in part, from the SARS-CoV-2-driven dysregulation of the master transcriptional factor STAT3. Pharmacological correction of STAT3 over-stimulation, which is at the root of acute respiratory distress syndrome (ARDS) and coagulopathy/thrombosis events, should be considered for treatment of severe COVID-19. In this perspective, we first review the current body of knowledge on the role of STAT3 in the pathogenesis of severe COVID-19. We then exemplify the potential clinical value of treating COVID-19 disease with STAT3 inhibitors by presenting the outcomes of two hospitalized patients with active cancer and COVID-19 receiving oral Legalon((R))-a nutraceutical containing the naturally occurring STAT3 inhibitor silibinin. Both patients, which were recruited to the clinical trial SIL-COVID19 (EudraCT number: 2020-001794-77) had SARS-CoV-2 bilateral interstitial pneumonia and a high COVID-GRAM score, and showed systemic proinflammatory responses in terms of lymphocytopenia and hypoalbuminemia. Both patients were predicted to be at high risk of critical COVID-19 illness in terms of intensive care unit admission, invasive ventilation, or death. In addition to physician's choice of best available therapy or supportive care, patients received 1050 mg/day Legalon((R)) for 10 days without side-effects. Silibinin-treated cancer/COVID-19+ patients required only minimal oxygen support (2-4 L/min) during the episode, exhibited a sharp decline of the STAT3-regulated C-reactive protein, and demonstrated complete resolution of the pulmonary lesions. These findings might inspire future research to advance our knowledge and improve silibinin-based clinical interventions aimed to target STAT3-driven COVID-19 pathophysiology.
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