butaprost

Butaprost is a chemical compound that functions as a selective agonist for the prostaglandin E receptor (EP2). It exhibits an EC50 of 33 nM and a Ki of 2.4 μM when interacting with the murine EP2 receptor. However, Butaprost demonstrates lower activity against murine EP1, EP3, and EP4 receptors. Furthermore, it effectively attenuates fibrosis by inhibiting the TGF-β/Smad2 signaling pathway [1] [2] [3].

(S)-Butaprost (free acid) is a highly potent and selective EP2 receptor agonist[1].

(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.

TG6-129 is an antagonist of the EP2 receptor. TG6-129 suppresses PGE2-induced elevation of cAMP in cells expressing EP2 with an IC50 value of 1.6 µM. TG6-129 reduces the expression of COX-2, IL-1β, IL-6, IL-12, IL-23 and TNF-α induced by the EP2-selective