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During the congress, E-Posters will be accessible to all participants on the congress website 24/7, as well as in the E-poster stations in the congress center.
Preparing your E-Poster
Please review the E-Poster format requirements carefully when preparing your E-Poster. Should your E-Poster not meet the mentioned requirements, it may not be displayed as described above.
E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
Please follow the instructions below to input your abstract title.
Abstract titles should be brief and reflect the content of the abstract.
Diabetic kidney disease remains the most frequent cause of end stage kidney disease requiring novel therapies to stabilize or improve eGFR and kidney function.
Varoglutamstat is an oral small molecule inhibitor of glutaminyl-cyclases, which has shown statistically significant and clinically meaningful improvement of eGFR in elderly participants (2.65 mL/min/1.73m2/year versus placebo), especially in those with a diabetic background (> 6 mL/min/1.73m2/year versus placebo) in a Phase 2b study with 259 participants with early Alzheimer´s Disease (VIVIAD, NCT04498650). The results have been confirmed in a second, independent Phase 2 study with 109 participants (VIVA-MIND, NCT03919162) with very similar inclusion criteria.
Participants with and without diabetes had a mean eGFR at baseline of about 80 mL/min/1.73m2 raising the question if a similar effect size can be expected in diabetic patients with CKD 3 and 4.
All participants from two Phase 2 programs in the varoglutamstat 600 mg BID (n=112) and placebo (n=174) groups were included into an analysis of interaction between baseline impairment of eGFR and treatment effect size using random coefficients analysis.
Additionally, a preclinical experiment of varoglutamstat in an advanced translational mouse model for DKD (Renin-encoding adeno-associated viral induction of hypertension and unilateral nephrectomy in db/db mice) was conducted.
Pooled data from VIVIAD and VIVA-MIND studies including only the participants with baseline eGFR <72 mL/min/1.73m2 (n=89; corresponding to the most severe tercile ≤33.3 percentile) with a mean eGFR at baseline of 62.8 mL/min/1.73m2 showed a treatment effect (difference between the eGFR slopes of placebo and varoglutamstat) of 3.2 mL/min/1.73m2/year, p=0.02, comparable to the difference in the total pooled population (3.2 mL/min/1.73m2/year, p=0.0001).
For participants with diabetes, mean eGFR at baseline was 60.5 mL/min/1.73m2 in the most severely impaired tercile (n=12). The treatment effect in this subgroup was 6.5 mL/min/1.73m2/year, also in line with results for the total population with diabetes (5.2 mL/min/1.73m2/year). When assessing the eGFR of the most severely affected 25% or even 20% diabetic patients, the treatment effect tended to increase (7.5 and 7.7 mL/min/1.73m2/year, respectively).
Results of the DKD mouse model confirmed the clinical findings showing a significant reduction of the average glomerulosclerosis (GS) index by 40% when treated with varoglutamstat compared to vehicle control, and even a reduction of the most severe GS categories 3 and 4 by over 60%. In addition, inflammatory macrophages (CD11c) in the kidney were reduced and serum creatinine decreased.
Treatment effects of varoglutamstat on eGFR are larger in diabetics than in elderly without diabetes. The effect size in diabetic participants with lower baseline eGFR (mean 60 mL/min/1.73m2) was comparable or higher than in the total population with diabetes. Correspondingly, the DKD mouse model showed significant improvements of inflammation, glomerulosclerosis and kidney function. This translates well to the results obtained earlier in humans showing reduced pE-CCL2 concentration and improved eGFR. These findings make varoglutamstat a promising candidate for further development in diabetic patients with CKD 3 and 4.
