17-phenyl trinor PGE ethyl amide is derived from 17-phenyl trinor PGE, a synthetic analog of PGE that acts as an agonist of EP and EP receptors in mice (K = 14 and 3.7 nM, respectively) and EP, EP, and EP in rats (K = 25, 4.3, and 54 nM, respectively). 17-phenyl trinor PGE causes contraction of guinea pig ileum at a concentration of 11 µM and is 4.4 times more potent than PGE as an antifertility agent in hamsters. Modification of the C-1 carboxyl group to an ethyl amide serves to increase lipid solubility, thereby improving uptake into tissues and further lowering the effective concentration. Ethyl amide groups are then removed by amidases, regenerating the active free acid.
17-Phenyl trinor prostaglandin E2 ethyl amide (17-Phenyl trinor PGE2 ethyl amide) is a EP1 receptor agonist. 17-Phenyl trinor prostaglandin E2 ethyl amide aggravates renal dysfunction and glomerulosclerosis.
体内研究
17-Phenyl trinor prostaglandin E2 ethyl amide (0.3 µg/g; i.p.; three times a week for 12 weeks) aggravates renal dysfunction and glomerulosclerosis in five-sixths nephrectomy renal fibrosis model mice.
Increased the plasma blood urea nitrogen (BUN) levels and plasma creatinine (Cr) concentration, increased the extracellular matrix and the area of collagen deposition, upregulated the protein of expression of Col1, GRP78, TRPC1 and PERK in 5/6 Nx mice.