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Updated: Feb 4, 2026
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Mouse Kidney Transplantation: Models of Allograft Rejection
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Fulacimstat Reduces Angiotensin II in Kidney Allografts in a Cross-Sectional Exploratory Study
Johannes J Kovarik1, Tarik Shoumariyeh1, Oliver Domenig2
1Division of Nephrology and Dialysis, Department of Medicine III, Medical University of Vienna, Vienna, Austria.
Kidney International Reports
|February 2, 2026
Summary
Chymase, not ACE, drives Ang II formation in aged kidney allografts. The chymase inhibitor fulacimstat effectively reduced Ang II production in human kidney allografts, suggesting therapeutic potential for kidney transplant recipients.
Area of Science:
- Nephrology
- Pharmacology
- Transplantation Immunology
Background:
- The role of renin-angiotensin system (RAS) blockade in kidney transplantation (KTx) is unclear.
- Chymase is a more efficient angiotensin (Ang) II-forming enzyme than angiotensin-converting enzyme (ACE).
Purpose of the Study:
- To investigate the efficacy of fulacimstat, a selective chymase inhibitor, in reducing Ang II formation in human kidney allograft biopsy tissue.
Main Methods:
- Analysis of biopsy samples from KTx recipients (n=55) and healthy donors (n=13).
- Mass spectrometry and enzyme inhibitors were used to assess ACE and chymase activity and their contribution to intrarenal Ang II formation.
- Metabolic assays were performed to study enzyme activities.
Main Results:
- A shift towards chymase-dependent Ang II formation was observed in kidney allografts older than 2 years, unlike in healthy kidneys.
- Fulacimstat demonstrated high efficacy in inhibiting chymase-dependent Ang II formation in human kidney allograft biopsies, regardless of RAS blockade.
Conclusions:
- Chymase is the primary enzyme for Ang II production in aged kidney allografts (>2 years).
- Selective chymase inhibition with fulacimstat effectively reduces Ang II formation in human kidney allografts, indicating potential therapeutic benefits.
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