Mechanism of protective actions of sparsentan in the kidney: lessons from studies in models of chronic kidney disease

Clin Sci (Lond). 2024 Jun 5;138(11):645-662. doi: 10.1042/CS20240249.

Abstract

Simultaneous inhibition of angiotensin II AT1 and endothelin ETA receptors has emerged as a promising approach for treatment of chronic progressive kidney disease. This therapeutic approach has been advanced by the introduction of sparsentan, the first dual AT1 and ETA receptor antagonist. Sparsentan is a single molecule with high affinity for both receptors. It is US Food and Drug Administration approved for immunoglobulin A nephropathy (IgAN) and is currently being developed as a treatment for rare kidney diseases, such as focal segmental glomerulosclerosis. Clinical studies have demonstrated the efficacy and safety of sparsentan in these conditions. In parallel with clinical development, studies have been conducted to elucidate the mechanisms of action of sparsentan and its position in the context of published evidence characterizing the nephroprotective effects of dual ETA and AT1 receptor inhibition. This review summarizes this evidence, documenting beneficial anti-inflammatory, antifibrotic, and hemodynamic actions of sparsentan in the kidney and protective actions in glomerular endothelial cells, mesangial cells, the tubulointerstitium, and podocytes, thus providing the rationale for the use of sparsentan as therapy for focal segmental glomerulosclerosis and IgAN and suggesting potential benefits in other renal diseases, such as Alport syndrome.

Keywords: Angiotensin II; Endothelin Type A receptor; Endothelin-1; FSGS; IgA nephropathy; Sparsentan.

Publication types

  • Review

MeSH terms

  • Angiotensin II Type 1 Receptor Blockers / pharmacology
  • Angiotensin II Type 1 Receptor Blockers / therapeutic use
  • Animals
  • Disease Models, Animal
  • Endothelin A Receptor Antagonists / pharmacology
  • Endothelin A Receptor Antagonists / therapeutic use
  • Humans
  • Kidney* / drug effects
  • Kidney* / metabolism
  • Renal Insufficiency, Chronic* / drug therapy
  • Renal Insufficiency, Chronic* / metabolism

Substances

  • Endothelin A Receptor Antagonists
  • Angiotensin II Type 1 Receptor Blockers

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