Butaprost is a selective agonist of the prostaglandin E receptor EP2 that exhibits an EC50 of 33 nM and a Ki of 2.4 μM toward the murine EP2 receptor, while showing markedly lower activity against murine EP1, EP3, and EP4 receptors. Butaprost effectively attenuates fibrotic responses by inhibiting the TGF-β/Smad2 signaling pathway, supporting its utility in fibrosis, inflammation, and prostaglandin receptor signaling research.

EP2:1-100 nM (EC50)

In hEP2-HEK293/EBNA cells, the compound (1-100 nM) induces a dose- and time-dependent increase in Nur77 mRNA (approx. 5-fold). In Madin-Darby canine kidney (MDCK) cells, treatment with 50 μM Butaprost counteracts TGF-β signaling by reducing fibronectin (FN) expression, inhibiting Smad2 phosphorylation (p-Smad2), and suppressing EMT [1][2][3][5].

In male C57BL/6 mice subjected to unilateral ureteral obstruction (UUO) surgery, Butaprost treatment (1-4 mg/kg; i.p.; twice daily; 7 days) was evaluated for its effects on renal fibrosis. Administration of the compound resulted in a reduction in the gene and protein expression levels of α-smooth muscle actin (α-SMA), fibronectin, and collagen 1A1 (Col1A1). These results indicate that Butaprost is associated with the attenuation of fibrosis development in this obstructive kidney injury model [1].