ArticleBMC nephrology2026
YS-1301 ameliorates crescentic glomerulonephritis by promoting immunoregulatory macrophages.
Article in BMC nephrology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundAnti-glomerular basement membrane (GBM) glomerulonephritis (GN) is a severe crescentic GN causing rapid renal failure. Despite extensive study of leukocyte-mediated injury, effective therapies that suppress inflammation and promote immunoregulation remain limited. YS-1301, a non-prostanoid prostacyclin receptor agonist and thromboxane synthase inhibitor, enhances tissue-protective factor release and modulates immune responses in other disease models. This study investigated whether YS-1301 ameliorates anti-GBM GN via immunomodulatory mechanisms.
methodsCrescentic GN was induced in WKY rats by intravenous injection of anti-GBM antibody clone TF78. YS-1301 (10 mg/kg/day) was administered intravenously after disease induction on days 0-2. Renal function and histologic injury were assessed on day 3, and additional cohorts were evaluated on day 7, the latest time point within the rapidly progressive GN phase of this model. Leukocyte infiltration and monocyte/macrophage phenotypes were evaluated by immunohistochemistry and flow cytometry.
resultsYS-1301 significantly reduced day-3 and day-7 blood urea nitrogen (BUN), serum creatinine, proteinuria, and crescent formation without altering initial glomerular antibody deposition. Total glomerular CD68
conclusionsWhen administered as an early post-induction intervention, YS-1301 ameliorated anti-GBM GN and was associated with localized accumulation of glomerular immunoregulatory macrophages rather than reduced total macrophage infiltration. These data support further evaluation of YS-1301 as an early immunomodulatory strategy for rapidly progressive GN.
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