Abstract. Prostaglandin E 2 -receptor subtypes, EP 1 , EP 2 , EP 3 , and EP 4 , are present in the kidney. The aim of this study was to elucidate the anti-nephritic effect of an EP 4 -receptor agonist on an experimental nephritic model. Mice were injected i.v. with anti-glomerulus antiserum to induce nephritis. Nephritic glomeruli generated more prostaglandin E 2 (2.6 and 0.7 ng) and less cyclic AMP than normal glomeruli (11 and 26 pmol). The production of cyclic AMP in nephritic glomeruli increased 67% in response to AE1-329, an EP 4 agonist, at 10 −5 M. Nephritic glomeruli expressed a lesser amount of mRNA of prostaglandin E 2 -receptor subtypes as compared with normal glomeruli. AE1-329 was administered s.c. at 100 µg/ kg per day for 3 weeks. AE1-329 suppressed the increase in creatinine and cholesterol compared to those in the control nephritic mice. AE1-329-treated nephritic mice had less crescentic glomeruli and less deposition of rabbit IgG (anti-glomerular basement membrane antibody) in glomeruli than the control mice. AE1-329 prevented the development of glomerulonephritis. These findings suggest that EP 4 -receptor agonists are a promising drug to prevent the development of glomerulonephritis.