https://www.selleckchem.com/products/unc3866.html
This was due to the fact that 2-APB restrained the expression fibrotic markers, α-SMA, fibronectin and vimentin through inhibiting TGF-β1/SMAD3 signaling. Thus, subcutaneous injection of 2-APB improved bleomycin-induced skin and pulmonary fibrosis. 2-APB is a potential candidate for treating fibrosis, by disrupting intracellular Ca regulation in SSc to induce the dedifferentiation of myofibroblasts and meliorates fibrosis pathogenesis via inhibiting TGF-β1/SMAD3 signaling. 2-APB is a potential candidate for treating fibrosis, by disrupt
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