Chronic kidney disease (CKD) has been recognized as a major public health problem with a prevalence of about 843.6 million cases worldwide, and it is one of the few non-communicable diseases with an increase in associated deaths over the past 2 decades.

Patients with impaired kidney function face a high risk of progressive renal function loss that may either lead to complete loss of kidney function requiring dialysis or transplantation, or to increased risk for cardiovascular complications and premature mortality even before life-saving transplantation. From a clinical point of view, CKD manifests with reduced glomerular filtration rate (GFR) and increased albuminuria. Since GFR is significantly affected by high blood pressure, blood pressure-lowering agents typically represent the therapy of first choice. Mineralocorticoid receptor antagonists (MRAs) have also gained a lot of attention, as numerous studies confirmed their anti-albuminuria effects. However, the use of MRAs is rather limited due to the risk of developing life-threatening hyperkalemia.


Therapeutic lead

OUR STRATEGY: The clinically complicated situation with CKD is partially offset by advances made in functional genomics, proteomics, and biofluid profiling, which have already uncovered several new candidates not only for predicting CKD progression but also as potential targets for therapy. Several Phase 3 clinical trials have though recently failed to provide improved renal outcomes, mostly because of poor drug efficacy, and inherent drug toxicity.

RENAL FIBROSIS is the final manifestation of CKD. Many efforts have been made to identify mediators and pathways participating in renal fibrosis development. Several mediators have been found upregulated in models of CKD and subsequent studies showed that inhibition of any of these mediators delayed the progression of renal disease and preserved renal structure and function, emphasizing their potential to constitute future therapeutic targets for CKD.

ASPER1 is a specific inhibitor of one of the key mediators of renal fibrosis and is currently under early-stage preclinical validation.

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