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https://www.selleckchem.com/products/l-685-458.html the prognosis. Studies have also shown an association between some of these markers and severe COVID-19 infection requiring admission to the intensive care unit or complicated by acute respiratory distress syndrome (ARDS). Since, so far, a vaccine is not available, prevention of the infection is based on the avoiding people affected and the spreading of the virus; the treatment, in the absence of an effective antiviral agent, is symptomatic, and, in addition to oxygen support, finds in the anti-inflammatory drugs and anticoagulation fundamental therapeutic lines. According to the American Society of Hematology (ASH), all hospitalized patients with COVID-19 should receive pharmacologic thromboprophylaxis with LMWH.β-thalassemia is a hereditary disorder caused by defective production of β-globin chains of hemoglobin (Hb) that leads to an increased α/β globins ratio with subsequent free α-globins. Alpha globin excess causes oxidative stress, red blood cells membrane damage, premature death of late-stage erythroid precursors, resulting in ineffective erythropoiesis. The transforming growth factor β (TGF-β) superfamily signaling acts on biological processes, such as cell quiescence, apoptosis, proliferation, differentiation, and migration, and plays an essential role in regulating the hematopoiesis. This pathway can lose its physiologic regulation in pathologic conditions, leading to anemia and ineffective erythropoiesis. Activin receptor-ligand trap molecules such as Sotatercept and Luspatercept downregulate the TGF-β pathway, thus inhibiting the Smad2/3 cascade and alleviating anemia in patients with β-thalassemia and myelodysplastic syndromes. In this review, we describe in extenso the TGF-β pathway, as well as the molecular and biological basis of activin receptors ligand traps, focusing on their role in various β-thalassemia experimental models. The most recent results from clinical trials on sotatercept and luspat

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