Esaxerenone |
| Catalog No.GC19143 |
Esaxerenone (CS-3150), a selective nonsteroidal mineralocorticoid receptor antagonist, has been shown to bind to mineralocorticoid receptors, thereby inhibiting aldosterone binding and activation of the receptor.
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Cas No.: 1632006-28-0
Sample solution is provided at 25 µL, 10mM.
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Esaxerenone (CS-3150), a selective nonsteroidal mineralocorticoid receptor antagonist, has been shown to bind to mineralocorticoid receptors, thereby inhibiting aldosterone binding and activation of the receptor [1]. Esaxerenone inhibited 3H-aldosterone binding to mineralocorticoid receptor in a concentration-dependent manner with IC50 of 9.4 nM. Esaxerenone inhibited aldosterone-induced human mineralocorticoid receptor activation in a concentration-dependent manner with IC50 of 3.7 nM. Esaxerenone showed antagonist activity for rat mineralocorticoid receptor with IC50 of 4.9 nM [1].
Esaxerenone (10,100nM) reversed the reduction in insulin-induced Akt phosphorylation caused by aldosterone in insulin target cells, such as adipocytes, hepatocytes, and myocytes. Pretreatment with esaxerenone significantly ameliorated insulin signaling in these cell types [2].
Esaxerenone (3 mg/kg) significantly inhibited DOCA/salt-loading induced elevation in systolic blood pressure compared with the control rats (DOCA-untreated) [1]. Esaxerenone (0.25-2 mg/kg) was orally administered once a day to DS rats fed a high salt diet for 7 weeks. The high salt diet significantly increased systolic blood pressure, which was prevented by treatment with Esaxerenone in a dose-dependent manner with no hyperkalemia (>5.5 mEq/L). Esaxerenone also suppressed proteinuria and renal hypertrophy induced by the high salt diet. Histopathological examination of kidneys showed that CS-3150 markedly ameliorated glomerulosclerosis, tubular injury and tubulointerstitial fibrosis. CS-3150 inhibited left ventricular hypertrophy and elevation of plasma brain natriuretic peptide level [3]. In preclinical models, the pharmacokinetic profile of esaxerenone is the basis for a long-lasting action (plasma half-life rats: 6.5-6.9 h), high oral bioavailability and predominant excretion via faeces [1,4]. A long plasma half-life of esaxerenone has been confirmed in healthy human volunteers (plasma half-life: 30 h) [5].
References:
[1]. Arai K, Homma T, Morikawa Y, et al. Pharmacological profile of CS-3150, a novel, highly potent and selective non-steroidal mineralocorticoid receptor antagonist[J]. European Journal of Pharmacology, 2015, 761: 226-234.
[2]. Bavuu O, Fukuda D, Ganbaatar B, et al. Esaxerenone, a selective mineralocorticoid receptor blocker, improves insulin sensitivity in mice consuming high-fat diet[J]. European Journal of Pharmacology, 2022, 931: 175190.
[3]. Arai K, Tsuruoka H, Homma T. CS-3150, a novel non-steroidal mineralocorticoid receptor antagonist, prevents hypertension and cardiorenal injury in Dahl salt-sensitive hypertensive rats[J]. European journal of pharmacology, 2015, 769: 266-273.
[4]. Wan N, Rahman A, Nishiyama A. Esaxerenone, a novel nonsteroidal mineralocorticoid receptor blocker (MRB) in hypertension and chronic kidney disease[J]. Journal of Human Hypertension. 2021 Feb;35(2):148-56.
[5]. Yamada, M., Mendell, J., Takakusa, H., Shimizu, T., & Ando, O. (2019). Pharmacokinetics, metabolism, and excretion of [14C] esaxerenone, a novel mineralocorticoid receptor blocker in humans[J]. Drug Metabolism and Disposition, 47(3), 340-349. Diseases, 2013, 72(Suppl 3): A129-A129.
Average Rating: 5 (Based on Reviews and 33 reference(s) in Google Scholar.)
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