» Articles » PMID: 39899058

Phase 1 Studies of the Safety, Tolerability, Pharmacokinetics, and Pharmacodynamics of BI 690517 (vicadrostat), a Novel Aldosterone Synthase Inhibitor, in Healthy Male Volunteers

Overview
Date 2025 Feb 3
PMID 39899058
Authors
Affiliations
Soon will be listed here.
Abstract

Purpose: In chronic kidney disease (CKD), raised plasma aldosterone levels are strongly associated with adverse cardiorenal outcomes. Current standard of care may improve outcomes; however, elevated aldosterone levels often persist. We report safety results for BI 690517 (vicadrostat), a potent, selective aldosterone synthase inhibitor under investigation for CKD.

Methods: Four phase 1 studies of BI 690517 conducted in healthy European/Chinese/Japanese men: two single rising dose (SRD) and two multiple rising dose (MRD) studies.

Primary Endpoint: proportion of participants with investigator-defined drug-related adverse events (AEs).

Results: Single and multiple doses of BI 690517 ≤ 80 mg (0.7-80 mg [European SRD]; 3-80 mg [Chinese/Japanese SRD and MRD]) were well tolerated. Proportions of participants with drug-related AEs: European SRD, 8.3% (4/48); Chinese/Japanese SRD, 21.4% (12/56); European MRD, 13.9% (10/72); Japanese MRD, 2.8% (1/36). No serious AEs, deaths, or AEs leading to treatment discontinuation were reported; one AE of severe orthostatic hypotension occurred (European SRD). Plasma exposure to BI 690517 increased dose dependently; median time to maximum concentration was 0.50-1.75 h and mean half-life was 4.4-6.3 h. Exposure was slightly higher in Asians versus Europeans and may relate to lower body weight in Asian participants. A standardized high-fat/high-calorie meal reduced the rate, but not extent, of BI 690517 absorption. Plasma aldosterone concentrations decreased markedly 1-2 h after BI 690517 administration; decreases were more pronounced with increasing BI 690517 doses.

Conclusion: BI 690517 was well tolerated and demonstrated dose-dependent inhibition of aldosterone synthesis. Larger studies are warranted to confirm these findings.

References
1.
Alicic R, Rooney M, Tuttle K . Diabetic Kidney Disease: Challenges, Progress, and Possibilities. Clin J Am Soc Nephrol. 2017; 12(12):2032-2045. PMC: 5718284. DOI: 10.2215/CJN.11491116. View

2.
Andersen K, Hartman D, Peppard T, Hermann D, Van Ess P, Lefkowitz M . The effects of aldosterone synthase inhibition on aldosterone and cortisol in patients with hypertension: a phase II, randomized, double-blind, placebo-controlled, multicenter study. J Clin Hypertens (Greenwich). 2012; 14(9):580-7. PMC: 8108872. DOI: 10.1111/j.1751-7176.2012.00667.x. View

3.
Bakris G, Agarwal R, Anker S, Pitt B, Ruilope L, Rossing P . Effect of Finerenone on Chronic Kidney Disease Outcomes in Type 2 Diabetes. N Engl J Med. 2020; 383(23):2219-2229. DOI: 10.1056/NEJMoa2025845. View

4.
Bogman K, Schwab D, Delporte M, Palermo G, Amrein K, Mohr S . Preclinical and Early Clinical Profile of a Highly Selective and Potent Oral Inhibitor of Aldosterone Synthase (CYP11B2). Hypertension. 2016; 69(1):189-196. PMC: 5142369. DOI: 10.1161/HYPERTENSIONAHA.116.07716. View

5.
Bomback A, Klemmer P . The incidence and implications of aldosterone breakthrough. Nat Clin Pract Nephrol. 2007; 3(9):486-92. DOI: 10.1038/ncpneph0575. View