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Kidney Week

Abstract: TH-PO1206

Correlation of eGFR and pE-CCL2 in Older Adult Patients Treated with Varoglutamstat: Data from VIVIAD, a Phase 2B Randomized Clinical Trial

Session Information

Category: Diabetic Kidney Disease

  • 702 Diabetic Kidney Disease: Clinical

Authors

  • Schaeffer, Michael Karl, Vivoryon Therapeutics N.V., Halle (Saale), Germany
  • Weber, Frank Thomas, Vivoryon Therapeutics N.V., Halle (Saale), Germany
  • Hoffmann, Torsten, Vivoryon Therapeutics N.V., Halle (Saale), Germany
  • Wenzkowski, Christine, Vivoryon Therapeutics N.V., Halle (Saale), Germany
  • Schell-Mader, Sylvia, Vivoryon Therapeutics N.V., Halle (Saale), Germany
  • Meyer, Antje, Vivoryon Therapeutics N.V., Halle (Saale), Germany
  • Tasler, Stefan, Vivoryon Therapeutics N.V., Halle (Saale), Germany
  • Fuchs, Katharina, Vivoryon Therapeutics N.V., Halle (Saale), Germany
  • Carroll, Kevin, KJC Statistics Ltd, Dublin, Ireland
  • Huber, Tobias B., Universitätsklinikum Hamburg-Eppendorf, Hamburg, Germany
Background

Varoglutamstat is an oral, small molecule inhibitor of glutaminyl cyclases (QPCT/L), which are involved in the maturation of biologically active peptides/proteins by catalyzing the formation of an N-terminal pyroglutamyl (pE) residue required for full activity and/or stability of the respective peptides.

Methods

VIVIAD (NCT04498650) is a randomized clinical trial (Phase 2b) in 259 patients with early Alzheimer’s disease treated with 300 or 600 mg varoglutamstat, or placebo, BID for 48-96 weeks. Measurement of eGFR and biomarkers of inflammation were prospectively defined. pE-CCL2 serum levels were measured at baseline and at week 48 with an ELISA. Individual patient slopes of eGFR (MDRD formula) were calculated using random-coefficient analysis. Spearman correlations were calculated with R.

Results

Varoglutamstat improved kidney function as judged by a significant and clinically meaningful increase of the estimated glomerular filtration rate (eGFR). This effect was dose-dependent. Statistically significant improvement of eGFR above baseline was replicated in a second RCT (VIVA-MIND, data not shown). Furthermore, a treatment-related reduction of mature pE-CCL2, a chemokine involved in inflammation and fibrosis, was observed.
Dose dependent increase of eGFR and reduction of pE-CCL2 was observed under treatment with varoglutamstat. Further analysis on patient level confirmed a moderate (Spearman’s rho = -0.38, p = 1.1*10-8) inverse correlation between change in pE-CCL2 serum levels at week 48 and the slope in eGFR over time. Accordingly, a decrease in pE-CCL2 serum levels is associated with an increase of the eGFR slope over time.

Conclusion

Base-level pyroglutamylation of CCL2 occurs mainly intracellularly in the Golgi apparatus. This transformation increases its inflammatory potency and renders it more resistant against degradation. The results show that a beneficial effect on eGFR and a reduction of pE-CCL2 serum levels, both effector parameters of the inhibition of glutaminyl cyclases, are well correlated. Glutaminyl cyclase inhibition which can combine anti-inflammatory effects via reduction of chemokine activity with direct effects of on kidney function is a promising new approach to treat diabetic kidney disease.

Digital Object Identifier (DOI)