Pentabromopseudilin (PBrP), a marine antibiotic derived from Pseudomonas bromoutilis and Alteromonas luteoviolaceus, demonstrates antimicrobial, antitumor, and phytotoxic properties. It acts as a reversible, allosteric inhibitor of myosin Va (MyoVa) and robustly inhibits transforming growth factor-β (TGF-β) activity. PBrP is utilized in researching fibrotic diseases and cancer [1].

Pentabromopseudilin (PBrP) at concentrations of 0.01-1 μM for 6 hours inhibited TGF-β-induced phosphorylation and nuclear translocation of Smad proteins [1]. Additionally, at 0.5 μM for 6 hours, PBrP suppressed the transcriptional response stimulated by TGF-β [1]. Furthermore, PBrP across a range of 0-1 μM for 6 hours impeded TGF-β-induced epithelial-mesenchymal transition (EMT) in A549 cells [1]. At a specific dose of 0.2 μM for 20 hours, PBrP obstructed cell migration prompted by TGF-β [1]. PBrP at 0.01-1 μM for 6 hours blocked TGF-β signaling by enhancing the degradation of TβRII [1]. At a concentration of 0.5μM and at time intervals of 0, 1, and 3 hours, PBrP disrupted TGF-β signaling by promoting TβRII degradation through caveolae-dependent endocytosis [1].