(r)-butaprost

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.

(R)-Butaprost (free acid) is a prostaglandin E2 (PGE2) analog exhibiting high EP2 receptor subtype selectivity, commonly used to delineate EP receptor expression in human and animal tissues and cells. In 1986, Gardiner induced significant confusion regarding its structure by incorrectly identifying the selective C-16 epimer as (R)-butaprost (refer to the British Journal of Pharmacology, page 46, as TR 4979, and notes). By removing the methyl ester and restoring the native carboxylic acid at C-1, the binding affinity for prostaglandin receptors was enhanced, given such free acids typically display 10 to 100 times greater affinity than their ester counterparts. Although not extensively studied pharmacologically, (R)-butaprost is generally viewed as the less active C-16 epimer, with careful studies conducted later in the United States and Japan ultimately establishing the correct active structure as the 16(S) epimer.