ArticleKidney international reports2026
Fulacimstat Reduces Angiotensin II in Kidney Allografts in a Cross-Sectional Exploratory Study.
Article in Kidney international reports, 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
Introduction: The nephroprotective effects of renin-angiotensin system (RAS) blockade after kidney transplantation (KTx) remain ambiguous. It has been shown that chymase and not angiotensin (Ang)-converting enzyme (ACE) is the most efficient Ang II-forming enzyme. Here, we investigated the efficacy of the novel and highly selective chymase inhibitor fulacimstat (BAY 1142524) on Ang II formation in human allograft biopsy tissue. Methods: In this cross-sectional, exploratory single-center study we analyzed biopsy samples of KTx recipients ( Results: In contrast to healthy kidneys, a distinct shift from ACE toward chymase-dependent Ang II formation was observed in aged (> 2 years) kidney allografts. Irrespective of RAS blockade, we demonstrated high efficacy of fulacimstat (BAY 1142524) to inhibit endogenous chymase-dependent Ang II formation in biopsy tissues of human kidney allografts. Conclusion: Chymase is the key enzyme for Ang II production in aged graft vintage (> 2 years). Selective inhibition of tissue-specific chymase with fulacimstat (BAY 1142524) inhibits Ang II formation in human kidney allografts, indicating potential therapeutic effects.
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